International Handbook on Psychopathic Disorders and the Law

The International Handbook of Psychopathic Disorders and the Law Volume I Diagnosis and Treatment Edited by Alan Felth...

Author: Alan Felthous | Henning Sass

307 downloads 1380 Views 5MB Size Report

This content was uploaded by our users and we assume good faith they have the permission to share this book. If you own the copyright to this book and it is wrongfully on our website, we offer a simple DMCA procedure to remove your content from our site. Start by pressing the button below!

Report copyright / DMCA form

DOWNLOAD PDF

The International Handbook of Psychopathic Disorders and the Law Volume I Diagnosis and Treatment

Edited by

Alan Felthous Department of Neurology and Psychiatry St Louis University School of Medicine, USA

and Henning Saß Medical Faculty University of Technology Aachen, Germany

The International Handbook of Psychopathic Disorders and the Law Volume I Diagnosis and Treatment

The International Handbook of Psychopathic Disorders and the Law Volume I Diagnosis and Treatment

Edited by

Alan Felthous Department of Neurology and Psychiatry St Louis University School of Medicine, USA

and Henning Saß Medical Faculty University of Technology Aachen, Germany

C 2007 Copyright John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex PO19 8SQ, England

Telephone (+44) 1243 779777 Email (for orders and customer service enquiries): [email protected] Visit our Home Page on www.wiley.com All Rights Reserved. No part of this publication may be reproduced, stored in a retrieval system or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, scanning or otherwise, except under the terms of the Copyright, Designs and Patents Act 1988 or under the terms of a licence issued by the Copyright Licensing Agency Ltd, 90 Tottenham Court Road, London W1T 4LP, UK, without the permission in writing of the Publisher. Requests to the Publisher should be addressed to the Permissions Department, John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex PO19 8SQ, England, or emailed to [email protected], or faxed to (+44) 1243 770620. Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The Publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the Publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought. Other Wiley Editorial Offices John Wiley & Sons Inc., 111 River Street, Hoboken, NJ 07030, USA Jossey-Bass, 989 Market Street, San Francisco, CA 94103-1741, USA Wiley-VCH Verlag GmbH, Boschstr. 12, D-69469 Weinheim, Germany John Wiley & Sons Australia Ltd, 42 McDougall Street, Milton, Queensland 4064, Australia John Wiley & Sons (Asia) Pte Ltd, 2 Clementi Loop #02-01, Jin Xing Distripark, Singapore 129809 John Wiley & Sons Canada Ltd, 6045 Freemont Blvd, Mississauga, ONT, L5R 4J3, Canada Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books. Anniversary Logo Design: Richard J. Pacifico Library of Congress Cataloging-in-Publication Data: The international handbook of psychopathic disorders and the law / edited by Alan Felthous, and Henning Sass. p. ; cm. Includes bibliographical references and indexes. ISBN 978-0-470-01185-0 (set : cloth) – ISBN 978-0-470-06638-6 (vol. 1 : cloth) – ISBN 978-0-470-06640-9 (vol. 2 : cloth) 1. Antisocial personality disorders–Handbooks, manuals, etc. 2. Psychopaths–Legal status, laws, etc.–Handbooks, manuals, etc. I. Felthous, Alan R. II. Sass, Henning. [DNLM: 1. Antisocial Personality Disorder. 2. Mentally Ill Persons–legislation & jurisprudence. 3. Forensic Psychiatry–methods. WM 190 I617 2007] RC555.I58 2007 616.85’82–dc22 2007039322 British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library ISBN 978-0-470-06638-6 (Volume I)

ISBN 978-0-470-01185-0 (Two Volume Set)

Typeset in 10/12pt Times by Aptara, New Delhi, India Printed and bound in Great Britain by Antony Rowe, Chippenham, Wiltshire This book is printed on acid-free paper responsibly manufactured from sustainable forestry in which at least two trees are planted for each one used for paper production.

To my parents Robert A. Felthous Agnetta W. Felthous

To my children Christian Saß Vera Saß

Contents

About the Editors

xi

Contributors

xiii

Preface to Volume I

xvii

Acknowledgments

xix

Introduction to Volume I

1

PART I Conceptual History Chapter 1 History and Conceptual Development of Psychopathic Disorders Henning Saß and Alan R. Felthous

9

PART II Assessment Chapter 2 Psychiatric Assessment Paul Hoff and Sabine C. Herpertz

33

Chapter 3 Psychological Instruments in the Assessment of Psychopathy Robert D. Hare

41

Chapter 4 Functional and Structural Brain Imaging Research on Psychopathy Yaling Yang and Adrian Raine

69

Chapter 5 Psychophysiological Correlates of Psychopathic Disorders Matthew S. Stanford, Rebecca J. Houston and Ernest S. Barratt

83

Chapter 6 Cognitive Correlates Herta Flor

103

Chapter 7 Violence: Psychopathology, Risk Assessment and Lawsuits Kenneth Tardiff

117

Chapter 8 Risks of Diagnosing Psychopathic Disorders Nobert Leygraf and Klaus Elsner

135

PART III Etiology and Pathogenesis Chapter 9 The Genetics of Psychopathic Disorders David Goldman and Francesca Ducci Chapter 10 Neuroimaging Perspectives in Pathogenesis and Therapeutic Strategies J¨urgen L. M¨uller

149

171

viii

CONTENTS

Chapter 11 Electrophysiology Sabine C. Herpertz Chapter 12 The Role of ADHD in the Etiology and Outcome of Antisocial Behavior and Psychopathy Beate Herpertz-Dahlmann, Kerstin Konrad and Sabine C. Herpertz Chapter 13 Brain Trauma Hannelore Ehrenreich, Henning Krampe and Anna-Leena Sir´en

187

199 217

Chapter 14 Acquired Psychopathy and the Assessment of Traumatic Brain Injury Robert P. Granacher and Manish A. Fozdar

237

Chapter 15 Comorbidities of Psychopathy and Antisocial Personality Disorder: Prevalence and Implications Elena Carmen Nichita and Peter F. Buckley

251

Chapter 16 The Paraphilias and Psychopathy John M.W. Bradford, Philip Firestone and A.G. Ahmed Chapter 17 Family Upbringing: Family Factors as Predictors for the Development of Antisocial Behavior and Psychopathy Dimensions Maya K. Krischer, Kathrin Sevecke and Gerd Lehmkuhl

275

291

Chapter 18 Discipline by Parents and Child Psychopathology Emily M. Douglas and Murray A. Straus

303

Chapter 19 Social Origins of Psychopathy David P. Farrington

319

Chapter 20 A Psychoanalytic View of the Psychopath J. Reid Meloy and Andrew Shiva

335

Chapter 21 Women and Girls with Psychopathic Characteristics Tonia L. Nicholls, Candice L. Odgers and David J. Cooke

347

Chapter 22 Educational Issues Franz Petermann and Ute Koglin

367

PART IV Intervention, Treatment and Management Chapter 23 Intervention, Treatment and Management of ADHD Beate Herpertz-Dahlmann, Kerstin Konrad and Sabine C. Herpertz

381

Chapter 24 Pharmacotherapy of Clinical Aggression in Individuals with Psychopathic Disorders F. Gerard Moeller and Alan C. Swann

397

Chapter 25 Treatment and Management of Conduct Disorders in Children and Adolescents Manfred Doepfner, Kerstin Adrian and Charlotte Hanisch

417

Chapter 26 Psychotherapy of Psychopathic Disorders Gill McGauley, Gwen Adshead and Sameer P. Sarkar

449

CONTENTS

Chapter 27 Comprehensive Outpatient Treatment and Management Andreas Hill, Peer Briken and Wolfgang Berner Chapter 28 Antisocial Disorders and Domestic Violence: Treatment Considerations L. Kevin Hamberger and Jennifer Langhinrichsen-Rohling

ix

467

497

Chapter 29 Workplace Violence Goes Beyond Psychopathology Michael H. Corcoran

519

Chapter 30 Addressing the Associated Conditions of Drug and Alcohol Abuse Falk Kiefer and Karl Mann

531

Chapter 31 Experiential and Community Treatment of Adult Antisocial Syndromes Stephen A. Thorne and William H. Reid

543

Chapter 32 Legal, Medical and Social Impediments to better Psychopaths: How Best to Deal with Persons with Psychopathic Disorders? J¨urgen. L. M¨uller

557

Chapter 33 Social Policy Considerations on Psychopathic Disorders Harald Dreßing, Hans Joachim Salize and Peter Gass

573

Index

587

About the Editors

Alan R. Felthous, M.D., is Professor and Director of Forensic Psychiatry in the Department of Neurology and Psychiatry, Saint Louis University School of Medicine. He received his Bachelor of Sciences degree at the University of Washington and his medical doctorate at the University of Louisville School of Medicine before interning at Roosevelt Hospital in New York City and completing a residency in psychiatry at McLean Hospital and Harvard Medical School. After two years as a staff psychiatrist at the Naval Regional Medical Center in Oakland, Dr. Felthous joined the staff at the Menninger Foundation in Topeka, Kansas. For nearly 15 years, he was Chief of the Forensic Services, the Department of Psychiatry and Behavioral Sciences at the University of Texas Medical Branch in Galveston, where he was the Marie B. Gale Centennial Professor of Psychiatry. Before coming to Saint Louis University, Dr. Felthous was Director of Forensic Psychiatry at Southern Illinois University School of Medicine and Medical Director of Chester Mental Health Center, the maximum security forensic hospital for the state of Illinois. Dr. Felthous is President of the American Academy of Psychiatry and the Law, Senior Editor of Behavioral Sciences and the Law and Past President of the American Board of Forensic Psychiatry. His research, scholarly and teaching interests focus on clinical aggression, the psychopathology of criminal behavior, legal requirements of clinicians in managing potentially violent patients, and jail and prison suicide. Henning Saß, M.D., is currently Medical Director and Chairman of the Board of Directors at the University Hospital of the University of Technology (RWTH) in Aachen/Aix-laChapelle, Germany. He studied medicine at the universities of Kiel, Vienna and Mainz. After passing the state examination in Kiel and receiving his medical doctorate in Mainz, he was a resident in the Department of Psychiatry at the University of Heidelberg. Having completed his training in clinical psychiatry and in psychotherapy, he concentrated on forensic psychiatry, general psychopathology, diagnostic research and personality disorders. His habilitation on Psychopathie, Soziopathie, und Dissozialitat (Psychopathy, Sociopathy and Dissocial Behaviors) was published as a Springer monograph in 1987. He was then appointed Professor of Forensic Psychiatry at the Ludwig-Maximilians-University in Munich, after which he was the Chair of Psychiatry and Psychotherapy at the medical faculty in Aachen for 10 years, before he was appointed to his current position. His research interests remain focused on forensic psychiatry, especially in the field of personality disorders. During his academic career, he was President of the German Society for Psychiatry, Psychotherapy and Nervous Diseases (DGPPN) and of the Association of European Psychiatrists (AEP). He is editor or co-editor of several scientific journals and member of numerous boards of scientific organizations including the European Brain Council and the Research Council of the German Ministry for Science, Research and Technology.

Contributors

Kerstin Adrian, University of Cologne, Department of Child and Adolescent Psychiatry, Robert-Koch-Str. 10, D-50931 K¨oln, Germany Gwen Adshead, Broadmoor Hospital, Crowthorne, Berkshire, RG45 7EG, UK A.G. Ahmed, Royal Ottawa Hospital, 1145 Carling Avenue, Ottawa, ON K1Z 7K4, Canada Ernest S. Barratt, The University of Texas Medical Branch, Department of Psychiatry and Behavioral Sciences, 301 University Blud., Galueston, TX 77555, USA Wolfgang Berner, University Hospital Hamburg-Eppendorf, Department of Sexual Research and Forensic Psychiatry, Martinistr. 52, D-20246 Hamburg, Germany John M.W. Bradford, Royal Ottawa Hospital, 1145 Carling Avenue, Ottawa, ON K1Z 7K4, Canada Peer Briken, University Hospital Hamburg-Eppendorf, Department of Sexual Research and Forensic Psychiatry, Martinistr. 52, D-20246 Hamburg, Germany Peter F. Buckley, Medical College of Georgia, 1515 Pope Avenue, Augusta, GA 30912, USA David J. Cooke, Douglas Inch Centre & Glasgow Caledonian University, 2 Woodside Terrace, Glasgow, G3 7UY, UK Michael H. Corcoran, Henley-Putnam University, 25 Metro Dr., San Jose, CA 95110, USA Manfred Doepfner, University of Cologne, Department of Child and Adolescent Psychiatry, Robert-Koch-Str. 10, D-50931 K¨oln, Germany Harald Dreßing, University of Heidelberg, Department of Forensic Psychiatry, Central Institute for Mental Health-Mannheim, J5, D-68159 Mannheim, Germany Emily M. Douglas, University of New Hampshire, Department of Family Studies, Pettee Hall, 55 College Road, Durham, NH 03824, USA Francesca Ducci, National Institutes of Health, NIAAA, Laboratory of Neurogenetics, 5625 Fishers Lane, Room 3S32, MSC 9412, Rockville, MD 20852, USA Hannelore Ehrenreich, Max-Planck Institute for Experimental Medicine, Hermann-ReinStr. 3, D-37075-G¨ottingen, Germany

xiv

CONTRIBUTORS

Klaus Elsner, University of Essen, Department of Forensic Psychiatry, Postfach 10 30 43, D-45030 Essen, Germany David P. Farrington, Institute of Criminology, Sidgwick Avenue, Cambridge CB3 9DT, UK Alan R. Felthous, Saint Louis University School of Medicine, Department of Neurology and Psychiatry, 1438 South Grand Blud., Saint Louis, MO 63104, USA Philip Firestone, Royal Ottawa Hospital, 1145 Carling Avenue, Ottawa, ON K1Z 7K4, Canada Herta Flor, University of Heidelberg, Department of Neuropsychology, Central Institute for Mental Health-Mannheim, D-68159 Mannheim, Germany Manish A. Fozdar, Triangle Forensic Neuropsychiatry, 1109 Chilmark Avenue, Wake Forest, NC 27587, USA Peter Gass, University of Heidelberg, Department of Forensic Psychiatry, Central Institute for Mental Health-Mannheim, J5, D-68159 Mannheim, Germany David Goldman, National Institutes of Health, NIAAA, Laboratory of Neurogenetics, 5625 Fishers Lane, Room 3S32, MSC 9412, Rockville, MD 20852, USA Robert P. Granacher, Jr., Lexington Forensic Institute, 1401 Harrodsburg Road, Suite A400, Lexington, KY 40502, USA L. Kevin Hamberger, Medical College of Wisconsin, Department of Family and Community Medicine, Racine Family Practice Center, 1320 Wisconsin Avenue, P.O. Box 548, Racine, WI 53401-0548, USA Charlotte Hanisch, University of Cologne, Department of Child and Adolescent Psychiatry, Robert-Koch-Str. 10, D-50931 K¨oln, Germany Robert D. Hare, 26 St. Martin’s Lane, 15020 27A Avenue, South Surrey, British Columbia, V4P 2Z9, Canada Beate Herpertz-Dahlmann, University Hospital Aachen, Department of Child and Youth Psychiatry and Psychotherapy, Pauwelsstraße 30, D-52074 Aachen, Germany Sabine C. Herpertz, University of Rostock, Department of Psychiatry and Psychotherapy, Gehlsheimer Strasse 20, D-18147 Rostock, Germany Andreas Hill, Klinikum Nord Hamburg, Department of Psychiatry and Psychotherapy – Forensic Psychiatry, Langenhorner Chaussee 560, D-22419 Hamburg, Germany Paul Hoff, University of Zurich, Department of General and Social Psychiatry, Lenggstrasse 31, P.O. Box 1931, CH-8032 Zurich, Switzerland Rebecca J. Houston, State University of New York at Buffalo, Research Institute on Addictions, 1021 Main Street, Buffalo, NY 14203, USA Falk Kiefer, University of Heidelberg, Department of Addictive Behavior and Addiction Medicine, Central Institute for Mental Health-Mannheim, J5, D-68159 Mannheim, Germany

CONTRIBUTORS

xv

Ute Koglin, University of Bremen, Center for Clinical Psychology and Rehabilitation, Grazer Straße 2 und 6, D-28359 Bremen, Germany Kerstin Konrad, University Hospital Aachen, Department of Child and Youth Psychiatry and Psychotherapy, Pauwelsstraße 30, D-52074 Aachen, Germany Henning Krampe, Max-Planck Institute for Experimental Medicine, Hermann-Rein-Str. 3, D-37075-G¨ottingen, Germany Maya K. Krischer, University Clinic of Cologne, Department of Child and Adolescent Psychiatry, Robert-Koch-Strasse 10, D-50935 K¨oln, Germany Jennifer Langhinrichsen-Rohling, University of South Alabama, Department of Psychology, Mobile, AL 36688-0002, USA Gerd Lehmkuhl, University Clinic of Cologne, Department of Child and Adolescent Psychiatry, Robert-Koch-Strasse 10, D-50935 K¨oln, Germany Norbert Leygraf, University of Essen, Department of Forensic Psychiatry, Postfach 10 30 43, D-45030 Essen, Germany Karl Mann, University of Heidelberg, Department of Addictive Behavior and Addiction Medicine, Central Institute for Mental Health-Mannheim, J5, D-68159 Mannheim, Germany Gill McGauley, Broadmoor Hospital, Crowthorne, Berkshire, RG45 7EG, UK F. Gerard Moeller, University of Texas Health Science Center at Houston, Department of Psychiatry and Behavioral Science, 1300 Moursund, Houston, TX 77030, USA Jurgen ¨ L. Muller, ¨ Georg August University of G¨ottingen, Department of Psychiatry and Psychotherapy, Von Siebold Str. 5, D-37075 G¨ottingen, Germany Elena Carmen Nichita, University of South Carolina, Department of Neuropsychiatry and Behavioral Science, School of Medicine, William S. Hall Psychiatric Institute, 2100 Bull Street, P.O. Box 119, Columbia, SC 29202, USA Tonia L. Nicholls, British Columbia Mental Health and Addiction Services, Forensic Psychiatric Hospital, 70 Colony Farm Road, Port Coguitlam, British Columbia, V3C5X9 CANADA Candice L. Odgers, University of California, Irvine, Psychology and Social Behavior, 3340 Social Ecology Building 11, Irvine, CA 92697, USA Franz Petermann, University of Bremen, Center for Clinical Psychology and Rehabilitation, Grazer Straße 2 und 6, D-28359 Bremen, Germany Adrian Raine, University of Southern California, Department of Psychology, Los Angeles, CA 90089-1061, USA William H. Reid, University of Texas Health Science Center at San Antonio, Clinical and Forensic Psychiatry, P.O. Box 4015, Horseshoe Bay, TX 78657, USA J. Reid Meloy, University of California, P.O. Box 90699, San Diego, CA 92169, USA

xvi

CONTRIBUTORS

Hans Joachim Salize, University of Heidelberg, Department of Forensic Psychiatry, Central Institute for Mental Health-Mannheim, J5, D-68159 Mannheim, Germany Sameer P. Sarkar, Broadmoor Hospital, Crowthorne, Berkshire, RG45 7EG, UK Henning Saß, University of Technology Aachen, University Hospital Aachen, Medical Faculty Pauwelsstraße 30, D-52074 Aachen, Germany. Kathrin Sevecke, University Clinic of Cologne, Department of Child and Adolescent Psychiatry, Robert-Koch-Strasse 10, D-50935 K¨oln, Germany Andrew Shiva, 40 Riverside Drive, New York, NY 10023, USA Anna-Leena Sir´en, University of W¨urzburg, Department of Neuro sergery, JosephSchneider Str. 11, 97080 W¨urzburg, Germany Matthew S. Stanford, Baylor University, Department of Psychology and Neuroscience, One Bear Place #97334, Waco, TX 76798-7334, USA Murray A. Straus, University of New Hampshire, Family Research Laboratory, 126 Horton Social Science Center, Durham, NH 03842-3586, USA Alan C. Swann, University of Texas Health Science Center at Houston, Department of Psychiatry and Behavioral Science, 1300 Moursund, Houston, TX 77030, USA Kenneth Tardiff, Weill Cornell Medical College, Department of Psychiatry, Box 140, 525 East 68th Street, New York, NY 10021, USA Stephen A. Thorne, 4810 B Spicewood Springs Road, Austin, TX 78759, USA Yaling Yang, University of Southern California, Department of Psychology, SGM610, Los Angeles, CA 90089-1061, USA

Preface to Volume I

The need for a comprehensive, international textbook on psychopathic disorders and the law was recognized when the co-editors prepared a special issue of Behavioral Sciences and the Law on ‘International Perspectives on Psychopathic Disorders’ published in 2000. Contributors to this issue addressed phenomenological, molecular, psychosocial, therapeutic and legal aspects of psychopathic disorders. From our work on this special issue, we came to realize three facts. First, the scientific advancements in understanding psychopathic disorders have been substantial in recent decades. Secondly, every society is burdened with the necessity of dealing with psychopathically disordered individuals. And, thirdly, the considerable literature on psychopathic disorders is extraordinarily compartmentalized, limiting its usefulness to practitioners and policymakers alike. The compartmentalization of knowledge on psychopathic disorders exists on several levels. Scientific disciplines tend to focus their methodologies on a single aspect or a few closely associated aspects of psychopathy. Consequently, attempts at broader, integrated views are relatively lacking. Literatures on phenomenology, pathogenesis and treatment are separate. Even more pronounced is the tremendous chasm that exists between printed knowledge of a clinical and scientific nature and that having to do with public policies and legal regulations. Yet psychopathic disorders impose a cost and stress on society, which responds with its frustrated attempts at correcting or at least ‘containing’ the problems secondary to psychopathic disorders. Finally, individual countries have a wealth of experience in studying, attempting to treat and manage and to limit harm and risks associated with psychopathy through legal regulations, but each country is left to its own with minimal international exchange, especially in public policy approaches. The time is ripe for a more comprehensive, encyclopedic treatment of psychopathic disorders, not limited by disciplinary or geopolitical boundaries. We initially planned the outline for this International Handbook during a meeting of the German Psychiatric Society (the Deutsche Gesellschaft f¨ur Psychiatrie, Psychotherapy und Nervenheilkunde) in Berlin. From our intense discussions, we agreed that the main purpose was to collect important bodies of knowledge and conceptual traditions within the Anglo-American and European realms. The rather independent developments in these two realms needed to be brought together. Another goal was to assemble the different scientific approaches to the problem of psychopathy including the psychological, sociological, medical and psychiatric approaches. Even if we could not achieve an integration of these approaches into a single unified theory or empirical design, we have at least endeavored to collect the most important and influential perspectives. This work may serve as a basis for future attempts at developing an integrated view. A third objective was to give expression to the challenging debate involving legal and mental health experts on the significance of neurobiological findings in addressing questions of criminal responsibility. This debate is

xviii

PREFACE TO VOLUME I

still unsettled and should continue and include considerations of biologically determined dispositions, deficiencies in psychological functions such as empathy, current conceptions of ‘free will’, neuroplasticity and the possibility of repairing deficits with origins in early modes of learning and developing bonding behavior and moral attitudes. We bring to this project our own overlapping, yet distinct experiences, interests and concepts. Over two decades, Henning Saß, M.D., has refined conceptualizations of psychopathic disorders, beginning with his monograph, Psychopathy, Sociopathy and Dissocial Conditions: Towards the Differential Typology of Personality Disorders (1987). Through original research and examination of the literature, he clarified important conceptual distinctions between these three concepts as well as the DSM concept of antisocial personality disorders, then following the DSM-III (1980). Dr. Saß’ continued study of psychopathic disorders emphasizes the importance of looking beyond mere behaviors and establishing presence of psychological dysfunctional symptoms such as the emotional deficiency of the psychopath (Herpertz & Saß, 2000). Alan R. Felthous, M.D., studied individual antisocial behavior, namely animal cruelty, which tends to be cavalierly de- or overvalued as a sign of antisocial personality disorder or psychopathy, but detailed inquiry should involve an assessment of the severity, motivation and mental state which in turn enhances or diminishes its pathological significance (Felthous & Kellert, 1987; Gleyzer, Felthous & Holzer, 2002). As a collaborative investigator, he participated with the late Dr. Ernest Barratt’s team in studying the nature and treatment of impulsive aggression. We have as well made our respective contributions to thought concerning the application of clinical skills to public policy. Dr. Saß (1985, 1991a,b), for example, has refined and explicated the ‘pathological reference system’, a concept and method for assessing psychopathology as it relates to criminal responsibility. Dr. Felthous (e.g., 1989, 2006) has written extensively on the clinician’s legal duty to warn or protect of patients who present a foreseeable danger to others. Collaboratively we wrote about forensic evaluations (Felthous, Kr¨ober & Saß, 2001) and treatment programs for offenders (Felthous & Saß, 2006). We both share an extensive experience in evaluating and treating mentally disordered individuals and in consulting to attorneys and courts. Importantly, we share a desire for improvements in treatment and sound public policies that take into account the deficiencies and needs of psychopathically disordered individuals as well as the security of society. We would be pleased if this two-volume work contributes toward bringing about such improvements. The present Volume I comprehensively addresses diagnosis and treatment of psychopathic disorders. Sections on the scientific and clinical aspects of psychopathic disorders include Conceptual History; Assessment; Etiology and Pathogenesis; and Intervention, Treatment and Management. Distinguished contributors for this volume represent five countries: Canada, Germany, India, the United Kingdom and the United States. Not every chapter is neatly, exclusively limited to its corresponding subheading topic and some chapters bridge over into public policies, the subject of Volume II. In order to encourage a variety of perspectives and rich discussion, authors were not restricted in terms and concepts referring to psychopathic disorders. In reading these chapters, one will recognize the therapeutic pessimism so commonly observed, but also much reason for hope that specific problems when accurately assessed can respond to specific interventions. Although this volume is available for purchase without its companion, we encourage those interested to obtain both volumes. The strength of this publication, as a text and a

PREFACE TO VOLUME I

xix

reference, we believe, is its comprehensive approach to psychopathic disorders, an approach that relates laws and public policies to diagnosis and treatment. Alan R. Felthous, M.D. Henning Saß, M.D.

REFERENCES American Psychiatric Association (1980). Diagnostic and Statistical Manual of Mental Disorders, 3rd edition (DSM-III). Washington, DC: American Psychiatric Association. Felthous, A.R. (1989). The Psychotherapist’s Duty to Warn or Protect. Springfield, IL: Charles C. Thomas. Felthous, A.R. (2006). Warning a potential victim of a person’s dangerousness: clinician’s duty or victim’s right? Journal of the American Academy of Psychiatry and the Law, 34, 338–48. Felthous, A.R. & Kellert, S.R. (1987). Childhood cruelty to animals and later aggression against people: a review. American Journal of Psychiatry, 144(6), 710–17. Felthous, A.R., Kr¨ober, S. & Saß, H.L. (2000). Forensic evaluations for civil and criminal competencies and criminal responsibility in German and Anglo-American legal systems. In F. Henn, N. Sartorius, H. Helmchen & H. Lauter (eds.), Psychiatry for Today (pp. 287–302). Heidelberg: Springer-Verlag. Felthous, A.R. & Saß, H. (2006). Behandlungs-programme f¨ur Straft¨ater in den Vereinigten Staaten und Kanada [Treatment programs for criminal offenders in the United States and Canada]. In H-L. Kr¨ober, D. D¨olling, N. Leygraf and H. Saß (eds.), Handbuch der forensischen Psychiatrie, Band 3: Psychiatrische Kriminal prognose und Kriminal therapie [Handbook of Forensic Psychiatry, Volume 3: Psychiatric Prognosis and Therapy of Criminals], 390–412. Gleyzer, R. Felthous, A.R. & Holzer, C.E. (2002). Psychiatric disorders and animal cruelty. Journal of the American Academy of Psychiatry and the Law, 30(2), 257–65. Herpertz, S.C. & Saß, H. (2000). Emotional deficiency and psychopathy. Behavioral Sciences and the Law, 18(5), 567–80. Saß, H. (1987). Psychopathie, Soziopathie, Dissozialit¨at [Psychopathy, Sociopathy and Dissocial Conditions]. Berlin: Springer-Verlag. Saß, H. (1991a). Ein psychopathologisches Referenzsystem zur Beurteilung der Schuldf¨aligkeit [A psychopathological reference system for the assessment of criminal responsibility]. Forensia, 6, 33–43. Saß, H. (1991b). Forensische Erheblichkeit seelischer St¨orungen in psychopathologischen Referenzsystem [The forensic relevance of mental disorders in the psychopathological reference system] (pp. 266–81). In H. Sch¨utz, H. Kaatsch & H. Thomsen (eds.), Festschrigt Schewe. Berlin: Springer.

Acknowledgments

Alan J. Tomkins, J.D., Ph.D., who was editor of Behavioral Sciences and the Law when our special issue on psychopathic disorders was published, gave us the idea and encouragement to edit this greatly expanded work in the form of an international handbook. Many others offered useful thoughts and suggestions. We thank in particular Charles Patrick Ewing, J.D., Ph.D., current editor of Behavioral Sciences and the Law, Michael L. Perlin, J.D., John Petrila, J.D., LL.M., Mark Heyrman, J.D. and Roy Lacoursiere, M.D. Sincerest thanks go to Felecia Rucker, Dr. Felthous’ extraordinarily proficient assistant, who was a key organizing force from the work’s inception to its publication. She essentially organized the project, corresponded with authors, tracked their progress, made corrections and sent the final products to John Wiley. Her support and energy for the project continued seamlessly even after Dr. Felthous relocated from Chester Mental Health Center and Southern Illinois University to Saint Louis University in Missouri. It is hard to imagine a more dedicated, capable assistant: it is hard to imagine successful completion of this work without Ms. Rucker’s invaluable participation. At the University of Technology (RWTH) in Aachen, it was Alex Morton, Stefan Galow and Annika Martens, who gave valuable technical support to Henning Saß. We express our heartfelt appreciation to our spouses, Mary Felthous and Isabella Saß, Ph.D., for their unwavering support and for allowing us the time to pursue this project. Finally, we thank our many outstanding authors for their excellent contributions. We thank them as well for their patience, their responsiveness, and their understanding whenever our communication with them was imperfect.

Introduction to Volume 1 Henning Saß University of Technology Aachen, Germany

and Alan R. Felthous Saint Louis University School of Medicine, USA

The amount of harm and suffering caused by individuals with psychopathic disorders must be incalculable. Beyond the obvious grief, fear and rage their acts engender in others, those afflicted pay a high price themselves for this disorder in terms of limited vocational success, empty or missing relationships, restricted freedom when subjected to criminal sentencing and a life devoid of meaning. The economic cost to a society must take into account, among others, the costs to the criminal justice system and correctional systems exacted by the acts of those with psychopathic disorders. A substantial proportion of imprisoned offenders have psychopathic disorders and antisocial personality disorders (DSM-IV-TR, American Psychiatric Association, 2000) in particular. Those with psychopathy a` la Hare, comprise a much smaller percentage of offenders, but are extraordinarily disposed to recidivism. Sociologist Marvin Wolfgang (Wolfgang, Figlio & Sellin, 1972) observed that a very small percentage of offenders are responsible for an exceptionally large share of serious crimes. If society could arrive at an effective approach for dealing with this hard core of extremely antisocial individuals, this alone would take a big bite out of crime. As of yet, satisfying solutions to the problems secondary to the disorders themselves, though pressing, remain disturbingly elusive. If psychopathic disorders are to be understood, if effective treatment and management approaches are to be discovered, if sound laws and public policies are to be formulated and implemented; we believe the solution will come from interdisciplinary and international collaboration. It is with the interest in moving this collaborative process forward that this International Handbook was conceived and developed. Our knowledge of psychopathic disorders will have little meaning and practical value unless it can be applied through effective legislation. Conversely, public policies will continue to fall short of their goals unless they are informed by the best, most current scientific knowledge and understanding of psychopathic disorders. Therefore, in this work, we have attempted to comprehensively address clinical and scientific aspects of psychopathic disorders on the one hand and legal

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

2

VOLUME I: DIAGNOSIS AND TREATMENT

and public policy issues on the other. Because this comprehensive approach to psychopathic disorders results in a much more extensive treatment of the topic than either realm alone, it is divided into two volumes. The reader can conveniently make good use of one volume and not the other as reading and referencing needs demand. This division of the work into two separate volumes is not thematically pure and absolute; some chapters in the first volume touch on public policy issues, and some in the second volume mention clinical issues. For the best contemporary understanding and most comprehensive reference of psychopathic disorders, the editors recommend the two volumes as a companion set. The reader will immediately recognize that we have not selected a single disorder to focus exclusively upon. Neither have we expanded this work to explicitly include all antisocial or criminal behaviors regardless whether a disorder exists. We have selected the term ‘psychopathic disorders’ to include both taxonomical and dimensional approaches, and to include diagnostic conditions characterized by antisocial behaviors. Authors were free to address primarily antisocial personality disorder (APD) or psychopathy or other related ‘antisocial’ disturbances, although most confined their discussion to the APD–psychopathy spectrum. What precisely is meant by psychopathic disorders, and by the major disorders themselves, is defined in the first part. We trace the history and development of the central diagnostic concepts. In so doing, specific defects and manifestations of psychopathy and related conditions are identified. Although this discussion is complete and describes the conditions to be discussed in the two volumes, we have allowed and even encouraged contributors to define the condition(s) that they address. By so doing, the authors clarify what they mean by diagnostic terms that, despite uniform nomenclature, can be understood somewhat differently by author or reader. Part II, Assessment, concerns the clinical evaluation of psychopathic disorders. This section will be particularly useful for clinicians who conduct diagnostic assessments. Professionals who deal with psychopathically disturbed individuals will also benefit from knowing how such disorders are evaluated and diagnosed. Moreover, an appreciation as to how these disorders are recognized should result in an improved understanding of their nature. A basic psychiatric or psychological assessment is most frequently required and often sufficient. In practice, other specialized or more focused assessments such as for clinical violence or for assessment of risk in general, are abbreviated or expanded, depending upon circumstances of individual cases. Because of the expense and need for further research, brain imaging is not considered standard practice, though in the future with cost reduction and the identification of specific, compelling indications, imaging techniques could eventually become diagnostically useful. Part III addresses research into the nature of psychopathic disorders, findings and conclusions of which should guide clinical practices and development of public policy. Like other mental disorders, the cause and progression of psychopathic disorders are complex and multidimensional. Investigations of stars and subatomic particles require different principles and technologies, but knowledge of both is needed to understand the universe. Likewise, the study of ‘experience’, ‘mind’ and ‘body’, though casually inseparable, require different disciplines with their different theories, technologies and languages. The best understanding of the origin of psychopathic disorders will eventually result from not only in-depth knowledge in relevant fields but also from a meaningful integration of the disparate contributions within a unified field theory that thus far does not exist. A human being with his or her predispositions, including the predisposition to develop a psychopathic disorder, begins with the genome. The relationships between genes and

INTRODUCTION TO VOLUME 1

3

psychology, behavior and mental disorder are established through study of familial inheritance patterns and techniques of molecular genetics. Genes give rise to molecules, which determine the structures and functions of the brain. Neuroimaging, its contributions and limitations, is identifying structural and functional deviations that pertain to psychopathic disorders. Neurophysiology in turn results in the electrical activity of the brain, but electrophysiological anomalies of psychopathy are evident in the body as well. A form of subtle but significant neurophysiological defect is manifested in attention deficit hyperactivity disorder (ADHD), the course of which can affect the development of a psychopathic disorder beyond symptoms limited to ADHD alone. ‘Pathological synergy’ or interaction between psychopathic and other comorbid disorders, certainly complicate and sometimes frustrate treatment efforts, but may also contribute to the understanding of the pathogenesis of psychopathic disorders as well. Recent studies that examined both genetic factors and environmental or experiential factors have helped to elucidate how they might interact to exacerbate or protect against the possible development of psychopathic disorders. Spheres of study on the experiential contributions include patterns of family upbringing, parental discipline and sociological factors in general. The psychoanalytic view examines the psychology, not just the behavior, of relationships as they relate to the individual. Although women are much less likely to have a psychopathic disorder, some do. The gender discrepancy and gender nonspecificity could suggest a role for gender in etiology. Here findings of psychopathy in women are summarized. Poor educational performance correlates with later development of psychopathic disorders. Academic underachievement is regarded as an early manifestation of a conduct or future psychopathic disorder; however, if specific clinical (e.g., ADHD), or educational needs are identified and addressed, such measures may provide hope for mitigation or prevention. Most important and challenging is the development of an integrated approach to understanding psychopathic disorders. An integrated approach to understanding the etiology of psychopathy will logically allow for integrated approaches to interventions, treatment and management. A common assumption is that those with psychopathic disorders are untreatable. Moreover, there is little expressed hope for developing effective treatment in the future. Today’s view is that the mentally ill should be treated within the mental health system and the psychopathically disordered should be dealt with within the criminal justice system. Without a better approach for the psychopathically disordered this seems to be a reasonable position. However, it is a gross oversimplification. An important purpose of the criminal justice system is reform or rehabilitation to improve the offender’s likelihood of succeeding in the community without reoffending. Rehabilitation requires various remedial measures including sometimes treatment. Though not typically considered in the abstract, professionals who provide clinical services ‘on the front line’ in both mental health and correctional settings are distressingly aware that the ‘mad or sad’ and ‘bad’ dichotomy has many exceptions. Many, though not most, who are mentally ill also have a psychopathic disorder and many with psychopathic disorders have one or more comorbid disorders. In fact, it is the comorbidity that can render their condition so difficult to treat or rehabilitate effectively, but the attempt must be made. A most common comorbidity of psychopathic disorders is substance abuse. Like psychopathic disorders, substance abuse is very common and probably a causal factor in the criminal behavior of criminal offenders in general. Nearly half of all state prisoners in the United States, for example, have a history of substance abuse, committed robbery or

4

VOLUME I: DIAGNOSIS AND TREATMENT

property offenses to support their habit/addictions or were under the influence of a chemical substance at the time of their offense (Califano, 1998). Therefore, addressing the psychopathic’s substance disorder should reduce the likelihood of recidivism. In impulse disorders in general, an important etiological question is whether an impulse is incapable of being resisted or simply not resisted. Thus, for purposes of treatment and rehabilitation, the co-occurrence of a sexual paraphilia and a psychopathic disorder can render the paraphilia especially difficult to treat, but treat to rehabilitate one must try. Perhaps more effective, in part because it can be started early, is the treatment of ADHD in childhood, which has the potential of lessening the severity of a pre-morbid psychopathic disorder. Psychopathically disturbed individuals not infrequently physically, sexually and/or emotionally abuse other members of the family, necessitating intervention. Although most approaches addressed in the volume are clinical, protection of society and maintenance of the social order are important considerations for individuals whose disorder predisposes them to violate other people’s rights and the law in general. The interests of society and purposes of the criminal justice system must be considered as well as the interests of the individual psychopathic offender. Whether the law allows and supports hospitalization and treatment of individuals who suffer only from psychopathic disorders, such individuals will end up in mental health settings, if only because they have a co-occurring and treatment qualifying disorder. Then the issue becomes how to maximize the likelihood of success and ensure that safety is preserved in the process. Today no psychopharmacologic agent has been developed to restore the psychopathic’s core defect in emotional experience. Pharmacotherapy can be an option, however, for bringing aggressive behavior under control, at least behavior that is impulsive or secondary in part to a co-occurring mental disorder for which efficacious medication exists. Some clinicians provide psychotherapy for individuals with personality and psychopathic disorders: Sarkar and colleagues describe their method and specific considerations for psychopathically disturbed individuals. Between outpatient psychotherapy and imprisonment, residential and activity programs have been developed that provide some support, structure and rehabilitation for individuals in the community who have shown significant antisocial behavior. Surprisingly, Thorne and Reid conclude that the worse the behavior, the better the prognosis; but this paradox may be the result of indexing behavior and not the diagnosis of psychopathy. Persons with psychopathic disorders can be the offenders in workplace violence, a social problem that demands an adequate response, and more effective preventive measures. Treatment programs for psychopathy itself are virtually nonexistent in prisons, hospitals or the community. Mental health systems are designed to treat mental illness, not psychopathic disorders. Correctional systems are designed to be secure and to maintain order, not to promote psychological growth. Mental hospitals on the other hand are patient-centered, and create opportunities for psychopathically disturbed individuals to exploit and disrupt, without consequence or safe containment. Recognizing the limitations of both mental health and correctional programs, M¨uller argues for the development of programs that are specially designed to treat and rehabilitate individuals with psychopathic disorders. Such programs must have a built-in research component to determine which measures are effective and which are ineffective or even counter-effective.

INTRODUCTION TO VOLUME 1

5

This first volume on Diagnosis and Treatment ends with a thoughtful analysis of social policy considerations. What is known, and indeed what is unknown, about the diagnosis and treatment of psychopathic disorders is meaningful if given practical application for the betterment of the afflicted and for society. More than a fitting ending to this volume, the concluding chapter also serves as a transition to the second volume, intended to directly address critical issues in law and social policy concerning psychopathic disorders.

REFERENCES American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders, 4th edition – Text Revision (DSM-IV-TR). Washington, DC: American Psychiatric Association. Califano, J.A., Jr. (1998). Forward and accompanying statement. In Behind Bars: Substance Abuse and America’s Prison Population (pp. iii–ix). New York: National Center on Addiction and Substance Abuse at Columbia University. Wolfgang, M.E., Figlio, R.M. & Sellin, T. (1972). Delinquency in a Birth Cohort. Chicago: University of Chicago Press.

PART I

Conceptual History

CHAPTER 1

History and Conceptual Development of Psychopathic Disorders Henning Saß Medical Faculty, University of Technology Aachen, Germany

and Alan R. Felthous Saint Louis University School of Medicine, USA

The fascination and risks inherent in psychiatric thinking lie in the complex nature of psychiatric disorders, which is characterized by an intricate interplay of somatic functions, learning processes, acquired attitudes and situation-specific influences. This is particularly evident with accentuated personality constitutions which conceptually, nosologically and diagnostically transcend and touch on various disciplines: the broad range between the healthy condition and a pathological development, between successful adaptation and dissocial development, and between constitutional temper and character variants and psychiatric illness. Moreover, the field dealing with deviant personalities is susceptible to misinterpretation in terms of anthropology, sociopsychology and criminological policy: instead of as a physician, the psychiatrist can be perceived as an instrument with which to implement law and order. This is particularly important when dealing with dissocial behavior, which is why, in Der Mann ohne Eigenschaften (‘The Man without Features’), Musil warned our profession against becoming the backup angel of justice. The concept of psychopathy results from a confluence of views entertained in the French, German and Anglo-American psychiatric traditions. Well into the twentieth century, sociocultural factors caused these concepts of psychopathy to develop more or less independently. This chapter deals with all three traditions – the development of standard nomenclatures and a brief enumeration of the main conceptual milestones is given in Table 1.1. A more detailed overview can be found in Saß (1987) and Saß and Herpertz (1995).

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

10

VOLUME I: DIAGNOSIS AND TREATMENT

Table 1.1 Milestones in the history of the concepts of personality disorders and psychopathy Concepts of personality disorders and psychopathy

Reference

French concepts Manie sans d´elire [Mania without delirium] Les Monomanies [Monomania] D´eg´en´er´es [Degenerates] Delinquente nato [The born criminal] D´es´equilibration mentale [Mental instability]

(Pinel, 1809) (Esquirol, 1839) (Morel, 1957) (Lombroso, 1876) (Dupr´e, 1925)

Anglo-American concepts Moral alienation of the mind Moral insanity Sociopathy Psychopathic states Anethopathy Semantic dementia

(Rush, 1812) (Prichard, 1835) (Partridge, 1930) (Henderson, 1939) (Karpman, 1941) (Cleckley, 1941)

German concepts Psychopathische Minderwertigkeiten [Psychopathic inferiorities] Der geborene Verbrecher [The born criminal] Konstitutionelle Degeneration (Constitutional degeneration) ¨ Psychopathische Personlichkeiten [Psychopathic personalities] ¨ Korperbau und Charakter [Body type and character] ¨ Psychopathische Personlichkeiten [Psychopathic personalities] Psychopathische Verbrecher [Psychopathic criminal]

(Koch, 1891/93) (Bleuler, 1896) (Ziehen, 1905) (Kraepelin, 1909/15) (Kretschmer, 1921) (Schneider, 1923) (Birnbaum, 1926)

THE FRENCH CONCEPT OF PSYCHOPATHY Mania without Delirium Pinel’s concept of a manie sans d´elire (mania without delirium) can be looked upon as the beginning of the scientific study of personality disorders (Pinel, 1809). For the first time in contemporary psychiatry the field of deranged personality was conceptualized as a nosologic entity. According to its rationalistic way of thinking, the eighteenth century regarded mental diseases exclusively as disturbances of the intellect. Pinel was one of the first to stress that in some disorders it was the emotions which are primarily involved while the intellectual functions are essentially undisturbed. In his well-known dissertation ‘Medico-Philosophical Treatise on Mental Derangement’ (Trait´e m´edico-philosophique sur l’ali´enation mentale) he distinguished between five nosological categories: melancholia, mania without delirium, mania with delirium, dementia and idiocy. Pinel gave some examples of what he regarded as mania without delirium; only one description of which stands out for extreme emotional instability, and dissocial tendency would probably fit our present diagnostic view, whereas today the other disorders would be considered to be cases of epilepsy and paranoid schizophrenia. Path-breaking was not Pinel’s diagnostic concept, but his empirical observation of a syndrome which shows disturbance of emotion and behavior without intellectual deficits.

DEVELOPMENT OF PSYCHOPATHIC DISORDERS

11

With respect to etiology, Pinel considered an inadequate education or a perverse, unrestrained constitution and therefore alluded to the discussion of whether psychopathy is the result of psychosocial development or is primarily endogenous and hereditary-based. Despite the efforts of nineteenth-century psychiatrists such as Pinel, the definition of madness remained in the main cognitive in nature (Berrios, 1985). Indeed, to this day, disorders of affect have been rather neglected in psychiatric phenomenology, at least in comparison to the intensive concern with cognition and perception.

Monomania Esquirol (1839), the most prominent student of Pinel, developed the idea of monomania, a diagnostic category, which in succession of his teacher also referred to disorders of the noncognitive side of personality. Esquirol presented his concept in his main work ‘Mental Diseases’ (Des Malades Mentales), wherein he proposed a distribution of mind in understanding, will and feeling. Defects of understanding were named ‘intellectual monomanias’. ‘Instinctive monomanias’ meant changes of will, so that subjects are forced to act and behave in a way that does not correspond to their wishes. The group of illnesses called ‘affective monomanias’ subsumed changes of emotions which cannot be controlled. Finally Esquirol extended his theory of monomania to the point of circularity. He worked out conceptions of circumscribed monomanias so that a single behavioral disturbance became the only criterion needed to diagnose the condition. Well-known examples are pyromania, kleptomania, erotomania and even homicidal monomania. His concept of monomanias is seen in present classification systems with their diagnostic categories of disorders of impulse control, kleptomania and pathological gambling, for example. The idea of monomania also had great influence on the further scientific work on psychopathy at the turn of the twentieth century: the instinctive monomanias transitioned easily into ‘Impulsives Irresein’, that is the impulsive insanity of German psychiatry; the affective monomanias were one of the roots of the British concept of moral insanity. Nevertheless, Esquirol’s concept of monomania also met with severe criticism from a psychopathological view as well as from medico-legal reasoning. One of the most significant critics was the great German psychiatrist Griesinger (1845), who can be looked upon as the founder of the biological epoch of psychiatric research. He emphasized that every single id´ee fixe is the expression of a deeply deranged psychic individuality and probably an indicator of an incipient form of mania. In regard to criminal law, he proposed that the procedure first look for evidence of a mental disease before and after the criminal act and not to consider the act itself as a significant criterion of a presumably abnormal state of mind.

The Theory of Degeneration A work which proved to be of great significance for further concepts of abnormal personalities was Morel’s ‘Treatise on the Physical, Intellectual and Moral Human Degenerates and the Causes which Produce these Various Diseases’ (Trait´e des d´eg´en´er´escences physiques, intellectuelles et morales de l’esp´ece humaine, 1857). Morel’s idea of degeneration was not primarily a scientific one but traced back to philosophical thinking and to a religious worldview. In close connection with Genesis, degeneration was looked upon as the true nature

12

VOLUME I: DIAGNOSIS AND TREATMENT

and destiny of mankind after the Fall. Morel worked out a theory of degeneration which included three characteristics: (i) Degenerative alterations are pathological deviations from normality. (ii) Mental diseases are mostly hereditary. Originally caused by harmful external influences, the disorders are inscribed into the biology of the subject and are passed on from generation to generation, with ever increasing pathological deviation and even progressive deterioration within one’s own lifetime (hence, the idea of progressive degeneration). (iii) Degeneration not only occurs quantitatively, with the same symptoms getting worse, but also qualitatively, resulting in completely new disorders. According to Morel’s model, all variants of mental and even neurological syndromes can be traced back to one common hereditary origin (the idea of polymorphic heredity). Consequently, his nosology of mental diseases was no longer symptom-based but was grounded in his hypothetical etiology of disorders. Morel divided the hereditary madnesses (les folies h´er´editaires) into different categories corresponding to an increasing degree of degeneration. He started with groups of individuals who presented with no severe defects of cognitive functions but rather stood out for their eccentricity, emotional instability, disregard for rules, unreliability and absence of sense of duty. They suffered from folie morale, a notion that was similar to the British concept of ‘moral insanity’. In the middle of the nineteenth century Morel’s conception of progressive and polymorphic degeneration was generally accepted as the source of most mental illnesses. Second only to Morel, the psychiatrist Magnan (Magnan & Legrain, 1895) was the most famous representative of the theory of degeneration in France. Magnan dissociated himself, however, from Morel’s religious point of view and regarded himself as a disciple of Darwin. It was Magnan who formulated the concept of predisposition as a result of hereditary transformations, which could be either latent (not yet expressing themselves in any symptoms) or manifest since birth. Mental disorder was thus an expression of degenerative changes of cerebro-spinal centers as its neurophysiological substrate. It induced a fateful, lifelong fragility, which made the individual vulnerable to fail through difficult environmental influences. In his opinion the progressive evolution of man was constantly endangered by destructive influences which caused degeneration by ruining man’s mental equilibrium. Magnan also distinguished different degrees of degeneration, the least degenerated class being the ‘higher degenerates’ (d´eg´en´eres sup´erieurs), who appeared to have significant affective disturbance but no intellectual deficits. Ideas of degeneration theory were also expressed by the well-known Italian psychiatrist Lombroso (1876) who developed the central idea of the ‘born criminal’ (delinquente nato). Inspired by Darwin’s evolutionism, he regarded a criminal individual as a form of human atavism, a step back in the phylogenesis of mankind. According to his opinion, criminal acts were rooted in biology and the criminal could be recognized by specific anatomical stigmata of degeneration. He was considered to lack higher nervous centers, which represent moral faculties. Social prognosis was very poor. Although Lombroso’s ‘social-Darwinistic’ concept was heavily criticized, his thoughts have obviously maintained some subliminal significance and have supported prejudice against mental illness and psychopathy. After the First World War, Dupr´e (1925) was the true founder of the concept of mental instability (d´es´equilibration mentale). However, within the beginning of the twentieth century the idea of degeneration was abandoned. Instead the doctrine of constitution, which is connected with German views of a hereditary-based psychopathic constitution, gained in importance.

DEVELOPMENT OF PSYCHOPATHIC DISORDERS

13

Summary The French psychiatry of the nineteenth and early twentieth centuries with its synthesis of doctrines of Pinel, Esquirol, Morel and Magnan gave momentum to the development of additional concepts of psychopathy. An important concept following that of mania without delirium was Prichard’s ‘moral insanity’ (1835), which as well was influenced by the French school, as it responded to the research on mental diseases in France. After other modifications by German psychiatry the process of development went on from the concept of ‘higher degenerates’ (d´eg´en´er´es sup´erieurs) to ‘unbalanced degenerates’ (d´es´equilibr´es d´eg´en´er´es) and eventually to the constitutionally unstable (d´es´equilibr´es). In regard to the classification of syndromes, the main element of the French concept is that psychopathy represents disorders of emotion and social behavior while intellectual functions remain undisturbed. From the pathogenetic point of view, the idea of an inborn constitution combined with psychic instability and fragility was favored.

THE ANGLO-AMERICAN CONCEPT OF PSYCHOPATHY Great Britain The Concept of Moral Insanity Prichard’s (1835) definition of ‘moral insanity’ was based in part on the earlier thoughts of French psychiatry. He gave the following definition of moral insanity: ‘. . . madness, consisting in a morbid perversion of the natural feelings, affections, inclinations, temper, habits, moral dispositions, and natural impulses, without any remarkable disorder or defect of the interest or knowing and reasoning faculties, and particularly without any insane illusion or hallucinations’ (p. 6). Lest ‘moral insanity’ be interpreted in purely moralistic terms, the reader must bear in mind that the word ‘moral’ has various meanings in different languages. These various possible meanings have given rise to confusion and misunderstandings. One can distinguish between the following meanings: (i) ‘Moral’ can describe a method of treatment which made use of psychological methods and environmental influences. (ii) In a nonbiased sense ‘moral’ was used for the affective and volitional, in contrast to the intellectual side of man’s nature. (iii) In its limited context ‘moral’ was a synonym for ‘ethical’, which is also the contemporary meaning of the word. Prichard’s ‘moral insanity’ essentially denoted the second broad meaning of the word, and can therefore be translated with terms such as ‘emotional’ and ‘affective’. Similar to Pinel, he relinquished the view that mental disorders were only disturbances of the intellect, but he considered other dysfunctions beyond just the cognitive (cf. Berrios, 1993). One might speculate that today’s shift in meaning favored an early tendency to restrict the concept of abnormal personality to a type of habitual social deviation and criminality. Etiologically Prichard considered different causes of moral insanity, ranging from cases in which the defect is constitutional to those with ‘a well-marked change of character’ resulting from ‘moral shock’ or from ‘fever’ (Tuke, 1884, p. 80). Epilepsy was associated with moral

14

VOLUME I: DIAGNOSIS AND TREATMENT

insanity as well. Therefore, it seems to have been a broad heterogeneous group of mental diseases under which Prichard subsumed this nosological entity. The well-known English psychiatrist Maudsley (1874) strove for clarification between evil as an expression of mental derangement in the sense of moral insanity on the one hand and as that of an eccentric and dissolute personality on the other hand. In his prominent medico-legal work, Responsibility in Mental Diseases, he resisted many lawyers of his day who considered moral insanity to be just a ‘groundless medical invention’ (p. 68) and argued for the acceptance of the concept of diminished criminal responsibility in English law. In contrast to his contemporaries, Maudsley believed that emotions and impulses alone, without disturbed reason, could drive one to commit criminal acts.

The Concept of Constitution and the Psychopathic State For a long time in the twentieth century, the British concept of psychopathy was shaped by Henderson (1939), a Scottish disciple of the American psychiatrist Adolf Meyer (1903), Henderson considered ‘psychopathic states’ to be constitutional abnormalities. In contrast to others, especially German psychiatrists, he conceived of the constitution as resulting from both heredity and environment. He defined three psychopathic conditions: Those that were (i) predominantly aggressive; (ii) predominantly inadequate and (iii) predominantly creative. While the third type was not commonly applied, the inadequate and aggressive types of psychopathy entered into the Anglo-Saxon concepts of personality disorders that were mainly characterized by dissocial traits. The British ‘Mental Health Act’ still uses the term ‘psychopathic disorder’ exclusively in the sense of abnormally aggressive and irresponsible behavior. The term ‘psychopathic disorder’ is also used in psychiatric literature to refer to aspects of personality that have relevance in forensic psychiatry (Saß & Herpertz, 1994). Even today the ambiguous meaning of the term ‘psychopathy’ has persisted. On the one hand it serves as a general term for different abnormalities of personality – both neurotic and psychopathic. On the other hand it is used as a specific term for the aggressive, dissocial type of offender who is prone to recidivism. Besides its legal significance, Henderson assumed that psychopathic conditions hold special importance with regard to the prognosis of mental diseases in general: ‘It is the underlying psychopathic state which constitutes the rock on which our prognosis and treatment in relation to many psychoneurotic and psychotic states becomes shattered’ (Henderson, 1941, p. 37).

Understanding Psychopathy as a Dissocial Disorder By providing inclusion and exclusion criteria, Craft (1966) formulated the first operational view of psychopathy in the sense of a dissocial disorder. As ‘primary’ features he identified lack of feeling towards other human beings and a tendency to act on impulse. As secondary features he listed aggressiveness, absence of shame and remorse, an inability to profit from experience and a deficit of drive or motivation. The presence of psychosis, a significant mental disability or normal criminal motivation excluded the diagnosis of psychopathy (Craft, 1966, p. 5).

DEVELOPMENT OF PSYCHOPATHIC DISORDERS

15

North America Disease of the Moral Faculty Benjamin Rush (1812), known as the ‘father of American psychiatry’, was the first AngloAmerican psychiatrist who studied individuals whose disturbances were primarily characterized by irresponsibility, unscrupulousness and aggressiveness. Rush spoke of ‘perversion of the moral faculties’ and of ‘moral alienation of the mind’. He believed that reprehensible acts were manifestations of mental diseases, which were committed without motive and were driven ‘by a kind of involuntary power’ (Rush, 1827, p. 261). As with historical British concepts, we find the main accent on dissocial and amoral aspects in early American ideas about psychopathy.

Moral Mania By the change of the century in America, it was Ray’s idea of ‘moral mania’ which was most closely associated with European concepts of psychopathy (Ray, 1838). Based on his familiarity with phrenology, he believed in well-defined cerebral localizations for both intellectual and emotional faculties. This facilitated his acceptance of the idea of ‘moral insanity’. However, a lively dispute took place around him, which not only involved scientific assessments but also religious and philosophical ideals.

The Difference between Constitutional Inferiority and Neurosis Adolf Meyer (1903) contributed to the subsequent distinction between psychopathy and neurosis. He designated neurasthenia, psychasthenia and hysteria as forms of neurosis that he distinguished from constitutional inferiority. Here he included a large group of various inferiorities, which were not sufficiently differentiated to be regarded as definite mental diseases. As views shifted away from the concept of definitely inherited conditions, the term constitution was conceived in the broad meaning of early and permanently fixed characteristics of the mind. Towards the end of the 1920s ‘constitutional inferiority’ was replaced by ‘psychopathic personality’ in the Anglo-American nomenclature. Partridge (1930) was one of the main advocates of the new concept of psychopathy. He described personalities whose abnormality was mainly expressed in impulsiveness and in moral deficiency.

Psychoanalytic Views on Psychopathy After Freud’s work on Character and Anal Eroticism (1908), Alexander (1928) and Reich (1933) proposed the concept of ‘character neurosis’. They argued that neurosis manifests itself not only in circumscribed symptoms but also in the character as a whole. Alexander limited his definition of ‘neurotic character’ to those cases wherein individuals act out their deviance with impulsive behavior. According to him most criminals suffer from

16

VOLUME I: DIAGNOSIS AND TREATMENT

an unconscious conflict between parts of the ego, and they surely possess a superego. But, instead of suffering from symptoms, they disturb other people (actions instead of symptoms). Later the difference between the ego-syntonic psychopath and the ego-dystonic neurotic became established. Reich (1933), in turn, regarded character primarily as a defensive structure against inner impulses and external stress. In contrast to Alexander, he rejected a principal difference between symptomatic neurosis and character neurosis and assumed that the neurotic character is the basis for every neurotic symptom. Based on this hypothesis, he developed a special form of character analysis. Reich was of the opinion that character neurosis stands for the integrated product of symptoms that can no longer be averted. Character neurosis can therefore be looked upon as the progressive effort at adjustment in contrast to the regressive symptom-neurosis.

Psychopathy and Sociopathy As explained above, the concept of psychopathic personality was increasingly narrowed until it basically meant dissocial behavior. Therefore it seems to be consequent that Partridge proposed the notion ‘sociopathy’ for this main psychopathic group. ‘Sociopathy’ was defined as a persistent maladjustment that cannot be corrected and brought into normal social patterns by ordinary methods of education or by punishment. Although the sociological perspective with its focus on behavioral disturbances had existed since the beginning of the development of psychopathy concepts, it now gained more and more importance. Patridge wrote: We might say that pragmatically the psychopath is mainly reduced to types which are of importance from the standpoint of society and the effect of personalities adversely upon the social life seems to be recognized as a justification for a category within the field of the psychopathological in its more individual and subjective aspects (p. 75).

From the time of Partridge, the emphasis has been on descriptions and etiological speculation has taken the back seat (e.g., concepts regarding degeneration, constitution, psychodynamic background). To this day the restriction of ‘psychopathy’ to the dissocial ‘sociopathy’ dominates the Anglo-Saxon sphere, so that both expressions and also the new term ‘antisocial personality disorder’, of DSM-III (American Psychiatric Association, 1980), and later on in DSM-IIIR/DSM-IV, are used virtually as synonyms.

Idiopathic and Symptomatic Forms of Psychopathy Karpman (1941) suggested a distinction between idiopathic and symptomatic forms of psychopathy. Under ‘symptomatic psychopathy’, he grouped all those reactions that were basically neurotic and therefore could be traced back to intra-psychic conflicts. According to Karpman there was another smaller group of true psychopaths whose behavior could not be explained by any psychodynamic formulations. He considered these ‘anethopaths’ to lack a conscience.

DEVELOPMENT OF PSYCHOPATHIC DISORDERS

17

The Idea of Semantic Dementia Cleckley (1976) had remarkable influence on American conceptualizations of psychopathy. His famous treatise, The Mask of Sanity, went through five editions, the last in 1976. It contained a number of case reports that reflected the clinical–intuitive procedure of the author and became the basis of empirical research on psychopathy in North America. Cleckley’s ‘psychopath’ was characterized by dissocial behavior which could not be deduced from any adequate motivation and which was caused neither by psychosis nor neurosis nor mental handicap. He listed 16 criteria which he thought to be typical and distinctive for psychopathy including: superficial charm and undisturbed intelligence; unreliability and insincerity; inability to accept blame or shame; failure to learn from experience; pathological egocentricity and incapacity for love; lack of emotions in general; impersonal and poorly integrated sexual relationships; inability to follow one’s aim in life. Indeed, the DSM-IV concept of antisocial personality disorder (American Psychiatric Association, 1994) includes most of these criteria. Cleckley was convinced that ‘psychopathy’ should be accepted as a ‘severe disease’ having the quality of a psychosis that had not manifested itself. Cleckley minted the speculative notion of ‘semantic dementia’. It described the incapacity of the psychopath to have central human experiences with any degree of emotional depth, even though intellectual understanding is undisturbed. A similar picture of the psychopath was offered by the sociologists McCord and McCord (1964) who researched the long-term association between psychopathy and criminality.

The Concept of Dissocial Personality Disorder In his well-known monograph Deviant Children Grown Up, Robins (1979) described a population of more than 500 males who were observed over a period of 30 years. This data gave the most important empirical basis for the current concept of antisocial personality disorder in the United States. The conclusion of a synopsis of 29 great inquiries about course and prognosis of dissocial personality disorder was as follows: The degree of dissocial and especially aggressive behavior in childhood and youth can be looked upon as the best early predictor for developing a sociopathic disorder. This finding also supported the wide-spread supposition that disordered personality traits are stable and enduring.

Summary The development of conceptions on ‘psychopathy’ proceeded quite homogeneously in the Anglo-American area. Significant was the early restriction of the concept of personality disorders to a type of habitual social deviation and criminality. This tendency already emerged in the narrow usage of the term ‘moral insanity’ and later in the concept of ‘psychopathy’ and finally ‘sociopathy’. Early on, American psychiatrists absorbed psychoanalytic views that were based on the idea that most abnormal personalities and even criminals suffer from a neurotic unconscious conflict. Therefore the differentiation between an idiopathic and a neurotic symptomatic form was accomplished. The basically neurotic psychopath

18

VOLUME I: DIAGNOSIS AND TREATMENT

was supposed to act out his impulses in deviance. Beside psychoanalytic ideas etiological speculations such as the concept of ‘anethopathy’ or ‘semantic dementia’ refer to the assumption of a basic mental and spiritual defect which cannot be explained by any psychodynamic formulation and which is regarded as responsible for the individual’s inability to have central human experiences.

THE GERMAN CONCEPT OF PSYCHOPATHY Psychopathic Inferiorities In Germany the term and concept of ‘psychopathy’ came to embrace most forms of abnormal personalities. Up to the 1840s ‘psychopathy’ meant what the etymologist would expect: for von Feuchtersleben (1845) ‘psychopathy’ meant a psychological defect, psychosis or illness of personality. However, the current German meaning is traceable to Koch (1889) who first applied the term ‘psychopathic inferiorities’ (Psychopathische Minderwertigkeiten) for anomalies of personality in his Handbook of Psychiatry. In Germany, through his monograph Psychopathische Minderwertigkeiten (1891–93), Koch gained recognition for his conceptualization of abnormal personalities, similar to his predecessors Pinel in France, Rush in the United States and Prichard in Great Britain. The German ideas of psychopathy influenced French and Anglo-American views. This was more noticeable after the 1930s when many German-speaking psychiatrists and psychoanalysts emigrated to these countries. In his group of ‘psychopathic inferiorities’ Koch included a wide range of conditions that mostly stood out because of minor mental defects. It is remarkable that he already described some definite forms of psychopathic inferiority in the sense of our present concepts of psychopathy. Therefore, it was Koch who not only established our present notion of psychopathy as an integral part of today’s use of language in psychiatry, but he also contributed to the currently still valid concept of psychopathy in the manner of a typology. Koch divided the ‘psychopathic inferiorities’ into congenital and acquired, and each of these categories into psychopathic predisposition, psychopathic defect and psychopathic degeneration. In his expositions many of the psychopathic types of later concepts were already identified. For example he referred to those individuals who are distinguished by psychic fragility (psychische Zartheit), as having a weak, vulnerable constitution. In the 1840s, Griesinger (1845) defined ‘nervous constitution’, the ‘sensitive weakness’, as that individual predisposition that can lead to mental suffering and to loss of mental stability. Griesinger and Koch’s concepts corresponded somewhat with the French ideas of mental instability (d´es´equilibration mentale) and to the idea of asthenia which gained considerable importance later in German psychiatry. In contrast to the Anglo-American sphere, the German concept of personality disorders was thus broader, and included far more than dissocial criteria. Nevertheless, Koch’s term ‘inferiority’ also led to negative connotations and even moral condemnation. Although one does not encounter explicitly pejorative intentions in the writings of Koch, it was probably also he who provided the unfortunate amalgamation of aspects of amorality, inferiority and socially harmful behavior.

DEVELOPMENT OF PSYCHOPATHIC DISORDERS

19

Psychopathic Constitutions Ziehen (1906) developed Koch’s views one step further but preferred to speak of ‘psychopathic constitutions’ which were also considered to be genetic in nature. In his writing Mental Diseases of Childhood (Geisteskrankheiten des Kindesalters), Ziehen presented 12 forms of psychopathic constitutions, among them the hysterical, the neurasthenic, the depressive, the hyperthymic, the paranoid and the obsessive types.

Psychopathic Personalities A Predominantly Social-Judgment Concept of Psychopathy Kraepelin’s concept of psychopathy was influenced by the French theory of degeneration (Kraepelin, 1896) and in turn formed the basis of Kurt Schneider’s typology, and through the latter, of today’s well-established German view of psychopathy. In successive editions of his textbook Kraeplin continued to develop his concept of ‘psychopathic conditions’ in the meaning of our current view on abnormal personalities. The expression Die psychopathischen Zust¨ande appeared for the first time in the fifth edition (1896) and consisted of compulsive conditions, impulsive insanity, homosexuality and disturbances of the mood, the so-called konstitutionellen Verstimmungen. In the seventh edition (Vol. 2, 1904), under the heading ‘Insanity of Degeneration’ (Entartungsirresein), he treated the anomalies of personality considerably in the tradition of the theory of degeneration. After that an innovation was introduced: henceforth, Kraepelin distinguished between ‘original disease conditions’ (Origin¨are Krankheitszust¨ande) – the group he had earlier called psychopathic states – and psychopathic personalities (Psychopathische Pers¨onlichkeiten). The latter were regarded as stable psychopathic conditions corresponding to personality defects. Kraepelin employed the term ‘psychopathic personalities’ in a predominantly socially judgmental sense. In the seventh edition he subsumed under this well-known designation the inborn delinquents, the unstable individuals, the liars, the swindlers and the pseudoquerulants. In the eighth edition (1909–15), he named the following types of psychopathic personalities besides those who were dissocial Gesellschaftsfeinde: the excitable, the unstable, the Triebmenschen (‘driven persons’, relating to impulsive insanity), the eccentrics, the liars and swindlers and the quarrelsome. It is remarkable that Kraepelin now considered the states of disturbed mood – today’s subaffective disorders – not to be psychopathic conditions but primarily attenuated phases of manic-depressive diseases. This change corresponds with current classification systems of mental diseases (cf. Akiskal, 1981). Birnbaum (1926) also researched the social aspects of psychopathy and in his monograph, The Psychopathic Offender (Die psychopathischen Verbrecher), he concerned himself with the forensic significance of abnormal personality. Birnbaum assumed that psychopathic personalities show constitutionally conditioned deviations in personality of a moderate degree. Following the French theory of degeneration, the criterion of an abnormal, inherited predisposition was of decisive importance for Birnbaum and the psychiatric schools in Germany that followed. Moreover, according to Dupr´e’s concept of mental instability (d´es´equilibration mentale), he also paid attention to disharmony of personality traits and abnormal lability of mental stability.

20

VOLUME I: DIAGNOSIS AND TREATMENT

The Relationship between Body Type and Personality During this period there also appeared various forms of systematic typologies. This means that the different psychopathic modes of appearance were inferred from prototypic ideas about the structure of personality. Foremost amongst these is Kretschmer’s konstitutionstypologisches Modell (1921). But there were many others. Gruhle (1956) deduced his types from fundamental characteristics of the human mind such as activity, basic mood, affective responsiveness, willpower and so on. Other psychiatrists such as Kahn (1928), Schultz (1928), Homburger (1929) and Rothacker (1947) proposed a hierarchical model of personality (Schichttypologien). Others such as Kretschmer (1925) and Ewald (1924) also introduced the notion of ‘Typologies of Reaction’ (Reaktionstypologien) which referred to different ways of digesting experiences. After Kurt Schneider’s monograph (1923) was published, the systematic typologies lost most of their significance. Kretschmer suggested that there was a specific correlation between body type and personality and he divided all people into one of three body types: the pyknic, the leptosomic and the athletic type. The pyknic body type was associated with the cyclothymic character. In Kretschmer’s opinion the boundaries between the normal cyclothymic character, the abnormal cycloid variant and the manic-depressive psychosis were fluid so that mental health and illness were regarded as a continuous phenomenon. Correspondingly the leptosomic and athletic body type were related to a schizothymic temperament and therefore to the schizoid form of psychopathy and finally to schizophrenia.

Abnormal Personalities and Psychopathic Personalities: An Attempt at Developing a Concept of Psychopathy that is Free from Value Judgments Kurt Schneider’s famous monograph, The Psychopathic Personalities (Die psychopathischen Pers¨onlichkeiten) (first published in 1923), takes root in his earlier studies on The Personality and Fate of Registered Prostitutes (Pers¨onlichkeit und Schicksal eingeschriebener Prostituierter) (1921) wherein he already recognized 12 characterological types. Schneider, like Kraepelin, used a typology approach. However, in contrast to Kraepelin’s predominantly socially judgmental concept with its sociological forms of psychopathic states, Schneider intended to maintain a value-free concept. Therefore, he also incorporated some non-dissocial forms into his typology. Approaching the problem of psychopathy from the perspective of the normal personality, Schneider regarded abnormal personalities as statistical deviations from an estimated average norm, although this norm was only vaguely conceptualized. For Schneider, however, who also regarded eminently creative or intelligent individuals as abnormal, not all abnormal personalities were of psychiatric significance: ‘Psychopathic personalities are those abnormal personalities that suffer from their abnormality or whose abnormality causes society to suffer‘ (1923, p. 6). Schneider did not consider psychopathy to be a mental illness because according to his idea illnesses were necessarily associated with somatic injury or disease process. In this he opposed Kretschmer and Bleuler who believed psychosis and psychopathy were just different degrees on a continuous scale of derangement.

DEVELOPMENT OF PSYCHOPATHIC DISORDERS

21

Schneider’s typology differentiated in detail 10 forms of psychopathic personalities which were based on clinical views and were not intended to be of systematic quality: the hyperthymic and depressive psychopaths with their stable deviations of mood and activity; the insecure psychopaths with their subgroups of the sensitive and anankastic psychopaths; the fanatics; the self-assertive psychopaths; the emotionally unstable psychopaths; the explosive; the callous; the weak-willed; and the asthenic psychopaths. Especially the subtle descriptions of Petrilowitsch (1966) deepened Schneider’s typology portrayals from the perspective of character pathology. Schneider’s doctrine influenced all future descriptive typologies. The current classification systems DSM-IV and ICD-10 have also integrated many essential parts of Schneider’s work on psychopathy into their conceptions of personality disorders.

Summary Our current connotations of the term ‘psychopathy’ trace back to Koch’s ‘psychopathic inferiorities’ which represented a first attempt at a descriptive typology. It is remarkable that already Koch addressed precursor concepts of psychasthenia. Early German writings on psychopathy were highly influenced by the French theory of degeneration. Later French concepts were replaced by German concepts in many respects. Kraepelin’s and Birnbaum’s writings focussed on the social aspects of psychopathy and especially Kraepelin’s dissocial psychopath – der Gesellschaftsfeind – gained special importance. Schneider intended to maintain a value-free concept of psychopathy, however, he did not completely succeed in erasing immoral and pejorative connotations. Until today Schneider’s unsystematic typology has received great interest and caused earlier systematic typologies to fade away. In contrast to Kretschmer and Bleuler, Schneider did not regard psychopathy as a mental disease but as a deviation from average. Thus, he gave up the idea of a continuous scale between psychopathy and psychosis. Up to the present day the German traditional views of psychopathy – especially in the form of Schneider’s concept – have continued to influence psychopathological research on abnormal personalities.

CONCLUSIONS This last section is intended to deal with some selected historical and conceptual aspects of psychopathy that have developed a special significance for today’s research on personality disorders.

The Strong Emphasis Placed on the Sociological Aspects of Personality Disorder As we have argued in detail, the concepts of personality disorders have tended towards an unfavorable amalgamation of psychopathological disturbances and social deviation through the nineteenth and twentieth century. Even though the sociological perspective especially dominated the Anglo-American sphere, this historical line of development was to be found

22

VOLUME I: DIAGNOSIS AND TREATMENT

in the French view of degeneration and in the German tradition as well. The strong emphasis placed on the sociological aspects of personality disorder can be demonstrated impressively by the concept of ‘moral insanity’. The disturbance of man’s affective side, in contrast to his intellectual side, was originally regarded as the characteristic of moral insanity. This idea evolved into a predominantly ethical insanity in the sense of a socially reprehensible propensity towards criminality. In spite of contrary intentions, which often remained only as lip service, the emphasis on the harmful social aspects also crept into the German view of psychopathy. Kraepelin explicitly gave up the differentiation between the sociological and psychopathological aspects. The different editions of his textbook present an increasing limitation on his own originally broader concept of socially harmful forms of psychopathy. In the course of time, some primarily psychopathic types, especially those with disturbed mood, were no longer subsumed under disorders of personality but were looked upon as preliminary stages of endogenous psychoses. In contrast to Kraepelin’s late writings Kurt Schneider favored a value-free psychological and characterological point of view that comprised subaffective disturbances. Distinguishing two forms of psychopaths – those who suffer from their psychic abnormality and those from whom society suffers – Schneider achieved a conceptual break and in this way also combined psychopathological and sociological aspects (cf. Saß, 1987). Nevertheless, the German tradition was constructed more broadly from the very beginning, by introducing a second significant type beside the dissocial forms. This type was the asthenic, feeble psychopath to whom the group of subaffective abnormalities of personality was added later on. One could suppose that this completion contributed to the greater significance the concept of psychopathy achieved in German-speaking countries. Probably in the Anglo-American sphere the early distinction between the suffering, egodystonic neurotic and the disturbing, ego-syntonic psychopath supported the American restriction of the concept of psychopathy to forms of persistent maladjustment to society. Contrary to American development, Schneider’s concept contains the two manifestations of psychopathy mentioned above which partly overlap with the Anglo-Saxon differentiation between neurosis and psychopathy. Thus many of the ego-dystonic neurotics correspond with Schneider’s criteria of psychopathy.

Personality Disorder and Endogenous Psychosis Psychiatric Concepts Personality disorders present conditions which belong to a border zone between mental health and current phenomena of everyday life on the one hand and specific mental diseases on the other hand. While fluid transitions between normal and slightly abnormal personalities are generally accepted, the borderland at the other end of the continuum of psychiatric disturbances – including most severe pathology of character and endogenous psychoses – causes greater difficulties (cf. Saß & Koehler, 1983). The different facets of an ‘idea of continuum’ especially concerned the German tradition of psychiatry beginning with the unitarian concepts of Zeller (1840) and Griesinger (1845) (cf. Saß, 1990). The French theory of degeneration and its idea of polymorphic heredity considered all varieties of mental and neurological syndromes to trace back to one unitary hereditary origin. The French notion of manie sans d´elire as the forerunner of the later term

DEVELOPMENT OF PSYCHOPATHIC DISORDERS

23

‘psychopathy’ stood for the broad field of mental derangement, which was not yet definitely conceptualized but represented a low level on a continuous scale of increasing degeneration. In the development of the German concept of psychopathy, two lines can be distinguished from one another. The first one, above all linked to Kretschmer, claimed gradual transitions between normal personality traits, psychopathies and endogenous psychoses. The other one, represented by Kurt Schneider but also by Birnbaum, Jaspers (1959) and Gruhle, rejected any possibility of a continuous development of endogenous psychosis through intensifying psychopathic traits but insisted on categorical differences. Conceding only a few cases of diagnostic doubt, Schneider challenged psychiatrists to reach a decision as to whether a patient has an abnormal personality or an endogenous psychosis. Empirical research over the recent decades did not find a significant accumulation of specific personality disorders in the approaches of schizophrenia, for instance in the sense of Kretschmer’s schizoid dimension. Nevertheless, characteristics of increased psychic vulnerability were found. In the field of affective psychoses, typical pre-morbid traits of personality could be ascertained more likely. (cf. Akiskal, Hirschfeld, Yerevanian, 1983) Already Kraepelin referred to subaffective states of disturbed mood as personality features in his early writings. In the discussion of the concept of unitary psychosis and the ‘idea of continuum’, the structural–dynamic concept, worked out by Janzarik (1988), is worth mentioning. This structural–dynamic approach differentiates the mental whole into two aspects, the dynamic and the structural. Simplistically, ‘dynamics’ means the vital, mostly constitutionally based affective side of man, whereas ‘structure’ refers to the intentions, attitudes and values that are determined to a large extent by life history. Pre-morbid traits of personality are characterized by dynamic and structural peculiarities. Considering the dynamic side, the vulnerability to developing an endogenous psychosis seems to be determined by a basic instability and proneness to psychic derailment. Whether instability leads to a mental disease or not, depends on the situational and personal history factors and on the qualities of the ‘structure’. It is also ‘structure’ which determines the kind of psychotic disorder (e.g., schizophrenic or affective) the individual displays (cf. Saß, 1992). The completion of purely criteria-based diagnostics of personality through fundamental and ganzheitliche models of personality could usher in a new access to the understanding of mental diseases. Faced with today’s level of knowledge, however, it seems to be useful to base diagnostic classification systems on a multiaxial assessment which registers ‘states’ and ‘traits’ independently and therefore enables further research on possible associations.

Psychoanalytic Theory of Infantile Development From 1913 until 1923 Freud worked out his conception of infantile psychological development which he described as a succession of organization forms of libido under the priority of erogenous (oral, anal, genital) areas. During recent decades psychoanalytic interest shifted from the dominance of sexual drive to the leading role of object relationship and its influence on emotional development. Common to all psychoanalytic schools is the thought that the roots of all psychiatric disorders lie in disturbances during the early formative years. That means specifically that distortions and arrests during these early developmental stages cause conflicts which arise over unresolved infantile sexual drives and especially relationships leading to neurotic or psychotic symptoms in adult life. In this special sense of an ‘idea of continuum’, psychoanalysts have established a continuous sequence of psychiatric

24

VOLUME I: DIAGNOSIS AND TREATMENT

disorders extending over neurosis, psychopathy and psychosis, the severity of the disorder depending on the time when significant traumas were experienced.

Categories and Dimensions: Two Different Models of Personality Historical concepts of personality disorders predominantly present classical typology descriptions of special types of personality. These categorical systems have developed naturalistically without a systematic and comprehensive scheme. Especially academic psychology promotes dimensional models of personality which conceptualize personality disorders in relation to normally occurring traits, and the dimensions therefore are better suited for empirical verification and broader generalizability. One of the best-known dimensional models of personality is that of Eysenck (1952), who, using factor analysis, reduced the variety of possible traits to the dimensions of extraversion, neuroticism and psychoticism. During the last decade some other dimensional models of personality were proposed which can be related to some extent to one another. Millon (1981) proposes the following three dimensions: ‘self–other orientations’, ‘activity–passivity’ and ‘pleasure–pain’. Widinger et al. (1987) present a differentiated, methodologically demanding attempt to dimensionalize personality disorders. He refers to the dimensions: ‘high social involvement vs. low social involvement’, ‘high assertion or dominance vs. low assertion or dominance’, ‘anxious rumination vs. behavioral acting out’. Cloninger (1987) correlates three dimensions of personality with the neurotransmitter systems and neurogenic mechanisms of learning: ‘novelty seeking’ (dopamergic system), ‘harm avoidance’ (noradrenergic system) and ‘reward dependence’ (serotonergic system). The five-factor model (McCrae & Costa, 1989) derives from Eysenck’s three dimensions and the two dimensions of the interpersonale circumplex model (Wiggins, 1982) and consists of neuroticism, extraversion, openness, agreeableness and conscientiousness. Because of their high level of abstraction, dimensional models still seem removed from clinical realities and remain of secondary importance in clinical usage in comparison with categorical models. New developments in personality research attempt to combine categorical and dimensional elements. Widinger (1991) for example proposes to retain the categorical format of today’s international classification systems but to add weighting diagnostic criteria including a measure of ‘prototypicality’. In this way dimensional elements could improve present categorical prototypic models that are characterized by a clear set of definitional features which ‘are not considered to be singly necessary or jointly sufficient’ (Widinger & Frances, 1985, p. 616). This polythetic rather than monothetic method permits multiple personality diagnoses. From the historical perspective, it is remarkable that the first conceptual roots of prototypic models can be found in the writings of Max Weber and Jaspers (1959) on ‘ideal’ personality types.

Standardization of Nomenclature Until the middle of the twentieth century no single standard nomenclature of mental disorders prevailed. In the United States at least three separate nomenclatures were in use: a standard nomenclature of disease, a project initiated by the New York Academy of Medicine in 1927; a nomenclature developed for use in the Armed Forces; and the Veterans Administration nomenclature (American Psychiatric Association, 1952). Clinicians tended to use diagnostic terms and concepts taught at their medical schools and residency programs,

DEVELOPMENT OF PSYCHOPATHIC DISORDERS

25

and the terminology of various educational centers was far from uniform. This frustrated attempts to learn and advance knowledge by sharing information through publications and seminars. It also impeded research because the resulting babble did not allow accurate comparisons of investigative results from different centers. Eventually the American Psychiatric Association developed its nomenclature in the form of its first edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-I, 1952). A challenge in gaining general acceptance of any new nomenclature was the disharmony in theoretical orientation of mental health professionals. Names and criteria of mental disorders can reflect etiological assumptions. Adolf Meyer’s psychobiological approach was thought to be more unifying than a strictly biological or psychodynamic model, for example, would have been. Thus, disorders were termed ‘reactions’. Symptoms and aberrant behaviors were considered to contribute to total adaptive reactions to internal (biological) or external (psychological) stresses. In the first DSM, personality disorders were considered to be pathological conditions, usually lifelong, with little stress or distress, characterized more by behavioral features than subjective symptoms. Three main groups within the category of personality disorders were the sociopathic personality disturbances characterized by failure to conform to social norms. Four disturbances within the sociopathic personality disturbance were antisocial reaction, dissocial reaction, sexual deviation and addiction. Antisocial reaction was described by Clecklian features, such as chronic antisocial behavior, failure to learn from adverse experience and callousness. The condition previously designated as ‘constitutional psychopathic state’ would henceforth be known as antisocial reaction (American Psychiatric Association, 1952). Less familiar to North Americans, because the term has long been discarded, was ‘dissocial reaction’,1 a condition wherein a person disregards norms of the prevailing culture, because he or she was brought up in a contrary moral environment. A Mafia family member, for example, would be considered a product of social learning from a deviant subculture rather than mentally disordered in a pathological sense. By 1968 the concept of dissocial reaction was dropped from the DSM, now in its second edition. The salient pathological antisocial condition, no longer a reaction, was now one of several personality disorders. The diagnostic criteria for the DSM II’s antisocial personality were essentially the same as those for the DSM I’s antisocial reaction. The condition, ‘group delinquent reaction of childhood’, which retained the etiological implication of a ‘reaction’, had to be ruled out before settling on the diagnosis of antisocial personality (DSM II, American Psychiatric Association, 1968). The most significant change in diagnostic criteria and method occurred in the third edition in which all pathological personality disturbances, indeed most mental conditions, became known as disorders. Reflecting the seminal research of Robins (1979) described above, the criteria for the DSM III’s antisocial personality disorder (American Psychiatric Association, 1980) included childhood behaviors that establish the lifelong course of the disorder. Out of concern that the diagnosis could be falsely made based on subjective impressions and unclear inferences about psychological functions, DSM III criteria were

1

‘Dissocial’ was not even included in the later DSM editions’ glossary of technical terms. A current definition from a psychology dictionary is: An obsolescent term for a personality disorder characterized by a seriously distorted sense of ethics and morality. Often applied to ‘professional criminals’ because, although they might display honoured values such as loyalty and courage, they tend to do so in socially undesirable ways’ (Reber & Reber, 2001, pp. 223–4).

26

VOLUME I: DIAGNOSIS AND TREATMENT

essentially behavioral. Methodological consistency in diagnosis and objective signs was thought to result in more accurate diagnoses and improved interrater reliability. Subsequent editions of the DSM have continued this basic methodological and conceptual approach to antisocial personality disorder. Antisocial personality disorder is not to be found in the current International Classification of Mental Disorders (ICD-10, World Health Organization, 1989). The closest diagnostic condition is dissocial personality disorder, the criteria of which are much more like those of the earlier DSM’s APD than those of dyssocial reaction in the first DSM. Included within the ICD-10’s concept of dissocial personality disorder are the sociopathic, asocial, dissocial and psychopathic disorders. Incidentally, the diagnostic method is much more like that in the pre-1980 versions of the DSM and, therefore, relatively flexible. Important to note, however, are the altogether different meanings of the earlier dyssocial reaction of the DSM and the current dissocial personality disorder of the ICD. Parenthetically, but importantly for conceptual clarity, the term ‘dissocial behavior’, as used in the final formulation of this chapter could be somewhat confusing to some readers for several reasons. At least in North American common and technical language usage, the term has all but disappeared. To English readers, the term is ambiguous, meaning neither ‘dyssocial reaction’ of the earlier DSM nor ‘dissocial personality disorder’ of the current ICD. In fact our use of dissocial behavior is not intended to suggest any disorder whatsoever. Finally, there is already a widely used term to mean essentially what is intended and that is ‘antisocial behavior’, behavior that may be criminal when produced by adults, delinquent when done by youths, but not necessarily in violation of the law. Basically it is behavior that is offensive to others and violates social norms. It may but does not have to be the result of a disorder. The behavior itself, not its cause, is indicated by the term. However, because the prefix ‘anti’ means ‘against’ and in keeping earlier writings of Saß’ formulation of concepts of psychopathic disorders (see Felthous, Kr¨ober & Saß, 2001, Vol. 1, p. 297), the seemingly less pejorative descriptor ‘dissocial’ is retained.

FINAL COMMENT Differentiation of Personality Disorders and Psychopathy The meshing of the concepts of abnormal personality and social deviance was treated in detail in the section on history of ideas (especially in discussing the Anglo-American theories of psychopathy). The socially deviant personalities are now described by different diagnostic criteria, that is, antisocial personality disorder (DSM-IV); dissocial personality disorder (ICD-10); and the core group ‘psychopathy’ in the sense of Hare (1970, 1991). The differentiation of personality disorders from only dissocial behavior without additional psychopathological peculiarities is of importance, especially in forensic psychiatry. This requires a differentiation into more pathological and more antisocial abnormal personality variants (Saß, 1987), thus yielding the following differentiations which we illustrated in Figure 1.1: 1. Personality disorders occur in individuals who suffer from their psychopathological peculiarities and/or whose social life is impaired by these peculiarities. Their symptoms resemble those of psychiatric patients in the strict sense.

DEVELOPMENT OF PSYCHOPATHIC DISORDERS

27

Personality Disorders Dissocial Behaviors

Psychopathy

Antisocial Personality Disorder

Figure 1.1 Personality disorders, psychopathy and the law

2. Moreover, some of these individuals show a potential for social conflict, as their behavior is marked by deviance and criminality and is evidently related to psychopathological abnormalities. Due to the close correlation between social deviance and psychopathological abnormalities, the designation antisocial personality disorder (DSM-IV-TR) would seem justified. 3. Some individuals show a clear and persistent disposition towards deviant and delinquent behavior without psychopathologically relevant abnormalities throughout their lives. This criminologically important core group corresponds to the ‘psychopathy’ described by Hare (1970, 1991) in the strict sense: it usually shows a ‘dissocial character structure’ and is now also defined quite well biologically (Herpertz and Saß, 1999b, Herpertz et al., 2001). Only by means of a differentiation such as this can forensic questions of culpability, prognosis and therapy (Saß, 1987) be settled. On no account should we speak of a personality disorder when dealing with only recurring social deviance and criminality, as shown by chronic repeat offenders or professional criminals, since this diagnostic term can lead to erroneous connotations of an illness-like disorder.

REFERENCES Akiskal, H.S. (1981). Subaffective disorders: dysthymic, cyclothymic and bipolar II disorders in the borderline realm. Psychiatric Clinics of North America, 4, 25–46. Akiskal, H.S., Hirschfeld, R.M.A., Yerevanian, B.J. (1983): The relationship of personality to affective disorders. Archives of General Psychiatry, 40:801–810. Alexander, F. (1928): Der neurotische Charakter [The neurotic character]. Seine Stellung in der Psychopathologie und in der Literatur. International Journal of Psychoanalysis, 14, 26–44. American Psychiatric Association (1952). Diagnostic and Statistical Manual of Mental Disorders. Washington, DC: American Psychiatric Association.

28

VOLUME I: DIAGNOSIS AND TREATMENT

American Psychiatric Association (1968). Diagnostic and Statistical Manual of Mental Disorders, 2nd edition, Washington, DC: American Psychiatric Association. American Psychiatric Association (1980). Diagnostic and Statistical Manual of Mental Disorders, 3rd edition. Washington, DC: American Psychiatric Association. American Psychiatric Association (1987). Diagnostic and Statistical Manual of Mental Disorders, 3rd edition, revised. Washington, DC: American Psychiatric Association. American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders, 4th edition. Washington, DC: American Psychiatric Association. Berrios, G.E. (1985). The psychopathology of affectivity: conceptual and historical aspects. Psychological Medicine, 15, 745–58. Berrios, G.E. (1993). European views on personality disorders: a conceptual history. Comprehensive Psychiatry, 34(1), 14–30. Birnbaum, K. (1926). Die psychopathischen Verbrecher [The Psychopathic Offenders], 2nd edition. Leipzig: Thieme. (1st edition, 1914). Bleuler, E. (1896). Der geborene Verbrecher. Eine kritische Studie [The Inborn Delinquent. A Critical Study]. M¨unchen: Lehmann. Cleckley, H. (1976). The Mask of Sanity: An Attempt to Clarify Some Issues About the So Called Psychopathic Personality, 5th edition. St Louis: Mosby (1st edition, 1941). Cloninger, C.R. (1987). A systematic method for clinical description and classification of personality variants. Archives of General Psychiatry, 44, 573–88. Craft, M. (1966). Psychopathic Disorders and their Assessment. Oxford: Pergamon Press. Dupr´e, E. (1925): La doctrine des constitutions. In Pathologie de l’imagination es de l’´emotivit´e. G¨ottingen: Ruprecht. Esquirol, E. (1839). Des Maladies Mentales Consid´er´ees sous les Rapports M´edical, Hygi´enique et M´edico-Legal [Mental Diseases under Medical, Hygienic and Medico-Legal Aspects]. Paris: Bailli´ere`e. Ewald, G. (1924). Temperament und Character [Temperament and character]. Berlin: Springer. Eysenck, H.J. (1952). The Scientific Study of Personality. London: Routledge & Kegan Paul. Felthous, A.R., Kr¨ober, H.L. & Saß, H. (2001). Forensic evaluations for civil and criminal competencies and criminal responsibility in German and Anglo-American legal systems. In F. Henn, N. Sartorius, H. Helmchen & H. Lauter (eds.) Contemporary Psychiatry, Vol. 1, Foundations in Psychiatry (pp. 287–302). Berlin: Springer. Feuchtersleben E. von (1845): Lehrbuch der a¨ rztlichen Seelenkunde [Textbook of Medical Mental Science]. Wien: Gerold. Freud, S. (1908). Charakter und Analerotik. GW VII. Frankfurt: Fischer. Griesinger, W. (1845). Die Pathologie und Therapie der psychischen Krankheiten. Stuttgart: Krabbe. Gruhle, H.W. (1956). Psychopathie [Psychopathy]. In W. Weygandt (ed.), Lehrbuch der Nerven- und Geisteskrankheiten (2nd edn.) (pp. 664–86). Halle: Marhold. Hare, R.D. (1970). Psychopathy: Theory and Research. New York: John Wiley & Sons, Inc. Hare, R.D. (1990). The Hare Psychopathy Checklist-Revised. Toronto: Multi-Health Systems. Henderson, D. (1939). Psychopathic States. New York: Norton. Herpertz, S. & Saß, H. (1999). Differentialtypologie der Pers¨onlichkeitsst¨orungen [Differential typology of personality disorders]. M¨unchener Medizinische Wochenschrift, 133(21), 337–41. Herpertz, S.C., Werth, U., Lukas, G., Qunaibi, M., Schuerkens, A., Kunert, H-J., Freese, R., Flesch, M., Mueller-Isberner, R., Osterheider, M. & Sass, H. (2001). Emotion in Criminal Offenders with Psychopathy and Borderline Personality Disorder. Archives of General Psychiatry, 58, 735–745. Homburger, A. (1929). Versuch einer Typologie der psychopathischen Konstitution [Attempt of a typology of psychopathic constitution]. Nervenarzt, 2, 134–6. Janzarik, W. (1988a). Strukturdynamische Grundlagen der Psychiatrie [Structural–Dynamic Foundations of Psychiatry]. Stuttgart: Enke. Jaspers, K. (1959): Allgemeine Psychopathologie [General Psychopathology]. 7th edition. Berlin: Springer. (1st edition, 1913). Kahn, E. (1928): Die psychopathischen Pers¨onlichkeiten [The Psychopathic Personalities]. In O. Bumke (ed.), Handbuch der Geisteskrankheiten, vol. 5 (pp. 227–487). Berlin: Springer. Karpman, B. (1941). On the need of separating psychopathy into two distinct clinical types: the symptomatic and the idiopathic. Journal of Criminal Psychopathology, 2, 112–37.

DEVELOPMENT OF PSYCHOPATHIC DISORDERS

29

Koch, J.L.A. (1889). Kurzgefaßter Leitfaden der Psychiatrie [Short Handbook of Psychiatry], 2nd edition. Ravensburg: Verlag d. Dorn’schen Buchhandlung. Koch, J.L.A. (1891–93). Die psychopathischen Minderwertigkeiten [The Psychopathic Inferiorities]. Ravensburg: Maier. ¨ Kraepelin, E. (1896): Psychiatrie. Ein Lehrbuch f¨ur Studirende und Arzte [Psychiatry. A Textbook for Students and Doctors], 5th edition. Leipzig: Barth. ¨ Kraepelin, E. (1904). Psychiatrie. Ein Lehrbuch f¨ur Studirende und Arzte [Psychiatry. A textbook for students and doctors]. Vol. 2, 7th edition. Leipzig: Barth. ¨ Kraepelin, E. (1909–15). Psychiatrie. Ein Lehrbuch f¨ur Studirende und Arzte [Psychiatry. A Textbook for Students and Doctors], 8th edition. Leipzig: Barth. Kretschmer, E. (1921): K¨orperbau und Character. Berlin: Springer. Kretschmer, E. (1925). Character and Physique. London: Kegan Paul. Lombroso, C. (1876). L’Uomo Delinquente. Mailand: Hoepli. Magnan, M. & Legrain, M. (1895). Les D´eg´en´er´es (´etat mental et syndromes e´ pisodiques) [The Degenerates (state of mind and episodical syndromes)]. Paris: Rueff. Maudsley, H. (1874). Responsibility in Mental Disease. London: King. McCord, W. & McCord, J. (1964). The Psychopath. An Essay on the Criminal Mind. (2nd edn.) Princeton: Van Norstrand. McCrae, R. & Costa, P. (1989). The structure of interpersonal traits: Wiggins’s circumplex and the five-factor model. Journal of Personality and Social Psychology, 56, 586–95. Meyer, A. (1903). An attempt at analysis of the neurotic constitution. American Journal of Psychiatry, 14, 354–67. Millon, T. (1981). Disorders of Personality. DSM-III: Axis II. New York: John Wiley & Sons, Inc. Morel, B.A. (1857). Trait´e des D´eg´en´erescences Physiques, Intellectuelles et Morales de l’Esp`ece Humaine et des Causes qui Produisent ces Vari´et´es Maladive [Treatise on the Physical, Intellectual and Moral Human Degenerates and the Causes which Produce these Various Diseases]. Paris: Bailli`ere. Partridge, G.E. (1930). Current conceptions of psychopathic personality. American Journal of Psychiatry, 10, 53–99. Petrilowitsch, N. (1966). Abnorme Pers¨onlichkeiten [Abnormal Personalities], 3rd edition. Basel: Karger. Pinel, P. (1809). Trait´e M´edico-Philosophique sur L’ali´enation Mentale [Medico-Philosophical Treatise on Mental Derangement]. 2nd edition. Paris: Brosson. Prichard, J.C. (1835). A Treatise on Insanity and Other Disorders Affecting the Mind. London: Sherwood, Gilbert & Piper. Ray, I. (1838). A Treatise on the Medical Jurisprudence of Insanity. Boston: Little. Reber, A.S. & Reber, E. (2001). The Penguin Dictionary of Psychology, 3rd edition. London: Penguin Books. Reich, W. (1933): Charakteranalyse. Technik und Grundlagen. Berlin: Selbstverlag. Robins, L.N. (1979). Deviant Children Grown Up: A Sociological and Psychiatric Study of Sociopathic Personality. Baltimore: Williams & Wilkens. Robins, L.N. (1979). Longitudinal methods in the study of normal and pathological development. In K.P Kisker et al. (ed.), Psychiatrie der Gegenwart, vol. 1, 2nd edition (pp 627–84). Berlin: Springer. Rothacker, E. (1947). Die Schichten der Pers¨onlichkeit [Layers of Personality], 3rd edition. Leipzig: Barth. Rush, B. (1812). Medical Inquiries and Observation upon the Diseases of the Mind. Philadelphia: Kimber & Richardson (Hafner Press, New York, 1962). Rush, B. (1827). Medical Inquiries and Observation upon the Diseases of the Mind. (3rd edn.) Philadelphia: Kimber & Richardson. Saß, H. (1986). Zur Klassifikation der Pers¨onlichkeitsst¨orungen [Classification of personality disorders]. Nervenarzt, 56, 193–203. Saß, H. (1987). Psychopathie – Soziopathie – Dissozialit¨at: Zur Differentialtypologie der Pers¨onlichkeitsst¨orungen [Psychopathy – Sociopathy – Dissociality: The Differential Typology of Personality Disorders]. Berlin: Springer.

30

VOLUME I: DIAGNOSIS AND TREATMENT

Saß, H. (1990). Einheitspsychose [Unitary psychosis]. In C.N. Stephanis, C.R. Soldatos & A.D. Rabavilas (eds.), Psychiatry: A World Perspective. Proceedings of the 8th World Congress of Psychiatry. Athens: Congress Series 900. Saß, H. (1992): Strukturelle und dynamische Pers¨onlichkeitsvarianten im Vorfeld idiopathischer Psychosyndrome [Structural and dynamic variants of personality in the run-up to idiopathical brain syndromes]. In Ch. Mundt & H. Saß (eds.), Einheitspsychose. Festschrift f¨ur W. Janzarik. Stuttgart: Thieme. Saß, H. & Herpertz, S. (1994). Psychopathic disorder. In A.R. Felthous & P. Bowden (eds.), Forensic Psychiatry. Current Opinion in Psychiatry, 7(6). Saß, H. & Herpertz, S. (1995). Personality disorders. In G. Berrios & R. Porter (eds.), A History of Clinical Psychiatry. The Origin and History of Psychiatric Disorders (pp. 633–44). London: The Athlone Press. Saß, H. & Koehler, K. (1983): Borderline-Syndrome: Grenzgebiet oder Niemandsland? Zur klinischpsychiatrischen Relevanz von Borderline-Diagnosen [Borderline syndromes: true borderland or no-man’s land?]. Nervenarzt, 54, 221–30. Schneider, K. (1921). Studiener¨ufer Pers¨onlichkeit eingeschriebener Prostitutierten. Springer: Berlin. Schneider, K. (1950). Die psychopathischen Pers¨onlichkeiten [The Psychopathic Personalities], 9th edition. Wien: Deuticke. (1st edn.1923, Thieme, Leipzig). Schultz, J.H. (1928). Die konstitutionelle Nervosit¨at [The constitutional nervosity]. In O. Bumke (ed.), Handbuch der Geisteskrankheiten, vol. 5 (pp. 28–111). Berlin: Springer. Tuke, D.H. (1884). Prichard and Symonds in Especial Relation to Mental Science with Chapters on Moral Insanity. London: J. & A. Churchill. Widinger, T.A. (1991). Personality disorder dimensional models proposed for DSM-IV. Journal of Personality Disorders, 5(4), 386–98. Widinger, T.A. & Frances, A. (1985): The DSM-III personality disorders: perspectives from psychology. Archives of General Psychiatry, 42, 615–23. Widinger, T.A., Trull, T., Hurt, S., Clarkin, J. & Frances, A. (1987): A multidimensional scaling of the DSM-III personality disorders. Archives of General Psychiatry, 44, 557–63. Wiggins, J. (1982): Circumplex models and interpersonal behavior in clinical psychology. In P. Kendall & J. Butcher (eds.), Handbook of Research Methods in Clinical Psychology (pp. 183– 221). New York: John Wiley & Sons, Inc. World Health Organization (1989). International Classification of Mental Disorders (ICD-10). Geneva: World Health Organization. Zeller, A. (1840). Med. Korr. Bl. d. W¨urttemb. Medizinvereins, 10, 17. Ziehen, T.H. (1905, 1907, 1908, 1912). Zur Lehre von den psychopathischen Konstitutionen [The Doctrine of the Psychopathic Constitutions]. Charit´e-Annalen 29, 31, 32, 36. Anfang Verzeichnis V.

PART II

Assessment

CHAPTER 2

Psychiatric Assessment Paul Hoff University of Zurich, Switzerland

and Sabine C. Herpertz University of Rostock, Germany

The psychiatric assessment of ‘psychopathy’ or antisocial personality is an especially delicate and complicated subject, regardless whether clinical, forensic or research issues are concerned. There are two main reasons for this: first, in the process of assessing or diagnosing antisocial personality we encounter the same methodological and theoretical problems as in the assessment of any other mental disorder. Second, the linkage to areas ‘outside’ psychiatry – especially jurisdiction, sociology and politics – is even more obvious when it comes to the psychiatric aspects of antisocial behavior. Therefore, the way the concept of antisocial personality is dealt with sheds some light on the question of whether psychiatry is responsible minded toward such critical issues or not. Four examples – each one in the form of a question – will elucidate how closely the practical aspect of assessing antisocial personality traits is linked to fundamental issues in psychiatry: 1. Is antisocial behavior closer to mental disorder or to mere social misconduct? The two extreme answers to this question will have significant, mainly negative consequences. First, if one identifies antisocial behavior as a special form of mental illness, it will be completely ‘located’ in the realm of psychiatry. Psychiatry, in turn, will then become the center of decision making not only regarding assessment, diagnosis, treatment and therapeutic prognosis, but also regarding criminal prognosis and aspects that are usually part of court decisions and mental health policy. Emil Kraepelin’s understanding of forensic psychiatry points in this direction, which is problematic since it disproportionately broadens the psychiatric field (Hoff, 1998; Kraepelin, 1907). Second, if the focus of attention is on the description of social misconduct without any links to medical or psychopathological criteria – as, for example, suggested by the ‘structural–social concept of illness’ (Rasch, 1986) – there will be the risk of overlooking treatable mental

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

34

VOLUME I: DIAGNOSIS AND TREATMENT

disorders underlying or, at least, modifying the overt behavior. Of course, there is a broad overlap between these two extremes. The concept of sociopathy, discussed in detail by Saß (1987), allows one to take into account both aspects, the psychopathological and the sociological. 2. Is antisocial behavior closer to mental disorder or to maladaptive types of character? This question does, of course, overlap with the one mentioned above. But the important difference is that ‘misconduct’ just addresses a certain type of overt behavior, whereas ‘character’ implies the existence of a complex psychological entity developing and enduring over the life span. Of course, both the descriptive misconduct approach and the psychological character approach are not only objective technical terms but also – like any other term in the psychiatric field – value-laden (Ernst, 1995; Fulford et al., 2005; Schwartz & Schwartz, 1976). 3. Is the etiology of antisocial personality disorder predominantly biological in nature, or psychological, or sociological? 4. Is the best approach to personality disorders, including antisocial personality disorder, a categorical one or a dimensional one? These last two questions center around the appropriateness of the ‘medical model’ for the understanding of mental disorders in general and personality disorders in particular. They have accompanied psychiatric nosology and research – in the clinical and forensic perspective – since the field defined itself as a scientific discipline in the late eighteenth century (Hoff, 2005). From a historical point of view, one can find all these positions in the literature, for example, the psychological and moralistic underpinnings of romantic psychiatry, the shift to a new scientific paradigm in psychiatry that was oriented on the quantitative natural sciences and was initiated by Wilhelm Griesinger, the increasingly close relation of personality disorder and especially psychopathy to the concept of degeneration in the second half of the nineteenth century and, finally, the pragmatic and much less speculative, descriptive models of personality disorders as suggested by Kurt Schneider and developed further up to the present day. We are still participating in the longstanding controversy as to which aspect has the lead within the bio–psycho–social paradigm, a paradigm which is widely accepted nowadays also in the field of personality disorders. Before addressing the actual diagnostic procedures in some detail, the complexity of this process, well beyond quantifying rating scales, should be emphasized. We face the typical dilemma of any psychiatric assessment: the tension between objective quantitative data that are reliable and reproducible on the one hand and subjective experiences of the patients that are perceived and, in the best case, understood by the diagnostician on the other hand. The relevance of this context becomes even more noticeable when, for the time being, we broaden the term ‘assessment’ beyond the description of the present status to include anamnestic, especially biographical data (Hoff, 2003). It is the wellbalanced application of flowing interviews, structured interviews and diagnostic criteria that – of course complemented by neuropsychological and somatic findings – will best serve the aim of an adequate scientific assessment of the patient’s status (Saß & Hoff, 2003).

PSYCHIATRIC ASSESSMENT

35

CONCEPTS OF ANTISOCIAL PERSONALITY Current psychiatric classification of legally relevant personality disorders is far from homogeneous. Three different diagnostic categories are now being used: the DSM-IV antisocial personality disorder; the ICD-10 dissocial personality disorder; and Hare’s psychopathy concept, which is based largely on Cleckley’s conceptualization by the same name (Cleckley, 1976). Particularly in Germany, Partridge’s concept of the sociopathic personality disorder (1930) is still being used by psychiatric experts-at-law in order to describe abnormal personalities showing deviant or delinquent behavior related to psychopathological phenomena. The DSM-IV concept of antisocial personality disorder is generally commended for good reliability (see Figure 2.1). This applies to both joint interview and test/retest designs over short and longer intervals. However, it has been criticized for overdiagnosis, temporal instability, inattentiveness to issues of symptom pervasiveness, and overlap with some of the symptoms of substance abuse disorders (Cunningham & Reidy, 1998; for a review see Herpertz & Saß, 1999). Among prison inmates the prevalence rates of the DSM-IV category range from 70 to 100 % (Widiger & Corbitt, 1993), however, prisoners show major decreases in the diagnoses above the age of 40 years. Moreover, the majority of items are restricted to describing criminal and socially damaging patterns of behavior which do not include indicators of profound disturbances of personality functioning which go beyond the criminal behavior itself. A further shortcoming could be gender bias, at least regarding the diagnostic criteria related to antisocial behavior in adolescence. Furthermore, among the DSM-IV criteria aggressive, violent and manifest criminal modes of behavior, which are much more common among men than females, are strongly weighted, whereas female forms of antisocial behavior, such as deficient care and responsibility for wards, are not taken Diagnostic criteria for 301.7 antisocial personality disorder A. There is a pervasive pattern of disregard for and violation of the rights of others occurring since age 15 years, as indicated by three (or more) of the following: (1) failure to conform to social norms with respect to lawful behaviors as indicated by repeatedly performing acts that are grounds for arrest (2) deceitfulness, as indicated by repeated lying, use of aliases, or conning others for personal profit or pleasure (3) impulsivity or failure to plan ahead (4) irritability and aggressiveness, as indicated by repeated physical fights or assaults (5) reckless disregard for safety of self or others (6) consistent irresponsibility, as indicated by repeated failure to sustain consistent work behavior or honor financial obligations (7) lack of remorse, as indicated by being indifferent to or rationalizing having hurt, mistreated, or stolen from another B. The individual is at least age 18 years. C. There is evidence of conduct disorder with onset before age 15 years. D. The occurrence of antisocial behavior is not exclusively during the course of schizophrenia or a manic episode. Figure 2.1 DSM-IV and DSM-IV-TR: antisocial personality disorder

36

VOLUME I: DIAGNOSIS AND TREATMENT

Diagnostic criteria for F60.2 dissocial personality disorder A. The general criteria of personality disorder (F60) must be met. B. At least three of the following must be present: (1) Callous unconcern for the feelings of others. (2) Gross and persistent attitude of irresponsibility and disregard for social norms, rules and obligations. (3) Incapacity to maintain enduring relationships, though having no difficulty to establish them. (4) Very low tolerance to frustration and a low threshold for discharge of aggression, including violence. (5) Incapacity to experience guilt, or to profit from adverse experience, particularly punishment. (6) Marked proneness to blame others, or to offer plausible rationalizations for the behaviour bringing the subject into conflict with society. Comments: Persistent irritability and the presence of conduct disorder during childhood and adolescence, complete the clinical picture but are not required for the diagnosis. It is suggested that subcriteria should be developed to operationalize behaviour patterns specific to different cultural settings concerning social norms, rules and obligations where needed (such as examples of diminished criminal responsibility and disregard of social norms). Figure 2.2 ICD-10: dissocial personality disorder

into consideration. Finally, several studies have demonstrated the existence of a substantial comorbidity between antisocial personality disorder (APD) and various substance abuse disorders (for a review see Weaver et al., 2003). There is considerable phenomenological overlap between these disorders, especially when one focuses on deviant modes of behavior. Thus, Widiger and Corbitt (1993) have suggested that the overemphasis on criminal acts and law breaking contributes to the difficult differentiation of APD from substance abuse disorders. The ICD-10 concept of dissocial personality disorder has some advantages compared to the DSM-IV category since in addition to the description of problematic modes of behavior it includes relevant traits such as the inability to learn from punishment, to take over responsibility for others or lack of empathy (see Figure 2.2). As standardized diagnostic instruments for the assessment of personality disorders, semi-structured interviews are favored, the International Personality Disorder Examination (IPDE) (Loranger et al., 1996) and the Structured Clinical Interview for Mental Disorders II (First et al., 1996), in particular. They include screening questionnaires, which help to provide first indications of an antisocial behavioral style. When performing these diagnostic interviews, the high face validity of related items has to be critically taken into consideration, because they may render authentic answers more difficult in the forensic-psychiatric context. Therefore, informants’ comments as a further independent source of information are of particular importance in this field. In addition to the classification systems, the concept of psychopathy is increasingly being recognized in clinical and research work as well as in the courtroom, because it is considered to reflect a more stable, trait-based concept which, moreover, is more neutral towards gender. Aside from an antisocial lifestyle, it is based on character features such as selfishness, callousness, emotional detachment, lack of empathy and remorse. Prevalence rates are much lower for psychopathy than for the two other current classification systems.

PSYCHIATRIC ASSESSMENT

37

In a Canadian prison population, diagnostic criteria according to the Psychopathy ChecklistRevised (PCL-R; Hare, 1991) were met by only 28 % (Widiger et al., 1996); in a Swedish forensic psychiatric population by 25 % (Stalenheim & Knorring, 1996); and in a British prison population by 26 % (Hobson & Shine, 1998). PCL scores appear not to be equivalent across cultures: in a study performed by Cooke et al. (2005), the same level of psychopathy was associated with lower PCL scores in the UK compared to North America, with affective symptoms having the highest cross-cultural stability. The diagnosis of antisocial disorders, including psychopathy, requires a comprehensive assessment of the individual’s history starting in early childhood and considering behavior and performance in school and adolescence in detail, and diagnosis demands a concise assessment of the mental state and the development of psychopathology. The diagnosis of psychopathy should be further based on the PCL-R, which collects information not only from self-report but also from informants’ comments and official reports, although its usage is still limited in practice. In its original version, this scale consists of two factors: Factor 1 with eight items that assess affective-interpersonal traits and Factor 2 with nine items that are related to antisocial traits, criminal behavior and substance abuse. There are three additional items, which are not related to this two-factor structure. Currently, there is an intense debate on the factorial structure of the psychopathy concept. While Hare (2003) claims a fourfactor model (interpersonal problems, affective features, impulsive/irresponsible modes of behavior, antisocial behavior), Cooke and Michie (2001; Cooke et al., 2004) regard antisocial behavior, not as a symptom but as a consequence of psychopathy and therefore establish a three-factor model of psychopathy: (i) arrogant and deceitful interpersonal style; (ii) deficient affective experience; and (iii) impulsive and irresponsible behavioral style, without items that describe antisocial behavior per se. A number of studies provided evidence for the predictive potency of the psychopathy concept with high PCL-R scores indicating high recidivism and severe violence (for a review see Hare et al., 2000). According to a study by Andersen et al. (1999), high scorers exhibited a higher degree of psychosocial maladjustment and had a history of more suicide attempts. A further interesting finding of this study concerns underlying temperamental factors: according to the three-factor model of Eysenck and Eysenck (1985), high scorers were characterized by high psychoticism in contrast to mid-range scorers, who showed high neuroticism and neurotic/stress-related disorders. Thus, mid-range scorers on the PCLR are reminiscent of the classical concept of the secondary neurotic sociopath (Meyer, 1903). Other authors regard ‘psychopathy’ as a causal model. According to this theory, psychopathy results in delinquency in cases wherein psychosocial disadvantages and/or low verbal intelligence co-occur; otherwise, this type of personality may lead to severe interpersonal dysfunction without manifest criminality (Cooke et al., 2004). There are also dimensional models of antisocial personality traits, which describe personality disorders as extreme variants of basic personality factors. According to the personality theory of Gray (1975), human behavior can be described by means of the behavioral approach system (BAS), which encourages behavior in expectation of reward leading to experiences of joy and other positive feelings, and the behavioral inhibition system (BIS), which induces the inhibition of behavior in response to punishment and frustration and is responsible for experiences of negative emotions such as fear. According to a recently published study by Newman et al. (2005), primary psychopathy is associated with a weak BIS while secondary psychopathy is predominantly associated with a strong BAS. For children

38

VOLUME I: DIAGNOSIS AND TREATMENT

with conduct disorder, a weak activity of the BIS has been suggested (Nigg, 2003). Psychopaths particularly fail to show response reversal when a stimulus previously associated with reward is now followed by aversive consequences, that is, they show an impaired ability to learn over the course of a task (Mitchell et al., 2002). Longitudinal studies have provided evidence that behavioral disinhibition, callousness, egocentricity and indifference are personality traits which indicate a risk for an antisocial development. Raine et al. (1998) were able to show that fearlessness and increased sensation seeking in three-year-old children predicted adult antisocial behavior, and Kerr et al. (1997) provided evidence that inhibited temperament, fearfulness and harm avoidance protect against antisocial development.

CONCLUDING REMARKS The assessment of antisocial behavior and the diagnosis of antisocial personality disorder including psychopathy is a difficult task. Like any other psychiatric diagnosis, it faces the problem of defining a cut-off between minor psychopathological or conduct-related symptoms and illness. As compared to other diagnoses, however, it is even more closely linked to social and political issues. Such an assessment will only be effective and scientifically sound if:

r internationally accepted methods and criteria are applied; r the subjective dimension in the assessment of the present status and the biographical data of the patient is acknowledged; and

r the complex theoretical background of the terms ‘personality disorder’ in general and ‘psychopathy’ in particular is reflected, thus enabling a responsible attitude toward the psychiatrist’s role both as a psychotherapist and as a forensic expert.

REFERENCES Andersen, H.S., Sestoft, D., Lillebaek, T., Mortensen, E.L. & Kramp, P. (1999) Psychopathy and psychopathological profiles in prisoners on remand. Acta Psychiatrica Scandinavica, 99, 33–9. Cleckley, H. (1976). The Mask of Sanity: An Attempt to Clarify Some Issues About the So Called Psychopathic Personality, 5th edition. St Louis: Mosby (1st edition, 1941). Cooke, D.J. & Michie, C. (2001) Refining the construct of psychopathy: towards a hierarchical model. Psychological Assessment, 13, 171–88. Cooke, D.J., Michie, C., Hart, S.D. & Clark, D.A. (2004). Reconstructing psychopathy: clarifying the significance of antisocial and socially deviant behavior in the diagnosis of psychopathic personality disorder. Journal of Personality Disorders, 18, 337–57. Cooke, D.J., Michie, C., Hart, S.D. & Clark, D. (2005). Assessing psychopathy in the UK: concerns about cross-cultural generalisability. British Journal of Psychiatry, 186, 335–41. Cunningham, M.D. & Reidy, T.J. (1998). Antisocial personality disorder and psychopathy: diagnostic dilemmas in classifying patterns of antisocial behavior in sentencing evaluations. Behavioral Sciences and the Law, 16, 333–51. Ernst, W. (1995). Personality disorders – social section. In G.E. Berrios & R. Porter (eds.) A History of Clinical Psychiatry. The Origin and History of Psychiatric Disorders (pp. 645–55). London: The Athlone Press. Eysenck, H.J. & Eysenck, M.W. (1985). Personality and Individual Differences: A Natural Science Approach. New York: Plenum.

PSYCHIATRIC ASSESSMENT

39

First, M.B., Spitzer, R.L., Gibbon, M. & Williams, J.B.W. (1996). Structured Clinical Interview for DSM-IV Personality Disorders. Washington, DC: American Psychiatric Press. Fulford, K.W.M., Broome, M., Stanghellini, G. & Thornton, T. (2005). Looking with both eyes open: fact and value in psychiatric diagnosis? World Psychiatry, 4, 78–86. Gray, J.A. (1975) Elements of a Two-Process Theory of Learning. New York: Academic Press. Hare, R.D. (1991). Manual for the Hare Psychopathy Checklist-Revised. Toronto: Multi-Health Systems. Hare, R.D. (2003). The Hare Psychopathy Checklist-Revised, 2nd edition. Toronto: Multi-Health Systems. Hare, R.D., Clark, D., Grann, M. & Thornton, D. (2000) Psychopathy and the predictive validity of the PCL-R: an international perspective. Behavioral Sciences and the Law, 18, 623–45. Herpertz, S. & Saß, H. (1999). Personality disorders and the law, with a German perspective. Current Opinion in Psychiatry, 12(11), 689–93. Hobson, J. & Shine, J. (1998). Measurement of psychopathy in a UK prison population referred for long-term psychotherapy. British Journal of Criminology, 38, 504–15. Hoff, P. (1998). Emil Kraepelin and forensic psychiatry. International Journal of Law and Psychiatry, 21, 343–53. Hoff, P. (2003). Biographische und Krankheitsanamnese. In H.J. M¨oller, G. Laux & H.P. Kapfhammer (eds.), Psychiatrie und Psychotherapie, 2nd edition. (pp. 364–72). Berlin: Springer. Hoff, P. (2005). Perspektiven der forensischen Psychiatrie – eine psychiatriehistorische und aktuelle Bestandsaufnahme. Nervenarzt, 76, 1051–61. Kerr, M., Tremblay, R.E., Pagani, L. & Vitaro, F. (1997). Boys’ behavioral inhibition and the risk of later delinquency. Archives of General Psychiatry, 54, 809–16. Kraepelin, E. (1907). Das Verbrechen als soziale Krankheit. Monatsschrift f¨ur Kriminalpsychologie und Strafrechtsreform, 3, 257–79. Loranger, A.W., Susman, V.L., Oldham, H.M. & Russakoff, L.M. (1996). International Personality Disorder Examination (IPDE): a structural interview for DSM-IV and ICD-10 personality disorders. German Translation by W. Mombour et al. New York: New York Hospital Cornell Medical Center. Meyer, A. (1903). An attempt at analysis of the neurotic constitution. American Journal of Psychiatry, 14, 354–67. Mitchell, D.G., Colledge, E., Leonhard, A. & Blair, R.J. (2002). Risky decisions and response reversal: is there evidence of orbitofrontal cortex dysfunction in psychopathic individuals? Neuropsychology, 40, 2013–22. Newman, J.P., MacCoon, D.G., Vaughn, L.J. & Sadeh, N. (2005). Validating a distinction between primary and secondary psychopathy with measures of Gray’s BIS and BAS contsructs. Journal of Abnormal Psychology, 114, 310–23. Nigg, J.T. (2003). Response inhibition and disruptive behaviors: toward a multiprocess conception of etiological heterogeneity for ADHD combined type and conduct disorder early-onset type. Annals of the New York Academy of Science, 1008, 170–82. Partridge, G.E. (1930). Current conceptions of psychopathic personality. American Journal of Psychiatry, 10, 53–99. Raine, A., Meloy, J.R., Bihrle, S. et al. (1998) Reduced prefrontal and increased subcortical brain functioning assessed using positron emission tomography in predatory and affective murderers. Behavioral Sciences and the Law, 16, 319–32. Rasch, W. (1986). Forensische Psychiatrie. Stuttgart: Kohlhammer. Saß, H. (1987). Psychopathie – Soziopathie – Dissozialit¨at: zur Differentialtypologie der Pers¨onlichkeitsst¨orungen [Psychopathy – Sociopathy – Dissociality: The Differential Typology of Personality Disorders]. Berlin: Springer. Saß, H. & Hoff, P. (2003). Deskriptiv-psychopathologische Befunderhebung. In H.J. M¨oller, G. Laux & H.P. Kapfhammer (eds.), Psychiatrie und Psychotherapie, 2nd edition (pp. 382–99). Berlin: Springer. Schwartz, R.A. & Schwartz, I.K. (1976). Are personality disorders diseases? Diseases of the Nervous System, 86, 613–17. Stalenheim, E.G. & Knorring, L. (1996) Psychopathy and axis I and axis II psychiatric disorders in forensic psychiatric population in Sweden. Acta Psychiatrica Scandinavica, 94, 217–23.

40

VOLUME I: DIAGNOSIS AND TREATMENT

Weaver, T., Madden, P., Charles, V. et al. (2003). Comorbidity of substance misuse and mental illness in community mental health and substance misuse services. British Journal of Psychiatry, 183, 304–13. Widiger, T.A., Cardoret, R., Hare, R. et al. (1996) DSM-IV antisocial personality disorder field trial. Journal of Abnormal Psychology, 105, 3–16. Widiger, T.A. & Corbitt, E.M. (1993). Antisocial personality disorder: proposals for DSM-IV. Journal of Personality Disorders, 7(1), 63–77.

CHAPTER 3

Psychological Instruments in the Assessment of Psychopathy Robert D. Hare University of British Columbia and Darkstone Research Group, Vancouver, Canada

This chapter draws on several more extensive discussions of the topics contained herein (Book et al., 2006; Hare, 2006; Hare & Neumann, 2006). I thank Kylie Neufeld for her help in preparing this chapter. Psychopathy is a personality disorder that includes a cluster of interpersonal, affective, lifestyle and antisocial traits and behaviors, including deception, manipulation, irresponsibility, impulsivity, stimulation-seeking, poor behavioral controls, shallow affect, a lack of empathy, guilt or remorse, promiscuity, and a range of unethical and antisocial behaviors, not necessarily criminal. Among the most devastating features of criminal psychopathy are a callous disregard for the rights of others and high risk for a variety of predatory and aggressive behaviors. In this chapter I outline procedures for the assessment of this disorder, with emphasis on the Psychopathy Checklist-Revised (PCL-R). I also provide a brief discussion of the implications of psychopathy for the criminal justice system.

PSYCHOLOGICAL INSTRUMENTS IN THE ASSESSMENT OF PSYCHOPATHY Throughout recorded history there have been many descriptions of individuals whose traits and behaviors were remarkably consistent with current clinical conceptions of psychopathy. However, it was only in the last several hundred years that psychopathy began to take shape as a formal psychiatric disorder, reflected in the clinical investigations and speculations of European and North American psychiatrists and psychologists (see Berrios, 1996; Cleckley, 1976; Hare, 2003; Herv´e, 2007a; Meloy, 1988; Millon et al., 1998). Millon, Simonsen and Birket-Smith (1998) noted that the concept of psychopathy ‘has a long historical and clinical tradition’ and ‘was the first personality disorder to be recognized in psychiatry’ (p. 28). The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

42

VOLUME I: DIAGNOSIS AND TREATMENT

The last quarter century has seen a dramatic increase in basic and applied research on psychopathy, due in large part to the development and validation of new assessment tools, including the Psychopathy Checklist-Revised (PCL-R; Hare, 1991, 2003). The basic research includes empirical investigations of etiology, measurement, developmental course, cross-cultural generalizability, issues related to cognitive/affective neuroscience and implications of, and for, general personality theory (Hare, 2003; Herv´e & Yuille, 2007; Patrick, 2006). Much of the applied work involves matters of interest to forensic psychology and psychiatry, including assessments of risk for violence and recidivism, civil commitment and dangerous offender proceedings, and evaluations of treatment suitability (Douglas, Vincent & Edens, 2006; Felthous & Saß, 2000; Hare, 2003; Monahan et al., 2001; Porter & Porter, 2007; Wong & Hare, 2005). A recent development is the use by law enforcement of psychopathy for crime scene analyses and the selection of interview strategies (O’Toole, 2007). Because of its pervasive influence, psychopathy has been described as the single most important clinical construct in the criminal justice system (Hare, 1996) and as what may be the most important forensic concept of the early twenty-first century (Monahan, 2006). The etiology, dynamics and conceptual boundaries of this personality disorder remain the subject of debate and research, but there is a rather consistent clinical (much of it psychodynamic; Meloy, 1988) and empirical tradition concerning its affective, interpersonal and behavioral attributes. The detailed clinical descriptions of Cleckley (1941, 1976) have been particularly influential in this regard, and have formed an important basis for North American research conducted over the last 50 years. We might describe psychopathic individuals as grandiose, arrogant, callous, dominant, superficial and manipulative. They are short-tempered, unable to form strong emotional bond with others, and lacking in empathy, guilt or remorse. They engage in a socially deviant (not necessarily criminal) lifestyle that includes irresponsible and impulsive behavior, and a tendency to ignore or violate social conventions and rules. Psychopathy cannot be understood solely, or even primarily, in terms of social and environmental forces and influences. It is likely that genetic factors play an important role in the formation of the personality traits and temperament considered essential to the disorder (Blonigen et al., 2005; Larsson, Andershed & Lichstenstien, 2006; Viding et al., 2005; Waldman & Rhee, 2006). However, its lifelong expression is a product of complex interactions between biological/temperamental predispositions and social forces (MacDonald & Iacono, 2006). For example, early child abuse has been posited as a contributor to the development of psychopathy (Weiler & Widom, 1996) but Poythress, Skeem and Lilienfeld (2006) reported that the association is weak and confined to the impulsive and irresponsible lifestyle (externalizing) features of psychopathy (see section on Factor Structure). Certainly, the traits and behaviors that help to define adult psychopathy begin to manifest themselves early in childhood (Frick, 2007; Frick & Marsee, 2006; Lynam, 1996). Blair and his colleagues (Blair, 2005; Blair, Mitchell & Blair, 2005) have provided an extensive discussion of current models of psychopathy based on cognitive/affective neuroscience. Kiehl (2006; also see Kiehl et al., 2006; Kiehl et al., 2004) has described a model in which ‘the relevant functional neuroanatomy of psychopathy includes limbic and paralimbic structures, which may be collectively termed the paralimbic system’. Newman and his colleagues (2006) have conducted an extensive program of research involving cognitive/emotional processing deficits in psychopathy. Although much of this research implies that psychopathy is related to abnormal brain function, the nature of this relationship is unclear. Is the abnormal brain

PSYCHOLOGICAL INSTRUMENTS AND ASSESSMENT

43

process structural or functional in nature? If the latter, do the underlying processes reflect a processing ‘defect’ or unusual (perhaps learned) processing strategies? Models based on evolutionary psychology view psychopathy as less a disorder than an evolved ‘cheater’ strategy for passing on one’s gene pool (Harris & Rice, 2006). Some investigators consider psychopathy to be a pathological variant of normal personality (Hicklin & Widiger, 2005), while others describe and account for psychopathy in terms of psychodynamic mechanisms and processes (see Kernberg, 1984; Meloy, 1988; Meloy & Shiva, Chapter 20, this volume). Whatever its etiology or psychobiological nature, psychopathy clearly presents society with a serious problem. Although not all psychopaths come into formal contact with the criminal justice system (Babiak, 2007; Babiak & Hare, 2006; Hare, 1998a), their defining features clearly place them at high risk for crime and violence. As Silver, Mulvey and Monahan (1999) put it, ‘Psychopathy’s defining characteristics, such as impulsivity, criminal versatility, callousness, and lack of empathy or remorse make the conceptual link between violence and psychopathy straightforward’ (p. 244). The problem is to assess psychopathy as professionally and accurately as possible, particularly in situations where such an assessment has serious implications for both individuals and society. Extensive accounts of the recent research and theory on psychopathy and its clinical and forensic measurement and applications are available elsewhere in the present volume and in other edited volumes (e.g., Gacono, 2000; Herv´e & Yuille, 2007; Patrick, 2006).

ASSESSMENT Because of space limitations I focus on the most widely accepted measure of psychopathy, the Psychopathy Checklist-Revised (PCL-R; Hare, 1991, 2003). Occasional references also are made to its direct derivatives, the Psychopathy Checklist: Screening Version (PCL: SV; Hart, Cox & Hare, 1995), the Psychopathy Checklist: Youth Version (PCL: YV; Forth, Kosson & Hare, 2003), and the Antisocial Process Screening Device (APSD; Frick & Hare, 2001), each supported by extensive evidence for their reliability and validity. I also briefly describe recent attempts to develop and validate self-report scales for the assessment of psychopathy.

PSYCHOPATHY CHECKLIST-REVISED (PCL-R) The PCL-R was designed to measure the construct of psychopathy. The extensive evidence for the reliability and validity of the PCL-R led the Buros 12th Mental Measurements Yearbook to describe it as ‘state of the art. . . both clinically and in research use’ (Fulero, 1995, pp. 453–54). Following publication of the second edition of the PCL-R (Hare, 2003), the 16th Mental Measurements Yearbook referred to it as ‘the gold standard for the assessment of psychopathy’ (Acheson, 2005, pp. 429–31). It is clear that this instrument has helped to fill a diagnostic and assessment void by providing researchers and clinicians with a common metric that has demonstrated reliability and validity in an array of populations and contexts. The past decade has seen a sharp rise in its use in the courts (Walsh & Walsh, 2006). The origins of the PCL-R have been described in detail elsewhere (Hare, 1991, 2003; Hare & Neumann, 2006). Briefly, in the 1970s my colleagues and I began work on what we hoped would be a useful research tool for the assessment of the traditional clinical construct

44

VOLUME I: DIAGNOSIS AND TREATMENT

of psychopathy (Hare, 1980). These efforts resulted in a draft manuscript first circulated in 1985 and published in 1991 as the PCL-R.

Administration The PCL-R is a 20-item construct rating scale widely used in research, clinical and forensic settings for the assessment of psychopathy in adults (see Table 3.1). The scale items measure personality traits and behaviors related to traditional conceptions of psychopathy, such as impulsivity, lack of empathy, lack of remorse, irresponsibility and grandiosity (see Berrios, 1996; Cleckley, 1976; Coid, 1993; Millon, Simonsen & Birket-Smith, 1998; Pichot, 1978). Each item is rated on a three-point scale (0, 1 or 2) according to the extent to which an individual exhibits the trait or behavior being rated. The Total score varies from 0 to 40, reflecting the degree to which the individual matches the ‘prototypical’ psychopath. The standard procedure for administration of the PCL-R involves a semi-structured interview and a review of available file and collateral information (Hare, 2003). The interview typically covers education, employment and family background, relationships, substance use and antisocial behaviors from adolescence on. It may be spread over several sessions, allowing for a more representative sample of the individual’s interactional style. The interview itself has several purposes. First, certain historical information about the individual is required for scoring PCL-R items. Second, the interview often provides clues as to the individual’s interpersonal style. It also gives the assessor a chance to evaluate consistency (and deception) within the interview and between the interview and collateral information. Finally, the use of an interview allows probes and challenges when further information is required, or inconsistencies are encountered. The latter purpose is facilitated if the file Table 3.1 Items and factors in the Hare PCL-R Interpersonal 1. Glibness/superficial charm 2. Grandiose self-worth 4. Pathological lying 5. Conning/manipulative

Affective 6. Lack of remorse 7. Shallow affect 8. Lack of empathy 16. Will not accept responsibility

Lifestyle

Antisocial

3. Need for stimulation 9. Parasitic lifestyle 13. Lack of goals 14. Impulsivity 15. Irresponsibility

10. Poor behavioral controls 12. Early behavioral problems 18. Juvenile delinquency 19. Revocation conditional release 20. Criminal versatility

Note: The items are from Hare (1991, 2003). Copyright 1991 R.D. Hare and Multi-Health Systems, 3770 Victoria Park Avenue, Toronto, Ontario, M2H 3M6. All rights reserved. Reprinted by permission. Note that the item titles cannot be scored without reference to the formal criteria contained in the PCL-R Manual. Item 11, Promiscuous sexual behavior, and Item 17, Many short-term marital relationships, contribute to the Total PCL-R score but do not load on any factors. The Interpersonal and Affective factors underpin a broad factor identical with the original Factor 1 described in the 1991 Manual. The Lifestyle and Antisocial factors underpin a broad factor identical with the original Factor 2 described in the 1991 Manual, but with the addition of item 20.

PSYCHOLOGICAL INSTRUMENTS AND ASSESSMENT

45

review is conducted prior to the interview, giving the interviewer bases for challenging or probing. The second part of the assessment involves reviewing any collateral and/or file information that is available; this is a mandatory aspect of the assessment. The use of collateral information allows the rater to evaluate the truth/reliability of the information given in the interview and to gain access to primary data for scoring several of the PCL-R items. Available collateral information will depend upon the setting in which the assessment is conducted. In correctional settings files typically contain a variety of official records that may be helpful in scoring the items of the PCL-R, and usually are adequate for collateral review (Hare, 2003). In forensic psychiatric and pretrial settings, raters may have access to official reports, but may also be able to examine reports of interviews with family members, friends and employers, as well as the results of medical and psychological assessments. When dealing with nonoffenders it may be difficult to obtain sufficient collateral information, although there may be methods available for accessing some useful information, such as telephone interviews, work records, peer ratings, and so forth. Regardless of the context in which the assessment is conducted, information should come from as many different sources as possible. Scores for items should not be calculated unless there is adequate collateral information.

PCL-R Second Edition The second edition of the PCL-R was published in 2003. Although the manual for the second edition was greatly expanded, the PCL-R items and their scoring criteria remained the same as they had been in the 1991 edition. The new edition was deemed necessary for several reasons. First, I provided some guidelines to prevent misuse of the PCL-R, especially where it is used to help with adjudication and treatment decisions. Second, it was apparent that many of those who produced psychological reports for the criminal justice system or who testified in court relied primarily on material published in the 1991 manual. The inclusion of more recent research in the 2003 manual was intended to provide users with more up-to-date information about the PCL-R assessment of psychopathy, and to encourage them to keep abreast of the current literature, especially with regards to its implications for minority and legal issues. The third reason for the revision was the fact that a large amount of data had been generated since the original manual was written. The explosion in research provided a large amount of data for establishing comparison tables and for addressing issues concerning the factor structure, reliability, validity and generalizability of the PCL-R. Psychometric analyses were conducted on more than 10,000 North American and European offenders and forensic patients, and are fully detailed in the manual (Hare, 2003). Extensive descriptions of the development and psychometric properties of the PCL-R are available (e.g., Bolt, 2007; Bolt et al., 2004; Hare, 2003; Hare & Neumann, 2005, 2006; Neumann, Kosson & Salekin, 2007) and only a brief outline is provided here.

Reliability Total PCL-R scores are highly reliable when used by trained and experienced raters. The intraclass correlation (ICC) typically exceeds .80 for a single rater (ICC1 ) and .90 for the

46

VOLUME I: DIAGNOSIS AND TREATMENT

average of two raters (ICC2 ). Internal consistency (alpha coefficients of .80+ and mean inter-item correlations of .20+) is also high. The standard error of measurement (SEM) of the PCL-R total score is approximately 3 for a single rating and 2 for the average of two ratings. This means that if 100 trained raters assessed the same subject at the same time, about 68 % of the scores would fall within ±1 SEM unit of the subject’s obtained total score, and about 95 % would fall within ±2 SEM units. The SEM can be used as an estimate of ‘the reasonable limits of the true score for (an individual) with any given obtained score’ (Anastasi, 1982).

Cut Scores Investigators often adopt upper (e.g., 30) and lower (e.g., 20) PCL-R cut scores in order to conduct extreme-group analyses. The practice has proven useful for comparing and evaluating findings obtained by different investigators, and has resulted in an increase in the replication of research findings. Some researchers use a cut score for psychopathy that reflects the distribution of PCL-R scores in their own jurisdiction. For example, PCL-R scores in the United Kingdom and some European countries tend to be lower than those in North America, leading some researchers to adopt a lower cut score for psychopathy, typically around 25. The assumption here is that such a score reflects much the same level of psychopathy as a North American score of 30, an assumption that may not be correct (see next section). Problems arise when clinicians and investigators treat a cut score as if it were a sharp (or even fuzzy) dividing line between offenders and patients who are psychopaths (members of a taxon) and those who are not. The problems are compounded when the judicial system makes the same assumption (Hare, 1998b). Recent research suggests that the construct underlying the PCL-R is dimensional in nature rather than taxonic (Edens, Skeem & Douglas, 2006; Guay et al., in press). Additional research with a range of other variables and procedures relevant to psychopathy is needed before we can determine whether the psychopathy construct itself (not only as measured by the PCL-R) is better viewed as a taxon or as a dimensional construct. Meanwhile, cut scores might be viewed primarily as a methodological convenience for facilitating communication among researchers. Their utility for clinical and forensic purposes will depend on the context in which the PCL-R is used (e.g., diagnosis, risk assessment, treatment options, and so forth), as well as an appreciation of the SEM and the issues associated with the use of cut scores (Hare, 2003). Many investigators prefer to use methods that do not rely on a set cut score, such as correlation analyses, multiple regression and structural equation modeling (Hare & Neumann, 2005). In risk assessment the predictive validity of the PCL-R and other scales increasingly is being evaluated with receiver operating characteristic (ROC) analyses (see section on Assessment of Risk).

Item Response Theory (IRT) Item response theory (IRT) provides a mathematical expression of the relationship between a score on an individual item or group of items (e.g., total score) and the underlying construct or latent trait of psychopathy. IRT analyses of the large data sets described in the second edition of the PCL-R Manual (Hare, 2003) and by Bolt and colleagues (2004) indicate that

PSYCHOLOGICAL INSTRUMENTS AND ASSESSMENT

47

a score of 30 represents much the same level of the latent trait of psychopathy in North American male offenders, female offenders, male forensic psychiatric patients and male offenders assessed from file reviews. IRT analyses (Cooke, Kosson & Michie, 2001) and a meta-analytic review (Skeem et al., 2004) indicate that the PCL-R functions the same in African-American and Caucasian offenders and patients. Similarly, scores in the mid to upper range (approximately 25+) appear to reflect much the same level of psychopathy in United Kingdom and European male offenders as they do in their North American counterparts (Bolt, Hare & Neumann, 2007; Cooke et al., 2005; Hare, 2003). Lower scores appear to reflect a somewhat greater level of psychopathy in offenders in the United Kingdom and Europe than in those in North America.

Factor Structure There is an extensive empirical literature indicating that in forensic populations the items in the PCL-R measures a unitary construct (e.g., Bolt et al., 2004; Cooke & Michie, 1997; Hare, 2003; Hare & Neumann, 2005; Neumann et al., 2005). Early factor analyses indicated that the items could be organized into two broad clusters or factors. Factor 1 reflected the interpersonal and affective components of the disorder, whereas Factor 2 was more closely allied with a socially deviant (externalizing) lifestyle. Recent confirmatory factor analyses of very large data sets (Hare, 2003; Hare & Neumann, 2005; Neumann et al., 2005; Neumann, Hare & Newman, 2007) clearly indicate that a superordinate four-factor model (18 items) fits the data well: Interpersonal (glibness/superficial charm, grandiose sense of self-worth, pathological deception, conning/manipulative); Affective (lack of remorse or guilt, shallow affect, callous/lack of empathy, failure to accept responsibility for actions); Lifestyle (need for stimulation/proneness to boredom, parasitic lifestyle, lack of realistic long-term goals, impulsivity, irresponsibility); and Antisocial (poor behavioral controls, early behavior problems, juvenile delinquency, revocation of conditional release, criminal versatility). Two other items (promiscuous sexual behavior and many short-term relationships) do not load on any factor but contribute to the total PCL-R score. The pattern of correlations among the four factors, as well as confirmatory factor analyses (Hare, 2003; Hare & Neumann, 2005; Neumann et al., 2006) also indicate the presence of two broad factors, one identical with the original Factor 1 (Interpersonal/Affective) and the other the same as the original Factor 2 (Lifestyle/Antisocial), but with the addition of one item (criminal versatility). The factor structure of the PCL-R does not necessarily mean that the construct of psychopathy is similarly organized. Factor analysis can only reflect the items that go into the mix, and the inclusion of additional or different items related to psychopathy might yield somewhat different factor structures. Even with the current set of items, the use of multidimensional scaling (MDS), while supporting the four-factor structure, also suggests that other dimensions might be useful in understanding the nature of psychopathy (Bishopp & Hare, in press). Similarly, the use of complementary measurement methods, such as self-reports (see below), may provide additional perspectives on the structure and nature of psychopathy. The factor structure of the PCL-R (and its derivatives; see below) is of more than academic interest. For example, clinicians may describe an individual offender, patient or client in terms of the score on each of the four factors, thus developing a profile that helps to provide a more finely detailed picture of the individual (Hare, 2003; Herv´e, 2007b; O’Toole, 2007).

48

VOLUME I: DIAGNOSIS AND TREATMENT

Further, recent evidence, discussed in the section on Assessment of Risk, indicates that the inclusion of the Antisocial factor changes the pattern of correlations that the other factors have with violent outcomes.

Generalizability Although developed primarily with data from North American male offenders and forensic patients, the psychometric and predictive properties of the PCL-R now are well established in a variety of other offender and patient populations, including females, substance abusers and sex offenders. The PCL-R and the PCL: SV have been translated into several languages, including Swedish, Norwegian, Dutch, German, Spanish, Portuguese, Bulgarian, Russian, Japanese and Korean. The available evidence indicates that these instruments have much the same psychometric properties and correlates in other countries as in North America. They have good cross-cultural generalizability, although IRT analyses suggest that there may be ethnic and cultural differences in the way some features of psychopathy are manifested (e.g., Bolt et al., 2004; Bolt, Hare & Neumann, 2007; Cooke et al., 2005; Hare, 2003; Sullivan & Kosson, 2006). The Interpersonal and Affective features appear to be more stable across cultures than are some of the Lifestyle and Antisocial features.

Validity The PCL-R was designed to measure the clinical construct of psychopathy. However, because of its demonstrated ability to predict recidivism, violence and treatment outcome in a variety of populations (criminal, forensic psychiatric, civil psychiatric) the PCL-R routinely is used in risk assessments, either on its own or, more appropriately, as part of a battery of variables and factors relevant to offending and violence. Because there are no exclusion criteria for its use offenders and patients with a variety of psychiatric disorders may be assessed with the PCL-R. This means that psychopathy might be viewed as co-morbid with other disorders, but the dimensional nature of the construct measured by the PCL-R and its factors (Edens et al., 2006; Guay et al., in press) suggests that a likely scenario is an overlap of symptoms. In any case, the combination of a history of violence, an Axis I disorder and a high PCL-R score has particular significance for the assessment of risk (see below). Evidence for the validity of the PCL-R and the construct it measures is extensive (see Hare, 2003; Herv´e &Yuille, 2007; Newman et al., 2007; Patrick, 2006), and comes from research examining relationships to a variety of other instruments and scales, associations with behavioral data, such as recidivism and violence, and basic laboratory research involving information processing, functional magnetic resonance imaging, electrocortical activity and biochemical correlates. This research is discussed in detail elsewhere (e.g., Blair, Mitchell & Blair, 2005; Hare, 2003; Herba et al., 2007; Herpertz & Saß, 2000; Kiehl, 2006; Patrick, 2006).

Associations With Other Measures The PCL-R is significantly correlated, in expected directions, with various self-report measures of psychopathy, and with relevant scales in omnibus personality inventories that

PSYCHOLOGICAL INSTRUMENTS AND ASSESSMENT

49

measure general and psychopathological personality characteristics (Hare, 2003; Lilienfeld & Fowler, 2006; Widiger, 2006). The pattern of correlations between the PCL-R and psychiatric diagnoses is consistent with the clinical conception of psychopathy. These psychiatric diagnoses include Axis I and II disorders in the various editions of the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSMIII, DSM-III-R, DSM-IV), as well as the personality disorders listed in the 10th edition of the International Classification of Diseases and Related Disorders (ICD-10; World Health Organization, 1990). Their associations with the PCL-R are summarized in Hare, 2003 (also see Hildebrand & de Ruiter, 2004; Ullrich & Marneros, 2004).

ICD-10 and DSM-IV The attributes measured by the PCL-R are similar in many respects to the diagnostic criteria for dissocial personality disorder listed in ICD-10 (Widiger et al., 1996). However, they differ in important ways from the criteria for antisocial personality disorder (APD) contained in DSM-IV (American Psychiatric Association, 1994). The diagnostic criteria for APD reflect the assumptions that it is difficult for clinicians to assess personality traits reliably, and that early-onset delinquency is a cardinal symptom of the disorder (Robins, 1978). These assumptions account for the heavy emphasis on delinquent and antisocial behavior in the criteria for APD (Hare & Hart, 1995; Rogers et al., 2000; Widiger et al., 1996). In forensic populations the prevalence of APD is much higher (> 50%) than the prevalence of psychopathy (< 30%), resulting in an asymmetric association between the PCL-R and APD. In this respect, it is noteworthy that APD is strongly associated with the PCL-R Lifestyle and Antisocial factors, but only weakly associated with the PCL-R Interpersonal and Affective factors. Most psychopaths meet the criteria for APD, but most of the offenders with APD are not psychopaths. Yet, DSM-IV says that APD ‘has also been referred to as psychopathy’ (p. 655), effectively equating the two constructs. The Associated Features and Disorders section for APD (both in DSM-IV and in the DSM-IV Text Revision; American Psychiatric Association, 2000) compounds the problem by suggesting that in forensic populations the diagnosis of APD may be facilitated by assessing traits and behaviors imported (without attribution or scoring instructions) from the 10-item Psychopathy Criteria Set that my colleagues and I had derived from the PCL-R and PCL: SV for use in the DSM-IV Field Trial for APD (Widiger et al., 1996). Had these imported traits been required for a diagnosis of APD, rather than being made optional in forensic contexts, the relation between psychopathy and APD would have been strengthened. Rogers et al. (2000) had this to say about the situation: ‘As noted by Hare (1998), DSM-IV does considerable disservice to diagnostic clarity in its equating of APD to psychopathy’ (pp. 236–37). Or, as Lykken (2006, p. 4) put it, ‘Identifying someone as “having” APD is about as nonspecific and scientifically unhelpful as diagnosing a sick patient as having a fever or an infectious or a neurological disorder.’ Following their analyses of ICD-10 personality disorders Ullrich and Marneros (2004) had this to say: ‘Although suggestions to replace ASPD in DSM-IV with the construct of psychopathy were previously rejected, its importance within forensic contexts is established. Against the background of our findings, we conclude that specific dimensions of personality disorders are strongly interrelated and show remarkable similarities to the personality features constituting psychopathy’ (pp. 211–12). A similar conclusion was drawn by Livesley and Schroeder (1991).

50

VOLUME I: DIAGNOSIS AND TREATMENT

As things stand, the PCL-R and its derivatives do not measure the same construct as does APD, either in males or in females (Warren & South, 2006). It is perhaps then ironic that the development of both the PCL-R and the DSM-III criteria for APD owe much to the NATO Advanced Study Institute (ASI) that I directed in Les Arcs, France in 1975 (see Hare, 1997, 2007; Hare & Schalling, 1978). The ASI made the attendees (including Lee Robins, who played an important role in DSM-III) painfully aware of the need for a sound measure of psychopathy. The DSM-III solution was to use readily scored antisocial items as diagnostic criteria, whereas my colleagues and I chose to develop procedures that would allow for the reliable assessment of both personality traits and behaviors relevant to traditional conceptions of psychopathy.

DERIVATIVE MEASURES The PCL-R has been used primarily with criminal and forensic psychiatric populations, with occasional extensions to the general community. Part of its strength is the requirement that in order to score an item the rater has to supplement an in-depth interview with extensive collateral information. During the planning phase in the late 1980s of what was to become the MacArthur Study of Mental Disorder and Violence in civil psychiatric patients (see Monahan et al., 2001), it became evident that a potentially important risk factor for violence was psychopathy. I was asked if it would be possible to develop a version of the PCL-R that reduced the amount of time, effort and information required for a reliable assessment. The result was the PCL: SV. As it turned out, the PCL: SV was the single most important risk factor for violence in the study population (Steadman et al., 1999).

PCL: SV The PCL: SV consists of 12 items derived from the PCL-R, each scored on a three-point scale (0, 1, 2) on the basis of interview and collateral information that is less extensive than that required for scoring the PCL-R. Total scores can vary from 0 to 24. It is conceptually and empirically related to the PCL-R (Cooke et al., 1999; Hart et al., 1995), and can be used as an effective screen for psychopathy in forensic populations (Guy & Douglas, 2006) or as a stand-alone instrument for research with noncriminals, including civil psychiatric patients (as in the MacArthur study). Its psychometric properties and four-factor structure (see Table 3.2) are much the same as those of the PCL-R (Hill, Neumann & Rogers, 2004; Vitacco, Neumann & Jackson, 2005). There is rapidly accumulating evidence for the construct validity of the PCL: SV, including its ability to predict aggression and violence in offenders and in both forensic and civil psychiatric patients (see below). In this respect, the correlates of the PCL: SV are much the same as those of the PCL-R.

PCL: YV The PCL: YV (Forth, Kosson, & Hare, 2003) is an age-appropriate modification of the PCL-R intended for use with adolescents. Like the PCL-R, it consists of 20 items and four factors (Jones et al., 2006; Neumann et al., 2006). The items are presented in Table 3.3. It

PSYCHOLOGICAL INSTRUMENTS AND ASSESSMENT

51

Table 3.2 Items and factors in the Hare PCL: SV Interpersonal

Lifestyle

1. Superficial 2. Grandiose 3. Deceitful

7. Impulsive 9. Lacks goals 10. Irresponsibility

Affective

Antisocial

4. Lacks remorse 5. Lacks empathy 6. Doesn’t accept responsibility

8. Poor behavioral controls 11. Adolescent antisocial behavior 12. Adult antisocial behavior

Note: The items are from Hart, Cox & Hare (1995). Copyright 1995 R.D. Hare and Multi-Health Systems, 3770 Victoria Park Avenue, Toronto, Ontario, M2H 3M6. All rights reserved. Reprinted by permission. Note that the item titles cannot be scored without reference to the formal criteria contained in the PCL:SV Manual.

appears to have much the same psychometric properties and much the same correlates as its adult counterpart (see Book et al., 2006; Salekin et al., 2004; Vitacco et al., 2006). Like the PCL-R, it appears to generalize well across ethnic groups and countries (e.g., Book et al., 2006; Dolan & Rennie, 2006; McCoy & Edens, 2006; Schrum & Salekin, 2006). Although there is little doubt about the reliability and validity of the PCL: YV, concerns arise with respect to its use in the criminal justice system. The main issues have to do with: (i) the dangers of labeling an adolescent as a psychopath; (ii) the implications of the PCL: YV for classification, sentencing and treatment; (iii) the possibility that some features measured by the PCL: YV are found in normally developing youth; and (iv) the degree of stability of psychopathy-related traits from late childhood to early adulthood. Extensive discussions of these issues are available elsewhere (e.g., Book et al., 2006; Forth & Book, 2007; Frick, 2007; Frick & Marsee, 2006; Lynam & Gudonis, 2005; Salekin, 2006; Vitacco & Vincent, Table 3.3 Items and factors in the PCL: YV Interpersonal 1. Impression management 2. Grandiose sense of self-worth 4. Pathological lying 5. Manipulation for personal gain

Affective 6. Lack of remorse 7. Shallow affect 8. Callous/lack of empathy 16. Will not accept responsibility

Behavioral

Antisocial

3. Need for stimulation 9. Parasitic orientation 13. Lack of goals 14. Impulsivity 15. Irresponsibility

10. Poor anger control 12. Early behavioral problems 18. Serious criminal behavior 19. Serious violations of release 20. Criminal versatility

Note: The items are from Forth, Kosson & Hare (2003). Copyright 2003 R.D. Hare and Multi-Health Systems, 3770 Victoria Park Avenue, Toronto, Ontario, M2H 3M6. All rights reserved. Reprinted by permission. Note that the item titles cannot be scored without reference to the formal criteria contained in the PCL: YV Manuals. Item 11, Impersonal sexual behavior, and Item 17, Unstable interpersonal relationships, contribute to the total PCL: YV score but do not load on any factors.

52

VOLUME I: DIAGNOSIS AND TREATMENT

2006). Briefly, although psychopathy and its features do not suddenly emerge in early adulthood, it nonetheless would be inappropriate to label an adolescent or to use a high PCL: YV score as a basis for a harsher sentence or for exclusion from treatment. Although some adolescents may exhibit some features of psychopathy in certain contexts or for a limited time, a high score on the PCL: YV requires evidence that the traits and behaviors are extreme and that they are manifested across social contexts and over substantial time periods. High ratings of psychopathic traits are rare in community youth (Forth et al., 2003). As Lynam and Gudonis (2005, pp. 401–2) put it following their review of the literature, ‘psychopathy in juveniles looks much like psychopathy in adults. The same traits characterize these individuals at different developmental time points. Additionally, juvenile psychopathy acts like adult psychopathy. Like their adult counterparts, psychopathic juveniles are serious and stable offenders. They are prone to externalizing disorders. . . .as far as has been observed, juvenile psychopathy appears quite stable across adolescence. All of these findings replicate those observed in studies using psychopathic adults’.

Antisocial Process Screening Device (APSD) The APSD (Frick & Hare, 2001) is a teacher/parent rating scale for use with children from 6 to 13 years of age. It consists of 20 scaled items that measure three dimensions of behavior thought to be precursors to psychopathic traits: Callous/unemotional (CU); Narcissism; and Impulsivity. Research with the APSD is increasing rapidly, with considerable evidence that CU traits in particular are related to a variety of disruptive behaviors, and are relatively stable over three- or four-year periods (Dadds et al., 2005; Frick & Marsee, 2006).

Self-Report Measures Self-report psychopathy scales are beginning to broaden the repertoire of available assessment tools, and show promise of helping us to understand better the construct they purport to measure. These include the Psychopathy Personality Inventory (PPI; Lilienfeld & Andrews, 1996); the Youth Psychopathic Traits Inventory (YPI; Andershed et al., 2002); and the experimental four-factor version of the Self-Report Psychopathy (SRP) scale (SRP-E; Williams, Paulhus & Hare, 2007). These and omnibus personality inventories, including the Multidimensional Personality Questionnaire (MPQ; Tellegen, in press) and the various instruments used in the Five-Factor Model (FFM) of personality (Costa & McCrae, 1992; Costa & Widiger, 2002; Lynam, 2002), are beginning to play an important role in delineating and elucidating the nomological network, behavioral genetics and early antecedents of psychopathy. Benning et al. (2005) suggest that the PCL-R can be used as an ‘anchor for the burgeoning nomological network of psychopathy’ (p. 271). Recent empirical research indicates that self-report scales related to psychopathy have moderate predictive validity with respect to recidivism (see Lilienfeld & Fowler, 2006). The SRP-III scale is a significant predictor of a variety of unethical and antisocial behaviors in college students (Nathanson, Paulhus, & Williams, 2007; Williams et al., 2007). There are several advantages and disadvantages to using specialized and general scales of this sort for the study of psychopathy (Lilienfeld & Fowler, 2006; Westen & Weinberger, 2004). They make it possible to use very large samples, in both forensic and other populations. They broaden the nomological network by extending to the general population some

PSYCHOLOGICAL INSTRUMENTS AND ASSESSMENT

53

of the research paradigms found useful in experimental/laboratory research with forensic populations. Further, by viewing psychopathy from different perspectives, including that of the individual under study (self-reports), these scales may lead to a more complete and accurate conceptualization of the construct when combined with other measures. And of course they also make the researcher’s task much easier, because most of the assessment work is done by the study participants, who provide their own managed view of themselves. However, we should recognize that psychopathic individuals are particularly prone to impression management (Cooper & Yuille, 2007). We also should take pains to ensure that the nomological net is not cast too wide or in the wrong place, and that the construct putatively under investigation really is what we think it is. As Rutter (2005) put it in his commentary on a special journal issue on adolescent psychopathy, some of the core features of psychopathy ‘. . . may not be best represented by scores on personality dimensions that are designed to pick up rather different features’ (p. 500).

PSYCHOPATHY AND CRIME In the past few years there has been a dramatic change in the perceived and actual role played by psychopathy in the criminal justice system. Formerly, a prevailing view was that clinical diagnoses such as psychopathy were of little value in understanding and predicting criminal behaviors. More recently, the importance of psychopathy, particularly as measured by the PCL-R and its derivatives, is widely recognized, both by forensic clinicians (e.g., Lally, 2003) and by the courts (e.g., Walsh & Walsh, 2006). This is not surprising, given that many of the characteristics important for inhibiting antisocial and violent behavior – empathy, close emotional bonds, fear of punishment, guilt – are lacking or seriously deficient in psychopaths. Moreover, their egocentricity, grandiosity, sense of entitlement, impulsivity, general lack of behavioral inhibitions and need for power and control, constitute what might be described as the perfect prescription for the commission of antisocial and criminal acts (Hare, 2003; Porter & Porter, 2007). This would help to explain why psychopaths make up only about 1 % of the general population but as much as a quarter of our prison populations. It also would explain why they find it so easy to victimize the vulnerable and to use intimidation and violence as tools to achieve power and control over others. Their impulsivity and poor behavioral controls may result in ‘reactive’ forms of aggression of violence, but other features (e.g., lack of empathy, shallow emotions) also make it relatively easy for them to engage in aggression and violence that is more predatory, premeditated, instrumental or ‘cold-blooded’ in nature (Cornell et al., 1996; Hare, 2003; Meloy, 2002; Porter & Woodworth, 2006; Williamson, Hare & Wong, 1987; Woodworth & Porter, 2002). Interestingly, some clinicians have reported that they feel uneasy or threatened while in the presence of a psychopath, feelings that Meloy and Meloy (2003, p. 21) describe as part of an evolutionary-based reaction to an ‘intraspecies predator’.

ASSESSMENT OF RISK Extensive discussions of the theories and methodologies of risk assessment are provided elsewhere (e.g., see Monahan & Steadman, 1994; Monahan et al., 2001; Quinsey et al., 1998). The latest generation of risk assessment instruments largely has dispelled the

54

VOLUME I: DIAGNOSIS AND TREATMENT

belief that useful predictions cannot be made about criminal behavior. Much of the recent debate is concerned with the relative effectiveness of actuarial instruments and structured clinical assessments. The former are empirically derived sets of static (primarily criminal history, demographic) risk factors, and include the Violent Risk Appraisal Guide (VRAG; Quinsey et al., 1998), and the Sex Offender Risk Appraisal Guide (SORAG; Quinsey, Rice & Harris, 1995), instruments that improve considerably on unstructured clinical judgments or impressions. However, procedures that include structured clinical decisions based on specific criteria, are proving to be at least as good as purely actuarial scales. For example, the HCR-20: Assessing Risk for Violence (Webster et al., 1997) assesses 10 historical (H) variables, five clinical (C) variables and five risk management (R) variables. Because of its importance in the assessment of risk, psychopathy, as measured by the PCL-R or the PCL: SV, is included in the VRAG, SORAG and HCR-20, as well as in the Sexual Violence Risk-20 (SVR-20; Boer et al., 1997). A detailed account of psychopathy as a risk for recidivism and violence is beyond the scope of this chapter. However, its significance as a robust risk factor for institutional problems, for recidivism in general, and for violence in particular, is now well established (see meta-analyses and reviews by Buffington-Vollum et al., 2002; Cunningham, Sorensen & Reidy, 2005; Dolan & Doyle, 2000; Douglas et al., 2006; Gendreau, Goggin & Smith, 2002; Hemphill, 2007; Hemphill & Hare, 2004; Porter & Woodworth, 2006; Salekin, Rogers & Sewell, 1996; Walters, 2003). The predictive value of psychopathy applies not only to adult male offenders but also to adult female offenders (e.g., Jackson & Richards, 2007; Verona & Vitale, 2006), adolescent offenders (e.g., Forth et al., 2003; Gretton, Hare & Catchpole, 2004; Stafford & Cornell, 2003), and forensic psychiatric patients, including those with Axis I disorders (e.g., Dolan & Davies, 2006; Doyle, Dolan & McGovern, 2002; Hill, Rogers & Bickford, 1996; Heilbrun et al., 1998; Rice & Harris, 1992; Tengstr¨om et al., 2004; Tengstr¨om et al., 2000; Tengstr¨om et al., 2006). Psychopathy also is increasingly being seen as an important factor in explaining domestic violence (Spidel et al., 2007). Leistico, Salekin, Decoster and Rogers (in press) recently have provided a comprehensive meta-analysis of psychopathy and antisocial conduct.

ROC Analyses Many investigators use receiver operating characteristic (ROC) analyses to determine the predictive ability of instruments (Mossman, 1994; Quinsey et al., 1998). An ROC curve is a plot of true positives (sensitivity) against false positives (1 minus specificity), with respect to an outcome variable, at different PCL-R (or other) scores. If the outcome variable is recidivism, for example, the area under the curve (AUC; the area between the curve and the diagonal) represents the probability that a randomly selected recidivist will have a higher PCL-R score than will a randomly selected nonrecidivist. AUCs for the PCL-R and PCL: SV in North American samples of offenders and forensic psychiatric patients typically fall between .70 and .80, and frequently are not significantly different from the AUCs obtained with purpose-built risk tools, such as the VRAG and the HCR-20, that include one of these measures of psychopathy (e.g., Douglas, Yeomans & Boer, 2005; Hare, 2003). Similar results have been obtained with the PCL-R or PCL: SV in studies of offenders and forensic psychiatric patients in Europe and the United Kingdom, including: violent recidivism by Dutch forensic psychiatric patients (de Vogel et al., 2004);

PSYCHOLOGICAL INSTRUMENTS AND ASSESSMENT

55

violent recidivism by German prison inmates and forensic psychiatric patients (Stadtland et al., 2005); general and violent recidivism by German prison inmates (Dahle, 2006); violent recidivism by Swedish rapists (Sj¨ostedt & L˚angstr¨om, 2002); violent recidivism by Belgium prison inmates and forensic psychiatric patients (Pham et al., 2005); violent recidivism by Swedish violent offenders (Tengstr¨om, 2001); and physical violence and institutional aggression by English forensic patients with schizophrenia (Dolan & Davies, 2006). There is some evidence that the predictive validity of the PCL-R and the HCR-20 among criminals (also see next section) can be improved by using them as part of a classification tree analysis (e.g., Dahle, 2006).

Civil Psychiatric Patients The predictive validity of psychopathy is not confined to forensic populations (Douglas, Ogloff & Nicholls, 1997; Steadman et al., 1999). The article by Steadman and colleagues (1999) was a report of the MacArthur Foundation’s findings on risk for violence in civil psychiatric patients. The most extensive and thorough study of its sort ever conducted, it evaluated 134 potential predictors of violence in 939 patients following discharge from a civil psychiatric facility. In presenting their results, the authors used a ‘classification tree’ approach in which a hierarchy of decisions is made about the risk posed by a given patient. The single best predictor was the PCL: SV, developed for use in the study. In this scheme, the first decision is whether or not the patient has a PCL: SV score of 13 or more. Silver et al. (1999) used a subsample of these patients to investigate the impact that neighborhood factors have on individual risk factors for violence in discharged patients. Again, the single best predictor of violence was the PCL: SV. Although patients discharged into neighborhoods with ‘concentrated poverty’ generally were at higher risk for violence than were those discharged into neighborhoods with less poverty, this did not apply to patients with high PCL: SV scores. That is, their risk of the latter patients was independent of the neighborhood into which they were discharged. In a recent reanalysis of the MacArthur data, Vitacco et al. (2005) found that when using the three-factor model only the Affective factor was significantly correlated with violence at 20 weeks. However, when the four-factor model was used the predictive power of the Affective factor increased and the Antisocial factor was a strong predictor. A similar result was obtained by Vitacco et al. (2006) in their analysis of the association between the PCL: YV and instrumental aggression. They reported that the association of the PCL: YV factors with instrumental aggression in the three-factor model changed with the addition of the Antisocial factor. Harris, Rice and Camilleri (2004) applied a modified 10-item version of the VRAG to the MacArthur data and reported that its predictive validity was almost as high as that of the classification tree approach used by Steadman and colleagues (1999). Of the items in this version of the VRAG, the PCL: SV was by far the best predictor. Harris and colleagues (2004) commented that even if the base rate of psychopathy or psychopathic features in a population is relatively low, ‘. . . the personality traits associated with psychopathy are among the most important causes of aggression’ (p. 1070). Indeed, a reanalysis of the Harris et al. (2004) data by Edens, Skeem and Douglas (2006) showed that the predictive power of the modified, 10-item version of the VRAG was entirely due to the presence of the PCL: SV.

56

VOLUME I: DIAGNOSIS AND TREATMENT

INSTITUTIONAL PROBLEMS There is a moderate association between PCL-R/PCL: SV scores and measures of institutional adjustment (see Hare, 2003. Also see meta-analyses by Buffington-Vollum et al., 2002; Cunningham, Sorenson & Reidy, 2005; Guy et al., 2005; Walters, 2003). Institutional misconduct includes a range of behaviors from verbal infractions to assault with a weapon. Guy and colleagues (2005) reported that the effect sizes for the PCL-R prediction of institutional misconduct were not as large in American institutions as are those typically obtained in other countries. The reasons for this finding are unclear, but it may be related to differences between America and other countries in the role of gangs in managing institutional behavior, and in base rates for psychopathy and institutional misconduct.

SEXUAL VIOLENCE The last few years have seen a sharp increase in public and professional attention paid to sex offenders, particularly those who commit a new offense following release from a treatment program or prison. It has long been recognized that psychopathic sex offenders present special problems for therapists and the criminal justice system. In general, the prevalence of psychopathy, as measured by the PCL-R, is much lower in child molesters than in rapists or ‘mixed’ offenders (Hare, 2003; Porter et al., 2000). Quinsey, Rice and Harris (1995) concluded from their research that psychopathy functions as a general predictor of sexual and violent recidivism. Not only are the offenses of psychopathic sex offenders likely to be more violent than those of other sex offenders, they tend to be more sadistic (Hare, 2003; Harris et al., 2003). In extreme cases – for example, among serial killers – co-morbidity of psychopathy and sadistic personality is very high (Hare, Cooke & Hart, 1999; Stone, 1998). In their PCL-R study of murderers, Porter et al. (2003) concluded that ‘not only are psychopathic offenders disproportionately more likely to engage in sexual homicide (than are other murderers), but, when they do, they use significantly more gratuitous and sadistic violence’ (p. 467).

Deadly Combination One of the most potent combinations to emerge from the recent research on sex offenders is psychopathy coupled with evidence of deviant sexual arousal. Rice and Harris (1997) reported that sexual recidivism was strongly predicted by a combination of a high PCLR score and deviant sexual arousal, defined by phallometric evidence of a preference for deviant stimuli, such as children, rape cues or nonsexual violence cues. Several studies indicate that psychopathy and behavioral or structured clinical evidence of deviant sexual arousal also is a strong predictor of sexual violence (Harris & Hanson, 1998; Hildebrand, de Ruiter & de Vogel, 2004; Serin, Mailloux & Malcolm, 2001). Gretton et al. (2001) found that this combination was highly predictive of general and violent re-offending in adolescent sex offenders. Recently, Harris and colleagues (2003) reported that in a large-sample study involving four sites the psychopathy–sexual deviance combination was predictive of violent recidivism in general, both sexual and nonsexual. The authors commented, ‘Because

PSYCHOLOGICAL INSTRUMENTS AND ASSESSMENT

57

of the robustness of this (psychopathy × sexual deviance) interaction and its prognostic significance, its inclusion in the next generation of actuarial instruments for sex offenders should increase predictive accuracy’ (p. 421) of general violent recidivism.

SOME CAUTIONS Although the research evidence for the reliability and validity of the PCL-R and its derivatives is extensive, this does not ensure that an individual assessment will be reliable or valid. In a research context misuse of these instruments will have few negative consequences for the individual. However, when the scores are used in clinical and criminal justice contexts the implications of misuse are potentially very serious, especially if the scores are used to guide treatment or adjudication decisions (Edens, 2001; Hare, 1998b, 2003). In addition, it is important when conducting an assessment to use all information available to provide a complete picture of the person. In each case the PCL-R must be used properly and in accordance with the highest ethical and professional standards. The items must be scored in accordance with the criteria listed in the Manual, or not scored at all. Clinicians who use the PCL-R or its derivatives must be prepared to outline the information used to score the items and to explain and justify the manner in which they scored the items. They must take into account measurement error (Hare, 2003) and the probabilistic nature of risk assessments. They also should be aware of the fact that many prosecutors and defense attorneys are familiar with the PCL-R, its uses and its limitations (see Book et al., 2006).

TREATMENT Unlike most other offenders, psychopaths suffer little personal distress, see little wrong with their attitudes and behavior, and seek treatment only when it is in their best interests to do so, such as when seeking probation or parole. They derive little benefit from traditional prison programs, particularly those aimed at the development of empathy, conscience and interpersonal skills (Harris & Rice, 2006, 2007; Richards, Casey & Lucente, 2003; Thornton & Blud, 2007; Wong & Hare, 2005). Indeed, there have been reports that some programs designed to modify the behavior of psychopathic offenders resulted in an increase in post-release criminal behavior (Hare et al., 2000; Rice, Harris & Cormier, 1992). These were group therapy and insight-oriented programs that presumably help psychopaths to develop better ways of manipulating, deceiving and using people, but do little to help them to understand themselves. Programs that do not take into account the nature of psychopathic offenders are unlikely to be effective. Hobson, Shine and Roberts (2000) found that offenders with high PCL-R scores obtained on admission to a well-developed prison therapeutic community program engaged in a variety of counter-productive behaviors during later therapy sessions. Their behaviors included manipulation of the system to satisfy a personal need for power, control and prestige, playing ‘head games’ with other inmates and staff, continually testing the boundaries, exploitation of other patients, and a lack of genuine interest in changing their own attitudes and behaviors. Nevertheless, they managed to manipulate and fool some staff into thinking their efforts were sincere and that they were making good progress. Not surprisingly, there is some evidence that psychopathic sex offenders are able to manipulate skilled therapists into concluding that they have made good progress (Looman et al., 2005).

58

VOLUME I: DIAGNOSIS AND TREATMENT

However, earlier reports of the unusually high sexual re-offense rate of sex offenders with elevated PCL-R scores who had been rated as having made good progress in therapy have not been replicated (Barbaree, 2005). Langton et al. (2006) reported that among treated sex offenders it is psychopathy, not ratings of treatment success, that is a significant predictor of post-release sexual behavior. Further, they reported that psychopathic offenders with poor treatment ratings re-offended faster than did other offenders. This does not mean that the attitudes and behaviors of psychopathic offenders and patients are immutable or that ‘nothing works’ (Wong & Burt, 2007; Wong & Hare, 2005; D’Silva, Duggan & McCarthy, 2004). But it is clear that traditional programs, particularly those that are emotion- or insight-oriented, are ineffective and that the task of bringing the behaviors of psychopathic individuals into line with societal expectations is a formidable one (Wong & Hare, 2005). What then? Do we simply keep them in prison until they are old enough to pose little risk to society? Do we ask psychopaths to participate in treatment programs that have little chance of success and that fool them and others into thinking that the exercise is worthwhile and of practical benefit to them? Rather than being discouraged, we should mount a concerted effort to develop innovative procedures designed specifically for psychopathic offenders. L¨osel (1998), Thornton and Blud (2007), and Wong and Hare (2005) have discussed the issues involved in the treatment and management of psychopathic and other offenders, and have outlined in some detail the requirements for an effective program. Thornton and Blud (2007) have discussed the implications of the four-factor model of psychopathy for working with offenders. An extensive set of program guidelines for development of a program specifically designed for psychopaths is now available (Wong & Hare, 2005). In brief, we propose that relapse-prevention techniques and risk/needs/responsivity principles (Andrews & Bonta, 2003; Andrews, Bonta & Wormith, 2006) should be integrated with elements of the best available cognitive-behavioral correctional programs. The program is less concerned with developing empathy and conscience or effecting changes in personality than with convincing participants that they alone are responsible for their behavior, and that they can learn more prosocial ways of using their strengths and abilities to satisfy their needs and wants. It involves use of relapse prevention and risk/needs/responsivity principles (Andrews & Bonta, 2003; Andrews, Bonta & Wormith, 2006), tight control and supervision, both in the institution and following release into the community, and comparisons with carefully selected groups of untreated offenders or offenders treated in standard correctional programs. The program would permit empirical evaluation of its treatment and intervention modules (what works and what doesn’t work for particular individuals). That is, some modules or components might be effective with psychopaths but not with other offenders, and vice versa. Because correctional programs are constantly in danger of erosion because of changing institutional priorities, community concerns and political pressures, we proposed stringent safeguards for maintaining the integrity of the program. A key element of any program that hopes to be effective with psychopathic offenders and patients is the availability of a highly trained staff and cooperation of all levels of administration. A recent study by Wong et al. (2006) offers some promise that such a program may have a beneficial effect on psychopathic offenders. Wong et al. (2006) found that although completion of the program did not reduce the recidivism rate or time to reoffense of psychopathic offenders, it appeared to reduce the seriousness of the offenses committed, as reflected in the average length of the sentence for a new offense.

PSYCHOLOGICAL INSTRUMENTS AND ASSESSMENT

59

CONCLUSIONS There is a substantial amount of empirical evidence that psychopathy, as measured by the PCL-R and its derivatives, is a predictor of recidivism and violence in prison, forensic psychiatric and civil psychiatric populations. Indeed, the PCL-R is one of the most generalizable of the risk factors identified thus far, and for this reason it is included in a variety of actuarial and structured-clinical risk assessment procedures. Although psychopathy is not the only risk factor for recidivism and violence, it is unusually pervasive and too important to ignore, particularly with respect to violence. Treatment and management are difficult, time-consuming and expensive, but new initiatives based on current theory and research on psychopathy and the most effective correctional philosophies may help to reduce the harm done by psychopaths.

REFERENCES Acheson, S.K. (2005). Review of the Hare Psychopathy Checklist-Revised, 2nd edition. In R.A. Spies & B.S. Plake (eds.), The Sixteenth Mental Measurements Yearbook (pp. 429–31). Lincoln, NE: Buros Institute of Mental Measurements. American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. Washington, DC: American Psychiatric Association. American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision. Washington, DC: American Psychiatric Association. Anastasi, A. (1982). Psychological Testing (5th edn.). London: Collier Macmillan. Andershed, H., Kerr, M., Stattin, H. & Levander, S. (2002). Psychopathic traits in non-referred youths: a new assessment tool. In E. Blauw & L. Sheridan (eds.), Psychopaths: Current International Perspectives (pp. 131–58). The Hague: Elsevier. Andrews, D.A. & Bonta, J. (2003). The Psychology of Criminal Conduct, 3rd edition. Cincinnati, OH: Anderson. Andrews, D.A., Bonta, J. & Wormith, J. S. (2006). The recent past and near future of risk and/or need assessment. Crime & Delinquency, 52, 7–27. Babiak, P. (2007). From darkness into light: psychopathy in industrial and organizational psychology. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 411–28). Mahwah, NJ: Lawrence Erlbaum. Babiak, P. & Hare, R.D. (2006). Snakes in Suits: When Psychopaths Go To Work. New York: Harper/Collins. Barbaree, H.E. (2005). Psychopathy, treatment behavior, and recidivism: an extended follow-up of Seto and Barbaree (1999). Journal of Interpersonal Violence, 20, 1115–31. Benning, S.B., Patrick, C.J., Salekin, R.T. & Leistico, A.M.R. (2005). Convergent and discriminant validity of psychopathy factors assessed via self-report: A comparison of three instruments. Assessment, 12, 270–89. Berrios, G.E. (1996). The History of Mental Symptoms: Descriptive Psychopathology since the Nineteenth Century. Cambridge, UK: Cambridge University Press. Bishopp, D. & Hare, R.D. (in press). A multidimensional scaling analysis of the Hare PCL-R. Psychology, Crime, and Law. Blair, R.J.R. (2005). Applying a cognitive neuroscience perspective to the disorder of psychopathy. Development and Psychopathology, 17, 865–91. Blair, R.J.R., Mitchell, D. & Blair, K. (2005). The Psychopath: Emotion and the Brain. New York: Blackwell. Blonigen, D.M., Hicks, B.R., Kreuger, R.F. et al. (2005). Psychopathic personality traits: heritability and genetic overlap with internalizing and externalizing psychopathology. Psychological Medicine, 35, 637–48.

60

VOLUME I: DIAGNOSIS AND TREATMENT

Boer, D.P., Hart, S.D., Kropp, P.R. & Webster, C.D. (1997). Manual for the Sexual Violence Risk20. Professional Guidelines for Assessing Risk of Sexual Violence. Vancouver, Canada: British Columbia Institute on Family Violence. Bolt, D.M. (2007). Analyzing the Psychopathy Checklist-Revised (PCL-R) using item response theory and factor analysis: overview and recent advances. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 105–39). Mahwah, NJ: Lawrence Erlbaum. Bolt, D.M., Hare, R.D. & Neumann, C.S. (2007). Score metric equivalence of the PCL-R across North American and UK criminal offenders: a critique of Cooke et al. (2005) and new analyses. Assessment, 14, 44–56. Bolt, D., Hare, R.D., Vitale, J. & Newman, J.P. (2004). Multigroup IRT analyses of the Hare Psychopathy Checklist-Revised (PCL-R). Psychological Assessment, 16, 155–68. Book, A.S., Clark, H.J., Forth, A.E. & Hare, R.D. (2006). The PCL-R and PCL: YV: forensic applications and limitations. In R.P. Archer (ed.), Forensic Uses of Clinical Assessment Instruments (pp. 147–79). Mahwah, NJ: Lawrence Erlbaum. Buffington-Vollum, J.K., Edens, J.F. et al. (2002). Psychopathy as a predictor of institutional misbehaviour in sex offenders: a prospective replication. Criminal Justice and Behavior, 29, 497–511. Cleckley, H. (1941). The Mask of Sanity. St. Louis, MO: Mosby. Cleckley, H. (1976). The Mask of Sanity, 5th edition. St. Louis, MO: Mosby. Coid, J.W. (1993). Current concepts and classifications of psychopathic disorder. In P. Tyrer & G. Stein (eds.), Personality Disorder Reviewed (pp. 113–64). London: Gaskell Press. Cooke, D.J., Kosson, D.S. & Michie, C. (2001). Psychopathy and ethnicity: structural, item, and test generalizability of the Psychopathy Checklist-Revised (PCL-R) in Caucasian and African American participants. Psychological Assessment, 13, 531–42. Cooke, D.J. & Michie, C. (1997). An item response theory analysis of the Hare Psychopathy ChecklistRevised. Psychological Assessment, 9, 3–14. Cooke, D.J., Michie, C., Hart, S.D. & Clarke, D. (2005). Searching for the pan-cultural core of psychopathic personality disorder. Personality and Individual Differences, 39, 283–95. Cooke, D.J., Michie, C., Hart, S.D. & Hare, R.D. (1999). Evaluation of the screening version of the Hare Psychopathy Checklist-Revised (PCL: SV): an item response theory analysis. Psychological Assessment, 11, 3–13. Cooper, B.S. & Yuille, J.C. (2007). Psychopathy and deception. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 487–503). Mahwah, NJ: Lawrence Erlbaum. Cornell, D.G., Warren, J., Hawk, G. et al. (1996). Psychopathy in instrumental and reactive violent offenders. Journal of Consulting and Clinical Psychology, 64, 783–90. Costa, P.T. & McCrae, R.R. (1992). The five-factor model of personality and its relevance to personality disorders. Journal of Personality Disorders, 6, 343–59. Costa, P.T., Jr., & Widiger, T.A. (eds.). (2002). Personality Disorders and the Five-Factor Model of Personality, 2nd edition. Washington, DC: American Psychological Association. Cunningham, M.D., Sorensen, J.R. & Reidy, T.J. (2005). An actuarial model for assessment of prison violence risk among maximum security inmates. Assessment, 12, 40–9. Dadds, M.R., Fraser, J., Frost, A. & Hawes, D.J. (2005). Disentangling the underlying dimensions of psychopathy and conduct problems in childhood: a community study. Journal of Consulting and Clinical Psychology, 73, 400–10. Dahle, K.P. (2006). Strengths and limitations of actuarial prediction of criminal reoffence in a German prison sample: a comparative study of LSI-R, HCR-20 and PCL-R. International Journal of Law and Psychiatry, 29, 431–42. de Vogel, V., de Ruiter, C., Hildebrand, M. et al. (2004). Type of discharge and risk of recidivism measured by the HCR-20: a retrospective study in a Dutch sample of treated forensic psychiatric patients. International Journal of Forensic Mental Health, 3, 149–65. Dolan, M. & Davies, G. (2006). Psychopathy and institutional outcome in patients with schizophrenia in forensic settings in the UK. Schizophrenia Research, 81, 277–81. Dolan, M. & Doyle, M. (2000). Violence risk prediction: clinical and actuarial measures and the role of the Psychopathy Checklist. British Journal of Psychiatry, 177, 303–11. Dolan, M. & Rennie, C.E. (2006). Reliability and validity of the Psychopathy Checklist: Youth Version in a UK sample of conduct disordered boys. Personality and Individual Differences, 40, 65–75.

PSYCHOLOGICAL INSTRUMENTS AND ASSESSMENT

61

Douglas, K.S. Ogloff, J.R.P. & Nicholls, T.L. (1997, June). Personality disorders and violence in civil psychiatric patients. Paper presented at the 5th International Congress on the Disorders of Personality, Vancouver, British Columbia. Douglas, K.S., Vincent, G.M. & Edens, J.F. (2006). Risk for criminal recidivism: the role of psychopathy. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 533–54). New York: Guilford Press. Douglas, K.S., Yeomans, M. & Boer, D.P. (2005). Comparative validity analysis of multiple measures of violence risk in a sample of criminal offenders. Criminal Justice and Behavior, 32, 479– 510. Doyle, M., Dolan, M. & McGovern, J. (2002). The validity of North American risk assessment tools in predicting in-patient violent behaviour in England. Legal and Criminological Psychology, 7, 141–54. D’Silva, K., Duggan, C. & McCarthy, L. (2004). Does treatment really make psychopaths worse? A review of the evidence. Journal of Personality Disorders, 18, 163–77. Edens, J.F. (2001). Misuses of the Hare Psychopathy Checklist-Revised in court: two case examples. Journal of Interpersonal Violence, 16, 1082–93. Edens, J.F., Marcus, D.K., Lillienfeld, S.O. & Poythress, N.G. (2006). Psychopathic, not psychopath: taxometric evidence for the dimensional structure of psychopathy. Journal of Abnormal Psychology, 115, 131–44. Edens, J.F., Skeem, J.L. & Douglas K.S. (2006). Incremental validity analyses of the Violence Risk Appraisal Guide and the Psychopathy Checklist: Screening Version in a civil psychiatric sample. Assessment, 13, 1–7. Felthous, A.R. & Saß, H. (2000). Introduction to this issue: international perspectives on psychopathic disorders. Behavioral Sciences and the Law, 18, 557–65. Forth, A.E. & Book, A.S. (2007). Psychopathy in youth: a valid construct. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 369–87). Mahwah, NJ: Lawrence Erlbaum. Forth, A.E., Kosson, D. & Hare, R.D. (2003). The Hare Psychopathy Checklist: Youth Version. Toronto, ON: Multi-Health Systems. Frick, P.J. (2007). Using the construct of psychopathy to understand antisocial and violent youth. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 343–67). Mahwah, NJ: Lawrence Erlbaum. Frick, P.J. & Hare, R.D. (2001). The Antisocial Process Screening Device. Toronto, ON: Multi-Health Systems. Frick, P.J. & Marsee, M.A. (2006). Psychopathy and developmental pathways to antisocial behavior in youth. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 353–74). New York: Guilford Press. Fulero, S. (1995). Review of the Hare Psychopathy Checklist-Revised. In J.C. Conoley & J.C. Impara (eds.), Twelfth Mental Measurements Yearbook (pp. 453–54). Lincoln, NE: Buros Institute of Mental Measurements. Gacono, C.B. (ed.). (2000). The Clinical and Forensic Assessment of Psychopathy: A Practitioner’s Guide. Mahwah, NJ: Lawrence Erlbaum. Gendreau, P., Goggin, C. & Smith, P. (2002). Is the PCL-R really the ‘unparalleled’ measure of offender risk? A lesson in knowledge cumulation. Criminal Justice and Behavior, 29, 397–426. Gretton, H.M., Hare, R.D. & Catchpole, R. (2004). Psychopathy and recidivism in adolescent offenders: a ten year follow up. Journal of Clinical and Consulting Psychology, 72, 636–45. Gretton, H.M., McBride, M., O’Shaughnessy, R. et al. (2001). Psychopathy and recidivism in adolescent sex offenders. Criminal Justice and Behavior, 28, 427–49. Guay, J.P., Ruscio, J., Hare, R.D. & Knight, R.A. (in press). A taxometric analysis of the latent structure of psychopathy: evidence for dimensionality. Journal of Abnormal Psychology. Guy, L.S. & Douglas, K.S. (2006). Examining the utility of the PCL: SV as a screening measure using competing factor models of psychopathy. Psychological Assessment, 18, 225–30. Guy, L.S., Edens, J.F., Anthony, C. & Douglas, K. S. (2005). Does psychopathy predict institutional misconduct among adults? A meta-analytic investigation. Journal of Consulting and Clinical Psychology, 73, 1056–64. Hare, R.D. (1980). A research scale for the assessment of psychopathy in criminal populations. Personality and Individual Differences, 1, 111–19.

62

VOLUME I: DIAGNOSIS AND TREATMENT

Hare, R.D. (1991). The Hare Psychopathy Checklist-Revised. Toronto: Multi-Health Systems. Hare, R.D. (1996). Psychopathy: a construct whose time has come. Criminal Justice and Behavior, 23, 25–54. Hare, R.D. (1997). The NATO Advanced Study Institute on psychopathy, Alvor, Portugal, 1995. Journal of Personality Disorders, 11, 301–3. Hare, R.D. (1998a). Without Conscience: The Disturbing World of the Psychopaths Among Us. New York: Guilford Press. Hare, R.D. (1998b). The Hare PCL-R: some issues concerning its use and misuse. Legal and Criminological Psychology, 3, 101–23. Hare, R.D. (2003). The Hare Psychopathy Checklist-Revised, 2nd edition. Toronto, ON: Multi-Health Systems. Hare, R.D. (2006). Psychopathy: a clinical and forensic overview. Psychiatric Clinics of North America, 29, 709–24. Hare, R.D. (2007). Forty years aren’t enough: recollections, prognostications, and random musings. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 3–28). Mahwah, NJ: Lawrence Erlbaum. Hare, R.D., Clark, D., Grann, M. & Thornton, D. (2000). Psychopathy and the predictive validity of the PCL-R: An international perspective. Behavioral Sciences and the Law, 18, 623–45. Hare, R.D., Cooke, D.J. & Hart, S.D. (1999). Psychopathy and sadistic personality disorder. In T. Millon, P. Blaney & R. Davis (eds.), Oxford Textbook of Psychopathology (pp. 555–84). Oxford: Oxford University Press. Hare, R.D. & Hart, S. D. (1995). A commentary on the Antisocial Personality Disorder Field Trial. In W.J. Livesley (ed.), The DSM-IV Personality Disorders (pp. 127–34). New York: Guilford Press. Hare, R.D. & Neumann, C.S. (2005). Structural models of psychopathy, Current Psychiatry Reports, 7, 57–64. Hare, R.D. & Neumann, C.S. (2006). The PCL-R assessment of psychopathy: development, structural properties, and new directions. In C. Patrick (ed.), Handbook of Psychopathy (pp. 58–88). New York: Guilford Press. Hare, R.D. & Schalling, D. (eds.) (1978). Psychopathic Behavior: Approaches to Research. Chichester, England: John Wiley & Sons, Ltd. Harris, A.J.R. & Hanson, R.K. (1998, October). Supervising the psychopathic sex deviant in the community. Paper presented at the 17th Annual Research and Treatment Conference, The Association for the Treatment of Sexual Abusers, Vancouver, Canada. Harris, G.T. & Rice, M.E. (2006). The treatment of psychopaths. In C. Patrick (ed.), Handbook of Psychopathy (pp. 555–72). New York: Guilford Press. Harris, G.T. & Rice, M.E. (2007). Psychopathy research at Oak Ridge: skepticism overcome. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 57–76). Mahwah, NJ: Lawrence Erlbaum. Harris, G.T., Rice, M.E. & Camilleri, J.A. (2004). Applying a forensic actuarial instrument (the Violence Risk Appraisal Guide) to nonforensic patients. Journal of Interpersonal Violence, 19, 1063–74. Harris, G.T., Rice, M.E., Quinsey, V.L., Lalumi`ere, M.L. & Boer, D. (2003). A multi-site comparison of actuarial risk instruments for sex offenders. Psychological Assessment, 15, 413–25. Hart, S.D., Cox, D.N. & Hare, R.D. (1995). The Hare Psychopathy Checklist: Screening Version. Toronto, ON: Multi-Health Systems. Heilbrun, K., Hart, S.D., Hare, R.D. et al. (1998). Inpatient and post-discharge aggression in mentally disordered offenders: the role of psychopathy. Journal of Interpersonal Violence, 13, 514– 27. Hemphill, J.F. (2007). The Hare Psychopathy Checklist and recidivism: methodological issues and critical evaluation of empirical evidence. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 141–70). Mahwah, NJ: Lawrence Erlbaum. Hemphill, J.F. & Hare, R.D. (2004). Some misconceptions about the Hare PCL-R and risk assessment: a reply to Gendreau, Goggin, and Smith. Criminal Justice and Behavior, 31, 203–43. Herba, C.M., Hodgins, S., Blackwood, N. et al. (2007). The neurobiology of psychopathy: a focus on emotional processing. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 253–83). Mahwah, NJ: Lawrence Erlbaum.

PSYCHOLOGICAL INSTRUMENTS AND ASSESSMENT

63

Herpertz, S.C. & Saß, H. (2000). Emotional deficiency and psychopathy. Behavioral Sciences and the Law, 18, 567–80. Herv´e, H. (2007a). Psychopathy across the ages. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 31–55). Mahwah, NJ: Lawrence Erlbaum. Herv´e, H. (2007b). Psychopathic subtypes: historical and contemporary perspectives. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 431–60). Mahwah, NJ: Lawrence Erlbaum. Herv´e, H. & Yuille, J.C. (eds.) (2007). The Psychopath: Theory, Research, and Practice. Mahwah, NJ: Lawrence Erlbaum. Hicklin, J. & Widiger, T.A. (2005). Similarities and differences among antisocial and psychopathic self-report inventories from the perspective of general personality functioning. European Journal of Personality, 19, 325–41. Hildebrand, M. & de Ruiter, C. (2004). PCL-R psychopathy and its relation to DSM-IV Axis I and Axis II disorders in a sample of male forensic psychiatric patients in the Netherlands. International Journal of Law and Psychiatry, 24, 233–48. Hildebrand, M., de Ruiter, C. & de Vogel, V. (2004). Psychopathy and sexual deviance in treated rapists: association with (sexual) recidivism. Sexual Abuse: Journal of Research and Treatment, 16, 1–24. Hill, C., Neumann, C.S. & Rogers, R. (2004). Confirmatory factor analysis of the Psychopathy Checklist: Screening Version (PCL: SV) in offenders with Axis I disorders. Psychological Assessment, 16, 90–5. Hill, C.D., Rogers, R. & Bickford, M.E. (1996). Predicting aggressive and socially disruptive behavior in a maximum security forensic psychiatric hospital. Journal of Forensic Sciences, 41, 56–9. Hobson, J., Shine, J. & Roberts, R. (2000). How do psychopaths behave in a prison therapeutic community? Psychology, Crime, and the Law, 6, 139–54. Jackson, R. & Richards, H. (2007). Psychopathy in women: a valid construct with clear implications. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 389–410). Mahwah, NJ: Lawrence Erlbaum. Jones, S., Cauffman, E., Miller, J.D. & Mulvey, E. (2006). Investigating different factor structures of the Psychopathy Checklist: Youth Version: Confirmatory factor analytic findings. Psychological Assessment, 18, 33–48. Kernberg, O. (1984). Severe Personality Disorders. New Haven: Yale University Press. Kiehl, K.A. (2006). A cognitive neuroscience perspective on psychopathy: evidence for paralimbic system dysfunction. Psychiatry Research, 142, 107–28. Kiehl, K.S., Bates, A.T., Laurens, K.R. et al. (2006). Brain potentials implicate temporal lobe abnormalities in criminal psychopaths. Journal of Abnormal Psychology, 115, 443–53. Kiehl, K.A., Smith, A.M., Mendrek, A. et al. (2004). Temporal lobe abnormalities in semantic processing by criminal psychopaths as revealed by functional magnetic resonance imaging. Psychiatry Research: Neuroimaging, 130, 27–42. Lally, S.J. (2003). What tests are acceptable for use in forensic evaluations? A survey of experts. Professional Psychology: Research and Practice, 34, 491–8. Langton, C.N., Barbaree, H.E., Harkins, L. & Peacock, E.J. (2006). Sex offenders’ response to treatment and its association with recidivism as a function of psychopathy. Sexual Abuse: Journal of Research and Treatment, 18, 99–120. Larsson, H., Andershed, H. & Lichtenstein, P. (2006). A genetic factor explains most of the variation in the psychopathic personality. Journal of Abnormal Psychology, 115, 221–30. Leistico, A.M., Salekin, R.T., Decoster, J., & Rogers, R. (in press). A meta-analysis relating the Hare measures of psychopathy to antisocial conduct. Law and Human Behavior. Lilienfeld, S.O. & Andrews, B.P. (1996). Development and preliminary validation of a self-report measure of psychopathic personality traits in noncriminal populations. Journal of Personality Assessment, 66, 488–524. Lilienfeld, S.O. & Fowler, K.A. (2006). The self-report assessment of psychopathy: problems, pitfalls, and promises. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 107–32). New York: Guilford Press. Livesley, W.J. & Schroeder, M.L. (1991). Dimensions of personality disorder: the DSM-III-R cluster B diagnoses. Journal of Nervous and Mental Disease, 179, 320–8.

64

VOLUME I: DIAGNOSIS AND TREATMENT

Looman, J., Abracen, J., Serin, R., & Marquis, P. (2005). Psychopathy, treatment change and recidivism in high risk high need sexual offenders. Journal of Interpersonal Violence, 20, 549– 68. L¨osel, F. (1998). Treatment and management of psychopaths. In D.J. Cooke, A.E. Forth & R.D. Hare (eds.), Psychopathy: Theory, Research, and Implications for Society (pp. 303–54). Dordrecht, The Netherlands: Kluwer. Lykken, D.T. (2006). Psychopathic personality: the scope of the problem. In C. Patrick (ed.), Handbook of Psychopathy (pp. 3–13). New York: Guilford Press. Lynam, D.R. (1996). Early identification of chronic offenders: who is the fledgling psychopath? Psychological Bulletin, 120, 209–34. Lynam, D.R. (2002). Fledgling psychopathy: a view from personality theory. Law and Human Behavior, 26, 255–9. Lynam, D.R. & Gudonis, L. (2005). The development of psychopathy. Annual Review of Clinical Psychology, 1, 381–407. MacDonald, A.W. & Iacono, W.G. (2006). Toward an integrated perspective on the etiology on psychopathy. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 375–85). New York: Guilford Press. McCoy, W.K. & Edens, J.F. (2006). Do black and white youths differ in level of psychopathic traits: a meta-analysis of the Psychopathy Checklist measures. Journal of Consulting and Clinical Psychology, 74, 386–92. Meloy, J.R. (1988). The Psychopathic Mind: Origins, Dynamics, and Treatment. Northvale, NJ: Aronson. Meloy, J.R. (2002). The ‘polymorphously perverse’ psychopath: understanding a strong empirical relationship. Bulletin of the Menninger Clinic, 66, 273–90. Meloy, J.R. & Meloy, M.R. (2003). Autonomic arousal in the presence of psychopathy: a survey of mental health and criminal justice professionals. Journal of Threat Assessment, 2, 21– 34. Millon, T., Simonsen, E. & Birket-Smith, M. (1998). Historical conceptions of psychopathy in the United States and Europe. In T. Millon, E. Simonsen, M. Birket-Smith & R.D. Davis (eds.), Psychopathy: Antisocial, Criminal, and Violent Behaviors (pp. 3–31). New York: Guilford Press. Millon, T., Simonsen, E., Birket-Smith, M. & Davis, R.D. (1998). Psychopathy: Antisocial, Criminal, and Violent Behaviors. New York: Guilford Press. Monahan, J. (2006). Comments on cover jacket of C.J. Patrick (ed.), Handbook of psychopathy. New York: Guilford Press. Monahan, J. & Steadman, H. (eds.) (1994). Violence and Mental Disorder: Developments in Risk Assessment. Chicago: University of Chicago Press. Monahan, J., Steadman, H.J., Silver, E. et al. (2001). Rethinking Risk Assessment: The McArthur Study of Mental Disorder and Violence. New York: Oxford University Press. Mossman, D. (1994). Assessing predictions of violence: being accurate about accuracy. Journal of Consulting and Clinical Psychology, 62, 783–92. Nathanson, C., Paulhus, D.L. & Williams, K.M. (2007). Personality and misconduct correlates of body modification and other cultural deviance markers. Journal of Research in Personality, 40, 779–802. Neumann, C.S., Hare, R.D. & Newman, J.P. (2007). The superordinate nature of psychopathy. Journal of Personality Disorders, 21, 102–17. Neumann, C.S., Kosson, D.S., Forth, A.E. & Hare, R.D. (2006). Factor structure of the Hare Psychopathy Checklist: Youth Version in incarcerated adolescents. Psychological Assessment, 18, 142–54. Neumann, C.S., Kosson, D.S. & Salekin, R.T. (2007). Exploratory and confirmatory factor analysis of the psychopathy construct: methodological and conceptual issue. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 79–104). Mahwah, NJ: Lawrence Erlbaum. Neumann, C.S., Vitacco, M.J., Hare, R.D. & Wupperman, P. (2005). Reconstruing the reconstruction of psychopathy. a comment on Cooke, Michie, Hart, and Clarke. Journal of Personality Disorders, 19, 624–40.

PSYCHOLOGICAL INSTRUMENTS AND ASSESSMENT

65

Newman, J.P., Brinkley, C.A., Lorenz, A.R. et al. (2007). Psychopathy as psychopathology: beyond the clinical utility of the Psychopathy Checklist–Revised. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 173–206). Mahwah, NJ: Lawrence Erlbaum. O’Toole, M.E. (2007). Psychopathy as a behavior classification system for violent and serial crime scenes. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 301–25). Mahwah, NJ: Lawrence Erlbaum. Patrick, C.J. (ed.) (2006). Handbook of Psychopathy. New York: Guilford Press. ´ du risque de r´ecidive au sein Pham, T.H., Ducro, C., Marghem, B. & R´eveill`ere, C. (2005). Evaluation d’une population de d´elinquants incarc´er´es ou intern´es en Belgique francophone. Annales M´edico Psychologiques, 163, 842–5. Pichot, P. (1978). Psychopathic behaviour: a historical overview. In R.D. Hare & D. Schalling (eds.), Psychopathic Behavior: Approaches to Research (pp. 55–70). Chichester, England: John Wiley & Sons, Ltd. Porter, S., Fairweather, D., Drugge, J. et al. (2000). Profiles of psychopathy in incarcerated sexual offenders. Criminal Justice and Behavior, 27, 216–33. Porter, S. & Porter, S. (2007). Psychopathy and violent crime. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 287–300). Mahwah, NJ: Lawrence Erlbaum. Porter, S. & Woodworth, M. (2006). Psychopathy and aggression. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 481–94). New York: Guilford Press. Porter, S., Woodworth, M., Earle, J. et al. (2003). Characteristics of sexual homicides committed by psychopathic and nonpsychopathic offenders. Law and Human Behavior, 27, 459–70. Poythress, N.G., Skeem, J.L. & Lilienfeld, S.O. (2006). Associations among early abuse, dissociation, and psychopathy in an offender sample. Journal of Abnormal Psychology, 115, 288–97. Quinsey, V.L., Harris, G.E., Rice, M.E. & Cormier, C. (1998). Violent Offenders: Appraising and Managing Risk. Washington, DC: American Psychological Association. Quinsey, V.L., Rice, M.E. & Harris, G.T. (1995). Actuarial prediction of sexual recidivism. Journal of Interpersonal Violence, 10, 85–105. Rice, M.E. & Harris, G.T. (1992). A comparison of criminal recidivism among schizophrenic and nonschizophrenic offenders. International Journal of Law and Psychiatry, 15, 397–408. Rice, M.E. & Harris, G.T. (1997). Cross-validation and extension of the Violence Risk Appraisal Guide for child molesters and rapists. Law and Human Behavior, 21, 231–41. Rice, M.E., Harris, G.T. & Cormier, C.A. (1992). An evaluation of a maximum security therapeutic community for psychopaths and other mentally disordered offenders. Law and Human Behavior, 16, 399–412. Richards, H.J., Casey, J.O. & Lucente, S.W. (2003). Psychopathy and treatment response in incarcerated female substance abusers. Criminal Justice and Behavior, 30, 251–76. Robins, L.N. (1978). Aetiological implications in studies of childhood histories relating to antisocial personality. In R.D. Hare & D. Schalling (eds.), Psychopathic Behavior: Approaches to Research (pp. 255–71). Chichester, England: John Wiley & Sons, Ltd. Rogers, R., Salekin, R.T., Sewell, K.W. & Cruise, K.R. (2000). Prototypical analysis of antisocial personality disorder: a study of inmate samples. Criminal Justice and Behavior, 27, 234–55. Rutter, M. (2005). Commentary: what is the meaning and utility of the psychopathy concept? Journal of Abnormal Child Psychology, 33, 499–503. Salekin, R.T. (2006). Psychopathy in children and adolescents. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 389–414). New York: Guilford Press. Salekin, R.T., Neumann, C.S., Leistico, A.M. et al. (2004). Psychopathy and comorbidity in a young offender sample: taking a closer look at psychopathy’s potential importance over disruptive behavior disorders. Journal of Abnormal Psychology, 113, 416–27. Salekin, R., Rogers, R. & Sewell, K. (1996). A review and meta-analysis of the Psychopathy Checklist and Psychopathy Checklist-Revised: predictive validity of dangerousness. Clinical Psychology: Science and Practice, 3, 203–15. Schrum, C.L. & Salekin, R.T. (2006). Psychopathy in adolescent female offenders: an item response theory analysis of the Psychopathy Checklist: Youth Version. Behavioral Sciences and the Law, 24, 39–63. Serin, R.C., Mailloux, D.L. & Malcolm, P.B. (2001). Psychopathy, sexual arousal, and recidivism. Journal of Interpersonal Violence, 16, 234–47.

66

VOLUME I: DIAGNOSIS AND TREATMENT

Silver, E., Mulvey, E.P. & Monahan, J. (1999). Assessing violence risk among discharged psychiatric patients: Toward an ecological approach. Law and Human Behavior, 23, 237–55. Sj¨ostedt, G. & L˚angstr¨om, N. (2002). Assessment of risk for criminal recidivism among rapists: a comparison of four different measure. Psychology, Crime & Law, 8, 25–40. Skeem, J.L., Edens, J.F., Camp, J. & Colwell, L.H. (2004). Are there ethnic differences in levels of psychopathy? A meta-analysis. Law and Human Behavior, 28, 505–27. Spidel, A., Vincent, G., Huss, M.T. et al. (2007). The psychopathic batterer: subtyping perpetrators of domestic violence. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 327–40). Mahwah, NJ: Lawrence Erlbaum. Stadtland, C., Kleindienst, N., Kr¨oner, C. et al. (2005). Psychopathic traits and risk of criminal recidivism in offenders with and without mental disorders. International Journal of Forensic Mental Health, 4, 89–97. Stafford, E. & Cornell, D. (2003). Psychopathy scores predict adolescent inpatient aggression. Assessment, 10, 102–12. Steadman, H.J., Silver, E., Monahan, J. et al. (1999). A classification tree approach to the development of actuarial violence risk assessment tools. Law and Human Behavior, 24, 83–100. Stone, M.H. (1998). The personalities of murderers: the importance of psychopathy and sadism. In A.E. Skodol (ed.), Psychopathology and Violent Crime (pp. 29–52). Washington, DC: American Psychiatric Association. Sullivan, E.A. & Kosson, D.S. (2006). Ethnic and cultural variations in psychopathy. In C. Patrick (ed.), Handbook of Psychopathy (pp. 437–58). New York: Guilford Press. Tellegen, A. (in press). MPQ (Multi-Dimensional Personality Questionnaire): Manual for Administration, Scoring, and Interpretation. Minneapolis, MN: University of Minnesota Press. Tengstr¨om, A. (2001). Long-term predictive validity of historical factors in two risk assessment instruments in a group of violent offenders with schizophrenia. Nordic Journal of Psychology, 55, 243–9. Tengstr¨om, A., Grann, M., L˚angstr¨om, N. & Kullgren, G. (2000). Psychopathy (PCL-R) as a predictor of violent recidivism among criminal offenders with schizophrenia. Law and Human Behavior, 24, 45–58. Tengstr¨om, A., Hodgins, S., Grann, M. et al. (2004). Schizophrenia and criminal offending: the role of psychopathy and substance use disorders. Criminal Justice and Behavior, 31, 367–91. Tengstr¨om, A., Hodgins, S., M¨uller-Isberner, R. et al. (2006). Predicting violent and antisocial behavior in hospital using the HCR-20: the effect of diagnoses on predictive accuracy. International Journal of Forensic Mental Health, 5, 39–53. Thornton, D. & Blud, L. (2007). The influence of psychopathic traits on response to treatment. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 505–39). Mahwah, NJ: Lawrence Erlbaum. Ullrich, S. & Marneros, A. (2004). Dimensions of personality disorders in offenders. Criminal Behaviour and Mental Health, 14, 202–13. Verona, E. & Vitale, J. (2006). Psychopathy in women: assessment, manifestations, and etiology. In C. Patrick (ed.), Handbook of Psychopathy (pp. 415–36). New York: Guilford Press. Viding, E., Blair, R.J.R., Moffitt, T.E. & Plomin, R. (2005). Evidence for substantial genetic risk for psychopathy in 7-year-olds. Journal of Child Psychology and Psychiatry, 46, 592–7. Vitacco, M.J., Neumann, C.S., Caldwell, M.F. et al. (2006). Testing factor models of the Psychopathy Checklist: Youth Version and their association with instrumental aggression. Journal of Personality Assessment, 87, 74–83. Vitacco, M.J., Neumann, C.S. & Jackson, R.L. (2005). Testing a four-factor model of psychopathy and its association with ethnicity, gender, intelligence, and violence. Journal of Consulting and Clinical Psychology, 73, 466–76. Vitacco, M.J. & Vincent, G.M. (2006). Understanding the downward extension of psychopathy to youth: Implications for risk assessment and juvenile justice. International Journal of Forensic Mental Health, 5, 29–38. Waldman, I.D. & Rhee, S.H. (2006). Genetic and environmental influences on psychopathy and antisocial behavior. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 205–28). New York: Guilford Press.

PSYCHOLOGICAL INSTRUMENTS AND ASSESSMENT

67

Walsh, T. & Walsh, Z. (2006). The evidentiary introduction of Psychopathy Checklist-Revised assessed psychopathy in U.S. courts: Extent and appropriateness. Law and Human Behavior, 30, 493–507. Walters, G.D. (2003). Predicting institutional adjustment and recidivism with the psychopathy checklist factor scores: a meta-analysis. Law and Human Behavior, 27, 541–58. Warren. J.I. & South, S.C. (2006). Comparing the constructs of antisocial personality disorder and psychopathy in a sample of incarcerated women. Behavioral Sciences and the Law, 24, 1–20. Webster, C., Douglas, K., Eaves, D. & Hart, S. (1997). HCR-20 Assessing Risk for Violence: Version II. Burnaby, BC: Mental Health, Law & Policy Institute, Simon Fraser University. Weiler, B. & Widom, C.S. (1996). Psychopathy and violent behaviour in abused and neglected young adults. Criminal Behaviour and Mental Health, 6, 253–71. Westen, D. & Weinberger, J. (2004). When clinical description becomes statistical prediction. American Psychologist, 59, 595–613. Widiger, T.A. (2006). Psychopathy and DSM-IV psychopathology. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 156–71). New York: Guilford Press. Widiger, T.A., Cadoret, R., Hare, R.D. et al. (1996). DSM-IV Antisocial Personality Disorder Field Trial. Journal of Abnormal Psychology, 105, 3–16. Williams, K.M., Paulhus, D.L. & Hare, R.D. (2000). Capturing the four-factor structure of psychopathy by self-report in a community sample. Journal of Personality Assessment, 88, 205–19. Williamson, S.E., Hare, R.D. & Wong, S. (1987). Violence: criminal psychopaths and their victims. Canadian Journal of Behavioral Science, 19, 454–62. Wong, S. & Burt, G. (2007). The heterogeneity of incarcerated psychopaths: differences in risk, need, recidivism, and management approaches. In H. Herv´e & J.C. Yuille (eds.), The Psychopath: Theory, Research, and Practice (pp. 461–84). Mahwah, NJ: Lawrence Erlbaum. Wong, S. & Hare, R.D. (2005). Guidelines for a Psychopathy Treatment Program. Toronto, ON: Multi-Health Systems. Wong, S., Witte, T.D., Gordon, A., Gu, D. & Lewis, K. (2006). Can a treatment program designed primarily for violent risk reduction reduce recidivism in psychopaths? Paper presented at the Annual Meeting of the Canadian Psychological Association, Calgary, Alberta. June 8–10, 2006. Woodworth, M. & Porter, S. (2002). In cold blood: characteristics of criminal homicides as a function of psychopathy. Journal of Abnormal Psychology, 111, 436–45. World Health Organization (1990). International Classification of Diseases and Related Health Problems (10th edn.). Geneva, Switzerland: World Health Organization.

CHAPTER 4

Functional and Structural Brain Imaging Research on Psychopathy Yaling Yang and Adrian Raine University of Southern California, USA

It has been 150 years since the famous case of Phineas Gage, a man who suffered severe personality and behavioral changes following an accident which damaged his prefrontal cortex. The tragedy provides the inspiration for exploring the neuroanatomical bases of decision making and social behaviors (Damasio, 1994). Brain imaging research has gone a long way since then. Today, an increasing body of brain imaging evidence now attests to the fact that links exist between brain deficits and psychopathic behavior. Most of this research has assessed the functioning of the brain using positron emission tomography (PET) to measure glucose metabolism, single photon emission computerized tomography (SPECT) to assess blood flow, and functional magnetic resonance imaging (fMRI) to measure blood flow. In terms of structural difference, recent studies have employed anatomical MRI (aMRI) to assess brain structure. To date, cumulative knowledge has indicated that the key brain areas shown to be abnormal in antisocial individuals include several prefrontal cortices, regions of the temporal cortex, the amygdala–hippocampal complex, the corpus callosum and the anterior cingulate gyrus. Despite this developing knowledge base on antisocial personality, there has been surprisingly little brain imaging research on the specific subgroup of antisocial individuals who are thought to be severely impaired in processing emotional thoughts, namely psychopaths. Not surprisingly therefore, within this modest body of imaging research there are very few imaging studies specifically on structural or functional brain impairments in psychopaths. Consequently, the empirical basis for any discussion of the neuroanatomical basis of psychopathy based on imaging is very limited. As such, this chapter will rely upon the somewhat larger database of brain imaging research on antisocial, violent and impulsive individuals. While the emphasis will be on structural and functional brain impairments in psychopaths as a group, a more symptom-based approach will be taken by examining the imaging correlates of specific psychopathic features in order to provide hypotheses to guide future research on psychopaths. It will also be discussed as findings from such research

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

70

VOLUME I: DIAGNOSIS AND TREATMENT

(A) 9 46

10

45

11

44

47

(B) 9 10

12 11

Figure 4.1 Proximal representation of Brodmann area numbers for the orbitofrontal regions (10, 11, 12, 47), ventromedial prefrontal cortex (44, 45, 47), and dorsolateral prefrontal cortex (9, 46) on a three-dimensional high-resolution surface model. (A) Lateral view of left hemisphere. (B) Medial view of right hemisphere. (Adapted from Brodmann, 1909). See also color plates

may provide a context within which to evaluate the more limited research on psychopathic behavior, and thus provide directions for future research on psychopaths. In order to facilitate anatomical and functional similarities, we group the structural and functional imaging findings into dorsolateral/ventrolateral prefrontal cortex, orbitofrontal/ventromedial frontal cortex, superior temporal cortex, medial temporal structures (amygdala/hippocampus), and other brain areas (corpus callosum/anterior cingulated gyrus). For the prefrontal cortex in particular, a major obstacle in drawing conclusions combining both structural and functional imaging has been the lack of a clear guideline for identifying regions, and clear communication amongst researches can been difficult. Consequently, we clarify here that the way key regions described in this chapter are delineated in terms of Brodmann area (BA) are as follows: dorsolateral prefrontal cortex: BA 9 and 46; ventrolateral prefrontal cortex: BA 44, 45 and 47; and orbitofrontal/ventromedial prefrontal cortex: BA 10, 11, 12 and 47 (see Figure 4.1).

DORSOLATERAL AND VENTROLATERAL PREFRONTAL CORTEX Some studies suggest that psychopathy is more associated with abnormalities in the ventromedial prefrontal (VMPFC) function than in the dorsolateral prefrontal (DLPFC) due the

FUNCTIONAL AND STRUCTURAL BRAIN IMAGING RESEARCH

71

fact that lesions to the dorsolateral frontal regions generally do not produce behavioral and personality changes that resemble psychopaths (Dolan & Park, 2002). Meta-analytical studies, however, suggest that APDs, including psychopaths, may be associated with DLPFC functions, and executive ability in particular (Brower & Price, 2001; Dolan & Park, 2002; Fishbein, 2000; Giancola & Mezzich, 2000; Ishikawa & Raine, 2003; Morgan & Lilienfeld, 2000; Stevens, Kaplan & Hesselbrock, 2003). In contrast, the VLPFC receives its input from the inferotemporal cortex and project to the striatum, and might lead to difficulties in learning stimulus–response and stimulus–reward associations as shown in several animal studies (Miyashita & Hayashi, 2000; Parker & Gaffan, 1998; Shohamy et al., 2004). The inability to make appropriate decisions in situations linked to punishment or reward outcomes may therefore contribute to the impulsive and irresponsible behaviors shown by psychopaths.

Findings on Psychopaths Very few studies have assessed structural integrity of the DLPFC and the VLPFC and psychopathy. Laakso and colleagues (Laakso et al., 2002) found reduced gray matter volumes in the left DLPFC, and orbitofrontal cortex (OFC) in alcoholics with antisocial personalities compared to controls. These authors argued for an abolition of these effects when duration of alcoholism was controlled, but because this covariate is very heavily correlated with group membership (i.e., all controls have a zero age of onset, all alcoholic antisocial subjects have some age of onset), the covariate is almost synonymous with group membership, and hence this conclusion does not seem entirely warranted. The finding of reduced prefrontal gray volume is consistent with several studies which have examined the association between widespread prefrontal gray volume and psychopathy. Reduced gray matter throughout the prefrontal cortex has found in those with APD who also have high Psychopathy ChecklistRevised (PCL-R) scores (Raine et al., 2000). Similarly, Kruesi et al. (2004) found a 14 % reduction in the volume of prefrontal gray in conduct-disordered children but the result was statistically nonsignificant. This effect may have failed to reach statistical significance due to the small sample size (N = 10). However, another study showed no correlations between prefrontal gray or white volume and PCL-R scores (Laakso et al., 2002). This null effect could be due to a restriction of range as the sample was restricted to violent offenders with APD and alcoholic diagnoses. By using a community sample with a wide range of psychopathy scores, Yang and colleagues (Yang et al., 2004) found significant negative correlations between prefrontal gray volume and PCL-R scores (Factor 1: arrogant/deceptive; Factor 2: affective; Factor 3: impulsive/unstable). In contrast to antisocial personality, there appear to be no structural imaging studies on DLPFC or VLPFC volumes in carefully defined institutional psychopaths. With regard to the DLPFC and VLPFC, inhibitory control is a cognitive process thought to be both governed by these regions and also linked to psychopathy. However, inconsistent results have been found in several studies on the existence of the DLPFC and/or VLPFC functional deficits in psychopathic individuals (Gorenstein, 1982; Hart, Forth & Hare, 1990; Lapierre, Braun & Hodgins, 1995). It is worth mentioning that the absence of healthy controls in these studies make it difficult to interpret whether DLPFC and/or VLPFC functioning is associated specifically with the antisocial behavior component of the psychopathy complex as opposed to interpersonal psychopathic features. Only one recent fMRI study showed

72

VOLUME I: DIAGNOSIS AND TREATMENT

APD patients activate a different neural network involving inferior, medial, superior frontal and anterior cingulate cortices during a response inhibition task compared to the activation pattern (the right DLPFC and OFC) of the normal controls (Vollm et al., 2004). This result supports the hypothesis that the core personality features of psychopathy may result from OFC dysfunction, but that the additional involvement of DLPFC dysfunction may lead in addition to externalizing behavior problems such as poor planning, disorganization and difficulty keeping in mind future consequences (Dinn & Harris, 2000).

Findings on Specific Psychopathic Features The DLPFC mediates executive functions such as the ability to plan, monitor and override a strong response tendency (Bunge, 2004; Smith & Jonides, 1999). On the other hand, several studies have tightly linked the VLPFC to rule retrieval and rule maintenance (Bunge et al., 2003; Crone & van der Molen, 2004). Several fMRI studies have tested the involvement of the DLPFC and VLPFC in the executive functions described above by using inhibition control tasks. For example, Konishi and colleagues (Konishi et al., 1998) first suggested that the right inferior frontal gyrus (particularly DLPFC) constitutes the neural underpinnings of response inhibition. Garavan, Ross and Stein (1999) showed that a more complicated cortical network underlies response inhibition, involving activation of the DLPFC and the VLPFC. Liddle, Kiehl and Smith (2001) again showed significant activation in the DLPFC and VLPFC during response inhibition trails. A more recent study has shown a similar result involving higher activation of the DLPFC, the lateral OFC, anterior-medial prefrontal cortex, superior temporal gyrus and cingulate gyrus during the response (Horn et al., 2003). They indicated that the onset of the ability to inhibit behavior is a milestone in cognitive development, and is considered to be partly due to frontal lobe maturation (Garavan et al., 1999). Another increasing perspective associates the DLPFC and VLPFC functions to another psychopathic characteristic – deception (lying), and is supported by several recent fMRI studies. Psychopathic individuals are considered not only to appear at ease while repeatedly lying, but also seldom experience embarrassment when caught in a lie (Hare, 2003). Spence and colleagues (Spence et al., 2001) showed that lying about autobiographical events was associated with greater activation bilaterally in the VLPFC, and suggests that this region is involved in response alternation and inhibition and may therefore support the telling of lies. Similar results were found in another study (Lee et al., 2002) in which feigning memory loss was associated with a widespread activation pattern including several frontal regions (particularly the DLPFC)), parietal and temporal cortices. Phan and colleagues (Phan et al., 2005) used novel real-time fMRI technology to simulate a polygraph experience in order to evoke performance anxiety about generating lies, and found strong associations between deceptive responses and activation of the DLPFC, VLPFC, DMPFC and the superior temporal sulcus. Again, Nunez and colleagues (Nunez et al., 2005) observed increased DLPFC, ACC, caudate and thalamic nuclei activation during false responses. Based on these fMRI studies, it could be speculated that chronic lying in psychopaths is paradoxically associated with proficient rule retrieval (VLPFC function) and the inhibition of wrongful behaviors based on one’s judgment (DLPFC function). Although important, to our knowledge, no fMRI study to date has evaluated which brain circuits are activated when psychopaths deliberately falsify information.

FUNCTIONAL AND STRUCTURAL BRAIN IMAGING RESEARCH

73

ORBITOFRONTAL AND VENTROMEDIAL PREFRONTAL CORTEX Ventral regions of the prefrontal area including the OFC and VMPFC are densely connected with many brain regions including the basal ganglia, amygdala and other prefrontal cortices. Both location and connectivity allow these areas to receive information concerning emotional content, to process the information and tag it with reward values, and to input information to the DLPFC and VLPFC for ultimate decision making. Deficits to these regions show symptoms parallel to the clinical profile of psychopathy, including irresponsibility, impulsivity and indifference to ethical conventions.

Findings on Psychopaths The importance of the roles the OFC and VMPFC play in this wider circuit have been reported in numerous patient studies describing the emergence of psychopathic behavior following damage to these regions. Before damage, these patients have relatively normal intelligence and social skills levels. After damage, they demonstrate a significant alternation in personality described as the ‘acquired sociopathic syndrome’, a syndrome that includes social disinhibition, shallow affect, decreased empathy, poor control over impulses and impaired ability to predict the future consequence of their actions (Bechara, Damasio & Damasio, 2000; Bechara, Dolan, & Hindes, 2002; Damasio, 1994). However, only one aMRI study has been conducted on antisocial personality disorder (Laakso et al., 2002). As described above, the results indicate reduced MRI left prefrontal gray volumes in the OFC, and DLPFC in alcoholics with antisocial personalities compared with controls. This result is consistent with several studies which tested the relationship between widespread prefrontal gray volume and psychopathy (Raine et al., 2000; Yang et al., 2005; Laakso et al., 2002). However, no aMRI study has been done on psychopaths examining the existence of the same correlation found in APDs. This region is specially involved in processing the reward value of environmental stimuli and affective cues that accompany decision attributes and the ‘gut feelings’ that are associated with the act of good decision making (Krawczyk, 2002). Those with antisocial personality disorder, particularly psychopathy, are thought to be deficient in this ability. Several fMRI studies on psychopaths have also focused on their inability to inhibit responses. One study showed different patterns of activation between normal controls and APD during an inhibition task: the control group showed right DLPFC and left OFC activation; while the patient group showed a more bilateral and extended activation pattern across frontal regions (Vollm et al., 2004). Also, one study showed greater activation of OFC during response inhibition in impulsive individuals, and suggested that this region is required in order to sustain behavioral inhibition (Horn et al., 2003). They also suggested that greater engagement of the right OFC was needed to maintain inhibition in impulsive individuals (Horn et al., 2003). With regard to abnormal affective information processing in psychopathy, one fMRI study found increased activation in right prefrontal regions and the amygdala during viewing negative visual content and left OFC during positive content in psychopathic individuals (Muller et al., 2003). One conclusion that could be drawn from these fMRI studies is that the functions of the orbitofrontal regions (OFC and VMPFC) are most directly involved in decision making that involves affective cues and behavioral

74

VOLUME I: DIAGNOSIS AND TREATMENT

inhibition. This leads us to believe that impairments in these regions may predispose to primary psychopathy and that an abnormal activation pattern would be found if similar tasks were administered to psychopaths.

Findings on Specific Psychopathic Features Evidence has begun to build up to suggest that in normals the OFC and VMPFC are involved in a complex chain of cognitive processes that includes information receiving, reward coding and decision making. Interestingly, this process also plays an important role in moral reasoning, a unique and crucial ability in human society. Even though patients with adult-acquired lesions to the orbitofrontal region show no disruption in moral reasoning, patients with similar damage acquired in early childhood fail to learn factual knowledge about accepted standards of moral behavior, resulting in both severely impaired social behavior and defective social and moral reasoning (Anderson et al., 1999). Recent fMRI studies have shown that the orbitofrontal regions, especially the VMPFC, are activated during ethical decision making and tasks during which mental states of others have to be modeled or attributed. Greene and colleagues (Greene et al., 2001) found that reasoning about ethical dilemmas that are emotionally engaging as compared to dilemmas that are less emotionally engaging activate the medial prefrontal cortex (MPFC), posterior cingulate cortex (PCC) and bilateral posterior superior temporal gyri. Moll and colleagues (2002) again reported that OFC as well as the posterior superior temporal gyrus are recruited by passively viewing scenes evocative of moral emotions (emotions involving the interests or welfare either of society or of other individuals). Heekeren and colleagues (Heekeren et al., 2003) showed activation in the bilateral VMPFC, left lateral PFC, and several temporal regions during simple moral decisions compared to semantic decisions. No fMRI study to date has been conducted on psychopaths using a moral reasoning task. The prediction that would be made from these fMRI studies conducted on normals is that psychopaths would show a hypo-activated response while making ethical decisions, and that this decrease in activation would be found in the OFC and VMPFC.

SUPERIOR TEMPORAL CORTEX The superior temporal cortex (particularly the auditory cortex and Wernicke’s area) is a key structure for processing auditory information and comprehending sound-based language presentation. If impaired, dysfunction in this region may predispose to difficulty in the processing of either affective or neutral semantic information, deficits which have been demonstrated in psychopaths (Hare & Jutai, 1988; Kiehl et al., 1999).

Findings on Psychopaths Early computed tomographic studies of antisocial adults found temporal lobe abnormalities in some cases, although methodological limitations and inconsistent findings make drawing conclusions difficult (Bassarath, 2001). Studies conducted mainly on aggressive and violent patients and offenders have observed reduced temporal lobe volumes (Amen et al., 1996; Dolan & Park, 2002; Hirono et al., 2000; Volkow et al., 1995; Wong et al., 1997). Only

FUNCTIONAL AND STRUCTURAL BRAIN IMAGING RESEARCH

75

one aMRI study observed a significant reduction in temporal lobe and gray matter volume in early onset conduct disorder (Kruesi et al., 2004). It should be noted that many of the reported temporal lobe functional abnormalities in aggressive populations may reflect fronto-temporal dysfunction, as evidenced by the fact that most of the above studies found coexisting frontal deficits. A second notable point is that different imaging technologies using different activation states may be sensitive to dysfunction in different brain regions. For example,() Gatzke-Kopp et al. (2001) found resting EEG abnormalities in the temporal lobes of murderers, even though PET activation testing did not reveal evidence for temporal lobe dysfunction. Relatively poor cortical functioning in the temporal lobe is another finding emerging from the brain imaging literature with respect to the psychopathic behaviors of affective and semantic information processing. Intrator and colleagues (1997) using SPECT found that psychopaths show increased bilateral blood flow in fronto-temporal regions during the processing of emotional words. Again by using SPECT, significant negative correlations were found between psychopathy (especially the Factor 1 interpersonal features) and frontal and temporal perfusion (Soderstrom et al., 2002). They found the correlation with Factor 1 psychopathy to be strongest for the left temporal blood flow. The difficulties that psychopaths experience when accessing and understanding affective stimuli are particularly evident during language tasks (Williamson, Harpur & Hare, 1991). The only fMRI study conducted on psychopaths during a semantic task found that psychopathic individuals failed to show the appropriate neural differentiation between abstract and concrete stimuli in the right anterior temporal gyrus and surrounding cortex (Kiehl et al., 1999).

Findings on Specific Psychopathic Features An increasing number of fMRI studies focused on functions other than language processing in the superior temporal cortex have revealed the involvement of this region in decision making and emotion regulation. These processes are in turn tightly aligned to the understanding of the neural processes that may underlie psychopathic characteristics. For example, several studies suggest that the superior temporal gyrus (STG), especially the posterior region, is activated during the process of moral decision making (Greene et al., 2001; Heekeren et al., 2003; Moll et al., 2002) and processes stimuli that signal the actions and intentions of another individual (Allison, Puce & McCarthy, 2000). Similarly, Frith and Frith (2003) argue that the posterior STG (together with the medial prefrontal cortex) is a critical component of ‘theory of mind’ (mentalizing), which in turn may underlie the dysfunctional interpersonal relations of psychopaths, including lack of empathy.

MEDIAL TEMPORAL STRUCTURES (AMYGDALA/HIPPOCAMPUS) Two regions of the medial temporal cortex, the amygdala and hippocampus, are the focus in this section. The amygdala is located in the medial temporal lobe and receives information from association cortices and the thalamus. It sends efferents to projection sites to mediate the behavioral response to perceptual and emotional stimuli. Psychopathic individuals show

76

VOLUME I: DIAGNOSIS AND TREATMENT

a generalized decrease in emotional responsibility especially when the emotional stimuli involve fear and threat. The hippocampus is a folded structure situated medial to the lateral ventricles. Densely interconnected with the adjacent amygdala, it may serve as a substrate to predispose individuals to psychopathic behavioral problems.

Findings on Psychopaths The medial temporal region, especially the amygdala and the hippocampus, has received particular attention in recent years. There is a growing body of data from a small group of human patients with discrete lesions in the amygdala that highlights the importance of this region for both the perception and production of negative affect and associative aversive learning (LeDoux, 1996). The association between abnormalities in the medial temporal region and individuals with antisocial behavior, particularly psychopathy, has been found in several aMRI studies. Laakso and colleagues (2000) demonstrated reduced right hippocampal volume reductions in violent offenders with APD who were also early-onset alcoholics compared to controls. Another study has also reported reduced amygdala volume to be associated with increased psychopathy scores within a sample of violent offenders (Tiihonen, Hodgins & Vaurio, 2000). With regard to psychopathy, one study found reductions in the volume of the posterior hippocampus to be associated with increased psychopathy scores in antisocial alcoholics (Laakso et al., 2001). A more complex result was reported by Raine and colleagues (2004) assessing left and right hippocampus volumes, finding that unsuccessful (caught) psychopaths showed an exaggerated anterior hippocampal asymmetry (right > left) relative to both successful psychopaths (not caught) and controls. Another study using PET on murderers found abnormal asymmetries of functioning, with murderers showing lower left and increased right functioning in both the amygdala and hippocampus compared to controls (Raine, Buchsbaum & LaCasse, 1997). Soderstrom and colleagues (2000) in a SPECT study found bilaterally reduced hippocampal functioning in violent offenders. A growing amount of fMRI research conducted on psychopathic individuals has also examined the nature of this emotional abnormality and has shown increased activity in the amygdala during the viewing of affective stimuli in psychopathic individuals compared to normal controls (Kiehl et al., 2001; Muller et al., 2003; Schneider et al., 2000). There are, however, some exceptions to this pattern of results, which show instead reduced activation in psychopaths and adolescents with conduct disorders (Veit et al., 2002; Sterzer et al., 2005). Psychopaths may paradoxically show enhanced activity because they have fear conditioning and emotion deficits, so that to perform the behavioral–emotional activation task as well as controls, greater neurophysiological activation may be required, particularly if there is structural impairment in the amygdala in psychopaths. This is, however, highly speculative. These findings suggest that while prefrontal dysfunction may play a role in psychopathy traits such as impulsivity and repeated lying, temporal lobe dysfunction may contribute crucially to key personality traits such as lack of empathy and shallow affect in psychopathy.

Findings on Specific Psychopathic Features The amygdala and hippocampus have long been considered part of the brain circuits implicated in processing affective stimuli and have shown abnormalities in psychopaths as

FUNCTIONAL AND STRUCTURAL BRAIN IMAGING RESEARCH

77

described above. The amygdala is particularly responsive to negative affective states such as threat, fear and anxiety (Davidson & Irwin, 1999), while the hippocampus plays an important role in the processing of moral cognition (Moll et al., 2003) and may facilitate conscious recollection of memories that allow past events to affect current decisions (Casebeer & Churchland, 2003). In contrast to normal individuals, psychopathy is particularly characterized by abnormal or deficient emotional responding leading to disturbed social interaction and diminished ability to learn from negative experiences (i.e., punishment). Recent fMRI studies using more specific affective stimuli have suggested that the amygdala and the hippocampus are associated with negative emotion in particular, such as fear and threat. For example, Hariri and colleagues (2002) found increased signal activation in the bilateral amygdala during perception of threatening pictures that induce subjects’ fearful responses. Kuchinke and colleagues (2005) showed a distinct activation pattern associated with negative words in the hippocampus, anterior and posterior cingulate gyrus, and lingual gyrus. Schienle et al. (2005) using fear-inducing pictures with phobic patients found significant fear-evoking activation involving the amygdala, the right hippocampus and the right DLPFC compared to controls. Whalen and colleagues (1998) similarly showed significantly increased amygdala activation in response to masked fearful faces and an activation decrease to masked happy faces. In conclusion, an underlying neural network is hypothesized in which amygdala functioning is responsible for threat-related emotional responding, fear conditioning, and the appraisal of fearful facial expressions (Heriri et al., 2002; Wehner et al., 1997); while the hippocampus is more responsible for remembering the declarative facts of negative stimuli and to establish their context (Shienle et al., 2005; Wehner et al., 1997). In psychopaths, different activation patterns would be expected while processing emotional stimuli and significantly higher activation may be found in the amygdala and hippocampus in response to negative emotional stimuli. In contrast, reduced activation would be expected in these regions while viewing positively valenced emotional stimuli.

OTHER BRAIN AREAS Several aMRI and functional imaging studies have suggested that the corpus callosum and anterior cingulate gyrus may be just as important to the understanding of psychopathy as prefrontal and temporal regions. There appears to be only one study on the corpus callosum in psychopaths. Raine and colleagues (2003) assessed 15 male subjects with both high psychopathy scores and antisocial personality disorder, and 25 matched controls (all selected from a larger sample of 83 community volunteers) on aMRI measures of the corpus callosum (volume estimate of callosal white matter, thickness, length, area of genu and splenium), electrodermal and cardiovascular activity during a social stressor, and personality measures of affective and interpersonal deficits. Compared with controls, psychopathic antisocial individuals showed a significant increase in estimated callosal white matter volume, callosal length and functional interhemispheric connectivity. Correlational analyses in the larger unselected sample of 83 subjects confirmed the association between psychopathic personality and callosal structural abnormalities. Larger callosal volumes were associated with affective and interpersonal deficits, low autonomic stress reactivity and low spatial ability. In the functional domain, one PET study found that murderers exhibited decreased metabolic activity in the corpus callosum compared to normal controls (Raine, Buchsbaum & LaCasse, 1997). These

78

VOLUME I: DIAGNOSIS AND TREATMENT

findings may be related in that reduced callosal glucose metabolism has been associated with increased callosal thickness and area (Wu et al., 1993). Recent neuroimaging research has suggested that another region – the anterior cingulate cortex (ACC) – may be related to psychopathy and may form a key element in the circuitry underlying positive and negative affect. Kiehl and colleagues (2001) found that criminal psychopaths showed significantly less affect-related activity in the amygdala, hippocampus, parahippocampus gyrus, ventral striatum and the anterior and posterior cingulate gyrus. Nonetheless, psychopaths also showed overactivation in the bilateral fronto-temporal cortex for processing affective stimuli. Sterzer and colleagues (2005) observed a reduced activation in the right dorsal anterior cingulate cortex and left amygdala during viewing of negative pictures in adolescents with severe conduct disorder. Furthermore, as indicated above, the anterior cingulate cortex has been shown in several studies to be activated during deception (Kozel et al., 2004; Langleben et al., 2002; Nunez et al., 2005). This suggests that abnormal activation in the ACC may underlie the pathological lying and deception found in psychopaths. Again, this hypothesis remains to be tested.

SUMMARY OF EMPIRICAL FINDINGS Structurally, psychopathic individuals show abnormalities in the prefrontal cortex, temporal cortex (including the hippocampus and amygdala) and the corpus callosum. Functionally, abnormal activation has been found in psychopaths in areas including the prefrontal cortex (while performing an inhibition task), superior temporal regions (while engaging in a semantic task), the amygdala and hippocampus (while processing affective stimuli), the corpus callosum and the anterior cingulate. These regions have been repeatedly found to be activated in normal controls in recent brain imaging studies during the control of impulsive behaviors, processing negative affective information and decision making. Given the above evidence, it could be hypothesized that the structural and functional abnormalities in frontal-temporal-subcortical circuits may be partially account for the impulsivity/lack of inhibition, reward dominance, lack of remorse/guilt and shallow affect found in psychopaths.

REFERENCES Allison, T., Puce, A. & McCarthy, G. (2000). Social perception from visual cues: role of the STS region. Trends in Cognitive Sciences, 7, 267–78. Amen, D.G., Stubblefield, M., Carmichael, B. & Thisted, R. (1996). Brain SPECT findings and aggressiveness. Annals of Clinical Psychiatry, 8, 129–37. Anderson, S.W., Bechara, A., Damasio, H., Tranel, D. & Damasio, A.R. (1999). Impairment of social and moral behavior related to early damage in human prefrontal cortex. Nature Neuroscience, 2, 1032–7. Bassarath, L. (2001). Neuroimaging studies of antisocial behavior. Canadian Journal of Psychiatry, 46, 728–32. Bechara, A., Damasio, H. & Damasio, A.R. (2000). Emotion, decision making and the orbitofrontal cortex. Cerebral Cortex, 10, 295–307. Bechara, A., Dolan, S. & Hindes, A. (2002). Decision-making and addiction (part II): myopia for the future or hypersensitivity to reward? Neuropsychologia, 40, 1690–705. Brodmann, K. (1909). Vergliechende lokalisationlehere der grosshirnrinde in ihren prinziien dargestellt auf grund des aellenbaues: Leipzig: Barth.

FUNCTIONAL AND STRUCTURAL BRAIN IMAGING RESEARCH

79

Brower, M.C. & Price, B.H. (2001). Neuropsychiatry of frontal lobe dysfunction in violent and criminal behavior: a critical review. Journal of Neurology, Neurosurgery, and Psychiatry, 7, 720– 6. Bunge, S.A. (2004). How we use rules to select actions: a review of evidence from cognitive neuroscience. Cognitive, Affective and Behavioral Neuroscience, 4, 564–79. Bunge, S.A., Kahn, I., Wallis, J.D., Miller, E.K. & Wagner, A.D. (2003). Neural circuits subserving the retrieval and maintenance of abstract rules. Journal of Neurophysiology, 90, 3419– 28. Casebeer, W.D. & Churchland, P.S. (2003). The Neural Mechanisms of Moral Cognition: A MultipleAspect Approach to Moral Judgment and Decision-Making. Amsterdam: Springer. Crone, E.A. & van der Molen, M.W. (2004). Developmental changes in real life decision making: performance on a gambling task previously shown to depend on the ventromedial prefrontal cortex. Developmental Neuropsychology, 25, 251–79. Damasio, A.R. (1994). Descartes’ error and the future of human life. Scientific American, 271, 144. Davidson, R.J. & Irwin, W. (1999). The functional neuroanatomy of emotion and affective style. Trends in Cognitive Sciences, 3, 11–21. Dinn, W.M. & Harris, C.L. (2000). Neurocognitive function in antisocial personality disorder. Psychiatry Research, 97, 173–90. Dolan, M. & Park, I. (2002). The neuropsychology of antisocial personality disorder. Psychological Medicine, 32, 417–27. Fishbein, D. (2000). Executive cognitive function: a public health perspective. Aggression and Violent Behavior, 7, 215–35. Frith, U. & Frith, C.D. (2003). Development and neurophysiology of mentalizing. Philosophical Transactions of the Royal Society of London, 358, 459–73. Garavan, H., Ross, T.J., Murphy, K., Roche, R.A.P., & Stein, E.A. (2002). Dissociable executive functions in the dynamic control of behavior inhibition, error detection and correction. Neuroimage, 17, 1820–9. Garavan, H., Ross, T.J. & Stein, E.A. (1999). Right hemispheric dominance of inhibition control: an event-related functional MRI study. Proceedings of the National Academy of Sciences of the USA, 96, 8301–6. Gatzke-Kopp, L.M., Raine, A., Buchsbaum, M. & LaCasse, L. (2001). Temporal lobe deficits in murderers: EEG findings undetected by PET. Journal of Neuropsychiatry and Clinical Neuroscience, 13, 486–91. Giancola, P.R. & Mezzich, A.C. (2000). Executive cognitive functioning mediates the relation between language competence and antisocial behavior in conduct-disordered adolescent females. Aggressive Behavior, 26, 359–75. Gorenstein, E.E. (1982). Frontal lobe functions in psychopaths. Journal of Abnormal Psychology, 91, 368–79. Greene, J.D., Sommerville, R.B., Nystrom, L.E., Darley, J.M. & Cohen, J.D. (2001). An fMRI investigation of emotional engagement in moral judgment. Science, 293, 2105–8. Hare, R.D. (2003). Manual for the Revised Psychopathy Checklist (2nd edn.) Toronto: Multi-Health Systems. Hare, R.D. & Jutai, J.W. (1988). Psychopathy and cerebral asymmetry in semantic processing. Journal of Personality Processes and Individual Differences, 9, 329–37. Hariri, A.R., Mattay, V.S., Tessitore, A., Fera, F. & Weinberger D.R. (2002). Neocortical modulation of the amygdala response to fearful stimuli. Biological Psychiatry, 53, 494–501. Hart, S.D., Forth, A.E. & Hare, R.D. (1990). Performance of criminal psychopaths on selected neuropsychological tests. Journal of Abnormal Psychology, 100, 391–8. Heekeren, H.R., Wartenburger, I., Schmidt, H., Schwintowski, H. & Villringer, A. (2003). An fMRI study of simple ethical decision-making. Neuroreport, 14, 1215–19. Hirono, N., Mega, M.S., Dinov, I.D., Mishkin, F. & Cummings, J.L. (2000). Left frontotemporal hypoperfusion is associated with aggression in patients with dementia. Archives of Neurology, 57, 861–6. Horn, N.R., Dolan, M., Elliott, R., Deakin, J.F.W. & Woodruff, P.W.R. (2003). Response inhibition and impulsivity: an fMRI study. Neuropsychologia, 41, 1959–66.

80

VOLUME I: DIAGNOSIS AND TREATMENT

Intrator, J., Hare, R., Stritzke, P. et al. (1997). A brain imaging (Single Photon Emission Computerized Tomography) study of semantic and affective processing in psychopaths. Biological Psychiatry, 42, 96–103. Ishikawa, S.S. & Raine, A. (2003). Contributions of prefrontal lobe subregions to antisocial and aggressive behavior. In D. Barch (ed.), Cognitive and Affective Neuroscience of Psychopathology. Oxford: Oxford University Press. Kiehl, K.A., Smith, A.M., Hare, R.D. et al. (2001). Limbic abnormalities in affective processing by criminal psychopaths as revealed by functional magnetic resonance imaging. Biological Psychiatry, 50, 677–84. Kiehl, K.A., Smith, A.M., Mendrek, A. et al. (1999). Temporal lobe abnormalities in semantic processing by criminal psychopaths as revealed by functional magnetic resonance imaging. Psychiatry Research Neuroimaging, 130, 27–42. Konishi, S., Nakajima, K., Uchida, L., Schihara, K. & Miyashita, Y. (1998). No-go dominant brain activity in human inferior prefrontal cortex revealed by functional magnetic resonance imaging. European Journal of Neuroscience, 10, 1209–13. Kozel, F.A., Revell, L.J., Lorberbaum, J.P. et al. (2004). A pilot study of functional magnetic resonance imaging bring correlates of deception in healthy young men. Journal of Neuropsychiatry and Clinical Neuroscience, 16, 295–305. Krawczyk, D.C. (2002). Contribution of the prefrontal cortex to the neural basis of human decision making. Neuroscience and Behavioral Review, 26, 631–64. Kruesi, M.J.P., Casanova, M.F., Mannheim, G. & Johnson-Bilder, A. (2004). Reduced temporal lobe volume in early onset conduct disorder. Psychiatry Research Neuroimaging, 132, 1–11. Kuchinke, L, Jacobs, A.M., Grubich, C. et al. (2005). Incidental effects of emotional valence in single word processing: an fMRI study. Neuroimage, 17, 1037–41. Laakso, M.P., Gunning-Dixon, F., Vaurio, O. et al. (2002). Prefrontal volume in habitually violent subjects with antisocial personality disorder and type 2 alcoholism. Psychiatry Research Neuroimaging, 114, 95–102. Laakso, M.P. Vaurio, O., Koivisto, E. et al. (2001). Psychopathy and the posterior hippocampus. Behavioral Brain Research, 118, 187–93. Laakso, M.P., Vaurio, O., Savolainen, L. et al. (2000). A volumetric MRI study of the hippocampus in type 1 and 2 alcoholism. Behavioral Brain Research, 109, 177–86. Langleben, D.D., Schroeder, L., Maldjian, J.A. et al. (2002). Brain activity during stimulated deception: an event-related functional magnetic resonance study. Neuroimage, 15, 727–32. Lapierre, D., Braun, C.M. & Hodgins, S. (1995). Ventral frontal deficits in psychopathy: neuropsychological test findings. Neuropsychologia, 33, 139–51. LeDoux, J.E. (1996). The Emotional Brain: The Mysterious Underpinnings of Emotional Life. New York: Simon and Schuster. Lee, T.M.C., Liu, H., Tan, L. et al. (2002). Lie detection by functional magnetic resonance imaging. Human Brain Mapping, 15, 157–64. Liddle, P.F., Kiehl, K.A. & Smith, A.M. (2001). Event-related fMRI study of response inhibition. Human Brain Mapping, 12, 100–9. Miyashita, Y. & Hayashi, T. (2000). Neutral representation of visual objects: encoding and top-down activation. Current Opinion in Neurobiology, 10, 187–94. Moll, J., de Oliveira-Souza, R., Eslinger, P.J. et al. (2002). The neural correlates of moral sensitivity: a functional magnetic resonance imaging investigation of basic and moral emotions. Journal of Neuroscience, 22, 2730–6. Morgan, B.A. & Lilienfeld, O.S. (2000). A meta-analytic review of the relation between antisocial behavior and neuropsychological measures of executive function. Clinical Psychology Review, 20, 113–36. Muller, J.L., Sommer, M., Wagner, V. et al. (2003). Abnormalities in emotion processing within cortical and subcortical regions in criminal psychopaths: evidence from a functional magnetic resonance imaging study using pictures with emotional content. Psychiatry Research Neuroimaging, 54, 152–62. Nunez, J.M., Casey, B.J., Egner, T., Hare, T. & Hirsch, J (2005). Intentional false responding shares neural substrates with response conflict and cognitive control. Neuroimage, 25, 267–77.

FUNCTIONAL AND STRUCTURAL BRAIN IMAGING RESEARCH

81

Parker, A. & Gaffan, D. (1998). Memory after frontal/temporal disconnection in monkeys: conditional and non-conditional tasks, unilateral and bilateral frontal lesions. Neuropsychologia, 36, 259–71. Phan, K.L., Magalhaes, A., Ziemlewicz, T.J. et al. (2005). Neural correlates of telling lies: a functional magnetic resonance imaging study at 4 Tesla. Academic Radiology, 12, 164–72. Raine, A., Buchsbaum, M. & LaCasse, L. (1997). Brain abnormalities in murderers indicated by positron emission tomography. Biological Psychiatry, 42, 495–508. Raine, A., Ishikawa, S.S., Arce, E. et al. (2004). Hippocampal structural asymmetry in unsuccessful psychopaths. Biological Psychiatry, 55, 185–91. Raine, A., Lencz, T., Bihrle, S., LaCasse, L. & Colletti, P. (2000). Reduced prefrontal gray matter volume and reduced autonomic activity in antisocial personality disorder. Archives of General Psychiatry, 57, 119–27. Raine, A., Lencz, T., Taylor, K. et al. (2003). Corpus callosum abnormalities in psychopathic antisocial individuals. Archives of General Psychiatry, 160, 1627–35. Schienle, A., Schafer, A., Walter, B., Stark, R. & Vaitl, D. (2005). Brain activation of spider phobics towards disorder-relevant, generally disgust- and fear-inducing pictures. Neuroscience Letter, 388, 1–6. Schneider, F., Habel, U., Kessler, C. et al. (2000). Functional imaging of conditioned aversive emotional responses in antisocial personality disorder. Neuropsychobiology, 42, 192–201. Shohamy, D. Myers, C.E., Grossman, S. et al. (2004). Cortico-striatal contributions to feedback-based learning: converting data from neuroimaging and neuropsychology. Brain, 127, 851–9. Smith, E.E. & Jonides, J. (1999). Storage and executive processes in the frontal lobes. Science, 283, 1657–61. Soderstrom, H., Hultin, L., Tullberg, M.et al. (2002). Reduced frontotemporal perfusion in psychopathic personality. Psychiatry Research, 114, 81–94. Spence, S.A., Farrow, T.F., Herford, A.E. et al. (2001). Behavioral and functional anatomical correlates of deception in humans. Neuroreport, 12, 2849–53. Sterzer, P., Stadler, C., Krebs, A., Kleinschmidt, A. & Poustka, F. (2005). Abnormal neural responses to emotional visual stimuli in adolescents with conduct disorder. Biological Psychiatry, 57, 7–15. Stevens, M.C., Kaplan, R.F. & Hesselbrock, V.M. (2003). Executive-cognitive functioning in the development of antisocial personality disorder. Addictive Behaviors, 28, 285–300. Tiihonen, J., Hodgins, S. & Vaurio, O. (2000). Amygdaloid volume loss in psychopathy. Society for Neurroscience Meeting, 2017. Veit, R., Flor, H., Erb, M. et al. (2002). Brain circuits involved in emotional learning in antisocial behavior and social phobia in humans. Neuroscience Letters, 328, 233–6. Volkow, N.D., Tancredi, L.R., Grant, C. et al. (1995). Brain glucose metabolism in violent psychiatric patients: a preliminary study. Psychiatry Research, 61, 243–53. Vollm, B., Richardson, P., Stirling, J. et al. (2004). Neurobiological substrates of antisocial and borderline personality disorders: preliminary result of a functional fMRI study. Criminal Behavior and Mental Health, 14, 39–54. Wehner, J.M., Radcliffe, R.A., Rosmann, S.T. et al. (1997). Quantitative trait locus analysis of contextual fear conditioning in mice. Nature Genetics, 17, 331–4. Whalen, P.J., Bush, G., McNally, R.J. et al. (1998). The emotional counting stroop paradigm: a functional magnetic resonance imaging probe of the anterior cingulated affective division. Biological Psychiatry, 44, 1219–28. Williamson, S., Harpur, T.J. & Hare, R.D. (1991). Abnormal processing of affective words by psychopaths. Psychophysiology, 28, 260–73. Wong, M.T., Fenwick, P.B., Lumsden, J. et al. (1997). Positron emission tomography in male violent offenders with schizophrenia. Psychiatry Research, 68, 111–23. Wu, J.C., Buchsbaum, M.S., Johnson, J.C. et al. (1993). Magnetic resonance and positron emission tomography imaging of the corpus callosum: size, shape and metabolic rate in unipolar depression. Journal of Affective Disorders, 28, 15–25. Yang, Y., Raine, A., Lencz, T. et al. (2005). Volume reduction in prefrontal gray matter in unsuccessful criminal psychopaths. Biological Psychiatry, 57, 1103–8.

CHAPTER 5

Psychophysiological Correlates of Psychopathic Disorders Matthew S. Stanford Baylor University, Texas, USA

Rebecca J. Houston University at Buffalo, New York, USA

and Ernest S. Barratt University of Texas Medical Branch, USA

Psychopaths exemplify the extreme of individuals who have problems following social rules. This has been hypothesized to be related in large part to their lack of emotional responsiveness in social situations. A multitude of studies from Cleckley (1941) through Hare (Hare et al., 1990), Lykken, Patrick and others have been conducted in an attempt to elucidate those factors that contribute to the development and treatment of the psychopathic individual. Despite its popularity in clinical research, a definitive understanding of the basic mechanisms underlying this complex construct remains elusive. In this vein, a number of studies have examined the neurobiological correlates of psychopathy (e.g., Arnett, 1997; Raine, 1989; Sonderstrom et al., 2002). One area that has been a popular and valuable approach for understanding the underlying mechanisms in psychopathy is the use of psychophysiological techniques. The goal of the present chapter is to review the psychophysiological literature related to the concept of psychopathy and related disorders. Previous reviews have been restricted to those studies using the traditional Hare two-factor designation of psychopathy (Hare et al., 1990) or to specific psychophysiological techniques (Raine, 1989) or systems (Arnett, 1997). In this chapter we have chosen to examine the psychophysiological literature as it relates to recent factor analytic research (Cooke & Michie, 2001) on psychopathy and related disorders (i.e., antisocial personality disorder and dissocial personality disorder).

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

84

VOLUME I: DIAGNOSIS AND TREATMENT

FACTOR STRUCTURE OF PSYCHOPATHY Traditionally, psychopathy has been hypothesized to reflect two correlated facets: Factor 1, pertaining to interpersonal and affective features; and Factor 2, reflecting social deviance (Harpur, Hakstian & Hare, 1988; Harpur, Hare & Hakstian, 1989). These factors are primarily based on research conducted using the Psychopathy Checklist (PCL; Hare, 1980) and the Psychopathy Checklist-Revised (PCL-R; Hare, 1991) developed by Robert Hare. The PCL, and variations of the PCL, have become the established tools for evaluating psychopathy and psychopathic features. Recently, Cooke and Michie (2001) conducted an extensive re-evaluation of the factor structure of the PCL-R. Their report, consisting of multiple studies, contained two notable conclusions that should have a significant impact on future work in this area. First, factor analyses of the PCL-R, based partly on the original standardization data, indicated that a two-factor solution did not provide an acceptable structural model. Instead, a hierarchical model was proposed with a superordinate Psychopathy factor underpinned by three distinct lower order factors (Figure 5.1). In this three-factor model, the original PCL-R Factor 1 actually included two separate factors. Cooke and Michie labeled the first factor Arrogant and Deceitful Interpersonal Style, and the second factor Deficient Affective Experience. The third factor was composed of five items from the original PCL-R Factor 2, and Cooke and Michie applied the label Impulsive and Irresponsible Behavioral Style. Two recent studies have further validated this three-factor approach using the PCL in psychiatric patients (PCL-SV; Skeem, Mulvey & Grisso, 2003a) and incarcerated offenders (PCL-R; Hall, Benning & Patrick, 2004). Cooke and colleagues (Cooke et al., 2005a,b) have shown the three-factor structure to have good cross-cultural generalizability and stability. Furthermore, these factors are consistent with studies in children using the Psychopathy Screening Device (Frick, Bodin & Barry, 2000; Frick & Hare, 2001). The analogous factors for the Psychopathy Screening Device are termed Narcissism, Callous-Unemotional and Impulsivity (Frick et al., 2000). A second important conclusion from Cooke and Michie’s (2001) report was derived from the examination of a model which incorporated the psychopathy criteria from the aforementioned three-factor solution as well as the criteria for the diagnoses of antisocial personality disorder (APD; American Psychiatric Association, 2000) and dissocial personality disorder (DPD; World Health Organization, 1992). This analysis demonstrated substantial overlap across the three-factors for the psychopathy, APD and DPD criteria (Figure 5.1). This overlap is not surprising as the original conception of the APD and DPD diagnoses were originally based, in part, on the construct of psychopathy as described by clinicians like Cleckley (1941). The exact relationship between these clinical manifestations has been frequently debated (Cooke & Michie 2001; Hare et al., 1991; Ottoson et al., 2002). Specifically, it has been suggested that the diagnosis of APD reflects Factor 2 (social deviance) of the original two-factor conceptualization, but ignores the callous and unemotional interpersonal style (Factor 1) seen in the psychopath (Harpur et al., 1989; Hare, 1991). Conversely, it has been suggested that the DPD criteria incorporate more features related to the original Factor 1 (interpersonal and affective features), but do not sufficiently acknowledge features related to social deviance (Ottosson et al., 2002). Clinically, the overlap of these three distinctions has long been recognized – in fact, the terminology is often used interchangeably. Unfortunately, this has resulted in empirical research that often overlooks the potential confounding influence of these discrepancies when examining potential causal mechanisms.

PSYCHOPHYSIOLOGICAL CORRELATES

85

Arrogant and deceitful interpersonal style (narcissism) PCL-R Glibness/superficial charm Grandiose sense of self-worth Pathological lying Conning/manipulative APD DSM-III-R No regard for the truth Impulsive and irresponsible behavioral style (impulsivity) PCL-R Need for stimulation/proneness to boredom Parasitic lifestyle Lack of realistic, long-term goals Impulsivity Irresponsibility APD DSM-III-R Fails to plan ahead or is impulsive DPD ICD-10 Gross and persistent attitude of irresponsibility and disregard for social norms Deficient affective experience (callous/unemotional) PCL-R Lack of remorse or guilt Shallow affect Callous/lack of empathy Failure to accept responsibility for own actions APD DSM-III-R Lacks remorse DPD ICD-10 Callous unconcern for the feelings of others Incapacity to experience guilt and to profit from experience Marked proneness to blame others Figure 5.1 Overlap of PCL-R items, antisocial personality disorder criteria and dissocial personality disorder criteria Note: Adapted from Cooke and Michie (2001); PCL-R: Psychopathy Checklist – Revised; APD: antisocial personality disorder; DPD: dissocial personality disorder

ANTISOCIAL AND DISSOCIAL PERSONALITY DISORDERS: RELATIONSHIP TO PSYCHOPATHY As noted, some commonality among psychopathy, APD and DPD is not coincidental. In the first two versions of the Diagnostic and Statistical Manual of Mental Disorders (DSM-I

86

VOLUME I: DIAGNOSIS AND TREATMENT

and –II; American Psychiatric Association, 1952, 1968), psychopathic personality disorder was a diagnosis based largely on the works of individuals like Cleckley (1941), McCord and McCord (1956) and Karpman (1948). Cleckley (1941) is credited with developing a comprehensive description of the psychopathy syndrome which covered 16 diagnostic criteria. The development of the PCL was based largely on Cleckley’s work, and the diagnosis of psychopathic personality disorder in the DSM also followed Cleckley’s example. As a result, the diagnosis in DSM-I and II included features related to both social deviance and affective and interpersonal functioning. However, concerns regarding the reliability in gauging the personality-related aspects of the diagnosis led to changes in the criteria for DSM-III (American Psychiatric Association, 1980). As a result, the criteria for the newly named antisocial personality disorder (APD) primarily relied on criminal and antisocial behaviors (failure to conform to social norms, deceitfulness, impulsivity or failure to plan ahead, etc.), thus eliminating most criteria related to affective or interpersonal functioning. This focus for the APD diagnosis has remained relatively constant through subsequent revisions of the DSM (III-R and IV-TR; American Psychiatric Association, 1987, 2000), resulting in the aforementioned criticism that APD reflects Factor 2 of the original psychopathy construct and neglects features associated with Factor 1. The criteria for dissocial personality disorder, the diagnosis considered to be analogous to APD in the International Classification of Diseases (ICD-10) taxonomy, are also loosely based on the original concept of psychopathy. Unlike the APD diagnosis, however, the DPD criteria appear to focus more on interpersonal and affective features such as a callous unconcern for the feelings of others, incapacity to maintain enduring relationships and incapacity to experience guilt (Table 1; World Health Organization, 1992). Some behavioral aspects are included such as a disregard for social norms and a low threshold for discharge of aggression. However, it appears that although DPD, APD and psychopathy are frequently considered to be analogous syndromes, the specific criteria for these distinctions do not seem to be consistent. Interestingly, the descriptions for both APD and DPD note that these personality patterns are also referred to as ‘psychopathy, sociopathy or dissocial personality disorder’ (DSMIV-TR, p. 702) or ‘amoral, antisocial, asocial, psychopathic, and sociopathic personality (disorder)’ (ICD-10, p. 226). In DSM-IV-TR, the accompanying text on associated features and disorders for the APD diagnosis notes that ‘individuals with Antisocial Personality Disorder frequently lack empathy and tend to be callous, cynical, and contemptuous of the feelings, rights, and sufferings of others. . . They may display a glib, superficial charm. . . .’ (p. 703). These features are clearly derived from the traditional conception of psychopathy (which is acknowledged in the DSM), but are not part of the criteria for APD. As a result, individuals characterized as psychopaths likely meet criteria for APD, but it is possible that a number of individuals diagnosed with APD would not be characterized as psychopaths. The same may also be true of the DPD diagnosis and psychopathy. Furthermore, the research on the relationship between the APD and DPD diagnoses indicates concordant rates significantly lower than those for other analogous personality disorder diagnoses measured by the DSM and ICD taxonomies (Loranger et al., 1994; Ottoson et al., 2002). Despite the fact that APD and DPD were originally derived from the psychopathy construct, it appears that these diagnoses have drifted from that original influence. Perhaps the most critical problem with this ‘drif’ is that these terms are still used interchangeably in both practice and research. This results in limitations with regard to replicating and extrapolating research findings as well as applying these findings to clinical practice and criminal justice settings.

PSYCHOPHYSIOLOGICAL CORRELATES

87

PERSONALITY PATHOLOGY AND PSYCHOPATHIC DISORDERS Blackburn and Coid (1998) have argued that the confusion within the psychopathy literature emerged as a result of a failure to distinguish between personality constructs and antisocial behavior. The results of Cooke and Michie (2001) ‘place the definition of psychopathy firmly within the domain of personality pathology’ (p. 185). Furthermore, it has been suggested that variants of psychopathy may be distinguished by differences in these underlying facets (Skeem et al., 2003b). Thus it appears that psychophysiological studies of features related to Cooke and Michie’s (2001) factors may contribute to our understanding of psychopathic disorders as a whole. The present review encompasses psychophysiological research pertaining to the three factors: Arrogant and Deceitful Interpersonal Style (Narcissism); Deficient Affective Experience (Callous-Unemotional); and Impulsive and Irresponsible Behavioral Style (Impulsivity). This approach is taken here, and encouraged in future work, for several reasons: (i) to gauge the potential usefulness of the broader three-factor model for conceptualizing psychopathic disorders as a whole; (ii) to extend our understanding of these features that underlie psychopathic disorders and how they may contribute to development of the disorder; (iii) to identify conflicting evidence and determine potential confounds, ultimately leading to more systematic, reliable research; and (iv) to indicate the importance of considering the similarities and discrepancies between psychopathy and related disorders. Finally, because a review of neuroimaging data can be found in an accompanying chapter, the present chapter will focus primarily on electrocortical and autonomic psychophysiological techniques used in relation to the three aforementioned factors.

ARROGANT AND DECEITFUL INTERPERSONAL STYLE (NARCISSISM) Within the three-factor structure of psychopathy/APD one of the underlying facets is characterized by superficial charm, grandiosity, deception and manipulation. This component is probably best summarized by Frick and colleagues (2000) who have labeled it narcissism. The narcissistic individual is characterized by a pervasive pattern of grandiosity, need for admiration, impulsivity and a lack of empathy (American Psychiatric Association, 2000). They believe they are superior and insist that others recognize them as such. When this does not happen they may display a hostile and aggressive interpersonal style (Kernis & Sun, 1994; Rhodewalt & Morf, 1998). While several studies have demonstrated a relationship between the characteristics of narcissism and psychopathy/APD (Blackburn & Coid 1998; Frick et al., 2000; Zagon & Jackson 1994), to date few studies have attempted to look at the psychophysiological substrates of narcissism itself (Kelsey et al., 2001; Kelsey et al., 2002). Using an aversive tone task Kelsey and colleagues (2001) found a complex psychophysiological profile related to narcissism. Individuals scoring high on the Narcissistic Personality Inventory (NPI; Raskin & Terry, 1988) showed significantly lower skin conductance response (SCR) reactivity, greater pre-ejection period (PEP) shortening and enhanced cardiac deceleration in anticipation of the aversive stimulus when compared to those who scored low. These effects were shown during both active and passive coping conditions.

88

VOLUME I: DIAGNOSIS AND TREATMENT

The Kelsey and colleagues (2001) SCR results are consistent with greater SCR habituation in anticipation of an aversive stimulus that has been consistently reported in psychopath samples (Fowles, 2000; Fowles & Missel, 1994). However, the enhanced cardiac deceleration seen in the narcissistics is opposite to the enhanced acceleration traditionally seen during anticipation of an aversive stimulus in psychopaths (Hare, 1978; Hare & Craigen, 1974; Hare, Frazelle & Cox, 1978). However, two studies have reported enhanced cardiac deceleration in psychopaths (Hare, 1982; Ogloff & Wong, 1990). A follow-up study by Kelsey and colleagues (Kelsey et al., 2002) examined two dimensions of narcissism and found that SCR hyporeactivity in anticipation of an aversive stimulus was significantly correlated with alienation (covert/deflated narcissism) while PEP hyperreactivity under the same conditions was significantly correlated with egocentricity (overt/inflated narcissism). PEP, which is a purported measure of ß-adrenergic sympathetic influence on the heart, has not been studied in psychopathy. Psychophysiologically, individuals high in narcissism show impairment in the processing of aversive events (SCR hyporeactivity) and a heightened fight/flight response (PEP hyperreactivity). These results are consistent with similar findings in psychopathic populations (SCR hyporeactivity, Fowles, 1993; Hare, 1978; Siddle & Trasler, 1981; Zahn, 1986; heightened fight/flight response, Schalling, 1978). While narcissism is a multidimensional construct with a complex psychophysiological profile it is clear that the psychophysiological substrates of narcissism and psychopathy overlap in a predictable way that may help explain similar behaviors displayed in these populations and lend support to Kernberg’s (1989) suggestion that narcissism is a core component of both psychopathy and antisocial personality disorder.

IMPULSIVE AND IRRESPONSIBLE BEHAVIORAL STYLE (IMPULSIVITY) This factor relates to personality and behavioral aspects such as impulsivity, sensation seeking and irresponsibility. Other criteria subsumed on this factor according to Cooke and Michie (2001) include a parasitic lifestyle, a lack of realistic, long-term goals and a disregard for social norms. All these criteria are underscored, at least in part, by personality dimensions related to impulsivity/sensation seeking. With this in mind, this section of the review focuses on those studies examining psychophysiological correlates of impulsivity and sensation seeking. Impulsivity and sensation seeking are significant factors in a range of behaviors and psychiatric disorders (Moeller et al., 2001; Zuckerman, 1979). The impulsive individual tends to act or react quickly (on impulse) without thought or conscious judgment of the outcome or consequences. Sensation seeking is the tendency to pursue novel and stimulating experiences – it is sometimes referred to as risk taking. Those high in sensation seeking have strong positive affective reactions to situations of novelty and risk, are more sensitive to internal sensations and choose environments that augment them. Despite the recognized importance of these personality constructs in psychiatry and psychology, the body of psychophysiological work in impulsive and sensation-seeking subjects is relatively small compared to other personality constructs such as anger and anxiety. The psychophysiological literature that does exist on impulsivity and impulsivity-

PSYCHOPHYSIOLOGICAL CORRELATES

89

like constructs (e.g., extraversion and sensation seeking) is limited mainly to electrocortical techniques.

Electroencephalography (EEG) Eysenck (1994) has argued that the EEG is the ‘standard’ for assessing cortical arousal. The seminal work of David Lindsley (Lansing, Schwartz & Lindlsey, 1959; Lindlsey, 1960) demonstrated the relationship between high amplitude, low frequency activity (e.g., alpha) in the EEG and low cortical arousal, while higher levels of cortical arousal or activation are related to low amplitude, high frequency activity (e.g., beta). Within the impulsivity and sensation-seeking literature the theory of physiological underarousal has long dominated the field (Barratt, 1985; Eysenck & Eysenck, 1985; Zuckerman, 1979). Originally, Eysenck posited that extraverts function at a lower level of resting arousal, and therefore seek out stimulation (Eysenck, 1967). In their early work, Eysenck and Eysenck (1985) contend that the influential component of their extraversion construct was impulsivity. In support of the under-arousal theory it has been demonstrated that individuals high in impulsivity generally show greater EEG slowing, reflecting lower cortical arousal, when compared to nonimpulsive subjects at rest (Barratt & Patton, 1983; O’Gorman & Lloyd, 1987), during eyelid conditioning (Barratt, 1971), and during emotional processing (Stenberg, 1992). Similar results have been shown in aggressive individuals (Convit, Czobor & Volavka, 1991; Fishbein et al., 1989; Gatzke-Kopp, et al., 2001). In an attempt to examine impulsivity separate from impulsive aggression, Houston and Stanford (2005) compared EEG activity at rest and during photic stimulation between impulsive subjects (those scoring high on the Barratt Impulsiveness Scale) who reported no history of reactive aggressive behavior and nonaggressive, nonimpulsive controls. The impulsive group exhibited significantly lower delta and theta activity at frontal sites during rest and across all stimulation conditions. Decreases in delta and theta activity are commonly associated with greater cortical activation (e.g., hypervigilance and alertness; Beatty et al., 1974; Knott & Harr, 1996; Pritchard, 1991; Valentino, Arruda & Gold, 1993; ). Therefore, this finding was in contrast to the aforementioned slowing reported in other studies of impulsivity, but is remarkably similar to the theory that psychopaths exhibit better processing of relevant stimuli or enhanced attention as indexed by larger P3 event-related potential and positive slow wave (PSW) amplitudes (Flor et al., 2002; Raine 1989; 1993; Raine & Venables 1988). Similarly, Blackburn (1979) found that primary psychopaths show less theta activity than secondary psychopaths suggesting higher levels of cortical activation and alertness in this group. The impulsive group in the Houston and Stanford (2005) study also showed a different topographic distribution of beta activity compared to controls (lower levels of beta activity in the frontal region compared to both central and parietal regions while frontal beta activity in the control subjects was lower in comparison to the parietal region only). Correlational analyses indicated a significant negative relationship between frontal beta power and antisocial behavior scores on the Lifetime History of Aggression Questionnaire (Coccaro, Berman & Karvoussi, 1997). This is consistent with previous research demonstrating less frontal beta reactivity in relation to antisocial behavior (Finn et al., 2000). Conversely, research on sensation seeking has suggested a positive correlation between beta reactivity and sensation-seeking scores (Golding & Richards, 1985).

90

VOLUME I: DIAGNOSIS AND TREATMENT

Event-Related Potential (ERP) Another measure of brain activity often used in the assessment of impulsivity and sensation seeking is the event-related potential (ERP). While derived from the EEG, which measures spontaneous brain activity, the ERP is generated by a response to a specific stimulus and averaged over a number of trials. The most common ERPs used in the study of personality features such as impulsivity and sensation seeking are the early sensory components (e.g., N1). This is likely due to the consistent finding of increased augmenting of the early sensory ERPs in impulsive and sensation-seeking individuals (Barratt, 1981; Brocke, Tasche & Beauducel, 1987; Brocke et al., 2000; Carrillo de la Pena & Barratt, 1993; Hergerl et al., 1989; Wang & Wang 2001; Zuckerman, 1990; Zuckerman, Murtaugh & Siegel, 1974). The augmenting/reducing dimension of sensory performance was originally described by Petrie (1960, 1967) on the basis of perceptual differences observed in subjects on the Kinesthetic Figural Aftereffects test. Buchsbaum and Silverman (1968) later developed a visual ERP technique for measuring augmenting/reducing. Impulsive, extraverted and sensationseeking individuals have consistently been shown to be ERP augmenters in response to increasing stimulus intensity (for review see Carrillo de la Pena, 1992). This result has been interpreted as supportive of the under-arousal theory of impulsiveness and suggests that impulsive individuals seek out stimulation in an attempt to increase their low physiological arousal to a more ‘optimal’ level (Zuckerman, 1990). The relationship between cortical augmenting and psychopathy remains contentious (Raine, 1989; Raine & Venables, 1990). While the results on sensory ERPs and impulsivity/sensation seeking appear consistent, the relationship between long-latency potentials remains unclear. Few studies examining long-latency ERPs have focused solely on impulsivity or sensation seeking. Those studies that have taken this approach differ significantly in their methodology. Unlike the early sensory ERPs, long-latency potentials are cognitive in nature and are influenced by task-relevant information (Donchin & Coles, 1988). The P3, thought to provide an index of cognitive resource allocation and processing, is probably the most studied ERP in psychological and psychiatric literatures. Some studies have shown a significant negative relationship between P3 amplitude and impulsivity (Harmon-Jones, Barratt & Wigg, 1997) or sensation seeking (Ratsma, van der Stelt & Schoffelmeer, 2001; Wang & Wang, 2001) and related constructs such as extraversion (Stelmack & Houlihan, 1995) and psychoticism (De Pascalis & Speranza, 2000). Other studies have reported opposite results (Brocke et al., 1997; Pierson et al., 1999; Stenberg 1994). This inconsistency in P3 results is remarkably similar to the results of P3 amplitude investigations in psychopathy. Investigators using the P3 in psychopathic samples have reported no significant P3 amplitude differences (Jutai, Hare & Connolly, 1987), higher P3 amplitude (Raine & Venables, 1988), and others have reported lower P3 amplitude (Kiehl et al., 1999a). However, P3 studies in individuals diagnosed with APD have consistently shown reduced P3 amplitude (Bauer, O’Connor & Hesselbrock, 1994; Costa et al., 2000; O’Conner et al., 1994) compared to controls. Unlike the P3, which requires voluntary attentional control, the mismatch negativity (MMN) provides an index of involuntary attentional processing or automatic deviance detection (Naatanen, 2004). In a recent study (Franken, Nijs & Van Strien, 2005), left hemispheric MMN amplitude was significantly negatively correlated with dysfunctional impulsivity on the Dickman Impulsivity Inventory (Dickman, 1990). The authors interpreted these results as evidence of enhanced preattentive processing of irrelevant stimuli in

PSYCHOPHYSIOLOGICAL CORRELATES

91

impulsive persons. They further emphasized the fact that this relationship is independent of motoric responses, which are often used as a measure of impulsivity. Several studies have also looked at response-related potentials such as the contingent negative variation (CNV) and error-related negativity (Ne/ERN) in impulsive individuals. The CNV is a steady, negative shift that develops in anticipation of a response after a warning signal and has been suggested to be a measure of prefrontal cortex activity (Rosahl & Knight, 1995). While impulsive individuals have been shown to have very low CNVs (Barratt & Patton, 1983; Brown, Fenwick & Howard, 1989; Howard, Fenton & Fenwick, 1982) psychopathic and APD populations are typically characterized by larger than normal negative potentials (Bauer, 2001; Fenton et al., 1978; Flor et al., 2002; Forth & Hare, 1989; Howard, Fenton & Fenwick, 1984). This difference maybe related to the low arousal and distractability of impulsive individuals and the enhanced attentional processing theorized to exist in the psychopath (Tecce & Cattanach, 1993). Ne/ERN is a negative potential that is time-locked to the execution of an incorrect response. Pailing and colleagues (Pailing et al., 2002) found that individuals who exhibit small Ne/ERN peak amplitudes show a less controlled response strategy and are thus more impulsive. Ruchsow et al. (2005) replicated this effect using a Go/NoGo task to elicit the Ne/ERN. Finally, Fallgatter and Herrmann (2001) have shown that impulsivity is significantly correlated with a more anterior location of the Go and NoGo brain electrical field centroids. This result suggests that impulsivity may be associated with differences in prefrontal activation during cognitive response control.

Autonomic Measures As mentioned earlier electrocortical measures have dominated the psychophysiological literature on impulsiveness. Few studies have looked at traditional autonomic measures (e.g., electrodermal activity, heart rate) in impulsive individuals. Electrodermal activity (EDA) is controlled by the sympathetic nervous system and can be measured at rest or in response to a particular stimulus. Jones (1950, 1960) found electrodermal hyporeactivity to be predictive of later impulsive behavior in a longitudinal study of adolescents. Impulsive individuals have also been shown to have higher autonomic nervous system (ANS) variability using an ANS index that included electrodermal response (Barratt, 1963). Electrodermal hyporeactivity has also been shown in individuals high on sensation seeking (Gatzke-Kopp et al., 2002; Plouffe & Stelmack, 1986) and extraversion (Smith, 1983). Similarly, electrodermal hyporeactivity is one of the most replicated psychophysiological results in psychopathy and APD (Arnett, 1997; Dinn & Harris, 2000; Flor et al., 2002; Fowles, 1980; Fung et al., 2005; Hare, 1978;). Fowles (2000) has suggested that electrodermal hyporeactivity shown in psychopaths is related to a dimension of impulsivity within the broader construct of psychopathy. Unlike electrodermal activity, heart rate (HR) is controlled by input from both the parasympathetic and sympathetic nervous systems. Only three studies have looked specifically at impulsivity and heart rate. Barratt (1963) and Rule and Fischer (1970) found increased variability in the heart rate of impulsive individuals. Mathias and Stanford (2003) measured heart rate at rest and during increasing levels of stress during the Paced Auditory Serial Attention Task (PASAT). Highly impulsive individuals were shown to have a significantly lower heart rate at rest and a greater magnitude of change from baseline during the initial trial of the task. While their change from baseline was of a greater magnitude, highly

92

VOLUME I: DIAGNOSIS AND TREATMENT

impulsive individuals showed a lower heart rate compared to controls at all levels of the task. Similarly, in antisocial and/or criminal populations low resting heart rate is a consistent finding (; Ishikawa & Raine, 2002; Raine & Jones, 1987; Raine, Venables & Williams, 1990a, 1990b). However, the results of heart rate studies using psychopaths are not quite so clear. Although a number of studies have reported increased heart rate acceleration in anticipation of an aversive stimulus (for review see Arnett, 1997) the overall results are variable at best (Kilzieh & Cloninger, 1993). We agree with Mawson and Mawson’s (1977) suggestion that the inconsistency seen in the psychopathy literature indicates a greater degree of heart rate variability in this population. This is consistent with similar results seen in impulsive populations (Barratt, 1963; Rule & Fischer, 1970). In summary, impulsive individuals differ significantly from those characterized as psychopathic on electrocortical measures (Table 5.1). However, there is an amazing degree of similarity between these two groups on autonomic measures. The psychophysiological profile of highly impulsive individuals shows a general low level of physiological arousal both centrally and peripherally. This under arousal has been suggested to limit information processing and create an unpleasant hedonic state from which the impulsive individual attempts to remove himself through stimulation-seeking behavior (Eysenck & Eysenck, 1985). In contrast, the results of electrocortical measures in psychopathic individuals suggest a high level of cortical activation and alertness. Although autonomic measures in psychopathy appear similar to those found in impulsive individuals, they may have very different etiologies. While the EDA hyporeactivity and low resting/variable heart rate in impulsive individuals is reflective of low physiological arousal, the same results in the psychopath are most likely due to emotional/affective processing deficits associated with the limbic system. Boucsein (1992) has proposed a two-system model of EDA central control. The first system is an ipsilateral limbic control system responsible for EDA in emotional situations and the second is a contralateral frontal cortical control system responsible for EDA during locomotion, orienting and cognition. It is suggested that psychopathic individuals have deficits in the limbic control system while impulsive individuals show deficits in the frontal cortical system. Similar dual-function control of heart rate has also been proposed (Hugdahl, 2001). So it appears that while psychopathic individuals are indeed often impulsive, their impulsiveness is more likely related to an underlying deficit in attending to and processing relevant (emotional) information (Fowles, 1993) than low physiological arousal as seen in Table 5.1 Comparison of psychophysiological results in impulsivity and psychopathy

Electrocortical measures EEG CNV A/R P3 Autonomic measures EDA HR

Impulsivity

Psychopathy

↑Slow wave activity ↓Amplitude Augmenters ↓Amplitude

↓Slow wave activity ↑Amplitude (Reducers) (↑Amplitude or Normal)

Hyporeactivity ↓Resting, ↑ Variability

Hyporeactivity ↑Variability

Note: (Italics): Majority of studies support; EEG: electroencephalograph; CNV; contingent negative variation; A/R: augmenting/reducing; EDA: electrodermal activity; HR: heart rate.

PSYCHOPHYSIOLOGICAL CORRELATES

93

the highly impulsive individual. Recent reviews (Lane et al., 2003; Reynolds et al., 2006; Swann et al., 2002) have suggested two models of impulsivity that may account for this difference, a rapid-response model, which may be more associated with psychopathology; and a reward-discounting model.

DEFICIENT AFFECTIVE EXPERIENCE (CALLOUS-UNEMOTIONAL) According to Cooke and Michie (2001), criteria for this factor include a lack of remorse or guilt, callous unconcern or lack of empathy for others, shallow affect, proneness to blame others and a failure to accept responsibility for own actions. Unlike the factors 1 and 3 of the model, this factor is not necessarily related to a specific underlying personality feature or behavior that can be an independent subject of research. Instead, these features seem to be considered hallmark features of psychopathy (particularly as compared to the APD diagnosis). As a result, this section focuses on affective processing and those psychophysiological studies that have examined it as it relates to the psychopathic disorders (e.g., psychopathy and APD). A deficit in emotional processing has long been considered a core characteristic of psychopathic disorders (Cleckley, 1941). In the classic two-factor model of psychopathy Factor 1 reflects emotional detachment and a lack of guilt while Factor 2 is related to an impulsive, antisocial and unstable lifestyle (Hare, 1991). Harpur and Hare (1994) have shown that Factor 2 scores decline with age while Factor 1 scores remain constant. Blair and Frith (2000) have suggested that this persistence in Factor 1 (emotional-processing deficits) closely reflects the neurocognitive impairments that result in the development of psychopathy. Brain structures involved in the processing of emotional stimuli include the amygdala, insula, ventral striatum, hippocampus, anterior cingulate gyrus and the prefrontal cortex (Phillips et al., 2003). Deficits in this complex fronto-limbic circuit have been hypothesized to result in aggressive (Davidson, Putnam & Larson, 2000) and psychopathic (Anderson et al., 1999; Blair, 2003) behavior. Indeed psychopathic individuals do show abnormal functioning in limbic structures that have been associated with emotional processing (Kiehl et al., 2001; Laasko et al., 2001; Muller et al., 2003; Viet et al., 2002). Studies looking at cortical areas related to emotional processing, particularly the prefrontal cortex, in psychopathy have tended to find an increased level of functioning during processing (Intrator et al., 1997; Kiehl et al., 2001; Muller et al., 2003). The literature is not consistent and contrary results have been found in psychopathy (Veit et al., 2002) and individuals diagnosed with APD (Raine et al., 2000; Schneider et al., 2000). In a recent SPECT study of psychopathy, Sonderstrom and colleagues (Sonderstrom et al., 2002) found significant negative correlations between frontal and temporal perfusion and Factor 1 (Arrogant and Deceitful Interpersonal Style) as well as Factor 2 (Deficient Affective Experience) of the Cooke and Michie (2001) three-factor model. Phillips and colleagues (2003) suggest that emotion perception consists of three main processes: (i) appraisal of the emotional significance of a stimulus; (ii) the production of an affective state; and (iii) the regulation of the affective state. Appraisal and the production of the affective state are predominately the function of a ventral system made up of the

94

VOLUME I: DIAGNOSIS AND TREATMENT

limbic structures mentioned above. Regulation of the affective state is an executive function preformed by areas in the prefrontal cortex (dorsal system). It has been suggested that the emotional-processing deficit seen in psychopathic individuals is related to deficient interaction between limbic (ventral system) and cortical structures (dorsal system) (Flor et al., 2002). More specifically this deficit involves an inability to effectively generate a state of anxiety or fear when presented or in anticipation of an aversive stimulus (Fowles, 1980; Hare, 1970; Lykken, 1957; Patrick, 1994). Psychophysiologically psychopathic individuals have been consistently shown to be electrodermally hyporeactive to aversive stimuli (Arnett, 1997; Hare, 1978; Fowles, 1980, 2000; Siddle & Trasler, 1981; Zahn, 1986). Patrick (1994) has argued that autonomic measures are not reliable indices of fear activation and has suggested the use of the startle probe paradigm as a more effective measure of emotional activation in the psychopath. In the startle probe paradigm an individual is presented with emotionally evocative and neutral slides. A sudden noise burst (acoustic startle probe) occurs unexpectedly during some of the slides and reflex blinks to the probes are measured. In normal individuals startle responses (reflex blinks) to pleasant slides are reduced while responses to aversive slides are potentiated compared to neutral slides. It has been shown that psychopaths lack startle potentiation to aversive slides (Flor et al., 2002; Patrick, 1994). Interestingly both electrodermal responding (Edelberg, 1966) and startle potentiation during aversive events (Davis, 1992) are mediated by the amygdala. Few studies have attempted to look at emotional processing in psychopathic disorders using ERPs. Williamson and colleagues (Williamson, Harpur & Hare, 1991) compared the ERP response of psychopathic and nonpsychopathic inmates to affective words, neutral words and pronounceable nonwords. Several components of the ERP differentiated between affective and neutral words in the nonpsychopaths but this discrepancy was greatly reduced in the psychopaths. Psychopaths also differed from nonpsychopaths in the overall amplitude of a negative frontal-central ERP component and the late positive complex. These results were replicated in a subsequent study by Kiehl and colleagues (1999b). Flor and colleagues (2002) recorded ERPs in noncriminal psychopaths and healthy controls during a differential Pavlovian conditioning task with a foul odor as the unconditioned stimulus and neutral faces as the conditioned stimuli (CS). Attentional resource allocation of conditioned stimuli as assessed by the ERP components CNV, N100, P200 and P300 was equal or superior in the psychopathic group compared to healthy controls. A lack of CS differentiation was found in the CNV of the psychopathic group. Previous research has shown that CNV amplitude is modulated by extensive amygdale–cortical back projections (Birbaumer et al., 1990). As a whole, results from studies looking at emotional processing in psychopathy suggest that deficits in the functioning of limbic structures, specifically the amygdala, make it difficult for these individuals to produce an appropriate affective state to unpleasant and/or aversive stimuli.

CONCLUSIONS This chapter has attempted to use the three-factor structure of psychopathy proposed by Cooke and Michie (2001) as a framework to help explain the psychophysiological data found in studies of the psychopathic disorders. The underlying factors of psychopathy, while having different psychophysiological profiles, overlap in a consistent manner suggesting

PSYCHOPHYSIOLOGICAL CORRELATES

95

that psychopathic behavior may result from a dysfunction of neural circuits related to the processing of aversive and affective stimuli. These circuits are associated with a number of CNS areas including prefrontal cortex, limbic system and brain stem reticular nuclei. Ideally, a better understanding of the underlying physiology of individuals who display psychopathic and antisocial behavior will lead to more effective treatments and interventions in both the mental health and criminal justice systems.

REFERENCES American Psychiatric Association (1952). Diagnostic and Statistical Manual of Mental Disorders (1st edn.). Washington, DC: American Psychiatric Association. American Psychiatric Association (1968). Diagnostic and Statistical Manual of Mental Disorders (2nd edn.). Washington, DC: American Psychiatric Association. American Psychiatric Association (1980). Diagnostic and Statistical Manual of Mental Disorders (3rd edn.). Washington, DC: American Psychiatric Association. American Psychiatric Association (1987). Diagnostic and Statistical Manual of Mental Disorders (3rd edn., rev.). Washington, DC: American Psychiatric Association. American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders (4th edn., text revision). Washington, DC: American Psychiatric Association. Anderson, S.W., Bechara, A., Damasio, H. et al. (1999). Impairment of social and moral behaviour related to early damage in the human prefrontal cortex. Nature Neuroscience, 2, 1032–7. Arnett, P.A. (1997). Autonomic responsivity in psychopaths: a critical review and theoretical proposal. Clinical Psychology Review, 17, 903–36. Barratt, E.S. (1963). Intra-individual variability of performance: ANS and psychometric correlates. Texas Reports on Biology and Medicine, 4, 496–504. Barratt, E.S. (1971). Psychophysiological correlates of classical eyelid conditioning among subjects selected on the basis of impulsiveness and anxiety. Biological Psychiatry, 3, 339–46. Barratt, E.S. (1981). Time perception, cortical evoked potentials and impulsiveness among three groups of adolescents. In J.R. Hays, T.K. Roberts & K.S. Solway (eds.), Violence and the Violent Individual (pp. 87–95). New York: SP Medical and Scientific Books. Barratt, E.S. (1985). Impulsiveness subtraits: arousal and information processing. In J.T. Spence & C.E. Izard (eds.), Motivation, Emotion and Personality (pp. 137–46). New York: Elsevier. Barratt, E.S. & Patton, J.H. (1983). Impulsivity: cognitive, behavioral and psychophysiological correlates. In M. Zuckerman (ed.), Biological Bases of Sensation Seeking, Impulsivity and Anxiety (pp. 77–121). Hillsdale, NJ: Lawrence Erlbaum. Barratt, E.S., Pritchard, W.S., Faulk, D.M. & Brandt, M.E. (1987). The relationship between impulsiveness subtraits, trait anxiety and visual N100 augmenting/reducing: a topographic analysis. Personality and Individual Differences, 8, 43–51. Bauer, L.O. (2001). Antisocial personality disorder and cocaine dependence: their effects on behavioral and electroencephalographic measures of time estimation. Drugs and Alcohol Dependence, 63, 87–95. Bauer, L.O., O’Connor, S. & Hesselbrock, V.M. (1994). Frontal P300 decrements in antisocial personality disorder. Alcoholism: Clinical and Experimental Research, 18, 1300–5. Beatty, J., Greenberg, A., Deibler, W.P. & O’Hanlon, J.F. (1974). Operant control of occipital theta rhythm affects performance in a radar monitoring task. Science, 183, 871–3. Birbaumer, N., Elbert, T., Canavan, A. & Rockstroh, B. (1990). Slow cortical potentials of the cerebral cortex and behavior. Physiological Review, 70, 1–41. Blackburn, R. (1979). Cortical and autonomic arousal in primary and secondary psychopaths. Psychophysiology, 16, 143–50. Blackburn, R. & Coid, J. W. (1998). Psychopathy and the dimensions of personality disorders in violent offenders. Personality and Individual Differences, 25, 129–45. Blair, R.J. (2003). Neurobiological basis of psychopathy. British Journal of Psychiatry, 182, 5–7.

96

VOLUME I: DIAGNOSIS AND TREATMENT

Blair, R.J. & Frith, U. (2000). Neurocognitive explanations of the antisocial personality disorders. Criminal Behaviour and Mental Health, 10, S66–S81. Boucsein, W. (1992). Electrodermal Activity. New York: Plenum Press. Brocke, B., Beauducel, A., John, R., Debener, S & Heilemann, H. (2000). Sensation seeking and affective disorders: characteristics in the intensity dependence of acoustic evoked potentials. Neuropsychobiology, 41, 24–30. Brocke, B., Tasche, K.G. & Beauducel, A. (1997). Biopsychological foundations of extraversion: differential effort reactivity and state control. Personality and Individual Differences, 22, 447–58. Brown, D., Fenwick, P. & Howard, R. (1989). The contingent negative variation in a Go/No-Go avoidance task: relationships with personality and subjective state. International Journal of Psychopharmacology, 7, 35–45. Buchsbaum, M. & Silverman, J. (1968). Stimulus intensity and the cortical evoked response. Psychosomatic Medicine, 30, 12–22. Carrillo de la Pena, M.T. (1992). ERP augmenting/reducing and sensation seeking: a critical review. International Journal of Psychophysiology, 12, 211–20. Carrillo de la Pena, M.T. & Barratt, E.S. (1993). Impulsivity and ERP augmenting/reducing. Personality and Individual Differences, 15, 25–32. Cleckley, H. (1941). The Mask of Sanity (1st edn.). St. Louis, MO: Mosby. Coccaro, E.F., Berman, M.E. & Karvoussi, R.J. (1997). Assessment of life history of aggression: development and psychometric characteristics. Psychiatry Research, 73, 147–57. Convit, A., Czobor, P. & Volavka, J. (1991). Lateralized abnormality in the EEG of persistently violent psychiatric inpatients. Biological Psychiatry, 30, 363–70. Cooke, D.J. & Michie, C. (2001). Refining the construct of psychopathy: towards a hierarchical model. Psychological Assessment, 13, 171–88. Cooke, D.J., Michie, C., Hart, S.D. & Clark, D. (2005a). Assessing psychopathy in the UK: concerns about cross-cultural generalisability. British Journal of Psychiatry, 186, 335–41. Cooke, D.J., Michie, C., Hart, S.D. & Clark, D. (2005b). Searching for the pan-cultural core of psychopathic personality disorder. Personality and Individual Differences, 39, 283–95. Costa, L., Bauer, L.O., Kuperman, S. et al. (2000). Frontal P300 decrements, alcohol dependence and antisocial personality disorder. Biological Psychiatry, 47, 1064–71. Davidson, R.J., Putnam, K.M. & Larson, C.L. (2000). Dysfunction in the neural circuitry of emotion regulation: A possible prelude to violence. Science, 289, 591–4. Davis, M. (1992). The role of the amygdala in fear-potentiated startle: implications for animal models of anxiety. Trends in the Pharmacological Sciences, 13, 35–41. De Pascalis, V. & Speranza, O. (2000). Personality effects on attentional shifts to emotional charged cues: ERP, behavioral and HR data. Personality and Individual Differences, 29, 217–38. Dickman, S.J. (1990). Functional and dysfunctional impulsivity: personality and cognitive correlates. Journal of Personality and Social Psychology, 58, 95–102. Dinn, W.M. & Harris, C.L. (2000). Neurocognitive function in antisocial personality disorder. Psychiatry Research, 97, 173–90. Donchin, E. & Coles, M.G.H. (1988). Is the P300 component a manifestation of context updating? Behavioral and Brain Science, 11, 355–72. Edelberg, R. (1966). Electrical activity of the skin: its measurement and uses in psychophysiology. In N.S. Greenfield & R.S. Sternbach (eds.), Handbook of Psychophysiology (pp. 367–409). New York: Holt, Rinehart and Winston. Eysenck, H.J. (1967). The Biological Basis of Personality. Springfield, IL: Charles C. Thomas. Eysenck, H.J. (1994). Personality: biological foundations. In P.A. Vernon (ed.), The Neuropsychology of Individual Differences (pp. 151–207). London: Academic Press. Eysenck, H.J. & Eysenck, M.W. (1985). Personality and Individual Differences: A Natural Science Approach. New York: Plenum. Fallgatter, A.J. & Herrmann, M.J. (2001). Electrophysiological assessment of impulsive behavior in healthy subjects. Neuropsychologia, 39, 328–33. Fenton, G.W., Fenwick, P.B., Ferguson, W. & Lam, C.T. (1978). The contingent negative variation in antisocial behaviour: a pilot study of Broadmoor patients. British Journal of Psychiatry, 132, 368–77.

PSYCHOPHYSIOLOGICAL CORRELATES

97

Finn, P.R., Ramsey, S.E. & Earleywine, M. (2000). Frontal EEG response to threat, aggressive traits and a family history of alcoholism: a preliminary study. Journal of Studies on Alcohol, 61, 38–45. Fishbein, D.H., Herning, R.I., Pickworth, W.B. et al. (1989). EEG and brainstem auditory evoked potential response potentials in adult male drug abusers with self-reported histories of aggressive behavior. Biological Psychiatry, 26, 595–611. Flor, H., Birbaumer, N., Hermann, C., Ziegler, S. & Patrick, C.J. (2002). Aversive Pavlovian conditioning in psychopaths: peripheral and central correlates. Psychophysiology, 39, 505–18. Forth, A.E. & Hare, R.D. (1989). The contingent negative variation in psychopaths. Psychophysiology, 26, 676–82. Fowles, D.C. (1980). The three arousal model: implications of Gray’s two-factor learning theory for heart rate, electrodermal activity and psychopathy. Psychophysiology, 17, 87–104. Fowles, D.C. (1993). Electrodermal activity and antisocial behavior: empirical findings and theoretical issues. In J.C. Roy, W. Boucsein, D.C. Fowles & J. Gruzelier (eds.), Progress in Electrodermal Research (pp. 223–8). London: Plenum. Fowles. D.C. (2000). Electrodermal hyporeactivity and antisocial behavior: does anxiety mediate the relationship. Journal of Affective Disorders, 61, 177–89. Fowles, D.C. & Missel, K.A. (1994). Electrodermal hyporeactivity. Motivation and psychopathy: theoretical issues. In D. Fowles, P. Sutker & S.H. Goodman (eds.), Progress in Experimental Personality and Psychopathology Research 1994. Special Focus on Psychopathy and Antisocial Behvavior: A Developmental Perspective (pp. 263–83). New York: Springer. Franken, I.H.A., Nijs, I. & Van Strien, J.W. (2005). Impulsivity affects mismatch negativity (MMN) measures of preattentive auditory processing. Biological Psychology, 70, 161–7. Frick, P.J., Bodin, S.D. & Barry, C.T. (2000). Psychopathic traits and conduct problems in community and clinic-referred samples of children: further development of the psychopathy screening device. Psychological Assessment, 12, 382–93. Frick, P.J. & Hare, R.D. (2001). The Antisocial Process Screening Device. Toronto: Multi-Health Systems. Fung, M.T., Raine, A., Loeber, R. et al. (2005). Reduced electrodermal activity in psychopathy-prone adolescents. Journal of Abnormal Psychology, 114, 187–96. Gatzke-Kopp, L., Raine, A., Buchsbaum, M.S. & LaCasse, L. (2001). Temporal lobe deficits in murderers: EEG findings undetected by PET. Journal of Neuropsychiatry and Clinical Neuroscience, 13, 486–91. Gatzke-Kopp, L., Raine, A., Loeber, R., Stouthamer-Loeber, M. & Steinhauer, S.R. (2002). Serious delinquent behavior, sensation seeking and electrodermal arousal. Journal of Abnormal Child Psychology, 30, 477–86. Golding, J.F. & Richards, M. (1985). EEG spectral analysis, visual evoked potential and photic-driving correlates of personality and memory. Personality and Individual Differences, 6, 67–76. Hall, J.R., Benning, S.D. & Patrick, C.J. (2004). Criterion-related validity of the three-factor model of psychopathy: personality, behavior and adaptive functioning. Assessment, 11, 4–16. Hare, R.D. (1970). Psychopathy: Theory and Research. New York: John Wiley & Sons, Inc. Hare, R.D. (1978). Electrodermal and cardiovascular correlates of psychopathy. In R.D. Hare & D. Schalling (eds.), Psychopathic Behavior: Approaches to Research (pp. 107–44). New York: John Wiley & Sons, Inc. Hare, R.D. (1980). A research scale for the assessment of psychopathy in criminal populations. Personality and Individual Differences, 1, 111–20. Hare, R.D. (1982). Psychopathy and physiological activity during anticipation of an aversive stimulus in a distraction paradigm. Psychophysiology, 19, 266–71. Hare, R.D. (1991). Manual for the Hare Psychoapthy Checklist – Revised. Toronto: Multi-Health Systems. Hare, R.D. & Craigen, D. (1974). Psychopathy and physiological activity in a mixed-motive game situation. Psychophysiology, 11, 197–206. Hare, R.D., Frazelle, J. & Cox, D.N. (1978). Psychopathy and physiological responses to threat of an aversive stimulus. Psychophysiology, 15, 165–72. Hare, R.D., Harpur, T.J., Hakstian et al. (1990). The revised psychopathy checklist: reliability and factor structure. Psychological Assessment, 2, 238–41.

98

VOLUME I: DIAGNOSIS AND TREATMENT

Hare, R.D., Hart, S.D. & Harpur, T.J. (1991). Psychopathy and the DSM-IV criteria for antisocial personality disorder. Journal of Abnormal Psychology, 100, 391–8. Harmon-Jones, E., Barratt, E.S. & Wigg, C. (1997). Impulsiveness, aggression, reading and the P300 of the event-related potential. Personality and Individual Differences, 22, 439–45. Harpur, T.J., Hakstian, A.R. & Hare, R.D. (1988). Factor structure of the psychopathy checklist. Journal of Consulting and Clinical Psychology, 56, 741–7. Harpur, T.J. & Hare, R.D. (1994). Assessment of psychopathy as a function of age. Journal of Abnormal Psychology, 103, 604–9. Harpur, T.J., Hare, R.D. & Hakstian, A.R. (1989). Two-factor conceptualization of psychopathy: construct validity and assessment implications. Psychological Assessment, 1, 6–17. Hergerl, R.J., Prochno, I., Ulrich, G. & Muller-Oerlinghauser, B. (1989). Sensation seeking and auditory evoked potentials. Biological Psychiatry, 25, 179–90. Houston, R.J. & Stanford, M.S. (2005). Electrophysiological substrates of impulsiveness: Potential effects on aggressive behavior. Progress in Neuropsychopharmacology and Biological Psychiatry, 29, 305–13. Howard, R.C., Fenton, G.W. & Fenwick, P.B. (1982). Event Related Brain Potentials in Personality and Psychopathology: A Pavlovian Approach. Letchworth: Wiley Research Studies Press. Howard, R.C., Fenton, G.W. & Fenwick, P.B. (1984). The contingent negative variation, personality and antisocial behaviour. British Journal of Psychiatry, 144, 463–74. Hugdahl, K. (2001). Psychophysiology: The Mind–Body Perspective. Cambridge, MA: Harvard University Press. Intrator, J., Hare, R., Stritzke, P. et al. (1997). A brain imaging (single photon emission computerized tomography) study of semantic and affective processing in psychopaths. Biological Psychiatry, 42, 96–103. Ishikawa, S.S. & Raine, A. (2002). Psychophysiological correlates of antisocial behavior: a central control hypothesis. In J. Glicksohn (ed.), The Neurobiology of Criminal Behavior (pp. 187–229). Boston, MA: Kluwer. Jones, H.E. (1950). The study of patterns of emotional expression. In M.L. Reymert (ed.), Feelings and Emotions: The Mooseheart Symposium (pp. 161–8). New York: McGraw-Hill. Jones, H.E. (1960). The longitudinal method in the study of personality. In I. Iscoe & H. W. Stevenson (eds.), Personality Development in Children (pp. 3–27). Chicago: University of Chicago Press. Jutai, J.W., Hare, R.D. & Connolly, J.F. (1987). Psychopathy and event-related brain potentials (ERPs) associated with attention to speech stimuli. Personality and Individual Differences, 8, 175–84. Karpman, B. (1948). The myth of the psychopathic personality. American Journal of Psychiatry, 104, 523–34. Kelsey, R.M., Ornduff, S.R., McCann, C.M. & Reiff, S. (2001). Psychophysiological characteristics of narcissism during active and passive coping. Psychophysiology, 38, 292–303. Kelsey, R.M., Ornduff, S.R., Reiff, S. & Arthur, C.M. (2002). Psychophysiological correlates of narcissistic traits in women during active coping. Psychophysiology, 39, 322–32. Kernberg, O. F. (1989). The narcissistic personality disorder and the differential diagnosis of antisocial behavior. Psychiatric Clinics of North America, 12, 553–70. Kernis, M. H. & Sun, C. (1994). Narcissism and reactions to interpersonal feedback. Journal of Research in Personality, 28, 4–13. Kiehl, K.A., Hare, R.D., Liddle, P.F. & McDonald, J.J. (1999a). Reduced P300 responses in criminal psychopaths during a visual oddball task. Biological Psychiatry, 45, 1498– 507. Kiehl, K.A., Hare, R.D., McDonald, J.J. & Brink, J. (1999b). Semantic and affective processing in psychopaths: an event-related potential (ERP) study. Psychophysiology, 36, 765–74. Kiehl, K.A., Smith, A.M., Hare, R.D. et al. (2001). Limbic abnormalities in affective processing by criminal psychopaths as revealed by functional magnetic resonance imaging. Biological Psychiatry, 50, 677–84. Kilzieh, N. & Cloninger, C.R. (1993). Psychophysiological antecedents of personality. Journal of Personality Disorders, Supplement, 100–17. Knott, V.J. & Harr, A. (1996). Assessing the topographic EEG changes associated with aging and acute/long-term effects of smoking. Neuropsychobiology, 33, 210–22.

PSYCHOPHYSIOLOGICAL CORRELATES

99

Laakso, M.P., Vaurio, O., Koivisto, E. et al. (2001). Psychopathy and the posterior hippocampus. Behavioural Brain Research, 118, 187–93. Lane, S.D., Cherek, D.R., Rhodes, H.M., Pietras, C.J. & Tcheremissine, O.V. (2003). Relationships among laboratory and psychometric measures of impulsivity: implications in substance abuse and dependence. Addictive Disorders & Their Treatment, 2, 33–40. Lansing, R.W., Schwartz, E. & Lindsley, D.B. (1959). Reaction time and EEG activation under alerted and nonalerted conditions. Journal of Experimental Psychology, 58, 1–7. Lindsley, D.B. (1960). Attention, consciousness, sleep and wakefulness. In J. Field, H.W. Magoun & V.E. Hall (eds.), Handbook of Physiology (Vol. 3, pp. 1553–93). Washington, DC: American Physiological Society. Loranger, A.W., Sartorious, N., Andreoli, A. et al. (1994). The International Personality Disorder Examination: The World Health Organization/Alcohol, Drug Abuse, and Mental Health Administration international pilot study of personality disorders. Archives of General Psychiatry, 51, 215–24. Lykken, D.T. (1957). A study of anxiety in the sociopathic personality. Journal of Abnormal and Social Psychology, 55, 6–10. Mathias, C.W. & Stanford, M.S. (2003). Impulsiveness and arousal: heart rate under conditions of rest and challenge in healthy males. Personality and Individual Differences, 35, 355–71. Mawson, A.R. & Mawson, C.D. (1977). Psychopathy and arousal: a new interpretation of the psychophysiological literature. Biological Psychiatry, 12, 49–74. McCord, W. & McCord, J. (1956). Psychopathy and Delinquency. New York: Grune & Stratton. Moeller, F.G., Barratt, E.S., Dougherty, D.M., Schmitz, J.M. & Swann, A.C. (2001). Psychiatric aspects of impulsivity. American Journal of Psychiatry, 158, 1783–93. Muller, J.L., Sommer, M., Wagner, V. et al. (2003). Abnormalities in emotion processing within cortical and subcortical regions in criminal psychopaths: evidence from a functional magnetic resonance imaging study using pictures with emotional content. Biological Psychiatry, 54, 152– 62. Naatanen, R., Pakarinen, S., Rinne, T. & Takegata, R. (2004). The mismatch negativity (MMN): towards the optimal paradigm. Clinical Neurophysiology, 115, 140–4. O’Conner, S., Bauer, L.O., Tasman, A. & Hesselbrock, V. (1994). Reduced P3 amplitudes are associated with both a family history of alcoholism and antisocial personality. Progress in Neuropsychopharmacology and Biological Psychiatry, 18, 1307–21. Ogloff, J.R. & Wong, S. (1990). Electrodermal and cardiovascular evidence of a coping response in psychopaths. Criminal Justice and Behavior, 17, 231–45. O’Gorman, J.G. & Lloyd, J.E.M. (1987). Extraversion, impulsiveness and EEG alpha activity. Personality and Individual Differences, 8, 169–74. Ottoson, H., Ekselius, L., Grann, M. & Kullgren, G. (2002). Cross-system concordance of personality disorder diagnoses of DSM-IV and diagnostic criteria for research of ICD-10. Journal of Personality Disorders, 16, 283–92. Pailing, P.E., Segalowitz, S.J., Dywan, J. & Davies, P.L. (2002). Error negativity and response control. Psychophysiology, 39, 198–206. Patrick, C. J. (1994). Emotion and psychopathy: Startling new insights. Psychophysiology, 31, 319–30. Petrie, A. (1960). Some psychological aspects of pain and relief of suffering. Annals of the New York Academy of Science, 86, 13–27. Petrie, A. (1967). Individuality in Pain and Suffering (2nd edn.). Chicago: University of Chicago Press. Phillips, M.L., Drevets, W.C., Rauch, S.L. & Lane, R. (2003). Neurobiology of emotion perception I: The neural basis of normal emotion perception. Biological Psychiatry, 54, 504–14. Pierson, A., le-Houezec, J., Fossaert, A., Dubal, S. & Jouvent, R. (1999). Frontal reactivity and sensation seeking in ERP study in skydivers. Progress in Psychopharmacology and Biological Psychiatry, 23, 447–63. Plouffe, L. & Stelmack, R.M. (1986). Sensation-seeking and the electrodermal orienting response in young and elderly females. Personality and Individual Differences, 7, 119–20. Pritchard, W.S. (1991). Electroencephalographic effects of cigarette smoking. Psychopharmacology, 104, 485–90.

100

VOLUME I: DIAGNOSIS AND TREATMENT

Raine, A. (1989). Evoked potentials and psychopathy. International Journal of Psychophysiology, 8, 1–16. Raine, A. (1993). The Psychopathology of Crime: Criminal Behavior as a Clinical Disorder. San Diego: Academic Press. Raine, A. & Jones, F. (1987). Attention, autonomic arousal and personality in behaviorally disordered children. Journal of Abnormal Psychology, 15, 583–99. Raine, A., Lencz, T., Bihrle, S., LaCasse, L. & Colletti, P. (2000). Reduced prefrontal gray matter volume and reduced autonomic activity in antisocial personality disorder. Archives of General Psychiatry, 57, 119–27. Raine, A. & Venables, P.H. (1988). Enhanced P3 evoked potentials and longer P3 recovery times in psychopaths. Psychophysiology, 25, 30–8. Raine, A. & Venables, P.H. (1990). Evoked potential augmenting-reducing in psychopaths and criminals with impaired smooth-pursuit eye movements. Psychiatry Research, 31, 85–98. Raine, A., Venables, P.H. & Williams, M. (1990a). Relationships between central and autonomic measures of arousal at age 15 years and criminality at age 24 years. Archives of General Psychiatry, 47, 1003–7. Raine, A., Venables, P.H. & Williams, M. (1990b). Autonomic orienting response in 15 year old male subjects and criminal behavior at age 24. American Journal of Psychiatry, 147, 933–7. Raskin, R. & Terry, H. (1988). A principal-components analysis of the Narcissistic Personality Inventory and further evidence of its construct validity. Journal of Personality and Social Psychology, 54, 890–902. Ratsma, J.E., van der Stelt, O. & Schoffelmeer, A.N.M. (2001). P3 event-related potential, dopamine D2 receptor A1 allele, and sensation-seeking in adult children of alcoholics. Alcoholism: Clinical and Experimental Research, 25, 960–7. Reynolds, B., Ortengren, A., Richards, J.B. & de Wit, H. (2006). Dimensions of impulsive behavior: personality and behavioral measures. Personality and IndividualDifferences, 40, 305–15. Rhodewalt, F. & Morf, C.C. (1998). On self-aggrandizement and anger: a temporal analysis of narcissism and affective reactions to success and failure. Journal of Personality and Social Psychology, 74, 672–85. Rosahl, S.K. & Knight, R.T. (1995). Role of prefrontal cortex in generation of the contingent negative variation. Cerebral Cortex, 2, 123–34. Rule, B.G. & Fischer, D.G. (1970). Impulsivity, subjective probability, cardiac response and risktaking: correlates and factors. Personality, 1, 251–60. Ruchsow, M., Spitzer, M., Gron, G., Grothe, J. & Kiefer, M. (2005). Error processing and impulsiveness in normals: evidence from event-related potentials. Cognitive Brain Research, 24, 317–25. Schalling, D. (1978). Psychopathy-related personality variables and the physiology of socialization. In R.D. Hare & D. Schalling (eds.), Psychopathic Behavior: Approaches to Research (pp. 85–106). New York: John Wiley & Sons, Inc. Schneider, F., Habel, U., Kessler, C. et al. (2000). Functional imaging of conditioned aversive emotional responses in antisocial personality disorder. Neuropsychobiology, 42, 192–201. Siddle, D.A.T. & Trasler, G. (1981). The psychophysiology of psychopathic behavior. In M.J. Christie & P.G. Mellett (eds.), Foundations of Psychosomatics (pp. 283–303). Chichester, England: John Wiley & Sons, Ltd. Skeem, J.L., Mulvey, E.P. & Grisso, T. (2003a). Applicability of traditional and revised models of psychopathy to the Psychopathy Checklist: Screening Version. Psychological Assessment, 15, 41–55. Skeem, J.L., Poythress, N., Edens, J.F., Lilienfeld, S.O. & Cale, E.M. (2003b). Psychopathic personality or personalities? Exploring potential variants of psychopathy and their implications for risk assessment. Aggression and Violent Behavior, 8, 513–46. Smith, B.D. (1983). Extraversion and electrodermal activity: arousability and the inverted U. Personality and Individual Differences, 4, 411–19. Sonderstrom, H., Hultin, L., Tullberg, M. et al. (2002). Reduced frontotemporal perfusion in psychopathic personality. Psychiatry Research Neuroimaging, 114, 81–94. Stelmack, R.M. & Houlihan, M. (1995). Event-related potentials, personality and intelligence: concepts, issues and evidence. In D. H. Saklofske & M. Zeldner (eds.), International Handbook of Personality and Intelligence (pp. 349–66). New York: Plenum.

PSYCHOPHYSIOLOGICAL CORRELATES

101

Stenberg, G. (1992). Personality and the EEG: arousal and emotional arousability. Personality and Individual Differences, 13, 1097–113. Stenberg, G. (1994). Extraversion and the P300 in a visual classification task. Personality and Individual Differences, 16, 543–60. Swann, A.C., Bjork, J.M., Moeller, F.G. & Dougherty, D.M. (2002). Two models of impulsivity: relationship to personality traits and psychopathology. Biological Psychiatry, 51, 988–94. Tecce, J.J. & Cattanach, L. (1993). Contingent negative variation. In E. Niedermeyer & F. Lopes da Silva (eds.), Electroencephalography: Basic Principles, Clinical Applications and Related Fields (3rd edn.) (pp. 887–910). Baltimore: Urban and Schwarzenberg, Valentino, D.A., Arruda, J.E. & Gold, S.M. (1993). Comparison of QEEG and response accuracy in good vs. poorer performers during a vigilance task. International Journal of Psychophysiology, 15, 123–34. Veit, R., Flor, H., Erb, M. et al. (2002). Brain circuits involved in emotional learning in antisocial behavior and social phobia in humans. Neuroscience Letters, 328, 233–6. Wang, W. & Wang, Y.H. (2001). Sensation seeking correlates of passive auditory P3 to a single stimulus. Neuropsychologia, 39, 1188–93. Williamson, S., Harpur, T.J. & Hare, R.D. (1991). Abnormal processing of affective words by psychopaths. Psychophysiology, 28, 260–73. World Health Organization (1992). The ICD-10 classification of mental and behavioral disorders: clinical descriptions and diagnostic guidelines (1st edn.). Geneva, Switzerland: World Health Organization. Zahn, T.P. (1986). Psychophysiological approaches to psychopathology. In M.G.H. Coles, S.W. Porges & E. Donchin (eds.), Psychophysiology: Systems, Processes and Applications, Vol. 1 (pp. 508– 610). New York: Guilford Press, . Zargon, I.K. & Jackson, H.J. (1994). Construct validity of a psychopathy measure. Personality and Individual Differences, 17, 125–35. Zuckerman, M. (1979). Sensation Seeking: Beyond the Optimal Level of Arousal. Hillsdale, NJ: Lawrence Erlbaum. Zuckerman, M. (1990). The psychophysiology of sensation seeking. Journal of Personality, 58, 313– 45. Zuckerman, M., Murtaugh, T. & Siegel, J. (1974). Sensation seeking and cortical augmentingreducing. Psychophysiology, 11, 535–42.

CHAPTER 6

Cognitive Correlates Herta Flor University of Heidelberg, Germany

A very vivid description of a psychopath was given by Thomas Mann in his novel about the con man Felix Krull. Psychopaths have been characterized as callous, lacking morality, guilt and empathy, with shallow feelings, manipulative and cold-hearted behaviors. In addition, they seem to be disproportionately involved in antisocial acts and social norm violations. At the same time, however, they come across as very charming, intelligent and socially adapted individuals, often with excellent manners. Both aspects, the affective-interpersonal and the antisocial are commonly summarized under the term of psychopathy (Hare, 1991, 2003). The original writings by Cleckley (1941, 1982) assigned a special role to a lack of conscience and empathy as well as the presence of shallow affect in psychopathy and focused less on the antisocial aspects that are more characteristic of antisocial personality disorder (see Part I for details on the differentiation). A number of cognitive processes have been examined in persons with psychopathy as well as those with antisocial personality disorder and – especially in early studies – the two diagnoses were not clearly differentiated thus making it difficult to determine to what extent observed cognitive abnormalities are more related to the dissocial or more to the emotional components of these disorders. In addition, often violent offenders were tested without a clear diagnosis of a personality disorder. In this chapter we will examine cognitive correlates of psychopathy. We will not focus on antisocial personality disorder, but will discuss it only when it was used as a comparison group. As pointed out by Habermeyer and Herpertz (2006), psychopathy must be considered as a subset of the wider construct of disorders related to antisocial behavior and deficient emotional processing and it seems to be of special relevance for problems with the legal system. Modern definitions of psychopathy are based on the Psychopathy Checklist-Revised as devised by Hare (1991, 2003), which differentiates a more affective-interpersonal and a more antisocial factor. More recent formulations of psychopathy have also used a threefactor or a two-factor four-facet model (cf. Hare, 2003), however, most studies reported here have not yet taken these subgroups into account. Since men and women with psychopathy seem to differ in many respects (e.g., Vitale & Newman, 2001) and most studies have so far been conducted with male psychopaths, we will limit our chapter to this group. By cognitive correlates we mean all the mental processes of an individual such as perception,

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

104

VOLUME I: DIAGNOSIS AND TREATMENT

information processing, learning and memory. Emotional processing will be included as one aspect of cognitive functioning. Before we discuss cognitive correlates of psychopathy, it should be noted that it is an interesting feature of the disorder that persons with psychopathy appear to be cognitively completely intact on a superficial level and that they often show a high level of intelligence and executive function (Hare, 2003). Changes in cognitive abilities are subtle and only detectable with intricate experimental paradigms and specific neuropsychological testing. Moreover, more general neuropsychological dysfunction seems to be related to antisocial behavior rather than the affective/interpersonal component of psychopathy (Morgan & Lilienfeld, 2000).

THEORY OF MIND AND EMOTIONAL EMPATHY One interesting more recent hypothesis for the behavioral deficits in psychopaths, specifically the lack of regard for others, is a disturbance in their theory of mind. This construct refers to the ability to understand other people’s state of mind and the ability for role-taking, and this has been viewed as a prerequisite for empathy as well as the inhibition of inappropriate social behavior. This assumption has been juxtaposed to models that assume that fear of punishment mediates the acquisition of social behavior since there is accumulating research evidence that socialization and moral behavior are better induced by strengthening empathic behavior than by punishing antisocial behavior (Blair, 2001). A frequently used test of theory of mind is the eyes test (Baron-Cohen et al., 1997; Baron-Cohen et al., 2001), which assesses an individual’s ability to infer another person’s mental state by making judgments based on photographs of the eye region. Several studies examined theory of mind in psychopathic individuals as defined by the Hare Psychopathy Checklist-Revised (cf. Hare, 1991, 2003) and found no generalized deficit (e.g., Blair et al., 1996; Richell et al., 2003). However, knowing an emotion and being able to cognitively process it does not necessarily mean that one can feel or experience the emotion. Thus, if psychopaths can cognitively accurately process the emotion but do not process it on an emotional level, they will not be empathic in the sense that they feel (rather than think) with another individual and may accordingly behave in an emotionally detached and socially inadequate manner. This was confirmed by a study by Dolan and Fullam (2004), who found no major deficits in theory of mind in persons with antisocial personality disorder with or without psychopathy, but these individuals seemed to be less concerned about the consequences of their actions. These authors also reported that nonpsychopathic persons with antisocial personality disorder had difficulties in identifying basic emotions. This is in accordance with the assumption of Blair (2005) that cognitive, motor and emotional empathy must be differentiated and that psychopaths are specifically dysfunctional with respect to emotional empathy and the identification of negative emotions (see below). A related model, that of a deficient violence inhibition mechanism, suggests that there is an early developing system, the violence inhibition mechanism, which responds to signals of distress in others by increased autonomic activation, attention and the mobilization of a threat response system. It was proposed that the violence inhibition mechanism involves three aspects: moral emotions, the inhibition of violent action and the moral/conventional distinction. It is assumed that this system is dysfunctional in psychopaths (Blair, 1995) and that they lack the ability for empathy and thus moral socialization as a consequence. Associated with this is the assumption that psychopaths show an inability to correctly

COGNITIVE CORRELATES

105

process indicators of fear or sadness in others as also suggested by the theory of mind models (see above). This has been associated with the idea that there is suboptimal functioning of the amygdala that would lead to a deficient processing of distress cues. However, so far the data on the processing of unconditioned stimuli suggest normal processing in psychopaths (e.g., Flor et al., 2002). It must be noted in this context that social distress cues (e.g., baby cries that have been employed as unconditioned stimuli in conditioning paradigms) have not been tested with psychopaths. The violence inhibition mechanism model has received some support (Blair, 1995), however, it was revised to account for additional specific neural deficits (Blair, 2004).

EMOTION RECOGNITION AND EMOTIONAL RESPONDING Several tests have shown that psychopaths lack the ability to correctly identify certain emotions, specifically sadness and fear (Blair et al., 2001), which has been linked to the observed lack of empathy discussed above as well as deficient amygdala processing (see Chapters 2 and 3), although this has not been consistently found in psychopaths (cf. Birbaumer et al., 2005). Figure 6.1 shows data from one of our own studies where psychopaths displayed a significant deficit in the identification of fear but not sadness from pictures of faces depicting various emotions. However, this lack of recognition of negative emotions could be less related to deficits in empathy and theory of mind but more to an inability to emotionally associate neutral cues with aversive outcomes (i.e., a deficit in associative learning, see below), which impairs conditioning and thus the association of an expression of fear with the fear-inducing event. This notion is substantiated by the fact that autonomic responses to the expression of sadness and fear as well as in the anticipation of aversive events are greatly reduced in psychopaths (e.g., Blair et al., 1997; Flor et al., 2002).

100 90 80 70 60

Psychopaths

50 40 30 20 10 0 l N

eu

tra

e is pr Su r

ar Fe

ss ne

y Sa d

D

is

gu

ge An

Jo

st

Control group

r

Hit rate in %

Recognition of Emotions on the Basis of Facial Expressions

Emotions

Figure 6.1 Comparison of the ability to identify emotion in facial expressions in criminal psychopaths and matched controls (* p < .05)

106

VOLUME I: DIAGNOSIS AND TREATMENT

In a study that used the modulation of the startle reflex by emotional background pictures, Patrick, Bradley and Lang (1993) showed that psychopaths display a deficit in the emotional modulation by negative pictures suggestive of a generalized deficit in the processing of negative emotions. Whereas in healthy subjects the blink response to a startling noise is potentiated when aversive pictures are presented in the background, psychopaths with high scores on Factor 1 of the PCL-R (Affective/Interpersonal) failed to show this increase in the startle response. Since this increase in responding is known to be mediated by the amygdala and can be viewed as an indicator of the mobilization of a defensive response, these data have been interpreted as indicative of a deficient defensive system as well as a deficient amygdalar system. A study by Patrick, Cuthbert and Lang (1994) further added to the picture of deficits in emotional responding in psychopaths. Psychopaths showed deficits in the processing of emotional imagery, indicative of a dissociation between emotional and semantic processing. Levenston et al. (2000) examined specific pleasant (erotic, thrilling) and unpleasant (victims, threat) pictures and compared them to neutral slides. The psychopaths (high on both factors) showed startle inhibition to the victim and weak potentiation to the threat scenes, whereas healthy controls showed normal startle potentiation to both types of scenes. This difference was especially notable in the time window 800 ms post-stimulus, where emotional rather than attentional modulation emerges (Bradley, Cuthbert & Lang, 1993). Psychopaths also showed more reliable startle inhibition to positive contents and more heart rate orienting to all positive pictures. The authors interpreted the findings as indicative of a heightened aversion threshold in psychopaths that was not only present in response to distress in others (victim scenes) but also in a situation of threat. Verona et al. (2004) showed diminished skin conductance responses to both pleasant and unpleasant sounds, suggesting a deficit in the action mobilization component of emotional responses in psychopaths with high scores on Factor 1. Offenders who scored high only on the social deviance factor showed a delay in heart rate differentiation between affective and neutral sounds. These findings indicate abnormal reactivity to both positive and negative emotional stimuli in psychopathic individuals, and suggest differing roles for the two facets of deviation in affective processing in psychopaths noted by the authors. In boys with conduct disorder with or without concomitant attention deficit hyperactivity disorder but not in boys with attention deficit hyperactivity disorder alone, Herpertz and colleagues (2005) observed reduced arousal ratings to negative as well as reduced autonomic responding (skin conductance responses) to all emotional slides, thus suggesting that this deficit in emotional processing exists already early on and may well be genetically mediated. Several studies examined the identification of affect from spoken words where neutral words were used that were spoken with intonations that conveyed various emotions such as joy, anger, sadness or fear. As shown with visual materials, the psychopaths were especially impaired in the recognition of fear from vocal affect (Blair et al., 2002). In line with these findings, Hare, Williamson and Harpur (1988) observed that psychopaths who were asked to group words together, grouped them according to the literal meaning (denotation), whereas nonpsychopathic controls tended to group them according to emotional meanings (connotation). These data were further supported by the inability of psychopaths to properly sort words according to their emotional meaning (Herv´e, Hayes & Hare, 2003) as well as data showing that the faster responses to emotional words that are characteristic of healthy people (along with larger slow waves in the EEG) were absent in psychopaths (Williamson, Harpur & Hare, 1991), although this may be limited to tasks that involve the left hemisphere (Lorenz & Newman, 2002).

COGNITIVE CORRELATES

107

Taken together these studies suggest that psychopaths do have processing deficits with respect to emotional stimuli and the present studies do not clearly indicate if this is limited to negative affective stimuli or if there is deviant processing of emotions in general. It is also not clear if the deficit is more related to acquired emotions or if it is also present with respect to biologically relevant unconditioned emotional stimuli. Further research must strive to disentangle these different facets of emotional processing.

PAVLOVIAN AND INSTRUMENTAL CONDITIONING In the previous section we already addressed the question to what extent the deficits in emotional processing observed in persons with psychopathy might be related to deficient learning processes rather than to an innate inability to correctly process emotions. The discussion on the role of learning processes in psychopathy goes back to Cleckley. In his original description of the psychopath, Cleckley (1941, 1982) argued that the psychopath is a person who has an inability to experience true emotions much similar to the phenomenon of semantic aphasia where a person hears and speaks the words but cannot understand them. He assumed that moral feeling must be learned and that psychopaths have deficits in this learning process. However, there is little evidence that the inability to experience emotions relates to all emotions, and, therefore, Lykken (1957) suggested that it is only negative, not positive, emotions that are deficient in psychopaths and that they lack especially the experience of fear. In line with these assumptions, Eysenck (1977) noted that persons with antisocial behaviors are characterized by a lack of classical conditioning that associates antisocial acts with punishment. He suggested that aggression and antisocial acts are naturally rewarding and will only be inhibited when punished. In addition, a nervous system that is responsive to punishment must be present for aversive learning to occur. He suggested that persons with antisocial behaviors tend to be extraverted, that is, chronically underaroused and underresponsive to environmental stimuli. This leads to increased antisocial acts (because they can raise the level of activation) but it also dampens the effects of environmental stimuli on their nervous system. Eysenck thus also argued that in persons with poor conditionability adverse social events might have less of an impact than in those with high conditionability. Mednick (1977) suggested that the core of the learning inability in persons with antisocial behaviors is really a lack of autonomic arousal and that they have especially a slow recovery of skin conductance responses. In line with this, Gray (1987) and Fowles (1980) discussed that defects in the behavioral inhibition and activation systems might be related to psychopathy and depending on the type of defect, different types of psychopathy could emerge. Specifically, they assumed that emotional behavior is controlled (in addition to a flight–fight system) by a behavioral inhibition system (BIS) that responds to signals for aversive events and a behavioral approach system (BAS) that responds to signals of reward or nonpunishment. People with an underactive BIS might become primary psychopaths (those who lack guilt and remorse and any indication of fear) and people with a normal BIS but a very active BAS might become secondary psychopaths (persons who experience anxiety and guilt although they are aggressive, impulsive and undersocialized). The behavioral inhibition system has especially been associated with the septohippocampal system and it was assumed that an underactive BIS might result from septohippocampal damage, a tenet that has received only insufficient support.

108

VOLUME I: DIAGNOSIS AND TREATMENT

Some of the strongest evidence for a weak BIS in psychopathy comes from studies that examined skin conductance responses in psychopaths that were uniformly found to be lower than normal both in the resting state and in anticipation of aversive events (e.g., Flor et al., 2002; Hare, Frazelle & Cox, 1978; Sutker, 1970). These studies are in accordance with earlier accounts of psychopathy, where a deficit in passive avoidance was postulated as core deficit (Lykken, 1957), and subsequently demonstrated in several studies that tested electric shock (e.g., Schmauk, 1970) or the loss of money (e.g., Newman & Kosson, 1986). Blair (2004) has suggested that individuals with psychopathy have a deficit in the formation of stimulus–reinforcement associations, which require an intact amygdala. This would explain the deficits in passive avoidance learning and aversive conditioning that are present in this population. In addition to instrumental conditioning, deficits in Pavlovian conditioning have been described in several studies. For example, Lykken (1957) reported already deficient aversive conditioning as indexed by the absence of conditioned skin conductance responses. Veit et al. (2002) as well as Birbaumer et al. (2005) found an absence of conditioned responses in emotional valence ratings, self-reported arousal, skin conductance and startle responses as well as in brain indicators of conditioning such as differential activation in the amygdala, the orbitofrontal cortex, the insula and the anterior cingulate cortex (see Figure 6.2). EEG recordings in a parallel sample (Flor et al., 2002) found no indications for cognitive processing deficits since event-related EEG responses to the stimuli were normal as were contingency ratings for the relationship of the neutral and the biologically relevant stimuli that were used as conditioned and unconditioned stimuli. In addition, the responses to the unconditioned stimuli (aversive odors or pain) were unaltered in the psychopaths. This confirms the notion that it is not the processing of emotions in general but the association of normally neutral stimuli with an emotional meaning that may be at the core of psychopathy. Moreover, psychopaths seem to have a completely normal cognitive evaluation of these stimulus associations, it is the connection to the emotional evaluation and emotional response that seems to be deficient, quite in line with the assumptions of Blair (2004). These assumptions have so far only been tested in cue conditioning paradigms. To what extent this deficit also applies to contexts has so far not been determined although this might shed more light on the inability to respond properly to varying contexts, which seems to be a problem for psychopaths. One model of psychopathy termed the integrated emotion systems (IES) model (Blair, 2004) suggests that a core deficit in psychopathy is related to a lack of activation of the amygdala and the ventrolateral and orbitofrontal cortex. Specifically, it was proposed that psychopaths show deficits in the association between stimuli and reinforcements and the selection of appropriate motor responses after changes in reinforcement contingencies. This study was based on findings that stimulus–reinforcement learning requires an intact amygdala (Burns, Everitt & Robbins, 1999) and that reversal learning requires an intact ventrolateral/orbitofrontal cortex (Rolls, 1996). In patients with either amygdala or orbitofrontal/ventrolateral prefrontal lesions and persons with psychopathy, Mitchell and colleagues (2006) tested the acquisition as well as the reversal of simple stimulus– reinforcement contingencies using the snake learning and response reversal task. In this task, the participant directs a snake around the computer screen that has to eat as many mice as possible, which are represented by tokens of different colors that indicate a certain value. The participants have to identify optimal stimulus–reinforcement relationships by

COGNITIVE CORRELATES Valence

9

SAM Rating (1 = pleasant, 9 = unpleasant)

109

CS + (pp) CS – (pp) CS + (hc) CS – (hc)

8

7

6

5

4

3

2

1 H1 H2

A1 A2 A3 A4 A5 A6 A7A8 A9 A10

E1 E2 E3 E4 E5

Figure 6.2 Habituation (H1–H2), acquisition (A1–A12) and extinction (E1–E5) phases in a differential Pavlovian conditioning paradigm where two different faces serves as CS+ (conditioned stimulus) or CS-, which were presented in random order. In the habituation and extinction phases, no unconditioned stimulus (US, aversive odor) was given, whereas in the acquisition phase the CS+ was always followed by a US and the CS– was never followed by a US. The data show that the healthy controls (hc) and the psychopaths (pp) were not significantly different in the emotional evaluation of the faces in the habituation phase (the numbers denote trial blocks, i.e., blocks of five trials). In the acquisition phase, the hc rated the CS+ as significantly more aversive than the CS–; this was not the case in the pp who failed to emotionally differentiate the two cues, one indicating danger (CS+), one safety (CS–). In the extinction phase, both groups returned to baseline

taking into account the feedback about their choice. An acquisition phase and two reversal phases are incorporated in the game. The authors showed that amygdala lesions are related to impaired acquisition and that ventrolateral/orbitofrontal cortex lesions are related to impaired reversal of stimulus–reinforcement associations and that this pattern of deficits is also present in subjects with psychopathy. In contrast to these findings, simple stimulus– response associations do not seem to be impaired in psychopaths (e.g., Blair, Colledge & Mitchell, 2001). Taken together these data suggest that there are deficits in both Pavlovian and instrumental learning paradigms that may underlie some of the emotional deficits that are seen in psychopaths. The core deficit seems to relate to an inability to associate negative emotions with formerly neutral cues as well as an inability of response reversal, behaviors that involve the orbitofrontal/ventrolateral cortex and the amygdala.

110

VOLUME I: DIAGNOSIS AND TREATMENT

EXECUTIVE FUNCTION AND RESPONSE MODULATION

2.5

2.5

2.0

2.0 Locations

Words

A general deficit in executive function has often been suggested as a core cognitive dysfunction in psychopathy, however, it seems to be more relevant for antisocial personality disorder (e.g., Morgan & Lilienfeld, 2000; Raine, 1997). Executive function refers to a set of interrelated cognitive abilities that include planning for the future, cognitive flexibility, goal monitoring and self-control; and involves a number of frontal regions such as the dorsolateral prefrontal cortex, the anterior cingulate cortex or the orbitofrontal cortex. There is converging evidence that functions involving the dorsolateral frontal cortex, which can be assessed by tests such as the Wisconsin Card Sorting Test (LaPierre, Braun & Hodgins, 1995) or the Controlled Oral Word Association Test (Smith, Arnett & Newman, 1992) are intact in persons with psychopathy but are rather disturbed in antisocial personality disorder. Tests that probe into anterior cingulate (ACC) functions such as the Stroop test did not consistently find abnormalities in psychopathic individuals (cf., Blair et al., 2006) although imaging studies reported an underactivation of the ACC in psychopaths (Birbaumer et al., 2005; Kiehl et al., 2006; see also chapter 3). Deficient response modulation in psychopaths was proposed in an influential model put forward by Patterson and Newman (1993). Specifically, they suggested that psychopaths might focus too much on the implementation of goal-directed behavior and too little on the evaluation of the behavior, which would require attention to contextual cues. The lack of adequate attention shifting may thus prevent psychopaths from stopping maladaptive behavior patterns and the regulation of ongoing behavior. This deficient response modulation may be especially evident with tasks that involve the left hemisphere (cf., Bernstein et al., 2000). For example, Bernstein and colleagues showed that psychopaths did worse at recalling word locations (secondary task to the primary task of recalling word order) when they were presented to the right spatial field (processed by the left hemisphere, see Figure 6.3), although they showed the right spatial field advantage for the processing of words in general.

1.5 1.0 Psychopaths Controls

0.5 0

1.5 1.0 Psychopaths Controls

0.5 0

LSF

RSF

LSF

RSF

Figure 6.3 Mean number of words (left panel) and locations (right panel) recalled by the psychopaths and control subjects on a serial recall task. LSF: left spatial field; RSF: right spatial field. From Bernstein et al. (2000)

COGNITIVE CORRELATES

111

Also tasks that involve the approach system may show more deficient response modulation, although psychopaths do not seem to be hypersensitive to reward per se (Newman et al., 1990). However, several recent studies found appropriate processing of incidental information also in psychopaths (e.g., Blair et al., 2006) and no evidence for impaired context or conflict monitoring that has been related to ACC function (Cohen, Botvinick & Carter, 2000). These differences might be related to the type of stimulus materials and type of task (decision making versus memory retrieval or association formation) used. For example, when Stroop interference was reduced when the word and the color were spatially separated (Hiatt, Schmitt & Newman, 2004). The authors suggested that the attentional deficit apparent in psychopaths might only be evident when the unattended information is not integrated in the attended information or is not compatible with ongoing goal-directed behavior.

SOMATIC MARKERS AND RISKY DECISIONS The somatic marker hypothesis (Damasio, 1994) suggests that behavior is guided by feedback from somatic or emotional states developing when individuals experience that certain stimuli are connected with distinct emotional and accompanying somatic states. This activation guides behavior by focusing attention on positive or negative outcomes of a certain behavior in a relatively automatic fashion. Based on neuropsychological findings in individuals with lesions of the ventromedial frontal cortex, who are unable to make advantageous selections, and were therefore termed acquired sociopaths, Damasio hypothesized that psychopaths might show a similar deficit. A test that has been frequently used to test this hypothesis is the Iowa gambling task (e.g., Bechara et al., 1994), where four decks of cards are presented and individuals have to choose one card at a time. Whereas decks A and B yield large rewards but also large unpredictable losses, decks C and D are more advantageous in the sense that they yield smaller rewards but more limited and predictable punishments. It was found that persons with ventromedial frontal lesions choose more disadvantageous decks and it has also been shown that they lack the physiological activation, most notably skin conductance responses that characterize risky decisions (e.g., Bechara et al., 1997). Further evidence for orbitofrontal dysfunction in psychopathy comes from Mitchell et al. (2002) who also found risky decision making in a gambling task and deficits in reversal learning, as well as van Honk et al. (2002) who observed the expected enhanced choice of disadvantageous cards in a subclinical sample. However, other findings in psychopaths are inconsistent. For example, Schmitt, Brinkley and Newman (1999) did not report more risk taking in psychopaths, but rather in those with low anxiety scores. Similarly, L¨osel and Schmucker (2004) observed no enhanced risk taking in psychopaths. Differences in samples, type and amount of reward and different instructions may play a role in the inconsistent outcomes. More evidence for dysfunction comes from neuropsychological tests that involve the ventrolateral orbitofrontal cortex such as the Porteus maze task, the one-pack card-playing task or the object alternating task (LaPierre et al., 1995; Blair et al., 2006), where severe deficits in psychopaths were observed. By contrast, no deficits were observed in tasks that involve the dorsolateral prefrontal or the anterior cingulate cortex such as spatial alternation or number Stroop reading and counting tasks (Blair et al., 2006). Similarly, Roussy and Toupin (2000) found more errors of commission on the go/no-go task and also on the stop/signal task, both also indicative of ventrolateral prefrontal cortical dysfunction.

112

VOLUME I: DIAGNOSIS AND TREATMENT

However, there are also clear differences between acquired sociopathy and the facets of psychopathy that make it difficult to draw a direct comparison and to limit the features of psychopathy to orbitofrontal and ventromedial dysfunctions. Damage to the orbitofrontal cortex typically yields behaviors such as enhanced reactive aggression, impulsivity, grandiosity and confabulation as well as inadequate social behaviors. Although some behaviors such as impaired affect recognition or impaired response reversal are similar, there are substantial differences between the two conditions that make it unlikely that frontal damage, as in the case of acquired sociopathy, could account for the cognitive changes observed in psychopathy.

ATTENTION AND ORIENTING Some of the response-modulation deficits discussed above might stem from general disabilities in attentional processes as also suggested by Lorenz and Newman (2002). Here we discuss some additional aspects of attention and orienting that were not yet covered in the preceding sections. Hare, Frazelle and Cox (1978) first suggested that psychopaths might have problems with orienting, i.e., they do not mount an adequate physiological response to novel or salient stimuli. This idea was supported in several studies that showed deficient skin conductance responses to the novel or aversive stimuli (e.g., Hare, Frazelle & Cox, 1978). In addition, Hare (1986) suggested that psychopaths might be unable to focus their attention on important matters, unless they are of immediate interest to them. This might explain why they have problems with passive avoidance tasks or ignore cues for punishment. In favor of this interpretation Jutai and Hare (1983) found that psychopaths were less distracted by interfering stimuli in a selective attention task as evidenced by the amplitude of the N100 response in the electroencephalogram. These authors suggested that psychopaths might allocate too much attention to stimuli of interest to them at the expense of seemingly irrelevant stimuli. In addition, several authors (e.g., Christianson et al., 1996; Newman, Schmitt & Voss, 1997; Smith et al., 1992) observed that psychopaths are less distracted in Stroop tasks if the interfering stimuli are outside of the focus of their attention (e.g., if they do not spatially overlap with the target stimuli), and, in addition, there seems to be some indication that psychopaths may be more attentive than others to the primary task (e.g., Forth & Hare, 1989). However, in very demanding dual-task paradigms, it was found that psychopaths seem to have more difficulty, speaking against the notion that they focus less on irrelevant information and pointing more toward an explanation that they may have difficulty shifting their attention in an appropriate manner. This is in accordance with less differentiation in P300 potentials of the electroencephalogram in psychopaths as reported by Kiehl et al. (1999b). They suggested that this might be indicative of problems with sustained attention and the refocusing of attention to relevant targets. Kosson and collegues (e.g., 1996) suggested that some of the attentional processing problems might be related to asymmetries in hemispheric processing with psychopaths showing a special deficit when left hemispheric activation is involved. This assumption was confirmed in studies of language processing that also showed special deficits related to left hemispheric processing (e.g., Hare & Jutai, 1988).

LANGUAGE PROCESSES We have already noted that psychopaths seem to have problems with the emotional meaning of words. However, several studies also identified additional problems in linguistic abilities

COGNITIVE CORRELATES

113

in psychopaths that go beyond emotional processing. For example, Hare and Jutai (1988) as well as Kiehl et al. (1999a) observed that psychopaths had more errors in tasks that required abstract semantic categorization. This might be related to deficits in the activation of the anterior temporal lobe that normally differentiates abstract and concrete word processing (cf. Kiehl et al., 2004). In addition, abnormal responses to linguistic stimuli have been identified in evoked response potential (ERP) studies where late frontal negativities were present in psychopaths (Kiehl et al., 1999b; Williamson, Harpur & Hare, 1991). This abnormal response might be related to deficits in semantic processing in psychopaths, although tests that specifically examined the N400 response in psychopaths (an indicator of semantic mismatch) showed no abnormality in psychopaths (Kiehl et al., 2006). However, semantic mismatch is not necessarily identical with categorization processes and the specific deficits in semantic processing in psychopaths need to be further elucidated. As noted above, differences in hemispheric processing might contribute to the observed problems with language processing in psychopaths. For example, Hare and Jutai (1988) found that psychopaths made less semantic categorization efforts when the words were presented to the left visual field (i.e., the right hemisphere) that the right visual field (i.e., the left hemisphere) whereas nonpsychopathic subjects show a right field (or left hemisphere) advantage in these tasks. It is not known to what extent structural alterations might account for these deficits, although the imaging data by Kiehl et al. (2004) point in this direction.

SUMMARY AND CONCLUSIONS This chapter has shown that psychopaths have a large number of cognitive deficits, however, they seem to be modulated by contextual variables. Across a wide array of deficits, a common thread seems to be a specific inability to correctly interpret and make use of emotionally relevant materials, especially if they are indicative of negative emotions such as fear. It is not quite clear to what extent this deficit is primary or results from an inability of psychopaths to form emotionally meaningful associations between neutral stimuli and reinforcers. In addition feedback from physiological arousal seems to be disturbed in psychopaths thus making it difficult for them to use anticipatory behavioral control. As noted by Kiehl et al. (2006) and Blair (2005) these deficits are consistent with a model of psychopathy that assumes major dysfunction of the paralimbic system including the orbitofrontal cortex, the amygdala, the insula, the anterior cingulate, the parahippocampal gyrus and the superior temporal gyrus. A number of genetic studies suggests that much of this dysfunction – especially that related to the affective/interpersonal factor (cf., Viding et al., 2005) – may stem from predisposing rather than acquired variables, although more research is needed to confirm this hypothesis.

REFERENCES Baron-Cohen, S., Joliffe, T., Mortimore, C. & Robertson, M. (1997). Another advanced test of theory of mind: evidence from very high functioning adults with autisms or Asperger syndrome. Journal of Child Psychology and Psychiatry, 38, 813–22. Baron-Cohen, S., Wheelwright, S., Hill, J., Raste, Y. & Plumb, I. (2001). The ‘Reading the Mind in the Eyes’ test revised version: a study with normal adults, and adults with Asperger syndrome or high functioning autism. Journal of Child Psychology and Psychiatry, 42, 241–51.

114

VOLUME I: DIAGNOSIS AND TREATMENT

Bechara, A., Damasio, A.R., Damasio, H. & Anderson, S.W. (1994). Insensitivity to future consequences following damage to human prefrontal cortex. Cognition, 50, 7–15. Bechara, A., Damasio, H., Tranel, D. & Damasio, A.R. (1997). Deciding advantageously before knowing the advantageous strategy. Science, 275, 1293–5. Bernstein, A., Newman, J.P., Wallace, J.F. & Luh, K.E. (2000). Left hemisphere activation and deficient response modulation in psychopaths. Psychological Science, 11, 414–18. Birbaumer, N., Veit, R., Lotze, M., Erb, M., Hermann, C., Grodd, W. & Flor, H. (2005). Deficient fear conditioning in psychopathy: a functional magnetic resonance imaging study. Archives of General Psychiatry, 62, 799–805. Blair, R.J.R (1995). A cognitive developmental approach to morality: investigating the psychopath. Cognition, 57, 1–29. Blair, R.J.R. (2001). Neurocognitive models of aggression, the antisocial personality disorders and psychopathy. Journal of Neurology, Neurosurgery & Psychiatry, 71, 727–31. Blair, R.J.R. (2004). The roles of orbital frontal cortex in the modulation of antisocial behavior. Brain and Cognition, 55, 198–208. Blair, R.J.R. (2005). Responding to emotions of others: dissociating forms of empathy through the study of typical and psychiatric populations. Consciousness and Cognition, 14, 698–718. Blair, R.J.R., Colledge, E. & Mitchell, D.G.V. (2001). Somatic markers and response reversal: is there orbitofrontal dysfunction in boys with psychopathic tendencies? Journal of Abnormal Child Psychology, 29, 499–511. Blair, R.J.R., Colledge, E., Murray, L. & Mitchell, D.G.V. (2001). A selective impairment in the processing of sad and fearful expressions in children with psychopathic tendencies. Journal of Abnormal Child Psychology, 29, 491–8. Blair, R.J.R., Jones, Clark, F. & Smith, M. (1997). The psychopathic individual: a lack of responsiveness to distress cues? Psychophysiology, 43, 192–8. Blair, R.J.R., Mitchell, D.G.V., Richell, R.A., Kelly, S., Leonard, A., Newman, C. & Scott, S. (2002). Turning a deaf ear to fear: impaired recognition of vocal affect in psychopathic individuals. Journal of Abnormal Psychology, 111, 682–6. Blair, K.S., Newman, C., Mitchell, D.G.V., Richell, R.A., Leonard, A. Morton, J. & Blair, R. J. R. (2006). Differentiating among prefrontal substrates in psychopathy: neuropsychological test findings. Neuropsychology, 20, 153–65. Blair, R.J., Sellars, C., Strickland, I., Clark, F., Williams, A., Smith, M. & Jones, L. (1996). Theory of mind in the psychopath. Journal of Forensic Psychiatry, 7, 15–25. Bradley, M.M., Cuthbert, B.N. & Lang, P.J. (1993). Pictures as prepulse: attention and emotion in startle modification. Psychophysiology, 30, 541–5. Burns, L. H., Everitt, B.J. & Robbins, T.W. (1999). Effects of excitotoxic lesions of the basolateral amygdala on conditional discrimination learning with primary and conditioned reinforcement. Behavioural Brain Research, 100, 123–33. Christianson, S.A., Forth, A.E., Hare, R.D., Strachan, C., Lidberg, L. & Thorell, L.H. (1996). Remembering details of emotional events: a comparison of psychopathic and non-psychopathic offenders. Personality and Individual Differences, 20, 437–43. Cleckley, H. (1941, 1982 rev. ed). The Mask of Sanity. St. Louis: C.V. Mosby. Cohen, J.D., Botvinick, M. & Carter, C.S. (2000). Anterior cingulate and prefrontal cortex: who’s in control? Nature Neuroscience, 3, 421–3. Damasio, A. (1994). Descartes’ Error: Emotion, Reason and the Human Brain. New York: Putnam. Dolan, M. & Fullam, R. (2004). Theory of mind and mentalizing ability in antisocial personality disorders with and without psychopathy. Psychological Medicine, 34, 1093–102. Eysenck, H.J. (1977). Crime and Personality (3rd edn). St Albans, England: Paladin. Flor, H., Birbaumer, N., Hermann, C., Ziegler, S. & Patrick, C.J. (2002). Aversive Pavlovian conditioning in psychopaths: peripheral and central correlates. Psychophysiology, 39, 505–18. Forth, A.E. & Hare, R.D. (1989). The contingent negative variation in psychopaths. Psychophysiology, 26, 676–82. Fowles, D.C. (1980). The three arousal model: implications of Gray’s two-factor learning theory for heart rate, electrodermal activity, and psychopathy. Psychophysiology, 17, 87–104. Gray, J.A. (1987). The Psychology of Fear and Stress (2nd edn.). Cambridge: Cambridge University Press.

COGNITIVE CORRELATES

115

Habermeyer, E. & Herpertz, S.C. (2006). Dissoziale Pers¨onlichkeitsst¨orung [Dissocial personality disorder]. Nervenarzt, 77, 605–17. Hare, R.D. (1986). Twenty years of experience with the Cleckley psychopath. In W.H. Reid, D. Dorr, J.I. Walker & J.W. Bonner, III (eds.), Unmasking the Psychopath: Antisocial Personality and Related Syndromes (pp. 3–27). New York: Norton. Hare, R.D. (1991, 2003). The Hare Psychopathy Checklist-Revised. Toronto: Multi-Health Systems. Hare, R.D., Frazelle, J. & Cox, D.N. (1978). Psychopathy and physiological responses to threat of an aversive stimulus. Psychophysiology, 15, 165–72. Hare, R.D. & Jutai, J.W. (1988). Psychopathy and cerebral asymmetry in semantic processing. Personality and Individual Differences, 92, 329–37. Hare, R.D., Wiliamson, S.E. & Harpur, T.J. (1988). Psychopathy and language. In T.E. Moffitt & S.A. Mednick (eds.), Biological Contributions to Crime Causation (pp. 68–92). Dordrecht, The Netherlands: Kluwer. Herpertz, S.C., Mueller, B., Qunaibi, M., Lichterfeld, C., Konrad, K. & Herpertz-Dahlmann, B. (2005). Response to emotional stimuli in boys with conduct disorder. American Journal of Psychiatry, 162, 1100–7. Herv´e, H.F., Hayes, J.P. & Hare, R.D. (2003). Psychopathy and sensitivity to the emotional polarity of methaphorical statements. Personality and Individual Differences, 35, 1497–507. Hiatt, K.D., Schmitt, W.A. & Newman, J.P. (2004). Stroop tasks reveal abnormal selective attention among psychopathic offenders. Neuropsychology, 18, 50–9. Jutai, J.W. & Hare, R.D. (1983). Psychopathy and selective attention during performance of a complex perceptual motor task. Psychophysiology, 20, 146–51. Kiehl, K.A., Hare, R.D., Liddle, P.F. & McDonald, J.J. (1999a). Reduced P300 responses in criminal psychopaths during a visual oddball task. Biological Psychiatry, 45, 1498–507. Kiehl, K.A., Hare, R.D., McDonald, J.J., & Brink, J. (1999b). Semantic and affective processing in psychopaths: an event-related potential (ERP) study. Psychophysiology, 36, 765–74. Kiehl, K.A., Smith, A.M., Hare, R.D., Mendrek, A., Forster, B.B., Brink, J., & Liddle, P.F. (2001). Limbic abnormalities in affective processing by criminal psychopaths as revealed by functional magnetic resonance imaging. Biological Psychiatry, 50, 677–84. Kiehl, K.A., Smith, A.M., Mendrek, A., Forster, B.B., Hare, R.D., & Liddle, P.F. (2004). Temporal lobe abnormalities in semantic processing by criminal psychopaths as revealed by functional magnetic resonance imaging. Psychiatry Research, 130, 27–42. Kiehl, K.A., Laurens, K.R., Bates, A.T. & Liddle, P.F. (2006). Psychopathy and semantic processing: an examination of the N400. Personality and Individual Differences, 40, 293–304. Kosson, D.S. (1996). Psychopathy and dual task performance under focusing conditions. Journal of Abnormal Psychology, 105, 391–400. LaPierre, D., Braun, C.M.J. & Hodgins, S. (1995). Ventral frontal deficits in psychopathy: neuropsychological test findings. Neuropsychologia, 33, 139–55. Levenston, G.K., Patrick, C.J., Bradley, M.M. & Lang, P.J. (2000). The psychopath as observer: emotion and attention in picture processing. Journal of Abnormal Psychology, 109, 373–85. L¨osel, F. & Schmucker, M. (2004). Psychopathy, risk taking, and attention: a differentiated test of the somatic marker hypothesis. Journal of Abnormal Psychology, 113, 522–9. Lorenz, A.R. & Newman, J.P. (2002). Deficient response modulation and emotion processing in low-anxious Caucasian psychopathic offenders: results from a lexical decision task. Emotion, 2, 91–104. Lykken, D. (1957). A study of anxiety in sociopathic personality. Journal of Abnormal and Social Psychology, 55, 6–10. Mednick, S.A. (1977). A biosocial theory of the learning of law-abiding behavior. In S.A. Mednick and K.O. Christiansen (eds.), Biosocial Basis of Criminal Behavior (pp. 1–8). New York: Gardner. Mitchell, D.G.V., Colledge, E., Leonard, A. & Blair, R.J.R. (2002). Risky decisions and response reversal: is there evidence of orbitofrontal cortex dysfunction in psychopathic individuals? Neuropsychologia, 40, 2013–22. Mitchell, D.G.V., Fine, C., Richell, R.A., Newman, C., Lumsden, J., Blair, K.S. & Blair, R.J.R. (2006). Instrumental learning and relearning in individuals with psychopathy and in patients with lesions involving the amygdala or orbitofrontal cortex. Neuropsychology, 20, 280–9.

116

VOLUME I: DIAGNOSIS AND TREATMENT

Morgan, A.B. & Lilienfeld, S.O. (2000). A meta-analytic review of the relation between antisocial behavior and neuropsychological measures of executive function. Clinical Psychology Review, 20, 113–36. Newman, J.P. & Kosson, D.S. (1986). Passive avoidance learning in psychopathic and nonpsychopathic offenders. Journal of Abnormal Psychology, 95, 257–63. Newman, J.P., Patterson, C.M., Howland, E.W. & Nichols, S.L. (1990). Passive avoidance in psychopaths: the effects of reward. Personality and Individual Differences, 11, 1101–4. Newman, J.P., Schmitt, W.A. & Voss, W.D. (1997). The impact of motivationally neutral cues on psychopathic individuals: assessing the generality of the response modulation hypothesis. Journal of Abnormal Psychology, 106, 563–75. Patrick, C.J., Bradley, M.M. & Lang, P.J. (1993). Emotion in the criminal psychopath: startle reflex modulation. Journal of Abnormal Psychology, 102, 82–92. Patrick, C.J., Cuthbert, B.N. & Lang, P.J. (1994). Emotion in the criminal psychopath: fear image processing. Journal of Abnormal Psychology, 103, 523–34. Patterson, C.M. & Newman, J.P. (1993). Reflectivity and learning from aversive events: toward a psychological mechanism for the syndromes of disinhibition. Psychological Review, 100, 716–36. Raine, A. (1997). The Psychopathology of Crime. New York: Academic Press. Richell, R.A., Mitchell, D.G.V., Newman, C., Leonard, A., Baron-Cohen, S. & Blair, R.J.R. (2003). Theory of mind and psychopathy: can psychopathic individuals read the ‘language of the eyes’? Neuropsychologia,41, 523–26. Rolls, E.T. (1996). The orbitofrontal cortex. Philosophical Transactions of the Royal Society,B 351, 1433–43. Roussy, S. & Toupin, J. (2000). Behavioral inhibition deficits in juvenile psychopaths. Aggressive Behavior, 26, 413–24. Schmauk, F.J. (1970). Punishment, arousal, and avoidance learning in sociopaths. Journal of Abnormal Psychology, 76, 325–55. Schmitt, W.A., Brinkley, C. & Newman, J.P. (1999). Testing Damasio’s somatic marker hypothesis with psychopathic individuals: risk takers or risk averse? Journal of Abnormal Psychology, 108, 538–43. Smith, S.S., Arnett, P.A. & Newman, J.P. (1992). Neuropsychological differentiation of psychopathic and nonpsychopathic criminal offenders. Personality and Individual Differences, 13, 1233–43. Sutker. P.B. (1970). Vicarious conditioning and sociopathy. Journal of Abnormal Psychology, 76, 380–6. van Honk, J., Hermans, E.J., Putman, P., Montagne, B. & Schutter, D.J. (2002). Defective somatic markers in sub-clinical psychopathy. Neuroreport, 13, 1025–7. Veit, R., Flor, H., Erb, M., Hermann, C., Lotze, M., Grodd, W. & Birbaumer, N. (2002). Brain circuits involved in emotional learning in antisocial behavior and social phobia in humans. Neuroscience Letters, 328, 233–6. Verona, E., Patrick, C.J., Curtin, J.J., Bradley, M.M. & Lang, P.J. (2004). Psychopathy and physiological response to emotionally evocative sounds. Journal of Abnormal Psychology, 113, 99–108. Viding, E., Blair, R.J., Moffitt, T.E. & Plomin, R. (2005). Evidence for substantial genetic risk for psychopathy in 7-year-olds. Journal of Child Psychology and Psychiatry, 46, 592–7. Vitale, J.E. & Newman, J.P. (2001). Response perseveration in psychopathic women. Journal of Abnormal Psychology, 110, 644–7. Williamson, S., Harpur, T.J. & Hare, R.D. (1991). Abnormal processing of affective words by psychopaths. Psychophysiology, 28, 260–73.

CHAPTER 7

Violence: Psychopathology, Risk Assessment and Lawsuits Kenneth Tardiff Weill Cornell Medical College, New York, USA

Violence is one of the frequent manifestations of psychopathic disorders that is a great threat to the persons in society and the fabric of society itself. This chapter will present physical violence as a clinical phenomenon that is displayed differently in a number of psychiatric disorders. In light of this chapter’s clinical focus, it will distill the complex nature of psychopathic disorders as presented in this book into the clinical construct of antisocial personality disorder and will compare violence manifested in that disorder to that in other personality disorders such as the borderline, narcissistic and paranoid personality disorders and the intermittent explosive disorder, as well as to violence in alcohol and substance abuse, schizophrenia, delusional disorder, mood disorders, mental retardation and some medical and neurological disorders. What is apparent in this list is the comorbidity of antisocial personality disorder with a number of these disorders. This chapter will present how the clinician should assess the short-term risk of violence given the disorder and circumstances of the situation. Last, this chapter will present some legal consequences of violence by patients, namely lawsuits against clinicians when patients are violent, separate from the legal aspects of violence discussed in other chapters such as involuntary hospitalization and involuntary inpatient and outpatient treatment.

PSYCHIATRIC DISORDERS AND VIOLENCE Antisocial Personality Disorder Violence is just one of many antisocial behaviors exhibited by patients with antisocial personality disorder. The patient with antisocial personality disorder repeatedly gets into physical fights and violence involving his or her spouse, children and individuals outside of the family. Other antisocial behaviors include destroying property, harassing others, stealing, engaging in illegal occupations, driving in a reckless or intoxicated manner and being involved in promiscuous relationships. The patient lies, does not honor financial The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

118

VOLUME I: DIAGNOSIS AND TREATMENT

obligations and is unable to sustain consistent employment. Alcohol and substance abuse are often a problem. The violence toward others and other aspects of antisocial behavior are not accompanied by remorse or guilt. Violence is accompanied by little display of emotion and seems cold-blooded. Issues of self-esteem and/or revenge frequently underlie the violence. The patient with antisocial personality disorder can resemble the narcissistic person described later, but the antisocial patient is more likely to be impulsive. In antisocial personality disorder, violence can be premeditated or impulsive and impulsive violence is thought to be more amenable to psychopharmacological treatment (American Psychiatric Association, 2000; Hare, Hart & Harper, 1991; Widiger, 2000).

Borderline Personality Disorder In the case of borderline personality disorder, in addition to exhibiting frequent displays of anger and recurrent physical violence toward others, the patient manifests other behavioral problems between the violent episodes. There is a wide range of impulsive behaviors, including suicidal or self-mutilating behaviors, excessive spending, indiscreet sexual behavior, drug abuse, shoplifting and reckless driving. In addition, there is a marked and persistent identity problem manifested by uncertainty about self-image, sexual orientation, career goals and other values. There are manipulative attempts to obtain caring and attention from others. Violence is characteristically in response to feelings of abandonment or rejection by someone from whom the patient wants love, caring or merely attention. Violence is accompanied by intense emotional displays and affective instability (American Psychiatric Association, 2000; Gunderson, 1996; Herpertz et al., 1997; Kemperman, Russ & Shearin, 1997).

Narcissistic Personality Disorder The patient with narcissistic personality feels he or she has a right to control others and to be the focus of their attention and admiration. The patient is exploitative in relations with others and has little or no remorse in doing so. The narcissistic patient, unlike the borderline patient, does not experience chaotic disruption of interpersonal relationships and, unlike the antisocial patient, exhibits little flagrant criminal activity (with the exception of professional killers with narcissistic personality). More often, violence results from the patient’s frustration and anger that the other person has not given the patient what the patient thinks he or she deserves (American Psychiatric Association, 2000; Gunderson, Ronningstam & Smith, 1991).

Paranoid Personality Disorder The patient with paranoid personality disorder is suspicious and believes that people, whether they are in government or other organizations or are members of a certain race or class, conspire against him or her. The patient may be racist or sexist and perceives others to be so. Patients with paranoid personality disorder, particularly men, may belong to militaristic organizations or be preoccupied with militaristic themes. The patient tends

PSYCHOPATHOLOGY, RISK ASSESSMENT AND LAWSUITS

119

to be preoccupied with firearms and often possesses them. A history of episodic violence is not common; however, a history of threats of violence against others, for example, against human resources personnel after being discharged from a job, is common. Most patients with paranoid personality will not be physically violent, but when violence does occur, it is often lethal and may be targeted toward multiple persons, as in the work environment (American Psychiatric Association, 2000; Bernstein, Useda & Siever, 1993).

Intermittent Explosive Disorder A key characteristic of intermittent explosive disorder is episodic, recurrent and discrete outbursts of aggression and violence that are grossly out of proportion to any precipitating psychosocial stressor. These episodes of violence stem from the failure to resist aggressive urges. The patient feels remorse and expresses it profusely following this violent episode (e.g., in the case of a husband who has attacked his wife or a mother who has severely beaten her child). There is little evidence of other behavioral problems between these violent episodes. The patient with intermittent explosive disorder usually appears ‘normal’ between the violent episodes in terms of employment, interpersonal relationships and other aspects of life. These episodes of violence are not accounted for by other mental disorders discussed in this chapter, however, the use of alcohol may play a part in the outbursts of violence (American Psychiatric Association, 2000; Lesch & Merschdorf, 2000; Tardiff, 1992).

Schizophrenia Schizophrenia can produce violence in a number of ways. First is psychosis. In violent schizophrenic patients with psychosis, there can be delusional thinking, particularly in terms of persecution. Patients may believe that people are trying to harm them, that the police, FBI or other organizations are spying on them, that some unknown mechanism is controlling their minds, or that the therapist is harming them (e.g., through medication). Patients with paranoid delusions in schizophrenia may react to these persecutory delusions by retaliating against the presumed source of this persecution. Patients with other types of schizophrenia may attempt to kill others because of some form of psychotic identification with the victim. Hallucinations associated with schizophrenia, particularly command hallucinations (e.g., the patient is commanded to kill someone), have been known to result in violent behavior and homicide. In addition, hallucinations in which people are cursing or insulting the patient may result in retaliation against the supposed source of the insults. There are aspects of schizophrenia, apart from psychotic processes, that can result in violence. Sudden, unpredictable changes in affect may be associated with anger, aggression and violent behavior. Some schizophrenic patients are violent because of generalized disorganization of thought and a lack of impulse control, accompanied by purposeless, excited psychomotor activity. Patients with schizophrenia may inadvertently provoke violence because of akathisia secondary to antipsychotic medication. With the agitation and restlessness from akathisia, they may inadvertently come into physical contact with other patients, which may lead to fights. Other disease processes superimposed on the schizophrenic disorder, rather than

120

VOLUME I: DIAGNOSIS AND TREATMENT

delusions per se, may be responsible for the violence. These include brain damage secondary to heavy drug or alcohol use, head trauma, or any other of the numerous neurological or systemic diseases discussed later in this chapter. Other psychiatric disorders, such as mental retardation or personality pathology, may be responsible for violence by patients with schizophrenia. Last, schizophrenic patients may be violent to attain what they want, to express anger, or to deliberately hurt others. It is very important for the clinician to determine the cause of violence by a schizophrenic patient and not to assume the violence is due to psychosis and to respond with increase or change of medication (American Psychiatric Association, 2000; Andreasen et al., 1995; Dixon et al., 1991; Modestin & Ammann, 1996; Tardiff, 1992).

Delusional Disorder Although delusional disorder is uncommon, it can often be associated with violence. Delusions in delusional disorder are not as bizarre as those in schizophrenia and involve situations that can conceivably occur in real life, for example being deceived by one’s lover, being followed by someone or infected with a disease. Persons with delusional disorder may appear normal in terms of behavior and appearance when their delusions are not being discussed. The persistent delusion held by patients with delusional disorder may be of the persecutory type, involving feelings of being conspired against, cheated, spied on, poisoned or otherwise harmed. In addition to resorting to legal action and appeal to government agencies, patients with this disorder often become resentful and angry and may become violent against those they believe are harming them. Delusional disorder of the jealous type involves the persistent belief that the patient’s spouse or lover is unfaithful. Patients with this type of delusional disorder attempt to restrict the activities of and follow the spouse or lover. They may resort to physical attacks on the spouse or lover or on someone who is identified as the ‘other partner’ in this ‘infidelity’ (American Psychiatric Association, 2000; Serretti, Lattuada & Cusin, 1999).

Mood Disorders Mania Mania is defined as a period of abnormally and persistently elevated, expansive or irritable mood. The manic patient often seeks pleasurable behaviors that may have painful consequences. Mania can be associated with violence that results from extreme psychomotor agitation or irritable mood associated with angry tirades. Most violence by manic patients is not premeditated and is purposeless. Rarely, a manic patient may become violent as a result of delusional thinking in which the patient believes he or she is being persecuted because of some special attribute. It is usually the case with the manic patient that all impulses are put into action. Therefore, violent impulses become actions. The typical situation in which manic patients erupt with violence is when they feel contained and not free to do what they want to do. This containment may be physical, as being contained in a small examining room in the emergency room, or interpersonal, as when a nurse insists that the patient take

PSYCHOPATHOLOGY, RISK ASSESSMENT AND LAWSUITS

121

medication immediately (American Psychiatric Association, 2000; Miller, Zadolinnyi & Hafner, 1993).

Depression Patients with manic symptoms have been found to display depression with episodes of rage and violence as well as suicidal attempts. Other patients with mood disorders are rarely violent. An infrequent exception is the psychotically depressed patient. This type of patient is delusional with extreme hopelessness, feelings that life is not worth living, or delusional feelings of profound guilt may result in violence, usually involving murder, followed by suicide. When this occurs, it most often involves a woman killing her children and then herself, or a man killing his family and then himself. Obviously, the clinician is not called on to evaluate such a patient unless the suicide attempt has failed (American Psychiatric Association, 2000; McElroy et al.; Rosenbaum & Bennett, 1986).

Psychoactive Substances Alcohol and drugs can cause violence through their pharmacological effects in persons with no other psychiatric disorder. They can exacerbate the psychopathology in other psychiatric disorders and produce violence. It is important to recognize that alcohol and many drugs can produce violence through intoxication as well as withdrawal. A number of individuals mix alcohol and drugs, which may make it difficult in an emergency situation, such as that involving violence, to differentiate whether the clinical situation is the result of intoxication with some substances and/or withdrawal from other substances. Last, heavy use of alcohol and drugs can cause changes in the brain that may lead to chronic impairment and psychiatric symptoms related to violent behavior (Tardiff et al., 2005; Volavka & Tardiff, 1999).

Alcohol The ingestion of alcohol often may be associated with aggression and violence as a result of disinhibition, particularly in the initial phase of intoxication. Intoxication is accompanied by emotional lability and impaired judgment. The patient may appear to have slurred speech, incoordination, unsteady gait, nystagmus and a flushed face. Violent behavior can also be found in persons who drink small amounts of alcohol that are insufficient to cause intoxication in most people, a phenomenon known as alcohol idiosyncratic intoxication. Violence may be associated with alcohol withdrawal after cessation of prolonged, heavy ingestion of alcohol. Withdrawal is manifested by coarse tremor of the hands, tongue or eyelids and at least one of the following: nausea or vomiting, weakness, autonomic hyperactivity, anxiety, depressed mood or irritability, hallucinations (which may be transient or more persistent), headache or insomnia. In some cases, alcohol withdrawal may be manifested by delirium. Violence may result from gross disorganization of behavior or may be in response to threatening auditory hallucinations or delusional thinking (American Psychiatric Association, 2000; Bushman, 1997; Langevin et al., 1987).

122

VOLUME I: DIAGNOSIS AND TREATMENT

Cocaine Cocaine, particularly when absorbed through the nasal route, initially produces a feeling of well-being and euphoria. With continued use, particularly when the cocaine is taken intravenously or smoked in the form of crack, the euphoria turns to grandiosity, psychomotor agitation, suspiciousness and, frequently, violence. With continued use, suspiciousness becomes paranoid ideation and, subsequently, paranoid delusional thinking. Thus, violence results from delusional thinking as well as from the stimulation effect of cocaine. There is evidence that the use of cocaine with alcohol involves a greater risk of violence than the use of these substances separately. A person using cocaine has pupillary dilatation, chills, nausea or vomiting, tachycardia and elevated blood pressure, and may be perspiring and have hallucinations, particularly visual or tactile hallucinations. Unlike withdrawal from alcohol and the sedative-anxiolytic substances, cocaine withdrawal is usually associated not with violence but with depression. In some cases of prolonged use, cessation of cocaine use can result in profound impairment in thinking, suicidal behavior, irritability and psychomotor agitation. Irritability, agitation, and, in some cases, paranoid ideation may result in violence. Intense craving for more cocaine when supplies have been exhausted may also lead to violence in the process of obtaining cocaine or money for its purchase (American Psychiatric Association, 2000; Denison, Paredes & Booth, 1997; McCormick & Smith, 1995).

Amphetamines With intense or prolonged amphetamine use, a feeling of well-being and confidence turns to confusion, rambling, incoherence, paranoid ideation and delusional thinking, which are accompanied by agitation, fighting and other forms of aggression and impaired social judgment. The patient appears to have pupillary dilatation, may be perspiring, or may have chills, nausea or vomiting, tachycardia and elevated blood pressure. Amphetamine withdrawal, like cocaine withdrawal, is usually manifested by depression and insomnia, although there may be psychomotor agitation and paranoid ideation following prolonged heavy use of amphetamines or similar substances. The symptoms may persist more than 24 hours after cessation of use of amphetamines (American Psychiatric Association, 2000; Miczek & Tidey, 1989).

Hallucinogens Hallucinogens such as lysergic acid diethylamide (LSD), dimethyltryptamine (DMT) and mescaline may result in impaired judgment and paranoid ideation in addition to other perceptual changes, including depersonalization, derealization, illusions, synesthesias and hallucinations. The hallucinations are usually visual. The person may experience marked anxiety and a fear of losing his or her mind; will appear with pupillary dilatation, sweating, tremors and incoordination; and may have tachycardia, palpitations and blurring of vision. Violence may occur during intoxication with the above-mentioned hallucinogens but is not as common as in phencyclidine (PCP) intoxication. Within 1 hour of oral use (5 minutes

PSYCHOPATHOLOGY, RISK ASSESSMENT AND LAWSUITS

123

if smoked or taken intravenously), PCP often produces marked violence, impulsivity, unpredictability and grossly impaired judgment. There may be delusional thinking or delirium. The patient may have vertical or horizontal nystagmus, be ataxic and dysarthric, and manifest increased blood pressure or heart rate, numbness or diminished responsiveness to pain, muscle rigidity and hyperacusis. The patient may manifest seizures. There may be persistent psychopathology following PCP use; with other hallucinogens, except for occasional flashbacks, there is little residual psychopathology after limited use. Although a source of great anxiety for the patient, flashbacks are not typically associated with violent behavior (American Psychiatric Association, 2000; Convit, Nemes & Volavka 1988).

Inhalants Inhalants are substances that contain hydrocarbons, such as gasoline, glue, paint and paint thinners, that are used by young children and early adolescents to produce intoxication. Inhalant intoxication may be characterized by belligerence and violence as well as impaired judgment. Chronic or heavy use of inhalants may produce neurological signs such as incoordination, general muscle weakness and psychomotor retardation. Even with mild use of inhalants, the patient may manifest dizziness, nystagmus, incoordination, slurred speech, unsteady gait, lethargy, depressed reflexes, psychomotor retardation, tremor, general muscle weakness, blurred vision, stupor and/or euphoria (American Psychiatric Association, 2000; Johnston, O’Malley & Bachman, 1997).

Anabolic Steroids Anabolic steroids are used by young men to enhance muscle growth and performance in athletics and bodybuilding. Reports and systematic studies have found that after several months of administrating these drugs, these men become irritable, combative and violent. Changes in mood primarily involve violent feelings, hostility, irritability and violence. The irritability and violence subside several months after discontinuation (Choi, Parrott & Cowan, 1989; Pope & Katz, 1994).

Mental Retardation Although most patients with mental retardation are not violent, when violence does occur, it is often difficult to manage and often is among patients in residential treatment facilities. Violence due to poor intellectual ability is associated with anger and frustration at not being able to obtain what is desired or to verbalize concerns and feelings. These feelings of anger and frustration are accompanied by poor impulse control and then violence toward others or the self. Among mild to moderate mentally retarded patients, there are some with antisocial personality who commit violent crimes. The causes of mental retardation can be subsumed under a number of genetic disorders as well as environmental factors such as head trauma during birth or as an adult, hypoxia and lead poisoning in childhood. There is thought that persons with Down’s syndrome are at a less risk for violence than those with other causes of mental retardation (Hurley & Sovner, 1995; Linaker, 1994).

124

VOLUME I: DIAGNOSIS AND TREATMENT

Medical and Neurological Disorders There are a number of medical and neurological disorders that occasionally can be associated with an increased risk of violence (Anderson & Silver, 1999). Psychotic patients with medical or neurological disorders are usually violent as a result of delirium or dementia. Delirious patients can be violent as a result of disorganized, out-of-control behavior or as a result of paranoid delusions. Patients with dementia often have delusional thoughts, even paranoid delusions, and can be violent. Some primary diseases of the brain can be associated with violent behavior such as infections of the brain, including viral encephalitis, acquired immunodeficiency syndrome (AIDS), tuberculosis and fungal meningitis, syphilis and herpes simplex, can be associated with violent behavior. Other primary diseases of the brain associated with violence include head trauma, normal pressure hydrocephalus, cerebrovascular diseases, tumors, Huntington’s chorea, multiple sclerosis, Alzheimer’s disease, Pick’s disease, multi-infarct dementia (vascular dementia), Parkinson’s disease, Wilson’s disease and postanoxic or posthypoglycemic states with brain damage. Numerous medical disorders can be associated with violence: hypoxia, electrolyte imbalances; hepatic disease; renal disease; vitamin deficiencies (B12 and folate, thiamine); systemic infections; hypoglycemia; Cushing’s disease; hyper- or hypothyroidism; systemic lupus erythematosus; disorders caused by heavy metals, insecticides and other poisons; and porphyria.

THE ASSESSMENT OF THE SHORT-TERM RISK OF VIOLENCE This section will present a model for the short-term risk of violence by patients. The prediction of violence by patients is expected of all clinicians who have a relationship with a patient, whether for evaluation and/or treatment. This includes psychiatrists, other physicians, psychologists, nurses, social workers, activity therapists and all other staff that have responsibilities for patients. This responsibility exists as clinicians evaluate patients in the emergency room and make decisions as whether to discharge or admit the patient to the hospital. It exists as the clinician sees the patient in an office setting for the first time and between outpatient visits. It exists when the clinician admits a patient to a hospital and orders level of observation and other immediate treatment as the patient enters the hospital. It exists in the hospital in terms of diagnosis and treatment, including monitoring the patient and whether seclusion or restraint should be used. It exists in the decision to discharge the patient and in the planning and implementation of care after discharge. The focus of this section is to evaluate the risk of violence in the short-term time period, with days or a week, since an increased risk of violence should result in preventative actions as soon as possible, such as change in medication, monitoring, admitting or discharge from a hospital and other clinical action to decrease the imminent risk of violence. Actuarial methods of assessment use the personal characteristics of the individual, such a demographic characteristics, diagnosis, the history of violence and other factors to predict the long-term risk of violence after discharge from prison or forensic psychiatric treatment facilities. The actuarial method has been applied to nonforensic psychiatric patients in the long-term prediction of violence, but this does not assist the clinician in the daily treatment

PSYCHOPATHOLOGY, RISK ASSESSMENT AND LAWSUITS

125

of potentially violent patients. A number of researchers recently have reviewed many instruments used to assess risk of violence using actuarial methods. They have found that there should be more progress in the integration of clinical, dynamic data in the prediction of violence in the short term that would be more relevant to general adult psychiatry (Harris, Rice & Camilleri, 2004; Kroner, Mills & Reddon, 2005; Kumar & Simpson, 2005; Mills, 2005)

Principles in the Assessment of the Risk of Violence A well-trained psychiatrist or other mental health professional should be able to predict a patient’s short-term violence potential with assessment techniques analogous to those used in the short-term prediction (again days or a week) of suicide potential. Beyond that time, many factors may intervene after the initial decision is made about risk, as in the case of the stabilized schizophrenic patient stopping medication or the abstinent spouse abuser resuming drinking. As in the prediction of suicide, the evaluator focuses on the clinical aspects of the evaluation, namely, psychopathology, but one must take into consideration demographic, historical and environmental factors that may be related to an increased risk of violence or suicide. The evaluation of homicide potential is analogous to that of suicide potential. Even if the patient does not express thoughts of violence, one should routinely ask as part of every evaluation the subtle question ‘Have you ever lost your temper?’ as one would check for suicide potential with ‘Have you ever felt that life was not worth living?’ If the answer is yes, then the evaluator should proceed with the evaluation in terms of how, when and so on about violence as one would proceed with the evaluation of suicide potential. When making a decision about violence potential, one should interview, in addition to the patient, family members, police and other persons with information about the patient and violent incidents to guard against the patient’s minimizing dangerousness. One should contact or attempt to contact current therapists and past therapists and review old charts for previous episodes of violence, arrest records and other records of judicial proceedings if such records are available.

Factors in the Assessment of the Risk of Violence The model presented in this section describes 10 factors that must be evaluated in determining whether a patient poses a short-term risk of violence. These factors are not scored to produce a global numerical indication of risk, for example 6 out of 10 would indicate risk but 4 out of 10 would not indicate a risk of short-term violence. Rather, information obtained in each area should be synthesized and weighed by the evaluator to form a clinical decision about short-term risk of violence, keeping in mind that change in some factors may be more important that others for the individual patient in an increased the risk of violence, for example, resumption of alcohol or drug use or a patient’s wife telling him that she wants a divorce after he is discharged from a hospital. This model represents a consensus among experts that has not been empirically tested, but has been used by the author and other psychiatrists as a standard in a number of malpractice suits.

126

VOLUME I: DIAGNOSIS AND TREATMENT

Appearance of the Patient The appearance of the patient may prompt further scrutiny of the potential for violence. This would apply to the loud, agitated, angry-appearing patient who is impatient and refuses to comply with the usual intake procedures in the emergency room or clinic, as well as the quiet, guarded patient to whom one must carefully listen to detect subtle violent ideation. Dysarthria, unsteady gait, dilated pupils, tremors and other signs of acute drug or alcohol intoxication dictate caution and serious consideration of the potential for violence, even though threats of violence may not have been expressed.

Presence of Violent Ideation and Degree of Planning/Formulation One begins with assessing whether the patient has thoughts of violence toward other persons. As in the evaluation of suicide ideation, evaluation of violent ideation includes assessment of how well planned is the ideation or threat, that is, the degree of formulation. Vague threats of killing someone, such as ‘I’m going to get even with her or she’ll be sorry to see me’, are not as serious, all things being equal, as the patient saying, ‘I’m going to kill my wife with a gun because she had an affair’.

Intent If a patient has thoughts of harming someone, it is important to explore whether he or she really intends to do something versus just having thoughts of violence. This may arise during an outpatient treatment session, as an off-hand comment on the inpatient unit or during any other contact with the patient. The patient’s mere thought of violence may not be sufficient for the clinician to take action, as in warning someone, changing medication or hospitalizing the patient. At times, thoughts of violence may seem intrusive, alien and very disturbing to patients and they say that they do not intend to do anything.

Available Means The availability of a means of inflicting injury or death is important in the assessment of violence potential. If the patient is thinking about getting a gun or has a gun, the clinician should obviously take a threat of violence more seriously. The clinician always should ask a potentially violent patient if he or she has a gun or has ready access to a gun. Vigorous efforts should be made to have the patient get rid of the gun or to have the gun taken from the patient. If a gun can be removed from the residence by the patient, family members or others, the potential for homicide will be reduced, however, obviously that does not preclude the patient attacking the victim in other less lethal ways. Available means also applies to the physical availability of the potential victim. This refers to the daily vulnerability of the potential victim as in living in a secluded place or in a city building without a doorman. Geography is another aspect of availability, for

PSYCHOPATHOLOGY, RISK ASSESSMENT AND LAWSUITS

127

example, whether a schizophrenic patient is threatening his father with whom he lives versus threatening his father who lives in a distant city away from the patient.

Past History of Violence of Impulsive Behaviors A past history of violence or other impulsive behaviors is often predictive of future violence. One should ask about injuries to other persons, destruction of property, suicide attempts, reckless driving, reckless spending, criminal offenses, sexual acting out and other impulsive behaviors. Past violence increases the risk of future violence by a patient. Episodes of past violence, for example, the most recent episode, should be ‘dissected’ in a detailed, concrete manner by the clinician. This includes details as to the time and place of past violence, who was present, who said what to whom, what the patient saw, what the patient remembers, what family members, friends or staff remember about the violent episode, why the patient was violent, for example, because of psychosis, and what could have been done to avoid the violence. Often there is a pattern of escalation of violence, whether it involves the dynamics of a couple in domestic violence or a schizophrenic patient on the inpatient unit becoming more agitated as interactions with other patients become too intense. The past history of violence should be treated as any other medical symptom. This includes the date of onset, frequency, place and severity of violence. Severity is measured by degree of injury to the victim, from pushing, to punching, to causing injuries such as bruises, to causing more serious injuries such as broken bones, lacerations, internal injuries or even death. Severity, target and frequency of violence can be measured by a written instrument such as the Overt Aggression Scale (Yudofsky, Silver & Jackson, 1986). Information about past history of violence should include prior evaluations such as psychological testing, imaging, laboratory testing and other evaluations as well as past treatment, hospitalizations and response to treatments.

Alcohol and Drug Use Intoxication with alcohol and a number of drugs increases the risk of violence while withdrawal from alcohol also can increase the risk of violence. The syndromes and clinical manifestations of the disorders of alcohol and drug abuse have been described earlier in this chapter. Alcohol intoxication increases the risk of violence by decreasing a person’s inhibitions. Furthermore, alcohol impairs cognition including the intellectual ability to argue in a marital conflict or bar fight, thus resulting in violent action in an attempt to cope with a dispute. Alcohol withdrawal can produce delirium with disorganized behavior and psychosis with paranoid delusional thinking and hallucinations. Intoxication with cocaine and amphetamines increases risk of violence through agitation and suspiciousness with continued use, which can lead to paranoid delusional thinking. Hallucinogens, particularly phencyclidine (PCP), can produce grossly impaired judgment, paranoid ideation and severe, unpredictable violent and/or self-destructive behaviors. Inhalants can produce belligerence and impaired judgment, usually in children and adolescents. Anabolic steroids produce episodic rage attacks in men who use them.

128

VOLUME I: DIAGNOSIS AND TREATMENT

Psychosis As in the assessment of suicide potential, the presence of psychosis should make the clinician take threats of violence very seriously and makes the formal assessment of violence potential essential, even if threats or ideas of violence are not apparent. Psychosis is defined in DSM-IV-TR as follows. ‘This term has historically received a number of different definitions, none of which has achieved universal acceptance. The narrowest definition of psychotic is restricted to delusions or prominent hallucinations, with the hallucinations occurring in the absence of insight into their pathological nature. A slightly less restrictive definition would also include prominent hallucinations that the individual realizes are hallucinatory experiences. Broader still is a definition that also includes other positive symptoms of schizophrenia (i.e., disorganized speech, grossly disorganized or catatonic behavior)’ (American Psychiatric Association, 2000). Psychosis is not a diagnosis, but a symptom that can be found in a number of disorders, including schizophrenia, delusional disorder, neurological and medical disorders, substance abuse disorders such with alcohol, cocaine, amphetamines, hallucinogens, inhalants and other substances and mood disorders with mania or depression. When psychosis is present, regardless of the disorder, it increases the risk of violence. Conversely, these disorders that are discussed earlier in this chapter can produce violence in the absence of psychosis, for example, the schizophrenic patient who is disorganized and angry, the alcoholic who in only intoxicated, the manic patient who has extreme psychomotor agitation and is not psychotic. The paranoid patient, regardless of diagnosis, poses a problem in that paranoid delusions may not be obvious, sometimes because the patient attempts to hide them. Therefore, the evaluator must listen for subtle clues and should follow up regarding the assessment of violence toward others. The evaluator should not confront the patient about the presence of paranoid delusions in an antagonistic manner, for example, citing collateral sources, or to confront the patient about the unreality of the paranoid beliefs since this can provoke the paranoid patient to respond in a violent manner (Taylor, 2006; Taylor & Felthous, 2006). Psychotic patients who have auditory hallucinations, regardless of diagnosis, pose an increased risk of violence, particularly with command auditory hallucinations.

Personality Disorders Violence by persons with antisocial personality disorder is often vicious and persistent with continued punching or hitting the victim with objects beyond what is necessary to subdue the victim and win the fight. There is no remorse and the victim is perceived as deserving the beating. The person with borderline personality disorder can be violent and make suicidal gestures when rejected or when feeling rejected by others. The violence and suicide attempts of borderline patients are part of a broad instability of interpersonal relationships and impulsivity. The person with narcissistic personality can be violent occasionally when angry at not being given what he or she deserves. The person with paranoid personality rarely attacks the people whom he thinks are persecuting him, but when violence occurs, it can be severe, as in mass murder. The person with intermittent explosive disorder frequently is violent during circumscribed episodes with little apparent precipitating cause or is out of proportion to any identifiable cause.

PSYCHOPATHOLOGY, RISK ASSESSMENT AND LAWSUITS

129

Noncompliance with Treatment A history of noncompliance with treatment should alert the clinician that the patient represents an increased risk of violence behavior. Noncompliance involves a history of irregular attendance at scheduled outpatient appointments or other appointments for treatment or laboratory tests and other clinical purposes. Noncompliance involves the refusal by the patient to take certain medications for a psychiatric or medical disorder or missed doses of medication. Blood levels of medication may assist the clinician in monitoring compliance with medication. Contact with the patient’s family, with the consent of the patient, may assist in determining whether the patient is taking medication as prescribed. The use of depot medication, particularly the antipsychotic medications in schizophrenia and other psychotic disorders can be used to assure compliance by these patients.

Demographic Characteristics Demographic characteristics of patients should be considered in the assessment of violence potential. Increased risk of violence has been found in the young, in males, and in persons coming from environments of poverty, disruption of families and decreased social control, where, in general, violence is a more acceptable means of attaining a goal than in other segments of society. The environment from which the patient comes is an important consideration in the determination of violence potential. Is it one in which violence is viewed as an accepted means of obtaining what one wants in the face of poverty or lack of other legitimate means, education, work and verbal skills?

LAWSUITS AGAINST CLINICIANS WHEN PATIENTS ARE VIOLENT The author has reflected on his participation in a number of malpractice lawsuits against clinicians and/or health facilities when a patient in treatment or evaluation was violent toward a person(s). Generally, clinicians have not been faulted for inaccurate prediction of violence but for failure to collect the data necessary for the prediction of violence and to use the data logically when making a decision about the risk of violence. A case exemplifying this involved an employee who killed his employer with a knife while working in a carpet installation business. The employee was a middle-aged man with a diagnosis of schizophrenia who had been in treatment in an outpatient clinic at a Veterans Administration Hospital for over 20 years. Prior to the homicide, he was seen by a psychiatric resident every month. His records revealed a persistent delusion, since medical discharge from the military, that he was a spy for the US government. His records revealed no history of violence and no ideas of violence against his employer or anyone else. The records included an in-depth assessment of violence and suicide potential by the resident initially on seeing the patient and a statement by the resident about no change in his potential for violence every session. There were periodic notes by the supervising attending psychiatrist in the records. The patient was compliant with treatment in terms of keeping his appointments and taking antipsychotic medication. The judicial decision in this case was in favor of the defendant

130

VOLUME I: DIAGNOSIS AND TREATMENT

and stated that there was no evidence on which the defendant could have predicted that the patient would be violent. Coincidentally, the author read the diary of the patient (which was not included in the author’s testimony) that revealed no delusions about the employer and no thoughts of killing him or anyone else. Another case illustrates the opposite, where a psychiatrist made a decision to allow a patient to leave an inpatient unit without assessing violence potential and not considering prior concerns about violence. A young man was brought to an emergency room by his father because of a recent onset of delusion thinking. There, his father denied any history of his threatening violence. He was referred to a day hospital and discharged. Within a few hours, the patient swung a baseball bat at his father and was taken back to the same emergency room. A psychiatric resident diagnosed a psychotic process and stated ‘pt must be considered potentially a danger to others, in particular he may be a danger to his parents’. The resident discussed the case with an attending psychiatrist in the emergency room, who agreed with the formulation and decision to admit the patient to a private inpatient service in the hospital. Once on the inpatient unit, the patient was uncooperative and demanded to leave. The private attending psychiatrist on the inpatient unit was notified in the late afternoon and ordered discharge of the patient against medical advice without ever seeing the patient. The patient did not return home after leaving the hospital and the parents were so frightened that they checked into a motel for a few days. Six weeks later, the patient appeared in his parents’ driveway, began shooting and killed his father. The court decision in the malpractice case was against the private attending psychiatrist who discharged the patient from the inpatient unit. There were cases that did not criticize the assessment of risk of violence directly. These cases involved lapses in the degree of control of the potentially violent patient in the emergency room or inpatient service, as in the presence of security staff, degree of monitoring such as constant observation, room restriction or seclusion or restraint. Placement of potentially violent patients with vulnerable patients on inpatient services has been the subject of a number of lawsuits seen by the author. Perhaps the most egregious case in this category involved a young man who was in a wheelchair in a medical/psychiatry unit due a leg injury. He was psychotic with a history of antisocial personality and polysubstance abuse. In the unit, there were a number of elderly patients with dementia and other psychiatric disorders as well as medical disorders. The young man made comments such as the patients ‘need a date with the coroner’ and would do things such as pull out a patient’s feeding tube. One day, an elderly woman was found beaten to death with a leg rest from a wheelchair. It could not be proven that he did it because the staff cleaned the premises immediately after she was found. Some lawsuits have involved questions about the adequacy of discharge planning and/or implementation of an aftercare plan. A middle-aged woman was admitted to a hospital with a psychotic depression involving delusional thinking about her daughter and suicidal ideation. She responded well to sertraline and thiothixene in regard to the depression and delusional thinking and was ready for discharge. At the time of discharge, she denied any ideation about suicide or violence. The patient and her husband were told to attend aftercare treatment in a ‘step down’ facility that was in the same building where she was evaluated before admission to the hospital. She was given an appointment for three weeks after discharge with a psychiatrist at the facility. Nothing about the aftercare plan was given to them in writing. The patient did not keep the appointment and called to the social

PSYCHOPATHOLOGY, RISK ASSESSMENT AND LAWSUITS

131

worker at the hospital to say that she had decided to get care elsewhere. No follow-up was done by the hospital. Two months later, the patient killed her daughter’s friend who was attending a sleepover at her home and shot her daughter, who survived. The patient had not sought treatment elsewhere and she was psychotic and depressed when evaluated after the homicide.

SUMMARY This chapter has described violence in patients with antisocial personality disorder and other psychiatric disorders. Violence differs among these disorders in terms of frequency, the manner in which it is expressed and the psychopathology and dynamics that produce violence. Violence is seen more frequently by clinicians and is more problematic in antisocial personality, borderline personality and intermittent explosive disorders, schizophrenia and other psychotic disorders, mania, alcohol and drug abuse, mental retardation and some medical and neurological disorders. This chapter has presented a model to assess the potential for violence among patients in the short term (days or a week), a period of time of great relevance in clinical decisions, to admit to a hospital, to monitor and medicate patients in hospital, to discharge patients from hospital, to develop an aftercare plan and, in the outpatient setting, to monitor the potential for violence from office visit to office visit. The model for the assessment of violence potential is analogous to that for the assessment of suicidal potential. The clinician assessing violence potential must rely on as many sources of data as possible, from interviews with the patient, friends, police, current and former clinicians who have treated the patient as well as past clinical and other types of records. The areas that must be covered are: 1. 2. 3. 4. 5. 6. 7. 8.

appearance of the patient presence of violent ideation and degree of planning and/or formulation intent to be violent available means and access to the potential victim past history of violence and other impulsive behaviors alcohol and drug use presence of psychosis presence of personality disorders, particularly antisocial personality, borderline personality disorders and intermittent explosive disorder 9. a history of noncompliance with treatment 10. demographic and socioeconomic characteristics. All 10 of the factors are weighed by the clinician in the final assessment of whether the patient poses a short-term risk of violence to others. If the patient poses a short-term risk of violence, some action is necessary on the part of the evaluator. Action may include changing the treatment plan, hospitalizing the patient, warning the intended victim and/or the police and other creative maneuvers to prevent the imminent violence by the patient. All of the data on which the decision that the patient is or is not a risk for violence was made must be documented in writing; the thinking process by which the decision was made must be evident in the written documentation. Reassessment

132

VOLUME I: DIAGNOSIS AND TREATMENT

of violence potential should be made at short intervals (e.g., from visit to visit or every few days) if the patient is to continue to be treated outside of the hospital or other institution. In the hospital and emergency room, safety and monitoring of a potentially violent patient is essential and treatment after discharge must be detailed, in writing and arranged in a timely manner.

REFERENCES American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision. Washington, DC: American Psychiatric Association. Anderson, K.E. & Silver, J.M. (1999). Neurological and medical diseases and violence. In K. Tardiff (ed.), Medical Management of the Violent Patient: Clinical Assessment and Therapy (pp. 87–124). New York: Marcel Dekker. Andreasen, N.C., Arndt, S., Alliger, R., Miller, D. & Flaum. M. (1995). Symptoms of schizophrenia: methods, meanings, and mechanisms. Archives of General Psychiatry, 52, 341–51. Bernstein, D.P., Useda, D. & Siever, L.J. (1993). Paranoid personality disorder: a review of its current status. Journal of Personality Disorders, 7, 53–62. Bushman, B.J. (1997). Effects of alcohol on human aggression: validity of proposed explanation. Recent Developments in Alcoholism, 13, 227–304. Choi, P.Y.L., Parrott, A.C. & Cowan, D. (1989). High dose anabolic steroids in strength athletes: effects upon hostility and aggression. Journal of Psychopharmacology, 3, 102–13. Convit, A., Nemes, Z.C. & Volavka, J. (1988). History of phencyclidine use and repeated assaults in newly admitted young schizophrenic men. American Journal of Psychiatry, 154, 1176–83. Denison, M.E., Paredes, A. & Booth, J.B. (1997). Alcohol and cocaine interactions and aggressive behaviors. Recent Developments in Alcoholism, 13, 283–91. Dixon, L, Haas, G., Weiden, P.H., Sweeney, J. & Frances, A.J. (1991). Drug abuse in schizophrenic patients: clinical correlates and reasons for use. American Journal of Psychiatry, 148, 224–30. Gunderson, J.G. (1996), The borderline patient’s intolerance of aloneness: insecure attachment and therapist availability. American Journal of Psychiatry, 153, 752–8. Gunderson, J.G., Ronningstam, E. & Smith, L.E. (1991). Narcissistic personality disorder: a review of data on DSM-III-R descriptions. Journal of Personality Disorders, 5, 167–77. Hare, R.D., Hart, S.D. & Harper, T.J. (1991) Psychopathy and the DSM-IV criteria for antisocial personality disorder. Journal of Abnormal Psychology, 100, 391–8. Harris, G.T., Rice, M.E. & Camilleri, J.A. (2004). Applying a forensic actuarial assessment (the Violence Risk Appraisal Guide) to nonforensic patients. Journal of Interpersonal Violence, 19, 1063–74. Herpertz, S., Gretzer, E.M., Steinmeyer, V. et al. (1997). Affective instability and impulsivity in personality disorder. Journal of Affective Disorders, 44, 31–7. Hurley, A.D. & Sovner, R. (1995). Six cases of patients with mental retardation who have antisocial personality disorder. Psychiatric Services, 46, 828–35. Johnston, L.D., O’Malley, P.M. & Bachman, J.G. (1997). National Annual High School Senior and Young Adult Survey. Washington, DC: US Government Printing Office. Kemperman, I., Russ, M.J. & Shearin, E. (1997). Self-injurious behavior and mood regulation in borderline patients. Journal of Personality Disorders, 11, 146–57. Kroner, D.G., Mills, J.F. & Reddon, J.R. (2005). A coffee can, factor analysis and prediction of antisocial behavior: the structure of criminal risk. International Journal of Law and Psychiatry, 28, 360–74. Kumar, S. & Simpson, A.I. (2005). Application of risk assessment for violence methods to general adult psychiatry: a selective review of the literature. Australian New Zealand Journal of Psychiatry, 39, 328–35. Langevin, R., Ben-Aron, G., Wortzman, R., Dickey, R. & Handy, L. (1987). Brain damage, diagnosis, and substance abuse among violent offenders. Behavioral Sciences and the Law, 5, 77–86.

PSYCHOPATHOLOGY, RISK ASSESSMENT AND LAWSUITS

133

Lesch, K.P. & Merschdorf, U. (2000). Impulsivity, aggression and serotonin: a molecular psychobiological perspective. Behavioral Sciences and the Law, 18, 581–604. Linaker, O.M. (1994). Assaultiveness among institutionalized adults with mental retardation. British Journal of Psychiatry, 164, 62–78. McElroy, S., Keck, P.E., Pope, H.G. et al. (1992). Clinical and research implications of the diagnosis of dysphoric or mixed mania or hypomania. American Journal of Psychiatry, 149, 1633–44. McCormick, R.A. & Smith, M. (1995). Aggression and hostility in substance abuser: the relationship to abuse patterns, coping style, and relapse trigger. Addictive Behaviors, 22, 555–64. Miczek, K.A. & Tidey, J.W. (1989). Amphetamines: aggressive and social behavior. NIDA Research Monographs, 94, 68–79. Miller, R.J., Zadolinnyi, K. & Hafner, R.J. (1993). Profiles and predictors of assaultiveness for different psychiatric, ward populations. American Journal of Psychiatry, 150, 1368–73. Mills, J.F. (2005). Advances in the assessment and prediction of interpersonal violence. Journal of Interpersonal Violence, 20, 236–41. Modestin, T. & Ammann, R. (1996). Mental disorders and criminality: male schizophrenia. Schizophrenia Bulletin, 22, 69–82. Pope, H.G. & Katz, D.L. (1994). Psychiatric and medical effects of anabolic-androgenic steroid use: a controlled study of 160 athletes. Archives of General Psychiatry, 51, 375–86. Rosenbaum, M. & Bennett, B. (1986). Homicide and depression. American Journal of Psychiatry, 143, 367–73. Serretti, A,, Lattuada, E. & Cusin, C. (1999). Factor analysis of delusional disorder symptomatology. Comprehensive Psychiatry, 40, 143–7. Tardiff, K. (1992). The current state of psychiatry in the treatment of violent patients. Archives of General Psychiatry, 49, 493–7. Tardiff, K., Wallace, Z., Tracy, M. et al. (2005). Drug and alcohol use as determinants of New York City homicide trends from 1990–1998, Journal of Forensic Sciences, 50, 1–5. Taylor, P.J. (2006). Delusional disorder and delusions: is there a risk of violence in social interactions about the core symptoms? Behavioral Sciences and the Law, 24, 313–32. Taylor, P.J. & Felthous, A.R. (2006). Introduction to this issue: international perspectives on delusional disorders and the law. Behavioral Sciences and the Law, 24, 235–40. Volavka, J. & Tardiff, K. (1999). Substance abuse and violence, In K. Tardiff (ed.), Medical Management of the Violent Patient: Clinical Assessment of Therapy (pp. 153–77). New York: Marcel Dekker. Widiger, T.A. (2000). Personality disorders in the 21st century. Journal of Personality Disorders, 14, 3–16. Yudofsky, S.C., Silver, J.M., Jackson, W. (1986). The Overt Aggression Scale for the objective rating of verbal and physical aggression. American Journal of Psychiatry, 143, 35–9.

CHAPTER 8

Risks of Diagnosing Psychopathic Disorders Nobert Leygraf and Klaus Elsner University of Essen, Germany

In recent years, the concept of psychopathy has obtained an important position in forensic psychiatry and psychology as well as in criminological research. This is demonstrated by the number of publications about psychopathy in the international literature. More important, however, is the degree to which psychopathy has found its way into the criminal justice and mental health systems. The construct of psychopathy is based largely on the work of Harvey Cleckley (1976). Utilizing Cleckley’s description of psychopathic personality characteristics, Hare developed the Psychopathy Checklist (PCL) during the early 1980s, and the Psychopathy ChecklistRevised (PCL-R) in 1991. These instruments led to the standardized and reliable diagnosis of psychopathy (Hare, 1991, 2003). ‘Psychopathy is a socially devastating disorder defined by a constellation of affective, interpersonal, and behavioral characteristics, including egocentricity, impulsivity, irresponsibility, shallow emotions, lack of empathy, guilt or remorse, pathological lying, manipulativeness and the persistent violation of social norms and expectations’ (Hare, 1996, p. 25). A screening version of the PCL-R was developed by Hart, Cox and Hare (1995), and a version for adolescents between 12 and 18 years of age was recently introduced (Forth, Kosson & Hare, 2003). Although the PCL-R was not developed to predict criminal relapse, various studies have demonstrated an association between the diagnosis of psychopathy and recidivism. Subsequently, Hare (1996) expected the PCL-R to establish itself as an important instrument in the forensic field. The PCL-R has been occasionally described as an ‘unparalleled’ measure for the prediction of recidivism (Salekin, Rogers & Sewell, 1996). The observed acceptance and dissemination of this construct are closely associated with an increasing need for safety in the community, as well as disillusionment and mistrust in the effectiveness of treatment for dangerous offenders. At the same time, victim protection has become an increasingly important topic in sociopolitical discussions. This led to crimino-political initiatives and legal reforms in which the protection of the community from dangerous offenders was of central importance. In 17 states in the United States, Sexually Violent Predator Acts exist which allow for the involuntary civil

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

136

VOLUME I: DIAGNOSIS AND TREATMENT

commitment of sexual offenders who pose a high risk of reoffending (e.g., see Douard, 2007; Fitch & Ortega, 2000). In Great Britain the legal definition of ‘dangerous severe personality disorder’ was introduced. This definition includes people with a serious personality disorder, ‘ . . . who pose a high risk to other people because of serious antisocial behavior resulting from their disorder’ (Home Office & Department of Health, 1999). In Germany, the criteria for preventive detention were eased and retrospective preventive detention was introduced. In Switzerland, a referendum passed on the petition, ‘Life-long detention for extremely dangerous and untreatable sexual and violent offenders’. According to Article 123a of the Swiss Federal Constitution, early release or temporary leave is not possible for these offenders (Frommel, 2004). Aside from these legal regulations, correctional and forensic psychiatric institutions experienced strong political and public pressures to improve their risk assessments of dangerous offenders. The criticisms over the quality of these assessments were partly correct. Previously the liberalization of criminal law and the heavy focus on treatment in correctional institutions meant that risk assessments were not always conducted with the necessary care. Within this social and crimino-political situation, it was only a matter of time before the expectations of Hare (1996) were fulfilled. The construct of psychopathy established its importance in legal and forensic practice. It promised to identify potentially dangerous offenders reliably and through this to satisfy the community’s need for security and ongoing separation from these people. A robust relationship between the diagnosis of psychopathy and general as well as violent recidivism is clearly evident in research findings. Most of this research was conducted in North America, but an increasing number of studies have also appeared in the international literature. Obviously, the PCL-R identifies a small group of individuals within the criminal population who are responsible for a large number of criminal acts. This small group also demonstrates a greater likelihood to recidivate violently after release from prison (Dolan & Doyle, 2000; Hemphill, Hare & Wong, 1998; Salekin, Rogers & Sewell, 1996). Sexual offenders with a diagnosis of psychopathy and a deviant sexual preference display an increased risk for sexual reoffending (Hildebrand, de Ruiter & Nijman, 2004). The presence of psychopathic personality traits in forensic patients also relates to an increased risk of future violent behavior (Tengstr¨om et al., 2000). ThePCL-R has established predictive validity not only for incarcerated offenders and forensic patients, but also for psychiatric patients. A higher score on the PCL-SV was the strongest predictor of future violent behavior in the MacArthur Risk Study (Monahan et al., 2001). Furthermore, there is little evidence to date that high PCL-R scorers can benefit from psychological treatment (D’Silva, Duggan & McCarthy, 2004).

THE SIGNIFICANCE OF PCL-R ASSESSED PSYCHOPATHY IN LEGAL AND FORENSIC PRACTICE In the US justice system, Walsh and Walsh (2006) found nine areas in which the diagnosis of psychopathy formed part of the legal decision process: commitment pursuant to sexual predator laws, parole hearings, death penalty sentencing, civil commitment, transfer from juvenile to adult court, termination of parental rights, sentence enhancement and sentence mitigation, competency to stand trial and determination of criminal responsibility. In most

RISKS OF DIAGNOSING

137

cases, the PCL-R was utilized in preventative detention hearings. Sexual predator laws permit continued detention for habitual sexual offenders upon the completion of their criminal sentences relying on the theory that such offenders suffer from an inability to control their dangerous impulses. A high score on the PCL-R was presented as evidence for a high risk of sexual reoffending and therefore as reason for continued incarceration. Risk of reoffending in these cases was established either solely with the PCL-R or with psychological or psychiatric assessments in which the PCL-R was embedded. In capital sentencing hearings, PCL-R diagnosed psychopathy is used as evidence that the defendant will likely commit further violent acts in prison. The likelihood for this is used to argue for the death penalty instead of a life-long prison sentence. In European countries the PCL-R is increasingly utilized for risk assessments of patients in forensic hospitals and prisons. These assessments are focused on aggressive and disruptive behaviors during the hospital or prison stay, as well as on decisions about release (Eher et al., 2006; Hildebrand et al., 2004; Tengstr¨om et al., 2006). In Germany, a critical attitude exists towards the use of standardized risk assessment instruments. The recently formulated minimum requirements for legal prognosis developed by judges, forensic psychiatrists and forensic psychologists (Boetticher et al., 2006) states: ‘Risk assessment instruments do not replace the hermeneutic or hypothesis guided individual prognosis. However, they help to make empirical knowledge useful for the prognosis and to maintain international prognosis standards’ (p. 542). Aside from the assessment of violent recidivism, the PCL-R or the diagnosis of psychopathy has increasing influence on aspects of treatment. The discussion focuses on treatment responses, methods of treatment and optimal institutional settings for psychopaths (Wong, 2000). In contrast to the use of the PCL-R in research, the diagnosis of psychopathy has significant influence in criminal and mental health systems on trial decisions, sentencing options and decisions concerning treatment options. As a result, the diagnosis has serious implications for the individual thusly diagnosed. It is therefore critical to question just how far the research findings can be used in individual cases.

STATISTICAL RESULTS FOR GROUPS AND RISK PREDICTION FOR INDIVIDUALS The predictive validity of the PCL-R for violent criminality has been supported by many studies. The structural limitations of the PCL-R (the prediction of rare occurrences and the high percentages of criminals with medium scores) will not be considered here (see Dahle, Schneider & Ziethen, 2007). However, it is important to note that the PCL-R, like other actuarial instruments, can only make statements about the mean scores for individual populations. This is certainly sufficient and sensible in order to make scientifically based statements about the characteristics of single populations. It is problematic when concrete statements about the future dangerousness of an individual offender are necessary for legal decisions or for release from prison. In contrast to the research field, prognostic statements are demanded in legal and forensic practices, which are not based on group statistics. The prognosis must be based on the dangerousness derived from the personality of the individual offender and his specific offenses. This problem was made clear in a minority opinion of

138

VOLUME I: DIAGNOSIS AND TREATMENT

the Minnesota Supreme Court: ‘Not only are the statistics concerning the violent behavior of others irrelevant, but it seems to me wrong to confine any person on the basis, not of that person’s own prior conduct, but on the basis of statistical evidence regarding the behavior of other people’ (cited in Edens & Petrila, 2006, p. 576). The issues with the predictive validity of the PCL-R will now be made clearer by using specific examples. Grann et al. (1999) found in a group of personality disordered offenders (n = 352) that 55 % of the diagnosed psychopaths violently recidivated in an average follow-up period of 44.2 months (SD = 27.4). In comparison, only 25 % of the offenders not diagnosed as psychopaths (cut-off ≥ 26) recidivated violently. Similar results were found in violent psychotic patients (Tengstr¨om et al., 2000). Sixty-six percent of the patients (n = 141) with a PCL-R score ≥ 26 violently reoffended and only 18 % of patients with a score ≤ 25 did so. Hare et al. (2000) reported that prisoners released from English prisons (n = 728) with a high PCL-R score (cut-off ≥ 25) violently recidivated at a significantly higher rate than prisoners with a low PCL-R score (38.2 % vs. 2.7 %). Although a strong relationship between PCL-R scores and violent recidivism exists, the results of the above studies indicate that many psychopaths do not recidivate with a violent offense. Thirty-five percent of the released personality disordered offenders with a PCL-R score > 32 (Grann et al., 1999), 34 % of the released psychotic offenders with a PCL-R score ≥ 26 (Tengstr¨om et al., 2000) and about 62 % of the released offenders with a PCL-R score ≥ 25 (Hare et al., 2000) did not violently reoffend in the follow-up period. Freedman (2001) has also criticized the PCL-R, stating that the positive predictive power of the PCL-R is not sufficient. ‘The evidence of intragroup statistics indicates poor prediction capacity concerning violence. The rate of false-positives associated with the use of the PCLR, although often unreported in favor of intergroup data, is strikingly consistent and very high, worse than a coin toss in predictive ability (p. 91). Freedman (2001) found in the seven studies that he reviewed a false-positive rate between 50 % and 75 % concerning violent reoffending. This means that at least half of the high PCL-R scorers were falsely classified as dangerous. Concerning the poor predictive validity of the PCL-R, the absence of a theoretically justified and clearly defined cut-off score for the diagnosis of psychopathy is problematic. Depending on the chosen cut-off score, the number of offenders classified as psychopaths increases or decreases. As the prevalence of psychopathy remains unchanged in the population, lower cut-off scores lead to an increase in false-positives. Varying cut-off scores in the research field are not seen as problematic, simply because they are not linked to concrete decisions. However, in practice the use of arbitrary cut-off scores cannot be accepted due to the possible real-life consequences. The use of the PCL-R for the prediction of violent reoffending in legal settings is therefore questionable. Clearly, given the high false-positive rates, the PCL-R should not be used in forensic or clinical settings where life and liberty decisions are at stake. The PCL-R may be, as its proponents argue, the strongest in a field of weaklings, but it is by no means reliable and valid in the prediction of future dangerousness (Freedman, 2001, p. 94). There are varied findings in relation to the use of the PCL-R for the prediction of institutional rule violations (violation of rules, verbal threat and physical violence). Hildebrand, de Ruiter and Nijman (2004) found a significant relationship between PCL-R scores and institutional rule violations. Factor 2 accounted for most of the relationship. In a meta-analysis, Factor 2 was again found to be a significant contributor to institutional rule violations

RISKS OF DIAGNOSING

139

and Factor 1 less so (Walters, 2003). In a study by Hare (2003), the number of previous convictions and age were better predictors than the PCL-R score for behavior in the institution. The PCL-R score was a better predictor only for assault. Additionally, the PCL-R demonstrated no predictive validity of violent behavior in a sample of forensic patients in a German forensic hospital (Tengstr¨om et al., 2006). The prediction of misbehavior in institutions, in particular future violence, is a decisive factor in various states of the USA for death penalty sentencing (e.g., Texas Statutes and Codes, 2000). However, to date no empirical studies exist on the predictive validity of the PCL-R with a sample of death row inmates. Edens et al. (2005) reported that only 5.2 % of Texas death row inmates (former, current and executed inmates, n = 155) committed a serious assault after their conviction, even though expert testimony reported a continuing threat to society in these cases. Edens and colleagues (2005) concluded that the PCL-R is not suitable for the prediction of aggression in institutions. The empirical evidence for a relationship between psychopathy and institutional violence is insufficient and the clinical judgments ‘highly inaccurate and ethically questionable at best’ (p. 55).

INTERCULTURAL ASPECTS In the past decade, research on the prevalence and predictive validity of psychopathy in Europe (Great Britain, Scandinavia, Holland, Germany and Switzerland) has been increasingly conducted and published. However, the development and standardization of the construct largely relied on white prisoners in the United States and Canada. If psychopathy is a universal construct, which can be used in different cultures without modification, then the prevalence rates in the different countries should be comparable. In contrast to this assumption, the prisoners in North America display significantly higher PCL-R scores than prisoners in the international and predominantly European studies. Consequently, the number of prisoners classified as psychopaths in North America is higher than in Europe. In a review of 19 international studies, Sullivan and Kossan (2006) report a mean PCL-R score of 17.5 (SD = 7.3) in predominantly European prisoners (n = 2046). They reported prevalence rates between 3 % and 49 %, depending on the various cut-off scores and samples. In comparison North American prisoners (n = 5408) had a mean score of 22.1 (SD = 7.9) and a prevalence rate of 20.5 %. However, no difference was reported for psychiatric patients. Four hundred and forty psychiatric patients from international studies had a mean score of 22.5 (SD = 8.0) and North American psychiatric (n = 1246) patients, a mean score of 21.5 (SD = 6.9). How can the variation in prevalence rates between European (international) and North American studies be explained? Certainly, one could consider, whether the higher prevalence rates in North America actually reflect cultural differences. In this respect Cooke (1998) states that the psychopathic characteristics of superficial relationships and an impulsive lifestyle could underlie an individual’s migration. The influence of culturally determined attitudes and opinions on the different results has seldom been researched. Additionally, the attitude toward dealing with offenders, which the different rates of incarceration in the US and Europe reflect, may play an important role in explaining the prevalence rates. Finally, attitudes towards the possibility of personality change may also influence the variation in prevalence rates.

140

VOLUME I: DIAGNOSIS AND TREATMENT

Indeed European studies also reveal differences within Europe in PCL-R scores and prevalence rates. Cooke (1995) found that Scottish prisoners had a mean PCL-R score of 13.8 (SD = 7.4) and a prevalence rate between 3 % and 8 % depending on the cut-off score (≥ 30 or ≥ 25). In a sample of British prisoners (Hare et al., 2000), a mean PCL-R score of 16.5 (SD = 7.8) was found. Using a cut-off of ≥ 30 or cut-off ≥ 25, the prevalence rates were 4.5 % and 13 %, respectively. In contrast, Hobson and Shine (1998) report much higher scores (M= 24.2; SD = 6.2) and prevalence rate (26% for a cut-off ≥ 30) in a sample of 104 British prisoners. However, in this study the sample involved prisoners diagnosed with a personality disorder. Hildebrand and colleagues (2002) found in a sample of Dutch forensic psychiatric patients a mean score of 21.3 (SD = 8.4) and prevalence rates of 20% or 33% depending on the cut-off scores of ≥ 30 or ≥ 26. In a Swiss study (Urbaniok et al., 2006) of 96 prisoners, a mean PCL-R score of 19 (SD = 7.88) was found. Using cut-off scores of ≥ 25 and ≥ 30, 27 % and 9 % respectively were diagnosed as psychopaths. Sample differences could certainly largely explain the different prevalence rates. In the individual studies, different populations are represented. These populations differ concerning their biographical, criminological and personality or character disorder profile. Blackburn and Coid (1998) noted that comorbid disorders, such as Cluster B DSM-IV personality disorders or substance abuse, are associated with psychopathy. Socioeconomic status possibly also plays a role as a moderating variable. Walsh and Kosson (as cited in Sullivan & Kosson, 2006, p. 453) reported that the PCL-R score was a significant predictor of recidivism for Americans with an African heritage independent of their socioeconomic status. For Americans with a European heritage, the PCL-R score was only predictive for those with low socioeconomic status. Despite the above-mentioned differences Cooke et al., (2005) were able to identify a similar factor structure in North American and British data. They concluded that the PCL-R was measuring the same construct in two different cultural settings. However, the PCL-R scores are not comparable. A cut-off of 30 in North America is metrically equivalent to a score of 25 in Scotland or England (Cooke, 1998).

PSYCHOPATHY AND DENIAL OF TREATMENT The diagnosis of ‘psychopath’ is associated with the not unlikely danger of receiving the label of untreatable, and, because of this, being refused the option of forensic treatment. The claim of untreatability is mostly derived from the results of a study by Rice, Harris and Cormier (1992). In a retrospective study of mentally disordered offenders who were in a social therapy unit in Penetanguishene (Canada) between 1968 and 1979, Rice and colleagues found that offenders without a diagnosis of psychopathy (cut-off ≥ 25) benefited from treatment. Thirty-nine percent of the untreated versus 22 % of the treated offenders reoffended or committed parole violations. Psychopaths displayed the reverse effect. Seventy-seven percent of treated versus 55 % of untreated psychopaths reoffended or committed parole violations. Since the Rice publication, various authors used these results to argue that treatment of psychopaths is not only ineffective, but also detrimental. In reality the treatment goals, contents and methods of the treatment program at that time did not correspond with currently accepted standards of offender treatment (L¨osel, 1998). What was really evaluated was a therapeutic community in which group treatment in the form of marathon sessions and

RISKS OF DIAGNOSING

141

encounter groups were conducted. In these groups the offenders worked largely without professional supervision and were encouraged to take on therapist roles. In this respect, it is not hard to see how offenders who have a tendency towards manipulative, egocentric and irresponsible behavior took this opportunity to maintain their antisocial patterns of behavior. Wong (2000) concluded therefore, ‘The results of this program provide a good lesson on what not to do in the treatment of institutionalized psychopaths’ (p. 98). As evidence of the poor treatment response of psychopaths, the study by Seto and Barbaree (1999) is also often cited. These authors found a sexual reoffense rate that was five times higher for high PCL-R scorers who were also rated as making positive treatment progress. As the cut-off score was 15, it is questionable whether the results relate to psychopathy at all. These results were later reanalyzed (Barbaree, 2005) with a longer follow-up period and therefore a more extensive reoffense database. This increased the statistical power of the analyses. In the reanalysis, the interaction between psychopathy and treatment behavior on reoffending was no longer evident. A higher PCL-R score remained predictive of greater recidivism. To reiterate, there is no support in these data for the notion that psychopaths who perform well in treatment should be considered at higher risk for reoffense compared with psychopaths who perform badly in treatment. Finally, there is no evidence in our data involving the follow-up of sex offenders treated in an institutional setting that psychological treatment caused psychopaths to reoffend at a higher rate. Salekin (2002) also found no evidence for pessimism about effective treatment of psychopaths in his review. He found good results for high frequency treatments that last more than one year. In contrast, the success for programs of less than six months duration was poorer. Both psychodynamic and cognitive behavioral approaches were successful. He indicated that for the complex problems, that present in the cases of psychopathy, an intensive intervention is necessary which includes individual and group treatment as well as the inclusion of the family in treatment. Obviously independent of the specific treatment method, it is necessary to prevent treatment dropout. Cretton et al. (2001) found significantly less violent recidivism by psychopaths who completed treatment in comparison with those who dropped out. Caldwell et al. (2006) were able to show that treatment dropout was due, not only to the characteristics of the psychopaths, but also to the treatment context. Treated juveniles incarcerated in a juvenile correctional institution were twice as likely to reoffend violently in a two-year follow-up period as those in a treatment center managed by the health department. In light of equally high PCL-YV scores, the treatment philosophy as a central influence was discussed. This philosophy involved, above all, a focus on maintaining treatment contact with the juveniles, particularly when they displayed aggressive and disruptive behaviors. From the literature, one gains the impression that the discussion about the possibilities and limitations of treatment for psychopaths is scientifically based. Above all, the aforementioned studies by Rice and colleagues (1992) and Seto and Barbaree (1999) are used to argue for the refusal to offer treatment to psychopaths. This leads to the paradoxical situation that offenders with a high PCL-R score cannot gain early release without treatment. However, they are refused treatment based on the argument that it would increase their risk of reoffending. This argument had and has a not to be underestimated effect on the financing of treatment in forensic institutions. This ideologically led discussion distorts the real possibilities and limitations of treatment for this small group of offenders. However, it cannot be denied that psychopaths

142

VOLUME I: DIAGNOSIS AND TREATMENT

create significantly more problems in treatment than do other offenders who have fewer psychopathic traits. Many of the traits of psychopaths limit the possibilities of the usual therapeutic techniques or lead to difficulties in the treatment, for example, limited treatment motivation, impulsivity, lack of empathy and the psychopaths’ difficulties in establishing emotional attachment. In support of this Ogloff, Wong and Greenwood (1990) found that psychopaths were less motivated, more likely to be thrown out of treatment and made less progress. Hobson, Shine and Roberts (2000) and Richards, Casey and Lucente (2003) reported similar results in that higher PCL-R scores were associated with poorer conformity to the treatment program. To summarize the present studies, there is no empirically based evidence to date that psychopaths generally do not benefit from treatment. The lack of evidence is not just due to the methodological weaknesses of the studies conducted to date. Another problem is that only treatment modalities that had been found to be effective for ‘normal’ offenders were considered. At the most this suggests that only programs for ‘normal’ offenders are not at all effective or function with limitations for psychopaths. Nobody would consider treating the different types of depression with only one form of treatment!

ASSESSMENT OF DANGEROUSNESS VERSUS MANAGEMENT OF RISK Several authors have criticized the PCL-R, mostly for its lack of sensitivity to change (e.g., Gendreau, Goggin & Smith, 2002; Ross & Pf¨afflin, 2005). According to this criticism, any change due to therapy cannot be assessed. It also remains unclear whether a critical cut-off score exists concerning treatment response and which role the individual factors of the PCL-R play. The restricted view relying on static risk factors implies furthermore the unchangeability of personality. This involves the danger of developing a negative professional attitude towards these offenders and supports their stigmatization. In relation to this problem, Rogers (2000) refers to the cut-throat competition that the forensic patients trigger among inpatient treaters when risk factors are over valued. The different crimino-political positions in relation to problematic and dangerous offenders are apparent in the conflict between Gendreau and colleagues (2002), who favor the LSI-R for the assessment of reoffense risk, and their opponents, Hemphill and Hare (2004). On the one hand, treatment and rehabilitation is associated with a ‘risk-needs orientation’; on the other, the identification and long-term incarceration of dangerous offenders is accomplished by selection of the static and unchangeable factors of psychopathy.

LABELING AN INDIVIDUAL AS A PSYCHOPATH It is not only in the forensic context that the diagnosis of psychopathy has negative connotations. It is also associated with criminal guilt and dangerousness. This degrading label can influence the decisions of judges and therapists. Such decisions can involve more severe legal sanctions or exclusion from therapy. There are no clear empirical findings concerning the effect of this label on the persons themselves or the judges and therapists who deal with

RISKS OF DIAGNOSING

143

them. Based on their study, Edens, Guy and Fernandez (2003) reported that students were more likely to demand the death penalty for juveniles with psychopathic characteristics than those without such features. In contrast, Murrie, Cornell and McCoy (2005) found that the diagnoses of conduct disorder and psychopathy in juveniles had less influence on criminal law or therapeutic recommendations by juvenile probation officers than did a history of antisocial behavior.

CONCLUDING REMARKS In individual cases, the diagnosis of psychopathy is fraught with risks. These risks concern mainly the predictions of future dangerousness and the subsequent decisions about legal interventions. High PCL scores serve as evidence for ongoing dangerousness and are the basis for long incarcerations and additional measures that result in loss of freedom. On occasion, PCL scores are used to justify the death penalty instead of life-long incarceration. In fact, no theoretically defined or empirically based cut-off score for the diagnosis of psychopathy exists. Recommendations and conventions that are unproblematic exist only in the field of research. It should be obvious that these are not transferable to concrete decisions about individuals. Psychopathic characteristics, as well as antisocial and criminal behaviors, are mixed in the construct of psychopathy. Consequently, it can be questioned what is actually being measured, the characteristics or the behaviors. The behaviors themselves appear to be the consequences of the characteristics. Antisocial or criminal behavior is at the same time a predictor and a criterion. This is not just an academic question. Due to unclearly defined cutoff scores, the diagnosis of psychopathy can involve subgroups of individuals who display quite different patterns of personality features. In the end, an assessment of an individual can conclude only that the offender shares a number of features that are common to a specifically defined group of offenders who reoffended over a specific period of time. It is not possible to make a categorical risk prediction about the dangerousness of a particular offender. The diagnosis of psychopathy is associated with the risk of being excluded from therapy. Psychopaths are thought either to not respond to treatment or to respond negatively with increased reoffending. There is a lack of empirical evidence for both claims. It remains to be seen how effective the treatment approaches, developed in recent decades, will be with this obviously difficult to treat group of offenders.

REFERENCES Barbaree, H.E. (2005). Psychopathy, treatment behavior, and recidivism. An extended follow-up of Seto and Barbaree. Journal of Interpersonal Violence, 20, 1115–31. Blackburn, R. & Coid, J.W. (1998). Psychopathy and the dimensions of personality disorders in violent offenders. Personality and Individual Differences, 25, 129–45. Boetticher, A., Kr¨ober, H.L., M¨uller-Isberner, R. et al. (2006). Mindestanforderungen f¨ur Prognosegutachten. Neue Zeitschrift f¨ur Strafrecht, 26, 537–44. Caldwell, M., Skeem, J., Salekin, R. & Van Rybroek, G. (2006). Treatment response of adolescent offenders with psychopathy features: a 2-year follow-up. Criminal Justice and Behavior, 33, 571– 97.

144

VOLUME I: DIAGNOSIS AND TREATMENT

Cleckley, H. (1976). The Mask of Sanity, 5th edition. St. Louis, MO: Mosby. Cooke, D.J. (1995). Psychopathic disturbance in the Scottish prison population: cross-cultural generalizability of the Hare Psychopathy Checklist. Psychology, Crime and Law, 2, 101– 18. Cooke, D.J. (1998). Psychopathy across cultures. In D.J. Cooke, A.E. Forth & R.D. Hare (eds.), Psychopathy: Theory, Research and Implications for Society (pp. 13–45). Dordrecht, The Netherlands: Kluwer. Cooke, D.J., Michie, C., Hart, S.D. & Clark, D. (2005). Assessing psychopathy in the UK: concerns about cross-cultural generalisability. British Journal of Psychiatry, 186, 335–41. Cretton, H.M., McBride, M., Hare, R.D., O‘Shaughnessy, R.O. & Kumka, G. (2001). Psychopathy and recidivism in adolescent sex offenders. Criminal Justice and Behavior, 28, 427–49. Dahle, K.P., Schneider, V. & Ziethen, F. (2007). Standardisierte Instrumente zur Kriminalprognose. Forensische Psychiatrie, Psychologie, Kriminologie, 1, 15–26. D’Silva, K., Duggan, C. & McCarthy, L. (2004). Does treatment really make psychopaths worse? A review of evidence. Journal of Personality Disorders, 18, 163–77. Dolan, M. & Doyle, M. (2000). Violence risk prediction: Clinical and actuarial measures and the role of the Psychopathy Checklist. British Journal of Psychiatry, 177, 303–11. Douard, J. (2007). Loathing the sinner, medicalizing the sin: why sexually violent predator statutes are unjust. International Journal of Law and Psychiatry, 30, 36–48. Edens, J.F., Buffington-Vollum, J.K., Keilen, A. et al. (2005). Predictions of future dangerousness in capital murder trials: is it time to ‘disinvent the wheel?’ Law and Human Behavior, 29, 55– 86. Edens, J.F., Guy, L.S. & Fernandez, K. (2003). Psychopathic traits predict attitudes toward a juvenile capital murderer. Behavioral Sciences and the Law, 19, 807–28. Edens, J.F. & Petrila, J. (2006). Legal and ethic issues in the assessment and treatment of psychopathy. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 573–88). New York: Guilford Press. Eher, R., Schilling, F., Graf, T., Fr¨uhwald, S. & Frottier, P. (2006). Die standardisierte Begutach¨ tung von Sexualstraft¨atern im Osterreichischen Strafvollzug – erste Ergebnisse und Ausblicke. Neuropsychiatrie, 20, 50–6. Fitch, W.L. & Ortega, R.J. (2000). Law and the confinement of psychopaths. Behavioral Sciences and the Law, 18, 663–78. Forth, A.E., Kosson, D. & Hare, R.D. (2003). The Hare PCL: Youth Version. Toronto: Multi-Health Systems. Freedman, D. (2001). False prediction of future dangerousness: error rates of the Psychopathy Checklist-Revised. Journal of the American Academy of Psychiatry and Law, 29, 89– 95. Frommel, M. (2004). Lebenslange Verwahrung angeblich nicht therapierbarer und extrem gef¨ahrlicher Sexualstraft¨ater seit 1998 in Deutschland und der Schweiz. Neue Kriminalpolitik, 16, 86–9. Gendreau, P., Goggin, C. & Smith, P. (2002). Is the PCL-R really the ‘unparalleled’ measure of offender risk? Criminal Justice and Behavior, 29, 397–426. Grann, M., L˚angstr¨om, N., Tengstr¨om, A. & Kullgren, G. (1999). Psychopathy (PCL-R) predicts violent recidivism among criminal offenders with personality disorders in Sweden. Law and Human Behavior, 23, 203–15. Hare, R.D. (1991). The Hare Psychopathy Checklist-Revised. Toronto: Multi-Health Systems. Hare, R.D. (1996). Psychopathy: a clinical construct whose time has come. Criminal Justice and Behavior, 23, 25–54. Hare, R.D. (2003). The Hare Psychopathy Checklist-Revised (2nd edn.). Toronto: Multi-Health Systems. Hare, R.D., Clark, D., Grann, M. & Thornton, D. (2000). Psychopathy and the predictive validity of the PCL-R: an international perspective. Behavioral Sciences and the Law, 18, 623–45. Hart, S.D., Cox, D.N. & Hare, R.D. (1995). Manual for the Psychopathy Checklist: Screening Version (PCL:SV). Toronto: Multi-Health Systems. Hemphill, J.F. & Hare, R.D. (2004). Some misconceptions about the Hare PCL-R and risk assessment: a reply to Gendreau, Goggin, and Smith. Criminal Justice and Behavior, 31, 203–43.

RISKS OF DIAGNOSING

145

Hemphill, J.F., Hare, R.D. & Wong, S. (1998). Psychopathy and recidivism: a review. Legal and Criminological Psychology, 3, 139–70. Hildebrand, M., de Ruiter, C., de Vogel, V. & van der Wolf, P. (2002). Reliability and factor structure of the Dutch language version of Hare’s Psychopathy Checklist-Revised. International Journal of Forensic Mental Health, 1, 139–54. Hildebrand, M., de Ruiter, C. & Nijman, H. (2004). PCL-R psychopathy predicts disruptive behavior among male offenders in a Dutch forensic psychiatric hospital. Journal of Interpersonal Violence, 19, 13–29. Hildebrand, M., de Ruiter, C. & de Vogel, V. (2004). Psychopathy and sexual deviance in treated rapists: association with sexual and non-sexual recidivism. Sexual Abuse: A Journal of Research and Treatment, 16, 1–24. Hobson, J. & Shine, J. (1998). Measurement of psychopathy in a UK prison population referred for long-term psychotherapy. British Journal of Criminology, 38, 504–16. Hobson, J., Shine, J. & Roberts, R. (2000). How do psychopaths behave in a prison therapeutic environment? Psychology, Crime, and Law, 6, 139–54. Home Office & Department of Health. (1999). Managing Dangerous People with Severe Personality Disorder. London. L¨osel, F. (1998). Treatment and management of psychopaths. In D.J. Cooke, A.E. Forth & R.D. Hare (Eds.), Psychopathy: Theory, Research and Implications for Society (pp. 303–54). Dordrecht, The Netherlands: Kluwer. Monahan, J., Steadman, H.J., Silver, E. et al. (2001). Rethinking Risk Assessment. Oxford: Oxford University Press. Murrie, D.C., Cornell, D.G. & McCoy, W.K. (2005). Psychopathy, conduct disorder, and stigma: does diagnostic labeling influence juvenile probation officer recommendations? Law and Human Behavior, 29, 323–42. Ogloff, J., Wong, S. & Greenwood, A. (1990). Treating criminal psychopaths in a therapeutic community program. Behavioral Sciences and the Law, 8, 81–90. Rice, M.E., Harris, G.T. & Cormier, C.A. (1992). An evaluation of a maximum security therapeutic community for psychopaths and other mentally disordered offenders. Law and Human Behavior, 16, 399–412. Richards, H.J., Casey, J.O. & Lucente, S.W. (2003). Psychopathy and treatment response in incarcerated female substance abusers. Criminal Justice and Behavior, 30, 251–67. Rogers, R. (2000). The uncritical acceptance of risk assessment in forensic practice. Law and Human Behavior, 24, 595–605. Ross, T. & Pf¨afflin, F. (2005). Risk Assessment im Maßregelvollzug: Grenzen psychometrischer Gef¨ahrlichkeitsprognose im therapeutischen Umfeld. Monatsschrift f¨ur Kriminologie und Strafrecht, 88, 1–11. Salekin, R.T. (2002). Psychopathy and therapeutic pessimism. Clinical lore or clinical reality? Clinical Psychology Review, 22, 79–112. Salekin, R., Rogers, R. & Sewell, K.W. (1996). A review and meta-analysis of the Psychopathy Checklist-Revised: predictive validity of dangerousness. Clinical Psychology: Science and Practice, 3, 203–15. Seto, M.C. & Barbaree, H.E. (1999). Psychopathy, treatment behavior, and sex offender recidivism. Journal of Interpersonal Violence, 14, 1235–48. Sullivan, E.A. & Kosson, D.S. (2006). Ethnic and cultural variations in psychopathy. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 437–58). New York: Guilford Press. Tengstr¨om, A., Grann, M., L˚angstr¨om, N. & Kullgren, G. (2000). Psychopathy (PCL-R) as a predictor of violent recidivism among criminal offenders with schizophrenia. Law and Human Behavior, 24, 45–58. Tengstr¨om, A., Hodgins, S., M¨uller-Isberner, R. et al. (2006). Predicting violent and antisocial behavior in hospital using the HCR-20: the effect of diagnosis on predictive accuracy. International Journal of Forensic Mental Health, 5, 39–53. Texas Statutes and Codes. (2000). Texas Code Criminal Procedure, Article 37.071. Urbaniok, F., Noll, T., Rosegger, A. & Endrass, J. (in press). Die pr¨adiktive Qualit¨at der Psychopathy Checklist-Revised (PCL-R) bei Gewalt- und Sexualstraft¨atern. Fortschritte der Neurologie Psychiatrie.

146

VOLUME I: DIAGNOSIS AND TREATMENT

Walsh, T. & Walsh, Z. (2006). The evidentiary introduction of Psychopathy Checklist-Revised assessed psychopathy in US courts: extent and appropriateness. Law and Human Behavior, 30, 493–507. Walters, G.D. (2003). Predicting institutional adjustment and recidivism with the psychopathy checklist factor scores: a meta-analysis. Law and Human Behavior, 27, 541–58. Wong, S. (2000). Psychopathic offenders. In S. Hodgins & R. M¨uller-Isberner (eds.), Violence, Crime and Mentally Disordered Offenders (pp. 87–112). Chichester, England: John Wiley & Sons, Ltd.

PART III

Etiology and Pathogenesis

CHAPTER 9

The Genetics of Psychopathic Disorders David Goldman and Francesca Ducci Laboratory of Neurogenetics, Rockville, USA

Psychopathy is a concept encompassing moral, legal and social issues and clinical psychiatric diagnoses, namely antisocial personality and conduct disorders. As such, psychopathy is a non-ideal phenotype for genetic investigations. The inheritance of psychopathy has mainly been researched using three definitions: violation of legal or social norms (e.g., criminality, delinquency), psychiatric diagnosis (e.g., antisocial personality disorder, conduct disorder) and personality traits (e.g., impulsiveness/aggression, low emotionality/detachment). Despite the socially influenced nature of each of these different but interrelated entities, a considerable body of research indicates that all have an important familial component. Heritability estimates from twin and adoption studies are on the order of 40–50 % but highly variable, reflecting methodological differences across studies, definitions of phenotype, composition of samples including age and gender, and random measurement variance. The relative importance of genetic factors in different environmental contexts, at different ages, and in different sexes remains unclear. Antisocial behavior disorders frequently coexist with other psychiatric diseases and are associated with an increased risk of suicide. The comorbidity of antisocial behavior disorders with other psychiatric disorders in large epidemiological samples and cross-transmission with these disorders in genetically informative constellations such as twins reveals a broad latent factor (termed externalizing) linking antisocial behavior disorders and addiction in adulthood and adolescence, and linking conduct disorder and attention deficit hyperactivity disorder in childhood. Also, this link is mainly genetic in nature. Molecular genetic studies identify several genes associated with increased vulnerability to antisocial behaviors and other externalizing syndromes. The ability to identify genes is further improved by considering gene–environment interaction and by the use of intermediate phenotypes which are related to antisocial behavior disorders but that are likely to have less complex and more homogeneous determinants.

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

150

VOLUME I: DIAGNOSIS AND TREATMENT

DEFINITIONS AND EPIDEMIOLOGY Heritability and linkage studies on the genetics of psychopathy and antisocial personality have used a variety of partially overlapping phenotypes, including dimensionally measured personality traits (e.g., impulsivity, aggressiveness), the antisocial personality disorder (APD) and conduct disorder (CD) diagnoses, and histories of criminality and delinquency in adults and youth. None of these are ideal as a genetic phenotype. Despite this, and despite the differences between the phenotypes, some findings have generalized. When we refer to antisocial behavior, as we do in this chapter, we access a broad category of behaviors. Psychopathic individuals have been traditionally identified on the basis of personality traits such as egocentricity, manipulativeness, lack of empathy and remorse, selfishness, low emotionality and detachment (Hare & Neumann, 2005). Central to the disorder is a defective ability in processing affective stimuli (Gordon et al., 2004). Neuroimaging studies have demonstrated that psychopathics display a reduced activation of limbic structure including amygdale in response to affective stimuli (Kiehl et al., 2001). With the advent of DSM-III, the diagnosis of APD was created, or substituted for psychopathy, depending on one’s view. However, an important effect of this change in diagnostic classification was to put psychopathy more firmly in the category of a socially defined behavior. The DSM definition of APD is mainly based on behaviors such as violation of social norms rather than on personality traits. Psychopathy today is therefore a concept encompassing moral, legal and social issues, as well as brain function and dysfunction. This shift in diagnostic criteria may make the diagnosis more reliable, because behaviors can be measured more objectively than can the reasons (e.g., personality traits) why they occur (Hare, 1996). However, this change has created some heterogeneity within this diagnostic category (e.g., different types of personality can actually satisfy criteria for APD), and indeed most individuals with APD do not reflect the traditional concept of psychopathy (Hare, 1996). Further, the inclusion of ‘illegal acts’ among DSM criteria for APD has linked this psychiatric disorder to criminality and delinquency. Approximately 47 % of male and 21 % of female criminals satisfy criteria for APD (Fazel & Danesh, 2002); on the other hand 55 % of males and 17 % of females with APD are criminals (Rhee & Waldman, 2002). According to the last edition of DSM (DSM-IV-TR, American Psychiatric Association, 2000), APD is defined as a ‘pervasive pattern of disregard for and violation of the rights of others beginning in childhood or early adolescence and persisting into adulthood’. It is characterized by three or more symptoms belonging to the following domains: failure to conform to social/legal norms; deceitfulness, impulsivity, irritability and aggressiveness; consistent irresponsibility and lack of remorse (see Figure 9.1). Conduct disorder (CD) is the childhood version of APD. It is defined as a ‘repetitive and persistent pattern of behaviors in which major societal rules are violated’. It is manifested as presence of three or more symptoms related to aggression to people or animals, destruction of property, deceitfulness or theft, and violation of family, school and societal rules (see Figure 9.2). The diagnosis of CD before the age of 15 is required for APD. Antisocial behavior not preceded by CD is sometimes referred to as adult antisocial behavior (Compton et al., 2005). According to the National Epidemiological Survey on Alcohol and Related Conditions, a large (N = 43, 093) nationally representative sample of the adult population of the United States, the lifetime prevalences of CD, APD and adult antisocial behavior were 1.1 %, 3.6 % and 12.3 %, respectively (Compton et al., 2005). All three antisocial syndromes were more common in men, younger individuals and those of lower socioeconomic status (Compton et al., 2005).

THE GENETICS OF PSYCHOPATHIC DISORDERS

151

There is a pervasive pattern of disregard for and violation of the rights of others occurring since age 18 years, as indicated by three or more of the following:

r Failure to conform to social norms with respect to lawful behaviors as indicated by repeatedly performing acts that are grounds for arrest.

r Deceitfulness, as indicated by repeated lying, use of aliases, or conning others for personal profit or pleasure.

r Impulsivity or failure to plan ahead. r Irritability and aggressiveness, as indicated by repeated physical fights or assaults. r Reckless disregard for safety of self or others. r Consistent irresponsibility, as indicated by repeated failure to sustain consistent work behavior or honor financial obligations.

r Lack of remorse, as indicated by being indifferent to or rationalizing having hurt, mistreated, or stolen from another.

r The individual is at least 18 years old. r There is evidence of conduct disorder with onset before 15 years. r The occurrence of antisocial behavior is not exclusively during the course of schizophrenia or manic episode.

Figure 9.1 Diagnostic criteria for antisocial personality disorder (APD) according to DSM-IV-TR

In this chapter we describe the contributions of genetic studies to our understanding of the etiological architecture of antisocial behavior, including the moderating effects of age and sex. We discuss the comorbidity of antisocial behavior with other psychiatric diseases and the role of shared genetic vulnerability in explaining comorbidity. We describe the utility of intermediate phenotypes predictive of vulnerability to identify genes involved in antisocial behavior and the progress via animal models and human genetic studies to identify genes and neurobiologies mediating antisocial behaviors.

A. A repetitive and persistent pattern of behavior in which the basic rights of others or major age-appropriate societal norms or rules are violated, as manifested by the presence of three (or more) of the following criteria: Aggression to people and animals (e.g., treating or intimidating others; often initiating physical fights; using weapon that can cause serious physical harm to others; being physically cruel to people or animals; forcing someone into sexual activities) Destruction of property (e.g., deliberately engaging in fire setting or other activities with the intention of causing serious damage or destroying others’ property) Deceitfulness or theft (e.g., breaking into someone else’s house, building, or car; lying often to obtain goods or favors or to avoid obligations; stealing items of nontrivial value) Serious violation of rules (e.g., staying out at night despite parental prohibitions; starting before age 13, running away from home overnight at least twice while living in paternal house; being often truant from school, beginning before age 13) B. Behavior disturbances causing clinically significant impairment in social, academic, or occupational functioning C. If the individual is age 18 years or older, criteria are not met for antisocial personality disorder

Figure 9.2 Diagnostic criteria for conduct disorder (CD) (Adapted from DSM-IV-TR)

152

VOLUME I: DIAGNOSIS AND TREATMENT

GENETIC AND ENVIRONMENTAL ARCHITECTURE OF ANTISOCIAL BEHAVIOR It has been well established that antisocial behavior in the form of juvenile delinquency (Rowe, Rodgers & Meseck-Bushey, 1992), adult criminality (Mednick, Gabrielli & Hutchings, 1984), APD (Cadoret, 1978) and CD (Jary & Stewart, 1985) runs in families. Familiality can arise from genetic influences transmitted from parents to offspring as well as from shared environmental influences that make members of the same family similar (e.g., overlapping groups of friends, sharing economical status). Studies on twins and adoptees can disentangle genetic from shared environmental influences by comparing the degree of resemblance for a trait between pairs of family members with different degree of relatedness. In twin studies the phenotypic resemblance of monozygotic (MZ) twins is compared to that of dizygotic (DZ) twins who on average share only 50 % of their genes. Since shared environmental influences are assumed to contribute equally to similarity in MZ and DZ twins, a greater resemblance of MZ than DZ twins indicates that the phenotype in question is genetically influenced. Twin-pair resemblance is attributed to two sources: (i) heritability (h 2 ), which is resemblance due to genetic sharing; and (ii) shared environmental influences (c2 ). Dissimilarity between twins is caused by unique environmental influences as well as measurement error, a component that is particularly important for imprecisely measured behavioral traits such as antisocial behavior. Furthermore, genetic influences can be distinguished as additive (i.e., genetic variants exerting a cumulative effect equivalent to the sum of the effects of individual variants) and non-additive (i.e. genetic variants exerting an effect greater or lesser than expected for additive interaction, and resulting from interactions between alleles at a single locus (i.e., dominance/recessivity) or at different loci (epistasis). In the adoptive paradigm the similarity between adoptees and their biological relatives and between adoptees and their adoptive relatives are evaluated. The resemblance of biological relatives to those adopted-away reveals genetic influences, because children given for adoption share genes but not familial environment with biological relatives. On the other hand, the similarities of adoptees to their rearing relatives reveal shared environmental influences. Published twin and adoptive studies on antisocial behaviors show that both genetic and environmental influences play important roles in individual differences. However, the heritability estimates are highly variable, reflecting differences across studies for definitions of phenotype, age and gender composition of samples as well as discrepancies in assessment methods and ordinary sampling variation. Recently, the results of behavior genetic studies on antisocial behavior has been summarized in a comprehensive meta-analysis including 51 independent twin and adoptive studies for APD, CD, criminality/delinquency or aggressiveness (Rhee & Waldman, 2002). Heritability estimates for antisocial behavior and, for comparison, for other psychiatric diseases are shown in Figure 9.3. Antisocial behavior is moderately heritable (h 2 = 41 %). Approximately 78 % of the genetic influences for antisocial behavior appear be additive, and the effect of non-additive genetic influences appears to be modest (9 % of the total variance). Shared and unique environmental influences accounted respectively for 16 % and 43 % of the variance of antisocial behaviors (Rhee & Waldman, 2002) (See Figure 9.4), respectively. A meta-analysis on the

THE GENETICS OF PSYCHOPATHIC DISORDERS

153

1 0.9 0.8 0.7 0.6 h2

0.5 0.4 0.3 0.2 0.1 0

Blood Generalized Major Antisocial Anxiety Depression Behavior Phobia

Panic Alcoholism Schizophrenia Autism Disorder

Figure 9.3 Heritability estimates for antisocial behavior (Rhee & Waldman, 2002) and other psychiatric disorders (Blood phobia: Kendler et al., 2001; generalized anxiety, panic disorder: Hettema et al., 2001; major depression: Sullivan et al., 2000; schizophrenia: Sullivan et al., 2003; alcoholism: Goldman et al., 2005; autism: Muhle et al., 2004)

personality construct of aggression was also conducted (Miles & Carey, 1997), using 24 adoption and twin studies in which aggression was assessed. Heritability of aggression was 50 %. Although antisocial behavior has been clearly demonstrated to be heritable, the relative importance of genes and environment in different environmental contexts, at different ages and in different sexes remains unclear. However, behavior genetic studies have made some contribution to our understanding of the moderating role of age and sex.

Environment and random error

Genes

a2 e2 c2

d2

Figure 9.4 Estimates of genetic and environmental influences acting on antisocial behavior. (Adapted from Rhee & Waldman, 2002). a2 = additive genetic influences; d2 = non-additive genetic influences; c2 = shared environment; e2 = unique environment

154

VOLUME I: DIAGNOSIS AND TREATMENT

EFFECT OF AGE Although childhood antisocial behavior is one of the strongest predictors of adult antisocial behavior and criminality, about two-thirds of individuals with CD do not develop APD in adult life (Storm-Mathisen & Vaglum, 1994). Further, the relative importance of genes and environment in the etiology of antisocial behavior changes during the lifespan. Most studies have shown that in children both genetic and shared environmental influences are important in the pathogenesis of antisocial behaviors. On the other hand, studies in adult cohorts have usually found that genes but not shared environment influences account for the familial aggregation of antisocial behaviors. For example, the meta-analysis of Miles and Carey (1997) found that in children genes and shared environment contributed approximately equally to the familiality of aggressive behavior. In contrast, effect of familial environment was insignificant in adults, among whom heritability was higher than in children. A more recent meta-analysis (Rhee & Waldman, 2002) also found that shared environmental influences are more important in younger cohorts. However, in this study heritability tended to decrease with age. Developmental changes in the etiological architecture of antisocial behaviors have been better understood by retrospective and longitudinal studies on twin pairs. These studies have evaluated whatever the same set of genetic and environmental factors influences a phenotype across different developmental periods or whatever there are factors that act during some life periods but not in others. Antisocial behavior in the Vietnam Twin Registry study (VETR) (Lyons et al., 1995) was retrospectively evaluated in 3226 male twin pairs. Heritability was much higher in adulthood (43 %) than in childhood (9 %). On the other hand shared environmental influences were more important at younger age (31 %) than in adulthood (7 %). In this study, there was no evidence for age-specific genetic influences; the same set of genetic factors appeared to account for inheritance in adulthood as well as childhood. Another large (6806 twin pairs) retrospective study was conducted by Jacobson and colleagues (Jacobson, Prescott & Kendler, 2002). Antisocial behavior was assessed during three different developmental periods: under 15 years (childhood); 15–17 years (adolescence)– and over 18 years (adulthood). Again, the relative importance of genetic factors increased and the role of shared environment decreased as individuals aged from childhood to adulthood (see Figure 9.5). However, in contrast to Lyons and colleagues, Jacobson did find evidence for genetic influences specific to adolescence. Such genes could be activated at this time or their functional context might change at puberty. Evidence for new genetic influences after the transition from adolescence to adulthood were also seen (Jacobson et al., 2002; Malone et al., 2004). In a longitudinal twin study, approximately 50 % of the genetic variance in antisocial behavior at age 24 was attributable to genetic influences other than those acting at age 17 (Malone et al., 2004). The lower heritability and higher shared environmental influences for antisocial behavior in youth as compared to adulthood, as well as the increase in prevalence of antisocial behavior during adolescence might indicate the existence of etiologically heterogeneous subtypes of antisocial behavior. Moffitt (1993) hypothesized the existence of two forms of antisocial behavior: ‘adolescence-limited’ – limited to adolescence and mainly influenced by familial environment – and ‘life-course persistent’ – highly heritable and persistent across life course. In line with this theory, persistent antisocial behavior has been reported to be more heritable than antisocial behavior that is limited to either childhood or adulthood. Another similar subclassification of antisocial behavior distinguishes aggressive from

THE GENETICS OF PSYCHOPATHIC DISORDERS

155

0.7 0. 6

Estimates

0. 5 0. 4

h2 h2

0. 3

c2 c2 e2 e2

0. 2 0. 1 0 Childhood

Adolescence

Adulthood

Figure 9.5 Estimates of genetic and environmental influences on antisocial behavior in different developmental periods. (Adapted from Jacobson et al., 2002). h2 = heritability; c2 = shared environment; e2 = unique environment

non-aggressive antisocial behavior (Eley, Lichtenstein & Stevenson, 1999). The former, including physical acts of aggression such as fighting, is more heritable, whereas the latter is characterized by rule breaking and is more influenced by shared environment (Eley et al., 1999; Eley, Lichtenstein & Moffitt, 2003). Aggression is not easy to define, but paradoxically it is a consistent and heritable component of antisocial behavior. In a longitudinal twin study, the within-person genetic correlation between aggressive antisocial behavior in childhood and adolescence was found to be as high as 99 %, indicating that almost exactly the same genes underlie aggressive antisocial behavior in both childhood and adolescence. Also, genes accounted for 84 % of the continuity in aggressive antisocial behavior moving from adolescence into adulthood. On the other hand, for non-aggressive antisocial behavior, roughly half of the genes were specific to either adolescence or childhood but did not have an influence at both ages. Furthermore, genes and shared environmental influences were almost equivalent in promoting the continuity of non-aggressive antisocial behavior from childhood to adolescence (Eley et al., 2003). Environmental variables that predict juvenile delinquency include family criminality, family poverty and poor parental child-rearing patterns such as authoritarian discipline, poor supervision, parental conflicts and separation from parents (Shepherd & Farrington, 1995). All these variables are likely to act as shared environmental influences, although some might actually reflect genetic influences. The decrease of the effect of shared environment with age might indicate that these variables are relevant for initiation and early maintenance of aggression but their effect might fade over time.

EFFECT OF GENDER It is well known that antisocial behavior, no matter how defined, is consistently more common in males. According to a recent epidemiological study, the risk of APD in males is three-fold that of females (Compton et al., 2005). However, it is less clear whatever sex

156

VOLUME I: DIAGNOSIS AND TREATMENT 0.5 0.4 0.3 F M

h2 0.2 0.1 0 Childhood

Adolescence

Adulthood

Figure 9.6 Heritability of antisocial behavior in males and females in different developmental periods. (Adapted from Jacobson et al., 2000). h2 = heritability; F = female; M = male

differences in the prevalence of antisocial behaviors are associated with sex differences in etiological factors underlying this trait. It is important to stress that gender differences can be quantitative (e.g., the same set of genes and environmental factors are important for men and women but their relative magnitude may differ) as well as qualitative (e.g., different familial factors influence the trait in one sex as compared to the other). Qualitative differences can be evaluated comparing correlations for the phenotype of interest between pairs of DZ twins (or siblings) concordant (same-sex twin pairs) and discordant (oppositesex twin pairs) for gender. For instance, a lower correlation for a trait in discordant pairs as compared to concordant pairs might indicate that different genes influence the trait in men as compared to women. Results from twin and adoption studies are overall controversial as to whether antisocial behavior is more heritable in one sex than in the other. In Miles and Carey’s meta-analysis (Miles & Carey, 1997), heritability of aggressive behavior was slightly higher in males. In contrast, another large meta-analysis did not find gender differences (Rhee & Waldman, 2002). Finally, Eley and colleagues (Eley et al., 1999) found higher heritability of nonaggressive antisocial behavior in females than males. The inconsistencies could be explained by differences in the effects of genetic influences during different developmental periods (Jacobson et al., 2002). During childhood, heritability was higher in females (29 %) as compared to males (6 %). However, heritability of antisocial behavior increased with age in both sexes and in adulthood became approximately equal (males: 52 %, females: 50 %) Twin studies also tend to converge in showing that shared environmental influences acting on antisocial behavior in youth are more important in males than females (Eley et al., 1999; Jacobson et al., 2002). These results indicate that genetic influences on antisocial behaviors might appear earlier in females than males and that in adulthood the role of genetic factors is equivalent in the two sexes (see Figure 9.6). Concerning qualitative gender differences, DZ opposite-sex correlations are overall similar to same-sex DZ correlations. These data suggest that sex-specific genetic influences do not have a large effect on antisocial behavior (Eley et al., 2003; Jacobson et al., 2002; Rhee & Waldman, 2002).

THE GENETICS OF PSYCHOPATHIC DISORDERS

157

COMORBIDITIES AND INTERMEDIATE PHENOTYPES Antisocial behavior disorders frequently coexist with other psychiatric diseases including addictions (Compton et al., 2005), attention deficit hyperactivity disorder (ADHD) and mood and anxiety disorders (Goodwin & Hamilton, 2003). Antisocial behaviors predict the development of substance use disorder in longitudinal studies. In the Yale Family Study, CD was the psychiatric disease with the highest odd ratio for predicting addiction. Also the attributable risk for substance dependence due to CD was as high as 86 % (Merikangas & Avenevoli, 2000). These data emphasize the importance of recognizing CD to prevent substance use disorders. Also, APD predicts suicidal ideation in males with substance use disorders (Cottler et al., 2005). Shifting from the externalizing domain to the internalizing domain, in the National Comorbidity Survey (Goodwin & Hamilton, 2003) more than a half of subjects with ASPD had at least one anxiety disorder on a life-time basis, with comorbidity being highest for post-traumatic stress disorder and social phobia. Also, individuals with both comorbid anxiety and APD had the highest odds of major depression, substance use disorders, suicidal ideation and attempts (Goodwin & Hamilton, 2003). Comorbidity can indicate the existence of etiological factors shared between different psychiatric diseases, and that promote their coexistence within individuals. Large twin studies reveal a genetic diathesis that encompasses CD, APD, ADHD, addiction and related personality traits such as novelty seeking (Hicks et al., 2004; Kendler et al., 2003; Krueger et al., 2002). These disorders have been broadly labeled as ‘externalizing’ and are all characterized by reduced ability to inhibit behaviors that are socially undesirable and that frequently have negative psychological, familial and legal consequences. Most of the genetic variance of externalizing syndromes was found to be traced to a highly heritable (h 2 approximately 80 %) common genetic factor (Hicks et al., 2004; Kendler et al., 2003; Krueger et al., 2002), although disease-specific genetic influences (e.g., genes that increase the risk for one disorder but not for the others) have been demonstrated for some disorders, particularly alcoholism and other addictions (Kendler et al., 2003) (See Figure 9.7). On the Specific

Shared

Additive genetic influences

1 0.8 0.6 0.4 0.2 0 APD

CD

Alcoholism

Other Addictions

Figure 9.7 Disorder-specific and shared genetic influences between externalizing syndromes. (Adapted from Kendler et al., 2003). APD = antisocial personality disorder; CD = conduct disorder

158

VOLUME I: DIAGNOSIS AND TREATMENT Specific

Shared

Unique environmental influences

1 0.8 0.6 0.4 0.2 0 APD

CD

Alcoholism

Other Addictions

Figure 9.8 Disorder-specific and shared unique environmental influences between externalizing syndromes. (Adapted from Kendler et al., 2003). APD = antisocial personality disorder; CD = conduct disorder

other hand, disease-specific unique environmental influences were found to be significant across all disorders (Hicks et al., 2004; Kendler et al., 2003; Krueger et al., 2002) (see Figure 9.8). General vulnerability to an externalizing syndrome may be transmitted from parent to offspring. On the other hand, environmental factors which are unique to the individual are mainly responsible for the differentiation between the different disorders. However, it is important to note that disease-specific unique environmental influences might be overestimated by twin studies because of measurement errors that increase dissimilarity between family members and therefore mimic unique environment effects. Some progress in identifying the genetic basis of complex phenotypes such as antisocial behavior has been made using intermediate phenotypes. Intermediate phenotypes and endophenotypes (e.g., heritable intermediate phenotypes) are measurable biochemical, endocrinological, neuroanatomical, cognitive and neuropsychological parameters (Gottesman & Gould, 2003) that mediate etiologically complex phenotypes. The use of intermediate phenotypes represents an attempt to deconstruct more complex phenotypes, thereby increasing the power to detect the effects of genetic variants or other determinants. One endophenotype shared between different externalizing syndromes is P300 event-related potential amplitude. Event-related potentials (ERPs) are EEG voltages induced by auditory, visual and somatosensory stimuli. P300 amplitude is a heritable (h 2 = 60 %) ERP which reflects attention and information processing (van Beijsterveldt & van Baal, 2002). Individuals affected by CD, ADHD, APD, as well alcoholism and other addictions, display low amplitude of the P300 as compared to controls (for review see Iacono, Malone & McGue, 2003). Both affected and unaffected sons of alcoholics have reduced amplitude of the P300, and the same trend is observed for affected and unaffected sons of individuals with APD (Iacono et al., 2003). Longitudinal studies have shown that low P300 predicts the development of externalizing syndromes (Iacono et al., 2003). Further supporting the validity of P300 as an endophenotype for externalizing syndromes, chromosomal regions linked to low P300 amplitude partially overlap with ones linked to alcoholism (Porjesz et al., 2002).

THE GENETICS OF PSYCHOPATHIC DISORDERS

159

GENES AND NEUROBIOLOGIES FOR ANTISOCIAL BEHAVIOR Despite the fact that antisocial behavior is a complex phenomenon that is substantially socially defined, it is heritable, indicating the existence of genetic functional loci that can eventually be tied to vulnerability. However, it is predictable that the genetic origins of antisocial behavior will be diverse. For one thing, evidence from studies in animals and humans indicates that several neurobiologies are important. These include emotional reactivity mediated by amygdala and other parts of the limbic system, cognitive control mediated by prefrontal cortex, learning and potentially other behaviors. Each of these neurobiologies has complex origins and is dependent on the actions of many genes. Therefore, and despite the moderate-high heritability of antisocial behavior, no single genetic marker may account for more than a small portion of the variance in this phenotype. Here, we discuss several monoamine neurotransmitter genes for which evidence of genetic association to antisocial behavior has been accumulated. As discussed below in specific relation to these genes involved in serotonin, dopamine and perhaps norepinephrine function, the genetic variants influencing antisocial behavior will be both rare and common, and both strong in their effect (if one is a carrier) and weak in their effect. Also, role of different genetic variants will vary according to the environmental context in which their effects are exerted.

Serotonin The serotonergic system is a key modulator of aggressive/impulsive behavior. Evidence supporting this idea comes from studies showing lower levels of 5-hydroxyindoleacetic acid (5-HIAA) (the major metabolite of serotonin) in the cerebrospinal fluid (CSF) of violent offenders (Virkkunen, Goldman & Linnoila, 1996b) and in suicide attempters (Mann et al., 1996; Placidi et al., 2001). Also, other markers of serotonergic activity, such as neuroendocrine response to a 5-HT agonist, are blunted in individuals with a history of aggressive behavior (Coccaro et al., 1997). Consistently, the serotonin system is the target of drugs commonly used to treat psychiatric disorders associated with aggressive features. For example, selective serotonin reuptake inhibitors (SSRIs) are recommended for the treatment of affective liability, impulsivity and aggression in patients with borderline personality disorder. Antagonists of serotonin receptor 2a and agonists of serotonin receptor 1b have anti-aggressive properties (Olivier, 2004). Furthermore, serotonin is well known to regulate the hypothalamic–pituitary–adrenal (HPA) axis, which in turns modulates central serotonergic activity (Chen et al., 2006). The HPA axis is a critical neuroendocrine system that responds to stress and abnormalities of this axis have been described in a variety of neuropsychiatric disorders including major depression and addiction. Therefore genetic variation of genes belonging to the serotonin system might partially account for interindividual differences in stress resiliency. It is in fact likely that diminished stress resiliency is a factor in several psychiatric diseases including diseases in the dyscontrol domain. Indeed, adverse early-life events such as maltreatment are well-known risk factors for antisocial behavior in both males and females (Caspi et al., 2001, Robin et al., 1997). HTR1B: Mice lacking the serotonin receptor 1B gene (HTR1B) are more aggressive (Saudou et al., 1994) in the resident-intruder test. In this behavioral test, mice are isolated and then exposed to a non-isolated male intruder, and the latency and frequency of attacks

160

VOLUME I: DIAGNOSIS AND TREATMENT

are recorded. In mice, the 5-HT1B receptor also modulates aggressive responses induced by alcohol. Activation of this receptor reduces alcohol-induced aggressive behavior (Miczek et al., 2004). HTR1B knock-out mice also self-administer more ethanol (Crabbe et al., 1996) and cocaine (Rocha et al., 1998). In the human, a synonymous mutation (G861C) of this intronless gene was associated to antisocial alcoholism (alcoholism + APD) in two independent populations, including a sample of criminal alcoholics (Lappalainen et al., 1998). However, subsequent studies have sometimes replicated (Soyka et al., 2004) and other times not confirmed. (Kranzler, Hernandez-Avila & Gelernter, 2002; Ickowicz et al., 2003) this finding. TPH2: Tryptophan hydroxylase (TPH) is the rate-limiting enzyme in the biosynthesis of serotonin. There are two TPH genes. TPH1 is predominantly expressed in peripheral tissues and the pineal gland, and TPH2 is preferentially expressed in the brain. In mice, a singlenucleotide polymorphism in the TPH2 gene has been associated with brain TPH activity. Further, male carriers of the variant associated with higher TPH2 expression displayed an increase in aggressive behavior (Kulikov et al., 2005). In the rhesus macaque monkey, functional polymorphisms located in the 3’-UTR of TPH2 gene were found to predict gene expression measured in vitro and were correlated with plasma cortisol level. This indicates that genetic variation in the TPH2 gene might regulate HPA function by modulating 5-HT synthesis (Chen et al., 2006). In the human, TPH2 was linked to auto-aggressive behaviors in the form of suicide attempts in four large independent populations including a sample of criminal alcoholics (Zhou et al., 2005). In the same study, the TPH2 risk haplotype was associated with lower 5-HIAA levels among controls without psychiatric diagnoses. Association between TPH2 genetic variation and suicide behaviors has been recently replicated in a population of depressed patients (Ke et al., 2006). Finally a single nucleotide polymorphism in the promoter region of human TPH2 was found to predict amygdala reactivity in response to emotional stimuli in two independent fMRI studies (Brown et al., 2005; Canli et al., 2005). HTT: The 5-hydroxytryptamin transporter (HTT) removes 5-HT from the synaptic cleft, regulating the duration of post-synaptic receptor stimulation. Mice lacking HTT are less aggressive in the resident-intruder test (Holmes, Murphy & Crawley, 2002). In the promoter region of the human serotonin transporter gene (HTT), there is a functional polymorphism (HTTLPR) that affects the transporter expression. The two alleles, both common across populations that have usually been studied at this locus are the L (long) and S (short) variants which differ in number of copies of a 21- to 23-bp imperfect repeat sequence (Lesch et al., 1996). A third functional allele due to an LA → LG single nucleotide polymorphism was recently described (Hu et al., 2006), and this allele is also common in most populations. The S allele, which contains 14 copies of the repeat sequence, is associated with lower transcription as compared to the L allele, which contains 16 copies. In a recent metaanalysis of 17 independent studies, the S allele was found to significantly increase the risk for alcohol dependence, especially when associated to antisocial or suicidal behaviors (Feinn et al., 2005). Also, an excess of the S allele and the S/S genotype was found in subjects with violent behavior in a sample of 153 male referred for a forensic psychiatric examination (Retz et al., 2004). The effect of this locus on complex phenotypes such as antisocial behavior and addiction is weak overall but effects are stronger at the neurobiological level. HTTLPR modulates the transporter expression in human brain (Heinz et al., 2000; Little et al., 1998) and carriers of the low function allele display increased amygdala reactivity in response to emotional stimuli (Hariri et al., 2000). The effects of HTTLPR and a single

THE GENETICS OF PSYCHOPATHIC DISORDERS

161

nucleotide polymorphism of the TPH2 gene were recently found to act addictively on amygdala response (Herrmann et al., 2006). Finally HTTLPR appears to be important in deterring stress resiliency. Caspi and collegues (2003) showed that individuals with one or two copies of the S allele were at higher risk of suicide when exposed to stressful life events than individuals homozygous for the L allele. There is also some evidence for a role of other serotonin genes in aggression. Animal studies suggest that 5-HT1A receptor stimulation decreases aggressive behavior. Patients with increased aggressiveness showed a blunted prolactin response to the 5-HT1A agonist buspirone (for review see Kavoussi, Armstead & Coccaro, 1997). A possible role for the 5-HT2a receptor is supported by the fact that antagonism of this receptor reduces aggressiveness. Novel antipsychotic agents such as clozapine and olanzapine (which, unlike older antipsychotic medications, block 5-HT2 receptors) have anti-aggressive properties that are independent from their antipsychotic effects. In fact, these drugs have been shown to reduce auto-aggressive (Modestin, Dal Pian & Agarwalla, 2005) and hetero-aggressive behaviors in schizophrenia (Bitter et al., 2005; Volavka et al., 2004) as well as other psychiatric diseases (Kraus & Sheitman, 2005).

Catecholamines Dopamine (DA) and norepinephrine (NE) both modulate aggressive behavior. Consistently, drugs enhancing dopaminergic and noradrenergic neurotransmission, such as amphetamine and cocaine, induce aggressiveness. Also, low levels of CSF homovanillic acid (HVA), the principal metabolite of dopamine, were reported in individuals with family history of alcoholism and violence (Virkkunen et al., 1996a) and in suicide attempters (Roy et al., 1986), although other studies failed to find any correlation between HVA and differently defined antisocial behaviors (Placidi et al., 2001). Two major enzymes involved in catecholamine metabolism, monoamine oxidase A (MAOA) and catechol-O-methyltransferase (COMT), have been implicated in aggression and antisocial behavior. MAOA is an X-linked gene encoding a mitochondrial enzyme that metabolizes NE and DA, as well as serotonin. Studies on animals and humans have consistently demonstrated relevance of this gene for aggressive behaviors. MAOA knockout mice have higher levels of DA, 5-HT and NE, and manifest increased aggressiveness (Cases et al., 1995). In the human, different MAOA genetic variants impair MAOA activity to different degrees and the reduction in enzyme activity appears to parallel the effect on behavioral phenotype. Brunner and colleagues (1993) identified a rare stop codon mutation of MAOA in a single Dutch family including several males affected by a syndrome characterized by borderline mental retardation and abnormal behaviors including impulsive aggression, arson, attempted rape and exhibitionism. This syndrome was associated with a complete deficiency of MAOA activity measured in skin fibroblasts. A common polymorphism of MAOA affects transcriptional activity (Sabol, Hu & Hamer, 1998) causing a partial MAOA deficiency. This is a variable number of tandem repeat (VNTR) locus in the promoter region of the gene. Alleles at this VNTR differ in number of copies (2, 3, 3.5, 4 or 5) of a 30-bp repeated sequence. This polymorphism has been variably associated with CD, APD and other antisocial related disorders. More recently, studies on humans and other primates have demonstrated that MAOA genotypes increase the risk for antisocial behavior contingent on exposure to

162

VOLUME I: DIAGNOSIS AND TREATMENT

Stressors (maternal rejection, loss of primary caregiver, harsh discipline, sexual abuse, other physical abuse)

G*E

Antisocial Behavior

MAOA genotype

Figure 9.9 Effect of MAOA genotype and stress exposure in the development of antisocial behavior. (Adapted from Caspi et al., 2002). G*E = gene–environment interaction

certain environmental influences. In other words these studies converge on the relevance of gene–environment interaction. Childhood maltreatment is an important risk factor for CD and antisocial symptoms in general, but not all maltreated subjects become antisocial. In a longitudinal sample of males, Caspi et al. (2002) demonstrated that maltreated children (who suffered maternal rejection, loss of primary caregiver, harsh discipline, physical abuse or sexual abuse), who also had a genotype conferring low levels of MAOA expression, were more likely to develop antisocial problems. There was also an independent effect of maltreatment on risk for antisocial behavior (e.g., maltreatment increased the risk for CD independently from MAOA genotype) but an independent effect of MAOA genotype was not detected (see Figure 9.9). This finding has been replicated in at least four studies (Foley et al., 2004; Kim-Cohen et al., 2006; Nilsson et al., 2006; Widom & Brzustowicz, 2006) and one study reported a nonsignificant trend in the same direction (Haberstick et al., 2005). These studies were all conducted on human males, except Widom et al. (2006) which included males and females. The effect of MAOA genotype on aggressive and antisocial behaviour in females appears to be less consistent (Sjoberg et al., 2006; Widom & Brzustowicz, 2006), however only a few studies so far have explored MAOA X environment interaction in females. In the rhesus monkey, a polymorphism of MAOA orthologous to the human VNTR polymorphism has also been associated to aggression, and this association depended on whether the monkey had been separated from the mother shortly after birth. The low activity genotype was associated with higher aggression only in mother-reared male monkeys (Newman et al., 2005). Finally in an fMRI study, the genotype associated with low MAOA expression predicted hyperresponsivity of the amygdala and diminished reactivity of regulatory prefrontal regions during emotional arousal, compared with the high expression allele (Meyer-Lindenberg et al., 2006).

THE GENETICS OF PSYCHOPATHIC DISORDERS

163

The involvement of X-linked genes such as MAOA might also help explain the higher prevalence of antisocial behavior and other externalizing disorders among men, because since males carry only one copy of the gene it is more likely that they will be homozygous (hemizygous) for a variant leading to behavioral variation. Sex differences in aggressive behavior might partially be due to hormonal differences. In this regard high levels of testosterone have been associated with antisocial behavior in humans (Virkkunen et al., 1994) and with aggression in animal studies (Archer, 1991). Recently it has been shown that testosterone acts on the MAOA promoter regulating MAOA expression (Ou, Chen & Shih, 2006). COMT catalyzes the transfer of a methyl group to catecholamines, including DA and NE. In the prefrontal cortex (PFC), which is a critical region modulating behavior control as well as cognitive functions; 60 % of DA is metabolized by COMT. For comparison only 15 % of DA is degraded by COMT in other brain regions such as nucleus accumbens (Karoum, Chrapusta & Egan, 1994). COMT plays a larger role in PFC, because in this region levels of DA transporter are low and the synaptic action of DA is mainly terminated by COMT, or by diffusion. COMT has a common functional polymorphism: Val158Met. The enzyme containing Met158 is unstable at 37˚C and is one-third to one-fourth as active as the Val158-containing enzyme. Therefore, Val158 is predicted to reduce dopamine levels in the PFC. Consistently, Val158 has been associated with impairment in prefrontal cognitive functions (see e.g., Egan et al., 2001; Goldberg et al., 2003). The relation between DA and aggression is more complex and higher as well as lower DA levels have been associated with aggressive behaviors. For example, mice lacking COMT have increased dopamine levels in the PFC and are more aggressive (Gogos et al., 1998). However, DA depletion increases aggressive behaviors (Pucilowski et al., 1982). There are several reasonable explanations for this difference, including neurodevelopmental effects and the relative impact of DA depletion and augmentation in different regions of the brain. Consistent with the idea that higher DA levels that are genetically determined and present from birth are related to aggression, the low-activity Met158 allele has been associated with violent auto-aggressive (Nolan et al., 2000) and hetero-aggressive (Kotler et al., 1999; Lachman et al., 1998) behaviors in schizophrenic and schizoaffective patients. Met158 also confers risk for anxiety-related behaviors (Enoch et al., 2003) and mood disorders (Ohara, Nagai & Suzuki, 1998). Neuroimaging studies have shown that the Met158 allele is associated with increased limbic and prefrontal response to unpleasant stimuli (Smolka et al., 2005). This alteration in the processing of affective stimuli probably explains the lower emotional resilience against negative mood states conferred by Met158. On the other hand, reduced DA levels in the PFC may also be associated with aggressiveness. Jones and colleagues (2001), in a sample of schizophrenics, found that homozygotes for the higher activity Val158 displayed more aggressive behaviors than the other genotypes. A possible explanation for these discrepancies is that DA modulates aggressive behaviors bidirectionally, reflecting the complex origins of aggressive behaviors. In line with this hypothesis, Rujescu and colleagues (2003) found that Met158 was associated with violent suicide, whereas Val158 was related to inward-expressed aggression and individuals homozygous for this allele reported more state anger. Other genes belonging to the DA system may also be involved in vulnerability to antisocial behaviors. For example, both the dopamine receptor D4 (DRD4) (Faraone et al., 2001; Rowe et al., 2001) and dopamine transporter (SLC6A3) (Rowe et al., 2001; Young et al., 2002) polymorphisms have been linked to ADHD and CD.

164

VOLUME I: DIAGNOSIS AND TREATMENT

Also polymorphisms in DRD2 have been controversially linked to antisocial behaviors. Some studies have found DRD2 associations to APD (Ponce et al., 2003), antisocial personality symptoms (Bau et al., 2000), and biological markers of antisocial behaviour such as low platelet monoamine oxidative-B activity (Eriksson et al., 2000), prolonged P300 latency (Blum et al., 1994) low harm avoidance (Hill et al., 1999) and high sensation seeking (Ratsma et al., 2001). However, other studies failed to find association (Gelernter & Kranzler, 1999; Parsian, Cloninger & Zhang, 2000). Linkage studies using haplotypes and all available functional loci at DRD2 may help clarify the discrepancies (e.g., Xu et al., 2004).

SUMMARY Antisocial behavior is common. In the United States, prevalences are 1 % for CD, 3.8 % for APD and 12.3 % for adult APD. Antisocial behavior is moderately heritable (0.40–0.50) in both sexes although genetic influences appear to act earlier in women than men. Based on twin data, the effects of most genes contributing to antisocial behavior increase with age and the effects of shared environment decrease. Antisocial behavior that appears early in life and persists during adulthood is more heritable than childhood conduct disorder. Family environment is relevant for the initiation and early maintenance of aggression, particularly in men, but its effect fades. While some genes influence antisocial behavior during the whole life course, others become important only during adolescence and adulthood. Some genetic determinants of antisocial behavior are shared between an externalizing cluster of diseases including APD, CD, ADHD, alcoholism and other addictions. All are marked by behavioral disinhibition. Intermediate phenotypes, including low amplitude of the P300 event-related potential, might capture some of the genetic diathesis shared between externalizing syndromes. Several genes have been implicated in the pathogenesis of antisocial behavior such as MAOA and COMT. These genes, none of which accounts for a large amount of phenotypic variance, illustrate effects of gene–environment interaction, include both rare and common functional alleles, of different effect sizes, and modulate different neurobiologies relevant to antisocial behavior.

REFERENCES American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders, fourth edition, Text Revision. Washington, DC: American Psychiatric Association. Archer, J. (1991). The influence of testosterone on human aggression. British Journal of Psychology, 1, 1–28. Bau, C.H., Almeida, S. & Hutz, M.H. (2000). The TaqI A1 allele of the dopamine D2 receptor gene and alcoholism in Brazil: association and interaction with stress and harm avoidance on severity prediction. American Journal of Medical Genetics, 96, 302–6. Bitter, I., Czobor, P., Dossenbach, M. & Volavka, J. (2005). Effectiveness of clozapine, olanzapine, quetiapine, risperidone and haloperidol monotherapy in reducing hostile and aggressive behavior in outpatients treated for schizophrenia: a prospective naturalistic study (IC-SOHO). European Psychiatry, 20, 403–8.

THE GENETICS OF PSYCHOPATHIC DISORDERS

165

Blum, K., Braverman, E.R., Dinardo, M.J. et al. (1994). Prolonged P300 latency in a neuropsychiatric population with the D2 dopamine receptor A1 allele. Pharmacogenetics, 4, 313–22. Brown, S.M., Peet, E., Manuck, S.B. et al. (2005). A regulatory variant of the human tryptophan hydroxylase-2 gene biases amygdala reactivity. Molecular Psychiatry, 10, 884–8. Brunner, H.G., Nelen, M., Breakefield, X.O. et al. (1993). Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A. Science, 262, 578–80. Cadoret, R.J. (1978). Psychopathology in adopted-away offspring of biologic parents with antisocial behavior. Archives of General Psychiatry, 35, 176–84. Canli, T., Congdon, E., Gutknecht, L. et al. (2005). Amygdala responsiveness is modulated by tryptophan hydroxylase-2 gene variation. Journal of Neural Transmission, 112, 1479–85. Cases, O., Seif, I., Grimsby, J. et al. (1995). Aggressive behavior and altered amounts of brain serotonin and norepinephrine in mice lacking MAOA. Science, 268, 1763–6. Caspi, A., McClay, J., Moffitt, T.E. et al. (2002). Role of genotype in the cycle of violence in maltreated children. Science, 297, 851–4. Caspi, A., Sugden, K., Moffitt, T.E. et al. (2003). Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene. Science, 301, 386–9. Chen, G.L., Novak, M.A., Hakim, S. et al. (2006). Tryptophan hydroxylase-2 gene polymorphisms in rhesus monkeys: association with hypothalamic-pituitary-adrenal axis function and in vitro gene expression. Molecular Psychiatry, 11, 914–28. Coccaro, E.F., Kavoussi, R.J., Trestman, R.L. et al. (1997). Serotonin function in human subjects: intercorrelations among central 5-HT indices and aggressiveness. Psychiatry Research, 73, 1–14. Compton, W.M., Conway, K.P., Stinson, F.S. et al. (2005). Prevalence, correlates, and comorbidity of DSM-IV antisocial personality syndromes and alcohol and specific drug use disorders in the United States: results from the national epidemiologic survey on alcohol and related conditions. Journal of Clinical Psychiatry, 66, 677–85. Cottler, L.B., Campbell, W., Krishna, V.A. et al. (2005). Predictors of high rates of suicidal ideation among drug users. Journal of Nervous and Mental Disease, 193, 431–7. Crabbe, J.C., Phillips, T.J., Feller, D.J. et al. (1996). Elevated alcohol consumption in null mutant mice lacking 5-HT1B serotonin receptors. Nature Genetics, 14, 98–101. Egan, M.F., Goldberg, T.E., Kolachana, B.S. et al. (2001). Effect of COMT Val108/158 Met genotype on frontal lobe function and risk for schizophrenia. Proceedings of the National Academy of Sciences of the USA, 98, 6917–22. Eley, T.C., Lichtenstein, P. & Stevenson, J, (1999). Sex differences in the etiology of aggressive and nonaggressive antisocial behavior: results from two twin studies. Advances in Child Development and Behavior, 70, 155–68. Eley, T.C., Lichtenstein, P. & Moffitt T.E. (2003). A longitudinal behavioral genetic analysis of the etiology of aggressive and nonaggressive antisocial behavior. Development and Psychopathology, 15, 383–402. Enoch, M.A., Xu, K., Ferro, E., et al. (2003), Genetic origins of anxiety in women: a role for a functional catechol-O-methyltransferase polymorphism. Psychiatric Genetics, 13, 33–41. Eriksson, M., Berggren, U., Blennow, K., et al. (2000) Alcoholics with the dopamine receptor DRD2 A1 allele have lower platelet monoamine oxidase-B activity than those with the A2 allele: a preliminary study. Alcohol and Alcoholism, 35, 493–8. Faraone, S.V., Doyle, A.E., Mick, E. & Biederman, J. (2001). Meta-analysis of the association between the 7-repeat allele of the dopamine D(4) receptor gene and attention deficit hyperactivity disorder. American Journal of Psychiatry, 158, 1052–7. Fazel, S. & Danesh, J. (2002). Serious mental disorder in 23000 prisoners: a systematic review of 62 surveys. Lancet, 359, 545–50. Feinn, R., Nellissery, M. & Kranzler, H.R. (2005), Meta-analysis of the association of a functional serotonin transporter promoter polymorphism with alcohol dependence. American Journal of Medical Genetics. Part B,Neuropsychiatric Genetics, 133, 79–84. Foley, D.L., Eaves, L.J., Wormley, B. et al. (2004). Childhood adversity, monoamine oxidase a genotype, and risk for conduct disorder. Archives of General Psychiatry, 61, 738–44. Gelernter, J. & Kranzler, H. (1999). D2 dopamine receptor gene (DRD2) allele and haplotype frequencies in alcohol dependent and control subjects: no association with phenotype or severity of phenotype. Neuropsychopharmacology, 20, 640–9.

166

VOLUME I: DIAGNOSIS AND TREATMENT

Gogos, J.A., Morgan, M., Luine, V. et al. (1998). Catechol-O-methyltransferase-deficient mice exhibit sexually dimorphic changes in catecholamine levels and behavior. Proceedings of the National Academy of Sciences of the USA, 95, 9991–6. Goldberg, T.E., Egan, M.F., Gscheidle, T. et al. (2003). Executive subprocesses in working memory: relationship to catechol-O-methyltransferase Val158Met genotype and schizophrenia. Archives of General Psychiatry, 60, 889–96. Goldman, D., Oroszi, G. & Ducci, F. (2005). The genetics of addictions: uncovering the genes. Nature Review Genetics, 6, 521–32. Goodwin, R.D. & Hamilton, S.P. (2003). Lifetime comorbidity of antisocial personality disorder and anxiety disorders among adults in the community. Psychiatry Research, 117, 159–66. Gordon, H.L., Baird, A.A. & End, A. (2004). Functional differences among those high and low on a trait measure of psychopathy. Biological Psychiatry, 56, 516–21. Gottesman, I.I. & Gould, T.D. (2003). The endophenotype concept in psychiatry: etymology and strategic intentions. American Journal of Psychiatry, 160, 636–45. Hare R.D. (1996). Psychopathy and antisocial personality disorder: a case of diagnostic confusion. Psychiatric Times, 13(2). Hare, R.D. & Neumann, C.S. (2005). Structural models of psychopathy. Current Psychiatry Reports, 7, 57–64. Hariri, A.R., Mattay, V.S., Tessitore, A. et al. (2000). Serotonin transporter genetic variation and the response of the human amygdala. Science, 297, 400–3. Haberstick, B.C., Lessem, J.M., Hopfer, C.J. et al. (2005). Monoamine oxidase A (MAOA) and antisocial behaviors in the presence of childhood and adolescent maltreatment. American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics, 135, 59–64. Heinz, A., Jones, D.W., Mazzanti, C. et al. (2000). A relationship between serotonin transporter genotype and in vivo protein expression and alcohol neurotoxicity. Biological. Psychiatry, 47, 643–9. Herrmann, M.J., Huter, T., Muller, F. et al. (2006). Additive effects of serotonin transporter and tryptophan hydroxylase-2 gene variation on emotional processing. Cerebral cortex. PMID: 16801378. 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, 1568–78. Hicks, B.M., Krueger, R.F., Iacono, W.G. et al. (2004). Family transmission and heritability of externalizing disorders: a twin-family study. Archives of General Psychiatry, 61, 922–8. Hill, S.Y., Zezza, N., Wipprecht, G. et al. (1999.) Personality traits and dopamine receptors (D2 and D4): linkage studies in families of alcoholics. American Journal of Medical Genetics, 88, 634–41. Holmes, A., Murphy, D.L. & Crawley, J.N. (2002). Reduced aggression in mice lacking the serotonin transporter. Psychopharmacology, 161, 160–7. Hu, X.Z., Lipsky, R.H., Zhu, G. et al. (2006). The serotonin transporter promoter polymorphism is functionally triallelic and the gain-of-function allele is linked to obsessive-compulsive disorder. American Journal of Human Genetics, 78, 815–26. Iacono, W.G., Malone, S.M. & McGue, M. (2003). Substance use disorders, externalizing psychopathology, and P300 event-related potential amplitude. International Journal of Psychophysiology, 48, 147–78. Ickowicz, A., Feng, Y., Wigg, K. et al. (2006). The serotonin receptor HTR1B: gene polymorphisms in attention deficit hyperactivity disorder. American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics PMID: 16958036. Jacobson, K.C., Prescott, C.A. & Kendler, K.S. (2002). Sex differences in the genetic and environmental influences on the development of antisocial behavior. Development and Psychopathology, 14, 395–416. Jary, M.L. & Stewart, M.A. (1985). Psychiatric disorder in the parents of adopted children with aggressive conduct disorder. Neuropsychobiology, 13, 7–11. Jones, G., Zammit, S., Norton, N. et al. (2001). Aggressive behaviour in patients with schizophrenia is associated with catechol-O-methyltransferase genotype. British Journal of Psychiatry, 179, 351–5. Karoum, F., Chrapusta, S.J. & Egan, M.F. (1994). 3-Methoxytyramine is the major metabolite of released dopamine in the rat frontal cortex: reassessment of the effects of antipsychotics on the dynamics of dopamine release and metabolism in the frontal cortex, nucleus accumbens, and striatum by a simple two pool model. Journal of Neurochemistry, 63, 972–9.

THE GENETICS OF PSYCHOPATHIC DISORDERS

167

Kavoussi, R., Armstead, P. & Coccaro, E. (1997). The neurobiology of impulsive aggression. The Psychiatric Clinics of North America, 20, 395–403. Ke, L., Qi, Z.Y., Ping, Y. & Ren, C.Y. (2006). Effect of SNP at position 40237 in exon 7 of the TPH2 gene on susceptibility tosuicide. Brain Research. PMID: 17011525. Kendler, K.S., Myers, J., Prescott, C.A. & Neale, M.C. (2001). The genetic epidemiology of irrational fears and phobias in men. Archives of General Psychiatry, 58, 257–65. Kendler, K.S., Prescott, C.A., Myers, J. & Neale, M.C. (2003). The structure of genetic and environmental risk factors for common psychiatric and substance use disorders in men and women. Archives of General Psychiatry, 60, 929–37. Kiehl, K.A., Smith, A.M., Hare, R.D. et al. (2001). Limbic abnormalities in affective processing by criminal psychopaths as revealed by functional magnetic resonance imaging. Biological Psychiatry, 50, 677–84. Kim-Cohen, J., Caspi, A., Taylor, A. et al. (2006).MAOA, maltreatment, and gene–environment interaction predicting children’s mental health: new evidence and a meta-analysis. Molecular Psychiatry, 11, 903–913. Kotler, M., Barak, P., Cohen, H. et al. (1999). Homicidal behavior in schizophrenia associated with a genetic polymorphism determining low catechol O-methyltransferase (COMT) activity. American Journal of Medical Genetics, 88, 628–33. Kranzler, H.R., Hernandez-Avila, C.A. & Gelernter, J. (2002). Polymorphism of the 5-HT1B receptor gene (HTR1B): strong within-locus linkage disequilibrium without association to antisocial substance dependence. Neuropsychopharmacology, 26, 115–22. Kraus, J.E. & Sheitman, B.B. (2005) Clozapine reduces violent behavior in heterogeneous diagnostic groups. Journal of Neuropsychiatry and Clinical Neurosciences, 17, 36–44. Krueger, R.F., Hicks, B.M., Patrick, C.J. et al. (2002). Etiologic connections among substance dependence, antisocial behavior, and personality: modeling the externalizing spectrum. Journal of Abnormal Psychology, 111, 411–24. Kulikov, A.V., Osipova, D.V., Naumenko, V.S. & Popova, N.K. (2005). Association between Tph2 gene polymorphism, brain tryptophan hydroxylase activity and aggressiveness in mouse strains. Genes, Brain, and Behavior, 4, 482–5. Lachman, H.M., Nolan, K.A., Mohr, P. et al. (1998). Association between catechol Omethyltransferase genotype and violence in schizophrenia and schizoaffective disorder. American Journal of Psychiatry, 155, 835–7. Lappalainen, J., Long, J.C., Eggert, M. et al. (1998). Linkage of antisocial alcoholism to the serotonin 5-HT1B receptor gene in 2 populations. Archives of General Psychiatry, 55, 989–94. Lesch, K.P., Bengel, D., Heils, A. et al. (1996). Association of anxiety-related traits with a polymorphism in the serotonin transporter gene regulatory region. Science, 274, 1527–31. Little, K.Y., McLaughlin, D.P., Zhang, L. et al. (1998). Cocaine, ethanol, and genotype effects on human midbrain serotonin transporter binding sites and mRNA levels. American Journal of Psychiatry, 155, 207–13. Lyons, M.J., True, W.R., Eisen, S.A. et al. (1995) Differential heritability of adult and juvenile antisocial traits. Archives of General Psychiatry, 52, 906–15. Malone, S.M., Taylor, J., Marmorstein, N.R. et al. (2004). Genetic and environmental influences on antisocial behavior and alcohol dependence from adolescence to early adulthood. Development and Psychopathology, 16, 943–66. Mann, J.J., Malone, K.M., Psych, M.R. et al. (1996). Attempted suicide characteristics and cerebrospinal fluid amine metabolites in depressed inpatients. Neuropsychopharmacology, 15, 576– 86. Mednick, S.A., Gabrielli, W.F. & Hutchings, B. (1984). Genetic influences in criminal convictions: evidence from an adoption cohort. Science, 224, 891–4. Merikangas, K.R. & Avenevoli, S. (2000). Implications of genetic epidemiology for the prevention of substance use disorders. Addictive Behaviour, 25, 807–20. Meyer-Lindenberg, A., Buckholtz, J.W., Kolachana, B. et al. (2006). Neural mechanisms of genetic risk for impulsivity and violence in humans. Proceedings of the National Academy of Sciences of the USA, 103, 6269–74. Miczek, K.A., Fish, E.W., Almedia, R.M. et al. (2004). Role of alcohol consumption in escalation to violence. Annals of the New York Academy of Sciences, 1036, 278–89.

168

VOLUME I: DIAGNOSIS AND TREATMENT

Miles, D.R. & Carey, G. (1997). Genetic and environmental architecture of human aggression. Journal of Personality and Social Psychology, 72, 207–17. Modestin, J., Dal Pian, D. & Agarwalla, P. (2005). Clozapine diminishes suicidal behavior: a retrospective evaluation of clinical records. Journal of Clinical Psychiatry, 66, 534–8. Moffitt, T.E. (1993). Adolescence-limited and life-course-persistent antisocial behavior: a developmental taxonomy. Psychological Review, 100, 674–701. Muhle, R., Trentacoste, S.V. & Rapin, I. (2004). The genetics of autism. Pediatrics, 113, 472–86. Newman, T.K., Syagailo, Y.V., Barr, C.S. et al. (2005). Monoamine oxidase A gene promoter variation and rearing experience influences aggressive behavior in rhesus monkeys. Biological Psychiatry, 57, 167–72. Nilsson, K.W., Sjoberg, R.L., Damberg, M. et al. (2006). Role of monoamine oxidase A genotype and psychosocial factors in male adolescent criminal activity. Biological Psychiatry, 59, 121–7. Nolan, K.A., Volavka, J., Czobor, P. et al. (2000). Suicidal behavior in patients with schizophrenia is related to COMT polymorphism. Psychiatric Genetics, 10, 117–24. Ohara, K., Nagai, M. & Suzuki, Y. (1998). Low activity allele of catechol-o-methyltransferase gene and Japanese unipolar depression. Neuroreport, 9, 1305–8. Olivier, B. (2004). Serotonin and aggression. Annals of the New York Academy of Sciences, 1036, 382–92. Ou, X-M., Chen, K. & Shih, J.C. (2006). Glucocorticoid and androgen activation of monoamine oxidase A is regulated differently by R1 and Sp1. Journal of Biological Chemistry, 281, 21512– 25. Parsian, A., Cloninger, C.R. & Zhang, Z.H. (2000). Functional variant in the DRD2 receptor promoter region and subtypes of alcoholism. American Journal of Medical Genetics, 96, 407–11. Placidi, G.P., Oquendo, M.A., Malone, K.M. et al. (2001). Aggressivity, suicide attempts, and depression: relationship to cerebrospinal fluid monoamine metabolite levels. Biological Psychiatry, 50, 783–91. Ponce, G., Jimenez-Arriero, M.A., Rubio, G. et al. (2003). The A1 allele of the DRD2 gene (TaqI A polymorphisms) is associated with antisocial personality in a sample of alcohol-dependent patients. European Psychiatry:Journal of the Association of European Psychiatrists, 18, 356–60. Porjesz, B., Almasy, L., Edenberg, H.J. et al. (2002) Linkage disequilibrium between the beta frequency of the human EEG and a GABAA receptor gene locus. Proceedings of the National Academy of Sciences of the USA, 99, 3729–33. Pucilowski, O., Kostowski, W., Bidzinski, A. & Hauptmann, M. (1982). Effect of 6-hydroxydopamineinduced lesions of A10 dopaminergic neurons on aggressive behavior in rats. Pharmacology and Biochemical Behavior, 16, 547–51. Ratsma, J.E., van der Stelt, O., Schoffelmeer, A.N. et al. (2001). P3 event-related potential, dopamine D2 receptor A1 allele, and sensation-seeking in adult children of alcoholics. Alcoholism, Clinical and Experimental Research, 25, 960–7. Retz, W., Retz-Junginger, P., Suppria,n T. et al. (2004). Association of serotonin transporter promoter gene polymorphism with violence: relation with personality disorders, impulsivity, and childhood ADHD psychopathology. Behavioral Sciences and the Law, 22, 415–25. Rhee, S.H. & Waldman, I.D. (2002). Genetic and environmental influences on antisocial behavior: a meta-analysis of twin and adoption studies. Academic Psychology Bulletin, 128, 490–529. Robin, R.W., Chester, B., Rasmussen, J.K. et al. (1997). Prevalence, characteristics, and impact of childhood sexual abuse in a Southwestern American Indian tribe. Child Abuse and Neglect, 21, 769–87. Rocha, B.A., Scearce-Levie, K., Lucas, J.J. et al. (1998). Increased vulnerability to cocaine in mice lacking the serotonin-1B receptor. Nature, 393, 175–8. Rowe, D.C., Rodgers, J.L. & Meseck-Bushey, S. (1992). Sibling delinquency and the family environment: shared and unshared influences. Child Development, 63, 59–67. Rowe, D..C, Stever, C., Chase, D. et al. (1986). Reduced CSF concentrations of homovanillic acid and homovanillic acid to 5-hydroxyindoleacetic acid ratios in depressed patients: relationship to suicidal behavior and dexamethasone nonsuppression. American Journal of Psychiatry, 143, 1539–45. Roy, A. (1986). Suicide in schizophrenia. In A. Roy (ed.), Suicide (pp. 97–112). London: Williams & Wilkins.

THE GENETICS OF PSYCHOPATHIC DISORDERS

169

Rujescu, D., Giegling, I., Gietl, A. et al. (2003). A functional single nucleotide polymorphism (V158M) in the COMT gene is associated with aggressive personality traits. Biological Psychiatry, 54, 34–9. Sabol, S.Z., Hu, S. & Hamer, D. (1998). A functional polymorphism in the monoamine oxidase A gene promoter. Human Genetics, 103, 273–9. Saudou, F., Amara, D.A., Dierich, A. et al. (1994). Enhanced aggressive behavior in mice lacking 5-HT1B receptor. Science, 265, 1875–8. Shepherd, J.P. & Farrington, D.P (1995). Preventing crime and violence. British Medical Journal, 310, 271–2. Smolka, M.N., Schumann, G., Wrase, J. et al. (2005). Catechol-O-methyltransferase val158met genotype affects processing of emotional stimuli in the amygdala and prefrontal cortex. Journal of Neuroscience, 25, 836–42. Sjoberg, R.L., Nilsson, K.W., Wargelius, H.L. et al. (2006). Adolescent girls and criminal activity: role of MAOA-LPR genotype and psychosocial factors. American Journal of Medical Genetics, Part B, Neuropsychiatric Genetics PMID: 17034017. Soyka, M., Preuss, U.W., Koller, G., et al. (2004). Association of 5-HT1B receptor gene and antisocial behavior in alcoholism. Journal of Neural Transmission, 111, 101–9. Storm-Mathisen, A. & Vaglum, P. (1994). Conduct disorder patients 20 years later: a personal followup study. Acta Psychiatryca Scandinava, 8, 416–20. Sullivan, P.F., Neale, M.C. & Kendler, K.S. (2000). Genetic epidemiology of major depression: review and meta-analysis. American Journal of Psychiatry, 157, 1552–62. Sullivan, P.F., Kendler, K.S. & Neale, M.C. (2003). Schizophrenia as a complex trait: evidence from a meta-analysis of twin studies. Archives of General Psychiatry, 60, 1187–92. van Beijsterveldt, C.E. & van Baal, G.C. (2002). Twin and family studies of the human electroencephalogram: a review and a meta-analysis. Biological Psychology, 61, 111–38. Virkkunen, M., Eggert, M., Rawlings, R. & Linnoila, M. (1996a). A prospective follow-up study of alcoholic violent offenders and fire setters. Archives of General Psychiatry, 53, 523–9. Virkkunen, M., Goldman, D. & Linnoila, M. (1996b). Serotonin in alcoholic violent offenders. Ciba Foundation Symposium, 194, 168–77. Virkkunen, M., Rawlings, R., Tokola, R. et al. (1994). CSF biochemistries, glucose metabolism, and diurnal activity rhythms in alcoholic, violent offenders, fire setters, and healthy volunteers. Archives of General Psychiatry, 51, 20–7. Volavka, J., Czobor, P., Nolan, K. et al. (2004). Overt aggression and psychotic symptoms in patients with schizophrenia treated with clozapine, olanzapine, risperidone, or haloperidol. Journal of Clinical Psychopharmacology, 24, 225–8. Widom, C.S. & Brzustowicz, L.M. (2006). MAOA and the ‘cycle of violence’: childhood abuse and neglect, MAOA genotype, and risk for violent and antisocial behavior. Biological Psychiatry, 60, 684–9. Young, S.E., Smolen, A., Corley, R.P. et al. (2002). Dopamine transporter polymorphism associated with externalizing behavior problems in children. American Journal of Medical Genetics, 114, 144–9. Xu, K., Lichtermann, D., Lipsky, R.H. et al. (2004). Association of specific haplotypes of D2 dopamine receptor gene with vulnerability to heroin dependence in 2 distinct populations. Archives of General Psychiatry, 61, 597–606. Zhou, Z., Roy, A., Lipsky, R., Kuchipudi, K. et al. (2005). Haplotype-based linkage of tryptophan hydroxylase 2 to suicide attempt, major depression, and cerebrospinal fluid 5-hydroxyindoleacetic acid in 4 populations. Archives of General Psychiatry, 62, 1109–18.

CHAPTER 10

Neuroimaging Perspectives in Pathogenesis and Therapeutic Strategies Jurgen ¨ L. Muller ¨ ¨ Georg August University of Gottingen, Germany

This chapter would appear to be one of the easiest to write, because one has only to address limitations and problems of recent studies on psychopathy, make some proposals on how to improve study designs, describe the most important topics to be addressed in the near future and and provide a brief outlook on upcoming trends. At a second glance, this chapter quickly becomes difficult once it becomes apparent that there must be some good explanations as to why such improvements have not yet been realized. To discuss neuroimaging perspectives in psychopathy, several questions must be addressed. The sample: what is psychopathy and how is it defined? This point sounds boring, since this entire handbook addresses psychopathy. Nevertheless, it is important because neuroscientific approaches postulate dinstinct and well-conceptualized study designs and in particular a distinct study sample. The results: neuroimaging results have helped to explain the underpinnnings of psychopathy. But how far can we trust these findings regarding stability and validity and what do these results mean for the individual psychopath? The techniques: how can we use adequate neuroimaging and neuroscientific methods to address the most important questions on the neurobiology of psychopathy?

LOOKING FOR A PSYCHOPATHIC SAMPLE FOR NEUROSCIENTIFIC RESEARCH In this handbook, the concept of ‘psychopathy’ is thoroughly discussed. For assessing psychopathy, the Psychopathy Checklist-Revised (PCL-R) has been found to be a gold standard for most researchers. It is important for this chapter that different and heterogeneous syndromes have been incorprated into the 20 items of the PCL-R (Hare, 1991, 2003). Using the

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

172

VOLUME I: DIAGNOSIS AND TREATMENT

PCL-R, neuroscientific research has been encouraged since a well-defined sample can be described. This facilitated empirical and neuroscientific studies on psychopathy. The PCLR based concept of psychopathy according to Robert Hare describes psychopathy using 20 items and a cut-off score of 30 from 40. At least a two-factor, and recently even a three- or a four-factor model, has been used to address the most important dimensions of psychopathy: emotional detachment and antisocial behavior. Regarding the PCL-R psychopathy, antisocial behavior matters since 6 points out of 40 deal with conviction and behavior on release. However, there is good evidence that antisocial behavior is not the most important feature in psychopathy, because criminality is only loosely linked to psychiatric disorders. Instead of antisocial behavior, emotional detachment, comprised in the factor 1 of the PCL-R, seems to be a more important hallmark: ‘glibness/superficial charm’, ‘grandiose sense of self-worth’, ‘pathological lying’, ‘cunning/manipulative behavior’, ‘lack of remorse and guilt’, ‘shallow affect’, ‘callous lack of empathy’, ‘failure to accept responsibilty for own actions’ contribute to factor 1 according to the PCL-R (Hare et al., 2000, 2003). Emotional detachment is the most challenging feature of psychopathy, and the most promising approach in the research on its neurobiological underpinnings. Historically, Robert Hare introduced the PCL-R for risk assessment in a prison setting; it was a second step to use it to describe a study sample for neuroscientific research. In line with this, most of the earlier studies on criminal inmates looked for abnormalities in emotional regulation, avoidance learning, fear response and startle reflex modulation. Recently, research interest has discovered community or successful psychopaths who are not criminal and who have not yet been convicted. For community or successful psychopaths, other checklists and other inclusion criteria have been introduced. Since all participants from heterogeneous studies are classified as psychopaths, it is difficult to compare results and outcome, because the samples are quite different. This heterogenity is not a new topic in the history of psychopathy (Herpertz & Saß, 2000). The difficulty in finding a consistent concept for psychopathy can be traced back to the early clinical descriptions. Emil Kraepelin (Kraepelin, 1909–15) and Kurt Schneider (Schneider, 1948) described clinically a psychopathic syndrome. Harvey Cleckley gave us clinical impressions of different successfull and unsucessfull psychopathic persons ‘behind a mask of sanity’ (Cleckley, 1988). Some of the properties described by Cleckley were incorporated into the PCL-R by Hare who focused on incarcerated criminal psychopaths. To avoid stigmatization, European and German classifications replaced the term and concept of ‘psychopathy’ with the concept of ‘personality disorders’. Personality disorders refer to a different clinical concept that requires the fulfillment of different items. Regarding the inclusion diagnostic criteria from ICD-10 and DSM-IV, there is considerable overlap, but the classification manuals differ regarding the impact of emotional and affective symptoms in psychopathy. It is important to acknowledge that different inclusion criteria affect the results of in particular neuroscientific studies. To facilitate research and the interpretation of the results, comparable models for sample desciption have to be introduced.

EMPIRICAL FINDINGS ON PSYCHOPATHY Ever since the early clinical descriptions, impaired emotional responsiveness has been considered to be the hallmark of psychopathy (Cleckley, 1988; Hare, 1991). In the meantime, a growing body of research has focused on the nature and bases of affective disturbances in

NEUROIMAGING PERSPECTIVES

173

psychopathy. It is suggested that the emotional deficits associated with psychopathy interfere with the development of moral reasoning and put the individual at risk for developing high levels of antisocial behavior. Exploring emotion-related brain function including a reduced function of the defensive reaction system might help to focus on the core syndrome of psychopathy independently of the different rating scales and checklists. Neurophysiological investigations revealed abnormalities that might help to characterize the study sample by assessing the function of the defensive reaction system. Using brain imaging techniques, different features of psychopathy have been linked to prefrontal, in particular to orbitofrontal and temporal, in particular amgdala and hippocampal, brain structures and functions. Genetic factors have been found to have a great influence on personality factors, on emotion-related brain function as well as on aggressive behavior. Thus, it is well known that personality disorders, genetic factors and brain structure and function are closely correlated. Nevertheless, a wide range of techniques and protocols were used to focus on a variety of personality aspects. This makes it difficult to compare the results and to integrate the results into a unified model. It would be a major step forward to combine the study protocols investigating the same psychopathic participants using additionally electrophysiological, genetic and brain imaging techniques (see chapters on genetics and empirical findings in this handbook). Recent results inspire continued studying of brain structure and function in psychopathy. Nevertheless, we must realize that there is a considerable heterogenity of the psychopathic samples in different studies. One way out of this limitation is to readdress the same participants using a second method. Due to the required methodological effort, up until now this approach has rarely been used successfully. In addition to the study sample, the choice of the control group is also problematic. It has proved extremely problematic to control for even the most obvious of potential confounders, since drug abuse, specific length of imprisonment, a certain biography with a difficult childhood and heredity are closely correlated with psychopathy.

FINDINGS ON PSYCHOPATHY ARE NO BETTER THAN THE METHODS USED In addition to the sample description, there are more fundamental methodological issues concerning neuroimaging studies of antisocial individuals to be addressed if the results are to be used in relation to important legal questions. In spite of the increase in neuroimaging literature in recent years, there are many conditions that influence hemodynamic response and fundamental underpinnings of data consistency that are not quite well understood even in a healthy population. The validity of activation patterns has seldom been verified through sophisticated stimulation designs. Indeed, methodological inconsistencies between the studies underlie, in part, the failure to replicate findings. Existing studies have used varying technical equipment and imaging modalities that reflect different physiological events and tasks that tap into a range of cognitive processes assumed to be abnormal in antisocial individuals. Current neuroimaging technics are nascent, but they are developing very fast. Methodological improvements are introduced very quickly. Reliability and validity are currently expected to have only minor impact. For clinical applications, however, these are most important values. Neuroimaging studies rely on a comparison between the

174

VOLUME I: DIAGNOSIS AND TREATMENT

experimental image and a normative template. The idea of such a template is itself problematic, and raises a number of issues that could impact on the ultimate interpretation of the data (for an overview see Eastman & Campbell, 2006). No gold standard exists, nor is there a consensus on which particular measure should be used as a normative standard, with the result that, in theory, any given brain might qualify as ‘normal’ on one measure but not on another. Morover the resulting, but potentially misleading, image is often visually persuasive because an image from an exemplary study is indistinguishable from one from a poorly designed study. Regarding functional imaging, an activation pattern is defined by a threshold for statistical significance, which is set by convention rather than as an absolute standard. Thus, activation patterns represent a statistical interpretation of a complex data set, which might be interpreted differently by different researchers. The selection of test and control conditions is also crucial, as different control conditions could produce different activation patterns during assessment with the same task. Summarizing, there are many unresolved questions regarding imaging research, all of which influence the validity of data in psychopathy. Therefore, in order to obtain hard data, we must improve inclusion criteria as well as study standards, investigate reliabilty and develop specific tests for forensic psychiatric questions (for an overview see Eastman & Campbell, 2006).

WHICH IS THE RIGHT TEST FOR PSYCHOPATHS? No single item on any given test proves the existence of psychopathy. Even factor 1 of the PCL-R, which assesses emotional detachment, consists of different and heterogeneous items. One step further would be to investigate specific psychopathic features. Thus, the items of the PCL-R must be transferred to a neuroscientific model. This is not a trivial effort to translate the PCL-R items to a specific empirical test that measures the interesting features. Some of the items allow for research more easily than others, but it is is still complicated to mix heterogeneous items and investigate the combination using highly sophisticated protocols. This heterogenity might help to explain the inconsistency of results. Some researchers linked psychopathy to a paralimbic syndrome (Kiehl, 2006), others attribute the most important features to prefrontal abnormalities (Raine et al., 2000, Yang et al., 2005), others favor the amygdala or temporal regions (Kiehl et al., 2004, M¨uller et al., 2003) for explaining psychopathy. Each hypothesis focused on different features of psychopathy addressing for example avoidance learning, emotion processing or fear response (Herpertz et al., 2001; Lang, Bradley & Cuthbert, 1993; Patrick, 1994; Patrick, Cuthbert & Lang, 1994). It is hypothesized that the emotional deficits associated with psychopathy interfere with the development of moral reasoning and place the individual at risk for developing high levels of antisocial behavior. Lack of empathy and lack of the abilility to experience deeper feelings such as love have been investigated studying the processing of emotions. Reduced fear has been addressed using the modulation of the startle response and avoidance learning. One of the earliest and most important symptoms of the psychopathic core syndrome is the poor legal prognosis. Psychopaths seem to be unable to learn from negative experiences. Revocation of conditional releases could correspond to the inability to benefit from negative experiences, in particular to learn from punishment. Negative experiences, in particular punishment, are correlated with the fear reaction system that might be hypofunctional in psychopathy (Cleckley, 1988; Hare, 1982, 1991). In line with this, results of neurophysiological studies suggest that autonomic reactivity is attenuated in psychopathy (Fowles,

NEUROIMAGING PERSPECTIVES

175

2000; Miranda et al., 2003; Patrick, 1994; Patrick, Cuthbert & Lang, 1994). The typical augmentation of the startle response during exposure to aversive stimuli has been found to be diminished or absent in psychopathy (Greenwald et al., 1998; Herpertz et al., 2001; Lang et al., 1993). This low defense reaction level is thought to be based on a general deficit in processing emotional contents that may impede the ability to learn from punishment and passive avoidance learning (Flor et al., 2002; Newman & Kosson, 1986). Thus, there is good empirical evidence that learning from punishment is abnormal in psychopathy due to deficits in emotional processing. Recent functional magnetic resonance imaging (fMRI) addressed how emotion is related to brain function and the neural underpinnings of learning from punishment (Birbaumer et al., 2005; Schneider et al., 2001).

COGNITION IMPAIRMENT IN PSYCHOPATHS? In addition to emotion-related brain dysfunction, varous studies show that psychopaths perform worse in executive functions. LaPierre, Braun & Hodgins (1995) found that psychopathic inmates are impaired on all neuropsychological tests sensitive to orbitofrontal and ventromedial dysfunction, but not to dorsolateral-prefrontal and posterorolandic function. Psychopathic individuals showed impaired extinction of previously rewarding responses in a single-back card playing task. Others reported on an impairment on the four-back gambling task given to boys with psychopathic tendencies. Mitchell and colleagues found that psychopathic individuals were less likely to avoid making risky selections over the course of the gambling task (Mitchell et al., 2002). In spite of these empirical findings, data on an impairment of cognitive function in psychopaths are still inconsistent (Sommer et al., 2004).

DO PSYCHOPATHS ACT IN COLD BLOOD – DUE TO DISTURBED INTERACTION OF EMOTION AND COGNITION? Emotion and cognition are closely intertwined. Cognitive processes are able to regulate emotions (Ochsner & Gross, 2005) and conversely, emotional and motivational factors can significantly affect cognitive performance (Davidson, 2002; Simpson et al., 2001a,b). Cognitive processes and emotional processing contribute to the control and regulation of behavior. Emotional states enhance or impair cognitive performance depending on the particular emotion and cognitive process involved; thus different emotional states can have opposites effects (Gray, 2001). Resource allocation models predict that all emotional states consume resources and that these resources are no longer available for controlled cognition (Ellis & Ashbrook, 2005). Until now very little empirical data has existed that characterize the neural basis of the interrelationship between cognition and emotion. For healthy subjects, studies with positron emission tomography (PET) or fMRI show a dynamic interplay between cognition and emotion with a reciprocal association between emotional and cognitive brain areas (Drevets & Raichle, 1992). Only a few studies that evaluated the effects of induced emotions on cognitive processes indicated a dynamic exchange between cognitive task performance and emotional states. Investigating the neural underpinnings, Gray and colleagues focused on the effect of cognitive tasks on emotional state manipulations and found an emotion–cognition interaction bilaterally in the prefrontal cortex (Gray, Braver & Raichle, 2002).

176

VOLUME I: DIAGNOSIS AND TREATMENT

In line with the evidence that the processing of emotions is critically out of balance in psychopathy and that emotional and cognitive processes are closely interwined, it can be assumed that the emotional impairment of psychopaths also influences their cognitive processing. In spite of good empirical evidence that emotion processing and executive functioning are critically unbalanced, only few studies addressed the impact of emotions on cognitive processes in psychopathy (Sommer et al., 2006). Low-anxiety psychopaths were impaired in using emotional information in an investigation on the influence of emotional cues on a lexical-decision task (Lorenz & Newman, 2002). In our study, we focused on the interaction of cognition and emotion evaluating behavioral data and brain function using fMRI (Belliveau et al., 1992; Kwong et al., 1992; Ogawa et al., 2000) and pictures from the International Affective Picture Set (IAPS; ()CESA-NIMH, 1999). We tested the impact of pleasant and unpleasant emotions on automatic and controlled information processing by a Simon paradigm (Sommer et al., 2004) in 10 totally right-handed male volunteers with psychopathy, according to PCL-R, in comparison to 12 controls. Whereas control subjects made more errors in the negative emotional context than in the positive or neutral context, psychopaths showed no influence of the induced emotion on their error rates, although they did not differ from healthy controls in their ratings of emotional valence. For healthy controls, a network of areas sensitive to ‘Emotion X Task’ interaction, including superior and inferior frontal gyri, anterior cingulate, putamen and thalamus were activated. Especially negative emotions led to less activation during incompatible trials compared to compatible trials. For psychopathic patients, no interactive effect was found (M¨uller et al., 2007). These results suggest that for psychopaths negative emotions do not drain attention and possibly require less ressources for emotional processing. Therefore, their regulatory influence on behavior is lower than in nonpsychopaths. Up until now, there has been no imaging investigation to show how emotion influences cognitive functions in psychopaths. This is of major interest since psychopaths have been found to act in ‘cold blood’, committing crimes without being warned by feelings of empathy or fear from punishment. If psychopaths cannot integrate feelings and cognitions because of their neurobiology, this could critically impact their therapy and prognoses.

COMBINING DIFFERENT METHODS: IN PSYCHOPATHY, VOLUME LOSS AND REDUCED EMOTION ARE RELATED TO BRAIN FUNCTION IN THE RIGHT SUPERIOR TEMPORAL GYRUS In spite of growing interest in psychopathy, only a few imaging studies have addressed brain structure. Some of these studies included subjects with antisocial personality disorder (APD), others addressed those with PCL-R psychopathy. Prefontal volume changes were found by Raine and colleagues in persons with APD without brain trauma (Raine et al., 2000). Laakso and colleagues found significantly smaller volumes of the left dorsolateral, medial frontal and orbitofrontal cortex in APD, but after controlling for differences in education and duration of alcoholism this significance disappeared. For the dorsolateral and orbitofrontal cortices, only duration of alcoholism was significantly associated with the observed volume deficit, and for the medial frontal cortex, the difference in education. Moreover, no significant correlations were found between any of the volumes and the degree of

NEUROIMAGING PERSPECTIVES

177

Table 10.1 Volume loss in right superior temporal gyrus in psychopathy– comparison between psychopaths and controls (two-sample t-test) x

y

z

t score

z score

p (corr)

p value

42

15

−32

6.1

4.93

0.002

0.0001

42

15

−32

6.1

4.93

0.002

0.05

Right superior temporal gyrus (BA 38) Bonferroni corrected

psychopathy (Laakso et al., 2000, 2002). Dolan and colleques looked for volume changes in incarcerated impulsive-aggressive personality-disordered (PD) offenders. Despite evidence of impairments in executive function, frontal lobe volume was not reduced (Dolan et al., 2002). In contrast, they found 20 % smaller temporal lobe volumes in comparison with those of control subjects. Hippocampal involvement in psychopathy has been found by Laasko and colleagues in APD associated with alcoholism (Laakso et al., 2000, 2002) and by Raine and colleagues in unsuccessful psychopaths (Raine et al., 2004). Additionally, Raine reported that the corpus callosum was affected in psychopathic antisocial individuals (Raine et al., 2003). These results confirmed the hypothesis that prefrontal and temporal lobe structures in particular are changed in psychopathy. The data were inconsistent due to different methodological approaches and different sample descriptions. In our study, we used voxel-based morphometry (Ashburner & Friston, 2001), a sophisticated objective wholebrain imaging technique, to investigate subtle, region-specific changes in gray and white matter by averaging results across 17 criminal psychopaths in comparison to 17 controls. We found a highly significant volume loss in the right superior temporal gyrus (BA 38) that survived Bonferroni correction (M¨uller et al., 2007) (see Table 10.1 and Figure 10.1).

Figure 10.1 Changes in brain structure and function in right superior temporal gyrus (STG) in psychopathy: volume loss is demonstrated in the right STG

178

VOLUME I: DIAGNOSIS AND TREATMENT

Figure 10.2 Hypofunction in the right STG in psychopathy while processing negative pictures

In addition, six criminal psychopaths from this study participated in an fMRI study on emotion (M¨uller et al., 2003). Thus, functional and structural data could be correlated in order to explore the role of structural changes in processing emotions. We found a significant volume loss and reduced emotion-related brain function in the right superior temporal gyrus of criminal psychopaths (Figure 10.2). This study showed a highly significant volume loss in the right superior temporal gyrus (Brodman Area 38) and a reduced emotion-related brain function in this area in psychopathy (Figure 10.3). The functional role of the right temporal region in psychopathy has been emphasized in different studies on brain function (Kiehl et al., 2004; M¨uller et al., 2003. In particular, to right superior temporal gyrus was connected to sharing feeling with others

tMRI response (% BOLD signal)

2

1

0

–1

–2

–6

6 0 12 Time [scans]

Figure 10.3 Reduced emotion related brain function in the right STG in psychopathy. Eventrelated averaged data comparing psychopaths (green) and controls (orange). See also color plates

NEUROIMAGING PERSPECTIVES

179

and empathy (Allison et al., 2000; Carmichael et al., 2004; Carr et al., 2004; Farrow et al., 2001; Moll et al., 2005).

PSYCHOPATHY AS A MODEL FOR MORALITY AND RESPONSIBILITY Moral cognitive neuroscience focuses on the neural basis of uniquely human forms of social cognition and behavior. Recent evidence from functional imaging and clinical reports indicates that a consistent network of brain regions is involved in moral cognition. In a review, Moll and colleagues hypothesized that moral phenomena could emerge from the integration of contextual social knowledge, represented as event knowledge in the prefrontal cortex (PFC); social semantic knowledge, stored in the anterior and posterior temporal cortex; and motivational and basic emotional states, which depend on cortical–limbic circuits (Moll et al., 2005). This field is of major interest in psychopathy since moral development, moral emotion and moral cognition are critically impaired in psychopaths. Moreover, as has been shown here earlier, in psychopathy these brain regions have been found to be abnormal in structure and function. According to Moll et al. (Moll, 2005) social behavior is related to morality that might be considered as the sets of customs and values that are embraced by a cultural group to guide social conduct. Moll and colleagues hypothesize an event–feature–emotion complex (EFEC) framework that postulates that moral cognitive and behavioral phenomena arise from the binding of three main components: structured event knowledge (provided by context-dependent representations in prefrontal subregions); social perceptual and functional features (stored in the posterior and anterior sectors of the temporal cortex); and central motive or basic emotional states (such as aggressiveness, sadness, attachment or sexual arousal, represented in limbic and paralimbic regions). Using this model, according to the authors it could be possible to predict prognostic developments perhaps after a brain lesion or after one has found a localized reduction in brain activity. Thus, changes in brain function or structure could predict behavior. For example, lesions of the dorsolateral prefrontal cortex (DLPFC would lead to behavioral impairments in unfamiliar situations, but would leave intact wellestablished social behaviors and attitudes. Lesions in the ventral sectors of the prefrontal cortex (PFC) would lead to severe social behavioral changes due to disruption of social– emotional contextual knowledge, with early lesions having more drastic effects as they impair the learning of moral values. Lesions in the ventromedial PFC would tend to impair adherence to well-established social norms and attitudes. Lesions in the lateral OFC are expected to impair behaviors that rely on dynamically comparing unmatched social– emotional cues with stored representations. Damage to the posterior STS would impair the ability to recognize socially relevant perceptual features leading to inadequate social behavior under circumstances that depend on the perception of these signals. Lesions in the anterior temporal lobe are expected to disrupt knowledge of social concepts and values that are more context-independent (such as ‘honor’ and ‘greed’), but to leave intact highly context-dependent knowledge of sequences of social events (e.g., ‘going to a supermarket’). Dysfunction of limbic or paralimbic regions is predicted to cause exaggeration or attenuation of basic motivational and emotional states. Lesions of the hypothalamus, septal nuclei, basal forebrain and neighboring structures are predicted to produce gross distortions of the

180

VOLUME I: DIAGNOSIS AND TREATMENT

valence of moral values, attitudes and moral emotions. This is in line with the observation that unprovoked rage, lack of empathy and abnormal sexual behaviors follow isolated damage to limbic and paralimbic regions (for the review see Moll et al., 2005). This approach is important because most of these brain regions have been found to be involved in the pathogenesis of psychopathy: different parts of the prefrontal cortex, the temporal lobe, the amygdala and the hypothalamus and the ventral striatum. It would be interesting to study the function of these regions in psychopaths using a task related to morality. By means of fMRI techniques, it is possible to investigate the neural basis of moral decisions, for example, using the prison dilemma or the ultimatum game. In this task, a proposer makes an offer to a responder on how to split an amount of money. If the responder accepts, the money is split as proposed. However, if the responder rejects the offer, both players end up with nothing. Brain areas activated during these interactions include the limbic and paralimbic regions, the anterior prefrontal cortex and the superior temporal sulcus. It is interesting that in psychopaths, these designs have been studied in the 1960s and the 1970s, but have not been investigated using modern imaging techniques. Currently, several research groups are focusing on such experiments including in particular so-called successful community psychopaths.

PSYCHOPATHS: ARE THEY A NEUROBIOLOGICAL MODEL FOR IRRESPONSIBILITY? Progress in neuroimaging techniques and recent neurobiological findings in particular on psychopathy led to an international debate on freedom of will and on the related forensic topic on legal reponsibilty. Most of the speakers and authors with a neuroscientific background argue that emotions, vision and decision making are based on neural activity that can be investigated by neuroscientific means. Recent progress in investigating the neural underpinnings of morals and social behavior supported the point of view that every decision and every action is determined by its neural underpinnings. Because it is known that in particular subcortical regions contribute to determining behavior unconsciously, no one should be blamed for his deeds. Thus, according to the protagonists, a neuroscientifically based penal law must be introduced. (As a matter of fact, to be consistent, this must be extended to civil law as well: ‘If I don’t pay this bill, obviously my limbic system has not agreed to the contract.’ So, who has to pay?) The debate was controversial. Lawyers picked up on the arguments, asking how neuroscience can answer specific questions from the court: it soon became apparent that different scientific systems were mixed up in the discussion. Neuroscientists dealt with the freedom of will generally and argued that human behavior is based on neurobiology. In contrast, lawyers had a different approach judging a concrete behavior with a practical decision with all consequences. Since psychopaths provided a neuroscientific model for criminal behavior consistent with a poor prognosis, psychopathy, an issue with which every legal court has frequently dealt, became a hot spot in this discussion, raising hopes and expectations that neuroscientific investigations could solve legal problems in predicting relapses and could lead to a reassessment of the need for preventive detention. In spite of expecting a great future for neuroscience in psychopathy, neuroscience will probably not solve legal problems for different reasons. Neuroscience is increasingly identifying associations between biology and different features of criminality.

NEUROIMAGING PERSPECTIVES

181

However, there is a mismatch between questions that the courts and society wish answered and those that neuroscience is capable of answering. This is very comforting since no one can give a concrete reaction time in a decision task or a percentage of activity change in a specific brain region that shows that the participant is irresponsible or dangerous and must be imprisoned for preventive detention. The gap between the different approaches of neuroscience and law will maintain. In spite of immense progress in neuroscientific research, the requirements for answering legal questions with the required accuracy and in the context of an individual behavior are too high. Science shows correlations of particular genes, or types of brain states with criminality or aggression, but the impact on criminal culpability is still unclear, because risk factors cannot cause a behavior. Science continues to seek risk factors for a distinct behavior, but when does a risk factor become so important or a correlation between brain and behavior so close that this may become a proper basis to place someone in preventive detention in the interest of public protection? Eastman and Campbell summarize that the law asks questions that science is at least currently unlikely to be able to answer; whereas science answers questions that the law does not pose (for a summary see Eastman & Campbell, 2006).

TREATMENT USING FMRT? In contrast to the assessment of responsibility, neuroimaging might become very helpful in diagnosis, in assessing treatment effects and perhaps as a tool for treatment itself (Mitterschiffthaler et al., 2006). The effects of a specific treatment can be evaluated using neuroimaging techniques. Different studies show a change in brain activation following therapeutic interventions. Psychopharmacological treatment influences brain activation patterns. This has been shown regarding newer and earlier neuroleptic drugs as well as regarding serotonin reuptake inhibitors (SSRI). Even a single administration of an SSRI antidepressant changes brain activation significantly (Loubinoux et al., 2002). Currently, psychopharmacological intervention is not the predominant kind of treatment for psychopathy, nevertheless aggression and impulsivity might be influenced pharmacologically. Since the prefrontal cortex is of major importance in psychopathy, it is noteworthy that orbitofrontal cortex (OFC) activity has been influenced through SSRIs in post-traumatic stress disorders. In line with the clinical improvement, OFC function increased as measured by using SPECT. Furthermore, the effect of psychotherapy has been illustrated using fMRI in a spider phobia (Paquette et al., 2003). Before the therapeutic intervention, there was an increased activity in the parahippocampal region and in the PFC. After psychotherapeutic intervention, brain activity was normalized in this participant. This study shows that pharmacological as well as psychotherapeutic treatment influence brain activation patterns. Consistent with the clinical improvement, brain activation patterns have been changing. This has to be expected. The results help to argue the other way round: if neuroimaging studies show dysfunctional activation patterns corresponding to a specific behavior, one might influence this behavior through changing brain activation patterns in specific brain regions. Psychopharamlogical and psychotherapeutic treatment have been addressed already. A newer technique using real-time fMRT has been introduced to influence brain activation by the participant himself. The participant was instructed to change his brain activity in distinct brain regions using a biofeedback approach (Weiskopf et al., 2004). This approach was successful in different studies. Nevertheless, it has yet to be shown whether changing brain activation

182

VOLUME I: DIAGNOSIS AND TREATMENT

leads to a change in behavior as well. Thus, studies designed to determine whether treatment influences behavior by changing activation, have to be performed. Finally there is another method to influence abnormal brain activation patterns. Repetitive transcranial magnetic stimulation (rTMS) has been used in treatment of depression as well as of tinnitus (Fregni et al., 2005; Herwig et al., 2001; Plewnia et al., 2007). Combining rTMS and fMRT, specific networks involved in the psychopathology might be used to change the neural underpinnings. Since neural activity and behavior are closely correlated, a change in impulsivity or emotion regulation could be demonstrated. These techniques and in particular combining different methods are promising; nevertheless, it has yet to be shown whether they can help in assessing and treating personality disorders and psychopathy in particular. Regarding diagnosis, the current results in psychopathy are encouraging but we are far from introducing imaging techniques for improving clinical work. Neither can we currently assess psychopathy using fMRI or structural MRI, nor have we currently a specific neuropsychological test to prove psychopathy and the corresponding behavior. Real-time fMRT might be helpful in the future, because sophisticated routines for data analysis will contribute to the evaluation of parameter-free data sets (Esposito et al., 2003). Using independent component analysis, independent statistical components could be related to a specific brain function, perhaps correlated with a distinct behavior. This would make it possible to discover whether subjects are hallucinating, even without their cooperation. Perhaps this fiction might become reality in the nearer furture. As a second step, the science and technology of neuroimaging could become transferable to the assessment of psychopathy.

REFERENCES Allison, T., Puce, A. & McCarthy, G. (2000). Social perception from visual cues: role of the STS region. Trends in Cognitive Sciences, 7, 267–78. Ashburner, J. & Friston, K.J. (2001) Why voxel-based morphometry should be used. Neuroimage, 14, 1238–43. Belliveau, J.W., Kwong, K.K., Kennedy, D.N. et al. (2005). Magnetic resonance imaging mapping of brain function. Human visual cortex. Investigative Radiology, 27(Suppl 2), S59–S65. Birbaumer, N., Veit, R., Lotze, M. et al. (2005). Deficient fear conditioning in psychopathy: a functional magnetic resonance imaging study. Archive of General Psychiatry, 62, 799–805. Carmichael, G. (2004). Left temporoparietal junction performs social reasoning. Lancet Neurology, 3, 328. Carr, L., Iacoboni, M., Dubeau, M.C. et al. (2003) Neural mechanisms of empathy in humans: a relay from neural systems for imitation to limbic areas. Proceedings of the National Academy of Science of the USA, 100, 5497–502. CESA-NIMH (Center for the Study of Emotion and Attention – National Institute of Mental Health) (1999). The International Affective Picture System: Digitized Photographs. Gainesville, FL: The Center for Research in Psychophysiology, University of Florida. Ref Type: Slide. Cleckley, H. (1988). The Mask of Sanity, 5th edition. Augusta: Mosby. Davidson, R.J. (2002). Anxiety and affective style: role of prefrontal cortex and amygdala. Biological Psychiatry, 51, 68–80. Dolan, M.C., Deakin, J.F., Roberts, N. & Anderson, I.M. (2002). Quantitative frontal and temporal structural MRI studies in personality-disordered offenders and control subjects. Psychiatry Research, 116, 133–49. Drevets, W.C. & Raichle, M.E. (1992). Neuroanatomical circuits in depression: implications for treatment mechanisms. Psychopharmacological Bulletin, 28, 261–74.

NEUROIMAGING PERSPECTIVES

183

Eastman, N. & Campbell, C. (2006). Neuroscience and legal determination of criminal responsibility. Nature Reviews Neuroscience, 7(4), 311–8. Ellis, H.C. & Ashbrook, P.W. (2005). Resource allocation model of the effects of depressed mood states on memory. In K. Fiedler & J. Forgas (eds.), Affect, Cognition and Social Behavior (pp. 25–43). Toronto: Hogrefe. Esposito, F., Seifritz, E., Formisano, E. et al. (2003). Real-time independent component analysis of fMRI time-series. Neuroimage, 20(4), 2209–24. Farrow, T.F., Zheng, Y., Wilkinson, I.D. et al. (2001). Investigating the functional anatomy of empathy and forgiveness. Neuroreport, 12, 2433–8. Flor, H., Birbaumer, N., Hermann, C. et al. (2002). Aversive Pavlovian conditioning in psychopaths: peripheral and central correlates. Psychophysiology, 39, 505–18. Fowles, D.C. (2000). Electrodermal hyporeactivity and antisocial behavior: does anxiety mediate the relationship? Journal of Affective Disorders, 61, 177–89. Fregni, F., Marcolin, M.A., Myczkowski, M. et al. (2005). Predictors of antidepressant response in clinical trials of transcranial magnetic stimulation. International Journal of Neuropsychopharmacology, 23, 1–14. Gray, J.R. (2001). Emotional modulation of cognitive control: approach-withdrawal states doubledissociate spatial from verbal two-back task performance. Journal of Experiment Psychology: General, 130, 436–52. Gray, J.R., Braver, T.S. & Raichle, M.E. (2002). Integration of emotion and cognition in the lateral prefrontal cortex. Proceedings of the National Academy of Sciences of the USA, 99, 4115–20. Greenwald, M.K., Bradley, M.M., Cuthbert, B.N. & Lang, P.J. (1998). Startle potentiation: shock sensitization, aversive learning, and affective picture modulation. Behavioral Neuroscience, 112, 1069– 79. Hare, R.D. (1982). Psychopathy and physiological activity during anticipation of an aversive stimulus in a distraction paradigm. Psychophysiology, 19, 266–71. Hare, R.D. (1991). Manual for the Hare Psychopathy Checklist-Revised. Toronto: Multi-Health Systems. Hare, R.D. (2003) Manual for the Hare Psychopathy Checklist-Revised (2nd edition). Toronto: MultiHealth Systems. Herpertz, S.C. & Saß, H. (2000). Emotional deficiency and psychopathy. Behavioral Sciences and the Law, 18, 567–80. Herpertz, S.C., Werth, U., Lukas, G. et al. (2001). Emotion in criminal offenders with psychopathy and borderline personality disorder. Archive of General Psychiatry, 58, 737–45. Herwig, U., Schonfeldt-Lecuona, C., Wunderlich, A.P. et al. (2001). The navigation of transcranial magnetic stimulation. Psychiatry Research, 108(2),123–31. Kiehl, K.A. (2006). A cognitive neuroscience perspective on psychopathy: evidence for paralimbic system dysfunction. Psychiatry Research, 142(2–3), 107–28. Kiehl, K.A., Smith, A.M., Hare, R.D. et al. (2001). Limbic abnormalities in affective processing by criminal psychopaths as revealed by functional magnetic resonance imaging. Biological Psychiatry, 50, 677–84. Kiehl, K.A., Smith, A.M., Mendrek, A. et al. (2004). Temporal lobe abnormalities in semantic processing by criminal psychopaths as revealed by functional magnetic resonance imaging. Psychiatry Research. Neuroimaging, 130, 27–42. ¨ Kraepelin, E. (1909–15). Psychiatrie. Ein Lehrbuch f¨ur Studierende und Arzte (8th edition). Leipzig: Ambosius Barth. Kwong, K.K., Belliveau, J.W., Chesler, D.A. et al. (1992). Dynamic magnetic resonance imaging of human brain activity during primary sensory stimulation. Proceedings of the National Academy of Science of the USA, 89, 5675–9. Laakso, M. P., Gunning-Dixon, F., Vaurio, O. et al. (2002). Prefrontal volume in habitually violent subjects with antisocial personality disorder and type 2 alcoholism. Psychiatry Research. Neuroimaging, 114, 95–102. Laakso, M.P., Vaurio, O., Koivisto, E. et al. (2001). Psychopathy and the posterior hippocampus. Behavioural Brain Research, 118, 187–93. Laakso, M.P., Vaurio, O., Savolainen, L. et al. (2000). A volumetric MRI study of the hippocampus in type 1 and 2 alcoholism. Behavioral Brain Research, 109, 177–86.

184

VOLUME I: DIAGNOSIS AND TREATMENT

Lang, P.J., Bradley, M.M. & Cuthbert, B.N. (1998). Emotion and motivation: measuring affective perception. Journal of Clinical Neurophysiology, 15, 397–408. Lang, P.J., Greenwald, M.K., Bradley, M.M. & Hamm, A.O. (1993). Looking at pictures: affective, facial, visceral, and behavioral reactions. Psychophysiology, 30, 261–73. Lapierre, D., Braun, C.M. & Hodgins, S. (1995). Ventral frontal deficits in psychopathy: neuropsychological test findings. Neuropsychologia, 33, 139–51. Loubinoux, I., Pariente, J., Boulanouar, K. et al. (2002). A single dose of the serotonin neurotransmission agonist paroxetine enhances motor output: double-blind, placebo-controlled, fMRI study in healthy subjects. Neuroimage, 15(1), 26–36. Lorenz, A.R. & Newman, J.P. (2002). Deficient response modulation and emotion processing in low-anxious Caucasian psychopathic offenders: results from a lexical decision task. Emotion, 2, 91–104. Miranda, R., Jr., Meyerson, L.A., Myers, R.R. & Lovallo, W.R. (2003). Altered affective modulation of the startle reflex in alcoholics with antisocial personality disorder. Alcohol and Clinical Experimental Research, 27, 1901–11. Mitchell, D.G., Colledge, E., Leonard, A. & Blair, R.J. (2002). Risky decisions and response reversal: is there evidence of orbitofrontal cortex dysfunction in psychopathic individuals? Neuropsychologia, 40(12), 2013–22. Mitterschiffthaler, M.T., Ettinger, U., Mehta, M.A. et al. (2006). Applications of functional magnetic resonance imaging in psychiatry. Journal of Magnetic Resonance Imaging, 23(6), 851–61. Moll, J., Zahn, R., de Oliveira-Souza, R. et al. (2005). The neural basis of human moral cognition. Perspectives. Nature Reviews Neuroscience, 6, 801–9. M¨uller, J.L., G¨anßbauer, S., Sommer, M. et al. (2007). Volumenverminderung und reduzierte emotionale Aktivierbarkeit des rechten superioren temporalen Gyrus bei krimineller Psychopathy. Untersuchungen mit Voxel –basierter Morphometrie und funktioneller Magnetresonanztomographie. Psychiatrische Praxis, 34(S1), 165–7. M¨uller, J.L., Sommer, M., Wagner, V. et al. (2003). Abnormalities in emotion processing within cortical and subcortical regions in criminal psychopaths: evidence from a functional magnetic resonance imaging study using pictures with emotional content. Biological Psychiatry, 54, 152–62. Newman, J.P. & Kosson, D.S. (1986). Passive avoidance learning in psychopathic and nonpsychopathic offenders. Journal of Abnormal Psychology, 95, 252–6. Ogawa, S., Lee, T.M., Stepnoski, R. et al. (2000). An approach to probe some neural systems interaction by functional MRI at neural time scale down to milliseconds. Proceedings of the National Academy of Science of the USA, 97, 11026–31. Ochsner, K.N. & Gross, J.J. (2005). The cognitive control of emotion. Trends in Cognitive Sciences, 9, 242–9. Paquette, V., Levesque, J., Mensour, B. et al. (2003). Change the mind and you change the brain: effects of cognitive-behavioral therapy on the neural correlates of spider phobia. Neuroimage, 18(2), 401–9. Patrick, C.J. (1994). Emotion and psychopathy: startling new insights. Psychophysiology, 31, 319–30. Patrick, C.J., Cuthbert, B.N. & Lang, P.J. (1994). Emotion in the criminal psychopath: fear image processing. Journal of Abnormal Psychology, 103, 523–34. Plewnia, C., Reimold, M., Najib, A. et al. (2007). Moderate therapeutic efficacy of PET-navigated repetitive transcranial magnetic stimulation against chronic tinnitus: a randomized, controlled pilot study. Journal of Neurology, Neurosurgery and Psychiatry, 78, 152–6. Raine, A., Ishikawa, S.S., Arce, E. et al. (2004). Hippocampal structural asymmetry in unsuccessful psychopaths. Biological Psychiatry, 55, 185–91. Raine, A., Lencz, T., Bihrle, S. et al. (2000). Reduced prefrontal gray matter volume and reduced autonomic activity in antisocial personality disorder. Archives of General Psychiatry, 57, 119–27. Raine A., Lencz, T., Taylor K. et al. (2003). Corpus callosum abnormalities in psychopathic antisocial individuals. Archives of General Psychiatry, 160, 1627–35. Schneider, F., Habel, U., Kessler, C. et al. (2000). Functional imaging of conditioned aversive emotional responses in antisocial personality disorder. Neuropsychobiology, 42,192–201. Schneider, K. (1948). Klinische Psychopathologie Thieme. Stuttgart.

NEUROIMAGING PERSPECTIVES

185

Simpson, J.R., Drevets, W.C., Snyder, A.Z. et al. (2001a). Emotion-induced changes in human medial prefrontal cortex: II. During anticipatory anxiety. Proceedings of the National Academy of Science of the USA, 98, 688–93. Simpson, J.R., Snyder, A.Z., Gusnard, D.A. & Raichle, M.E. (2001b). Emotion-induced changes in human medial prefrontal cortex: I. During cognitive task performance. Proceedings of the National Academy of Science of the USA, 98, 683–7. Sommer, M., Hajak, G., Dohnel, K. et al. (2006). Integration of emotion and cognition in patients with psychopathy. Progress in Brain Research, 156C, 457–66. Sommer, M., M¨uller, J., Weber, T. & Hajak, G. (2004). Die Bedeutung von Affekt und Emotion f¨ur psychiatrische Erkrankungen (The role of emotions in psychopathology). Psychiatrische Praxis, 31(Supplement 1), S64–S65. Weiskopf, N., Scharnowski, F., Veit, R. et al. (2004). Self-regulation of local brain activity using realtime functional magnetic resonance imaging (fMRI). Journal of Physiology, 98(4–6), 357–73. Yang, Y., Raine, A., Lencz, T. et al. (2005). Volume reduction in prefrontal gray matter in unsuccessful criminal psychopaths. Biological Psychiatry, 57, 1103–8.

CHAPTER 11

Electrophysiology Sabine C. Herpertz University of Rostock, Germany

The electrophysiological correlates of psychopathic disorders or in a broader sense antisocial spectrum behavior – including aggression, psychopathy, antisocial personality disorder and conduct disorder – have been the subject of a number of studies and theories since the 1960s. Links between antisocial spectrum behavior and electrophysiological measurements might help to understand temperamental characteristics of antisocial offenders and to elucidate relevant biological mechanisms underlying antisocial behavior. There is quite a large and convincing empirical database which provides evidence of abnormalities in autonomic and cortical physiology in subjects of different ages who repeatedly or habitually perform antisocial modes of behavior. However, clear interpretation of the literature has proved elusive in the face of a mixed pattern of results and many different theories that make related or competing predictions. In a first step, this chapter aims to summarize and review data collected for a number of different electrophysiological parameters which have been assessed in subjects of different age in the antisocial realm. Heterogeneity and inconsistencies in data will be elucidated with regard to several potential modulators: variety of diagnostic categories and behavioral constructs, differences in age, and heterogeneity in experimental paradigms (Lorber, 2004). In a second step, these data will be discussed in the context of different biosocial theories of the etiology of psychopathic disorders.

PERIPHERAL AUTONOMOUS PARAMETERS Of the many psychophysiological processes that have been investigated in psychopathic disorders, studies on autonomic functioning have been of particular interest over decades of research. Psychophysiological characteristics have been argued to ‘tap the dynamic interface between psychological processes and physiological processes’ (Raine, 2002, p. 314) and to particularly fit in the biopsychosocial models of the etiology of antisocial behavior. On the one hand, autonomic responses have significant heritability and establish one of the factors incorporated in models of temperament (Rothbart & Bates, 1998). On the other hand, psychosocial variables clearly modulate autonomic responses (see below). The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

188

VOLUME I: DIAGNOSIS AND TREATMENT

Heart Rate Heart rate is influenced through the sympathetic and parasympathetic branches of the autonomic nervous system with the parasympathetic system particularly controlling chronotropic, rate-related cardiac effects. Regarding brain correlates of task-induced cardiac changes, concurrent increases and decreases in the medial-prefrontal, insular and anterior cingulate cortices in addition to the amygdala–hippocampal complex have been reported (Critchley et al., 2003; Gianaros et al., 2004). In the realm of antisocial behavior, resting heart rate and phasic measurements to specific, well-defined events have been assessed.

Resting Heart Rate Low resting heart rate is a highly considered indicator of low autonomic arousal and is thought to be the best replicated biological correlate of antisocial behavior in child and adolescent samples (Raine, 2002). In a meta-analysis incorporating 29 independent samples of male and female children and adolescents with conduct problems, the average effect size was calculated at 0.56 (Raine, 1996). Different from most other biological markers, low heart rate is diagnostically specific of conduct disorder. In addition, it has been shown to have predictive value. While low resting heart rate in childhood has been shown to be a predictor of adolescent aggressive behavior (Raine, 1996) and a life course of persistent antisocial behavior (Moffitt & Caspi, 2001), high heart rate appears to protect against an unfavorable criminal development (Raine, Venables & Williams, 1995). Low heart rate may be at least partly genetically determined, because twin studies found substantial heritability for resting heart rate (Ditto, 1993; Thorell, de Faire & Fagrell, 1978) and as high father–son correlations were reported from high-risk families (Herpertz et al., 2007). However, low resting heart rate has not been found to be a stable characteristic of adult antisocial samples. Lorber’s meta-analysis (2004) across 17 studies did not confirm a clear association between low heart rate and psychopathy in adults, but they did find a correlation with adult aggression. Therefore, low heart rate may reflect high vagal or low noradrenergic functioning (see below) in high-aggressive subjects but not in the subgroup of psychopaths who have further temperamental characteristics in addition to an inclination towards aggressive behavior.

Heart Rate Responses Heart rate has been assessed in response to nonsignal, neutral stimuli (i.e., tones in an orienting paradigm) as well as to emotionally arousing stimuli (aversive tones in a startle paradigm, electric shocks and emotional pictures). On the whole, evidence of abnormal heart-rate reactivity is not very convincing. Although in children with conduct disorder higher heart-rate reactivity was demonstrated compared to age-matched controls, no significant data on heart-rate change to stimuli were found in adult subjects with psychopathy or antisocial personality disorder (Lorber, 2004).

Electrodermal Activity Electrodermal activity is assessed by means of the measurement of the electrical conductance of a small current passed through two electrodes. Electrodes can be placed at any place with a high density of sweat glands, usually the palmar hands (see Figure 11.1).

ELECTROPHYSIOLOGY

189

Mediale Phalanx

C7 Thenar

Hypothenar

C6

C8

Figure 11.1 Recording of electrodermal activity: typical electrode placements in the palmar hand (volar surfaces on medial phalanges as well as thenar and hypothenar eminences) Source: Cacioppo, J.T., Tassinary, L.G. & Bernston, G.G. (2000). Handbook of Psychophysiology, Figure 3, p. 2005. Reproduced by permission of Cambridge University Press

Electrodermal activity is exclusively controlled by the sympathetic nervous system. There are, for example, excitatory hypothalamic descending pathways controlling electrodermal activity and excitatory influences from the amygdala. Cortical pathways involve excitatory control from the premotor cortex and both excitatory and inhibitory influences originate in the frontal cortex. Skin conductance responses in an orienting task are associated with activity in the anterior cingulate and ventromedial prefrontal areas and therefore cortical areas of attentional processing (Williams et al., 2001), while responses elicited by fear faces were accompanied by left-sided amygdala activation together with medial frontal activity (Williams et al., 2004). Psychophysiological studies have been concerned with electrodermal responses to neutral (orienting) stimuli, to aversive, startling tones and to pleasant and unpleasant emotional pictures.

Resting Electrodermal Parameters In studies on antisocial behavior, skin conductance level and nonspecific skin conductance fluctuations have been evaluated as indicators of autonomic arousal. Significantly fewer skin conductance fluctuations have been reported from boys with conduct disorder (Herpertz et al., 2005) as well as from adult psychopaths (Hare, 1978; Raine, 1996), while results on skin conductance level are less consistent across studies. Nonspecific fluctuations may produce stronger support for skin conductance underarousal compared to skin conductance level, since the latter is more likely to be influenced by local conditions of the skin. Additional studies suggest that low skin conductance level and a low number of nonspecific fluctuations found in childhood may be a risk factor for criminal behavior in adulthood (Raine, 2002; Kruesi et al., 1992).

190

VOLUME I: DIAGNOSIS AND TREATMENT

Electrodermal Activity Changes Regarding phasic electrodermal activity, changes of electrical activity occur in response to novel stimuli, that is, the orienting response. Typical orienting stimuli are nonsignal, hardly motivating tones of 60 to 70 dB. Other studies made use of startling aversive nonconditioned stimuli of high intensity (90 to 110 dB). Orienting and startle responses reflect two different components of attentional capacity: while orienting reflects the allocation of attentional resources to a novel external stimulus and, thus, involves attentional engagement, startle represents the interruption of an ongoing activity (i.e., attentional disengagement) which is followed by avoidance or escape (Lang, Bradley & Cuthbert, 1997; Turpin, Schaefer & Buocsein, 1999). According to the defense cascade hypothesis (Lang et al., 1997), physiological responses to a threatening stimulus shift from selective attention/heightened vigilance expressed by heart-rate deceleration and skin conductance reactivity to a defensive action which, among others, is reflected in a priming of defensive reflexes, such as the eyeblink (see below). Concerning skin conductance orienting response, the majority of studies found evidence for an orienting deficit in children with conduct disorder (Herpertz et al., 2003) as well as in antisocial adults, at least if they additionally exhibited schizoid or schizotypal features (Raine & Venables, 1984). In addition, increased response habituation to a series of nonsignal tones has been reported consistently from a number of studies (Hare, 1978; Herpertz et al., 2003). The meta-analysis by Lorber (2004), based on 14 studies, reports a clear negative relationship between electrodermal activity (EDA) reactivity and psychopathy with studies included that used nonsignal or aversive stimuli. Hare (1978) reported smaller increases in skin conductance in anticipation of aversive stimuli in psychopathic subjects than in other inmates. Boys with conduct disorder (with and without a comorbid condition of attention deficit hyperactivity disorder) exhibited a decrement of the overall skin conductance response amplitude and stronger habituation compared to healthy controls and ADHD children to nonsignal orienting stimuli as well as in a startle paradigm (Herpertz et al., 2003). Since their autonomic responses were deficient to orienting and startling probes, CD children with and without ADHD appeared to have a deficit in allocating attention to nonsignal stimuli and in disengaging from an ongoing activity when faced with an aversive event. These data, however, suggest that deficient orienting does not result from a fundamental cognitive deficit, which should have been prominent in children with pure ADHD rather than in those with pure CD, but is more likely to indicate decreased attention to low-level, boring stimuli, an interpretation also suggested by Raine and Jones (1987). Fowles (2000) suggested that there may be two attentional deficits in antisocial individuals of any age: one deficit with respect to attending to neutral stimuli and another deficit with respect to the anticipation of aversive events. It has been repeatedly hypothesized that the presentation of negatively valenced stimuli would be associated with stronger effects in antisocial samples compared to normal controls than studies involving non-negative stimuli. However, no broad support can be found for this hypothesis (Lorber, 2004). The general autonomic hyporeactivity to pictorial stimuli of positive and neutral in addition to negative valence, that Herpertz and colleagues (2001a, 2005) found in samples of both adult psychopathic subjects and children diagnosed with conduct disorder may rather reflect a deficit in associative processing systems that respond more to complex cueing contexts than to specifically aversive cues.

ELECTROPHYSIOLOGY

191

Electromyographic Responses as Part of Defensive Reflexes In contrast to electrodermal activity, which reflects the arousal dimension of emotion (activation vs. calmness), the electromyographic blink response to a sudden, intense acoustic probe is primarily considered to be a measure of valence (pleasure vs. aversion). In addition to attentuated autonomic reactivity, an absence of the typical augmentation of startle response during exposure to aversive stimuli was reported in criminal psychopaths (Patrick et al., 1993, 1994). The startle probe is an aversive stimulus that elicits a defensive withdrawal response, one component of which is the eyeblink reflex. The blink or startle reflex is one of the first, fastest and most stable elements in the startle sequence namely the sudden closure of the eyelids 30 to 50 ms after the onset of the abrupt acoustic stimulus, assessed by means of the electromyographic measurement of the orbicularis oculi muscle directly beneath the eye (see Figure 11.2). Lang and colleagues (1990) explained the affect–startle effect in terms of synergistic response matching: unpleasant slides prompt a state of defensive readiness that is synchronous with the response to the startle probe, producing a larger startle reflex. A sample of convicted male sexual offenders scoring high on the factor 1 of the Psychopathy Checklist showed no potentiation of the startle response while viewing aversive slides. These findings suggest that psychopaths show an incapacity of an aversive affective state to prime aversion actions, namely to increase the strength of a defensive reflex ( et al., 1993). The lack of startle potentiation to aversive slides was specifically related to the emotional detachment component of psychopathy and not to the antisocial behavior component. Herpertz and colleagues (2001b) found an abnormal startle response pattern not only in the context of fear-related stimuli, but in relation to any kind of emotional stimulus, whether it was related to feelings of fear or threat or to sympathy with others. In their study, psychopaths not only showed an absence of startle potentiation when viewing aversive slides, but psychopaths were also characterized by deficient startle

musculus corrugator supercilii

electrode placement

musculus orbicularis oculi

Figure 11.2 Recording of the eyeblink reflex: typical electrode placements beneath the eye

192

VOLUME I: DIAGNOSIS AND TREATMENT

inhibition in reaction to stimuli inductive of an appetitive response. On the whole, startle data suggest a prominent fearlessness to aversive, frightening events, but beyond that, also a general deficit of psychopathic individuals in processing affective information. From the neurobiological perspective, these data suggest that psychopaths might exhibit a deficit in amygdala activation known to modulate the startle reflex. Van Goozen et al. (2004) performed a startle paradigm in children with disruptive behavior disorder, a diagnostic category, which includes oppositional defiant as well conduct disorders. Although these patients showed a similar linear relationship between slide valence and startle magnitude as the control children, the startle-elicited blinks were significantly smaller for all slide categories in children with disruptive behavior disorder than in healthy age-matched controls. Since larger startle responses have been shown to be linked to fear states (Greenwald, Cook III & Lang, 1989), the authors interpret their findings as supporting the fearlessness theory of antisocial behavior (see below).

ELECTROENCEPHALOGRAPHIC POTENTIALS Attempts to correlate specific electroencephalographic (EEG) abnormalities with aspects of behaviors have failed to produce conclusive results. However, the finding of frontal EEG slowing in waking psychopaths is the most robust finding and has been interpreted as reflecting cortical immaturity, cortical underarousal and an intense need for stimulus seeking; on the contrary, regression analyses found increased frontal left-hemisphere EEG activation to be associated with a decreased likelihood of psychopathy and antisocial personality disorder (Deckel, Hesselbrock & Bauer, 1996). Recently, quantitative analyses of EEG activity in homicidal men with antisocial personality disorder indicated an overall reduction of alpha power, together with a bilateral increase in occipital delta and theta power again supporting the theory of cortical underarousal and decreased daytime vigilance in antisocial individuals (Lindberg et al., 2005). Other researchers have investigated event-related potentials in response to visual or acoustic stimuli in psychopaths, but failed to demonstrate indicators of low cortical arousal (N100) or of an incapability to attend attentional resources to task-relevant events in a classical oddball task (P300) (Dolan, 1994). However, concerning the frontal P300, reduced amplitudes have been found in conduct disorder and antisocial personalities in early adulthood (Costa et al., 2000), suggesting that the P300 decrement might reflect the absence of normal maturation in frontal generators of the P300 amplitude in adolescence (Bauer & Hesselbrock, 2003). In addition, adult psychopaths show marked reduction in the frontal N275 eventrelated component during a Go/NoGo task, which is assumed to reflect the neural activity involved in response inhibition (Kiehl et al., 2000). Therefore, adult psychopathic subjects may have frontal deficits which interact with the capability to inhibit responses more than with attentional functioning in general. In addition, large contingent negative variation (CNV) during forewarned reaction time tasks in psychopathic offenders support the hypothesis that psychopaths are proficient at focusing attention on events that interest them (Forth & Hare, 1989). There have been some findings concerning the processing of emotional stimuli in psychopaths. Behavioral results suggest that psychopaths exhibit deficiencies in the detection of emotional faces (Kosson et al., 2002). This emotional deficit was neurophysiologically indexed by a decreased N300 component while processing faces of positive and negative valence (Campalla, Vanhoolandt & Philippot, 2005). This N300 component is thought to be particularly sensitive to affective features of stimuli.

ELECTROPHYSIOLOGY

193

Investigations on psychopathy and antisocial personality disorder may be confounded with the personality dimension of impulsivity that occurs in the majority of psychopaths and even contributes to Hare’s diagnostic criteria of psychopathy. However, the concept of impulsivity is rather heterogeneous. Within the concept of psychopathy, impulsivity is conceptualized as a lack of responsibility, deferred gratification pattern and planning behavior that increases the risk of non-premeditated, ‘impulsive’ aggression. This pattern of impulsive behavior appears to be different from ‘impulsive’, reactive aggression that results from intense feelings of anger in the context of frustration or rejection, as found in the concept of the impulsive subtype of the ICD-10 emotional unstable personality disorder. Violent behavior associated with anger and emotional aggression is thought to have different psychophysiological underpinnings from those of psychopaths (Scarpa & Raine, 1997) with, for example, an increment rather than a decrement of left frontal activity (Rybak et al., 2006) and with normal autonomous responses (Herpertz et al., 2001b). Barratt and colleagues (1997) follow the approach of differentiating subtypes of offenders as a function of the kind of aggressive behavior they display, that is, whether they show impulsive or premeditated aggression. They found abnormal P300 evoked potentials only in the group of antisocial offenders with impulsive but not in the one with premeditated aggression and they could provide evidence that electrical potentials were normalized with phenytoin at the same time their impulsive aggression improved. In summary, the role of impulsivity in biological underpinnings of antisocial behavior is far from clear and has to be further focused on in the future.

THEORIES EXPLAINING HOW ELECTROPHYSIOLOGICAL ABNORMALITIES PREDISPOSE TO ANTISOCIAL BEHAVIOR Data provide strong support for the significance of psychophysiological processes underlying antisocial and psychopathic behavior in both children and adolescents. Genes are known to contribute to characteristics of psychophysiological functioning, and autonomic responses have been suggested to act as biological mediators through which genetic influences operate on antisocial behavior (Raine, 2002). There is some evidence from the comparison of monozygotic and dizygotic twin pairs that genes may influence electrodermal activity. Crider and colleagues (2004) recently revealed heritabilities between 0.40 and 0.50 for phasic electrodermal activity measures. They replicated earlier findings by Lykken and colleagues (1988), who noticed similar additive genetic influences on initial skin conductance response (SCR) as well as habituation speed to a series of loud tones. However, autonomic responsiveness is also sensitive to environmental processes, e.g. by psychic trauma in the negative direction (Carrey et al., 1995) or by educational enrichment in the positive direction (Raine et al., 2001). However, what is less clear are the mechanisms of action that underlie the association between psychophysiological abnormalities and antisocial behavior.

Theory of Low Arousal and Sensation Seeking Reduced electrodermal and cardiovascular arousal functioning has been interpreted in different ways. The sensation or stimulation-seeking theory argues that low arousal is an aversive psychophysiological state that is compensated for by seeking stimulation, thrill and risk (Zuckerman, 1974). According to this theory, antisocial behavior is viewed as a form of stimulation seeking, in that committing crimes could be stimulating for some

194

VOLUME I: DIAGNOSIS AND TREATMENT

individuals. Another theory has linked reduced arousal levels with poor conditionability followed by poor socialization to punishment (Eysenck, 1987; Raine, 2002). Consistent with this view, Flor and colleagues (2002) found that psychopaths failed to exhibit a conditioned response although they showed no deficits in information processing in general. Data from this study were based on peripheral measurements and event-related potential data. Furthermore, autonomic underarousal may reflect a disinhibited temperament, predisposing to exploratory behavior already in childhood and aggressive, antisocial behavior through life. In accordance with this assumption, Caspi and colleagues (1996) provided some support that children characterized by an undercontrolled temperament at age three were more likely to fulfill the criteria of conduct disorder at age 15 years. Underarousal in subjects prone to antisocial and violent behavior is thought to reflect reduced noradrenergic functioning (Raine, 2002), although increased vagal tone cannot be completely excluded to underlie the heart rate – antisocial linkage. Accordingly Rogeness, Cepeda and Macedo (1990) found reduced heart rate and reduced levels of noradrenaline in children diagnosed with conduct disorder. Raine (1993) published a meta-analysis with a significantly negative effect size between reduced central measures of norepinephrine and increased antisocial behavior.

Theory of Fearlessness According to this theory, low levels of arousal indicated by low heart rate and low electrodermal resting activity as well as low autonomic responses to aversive stimuli are markers of low levels of fear. A particular inclination towards fearlessness is also supported by the absence of startle modulation in psychopaths and by lower magnitudes of startle responses in children with disruptive behaviors. Fearlessness is thought to result from deficient emotional learning, poor conditioning processes, in particular, and may lead to deficient avoidance behavior and a lack of conscience development (Raine, 1993). Similar to the hypoarousal theory, fearlessness is thought to rely on psychopaths’ weak response to aversive unconditioned stimuli and their incapability to establish an association between conditioned and unconditioned stimuli. Deficient conditioning may lead to an inability to learn from punishment and to develop passive avoidance learning. In addition, low experiences of fear would predispose to antisocial behavior inasmuch as such behavior requires a degree of fearlessness to execute (Raine, 1996). Both theories, the one of disinhibited, sensation-seeking temperament and the one of fearlessness may be complementary, because reduced autonomic arousal may predispose to antisocial behavior and crime because it produces fearlessness and because it encourages exploratory and antisocial sensation seeking (Raine, 2002). Other electrophysiological findings, such as those by Campalla and colleagues (2005) or Herpertz and colleagues (2001b), suggest that abnormal emotional processing in psychopaths may not be restricted to fear, but may include negative and even positive emotions in general. They therefore claim emotional detachment, instead of a specific lack of fear, to be the emotional characteristic of psychopathy.

Frontal Dysfunction Reduced skin conductance orienting has been interpreted with respect to a prefrontal dysfunction hypothesis of antisocial behavior (Raine, 2002), which is also supported by data from lesion studies (Damasio, Tranel & Damasio, 1990). Damage to prefrontal regions

ELECTROPHYSIOLOGY

195

was shown to lead to psychophysiological abnormalities, for example, reduced orienting (Damasio et al., 1990) and the prefrontal cortex is known to be involved in arousal regulation and stress responsivity. Data indicating prefrontal cortex dysfunction may be particularly interesting from a developmental process, because the prefrontal cortex is the latest structure to mature up into the early twenties or even the thirties. Therefore, late-maturing prefrontal cortex may contribute to a cessation of antisocial behavior in adulthood. Theories centered on prefrontal dysfunction in the sense of attentional deficits and other fundamental deficits in processing external information are less likely to sufficiently explain antisocial behavior, since even stronger attentional and executive deficiencies are found in ADHD subjects who exhibit quite a normal psychophysiological response pattern (Herpertz et al., 2001b). There is no doubt, however, that prefrontal areas – in addition to the amygdala – play a central role in processing autonomic responses. One neuroimaging study assessed neuronal correlates of cardiac and electrodermal autonomic responses within one design, and suggests neuroanatomical differences in cortical representations between the two autonomic measurements. This study, performed by Raine et al. (2000), found a significant association between reduced prefrontal cortex volume evaluated by means of magnetic resonance imaging, and fewer orienting responses in healthy subjects and they found that prefrontal gray matter deficits were linked to electrodermal, but not to cardiovascular deficits in a stressor task within a group of subjects with antisocial personalities. To be more specific about which prefrontal areas are dysfunctional in psychopaths, failure of conditional learning tends to suggest deficits in orbitofrontal areas, which are closely interconnected with extensive amygdala projections, than in the more dorsally located cortical areas. This assumption is supported by increasing neuroimaging data collected in psychopaths and antisocial personalities. Hemispheric dominance of brain dysfunction has also been studied in psychopathic disorders, particularly with regard to emotional processing. These data suggest that psychopaths compared to nonpsychopathic individuals rely less on connotative-emotional processes based in the right hemisphere than on denotative-linguistic processes based in the left hemisphere. In a tachistoscopic task, psychopaths showed neither higher accuracy nor lower reaction times when processing negative emotional words in the left instead of the right visual field, a finding replicated several times in normal controls (Silberman & Weingartner, 1986). These findings suggest impairment in right-hemisphere function which is thought to be specialized in decoding emotional stimuli by actually felt emotional reactions to the stimuli. The conclusion that right-hemisphere functioning in particular is reduced in antisocial subjects, however, may be premature, because superior right-hemispheric functioning has been reported from our studies.

CONCLUSIONS AND PERSPECTIVES FOR THE FUTURE With heart rate and electrodermal activity significant autonomic markers of antisocial spectrum disorders are available. While low resting heart rate appears to be the best replicated and most easily measured parameter in child and adolescent samples of antisocial behavior, abnormalities of electrodermal activity in resting states as well as in response to stimuli are suggested to be rather stable in antisocial samples of any age. Psychopathy appears to be more tied to electrodermal than to cardiovascular activity. In addition, a lack of emotional modulation of the startle (blink) reflex represents a characteristic of psychopathic individuals

196

VOLUME I: DIAGNOSIS AND TREATMENT

which is more related to emotional detachment than to antisocial behavior itself. The majority of studies, which have been published up to now, were conducted exclusively with male children and adults, so that little knowledge exists on the influence gender might exert on electrophysiological processes. Psychophysiological markers appear to indicate a risk for antisocial behavior in general, but it is far from clear which parameters might predict the transition from childhood conduct problems to adult psychopathy and which might precede other forms of aggressive or antisocial behavior. Longitudinal or cross-sectional studies with multiple age cohorts which combine the assessment of both aggressive/antisocial behavior and autonomic patterns at several points in time are needed for clarifying these important research questions. Psychophysiological research of antisocial behavior should not be restricted to identifying risk and protective factors but should also consider prevention implications. Raine and colleagues (2001) provided evidence that environmental enrichment at ages three to five years resulted in an increment of autonomic arousal in children at age 11 years. Therefore, early interventions of high-risk children may provide the most effective way of reversing or compensating the biological deficits that predispose to an antisocial, psychopathic development.

REFERENCES Barratt, E.S., Stanford, M.S., Felthous, A.R. & Kent, T.A. (1997). The effects of phenytoin on impulsive and premediated aggression: a controlled study. Journal of Clinical Psychopharmacology, 17, 341–9. Bauer, L.O. & Hesselbork, V.M. (2003). Brain maturation and subtypes of conduct disorder: interactive effects on P300 amplitude and topography in male adolescents. Journal of the American Academy of Child and Adolescence Psychiatry, 42, 106–15. Campalla, S., Vanhoolandt, M.E. & Philippot, P. (2005). Emotional deficit in subjects with psychopathic tendencies as assessed by the minnesota multiphasic personality inventory-2, an eventrelated potentials study. Neuroscience Letters, 373, 26–31. Carrey, N.J., Butter, H.J., Persinger, M.A., & Bialik, R.J. (1995). Physiological and cognitive correlates of child abuse. Journal of the American Academy of Child and Adolescence Psychiatry, 34, 1067– 75. Caspi, A., Moffitt, T.E., Newman, D.L. & Dilva, A. (1996). Behavioral observations at age 3 years predict adult psychiatric disorders. Archives of General Psychiatry, 53,1033–9. Costa, L., Bauer, L., Kuperman, S. et al. (2000). Frontal P3000 decrements, alcohol dependence, and antisocial personality disorder. Biological Psychiatry, 47, 1064–71. Crider, A., Kremen, W.S., Xian, H. et al. (2004). Stability, consistency, and heritability of electrodermal response lability in middle-aged male twins. Psychophysiology, 41, 501–9. Critchley, H.D., Mathias, C.J., Josephs, O. et al. (2003). Human cingulate cortex and autonomic control, converging neuroimaging and clinical evidence. Brain, 126, 2139–52. Damasio, A.R., Tranel, D. & Damasio, H. (1990). Individuals with sociopathic behavior caused by frontal damage fail to respond autonomically to social stimuli. Behavioral Brain Research, 41, 81–94. Deckel, A.W., Hesselbrock, V. & Bauer, L. (1996). Antisocial personality disorder, childhood delinquency, and frontal brain functioning: EEG and neuropsychological findings. Journal of Clinical Psychology, 52, 639–50. Ditto, B. (1993). Familial influences on heart rate, blood pressure, and selfreport anxiety responses to stress, results from 100 twin pairs. Psychophysiology, 30, 635–45. Dolan, M. (1994). Psychopathy – a neurobiological perspective. British Journal of Psychiatry, 165, 151–9.

ELECTROPHYSIOLOGY

197

Eysenck, H.J. (1987). Comments on ‘The orthogonality of extraversion and neuroticism scales’. Psychology Reports, 61, 50. Flor, H., Birbaumer, N., Herman, C. et al. (2002). Aversive pavlovian conditioning in psychopaths, peripheral and central correlates. Psychophysiology, 39, 505–18. Fowles, D.C. (2000). Electrodermal hyporeactivity and antisocial behavior: does anxiety mediate the relationship? Journal of Affective Disorders, 61, 177–89. Forth, A.E. & Hare R.D. (1989). The contingent negative variation in psychopaths. Psychophysiology, 26, 676–82. Gianaros, P.J., Van Der Veen, F.M. & Jennings, J.R. (2004). Regional cerebral blood flow correlates with heart period and high-frequency heart period variability during working-memory tasks: implications for the cortical and subcortical regulation of cardic autonomic activity. Psychophysiology, 41, 521–30. Greenwald, M.K., Cook III, E.W. & Lang, P.J. (1989). Affective judgment and psychophysiological response, dimensional covariation in the evaluation of pictorial stimuli. Journal of Psychophysiology, 3, 51–64. Hare, R.D. (1978). Electrodermal and cardiovascular correlates of psychopathy. In R.D. Hare & D. Schalling (eds.), Psychopathic Behavior: Approaches to Research. New York: John Wiley & Sons, Inc. Herpertz, S.C., Mueller, B., Wenning, B. et al. (2003). Autonomic responses in boys with externalizing disorders. Journal of Neural Transmission, 110, 1181–95. Herpertz, S.C., Mueller, B., Qunaibi, M. et al. (2005). Emotional responses in boys with conduct disorder. American Journal of Psychiatry, 162, 1100–7. Herpertz, S.C., Vloet, T., Mueller, M. et al.. (2007). Similar autonomic responsivity in boys with conduct disorder and their fathers. American Academy of Child Adolescence Psychiatry, 46, 535– 44. Herpertz, S.C., Wenning, B., Mueller, B. et al. (2001a). Psychophysiological responses in ADHD children with and without conduct disorder – implications for adult antisocial behavior. Journal of the American Academy of Child Adolescence Psychiatry, 40, 1222–30. Herpertz, S.C., Werth, U., Lukas, G. et al. (2001b). Emotion in criminal offenders with psychopathy and borderline personality disorder. Archives of General Psychiatry, 58, 737–45. Kiehl, K.A., Smith, A.M., Hare, R.D. & Liddle, P.F. (2000). An event-related potential investigation of response inhibition in schizophrenia and psychopathy. Biological Psychiatry, 48, 210–21. Kosson, D.S., Suchy, Y., Mayer, A.R. & Libby, J. (2002). Facial affect recognition in criminal psychopaths. Emotion, 2, 398–411. Kruesi, M.J., Hibbs, E.D., Zahn, T.P. et al. (1992). A 2-year prospective follow-up study of children and adolescents with disruptive behavior disorders. Prediction by cerebrospinal fluid 5hydroxindoleacetic acid, homovanillic acid, and autonomic measures? Archives of General Psychiatry, 49, 429–35. Lang, P.J., Bradley, M.M. & Cuthbart, B.N. (1997). Motivated attention, affect, activation, and action. In P. Lang, R. Simons & M. Balaban (eds.), Attention and Orienting, Sensory and Motivations Processes (pp. 97–136). New York: Erlbaum. Lang, S.F., Nelson, C.A. & Collins, P.F. (1990). Event-related potentials to emotional and neutral stimuli. Journal of Clinical and Experimental Neuropsychology, 12, 946–58. Lindberg, N., Taini, P., Virkkunen, M. et al. (2005). Quantitative electroencephalographic measures in homicidal men with antisocial personality disorder. Psychiatry Research, 136, 7–15. Lorber, M.F. (2004). Psychophysiology of aggression, psychopathy, and conduct problems, a metaanalysis. Psychological Bulletin, 130, 531–52. Lykken, D.T., Iacono, K.H., Haroian, K. et al. (1988). Habituation of the skin conductance response to strong stimuli, a twin study. Psychophysiology, 25, 849–54. Moffitt, T.E. & Caspi, A. (2001). Childhood predictors differentiate life-course persistent and adolescence-limited antisocial pathways among males and females. Develpmental Psychopathology, 13, 355–75. Patrick, C.J., Bradley, M.M. & Lang, P.J. (1993). Emotion in the criminal psychopath, startle reflex modulation. Journal of Abnormal Psychology, 102, 82–92. Patrick, C.J., Cuthbert, B.N. & Lang, P.J. (1994). Emotion in the criminal psychopath, fear image processing. Journal of Abnormal Psychology, 103, 523–34.

198

VOLUME I: DIAGNOSIS AND TREATMENT

Raine, A. (1993). Psychophysiology. In A. Raine (ed.), The Psychopathology of Crime (pp. 157– 90).San Diego: Academic Press. Raine, A. (1996). Autonomic nervous system factors underlying disinhibited, antisocial, and violent behavior. Annals of the New York Academy of Science, 794, 46–59. Raine, A. (2002). Annotation: the role of prefrontal deficits, low autonomic arousal, and early health factors in the development of antisocial and aggressive behavior in children. Journal of Child Psychology and Psychiatry, 43, 417–34. Raine, A. & Jones, F. (1987). Attention, autonomic arousal, and personality in behaviorally disordered children. Journal of Abnormal Child Psychology, 15, 583–99. Raine, A., Lencz, T., Bihrle, S. et al. (2000). Reduced prefromtal grey matter volume and reduced autonomic activity in antisocial personality disorder. Archives of General Psychiatry, 57, 119–27. Raine, A. & Venables, P.H. (1984). Electrodermal responding, antisocial behavior, and schizoid tendencies in adolescence. Psychophysiology, 21, 424–33. Raine, A., Venables, P.H., Dalais, C. et al. (2001). Early educational and health enrichment at age 3–5 years is associated with increased autonomic and central nervous system arousal and orienting at age 11 years, evidence from the Mauritius Child Health Project. Psychophysiology, 38, 254–66. Raine, A., Venables, P.H. & Williams, M. (1995). High autonomic arousal and electrodermal orienting at age 15 years as protective factors against criminal behavior at age 29 years. American Journal of Psychiatry, 152, 1595–600. Rogeness, G.A., Cepeda, C. & Macedo, C.A. (1990). Differences in heart rate and blood pressure in children with conduct disorder, major depression, and separation anxiety. Psychiatry Research, 33, 199–206. Rothbart, M.K. & Bates, J.E. (1998). Temperament. In W. Damon & N. Eisenberg (eds.), Handbook of Child Psychology. Social Emotional and Personality Development (Volume 3, pp. 105–76). New York: John Wiley & Sons, Inc. Rybak, M., Crayton, J.W., Young, I.J. et al. (2006). Frontal alpha power asymmetry in aggressive children and adolescents with mood and disrutpive behavior disorders. Clincal EEG and Neuroscience, 37, 16–24. Scarpa, A. & Raine, A. (1997). Psychophysiology of anger and violent behavior. Psychiatric Clinics of North America, 20, 375–94. Silberman, E.K. & Weingartner, H. (1986). Hemispheric lateralization of functions related to emotion. Brain and Cognition, 5, 322–53. Thorell, T., de Faire, U. & Fagrell, B. (1978). Cardiovascular reactions during psychiatric interview. A non-invasive study on a twin sample. Journal of Human Stress, 4, 27–31. Turpin, G., Schaefer, F. & Boucsein, W. (1999). Effects of stimulus intensity, risetime, and duration on autonomic and behavioral responding: implications for the differentiation of orienting, startle, and defense responses. Psychophysiology, 36, 453–63. van Goozen, S.H., Snoek, H., Matthys, W. et al. (2004). Evidence of fearlessness in behaviourally disordered children, a study on startle refelx modulation. Journal of Child Psychology and Psychiatry, 45, 884–92. Williams, L.M., Brown, K.J., Das, P. et al. (2004). The dynamics of cortico-amygdala and autonomic activity over the experimental time course of fear perception. Journal of Brain Research and Cognition, 21, 114–23. Williams, L.M., Phillips, M.L., Brammer, M.J. et al. (2001). Arousal dissociates amygdala and hippocampal fear respondes, evidence from simultaneous fMRI and skin conductance recording. Neuroimage, 14, 1070–9. Zuckerman, M., Murtaugh, T. & Siegel. J. (1974). Sensation seeking and cortical augmentingreducing. Psychophysiology, 11, 535–42.

CHAPTER 12

The Role of ADHD in the Etiology and Outcome of Antisocial Behavior and Psychopathy Beate Herpertz-Dahlmann and Kerstin Konrad Technical University of Aachen, Germany

and Sabine C. Herpertz University of Rostock, Germany

INTRODUCTION Attention deficit hyperactivity disorder (ADHD) and conduct disorder (CD) represent two of the most common neurobehavioral disorders of childhood, affecting children persistently through school and into adulthood, albeit with age- and gender-related changes in its manifestations. Both disorders co-occur greater than would be expected by chance in both clinical and epidemiological samples. The comorbid condition impacts significantly on the treatment outcome and long-term prognosis of the affected patients. Despite the high comorbidity rate both disorders can be reliably diagnosed and differentiated according to DSM IV (American Psychiatric Association, 1994) and ICD-10 (World Health Organization, 1991). In addition to some shared neurocognitive, psychophysiological and structural and functional brain abnormalities, there are also some syndrome-specific profiles associated with either ADHD or CD only. In this chapter, we will first summarize diagnostic criteria and epidemiological data as well as data on the symptomatology and course of antisocial behavior, before describing the role of ADHD in the etiology and pathogenesis of antisocial behavior. Particular emphasis will be given to recent genetic findings and the effects of other biological risk factors. Finally, data from neurocognitive, neuroimaging and psychophysiological studies will be discussed in reference to comorbidity and etiological models of antisocial behavior.

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

200

VOLUME I: DIAGNOSIS AND TREATMENT

DEFINITION AND CLASSIFICATION The term ‘antisocial behavior’ is used to describe a way of acting, which deviates from generally accepted social norms, whereas the term ‘delinquency’ is used to describe breaches of law. In international classification systems like ICD-10 and DSM-IV antisocial behavior characterizes different mental disorders, primarily conduct disorders of childhood and adolescence and antisocial personality disorder (ASPD) of adulthood. In ICD-10 six types of conduct disorder (CD) can be distinguished. These are ‘conduct disorders confined to the family context’, ‘socialized conduct disorder’, ‘unsocialized conduct disorder’, ‘oppositional defiant disorder’ (ODD) and two remaining categories for ‘other’ and ‘unspecified conduct disorder’. ‘Conduct disorders confined to the family context’ and ‘oppositional defiant disorder’ mostly occur in younger children and may have a better prognosis (Herpertz-Dahlmann, 2001). ‘Socialized conduct disorder’ and ‘unsocialized conduct disorder’ are determined by the nature of the child’s or adolescent’s bonding, rather than whether the antisocial behavior occurs alone or in a group. In DSM-IV three diagnoses for antisocial behavior in childhood and adolescence can be differentiated: 1. conduct disorder; 2. oppositional defiant disorder; and 3. disruptive behavior disorder not otherwise specified. Oppositional defiant disorder usually becomes evident before the age of eight and mostly emerges in the home setting. In several children oppositional defiant disorder is a developmental antecedent to conduct disorder. For a diagnosis of CD in DSM-IV four general criteria have to be fulfilled from which three must be present in the past 12 months, one must be present in the past six months:

r aggression to people or animals (like bullying or threatening); r destruction of property; r deceitfulness or theft; r severe violation of rules (like staying out at night, skipping school). For a more extensive review see Barrickman (2003). DSM-IV also differentiates between two types of antisocial behavior based on age at onset, which is the childhood-onset type (symptoms beginning before the age of 10 years) and the adolescent-onset type starting at or after age 10 (see below). The term psychopathy is not a synonym for either a diagnosis of conduct disorder or for a diagnosis of adult antisocial personality disorder. It should rather be seen as an extension for both of them (Blair, 2003). The term was defined by Cleckley (1941) and refers to an additional emotional impairment, particularly a diminished capacity for remorse, callousness, emotional detachment and lack of empathy (for a more extensive description see Chapter 2 in this book). These characteristics in adults have proven to describe a severe, chronic and difficult-to-treat type of antisocial behavior. The current diagnostic criteria for attention deficit hyperactivity disorder according to DSM-IV imply six or more symptoms of inattention and hyperactivity/impulsivity, an onset

ADHD AND ANTISOCIAL BEHAVIOR AND PSYCHOPATHY

201

of symptoms before age seven, a pervasiveness of symptoms (that is symptoms are evident in more than one single setting) and a clinically significant impairment in social/academic or occupational functioning. DSM-IV also discriminates between three subtypes: in the combined type both symptoms of inattention and hyperactivity/impulsivity are prominent; in the predominantly inattentive subtype only symptoms of inattention are met; while in the predominantly hyperactive-impulsive type criteria for inattention are not fulfilled. Diagnostic criteria of hyperkinetic disorder (HD) according to ICD-10 differ in important ways. Excessive talking is one of the items for hyperactivity in DSM-IV, but considered a manifestation of impulsiveness in ICD-10. In addition, DSM-IV and ICD-10 have different requirements for pervasiveness. According to the criteria for HD in ICD-10 inattentive/hyperactive symptoms must be evident at home and at school, whereas DSM-IV is less specific in defining the setting, and criteria have to be met either at home or at school (Schachar & Sergeant, 2002). Additionally, subtypes differ between DSM-IV and ICD-10: in ICD-10 a child or an adolescent who is solely inattentive or exclusively hyperactive/impulsive would not be diagnosed as hyperkinetic in contrast to DSM-IV. Both classification systems have in common that they are not adjusted to girls and very young children (Schachar & Sergeant, 2002). Several years ago there was an extensive debate as to whether conduct disorders and attention deficit hyperactivity disorder truly constitute separate nosological entities. The overlap of these disorders in both clinical and epidemiological studies is so far above the level of chance that ICD-10 included a category of hyperactive conduct disorder (F 90.1). The broad majority of children under the age of 12 who meet the criteria for conduct disorder also meet the criteria for ADHD (Reeves et al., 1987). Klein et al. (1997), who sought to find a group of children with pure conduct disorder for a research study, discovered that 69 % of the conduct disorder group concurrently had ADHD. In our own study on autonomic reactivity in boys with conduct disorder (Herpertz et al., 2005) only 13 % met criteria for pure CD. In sum there are rather few cases of pure ODD or CD in preadolescence while in adolescent populations pure CD is more common (Pliszka, Carlson & Swanson, 1999).

EPIDEMIOLOGY In the United States and Western Europe general population prevalence rates for conduct disorder are approximately 10 % (Lahey et al., 1999). Antisocial personality disorder is apparent in 3–7 % of the general male population. While one-quarter to one-third of individuals with antisocial personality disorder also meets the criteria for psychopathy (Lorber, 2004), prevalence rates of psychopathy in children with conduct disorder are not clear. As a result of different classification criteria in DSM-IV and ICD-10 prevalence rates of ADHD and HD vary. While ADHD is diagnosed in 5–10 % of the general population, HD is observed in only 1–3 %. Adults with ASPD typically have a history of aggressive and disruptive behavior and a failure to conform to social norms during childhood or adolescence. Approximately 50 % of adults with a diagnosis of ASPD already fulfilled diagnostic criteria of CD before age 18 (Barrickman, 2003). On the other hand about one-quarter to one-third of CD cases will develop ASPD as adults (Robins, Tipp & McEvoy 1991; Hechtman & Ozonoff, 1994). In a recent study by Simonoff et al. (2004) 39 % of male and 19 % of female twins treated for antisocial behavior in childhood at the Maudsley Hospital, London between 1948 and 1982

202

VOLUME I: DIAGNOSIS AND TREATMENT

were diagnosed with ASPD at 22 to 30 years of age, and 18.3 % had committed violent offenses. In the NIMH Epidemiological Catchment Area project the rate of subsequent antisocial personality disorder for children with eight or more CD symptoms was 71 % if symptoms appeared before the age of 6, 53 % if they appeared between the ages of 6 and 12, and 48 % if they appeared after 12 (Robins, Tipp & McEvoy, 1991). Hechtman & Offord (1994) emphasized that, in addition to criminality and mental illness, early disorders of conduct also predict ‘widespread social malfunction, as seen in high rates of divorce and separation, poor work history, and unsatisfactory social relationships’. In a prospective study of 89 hyperactive boys diagnosed between the ages of 6 and 12 years and 87 normal controls official arrest records were obtained for the time of adolescence and young adulthood. Hyperactive individuals had significantly higher juvenile (46 % versus 11 %) and adult (21 % versus 1 %) arrest rates. Juvenile and adult incarceration rates were also significantly higher (22 % versus 1 % and 12 % versus 1 %, respectively) (Satterfield & Schell, 1997). In a more recent young adult follow-up of 147 hyperactive children 40 % of the hyperactive group had been arrested at least two or more times compared to 12 % of a normal control group (Barkley et al., 2004).

SYMPTOMATOLOGY AND COURSE OF ANTISOCIAL BEHAVIOR IN CHILDHOOD AND ADOLESCENCE Numerous prospective studies have demonstrated different trajectories to different types of later antisocial behavior. Most authors and researchers agree on two distinct pathways: the first one emerging early in childhood (often already beginning in preschool years) called early starter and the second one beginning in late childhood or early adolescence, called late starter. Both types already delineated in the DSM-IV (see above) have been followed up by the research group of Moffitt and coworkers in the so-called Dunedin Study. The Moffitt group (research teams from the Institute of Psychiatry, King’s College, London, the Department of Psychology, University of Wisconsin, Madison, USA and the Dunedin School of Medicine, Otago, New Zealand) followed up a whole birth cohort of 1037 children born in 1972 from age 3 to age 18 and then again 96 % of the original sample at age 26 (Moffitt et al., 2002). They complemented the developmental taxonomy by describing two subtypes: (a) the life-course persistent offenders starting early in childhood (early starter) with high levels of aggression throughout development and continuation of violence in adulthood in contrast to (b) adolescent-limited offenders in whom antisocial behavior was limited to the life period of puberty and late adolescence (Moffit 1993; Moffit & Caspi, 2001). Children with early beginning of misconduct and aggression tended to demonstrate more pervasive and crueler antisocial behavior, for example, being physically cruel to animals and other children or causing harm by serious physical fights. At the age of 26 the childhood-onset delinquents were the most elevated on psychopathic personality traits, mental health problems, substance abuse and dependence, financial problems and violent crime in comparison to adolescent-onset offenders and normal children. Although the percentage of past-year DSM-IV diagnosis in the childhood-onset, life-time persistent type did not differ significantly from that of the adolescent-limited type (19 % versus 13 %, respectively) the early beginners scored much higher on the antisocial personality score according to the Diagnostic Interview Schedule for DSM-IV ( p = 0.006, Moffit et al., 2002).

ADHD AND ANTISOCIAL BEHAVIOR AND PSYCHOPATHY

203

Their aggression was obvious in several everyday situations: they had higher rates of hitting their children, more arguments with their coworkers and superiors and a higher probability of using controlling violence in their partner relationships. These subtypes primarily defined by Robins, Tipp & McEvoy (1991) and Moffitt, Lynam & Silva (1994) were confirmed by Lahey et al. (1998) in two large studies. The latter also demonstrated the strong association between very early antisocial behavior and subsequent serious aggressive behavior and psychiatric problems in four US communities.

ETIOLOGY AND PATHOGENESIS OF ANTISOCIAL BEHAVIOR AND THE ROLE OF ADHD The developmental taxonomy based on the two subtypes defined by age of onset hypothesizes two different etiological pathways with the childhood-onset disorder based more on neurobiological risk factors.

Temperament and Comorbidity with ADHD Behavioral inhibition as a dimension of temperament is a protective factor in the development of delinquency. There are probably two ways: (i) in unknown situations, behaviorally inhibited children may be less likely to perform socially deviant acts, because they react fearfully to the threat of punishment and to strange people; (ii) in addition behavioral inhibition may protect by preventing friendship with deviant peers (Kerr et al., 1997), which increases the risk for delinquency. In boys with ADHD the onset of CD is particularly early and often preceded by ODD (Loeber et al., 2000). In more than 90 % of a clinical sample with ADHD and comorbid CD the symptoms of CD were evident prior to age 12 (Biederman et al., 1996). A British epidemiological study observed that all preadolescents with CD also had ADHD (McArdle, O’Brien & Kolvin, 1995). Thus ADHD and CD particularly co-occur in the early-onset type of CD. Although long-term studies are generally consistent that ADHD in childhood increases the probability for later antisocial behavior, it is very difficult to determine whether ADHD or CD is the more prominent risk factor for later ASPD. One reason is that in these studies no clear effort was made to differentiate children with pure ADHD from those with comorbid CD/ADHD. There are only two follow-up studies that tried to exclude CD children at the initial assessment (Gittelman et al., 1985; Mannuzza et al., 1991). In these two reports individuals with childhood ADHD were much more likely to suffer from antisocial personality disorder in adult life than those without ADHD (in the first study 27 % of those with ADHD versus 8 % without; in the second study 32 % versus 8 %). Nevertheless these investigations did not exclude boys with ODD which is a frequent precursor of later CD. In other studies an association between ADHD in childhood and antisocial personality disorder could not be established (Loeber et al., 1995). Babinski, Hartsough and Lampert (1999) distinguished between DSM-IV criteria of inattention and those of hyperactivity/impulsiveness and stated that only the latter contributed to a higher risk for later criminal involvement. In a model on the relationship between both disorders elaborated by Lahey and Loeber it is hypothesized that only children with ADHD and the comorbid condition of ODD will

204

VOLUME I: DIAGNOSIS AND TREATMENT

develop CD in childhood, with a subgroup of CD children later exhibiting ASPD. ADHD is thought to have a mediator role influencing the developmental progress from less severe to very serious forms of CD (Loeber et al., 2000). In their prospective study Satterfield and Schell (1997) pointed out that only one conduct problem was needed to identify an increased risk for serious antisocial behavior in adolescence and adulthood. In the light of their findings the threshold set to identify conduct disorder according to DSM-IV (three or more CD) symptoms may be too high for children with ADHD. In a fairly recent work by Simonofff et al. (2004) 107 male and female twin pairs who had been systematically investigated in childhood were followed up personally 10–25 years later. The results demonstrated that childhood hyperactivity and conduct disorder were equally strong risk factors for antisocial personality disorder and criminality in early and mid-adult life. Nevertheless, multivariate analysis revealed that both disorders were independently associated with later antisocial behavior. In this sample, however, based on a clinical population, only 13 % of the participants below the threshold for both hyperactivity and conduct disorder in childhood were diagnosed with early adult ASPD in contrast to 65 % of those in whom both disorders were present.

Familial Transmission and Heritability In families of male probands with ADHD prevalence rates of this disorder have been observed to be seven times higher than in normal control families (Biederman et al., 1992). It is supposed to be one of the most heritable disorders in child and adolescent psychiatry, the recurrence risk in siblings estimated in the range of 5 (Biederman et al., 1992). Four genome-wide scans including one of our group detected significant large signals in the distal region of chromosome 5p despite differences in ethnicity, ascertainment and phenotyping schemes of the samples (Arcos-Burgos et al., 2004; Bakker et al., 2003; Fisher et al., 2002; Hebebrand et al., 2006). In addition to the locus on chromosome 5p the genome scans for ADHD found linkages to chromosomes 6q, 7p, 9q, 11q, 12q and 17q. It seems rather probable that ADHD DSM-IV subtypes of inattention and hyperactivity/impulsivity are linked to different gene loci. The most susceptible candidate genes are those important for dopamine transmission: the dopamine D4 receptor gene (DRD4) und the dopamine transporter gene (DAT1). Stimulant medications with good effects on both inattention and hyperactivity in ADHD block binding of dopamine to the dopamine transporter, and imaging studies have detected reduced dopamine transporter binding in adults with ADHD. While meta-analyses have revealed significant results for DRD4, there were only negative results for the DAT1 VNTR (variable number tandem repeat) polymorphism (Hebebrand et al., 2006). Antisocial and criminal behavior also occurs more frequently within families and is seen to be highly transmitted from one generation to the next. Several disorders in the parents increase the risk for children to develop CD: schizophrenia, substance abuse, depression (especially in mothers) and antisocial personality disorder in fathers (Hinshaw & Anderson, 1996). Farrington (1997) found that 63 % of boys with delinquent fathers had been convicted of criminal behavior, compared to only 30 % where the fathers had never been accused of any criminal act. However, there seem to exist several different pathways for transmission: one may represent a major genetic effect, in others environmental influences are of great importance like an excessively hard or inconsistent style of upbringing, inadequate control or supervision and acceptance and reward within the family of selfish and aggressive behavior.

ADHD AND ANTISOCIAL BEHAVIOR AND PSYCHOPATHY

205

The role of genetic factors had already been demonstrated in the early studies by Cloninger et al. (1982). In these long-term Swedish investigations 862 illegitimate boys adopted by nonrelatives were followed up. Individuals with one delinquent but nonalcoholic, biological parent were at a 1.9 times greater risk for delinquency than individuals from the control group. A history of parental antisocial behavior is thought to be particularly associated with the childhood and life-persistent type of antisocial behavior. Heritability rates for conduct disorder are generally higher in children samples than in juvenile samples (for a review see Pennington, 2002). Age and gender effects on the heritability of the aggression and delinquency subscales of the Child Behavior Checklist (CBCL) were studied by Eley, Lichtenstein and Stevenson (1999). In this study delinquency was more heritable in females than in males, while it was similar for aggression in both genders. In concordance with the theory of Moffitt (life-persistent versus adolescent-limited subtype) delinquency was also more heritable in children than in adolescents. Many of the risks deriving from adverse life experiences like harsh punishment and social disorganization depend on the vulnerability of the child to cope with these risk factors, for example, they are reliant of nature–nurture interplay (Rutter, 2005). In other words genetic liability plays a major role in mediating environmental effects. The importance of gene x environment interactions (epigenetic effects) was demonstrated in another paper of the Dunedin Longitudinal Study. Caspi et al. (2002) investigated the role of either maltreatment or upbringing without assault as experienced by boys between the age of 3 and 11 years and the existence of a specific polymorphism of the monoaminooxidase A (MAO A gene) which is located on the X chromosome. The MAO A enzyme metabolizes monoamines such as norepinephrine, serotonin and dopamine. There was no significant main effect of the gene when this was analyzed without reference to a history of maltreatment. There was a significant association between later antisocial behavior and maltreatment, but the strongest effect came from the gene x environment interaction. Boys with low MAO A activity who had suffered from childhood maltreatment were at the highest risk for later antisocial behavior: 12 % of the sample with low MAO A activity and assault in childhood accounted for 44 % of the violent convictions. At the age of 26 these 55 boys were three times more likely to have been sentenced of a violent crime than the resting 99 boys with high MAO A activity and assault. This study was replicated by Foley et al. (2004), but only in part supported by Haberstick et al. (2005). In a study by Thapar et al. (2005) a specific polymorphism of the catechol-Omethyltransferase (COMT) gene increased the effects of prenatal adversities measured by low birth weight. Different studies reported associations of the COMT valin/methionin (val/met) variant with prefrontal cognitive function. In these studies possession of the met allele (met/met and met/val genotype) was linked to better performance of prefrontal cognitive functions than the exclusive val allele, for example, in patients with schizophrenia and their siblings. In the study by Thapar and coworkers the valin/valin genotype and low birth weight (as a further example for gene–environment interaction) predicted early onset of antisocial behavior in children with ADHD. Recent studies have also examined the etiological relations between ADHD and CD/ODD. Family and twin study results suggest that much of the overlap between ADHD and CD is due to a common genetic etiology (Faraone et al., 1998), which also refers to ODD (Waldman et al., 2001). Conduct disorders, but not anxiety and affective disorders, cosegregate within families of ADHD probands. However, another finding by Faraone,

206

VOLUME I: DIAGNOSIS AND TREATMENT

Biederman and Monuteaux (2000) suggest that the comorbid disorder of ADHD and CD represents a distinct familial subtype of ADHD. In a research project by Thapar, Harrington and McGuffin (2001) parent-rated data were obtained for more than 2000 twin pairs. The overlap between ADHD and conduct problems was explained by common genetic and nonshared environmental factors. In accordance with other studies the authors concluded that CD was supported by additional environmental adversity factors; however, they also found that the comorbid condition had a higher genetic loading and clinical severity. The results by Thapar support the classificatory system of ICD-10 whereby ADHD/CD is a subcategory of ADHD with higher heritability and greater difficulty to treat. According to these results ADHD/CD would be a ‘true hybrid’ of hyperkinetic and conduct disorder. In addition to shared genetic risk factors ADHD/CD has similar cognitive and developmental impairments as ADHD and social adversities that correspond to those of CD. In addition patients with the comorbid condition respond fairly well to stimulant and atomoxetine medication as do children with pure ADHD (Schachar & Sergeant, 2002). However, other authors deny the hybrid hypothesis of both disorders because they found a distinct course (early beginning, high persistence) for each disorder and a different familial transmission (for a review see Schachar & Sergeant, 2002).

Other Biological Risk Factors There are several further prenatal and postnatal risk factors that might enhance the risk for conduct disorders, adult ASPD and ADHD. Maternal smoking during pregnancy has been found to be associated with conduct disorder and juvenile delinquency among male offspring (for a review see Wakschlag et al., 2002). This association between maternal smoking and antisocial behavior is consistent across different populations and social backgrounds. There is well-established evidence that nicotine and other substances of cigarette smoke are behavioral teratogens. Despite great variability of experimental paradigms used in animal studies several physical and cognitive effects of exposure to nicotine in utero have been observed, for example, low birth weight, enhanced locomotor activity and cognitive impairment. On the molecular level disturbances in neuronal pathfinding, abnormalities in cell proliferation and differentiation, and disruptions in the development of the cholinergic and catecholaminergic transmission have been observed (for a review see Ernst, Moolchan & Robinson, 2001). However, it is still unresolved whether prenatal smoking is independently associated with ADHD, particularly when covariations with conduct disorder symptoms are taken into account. Some studies found that maternal smoking during pregnancy is associated with ADHD symptoms in offspring not accounted for by genetic factors (Thapar et al., 2003), others could not confirm this relationship (Wakschlag & Hans, 2002). In a recent project of the Pittsburgh Youth Study boys that were exposed to nicotine during pregnancy had a significantly higher risk to develop ODD and the comorbid condition of ODD and ADHD, but not ADHD alone (Wakschlag et al., 2006). The authors investigated a sample with an average age of seven so that the authors concluded that maternal smoking is particularly associated with the early starter ‘life-persistent’ pattern of antisocial behavior. This is in accordance with the importance of neurobiological factors in the etiology of early-onset CD. Previously documented additional risk factors for ADHD are prenatal exposure to alcohol and drugs. Children with fetal alcohol syndrome tend to be hyperactive, exhibit cognitive,

ADHD AND ANTISOCIAL BEHAVIOR AND PSYCHOPATHY

207

particularly attention deficits, and deficits in adaptive behavior. In a case-control study ADHD cases were more than twice as likely to have been exposed to nicotine and alcohol in utero than control children (Mick et al., 2002). In a study by Liu et al. (2004) children with malnutrition at age three were more aggressive or hyperactive at age eight, had more disruptive disorders at age eight and more severe conduct disorder and motor restlessness at age 17 than adequately nourished children.

Childhood Trauma New investigations into the consequences of childhood traumatic experiences have revealed a strong link to the development of several psychiatric problems in adolescence and adulthood, including aggression, impulsiveness, delinquency and hyperactivity. Particularly chronic abuse, maltreatment and neglect may cause permanent damage to the neural structure and function of the developing brain that may in turn enhance genetic and environmental risk factors for ADHD and CD (for a review see Teicher et al., 2003).

Neurocognitive Impairment In recent years growing literature on cognitive functioning in children and adults with antisocial behavior reveals that conduct problems are associated with neurocognitive impairment (Lynam & Henry, 2001). Low intelligence is often considered to be linked to antisocial behavior; however, several studies failed to control for ADHD (Burke, Loeber & Birmaher, 2002). Particularly, conductdisordered children have deficits in verbal skills and verbal memory (Moffitt, Lynam & Silva, 1994), especially those with ADHD. In comparison to antisocial children with better verbal skills, poor performance in verbal tasks increases the likelihood for delinquency in late adolescence und young adulthood (Moffitt, Lynam & Silva, 1994). Reading problems have also been frequently linked to CD and may be connected to abnormal language processing in the left temporal cortex (Pine et al., 1997, also see ‘Neuroimaging’). In ADHD children the prevalence of learning disorders, especially reading and spelling disorders, is significantly higher than in normal controls; a comorbidity of ADHD with learning disorders seems to worsen the individual’s prognosis. However, these findings raised some opposition. In a later study by Aguilar et al. (2000) in high-risk children, verbal abilities in antisocial groups did not differ from those in nonantisocial individuals. In addition high intelligence does not prevent conduct disorder. Boys with conduct disorder and psychopathic tendencies, who also had a father with antisocial personality disorder, had no lower IQs than normal boys, but their IQ was higher than in boys with conduct disorder and no parental antisocial personality disorder (Christian et al., 1997) In a very recent study boys with early-onset life-course persistent antisocial behavior were compared to boys with childhood-limited and to boys with adolescent-limited antisocial behavior on several neuropsychological tasks, particularly verbal and spatial IQ and memory. Life-course persistent offenders had a lower verbal and total IQ than normal controls and lower verbal abilities than the adolescent-limited antisocial boys. They also had significantly more spatial memory impairment than controls. However the childhood-limited group also was not free of neurocognitive deficits. These lower neurocognitive capacities were independent of comorbid ADHD and psychosocial adversities (Raine et al., 2005).

208

VOLUME I: DIAGNOSIS AND TREATMENT

In addition, there is still a controversy on whether deficits in executive functions (EF), that is, in inhibitory control and working memory, are associated with ADHD only, CD only or are worse in children and adolescents of the comorbid condition. In contrast to the extensive literature on EF deficits in ADHD, which has relatively consistently indicated that about 60 to 70 % of all ADHD subjects suffer from deficits in inhibitory control (Nigg, 2005), studies on EF deficits in ODD/CD are scarce. However, indirect support for EF deficits in ODD/CD comes from studies of antisocial behavior in adults (Morgan & Lilienfeld, 2000). In children and adolescents, those studies finding support for EF deficits in ODD/CD often failed to control for comorbid ADHD (Pennington & Ozonoff, 1996), thus the presence of comorbid ADHD may have accounted for the EF deficits in children with ODD/CD. Osterlaan, Scheres and Sergeant (2005) investigated three putative domains of EF using well-validated tests: verbal fluency; working memory; and planning in children aged 6– 12 years. Independent of ODD/CD, ADHD was associated with deficits in planning and working memory, but not in verbal fluency. Only teacher-rated ADHD, but not parent-rated ADHD, significantly contributed to the prediction of EF task performance. No EF deficits were associated with ODD/CD. Thus in contrast to some prior results, here the presence of comorbid ADHD accounts for the EF deficits in children with comorbid ADHD+ODD/CD. These results suggest that EF deficits are unique to ADHD.

Neuroimaging Findings In ADHD, many studies have identified structural and functional brain abnormalities in the frontal-striatal circuitry (Durston, 2003). However, a recent review demonstrated the most replicated morphometrical alterations in ADHD include significantly smaller volumes in the dorsolateral prefrontal cortex, caudate, pallidum, corpus callosum and cerebellum, indicating that the brain in ADHD is altered in a more widespread manner than has been previously hypothesized (Seidman, Valera & Markis, 2005, for a review) (see Figure 12.1). Functional imaging studies have relatively consistently shown dysfunction of fronto-striatal structures (lateral prefrontal cortex, dorsal anterior cingulate cortex, caudate and putamen)

Figure 12.1 Group-difference map shows differences in gray-matter density (% difference) between ADHD patients and controls. Warmer colors (above O on the color bar) are regions in which gray-matter density is greater in patients than controls, and cooler colors (below O) are regions in which controls have greater gray-matter density than patients. Note the roughly 20–30 % increase in gray-matter density in temporal and inferior parietal regions bilaterally (from Sowell et al., 2003). See also color plates

ADHD AND ANTISOCIAL BEHAVIOR AND PSYCHOPATHY

209

(see Bush, Valera & Seidman, 2005, for a review). The majority of these studies has focused on brain dysfunctions during cognitive tasks with demands on attention and inhibition, such as the Go/NoGo task (Tamm et al., 2004), the Stop task (Rubia et al., 1999), the Stroop task (Bush et al., 1998) or the Attention Network test (Konrad et al., 2006). By contrast, neuroimaging studies focusing on patients with CD are still rare and most findings of antisocial behavior derive from adult samples. Early hints of an association between certain brain regions and antisocial behavior were given by case reports of adult subjects, which indicate that the prefrontal cortex (PFC) plays an important role in the modulation of social behavior (Harlow, 1868). Individuals with lesions in this area typically show disinhibited, impulsive and aggressive behavior and the PFC has been associated with the anticipationof punishment and reward. In addition, lesions in the amygdala seem to impair the ability to interpret social signs (Adolphs, Tranel & Damasio, 1998) and thereby might lead to inadequate fear responses. Since the amygdala has strong anatomical connections with frontal regions, it is likely that the connectivity between the frontal and limbic system plays a crucial role for antisocial pathology. Morphological abnormalities in the frontal lobe might impact on the modulatory role on amygdala activity, which in turn may affect fear-related processes (Hoptman, 2003). Other parts of the limbic system that have been investigated are the temporal lobes and hippocampus. Structural studies implicate that morphometric abnormalities of the temporal lobes, especially frontotemporal areas are associated with delinquent behavior in adults (Hoptman, 2003). In line with this, functional imaging studies of adult psychopaths indicate dysfunction of particular frontal and temporal lobe structures during classical conditioning (Birbaumer et al., 2005), response inhibition tasks (Kiehl et al., 2004) and in the processing of emotional words and pictures (Muller et al., 2003), although the direction of change differed among the studies. In children, some case reports of acquired frontal lobe damage also demonstrated that the majority of affected children displayed later significant conduct disorder symptoms (Pennington & Bennetto 1993). Only two structural imaging studies investigated children and adolescents with CD and ADHD. Bussing et al. (2002) found no cortical differences between a sample of seven children with CD, five children with ADHD alone and 19 healthy controls by using structural MRI, but reported smaller posterior volumes of the cerebellum for both pure ADHD and comorbid children compared to controls. In another morphometric study Kruesi et al. (2004) investigated regional brain volumes derived from 10 subjects aged 9 to 20 years with CD and a history of ADHD and compared them with a group of healthy age- and gender-matched controls. The right temporal lobe and right temporal gray-matter volumes were significantly reduced in the clinical group compared with the control group and prefrontal volumes tended to be smaller than in controls. A recent fMRI study including adolescents with CD (most of them with a comorbid condition of ADHD) suggested a pronounced deactivation within the dorsal anterior cingulate gyrus (ACC) during passive viewing of strongly negative compared to neutral pictures. When correcting for anxiety and depressive symptoms, additionally a reduced responsiveness of the left amygdala to negative pictures was found in patients compared with control subjects (Sterzer et al., 2005). The temperament dimension ‘novelty seeking’ was a significant predictor for ACC responsiveness to affective pictures as revealed by a stepwise multiple regression analysis. To date, it remains unclear to which extent these functional and structural brain abnormalities observed in patients with ADHD/CD are explained by genetics and/or by other

210

VOLUME I: DIAGNOSIS AND TREATMENT

biological risk factors (such as prenatal exposure to nicotine, alcohol). For example, longterm effects on the human brain development of children prenatally exposed to nicotine have not been investigated yet, perhaps because of the difficulty of separating the impact of drug exposure from other genetic and environmental factors. However, recently it has been shown that even relatively mild forms of fetal alcohol exposure may be associated with microstructural abnormalities in the posterior corpus callosum that are detectable with DTI in humans (Wozniak et al., 2006). Taken together, neuroimaging studies suggest in particular abnormal fronto-striatal processing in ADHD and fronto-temporal processing in CD, however, since the majority of previous studies has failed to adequately control for effects of comorbidity, future research has to focus on the identification of shared and disease-specific brain abnormalities between ADHD and disruptive behavior. This might also help to explain similarities and differences in the neurocognitive profiles of ADHD and CD patients and thereby point to interesting neuobiological endophenotypes on the brain level across diagnostic categories.

Psychophysiology and Antisocial Behavior in Children and Adolescents Autonomic underarousal and low autonomic responses have been shown to be predictive of adult antisocial behavior (Scarpa & Raine, 2004; for a further review see Chapter 11 in this book). The strength of this predictor is stronger in boys without psychosocial disadvantages compared to those boys with unfavorable social backgrounds and may therefore particularly reflect the biology–antisocial behavior relationship. Autonomic responses have been suggested to act as biological mediators through which genetic influences operate on antisocial behavior (Raine, 2002). Our own group assessed arousal measures and electrodermal responses to orienting and startling stimuli in 8–13-year-old boys diagnosed with ADHD, CD, the comorbid condition of ADHD + CD, and in controls. CD boys with and without ADHD, but not those with ADHD alone or controls showed decreased electrodermal responses and accelerated habituation which was highly similar to those found in antisocial adults. These data suggest that it is CD that sharply raises the risk of unfavorable, antisocial development, whether it occurs alone or comorbid with ADHD (Herpertz et al., 2003). There is some first evidence from the comparison of monozygotic and dizygotic twin pairs that genes may influence electrodermal activity with heritability estimations between 0.40 and 0.50 for phasic electrodermal activity measures (Crider et al., 2004). However, autonomic responsiveness is also sensitive to environmental processes (Carrey et al., 1995). In a study of our group (Herpertz et al., 2007) we examined the transmission of autonomic activity characteristics in families of boys with CD by investigating their biological fathers in the same experimental design. Parameters of autonomic arousal (resting heart rate and nonspecific skin conductance fluctuations) as well as electrodermal responsivity to pictorial stimuli proved to be highly correlated between fathers and sons. Searching for behavioral dimensions which could contribute to high father/son correlations of psychophysiological characteristics, correlations were found to be rather independent of fathers’ trait aggression or self-reported antisocial behavior. Future research will have to pursue the question whether autonomic hyporesponsiveness can be regarded as an endophenotype which provides one of the routes through which genetic influences on antisocial disorders find expression.

ADHD AND ANTISOCIAL BEHAVIOR AND PSYCHOPATHY

211

CONCLUSIONS Although it is not generally accepted that ADHD/CD is a ‘true hybrid’ of both disorders, there is broad consent that the comorbid disorder is a more severe condition than either disorder alone. ADHD/CD is more resistant to treatment than pure ADHD. Both disorders seem to constitute a synergistic and interactive relationship (Jensen, Martin & Cabtwekk, 1997), in that each disorder aggravates the other. In the context with ADHD very few conduct disorder symptoms already increase the risk for later ASPD. In most cases ADHD is associated with the early beginning, life-time persistent course of conduct disorder which is highly predictive of school failure, other psychiatric disorders and delinquency. It is associated with more neurobiological risk factors and characterized by a higher range and severity of conduct disorder symptoms. In particular, individuals with antisocial behavior beginning early in life are more prone to show psychopathic traits than those with conduct problems starting in adolescence. Although the distinction of an early beginning subtype of conduct disorder is a well supported and a high-fitting model for the role of ADHD in the development of antisocial personality disorder, it is not undisputed. In a recent follow-up of the Dunedin cohort where the distinction of earlyonset/adolescent-limited antisocial behavior was originally made it had to be stated that the adolescent-onset delinquents were in fact less extreme than the childhood-onset type, but demonstrated more impulsive personality traits, mental health problems, substance dependence, financial problems and property offenses than controls without remarkable delinquency history (Moffitt et al., 2002). The adolescent-onset offenders described themselves as ‘agreeable (not callous) and extraverted’ as the average male in contrast to the early-onset offenders, who rated themselves high on negative emotionality and callousness, the latter representing a trait of the psychopathic cluster. However the adolescent-onset sample accounted for twice their portion for convictions of property and drug offenses of the whole cohort during the period of adulthood. The less benign prognosis than previously hypothesized was confirmed by the investigation of Simonoff et al. (2004) who could not detect any difference in outcome between childhood-onset and adolescent-onset conduct disorder. Several findings suggest that high-quality treatments may have considerable impact on restoring ADHD children to better functioning. The results of a big multicenter trial (MTA Study group, e.g., Jensen et al., 2001) demonstrated that in children with ADHD only or with combined ADHD/CD medication is especially indicated; for children with a comorbid condition additional behavior therapy may offer additional benefit, especially in global functioning (Jensen et al., 2001).

REFERENCES Adolphs, R., Tranel, D. & Damasio, A.R. (1998). The human amygdala in social judgment. Nature, 393, 470–4. Aguilar, B., Sroufe, L.A., Egeland, B. & Carlson, E. (2000). Distinguishing the early-onset/persistent and adolescence-onset antisocial behavior types: from birth to 16 years. Development and Psychopathology, 12, 109–32.

212

VOLUME I: DIAGNOSIS AND TREATMENT

American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders (4th edition). Washington, DC: American Psychiatric Association. Arcos-Burgos, M., Castellanos, F.X., Pineda, D. et al. (2004). Attention-deficit/hyperactivity disorder in a population isolate: linkage to loci at 4q13.2, 5q33.3, 11q22 and 17p11. American Journal of Human Genetics, 75, 998–1014. Babinski, L.M., Hartsough, C.S., & Lambert, N.M. (1999). Childhood conduct problems, hyperactivity-impulsivity, and inattention as predictors of adult criminal activity. Journal of Child Psychololgy and Psychiatry, 40, 347–55. Bakker, S.C., van der Meulen, E.M., Buitelaar, J.K. et al. (2003). A whole-genome scan in 164 Dutch sib pairs with attention-deficit/hyperactivity disorder: suggestive evidence for linkage on chromosomes 7p and 15q. American Journal of Human Genetics, 72, 1251– 60. Barkley, R., Fischer, M., Smallish, L. & Fletcher, K. (2004). Young adult follow-up of hyperactive children: antisocial activities and drug use. Journal of Child Psychology and Psychiatry, 45, 195– 211. Barrickman, L. (2003). Disruptive behavioral disorders. Pediatric Clinics of North America, 50, 1005–17. Biederman, J., Faraone, S.V., Keenan, K. et al. (1992). Further evidence for family-genetic risk factors in attention deficit hyperactivity disorder: patterns of comorbidity in probands and relatives in psychiatrically and pediatrically referred samples. Archives of General Psychiatry, 49, 728–38. Biederman, J., Faraone, S.V., Milberger, S. et al. (1996). Is childhood oppositional defiant disorder a precursor to adolescent conduct disorder? Findings from a four-year follow-up of children with ADHD. Journal of the American Academy of Child and Adolescent Psychiatry, 35, 193–204. Birbaumer, N., Veit, R., Lotze, M. et al. (2005). Deficient fear conditioning in psychopathy: a functional magnetic resonance imaging study. Archives of General Psychiatry, 62, 799–805. Blair, R.J. (2003). Neurobiological basis of psychopathy. British Journal of Psychiatry, 182, 5–7. Burke, J.D., Loeber, R. & Birmaher, B. (2002). Oppositional defiant and conduct disorder: a review of the past 10 years, part II. Journal of the American Academy of Child and Adolescent Psychiatry, 41, 1275–93. Bush, G., Valera, E.M. & Seidman, L.J. (2005). Functional neuroimaging of attentiondeficit/hyperactivity disorder: a review and suggested future directions. Biological Psychiatry, 57, 1273–84. Bush, G., Whalen, P.J., Rosen, B.R. et al. (1998). The counting Stroop: an interference task specialized for functional neuroimaging – validation study with functional MRI. Human Brain Mapping, 6, 270–82. Bussing, R., Grudnik, J., Mason, D. et al. (2002). ADHD and conduct disorder: an MRI study in a community sample. The World Journal of Biological Psychiatry, 3, 216–20. Carrey, N.J., Butter, H.J., Persinger, M.A. & Bialik, R.J. (1995). Physiological and cognitive correlates of child abuse. Journal of the American Academy of Child and Adolescent Psychiatry, 34, 1067–75. Caspi, A., McClay, J., Moffitt, T.E. et al. (2002). Role of genotype in the cycle of violence in maltreated children. Science, 97, 851–4. Christian, R.E., Frick, P.J., Hill, N.L. et al. (1997). Psychopathy and conduct problems in children, II: implications for subtyping children with conduct problems. Journal of the American Academy of Child and Adolescent Psychiatry, 36, 233–41. Cleckley, H.C. (1941). The Mask of Sanity. St. Louis, MO: Mosby. Cloninger, C.R., Sigvardsson, S., Bohman, M. & von Knorring A.L. (1982). Predisposition to petty criminality in Swedish adoptees: II. Gross-fostering analysis of gene environment interaction. Archives of General Psychiatry, 39, 1242–7. Crider, A., Kremen, W.H., Xian, H. et al. (2004). Stability, consitency, and heritability of electrodermal response lability in middle-aged male twins. Psychophysiology, 41, 501–9. Durston, S. (2003). A review of the biological bases of ADHD: what have we learned from imaging studies? Mental Retardation and Developmental Disabilities Research Reviews, 9, 184–95. Eley, T.C., Lichtenstein, P. & Stevenson, J. (1999). Sex differences in the etiology of aggressive and nonaggressive antisocial behavior: results from two twin studies. Child Development, 70, 155–68.

ADHD AND ANTISOCIAL BEHAVIOR AND PSYCHOPATHY

213

Ernst, M., Moolchan, E. & Robinson, M. (2001). Behavioral and neural consequences of prenatal exposure to nicotine. Journal of the American Academy of Child and Adolescent Psychiatry, 40, 630–41. Faraone, S.V., Biederman, J., Mennin, D. et al. (1998). Familial subtypes of attention deficit hyperactivity disorder: a 4-year follow-up study of children from antisocial ADHD families, Journal of Child Psychology and Psychiatry, 39, 1045–53. Faraone, S.V., Biederman, J. & Monuteaux, M.C. (2000). Toward guidelines for pedigree selection in genetic studies of attention deficit hyperactivity disorder.Genetic Epidemiology, 18, 1–16. Farrington, D.P. (1997). A critical analysis of research on the development of antisocial behavior from birth to adulthood. In D.M. Stoff, J. Breiling & J.D. Maser (eds.), Handbook of Antisocial Behavior (pp. 234–40). Chichester: John Wiley & Sons, Ltd. Fisher, S.E., Francks, C., McCracken, J.T. et al. (2002). A genomewide scan for loci involved in attention-deficit/hyperactivity disorder.American Journal of Human Genetics, 70, 1183–96. Foley, D.L., Eaves, L.J., Wormley, B. et al. (2004). Childhood adversity, monoamine oxidase: a genotype, and risk for conduct disorder. Archives of General Psychiatry, 61, 738–44. Gittelmann, R., Mannuzza, S., Shenker, R. & Bonagura, N. (1985). Hyperactive boys almost grown up. Archives of General Psychiatry, 42, 937–47. Haberstick, B.C., Lessem, J.M., Hopfer, C.J. et al. (2005). Monoamine oxidase A (MAOA) and antisocial behaviors in the presence of childhood and adolescent maltreatment. American Journal of Medicine Genetics. Part B, Neuropsychiatric Genetics, 135, 59–64. Harlow, J.M. (1868). Recovery after severe injury to the head. Publications of the Massachusetts Medical Society, 2, 327–47. Hebebrand, J., Dempfle, A., Saar, K. et al. (2006). A genome-wide scan for attentiondeficit/hyperactivity disorder in 155 German sib-pairs. Molecular Psychiatry, 11, 196– 205. Hechtman, L. & Offord, D.R. (1994). Long-term outcome of disruptive disorders. Child and Adolescent Psychiatry Clinics of North America, 3, 379–403. Herpertz, S.C., M¨uller, B., Qunaibi, M. et al. (2005). Response to emotional stimuli in boys with conduct disorder. American Journal of Psychiatry, 162, 1100–7. Herpertz, S.C., M¨uller, B., Wenning, B. et al. (2003). Autonomic responses in boys with externalizing disorders. Journal of Neural Transmission, 110, 1181–95. Herpertz, S.C., Vloet, T., M¨uller, B. et al. (2007). Similar autonomic responsivity in boys with conduct disorder and their fathers. Journal of the American Academy of Child and Adolescent Psychiatry, 46(4), 535–44. Herpertz-Dahlmann, B. (2001). Conduct disorders, antisocial behavior, delinquency. In H. Remschmidt (ed.),Psychotherapy with Children and Adolescents (pp. 498–511). Cambridge: Cambridge University Press. Hinshaw, S.P. & Anderson, C.A. (1996). Conduct and oppositional defiant disorders. In E.J. Mash & R.A. Barkley (eds.), Child Psychopathology (pp. 113–49). New York: Guilford Press. Hoptman, M.J. (2003). Neuroimaging studies of violence and antisocial behavior. Journal of Psychiatric Practice, 9, 265–78. Jensen, P.S., Martin, D. & Cabtwekk, D.O. (1997). Comorbidity in ADHD: implications for reserach, practice, and DSM-V. Journal of the American Academy of Child and Adolescent Psychiatry, 36, 1065–79. Jensen, P.S., Hinshaw, S.P., Kraemer, H.C. et al. (2001). ADHD comorbidity findings from the MTA study: comparing comorbid sub-groups. Journal of the American Academy of Child and Adolescent Psychiatry, 40, 147–58. Kerr, M., Tremblay, R.E., Pagani, L. & Vitaro, F. (1997). Boys’ behavioral inhibition and the risk of later delinquency. Archives of General Psychiatry, 54, 785–9. Kiehl, K.A., Smith, A.M., Mendrek, A. et al. (2004). Temporal lobe abnormalities in semantic processing by criminal psychopaths as revealed by functional magnetic resonance imaging. Psychiatry Research, 130, 297–312. Klein, R.G., Abikoff, H., Klass, E. et al. (1997). Clinical efficacy of methylphenidate in conduct disorder with and without attention deficit hyperacitivy disorder. Archives of General Psychiatry, 54, 1073–80.

214

VOLUME I: DIAGNOSIS AND TREATMENT

Konrad, K., Neufang, S., Hanisch, C. et al. (2005). Dysfunctional attentional networks in children with attention deficit hyperactivity disorder (ADHD) – evidence from an event-related fMRI study. Biological Psychiatry, 59, 643–51. Kruesi, M.J., Casanova, M.F., Mannheim, G. & Johnson-Bilder, A. (2004). Reduced temporal lobe volume in early onset conduct disorder. Psychiatry Research, 132, 1–11. Lahey, B.B., Miller, T.L., Gordon, R.A. & Riley, A.W. (1999). Developmental epidemiology of the disruptive behavior disorders. In H.C. Quay & A.E. Hogan (eds). Handbook of Disruptive Behavior Disorders in Childhood and Adolescence (pp. 449–77). New York: Kluwer Academic/Plenum. Lahey, B.B., Loeber, R., Quay, H.C. et al. (1998). Validity of DSM-IV subtypes of conduct disorder based on age of onset. Journal of the American Academy of Child and Adolescent Psychiatry, 37, 435–42. Liu, J., Raine, A., Venables, P. & Mednik, S. (2004). Malnutrition at age 3 years and externalizing behavior problems at ages 8, 11, and 17 years. American Journal of Psychiatry, 161, 2005–13. Loeber, R., Green, S.M., Keenan, K. & Lahey, B.B. (1995). Which boys will fare worse? Early predictors of the onset of conduct disorder in a six-year longitudinal study. Journal of the American Academy of Child and Adolescent Psychiatry, 34, 499–509. Loeber, R., Burke, J.D., Lahey, B.B. et al. (2000). Oppositional defiant and conduct disorder: a review of the past 10 years, part I. Journal of the American Academy of Child and Adolescent Psychiatry, 39, 1468–84. Lorber, M.F. (2004). Psychophysiology of aggression, psychopathy, and conduct problems: a metaanalysis. Psychological Bulletin, 130, 531–52. Lynam, D.R. & Henry, V. (2001). The role of neuropsychological deficits in conduct disorders. In J. Hill & B. Maughan (eds.). Conduct Disorders in Childhood and Adolescence. Cambridge: Cambridge University Press. Mannuzza, S., Klein, R.G., Bonagura, N. et al. (1991). Hyperactive boys almost grown up: replication of psychiatric status. Archives of General Psychiatry, 48, 77–83. McArdle, P., O’Brien, G. & Kolvin, I. (1995). Hyperactivity: prevalence and relationship with conduct disorder. Journal of Child Psychology and Psychiatry, 36, 279–303. Mick, E., Biederman, J., Faraone, S. et al. (2002). Case-control study of attention-deficit hyperactivity disorder and maternal smoking, alcohol use, and drug use during pregnancy. Journal of the American Academy of Child and Adolescent Psychiatry, 41, 378–85. Moffitt, T.E. (1993). Adolescence-limited and life-course-persistent antisocial behavior. A developmental taxonomy. Psychological Review, 100, 674–701. Moffitt, T.E. & Caspi, A. (2001). Childhood predictors differentiate life-course persistent and adolescence-limited pathways, among males and females. Development and Psychopathology, 13, 355–75. Moffitt, T.E., Caspi, A., Harrington, H. & Milne, B.J. (2002). Males on the life-course-persistent and adolescence-limited antisocial pathways: follow-up at age 26 years. Developmental Psychopathy, 14, 179–207. Moffitt, T.E., Lynam, D.R. & Silva, P.A. (1994). Neuropsychological tests predicting persistent male delinquency. Criminology, 32, 277–300. Morgan, A.B. & Lilienfeld, S.O. (2000). A meta-analytic review of the relation between antisocial behavior and neuropsychological measures of executive function. Clinical Psychology, 200, 113– 36. Muller, J.L., Sommer, M., Wagner, V. et al. (2003). Abnormalities in emotion processing within cortical and subcortical regions in criminal psychopaths: evidence from a functional magnetic resonance imaging study using pictures with emotional content. Biological Psychiatry, 54, 152– 62. Osterlaan, J., Scheres, A. & Sergeant, J.A. (2005). Which executive functioning deficits are associated with AD/HD, ODD/CD and comorbid AD/HD+ODD/CD? Journal of Abnormal Child Psychology, 33, 69–85. Nigg, J.T. (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, 1424–35. Pennington, B.F. (2002). Nature and Nurture, the Development of Psychopathology. New York: Guilford Press.

ADHD AND ANTISOCIAL BEHAVIOR AND PSYCHOPATHY

215

Pennington, B.F. & Bennetto, L. (1993). Main effects or transactions in the neuropsychology of conduct disorder. Development and Psychopathology, 5, 153–64. Pennington, B.F. & Ozonoff, S. (1996). Executive functions and developmental psychopathology. Journal of Child Psychology and Psychiatry, 37, 51–87. Pine, D.S., Bruder, G.E., Wasserman, G.A. et al. (1997). Verbal dichotic listening in boys at risk for behavior disorders. Journal of the American Academy of Child and Adolescent Psychiatry, 36, 1465–73. Pliszka, S.R., Carlson, C.L. & Swanson, J.M. (1999). ADHD with Comorbid Disorders – Clinical Assessment and Management. New York: Guilford Press. Raine, A. (2002). Biosocial studies of antisocial and violent behavior in children and adults: a review. Journal of Abnormal Child Psychology, 30, 311–26. Raine, A., Moffitt, T.E., Caspi, A. et al. (2005). Neurocognitive impairments in boys on the life-course persistent antisocial path. Journal of Abnormal Psychology, 114, 38–49. Reeves, J.C., Werry, J.S., Elkind, G.S. & Zametkin A (1987). Attention deficit, conduct, oppositional, and anxiety disorders in childre, II: clinical characteristics. Journal of the American Academy of Child and Adolescent Psychiatry, 26, 144–55. Robins, L.N., Tipp, J. & McEvoy, L. (1991). Antisocial personality. In L.N. Robins & D. Regier (eds.).Psychiatric Disorders in America (pp. 258–90). New York: Free Press. Rubia, K., Overmeyer, S., Taylor, E. et al. (1999). Hypofrontality in attention deficit hyperactivity disorder during higher-order motor control: a study with functional MRI. American Journal of Psychiatry, 156, 891–6. Rutter, M. (2005). Environmentally mediated risks for psychopathology: research strategies and findings. Journal of the American Academy of Child and Adolescent Psychiatry, 44, 3–18. Satterfield, J.H. & Schell, A. (1997). A prospective study of hyperactive boys with conduct problems and normal boys: adolescent and adult criminality. Journal of the American Academy of Child and Adolescent Psychiatry, 36, 1726–735. Scarpa, A. & Raine, A. (2004). The psychophysiology of child misconduct. Pediatric Annals, 33, 296–304. Schachar, R. & Sergeant, J.A. (2002). Classification issues. In S. Sandberg (ed.),Hyperactivity and Attention Disorders of Childhood (pp. 126–61). Cambridge: Cambridge University Press. Seidman, L.J., Valera, E.M. & Markis, N. (2005). Structural brain imaging of attentiondeficit/hyperactivity disorder. Biological Psychiatry, 57, 1263–72. Simonoff, E., Elander, J., Holmshaw, J. et al. (2004). Predictors of antisocial personality. Continuities from childhood to adult life. British Journal of Psychiatry, 184, 118–27. Sowell, E.R., Thompson, P.M., Welcome, S.E., Henkenius, A.L., Toga, H.W., Peterson, B.S. (2003). Cortical anomalies in children and adolescents with attention-deficit hyperactivity disorder. The Lancet, 362, 1699–707. Sterzer, P., Stadler, C., Krebs, A. et al. (2005) Abnormal neural responses to emotional visual stimuli in adolescents with conduct disorder. Biological Psychiatry, 57, 7–15. Tamm, L., Menon, V., Ringel, J. & Reiss, A.L. (2004). Event-related FMRI evidence of frontotemporal involvement in aberrant response inhibition and task switching in attention-deficit/hyperactivity disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 43, 1430–40. Teicher, M., Andersen, S., Polcari, A. et al. (2003). The neurobiological consequences of early stress and childhood maltreatment. Neuroscience and Biobehavioral Review, 27, 33–44. Thapar, A., Harrington, R. & McGuffin, P. (2001). Examining the comorbidity of ADHD-related behaviours and conduct problems using a twin study design. Britisch Journal of Psychiatry, 179, 224–9. Thapar, A., Fowler, T., Rice, F. et al. (2003). Maternal smoking during pregnancy and attention deficit hyperactivity disorder symptoms in offspring. American Journal of Psychiatry, 160, 1985–9. Thapar, A., Langley, K., Fowler, T. et al. (2005). Catechol-O-methyltransferase gene variant and birth weight predict early-onset antisocial behavior in children with attention-deficit/hyperactivity disorder. Archives of General Psychiatry, 62, 1275–8. Wakschlag, L. & Hans, S. (2002). Maternal smoking during pregnancy and conduct problems in high-risk youth: a developmental framework. Development and Psychopathology, 14, 351–69.

216

VOLUME I: DIAGNOSIS AND TREATMENT

Wakschlag, L., Pickett, K., Kasza, K. & Loeber, R. (2006). Is prenatal smoking associated with a developmental pattern of conduct problems in young boys? Journal of the American Academy of Child and Adolescent Psychiatry, 45, 461–7. Waldman, I., Rhee, S.H., Levy, F. & Hay, D.A. (2001). Causes of the overlap among symptoms of ADHD, oppositional defiant disorder and conduct disorder. In F. Levy & D.A. Hay (eds.).Attention, Genes and ADHD (pp. 115–38). East Sussex, UK: Brunner-Routledge. World Health Organization (1993). The ICD-10 Classification of Mental and Behavioral Disorders: Diagnostic Criteria for Research. Genf. Wozniak, J., Mueller, B., Chang, P. et al. (2006). Diffusion tensor imaging in children with fetal alcohol spectrum disorders. Alcoholism, Clinical and Experimental Research, 30, 1799–806.

CHAPTER 13

Brain Trauma Hannelore Ehrenreich and Henning Krampe ¨ Max-Planck Institute of Experimental Medicine, Gottingen, Germany

Anna-Leena Sir´en ¨ Department of Neurosurgery, University of Wurzburg, Germany

The present chapter is devoted to brain trauma as it relates to psychopathic disorders. Screening the literature in a narrow, topic-pertinent way yields a small number of relevant articles, many of them case reports, only few with substantial and scientifically sound information. Therefore, this chapter will provide a short overview of the state-of-the-art knowledge on etiology and pathogenesis of brain trauma, ranging from epidemiology to molecular biology, which may be helpful for understanding psychopathy as potential consequence and/or predisposing factor of brain trauma. Brain trauma can be defined as an external influence, physical or psychological, on the brain that either temporarily or permanently leads to functional and/or morphological damage to the brain. This definition allows for the integration of both traumatic brain injury (neurotrauma) and psychotrauma under the common umbrella of ‘brain trauma’, thereby the reconsideration of recent developments of biological research. Psychotrauma is the term for all kinds of psychological injuries to the brain whereas the term neurotrauma is the term usually applied to any kind of physical brain damage ranging from traumatic brain injury to sudden, noise-induced hearing loss. Brain trauma can be direct or indirect, acute, chronic or recurrent. For overview see Figure 13.1. Brain trauma has to be recognized not only as a whole-brain disease, but even a wholebody disease. The cellular and/or molecular response of the brain and the entire organism to brain injury, physical or psychological, appears to be relatively uniform. Over all, there is a vast array of risk and protective factors, some of them genetically determined, which play an important modifying role for the course and outcome of brain trauma.

EPIDEMIOLOGY AND RISK FACTORS According to the Brain Injury Association of America, more than 2 % of the US population currently live with disabilities resulting from traumatic brain injury (Kraus & McArthur, 1999). Over one million US Americans sustain a traumatic brain injury each year with only The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

218

VOLUME I: DIAGNOSIS AND TREATMENT

- RISK FACTORS -

(genetic and environmental)

BRAIN TRAUMA

Physical

indirect

"Neurotrauma" "Brain Injury"

Psychological "Psychotrauma"

acute – chronic - recurrent

- MODIFIERS -

(enhancers and protective factors)

immediate consequences initiation of molecular - cellular cascades early (weeks)

acute psychopathology organ dysfunction delayed (up to 1 year)

cognitive alterations psychiatric comorbidity brain atrophy physical disability late (years to decades)

personality changes “enhancement” of personality disorders cognitive decline degenerative brain disease persistent physical disability

enormous individual, familial and societal costs

very early (minutes → ongoing)

Figure 13.1 Overview of brain trauma – flowchart of consequences

10 % of cases resulting in severe long-term disability or death. The remaining cases may or may not recover. With an incidence of 235 cases per 100,000 inhabitants per year, a prevalence of around 7.8 million cases and an estimation of 6.3 million people living with some level of disability or handicap, the numbers in Europe are comparable (Tagliaferri et al., 2006). Consequences apart from death and severe disability are neither accurately followed nor reliably estimated. These, however, may be most relevant in the context of this book. An important field in brain trauma research is the detection and definition of risk and protective factors. Table 13.1 gives an overview of identified risk factors in both neurotrauma and psychotrauma patients. Logically, the absence of a potential predisposing factor or the presence of a specific risk factor may be considered as at least partially being protective, for example, the risk for developing post-traumatic stress disorder (PTSD) may be less for

BRAIN TRAUMA

219

Table 13.1 Overview of the most important identified predisposing/risk factors of brain trauma Neurotrauma /Brain injury

Psychotrauma /PTSD

Biological risk factors

Genetic risk factors, gender (male:female = 2:1), age (highest risk at age 15–24 years and >75 years)

Social and economic risk factors

Lower socioeconomic status, inner city residence, marital status (unmarried, singles), risky behavior (risky sports, negligent use of protection such as seat belts, helmets), increased professional risk Earlier head trauma, family psychiatric history, e.g., schizophrenia; pre-existing history of own psychiatric illness, e.g., schizophrenia, conduct disorder, substance use disorder, especially alcohol use

Genetic risk factors, female gender, smaller hippocampal volume, increased presence of neurological soft signs, presence of abnormal cavum septum pellucidum Lower socioeconomic status, less education, lack of social support, risky behavior, professional exposure

Prior historyrelated risk factors

Negative modifiers of course and outcome

Genetic factors (APOE genotype), greater trauma severity, multiple trauma exposure, quality of intensive care treatment, complications and comorbidity

Multiple trauma exposure; family psychiatric history, e.g., depression; lower intelligence; early life trauma, e.g., childhood abuse; pre-existing history of psychiatric illness, e.g., anxiety disorder, mood disorder, conduct disorder, substance use disorder Greater trauma severity, group C symptoms after exposure to a disaster, act of terrorism or combat, subsequent life stress, lack of coping strategies, quality of early intervention

Sources: Andrews et al. (2003), Bazarian et al. (2005), Brewin et al. (2000), Chan et al. (1989), Fann et al. (2004), Fearnside & Simpson (1997), Koenen et al. (2002), Kraus et al. (1984), Kraus & Nourjah (1988), Kraus & McArthur (1996), Malaspina et al. (2001); Nemeroff et al. (2006), North et al. (2001), Pitman et al. (2006), Segman & Shalev (2003), Solomon & Mikulincer (2006), Tagliaferri et al. (2006), Winqvist et al. (2006)

individuals who are male and have neither a psychiatric history in their family nor a history of psychiatric illness themselves. The risk of traumatic brain injury is highest among adolescents, young adults (peaking in the age group 15–24 years) and those older than 75 years of age. Men are approximately twice as likely as women to sustain traumatic brain injury. This ratio approaches parity as age increases because of the increased likelihood of brain injury caused by falls, for which members of both sexes have similar risks later in life (Fearnside & Simpson, 1997; Kraus et al., 1984; Kraus & McArthur, 1996). Other risk factors include socioeconomic factors such as low income, marital status (unmarried > married), residence in inner cities, as well as history of previous brain injury, psychiatric illness and substance abuse (Kraus et al., 1984; Kraus & McArthur, 1996). Especially alcohol is a major factor in traumatic brain injuries (Tagliaferri et al., 2006) (Table 13.1). In a recent study, adolescents who drank alcohol once a month or more often (frequent drinkers) or who had sometimes been drunk before the age of 14 years, were compared with adolescents who never consumed alcohol. Alcohol use in this cohort of 10,424 14-yearold adolescents born in 1966 in Northern Finland was associated with an increased rough

220

VOLUME I: DIAGNOSIS AND TREATMENT

relative risk of traumatic brain injury during the follow-up period of 21 years (Winqvist et al., 2006). In a retrospective study exploring genetic risk factors, history of traumatic brain injury and diagnosis of 1275 individuals with multiplex bipolar disorder pedigrees were compared with 565 individuals of multiplex schizophrenia pedigrees. Family members of those with schizophrenia were more likely to have had traumatic brain injury than were members of the bipolar disorder pedigrees. Interestingly, members of the schizophrenia pedigrees failed to show the typical gender difference for traumatic brain injury in the general population (twice as common in men as in women) that was present in the bipolar disorder pedigrees (Malaspina et al., 2001). With each brain injury, the risk for a second or a third increases dramatically (Fearnside & Simpson, 1997; Kraus et al., 1984; Kraus & McArthur, 1996). In contrast to traumatic brain injury, reliable numbers on psychotrauma victims are missing. The vast majority of people suffering from psychotrauma do not seek professional help, partly due to lack of knowledge even among professionals. For instance, in a recent study comparing neuropsychological and psychopathological development of two groups of victims of vehicular accidents, those with severe brain injury and those with multiple traumas excluding the brain, yielded unexpected results for the multiple trauma group. Upon follow-up, multiple trauma patients suffered from memory loss, concept disorganization, loss of initiative, irritability, unusual thought content, mood swings, attention difficulties, suspiciousness and feelings of guilt (Frenisy et al., 2006). The study suggests that neurobehavioral and psychopathological disorders of polytraumatized patients without brain injury may at least in part reflect severe psychotraumatization of these subjects. Relatively accurate numbers at least on subgroups of psychotraumatized patients may be obtained from studies on post-traumatic stress disorder (PTSD). The most comprehensive epidemiological data on PTSD were obtained in the National Comorbidity Survey (NCS) in which a representative US sample of 5877 persons, ages 15 to 54, was interviewed (Kessler et al., 1995). The estimated lifetime prevalence of PTSD is 7.8 %, with women being over twice as likely as men to have suffered from this condition (10.4 % versus 5.0 %). The traumas most commonly associated with PTSD are interpersonal violence (e.g., rape, assault, torture), exposure to life-threatening accidents (e.g., car accidents) and disasters (e.g., fires, earthquakes). Table 13.2 shows that there is a considerable variation between the prevalence of specific traumatic events in the general population, the rates of the most upsetting traumas reported by persons with PTSD, and the rates of subjects who developed PTSD in response to a specific traumatic event. Importantly, there is also a different distribution of prevalence rates among men and women. The greater exposure to more distressing traumas and the greater likelihood of developing PTSD once exposed are among the reasons for the higher lifetime prevalence of PTSD in women. Witnessing someone being badly injured or killed (35.6 %) and accidents (25 %) are the most frequent traumas experienced by men, and the most upsetting traumas reported in male persons with PTSD are combat (28.8 %) and witnessing (24.3 %). However, the experience of rape (65 %) and combat (38.8 %) resulted in the highest probability for PTSD in men. Whereas natural disasters (15.2 %) and witnessing (14.5 %) show the highest prevalence rates in women, rape (29.9 %) and sexual molestation (19.1 %) were reported as the most upsetting traumas of women with PTSD. Finally, physical abuse (48.5 %) and rape (45.9 %) result in the highest probability of PTSD in women. The National Comorbidity Survey also investigated psychiatric comorbidity and the duration of PTSD. In fact, 88 % of men and 79 % of women with PTSD showed a lifetime history of at least one other psychiatric disorder. The

BRAIN TRAUMA

221

Table 13.2 Prevalence of psychotrauma/PTSD Prevalence of traumatic event in the general population (%)

Most upsetting traumas reported in persons with PTSD (%)

Persons who developed PTSD in response to a specific event (%)

Traumatic event

Men

Women

Men

Women

Men

Women

Rape Molestation Physical attack Combat Shock Threat with weapon Accident Natural disaster with fire Witness Neglect Physical abuse Other qualifying trauma Any trauma

0.7 2.8 11.1 6.4 11.4 19.0

9.2 12.3 6.9 0.0 12.4 6.8

5.4 1.8 1.4 28.8 4.5 2.5

29.9 19.1 5.9 — 6.8 7.7

65.0 12.2 1.8 38.8 4.4 1.9

45.9 26.5 21.3 — 10.4 32.6

25.0 18.9

13.8 15.2

12.1 5.2

5.1 3.5

6.3 3.7

8.8 5.4

35.6 2.1 3.2 2.2

14.5 3.4 4.8 2.7

24.3 2.8 7.4 3.8

4.9 1.8 8.2 7.0

6.4 23.9 22.3 12.7

7.5 19.7 48.5 33.4

60.7

51.2

100.0

100.0

8.1

20.4

Source: Kessler et al. (1995)

retrospective data suggest that PTSD usually occurs subsequent to at least one previous disorder and is often associated with the subsequent onset of other disorders. While major depression (48 %), alcohol abuse/dependence (52 %) and conduct disorder (43 %) are the most frequent comorbid diagnoses in men, major depression (49 %), simple phobia (29 %) and social phobia (28 %) are the most prevalent comorbid disorders in women. The remission of PTSD is strongest in the first 12 months after onset of symptoms and proceeds for approximately six years, resulting in a median duration of PTSD between three years (among individuals who obtained treatment) and five years (among individuals who did not receive treatment). However, one-third of persons with PTSD never fully remit even after many years and irrespective of whether they are in treatment (Kessler et al., 1995).

CAUSES AND SEVERITY OF BRAIN TRAUMA An overview of causes of psycho- and neurotrauma is given in Table 13.3. Whereas automobile accidents are the leading cause of neurotrauma, followed by falls as a second leading cause, the most prominent cause for psychotrauma is rape (Yehuda, 2002). A large number of classification systems have been described, predominantly aiming at a more objective rating of the severity of trauma that might allow one to estimate the intensity of therapy and rehabilitation required as well as the potential prognosis. Regarding traumatic brain injury, the Glasgow Coma Scale and the Glasgow Outcome Scale are perhaps the most frequently used instruments. Although useful in many ways, these and other scales in the field did not

222

VOLUME I: DIAGNOSIS AND TREATMENT

Table 13.3 Most important causes of neuro- and psychotrauma Neurotrauma/Traumatic brain injury

Psychotrauma/PTSD

Traffic accidents (> 90 % of all in age group 15–24) (road crashes: automobiles >> motorcycles > pedestrians > bicyclists) Falls Physical assault (firearms) Sports (horseback riding, military, bicycle riding, soccer, football, boxing) * Other recreation-related causes

Rape Molestation Physical assault, combat Sudden death of loved one Accident, natural disaster Witnessed death or injury

∗ Sports and bicycle riding account for about 26 % of mild head injuries among children aged 5–14 years Sources: Bazarian et al. (2005), Chan et al. (1989), Fearnside & Simpson (1997), Kraus et al. (1984), Kraus & Nourjah (1988), Kraus & McArthur (1996), Tagliaferri et al. (2006), Yehuda (2002)

prove to be very helpful in predicting outcome when applied in acutely traumatized patients (van der Naalt, 2001). Table 13.4 summarizes the items included in these scales. The accurate diagnosis of PTSD is based on the diagnostic criteria for PTSD of the DSM-IV (American Psychiatric Association, 2000) (Figure 13.2). It is made with general structured clinical interviews, for example, the Structured Clinical Interview for DSM-IV (SCID) (Spitzer et al., 1994), or with interviews that are dedicated to PTSD, for example, the Clinician-Administered PTSD Scale, (CAPS) (Blake et al., 1990, 1995). In addition to the structured clinical interviews, PTSD questionnaires are used to assess self-reports of patients’ symptom severity. Among the most frequently employed instruments is the PTSD Symptom Scale (PSS), a psychometrically sound measure of symptom frequency and diagnostic status (Foa et al., 1993). Despite all efforts at developing suitable instruments, there are as yet no reliable predictors of the course of disease and outcome after brain trauma.

MOLECULAR PATHOGENESIS Neurotrauma and psychotrauma share a large number of pathogenetic and pathophysiological features, especially regarding the more delayed consequences of brain trauma. Physical forces at the moment of injury directly damage brain parenchyma, that is, neurons, glial cells and cerebral vasculature. Regardless of the type of this initial traumatic brain injury (focal mechanical blow/crash, penetrating gunshot, stab wound or thermal injury), an evolving sequence of secondary events (gene expression, metabolic, neurochemical, inflammatory, hypoxic-ischemic events and edema formation) is set in motion that spreads from the original lesion site to induce a global disturbance in brain function (Bullock, 1997; Dash, Kobori & Morre, 2004; Goerlach et al., 1998; Knerlich et al., 1999; Michael, Byers & Irwin, 2005; Raghupathi, 2004; Shapira & Shohami, 1993; Shohami et al., 1999; Sir´en et al., 2000; Sullivan et al., 2005). Recent advances in genomic technology have resulted in attempts at a molecular description of brain injury. Microarray analyses, confirmed either by real-time polymerase chain reaction (PCR), Northern blotting or in-situ hybridization of rat and mouse brain tissue in several models of experimental brain injury, have identified a great number of differentially expressed genes in the injured brain (Dash, Kobori & Moore, 2004). Over 50 % of the differentially expressed genes both during the acute (less than 24 hours after injury) and subacute (more than 24 hours after injury) response to brain injury were genes

BRAIN TRAUMA

223

Table 13.4 Established instruments for severity rating of traumatic brain injury Glasgow Coma Score The GCS is scored between 3 and 15, 3 being the worst, and 15 the best. It is composed of three parameters: Best Eye Response, Best Verbal Response, Best Motor Response, as given below: Best Eye Response (4) Score 1 2 3 4

Rating No eye opening Eye opening to pain Eye opening to verbal command Eyes open spontaneously

Best Verbal Response (5) Score 1 2 3 4 5

Rating No verbal response Incomprehensible sounds Inappropriate words Confused Orientated

Best Motor Response (6) Score 1 2 3 4 5 6

Rating No motor response Extension to pain Flexion to pain Withdrawal from pain Localising pain Obeys commands

Glasgow Outcome Score Score

Rating

Definition

5 4

Good recovery Moderate disability

3

Severe disability

2 1

Persistent vegetative Death

Resumption of normal life despite minor deficits Disabled but independent. Can work in sheltered setting Conscious but disabled. Dependent for daily support Minimal responsiveness Non survival

Note that the phrase ‘GCS of 11’ is essentially meaningless, and it is important to break the figure down into its components, such as E3V3M5 = GCS 11. A Coma Score of 13 or higher correlates with a mild brain injury; 9 to 12 is a moderate injury and 8 or less a severe brain injury. Source: Teasdale & Jennett (1974)

224

VOLUME I: DIAGNOSIS AND TREATMENT

A. Person has been exposed to a traumatic event with both of the following present: (1) the person experienced, witnessed, or was confronted with event(s) that involved actual or threatened death or serious injury; (2) the person’s response involved intense fear, helplessness, or horror. B. The traumatic event is persistently reexperienced in one (or more) of following ways: (1) recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions; (2) recurrent distressing dreams of the event; (3) acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative flashback episodes, including those that occur on awakening or when intoxicated); (4) intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event; (5) physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event. C. Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by three (or more) of the following: (1) efforts to avoid thoughts, feelings, conversations associated with the trauma; (2) efforts to avoid activities, places, people that arouse recollections of trauma; (3) inability to recall an important aspect of the trauma; (4) markedly diminished interest or participation in significant activities; (5) feeling of detachment or estrangement from others; (6) restricted range of affect (e.g., unable to have loving feelings); (7) sense of a foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span). D. Persistent symptoms of increased arousal (not present before the trauma), as indicated by two (or more) of the following: (1) difficulty falling or staying asleep; (2) irritability or outbursts of anger; (3) difficulty concentrating; (4) hypervigilance; (5) exaggerated startle response. E. Duration of the disturbance is more than one month. Figure 13.2 Diagnostic criteria for post-traumatic stress disorder (DSM-IV)

involved in regulation of signal transduction, neuronal plasticity and brain metabolism (Dash, Kobori & Moore, 2004). Analysis of pericontusional tissue taken during surgery from patients with severe head injury found 104 out of 12,000 analyzed genes to be differentially expressed in brain samples of brain injury patients as compared to control samples of presumably normal brain tissue from a patient with vasculitis and one with meningeoma (Michael, Byers & Irwin, 2005). Out of these, only the expression of four immediate early genes (c-fos, Jun-B, HSP70 and Zif/268) have been verified by Northern blotting (Michael, Byers & Irwin, 2005). Upregulation of the immediate early genes has been a consistent finding in the previous animal models (Dash, Kobori & Moore, 2004). Using in-situ

BRAIN TRAUMA

225

hybridization, we found an immediate c-fos upregulation at 30 seconds after parietal cortical freezing the lesion in the perilesional tissue. Starting at six hours and extending until 24 hours after injury, a profound bilateral hippocampal expression of c-fos mRNA was observed, indicating a widespread activation of gene expression after a small, focal cortical injury in a highly standardized model free of a primary contre-coup damage (Sir´en et al., 2000). A mechanical trauma on the other hand always leads to diffuse axonal and vascular injury due to primary cerebral laceration and to contre-coup damage (Blumbergs, 1997; Gennarelli et al., 1982; Ommaya, Grugg & Naumann, 1971). The degree and pattern of this injury depends on the manner and duration in which kinetic energy impacts the cranium: typical to motor vehicle accidents is a long duration of acceleration/deceleration force leading to severe diffuse axonal injury whereas brief duration of shear force (e.g., slow crush injury) produces massive skull fractures, subdural hematomas and contusion (Bullock, 1997). The immediate pathophysiological sequelae after a head injury inevitably lead to a chronic neurodegeneration manifesting months to years after injury as global brain atrophy, cognitive impairments, deficits in attention and motivation and personality changes (Arciniegas et al., 1999; Finset et al., 1999; Geuze et al., 2005; Jennett, 1997; MacKenzie et al., 2002; Malaspina et al., 2001; Max et al., 2004; McAllister & Green, 1998; McKinlay et al., 2002; Milman et al., 2005; Parker & Rosenblum, 1996; Piazza, Sir´en & Ehrenreich, 2004; Sir´en et al., 2006). The mechanisms involved in the initiation of the chronic events are complex and may include disruption of the blood–brain barrier, overall microglia activation and excessive oxidative stress characterized by reduced antioxidative capacity, increased production of oxygen radicals and alterations in excitatory neurotransmitter release/receptor expression (Biegon et al., 2004; Ezra et al., 2003; Genis et al., 2000; Knerlich et al., 1999; Panikashvili et al., 2001; Shohami et al., 1994, 1999; Sir´en et al., 2000). These mechanisms add up to tissue damage and mortality in the acute phase following head injuries. How these acute events actually lead to chronic functional impairments, however, is not well understood. Massive acute cell loss through apoptosis/necrosis does not seem to be the only contributing factor for the late functional impairments, because gradually accelerating brain atrophy and cognitive decline can be observed as late consequences of mild to moderate head injuries that do not cause acute excessive neuronal loss (Bigler et al., 2006; MacKenzie et al., 2002; McKinlay et al., 2002; Milman et al., 2005; Skelton et al., 2000; Zohar et al., 2003). Therefore, other possible pathophysiological mechanisms may be considered. For example, even slightly damaged neurons may exhibit reduced plasticity with reduced synaptic/axonal sprouting which eventually leads to reduced synaptic function and connectivity. Recent experimental studies have indeed revealed impaired synaptic plasticity and widespread synaptic dysfunction after a freeze-induced cortical lesion in rats (Peters et al., 2004; Redecker et al., 2000). We found global brain atrophy months after discrete unilateral parietal cortical freezing lesion when it was applied in juvenile (four-week-old) mice (Sir´en et al., 2006). As illustrated in Figure 13.3, significant enlargement of cerebral ventricles and reduction in brain-matter volume was evident six months after lesioning. In mice, the developmentally regulated loss of cortical synapses occurs during the juvenile period (four weeks of age) of postnatal life (Zuo et al., 2005). Brain injury at this vulnerable period might lead to an exaggerated loss of synapses and unfavorable metabolic alterations which set off the late cognitive decline and brain atrophy. In this respect, the consequences of traumatic brain injury in childhood and early adolescence share many features of psychotrauma (e.g., hippocampal dysfunction, impairments in attention and motivation).

226

VOLUME I: DIAGNOSIS AND TREATMENT p<0.05

p<0.05 sham lesion n=12 97

96

3 ventricles (%total brain)

brain matter (%total brain)

98

sham lesion n=12

2

1

0

0

sham

lesion

Figure 13.3 Brain atrophy six months after parietal cortical injury. Shown are bar graphs of volumetrical quantification and representative magnetic resonance images illustrating ventricular enlargement six months after standardized unilateral parietal cortical freeze lesion

Long-term outcome after brain injury depends on the extent of neuronal loss, regeneration and plasticity (Giza & Prins, 2006; Palop, Chin & Mucke, 2006). These functions are under the control of multiple internal and external factors that influence gene expression and biochemical homeostasis in the brain (compare also Table 13.1). Therefore, outcome depends not solely on the severity of the primary brain injury but can be modified by genetic and environmental factors. For example, possession of the apolipoprotein E (APOE ε4) allele reduces the prospect of a favorable outcome in children and young adults (Teasdale, Murray & Nicoll, 2005). Increased mortality after closed head injury has been reported in mice overexpressing the human APOE ε4, whereas the allele ε3 is protective (Sabo et al., 2000). Even though the presence of the APOE ε4 allele is associated with the severity of atherosclerosis and cerebrovascular impairment, the negative influence of the APOE ε4 allele can also be explained by impaired functioning of apolipoprotein E (APOE) in the brain (White et al., 2001a). APOE, the most prevalent lipoprotein in the nervous tissue, is known to be involved in lipid debris clearance and recycling of lipids to sprouting neurons during recovery after neuronal injury (White et al., 2001a). Interestingly, APOE ε4 overexpressing mice not only show an impaired capacity to clear lipid cell debris and to recycle lipids

BRAIN TRAUMA

227

to damaged neurons for sprouting and synaptogenesis but also exhibit drastically reduced neuronal plasticity after brain injury (White et al., 2001a, 2001b). Pituitary dysfunction following traumatic brain injury may lead to growth hormone insufficiency which can contribute to reduced synaptic plasticity and worsen neurobehavioral recovery after head injury (Bondanelli et al., 2004; Kelly et al., 2006). In this context, it is important to note that while post-traumatic hypopituitarism was described more than 80 years ago (Cryan, 1918), its clinical significance and high incidence (50 % of head injury victims) has been recognized only recently (Agha et al., 2004; Lieberman et al., 2001; Powner et al., 2006). To summarize, the long-term neuropsychological alterations after mild to moderate brain injury may reflect complex functional impairments which are the result of processes impairing neuronal plasticity and the integrity of the neuronal network. The molecular pathophysiology of psychotrauma has been much less studied than that of traumatic brain injury. Neuroimaging studies have identified specific alterations in the hippocampus and amygdala in patients with post-traumatic stress disorder (Hull, 2002; Yehuda, 2002), at least in part resembling the sequence of events late after traumatic brain injury. The most replicated finding in neuroimaging studies in adults has been a volume reduction of the hippocampus (Hull, 2002), fitting conceptually well with the animal studies demonstrating that exposure to chronic severe stress leads to marked hippocampal damage (de Kloet, Joels & Holsboer, 2005; Miller & McEwen, 2006; Sapolsky et al., 1990). However, a hippocampal volume reduction has neither been seen in children and adolescents with PTSD (Hull, 2002; Tupler & De Bellis, 2006) nor with studies that have rigorously excluded comorbid alcohol abuse (Gilbertson et al., 2002; Woodward et al., 2006). On the other hand, a pre-existing smaller hippocampal size has shown to increase the risk for development of PTSD (Gilbertson et al., 2002; Pitman et al., 2006). Patients with PTSD exhibit distinct neurochemical and neuroendocrine alterations, including increased circulating norepinephrine levels and an increased reactivity to alphaadrenergic drugs (Yehuda, 2002). Specific alterations in the stress response in patients with PTSD include low serum cortisol, high cerebrospinal fluid corticotropin releasing factor (CRF) and an enhanced responsiveness of the hypothalamic–pituitary–adrenal axis to glucocorticoid challenge (Yehuda, 2002). The most relevant animal models that have been developed to elucidate the biological mechanisms of PTSD use acute and chronic stressors such as restraint or immobilization (Miller & McEwen, 2006; Siegmund & Wotjak, 2006) which target amygdala, frontal cortex and hippocampus (Elzinga & Bremner, 2002). In the hippocampus, chronic stress leads to morphological (inhibition of dentate neurogenesis, increased neuronal death, reduced synaptic density and dendritic length) and functional (hippocampal memory tasks) deficits (de Kloet et al., 2005; Miller & McEwen, 2006) similar to those seen as late consequences after neurotrauma (see above). The hypothalamic– pituitary–adrenal axis seems to play a complex role in the stress effects in rodents, with very low and very high circulating glucocorticoid levels having a negative effect on neural plasticity and memory (de Kloet et al., 2005; Miller & McEwen, 2006; Siegmund & Wotjak, 2006). Interestingly, inhibition of protein synthesis with anisomycin can in an animal model reduce the anxiety-related behavior when applied before or shortly after predator stress, suggesting that disruption of the consolidation of traumatic memory may alleviate symptoms of PTSD (Cohen et al., 2006). Similar findings have been reported in the use of beta-adrenergic receptor blockers; propranolol can block reconsolidation of fear memory and prevent stress-related hippocampal memory (Miller & McEwen, 2006). Dysfunction of the autonomic nervous system is a feature of clinical PTSD (Elzinga & Bremner, 2002;

228

VOLUME I: DIAGNOSIS AND TREATMENT

Yehuda, 2002). An overactive adrenergic system seems to be involved also in the aggression and irritability seen in head injury victims as these symptoms respond well to treatment with propranolol and other beta-adrenergic receptor blockers (Warden et al., 2006). In this respect both psychotrauma and neurotrauma share most features of global brain and perhaps even whole-body dysfunction. Interestingly, a general reduction in gene expression of transcription activators was recently observed in peripheral blood mononuclear cells from trauma survivors who had developed PTSD (Segman et al., 2005).

CONSEQUENCES OF BRAIN TRAUMA Outcome after brain injury is certainly dependent on quality and efficiency of early intervention. This includes the intensive care setting where (multi-)organ dysfunction and secondary complications can be coped with (Jennett, 1997; Levin & Grossman, 1978; Levin et al., 1979). In the case of psychotrauma it means immediate attention and psychotherapeutic support (Nemeroff et al., 2006; Vieweg et al., 2006). Immediate re-exposure during crisis intervention, however, has proven to be damaging rather than helpful (McNally, Bryant & Ehlers, 2003).

Early Consequences Psychopathological features during the early post-trauma phase include confusion, psychomotor slowing, amnesia and aggression (Warden et al., 2006). During acute post-trauma recovery, 35–96 % of brain injury victims exhibit aggressive behavior (Brooke et al., 1992; Levin & Grossman, 1978; Rao, Jellinek & Woolston, 1985; Tateno, Jorge & Robinson, 2003). Agitation and irritability often prevail with estimates of 67–71 % of victims showing these symptoms for up to 15 years after injury (Levin et al., 1979; Rao, Jellinek & Woolston, 1985; Thomsen, 1984).

Delayed Consequences Delayed consequences of brain trauma occurring after the acute phase (up to one year after injury or psychotrauma) include increasing awareness of disability (causing additional psychotraumatization) and decreased quality of life, sustained hyperactivity/agitation and irritability, mental fatigue, motor slowing, mood swings, depression and suicidality. Unusual thought content, hostility and suspicion may also be present (Anstey et al., 2004; Brooke et al., 1992; Jorge et al., 2004; Levin & Grossman, 1978; Levin et al., 1979; Rao, Jellinek & Woolston, 1985; Tateno, Jorge & Robinson, 2003; Thomsen, 1984). A recent study, assessing phenomenology and predictive factors of personality features following traumatic brain injury in 177 children, ages 5–14 years, found personality changes in 22 % of participants in the first six months after injury (Max et al., 2005). Similarly, survival analyses showed that individuals with active PTSD are substantially more likely than those without PTSD to develop other anxiety, mood and substance use disorders (Kessler, 2000). For example, men and women with PTSD are 5.7 and 3.4 times, respectively, as likely as demographically matched controls to develop subsequent major depression. The corresponding odds ratios are equally high for other disorders, for example, dysthymia (5.3 in men, 4.4 in women), panic disorder (4.6 in men, 3.1 in women), or alcohol

BRAIN TRAUMA

229

dependence (3.0 in men, 3.2 in women). Importantly, people with PTSD are six times as likely as people without PTSD to attempt suicide (Kessler, 2000). Disinhibition and sex offending are a significant problem among a minority (6–7 %) of mostly male traumatic brain injury victims (Frenisy et al., 2006; Simpson, Blaszczynski & Hodgkinson, 1999). Most commonly, touching offenses, followed by exhibitionism and, rarely, overt sexual aggression are observed, and attributed to lesions of the frontal or frontotemporal cortex and the limbic system (Simpson et al., 1999). Persistent cognitive dysfunction following traumatic brain injury becomes typically evident after resolution of acute post-traumatic amnesia (Levine et al., 2005; McAllister, 1992). Basically all cognitive domains (attention and speed of processing, flexibility, memory and executive functions) are affected (McAllister, 1992; McAllister & Green, 1998). In fact, gray matter reduction and ventricular enlargement (as revealed by MRI) are observed even after mild to moderate traumatic brain injury and correlate with cognitive and functional outcome (MacKenzie et al., 2002; Parker & Rosenblum, 1996). Regarding psychotrauma, two recent reviews conclude that there is evidence for at least mild impairment in attention and immediate memory in individuals with chronic PTSD (Golier & Yehuda, 2002; Horner & Hamner, 2002). However, both reviews emphasize that any conclusions regarding deficits in other cognitive domains are premature because of the inconsistency of findings and methodologically confounding factors. In addition, it remains unclear to which extent the high psychiatric comorbidity, especially long-term substance abuse and dependence, might contribute to the cognitive deficits in chronic PTSD patients. Other important confounders are motivational issues, the extent of chronicity, and the role of possible cognitive deficits that antedate trauma experience and might be among the risk factors for development of PTSD (Golier & Yehuda, 2002; Horner & Hamner, 2002).

Late Consequences In respect to personality disorders and psychopathy, both neuro- and psychotrauma may be regarded as ‘enhancers’ of pre-existing personality features, both normal and abnormal (Figure 13.1, see also Ehrenreich and Sir´en (2001)). In a recent prospective study in which psychiatric illness was investigated over three years after traumatic head injury, mild head injury seemed to be associated with higher persistent risk for psychiatric illness as contrasted to the initially higher risk for psychiatric illness in the severe to moderate head injury group (Fann et al., 2004). Depression after head injury is common, with published estimates of about 25–60 % of brain injury victims developing a depressive episode within eight years after their injury (Jorge et al., 2004; Warden et al., 2006). Depression may persist and contribute to the increased suicide rate, suicide ideation and hopelessness which have been documented several years after brain trauma (Achte et al., 1969; Simpson & Tate, 2002; Teasdale & Engberg, 2001). Regarding very late consequences of brain injury, there is an increasing amount of literature documenting neurotrauma as a risk factor for Alzheimer’s disease, Parkinson’s disease and schizophrenia (AbdelMalik et al., 2003; Arciniegas et al., 1999; Finset et al., 1999; Jennett, 1997; Koponen et al., 2002; Max et al., 2004; McAllister & Green, 1998; McKinlay et al., 2002; Milman et al., 2005; Nemetz et al., 1999; Parker & Rosenblum, 1996; Smith et al., 1997). The potential risk for the development of other diseases like amyotrophic lateral sclerosis is still a matter of discussion (Piazza, Sir´en & Ehrenreich, 2004). In all degenerative diseases developing in a person who underwent a brain trauma, the genetic

230

VOLUME I: DIAGNOSIS AND TREATMENT

predisposition might play an important role. In other words, a person without any genetic predisposition for schizophrenia, for example, will not develop the disease even after being exposed to trauma as a known environmental risk factor. The role of previous psychotrauma (PTSD) in the development of degenerative brain disease is still a matter of speculation, although from a biological point of view one might expect that there is as much an enhancer function of psychotrauma as it is of neurotrauma. Interesting in this respect is the observation that depression has been reported to confer an increased risk for Alzheimer’s disease (Ownby et al., 2006).

Effects of Brain Trauma on Occupational and Social Functioning Individuals with brain trauma suffer from widespread occupational and social dysfunction. For instance, a PTSD study that investigated 182 survivors of the bombing of the Alfred P. Murrah Federal Building in Oklahoma City six months after the disaster, also assessed indicators of social and occupational functioning (North et al., 1999). Of the subjects with PTSD alone, 52 % reported that their PTSD interfered with their activities, and 53 % were dissatisfied with their work performance. With 87 % and 78 %, respectively, the rates of functional interference and work dissatisfaction were even higher for those with PTSD and comorbid depression. About 75 % of the individuals with PTSD had negative changes in personal relationships as a result of the bombing. Survivors without PTSD showed, on the contrary, lower rates of functional interference (17 %), dissatisfaction with work performance (40 %) and worsened personal relationships (27 %). PTSD patients with comorbid depression had particularly higher rates of negative changes of personal relationships with spouses (32 %), household members (23 %) and relatives or friends (43 %), compared with subjects without PTSD who showed rates of 5 %, 2 % and 10 %, respectively (North et al., 1999).

Socioeconomic Costs of Brain Trauma The cost of traumatic brain injury in the United States is estimated to be almost $50 billion annually (Kraus & McArthur, 1999). For a person with severe head injury the lifetime costs are over $3 million; for moderate injury, $941,000; and for mild trauma, $85,000. Only a few studies on the socioeconomic burden of PTSD are available in contrast to major depression, for example, which is supposed to be among the most burdensome diseases in the world (Kessler, 2000). Thus, estimates of socioeconomic costs of PTSD should be considered as preliminary and interpreted with caution. Analyses based on the National Comorbidity Survey data found that the amount of work impairment associated with PTSD (0.8 days/month of work loss, 2.8 days/month of work cutback) is very similar to that associated with major depression (0.4 days/month of work loss, 2.8 days/month of work cutback), but less than that associated with panic disorder (1.4 days/month of work loss, 4.9 days/month of work cutback), translating into an annual productivity loss over $3 billion in the United States. In addition, NCS respondents with PTSD had 40 % elevated odds of high school and college failure, 30 % elevated odds of teenage childbearing, 60 % elevated odds of marital instability and 150 % elevated odds of being unemployed compared to individuals without PTSD (Kessler, 2000). The findings of three recent studies suggest that among patients with anxiety disorders, those with PTSD cause the highest treatment

BRAIN TRAUMA

231

costs: Greenberg et al. (1999) estimated that PTSD is the strongest cost driver with respect to service use and workplace costs compared to other anxiety disorders, and thus is among the most expensive anxiety disorders, which in total caused an economic burden of approximately $42.3 billion in 1990 (Greenberg et al., 1999). An examination of medical-care costs associated with PTSD in Vietnam veterans found that a diagnosis of PTSD was associated with medical costs 60 % higher than average (Marshall et al., 2000). This result is in accordance with a more recent study which estimated that mean total medical costs for individuals diagnosed with an anxiety disorder is approximately $6475, and that PTSD is the anxiety disorder with the highest increase in total medical costs (Marciniak et al., 2005).

SUMMARY AND CONCLUSIONS Despite different causes, both neurotrauma and psychotrauma lead to a similar cascade of events ranging from biomedical to socioeconomic consequences that ultimately influence personality through alterations in cognition, emotions and behavior, in addition to potential physical disability. The degree of personality change may ultimately depend not only on the severity of the trauma (with mild to moderate injuries having even more pronounced and lasting effects on personality than severe injuries), but also on the individual genetic background and modifying environmental factors. Regarding delayed and late consequences of mild to moderate traumatic brain injury or of psychotrauma, a vast array of similarities are detectable. The same holds true when predisposing/risk factors are compared. Altogether, there is still important information missing, particularly in light of potential preventive strategies, which points to the need, in parallel with more relevant animal experiments, for comprehensive prospective studies on the course of neuro- and psychotrauma.

REFERENCES AbdelMalik, P., Husted, J., Chow, E.W.C. & Bassett, A.S. (2003). Childhood head injury and expression of schizophrenia in multiply affected families. Archives of General Psychiatry, 60, 231–6. Achte, K.A., Hillbom, E. & Aalberg, V. (1969). Psychoses following war brain injuries. Acta Psychiatrica Scandinavica, 45, 1–18. Agha, A., Rogers, B., Sherlock, M. et al. (2004). Anterior pituitary dysfunction in survivors of traumatic brain injury. Journal of Clinical Endocrinology and Metabolism, 89, 4929–36. Andrews, B., Brewin, C. & Rose, S. (2003). Gender, social support, and PTSD in victims of violent crime. Journal of Traumatic Stress, 16, 421–7. American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders: DSM-IV-TR. Washington, DC: American Psychiatric Association. Anstey, K.J., Butterworth, P., Jorm, A.F. et al. (2004). A population survey found an association between self-reports of traumatic brain injury and increased psychiatric symptoms. Journal of Clinical Epidemiology, 57, 1202–9. Arciniegas, D., Adler, L., Topkoff, J. et al. (1999). Attention and memory dysfunction after traumatic brain injury: cholinergic mechanisms, sensory gating, and a hypothesis for further investigation. Brain Injury, 13, 1–13. Bazarian, J.J., McClung, J., Shah, M.N. et al. (2005). Mild traumatic brain injury in the United States, 1998–2000. Brain Injury, 19, 85–91.

232

VOLUME I: DIAGNOSIS AND TREATMENT

Biegon, A., Fry, P.A., Paden, C.M. et al. (2004). Dynamic changes in N-methyl-D-aspartate receptors after closed head injury in mice: implications for treatment of neurological and cognitive deficits. Proceedings of the National Academy of Sciences of the USA, 101, 5117–22. Bigler, E.D., Ryser, D.K., Gandhi, P. et al. (2006). Day-of-injury computerized tomography, rehabilitation status, and development of cerebral atrophy in persons with traumatic brain injury. American Journal of Physical Medicine and Rehabilitation, 85, 793–806. Blake, D., Weathers, F., Nagy, L. et al. (1990). A clinician rating scale for assessing current and lifetime PTSD: the CAPS-1. Behavior Therapist, 13, 187–8. Blake, D., Weathers, F., Nagy, L. et al. (1995). The development of a clinician-administered PTSD scale. Journal of Traumatic Stress, 8, 75–90. Blumbergs, P.C. (1997). Pathology. In P. Reilly & R. Bullock (eds.), Head Injury (pp. 39–70). London: Chapman & Hall. Bondanelli, M., De Marinis, L., Ambrosio, M.R. et al. (2004). Occurrence of pituitary dysfunction following traumatic brain injury. Journal of Neurotrauma, 21, 685–96. Brewin, C., Andrews, B. & Valentine, J. (2000). Meta-analysis of risk factors for posttraumatic stress disorder in trauma-exposed adults. Journal of Consulting and Clinical Psychology 68, 748–66. Brooke, M.M., Patterson, D.R., Questad, K.A. et al. (1992). The treatment of agitation during initial hospitalization after traumatic brain injury. Archives of Physical Medicine and Rehabilitation, 73, 917–21. Bullock, R. (1997). Injury and cell function. In P. Reilly & R. Bullock (eds.), Head Injury (pp. 121–41). London: Chapman & Hall. Chan, B.S., Walker, P.J. & Cass, D.T. (1989). Urban trauma: an analysis of 1,116 paediatric cases. Journal of Trauma-Injury Infection and Critical Care, 29, 1540–7. Cohen, H., Kaplan, Z., Matar, M.A. et al. (2006). Anisomycin, a protein synthesis inhibitor, disrupts traumatic memory consolidation and attenuates posttraumatic stress response in rats. Biological Psychiatry, 60, 767–76. Cryan, E. (1918). Hypophysensch¨adigung durch Sch¨adelbasisfraktur. Deutsche Medizinische Wochenschrift, 44, 1261. Dash, P.K., Kobori, N. & Moore, A.N. (2004). A molecular description of brain trauma pathophysiology using microarray technology: an overview. Neurochemical Research, 29, 1275–86. de Kloet, E.R., Joels, M. & Holsboer, F. (2005). Stress and the brain: from adaptation to disease. Nature Reviews Neuroscience, 6, 463–75. Ehrenreich, H. and Sir´en, A.-L. (2001). Neuroprotection – what does it mean? – What means do we have? European Archives of Psychiatry and Clinical Neuroscience, 251, 149–51. Elzinga, B.M. & Bremner, J.D. (2002). Are the neural substrates of memory the final common pathway in posttraumatic stress disorder (PTSD)? Journal of Affective Disorders, 70, 1–17. Ezra, Y., Oron, L., Moskovich, L. et al. (2003). Apolipoprotein E4 decreases whereas apolipoprotein E3 increases the level of secreted amyloid precursor protein after closed head injury. Neuroscience, 121, 315–25. Fann, J., Burington, B., Leonetti, A. et al. (2004). Psychiatric illness following traumatic brain injury in an adult health maintenance organization population. Archives of General Psychiatry, 61, 53–61. Fearnside, M. & Simpson, D. (1997). Epidemiology. In P. Reilly & R. Bullock (eds.), Head Injury (pp. 2–24). London: Chapman & Hall. Finset, A., Anke, A.W., Hofft, E. et al. (1999). Cognitive performance in multiple trauma patients 3 years after injury. Psychosomatic Medicine, 61, 576–83. Foa, E., Riggs, D., Dancu, C. & Rothbaum, B. (1993). Reliability and validity of a brief instrument for assessing post-traumatic stress disorder. Journal of Traumatic Stress, 6, 459–73. Frenisy, M.C., Benony, H., Chahraoui, K. et al. (2006). Brain injured patients versus multiple trauma patients: some neurobehavioral and psychopathological aspects. Journal of Trauma-Injury Infection and Critical Care, 60, 1018–26. Genis, L., Chen, Y., Shohami, E. & Michaelson, D.M. (2000). Tau hyperphosphorylation in apolipoprotein E-deficient and control mice after closed head injury. Journal of Neuroscience Research, 60, 559–64. Gennarelli, T.A., Thibault, L.E., Adams, J.H. et al. (1982). Diffuse axonal injury and traumatic coma in the primate. Annals of Neurology, 12, 564–74.

BRAIN TRAUMA

233

Geuze, E., Vermetten, E. & Bremner, J.D. (2005). MR-based in vivo hippocampal volumetrics: 2. Findings in neuropsychiatric disorders. Molecular Psychiatry, 10, 160–84. Gilbertson, M.W., Shenton, M.E., Ciszewski, A. et al. (2002). Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Nature Neuroscience, 5, 1242–7. Giza, C.C. & Prins, M.L. (2006). Is being plastic fantastic? Mechanisms of altered plasticity after developmental traumatic brain injury. Developmental Neuroscience, 28, 364–79. Goerlach, C., Sir´en, A.L., Knerlich, F. et al. (1998). Delayed loss of ETB receptor-mediated vasorelaxation after cold lesion of the rat parietal cortex. Journal of Cerebral Blood Flow and Metabolism, 18, 1357–64. Golier, J. & Yehuda, R. (2002). Neuropsychological processes in post-traumatic stress disorder. Psychiatric Clinics of North America, 25, 295–315. Greenberg, P.E., Sisitsky, T., Kessler, R.C. et al. (1999). The economic burden of anxiety disorders in the 1990s. Journal of Clinical Psychiatry, 60, 427–35. Horner, M.D. & Hamner, M.B. (2002). Neurocognitive functioning in posttraumatic stress disorder. Neuropsychology Review, 12, 15–30. Hull, A.M. (2002). Neuroimaging findings in post-traumatic stress disorder – Systematic review. British Journal of Psychiatry, 181, 102–10. Jennett, B. (1997). Outcome after severe head injury. In P. Reilly & R. Bullock (eds.), Head Injury (pp. 439–61). London: Chapman & Hall. Jorge, R.E., Robinson, R.G., Moser, D. et al. (2004). Major depression following traumatic brain injury. Archives of General Psychiatry, 61, 42–50. Kelly, D.F., McArthur, D.L., Levin, H. et al. (2006). Neurobehavioral and quality of life changes associated with growth hormone insufficiency after complicated mild, moderate, or severe traumatic brain injury. Journal of Neurotrauma, 23, 928–42. Kessler, R. (2000). Posttraumatic stress disorder: the burden to the individual and to society. Journal of Clinical Psychiatry, 61, 4–14. Kessler, R.C., Sonnega, A., Bromet, E. et al. (1995). Posttraumatic stress disorder in the National Comorbidity Survey. Archives of General Psychiatry, 52, 1048–60. Knerlich, F., Schilling, L., Goerlach, C. et al. (1999). Temporal profile of expression and cellular localization of inducible nitric oxide synthase, interleukin-1beta and interleukin converting enzyme after cryogenic lesion of the rat parietal cortex. Brain Research. Molecular Brain Research, 68, 73–87. Koenen, K.C., Harley, R., Lyons, M.J. et al. (2002). A twin registry study of familial and individual risk factors for trauma exposure and posttraumatic stress disorder. Journal of Nervous and Mental Disease, 190, 209–18. Koponen, S., Taiminen, T., Portin, R. et al. (2002). Axis I and II psychiatric disorders after traumatic brain injury: a 30-year follow-up study. American Journal of Psychiatry, 159, 1315–21. Kraus, J.F., Black, M.A., Hessol, N. et al. (1984). The incidence of acute brain injury and serious impairment in a defined population. American Journal of Epidemiology, 119, 186–201. Kraus, J.F. & McArthur, D.L. (1996). Epidemiologic aspects of brain injury. Neurologic Clinics, 14, 435–50. Kraus, J.F. & McArthur, D.L. (1999). Incidence and prevalence of and costs associated with traumatic brain injury. In M. Rosenthal, E. Griffith, J. Kreutzer & B. Pentland (eds.), Rehabilitation of the Adult and Child with Traumatic Brain Injury, 3rd edition (pp. 3–18). Philadelphia: F.A. Davis. Kraus, J.F. & Nourjah, P. (1988). The epidemiology of mild, uncomplicated brain injury. Journal of Trauma-Injury Infection and Critical Care, 28, 1637–43. Levin, H.S. & Grossman, R. (1978). Behavioral sequelae of closed head injury. A quantitative study. Archives of Neurology, 35, 720–7. Levin, H.S., Grossman, R.G., Rose, J.E. & Teasdale, G. (1979). Long-term neuropsychological outcome of closed head injury. Journal of Neurosurgery, 50, 412–22. Levine, S.C., Kraus, R., Alexander, E. et al. (2005). IQ decline following early unilateral brain injury: A longitudinal study. Brain and Cognition, 59, 114–23. Lieberman, S., Oberoi, A., Gilkison, C. et al. (2001). Prevalence of neuroendocrine dysfunction in patients recovering from traumatic brain injury. Journal of Clinical Endocrinology and Metabolism, 86, 2752–6.

234

VOLUME I: DIAGNOSIS AND TREATMENT

MacKenzie, J.D., Siddiqi, F., Babb, J.S. et al. (2002). Brain atrophy in mild or moderate traumatic brain injury: a longitudinal quantitative analysis. American Journal of Neuroradiology, 23, 1509–15. Malaspina, D., Goetz, R.R., Friedman, J.H. et al. (2001). Traumatic brain injury and schizophrenia in members of schizophrenia and bipolar disorder pedigrees. American Journal of Psychiatry, 158, 440–6. Marciniak, M.D., Lage, M.J., Dunayevich, E. et al. (2005). The cost of treating anxiety: the medical and demographic correlates that impact total medical costs. Depression and Anxiety, 21, 178–84. Marshall, R.P., Jorm, A.F., Grayson, D.A. & O’Toole, B.I. (2000). Medical-care costs associated with posttraumatic stress disorder in Vietnam veterans. Australian and New Zealand Journal of Psychiatry, 34, 954–62. Max, J.E., Lansing, A.E., Koele, S.L. et al. (2004). Attention deficit hyperactivity disorder in children and adolescents following traumatic brain injury. Developmental Neuropsychology, 25, 159–77. Max, J.E., Levin, H.S., Landis, J. et al. (2005). Predictors of personality change due to traumatic brain injury in children and adolescents in the first six months after injury. Journal of the American Academy of Child and Adolescent Psychiatry, 44, 434–42. McAllister, T.W. (1992). Neuropsychiatric sequelae of head injuries. Psychiatric Clinics of North America, 15, 395–413. McAllister, T.W. & Green, R.L. (1998). Traumatic brain injury: a model of acquired psychiatric illness? Seminars in Clinical Neuropsychiatry, 3, 158–9. McKinlay, A., Dalrymple-Alford, J.C., Horwood, L.J. & Fergusson, D.M. (2002). Long term psychosocial outcomes after mild head injury in early childhood. Journal of Neurology, Neurosurgery, and Psychiatry, 73, 281–8. McNally, R.J., Bryant, R.A. & Ehlers, A. (2003). Does early psychological intervention promote recovery from posttraumatic stress? Psychological Science, 45–79. Michael, D.B., Byers, D.M. & Irwin, L.N. (2005). Gene expression following traumatic brain injury in humans: analysis by microarray. Journal of Clinical Neuroscience, 12, 284– 90. Miller, M.M. & McEwen, B.S. (2006). Establishing an agenda for translational research on PTSD. Annals of the New York Academy of Sciences, 1071, 294–312. Milman, A., Rosenberg, A., Weizman, R. & Pick, C.G. (2005). Mild traumatic brain injury induces persistent cognitive deficits and behavioral disturbances in mice. Journal of Neurotrauma, 22, 1003–10. Nemeroff, C., Bremner, J., Foa, E. et al. (2006). Posttraumatic stress disorder: a state-of-the-science review. Journal of Psychiatric Research, 40, 1–21. Nemetz, P.N., Leibson, C., Naessens, J.M. et al. (1999). Traumatic brain injury and time to onset of Alzheimer’s disease: a population-based study. American Journal of Epidemiology, 149, 32–40. North, C.S., Nixon, S.J., Shariat, S. et al. (1999). Psychiatric disorders among survivors of the Oklahoma City bombing. Journal of the American Medical Association, 282, 755–62. North, C., Spitznagel, E. & Smith, E. (2001). A prospective study of coping after exposure to a mass murder episode. Annals of Clinical Psychiatry, 13, 81–7. Ommaya, A.K., Grubb, R.L., Jr. & Naumann, R.A. (1971). Coup and contre-coup injury: observations on the mechanics of visible brain injuries in the rhesus monkey. Journal of Neurosurgery, 35, 503–16. Ownby, R., Crocco, E., Acevedo, A. et al. (2006). Depression and risk for Alzheimer disease: systematic review, meta-analysis, and metaregression analysis. Archives of General Psychiatry, 63, 530–8. Palop, J.J., Chin, J. & Mucke, L. (2006). A network dysfunction perspective on neurodegenerative diseases. Nature, 443, 768–73. Panikashvili, D., Simeonidou, C., Ben-Shabat, S. et al. (2001). An endogenous cannabinoid (2-AG) is neuroprotective after brain injury. Nature, 413, 527–31. Parker, R. S. & Rosenblum, A. (1996). IQ loss and emotional dysfunctions after mild head injury incurred in a motor vehicle accident. Journal of Clinical Psychology, 52, 32–43. Peters, O., Redecker, C., Hagemann, G. et al. (2004). Impaired synaptic plasticity in the surround of perinatally acquired dysplasia in rat cerebral cortex. Cerebral Cortex, 14, 1081–7. Piazza, O., Sir´en, A.-L. & Ehrenreich, H. (2004). Soccer, neurotrauma and amyotrophic lateral sclerosis: is there a connection? Current Medical Research and Opinion, 20, 505–8.

BRAIN TRAUMA

235

Pitman, R.K., Gilbertson, M.W., Gurvits, T.V. et al. (2006). Clarifying the origin of biological abnormalities in PTSD through the study of identical twins discordant for combat exposure. Annals of the New York Academy of Sciences, 1071, 242–54. Powner, D., Boccalandro, C., Alp, M. & Vollmer, D. (2006). Endocrine failure after traumatic brain injury in adults. Neurocritical Care, 5, 61–70. Raghupathi, R. (2004). Cell death mechanisms following traumatic brain injury. Brain Pathology, 14, 215–22. Rao, N., Jellinek, H.M. & Woolston, D.C. (1985). Agitation in closed head injury: haloperidol effects on rehabilitation outcome. Archives of Physical Medicine and Rehabilitation, 66, 30–4. Redecker, C., Luhmann, H.J., Hagemann, G. et al. (2000). Differential downregulation of GABAA receptor subunits in widespread brain regions in the freeze-lesion model of focal cortical malformations. Journal of Neuroscience, 20, 5045–53. Sabo, T., Lomnitski, L., Nyska, A. et al. (2000). Susceptibility of transgenic mice expressing human apolipoprotein E to closed head injury: the allele E3 is neuroprotective whereas E4 increases fatalities. Neuroscience, 101, 879–84. Sapolsky, R.M., Uno, H., Rebert, C.S. & Finch, C.E. (1990). Hippocampal damage associated with prolonged glucocorticoid exposure in primates. Journal of Neuroscience, 10, 2897–902. Segman, R.H. & Shalev, A.Y. (2003). Genetics of posttraumatic stress disorder. CNS Spectrums, 8, 693–8. Segman, R.H., Shefi, N., Goltser-Dubner, T. et al. (2005). Peripheral blood mononuclear cell gene expression profiles identify emergent post-traumatic stress disorder among trauma survivors. Molecular Psychiatry, 10, 425, 500–13. Shapira, Y. & Shohami, E. (1993). Experimental studies on brain oedema after blunt head injury: experimental approaches from animal experimentation to actual or possible clinical application. European Journal of Anaesthesiology, 10, 155–73. Shohami, E., Gati, I., Beit-Yannai, E. et al. (1999). Closed head injury in the rat induces whole body oxidative stress: overall reducing antioxidant profile. Journal of Neurotrauma, 16, 365–76. Shohami, E., Novikov, M., Bass, R. et al. (1994). Closed head injury triggers early production of TNF alpha and IL-6 by brain tissue. Journal of Cerebral Blood Flow and Metabolism, 14, 615–19. Siegmund, A. & Wotjak, C. T. (2006). Toward an animal model of posttraumatic stress disorder. Annals of the New York Academy of Sciences, 1071, 324–34. Simpson, G., Blaszczynski, A. & Hodgkinson, A. (1999). Sex offending as a psychosocial sequela of traumatic brain injury. Journal of Head Trauma Rehabilitation, 14, 567–80. Simpson, G. & Tate, R. (2002). Suicidality after traumatic brain injury: demographic, injury and clinical correlates. Psychological Medicine, 32, 687–97. Sir´en, A.-L., Knerlich, F., Schilling, L. et al. (2000). Differential glial and vascular expression of endothelins and their receptors in rat brain after neurotrauma. Neurochemical Research, 25, 957–69. Sir´en, A.-L., Radyushkin, K., Boretius, S. et al. (2006). Global brain atrophy after unilateral parietal lesion and its prevention by erythropoietin. Brain, 129, 480–9. Skelton, R.W., Bukach, C.M., Laurance, H.E. et al. (2000). Humans with traumatic brain injuries show place-learning deficits in computer-generated virtual space. Journal of Clinical and Experimental Neuropsychology, 22, 157–75. Smith, D.H., Chen, X.H., Pierce, J.E. et al. (1997). Progressive atrophy and neuron death for one year following brain trauma in the rat. Journal of Neurotrauma, 14, 715–27. Solomon, Z. & Mikulincer, M. (2006). Trajectories of PTSD: a 20-year longitudinal study. American Journal of Psychiatry, 163, 659–66. Spitzer, R., Williams, J., Gibbon, M. & First, M. (1994). Structured Clinical Interview for DSM-IV (SCID-IV). New York: Biometric Research, New York State Psychiatric Institute. Sullivan, P.G., Rabchevsky, A.G., Waldmeier, P.C. & Springer, J.E. (2005). Mitochondrial permeability transition in CNS trauma: cause or effect of neuronal cell death? Journal of Neuroscience Research, 79, 231–9. Tagliaferri, F., Compagnone, C., Korsic, M. et al. (2006). A systematic review of brain injury epidemiology in Europe. Acta Neurochirurgica, 148, 255–68. Tateno, A., Jorge, R.E. & Robinson, R.G. (2003). Clinical correlates of aggressive behavior after traumatic brain injury. Journal of Neuropsychiatry and Clinical Neurosciences, 15, 155–60.

236

VOLUME I: DIAGNOSIS AND TREATMENT

Teasdale G.M. & Jennett B. (1974). Assessment of coma and impaired consciousness. A practical scale. Lancet, (ii), 81–4. Teasdale, G.M., Murray, G.D. & Nicoll, J.A. (2005). The association between APOE epsilon4, age and outcome after head injury: a prospective cohort study. Brain, 128, 2556–61. Teasdale, T.W. & Engberg, A.W. (2001). Suicide after traumatic brain injury: a population study. Journal of Neurology, Neurosurgery and Psychiatry, 71, 436–40. Thomsen, I. (1984). Late outcome of very severe blunt head trauma: a 10-15 year second follow-up. Journal of Neurology Neurosurgery and Psychiatry, 47, 260–8. Tupler, L.A. & De Bellis, M.D. (2006). Segmented hippocampal volume in children and adolescents with posttraumatic stress disorder. Biological Psychiatry, 59, 523–9. van der Naalt, J. (2001). Prediction of outcome in mild to moderate head injury: a review. Journal of Clinical and Experimental Neuropsychology 23, 837–51. Vieweg, W.V.R., Julius, D.A., Fernandez, A. et al. (2006) Posttraumatic stress disorder: Clinical features, pathophysiology, and treatment. American Journal of Medicine, 119, 383–90. Warden, D.L., Gordon, B., McAllister, T.W. et al. (2006) Guidelines for the pharmacologic treatment of neurobehavioral sequelae of traumatic brain injury. Journal of Neurotrauma, 23, 1468–501. White, F., Nicoll, J.A. & Horsburgh, K. (2001a). Alterations in ApoE and ApoJ in relation to degeneration and regeneration in a mouse model of entorhinal cortex lesion. Experimental Neurology, 169, 307–18. White, F., Nicoll, J.A., Roses, A.D. & Horsburgh, K. (2001b). Impaired neuronal plasticity in transgenic mice expressing human apolipoprotein E4 compared to E3 in a model of entorhinal cortex lesion. Neurobiological Disorders, 8, 611–25. Winqvist, S., Jokelainen, J., Luukinen, H. & Hillbom, M. (2006). Adolescents’ drinking habits predict later occurrence of traumatic brain injury: 35-year follow-up of the northern Finland 1966 birth cohort. Journal of Adolescent Health, 39, 275. Woodward, S.H., Kaloupek, D.G., Streeter, C.C. et al. (2006). Hippocampal volume, PTSD, and alcoholism in combat veterans. American Journal of Psychiatry, 163, 674–81. Yehuda, R. (2002). Post-traumatic stress disorder. New England Journal of Medicine, 346, 108–14. Zohar, O., Schreiber, S., Getslev, V. et al. (2003) Closed-head minimal traumatic brain injury produces long-term cognitive deficits in mice. Neuroscience, 118, 949–55. Zuo, Y., Yang, G., Kwon, E. & Gan, W.B. (2005) Long-term sensory deprivation prevents dendritic spine loss in primary somatosensory cortex. Nature, 436, 261–5.

CHAPTER 14

Acquired Psychopathy and the Assessment of Traumatic Brain Injury Robert P. Granacher University of Kentucky College of Medicine, USA

and Manish A. Fozdar Duke University Medical Center, USA

One of the most intriguing observations of patients with ventromedial prefrontal cortex lesions pertains to the realm of personality. The development of certain maladaptive personality features following the onset of damage to this brain region has been noted repeatedly throughout the history of neuropsychiatry. This chapter will review the history of Phineas Gage, and cover the characteristics of the syndrome of acquired psychopathy following traumatic brain injury. This discussion includes analysis of this syndrome and principles of traumatic brain-injury assessment. General issues of impairment of social and moral behavior following early damage to prefrontal cortex are discussed. Psychopathy has been an academic and clinical subject of interest to psychiatric and psychological professionals for many years. Cleckley (1976) provided one of the early clinical and practical descriptions of psychopathic lives and behaviors. Since Cleckley’s book was published, Hare (1991) has published the Hare Psychopathy Checklist-Revised; this is a useful standardized method for assessing clinically the presence of psychopathic traits. The most recently defined criteria for antisocial or psychopathic personality disorder are within the DSM-IV-TR (American Psychiatric Association, 2000). However, acquired psychopathy presents a dual-diagnosis issue. The behavioral characteristics – at least in part – can be represented by the DSM-IV-TR criteria for antisocial personality disorder. On the other hand, since acquired psychopathy from traumatic brain injury or other brain-injury disorders usually results in a cognitive impairment as well, it is probably more accurate to use the diagnostic term, ‘personality change, due to traumatic brain injury’, from the DSMIV-TR criteria to characterize acquired psychopathy. Moreover, it has been argued that antisocial personality disorder, as described in DSM-IV-TR, is broader and more inclusive The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

238

VOLUME I: DIAGNOSIS AND TREATMENT

in nature, and does not represent true psychopathy, as described by Cleckley and Hare (Reid & Ruiz-Sweeney, 2003). This chapter will review the neuropsychiatry of acquired psychopathy as specifically related to lesions of the ventromedial prefrontal cortex (VMPF). The pathogenesis and manifestations of acquired psychopathy will be discussed. Little information on the prognosis of acquired psychopathy is available in the medical literature, but it may persist for 10 years or more (Tranel, 2002). Methods for assessment of acquired brain injury causing psychopathy will follow the models for assessing any form of acquired brain injury, whether specific for acquired psychopathy or not.

THE NATURE OF ACQUIRED PSYCHOPATHY Deficits of higher cognition and social behavior are common sequelae of acquired lesions of the prefrontal brain cortex. These behavioral changes have been linked specifically with damage to the orbitofrontal or ventromedial prefrontal cortex. Historically, the specific emotional, cognitive or physiological processes of these sequelae have not been well delineated (Mah, Arnold & Grafman, 2005). One of the best historical representations of acquired psychopathy is the famous case of Phineas Gage, made relevant to us by the astute clinical observations of his physician, John Harlow (1848). On September 13, 1848, Phineas Gage was using a tamping iron, which struck an unexploded piece of dynamite while he worked on a Vermont railroad. The tamping iron exploded forcefully under his left zygoma, and exited through his right medial-frontal skull. Recently, Gage’s skull was analyzed by using modern computer-assisted reconstruction by Damasio et al. (1994). Figure 14.1 demonstrates the inferior medial frontal anatomy that was injured by the tamping rod and is the locus of the VMPF. As Harlow outlined 20 years after his first publication (1868), Gage displayed a profound change in personality and social conduct following this injury. Prior to this injury, he was described as a responsible, socially well-adjusted and popular person with coworkers and supervisors. After his injury, he became irresponsible, untrustworthy, irreverent, capricious, unreliable and callous (Harlow, 1868). Harlow went on to say that Gage was ‘fitful, irreverent, indulging at times in the grossest profanity (which was not previously his custom), manifesting but little deference for his fellows, impatient of restraint or advice when it conflicts with his desires, at times pertinaciously obstinate, yet capricious and vacillating, devising many plans of future operation, which are no sooner arranged than they are abandoned and turned for others appearing more feasible’ (Harlow, 1868). The University of Iowa group has called our attention to the bizarre development of personality changes and abnormal social behavior that occurs following prefrontal brain injury (Tranel, 2002). After prefrontal brain injury, patients display a number of characteristic features: inability to organize future activity and hold gainful employment; diminished capacity to respond to punishment; a tendency to present an unrealistic, favorable view of themselves; and a tendency to display inappropriate emotional reactions. Thirty years ago, Blumer and Benson (1975) characterized these same personality features as ‘pseudopsychopathic’; they characterized the behavior of afflicted persons as puerile, jocular in attitude, displaying sexually disinhibited humor, demonstrating inappropriate and near-total selfindulgence and a complete lack of concern for others. Stuss and Benson (1986) described further that these patients demonstrate a remarkable lack of empathy and show a general

ACQUIRED PSYCHOPATHY

239

Figure 14.1 Phineas Gage. Reprinted with permission from Damasio, H. et al. (1994). The return of Phineas Gage: clues about the brain from a famous patient. Science, 264, 1102–5, c 1994. Courtesy of Dr. Hanna Damasio, the Dana and David Dornsife Cognitive Neuro science Imaging Center and Brain and Creativity Institute, University of Southern California

lack of concern about others; they describe patients as showing boastfulness, unrestrained and tactless behavior, impulsiveness, facetiousness, and diminished anxiety and concern for the future. These antisocial personality characteristics and profiles bear some striking similarities to those described by Cleckley (1976), Hare (1991) and the DSM-IV-TR (American Psychiatric Association, 2000). Interestingly, when an attempt was made to measure the characteristics of ventromedial prefrontal patients, using standardized personality instruments, the endeavor was a complete failure. Barrash, Tranel and Anderson (1994) administered to a group of patients demonstrating ventromedial prefrontal damage several psychometric instruments, including the MMPI-2, the Eysenck Personality Questionnaire, the Structured Interview for the DSMIII-R and the Hare Psychopathy Checklist-Revised. The VMPF patients generated normal personality profiles on these instruments, or produced profiles that were in no way faithful to the real-world personality manifestations of the patients. Barrash and his group argue that this outcome may be explained by the fact that many of these instruments rely on the

240

VOLUME I: DIAGNOSIS AND TREATMENT

self-report of the patient. It is well known that VMPF patients have significant anosognosia (organically based lack of insight) for their condition. It is also well known that VMPF patients have normal personalities prior to the onset of their brain injuries, for the most part.

THE PATHOGENESIS OF ACQUIRED PSYCHOPATHY It is presumed that since the human prefrontal cortex produces the type of higher order cognitive processes that distinguish humans from other primates, an understanding of its underlying cognitive and neurological architecture can only come from the study of humans. Persons who sustain frontal-lobe lesions generally are able to understand conversation, commands, recognize and use objects, and express themselves adequately enough to interact socially; they can learn and remember geographic routes, and they can make decisions. However, they do present themselves with defects of attention, and they have difficulty anticipating what will happen next (seeing to the future) and in dividing their resources. They often demonstrate difficulty adjusting to situations requiring social cognition, and they often show problems with processing the theme or the moral of a story line. They generally demonstrate impairment in forming concepts, abstracting, reasoning and planning. These deficits have been observed and confirmed by investigators with clinical and experimental research over the last 40 years (Grafman, 2002). The human prefrontal cortex (PFC) can be described as composed of a number of functional domains; these include working memory, executive function, attentional-control processing, social cognition and somatic marking, action sequencing and computational frame working (Grafman, 2002). Baddely (1998a) notes that human working memory was first proposed some 30 years ago. This term was used to account for a variety of human memory data that was not addressed by the models of short-term memory in use at that time. Working memory has been noted recently to contain slave systems, which are employed by working memory to allow for the maintenance of stimuli in a number of different forms that can be manipulated by the central-executive component of the working-memory system (Baddely, 1998b). Working memory can be thought of in a simplified schema as the random-access memory to be provided to the hard disc in computer conceptualization. With regard to executive function, Norman and Shallice (1986) argue that the PFC is primarily specialized for the supervision of attention towards unexpected occurrences. They have also hypothesized the presence of a scheduling system that is specialized for the initiation and efficient running of automatized behaviors, such as repetitive routines, procedures and skills. Burgess (2000) has expanded the idea that the prefrontal cortex is a voluntary-control device, and that the supervisory-attention system is fractionated into a set of parallel-attention processors that work together to manage complex, multitask behaviors. For the control of social and emotional behavior, there is substantial evidence that the prefrontal cortex is involved in these functions. Damasio and his University of Iowa colleagues have repeatedly confirmed the association of VMPF lesions and abnormalities of social behavior and decision making. Convincing evidence is emerging that the VMPF serves to associate somatic markers (autonomic nervous system modulators that bias activation and decision making) with social knowledge; this enables rapid social decision making, particularly for overlearned associative knowledge. Damasio (1996) has noted that these markers are distributed across a large system of brain regions, including the limbic system and its substructures, such as the amygdala.

ACQUIRED PSYCHOPATHY

241

It has been conceptualized that the PFC is the cognitive extension of the specialized motor areas of the frontal lobes (Gomez Beldarrain et al., 1999). This cognitive system is thought to play an essential role in determining action sequences in the real world. Clinical examples of deficits of action in patients with frontal-lobe lesions include ideomotor or ideation dyspraxia, and can be demonstrated in patients by asking them to mimic brushing their teeth or to demonstrate how to saw an imaginary piece of wood. However, it is not clear whether evidence of this error of praxis has ecological validity in predicting whether patients would be able to carry action to a higher level, such as planning a vacation (Grafman, 2002). How is it then that damage to the VMPF can produce the syndrome of acquired psychopathy? Grafman (2002) describes the structured parts of complex social behavior as a structured-event complex (SEC). He defines an SEC as a set of events, structured in a particular sequence, that as a complex, composes a particular kind of activity that is usually goal oriented. For instance, the complex events that would be necessary to pursue a goal of developing a relationship with the opposite sex, or planning and carrying out a complex social event, such as a dinner at a restaurant with a friend would represent an SEC. This level of complexity becomes even more challenging to persons with VMPF lesions when the moral aspects of behavior are coupled with behaviors necessary to plan and carry out a structured event. Even if an individual possessed sufficient cognitive capacity to carry out a structured event, an individual with a VMPF lesion may have such a profound inability to express emotion, and to experience feeling relative to these complex personal and social situations, that he cannot function in a morally acceptable social manner. Tranel’s research (2002) has noted differences between developmental psychopaths and early-onset VMPF patients, in that the patterns of aggression in the latter seem impulsive, rather than goaldirected, and have a highly transparent, almost childlike nature to them. The behavior of VMPF patients is even more puzzling, when compared to the fact that they usually are capable of performing normally on many conventional neuropsychological procedures. They do not manifest defects of intellectual function, generally. If the lesion is confined closely to the VMPF, their working memory, attention and concentration may seem relatively normal. Moreover, they often perform well on many so-called frontal-lobe tests, such as the Wisconsin Card Sorting Test, the Category Test and the Tower of Hanoi (Tranel, Anderson and Benton, 1994). VMPF-damaged patients manifest a profound inability to express emotion and to experience feeling, relative to complex personal and social situations; they lack in ability to express or experience embarrassment or guilt. Thus, these severe defects of social feeling and behavior cannot be explained by basic neuropsychological impairments of intellect, memory, working memory, language or attention, even if these deficits are present. The University of Iowa group proposes that deficits in bioregulatory responses might provide a plausible explanation for these deficits of behavior; this has been described earlier as the somatic-marker hypothesis (Damasio, 1996). These researchers propose five principles to explain the somatic-marker hypothesis (Tranel, 2002): 1. Certain structures in prefrontal cortex are necessary for learning the associations between complex stimuli and internal states of the organism (such as emotions). 2. When a particular class of complex social stimuli recurs during a person’s ongoing experience, systems in the VMPF region trigger the reactivation of the somatosensory pattern that depicts the appropriate somatic state.

242

VOLUME I: DIAGNOSIS AND TREATMENT

3. The somatic-marker process functions either as an incentive or a deterrent to social or moral behavior as good or bad (moral valence). 4. The somatosensory-activity pattern facilitates attentional and working-memory systems to provide an indirect influence on the decision-making process. 5. Logical reasoning is facilitated by the steps in 3 and 4. Emotion is a crucial component of the process of reasoning and decision making. In summary, somatic markers – regardless of whether they are perceived consciously in the form of feelings – provide critical signals that are needed in many situations of reasoning and decision making, and especially those that occur in a social context. Injury to the VMPF interferes with the expression of these somatic markers necessary for social control and the accurate perception of social feedbacks.

MANIFESTATIONS OF ACQUIRED PSYCHOPATHY Tranel (2002) studied 57 brain-damaged subjects, seven of whom had bilateral VMPF damage. Personality characteristics that were rated as significantly more severe in the VMPF subjects included, in descending order of severity, lack of insight, lack of initiative, irritability, social inappropriateness, poor judgment, lack of persistence, indecisiveness, lability, blunted emotional experience, apathy, inappropriate affect, poor frustration tolerance and inflexibility. As a result of this study, Tranel identified a set of personality and behavioral characteristics that comprise the core of a syndrome that the University of Iowa group has termed ‘acquired sociopathy’. This syndrome of acquired sociopathy (psychopathy) has the following characteristics:

r general damping of emotional experience; r poorly modulated emotional reactions; r disturbances in decision making; r disturbances in goal-directed behavior; r disturbances in social behavior; and r marked lack of insight into acquired changes. This syndrome was found to be highly and specifically associated with VMPF damage, and not with brain damage outside the ventromedial prefrontal region, or with brain damage in general. Moreover, the syndrome of acquired sociopathy was found to be enduring in the VMPF patients, as on average, they had manifested these characteristics for more than 10 years after the onset of brain injury. Since many patients with VMPF damage do not demonstrate impairments on conventional neuropsychological procedures – including, so-called ‘frontal-lobe’ tasks, such as the Wisconsin Card Sorting Test or the Category Test – Tranel and his University of Iowa Group developed a card game (the Gambling Task) to provide a valid analog to real-world decision making, by making unpredictable rewards and punishments an explicit aspect of the situation, and by requiring delayed-response gratification (Tranel, 2002). As Tranel describes this test, in the basic version of the Gambling Task, subjects are presented four decks of

ACQUIRED PSYCHOPATHY

243

cards, and are given a $2000 startup loan. Subjects are told that the game requires a long series of card selections, one card at a time, from any of the decks, until the experimenter ends the game. After each card selection, subjects receive a monetary reward; the amount is announced after the card selection, and varies from deck to deck. After some card selections, subjects are given money and asked to pay a penalty; again, the amount is announced only after the card selection, and it varies from deck to deck and from position to position within a given deck. Subjects are told that the goal of the task is to maximize their profit; they are free to switch from any deck to another, at any time, as often as they wish. The task is discontinued after 100 card selections (subjects are not informed of this beforehand). The Gambling Task is rigged, so that two of the decks (the disadvantageous decks) yield higher immediate rewards, but higher long-term penalties, such that selecting frequently from these decks will result in a net long-term monetary loss. The other two decks (the advantageous decks) yield lower immediate rewards, but also lower long-term penalties, such that selecting frequently from these decks will result in a net long-term financial gain (Tranel, 2002). Six subjects with bilateral VMPF lesions were compared against six braindamaged controls, who had lesions outside the VMPF, and 44 normal controls who were free of neurologic or psychiatric disease. As the Gambling Task progressed, normal and brain-damaged controls gradually shifted their selections toward the advantageous decks, and by the last two blocks (trials 61–100), the subjects were choosing almost exclusively from these decks. On the other hand, the VMPF subjects failed to demonstrate this shift: in all but one trial block, they selected more cards from the disadvantageous decks, and on the last two trial blocks, they continued to select more frequently from the disadvantageous decks. This same pattern of performance has been demonstrated in follow-up studies using different permutations of the Gambling Task within larger groups of subjects (Bechara, Tranel & Damasio, 2000). These findings suggest that patients with VMPF lesions have a fundamental insensitivity to the future consequences of their choices – whether these consequences are positive or negative – and are guided by the immediate prospects of their behavior. In another effort to measure the deficits in decision making of VMPF patients, Mah’s group (2005) compared the performance of patients with ventromedial prefrontal cortex or dorsal-lateral prefrontal cortex lesions with healthy volunteers on the Tests of Social Intelligence (TSI) (O’Sullivan & Guilford, 1976). The TSI consists of four different subtests (expression, missing cartoons, social translations and cartoon predictions), designed to measure the ability to understand the thoughts, feelings and intentions of other people, as expressed in visually observed behavior. In Mah’s group, there were 20 ventromedial frontal-lobe patients, nine dorsolateral frontal-lobe patients (who generally score poorly on the Wisconsin Card Sorting Test), and 23 normal-comparison persons. All subjects performed at above-chance levels, indicating that errors were not due simply to guessing at random; this was considered to be very important in this study, because ventromedial patients may make errors by guessing, due to difficulties in inhibiting selection responses. Ventromedial patients had lower total TSI scores, when compared with either the normalcomparison group or the dorsolateral group; the dorsolateral group did not vary significantly from the normal-comparison group. This study found objective evidence of deficits in social knowledge in patients with ventromedial prefrontal cortex damage, as compared with normal-comparison subjects. The results of this study suggest that deficits in social knowledge – namely, difficulty interpreting nonverbal emotional expression – contribute to the aberrant social behavior observed following ventromedial prefrontal cortex lesions.

244

VOLUME I: DIAGNOSIS AND TREATMENT

PROGNOSIS OF ACQUIRED PSYCHOPATHY Since acquired psychopathy is almost always caused by head and brain trauma, there is insufficient information in the medical literature to give prognostic guidelines on other potential causes of acquired psychopathy. These other causes would include brain infections, hypoxia-ischemia or ventromedial space-occupying masses. In the United States, braininjury occurrence rates range from a low of 92 per 100,000 population, to a high of 618 per 100,000 population (Kraus & Chu, 2005). There are no estimates of incidence in the United States of acquired psychopathy following traumatic brain injury or other causes. The prediction of long-term consequences following traumatic brain injury is difficult. The Glasgow Outcome Scale (Jennett & Teasdale, 1981) has been used as a predictor, but it is quite crude; it may have some validity in population studies, but its application to individual cases is poor at best. Moreover, the research criteria for defining outcome also are poor. There are broad ranges for outcome based on length of loss of consciousness, the Glasgow Coma Scale score, and other highly variable indices. These do not allow accurate outcome prediction based upon injury data at this time. There is currently at the Center for Disease Control in Atlanta an expert working group on mild traumatic brain injury; to this date, a consensus definition of mild traumatic brain injury has not been completed. Recent published guidelines for treatment of severe traumatic brain injury (Bullock et al., 1996) have demonstrated that poor outcome is increased by older age, low blood pressure, CT-scan irregularities, abnormal pupillary responses and Glasgow Coma Scale score of 3–5. There are no known specific cutoff points for age or level of hypotension. Data to predict outcomes for moderate and milder forms of traumatic brain injury are not presently available. Again, no reported studies of traumatic brain injury define specifically acquired psychopathy or lesions of the ventromedial prefrontal cortex as predictors. A meta-analysis of 14 studies of traumatic injury has demonstrated that when brain-injured patients are measured against control subjects, brain-injury patients score lower than control subjects for general intelligence 80 % of the time; language, 80 % of the time; learning and motor skills, 58 % of the time; motor skills, 42 % of the time, and spatial skills, 35 % of the time (Kraus & Chu, 2005). Thus, general intelligence, language and learning appear more affected by traumatic brain injury than motor skills and spatial skills. This is phylogenetically consistent, as motor skills and spatial skills would be much more necessary for survival of the species than general intelligence, language or learning. There has been association made between a brain trauma and the onset of neurological disease. Diseases in which a possible connection with head trauma has been reported include Pick’s disease, Parkinson’s disease, motor-neuron disease and Creutzfeldt–Jakob disease (Graham, Gennarelli & McIntosh, 2002). The most convincing synergistic interaction between traumatic brain injury and neurodegeneration is possession of the e4 allele of the apolipoprotein E gene. There is increasing evidence at this time that possession of the apolipoprotein E e4 allele is a risk factor for developing Alzheimer’s disease following traumatic brain injury (Graham, McIntosh & Maxwell, 2000; Mayeux, Ottman & Maestre, 1995). There is no available research data to demonstrate whether or not traumatic-induced acquired psychopathy will be associated with a later risk of Alzheimer’s disease. However, based upon the available data of traumatic brain injury, in general, and the relationship between apolipoprotein E e4 and brain trauma specifically, it is reasonable to conclude that a person who develops post-traumatic acquired psychopathy, and is found to possess an

ACQUIRED PSYCHOPATHY

245

allele of apolipoprotein E e4, carries a greater risk of developing Alzheimer’s disease in association with his psychopathy.

ASSESSMENT OF ACQUIRED BRAIN INJURY A method for assessing acquired brain injury has been published previously (Granacher, 2003), and is the guide used for this chapter. Major elements within a comprehensive assessment of acquired brain injury are:

r review of pertinent medical, historical and legal records; r neuropsychiatric history; r neuropsychiatric mental-status examination; r neurological examination; r structural and functional brain imaging; r standardized neurocognitive assessment; r standardized behavioral assessment; and r neurobehavioral analysis, causation analysis, impairment rating and prognosis. Analysis and review of the original-injury records are critical to understanding acquired brain injury within a personal-injury litigation. If the injury occurred on the highway, or other location requiring police confirmation, the police record can be most helpful to the injury investigation. For instance, it will document whether the injured party was able to provide a history to the investigating police officer; this will demonstrate early indicia of the injured party’s cognitive state immediately following the accident. It is important to review the ambulance record or the record of emergency medical technicians providing initial services. In most English-speaking countries, the Glasgow Coma Scale (Jennett & Teasdale, 1981) will be administered; it may not be stated as such explicitly in the record, and the examiner should look for either ‘GCS’ or ‘EMV’. EMV represents eyes, motor, verbal, and will be included in the medical record with appropriate scoring. The Glasgow Coma Scale ranges from a low of 3 (coma), to a high of 15 (full eye, motor and verbal function). If the person is transported to an emergency department of a hospital, it is important to review the early hospital records – again, for the Glasgow Coma Scale – to see if there have been changes in the score value. For instance, an emerging epidural hematoma will generally show a longitudinal decline in the Glasgow Coma Scale score; whereas, a person with minimal-to-no injury will probably score GCS = 15, and that score will remain stable over time. The hospital records will allow the examiner to determine whether neurosurgical care was required, and whether secondary traumatic issues, such as hemorrhagic shock or respiratory failure, played a role in the genesis of potential acquired brain injury. If the person required placement in an intensive care unit, it is important to review these records as often serial Glasgow Coma Scales are obtained within the course of intensive-care treatment. At discharge, the records should be reviewed to determine whether a rehabilitation unit was required, and thereafter one should seek outpatient-care records. Most forensic examinations of acquired brain injury will occur months to years following the original trauma. The mental-status examination should follow standard examination techniques. The reader may refer to Strub and Black (2000) or Trzepacz and Baker (1993) for more complete

246

VOLUME I: DIAGNOSIS AND TREATMENT

mental-status examination techniques. Likewise, the neurological examination of the adult or child should be performed by following standard neurological procedures (Bradley et al., 2000; Menkes, 1995). The management and evaluation of acquired brain injury has been revolutionized in the last 25 years, with the advent of structural imaging, such as computerized tomography (CT) and magnetic resonance imaging (MRI). More recently, functional imaging by single-photon-emission tomography (SPECT) and positron-emission tomography (PET) has been added to the evaluation armamentarium. In addition to the nuclear techniques of SPECT and PET, functional magnetic resonance imaging (fMRI) shows promise for correlating brain function with structure, and magnetic resonance spectroscopy (MRS) is becoming useful in identifying patients with neuronal injuries after acquired brain injury. For instance, the detection of N-acetylaspartate levels by MRS is a sensitive indicator of neuronal damage that results in worst-outcome brain injury (Granacher, 2003). Whereas, the neurological examination and structural or functional brain imaging can indicate acquired brain injury, these techniques cannot detect whether a person can think, reason or calculate following acquired brain injury; that is best detected by a standardized neurocognitive assessment. A standardized assessment of cognitive function following acquired brain injury should usually contain measurements of the following:

r cognitive forensic distortion; r psychological forensic distortion; r preinjury cognitive baseline estimation; r attention; r memory; r language; r visuoperceptual ability; r sensorimotor function; r executive function; r intellectual function; and r behavioral function. All standardized neuropsychological test instruments are effort-dependent; therefore, it is incumbent upon the forensic examiner to determine whether optimal cognitive effort has been provided during a neurocognitive examination. Moreover, attempts should be made to measure tendencies to malinger, symptom-magnify or otherwise bias the cognitive examination. Measurement of cognitive distortion should be based on binomial probability theory. It is wise to avoid using cognitive-effort tests, such as the Rey 15-Item Figure Memory Test or Dot-Counting Test (Lezak, 1995). There are many test instruments available to measure cognitive effort during neuropsychological examination; thus, the examiner has a wide choice of validity instruments available. These include such tests as the Portland Digit Recognition Test (Binder, 1993), the Test of Memory Malingering (Tombaugh, 1996), or the Victoria Symptom Validity Test (Slick et al., 1997). Since a neuropsychological examination is a present-state examination, it detects evidence of acquired brain injury after the fact. It is very important to establish a person’s preinjury cognitive baseline, in order to determine accurately deficits that are a result of acquired brain injury, and to distinguish these from those deficits that may have been present prior to acquired brain injury. Many tests are available for determining preinjury mental abilities, and these are generally based on demographic tests, such as the Barona Index,

ACQUIRED PSYCHOPATHY

247

the Oklahoma Estimate, or Wilson’s Formula (Granacher, 2003), or are based upon reading ability, such as the National Adult Reading Test (NART), North American Adult Reading Test (NAART), Wechsler Test of Adult Reading (WTAR), or Wide Range Achievement Test (WRAT) (Granacher, 2003). A test widely used by neuropsychologists in North America is the Wechsler Test of Adult Reading (2001), which was developed specifically to provide clinicians with an assessment tool for estimating premorbid intellectual functioning of adults ages 16–89; it has been developed and standardized with the Wechsler Adult Intelligence Scale-III (WAIS-III) and the Wechsler Memory Scale-III (WMS-III). With regard to acquired brain injury, this test has been specifically standardized in persons who have sustained traumatic brain injury, suffer from Parkinsonism, Huntington’s disease, or Alzheimer’s disease. The WTAR is probably the most powerful test available at this time for estimation of premorbid intellectual and memory abilities in persons with acquired brain injury. The predictions are based not only upon reading scores, but the WTAR also specifically includes a combination of WTAR reading scores and a demographics prediction of WAIS-III and WMS-III scores. The forensic examiner must also keep in mind that if a person is being retested on instruments administered at a prior time following acquired brain injury, the scores may inflate, due to the practice effect (Lezak, Howieson & Loring, 2004). Practice effects occur as a result of repeated psychological examinations. The general rule for practice effects is that psychological test instruments having a large speed component, that require an unfamiliar or infrequently practiced mode of response, or have a single solution – particularly, if it can be easily conceptualized once it is attained – are much more likely to show significant elevation of scores than tests that do not have these features. There are texts available, which may be consulted to determine the effect of practice on certain psychological test instruments (McCaffrey, Duff & Westervelt, 2000). After the cognitive effort of the individual being examined has been established, and after a preinjury cognitive baseline has been established, neuropsychological testing should be undertaken to measure the various cognitive domains tabulated above. Some neuropsychologists will follow a format using batteries, such as the Halstead–Reitan Test Battery (Reitan & Wolfson, 1993), Luria–Nebraska Neuropsychological Battery for Adults (Golden, Purisch & Hammeke, 1991), and the NEPSY for children (Korkman, Kirk & Kemp, 1998). Other neuropsychological approaches may use the deficit-measurement technique (Lezak, Hoieson & Loring, 2004) or the Boston process approach (Milberg, Hebben & Kaplan, 1996). A comprehensive evaluation of acquired brain injury also includes a standardized behavioral assessment. In the United States, most neuropsychologists will use either the Minnesota Multiphasic Personality Inventory-2 (Graham, 2006) or the Personality Assessment Inventory (Morey, 1996); these can provide important ancillary information about behavioral functioning following acquired brain injury. They also provide a screen for psychological forensic distortion in personal-injury litigation, as they are capable of measuring negativeresponse bias producing a malingering or symptom-magnification pattern. Since mental malingering can occur either as cognitive distortion, psychological distortion or distortion of both cognitive and psychological aspects of an examination, it is necessary to have an independent assessment of psychological test effort, as well as an independent assessment of cognitive test effort. After the neuropsychiatric evaluation is completed, neurobehavioral analysis should be applied to the data. At this point, it is necessary to return to the original-injury records and

248

VOLUME I: DIAGNOSIS AND TREATMENT

determine the exact nature of the injury and the severity of the injury, from the perspective of those providing immediate care and treatment. Once the litigation process is undertaken, bias is much more likely to be introduced into the evaluations, and expert opinions tend to become polarized. Following review of the injury record, the examiner should review his or her mental status and neurological evaluations to determine whether focal mental or neurological deficits are obvious. Brain neuroimaging should be consulted to review for the presence of structural or functional deficits. Neurocognitive and behavioral measures should be reviewed, as well, in an effort to confirm the differential diagnosis established following the mental, neurological and brain-imaging evaluations. If possible, collateral information should be obtained, to see what the impact of the person’s brain injury is upon caregivers. Moreover, if necessary, a determination should be made of the level of impairment – both social and physical – caused by the acquired brain injury. After all is said and done during assessment, the most likely DSM IV-TR diagnosis appropriate for persons with acquired psychopathy will be ‘personality change due to traumatic brain injury’ (American Psychiatric Association, 2000). To determine the level of competency and impairment following acquired brain injury, one can consult methods for measuring these, discussed previously by Granacher (2003, in press). Sometimes in personal-injury litigation, it is necessary first to determine the level of competency of an individual, to determine whether or not guardianship is required. The examiner can receive assistance in this regard by using the McArthur Competence Assessment Tool (Grisso & Applebaum, 1998). Determining impairment can be enhanced by consulting the American Medical Association Guides to the Evaluation of Permanent Impairment (Guides) (2000). The Guides contains a chapter for each body system, outlining methods for determining whole-body impairment, based upon impairment within a singlebody system. For instance, the fifth edition of the Guides details ratings for central nervous system impairment in chapter 13 and psychiatric impairment in chapter 14.

REFERENCES American Medical Association (1984). Guides to the Evaluation of Permanent Impairment (2nd edition). Chicago, IL: American Medical Association. American Medical Association (2000). Guides to the Evaluation of Permanent Impairment (5th edition). Chicago, IL: American Medical Association. American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders (4th edition, Revised). Washington, DC: American Psychiatric Association. Baddely, A. (1998a). Recent developments in working memory. Journal of the International Neuropsychological Society, 8, 234–8. Baddely, A. (1998b). The central executive: a concept and some misconceptions. Journal of the International Neuropsychological Society, 4, 523–6. Barrash, J., Tranel, D. & Anderson, S. (1994). Assessment of dramatic personality changes after ventromedial frontal lesions. Journal of Clinical and Experimental Neuropsychology, 16, 66–78. Bechara, A., Tranel, D. & Damasio, H. (2000). Characterization of the decision-making deficit of patients with ventromedial prefrontal cortex lesions. Brain, 123, 2198–202. Binder, L. (1993). Portland Digit Recognition Test manual (2nd edition). Beaverton, OR: L. Binder. Blumer, D. & Benson, D. (1975). Personality changes with frontal and temporal-lobe lesions. In D. Benson & D. Blumer (eds.), Psychiatric Aspects of Neurologic Disease (pp. 151–69). New York: Grune and Stratton. Bradley, W., Daroff, R., Fenichel, G. & Marsden, C. (eds.) (2000). Neurology in Clinical Practice. Boston, MA: Butterworth Heinemann.

ACQUIRED PSYCHOPATHY

249

Bullock, R., Chestnut, R., Clifton, G. & Ghajar, J. (1996). Guidelines for the management of severe head injury. Journal of Neurotrauma, 11, 639–734. Burgess, P. (2000). Strategy application disorder: the role of the frontal lobes in human multitasking. Psychological Research, 63, 279–88. Cleckley, H. (1976). The Mask of Sanity (5th edition). St. Louis: C.V. Mosby. Damasio, A. (1996). The somatic marker hypothesis and the possible functions of the prefrontal cortex. Philosophical Transactions of the Royal Society of London, series B: Biological Sciences, 351, 1413–20. Damasio, H., Grebowski, T., Frank, R. et al. (1994). The return of Phineas Gage: clues about the brain from the skull of a famous patient. Science, 264, 1102–5. Golden, C., Purisch, A. & Hammeke, T.C. (1991). Luria-Nebraska Neuropsychological Battery: Form I and II Manual. Los Angeles: Western Psychological Services. Gomez Beldarrain, M., Grafman, J., Pascual-Leone, A. & Garcia-Monco, J. (1999). Procedural learning is impaired in patients with prefrontal lesions. Neurology, 52, 1853–60. Grafman, J. (2002). The structured-event complex and the human prefrontal cortex. In D. Stuss & R. Knight (eds.), Principles of Frontal Lobe Function (pp. 292–310). New York: Oxford University Press. Graham, J. (2006). MMPI-2: Assessing Personality and Psychopathology (4th edition). New York: Oxford University Press. Graham, D., Gennarelli, T. & McIntosh, T. (2002). Trauma. In D. Graham & P. Lantos (eds.), Greenfield’s Neuropathology (7th edition) (pp. 821–98). London: Arnold. Graham, D., McIntosh, T. & Maxwell, W. (2000). Recent advances in neurotrauma. Journal of Neuropathology and Experimental Neurology, 59, 641–51. Granacher, R. (2003). Traumatic Brain Injury: Methods for Clinical and Forensic Neuropsychiatric Assessment. Boca Raton: CRC Press. Granacher, R. (in press). The forensic neuropsychiatric assessment of traumatic brain injury. In G. Murray & D. Starzinski (eds.), The Forensic Evaluation of Traumatic Brain Injury: A Handbook for Clinicians and Attorneys, Boca Raton, CRC Press. Grisso, T. & Applebaum, P. (1998). Assessing Competence to Consent to Treatment: A Guide for Physicians and Other Health Professionals. New York: Oxford University Press. Hare, R. (1991). The Hare Psychopathy Checklist (revised edition). Toronto: Multi-Health Systems. Harlow, J. (1848). Passage of an iron rod through the head. Boston Medical and Surgical Journal, 39, 389–93. Harlow, J. (1868). Recovery from the passage of an iron bar through the head. Publications of the Massachusetts Medical Society, 2, 327–47. Jennett, B. & Teasdale, G. (1981). Management of Head Injuries. Philadelphia: F.A. Davis. Korkman, M., Kirk, V. & Kemp, S. (1998). NEPSY: A Developmental Neuropsychological Assessment Manual. San Antonio, TX: The Psychological Corporation. Kraus, J. & Chu, L. (2005). Epidemiology. In J. Silver, T. McAllister & S. Yudofsky (eds.), Textbook of Traumatic Brain Injury (pp. 3–26). Washington, DC: American Psychiatric Publishing. Lezak, M. (1995). Neuropsychological Assessment (3rd edition). New York, Oxford University Press. Lezak, M., Howieson, D. & Loring, D. (2004). Neuropsychological Assessment (4th edition). New York: Oxford University Press. Mah, L., Arnold, M. & Grafman, J. (2005). Deficits in social knowledge following damage to ventromedial prefrontal cortex. Journal of Neuropsychiatry and Clinical Neuroscience, 17, 66–74. Mayeux, R., Ottman, R. & Maestre, G. (1995). Synergistic effects of traumatic head injury and apolipoprotein E-4 in patients with Alzheimer’s disease. Neurology, 45, 555–7. McCaffrey, R., Duff, K., & Westervelt, H. (eds.). (2000). Practitioner’s Guide to Evaluating Changes with Neuropsychological Assessment Instruments. New York: Kluwer Academic. Menkes, J. (1995). Textbook of Child Neurology (5th edition). Baltimore, MD: Williams and Wilkins. Milberg, W., Hebben, N. & Kaplan, E. (1996). The Boston process approach to neuropsychologicalassessment. In I. Grant & K. Adams (eds.), Neuropsychological Assessment of Neuropsychiatric Disorders (2nd edition). New York: Oxford University Press. Morey, L. (1996). An Interpretive Guide to the Personality Assessment Inventory. Odessa, FL: Psychological Assessment Resources.

250

VOLUME I: DIAGNOSIS AND TREATMENT

Norman, D. & Shallice, E, T. (1986). Attention to action: willed and automatic control of behavior. In R. Davidson, G. Schwartz & D. Shapiro (eds.), Consciousness and Self-Regulation (Vol. 4, pp. 1–18). New York: Plenum Press. O’Sullivan, M. & Guilford, J. (1976). Four Factor Tests of Social Intelligence: Manual of Instructions and Interpretations. Palo Alto: Consulting Psychologist Press. Reid, W. & Ruiz-Sweeney, M. (2003). Antisocial personality, psychopathy, and forensic psychiatry. In R. Rosner (ed.), Principles and Practice of Forensic Psychiatry (2nd edition) (pp. 555–63). London: Arnold. Reitan, R. & Wolfson, D. (1993). The Halstead–Reitan Neuropsychological Test Battery: Theory and Clinical Interpretation. Tuscon, AZ: Neuropsychology Press. Slick, D., Hopp, G., Strauss, E. & Thompson, G. (1997). Victoria Symptom Validity Test Manual. Odessa, FL: Psychological Assessment Resources. Strub, R. & Black, F. (2000). The Mental Status Examination in Neurology (4th edition). Philadelphia, PA: F.A. Davis. Stuss, D. & Benson, D. (1986). The Frontal Lobes. New York: Raven Press. Tombaugh, T. (1996). Test of Memory Malingering Manual. Toronto: Multi-Health Systems. Tranel, D. (2002). Emotion, decision-making, and the ventromedial prefrontal cortex. In D. Stuss & R. Knight (eds.), Principles of Frontal-Lobe Function (pp. 338–53). New York: Oxford University Press. Tranel, D., Anderson, S. & Benton, A. (1994). Development of the concept of ‘executive function’ and its relationship to the frontal lobes. In F. Boller & J. Grafman (eds.), Handbook of Neuropsychology (Vol. 9, pp. 125–48). Amsterdam: Elsevier. Trzepacz, P. & Baker, R. (1993). The Psychiatric Mental Status Examination. New York, Oxford University Press. Wechsler, D. (2001). Wechsler Test of Adult Reading Manual. San Antonio, Texas: The Psychological Corporation.

CHAPTER 15

Comorbidities of Psychopathy and Antisocial Personality Disorder: Prevalence and Implications Elena Carmen Nichita and Peter F. Buckley Medical College of Georgia, USA

Comorbidity with other mental disorders in patients with antisocial personality disorder (APD) is underappreciated despite compelling evidence that such comorbidities are more the rule than the exception in clinical practice. The most common disorders that co-occur in individuals diagnosed with APD are major mental disorders, such as schizophrenia and affective disorders, as well as substance abuse and anxiety disorders. Estimating the prevalence of such comorbidities is complicated by variations in nomenclature and classification criteria, the most prominent being across the definitions of conduct disorder, APD and antisocial behavior itself. Since the diagnosis of conduct disorder must precede that of APD, the comorbidities and trajectory of conduct disorder, attention deficit hyperactivity disorder, and substance abuse in children is another salient consideration. Explanations for the comorbidities associated with adult APD include shared genetics, shared vulnerability, shared environment and learned behavior. Additionally, the overlapping features and core constructs of these disorders might contribute the high expression of comorbid diagnoses in APD. Although there are inherent limitations in the evaluation and current treatment of comorbidities in patients with APD, it is important to recognize these and to appreciate the reciprocal influences of APD and psychiatric comorbidities upon the treatment and outcome in patients with persistent mental illnesses. This chapter reviews the prevalence of comorbidities in APD, potential etio-pathological explanations for the frequent co-occurrence of psychiatric disorders in APD, and the impact thereupon on management of these patients in clinical practice. Comorbidities of APD with major mental illnesses coded on Axis I of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR, American Psychiatric Association, 2000) are more the rule than the exception. Comorbidities stem from multiple mechanisms such as shared genetic risk, shared vulnerability, shared environment influences, or a The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

252

VOLUME I: DIAGNOSIS AND TREATMENT

combination of them. Adoption and twin studies have found evidence of both genetic and environmental factors in both APD and substance use disorders (Bree, Svikis & Pickens, 1998). Additionally, there is a diagnostic overlap with conditions which contribute to such comorbidity. One explicit example of overlap in symptoms is the case with APD and substance abuse, where individuals disregard commitments and obligations (due to substance use), engage in hazardous behavior (such as driving under influence), have criminal behaviors and arrests (related to substance use), or continue to use alcohol or drugs despite social and interpersonal problems. With such a presentation, it is hardly surprising that the occurrence of substance abuse and APD comorbidity would be so common (Robins, 1998). Although the last criteria listed in the DSM-IV-TR used to diagnose somebody with any personality disorder in general excludes the pattern of behavior that is the ‘direct psychological effect of a substance or medical condition’, and to diagnose APD in particular excludes behavior that occurs exclusively during schizophrenia or a manic episodes, it is still common to see these diagnoses associated for a good reason. Should we identify all the potential diagnoses in an individual or not? Would that be helpful for treatment or not? While clinicians want to be thorough and not overlook an important symptom or diagnosis, labels such as ‘antisocial personality disorder’ or ‘psychopath’ have a high impact on the care of such an individual. When a psychiatrist evaluates a patient who already carries an Axis II diagnosis (especially from cluster B) there is a higher risk of bias and negative counter-transference that could affect the diagnosis process and the subsequent treatment. Additionally, careful inquiry into symptoms would clarify whether the criteria used to diagnose conduct disorder or antisocial personality disorder was a valid one or not. For example, simply asking about running away from home, being truant from school, or stealing as a child may endorse positive answers and lead to a diagnosis of conduct disorder. After careful questioning the interviewer could unmask that severe abuse and/or neglect in the parental home was the reason for running away to escape physical or sexual abuse. Similarly, parents could prohibit children from attending school when they had visible signs of parental violence. On the same note, neglect would prompt somebody to steal food or clothes in order to survive. In a legal setting, especially in capital cases, diagnosing somebody with psychopathy or APD without careful consideration could be very damaging.

MOST COMMON COMORBIDITIES IN ADULTS Schizophrenia Although violence among persons with schizophrenia (‘split mind’) is much less common than the public perception, it is clear that a proportion of patients engages in violent behavior. A major question for the public and for clinicians would be: Is this patient ‘bad’ or ‘mad’? Translating this into clinical parlance: Is the patient’s violent behavior due to his illness (psychosis driven) or is it more willful (antisocial) behavior? Violence invariably occurs during a period of florid psychosis and is most often associated with medication noncompliance and with active substance abuse. There are also longstanding and complex associations between particular symptoms (e.g., command hallucinations or delusions) and the risk of violence (Taylor & Estroff, 2003). For example (Taylor et al., 1998), from a sample of patients in a high security hospital (1015 patients),

COMORBIDITIES OF PSYCHOPATHY AND APD

253

58 % had functional psychoses, 26 % had personality disorders alone, and 16 % had learning disabilities. A quarter of the patients with psychosis also had an additional personality disorder. Direct personal violence was more common among men and fire setting more common among women. Schizophrenia was mostly associated with personal violence and three-quarters of the subjects were mostly driven by their delusions in their acts of violence (often minor violence). A recent study (Swanson et al., 2006) evaluated the six-month prevalence of violence in participants enrolled in the National Institute of Mental Health Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE study), conducted at 56 sites within the United States. Data from 1410 patients with schizophrenia were assessed using the McArthur Community Violence interview for minor violence and serious violence over the past six months. Serious violence was reported by 3.6 % of the participants, but 19.1 % reported any kind of violence. Delusions increased the risk for violence (minor or serious), but negative symptoms (‘deficit’ symptoms) lowered the risk of violence. Living alone had a lower risk of violence than residing with families of others. The seminal, McArthur Study (Steadman et al., 1998) monitored violence to others every 10 weeks for a year after discharge from the hospital of 1136 patients with mental disorders. There was a control group composed of 519 people living in the same neighborhoods as the patients. There was no significant difference in the rate of violence by patients without symptoms of substance abuse and their match-controls without substance abuse. The abuse of drugs or alcohol significantly raised the rate of violence in both groups. Trying to assess the violence in the general population reported to violence in patients with schizophrenia, the criminal records of 2861 patients with schizophrenia were compared to those of matched controls in Australia (Wallace, Mullen & Burgess, 2004). The schizophrenia patients accumulated a greater total number of criminal convictions (8791 compared with 1119) and a higher rate of convictions for a criminal offense (21.6 % versus 7.8 %) and an offense involving violence (8.2 % as opposed to 1.8 %). Significantly higher rates of criminal convictions were found for patients with substance abuse than for those without substance use disorders (68.1 % versus 11.7 %). Undeniably, the co-occurrence of alcohol and drugs increases the incidence of violent behavior in patients with schizophrenia. Data from the Epidemiologic Catchment Area (Swanson et al., 1990) showed that subjects who reported violent behavior during the preceding year were young, male, with low socioeconomic status, and more than half had a psychiatric diagnosis. Individuals with alcohol and drug use were twice as likely as those with schizophrenia alone to report violent behavior. A significant interaction was found between schizophrenia and substance use disorders. The higher the number of psychiatric disorders the higher the risk of violence was in the population. After 30 males with affective disorders and 74 males with schizophrenia were followed for two years, 33 % of the patients with affective disorders and 15 % with schizophrenia had committed violent crimes. Comorbid antisocial personality disorder was associated with criminality among patients with schizophrenia, while drug use and intensity of the outpatient treatment were associated with violent acts in patients with affective disorders (Hodgins, Lapalme & Toupin, 1999). An Austrian study (Stompe, Ortwein-Swoboda & Schanda, 2004) compared a group of male offenders (119) with schizophrenia who were acquitted by reason of insanity (NGRI) with a control group of nonoffending patients with schizophrenia (105). Although they were found NGRI for serious violence, there was no significant difference in the threat/override symptoms in the course of the illness of offending and nonoffending individuals with schizophrenia. What discriminated among them was substance abuse and social origin.

254

VOLUME I: DIAGNOSIS AND TREATMENT

Similarly, a study (Caton et al., 2005) of 400 subjects who presented to the emergency department with psychotic symptoms and followed afterwards found that 217 had a primary psychotic disorder and 169 had a substance induced psychosis. The first group had a comorbid APD in 8.3 % of the cases and the second group in 17.2 %. On the other hand, there is also emerging evidence that people with schizophrenia who are violent may have had troubled childhoods and even exhibited antisocial traits during childhood. This suggests a premorbid pattern of antisocial behavior and raises the likelihood of comorbid APD in some patients with schizophrenia. In a British study (Walsh et al., 2004), 271 patients with schizophrenia were followed for two years to assess the prevalence of violence. Of these 271 patients 22 % (62 patients) received a violent conviction and 34 % (93 patients) a nonviolent conviction prior to this study. Twenty-five percent physically assaulted another person, 14 % reported violent behavior, 12 % were reported violent in their case notes, and 13 % were reported violent by their case manager. Those who assaulted others were more likely to be younger than 40 years of age, to have received special education in school, to have committed assault in the last two years, to have had previous (violent and nonviolent) convictions, and to have had a history of alcohol abuse. Similarly (Hodgins & Cote, 1993a,b) in a representative prison population in Quebec, the association of a major mental illness with APD was found in individuals with juvenile delinquency, earlier age of first conviction, and more total convictions especially for nonviolent crimes. The offenders with major mental illness had similar number of convictions, regardless of the presence of APD. The most popular hypothesis is that the antisocial behavior is present in children long before the onset of the major mental illness. The violent patients with schizophrenia were more likely to have a history of childhood and adolescent antisocial behavior. Several studies address such antecedents of violent behavior. A Danish study (Gosden et al., 2005) examined the outcomes of 780 subjects (ages 15–19 years old), drawn from a national cohort of young convicted criminals. At the nine-year follow-up, 3.3 % of them were diagnosed with schizophrenia and 4.5 % with any psychosis. Violence in late adolescence was significantly associated with future diagnosis of schizophrenia (odds ratio of 4.59). These studies suggest that antisocial traits, likely preceding the ones of schizophrenia, may play a prominent role in violence in this patient group. Another large study in Denmark (Munker et al., 2003) identified everyone diagnosed with schizophrenia from 1963 to 1999 and searched for them in the crime register. Fortyone percent of the schizophrenic patients had been convicted for at least one offense; 22 % of the male and 5 % of the female patients with schizophrenia had at least one violent conviction. Among the male population of violent schizophrenic offenders 58 % had committed the offense before they had psychiatric care and 17 % before they were diagnosed with schizophrenia. For women the percentages were 21 % and 28 %. One hypothesis may be that there is a subgroup with presymptomatic pattern of antisocial behavior or violence and these could be signs of illness. There is a significant positive relationship between major mental disorders that led to hospitalization and criminal violence (odds ratios 2.0–8.8 for men and 3.9–23.2 for women) (Brennan, Mednick & Hodgins, 2000). The results of these Danish studies are similar to those from other countries, but the crime rate among psychiatric patients is higher in Denmark possibly due to deinstitutionalization (Kramp, 2004). Another complimentary strategy that has been used was to formally evaluate psychopathy in patients with schizophrenia using the psychopathy scales. Several studies describe high psychopathy scores in patients with schizophrenia. Among 202 men with schizophrenia

COMORBIDITIES OF PSYCHOPATHY AND APD

255

and 78 men with a primary diagnosis of psychopathy (Tengstrom et al., 2004), nonmentally ill offenders diagnosed with psychopathy committed the highest numbers of offenses per year. Among offenders with schizophrenia, those with high psychopathy scores committed more crimes than those with low psychopathy scores. The nonmentally ill offenders with psychopathy and schizophrenic offenders with high psychopathy scores, committed similar number of offenses regardless of the presence of a substance use disorder. When Nolan and colleagues compared psychopathy and violent behavior among patients with schizophrenia and schizoaffective disorder, they found that violent patients with schizophrenia who score high on measures of psychopathy may have a personality disorder that precedes the emergence of psychotic symptoms, or they may constitute a previously unclassified subtype of schizophrenia, characterized by early symptoms of conduct disorder traits and persistent violent behavior (Nolan et al., 1999). Tengstrom and colleagues used Hare’s Psychopathy Checklist-Revised (PCL-R; 1991) to assess for violent recidivism in violent offenders with schizophrenia. A total of 30 (21 %) of the 141 individuals in the follow-up group were convicted of at least one new violent crime: murder (7 %), assault (90 %), or armed robbery (3 %). Among psychopaths (PCL-R score greater than 26), the violent recidivism rate was 48 % and among the nonpsychopaths was 14 %. The psychopaths were four times at higher risk of recidivism than nonpsychopaths. The PCL-R explained the violent recidivism rate better than teen substance abuse, early behavior problems (conduct disorder), behavioral problems in school, number of violent acts, age or marital status. Substance abuse/dependence remained a significant factor when controlling for psychopathy (Tengstrom et al., 2000). This finding was concordant with a previous study performed by Rice. From a sample of 618 individuals at risk (Rice & Harris, 1995), 191 failed violently. Of them 51 % had an alcohol problem, 24 % had schizophrenia, and 22 % were psychopaths. The association of psychopathy with schizophrenia in the absence of an alcohol disorder was lower than expected. Psychopaths were more likely to have an alcohol problem and they were positively related to violent recidivism. Schizophrenia alone was inversely related to violent recidivism. Another approach to determine violence and eventually APD comorbidity in schizophrenia was to study rates of schizophrenia and other mental illnesses among homicide populations. A group of researchers in Finland (Putkonen et al., 2004) initially looked at comorbidities found in mentally ill homicide offenders. They found that out of a nationally representative sample of men (n = 90) with a major mental illness (78 % with schizophrenia, 17 % with schizoaffectve disorder and 5 % with other psychosis), one-half had triple diagnosis (APD with substance use disorder and major mental illness), one-quarter had dual diagnosis (substance abuse and major mental illness) and one-quarter had only mental illness. The association of major mental illness with APD alone, without substance use, was not found. Later, Joyal et al. studied the circumstances of the homicidal acts in patients with schizophrenia. The participants in the study were selected from a pool of all-male homicide offenders in Finland between 1984 and 1991. Only 58 individuals who received a diagnosis of schizophrenia or schizoaffective disorder were selected (6.4 % of all homicide charges). Of them, 35 patients also had a diagnosis of APD. Those with schizophrenia and APD tended to assault nonmembers of the household (69 %) and nonmembers of their family (77 %). Twenty-six patients had paranoid schizophrenia and 60 % of the homicides followed delusions and/or hallucinations directly related to them. A higher proportion of patients with schizophrenia only, without APD (83 %) was found to be influenced by psychotic symptoms

256

VOLUME I: DIAGNOSIS AND TREATMENT

while committing their crimes, as opposed to only 46 % of those with both diagnoses (Joyal et al., 2004). Hodgins and Muller-Isberner (2004) examined 232 men with schizophrenia disorders that were discharged from general and forensic psychiatric hospitals. Almost 40 % (39.8 %) of the forensic patients and 10.8 % of the general psychiatric patients before their first admission to a general psychiatric hospital had committed offenses. They committed 195 nonviolent and 59 violent offenses after their first admission. Subsequently, 49 of these patients committed serious violent offenses that led to forensic psychiatric hospitalizations. The offenders were distinguished by a pervasive and stable pattern of antisocial behavior evident from at least mid-adolescence, antisocial personality disorder (increased the risk of offending 6.05 times), being institutionalized before age 18 (increased the risk 2.89 times), and alcohol abuse or dependence at first admission (4.06 times higher the risk) (Hodgins & Muller-Isberner, 2004). From the same sample of 232 men with schizophrenia, threequarters had committed at least one crime; the presence or absence of APD did not influence the course and symptoms of schizophrenia. At first admission for their mental illness they had already displayed a long history of antisocial behavior and emotional dysfunction that can increase the risk of violence (Moran & Hodgins, 2004). There is some evidence that cognitive processing may differ between violent and nonviolent patients with schizophrenia, perhaps suggestive of some basic neurobiological difference between the two groups. Evidence includes deficits in facial recognition, deficits in insight and in cognitive performance. Violent schizophrenia patients (Silver et al., 2005) may have a higher ability to identify facial emotional cues than the nonviolent schizophrenia patients, but are less able to assess the intensity of these cues. This trait may contribute to conflict generation and failure to recognize resolution signals, leading to conflict escalation and aggression in violence-prone patients. There was no difference in cognitive performance in these two groups. Patients with schizophrenia and schizoaffective disorder have not only poor insight into their illness, but also they lack insight into the legal consequences of their violent acts. The violent schizophrenia group (Buckley et al., 2004) showed evidence of active psychotic symptoms and 55 % were abusing substances at the time of the violent offense. The violent patients with schizophrenia had higher scores for the positive and general psychopathology (but not negative symptoms), poorer functioning, and greater deficits in insight than the nonviolent schizophrenia patients. The cognitive differences in schizophrenia and APD (Barkataki et al., 2005) are in different spheres, suggesting differences in underlying pathology. Among individuals from an incarcerated sample population with schizophrenia, APD and violent behavior, divided in three groups and compared with a control group from general public, the cognitive deficits were more widespread among persons with schizophrenia regardless of history of violence, when compared with APD individuals. When schizophrenia and violence were present concomitantly, patients had poorer performance than patients with schizophrenia alone on executive functioning. Individuals with a diagnosis of APD alone showed impairment in processing speed. In summary, evidence from multiple studies points to a relationship between florid symptoms of psychosis and propensity for violence. A diagnosis of psychosis alone (schizophrenia and other psychotic disorders) increases the risk of violence when positive symptoms are present, when there is poor compliance with medications, and when there is substance use, especially alcohol. Schizophrenia alone was inversely related to violent recidivism. There is also emerging evidence that some of these patients may have a lifelong trajectory of antisocial behavior and psychopathy traits, which is further exacerbated by active

COMORBIDITIES OF PSYCHOPATHY AND APD

257

psychosis. Psychopaths are more likely to have an alcohol problem and they are more likely to be positively related to violent recidivism. Since a personality disorder has a pervasive pattern throughout life, the antisocial behavior may be present in children long before the onset of the major mental illness in late teens and early adulthood. When a psychotic disorder is grafted on antisocial/psychopathic personality traits/disorder, the likelihood of these patients being involved in violent acts increases considerably. This may not only be due to their innate impulsivity and other maladaptive personality features, but also due to active symptoms of psychosis (especially positive symptoms, hallucinations and/or delusions). The highest propensity for violent acts would be seen in the triad psychotic illness–antisocial personality disorder/psychopathy–drug and alcohol use (see Table 15.1).

Affective Disorders Overall, people with mood disorders are less violent than patients with schizophrenia and when they become violent it is usually during a manic episode and is characterized by agitated (most often low-lethality) behavior. Corrigan and Watson used data from the National Comorbidity Survey to evaluate the relationship between violent behavior and mood disorders. The odds ratio for violence in the group of individuals with bipolar disorder was 9.5 and in the groups with dysthymia and depression was 4.8 and 3.9 respectively when compared with the ‘no disorder’ group (Corrigan & Watson, 2005). Violence is random and not goal directed. Among 419 persons involved in hostage/barricade situations 88 % met DSM-IV criteria for a psychiatric illness: 34 % had an affective disorder (31 % depression and 3 % bipolar disorder). The affective group had higher rates of violence (including suicide) than other diagnostic groups. The other study by the same author looked at 877 workplace violence offenders and 21.6 % had an affective diagnosis. Workplace violence offenders with affective disorders were less violent than offenders with Axis II or substance abuse diagnoses (Feldmann, 2001). Another study (Pelissier & O’Neil, 2000) looked at a sample of federal inmates who participated in a residential or outpatient drug and alcohol program. They found that the most common comorbidities among incarcerated substance use individuals were depression and APD. A number of inmates (633 males and 156 females) enrolled in a residential drug and alcohol treatment program were assessed for the presence of depression and APD. Dependence on one or more drugs was found in 74 % of males and 91 % of female inmates. Among them, 38 % males and 43 % females had a diagnosis of APD and 17 % of men and 33 % of women had a lifetime diagnosis of depression. Rates of APD were highest among those persons dependent on heroin, cocaine and alcohol (60 %), while heroin-only dependent individuals had a rate of 27 % for APD. The latter had the lowest rates of depression (7 %) and generalized anxiety (2 %). The prevalence of lifetime major depression in general population ranged between 3.7 and 6.7 % while the prevalence of major depression in male inmates was 5.75 % as opposed to 3.15 % in the general population. The general female population has a lifetime prevalence for major depressive disorder ranging from 6.8 % to 12.8 % while in the jail setting reaches 15.3 % to 24.8 % (Robins et al., 1984; Teplin, 1990 Teplin et al., 1996). Alcoholic suicide attempters have been found to have more comorbid diagnoses than nonattempters (multiple drug use, depression, antisocial characteristics) and a poorer prognosis (Roy et al., 1990). Of the 66 inmates in jail who had a previous diagnosis of bipolar disorder 74.2 % were found to have been manic and 59 % psychotic at the time of the arrest. They had

Swanson et al., 2006

Walsh et al., 2004 Gosden et al.,2005 Tengstrom et al., 2000 Putkonen et al., 2004 Hodgins et al., 2004 Munker et al., 2003

90

780

Number 271 3.3 % 141 78 % 232 All patients 1963–99 1410

Schizophrenia

4.5 % 30 (21%) 22 %

Any psychosis

3.6 %

49 27 %

62 (22 %)

Violent convictions

Table 15.1 Comparison on schizophrenia, psychosis, psychopathy and violence

19.1 %

93 (34 %)

Nonviolent convictions

48 %

Psychopathy present

14 %

Psychopathy absent

COMORBIDITIES OF PSYCHOPATHY AND APD

259

a higher rate of comorbid substance abuse than 54 bipolar patients hospitalized in the community who did not have a history of legal charges (75.8 % versus 18.5 %) (Quanbeck et al., 2004). When assessing the relationship between bipolar disorder and antisocial personality disorder, the overlap in the symptoms of these two disorders should be considered (Swann, 2005). The lack of insight, impulsivity, poor judgment, grandiosity, reckless behavior and irritability could predispose individuals to assaultive or threatening behavior and increased risk of criminal offending and legal charges. In this regard, a study of 325 parolees with a mental illness found that the number of lifetime manic episodes and frequency of psychiatric hospitalizations were associated significantly with the number of lifetime arrests (Solomon & Draine, 1999). There is less information on the trajectory of childhood/adolescence in bipolar patients and the antecedents of violent/antisocial behavior, since the behaviors in these patients has been less systematic studied than in patients with schizophrenia.

Substance Use Disorder The most compelling comorbidity of APD is with substance abuse. In the general population the lifetime prevalence for APD ranges from 2.6 % to 3.5 %, while the lifetime prevalence for substance use disorder is 16.7–26.6 % (DSM-IV-TR). Among individuals with a drug use disorder 18 % have APD, and 14 % of individuals with an alcohol diagnosis have APD. Approximately 70 % of patients with APD criteria also have an alcohol diagnosis and 30–40 % have a comorbid drug use diagnosis (Regier et al., 1990). These figures alone speak to a compelling relationship. Additionally, substance abusers with a diagnosis of CD or APD have an earlier onset of abuse, more severe abuse and more severe psychiatric symptoms, as well as social impairment. From a sample of patients with schizophrenia or schizoaffective disorder, associated with a substance use disorder, APD patients scored lower on personality measures related to socialization and higher on antisocial behavior, psychopathy and aggression (Mueser et al., 1997). A study conducted at a state hospital (Mueser et al., 1999) looked at the association of a major mental illness, a substance use disorder and conduct disorder, adult antisocial behavior, full APD, and none of the antisocial traits as a child or adult. Of 293 patients with schizophrenia spectrum and affective disorders, substance use disorders were strongly associated with full APD. The odds ratio ranged from 3.96 for lifetime cannabis use to 11.35 for recent cocaine use. Patients with CD and adult antisocial behavior only were at increased risk of having a substance use disorder when compared with the patients without antisocial characteristics, but their risk was lower than for patients with concomitant full APD. Childhood CD and adult antisocial behavior were considered to be a risk for the development of substance abuse in patients with major mental illnesses. Mueser later replicated the study (Mueser et al., 2006) and found that among the 176 clients with dual diagnosis, the most severe drug abuse, homelessness and increased number of lifetime sexual partners was in the group with adult APD only, followed by the group with full APD. Another state hospital study (Windle, 1999) of 740 patients admitted for alcohol treatment, concluded that alcoholics with a comorbid APD had an earlier onset of problem drinking, higher levels of pathological drinking and social impairment, and a higher prevalence of familial alcoholism when compared with the alcohol abusers without APD. These findings

260

VOLUME I: DIAGNOSIS AND TREATMENT

did not replicate for the psychopaths versus nonpsychopaths with a drinking problem. APD alcoholics had a higher prevalence of substance abuse disorder and psychopaths had a more frequent association with generalized anxiety disorder, panic disorder and schizophrenia. Also alcoholics with APD engaged in criminal activities and violent acts more often. In an outpatient study (Grella, Joshi & Hser, 2003) of 453 men and 254 women enrolled in treatment for cocaine dependence, 47.2 % of men and 34.3 % of women met criteria for APD. At a five-year follow-up, the existence of APD diagnosis was associated with increased likelihood of alcohol and other substances use among men, while APD in women was associated with increased rates of psychological problems that required mental health treatment. A Greek study (Hatzitaskos et al., 1999) showed that a higher percentage of patients with APD have a lifetime history of alcohol and drug use, finding that was consensual with numerous other studies. They studied 44 hospitalized male patients who met the diagnostic criteria for APD. Of them 95.5 % of the patients with APD abused one or more substances; only two subjects were free of any substance use. Among these 44 patients, one (2.3 %) abused only one substance, six (13.6 %) used a combination of two substances, and 20 (45.5%) abused four substances. Schuckit assessed the relationship between the drinking behavior and APD in 577 people who entered a treatment program. He found that people who had APD and drug use before they developed the drinking problems consumed more alcohol per day and experienced more alcohol-related legal and social problems than drinkers without APD (Schuckit, 1985). These findings suggest that individuals with APD have higher rates of alcohol abuse and dependence than the general population and they experience more alcohol-related problems than other alcoholics. Studies have shown that the rates of comorbidity of APD with substance use differ by gender: men with APD are three times more likely to abuse alcohol and five times more likely to abuse drugs than men without APD. Women with APD have an increased likelihood of having an alcohol diagnosis by 13 times and a drug use diagnosis by 12 times when compared with women without APD (Robins, Tipp & Przybeck, 1991). The relationship between alcohol abuse and APD could also be applied to populations who abuse illicit drugs. King and colleagues studied 513 patients who were newly admitted to a methadone maintenance treatment program. They were classified into four groups: (i) substance use and APD (APD ONLY); (ii) substance use, APD and other psychiatric disorder (APD MIXED); (iii) substance use and other psychiatric disorder but no APD (OTHER); and (iv) substance use only (NONE). The APD ONLY group had a higher proportion of male subjects than the other groups. The NONE group had nearly one year more formal education than the APD MIXED group. The APD ONLY group had a higher rate of opioid positive urine drug screen than the APD MIXED and OTHER groups. The APD ONLY group had a higher rate of cocaine-positive specimens. The APD MIXED and OTHER groups had higher rates of benzodiazepine positive urine drug screen. Interestingly, there were no significant group differences for treatment retention among the four subgroups (King et al., 2001). The conclusions from these studies are clear. There is a high comorbidity between substance abuse and APD. It is also evident that substance abuse heightens the propensity for violent behavior in APD patients and that this comorbidity is associated with poorer long-term outcome. People with APD may be more prone to alcohol-related aggression than people without APD. Individuals with APD have higher rates of alcohol dependence and more alcohol-related problems than people without APD. In laboratory studies, people

COMORBIDITIES OF PSYCHOPATHY AND APD

261

Table 15.2 Substance use and antisocial personality disorder APD Grella et al., 2003 Hatzitaskos et al., 1999 Schuckit, 1985 King et al., 2001 Regier et al., 1990

Alcohol

47.2 % men 34.3 % women 44 men Increased risk Increased risk 70 %

SUD

95.5 % 577 Any diagnosis

30–40 %

Cocaine

Opioid

453 men 254 women

Increased risk

513

SUD = substance use disorder; APD = antisocial personality disorder

with APD show greater increase in aggressive behavior after consuming alcohol than people without APD (Moeller & Dougherty, 2001). See Table 15.2.

Anxiety Disorders In contrast to the well-appreciated relationship between substance abuse comorbidity and APD, the extent of comorbidity between anxiety disorders and APD is underappreciated. An analysis of data from the National Comorbidity Survey by Corrigan and Watson showed that people with an anxiety disorder were almost four times more likely to engage in violent behavior than people who did not have a psychiatric diagnosis (Corrigan & Watson, 2005). Another analysis of data from the National Comorbidity Survey (Goodwin & Hamilton, 2003) is also informative. They looked at a sample of 5877 subjects (ages 15–54). Out of 3.3 % adults with APD 54.33 % had an anxiety disorder and out of 9.4 % adults who had CD, but did not meet criteria for APD, 42.31 % had a lifetime anxiety disorder. Social phobia and post-traumatic stress disorder (PTSD) increased the likelihood of having APD, after adjusting for differences in sociodemographic characteristics and associated psychiatric disorders (other than an anxiety disorder). The association between APD and anxiety increases the risk of affective disorders and substance use disorders. There are increased rates of suicidal ideations and suicide attempts in individuals with APD and anxiety than in those with either one alone or neither disorder. The co-occurrence of APD and anxiety disorder was more common in women and people who were separated or divorced. Sareen and colleagues also found a significant association between anxiety disorders and antisocial diagnosis, which was still considerable after adjusting for sociodemographics, depression and alcohol and drug use disorders. Social phobia and PTSD had the strongest association with antisocial behavior, which was consistent with the observations from Goodwin and Hamilton’s study. Also people with comorbid anxiety and antisocial behavior have greater levels of distress, dysfunction, poor quality of life and suicidal ideations than people with either disorder alone (Sareen et al., 2004). These conclusions are valid for APD only (as it appears in DSM-IV) and might not be true for psychopathic people (the narrower and worse subcategory of people who would qualify for APD), who have been thought to have lower than normal levels of anxiety. This thought was based on a significant finding on biological electrodermal hyporeactivity

262

VOLUME I: DIAGNOSIS AND TREATMENT

in the anticipation to aversive stimuli. Electrodermal hypoactivity is associated with low anxiety and disinhibition and poor control of emotional expression. It appears to relate to an impulsivity dimension among psychopaths rather than the core personality features of psychopaths (Fowles, 2000).

Post-Traumatic Stress Disorder (PTSD) It might be anticipated that individuals who have been exposed to violent trauma might be at risk of violence and antisocial behaviors in correlation with post-traumatic stress disorder. To test this relationship, Koenen used data from the Harvard Twin Study of Drug Abuse and Dependence (1992), where 8039 male–male twin pairs were interviewed by telephone. The analysis showed not only that PTSD (in Vietnam veterans) was significantly associated with conduct disorder and APD, but also their families had an increased occurrence of conduct disorder and APD. Individuals with PTSD were twice more likely to have a lifetime diagnosis of conduct disorder and five times more likely to have APD. Combat exposure was a significant predictor of adult antisocial behavior, even after adjustment for familial influences and genetic factors (Koenen, 1999). In contrast with this finding, a study done at a Swiss correctional facility (Moeller & Hell, 2003) on 102 young male inmates (ages 17–27) did not find a diagnosis of PTSD in the psychopathic population, even though 12 % indicated sexual abuse and a significant number reported a traumatic event; the PCL-R scores were directly correlated with the number of traumatic events. Affective disorders were present in 28 % of inmates and 28 % had at least one suicide attempt. Abuse or dependency on a psychotropic substance was found in 82 % of the inmates. A psychopathic score above 25 was found in 16 % of the subjects.

Sexual Disturbances and Paraphilias Door (1998) advocates the idea that the majority of pedophiles is psychopathic. He bases his theory on the fact that the criteria for diagnosing these disorders greatly overlap. The lack of remorse, manipulation, lying, lack of empathy, poor behavioral control and promiscuous behavior seen in psychopath, could be transcribed in the primary goal of the pedophile: to use another to satisfy the grandiose self. The MMPI profiles of 90 child molesters were assessed and they revealed eight clusters; in the first four the MMPI Psychopathic Deviate peaked, in the company of other scales, other two clusters were ‘normal episodic offender cluster’. On the other two clusters the elevations were not as high, but elevated enough (Duthie & McIvor, 1990). McAnulty, who expressed disapproval of the use of MMPI in the pedophile, used two groups of sexual offenders to prove the lack of psychopathy in some pedophiles. Contrary to his hypothesis, both subtypes of pedophiles showed psychopathic tendencies on MMPI (McAnulty, Adams & Wright, 1994). A subgroup of 15 men with schizophrenia who committed sexual offenses or had shown antisocial sexual behavior (Phillips et al., 1999) was compared with 55 males with schizophrenia and violent behavior treated at the same secure hospital. Seven of them had committed a total of 14 offenses of rape or attempted rape and eight indecent assaults. In addition they had seven other offenses, including two homicides. For these men the pattern

COMORBIDITIES OF PSYCHOPATHY AND APD

263

showed escalation in the severity of offending. Eight other men had a history of antisocial sexual behavior prior to admission (inappropriately touching of women while demanding sexual intercourse and sexual assault), but did not incur charges for these acts. They were in the hospital on other charges such as attempted murder, bodily harm and other minor offenses. The majority of patients (12) appeared to be psychotic at the time of the sexual offenses/behavior, which was rather their baseline than deterioration of their illness. Two studies performed in Ohio in 1999 and 2004 (Dunsieth et al., 2004 and McElroy et al., 1999) used the same method to evaluate the psychiatric and legal features of men convicted of sexual offenses. The first study looked at 36 subjects and found that 83 % had a substance use disorder, 58 % had a paraphilia, 61 % a mood disorder 36 % an impulse disorder, 17 % an eating disorder and, importantly, 72 % met DSM-IV criteria for antisocial personality disorder. The subjects with paraphilia had higher rates of comorbidities that the ones without paraphilia. The second study, with 113 subjects, largely replicated the 1999 study, but the rates of paraphilia were higher (74 %), while the rates of antisocial personality disorder were lower (56 %). Paraphilic offenders reported more victims, started offending at a younger age, were more likely to perpetrate incest, and were more likely to admit to sexual offenses involving minors. Fifty percent of the individuals met DSM-IV criteria for pedophilia, 17.8 % for sexual sadism, 22.6 % for frotteurism, and 19 % for voyeurism. Berger et al. (1999) studied an Austrian sample involving 70 sex offenders (27 child molesters, 33 rapists and 10 murderers). From the total sample, 27.2 % met DSM-III criteria for sadistic personality disorder and the highest overlap was with APD (in 42.1 % of the cases). Criteria for sexual sadism, as defined in DSM-III-R, were met by 42.1 % of the subjects with sadistic personality disorder. Later, other authors (Myers, Burkett & Husted, 2006) tried to make a parallel between the sadistic personality disorder as it appeared in the DSM-III and antisocial personality disorder as defined in the DSM-IV and their associated comorbidities in a sample of adolescent inpatients. Out of their 56 subjects, 8 met full criteria and 10 had traits for sadistic personality disorder (sadistic group). Since they were admitted to the adolescent unit (maximum age was 18) they could not be diagnosed with APD, but 12 out of the 18 individuals in the sadistic group met criteria for conduct disorder. Another study done by a group of researchers in Oregon (Freeman, Dexter-Mazza & Hoffman, 2005) evaluated 36 adolescents admitted to a residential program for delinquent youth to assess different characteristics of juvenile sex offenders compared to non-sex-offending delinquent adolescents. The juvenile sex offenders had lower scores on the Psychopatic Deviant Scale of the adolescent version of the MMPI than their nonsex-offender counterparts. Although 77.78 % of the entire sample had a primary diagnosis of conduct disorder, possible paraphilias were not assessed. At a maximum security prison 41 inmates were assessed and classified as psychopathic or nonpsychopathic and violent or sexually violent (Holt, Meloy & Strack ,1999). Psychopaths were found to be more sadistic than nonpsychopaths, however, only three individuals could be diagnosed with sexual sadism. A Canadian study published by Firestone and colleagues in 1999 compared 48 homicidal sex offenders with incest offenders. The homicidal sex offenders had higher levels of response to pedophilic stimuli and assaultive acts to children. They were also diagnosed with psychosis, APD, paraphilia, sexual sadism, sexual sadism with pedophilia and substance abuse. Additionally the homicidal sex offenders had higher PCL-R scores than the incest offenders (Firestone et al., 1999). Porter and colleagues (2003) concluded after they studied 125 males who committed homicide that 38/125 (30.4 %) exhibited sexual behavior in the

264

VOLUME I: DIAGNOSIS AND TREATMENT

Table 15.3 Correlation of paraphilia, sexual offenses and psychopathy/antisocial personality disorder

McElroy et al., 1999 Dunsieth et al., 2004 Berger et al., 1999 Myers et al., 2006 Porter et al., 2003

Sexual offenses

SUD

Paraphilia

Mood disorder

APD/psychopathy/ conduct disorder

36

83 %

58 %

61 %

72 %

113

∼Same

74 %

∼Same

56 %

70

42 %

56

12

38

18

context of their homicide. Out of the 38 subjects 18 had a PCL-R score above 30, placing them into the psychopathic range; the rest of 20 subjects were classified as nonpsychopaths. Overall, there was evidence for the use of gratuitous and sadistic violence by 82.4 % of psychopaths and 52.6 % of nonpsychopaths (Porter et al., 2003). Different authors have tried to define different categories of rapists. Some of them found as many as nine types, others tried to collapse them into fewer classes. In 1997 Brown and Forth assessed a sample of 60 incarcerated rapists and divided them into five types, according to the Massachusetts Treatment Center: Revised Rapist Typology, Version 3: opportunistic; nonsadistic-sexual; sadistic sexual; anger; and vindictive. The ones who had higher psychopathy scores were the one from the opportunistic and pervasively angry group. Later, an Australian study (McCabe & Wauchope, 2005) tried to determine behavioral characteristics of different types of rapists cluster into four groups: anger; power exploitative; power reassurance; and sadistic. However, they did not look at associated psychopathy or antisocial personality disorder. See Table 15.3.

Organic Brain Syndrome Patients with organic brain syndrome are known to be at greater risk of becoming violent. The extent to which the brain trauma unmasks underlying antisocial tendencies is unclear. On the other hand, individuals with violent and antisocial behavior are more prone to different kind of injuries, including head injuries. There is a well-known association between frontal-lobe dysfunction and increased aggressive and antisocial behavior. The evidence appears to be strongest for the association of focal prefrontal damage and an impulsive subtype of aggressive behavior (Brower & Price, 2001). There was one case report (Meyers et al., 1992) of ‘acquired antisocial behavior’ after unilateral frontal-lobe damage post resection of a pituitary tumor. The change in behavior after the surgery included irresponsible behavior at work and at home, impulsivity and disinhibition. These changes were called ‘pseudosociopathic’ or ‘pseudopsychopathic’ by Benson and Blumer in 1975. Another similar case was published by Blair and Cipolotti in 2000 and involved an engineer who sustained a head trauma in the right frontal region. He became assaultive, irritable and aggressive, which

COMORBIDITIES OF PSYCHOPATHY AND APD

265

was a change from his previous level of functioning and behavior. In addition he showed no remorse for his behavior. He was thought to have ‘acquired sociopathy’. In contrast, individuals who sustain cerebrovascular accidents tend to develop symptoms of depression rather than aggressive behavior. A link between traumatic brain injury (TBI), substance use disorders and APD was established in a study published in 2006 (Felde, Westermeyer & Thuras, 2006). From 550 patients enrolled in a drug rehabilitation program 218 (40 %) reported TBI (with loss of consciousness). Patients with TBI were more likely to have a more severe drug problem, more anxiety and depressive symptoms, attempted suicide and APD. It appears that childhood conduct disorder may predict risk-taking behavior that can lead to TBI. In one study of criminals with organic brain syndrome, ‘early starters’ were significantly more likely than ‘late starters’ to be arrested before the onset of organic brain syndrome, to show a higher rate of offending before, but not after the onset of the organic brain syndrome, be both recidivists and violent recidivists, and have a diagnosis of antisocial personality disorder. Early starters show a more global, persistent and stable pattern of offending than late starters (Grekin et al., 2001).

COMORBIDITIES IN CHILDREN Since the diagnosis of conduct disorder must precede that of APD, the comorbidities and trajectory of conduct disorder, attention deficit hyperactivity disorder (ADHD) and substance abuse in children is another salient consideration. About half of the children who have ADHD will also meet criteria for oppositional defiant disorder (ODD) or conduct disorder (CD). ADHD alone and ADHD with CD appear to be two distinctive subtypes, with possibly different etiologies. While both groups respond similarly to stimulants in the short term, children with ADHD and CD have higher rates of APD as adults (Pliszka, 1998). ADHD with antisocial comorbidity might be different from other forms of ADHD. Families with ADHD (140) and control families (120) participated in a study that concluded that antisocial ADHD and bipolar ADHD are different subtypes of manifestation of the same family condition (Faraone et al., 1998). Several studies have evaluated the extent of substance abuse among juvenile offenders. The incidence of psychopathy in incarcerated male offenders is estimated to be 34 %, but its comorbidity with substance use is not known. A study done in a secure facility in Ontario (Mailloux, Forth & Kroner, 1997) looked at 40 male adolescents. Their mean age was 17, the majority was convicted of a violent crime, and 75.6 % of them were white. They were given the Psychopathy Check List: Youth Version as well as the Michigan Alcohol Screening Test (MAST) and the Drug Abuse Screening Test (DAST). The results for adolescent male offenders replicated the ones found for adult male offenders. The subjects who scored higher on the PCL tended to have higher scores on both screening tests: for alcohol and for drug use. Also they started to use at a younger age and tried a greater variety of drugs than those with lower scores on the PCL. These correlations were strongest with the behavioral characteristics of psychopathy. Studies show that juvenile delinquents represent a highly traumatized group with rates of PTSD approaching 30 % (Carrion & Steiner, 2000; Cauffman et al., 1998; Steiner, Garcia & Matthews, 1997). Eighty-five incarcerated boys (mean age 16.6) charged with violent offenses were questioned to assess the rates of PTSD. The prevalence of PTSD in the

266

VOLUME I: DIAGNOSIS AND TREATMENT

incarcerated sample was higher than the rates of PTSD in the adolescent population in the community and the adolescents from county probation camps. The full PTSD criteria were met by 22 % of the subjects in the incarcerated sample; 20 % met only partial criteria. They displayed elevated distress, anxiety, depression and lower threshold for impulse control and suppression of aggression (Steiner, Garcia & Matthews, 1997). They also had more immature defense mechanisms such as somatization, conversion, projection or dissociation. Out of 64 adolescents in a juvenile probation hall, 28.3 % met criteria for dissociative disorder and 96.8 % endorsed a history of traumatic event (Carrion & Steiner, 2000). A small sample study of 39 adolescent inpatients with psychosis, divided in two subgroups, ‘violent’ and ‘nonviolent’ replicated the studies showing that the criminal behavior was associated with a history of emotional or physical abuse, previous contact with social or mental health services, and previous criminal behavior (Clare, Bailey & Clark, 2000). It failed to replicate though the results of most studies in adult schizophrenia. The rate for PTSD is higher among female young offenders than in the general or male incarcerated population. Ninetysix female offenders ages 13–22 years were compared with a male sample from another study. While the percentage of lifetime PTSD in the female population was 65.3 % and for current PTSD was 48.9 %, the PTSD in the male population was 32.3 % (Cauffman et al., 1998). Among the 351 subjects selected from a pool of juvenile inmates in Northern Russia (Ruchkin et al., 2002), who reported at least one traumatic event, the rates of PTSD were as following: 33.6 % had no symptoms of PTSD; 41.6 % had partial PTSD (had at least three threshold ratings but did not meet full DSM-IV criteria); and 24.8 % met full PTSD criteria. Conduct disorder was present in 259 subjects (73.8 %): 80 with no PTSD symptoms; 107 with partial PTSD; and 72 with full PTSD. A small sample of 50 youths (ages 11–17) admitted to a juvenile detention center was screened for psychiatric disorders. Affective disorders were found in 42 % of the cases: 20 cases met the DSM-IV criteria for mania; 20 for depression; and one for a mixed episode. Conduct disorder was present in 60 % of the juveniles. The same sample had an increased rate of alcohol, cannabis and other substances dependence (Pliszka et al., 2000). The rate of mania was much higher in the juvenile detention center (22 %) compared with the rate in the general teenager population (1 %) (Lewinsohn, Klein & Seeley, 1995). Childhood CD and adult psychopathic traits were the main links to repeated violent crimes and aggression among offenders under forensic psychiatric investigation in Sweden (Soderstrom et al., 2005). Both, PCL-R and DSM-IV were used in assessing these diagnoses. Psychopathic traits were positively correlated with bipolar disorder and negatively with unipolar depression. ‘Unemotionality’ and ‘behavioral dyscontrol’ factors and PCL-R scores were correlated with ADHD, Asperger’s syndrome/high functioning autistic traits, CD, substance abuse and Cluster B personality disorder traits. After following a group of 137 adolescents (average age 15.9 years) who attended a drug treatment program for four years, Myers and colleagues (1998) found that 61 % met DSM-III criteria for antisocial personality disorder. They displayed more involvement with drugs or alcohol and poorer social functioning. These adolescents exhibited an earlier age of deviant behavior, a greater diversity of deviant behavior and more extensive pretreatment drug use. All these factors best predicted the progression to antisocial personality disorder (Myers, Stewart & Brown, 1998). The co-occurrence of APD and mental retardation was limited (2.4 %) in a sample of murder defendants referred for pretrial evaluation in South Carolina over a five-year period (Dwyer, 2006). Three groups of offenders with intellectual disabilities were studied by

COMORBIDITIES OF PSYCHOPATHY AND APD

267

Table 15.4 Childhood diagnoses and conduct disorder/psychopathy Number Mailloux et al., 1997 Steiner et al., 1997 Cauffman et al., 1998 Ruchkin et al., 2002 Pliszka, 1998 Myers et al., 1998

ADHD

PTSD

40

Increased risk

85

22 %

96

65.3 %

351

24.8 %

137

SUD

Total number

Psychopathy/CD/ODD Higher scores

259 (73.8 %) 137

∼50% CD or ODD 61 %

ADHD = attention deficit hyperactivity disorder; SUD = substance use disorder; PTSD = post-traumatic stress disorder; ODD = oppositional defiant disorder

Hogue and colleagues (2006) and it was found that offenders from the high-level security facility had more extensive forensic history prior to age 18 than the ones from a low security. They were also more likely to have a psychopathic disorder (26 %) and mental illness (19 %) than their counterparts from the low security facility. See Table 15.4.

WHY IS THERE AN ASSOCIATION BETWEEN APD AND OTHER MENTAL ILLNESSES? Explanations for the comorbidities associated with adult APD include shared genetics, shared vulnerability, shared environment and learned behavior. For example, it is known that schizophrenia has a strong (but complex) genetic heritability. It is plausible that the comorbidity of APD and schizophrenia may have some underlying genetic basis. In this regard, trying to elucidate the biological basis of violence, Strous and colleagues screened 37 patients with schizophrenia to determine the association between catechol-O-methyltransferase (COMT) polymorphism and dangerousness (as assessed by violent and threatening behavior, crime, drug and alcohol use and other antisocial behaviors). Schizophrenia patients who were homozygous for the low-activity allele were considered by their psychiatrists to be at higher risk for aggressive and dangerous behavior than the ones who were homozygous for the high-activity allele (Strous et al., 1997). Additionally Caspi and colleagues have recently demonstrated an intriguing relationship between childhood cannabis abuse, COMT polymorphism and later risk for developing schizophrenia (Caspi et al., 2005). Swann has also postulated that impulsivity represents a dimensional construct seen in many conditions including ADHD, bipolar disorder, APD and substance abuse. He has suggested that there is a fundamental neurobiological deficit underlying impulsivity. Such a scheme may also explain the comorbidities of APD with mood or anxiety disorders and with substance abuse disorders (Swann, 2005). Similar studies tried to find shared genetics among APD, major depressive disorder and substance use disorder (Fu et al., 2002). Genetic effects on APD accounted for 38 %, 50 % and 58 % of the total genetic variance in risk for major depression, alcohol dependence and

268

VOLUME I: DIAGNOSIS AND TREATMENT

cannabis dependence, but after controlling for genetic effects on APD the partial genetic correlations for the other disorder were no longer significant. This finding could mean that the existence of one disorder greatly influences the others.

LIMITATIONS The common misuse of the term antisocial behavior creates a bias for the diagnosis of APD and possible for its worse and narrower subcategory, psychopathy. While APD (according to DSM-IV-TR) is broader, more inclusive, based on visible consequences of unsocialized behavior (‘conduct’) and focuses on antisocial issues and behaviors, psychopathy (according to Hare and Cleckley) is more severe, more likely to result in criminality, is based on personality dynamics, with a callous, remorseless style of relating to others. Psychopathy includes characteristics not only from the DSM-IV criteria for all personality disorders gathered under Cluster B; it also has some characteristics of paranoid and schizotypal personality disorder (Reid & Ruiz-Sweeney, 2003). Classifications of psychopathy are not synonymous with diagnoses of conduct disorder or APD, but represent an extension. The rate of conduct disorder is 16 % in boys attending mainstream education and above 80 % for APD in adult forensic institutions. Antisocial behavior of psychopaths is toward achieving money, sexual opportunities or increased status. In addition to antisocial behavior, the psychopath has emotional impairment such of lack of guilt as well as difficulties in processing the fearfulness and sadness of others. The emotional impairment interferes with socialization and the individual cannot learn to avoid antisocial behavior (Blair, 2003). The extent to which such nosological nuances are considered in assigning a comorbid diagnosis of APD among patients with serious mental illness is unclear. The studies cited earlier in the text of psychopathic ratings would suggest validity to one ascribing the diagnosis of APD in such patients. However, many clinicians consider violence as synonymous with antisocial personality. This may result in elevated rates of comorbidity. On the other hand, it is very difficult to disentangle where a psychiatric disorder ends and another one starts. Psychiatric disorders are of course grafted on pre-existing personalities. Texts on APD concern a prototypic case in isolation from other personality disorders, but the presence of narcissistic, paranoid, histrionic or borderline traits add a different course, presentation or even etiology than APD alone. Co-occurrence with histrionic personality would represent the different representation of APD in men and women, while the presence of narcissistic traits in APD population would define psychopathy. The prison setting may have a higher rate of APD comorbid with narcissistic traits than the general population (Widiger & Corbitt, 1997). Warren and colleagues (2003) found similarity in the prevalence and structure of the psychopathy construct among men and women: 15–25 % incarcerated men at a maximum security prison had PCL-R of 30 and higher while 17.4 % of a female sample met the same criteria. The comorbidity of other personality disorders with APD would define psychopathy (Warren et al., 2003).

IMPLICATIONS FOR TREATMENT A major implication of comorbidity with APD is its impact upon treatment and long-term outcome. There is ample and compelling evidence that APD comorbidity with substance use complicates treatment and inevitably confers a poorer outcome. In one study of 252

COMORBIDITIES OF PSYCHOPATHY AND APD

269

substance dependent patients, 50 % of them were found to have one or more personality disorders, which increased the likelihood of relapse. After one year only 6 % of patients with comorbid personality disorders were maintaining sobriety as compared to 44 % of patients without a personality disorder (Thomas, Melchert & Banken, 1999). Compared with substance abusers without APD, antisocial substance abusers have more severe use and worse treatment prognosis (Brooner, 1993, 1997; Woody et al., 1985). Intravenous drug use and sexual behavior of drug abusers who are comorbid with APD put them at increased risk to acquire HIV (Brooner, 1993; Compton, 1995; Gill, 1992). Male opioid users with APD had a poorer outcome to psychotherapy, but responded more favorably when APD was associated with depression (Woody et al., 1985). The key features of APD such as disruptiveness, impulsivity and general disregard for others conflict with the ability to engage in and respond positively to treatment. Not surprisingly then, these patients achieve lower rates of treatment retention and completion and poorer post-treatment outcomes. APD has been associated with higher rates of treatment drop-out for substance abusers in an inpatient dual diagnosis unit (Greenberg, Otero & Villanueva, 1994). It has been shown that the greater the severity of psychopathology and drug use, the poorer the treatment outcomes for cocaine abusers at one-year follow-up was the conclusion of another study (Carroll et al., 1993). Treatment milieu and aspects of care for persons with APD are covered in several other chapters of this book.

CONCLUSIONS In conclusion, comorbidity between APD and serious mental illness is common and is not confined to a simple diagnostic category. Moreover, the triad of antisocial behavior– exacerbated symptom of a major mental illness–substance abuse is so common and overlapping across each condition that this appears to be a fundamental relationship. Swann has suggested that impulsivity is the core construct that underlies these interrelationships. While this hypothesis is intuitively appealing, we presently know very little of potential neurobiological differences between patients with comorbid APD and those with only one primary mental disorder.

REFERENCES American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision. Washington, DC: American Psychiatric Association. Barkataki, I., Kumari, V., Das, M. et al. (2005). A neuropsychological investigation into violence and mental illness. Schizophrenia Research, 74, 1–13. Berger, P., Berner, W., Bolterauer, J. et al. (1999). Sadistic personality disorder in sex offenders: relationship to antisocial personality disorder and sexual sadism. Journal of Personality Disorders, 13(2), 175–86. Blair, R.J.R. (2003). Neurobiological basis of psychopathy. British Journal of Psychiatry, 182, 5–7. Blair, R.J.R. & Cipolotti, L. (2000). Impaired social response reversal. A case of ‘acquired’ sociopathy. Brain, 123, 1122–41. Bree, M.B.M., Svikis, D.S. & Pickens, R.W. (1998). Genetic influences in antisocial personality and drug use disorders. Drug and Alcohol Dependence, 49, 177–87.

270

VOLUME I: DIAGNOSIS AND TREATMENT

Brennan, P.A., Mednick, S.A. & Hodgins, S. (2000). Major mental illness and criminal violence in a Danish birth cohort. Archives of General Psychiatry, 57, 494–500. Brooner, R.K., Greenfield, L., Schmidt, C.W. & Bigelow, G.E. (1993). Antisocial personality disorder and HIV infection among intravenous drug abusers. American Journal of Psychiatry, 150, 53–8. Brooner, R.K., King, V.L., Kidorf, M. et al. (1997). Psychiatric and substance use comorbidity among treatment-seeking opioid abusers. Archives of General Psychiatry, 54(1),71–80. Brower, M.C. & Price, B.H. (2001). Neuropsychiatry of frontal lobe dysfunction in violent and criminal behavior: a critical review. Journal of Neurology, Neurosurgery and Psychiatry, 71, 720–6. Brown, S.L. & Forth, A.E. (1997). Psychopathy and sexual assault: static factors, emotional precursors, and rapist subtypes. Journal of Consulting and Clinical Psychology, 65(5),848–57. Buckley, P.F., Hrouda, D.R., Friedman, L. et al. (2004). Insight and its relationship to violent behavior in patients with schizophrenia. American Journal of Psychiatry, 161(9),1712–14. Carroll, K.M., Power, M.D., Bryant, K. & Rousanville, B.J. (1993). One-year follow-up status of treatment-seeking cocaine abusers: psychopathology and dependence severity as predictors of outcome. Journal of Nervous and Mental Disease, 181, 71–9. Carrion, V.G. & Steiner, H. (2000). Trauma and dissociation in delinquent adolescents. Journal of the American Academy of Child and Adolescent Psychiatry, 39(3), 353–9. Caspi, A., Moffitt, T.E., Cannon, M. et al. (2000). Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-metyltransferase gene: longitudinal evidence of a gene X environment interaction. Biological Psychiatry, 57(10), 1117–27. Caton, C.L.M., Drake, R.E., Hasin, D.S. et al. (2005). Differences between early phase primary psychotic disorders with concurrent substance use and substance induced psychoses. Archives of General Psychiatry, 62, 137–45. Cauffman, E., Feldman, S., Wateman, J. & Steiner, H. (1998). Post-traumatic stress disorder among female juvenile offenders. Journal of the American Academy of Child and Adolescent Psychiatry, 37(11), 1209–18. Clare, P., Bailey, S. & Clark, A. (2000). Relationship between psychotic disorders in adolescence and criminally violent behaviour. British Journal of Psychiatry, 177, 275–9. Compton, W.M., Cottler, L.B., Shillington, A.M. & Price, R.K. (1995). Is antisocial personality disorder associated with increased HIV risk behaviors in cocaine users? Drug and Alcohol Dependence, 37, 37–44. Corrigan, P.W. & Watson, A.C. (2005). Findings from the National Comorbidity Survey on the frequency of violent behavior in individuals with psychiatric disorders. Psychiatry Research, 136(2–3), 153–62. Door, D. (1998). Psychopathy in the pedophile. In T. Millon & E. Simonsen (eds.), Psychopathy: Antisocial, Criminal, and Violent Behavior (pp. 304–20). New York: Guilford Press. Dunsieth, N.W., Nelson, E.B., Brusman-Lovins, L.A. et al. (2004). Psychiatric and legal features of 113 men convicted of sexual offenses. Journal of Clinical Psychiatry, 65, 293–300. Duthie, B. & McIvor, D.L. (1990). A new system for cluster-coding child molester MMPI profile types. Criminal Justice and Behavior, 17(2), 199–214. Dwyer, R.G. & Frierson, R.L. (2006). The presence of low IQ and mental retardation among murder defendants referred for pretrial evaluation. Journal of Forensic Sciences, 51(3), 678–82. Faraone, S.V., Biderman, J., Mennin, D. & Russell, R. (1998). Bipolar and antisocial disorders among relatives of ADHD children: Parsing familial subtypes of illness. American Journal of Medical Genetics (Neuropsychiatric Genetics), 81, 108–16. Felde, A.B., Westermeyer, J. & Thuras, P. (2006). Co-morbid traumatic brain injury and substance use disorder: childhood predictors and adult correlates. Brain Injury, 20(1), 41–9. Feldmann, T.B. (2001). Bipolar disorder and violence. Psychiatric Quarterly, 72, 119–29. Firestone, P., Bradford, J.M., Greenberg, D.M. & Larose, M.R. (1998). Homicidal sex offenders: psychological, phallometric, and diagnostic features. Journal of the American Academy of Psychiatry and the Law, 26(4), 537–52. Fowles, D.C. (2000). Electrodermal hyporeactivity and antisocial behavior: does anxiety mediate the relationship? Journal of Affective Disorders, 61, 177–89.

COMORBIDITIES OF PSYCHOPATHY AND APD

271

Freeman, K.A., Dexter-Mazza, E.T. & Hoffman, K.C. (2005). Comparing personality characteristics of juvenile sex offenders and non-sex offending delinquent peers: a preliminary investigation. Sexual Abuse: A Journal of Research and Treatment, 17(1),3–12. Fu, Q., Heath, A.C., Bucholz, K.K. et al. (2002). Shared genetic risk of major depression, alcohol dependence and marijuana dependence. Contribution of antisocial personality disorder in men. Archives of General Psychiatry, 59, 1125–32. Gill, K., Nolimal, D. & Crowley, T. (1992). Antisocial personality disorder, HIV risk behavior and retention in methadone maintenance therapy. Drug and Alcohol Dependence, 30, 247–52. Goodwin, R.D. & Hamilton, S.P. (2003). Lifetime comorbidity of antisocial personality disorder and anxiety disorders among adults in the community. Psychiatry Research, 117, 159–66. Gosden, N.P., Kramp, P., Gabrielsen, G. et al. (2005). Violence of young criminals predicts schizophrenia: a 9-year register-based follow up of 15 to 19 year old criminals. Schizophrenia Bulletin, 31(3), 759–68. Greenberg, W.M., Otero, J. & Villanueva, L. (1994). Irregular discharges from a dual diagnosis unit. American Journal of Drug and Alcohol Abuse, 20(3), 355–71. Grekin, E.R., Brennan, P.A., Hodgins, S. & Mednick, S.A. (2001). Male criminals with organic brain syndrome: two distinct types based on age at first arrest. American Journal of Psychiatry, 158, 1099–104. Grella, C.E., Joshi, V. & Hser, Y.I. (2003). Follow-up of cocaine-dependent men and women with antisocial personality disorder. Journal of Substance Abuse Treatment, 25, 155–64. Hare, R.D. (1991). The Hare Psychopathy Checklist-Revised, 2nd edition. Toronto: Multi-Health Systems. Hatzitaskos, P., Soldatos, C.R., Kokkevi, A. & Stefanis, C.N. (1999). Substance abuse patterns and their association with psychopathology and type of hostility in male patients with borderline and antisocial personality disorder. Comprehensive Psychiatry, 40(4), 278–82. Hodgins, S. & Cote, G. (1993a). The criminality of mentally disordered offenders. Criminal Justice and Behavior, 28, 115. Hodgins, S. & Cote, G. (1993b). Major mental disorder and APD: a criminal combination. Bulletin of the American Academy of Psychiatry and the Law, 21, 155. Hodgins, S., Lapalme, M. & Toupin, J. (1999). Criminal activities and substance use of patients with major affective disorders and schizophrenia: a 2-year follow-up. Journal of Affective Disorders, 55(2–3), 187–202. Hodgins, S. & Muller-Isberner, R. (2004). Preventing crime by people with schizophrenic disorders: the role of psychiatric services. British Journal of Psychiatry, 185, 245–50. Hogue, T., Steptoe, L., Taylor, J.L. et al. (2006). A comparison of offenders with intellectual disability across three levels of security. Criminal Behaviour and Mental Health, 16(1), 13–28. Holt, S.E., Meloy, J.R. & Strack, S. (1999). Sadism and psychopathy in violent and sexually violent offenders. Journal of the American Academy of Psychiatry and the Law, 27(1), 23–32. Joyal, C.C., Putkonen, A., Paavola, P. & Tiihonen, J. (2004). Characteristics and circumstances of homicidal acts committed by offenders with schizophrenia. Psychological Medicine, 34(3), 433–42. King, V.L., Kindorf, M.S., Stoller, K.B. et al. (2001). Influence of antisocial personality subtypes on drug abuse treatment response. Journal of Nervous and Mental Disease, 189, 593–601. Koenen, K.C. (1999). The comorbidity of post traumatic stress disorder and antisocial personality disorder: an epidemiological and genetic study (men, twins). Dissertation thesis (abstract only). Kramp, P. (2004). Editorial: schizophrenia and crime in Denmark. Criminal Behaviour and Mental Health, 14(4), 231–7. Lewinsohn, P.M., Klein, D.N. & Seley, J.R. (1995). Bipolar disorders in a community sample of older adolescents: prevalence, phenomenology, comorbidity, and course. Journal of the American Academy of Child and Adolescent Psychiatry, 34, 454–63. Mailloux, D.L., Forth, A.E. & Kroner, D.G. (1997). Psychopathy and substance use in adolescent male offenders. Psychological Reports, 81(2), 529–30. McAnulty, R.D., Adams, H.E. & Wright, L.W. (1994). Relationship between MMPI and penile plethysmograph in accused child molesters. Journal of Sex Research, 31(3), 179–84. McCabe, M.P. & Wauchope, M. (2005). Behavioral characteristics of men accused of rape: evidence for different types of rapists. Archives of Sexual Behavior, 34(2), 241–53.

272

VOLUME I: DIAGNOSIS AND TREATMENT

McElroy, S.L., Soutullo, C.A., Taylor, P. et al. (1999). Psychiatric features of 36 men convicted of sexual offenses. Journal of Clinical Psychiatry, 60, 414–20. Meyers, C.A., Berman, S.A., Scheibel, R.S. & Hayman, A. (1992). Case report: acquired antisocial personality disorder associated with unilateral left orbital frontal lobe damage. Journal of Psychiatry and Neuroscience, 17(3), 121–5. Moeller, A.A. & Hell, D. (2003). Affective disorder and ‘psychopathy’ in a sample of younger male delinquents. Acta Psychiatrica Scandinavica, 107, 203–7. Moeller, F.G. & Dougherty, D.M. (2001). Antisocial personality disorder, alcohol, and aggression. Alcohol Research and Health, 25(1),5–11. Moran, P. & Hodgins, S. (2004). The correlates of comorbid antisocial personality disorder in schizophrenia. Schizophrenia Bulletin, 30(4), 791–802. Mueser, K.T., Crocker, A.G., Frisman, L.B. et al. (2006). Conduct disorder and antisocial personality disorder in persons with severe psychiatric and substance use disorders. Schizophrenia Bulletin, 32(4), 626–36. Mueser, K.T., Drake, R.E., Ackerman, T.H. et al. (1997). Antisocial personality disorder, conduct disorder and substance abuse in schizophrenia. Journal of Abnormal Psychology, 106(3), 473–7. Mueser, K.T., Rosenberg, S.D., Drake, R.E. et al. (1999). Conduct disorder, antisocial personality disorder and substance use disorders in schizophrenia and major affective disorders. Journal of Studies on Alcohol, 60(2), 278–84. Munker, R., Haastrup, S., Joergensen, T. & Kramp, P. (2003). The temporal relationship between schizophrenia and crime. Social Psychiatry and Psychiatric Epidemiology, 38, 347–53. Myers, M.G., Stewart, D.G. & Brown, S.A. (1998). Progression from conduct disorder to antisocial personality disorder following treatment for adolescent substance abuse. American Journal of Psychiatry, 155, 479–85. Myers, W.C., Burkett, R.C. & Husted, D.S. (2006). Sadistic personality disorder and comorbid mental illness in adolescent psychiatric inpatients. Journal of the American Academy of Psychiatry and the Law, 34, 61–71. Nolan, K.A., Volavka, J., Mohr, P. & Czobor, P. (1999). Psychopathy and violent behavior among patients with schizophrenia or schizoaffective disorder. Psychiatric Services, 50(6), 787–92. Pelissier, B.M.M. & O’Neil, J.A. (2000). Antisocial personality and depression among incarcerated drug treatment participants. Journal of Substance Abuse, 11(4), 379–93. Phillips, S.L., Heads, T.C., Taylor, P.J. & Hill, G.M. (1999). Sexual offending and antisocial sexual behavior among patients with schizophrenia. Journal of Clinical Psychiatry, 60, 170–5. Pliszka, S.R. (1998) Comorbidity of attention-deficit/hyperactivity disorder with psychiatric disorder: an overview. Journal of Clinical Psychiatry, 59(Supplement 7), 50–8. Pliszka, S.R., Sherman, J.O., Barrow, M.V. & Irick, S. (2000). Affective disorder in juvenile offenders: a preliminary study. American Journal of Psychiatry, 157, 130–2. Porter, S., Woodworth, M., Earle, J. et al. (2003). Characteristics of sexual homicides committed by psychopathic and nonpsychopathic offenders. Law and Human Behavior, 27(5), 459–70. Putkonen, A., Kotilainen, I., Joyal, C.C. & Tiihonen, J. (2004). Comorbid personality disorders of mentally ill homicide offenders: a structured clinical study on dual and triple diagnoses. Schizophrenia Bulletin, 30(1), 59–72. Quanbeck, C.D., Stone, D.C., Scott, C.L. et al. (2004). Clinical and legal correlates of inmates with bipolar disorder at the time of criminal arrest. Journal of Clinical Psychiatry, 65, 198–203. Regier, D.A., Farmer, M.E., Rae, D.S. et al. (1990). Comorbidity of mental disorders with alcohol and other drug abuse. Journal of the American Medical Association, 264, 2511–18. Reid, W.H. & Ruiz-Sweeney, M.S. (2003). Antisocial personality, psychopathy and forensic psychiatry. In R. Rosner (ed.), Principle and Practice of Forensic Psychiatry, 2nd edition (pp. 555–63). Rice, M.E. & Harris, G.T. (1995) Psychopathy, schizophrenia, alcohol abuse, and violent recidivism. International Journal of Law and Psychiatry, 18(3), 333–42. Robins, L.N. (1998). The intimate connection between antisocial personality disorder and substance abuse. Social Psychiatry and Psychiatric Epidemiology, 33, 393–9. Robins, L.N., Helzer, J.E., Weissman, M.M. et al. (1984). Lifetime prevalence of specific psychiatric disorders in three sites. Archives of General Psychiatry, 41, 949–58. Robins, L.N., Tipp, J. & Przybeck, T. (2001). Antisocial personality. In L.N. Robins & D.A. Regier (eds.), Psychiatric Disorders in America: The Epidemiologic Catchment Area Study (pp. 258–90). New York: Free Press.

COMORBIDITIES OF PSYCHOPATHY AND APD

273

Roy, A., Lamparski, D., DeJong, J. et al. (1990). Characteristics of alcoholics who attempt suicide. American Journal of Psychiatry, 147, 761–5. Ruchkin, V.V., Schwab-Stone, M., Koposov, R. et al. (2002). Violence exposure, posttraumatic stress, and personality in juvenile delinquents. Journal of the American Academy of Child and Adolescent Psychiatry, 41, 322–9. Sareen, J., Stein, M.B., Cox, B.J. & Hassard, S.T. (2004). Understanding comorbidity of anxiety disorders with antisocial behavior. Journal of Nervous and Mental Disease, 192, 178–86. Schuckit, M.A. (1985). The clinical implications of primary diagnostic groups among alcoholics. Archives of General Psychiatry, 42(11), 1043–9. Silver, H., Goodman, C., Knoll, G. et al. (2005). Schizophrenia patients with a history of severe violence differ from nonviolent schizophrenia patients in perception of emotions but not cognitive functioning. Journal of Clinical Psychiatry, 66, 300–8. Soderstrom, H., Nilsson, T., Sjodin, A.K. et al. (2005).The childhood onset neuropsychiatric background to adulthood psychopathic traits and personality disorders. Comprehensive Psychiatry, 46, 111–16. Solomon, P. & Draine, J. (1999). Explaining lifetime criminal arrests among clients of a psychiatric probation and parole service. Journal of the American Academy of Psychiatry and the Law, 27, 239–51. Steadman, H.J., Mulvey, E.P., Monahan, J. et al. (1998). Violence by people discharged from acute psychiatric inpatient facilities and by others in the same neighborhoods. Archives of General Psychiatry, 55(5), 393–401. Steiner, H., Garcia, I.G. & Matthews, Z. (1997). Posttraumatic stress disorder in incarcerated juvenile delinquents. Journal of the American Academy of Child and Adolescent Psychiatry, 36(3), 357–65. Stompe, T., Ortwein-Swoboda, G. & Schanda, H. (2004). Schizophrenia, delusional symptoms, and violence: the threat/control override concept reexamined. Schizophrenia Bulletin, 30(1), 31–44. Strous, R.D., Bark, N., Parsia, S.S. et al. (1997). Analysis of a functional catechol-O-metyltransferase gene polymorphism in schizophrenia: evidence for association with aggressive and antisocial behavior. Psychiatry Research, 69, 71–7. Swann, A.C. (2005). Bipolar disorder and substance abuse: two disorders or one? Journal of Dual Diagnosis, 1(3), 9–23. Swanson, J.W., Holzer, C.E. 3rd, Ganju, V.K. & Jono, R.T. (1990). Violence and psychiatric disorder in the community: evidence from the Epidemiologic Catchment Area surveys. Hospital and Community Psychiatry, 41(7), 761–70. Swanson, J.W., Swartz, M.S., Van Dorn, R.A. et al. (2006). A national study of violent behavior in persons with schizophrenia. Archives of General Psychiatry, 63, 490–9. Taylor, P.J. & Estroff, S.E. (2003). Schizophrenia and violence. In S.R. Hersch & D. Weinberger (eds.), Schizophrenia (pp. 591–612). Massachusetts: Blackwell Science. Taylor, P.J., Leese, M., Williams, D. et al. (1998). Mental disorder and violence. A special (high security) hospital study. British Journal of Psychiatry, 172, 218–26. Tengstrom, A., Grann, M., Langstrom, N. & Kullgren, G. (2000). Psychopathy (PCL-R) as a predictor of violent recidivism among criminal offenders with schizophrenia. Law and Human Behavior, 24(1), 45–58. Tengstrom, A., Hodgins, S., Grann, M. et al. (2004). Schizophrenia and criminal offending. The role of psychopathy and substance use disorders. Criminal Justice and Behavior, 31(4), 367–91. Teplin, L.A. (1990). The prevalence of severe mental disorder among male urban jail detainees; comparison with the epidemiologic catchment area program. American Journal of Public Health, 80, 663–9. Teplin, L.A., Abram, K.M. & McClelland, G.M. (1996). Prevalence of psychiatric disorders among incarcerated women. Archives of General Psychiatry, 53, 505–12. Thomas, V.H., Melchert, T.P. & Banken, J.A. (1999). Substance dependence and personality disorders: Comorbidity and treatment outcome in an inpatient treatment population. Journal of Studies on Alcohol, 60(3), 271–82. Wallace, C., Mullen, P.E. & Burgess, P. (2004). Criminal offending in schizophrenia over a 25-year period marked by deinstitutionalization and increasing prevalence of comorbid substance use disorders. American Journal of Psychiatry, 161, 716–27.

274

VOLUME I: DIAGNOSIS AND TREATMENT

Walsh, E., Gilvarry, C., Samele, C. et al. (2004).Predicting violence in schizophrenia: a prospective study. Schizophrenia Research, 67(2–3), 247–52. Warren, J.I., Burnette, M.L., South, S.C. et al. (2003). Psychopathy in women: structural modeling and comorbidity. International Journal of Law and Psychiatry, 26, 223–42. Widiger, T.A. & Corbitt, E.M. (1997). Comorbidity of antisocial personality disorder with other personality disorders. In D.M. Stoff, J. Breiling & J.D. Maser (eds.), Handbook of Antisocial Behavior (pp. 75–82). New York: John Wiley & Sons, Inc. Windle, M. (1999). Psychopathy and antisocial personality disorder among alcoholic inpatients. Journal of Studies on Alcohol, 60(3), 330–42. Woody, G.E., McLellan, A.T., Luborsky, L. & O’Brian, C. (1985). Sociopathy and psychotherapy outcome. Archives of General Psychiatry, 42, 1081–6.

CHAPTER 16

The Paraphilias and Psychopathy John M.W. Bradford, Philip Firestone and A.G. Ahmed University of Ottawa, Canada

There has been a long association and some confusion between the paraphilias and personality disorders in general and psychopathy in particular. The term ‘paraphilias’ was only introduced in 1980 into the diagnostic classification. The sexual deviations (paraphilias) were initially regarded as personality disorders. In DSM-I and II the sexual deviations were classified as part of personality disorders (‘Sociopathic Personality Disturbances’) as opposed to a separate diagnostic classification. In DSM-III, first published in 1980, the ‘Psychosexual Disorders’ were included in the classification and this included the sexual dysfunctions, gender identity disorders, paraphilias, as well as egodystonic homosexuality. Starting with DSM-III-R and continuing with DSM-IV the full classification of the paraphilias were included. This long-standing association and confusion with personality disorders has led to difficulties in accepting the paraphilias as Axis 1, psychiatric disorders, and this has resulted in difficulties in setting up treatment programs and some rejection by mainstream psychiatry. It has also led to misunderstanding by the criminal justice system particularly in the United States. This chapter will attempt to explore the relationship between the paraphilias and psychopathy within a broad framework of clinical practice. In pursuing this goal, the chapter begins by reviewing the clinical features of paraphilias. This is followed by section on the features and diagnosis of psychopathy. In the next section there is a review of the association of psychopathy with the paraphilias in particular and sexual offending behavior in general. The chapter concludes by reviewing sexual recidivism studies and the role that psychopathy plays in sexual offense recidivism. The paraphilias were included in DSM-III-R and have continued in DSM-IV and DSMIV TR. They are characterized by ‘recurrent, intense sexually arousing fantasies, sexual urges, or behaviors generally involving 1) nonhuman objects 2) the suffering or humiliation of oneself or one’s partner 3) children or other nonconsenting persons that occur over the period of at least six months’ (American Psychiatric Association, 1994, 2000). Initially the sexual deviations were regarded as personality disorders and were classified in DSM 1 under

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

276

VOLUME I: DIAGNOSIS AND TREATMENT

‘Sociopathic Personality Disturbance’. In DSM-II the sexual deviations were again classified as personality disorders and were included in the diagnostic system as ‘Personality Disorders’. For the first time definitions of sexual deviations were included in this classification. As the diagnostic and classification system evolved with DSM-III, first published in 1980, the sexual deviations were classified for the first time under ‘Psychosexual Disorders’. This classification was continued in DSM-III-R; DSM-IV and now in DSM-IV TR (American Psychiatric Association, 1994, 2000). The psychosexual disorders have included a series of sexual disorders ranging from sexual dysfunctions, gender identity disorders and the paraphilias. Initially in DSM-III egodystonic homosexuality was included. The definition for a deviant sexual preference being the use of nonhuman objects necessary for achieving sexual arousal became an important part of the definition of the paraphilias. This was expanded to include sexual suffering and sexual acting out with nonconsenting partners. The paraphilias were included in DSM-III-R and have continued in DSM-IV and DSM-IV TR. (American Psychiatric Association, 1994, 2000). DSM-IV is the official nomenclature for the diagnosis and classification of mental disorders. The fourth edition also correlates with the tenth revision of the World Health Organization’s International Classification of Diseases and Related Health Problems (ICD 10). This ensures that the diagnostic systems used in the United States are compatible with ICD 10 to achieve uniform reporting of both national and international statistics on mental disorders. This has meant that the paraphilias are now an accepted diagnostic classification internationally both within DSM-IV trace and ICD 10. The paraphilias are classified as exhibitionism, fetishism, frotterism, pedophilia, sexual masochism, sexual sadism, transvestitic fetishism, voyeurism, and paraphilias not otherwise specified. The main characteristics of the subclasses of paraphilias are outlined in Table 16.1.

PSYCHOPATHY The concept of psychopathy has intrigued the academic and popular press for centuries. The definition of psychopathy has both historical and current conceptions which is beyond the scope of this chapter but has been extensively covered in literature elsewhere (Blackburn, 1998; Hare, 1996, 2003). This is a concept that has developed historically from extensive clinical research by American and European psychiatrists and psychologists. It continues to develop from a clinical and research standpoint although there is a significant body of knowledge supporting the core attributes of the concept of psychopathy (Cleckley, 1976; Hare, 2003). Psychopathy as a concept is widely recognized by the mental health professions, psychiatry and psychology, as well as the criminal justice system and is also a term recognized by the lay public. The term psychopathy is broadly used in Europe to cover personality disorder and there is a debate as to whether it should be defined as an abnormal personality or abnormal behavior (Coid, 1993; Hare, 2003). While many definitions of psychopathy have been proffered, the Cleckley concept (1941) as operationalized in the Hare Psychopathy Checklist (PCL-R) is currently the most reliable means of identifying psychopathic traits. Psychopathy is characterized by antisocial behavior, ‘superficial charm’, unreliability, insincerity, inability to accepted blame or shame, impulsivity, failure to learn from experience, egocentricity and a lack of capacity to love, a general lack

Egosyntonic Exclusive and caring relationship with the victim

Egosyntonic ???

Egosyntonic Exposing self and or observer may be sexually aroused

Paraphilic fantasies and urges

Sexual activity with a prepubescent child (13 yrs or younger) *Perpetrator must 16 years or older or 5 years older than child victim Egosyntonic Sexual activity with a prepubescent child (13 years or younger)

Touching and rubbing against a nonconsenting person

Use of nonliving objects

Pedophilia

Frotteurism

Fetishism

Exposure of genitals to a stranger

Exhibitionism

Paraphilic focus

Main characteristics

Acts of observing unsuspecting individuals naked disrobing or engaging in sexual activities

Egosyntonic Having sexual experience with the observed person

Cross-dressing by males in women’s attire

Egosyntonic Person as female (autogynephilia)

Acts (real or simulated) of inflicting psychological or physical suffering (including humiliation) on the victim Egosyntonic or egodystonic especially if they occur during sexual intercourse Fantasy of complete victim control and dominance

Acts (real or simulated) of being humiliated, beaten bound or otherwise made to suffer

Egosyntonic or egodystonic especially if they occur during sexual intercourse

Voyeurism

Transvestic fetishism

Sexual sadism

Sexual masochism

Paraphilias

Table 16.1 Main characteristics of the paraphilias (Adapted from DSM- 1V-TR, American Psychiatric Association, 2000)

(Continued)

Include the following: telephone scatologia, necrophilia, partialism, zoophilia, coprophilia, klismaphilia, urophilia

Paraphilia NOS

Yes (while fantasizing or exposing)

No attempt

Sexual activity with object of fantasy

Exhibitionism

Masturbation

Main characteristics

Table 16.1 (Continued )

Maybe when the favored article becomes erotic in itself Rare

Yes during act or fantasy

Mostly with nonconsenting or consenting partner (sexual masochism)

Yes during act or fantasy

May act on fantasies or urges by self inflicted aggression or with a partner

In the presence of the child

Undressing and looking, self-exposure, gentle touching and fondling, fellatio or cunnilingus, vaginal, anal or mouth penetration (with finger, foreign objects or penis)

Maybe while fantasizing ???

Transvestic fetishism

Yes (while holding, rubbing or smelling object) Fetish may be used in sexual encounter

Sexual sadism

Sexual masochism

Pedophilia

Frotteurism

Fetishism

Paraphilias

During actual voyeuristic activity or later recollection of same Rare

Voyeurism

Paraphilia NOS

Rare ????

Usually before age 18

Gradual decline after age 40

Usually before age 40

Use of force

Onset

Course

Arrest

Usually results from stealing women’s clothing items

Chronic

Usually in adolescence

Rare ???

Likely

Gradual decline

Usually in adolescence (15–25)

Body contact in crowds

Chronic. May fluctuate with psychosocial stress Highly likely. Recidivism very high especially with female preference subtype

May threaten and assault victim to prevent disclosure Usually in adolescence (may start in middle age) Childhood or early adolescence. Public cross-dressing in adulthood Chronic

Fantasies usually in childhood. Activities early adulthood Chronic

Likely. Recidivism is high until arrest

Chronic

Unlikely ???

??? Public nuisance

Rare

Main characteristic directed at the victim

Self-directed unless associated with sexual sadism Fantasies usually in childhood. Activities early adulthood

Possible

Chronic

(Continued )

Almost never. Observation usually the exclusive sexual activity Before age 15years

Others

Main characteristics

Marked distress or interpersonal difficulty Goal is to surprise or shock observer

Exhibitionism

Table 16.1 (Continued )

Pedophilia Subtypes include: – exclusive and nonexclusive – sexually attracted to male, to female, to both

Frotteurism Fondling of victims body or gentalia Usually in crowded places

Fetishism

Fetish required or preferred for sexual excitement. May have erectile dysfunction without

Transvestic fetishism Women’s garments are arousing as symbols of the individual’s femininity rather than fetishes Described only in heterosexual males *Not diagnosed when it occurs exclusively in the context of gender identity disorder May be associated with sexual masochism Cross-dressing may become anxiolytic or antidysphoric without sexual arousal Association with gender dysphoria when under stress

Sexual sadism Severity of sadistic acts increase over time. When severe or associated with antisocial personality disorder it may result in serious injuries or victim’s death

Sexual masochism May be associated with infantilism, hypoxyphilia which result in death (1–2 deaths/million/ year) May be associated with fetishism, transvestic fetishism or sexual sadism

Paraphilias

‘Peeping Tom’

Voyeurism

Paraphilia NOS

THE PARAPHILIAS AND PSYCHOPATHY

281

of a capacity to emote, poor integration into sexual relationships and inability to follow life goals. Since it was first published in 1991, the Hare Psychopathy Checklist has become the most important tool in assessing psychopathic personality. The instrument is easy to use, easy to understand and has been supported by significant scientific research into its validity (Hare, 1996, 2003). The reliability and validity of the PCL-R is extensively covered in the latest edition of the manual of the Hare Psychopathy Checklist Revised and will not be covered in a detailed in this chapter and is beyond the scope of this chapter (Hare, 2003). The Psychopathy Checklist-Revised (PCL-R) consists of 20 clinical rating scales designed to assess behaviors and personality characteristics considered fundamental to psychopathy that are rated through a semistructured interview (Hare, 2003). Rigorous testing has indicated that the PCL-R is a psychometrically sound instrument; the reported alpha coefficient, aggregated across seven samples of incarcerated males from Canada, the United States and England was .87 (Hare, Forth & Strachan, 1992) The existence of two factors was replicated using various samples: (i) the degree of personality, interpersonal and affective traits deemed significant to the construct of psychopathy; and (ii) the degree of antisocial behavior, unstable and corrupted lifestyle (Harpur, 1989). Hare et al. (1990), using five prison samples (N = 925) and three forensic samples (N = 356), found the correlation between the two factors averaged .48. Previous studies have found the interrater reliability and internal consistency of both factors to be high despite the small number of items per factor (Hare, 2003; Hare et al., 1990). The reliability of the PCL-R in clinical work has been enhanced since the publishers and developers of the scale require that those using it undergo specialized training. The principal authors of this chapter, with colleagues, have used the Hare Psychopathy Checklist-Revised extensively in studying sexual offender recidivism as well in other related studies because of its acceptance in the scientific literature from the standpoint of reliability and validity. The experience gained in using it in scientific studies has resulted in the principal authors strongly endorsing this instrument. In fact, the principal authors believe that every forensic psychiatric program should use this instrument on a routine basis in forensic psychiatric assessments. It is a fundamental tool in forensic psychiatric risk assessment. The PCL-R and the DSM-IV classification of antisocial personality disorder have a number of overlapping diagnostic features. The fact that psychopathy should be considered both in terms of personality traits and behavior is reflected in the operational definition of antisocial personality disorder in DSM-IV (American Psychiatric Association, 2000; Hare, 2003). The difference appears to be that DSM-IV relies heavily on behavior including the evidence of conduct disorder prior to age 15 and then ongoing antisocial behavior, which shows a pervasive pattern of the violation of and disregard for the rights of others after age 15 years. The PCL-R and the traditional concept of psychopathy as defined by Cleckley focuses more on the personality traits associated with psychopathy. Many of the core psychopathic traits are seen as associated features to antisocial personality disorder in DSM-IV (Cleckley, 1976; Hare, 1996, 2003). It is the PCL-R as opposed to the DSM-IV operational definition of antisocial personality disorder that has dominated the research into sexual offending behavior and paraphilic behavior as its overlaps with this type of behavior and sexual offender recidivism specifically.

282

VOLUME I: DIAGNOSIS AND TREATMENT

PSYCHOPATHY AND THE PARAPHILIAS The main association between psychopathy and the paraphilias has been through studies on sexual offenders. Sexual offenders are mostly men who have a paraphilia but this is not consistent depending on the type of sexual offender or the type of paraphilia. For example, pedophiles molest children and this activity brings them into conflict with the law where they would then be classified as sexual offenders. Having a sexual preference for children, as opposed to a sexual preference for adults, is fundamental to pedophilia. It is the most common mechanism leading to child-molesting behavior but it is not the only mechanism where adults may molest children. Sexual abuse of children may occur secondary to disturbed mental states such as psychosis and dementia in individuals who do not have a sexual preference for children. As with all sexual offenders, alcohol and substance abuse are problematic as they may act as behavioral disinhibitors or contribute to emotional dyscontrol. Incest perpetrators, a subcategory of pedophilia, may have a sexual preference for children but some of them do not and their incestuous sexual behavior against children occurs for other reasons. In theory, alcoholism and marital dysfunction may lead to men sexually acting out with their daughters rather than specifically a sexual preference for children. In the case of sexual offenses against adult females (rape) it is even more complicated. Rape may occur because of opportunity and is associated with a severe personality disorder without having a sexual preference for coercive sex. At the same time certain individuals have a sexual preference for coercive sex that may show as rape or may be classified as sexual sadism. The actual prevalence of the paraphilias within the general population is unknown although some attempts to estimate the prevalence have used criminal justice statistics and specifically convictions for sexual offenses. It has been estimated that 1–2 % of the male population will eventually be convicted of a sexual offense (Marshall, 1997). The diagnostic problems with sexual offenders are more extensive when many clinicians and researchers do not consider DSM-IV criteria for the diagnosis. This leads to many people being classified as child molesters, some of whom are pedophiles and some who may have molested postpubescent children and are technically hebephiles (Marshall, 2006). Marshall (2006) has dealt with this issue in detail in relation to pedophilia and sexual sadism (Marshall, 2006). One of the main areas of difficulty relates to a group of offenders against adult females (rapists) who should be considered to have a paraphilia. A number of experts in the field concluded that the weight of scientific evidence supported the inclusion of this group in the paraphilias with a new diagnosis of a coercive paraphilic disorder. This was a recommendation of a committee working on DSM-III R but was not supported by the Council of the American Psychiatric Association, despite the empirical evidence, because of concerns of the potential misuse in forensic psychiatric situations (Abel, 1989; American Psychiatric Association, 1999). A Task Force of the American Psychiatric Association also addressed the issue of psychopathology among sexual offender populations and concluded that there was a lack of reliable data on the actual prevalence of sexual offending; a lack of reliable data on the rates of sexual deviations, defined in clinical terms, in the general population and the rates of sexual deviation and other psychopathology in sexual offender populations (American Psychiatric Association, 1999). There is also evidence that multiple paraphilias usually are present in any given individual who is diagnosed as having a paraphilia (Abel et al., 1988; Bradford, Boulet & Pawlak, 1992). There is also a concern over other competing typologies to DSM-IV which further complicates this picture (American Psychiatric

THE PARAPHILIAS AND PSYCHOPATHY

283

Association, 1999). Although these concerns are real, there is considerable scientific literature related to sexual offenders and sexual offense recidivism that includes accurate data on psychopathy, most commonly based on the measurement of psychopathy using the PCL-R. For a substantial period of time there has been the recognition that certain sex offenders are psychopathic and that they present special problems or difficulties for the criminal justice system, the general public as well as treatment providers. Various studies of sexual offenders have shown mixed results, with the PCL-R being strongly correlated with general and violent criminal behavior and less strongly correlated with sexual offending behavior (Hare, 2003). This in part is based on studies not differentiating different types of sexual offenders, and this includes child molesters, the majority of whom were not psychopathic. These undifferentiated studies of sexual offenders therefore weaken the possible correlations between the PCL-R and sexual violence (Hare, 2003). A recent comprehensive meta-analysis found that only six of 61 studies which met inclusion criteria were concerned with child molesters, and fewer studied groups of incest offenders (Hanson & Bussiere, 1998; Quinsey et al., 1995). Quinsey and colleagues reviewed published articles on recidivism in sexual offenders and were able to locate four studies where incest offenders specifically were studied, published between 1962 and 1991 (Quinsey et al., 1995) They reported the average reported sexual reoffense rate for these studies was 8.5 % (Quinsey et al., 1995). This limited research indicates incest offenders recidivate at a lower rate than extrafamilial child molesters, and suggests variables predicting recidivism differs between these two groups of child molesters (Hanson & Bussiere, 1998; Quinsey et al., 1995). Recidivism was divided into three categories in a fashion similar to Proulx et al. (1997) and Rice, Quinsey and Harris (1991). Sexual recidivism was defined as any charge or conviction for sexual offense, after the index offense. Violent recidivism included any charge or conviction for nonsexual violent and sexual offenses. Criminal recidivism was defined as any charge or conviction noted in the Canadian Police Information Center’s (CPIC) documentation. A cumulative hierarchy in which each additional category subsumes that of the previous was adopted to account for plea-bargaining distortions and to allow comparison with previous recidivism research with child molesters (Rice et al., 1991). The principal authors of this chapter, with colleagues, have completed a number of studies on sexual offenders where sexual offense recidivism and the factors associated with it have been analyzed (Firestone, Wexler & Bradford, 2006; Firestone, Bradford, McCoy et al., 1998, 2000; Firestone et al., 1999; Greenberg et al., 2002). One of the recidivism studies looked at incest offenders. Two hundred and fifty-one incest offenders were followed for an average of 6.7 years after their conviction, while at risk to reoffend in the community. The percentage of men who had committed a sexual, violent, or any criminal offense by the twelfth year of follow-up was 6.4 %, 12.4 % and 26.7%, respectively (Firestone et al., 1999) . The sexual recidivists scored higher on the Michigan Alcohol Screening Test (MAST) (Firestone et al., 1999; Gibbs, 1983), and the PCL-R (Hare, 2003). The violent recidivists had higher MAST and PCL-R scores as well as more violence in their police records (Firestone et al., 1999). In terms of any criminal recidivism, recidivists were several years older, their families of origin were more disturbed and they reported higher rates of being physically abused and being removed from their homes prior to 16 years of age. In addition, recidivists demonstrated more general hostility on the Buss–Durkee Hostility Inventory, higher MAST and PCL-R scores (Firestone et al., 1999). They also had more charges or convictions for sexual, violent and any criminal acts on their police

284

VOLUME I: DIAGNOSIS AND TREATMENT

records. The small number of significant differences between recidivists and nonrecidivists in the sexual and violent categories precluded an attempt to determine which combination of factors meaningfully predicted reoffending. However, for criminal recidivism, a stepwise discriminant function analysis to assess the combination of factors that most successfully distinguished between groups was significant. A combination of total criminal offenses, PCL-R, age and the number of previous sexual offenses correctly classified 97.6 % of the nonrecidivists and 35.4 % of the recidivists. This represents a rate of improvement over chance of 20.7 % for nonrecidivists and 12.3 % for recidivists (Firestone et al., 1999). In studying these results one must be careful to take into account that the actual recidivism rates of sex offenders are underrepresentations of the real number of sexual offenses committed, no matter what criteria are used (Furby, Weinrott & Blackshaw, 1989; Hanson & Bussiere, 1998). Many sexual offenses are not reported, therefore this study and the other recidivism studies identified the recidivism risk and clinical factors associated with various types of offenders, who also have different types of paraphilias, appearing before the courts. Further, this represented a sample of men who were purely incest perpetrators and not extrafamilial child molesters or offenders against adult females. In addition, the majority of recidivists did so by the fifth year, as the respective rates at that time were 4.8 %, 9.2 % and 22.3 %, for sexual, violent and general recidivism, respectively. As a group, the incest offenders were considerably less antisocial than previously studied groups of extrafamilial child molesters, where only 6 % had a previous sexual offense conviction compared to other studies where this varied between 15 % and 41.9 % (Firestone et al., 2000; Hanson & Bussiere, 1998). The recidivism rates for these incest offenders were also considerably lower than previously published Canadian rates for men who sexually offended against children (Hanson & Bussiere, 1998) and close to a similar Canadian study (Quinsey et al., 1995). In terms of sexual recidivism, our 6.4 % reoffense rate is remarkably similar to the 8.5 % computed by Quinsey and colleagues (1995). In the present study, one of only four of the measures that discriminated sexual recidivists from nonrecidivists was the PCL-R total score. The others were the MAST, age and the number of previous sexual charges/convictions. Although alcohol abuse has been reported as occurring in a high proportion of sexual sadists and other sexual offenders (Allnutt et al., 1996), the documented evidence for alcohol abuse and alcoholism in sexual recidivism is limited (Hanson & Bussiere, 1998). In this study the mean score on the MAST was in the alcoholism range. Psychopathy as measured by the PCL-R total score continues to demonstrate its potency as a measure in the prediction of criminal behavior. The PCL-R total scores of 21.7 and 17.9 for sexual offender recidivists versus nonrecidivists show the importance of the PCL-R in evaluating sexual offenders, even though, due to the small number of subjects in the sexual recidivism category, the discriminant function was of little value in predicting which men would reoffend based on these variables. As with sexual recidivism, measures related to alcohol abuse, psychopathy and previous offending differentiated violent offenders from those that did not reoffend. It is interesting, but not surprising, that the PCL-R, Factor 2 differentiated recidivists from nonrecidivists, as did the total score. Factor 2 is related to criminal lifestyle, as are the CPIC data. Once again, due to the low base rate problem, the discriminant function was of little value in assisting in the prediction of violent recidivism. The PCL-R was also successful in discriminating between criminal recidivists and nonrecidivists. The role of phallometric measures in the assessment and treatment of sex offenders is a matter of controversy and debate. A

THE PARAPHILIAS AND PSYCHOPATHY

285

recent meta-analysis suggested that sexual preference for children, as measured by phallometric methods, was the single largest predictor of sexual recidivism for child molesters (Hanson & Bussiere, 1998). Many of the studies reviewed did not differentiate between child molesters and incest offenders. The findings from the present study suggested that deviant sexual arousal was not useful for predicting recidivism in incest offenders. The phallometric assessments were helpful in demonstrating that, as a group, incest offenders show considerable deviant arousal. In our clinic a pedophile index greater than 1 indicates a deviant sexual preference for children, a pedophilic assault index, an indication that sexual sadism is associated with a deviant sexual preference for children is of significant concern and an index of .75 and above would be of serious concern. The fact that for sexual, violent and criminal offenses, both recidivists and nonrecidivists had mean pedophile and pedophile assault indices ranging from .7 to 1.2, reveals their deviant sexual arousal is disturbingly high, even though not related to recidivism. This means this group clearly had a deviant sexual preference for children, as measured using penile tumescence techniques, and therefore were clearly pedophilic. Even though this is important clinically in terms of the definition of the pathology of the incest offenders it did not help in the prediction of recidivism (Firestone et al., 1999). The discriminant function based on age, PCL-R total score and history of sexual offenses and all criminal offenses was successful in improving prediction over chance by 20.7 % for the nonrecidivists and 12.3 % for the recidivists. Our better rates of prediction for nonrecidivists compared to recidivists was common in the sex offender literature and are largely a function of the low base rates of sex offenses. Similar to incest offenders, research has attempted to identify the variables which accurately predict recidivism in extrafamilial child molesters. As already outlined these two groups of child molesters need to be seen as independent groups for research and clinical purposes. Studies that have differentiated these groups show that extrafamilial child molesters recidivate at a considerably higher level than incest perpetrators (Hanson & Bussiere, 1998; Quinsey et al., 1995). Two of the authors of this chapter with colleagues completed a study wherein any child molesters who had ever been charged with an incest offense or an offense against an adult female were specifically excluded in the sample. There were 192 male subjects, 18 years or older at the time of their index offense, who had been convicted of a hands-on sexual offense against an unrelated male or female child who were followed for an average of 7.8 years while at risk in the community. The percentage of the sample that had committed a sexual, violent and any criminal offense by the end of 12 years of follow-up was 15.1 %, 20.3 % and 41.6%, respectively (Firestone et al., 2000). Recidivism here, similar to the incest study, was cumulative. By the end of the fifth year of follow-up recidivism rates for sexual, violent and any criminal act were 9.4 %, 14.1 % and 30.7 %, respectively. A five-year period at risk in the community is the important minimum benchmark for evaluating recidivism. The sexual recidivists, when compared to the nonrecidivists, demonstrated more difficulties with alcohol and showed greater sexual arousal to assault (coercive or violent) stimuli involving sex with children when compared to stimuli where the interaction between adults and children would present as a being consenting (nonviolent, noncoercive). This means the pedophilic arousal that was present in the recidivists was significantly more violent and coercive. The violent recidivists, when compared to nonrecidivists, were more likely to have a history of violence within the families they were raised and were significantly more psychopathic on the PCL-R. This group of recidivists was significantly more pedophilic in their sexual arousal patterns than the nonrecidivists.

286

VOLUME I: DIAGNOSIS AND TREATMENT

When any criminal recidivism was considered, the recidivists were younger, less educated, came from more psychologically harmful families, were more likely to have been physically abused, and removed from their families prior to 16 years of age. In addition, they showed high levels of hostility and high levels of psychopathy on the PCL-R. The mean total PCL-R score for the sexual recidivists was 19.8 compared to the mean total PCL-R score of 18.1 for the nonrecidivists. When violent recidivists were compared to nonrecidivists, the mean total PCL-R score was 21.1 versus 17.6, and criminal recidivists versus nonrecidivists, the mean total PCL-R scores were 22.1 and 15.6, respectively. The criminal recidivists compared to the nonrecidivists also had high Factor 1 and Factor 2 scores. The small number of significant differences between recidivists and nonrecidivists in the sexual and violent categories prevented any further analysis of combination of factors that would meaningfully predict reoffending. However, in the criminal recidivism group, a number of factors including age, level of education, MAST score, PCL-R total score, various sexual arousal indices and previous violent and criminal offenses were included in the discriminant function analysis which was significant at a p < .001 level. The rate of prediction as an improvement over chance was 30.86 %. When the PCL-R total score was used alone, this was 34.03 % (Firestone et al., 2000). PCL-R scores were very successful in discriminating between recidivists and nonrecidivists in the criminal recidivism category. The PCL-R total scores 22.1 and 15.6 respectively placed them at the 57th and 26th percentiles of forensic psychiatric patients. These results, highlighting the usefulness of the PCL-R in recidivism research, are similar to what has been seen previously in other studies (Firestone, Bradford, McCoy et al., 1998; Quinsey et al., 1995). In sexual offense, recidivism rapists are generally regarded as being more psychopathic or having high antisocial traits compared to incest perpetrators and extrafamilial child molesters. It would follow therefore that the PCL-R should be very useful in predicting recidivism in this group. In a study completed by two of the authors of this chapter on recidivism in convicted rapists this proved not to be the case (Firestone, Bradford, McCoy et al., 1998). Eighty-six rapists who had been out of prison for the 12 years, with the mean follow-up period of 7.6 years, were studied in detail with information of typing from the sexual behaviors clinic where they had been evaluated in depth. The ability to predict sexual and violent recidivism was poor. More sexual recidivists compared to nonrecidivists had been removed from their family home prior to age 16. Violent recidivists compared to nonrecidivists were also more frequently removed from their homes prior to 16 years of age and showed significantly more problems with alcohol. Criminal recidivists compared to nonrecidivists were younger and had high scores on the Michigan Alcohol Screening Test, as well as more previous criminal convictions (Firestone, Bradford, McCoy et al., 1998). In this study the level of psychopathy was moderately high and consistent across all groups. The mean total PCL-R scores for sexual recidivism versus nonrecidivists were 25.2 and 25.2, respectively; for violent recidivists versus nonrecidivists, 26.1 and 24.8, respectively; and criminal recidivists versus nonrecidivists, 26.7 and 23.3, respectively. This distribution of scores being so close and moderately high shows the significant levels of psychopathy amongst rapists compared to child molesters and incest perpetrators even though in this instance it does not discriminate between the recidivists and nonrecidivists in the various categories (Firestone, Bradford, McCoy et al., 1998, 2000; Firestone et al., 1999). Exhibitionism has generally been regarded as a public nuisance as opposed to being a serious criminal offense or even in some cases not even regarded as being a sexual offense. Studies have shown, however, that exhibitionists can escalate into more serious crimes of

THE PARAPHILIAS AND PSYCHOPATHY

287

hands-on sexual offenders. Two of the authors of this chapter conducted a study to examine recidivism in exhibitionists and also to study who recidivated with a ‘hands-on’ sexual offense as opposed to a ‘hands-off’ or nontouching sexual offense. The study followed 221 exhibitionists for a mean follow-up period of 6.83 years (Greenberg et al., 2002). The rate of recidivism for sexual, violent and criminal recidivism was 11.7 %, 16.8 % and 32.7 %, respectively. Sexual offender recidivists were less educated and had a higher number of sexual and criminal offenses. Violent recidivists were also less educated and had higher total PCL-R scores as well as some other differences on sexual dysfunction and previous criminal offenses. Criminal recidivists also had higher total PCL-R scores as well as some other differences. The more serious recidivists with ‘hands-on’ sex offenses when compared to ‘hands-off’ sexual offender recidivists had higher PCL-R scores, higher sexual arousal deviant indices, as well as a history of more prior sexual, violent and criminal offenses (Greenberg et al., 2002). A recently published long-term follow-up study of exhibitionists over a mean follow-up period of 13.24 years found that 23.6 %, 31.3 % and 38.9 % of exhibitionists were convicted or charged with a new sexual, violent and criminal offense (Firestone, Wexler & Bradford, 2006). Sexual recidivists, when compared to nonrecidivists, were less educated, scored higher on the Michigan Alcohol Screening Test and the PCL-R score, as well as the Pedophile Index, a measure of sexual deviance and deviance sexual preference. Violent recidivists compared to nonrecidivists were less educated, scored higher on the MAST score, had high scores on the PCL-R and the Pedophile Index. Criminal recidivists were also less educated and scored higher on the MAST score, PCL-R and Pedophile Index as well as having a higher number of previous sexual, violent and criminal charges (Firestone, Wexler & Bradford, 2006). The PCL-R, once again featured prominently in differentiating recidivists from nonrecidivists across the various categories of offenses. The comorbidity of personality disorder (including antisocial personality disorder diagnosed using DSM IV rather than the PCL-R) as well as high rates of mental illness substance abuse and paraphilias have been described in other samples of sexual offenders where the clinical features were the object of the study as opposed to recidivism (Dunsieth et al., 2004). Although a rare occurrence, pedophiles committing sexually motivated homicides cause significant distress in the general public because of the very nature of this type of offense. If there was any way of differentiating homicidal child molesters from nonhomicidal child molesters, this would be seen as a very important development. The principal authors of this chapter studied the psychological, phallometric and criminal features in a sample of homicidal and nonhomicidal child molesters (Firestone, Bradford, Greenberg & Larose, 1998; Firestone, Bradford, Greenberg & Nunes, 2000). In the 1998 study the PCL-R total score, Factor 1 and Factor 2 scores were high in both samples of homicidal and nonhomicidal child molesters with the homicidal child molesters having significantly higher PCL-R Factor 1 and Factor 2 scores at the 93rd and 82nd percentiles respectively compared to the published norms for forensic psychiatric patients (Firestone, Bradford, Greenberg & Larose, 1998). The larger proportion of the homicidal child molesters suffered from antisocial personality disorder and the paraphilias, specifically sexual sadism. It was the PCL-R scores that significantly differentiated the groups (Firestone, Bradford, Greenberg & Larose, 1998). In a similar study, homicidal child molesters, nonhomicidal child molesters and a nonoffender control group were investigated. Various measures of deviant sexual preference were obtained using a penile tumescence technique and were studied in the three groups. The homicidal child molesters showed a significantly higher

288

VOLUME I: DIAGNOSIS AND TREATMENT

Pedophile Assault Index (arousal to sexual sadism and violence directed towards children) when compared to the other groups (Firestone, Bradford, Greenberg & Nunes, 2000). The PCL-R and the standardized use of phallometric testing in combination is a very promising in identifying homicidal child molesters, a rare but extremely dangerous subcategory of child molesters. To summarize the PCL-R is extremely important in differentiating recidivists from nonrecidivists across a spectrum of paraphilias. In general terms the higher the recidivism or the higher the risk of violence of the subcategory the higher the PCL-R score (see Figure 16.1). The treatment of the paraphilias is beyond the scope of this chapter, however, it is important to note that the pharmacological treatment of the paraphilias is well established and has a significant impact on recidivism regardless of the levels of psychopathy as measured by the PCL-R or other measures. Further, comorbidity of personality disorders with the paraphilias has been well established (Bradford, 2001). The pharmacological treatment regime is geared towards reducing deviant sexual arousal but it is possible that the pharmacological treatments also have an impact on associated features of psychopathy such as impulsivity (Bradford, 1996; Bradford & Gratzer, 1995; Bradford & Pawlak, 1993a, 1993b). This may contribute to the successful outcomes in the pharmacological treatments of the paraphilias. As serotonin reuptake inhibitors can be used to successfully treat pedophilia and other paraphilias and some treatment success has been documented for the symptomatic treatment of some features of antisocial personality disorder, this may be a further indication of successful treatment of the comorbid conditions (Bradford, 1999, 2000; Greenberg & Bradford, 1997). Research into the neurobiology of serotonin in the paraphilias and psychopathy could be a useful research strategy in the future looking at possible causal relationships as well as exploring new treatment options (Coccaro, 1992; Coccaro & Kavoussi, 1997; Coccaro et al., 1997; Lee & Coccaro, 2001).

PCL-R Score

40

20

0 Incest

CM

Rapist

Homicidal SO

Paraphillias

Figure 16.1 Mean PCL-R scorce in different Paraphillias

Homicidal CM

THE PARAPHILIAS AND PSYCHOPATHY

289

REFERENCES Abel, G.G. (1989). Paraphilias. In H.I. Kaplan, Sadock, B.J. (eds.), Comprehensive Textbook of Psychiatry V (5th edition, pp. 1069–85). Baltimore: Williams & Wilkins. Abel, G.G., Becker, J.V., Cunningham-Rathner, J. et al. (1988). Multiple paraphilic diagnoses among sex offenders. Bulletin of the American Academy of Psychiatry and the Law, 16(2), 153–68. Allnutt, S.H., Bradford, J.M., Greenberg, D.M. & Curry, S. (1996). Co-morbidity of alcoholism and the paraphilias. Journal of Forensic Science, 41(2), 234–9. American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders: DSM-IV (4th edition). Washington, DC: American Psychiatric Association. American Psychiatric Association (1999). Dangerous Sex Offenders: A Task Force Report of the American Psychiatric Association (1st edition). Washington, DC: American Psychiatric Association. American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders: DSM-IV-TR (4th edition). Washington, DC: American Psychiatric Association. Blackburn, R. (1998). Psychopathy and personality disorder: implications of interpersonal theory. In D. Cooke, A.E. Forth & R.D. Hare (eds.), Psychopathy: Theory, Research, and Implications for Society (pp. 269–301). Dordrecht: Kluwer Academic. Bradford, J.M. (1996). The role of serotonin in the future of forensic psychiatry. Bulletin of the American Academy of Psychiatry and the Law, 24(1), 57–72. Bradford, J.M. (1999). The paraphilias, obsessive compulsive spectrum disorder, and the treatment of sexually deviant behaviour. Psychiatry Quarterly, 70(3), 209–19. Bradford, J.M. (2000). The treatment of sexual deviation using a pharmacological approach. Journal of Sex Research, 37, 248–57. Bradford, J.M. (2001). The neurobiology, neuropharmacology, and pharmacological treatment of the paraphilias and compulsive sexual behaviour. Canadian Journal of Psychiatry, 46(1), 26–34. Bradford, J.M., Boulet, J. & Pawlak, A. (1992). The paraphilias: a multiplicity of deviant behaviours. Canadian Journal of Psychiatry, 37(2), 104–8. Bradford, J.M. & Gratzer, T.G. (1995). A treatment for impulse control disorders and paraphilia: a case report. Canadian Journal of Psychiatry, 40(1), 4–5. Bradford, J.M. & Pawlak, A. (1993a). Double-blind placebo crossover study of cyproterone acetate in the treatment of the paraphilias. Archives of Sexual Behaviour, 22(5), 383–402. Bradford, J.M. & Pawlak, A. (1993b). Effects of cyproterone acetate on sexual arousal patterns of pedophiles. Archives of Sexual Behaviour, 22(6), 629–41. Cleckley, H. (1976). The Mask of Sanity (5th edition). St. Louis: Mosby. Coccaro, E.F. (1992). Impulsive aggression and central serotonergic system function in humans: an example of a dimensional brain–behavior relationship. International Clinical Psychopharmacology, 7(1), 3–12. Coccaro, E.F. & Kavoussi, R.J. (1997). Fluoxetine and impulsive aggressive behavior in personalitydisordered subjects. Archives of General Psychiatry, 54(12), 1081–8. Coccaro, E.F., Kavoussi, R.J., Sheline, Y.I. et al. (1997). Impulsive aggression in personality disorder correlates with platelet 5-HT2A receptor binding. Neuropsychopharmacology, 16(3), 211–16. Coid, J. (1993). Current concepts and classifications of psychopathic disorder. In P.S. Tyrer (ed.), Personality Disorder Reviewed. London: Gaskell Press. Dunsieth, N.W., Jr., Nelson, E.B., Brusman-Lovins, L.A. et al. (2004). Psychiatric and legal features of 113 men convicted of sexual offenses. Journal of Clinical Psychiatry, 65(3), 293–300. Firestone, P., Bradford, J.M., Greenberg, D.M. & Larose, M.R. (1998). Homicidal sex offenders: psychological, phallometric, and diagnostic features. Journal of American Academy of Psychiatry and the Law, 26(4), 537–52. Firestone, P., Bradford, J.M., Greenberg, D.M. & Nunes, K.L. (2000). Differentiation of homicidal child molesters, nonhomicidal child molesters, and nonoffenders by phallometry. American Journal of Psychiatry, 157(11), 1847–50. Firestone, P., Bradford, J.M., McCoy, M. et al. (1998). Recidivism in convicted rapists. Journal of American Academy of Psychiatry and the Law, 26(2), 185–200. Firestone, P., Bradford, J.M., McCoy, M. et al. (2000). Prediction of recidivism in extrafamilial child molesters based on court-related assessments. Sex Abuse, 12(3), 203–21.

290

VOLUME I: DIAGNOSIS AND TREATMENT

Firestone, P., Bradford, J.M., McCoy, M. et al. (1999). Prediction of recidivism in incest offenders. Journal of Interpersonal Violence, 14(5), 511–31. Firestone, P., Wexler, A. & Bradford, J.M. (2006). Long-term follow-up of exhibitionists: psychological, phallometric, and offense characteristics. Journal of the American Academy of Psychiatry and the Law, 34(3), 349–59. Furby, L., Weinrott, M.R. & Blackshaw, L. (1989). Sex offender recidivism: a review. Psychology Bulletin, 105(1), 3–30. Gibbs, L.E. (1983). Validity and reliability of the Michigan alcoholism screening test: a review. Drug and Alcohol Dependency, 12(3), 279–85. Greenberg, D. & Bradford, J.M. (1997). Treatment of the paraphilic disorders: a review of the role of the selective serotonin reuptake inhibitors. Sex Abuse, 9, 349–61. Greenberg, S.R., Firestone, P., Bradford, J.M. & Greenberg, D.M. (2002). Prediction of recidivism in exhibitionists: psychological, phallometric, and offense factors. Sex Abuse, 14(4), 329–47. Hanson, R. & Bussiere, M.T. (1998). Predicting relapse: a meta-analysis of sexual offender recidivism studies. Journal of Consulting and Clinical Psychology, 66(2), 348–2. Hare, R. (1996). Psychopathy: a clinical construct whose time has come. Criminal Justice and Behavior, 23, 25–54. Hare, R. (2003). Hare Psychopathy Checklist Revised (PCL-R) (2nd edition). Toronto: Multi-Health Systems. Hare, R.D., Forth, A.E. & Strachan, K.E. (1992). Psychopathy and crime across the life span. In R. Peters, R.J. McMahon & V.L. Quinsey (eds.), Aggression and Violence Throughout the Lifespan (pp. 285–300). Newbury Park: Sage. Hare, R.D., Harpur, T.J., Hakstian, A.R. et al. (1990). The Revised Psychopathy Checklist: descriptive statistics, reliability and factor structure. Psychological Assessment: A Journal of Consulting and Clinical Psychology, 338–41. Harpur, T., Hare, R.D. & Hakstian, A.R. (1989). Two-factor conceptualization of psychopathy: construct validity and assessment implications. Psychological Assessment: A Journal of Consulting and Clinical Psychology, 1(1), 6–7. Lee, R. & Coccaro, E. (2001). The neuropsychopharmacology of criminality and aggression. Canadian Journal of Psychiatry, 46(1), 35–44. Marshall, P. (1997). The Prevalence of Convictions for Sexual Offending. London: Home Office Research and Statistics Directorate. Marshall, W.L. (2006). Diagnostic problems with sexual offenders. In W.L.F. Marshall, Y.M. Marshall & G.A. Serran (eds.), Sexual Offender Treatment, Controversial Issues (pp. 33–45). Chichester, England: John Wiley & Sons, Ltd. Proulx, J., Pellerin, B., Paradis, Y. et al. (1997). Static and dynamic predictors of recidivism in sexual aggressors. Sexual Abuse: A Journal of Research and Treatment, 9, 7–27. Quinsey, V., Lalumiere, M.L., Rice, M.E. & Harris, G.T. (1995). Predicting sexual offenses. In J. Campbell (ed.), Assessing Dangerousness. Violence by Sexual Offenders, Batterers, and Child Abusers. Thousand Oaks: Sage. Rice, M.E., Quinsey, V.L. & Harris, G.T. (1991). Sexual recidivism among child molesters released from a maximum security psychiatric institution. Journal of Consulting Clinical Psychology, 59(3), 381–6.

CHAPTER 17

Family Upbringing: Family Factors as Predictors for the Development of Antisocial Behavior and Psychopathy Dimensions Maya K. Krischer, Kathrin Sevecke and Gerd Lehmkuhl The University of Cologne, Germany

Educational, social and psychiatric factors within a family play an important role for the development of antisocial behavior. Financial problems of the family, the lack of warmth in family relationships, abusive behavior on the part of a parent as well as psychopathology of either the parents or siblings are factors that have an impact on the etiology of aggressive or antisocial behavior of a child and juvenile. This chapter will present an overview of current findings on early familial factors as predictors for the development of antisocial behavior and the syndrome of psychopathy. Psychopathy is defined as a constellation of personality traits and behavioral indicators that can strongly predict future violent and aggressive behavior. Like most personality disorders, the syndrome of psychopathy is believed to consist of a stable set of maladaptive personality traits, attitudes and behaviors, such as affective deficits, interpersonal deceptiveness, impulsive and antisocial tendencies, that began in childhood. In this text the terms antisocial and dissocial behavior are used as generic terms to describe criminal and aggressive conduct that is often existent in children and juveniles, whether it is a persistent behavior (an antisocial pathway) or only a temporary phenomenon during adolescence. In addition to structural family factors during upbringing, this chapter reports on current findings regarding the impact of early traumatization and biological vulnerability as essential risk factors for a deviant social and especially psychopathic development. Moreover, in this chapter we report on findings pertaining to early physical punishment within a German sample of delinquent adolescents.

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

292

VOLUME I: DIAGNOSIS AND TREATMENT

FAMILY UPBRINGING AND AN ANTISOCIAL PATHWAY Intra- and Extrafamilial Factors During Upbringing Two categories of structural factors during upbringing are regarded as influential for the development of an antisocial or psychopathic pathway. First, intrafamilial elements include the socioeconomic status of the family, parental divorce, single motherhood or the number of children in the household. Secondly extrafamilial factors are identified, such as peer group and school influence. In reference to the intrafamilial factors, Loeber et al. (1993) suggest that the continuance of delinquency from childhood and adolescence into adulthood can be attributed to a lack of parental presence during upbringing. Consistent adverse family conditions as well as an early diagnosed developmental delay significantly increase the risk of ongoing delinquency. Adverse social conditions during adolescence have a greater prognostic value than early childhood risk factors, and especially in developmentally delayed juveniles, play an important role for a poor prognosis of ongoing criminal behavior. Deviant peer affiliation as an extrafamilial factor has been shown to increase the likelihood of aggressive behavior during adolescence and even for an ongoing adult antisocial lifestyle (Lambert et al., 2005; Shortt et al., 2003). Different studies suggest the amplification of the individual risk for maladaptive behavior by deviant friendships with peers, independent of the child’s ethnicity (Dishion et al., 2004; Dekovic, Wissink & Marie Mejier, 2004). At the same time, this phenomenon may correspond with family management practices and parental disengagement (Dishion, Winter & Bullock, 2004). In a German prospective study with 321 subjects who were followed up to the age of 25, Laucht and coworkers (2001) demonstrated that almost every environmental stress factor was associated with a heightened risk for antisocial behavior. These findings indicate that when taking all predictive variables into consideration, besides early developmental disorders, adverse family conditions at least until the age of 13 years are of special importance. Within the realm of socioeconomic factors, Laucht lists, for example, cramped/choked living conditions, constant marital strife, an incomplete family and a foster home placement for the child. Various recent findings showed that low socioeconomic status of the family or single-parent mothers predicts antisocial problems in adolescence (Marmorstein & Iacono, 2005; van Bokhoven et al., 2005).

Parental Disposition Many studies investigated parental dispositional factors among the potential early risk factors for antisocial behavior. The most common variables that have been investigated are psychiatric problems of a parent, especially maternal depression, parental criminal behavior or a history of substance abuse. Children of depressed mothers have elevated conduct problems, presumably due to the fact that depression disrupts the care-giving environment (Kim-Cohen et al., 2005; Marmorstein & Iacono, 2004). Interestingly, based on their findings, researchers explained this phenomenon by noting the tendency of depressed mothers to partner with antisocial fathers and their own likelihood of having comorbid antisocial personality traits (Marmorstein, Malone & Iacono, 2004). An important parental factor is linked to paternal substance abuse

FAMILY UPBRINGING

293

that influences the child’s externalizing psychopathology (Moss et al., 2002). Furthermore, parental imprisonment was found to have an important impact on the risk of a child becoming antisocial (Lahey et al., 2002; Murray & Farrington, 2005). Prisoners’ children are considered a highly vulnerable group with multiple risk factors for adverse outcomes due to early separation experience, reduction in family income and reduced quality of care. Similarly, other problems of the biological parents, such as their personality traits, were associated with later antisocial behavior in the adolescent, presumably due to traits such as high neuroticism and low conscientiousness impairing the parent’s ability to provide adequate child care (Nigg & Hinshaw, 1998; Pevalin, Wade & Brannigan, 2003).

The Parent–Child Interaction An important predictor for an antisocial pathway seems to lie in the parent–child interaction. Some research demonstrates that these so-called proximal factors which operate within a family are significant predictors of antisocial behavior (Dekovic, Janssens & Van As, 2003). Other results indicate parenting practices to be relatively poor predictors of antisocial behavior (Bor, McGee & Fagan, 2004). In a longitudinal study parental rejection, insufficient parental monitoring and a deficit in the parent–child interaction were suggested as strong predictors for adolescent delinquency and antisocial behavior (Loeber et al., 1993; Loeber & Stouthamer-Loeber, 1998). As shown by different studies, antisocial behavior with respect to aggression against others is associated with a rough and unloving parental style of upbringing, disharmony and discord between the parents and parental rejection of the child. Larceny and property-related crimes are also associated with a lack of parental consequence and care. Correlations with lack of parental monitoring and consequences were found not only for antisocial behavior in general, but also specifically for the development of psychopathy (Block, 1993). Furthermore, based on the parent–child relationship some authors include insecure attachment, deficient competence in child upbringing (Patterson, Capaldi & Bank, 1991) and negative child-rearing practices (Dodge et al., 1995) as influencing factors for an antisocial pathway. Moreover, parents (N = 109) who reported having been victims themselves, of physical abuse in childhood, are significantly more likely to engage in abusive behaviors towards the next generation than parents who have not been abused (Pears & Capaldi, 2001). This brings us to the influence of exposure to trauma.

THE IMPACT OF TRAUMA EXPOSURE FOR THE DEVELOPMENT OF ANTISOCIAL BEHAVIOR In addition to these family-related factors, during upbringing the impact of traumatic experiences plays an important role for antisocial and especially aggressive behavior. Traumatic experiences usually mentioned as stressful life events include experiencing early physical and emotional deprivation, as well as experiencing or observing physical or sexual abuse within or outside the family (Egle et al., 2002). Early traumatization is commonly regarded a causal or mediating risk factor for aggressive and violent behavior (Pollock, 1999). Researchers agree that violence leads to violence and that children with conduct disorder suffer disproportionately often from traumatization or

294

VOLUME I: DIAGNOSIS AND TREATMENT

trauma symptoms (Soberman, Greenwald & Rule, 2002). Other authors argue that early broken trust has a negative influence on the ability to feel empathy (James, 1989) and that this phenomenon lowers the threshold to commit criminal deeds. Ongoing heightened hyperarousal during early childhood, which is typical for an upbringing within a traumatic environment, leads to affective and violent outbursts and deficient impulse control (Erwin et al., 2000). Novaco and Chemtob (1998) suggest that early traumatic experiences have a negative impact on anger regulation, which is the basis for aggressive behavior. Furthermore, emotional numbing, a typical symptomatic reaction to early traumatization, appears to be a causal factor for a heightened tendency of sensation seeking and therefore risky behavior in these children. Some researchers understand sensation seeking as a reflection of emotional numbness and the attempt to overcome one’s lack of feeling (Baker & Alfonso, 2003; Zuckerman, 1979). A variety of studies with delinquent and incarcerated juveniles demonstrated a heightened prevalence of post-traumatic stress symptoms and early traumatic experiences. Most studies with violent criminal offenders found higher prevalence rates than studies with nonviolent delinquents (Erwin et al., 2000, n = 51; Steiner et al., 1997, n = 85). In their Chicago study with incarcerated children and juveniles, Abram and coworkers (2004) showed that almost all participants (N = 898) experienced at least one or more traumatic incidents during upbringing. Of all male and female subjects, 74 % reported confrontation with violence as their most severe traumatic experience, 58 % said they were threatened by a weapon, and 53 % mentioned a traumatic situation in which they expected themselves or a significant other to be severely hurt or to die. In this study, no significant sex differences were found. Other researchers referred to heightened prevalence rates of traumatic symptoms in female delinquents compared to male delinquents. Based on clinical interviews, Cauffman and coworkers (1998) suggested that almost 50 % of female juvenile delinquents (n = 96) had not only experienced a traumatic incident, but had also suffered from post-traumatic stress disorder. Most of these girls claimed to have been a victim of a violent crime. Some researchers estimate the prevalence of abuse in female delinquents as high as 90 %, with rates as high as 83 % for sexual abuse (Odgers, Reppucci & Moretti, 2005). Similarly, an Australian study reported a heightened prevalence of traumatization and post-traumatic symptoms in 100 female incarcerated adolescents compared to a control group, matched on age and socioeconomic status (Dixon, Howie & Starling, 2004). These findings indicate a gender effect pertaining to higher mental health problems and a greater number of comorbid disorders applicable to female than to male adolescent offenders (Abram et al., 2004; Timmons-Mitchell et al., 1997). In a prospective study, Widom detected that neglected or physically abused children have a 30 % heightened risk of committing a violent crime in adolescence (1992, 2001). Furthermore, abused children were younger when first incarcerated and committed many more crimes than those children who had never been abused. A German study similarly reported that the frequency and severity of intrafamilial violent experiences have a general impact on the rates of juvenile violent crimes (Wetzels et al., 2001, n = 3600). Of the group of victims of parental physical abuse, 34 % committed violent deeds whereas the percentage in the non-abused group was only 17 %. With their results in a high-risk representative cohort of 1116 twin pairs between five and seven years, using age of the mother at first child as the risk-stratification variable, Jaffee et al. (2004) support the hypothesis that physical maltreatment plays a causal role in the development of children’s antisocial behavior.

FAMILY UPBRINGING

295

The role of early sexually abusive experiences as an important impact factor for an antisocial pathway remains unclear. A large Australian community study of adolescents (n = 7361) described childhood sexual abuse as a risk factor for the development of antisocial behavior, with increased risks of three- to eightfold for sexually abused boys, and two- to threefold for sexually abused girls, compared to non-abused controls (Bergen et al., 2004). Other studies arrived at the conclusion that childhood sexual experience is related to becoming a child molester in adulthood (Coxe & Holmes, 2001). In contrast Zlotnick (1999) stated, based on a study of 85 incarcerated women with a history of childhood abuse, sexual abuse was not significantly associated with the diagnosis of antisocial personality disorder (APD) in adulthood. A control group was not included into this study.

PSYCHOPATHY AND TRAUMATIZATION DURING UPBRINGING Thus far, few studies have focused on the influence of early traumatic experiences on the syndrome of psychopathy specifically within the realm of antisocial personality pathology. Like most personality disorders diagnosed in adulthood, the syndrome of psychopathy is believed to consist of a stable set of maladaptive personality traits, attitudes and behaviors that began in childhood (i.e., Farrington, 1995; Forth, Kosson & Hare, 2003; Loeber & Farrington, 1998). Recently, in part due to its utility in predicting aggressive and violent behavior, researchers and clinicians have manifested increasing interest in the construct of ‘juvenile psychopathy’ (Edens, Skeem & Cruise, 2001). Forth et al. (2003) developed a specific version of the Psychopathy Checklist (PCL) – the Psychopathy Checklist: Youth Version (PCL: YV) – identifying adolescents with psychopathic traits. The few studies that used the PCL: YV have shown that incarcerated adolescent males with high PCL: YV scores display more violent behavior and more conduct disorder symptoms compared to low-scoring adolescent males (Forth & Burke, 1998). As suggested by different theories, early child maltreatment is expected to play an important causal role in the development of personality pathology, but few studies exist that investigated its empirical evidence in reference to the development of psychopathy. Campbell and colleagues (Campbell, Porter & Santor, 2004) evaluated the clinical, psychosocial and criminal correlates of psychopathic traits in a sample of 226 male and female incarcerated adolescent offenders. They demonstrated that although higher PCL: YV scores were associated with having experienced physical abuse, the only psychosocial factor that predicted elevated PCL: YV scores was a history of nonparental living arrangements (e.g., foster care). Marshall and Cooke (1999) demonstrated in their factor analysis of childhood experience variables two distinct factors, familial and societal, both of which were highly correlated with adult psychopathy scores of male prisoners. In a substance-abusing population (n = 339), Bernstein, Stein and Handelsman (1998) revealed several significant paths between types of maltreatment and personality disorder cluster: physical abuse and physical neglect were related to a subcategory of ‘psychopathic’ personality disorders consisting of childhood and adult antisocial personality traits and sadistic traits. Emotional abuse emerged as a broad risk factor for personality disorders in Clusters A, B and C. Emotional neglect was related to the traits of schizoid personality disorder. Finally, sexual abuse, which had

296

VOLUME I: DIAGNOSIS AND TREATMENT

been expected to predict borderline personality disorder traits, was in this sample unrelated to any personality disorder cluster. Marshall and Cooke (1999) found a high correlation between negative family and social childhood experiences and heightened scores on the psychopathy checklist in adults (PCL-R; Hare et al., 2000). In a Swiss sample of male inmates aged 17–27 years, the prevalence of affective disorder was significantly higher in the ‘non-psychopathic’ group. The total score on the Psychopathy Checklist Revised (PCL-R) was significantly correlated with the number of prior threatening events, but post-traumatic stress syndrome (PTSD) could not be diagnosed in the ‘psychopathic group’ (Moeller & Hell, 2003). In a Swedish longitudinal project, possible implications of childhood neglect and/or abuse on adult PCL scores and violent offending were studied in a socially high-risk neighborhood (Lang, Klinteberg & Alm, 2002). The high victimization subjects exerted significantly more violence, as did subjects with high PCL scores. Furthermore, they applied a configurational frequency analysis and found two significant ‘types’: in type one ‘high’ victimization in childhood is closely linked with later, ‘extensive’ violence and with ‘high’ PCL scores (over 25 points) at adult age; the other type had a frequent co-occurrence of ‘low’ victimization in childhood, ‘no or minor’ later signs of violence and ‘low’ adult PCL scores. To our knowledge, findings in female delinquent juveniles with psychopathic traits in relation to early traumatization are so far missing.

ORIGINAL RESEARCH RESULTS ON TRAUMA AND PSYCHOPATHY The authors’ own research (Krischer & Sevecke, in preparation) supports other findings that traumatization occurs significantly more often in delinquent juveniles (n = 178) than nondelinquent school juveniles, enrolled in public schools (n = 98; mean age of 16–17 years). Furthermore, consistent with other recent studies, we also found that detained girls (n = 87) reported significantly more often having experienced emotional, sexual and physical abuse than detained boys (n = 91; Krischer & Sevecke in preparation, see Table 17.1). In this study of incarcerated male and female German juveniles the authors found mainly positive intercorrelations between abuse scales and the psychopathy dimension ‘Early Behavior Problems’. Only physical neglect showed a slight correlation with the PCL: YV total score. Furthermore, results indicate that traumatization has a different influence in girls Table 17.1 Trauma experiences in our sample of incarcerated juveniles compared with school juveniles (average age: 17.2 years) % ( p)

Delinquent girls (n = 71)

Delinquent boys (n = 75)

Emotional abuse Physical abuse Sexual abuse Emotional neglect Physical neglect

28.3 % ( p = .016) 34.3 % ( p < .001) 16.4 % ( p = .05) 43.3 % ( p < .001) 12.5 % ( p = .002)

15.6 % ( p = .002) 16.8 % ( p = .001) 4.8 % n.s. 34.9 % ( p = .03) 7.2 % n.s.

School girls (n = 46)

School boys) (n = 52)

14.9 % 2.7 % 6.9 % 13.6 % 0%

1.4 % 1.4 % 1.4 % 19.2 % 8.2 %

Source: n.s. means not significant, comparing delinquent with nondelinquent girls/boys; traumatization was measured with the self-report instrument Childhood Trauma Questionnaire by Bernstein and Fink (2001).

FAMILY UPBRINGING

297

than boys with respect to developing psychopathic traits. Regarding sexual abuse, girls with reported abuse experience tended to have lower scores on the Psychopathy Checklist; in boys no differences were found in the non-abused compared to the abused group. These findings show, however, that physically abused boys tended to score significantly higher on the PCL: YV than delinquent male adolescents who denied the experience of maltreatment during their childhood. As hypothesized, the physically traumatized boys showed more problems regarding interpersonal and affective psychopathic traits, such as shallow affect and poor anger control. Moreover, this group of maltreated boys scored significantly higher in terms of antisocial behavior, such as ‘Serious Criminal Behavior’, ‘Criminal Versatility’ and ‘Failure to Accept Responsibility’. A similar difference was found for delinquent boys who reported emotional abuse. Consistent with other findings our results indicate that although traumatization is higher in delinquent girls than boys, especially physical maltreatment can be regarded as one upbringing factor that can cause the development of a psychopathic pathway for boys. Our results suggest that for girls traumatization plays less of a role for the development of psychopathy than for boys. Further research is needed to identify etiological factors which lead to psychopathic traits in girls.

BIOLOGICAL FEATURES AS VULNERABILITY AND PROTECTIVE FACTORS DURING UPBRINGING The importance of biological or psychobiological markers is based on their presumed influence on the ability to cope with stress. Some researchers argue that favorable temperament and intelligence (derived from biological or genetic factors) can improve the resilience against stressors and can protect against a maladaptive development or post-traumatic stress disorders (Bender & L¨osel, 1997; Werner, 1997). Other studies point out that early stressors, and especially the constant influence of a traumatic environment during childhood, can cause heightened glucocorticoid levels (De Bellis et al., 1994) as well as heightened dopamine/noradrenaline levels (Arnsten, 1997; Schore, 1997), both of which can harm the prefrontal cortex. It is established knowledge that dysfunction in the prefrontal cortex can cause heightened impulsivity and therefore problems with respect to coping with stress and inhibition of behavior (Arnsten, 2000; Dolan & Park, 2002). This leads to the so-called ‘attention to distraction’ that is typical for children with attention deficit hyperactivity disorder and to aggressive and self-destructive behavior in adolescents and adults (Castellanos & Tannock, 2002; van der Kolk & Fisler, 1994). Another current longitudinal study with a sample of 975 seven-year-old boys showed that the monoamine oxidase A (MAOA) polymorphism moderates the development of psychopathology after exposure to physical abuse, meaning that the MAOA gene influences vulnerability to environmental stress (Kim-Cohen et al., 2006). These findings indicate that, beside traumatic incidents during upbringing, biological factors play an important role either as protective or risk factors for a maladaptive pathway. Researchers studying the etiology of aggressive behavior point to the importance of biological markers. Raine, for example, demonstrated that hypoarousal, a biological risk marker of criminal behavior, is more prevalent in delinquents coming from middle or higher socioeconomic levels than those from the lower levels (Raine, 1997). These subjects interact

298

VOLUME I: DIAGNOSIS AND TREATMENT

with their parental figures, but cannot adapt their behavior in relation to authorities, social norms or the rights of others (Moffitt, 1993). Their behavior is based on their temperament as well as their underarousal. Therefore, the etiology of psychopathy is nowadays considered to be an interaction of biological vulnerability and the social environment or milieu of the child during upbringing. Children of higher socioeconomic level are less affected by adverse environmental factors, but are more vulnerable to biological risk factors (Loeber, 1990; Raine, Brennan & Mednick, 1997). Due to their biological basis, extreme aggressive disorders in children and adolescents are considered the most stable personality traits over the lifespan (Krischer et al., 2006; Lehmkuhl, 2006): Forty percent of the children who show such behavior in different situations continued to have such difficulties in adulthood. Temper tantrums, damage to property, aversion to learn, short attention span, distractibility and substance abuse are typical for such youths. Not to serve their own advantage, but especially to harm another person or thing is the goal of their aggression. It seems to be secondary, whether the aggressive deed benefits themselves or not. An early hyperactive or conduct disorder before the age of eight years appears to be the greatest risk factor for a prolonged delinquency. Block (1993) showed in his longitudinal study a significant association between childhood conduct disorder and later antisocial behavior. Robins found an association between aggressive oppositional behavior during childhood and the development of an antisocial personality disorder as well as substance abuse during adulthood (1991, 1996). Therefore, the practical relevance of these etiological research results lies in interventions that can halt or influence the development of antisocial behavior and psychopathy in children and juveniles who are at risk due to specific family, biological and social factors (Marshall & Cooke, 1999).

CONCLUSION So far research demonstrates an association between upbringing factors and the development of an antisocial pathway. Existing studies point to intra- and extrafamilial as well as biological factors that influence the development of antisocial behavior, factors such as peer groups, environmental factors, the parental disposition or trauma exposure. Especially the influence of early traumatization, including its biological impact on the child, is emphasized as an important risk factor for developing an antisocial personality disorder or psychopathy. Furthermore, early aggressive behavioral problems are considered to be the most stable personality traits that are associated with the development of an antisocial personality disorder and a psychopathic disorder. More follow-up studies are important to study the influence of different child-upbringing factors in girls and boys for developing a stable maladaptive antisocial or psychopathic pathway. Although many early influential factors are identified that predict antisocial behavior in adolescence, we still do not know enough about different patterns of pathways into adulthood to create meaningful intervention strategies. Therefore, we need more research that attempts to examine familial, social and biological dimensions with the aim of developing a meaningful theory on the etiology of antisocial disorders that integrates these fields.

FAMILY UPBRINGING

299

REFERENCES Abram, K.M., Teplin, L.A., Charles, D.R. et al. (2004). Post-traumatic stress disorder and trauma in youth in juvenile detention. Archives of General Psychiatry, 61, 403–10. Arnsten, A.F. (1997). Catecholamine regulation in the prefrontal cortex. Journal of Psychopharmacology, 11, 151–62. Arnsten, A.F. (2000). Genetics of childhood disorders: XVIII. ADHD, Part.2: norepinephrine has a critical modulatory influence on prefrontal cortical function. Journal of the American Academy of Child and Adolescent Psychiatry, 39, 1201–3. Baker, C. & Alfonso, C. (2003). PTSD and Criminal Behavior: A National Center for PTSD Fact Sheet. United States Department of Veterans Affairs. Bender, D. & L¨osel, F. (1997). Protective and risk effects of peer relations and social support on antisocial behavior in adolescents from multi-problem milieus. Journal of Adolescence, 20, 661– 78. Bergen, H.A., Martin, G., Richardson, A.S. et al. (2004). Sexual abuse, antisocial behavior and substance use: gender differences in young community adolescents. Australian and New Zealand Journal of Psychiatry, 38, 34–41. Bernstein, D.P., Stein, J.A. & Handelsman, L. (1998). Predicting personality pathology among adult patients with substance use disorders: effects of childhood maltreatment. Addictive Behaviors, 23, 855–68. Block, J. (1993). Studying personality the long way. In D. Furder, R. Parke, C. Tomlinson-Keasy & K. Widamen (eds.), Studying Lives Through Time: Personality and Development (pp. 9–41). Washington DC: American Psychological Association. Bor, W., McGee, T.R. & Fagan, A.A. (2004). Early risk factors for adolescent antisocial behavior: an Australian longitudinal study. Australian and New Zealand Journal of Psychiatry, 38(5), 365–72. Campbell, M.A., Porter, S. & Santor, D.S. (2004). Psychopathic traits in adolescent offenders: an evaluation of criminal history, clinical, and psychosocial correlates. Behavioral Science and the Law, 22(1), 23–47. Cauffman, E., Feldman, S.S., Waterman, J. & Steiner, H. (1998). Post-traumatic stress disorder among female juvenile offenders. Journal of the American Academy of Child and Adolescent Psychiatry, 37(11), 1209–16. Castellanos, F.X. & Tannock, R. (2002). Neuroscience of attention-deficit/hyperactivity disorder: the search for endophenotypes. Nature Reviews Neuroscience, 3(8), 617–28. Coxe, R. & Holmes, W. (2001). A study of the cycle of abuse among child molesters. Journal of Child Sexual Abuse, 10(4), 111–8. De Bellis, M.D., Chrousos, G.P., Dorn, L.D. et al. (1994). Hypothalamic–pituitary–adrenal axis dysregulation in sexually abused girls. Journal of Clinical Endocrinology and Metabolism, 78, 249–55. Dekovic, M., Janssens, J.M. & Van As, N.M. (2003). Family predictors of antisocial behavior in adolescence. Family Process, 42(2), 223–35. Dekovic, M., Wissink, I.B. & Marie Mejier, A. (2004). The role of family and peer relations in adolescent antisocial behavior: comparison of four ethnic groups. Journal of Adolescence, 27(5), 497–514. Dishion, T.J., Nelson, S.E. & Bullock, B.M. (2004). Premature adolescent autonomy: parent disengagement and deviant peer process in the amplification of problem behavior. Journal of Adolescence, 27(5), 515–30. Dishion, T.J., Nelson, S.E., Winter, C.E. & Bullock, B.M. (2004). Adolescent friendship as a dynamic system: entropy and deviance in the etiology and course of male antisocial behavior. Journal of Abnormal Child Psychology, 32(6), 651–63. Dixon, A., Howie, P. & Starling, J. (2004). Psychopathology in female juvenile offenders. Journal of Child Psychology and Psychiatry, 45(6), 1150–8. Dodge, K.A., Bates, J.E., Pettit, G.S. & Valente, E. (1995). Social information-processing patterns partially mediate the effect of early physical abuse on later conduct problems. Journal of Abnormal Psychology, 104, 632–43.

300

VOLUME I: DIAGNOSIS AND TREATMENT

Dolan, M. & Park, I. (2002). The neuropsychology of antisocial personality disorders. Psychological Medicine, 32(3), 417–27. Edens, J.F., Skeem, J.L. & Cruise, K.R. (2001). Assessment of juvenile psychopathy and its association with violence: a critical review. Behavioral Sciences and the Law, 19(1), 53–80. Egle, U.T., Hardt, J., Nickel, R. et al. (2002). Long-term effects of adverse childhood experiences – actual evidence and needs for research. Zeitschrift f¨ur Psychosomatische Medizin und Psychotherapie, 48, 411–34. Erwin, B.A., Newman, E., McMackin, R. et al. (2000). PTSD, malevolent environment, and criminality among criminally involved male adolescents. Criminal Justice and Behavior, 27, 196– 215. Farrington, D.P. (1995). The development of offending and antisocial behavior from childhood: key findings from the Cambridge Study in Delinquent Development. Journal of Child Psychology and Psychiatry, 36(6), 929–64 Forth, A.E. & Burke, H.C. (1998). Psychopathy in adolescence: assessment, violence and developmental precursors. In D.J. Cooke, A.E. Forth & R.D. Hare (eds.), Psychopathy: Theory, Research and Implications for Society (pp. 205–29). Boston: Kluwer Academic. Forth, A., Kosson, D. & Hare, R. (2003). The Hare Psychopathy Checklist: Youth Version. New York: Multi-Health Systems. Hare, R.D., Clark, D., Grann, M. & Thornton, D. (2000) Psychopathy and the predictive validity of the PCL-R: an international perspective. Behavioral Sciences and the Law, 18, 623–45. Jaffee, S.R., Caspi, A., Moffitt, T.E. & Taylor, A. (2004). Physical maltreatment victim to antisocial child: evidence of an environmentally mediated process. Journal of Abnormal Psychology, 113(1), 44–55. James, B. (1989). Treating Traumatized Children. New Insights and Creative Interventions. Lexington, MA: Lexington Books. Kim-Cohen, J., Moffitt, T.E., Taylor, A. et al. (2005). Maternal depression and children’s antisocial behavior: nature and nurture effects. Archives of General Psychiatry, 62(2), 173–81. Kim-Cohen, J., Caspi, A., Taylor, A. et al. (2006). MAOA, maltreatment, and gene–environment interaction predicting children’s mental health: new evidence and a meta-analysis. Molecular Psychiatry, 11, 903–13. Krischer, M. & Sevecke, K. (in preparation). The influence of early traumatization on psychopathy dimensions in female and male juvenile offenders. Krischer, M., Sevecke, K., Doepfner, M. & Lehmkuhl, G. (2006). Personality disorder traits in childhood and adolescence: concepts, methodological approaches and empirical results. Zeitschrift f¨ur Kinder- und Jugendpsychiatrie und –psychotherapie, 34(2), 87–100. Lahey, B.B., Loeber, R., Burke, J. & Rathouz, P.J. (2002). Adolescent outcomes of childhood conduct disorder among clinic-referred boys: predictors of improvement. Journal of Abnormal Child Psychology, 30(4), 333–48. Lambert, S.F., Ialongo, N.S., Boyd, R.C. & Cooley, M.R. (2005). Risk factors for community violence exposure in adolescence. American Journal of Community Psychology, 36(1–2), 29–48. Lang, S., Klinteberg, B. & Alm, P.O. (2002). Adult psychopathy and violent behavior in males with early neglect and abuse. Acta Psychiatrica Scandinavia, 412, 93–100. Laucht, M., Esser, G. & Schmidt, M.H. (2001). Differential development of infants at risk for psychopathology: the moderating role of early maternal responsivity. Developmental Medicine and Child Neurology, 43, 292–300. Lehmkuhl, G. (2006). The development of personality traits and personality disorders during childhood and adolescence. In A. Remmel, O.F. Kernberg, W. Vollmoeller & B. Strauss (eds.), Handbuch Koerper und Persoenlichkeit (pp. 91–101). Stuttgart: Schattauer. Loeber, R. (1990). Development and risk factors of juvenile antisocial behavior and delinquency. Clinical Psychology Review, 10, 1–41. Loeber, R. & Farrington, D.P. (1998). Serious and Violent Juvenile Offenders: Risk Factors and Successful Interventions. Thousand Oaks, CA: Sage. Loeber, R. & Stouthamer-Loeber, M. (1998). Development of juvenile aggression and violence. Some common misconceptions and controversies. American Psychologist, 53(2), 242–59. Loeber, R., Wung, P., Keenan, K. et al. (1993). Development pathways in disruptive child behavior. Journal of Development and Psychopathology, 5, 103–33.

FAMILY UPBRINGING

301

Marmorstein, N.R. & Iacono, W.G. (2004). Major depression and conduct disorder in youth: associations with parental psychopathology and parent–child conflict. Journal of Child Psychology and Psychiatry, 45(2), 377–86. Marmorstein, N.R. & Iacono, W.G. (2005). Longitudinal follow-up of adolescents with late-onset antisocial behavior: a pathological yet overlooked group. Journal of the American Academy of Child and Adolescent Psychiatry, 44(12), 1284–91. Marmorstein, N.R., Malone, S.M. & Iacono, W.G. (2004). Psychiatric disorders among offspring of depressed mothers: associations with paternal psychopathology. American Journal of Psychiatry, 161(9), 1588–94. Marshall, L.A. & Cooke, D.J. (1999). The childhood experiences of psychopaths: a retrospective study of familial and societal factors. Journal of Personality Disorders, 13(3), 211–25. Moeller, A.A. & Hell, D. (2003). Affective disorder and psychopathy in a sample of younger male delinquents. Acta Psychiatrica Scandinavia, 107(3), 203–7. Moffitt, T.E. (1993). Adolescence-limited and life-course persistent antisocial behaviour: a developmental taxonomy. Psychology Review, 100, 674–701. Moss, H.B., Lynch, K.G., Hardie, T.L. & Baron, D.A. (2002). Family functioning and peer affiliation in children of fathers with antisocial personality disorder and substance dependence: associations with problem behaviors. American Journal of Psychiatry, 159(4), 607–14. Murray, J. & Farrington, D.P. (2005). Parental imprisonment: effects on boys’ antisocial behavior and delinquency through the life-course. Journal of Child Psychology and Psychiatry, 46(12), 1269–78. Nigg, J.T. & Hinshaw, S.P. (1998). Parent personality traits and psychopathology associated with antisocial behaviors in childhood attention-deficit hyperactivity disorder. Journal of Child Psychology and Psychiatry, 39(2), 145–59. Novaco, R.W. & Chemtob, C.M. (1998). Anger and trauma. Conceptualization, assessment, and treatment. In V.M. Follette, J.I. Ruzek & F.R. Abueg (eds.), Cognitive-Behavioral Therapies for Trauma (pp. 162–90). New York: Guilford. Odgers, C.L., Reppucci, N.D. & Moretti, M.M. (2005). Nipping psychopathy in the bud: an examination of the convergent, predictive, and theoretical utility of the PCL: YV among adolescent girls. Behavioral Sciences and the Law, 23, 1–21. Patterson, G.R., Capaldi, D. & Bank, L. (1991). An early starter model for predicting delinquency. In D.J. Pepler & K.H. Rubin (eds.), The Development and Treatment of Childhood Aggression (pp. 139–68). Hillsdale, NY: Erlbaum. Pears, K.C. & Capaldi, D.M. (2001). Intergenerational transmission of abuse: a two-generational prospective study of an at-risk sample. Child Abuse and Neglect, 25(11), 1439–61. Pevalin, D.J., Wade, T.J. & Brannigan, A. (2003). Precursors, consequences and implications for stability and change in pre-adolescent antisocial behaviors. Prevention Science, 4(2), 123–36. Pollock, P.H. (1999). When the killer suffers. Post-traumatic stress reactions following homicide. Legal and Criminological Psychology, 4, 185–202. Raine, A. (1997). Antisocial behavior and psychophysiology: a biosocial perspective and a prefrontal dysfunction hypothesis. In D.M. Stoff, J. Breiling & J.D. Maser (eds.), Handbook of Antisocial Behavior (pp. 289–304). New York: John Wiley & Sons, Ltd. Raine, A., Brennan, P. & Mednick, S.A. (1997). Interaction between birth complications and early maternal rejection in predisponding individuals to adult violence: specificity to serious, early-onset violence. American Journal of Psychiatry, 154, 1265–71. Robins, L.N. (1991). Conduct disorder. Journal of Child Psychology and Psychiatry, 32, 193–212. Robins, L.N. (1996). Deviant Children Grown Up. Baltimore: Williams & Wilkins. Schore, A.N. (1997). Early organization of the nonlinear right brain and development of a predisposition to psychiatric disorders. Developmental Psychopathology, 9, 595–631. Shortt, J.W., Capaldi, D.M., Dishion, T.J. et al. (2003). The role of adolescent friends, romantic partners, and siblings in the emergence of the adult antisocial lifestyle. Family Psychology, 17(4), 521–33. Soberman, G.B., Greenwald, R. & Rule, D.L. (2002). A controlled study of eye movement desensitization and reprocessing (EMDR) for boys with conduct problems. In R. Greenwald (ed.), Trauma and Juvenile Delinquency. Theory, Research, and Interventions (pp. 217–36). Binghampton, NY: The Haworth Maltreatment & Trauma Press.

302

VOLUME I: DIAGNOSIS AND TREATMENT

Steiner, H., Garcia, I.G. & Matthews, Z. (1997). Post-traumatic stress disorder in incarcerated juvenile delinquents. Journal of the American Academy of Child and Adolescent Psychiatry, 36, 357–65. Timmons-Mitchell, J., Brown, C., Schulz, S.C. et al. (1997). Comparing the mental health needs of female and male incarcerated juvenile delinquents. Behavioral Sciences and the Law, 15, 195–202. van Bokhoven, I., Matthys, W., van Goozen, S.H. & van Engeland, H. (2005). Prediction of adolescent outcome in children with disruptive behavior disorders – a study of neurobiological, psychological and family factors. European Child and Adolescent Psychiatry, 14(3), 153–63. van der Kolk, B.A. & Fisler, R.E. (1994). Childhood abuse and neglect and loss of self-regulation. Bulletin of the Menninger Clinic, 58, 145–68. Wetzels, P., Enzman, D., Mecklenburg, E. & Pfeiffer, C. (2001). Jugend und Gewalt. Baden-Baden: Nomos. Werner, E.E. (1997). Vulnerable but invincible: high-risk children from birth to adulthood. Acta Paediatrica Supplement, 422, 103–5. Widom, C.S. (1992). The Cycle of Violence (Research in Brief, October). Washington, DC: National Institute of Justice. Widom, C.S. (2001). An Update on the ‘Cycle of Violence’ (Research in Brief, February). Washington, DC: National Institute of Justice Zlotnick, C. (1999). Antisocial personality disorder, affect dysregulation and childhood abuse among incarcerated women. Journal of Personality Disorders, 13(1), 90–5. Zuckerman, M. (1979). Sensation Seeking. Beyond the Optimal Level of Arousal. Hillsdale, NJ: Erlbaum.

CHAPTER 18

Discipline by Parents and Child Psychopathology Emily M. Douglas Bridgewater State College, USA

and Murray A. Straus University of New Hampshire, USA

There is wide consensus that parental discipline can have important affects on the psychological well-being of children, but there is little consensus on what constitutes discipline. For many parents, ‘discipline’ is a euphemism for spanking and other legal and culturally approved forms of corporal punishment. At the other extreme, for many professionals, ‘discipline’ is anything done to raise a well-adjusted child. The first of these conceptualizations of discipline is too narrow because spanking is only one of many modes of correcting misbehavior. The second conceptualization is too broad. It covers almost everything done as a parent. This chapter addresses how the topic of discipline is handled in psychiatric and other professional sources and presents a definition that avoids the two extremes. The chapter emphasizes research on a specific form of discipline, corporal punishment, because there is sufficient research to support an evidence-based analysis and because it is an aspect of discipline that has been the focus of controversy and legislation in many nations.

DEFINITION OF DISCIPLINE We examined 10 child psychiatry textbooks published between 1996 and 2006, and found that none defined it. Parallel to the absence of a definition is the disparate content discussed under ‘discipline’. It ranges from anything parents do to bring up a well-behaved child, such as providing love and support and moral guidance, to specific acts in response to misbehavior such as explaining, spanking or scolding. Although none of the 10 child psychiatry textbooks defined discipline, seven included a discussion of discipline. The most frequently occurring theme was the importance of avoiding harsh punishment, including spanking. We also

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

304

VOLUME I: DIAGNOSIS AND TREATMENT

examined 10 ‘child development’ and child psychology textbooks and found that three included a definition of discipline. All of the three, however, equate discipline with whatever it takes to bring up a child ‘properly’. For example, ‘The word discipline means instruction or training. In the field of child development, discipline refers to methods of modeling character and of teaching self-control and acceptable behavior’ (Papalia, Wendkos Olds & Duskin Feldman, 2006). Defining discipline as anything a parent does that affects a child’s moral and psychological development is too encompassing to be useful. Therefore, for purposes of this chapter, discipline is defined as behavior by parents in response to and intended to correct misbehavior by the child. Examples of such corrective behavior by parents include spanking, deprivation of privileges or material objects, diversion to socially acceptable tasks, explaining and instructing, ignoring misbehavior in order to not reinforce it, psychological aggression such as yelling and screaming at the child and rewarding the child for ceasing misbehavior. One of the strengths of using this definition is that it refers to specific parent behaviors that can be objectively measured (Straus, 2006). The focus on discipline as behaviors intended to correct a child’s misbehavior does not deny that almost everything parents do can affect the psychological development and mental health of a child. What this definition does is to identify one type of parent behavior as discipline so that readers can know what is being discussed.

COVERAGE OF DISCIPLINE IN CHILD PSYCHIATRY TEXTBOOKS We used this definition as the basis for examining the discussion of discipline in our sample of 10 child psychiatry textbooks. Of the seven that discussed discipline, all focused on the authoritarian, permissive and authoritative parenting styles identified by Diana Baumrind (1991) and the effect of these styles on child mental health. Discipline in the sense of actions taken to correct misbehavior is a key component of these parenting styles, but is only one of the components of parenting styles. Other components include parental warmth, acceptance and sensitivity to the child’s needs, and the degree to which parents grant autonomy to the child. The Baumrind parenting styles thus encompass more than discipline as defined for this chapter. Consequently, links between these parenting styles and mental health problems, although extremely important, do not provide evidence on the effects of the discipline component per se. When diagnosing and treating child mental health problems, it is important to be able to identify both the overall parenting style and also specific components such as discipline.

CORPORAL PUNISHMENT Corporal punishment such as spanking and slapping a child is the component of parenting that has been the most consistently controversial aspect of discipline. Corporal punishment (CP from here on) is ‘the use of physical force with the intention of causing the child to experience pain, but not injury, for purposes of correction or control of the child’s behavior’ (Straus, 2001). In practice, the difference between corporal punishment and physical abuse

DISCIPLINE BY PARENTS

305

hinges on whether the child is injured seriously enough for the case to be classified as ‘abuse’ by child protective services, regardless of the intent of the parent. This is shown by research showing that about two-thirds of cases of physical abuse begin as corporal punishment, but due to circumstances such as a defiant child or the child hitting the parent, escalate out of control and the child is injured (Straus, 2001). This chapter focuses on CP rather than physical abuse for several reasons. First, CP is used by almost all parents, although the frequency and severity varies greatly. Study after study has shown that over 90 % of parents in the United States and the United Kingdom use CP with children ages 2–5 (Newson & Newson, 1968; Straus & Stewart, 1999) and several studies show that at least a third of parents in the US and the UK slap or spank infants (Newson & Newson, 1963; Straus & Stewart, 1999). Therefore, it is important for child psychiatrists, and mental health professionals, in general, to have more information about something this widespread, and potentially harmful, in the lives of children. Second, in contrast to other discipline behaviors, there is a large body of high-quality and well-controlled research showing adverse mental health effects of CP, including prospective studies. This enables evaluation of this mode of discipline to be evidence-based. Third, a focus on CP is necessitated by the public health principle that removing a risk factor with a small effect size, but which is broadly prevalent (such as CP), can result in a much larger reduction in illness rates than removing a risk factor such as physical abuse, which has more damaging effects on individuals, but occurs relatively rarely (Rose, 1985). Fourth, is the cultural myth that CP is ‘sometimes necessary’. This is based on the belief that CP is effective when other methods have failed. We label this as a myth because research shows that, although CP is effective in stopping misbehavior in the immediate situation, these studies also show that it is not more effective than other modes of discipline, even in the immediate situation. Well-designed and executed research, including experimental studies that randomly assigned some parents to a spanking condition find that, even when the criterion is immediate compliance, nonphysical strategies work just as well as corporal punishment (Larzelere et al., 1996, 1998; Roberts, 1988; Roberts & Powers, 1990). Moreover, in the longer run, CP is not only less effective; it is counter-productive, as will be explained in the section on longitudinal studies. The belief that spanking is sometimes necessary persists because it is deeply ingrained in the culture of most societies and because the results of research which shows that other methods of discipline work just as well as CP are not reported in child development and child psychiatry textbooks. Child psychiatrists and other professionals who work with parents need to know the results of this extensive body of research. Finally, CP was discussed in seven of the 10 child psychiatry textbooks we surveyed, indicating its importance of CP for child psychiatry. Despite this, none of the 10 child psychiatry textbooks covered the extensive body of high-quality research on CP. The same situation applies to child psychology textbooks. This chapter is intended to help fill that gap.

CORPORAL PUNISHMENT AND PSYCHOPATHOLOGY It is well established that ‘physical abuse’ of a child results in psychological, as well as physical injury. Attitudes toward less severe parental violence in the form of CP, however, vary considerably. During the past three decades, there has been a large increase in research

306

VOLUME I: DIAGNOSIS AND TREATMENT

on CP. Using a large social science referencing database, we determined that between 1976 and 1986, only 60 articles with ‘CP’ or synonyms in the title were published in peerreviewed sources. In the next decade, 1986–96, this number increased to 137. In the most recent decade, 1996–2006, 240 articles with ‘CP’ in the title were published. There were likely many more publications that addressed CP, but were not indicated in the title. Despite the large body of evidence about the short- and long-term negative effects of CP, the research on the adverse mental health effects of CP, as previously noted, has not found its way into child psychiatry or child development textbooks. The studies reviewed in the following sections are restricted to those that assessed legal CP. To do this, studies that included parents who engaged in acts with a high risk of causing injury, such as kicking, punching or burning a child were excluded. The intent of the parents in these studies was not explicitly investigated. Rather, if the acts were legal forms of CP such as slapping or spanking a child, it is assumed that the intent was to cause pain for purposes of correction and control, and not to injure. Obviously, there are many cases of mixed motives because parents typically spank when they are angry and frustrated, and they may be motivated as and derive satisfaction from causing the child to experience pain, as well as being motivated to correct and control.

Meta-analysis The most comprehensive overview of the effects of CP by parents is a meta-analysis of 88 studies by Gershoff (2002), where there were a number of important findings concerning CP and psychopathology. Twelve of the studies examined the relation of CP to mental health problems of children, such as anxiety and depression, and eight examined the relation of childhood CP to adult mental health problems. Without exception, these 20 studies found that CP was associated with an increased probability of mental health problems. Thirteen studies investigated delinquent behavior. It is widely believed that CP ‘teaches the child a lesson’ and therefore reduces delinquency. Instead, in 12 of the 13 studies CP was found to be associated with a higher probability of delinquent and antisocial behavior. The same results were found for four of the five studies which investigated the relation between CP as a child and adult criminal behavior. The following sections describe and illustrate some specific studies of the relation of CP to child mental health problems.

General Population Studies Coyl, Roggman and Newland (2002) examined the relation of spanking and infant attachment for 169 mothers of 14-month-old children. They found that the more spanking within the past week, the less securely attached children were to their mothers. This has important mental health implications because of the research showing that a secure attachment is related to less problem behavior later in childhood (Elicker, Englund & Sroufe, 1992). Turner and Finkelhor (1996) studied 2000 youth who participated in the National Youth Victimization Prevention Study. They found that approximately 30 % had experienced CP within the past year, of which only 17 % experienced very low levels of CP, defined as once or twice within the past year. After controlling for parental income, physical abuse (such as a beating), and the sex and age of the child, even modest levels of CP were associated

DISCIPLINE BY PARENTS

307

with greater psychological distress including depressive symptoms. Moreover, children who experienced frequent CP from parents who they described as supportive were more likely to experience psychological distress than children who experienced lower levels of CP in combination with high levels of parental support. These findings dispute the notion that CP conducted in the context of a loving, supportive home environment is not harmful. A study of 134 adolescents, aged 10–15, from urban and suburban offices of pediatricians (Ohene et al., 2006) found that the more CP these adolescents experienced, the more likely they were to approve of peer violence. While approval of peer violence is not psychopathology, it is part of a constellation of cognitive and behavioral characteristics, such as negative attributions about the behavior of peers and physical aggression that can set in motion a developmental trajectory that is associated psychopathology. Using data from the 1985 National Family Violence Survey, Straus and Yodanis (1996) found that women who experienced CP as an adolescent by either their mothers or fathers, had an increased probability of depression during adulthood. Men who experienced CP during adolescence by their mothers, but not their fathers, had a smaller, but still statistically significant, increase in the probability of depression during adulthood. These analyses controlled for socioeconomic status, race and age. Using this same dataset and demographic controls, Straus and Kantor (1994) found that CP was associated with suicidal thoughts, alcohol abuse and perpetration of child abuse. Another retrospective study of 277 adults found that those who had experienced CP in childhood were more likely to report feelings of depression, attempted suicide and to report feelings that are consistent with being detached from or unconcerned with their life events (Good, 1999). A study of a representative sample of 933 mothers of children age 2–14 in two American cities (Straus & Mouradian, 1998) found that the more CP experienced by the child, the greater the tendency for the child to engage in antisocial behavior and to act impulsively. These relationships held after controlling for family socioeconomic status, the age and sex of the child, nurturance by the mother and the level of noncorporal intervention by the mother. When CP was carried out impulsively, the link between CP and child impulsiveness and antisocial behavior was stronger. This study indicates that the harmful effects of CP are increased when the violence is impulsive and expressive of anger, even though the intent was also to train and educate the child.

Clinical Populations Studies have found that highly aggressive and antisocial children have typically experienced exceptionally high rates of corporal punishment (Capaldi et al., 2003; Patterson, 1995; Patterson, Reid, & Dishion, 1992; Webster-Stratton, 1990; Welsh, 1976). For example, Mahoney and colleagues assessed the prevalence of CP among 390 clinic-referred youth, ages 2–17, whose problems included adjustment disorder, ADHD/disruptive behavior disorder and mood/anxiety disorder (Mahoney et al., 2000). When compared with a 1995 national sample that used the same instrument to measure CP, the clinic sample was much more likely to have experienced CP than the national sample. Multivariate analysis found that the more CP experienced, the higher the child’s externalizing behavioral problems. It is possible that clinic-referred youth are more difficult to parent and may elicit more harsh parenting styles. In fact there are a number of studies have found that children with a more difficult temperament are at a higher risk for being maltreated by their parents or

308

VOLUME I: DIAGNOSIS AND TREATMENT

the recipients of dysfunctional parenting (Blackson, Tarter & Maezzich, 1996; Engfer & Schneewind, 1982; Sherrod et al., 1984; Tourigny, 2006). Some research has demonstrated that training parents to avoid corporal punishment may be one of the key components to more successfully parenting a ‘difficult child’ (Patterson, 1995; Patterson et al., 1992; Webster-Stratton, 1990).

Cultural Context Effects Somewhat paradoxically, it is possible that the adverse effects of CP on mental health found in so many American studies result from the fact that the former universal approval of CP is on the decline. Consequently, children who are currently being spanked may perceive this as rejection rather than legitimate discipline. A 1968 survey of a large and representative national sample found that 94 % of American adults agreed that ‘a good hard spanking is sometimes necessary’. By 1999 the percentage had dropped by almost half, but was still a majority – 52 % (Straus & Yodanis, 1996). There have probably been further decreases since then. A much larger proportion of African Americans believe in the necessity of CP (Straus & Mathur, 1996). It has been argued that in such a cultural context, CP is not harmful because children will not mistake it for rejection. Some studies have tested the mitigating effect of a cultural context in which CP is the cultural norm, and have found results that are consistent with the theory, but most of the studies have found harmful effects, including studies of African American children. For example, DuRant and colleagues (1995) examined the role of CP in the overall well-being of 225 low-income, black youth living in and around public housing, they found that CP was a stronger predictor of depression than any of the other hypothesized risk factors, including family conflict, education level of the head of household, the child’s perception of the probability of being alive at age 25, witnessing community violence and unemployment of parent. Another study that examined the role of CP in the adjustment of African American youth (McCabe, Clark & Barnett, 1999) examined a smaller but more economically diverse sample than the previously mentioned study. They studied 64 sixth-grade children and found that parents who used more CP were more likely to describe their children as having behavioral, acting-out problems. They found no relationship between CP and shy or anxious behavior, or in having a social skills deficit. Adverse effects on children’s psychological well-being have also been demonstrated outside of the United States and in cross-national comparative studies. Lau and colleagues (1999) examined a sample of 3355 Chinese adolescents. Students who had experienced CP were more likely to suffer from indicators of anxiety and stress, and were more likely to report problems concerning feelings of happiness, feelings of worthiness and anxiety regarding puberty. Students who experienced CP were also more likely to engage in risky behavior and to report suffering from a host of physical conditions. These students were more likely to consume alcohol, to smoke and to have engaged in physical fights with others. Moreover, these students were more at risk for experiencing a host of health problems including asthma, anxiety, dizziness, to have been sick with a common cold or the flu, to have fallen down, to have burned oneself, or to have been hospitalized within the past three months. All of the analyses controlled for the gender and age of the student.

DISCIPLINE BY PARENTS

309

Rohner, Kean and Cournoyer (1991) studied 349 children age 9 to 16 in St. Kitts, West Indies. They found that, after controlling for many other variables, CP was associated with an increase in feelings of rejection by the child. This study is particularly important because the right of parents, in fact the obligation, to use CP is strongly embedded in the culture of that society, and many of the children shared this cultural belief. They found that the tendency for CP to be associated with feelings of rejection applied regardless of whether the children studied accepted the cultural belief that CP is appropriate. A study of 336 children in China, India, Italy, the Philippines and Kenya examined the relation of CP to anxiety and aggressiveness of the children (Lansford et al., 2005) and found that countries with the lowest use of physical discipline demonstrated the strongest relationship between mothers’ use of CP and children’s behavior problems. In all countries, however, higher use of physical discipline was associated with more child aggression and more anxiety. Finally, a study that used macro-level data from the International Dating Violence Study, and that was based on more than 9500 university students from 19 nations, examined the link between CP experienced prior to age 12 and later-life partner violence. The findings indicated that the higher the rate of CP prior to age 12, the higher the rate of hitting a dating partner in the past year. This finding applied to both males and females. The rate of injuries inflicted by females on their partners was lower than the rate of injuries inflicted by males, the relationship between CP and injury was stronger for females than for males (Douglas & Straus, 2006).

Longitudinal Studies Although many of the studies reviewed up to this point controlled for possible confounds, none were prospective studies in the sense of being able to control for the Time 1 level of aggression that might have led parents to use CP. Consequently, a major problem is that the child’s subsequent behavior problem, rather than being an effect of CP, may reflect a pre-existing behavior problem which led the parents to use CP. The publication of six longitudinal studies since 1997 that controlled for the child’s problem behavior at Time 1, therefore, constitutes a landmark in scientific knowledge of the unintended effects of CP. All six were based on large and nationally representative samples of children, and none were adult retrospective studies. All six show that CP has an adverse effect on child mental health.

CP And Subsequent Antisocial Behavior This research studied over 3000 children in the National Longitudinal Survey of Youth (Straus, Sugarman & Giles-Sims, 1997). The children were in three age groups: 3–5, 6–9 and 10–14. The mothers of all three groups of children were interviewed at the start of the study in 1988 to find out how often the focal child had been spanked in the seven days prior to the interview. The study controlled several variables that could affect antisocial behavior by the child: the sex of child, cognitive stimulation provided by the parents, emotional support by the mother, ethnic group of the mother and socioeconomic status of the family.

310

VOLUME I: DIAGNOSIS AND TREATMENT

Figure 18.1 Change in antisocial behavior from 1988 to 1990 by spanking in 1988 (children age 6–9)

Figure 18.1 shows that the more CP used during the first year of the study, the greater the tendency for antisocial behavior to have increased two years later. It also shows that this effect applied to both Euro American children and children of other ethnic groups.

A Second Study of CP and Antisocial Behavior Gunnoe and Mariner (1997) analyzed data from another large and representative sample of American children. They studied 1112 children in two age groups: 4–7 and 8–11. The parents were first interviewed in 1987–8, and then five years later. The measure of CP was the same as in the previously described study. They found that the more CP in 1987–8, the greater the amount of fighting at school five years later. However, for toddlers and for African American children, they found the opposite, that is, CP is associated with less fighting five years later. The opposite finding for these two subgroups might have occurred because CP of toddlers and African American children is so nearly universal in the USA that no CP might indicate a lack of guidance and nonphysical discipline. Gunnoe and Mariner also examined the relation of CP to score on an antisocial behavior scale. They found that the more CP experienced in year 1, the higher the level of antisocial behavior five years later. Moreover, they found that the harmful effect of CP applies to all children regardless of age, races and gender. Thus, the antisocial behavior part of Gunnoe and Mariner’s study, like the previously described study found that, although CP may work in the short run, in the long run it can boomerang and increase the probability of behavior problems.

DISCIPLINE BY PARENTS

311

CP and Child-to-Parent Violence Brezina (1999) analyzed data on a nationally representative sample of 1519 adolescent boys who participated in the Youth in Transition Study. This is a three-wave panel study that was begun in 1966. CP was measured by asking the boys ‘How often do your parents actually slap you?’ The response categories ranged from 1 (never) to 5 (always). Twentyeight percent of the boys reported being slapped by their parents during the year of the first wave of the study when their average age was 15, and 19 % were slapped during the wave 2 year (a year and half later). Brezina found that CP at Time 1 was associated with an increased probability of a child assaulting the parent a year and a half later. As with the other three prospective studies, the data analysis controlled for socioeconomic status and race of the family, the age of the parents, the child’s attachment to the parent, child’s attitude toward aggression and child’s physical size.

CP and Dating Violence Simons, Lin and Gordon (1998) tested the theory that CP by parents increases the probability of later hitting a partner in a dating relationship. They studied 113 boys in a rural area of the state of Iowa, beginning when the boys were in the seventh grade or about age 13. The mothers and the fathers of these boys were asked how often they spanked or slapped the child when he did something wrong, and how often they used a belt or paddle for CP. More than half of the boys experienced CP during those years. Consequently, the findings about CP apply to the majority of boys in that community, not just to the children of a small group of violent parents. The study controlled for delinquency at Time 1 and the extent to which the parents showed warmth and affection, were consistent in their discipline, monitored and supervised the child, explained rules and expectations, and also controlled for witnessing violence between the parents. Simons and colleagues found that the more CP, the greater the probability of the boys subsequently assaulting a girlfriend.

CP and Cognitive Development A study by Straus and Paschall (2007) was prompted by research showing that talking to children (including pre-speech infants) is associated with an increase in neural connections in the brain and in cognitive performance (Blakeslee, 1995). Straus and Paschall assumed that when parents avoid corporal punishment, they are more likely to engage in verbal methods of behavior control such as explaining to the child. If that is correct, the increased verbal interaction with the child will enhance the child’s cognitive ability. This theory was tested on 806 children of mothers in the National Longitudinal Study of Youth who were age 2 to 4 in the first year of the study and for 704 children who were age 5 to 9 in the first year. Corporal punishment was measured by whether the mother was observed hitting the child during the interview and by a question on frequency of spanking in the past week. Cognitive ability was measured in year 1 and two years later by tests appropriate for the age of the child at the time of testing such as the Peabody Picture Vocabulary Test. The study took into account the mother’s age and education, whether the father was present

312

VOLUME I: DIAGNOSIS AND TREATMENT

in the household, number of children in the family, mother’s supportiveness and cognitive stimulation, ethnic group, and the child’s age, gender and birth weight. The 2-to-4-year-old children in the high CP group experienced a slower rate of cognitive development than did the children in the middle CP group. The children in the low CP group experienced slightly faster than average cognitive development. The most dramatic results were for the small minority of children (10 %) who were not hit in either of the two baseline weeks. They gained an average of 5.5 points relative to the average cognitive ability of children their age. Similar but less strong relationships were found for the 5-to-9-year-old children. Maximizing cognitive ability is extremely important for many reasons, not the least of which is that lower than average cognitive ability is a risk factor for many types of psychosocial and psychiatric problems, both in childhood and adulthood (David et al., 1997; Gjaerum & Bjornerem, 2003; Kjelsberg, 1999; Taylor et al., 1991; Woodward & Fergusson, 2000).

CP and Child Behavior Problems An analysis of over 11,000 children aged 4 to 11 in the Canadian Longitudinal Study of Children (Millar, 2006) measured change in child behavior problems subsequent to CP at Time 1. The study also examined the effect of and controlled for five other variables: parental socioeconomic status; maternal depression; yelling at the child; consistency of discipline; and positive interaction with the child. After controlling for all these variables, children who were spanked had increases in emotional disorder, physical aggression and property offenses. In fact, the increase in physical aggression associated with spanking was greater than the increase associated with any of the other five risk factors. The literature reviewed indicates that CP is a risk factor for many psychological problems, both externalizing and internalizing problems, that can manifest during childhood, adulthood, or both. The research consistently shows that multiple types of problems can develop, but there has been little research that has explored to what extent and under what conditions externalizing or internalizing problems are more or less likely to develop. Future research in this area is clearly needed to better understand the effects of CP.

LEGAL STATUS OF CORPORAL PUNISHMENT Corporal punishment in schools, once almost universally practiced, is now banned by most industrial societies and half the states in the United States. However, CP by parents is legal in every American state and in most other nations. Americans remain committed to the idea that CP by parents may ‘sometimes be necessary’. Despite the reluctance of the United States to embrace a position of no physical discipline by parents, many other countries have done so. The organization EPOCH-Worldwide (End Physical Punishment of Children Worldwide) (http://stophitting.org/laws/) and the Global Initiative to End All Corporal Punishment (www.endcorporalpunishment.org) indicate that 15 countries have outlawed the use of corporal punishment over the last three decades: Austria (1989), Finland (1983), Latvia (1998), Croatia (1999), Germany (2000), Norway (1987), Cyprus (1994), Israel (2000), Sweden (1979), Denmark (1997), Iceland (2003), Ukraine (2004), Romania (2004), Bulgaria (2000) and Hungary (2005). Moreover, case law in Belgium, Italy and

DISCIPLINE BY PARENTS

313

Portugal indicate that these countries may be moving toward a position of no tolerance of CP. Ending the use of CP is also supported by the United Nations Educational, Scientific, and Cultural Organization (Hart et al., 2005). In June 2006, the United Nations Committee on the Rights of the Child issued a statement declaring that it is ‘the obligation of all States parties to move quickly to prohibit and eliminate all corporal punishment and all other cruel or degrading forms of punishment of children’ (United Nations Committee on the Rights of the Child, 2006, pp. 2–3). The Committee also outlines necessary legislative and public education steps that should be taken in order to eliminate corporal punishment in all settings, including families and schools. The effect of these laws and their ability to change attitudes and parental behavior is not well known. Sweden was, in 1979, the first country to ban CP by parents. Studies have found large decreases in both the approval of and actual use of CP (Durrant, 1999). These decreases, however, could reflect a continuation of a trend that originated decades earlier rather than an effect of the legislation (Roberts, 2000). In Sweden, the ban on CP is part of the civil code, not the criminal code, and there is no criminal penalty for using CP. Even where the criminal code has been revised to remove the exemption of parents from prosecution for assault (as in Germany), the value may not be as a threat of prosecution, but as a means to educate parents and caregivers about the harmful effects of CP.

CONCLUSIONS In light of the overwhelming empirical evidence on the harmful effects of CP, textbooks and other professional sources appear to inadequately prepare mental health professionals to help parents avoid using CP. In 1988, the American Academy of Child and Adolescent Psychiatry and the American Psychiatric Association issued a strong statement against the use of CP in schools. It is argued that children who are subjected to CP by teachers may learn to settle interpersonal disputes through the infliction of physical force and pain on others (American Academy of Child and Adolescent Psychiatry, 1988; American Psychiatric Association, 1988). Neither, however, mentions the use of CP by parents or family caregivers. None of the 10 child psychiatry textbooks examined for this chapter advised telling parents to ‘never spank’ their children. An article by Banks in American Family Physician (2002) states that other methods of discipline are more effective and cites numerous studies that have linked negative outcomes to CP. Yet, he also states that ‘spanking is inappropriate in children younger than 18 months’ (p. 1450). This implies that it is appropriate for children over the age of 18 months. Similarly, Forehand and McKinney (1993) provide an historical overview of child discipline in the United States and the role that mental health professionals can potentially play in shaping public understanding of the harmful effects of corporal punishment. But they too fail to suggest that mental health professionals embrace the policy of advising parents and caregivers to never hit a child as a form of discipline, unlike the ‘never shake a child’ public education campaigns supported by professional medical associations (American Academy of Pediatrics, n.d.; Canadian Paediatric Society Psychosocial Paediatrics Committee, 1997). A start in that direction, however, was made by the American Academy of Pediatrics which published ‘Guidelines for Effective Discipline’ that advises parents to avoid spanking (American Academy of Pediatrics, 1998). It is important to recognize that not all research shows a link between CP and psychopathology. Moreover, even the six longitudinal studies reviewed in this chapter have

314

VOLUME I: DIAGNOSIS AND TREATMENT

their imperfections and they could be picked apart one by one by their ideological critics, as can most epidemiological studies. This is what the tobacco industry did for many years (Geyelin, 1996a, 1996b; Ong & Glantz, 2000). In 1964 the US Surgeon General’s Committee on Smoking and Health, however, did the opposite. Their review of the research acknowledged the limitations of the studies when taken one by one. But the committee concluded that despite the defects of the individual studies, the cumulative evidence indicated that smoking is a risk factor for lung cancer and other diseases and called for an end to smoking (US Surgeon General, 1964). As a result, today, no health professional would shrink from advising a patient to never, under any circumstances, smoke. The cumulative weight of the evidence indicates a need for psychiatrists to take the same approach in respect to corporal punishment, as we have taken for smoking and shaking a baby.

REFERENCES American Academy of Child and Adolescent Psychiatry (1988). Policy Statement: Corporal Punishment in Schools. Retrieved June 5, 2006, from http://www.aacap.org/publications/policy/ps14. htm#TOP. American Academy of Pediatrics (1998). Guidance for effective discipline (RE9740). Pediatrics, 101(4), 723–8. American Academy of Pediatrics. (n.d.). Shaken Baby Syndrome. Retrieved September 3, 2006, from http://www.aap.org/pubed/ZZZM8JMMH4C.htm?&sub cat=355. American Psychiatric Association (1988). Corporal Punishment in Schools: Position Statement. Retrieved June 5, 2006, from http://www.psych.org/edu/other res/lib archives/archives/198901.pdf. Banks, J.B. (2002). Childhood discipline: challenges for clinicians and parents. American Family Physician, 66(8), 1447–52. Baumrind, D. (1991). The influence of parenting style on adolescent competence and substance use. Journal of Early Adolescence, 11, 56–95. Blackson, T.C., Tarter, R.E. & Maezzich, A.C. (1996). Interaction between childhood temperament and parental discipline practices on behavioral adjustment in preadolescent sons of substance abuse and normal fathers. American Journal of Drug and Alcohol Abuse, 22(3), 335–48. Brezina, T. (1999). Teenage violence toward parents as an adaptation to family strain: evidence from a national survey of male adolescents. Youth and Society, 30(4), 416–44. Canadian Paediatric Society Psychosocial Paediatrics Committee (1997). Never Shake a Baby. Retrieved September 3, 2006, from http://www.caringforkids.cps.ca/babies/SBS.htm. Capaldi, D.M., Pears, K.C., Patterson, G.R. & Owen, L.D. (2003). Continuity of parenting practices across generations in an at-risk sample: a prospective comparison of direct and mediated associations. Journal of Abnormal Child Psychology, 31(2), 127–42. Coyl, D.D., Roggman, L.A. & Newland, L.A. (2002). Stress, maternal depression, and negative mother–infant interactions in relation to infant attachment. Infant Mental Health Journal, 23(1), 145–63. David, A.S., Malmberg, A., Brandt, L. et al. (1997). IQ and risk for schizophrenia: a population-based cohort study. Psychological Medicine, 27(6), 1131–3. Douglas, E.M. & Straus, M.A. (2006). Assault and injury of dating partners by university students in 19 nations and its relation to corporal punishment experiences as a child. European Journal of Criminology, 3, 259–92. DuRant, R.H., Getts, A., Cadenhead, C. & Emans, S.J. (1995). Exposure to violence and victimization and depression, hopelessness, and purpose in life among adolescents living in and around public housing. Journal of Developmental and Behavioral Pediatrics, 16(4), 233–7. Durrant, J.E. (1999). Evaluating the success of Sweden’s corporal punishment ban. Child Abuse and Neglect, 23(5), 435–48.

DISCIPLINE BY PARENTS

315

Elicker, J., Englund, M. & Sroufe, L.A. (1992). Predicting peer competence and peer relationships in childhood from early parent–child relationships. In P. Parke & G. Ladd (eds.), Family-Peer Relationships: Models of Linkage. Hillsdale, NJ: Erlbaum. Engfer, A. & Schneewind, K. (1982). Causes and consequences of harsh parental punishment: an empirical investigation in a representative sample of 570 German families. Child Abuse and Neglect, 6(2), 129–39. Forehand, R. & McKinney, B. (1993). Historical overview of child discipline in the United States: implications for mental health clinicians and researchers. Journal of Child and Family Studies, 2(3), 221–8. Gershoff, E.T. (2002). Corporal punishment by parents and associated child behaviors and experiences: a meta-analytic and theoretical review. Psychological Bulletin, 128(4), 539–79. Geyelin, M. (1996a, October 1). Papers dispute tobacco research claims. Wall Street Journal, p. B6. Geyelin, M. (1996b, May 6). RJR ordered to turn over documents on tobacco industry-funded research. Wall Street Journal, p. B5. Gjaerum, B. & Bjornerem, H. (2003). Psychosocial impairment is significant in young referred children with and without psychiatric diagnoses and cognitive delays: applicability and reliability of diagnoses in face of co-morbidity. European Child and Adolescent Psychiatry, 12(5), 239–48. Good, J.A. (1999). Shame, Images of God and the Cycle of Violence in Adults who Experienced Childhood Corporal Punishment. Lanham, MD: University Press of America. Gunnoe, M.L. & Mariner, C.L. (1997). Towards a developmental-contextual model of the effects of parental spanking on children’s aggression. Archives of Pediatric and Adolescent Medicine, 151, 768–75. Hart, S.N., Durrant, J., Newell, P. & Power, F.C. (eds.). (2005). Eliminating Corporal Punishment: The Way Forward to Constructive Child Discipline. Paris: UNESCO. Kjelsberg, E. (1999). A long-term follow-up study of adolescent psychiatric in-patients. Part III. Predictors of disability. Acta Psychiatrica Scandinavica, 99(4), 243–6. Lansford, J.E., Chang, L., Dodge K.A. et al. (2005). Physical discipline and children’s adjustment: cultural normativeness as a moderator. Child Development, 76(6), 1234–46. Larzelere, R.E., Sather, P.R., Schneider, W.N. et al. (1998). Punishment enhances reasoning’s effectiveness as a disciplinary response to toddlers. Journal of Marriage and the Family, 60(2), 388–403. Larzelere, R.E., Schneider, W.N., Larson, D.B. & Pike, P.L. (1996). The effects of discipline responses in delaying toddler misbehavior recurrences. Child and Family Therapy, 18, 35–7. Lau, J.T.F., Liu, J.L., Cheung, J.C. et al. (1999). Prevalence and correlates of physical abuse in Hong Kong Chinese adolescents: a population-based approach. Child Abuse and Neglect, 23(6), 549–57. Mahoney, A., Donnelly, W.O., Lewis, T. & Maynard, C. (2000). Mother and father self-reports of corporal punishment and severe physical aggression toward clinic-referred youth. Journal of Clinical Child Psychology, 29(2), 266–81. McCabe, K.M., Clark, R. & Barnett, D. (1999). Family protective factors among urban African American youth. Journal of Clinical Child Psychology, 28(2), 137–50. Millar, P. (2006). The Effect of Family Law on Canadian Children. Calgary, Canada: University of Calgary. Newson, J. & Newson, E. (1963). Patterns of Infant Care in an Urban Community. Baltimore, MD: Penguin. Newson, J. & Newson, E. (1968). Four Years Old in an Urban Community. London: George Allen and Unwin. Ohene, S.-A., Ireland, M., McNeely, C. & Borowsky, I. W. (2006). Parental expectations, physical punishment, and violence among adolescents who score positive on a psychosocial screening test in primary care. Pediatrics, 117(2), 441–7. Ong, E.K. & Glantz, S.A. (2000). Tobacco industry efforts subverting International Agency for Research on Cancer’s second-hand smoke study. Lancet, 355(9211), 1253–9. Papalia, D.E., Wendkos Olds, S. & Duskin Feldman, R. (2006). A Child’s World Infancy Through Adolescence, 10th edition. New York: McGraw-Hill. Patterson, G.R. (1995). Coercion – a basis for early age of onset for arrest. In J. McCord (ed.), Coercion and Punishment in Long-Term Perspective (pp. 81–124). New York: Cambridge University Press.

316

VOLUME I: DIAGNOSIS AND TREATMENT

Patterson, G.R., Reid, J.B. & Dishion, T.J. (1992). Antisocial Boys: A Social Interactional Approach (Vol. 4). Castalia Publishing Company. Roberts, J.V. (2000). Changing public attitudes toward corporal punishment: the effects of statutory reform in Sweden. Child Abuse and Neglect, 24(8), 1027–35. Roberts, M.W. (1988). Enforcing timeouts with room timeouts. Behavior Modifications, 4, 353–70. Roberts, M.W. & Powers, S.W. (1990). Adjusting chair timeout enforcement procedures for oppositional children. Behavior Therapy, 21, 257–71. Rohner, R.P., Kean, K.J. & Cournoyer, D.E. (1991). Effects of corporal punishment, perceived caretaker warmth, and cultural beliefs on the psychological adjustment of children in St. Kitts, West Indies. Journal of Marriage and Family, 53, 681–9. Rose, G. (1985). Sick individuals and sick populations. International Journal of Epidemiology, 14(1), 32–8. Sherrod, K.B., Altemeier, W.A., O’Connor, S. & Vietze, P.M. (1984). Early prediction of child maltreatment. Early Child Development and Care, 13(3–4), 335–50. Simons, R.L., Lin, K. & Gordon, L.R. (1998). Socialisation in the family of origin and male dating violence: A prospective study. Journal of Marriage and Family, 60, 467–78. Straus, M.A. (2001). Beating the Devil Out of Them: Corporal Punishment in American Families and its Effects on Children. New Brunswick, NJ: Transaction Publishers. Straus, M.A. (2006). Manual for the Dimensions of Discipline Inventory. Durham, NH: Family Research Laboratory, University of New Hampshire. Straus, M.A. & Kantor, G.K. (1994). Corporal punishment of adolescents by parents: a risk factor in the epidemiology of depression, suicide, alcohol abuse, child abuse, and wife beating. Adolescence, 29(115), 543–61. Straus, M.A. & Mathur, A.K. (1996). Social change and trends in approval of corporal punishment by parents from 1968 to 1994. In D. Frehsee, W. Horn & K.-D. Bussmann (eds.), Family Violence Against Children: A Challenge for Society (pp. 91–105). New York: Walter deGruyter. Also an updated version in M.A. Straus & R.A. Maderios (eds.), (in press). The decline in public support. The Primordial Violence: Corporal Punishment by Parents, Cognitive Development, and Crime. Walnut Creek, CA: AltaMira Press. Straus, M.A. & Mouradian, V.E. (1998). Impulsive corporal punishment by mothers and antisocial behavior and impulsiveness of children. Behavioral Sciences and the Law, 16(3), 353–74. Straus, M.A. & Paschall, M.J. (2007). Corporal punishment by mothers and children’s cognitive development: A longitudinal study of two age cohorts. In M.A. Straus & R.A. Maderios (eds.), The Primordial Violence: Corporal Punishment by Parents, Cognitive Development, and Crime. Walnut Creek, CA: AltaMira Press. Straus, M.A. & Stewart, J.H. (1999). Corporal punishment by American parents: national data on prevalence, chronicity, severity, and duration, in relation to child, and family characteristics. Clinical Child and Family Psychology Review, 2(2), 55–70. Also an updated version in M.A. Straus & R.A. Maderios (eds.), (in press). Prevalence, chronicity, and severity. The Primordial Violence: Corporal Punishment by Parents, Cognitive Development, and Crime. Walnut Creek, CA: AltaMira Press. Straus, M.A., Sugarman, D.B. & Giles-Sims, J. (1997). Spanking by parents and subsequent antisocial behavior of children. Archives of Pediatric and Adolescent Medicine, 151, 761–7. Also an updated version in M.A. Straus & R.A. Maderios (eds.), (in press). The boomerang effect. The Primordial Violence: Corporal Punishment by Parents, Cognitive Development, and Crime. Walnut Creek, CA: AltaMira Press. Straus, M.A. & Yodanis, C.L. (1996). Corporal punishment in adolescence and physical assaults on spouses in later life: What accounts for the link? Journal of Marriage and the Family, 58(4), 825–41. Taylor, C.G., Norman, D.K., Murphy, J.M. et al. (1991). Diagnosed intellectual and emotional impairment among parents who seriously mistreat their children: prevalence, type, and outcome in a court sample. Child Abuse and Neglect, 15(4), 389–401. Tourigny, J.A. (2006). High-risk Environments and Infant Health: Predicting Psychological and Physical Health Outcomes with Maternal, Child, and Parenting Variables. University of Saskatchewan, Canada.

DISCIPLINE BY PARENTS

317

Turner, H.A. & Finkelhor, D. (1996). Corporal punishment as a stressor among youth. Journal of Marriage and the Family, 58(1), 155–66. US Surgeon General (1964). Reducing the health consequences of smoking. Retrieved September 3, 2006, from http://www.cdc.gov/tobacco/sgr/sgr 1964/sgr64.htm. United Nations Committee on the Rights of the Child. (2006). The right of the child to protection from corporal punishment and other cruel or degrading forms of punishment; General comment no. 8. Retrieved June 28, 2006, from http://www.ohchr.org/english/bodies/crc/docs/co/CRC.C.GC.8.pdf. Webster-Stratton, C. (1990). Enhancing the effectiveness of self-administered videotape parent training for families with conduct-problem children. Journal of Abnormal Child Psychology, 18(5), 479–92. Welsh, R.S. (1976). Severe parental punishment and delinquency: a developmental theory. Journal of Clinical Child Psychiatry, spring, 17–21. Woodward, L.J. & Fergusson, D.M. (2000). Childhood and adolescent predictors of physical assault: a prospective longitudinal study. Criminology, 38(1), 233.

CHAPTER 19

Social Origins of Psychopathy David P. Farrington Institute of Criminology, Cambridge University, UK

Psychopathy, at least as operationally defined by the family of PCL measures, is not a unitary construct. It includes explanatory elements such as low empathy, impulsiveness, and a cold, callous and conning personality, as well as behavioral elements such as antisocial and criminal conduct. Cooke et al. (2004) suggested that psychopathy should be operationally defined only by the personality trait elements of an arrogant and deceitful interpersonal style (ADI), deficient affective experience (DAE) and an impulsive and irresponsible lifestyle (IIB), and that these personality factors caused criminal and antisocial behavior. In this chapter, I will review and present new findings on social predictors of these three facets of psychopathy, and of the fourth facet of antisocial behavior (ANT). Social predictors include parental, child-rearing, family, socioeconomic, peer, school and neighborhood factors. Traditionally, ADI and DAE have been combined into the affective-interpersonal component of psychopathy (Factor 1), and IIB and ANT have been combined into the antisocial lifestyle component (Factor 2); for a review of predictors of these two components, see Farrington (2006).

LONGITUDINAL SURVEYS The best method of establishing that a social factor predicts later psychopathy is to carry out a prospective longitudinal survey, and the emphasis in this chapter is on results obtained in such surveys (see Kalb, Farrington & Loeber, 2001; Loeber & Farrington 1997). They avoid retrospective bias (e.g., where the recollections of parents about their child-rearing methods are biased by the knowledge that their child has become a psychopath) and help in establishing causal order. Also, psychopaths emerge naturally from an initially nonpsychopathic population in community surveys, avoiding the problem of how to choose a control group of nonpsychopaths. If extreme groups (e.g., psychopaths versus well-behaved nonoffenders) are compared, this will lead to an overestimate of the strength of relationships between explanatory variables and psychopathy. Retrospective case-control studies of psychopaths (cases) and nonpsychopathic offenders (controls) are questionable, because retrospective bias is problematic, causal ordering is unclear, and they may not shed much light on the development of psychopathy in the general The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

320

VOLUME I: DIAGNOSIS AND TREATMENT

population. In investigating the causes of psychopathy, prospective probabilities (e.g., the proportion of poorly supervised children who become psychopaths) are more relevant than retrospective probabilities (e.g., the proportion of psychopaths who were poorly supervised by their parents). Only risk factors that can vary over time within individuals can be causes (Kraemer et al., 1997). Hence, I will not review unchangeable factors such as gender and race (for gender and psychopathy, see two special issues of Behavioral Sciences and the Law, 23(6), 2005, and 24(1), 2006; for race and psychopathy, see Sullivan & Kosson, 2006). Unfortunately, there are very few prospective longitudinal surveys that specifically investigate the development of psychopathy in adults. (I am focusing on adult psychopathy because the extension of the term ‘psychopathy’ to children and adolescents is controversial; see Farrington, 2005b, and Johnstone & Cooke, 2004). Consequently, much of this chapter reviews knowledge gained in longitudinal surveys of criminal behavior. In my opinion, these surveys are more relevant than retrospective studies of psychopathy, especially since psychopathy is highly correlated with persistent, serious and violent offending. As Hart and Hare (1997, p. 22) pointed out: Many psychopaths engage in chronic criminal conduct and do so at a high rate, whereas only a small minority of those who engage in criminal conduct are psychopaths. This means that psychopaths are responsible for a disproportionate amount of crime in our society.

The Cambridge Study This chapter presents new results obtained in the Cambridge Study in Delinquent Development, which is a 40-year prospective longitudinal survey of the development of offending and antisocial behavior. In this survey, 411 London boys have been followed up by personal face-to-face interviews from age 8 to age 48 (Farrington, 2003; Farrington et al., 2006). Various individual, family and socioeconomic risk factors were measured at age 8 to 10, before any of the boys could be convicted. At age 48, 365 of the 394 men who were still alive were interviewed (93 %). Of the 365 who completed a social interview, 304 (83 %) also completed a medical interview including the SCID-II and the PCL-SV. Scores on the 12-item PCL-SV ranged from 0 to 17 (out of a possible maximum of 24), with a mean of 3.5 and a standard deviation of 3.8. Up to age 50, 167 men (41 %) were convicted out of 404 at risk (that is, excluding seven men who emigrated permanently before age 21 and therefore could not be searched for convictions). Convictions were only counted for the more serious ‘standard list’ offenses, excluding motoring and other minor crimes. Most offenses were of theft, burglary, violence, vandalism, fraud or drug use. Of the convicted men, 28 were defined as chronic offenders because they had 10 or more convictions. These chronic offenders (7 % of the sample) accounted for 52 % of all convictions.

Psychopathy versus Convictions When PCL-SV scores were compared with numbers of convictions, it was clear that there were qualitative differences between those scoring 10 or more on the PCL-SV and the remainder: all except one (97 %) of the 33 men scoring 10 or more (11 % of the sample)

SOCIAL ORIGINS OF PSYCHOPATHY

321

Table 19.1 PCL-SV scores versus convictions % Convicted

% Chronic

Score

%

Low

High

OR

Low

High

OR

Total ADI DAE IIB ANT

11 13 18 15 19

33 36 34 34 29

97 69 69 74 86

65.1 4.1 4.3 5.8 15.3

2 3 3 2 0.4

45 28 22 30 33

44.2 11.1 8.6 17.7 118.9

Notes: OR = odds ratio (all p < .05); ADI = arrogant, deceitful interpersonal style; DAE = deficient affective experience; IIB = impulsive or irresponsible behavioral style; ANT = antisocial behavior; % Convicted and % Chronic among low versus high scorers. (High scores on total PCL-SV = 10 or more out of 24; high scores on ADI, DAE, and IIB = 2 or more out of 6; high scores on ANT = 4 or more out of 6.)

were convicted, compared with 46 out of 73 men scoring 4–9 (63 %) and only 43 out of 197 men scoring 0–3 (22 %). Nearly half (45%) of the men scoring 10 or more were chronic offenders, compared with 2 % of the remainder (Table 19.1). The vast majority of chronic offenders who completed the medical interview (15 out of 20) scored 10 or more on the PCL-SV. Of course, it must be admitted that even the ‘most psychopathic’ males in this community sample would not necessarily be classified as clinical ‘psychopaths’. According to the PCL-SV manual (Hart, Cox & Hare, 1995), a ‘high’ score in a community sample is 16 or above. Only two men at age 48 achieved this score, suggesting that few of the ‘most psychopathic’ men suffered from a severe personality disorder. Nevertheless, based on the distribution of PCL-SV scores within this sample, it is correct to say that 33 males were the ‘most psychopathic’ at age 48 according to this measure of psychopathy. There is no other longitudinal study that has related childhood risk factors to measures of psychopathy or antisocial personality 40 years later. Table 19.1 also shows relationships between the four facets and convictions. Scores on all four facets were dichotomized; 39 men (13 %) scored 2 or more out of 6 on ADI; 54 men (18 %) scored 2 or more out of 6 on DAE; 47 men (15 %) scored 2 or more out of 6 on IIB; and 58 men (19 %) scored 4 or more out of 6 on ANT. Not surprisingly, ANT was most strongly related to convictions (Odds Ratio or OR = 15.3). ADI (OR = 4.1) and DAE (OR = 4.3) were rather similarly related to convictions, and IIB (OR = 5.8) had the strongest relationship. Not surprisingly, ANT was strongly related to chronic offending; 19 out of 20 chronic offenders were high on ANT. Of the other three facets, IIB was the most strongly related to chronic offending. (Unless otherwise stated, all ORs in this chapter are significant at p = .05. Confidence intervals can be obtained from the author.)

SOCIAL FACTORS Child-Rearing Methods Parental discipline refers to how parents react to a child’s behavior. It is clear that harsh or punitive discipline (involving physical punishment) predicts offending, as the review

322

VOLUME I: DIAGNOSIS AND TREATMENT

by Haapasalo and Pokela (1999) showed. In a follow-up study of nearly 700 Nottingham children, John and Elizabeth Newson (1989) found that physical punishment at ages 7 and 11 predicted later convictions; 40 % of offenders had been smacked or beaten at age 11, compared with 14 % of nonoffenders. Erratic or inconsistent discipline also predicts delinquency (West & Farrington, 1973, p. 51). This can involve either erratic discipline by one parent, sometimes turning a blind eye to bad behavior and sometimes punishing it severely, or inconsistency between two parents, with one parent being tolerant or indulgent and the other being harshly punitive. Just as inappropriate methods of responding to bad behavior predict offending, low parental reinforcement (not praising) of good behavior is also a predictor (Farrington & Loeber, 1999). Cold, rejecting parents tend to have delinquent children, as McCord (1979) found in the Cambridge-Somerville study in Boston. She also concluded that parental warmth could act as a protective factor against the effects of physical punishment (McCord, 1997). Whereas 51 % of boys with cold physically punishing mothers were convicted in her study, only 21 % of boys with warm physically punishing mothers were convicted – similar to the 23 % of boys with warm nonpunitive mothers who were convicted. The father’s warmth was also a protective factor against the father’s physical punishment. Low parental involvement in the child’s activities predicts subsequent offending, as the Newsons found in their Nottingham survey (Lewis, Newson & Newson, 1982). In the Cambridge Study, having a father who never joined in the boy’s leisure activities doubled his risk of conviction (West & Farrington, 1973, p.57), and this was the most important predictor of persistence in offending after age 21 as opposed to desistance (Farrington & Hawkins, 1991). Similarly, poor parent–child communication predicted offending in the Pittsburgh Youth Study (Farrington & Loeber, 1999), and low family cohesiveness was the most important predictor of violence in the Chicago Youth Development Study (GormanSmith et al., 1996). Marshall and Cooke (1999) compared psychopathic and nonpsychopathic prisoners in Scotland using the PCL-R and found that significantly more of the psychopathic prisoners had experienced parental indifference or neglect, poor parental supervision and poor parental discipline. In the Cambridge Study, poor parental supervision, measured at age 8, significantly predicted high psychopathy scores at age 48 (actually based on information between ages 18 and 48); 24 % of boys who were poorly supervised at age 8 (because their parents did not know where they were when they went out) had high psychopathy scores at age 48, compared with 8 % of the remainder (OR = 3.6, z = 3.22, p = .0006, one-tailed tests used in light of directional predictions). Generally, an OR of 2.0 or greater indicates a strong relationship (Cohen, 1996). Interestingly, poor parental supervision was related to IIB and ANT but not to ADI or DAE (Table 19.2). Harsh or erratic parental discipline at age 8 also predicted high psychopathy scores (OR = 2.6), but was significantly related only to the ANT facet. Low paternal involvement with the boy (the father not joining in the boy’s activities) was a strong predictor of high psychopathy scores (OR = 6.5) and it predicted DAE, IIB and ANT (Table 19.2).

Child Abuse and Neglect Children who are physically abused or neglected tend to become offenders later in life. The most famous study of this phenomenon was carried out by Widom (1989) in Indianapolis.

SOCIAL ORIGINS OF PSYCHOPATHY

323

Table 19.2 Early predictors of psychopathy at age 48 Odds ratio Age 8–10: Risk factor

PCL-SV

ADI

DAE

IIB

ANT

Poor supervision Harsh discipline Father uninvolved Physical neglect Disrupted family Parental disagreement Large family size Convicted father Convicted mother Delinquent sibling Young mother Depressed mother Low family income Low social class Poor housing Unpopular Delinquent school Low nonverbal IQ Low verbal IQ Low junior attainment Low school track record High daring Poor concentration High impulsivity Dishonest Troublesome

3.6* 2.6* 6.5* 5.9* 4.3* 3.0* 3.5* 5.1* 4.5* 4.0* 2.4* 2.7* 4.6* 3.1* 3.0* 1.9 3.9* 2.4* 2.7* 1.7 3.0* 3.6* 3.6* 2.4* 4.1* 3.4*

1.0 1.7 1.5 2.7* 1.5 1.9* 1.7 2.1* 1.8 2.6* 1.0 1.0 1.9* 2.0* 1.4 2.0* 2.4* 1.8 1.9* 1.5 2.4* 1.5 2.7* 1.2 2.0* 2.2*

1.4 1.6 2.6* 2.4* 1.7 1.6 2.4* 3.1* 2.2* 3.3* 2.1* 1.7 2.7* 1.6 2.0* 1.4 2.1* 2.0* 2.0* 2.0* 2.6* 2.3* 2.5* 1.6 2.3* 1.7

2.6* 1.6 2.0* 4.7* 2.8* 2.1* 2.6* 2.9* 2.2* 2.9* 1.5 2.1* 3.6* 2.0* 2.6* 1.2 2.2* 2.1* 1.9* 1.6 1.5 2.3* 1.9* 1.6 2.7* 1.8*

3.4* 2.6* 3.1* 4.0* 2.9* 2.9* 2.8* 4.0* 3.3* 4.7* 1.9* 2.0* 3.2* 2.3* 2.2* 2.0* 3.0* 2.6* 2.6* 3.0* 2.9* 2.9* 3.0* 1.9* 3.5* 3.5*

Notes: Dichotomized risk factors are compared with dichotomized scores; PCL-SV = total PCL-SV score; ADI = arrogant, deceitful interpersonal style; DAE = deficient affective experience; IIB = impulsive or irresponsible behavioral style; ANT = antisocial behavior; * p < .05, one-tailed; nonsignificant predictors: authoritarian parents, depressed father.

She used court records to identify over 900 children who had been abused or neglected before age 11, and compared them with a control group matched on age, race, gender, elementary school class and place of residence. A 20-year follow-up showed that the children who were abused or neglected were more likely to be arrested as juveniles and as adults than were the controls, and they were more likely to be arrested for juvenile violence (Maxfield & Widom, 1996). Child sexual abuse, and child physical abuse and neglect, also predicted adult arrests for sex crimes (Widom & Ames, 1994). Most importantly, Luntz and Widom (1994) showed that child abuse predicted adult antisocial personality disorder, and Weiler and Widom (1996) found that child abuse predicted high PCL-R scores in adulthood, for males and females and African American and white children. Similar results have been obtained in other studies. An extensive review by MalinoskyRummell and Hansen (1993) confirmed that being physically abused as a child predicted later violent and nonviolent offending. For example, in the Cambridge-Somerville study in Boston, McCord (1983) found that about half of the abused or neglected boys were convicted for serious crimes, became alcoholics or mentally ill, or died before age 35. In Stockholm,

324

VOLUME I: DIAGNOSIS AND TREATMENT

Lang, af Klinteberg and Alm (2002) reported that boys who were abused or neglected at age 11–14 tended to become violent and to have high PCL scores at age 36. Retrospective studies of offenders by Koivisto and Haapasalo (1996) in Finland and by Patrick, Zempolich and Levenston (1997) in Florida found correlations between early child abuse and high PCL-R scores, but Marshall and Cooke (1999) in Scotland reported no difference in physical abuse histories between psychopathic and nonpsychopathic prisoners. In the Cambridge Study, physical neglect of the boy at age 8 predicted his high psychopathy scores (OR = 5.9), and also predicted all four facets.

Disrupted Families and Parental Conflict Most studies of broken homes have focused on the loss of the father rather than the mother, because the loss of a father is much more common. In general, it is found that children who are separated from a biological parent are more likely to offend than children from intact families. For example, in a birth cohort study of children born in Newcastle-upon-Tyne, Kolvin et al. (1988b) discovered that boys who experienced divorce or separation in their first five years of life had a doubled risk of conviction up to age 32 (53 % as opposed to 28 %). McCord (1982) carried out an interesting study in Boston of the later serious offending (up to age 45) of boys from homes broken by loss of the biological father. She found that the prevalence of offending was high for boys from broken homes without affectionate mothers (62 %) and for those from unbroken homes characterized by parental conflict (52 %), irrespective of whether they had affectionate mothers. The prevalence of offending was low for those from unbroken homes without conflict (26 %) and – importantly – equally low for boys from broken homes with affectionate mothers (22 %). These results suggest that it might not be the broken home that is criminogenic but rather the parental conflict that often contributes to family breakdown. They also suggest that a loving mother might to some degree be able to compensate for the loss of a father. A meta-analysis by Wells and Rankin (1991) showed that broken homes were more strongly related to delinquency when they were caused by parental separation or divorce rather than by death. In the Cambridge Study, coming from a disrupted family (separation from a parent before the tenth birthday for reasons other than death or hospitalization) predicted high antisocial personality scores at age 32 (Farrington, 2000) and high psychopathy scores at age 48 (OR = 4.3; Table 19.2). Coming from a disrupted family predicted the IIB and ANT facets but not the ADI and DAE facets. While the retrospective study by Koivisto and Haapasalo (1996) in Finland found a correlation between broken homes and high PCL-R scores, Patrick, Zempolich and Levenston (1997) in Florida reported that psychopathic prisoners were less likely than nonpsychopathic prisoners to come from single-parent homes. Many studies show that parental conflict and interparental violence predict later antisocial behavior (see Buehler et al., 1997; Kolbo, Blakely & Engleman, 1996). In the Christchurch Health and Development Study in New Zealand, children who witnessed violence between their parents were more likely to commit both violence and property offenses according to their self-reports (Fergusson & Horwood, 1998). The predictability of witnessing fatherinitiated violence held up after controlling for other risk factors such as parental criminality, parental substance abuse, parental physical punishment, a young mother and low family

SOCIAL ORIGINS OF PSYCHOPATHY

325

income. Parental conflict also predicted offending in both the Cambridge and Pittsburgh studies (Farrington & Loeber, 1999). Table 19.2 shows that parental disagreement at age 8 significantly predicted high psychopathy scores (OR = 3.0), and predicted the ADI, IIB and ANT facets.

Large Family Size Large family size (a large number of children in the family) is a relatively strong and highly replicable predictor of offending (Ellis, 1988; Fischer, 1984). It was similarly important in the Cambridge and Pittsburgh studies, even though families were on average smaller in Pittsburgh in the 1990s than in London in the 1960s (Farrington & Loeber, 1999).In the Cambridge Study, if a boy had four or more siblings by his tenth birthday, this doubled his risk of being convicted as a juvenile (West & Farrington, 1973, p. 31). Large family size was the most important independent predictor of convictions up to age 32 in a logistic regression analysis; 58 % of boys from large families were convicted up to this age (Farrington, 1993). Large family size at the tenth birthday also predicted chronic offenders (Farrington & West, 1993), high antisocial personality scores at age 32 (Farrington, 2000), and high psychopathy scores at age 48 (OR = 3.5; Table 19.2). Large family size also predicted the DAE, IIB and ANT facets.

Crime Runs in Families Criminal and antisocial parents tend to have criminal and antisocial children, as shown in the classic longitudinal surveys by McCord (1977) in Boston and Robins (1979) in St. Louis. The most extensive research on the concentration of offending in families was carried out in the Cambridge Study. Having a convicted father, mother, brother or sister predicted a boy’s own convictions, and all four relatives were independently important as predictors (Farrington, Barnes & Lambert, 1996). For example, 63 % of boys with convicted fathers were themselves convicted up to age 32, compared with 30 % of the remainder. Samesex relationships were stronger than opposite-sex relationships, and older siblings were stronger predictors than younger siblings. Only 6 % of the families accounted for half of all the convictions of all family members. Similar results were obtained in the Pittsburgh Youth Study, which is a prospective longitudinal survey of Pittsburgh males from age 7 to age 25. Arrests of fathers, mothers, brothers, sisters, uncles, aunts, grandfathers and grandmothers all predicted the boy’s own delinquency (Farrington et al., 2001). The most important relative was the father; arrests of the father predicted the boy’s delinquency independently of all other arrested relatives. Only 8 % of families accounted for 43 % of arrested family members. There seems to be no longitudinal study specifically relating psychopathy of parents to psychopathy of children, but in Copenhagen Brennan, Mednick and Mednick (1993) found that parental psychopathology (including psychopathy) significantly predicted violence by sons up to age 22. Also, Harris, Rice and Lalumiere (2001) showed that antisociality in parents (identified on the basis of a composite measure incorporating parental criminality and alcoholism along with child abuse and neglect) was related to higher psychopathy in a sample of violent offenders drawn from a Canadian maximum security psychiatric hospital.

326

VOLUME I: DIAGNOSIS AND TREATMENT

In the Cambridge Study, having a convicted parent or a delinquent older sibling by the tenth birthday were consistently among the best age 8–10 predictors of the boy’s later offending and antisocial behavior. Apart from behavioral measures such as troublesomeness and daring, they were the strongest predictors of juvenile convictions (Farrington, 1992a) and chronic offending (Farrington & West, 1993). Having a convicted parent was the best predictor of high antisocial personality scores at age 32 (Farrington, 2000). Table 19.2 shows that having a convicted father (OR = 5.1), a convicted mother (OR = 4.5), or a delinquent sibling (OR = 4.0) by the tenth birthday significantly predicted high psychopathy scores at age 48. All of these factors predicted all four facets, with the single exception that a convicted mother did not significantly predict high ADI scorers.

Other Parental Features Numerous other parental features predict antisocial behavior. For example, early childbearing or teenage pregnancy is a risk factor. Morash and Rucker (1989) analyzed results from four surveys in the United States and England (including the Cambridge Study) and found that teenage mothers tended to coincide with low income families, and tended to have welfare support and absent biological fathers. In addition they tended to use poor childrearing methods, and their children were often characterized by low school attainment and delinquency. However, the presence of the biological father mitigated many of these adverse factors and generally seemed to have a protective effect (see below). Similarly, a large-scale study in Washington State showed that children of teenage or unmarried mothers had a significantly increased risk of offending (Conseur et al., 1997). Boys born to unmarried mothers aged 17 or less showed an eleven-fold increase in the risk of chronic offending compared with boys born to married mothers aged 20 or more. In the Cambridge and Pittsburgh studies, the age of the mother at her first birth was only a moderate predictor of the boy’s later delinquency (Farrington & Loeber, 1999). In the Cambridge Study, for example, 27 % of sons of young mothers were convicted as juveniles, compared with 18 % of the remainder. More detailed analyses in this study showed that teenage mothers who went on to have large numbers of children were especially likely to have convicted children (Nagin, Pogarsky & Farrington, 1997). Table 19.2 shows that boys born to mothers who were teenagers at the time of their first birth were significantly likely to have high psychopathy scores at age 48 (OR = 2.4). Young mothers predicted high scores on the DAE and ANT facets. Young mothers also predicted high antisocial personality scores at age 32 (Farrington, 2000). High parental stress, and parental anxiety or depression, also predicted delinquency in the Pittsburgh Youth Study (Loeber et al., 1998). In the Cambridge Study, having a mother who was anxious or depressed (according to psychiatric social worker ratings, a health questionnaire, or psychiatric records) predicted high antisocial personality scores at age 18, but not at age 32 (Farrington, 2000). However, having an anxious or depressed mother predicted high psychopathy scores at age 48 (OR = 2.7; Table 19.2), and predicted the IIB and ANT facets. Depressed fathers did not significantly predict psychopathy. Substance use by parents also predicts antisocial behavior by children, according to findings in the Pittsburgh Youth Study (Loeber et al., 1998). Smoking by the mother during pregnancy is a particularly important risk factor. A large-scale follow-up of a general population cohort in Finland showed that maternal smoking during pregnancy doubled the risk of

SOCIAL ORIGINS OF PSYCHOPATHY

327

violent or persistent offending by male offspring, after controlling for other biopsychosocial risk factors (Rasanen et al., 1999). When maternal smoking was combined with a teenage mother, a single-parent family and an unwanted pregnancy, the risk of offending increased ten-fold.

Socioeconomic Factors In general, coming from a low social class family predicts later violence. For example, in the US National Youth Survey, prevalence rates for self-reported assault and robbery were about twice as high among lower-class youth as among middle-class youth (Elliott, Huizinga & Menard, 1989). In Project Metropolitan in Stockholm (Wikstr¨om, 1985) and in the Dunedin study in New Zealand (Henry et al., 1996), the socioeconomic status of a boy’s family – based on the father’s occupation – predicted his later violent crimes. Low socioeconomic status is a less consistent predictor of offending. One source of variability depends on whether it is measured by income and housing or by occupational prestige. In the Cambridge Study, low family income and poor housing predicted official and self-reported, juvenile and adult offending, but low parental occupational prestige predicted only self-reported offending (Farrington, 1992a, 1992b). Also, low family income and low socioeconomic status (but not poor housing) significantly predicted chronic offending (Farrington & West, 1993) and high antisocial personality scores at age 32 (Farrington, 2000). Table 19.2 shows that low family income at age 8 (OR = 4.6), low social class at age 8–10 (based on occupational prestige; OR = 3.1), and poor housing at age 8–10 (OR = 3.0) all predicted high psychopathy scores at age 48. Low family income also predicted all four facets. Low social class predicted ADI, IIB and ANT, while poor housing predicted DAE, IIB and ANT.

Peer Influence It is well established that having delinquent friends is an important predictor of offending (Lipsey & Derzon, 1998). What is less clear is whether antisocial peers encourage and facilitate adolescent antisocial behavior, or whether it is merely the case that ‘birds of a feather flock together’. Delinquents may have delinquent friends because of co-offending, which is particularly common under age 21 (Reiss & Farrington, 1991). However, Elliott and Menard (1996) in the US National Youth Survey concluded that delinquent friends influenced an adolescent’s own delinquency and that the reverse was also true: more delinquent adolescents were more likely to have delinquent friends. Delinquent friends were not measured until age 14 in the Cambridge Study, but chronic offenders significantly tended to have them (Farrington & West, 1993). There is no doubt that highly aggressive children tend to be rejected by most of their peers (Coie, Dodge & Kupersmidt, 1990). In the Oregon Youth Study, peer rejection at age 9–10 significantly predicted adult antisocial behavior at age 23–24 (Nelson & Dishion, 2004). In Stockholm, Freidenfelt and af Klinteberg (2003) found that unpopularity predicted high PCL scores among hyperactive boys but not among nonhyperactive boys. Low popularity at age 8–10 was only a marginal predictor of adolescent aggression and teenage violence in the Cambridge Study (Farrington, 1989). It significantly predicted chronic offending (Farrington & West, 1993) but not high antisocial personality scores at age 32 (Farrington,

328

VOLUME I: DIAGNOSIS AND TREATMENT

2000). Low popularity did not significantly predict high psychopathy scores at age 48 (OR = 1.9), but it did significantly predict ADI and ANT (Table 19.2). Coie and Miller-Johnson (2001) found that it was the boys who were both aggressive and rejected by their classmates who became the self-reported and official offenders.

School and Neighborhood Factors It is also well established that delinquents disproportionately attend high delinquency-rate schools, which have high levels of distrust between teachers and students, low commitment to the school by students, and unclear and inconsistently enforced rules (Graham, 1988). In the Cambridge Study, attending a high delinquency-rate school at age 11 significantly predicted a boy’s own delinquency (Farrington, 1992a), as well as his chronic offending (Farrington & West, 1993) and high antisocial personality scores at age 32 (Farrington, 2000). Table 19.2 shows that attending a high delinquency-rate school significantly predicted high psychopathy scores at age 48 (OR = 3.9) and all four facets. Many studies show that boys living in urban areas are more violent than those living in rural ones. In the US National Youth Survey, the prevalence of self-reported assault and robbery was considerably higher among urban youth (Elliott, Huizinga & Menard, 1989). Within urban areas, boys living in high-crime neighborhoods are more violent than those living in low-crime neighborhoods. In the Rochester Youth Development Study, living in a high-crime neighborhood significantly predicted self-reported violence (Thornberry, Huizinga, & Loeber, 1995). Similarly, in the Pittsburgh Youth Study, living in a bad neighborhood (either as rated by the mother, or based on census measures of poverty, unemployment and female-headed households) significantly predicted official and reported violence (Farrington, 1998).

Other Risk Factors Table 19.2 also shows the degree to which other well-known risk factors, measured at age 8–10 in the Cambridge Study, predicted high psychopathy scores at age 48. Low nonverbal IQ, low verbal IQ and low school track (but not low junior school attainment) predicted high psychopathy scores at age 48. All four of these factors predicted DAE and ANT, but only two (low verbal IQ and low school track) predicted ADI, and similarly only two (low nonverbal IQ and low verbal IQ) predicted IIB. High daring (taking many risks), poor concentration or restlessness, and high impulsivity on psychomotor tests all predicted the most psychopathic males. Poor concentration predicted all four facets, while high daring predicted DAE, IIB and ANT, and high psychomotor impulsivity predicted only ANT (not very strongly). High dishonesty (rated by peers) and high troublesomeness (rated by peers and teachers) also significantly predicted high psychopathy scores at age 48. High dishonesty predicted all four facets, while high troublesomeness predicted ADI, IIB and ANT.

EXPLAINING THE DEVELOPMENT OF PSYCHOPATHY It is difficult to determine what the precise causal mechanisms are that link family factors – such as parental criminality, young mothers, large family size, poor parental supervision, child abuse or disrupted families – to later antisocial behavior or psychopathy. This is

SOCIAL ORIGINS OF PSYCHOPATHY

329

because these factors tend to be related not only to each other but also to other risk factors such as low family income, poor housing, impulsiveness, low IQ and low school attainment. Just as it is hard to know what the key underlying family constructs are, it is equally hard to know what the key underlying constructs are in other domains of life. It is important to investigate what family factors predict psychopathy independently of other family factors, independently of genetic and biological factors and independently of nonfamily factors (e.g., individual, peer, neighborhood and socioeconomic). It is important to investigate sequential effects of risk factors on psychopathy. Several researchers have concluded that socioeconomic factors have an effect on offending through their effect on family factors (see Dodge, Pettit & Bates, 1994; Larzelere & Patterson, 1990; Stern & Smith, 1995). In the Pittsburgh Youth Study, it was proposed that socioeconomic and neighborhood factors (e.g., poor housing) influenced family factors (e.g., poor supervision) which in turn influenced child factors (e.g., low guilt) which in turn influenced offending (Loeber et al., 1998, p. 10). There may also be sequential effects of some family factors on others (e.g., if young mothers tend to use poor child-rearing methods: see Conger, Patterson & Ge, 1995), or of family factors on other risk factors (e.g., if antisocial parents tend to have low incomes and live in poor neighborhoods). More research is needed to discover protective factors that might decrease the likelihood of psychopathy in people who are at risk. For example, in Hawaii, Werner and Smith (1982) studied children who possessed four or more risk factors for offending before age two but who nevertheless did not develop behavior problems during childhood or adolescence. They found that the major protective factors included being first-born, being active and affectionate during infancy, small family size, and receiving a large amount of attention from caretakers. In the Newcastle Thousand-Family Study, Kolvin et al. (1988a) investigated high-risk boys from deprived backgrounds who did not become delinquents. The major protective factors under age 5 were good mothering, good maternal health, an employed head of household and being an oldest child. Based on the OR, the best predictors at age 8–10 of high psychopathy scores at age 48 were low involvement of the father with the boy, physical neglect, a convicted father, low family income, a convicted mother and a disrupted family. The best predictors of ADI were poor concentration or restlessness, physical neglect, a delinquent sibling, attending a high delinquency-rate school, and being in a low school track.1 The best predictors of DAE were a delinquent sibling, a convicted father, low family income, low involvement of the father with the boy and being in a low school track. The best predictors of IIB were physical neglect, low family income, a convicted father, a delinquent sibling and a disrupted family. The best predictors of ANT were a delinquent sibling, a convicted father, physical neglect, troublesomeness and dishonesty. Table 19.3(a) shows the results of a logistic regression analysis to investigate the independent predictors of the personality features of psychopathy (that is, ADI + DAE + IIB, dichotomized into a score of 6 or more versus a score of 0–5). For ease of exposition, I will refer to this as ‘psychopathic personality’. The best predictors at age 8–10 were low family income, high daring, a convicted father, an anxious or depressed mother, a delinquent sibling, and poor concentration or restlessness. Theories of the development of psychopathy need to take account of these results.

1

A low school track, in the UK called a law school stream is a grouping of children, within a year of school or age cohort, based on educational attainment.

330

VOLUME I: DIAGNOSIS AND TREATMENT

Table 19.3 Prediction of psychopathic personality (a) Independent predictors Low family income High daring Convicted father Depressed mother Delinquent sibling Poor concentration (b) Risk score 0 1 2 3 4–6 Total

LRCS change

p

Partial OR

20.26 5.32 5.75 3.57 2.58 2.03

.0001 .011 .008 .029 .054 .077

3.6 3.5 3.0 2.5 2.5 2.2

LPP

HPP

% HPP

93 92 45 31 15 276

4 2 3 7 12 28

4.1 2.1 6.3 18.4 44.4 9.2

Notes: HPP=high psychopathic personality (score 6 or more on ADI + DAE + IIB); ADI = arrogant deceitful interpersonal style; DAE = deficient affective experience; IIB = impulsive or irresponsible behavioral style; LPP = low psychopathic personality; LRCS = likelihood ratio Chi-squared; OR = odds ratio. For (b), area under ROC curve = .782, SD = .056

In general, the likelihood of an undesirable outcome such as psychopathy increases with the number of risk factors that a person possesses. For example, in the Cambridge Study Farrington (2000) found that the percentage of boys who were antisocial at age 32 increased from 13 % of those with no risk factors at age 8–10 to 61 % of those with three or four risk factors at age 8–10. Table 19.3(b) shows how the probability of psychopathic personality (based on ADI + DAE + IIB) increased with the number of independent predictors, from 0 to 6. Whereas the base rate in the sample was only 9 %, 44 % of those with four or more of these risk factors at age 8–10 had high psychopathic personality scores.

CONCLUSIONS AND FUTURE DIRECTIONS More explanatory research is needed on the development of psychopathic personality. More efforts should be made to integrate the personality constructs underlying psychopathy – an arrogant and deceitful interpersonal style, deficient affective experience, and an impulsive and irresponsible lifestyle – with larger systems of personality constructs (Salekin et al., 2005; Widiger, 1998). More research is needed on the development of more unbiased, valid and reliable instruments to measure psychopathy – preferably measures that are not contaminated by antisocial behavior and that do not rely on open-ended questions. It is important to supplement self-report data with other information (e.g., from case files). The aim should be to propose and test developmental theories of psychopathy and of its core constructs such as low empathy and high impulsiveness (for developmental theories of offending, see Farrington, 2005a). There is a great need to carry out prospective longitudinal surveys with high-risk community samples to investigate the development of psychopathy, and the link between psychopathic parents and psychopathic children. More randomized experiments are needed to evaluate psychosocial interventions (see Farrington & Welsh,

SOCIAL ORIGINS OF PSYCHOPATHY

331

2005), with large samples and long-term follow-up periods, incorporating outcome measures of psychopathy. In principle, a great deal can be learned about causal effects of social factors from these experiments (Robins, 1992). No one can doubt the importance of the construct of psychopathy, the need to develop better operational definitions of the underlying constructs, and the pressing need to advance knowledge about its development, explanation, prevention and treatment. The time is ripe for western countries to mount an ambitious coordinated program of research on psychopathy, focusing on international multidisciplinary collaboration and aiming to train a new generation of biopsychosocial researchers. Given the enormous social costs of psychopathy, the benefits of such a large-scale coordinated program of research should easily outweigh its costs. And, of course, a reduction in the number of psychopathic individuals and in the number of their victims would greatly increase the sum of human happiness.

ACKNOWLEDGMENTS The age 8–10 data collection of the Cambridge Study in Delinquent Development was funded by the Home Office and directed by Professor Donald West. The medical interview at age 48 was funded by the UK National Programme on Forensic Mental Health. The interview was conducted by Dr. Crystal Romilly under the supervision of Professor Jeremy Coid. The PCL-SV was scored by Dr. Crystal Romilly and Dr. Simone Ullrich.

REFERENCES Brennan, P.A., Mednick, B.R. & Mednick, S.A. (1993). Parental psychopathology, congenital factors, and violence. In S. Hodgins (ed.), Mental Disorder and Crime (pp. 244–61). Newbury Park, CA: Sage. Buehler, C., Anthony, C., Krishnakumar, A. et al. (1997). Interparental conflict and youth problem behaviors: A meta-analysis. Journal of Child and Family Studies, 6, 233–47. Cohen, P. (1996). Childhood risks for young adult symptoms of personality disorder. Multivariate Behavioral Research, 31, 121–48. Coie, J.D., Dodge, K.A. & Kupersmidt, J. (1990). Peer group behavior and social status. In S.R. Asher & J.D. Coie (eds.), Peer Rejection in Childhood (pp. 17–59). Cambridge: Cambridge University Press. Coie, J.D. & Miller-Johnson, S. (2001). Peer factors and interventions. In R. Loeber & D.P. Farrington (eds.), Child Delinquents: Development, Intervention, and Service Needs (pp. 191–209). Thousand Oaks, CA: Sage. Conger, R.D., Patterson, G.R. & Ge, X. (1995). It takes two to replicate: A mediational model for the impact of parents’ stress on adolescent adjustment. Child Development, 66, 80–97. Conseur, A., Rivara, F.P., Barnoski, R. & Emanuel, I. (1997). Maternal and perinatal risk factors for later delinquency. Pediatrics, 99, 785–90. Cooke, D.J., Michie, C., Hart, S.D. & Clark, D.A. (2004). Reconstructing psychopathy: clarifying the significance of antisocial and socially deviant behavior in the diagnosis of psychopathic personality disorder. Journal of Personality Disorders, 18, 337–57. Dodge, K.A., Pettit, G.S. & Bates, J.E. (1994). Socialization mediators of the relation between socioeconomic status and child conduct problems. Child Development, 65, 649–65. Elliott, D.S., Huizinga, D. & Menard, S. (1989). Multiple Problem Youth. New York: Springer-Verlag. Elliott, D.S. & Menard, S. (1996). Delinquent friends and delinquent behavior: temporal and developmental patterns. In J.D. Hawkins (ed.), Delinquency and Crime: Current Theories (pp. 28–67). Cambridge: Cambridge University Press.

332

VOLUME I: DIAGNOSIS AND TREATMENT

Ellis, L. (1988). The victimful–victimless crime distinction, and seven universal demographic correlates of victimful criminal behavior. Personality and Individual Differences, 3, 525–48. Farrington, D.P. (1989). Early predictors of adolescent aggression and adult violence. Violence and Victims, 4, 79–100. Farrington, D.P. (1992a). Explaining the beginning, progress, and ending of antisocial behavior from birth to adulthood. In J. McCord (ed.), Facts, Frameworks and Forecasts: Advances in Criminological Theory (Vol. 3, pp. 253–86). New Brunswick, NJ: Transaction. Farrington, D.P. (1992b). Juvenile delinquency. In J.C. Coleman (ed.), The School Years (2nd edition, pp. 123–63). London: Routledge. Farrington, D.P. (1993). Childhood origins of teenage antisocial behaviour and adult social dysfunction. Journal of the Royal Society of Medicine, 86, 13–17. Farrington, D.P. (1998). Predictors, causes, and correlates of youth violence. In M. Tonry & M.H. Moore (eds.), Youth Violence (pp. 421–75). Chicago: University of Chicago Press. Farrington, D.P. (2000). Psychosocial predictors of adult antisocial personality and adult convictions. Behavioral Sciences and the Law, 18, 605–22. Farrington, D.P. (2003). Key results from the first 40 years of the Cambridge Study in Delinquent Development. In T.P. Thornberry & M.D. Krohn (eds.) Taking Stock of Delinquency (pp. 137–83). New York: Kluwer/Plenum. Farrington, D.P. (ed.) (2005a). Integrated Developmental and Life-Course Theories of Offending. (Advances in Criminological Theory, vol. 14.) New Brunswick, NJ: Transaction. Farrington, D.P. (2005b). The importance of child and adolescent psychopathy. Journal of Abnormal Child Psychology, 33, 489–97. Farrington, D.P. (2006). Family background and psychopathy. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 229–50). New York: Guilford Press. Farrington, D.P., Barnes, G. & Lambert, S. (1996). The concentration of offending in families. Legal and Criminological Psychology, 1, 47–63. Farrington, D.P., Coid, J.W., Harnett, L. et al. (2006). Criminal careers and Life Success: New Findings from the Cambridge Study in Delinquent Development. London: Home Office (Findings No. 281). Farrington, D.P. & Hawkins, J.D. (1991). Predicting participation, early onset, and later persistence in officially recorded offending. Criminal Behavior and Mental Health, 1, 1–33. Farrington, D.P., Jolliffe, D., Loeber, R. et al. (2001). The concentration of offenders in families, and family criminality in the prediction of boys’ delinquency. Journal of Adolescence, 24, 579–96. Farrington, D.P. & Loeber, R. (1999). Transatlantic replicability of risk factors in the development of delinquency. In P. Cohen, C. Slomkowski & L.N. Robins (eds.), Historical and Geographical Influences on Psychopathology (pp. 299–329). Mahwah, NJ: Erlbaum. Farrington, D.P. & Welsh, B.C. (2005). Randomized experiments in criminology: what have we learned in the last two decades? Journal of Experimental Criminology, 1, 9–38. Farrington, D.P. & West, D.J. (1993). Criminal, penal, and life histories of chronic offenders: risk and protective factors and early identification. Criminal Behavior and Mental Health, 3, 492–523. Fergusson, D.M. & Horwood, L.J. (1998). Exposure to interparental violence in childhood and psychosocial adjustment in young adulthood. Child Abuse and Neglect, 22, 339–57. Fischer, D.G. (1984). Family size and delinquency. Perceptual and Motor Skills, 58, 527–34. Freidenfelt, J. & af Klinteberg, B. (2003). Are negative social and psychological childhood characteristics of significant importance in the development of psychosocial functioning? International Journal of Forensic Mental Health, 2, 181–93. Gorman-Smith, D., Tolan, P., Zelli, A. & Huesmann, L.R. (1996). The relation of family functioning to violence among inner-city minority youths. Journal of Family Psychology, 10, 115–29. Graham, J. (1988). Schools, Disruptive Behaviour and Delinquency. London: Her Majesty’s Stationery Office. Haapasalo, J. & Pokela, E. (1999). Child-rearing and child abuse antecedents of criminality. Aggression and Violent Behavior, 1, 107–27. Harris, G.T., Rice, M.E. & Lalumiere, M. (2001). Criminal violence: the roles of psychopathy, neurodevelopmental insults, and antisocial parenting. Criminal Justice and Behavior, 28, 402–26. Hart, S.D., Cox, D.N. & Hare, R.D. (1995). The Hare Psychopathy Checklist: Screening Version. Toronto: Multi-Health Systems.

SOCIAL ORIGINS OF PSYCHOPATHY

333

Hart, S.D. & Hare, R.D. (1997). Psychopathy: assessment and association with criminal conduct. In D.M. Stoff, J. Breiling, & J.D. Maser (eds.), Handbook of Antisocial Behavior (pp. 22–35). New York: John Wiley & Sons, Inc. Henry, B., Caspi, A., Moffitt, T.E. & Silva, P.A. (1996). Temperamental and familial predictors of violent and nonviolent criminal convictions: age 3 to age 18. Developmental Psychology, 32, 614–23. Johnstone, L. & Cooke, D.J. (2004). Psychopathic-like traits in childhood: conceptual and measurement concerns. Behavioral Sciences and the Law, 22, 103–25. Kalb, L.M., Farrington, D.P. & Loeber, R. (2001). Leading longitudinal studies on delinquency, substance use, sexual behavior, and mental health problems with childhood samples. In R. Loeber & D.P. Farrington (eds.), Child Delinquents: Development, Intervention, and Service Needs (pp. 415–23). Thousand Oaks, CA: Sage. Koivisto, H. & Haapasalo, J. (1996). Childhood maltreatment and adulthood psychopathy in light of file-based assessments among mental state examinees. Studies on Crime and Crime Prevention, 5, 91–104. Kolbo, J.R., Blakely, E.H. & Engleman, D. (1996). Children who witness domestic violence: a review of empirical literature. Journal of Interpersonal Violence, 11, 281–93. Kolvin, I., Miller, F.J.W., Fleeting, M. & Kolvin, P.A. (1988a). Risk/protective factors for offending with particular reference to deprivation. In M. Rutter (ed.), Studies of Psychosocial Risk (pp. 77–95). Cambridge: Cambridge University Press. Kolvin, I., Miller, F.J.W., Fleeting, M. & Kolvin, P.A. (1988b). Social and parenting factors affecting criminal-offence rates: Findings from the Newcastle Thousand Family Study (1947–1980). British Journal of Psychiatry, 152, 80–90. Kraemer, H.C., Kazdin, A.E., Offord, D.R. et al. (1997). Coming to terms with the terms of risk. Archives of General Psychiatry, 54, 337–43. Lang, S., af Klinteberg, B. & Alm, P-O. (2002). Adult psychopathy and violent behavior in males with early neglect and abuse. Acta Psychiatrica Scandinavica, 106, 93–100. Larzelere, R.E. & Patterson, G.R. (1990). Parental management: mediator of the effect of socioeconomic status on early delinquency. Criminology, 28, 301–24. Lewis, C., Newson, E. & Newson, J. (1982). Father participation through childhood and its relationship with career aspirations and delinquency. In N. Beail & J. McGuire (eds.) Fathers: Psychological Perspectives (pp. 174–93). London: Junction. Lipsey, M.W. & Derzon, J.H. (1998). Predictors of violent or serious delinquency in adolescence and early adulthood: a synthesis of longitudinal research. In R. Loeber & D.P. Farrington (eds.), Serious and Violent Juvenile Offenders: Risk Factors and Successful Interventions (pp. 86–105).Thousand Oaks, CA: Sage. Loeber, R. & Farrington, D.P. (1997). Strategies and yields of longitudinal studies on antisocial behavior. In D.M. Stoff, J. Breiling & J.D. Maser (eds.), Handbook of Antisocial Behavior (pp. 125–39). New York: John Wiley & Sons, Inc. Loeber, R., Farrington, D.P., Stouthamer-Loeber, M. & van Kammen, W.B. (1998). Antisocial Behavior and Mental Health Problems. Mahwah, NJ: Erlbaum. Luntz, B.K. & Widom, C.S. (1994). Antisocial personality disorder in abused and neglected children. American Journal of Psychiatry, 151, 670–4. McCord, J. (1977). A comparative study of two generations of native Americans. In R.F. Meier (ed.), Theory in Criminology (pp. 83–92). Beverly Hills, CA: Sage. McCord, J. (1979). Some child-rearing antecedents of criminal behavior in adult men. Journal of Personality and Social Psychology, 37, 1477–86. McCord, J. (1982). A longitudinal view of the relationship between paternal absence and crime. In J. Gunn & D.P. Farrington (eds.), Abnormal Offenders, Delinquency, and the Criminal Justice System (pp. 113–28). Chichester, England: John Wiley & Sons, Ltd. McCord, J. (1983). A forty year perspective on effects of child abuse and neglect. Child Abuse and Neglect, 7, 265–70. McCord, J. (1997). On discipline. Psychological Inquiry, 8, 215–17. Malinosky-Rummell, R. & Hansen, D.J. (1993). Long-term consequences of childhood physical abuse. Psychological Bulletin, 114, 68–79. Marshall, L.A. & Cooke, D.J. (1999). The childhood experiences of psychopaths: a retrospective study of familial and social factors. Journal of Personality Disorders, 13, 211–25.

334

VOLUME I: DIAGNOSIS AND TREATMENT

Maxfield, M.G. & Widom, C.S. (1996). The cycle of violence revisited six years later. Archives of Pediatrics and Adolescent Medicine, 150, 390–5. Morash, M. & Rucker, L. (1989). An exploratory study of the connection of mother’s age at childbearing to her children’s delinquency in four data sets. Crime and Delinquency, 35, 45–93. Nagin, D.S., Pogarsky, G., & Farrington, D.P. (1997). Adolescent mothers and the criminal behavior of their children. Law and Society Review, 31, 137–62. Nelson, S.E. & Dishion, T.J. (2004). From boys to men: Predicting adult adaptation from middle childhood sociometric status. Development and Psychopathology, 16, 441–59. Newson, J. & Newson, E. (1989). The Extent of Parental Physical Punishment in the UK. London: Approach. Patrick, C.J., Zempolich, K.A. & Levenston, G.K. (1997). Emotionality and violent behavior in psychopaths: a biosocial analysis. In A. Raine, P.A. Brennan, D.P. Farrington & S.A. Mednick (eds.), Biosocial Bases of Violence (pp. 145–61). New York: Plenum. Rasanen, P., Hakko, H., Isohanni, M. et al. (1999). Maternal smoking during pregnancy and risk of criminal behavior among adult male offspring in the Northern Finland 1966 birth cohort. American Journal of Psychiatry, 156, 857–62. Reiss, A.J. & Farrington, D.P. (1991). Advancing knowledge about co-offending: results from a prospective longitudinal survey of London males. Journal of Criminal Law and Criminology, 82, 360–95. Robins, L.N. (1979). Sturdy childhood predictors of adult outcomes: replications from longitudinal studies. In J.E. Barrett, R.M. Rose, & G.L. Klerman (eds.), Stress and Mental Disorder (pp. 219–35). New York: Raven Press. Robins, L.N. (1992). The role of prevention experiments in discovering causes of children’s antisocial behavior. In J. McCord & R.E. Tremblay (eds.) Preventing antisocial behavior (pp. 3–18). New York: Guilford Press. Salekin, R.T., Leistico, A-M.R., Trobst, K.K. et al. (2005). Adolescent psychopathy and the interpersonal circumplex: expanding evidence of a nomological net. Journal of Abnormal Child Psychology, 33, 445–60. Stern, S.B. & Smith, C.A. (1995). Family processes and delinquency in an ecological context. Social Service Review, 69, 705–31. Sullivan, E.A. & Kosson, D.S. (2006). Ethnic and cultural variations in psychopathy. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 437–58). New York: Guilford. Thornberry, T.P., Huizinga, D. & Loeber, R. (1995). The prevention of serious delinquency and violence: implications from the program of research on the causes and correlates of delinquency. In J.C. Howell, B. Krisberg, J.D. Hawkins & J.J. Wilson (eds.), Sourcebook on Serious, Violent and Chronic Juvenile Offenders (pp. 213–37). Thousand Oaks, CA: Sage. Weiler, B.L. & Widom, C.S. (1996). Psychopathy and violent behavior in abused and neglected young adults. Criminal Behavior and Mental Health, 6, 253–71. Wells, L.E. & Rankin, J.H. (1991). Families and delinquency: A meta-analysis of the impact of broken homes. Social Problems, 38, 71–93. Werner, E.E. & Smith, R.S. (1982). Vulnerable but Invincible: A Longitudinal Study of Resilient Children and Youth. New York: McGraw-Hill. West, D.J. & Farrington, D.P. (1973). Who Becomes Delinquent? London: Heinemann. Widiger, T. (1998). Psychopathy and normal personality. In D.J. Cooke, A.E. Forth, & R.D. Hare (eds.), Psychopathy: Theory, Research, and Implications for Society (pp. 47–68). Dordrecht, Netherlands: Kluwer. Widom, C.S. (1989). The cycle of violence. Science, 244, 160–6. Widom, C.S. & Ames, M.A. (1994). Criminal consequences of childhood sexual victimization. Child Abuse and Neglect, 18, 303–18. Wikstr¨om, P-O.H. (1985). Everyday Violence in Contemporary Sweden. Stockholm: National Council for Crime Prevention.

CHAPTER 20

A Psychoanalytic View of the Psychopath J. Reid Meloy University of California, San Diego, USA

and Andrew Shiva John Jay College of Criminal Justice, City University of New York, USA

We are just beginning to understand the brain of the psychopath. His mind is another matter. Recent neuroimaging research has begun to functionally map the abnormalities of the psychopath’s brain (Kiehl et al., 2001, 2003), and such findings help us to biologically ground the clinical and forensic extremes of his behavior. But a theory of the psychopath’s mind is also important (Meloy, 1988). It guides empirical research. It puts flesh on the bone of empirical findings. It specifies the motivation and meaning of the psychopath’s behavior. And most importantly, it helps us understand his discrete experience of the world, and thus shapes our realistic perception of the risks he poses to himself and others. Freud understood the psychopath, but devoted little time and thought to investigating his mind. He wrote in 1928, ‘two traits are essential in a criminal: boundless egoism and a strong destructive urge. Common to both of these, and a necessary condition for their expression, is absence of love, lack of an emotional appreciation of (human) objects’ (p. 178). We define the psychopath’s personality nearly 80 years later in essentially the same twofold manner: his pathological narcissism and his cruel aggression. There is also a general recognition that both of these characteristics are fueled by an absence of emotional attachment to others: the bond that keeps most people from hunting those whom they love. These central traits of the psychopath are also empirically measured in contemporary science through the use of the Psychopathy Checklist-Revised (PCL-R; Hare, 2003), which has identified two factors in the construct of psychopathy, interpersonal/affective deficiencies and social deviancy. The current of psychoanalysis runs deep in our scientific understanding of the psychopath, and since we are all products of our history, it begins with his early development.

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

336

VOLUME I: DIAGNOSIS AND TREATMENT

ATTACHMENT, AROUSAL AND ANXIETY The ‘house of psychopath’ is constructed on a foundation of no attachment, underarousal and minimal anxiety. These appear to be necessary, related, but insufficient characteristics that provide certain biological predispositions for the development of the psychopathic character. Attachment is a biologically based, species-specific behavioral system which serves the survival of the infant by maintaining the closeness of the caretaker. First conceptualized and investigated by the British psychoanalyst John Bowlby and his colleagues (Robertson & Bowlby, 1952), it is deeply rooted in mammals, but absent in reptiles. The human infant first expresses his object-seeking through sucking and crying, behaviors which maintain his physiological balance by obtaining warmth, touch and food. During the first few months of life, this proximity seeking becomes more object specific and emotionally refined as the infant attaches most readily to his mother, and cries when she deserts him while in a state of need, even if it is momentary. It is during this time when object permanence is observed: the infant can anticipate the presence of an object that was just perceived, and squeals with delight when peek-a-boo is played; or when shown a photograph of mother in her absence, will react emotionally to an external image that is also found in the child’s mind. As psychoanalysts, we infer that this object representation can be held in the child’s mind as a memory for the first time, and is one manifestation of attachment. Attachment is often defined as a strong affectional bond in both children and adults. It was extensively researched during the last half century because it can be relatively easily measured: proximity seeking to an object, distress when the object leaves, and certain characteristic behaviors when the object returns. It is a stable characteristic in both children and adults, and most human beings with the requisite biology and loving, dependable parents will grow up to be able to form secure attachments throughout their lifespan (Cassidy & Shaver, 1999). Pathologies of attachment, however, have been identified and measured: they are typically labeled fearful, preoccupied, disorganized and dismissive (Meloy, 2002). Most salient to the psychopath’s mind is the latter pathology, characterized by behavior that indicates a chronic emotional detachment from others. Bowlby (1969) regarded the elements of detachment to be apathy, self-absorption, preoccupation with nonhuman objects and no displays of emotion. He initially described it as ‘affectionless psychopathy’ (Bowlby, 1944) in a sample of juvenile thieves, and believed it was caused by constant maternal rejection. Bender (1947), referring to a child inpatient sample at Bellevue Hospital, regarded emotional deprivation during infancy as a causal factor of ‘psychopathic behavior disorder in children’ (p. 361). Research supports that this pathology of attachment is correlated with conduct disorder and antisocial personality disorder (Allen, Hauser & Borman-Spurrell, 1996). Bartholomew (1997) found that dismissive individuals have a positive perception of self and a negative perception of others, and have managed rejecting parents by distancing and becoming selfreliant, inoculating themselves against the devaluation they have learned to expect. Fonagy (1999) argued that weak bonding and the dismissal of objects is a risk factor for violent criminality because there is an absence of an ability to ‘mentalize’: to conceive of the other as having a separate, unique mind. Raine, Brennan and Mednick (1997) demonstrated in a large cohort of Danish adult males that birth complications and maternal rejection during the first year of life predisposed them to the early onset and sustained patterns of violent criminality. Gacono and Meloy (1994) found in multiple samples of antisocial children,

A PSYCHOANALYTIC VIEW OF THE PSYCHOPATH

337

adolescents and adults that the texture response, a Rorschach measure of attachment, was less frequent than normals. Meloy (1988) described this measure as a somatosensory analog for early skin contact with the mother, the first means of affectional relatedness and perhaps the genesis of secure attachment, albeit missing in the psychopath. The second corner of the foundation is the psychopath’s underarousal, particularly to punishment. Hare (1970) conducted the early work on this phenomenon, which demonstrated peripheral autonomic hyporeactivity to aversive events. The direct measure utilized in these experiments was skin conductance, or galvanic skin response. His work has been replicated by other researchers throughout the world (Raine, 1993), and has stimulated a most intriguing body of work which has found that habitual criminals are ‘chronically cortically underaroused’ (Raine, 1993). The combined measures of cortical underarousal include three variables – slow wave (theta) EEG activity, low resting heart rate and poor skin conductance – and appear to have a predictive power that can override the influence of the environment, especially when the latter is considered normal or ‘good enough’ (Winnicott, 1965). Subsequent research also suggests a link between corpus callosum abnormalities and associated behavioral symptoms, such as lack of remorse and social closeness, and neurological responses, including reduced heart rate and skin conductance (Raine et al., 2003). Low levels of cortical arousal – which have nothing to do with intelligence – have also been implicated in research with children and adolescents who display ‘callous-unemotional’ traits and represent about one-third of children diagnosed with childhood-onset conduct disorder (Frick et al., 2003). Such children evidence thrill-seeking and fearlessness (Frick et al., 2003), show deficits in responding to negative stimuli (Frick et al., 2003), habituate more easily to distress in others (Kimonis et al., 2005), and show lower autonomic reactivity to negative emotional stimuli (Blair, 1999). This unique temperamental style may predispose to psychopathy in adulthood, but this has yet to be demonstrated. However, heritability of these ‘callous-unemotional’ traits appears to be substantial (Viding et al., 2004). Extending their work on the relationship between chronic cortical underarousal and aggression, Raine and his colleagues (Raine, 1993; Raine, Venables & Mednick, 1997; Raine, Reynolds, et al., 1998; Scarpa et al., 1997) have published a series of longitudinal studies of a large cohort of children born on Mauritius, an island in the Indian Ocean off the east coast of Africa. This location was selected to test hypotheses in a setting removed from westernized culture and to minimize the effects of a criminogenic environment. Their longitudinal study, now in its fourth decade, continues to support the power of biological variables to predict aggression despite other potentially mediating social and environmental factors. The third corner of the foundation is minimal anxiety. Anxiety is an unpleasant feeling that usually signals danger from within or without. When it defends against other affects from a structural perspective (Freud, 1926), we refer to it as signal anxiety. When it is specifically object related, we refer to it as fear. When the feared object is patently unreasonable, we may see the patient as phobic or delusional. Anxiety emerges during development in the service of safety and survival. When an infant sees a stranger’s face for the first time, she is likely to view it with rapt attention and curiosity, especially while held in the arms of her parent. If the child is handed too quickly to the stranger, however, the infant will immediately become distressed, often triggering a reaction in the parent to recapture the infant in his arms. The distress immediately ceases, because the potential danger has subsided. Bowlby argued that the evolutionary basis of

338

VOLUME I: DIAGNOSIS AND TREATMENT

the causes of anxiety – the appearance of a stranger, actual separation, the anticipation of loss – keeps the mother in close proximity to the child and the child safe from predators. Anxiety is minimal or absent in psychopathy. Lykken (1957) first discovered this when he differentiated between secondary (anxious) and primary (nonanxious) psychopaths in his laboratory at the University of Minnesota. Blackburn (1998) in the UK has followed suit with his demarcation between the anxious, moody, withdrawn psychopath and the hostile, extraverted and low anxiety psychopath. Other laboratory and clinical studies support this finding (Gacono & Meloy, 1991; Ogloff & Wong, 1990). Most notably, in conduct disordered children, there is a strong negative relationship between ‘callous-unemotional’ traits and anxiety (Frick et al., 1999). During a recent assessment conducted by one of the authors (AS), a psychopath spent two hours completing the MMPI-2. He frequently read the items aloud, providing commentary on whether or not they bore any relevance to his life. His response to an item regarding physical altercations (item 548) is illustrative of the underarousal and minimal anxiety level often observed in psychopaths. ‘When I’ve had to defend myself, I become more calm and relaxed in a fight. My strategy is to antagonize them. I don’t have anger, I get them angry. I take emotions away from myself to handle things cooler. It’s not me being angry. I smile and laugh during the whole damn fight’. The psychopath paused, and with a chopping gesture added, ‘Take out the knees and go to work’. Chronic emotional detachment, cortical underarousal and minimal anxiety biologically anchor the foundation of the ‘house of psychopath’. These substrates manifest in adult psychopathy as a fearless and sensation-seeking lifestyle, one that is unfettered by worry or concern about the rights and feelings of others.

FAILURES OF INTERNALIZATION Although the conventional belief is that a neglectful and abusive environment is central to the development of the psychopath, research has increasingly called this into question. Marshall and Cooke (1999) found a negative curvilinear relationship between such family experiences and psychopathy. In other words, if we measure psychopathy on a unidimensional scale such as the PCL-R (Hare, 2003), as adult psychopathy increases into the mild to moderate range, we do see a historical increase in neglect and abuse while growing up. As psychopathy increases into the severe range, however, we see a decrease in neglect and abuse while growing up. In related research, Raine, Stoddard et al. (1998) found that functional deficits measured by radioactively tagged glucose activation (positron emission tomography, PET) in the brains of samples of murderers with extensive criminal histories were more pronounced among those from good rather than poor home environments. The suggestive findings of these and other studies (Raine, 1993) is that the more severe the psychopathy, the more psychobiologically rooted is the cause. Some still wonder how Louise Bundy and her husband could produce such a child as Ted Bundy, who grew up to be one of the most notorious serial murderers in criminal history; yet most do not know that the man who raised him was actually his stepfather, and his mother had been impregnated by a wayfaring stranger who briefly passed through her life when she was young (Rule, 1980) – perhaps the carrier of the bad seed. Psychological failures appear to parallel the biological anomalies of the psychopath as he matures, regardless of the quality of his parenting. These are failures of internalization, which Hartmann (1939) described as the evolutionary and phylogenetic transfer of

A PSYCHOANALYTIC VIEW OF THE PSYCHOPATH

339

functional-regulatory mechanisms from outside to inside. Piaget (1954) called this process assimilation. Failures of internalization begin with an organismic distrust of the environment and early incorporative deficiencies. Incorporation is the most developmentally primitive or early form of internalization, and is most apparent in the normal infant’s desire to take everything in through its mouth, whether mother’s nipple or a piece of lint on the floor once his pincer grasp has developed. The instinct is to suck and swallow, and then within the first year, to tear, bite, chew and swallow. If normal development proceeds, these incorporative experiences are mostly pleasurable, gratifying, predictable and physiologically stabilizing. The infant develops a basic trust of the environment (Erikson, 1950). In psychopathy, however, these incorporative failures predict subsequent problems with two kinds of internalizations: identifications and introjections. Identifications are ways in which the self or behavior are modified to increase resemblance to the object (Schafer, 1968). Introjections are internalized objects that maintain a relationship to the self and are structurally a part of the superego. Introjections are most apparent in clinical settings when a patient reports that he ‘sees’ or ‘hears’ things in his mind that are not considered a part of himself. They are subjectively experienced as ‘not-I’ (Meloy, 1985). Borderline personality disordered subjects will complain of such persecutory ‘voices’, but they are not experienced as sensory-perceptual stimuli from the outside, as one would see in a psychotic individual. In the psychopath, identifications and introjects are either absent, unavailable when wanted, or harsh and unpleasant. There is a paucity of soothing internalization experiences, and the child may come to anticipate hard, aggressive objects from the outside with which he then identifies for both adaptation and defense. These objects may be the product of real assaults from the caretakers, or they may be re-internalized projections of his own intense aggressive impulses, despite the best nurturing efforts of the parents. Freud (1936) first noted this phenomenon and called it identification with the aggressor. It is most apparent in the degree to which abused children will closely bond to their abusive parent, and their own risk of aggressing in adulthood toward their offspring. Meloy (2001) referred to this identification in psychopathy as a predator part-object, the primary internalization and core narcissistic identification of the psychopath’s grandiose self-structure (Kernberg, 1984) – which may or may not be a partial product of parental abuse. How is this clinically apparent? Psychopathic adults will often transform benign percepts during Rorschach testing into predatory ones: ‘It’s a butterfly . . . with claws’; ‘It’s a whale . . . with a shark fin’; ‘I see two carnivorous wolves . . . I wish I could see doves mating’; ‘A bat or evil moth, a furry animal that doesn’t suckle to its mom’ (Gacono & Meloy, 1994; Meloy & Gacono, 1992; Meloy, 2001). Such identifications in the real world are manifest in the psychopath’s propensity to engage in planful, deliberate and emotionless violence (Meloy, 2006); and the strong association between sadism and psychopathy (Holt, Meloy & Strack, 1999). The central motivation of the psychopath is to dominate his objects. There is no desire for affectional relating, or reciprocal altruism. He operates from within a dominance-submission paradigm, and identifies in a conflict-free manner with the predator. This prey–predator dynamic (Meloy, 1988) is most apparent in our counter-transference responses to psychopathic adults. In a large survey study (N = 584) of mental health and criminal justice professionals, Meloy and Meloy (2002) found that 77.3 % who had interviewed an adult psychopath reported a physiological reaction that was likely due to sympathetic activation of their autonomic nervous system. It was typically a dermatological response: ‘my skin was crawling’; ‘he got my hackles up’; ‘he made the hair stand up on my neck’. Other reactions included perceptual, ‘felt outside myself . . . numb’; gastrointestinal,

340

VOLUME I: DIAGNOSIS AND TREATMENT

‘stomach felt like I swallowed cement’; muscular, ‘frozen with fear’; pulmonary, ‘I couldn’t catch my breath’; and cardiovascular, ‘my heart was pounding’. These are all primitive, atavistic responses that signal danger, the anticipation of being prey to an intraspecies predator. When experienced as anger, the counter-transference is likely to be sadistic in nature (Meloy, 1988; Symington, 1980).

THE GRANDIOSE SELF AND OMNIPOTENT FANTASY Central to psychopathy is a variation of the grandiose self-structure, delineated by Kernberg (1974) in his theoretical understanding of the narcissistic personality disorder. The term grandiose self was originated by Kohut (1968), who previously employed the term narcissistic self (Kohut, 1966). The grandiose self-structure, however, is a pathological formation, not a normal developmental fixation as argued by the self psychologists. The latter group see the grandiose self as one polarity which is in a tension arc with the idealized parent imago, a normal state of development which they believe can become a developmental fixation in adulthood (Kohut, 1968). They ignore aggression. Self psychology sheds little light on psychopathy, thus the absence of any writing on this topic by the self psychologists. The grandiose self-structure has three condensed components: a real self – the actual specialness of the child; the ideal self – a fantasized image which compensates for oral rage and envy; and an ideal object – a fantasized image of a completely loving and accepting parent, often at odds with the actual behavior of the devalued real parent. Narcissistic psychopathology is fundamental to psychopathy, and the grandiose self is the cognitive and affective core of the character disorder (Meloy, 1988). The development of the grandiose self-structure – a construct which theoretically remains unconscious while filled with stable, conscious images (representations) of the self and others – is the framing, drywall and wetwork that continues the construction of the house of psychopath. The dominant idealization of the self is that of a predator, which diminishes rage and envy toward others; the dominant idealization of the object is one who will perfectly serve the interests of the psychopath, often as prey. Occasionally we will see the psychopath identify himself with certain omnipotent religious figures to advance his desires, who then also become idealized objects within his grandiose self-structure, but are consciously used to rationalize extreme aggression. A charismatic psychopath identified himself to his family as ‘Walking in Christ,’ or Christ, or the Lord. He also coerced and persuaded them to believe that God would communicate his pleasures and displeasures only through him to his family members. Over the course of thirty years he kept his family isolated and mobile, impregnated his daughters and nieces who eventually gave birth, sexually molested the minor females in his family, and physically assaulted and battered them over the years when they displeased the Lord. He eventually murdered nine of his offspring when he was faced with losing some of his children to the police and child protective services (JRM case files).

The behavioral devaluation of others, amply illustrated by this case vignette, is the means by which the psychopath maintains a stable grandiose self-structure. Unlike the narcissistic personality disorder who can nurture within himself a special fantasy for years without revealing it to anyone, the psychopath cannot do this solely with fantasy, but instead must aggressively derogate and dismiss others in order to shore up his grandiosity. Such devaluation may run the gamut from cruel teasing to torture and murder.

A PSYCHOANALYTIC VIEW OF THE PSYCHOPATH

341

PRIMITIVE INTERNALIZED OBJECT RELATIONS As Meloy (2001, p. 13) wrote, ‘when one gazes upon the psychopath, there is less there than meets the eye.’ Regardless of his IQ – intelligence is normally distributed among psychopaths (Hare, 2003) – his personality is organized at a preoedipal or borderline level. This has been empirically demonstrated in extensive research utilizing the Rorschach and various measures of object relations in more than 400 antisocial and psychopathic children, adolescents and adults, both male and female (Gacono & Meloy, 1994; Meloy & Gacono, 1998). The neurotically organized psychopath is an oxymoron. There is no tripartite structure (id, ego, superego) to the psychopath’s personality. Internalized objects remain part objects in the sense that good and bad aspects are not integrated into a whole object or representation. Conception of self and others is either good or bad, but is tenuously maintained through the use of primitive defenses so that self-representations are always enhanced and object representations are always devalued. A dyadic part-self and part-object world exists without, or because of, the absence of more mature defenses, such as repression or sublimation. This state of mind is central to the preoedipal theory of Klein (1964), Jacobson (1964) and Kernberg (1980), and is often misunderstood by those who attempt to apply a tripartite structural theory to clinical understanding of primitive object relations. Repression must be an active defense in order for there to be a differentiated ego and id, and ideal selfrepresentations must integrate with ideal object representations as an ego ideal if a mature superego is to be realized. In the psychopathic character organized at a borderline level, dyad self and object representations are either condensed in the grandiose self-structure or displaced somewhere else, often outside the self via projection or projective identification. One 34-year-old serial murderer, although both moderately psychopathic and pathologically narcissistic, could not completely rid himself of his bad objects. He was clinically depressed and had very low self-esteem. He had abducted, raped and killed two young women and readily referred to the ‘sick fuck’ part of himself that committed these acts. He hated his mother owing to her abandonment of him and her drunken promiscuities with many men. He selected intoxicated victims his mother’s approximate age when she left him and reported rape fantasies toward his mother when he was 13 or 14 years old. He believed he should be executed – he was subsequently sentenced to death – and wished his father had killed him when he beat him as a boy (Meloy, 2001, p. 14).

SUPEREGO ABNORMALITIES Without attachment or anxiety, identifications or introjects that carry with them certain guides to behavior, are weakly cathected or nonexistent. With such failures of internalization that often begin with imitation of the parents’ behaviors, but then expand to include family, school and community norms and rules, there is a failure to internalize values. The psychopathic adult is a valueless person. The only vestiges of conscience in the psychopathic character are best described by Jacobson (1964) as sadistic superego precursors, which she defined as projected aspects of early persecutory objects, attributed to others to deny aggression in the midst of frustration. Kernberg (1984) defined this first superego layer as one of six levels of superego pathology. Such precursors in the child psychopath are most evident in his callous-unemotional traits

342

VOLUME I: DIAGNOSIS AND TREATMENT

(Frick, 1998), which have been empirically associated with impaired conscience. Psychopathic children are less distressed by the negative effects of their behavior on others (Frick et al., 2003); they show impaired moral reasoning and empathic concern (Blair, 1999); and they have difficulty recognizing expressions of sadness in faces and vocalizations of other children (Stevens, Charman & Blair, 2001) as well as facial expressions of fear (Blair et al., 2001) and, at times, disgust (Kosson et al., 2002). Sadism, the experience of pleasure through the dominance and suffering of another, is most clinically evident in childhood cruelty toward animals, particularly domestic pets. The infliction of suffering is the child’s attempt to defend against his own helplessness through the exercise of omnipotent control over another object. Felthous and Kellert (1986) demonstrated a significant correlation between the abuse of animals in childhood and protean violence in adulthood. In a more recent study, Gleyzer, Felthous and Holzer (2002) showed that a history of animal cruelty is significantly associated with an adult diagnosis of antisocial personality disorder and polysubstance abuse. Various measures of sadism have also been shown to be strongly associated with psychopathy (Holt, Meloy & Stack, 1999).

AFFECTS The psychopath lives in a presocialized emotional world (Meloy, 1988, 2001). He has a range and depth of feeling that is similar to that of a young toddler prior to his sustained interaction with peers. Consciously felt emotions include excitement, frustration, rage, boredom, envy, dysphoria and shame. Such feelings do not require whole-object relatedness wherein both self and others are conceived as whole, separate and meaningful individuals. Such emotions are related to part objects, or self objects in Kohutian (1968) terms, and are felt quickly, expressed coarsely and dissipated rapidly. This process, which is empirically referred to as modulation of affect, remains the same into adulthood. Psychopathic men typically modulate affect like five-to-seven-year-old boys (Gacono & Meloy, 1994). Kernberg (1974) noted important differences between the feelings supporting the pathological narcissism of the adult and the normal narcissism of the toddler: angry efforts to control his mother and to keep himself the center of attention have a far more realistic quality than the adult narcissist; the toddler’s sensitivity to criticism and strong need to be admired and loved coexist with spontaneous expressions of genuine love and gratitude toward the object, and a clear willingness to trust and depend on the object even during the first year of life, features which are absent in the adult narcissist; a child’s narcissism is related to the demand for the satisfaction of real needs, while an adult narcissist’s demands are excessive, never fulfilled, and secondary to the internal destruction of such received supplies from others; the warm quality of the child’s self-centeredness is in striking contrast to the coldness and aloofness of the adult narcissist and his contempt and devaluation of others; and the developing child, despite his fantasies of power, wealth and beauty, does not believe that he is the ‘exclusive owner of such treasures’ (p. 220), as one sees in the adult narcissist. What is emotionally absent in the psychopath is most important. More mature feelings that require whole-object relatedness and a capacity for secure attachment are missing. These include anger, fear, guilt, depression, sympathy, gratitude, empathy, remorse, sadness, loneliness and reciprocal joy – emotions that are broad, deep and complex. Instead, the emotional life of the psychopath centers on his internal management of envy (Kernberg, 1984) and shame (Kohut, 1968), two affects that often precede intentional destruction of

A PSYCHOANALYTIC VIEW OF THE PSYCHOPATH

343

the object in real life. The damaged object diminishes envy since there are no longer any qualities worth possessing; the damaged object diminishes shame since it can no longer threaten as a source of humiliation.

AGGRESSION Psychopathic individuals do not struggle with tensions of ego-dystonic aggression, since the impulse to aggress is either immediately acted out, or remains a source of aggressive fueling of the grandiose self-structure without conflict or ambivalence. Rorschach research has counter-intuitively found that antisocial and psychopathic individuals at all ages do not see percepts engaging in aggression as often as normals. They do, however, produce more aggressive objects with which they identify (Gacono & Meloy, 1994). Empirical research has established that psychopaths engage in two modes of violence more frequently than other nonpsychopathic criminals (Meloy, 2006). Affective violence, characterized by an emotional reaction to an imminent threat, is common among psychopaths, especially in the face of immediate frustration or humiliation. Predatory violence, characterized by a lack of emotion, careful planning and preparation, and the lack of autonomic arousal, is also frequent among psychopaths, and is emblematic of the homicides and sexual homicides which a few of them commit (Woodworth & Porter, 2002; Porter et al., 2003).

CONCLUSIONS A clinically based theory of the psychopathic mind is beginning to be delineated through a psychoanalytic understanding of his chronic emotional detachment, cortical underarousal, minimal anxiety, failures of internalization, grandiose self-structure, primitive object relations, sadistic superego precursors, narcissistically defined affects and modes of aggression. He remains a frightening member of our species, present in all walks of life. Understanding the motivation and meaning of his behavior helps our community and society to manage the risks he poses toward others.

NOTE This work is funded by a grant from Forensis, Inc. (www.forensis.org).

REFERENCES Allen, J., Hauser, S. & Borman-Spurrell, E. (1996). Attachment theory as a framework for understanding sequelae of severe adolescent psychopathology: an 11-year follow-up study. Journal of Consulting and Clinical Psychology, 64, 254–63. Bartholomew, K. (1997). Adult attachment processes: individual and couple perspectives. British Journal of Medical Psychology, 70, 249–63. Bender, L. (1947). Psychopathic behavior disorders in children. In R. Lindner & R. Seliger (eds.), Handbook of Correctional Psychology (pp. 360–77). New York: Philosophical Library.

344

VOLUME I: DIAGNOSIS AND TREATMENT

Blackburn, B. (1998). Psychopathy and personality disorder: implications of interpersonal theory. In D. Cooke, A. Forth & R. Hare (eds.), Psychopathy: Theory, Research and Implications for Society (pp. 269–302). London: Kluwer. Blair, R. (1999). Responsiveness to distress cues in the child with psychopathic tendencies. Personality and Individual Differences, 27, 135–45. Blair, R, Colledge, E. Murray, L. & Mitchell, D. (2001). A selective impairment in the process of sad and fearful expressions in children with psychopathic tendencies. Journal of Abnormal Child Psychology, 29, 491–8. Bowlby, J. (1944). Forty-four juvenile thieves: their characters and homelife. International Journal of Psychoanalysis, 25, 121–4. Bowlby, J. (1969). Attachment and Loss, Volume 1: Attachment. New York: Basic Books. Cassidy, J. & Shaver, P. (eds.) (1999). Handbook of Attachment. New York: Guilford Press. Erikson, E. (1950). Childhood and Society. New York: Norton. Felthous, A. & Kellert, S. (1986). Violence against animals and people: is aggression against living creatures generalized? Bulletin of the American Academy of Psychiatry and the Law, 14, 55–69. Fonagy, P. (1999). Attachment, the development of the self, and its pathology in personality disorders. In J. Derksen, C. Maffei & H. Groen (eds.), Treatment of Personality Disorders (pp. 53–68). New York: Kluwer Academic/Plenum. Freud, S. (1926). Inhibitions, Symptoms, and Anxiety. Standard Edition, XX. London: Hogarth Press. Freud, S. (1928). Dostoevsky and Parricide. Standard Edition, XXI. London: Hogarth Press. Freud, A. (1936). The Ego and the Mechanisms of Defense. New York: International Universities Press (1966, revised edition). Frick, P. (1998). Conduct Disorders and Severe Antisocial Behavior. New York: Plenum. Frick, P., Cornell, D., Barry, C. et al. (2003). Callous-unemotional traits and conduct problems in the prediction of conduct problem severity, aggression, and self-report of delinquency. Journal of Abnormal Child Psychology, 31, 457–70. Frick, P., Lilienfeld, S., Ellis, M. et al. (1999). The association between anxiety and psychopathy dimensions in children. Journal of Abnormal Child Psychology, 27, 381–90. Gacono, C.B. & Meloy, J.R. (1991). A Rorschach investigation of attachment and anxiety in antisocial personality disorder. Journal of Nervous and Mental Disease, 179, 546–52. Gacono, C.B. & Meloy, J.R. (1994). The Rorschach Assessment of Aggressive and Psychopathic Personalities. Hillsdale, NJ: Erlbaum. Gleyzer, R., Felthous, A. & Holzer, C. (2002). Animal cruelty and psychiatric disorders. Journal of the American Academy of Psychiatry and the Law, 30, 257–65. Hare, R.D. (1970). Psychopathy: Theory and Research. New York: John Wiley & Sons, Inc. Hare, R.D. (2003). The Hare Psychopathy Checklist-Revised, 2nd Edition Technical Manual. Toronto: Multihealth Systems. Hartmann, H. (1939). Ego Psychology and the Problem of Adaptation. New York: International Universities Press. Holt, S., Meloy, J.R. & Strack, S. (1999). Sadism and psychopathy in violent and sexually violent offenders. Journal of the American Academy of Psychiatry and the Law, 27, 23–32. Jacobson, E. (1964). The Self and the Object World. New York: International University Press. Kernberg, O. (1974). Further contributions to the treatment of narcissistic personalities. International Journal of Psychoanalysis, 55, 215–40. Kernberg, O. (1980). Internal World and External Reality. New York: Aronson. Kernberg, O. (1984). Severe Personality Disorders. New Haven: Yale University Press. Kiehl, K., Smith, A., Hare, R.D. et al. (2001). Limbic abnormalities in affective processing by criminal psychopaths as revealed by functional magnetic resonance imaging. Biological Psychiatry, 50, 677–84. Kiehl, K., Smith, A., Mendrek, A. et al. (2003). Temporal lobe abnormalities in semantic processing by criminal psychopaths as revealed by functional magnetic resonance imaging. Psychiatry Research: Neuroimaging, 130, 27–42. Kimonis, E., Frick, P., Fazekas, H. & Loney, B. (2005). Psychopathy, aggression, and the processing of emotional stimuli in non-referred boys and girls. Manuscript submitted. Klein, M. (1964). Contributions to Psychoanalysis: 1920–1945. New York: McGraw-Hill.

A PSYCHOANALYTIC VIEW OF THE PSYCHOPATH

345

Kohut, H. (1966). Forms and transformations of narcissism. Journal of the American Psychoanalytic Association, 14, 243–72. Kohut, H. (1968). The psychoanalytic treatment of narcissistic personality disorders: Outline of a systematic approach. Psychoanalytic Study of the Child, 23, 86–113. Kosson, D., Suchy, Y., Mayar, A. & Libby, J. (2002). Facial affect recognition in criminal psychopaths. Emotion, 2, 398–411. Lykken, D. (1957). A study of anxiety in the sociopathic personality. Journal of Abnormal and Social Psychology, 55, 6–10. Marshall, L. & Cooke, D. (1999). The childhood experiences of psychopaths: a retrospective study of familial and societal factors. Journal of Personality Disorders, 13, 211–25. Meloy, J.R. (1985). Concept and percept formation in object relations theory. Psychoanalytic Psychology, 2, 35–45. Meloy, J.R. (1988). The Psychopathic Mind: Origins, Dynamics, and Treatment. Northvale, NJ: Aronson. Meloy, J.R. (2001). The Mark of Cain. Hillsdale, NJ: The Analytic Press. Meloy, J.R. (2002). Pathologies of attachment, violence, and criminality. In A. Goldstein (ed.), Handbook of Psychology, Volume 11. Forensic Psychology (pp. 509–26). New York: John Wiley & Sons, Inc. Meloy, J.R. (2006). The empirical basis and forensic application of affective and predatory violence. Australian and New Zealand Journal of Psychiatry, 40, 539–47. Meloy, J.R. & Gacono, C.B. (1992). The aggression response and the Rorschach. Journal of Clinical Psychology, 48, 104–14. Meloy, J.R. & Gacono, C.B. (1998). The internal world of the psychopath. In T. Millon, E. Simonsen, M. Birket-Smith & R. Davis (eds.), Psychopathy: Antisocial, Criminal, and Violent Behavior (pp. 95–109). New York: Guilford Press. Meloy, J.R. & Meloy, M.J. (2002). Autonomic arousal in the presence of psychopathy: a survey of mental health and criminal justice professionals. Journal of Threat Assessment, 2, 21–33. Ogloff, J. & Wong, S. (1990). Electrodermal and cardiovascular evidence of a coping response in psychopaths. Criminal Justice and Behavior, 17, 231–45. Piaget, J. (1954). The Construction of Reality in the Child. New York: Basic Books. Porter, S., Woodworth, M., Earle, J. et al. (2003). Characteristics of sexual homicides committed by psychopathic and nonpsychopathic offenders. Law and Human Behavior, 27, 459–70. Raine, A. (1993). The Psychopathology of Crime. San Diego: Academic Press. Raine, A., Brennan, P. & Mednick, S. (1997). Interaction between birth complications and early maternal rejection in predisposing individuals to adult violence: specificity to serious, early-onset violence. American Journal of Psychiatry, 154, 1265–71. Raine, A., Lencz, T., Taylor, K. et al. (2003). Corpus callosum abnormalities in psychopathic antisocial individuals. Archives of General Psychiatry, 60, 1134–42. Raine, A., Reynolds, C., Venables, P. et al. (1998). Fearlessness, stimulation-seeking, and large body size at age 3 years as early predispositions to childhood aggression at age 11 years. Archives of General Psychiatry, 55, 745–51. Raine, A., Stoddard, J., Bihrle, S. & Buchsbaum, M. (1998). Prefrontal glucose deficits in murderers lacking psychosocial deprivation. Neuropsychiatric, Neuropsychological, and Behavioral Neurology, 11, 1–7. Raine, A., Venables, P. & Mednick, S. (1997). Low resting heart rate at age 3 years predisposes to aggression at age 11 years: evidence from the Mauritius Child Health Project. Journal of the American Academy of Child and Adolescent Psychiatry, 36, 1457–64. Robertson, J. & Bowlby, J. (1952). Responses of young children to separation from their mothers. Courr Centre International de l’Enfance, 2, 131–42. Rule, A. (1980). The Stranger Beside Me. New York: Norton. Scarpa, A., Raine, A., Venables, P. & Mednick, S. (1997). Heart rate and skin conductance in behaviorally inhibited Mauritian children. Journal of Abnormal Psychology, 106, 182–90. Schafer, R. (1968). Aspects of Internalization. New York: International Universities Press. Stevens, D., Charman, T. & Blair, R. (2001). Recognition of emotion in facial expressions and vocal tones in children with psychopathic tendencies. Journal of Genetic Psychology; Child Behavior, Animal Behavior, and Comparative Psychology, 16, 201–11.

346

VOLUME I: DIAGNOSIS AND TREATMENT

Symington, N. (1980). The response aroused by the psychopath. International Review of PsychoAnalysis, 7, 291–8. Viding, E., Blair, R., Moffitt, T. & Plomin, R. (2004). Psychopathic syndrome indexes strong genetic risk for antisocial behavior in 7 year-olds. Journal of Child Psychology and Psychiatry and Allied Disciplines, 45, 1–6. Winnicott, D. (1965). The Maturational Processes and the Facilitating Environment. New York: International Universities Press. Woodworth, M. & Porter, S. (2002). In cold blood: characteristics of criminal homicides as a function of psychopathy. Journal of Abnormal Psychology, 111, 436–45.

CHAPTER 21

Women and Girls with Psychopathic Characteristics Tonia L. Nicholls University of British Columbia, Canada

Candice L. Odgers University of California Irvine, USA

and David J. Cooke Douglas Inch Centre and Glasgow Caledonian University, United Kingdom

Since its inception, descriptions of psychopathy have included references to females with the disorder (e.g., Cleckley, 1988; Pinel, 1801); however, early clinical descriptions of females with psychopathic traits were sparse. For instance, Cleckley (1988) referred to just two female case studies. Similarly, preliminary efforts to measure psychopathy included discussions of gender differences and similarities, but women always have been considered as an afterthought or included as a footnote (PCL, Hare, 1980; PCL-R, Hare, 1991; PCL:SV, Hart, Cox & Hare, 1995). The exclusion of women is chiefly evident when one considers the proportion of research attention devoted to males versus females (see Hare, 2003). Overall, there has been a lack of both theoretical (Forouzan & Cooke, 2005) and empirical examination of psychopathy in women (Nicholls et al., 2005; Verona & Vitale, 2006) and girls (Odgers, Moretti & Reppucci, 2005); yet, the assumption is that assessment tools should function equally well within female and male populations (Forth, Kosson & Hare, 2003; Hare, 2003). This chapter will examine the utility of extending psychopathy, both as a construct and as a risk assessment tool, into female populations. Although there is good reason to consider the relevance of psychopathy to females, research and clinical experience with related personality disorders and related traits provide evidence to expect marked gender differences in the manifestation and prevalence rates of psychopathy among females. Over the last decade, there has been both a lateral and downward extension of psychopathy to women and girls. Much of the momentum behind the recent focus on psychopathy among females reflects persuasive evidence among adult male populations that psychopathy is associated with aggression and criminal offending (for a review, see Douglas, Vincent The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

348

VOLUME I: DIAGNOSIS AND TREATMENT

& Edens, 2006). For the most part, an ‘add and stir’ approach has been adopted when considering the extension of psychopathy to females. Instruments calibrated for use with male forensic populations, such as the Psychopathy Checklist-Revised (PCL-R, Hare, 1991, 2003) and Psychopathy Checklist: Youth Version (PCL:YV, Forth, Kosson & Hare, 2003) have been extended into female populations, with little theoretical or conceptual integration of what we know about the role of gender in personality, personality disorders (PDs), development or clinical assessment contexts. As a result, the field continues to grapple with basic conceptual and assessment issues. It is necessary, therefore, to take a step back and evaluate whether psychopathy is a useful theoretical and clinical construct within female populations. In particular, we need to demonstrate whether or not psychopathy is manifested distinctly across gender and evaluate how the cardinal features of this disorder may be expressed differently among females versus males and what that means for measurement and assessment with females. The first section of this chapter will apply what is known about gender differences in relation to other PDs, risk exposure and gender-role socialization to understanding the expression of psychopathy among females. Next, the small, albeit growing, body of research assessing psychopathy in females via the PCL and its descendents (PCL-R, PCL:SV, PCL:YV) will be reviewed; with an eye toward detecting measurement bias and the potential for construct drift. Finally, we consider whether psychopathy may be a useful risk marker for serious forms of aggression and antisocial behavior among women and girls, and whether such information can inform decision making in clinical-forensic settings. Although psychopathy has become a dominant personality construct in risk assessments with men there is considerable reluctance to apply the stigmatizing and controversial label to females (e.g., Laishes, 2002). With ethical considerations and empirical limitations in mind, we will conclude with recommendations for future research and clinical practice.

QUESTION I: IS THERE A FIT BETWEEN THE UNDERLYING THEORY OF PSYCHOPATHY AND PERSONALITY FEATURES IN FEMALES? Psychopathy appears to be a disorder found primarily in men (Hare, 2003; Nicholls et al., 2005), though an appreciation of the reasons for this gender gap are lacking (Cale & Lilienfeld, 2003). Several scholars have postulated that the current primary operationalization of psychopathy (i.e., PCL-R, Hare, 2003 and its variants) may not necessarily apply to women (Forouzan & Cooke, 2005) and that gender equivalence must be demonstrated, not assumed (Nicholls & Petrila, 2005; Vitale & Newman, 2001a). Psychopathy is a highly pejorative diagnosis with potentially severe consequences for the individual assessed. The possibility that the diagnosis of psychopathy is gender-biased is highly controversial and would constitute a major defect in that the diagnosis would contribute to, rather than alleviate, misdiagnosis and treatment errors (also see Widiger & Spitzer, 1991). Forouzan and Cooke (2005) similarly argued that a failure to consider gender might give rise to human rights concerns given the potentially serious implications of the diagnosis for civil rights (e.g., prolonged detention, exclusion from treatment). Conversely, a failure to identify individuals with the disorder could place others (i.e., the individual’s family members, community

WOMEN AND GIRLS WITH PSYCHOPATHIC CHARACTERISTICS

349

members) at substantial risk. At a theoretical rather than a practice level, the extent that a measure or diagnosis has inconsistent meaning across the genders makes it difficult to evaluate the meaningfulness of the construct (Sue, 1999, cited in Verona & Vitale, 2006) by limiting our understanding of the disorder and its etiology. In short, an examination of gender equivalence is essential to ensure that clinicians are meeting legal and ethical standards (e.g., when making recommendations to tribunals) and to advance theory and practice (e.g., reduce (re)offending, increase treatment responsivity, improve mental health). There are a number of reasons why we may expect to see gender differences in the core traits or expression of the disorder. The following section outlines four of the primary ways in which gender may matter when extending psychopathy to females.

Gender Differences are Common in the Manifestation of Personality Traits and Personality Disorders Scholars have long asserted that there are gender differences in the diagnostic rates of several personality disorders (PDs) and potential gender bias in the diagnosis of mental disorders (Ford & Widiger, 1989; Warner, 1978; Widigier & Spitzer, 1991). Gender plays a role in the expression (Goldstein et al., 1996) and identification of personality pathology (Elbogen et al., 2001; Lidz, Mulvey & Gardner, 1993; Skeem et al., 2005); there is no reason to suggest that psychopathy would be different. Personality disorders are expressed through interpersonal interactions, displays of affect and behaviors. Research points to important gender differences in manifestations of personality pathology and personality traits; it provides insight into how biological and psychosocial gender differences might alter the appearance of psychopathic characteristics in females versus males. Moreover, there are well-documented gender differences from epidemiological (e.g., Kessler et al., 1994) and clinical research with other disorders, that lend support to the hypothesis that the prevalence – and expression – of psychopathic traits may vary by gender. From an early age, females are found to show more empathy, accuracy in detecting facial expressions and a more developed ‘theory of mind’ than males (for a review see Baron-Cohen, 2002); while males have been found to have higher rates of sensation-seeking and risk-taking behavior (Rosenblitt et al., 2001), with girls consistently demonstrating a greater ability to regulate attention and impulses from an early age (for a meta-analysis see Else-Quest et al., 2006). As such, the higher prevalence rates of externalizing disorders among males come as no surprise. For instance, conduct disorder in youths is considerably less prevalent in girls than in boys; indeed, these gender differences extend into adulthood when antisocial personality disorder (APD) remains more common in men than in women (Cale & Lilienfeld, 2002a; Robins, Tipp & Przybeck, 1991; Silverthorn, Frick & Reynolds, 2001). Conversely, borderline personality disorder (BPD) is more commonly diagnosed in women than in men at a 3:1 ratio (Bjorklund, 2006). Paris (1997) noted that 80 % of BPDs are female and 80 % of APDs are male. Differences in the gender distribution of PDs have been attributed to: (i) the theoretical construction of the disorders (i.e., the superficial imposition of gender-specific characteristics associated with specific disorders); (ii) insufficiently sensitive criteria; (iii) meaningful differences in the latent variables (i.e., true gender differences); and (iv) gender bias on the part of assessors (e.g., Cale & Lilienfeld, 2002a; Ford & Widiger, 1989; Widiger & Spitzer, 1991). It is noteworthy that many tests of both personality and personality pathology (e.g.,

350

VOLUME I: DIAGNOSIS AND TREATMENT

Millon Clinical Multiaxial Inventory (MCMI), Minnesota Multiphasic Personality Inventory (MMPI), NEO Personality Inventory) take gender into account when they are scored, it is thus likely that pathology of personality will be gender linked. This is because a person’s gender influences their responses to test items, and presumably, this reflects the expression of their disorder. There are no a priori reasons to suspect that gender will not influence the expression of psychopathy. Indeed, it remains to be seen to what degree apparent gender differences in psychopathy reflect actual differences in the prevalence of the disorder and/or manifestation of the disorder as opposed to variations in raters’ perceptions of symptoms. Little relevant research is currently available.

Gender could be Relevant to Prevailing Theories and Etiological Explanations for the Disorder Whether one adheres to the view that psychopaths are different ‘by design’ (i.e., evolutionary biological differences, e.g., Lalumiere, Harris & Rice, 2001) or that the syndrome is a virulent PD reflecting severely disturbed moral development (e.g., Blackburn, 2006; Fowles & Dindo, 2006; Patrick, 2006), gender would seem to be a relevant consideration. In general, behavioral, cognitive and personality differences observed across the genders are assumed to be determined by both genetic and environmental factors. Indeed, there is a considerable body of research documenting the genetic mechanisms and biological substrates that are involved in sexual differentiation and behavioral dimorphism. These differences range from trajectories of brain development across the genders (e.g., amount of gray matter) to specific cognitive functions that are linked to the X chromosome (for a review see Craig, Harper & Loat, 2004). While research from animal models has supported a relationship between hormones (e.g., testosterone) and aggression, research with humans has produced inconsistent results. For example, meta-analyses summarizing the relationship between testosterone and aggression have highlighted weak to nonexistent effects across studies (see Archer, 1991; Book, Starzyk & Quinsey, 2001). Important, although indirect effects have been found for the hypothalamus–pituitary–adrenal (HPA) axis on the onset and maintenance of persistent and violent antisocial behavior in young boys, although the role of the HPA axis as a cause, consequence or mediator of aggression is not entirely clear (for a review see Ramirez, 2003). The picture is likely more complicated, however, as researchers have begun to document the importance of gene–environment interactions in antisocial behavior (Caspi et al., 2002; Moffitt, 2005), suggesting that research on the interplay between hormones and behavior has ‘miles to go’ as the presence or absence of environmental stimuli may be critical to understanding whether biological substrates are indeed linked to aggression – and moreover, if these relationships are responsible for observed differences between males and females. Regardless of the inconsistent research at this point, it is likely that genes on the sex chromosomes have evolved along divergent paths due to evolutionary and socialization pressures, and as such are likely to influence behavior, both directly and indirectly, through the control of hormones on brain maturation and other biologically plausible mechanisms (Craig et al., 2004). Even without considering the complicating factor of gender, the etiology of psychopathy and developmental aspects of the disorder are poorly understood. Because the lion’s share of psychopathy research has been conducted on males, we know especially little about the

WOMEN AND GIRLS WITH PSYCHOPATHIC CHARACTERISTICS

351

etiology of the disorder and the characteristics of women who meet diagnostic criteria; the same is true of girls. A consideration of the developmental literature suggests that the mechanisms or pathways leading to conduct problems (among children and adolescents) and personality dysfunction (among adults) are invariant across gender but are likely acting on vulnerabilities that differ across sex. For example, when discussing the role of gender in one of the most prominent theories of the developmental course of antisocial behavior, Moffitt (2004) asserts that females on the life-course persistent (LCP) pathway have the same pattern of childhood social, familial and neuro-developmental deficits that have been documented among their male LCP counterparts. Given the lower rates of neuro-developmental deficits in girls, however, the process of cumulative continuity operates to ensure that fewer females than males are on the LCP pathway (Moffitt & Caspi, 2001a; Moffitt et al., 2001b; Odgers et al., submitted). Some researchers, however, have challenged the notion that the mechanisms are the same across the genders; arguing instead that females require a theory of their own (Silverthorn & Frick, 1999; Silverthorn, Frick & Reynolds, 2001). Despite the ongoing debate in this area, there is virtual consensus regarding the need to assemble the type of prospective longitudinal data required to understand the role of gender differences in developmental patterns of antisocial behavior and related personality traits. With respect to psychopathy, these types of large-scale epidemiological studies (with adequate numbers of females – or indeed males – and developmentally appropriate measures) simply do not exist at this time. As such, many of the conclusions made regarding etiology have been derived from selective high-risk samples, which are likely to have limited value when trying to understand the developmental course of the disorder.

Sociocultural Determinants Have a Hand in the Expression of Diseases and Mental Disorders Phenotypic variations in psychopathy are anticipated across age, gender, ethnic and cultural groups (see generally, Patrick, 2006). Because the features that comprise the disorder have been derived primarily from scientific work with adult males, it remains to be seen if current descriptions are the most appropriate indicators of psychopathy in women and girls. The extension of psychopathy to girls is further complicated by the fact that features of the disorder are a part of normal adolescence (e.g., egocentricity, Hart, Watt & Vincent, 2002; Seagrave & Grisso, 2002). Gender differences are anticipated given that sociocultural determinants are widely recognized to influence the expression of diseases and mental disorders (Bjorklund, 2006; Draguns & Tanaka-Matsumi, 2003; Marsella, 1998). Consider, for instance, the cultural gap in disorders such as narcissism, borderline and schizoid personality disorders. Akhtar (1995, cited in Bjorklund, 2006) proposed cultural disparities in the prevalence of mental disorders might reflect varying child-rearing practices in combination with more or less permissive social mores. Societies with freer expression of affect, individuation and spirituality are known to have more flagrant and overt borderline and narcissistic individuals in comparison with more reserved and less permissive societies where muted manifestations of the same disorders are found. In much the same way, gender-role socialization is hypothesized to influence the expression of psychopathy and, thus, existing criteria might not be sensitive enough to identify women and girls with the disorder. Many experts have argued that psychopathic characteristics are at greater opposition with feminine than with masculine socialization (Cale & Lilienfeld, 2002b; Verona & Vitale, 2006; Vitale

352

VOLUME I: DIAGNOSIS AND TREATMENT

& Newman, 2001b). In a manner consistent with cross-cultural differences, we may see that at the same degree of the latent trait women and girls receive lower scores on psychopathy measures (Cooke, 2001; Cooke & Michie, 1999).

Psychopathic Traits could be Expressed Differently in Females: The Risk of Misdiagnosis Hare (1991, p. 64) acknowledged that the expression of psychopathy could be different in women than in men. Like most psychological traits, psychopathy is unobserved and inferences regarding the underlying latent trait (i.e., psychopathy) must be made through the expression of manifest traits (e.g., behaviors, observable characteristics). It is possible, therefore, that although the underlying trait of psychopathy may be invariant across males and females, the manifest markers of the disorder may be differentially expressed. Biological gender differences (e.g., sex hormones) and psychosocial gender differences (e.g., genderrole socialization) alike could color the expression of psychopathy. Paris (1997) proposed that ‘the same underlying dimensions could lead to different forms of psychopathology in the two genders’ (p. 240). Similarly, Grann (2000) postulated that manipulation may be expressed as sexual seductivity in women as opposed to men who may be more inclined to use wit or superficial charm to manipulate others. Reflecting differences in gender roles and socialization, glibness/superficial charm (i.e., PCL-R item 1) in females may be less likely to be evidenced by verbal facility and entertaining conversation as it might be by exaggerated attentiveness to people in positions of power and authority. High self-regard and mastery are more stereotypically socialized in boys than in girls; thus, grandiosity might be less overt or extreme in female psychopaths (see Forouzan & Cooke, 2005; Rutherford et al., 1996; Zagon & Jackson, 1994). The last two decades have substantially increased our appreciation of gender differences in the development and manifestation of antisocial behavior and aggression in females (e.g., Crick & Grotpeter, 1995; Eagly & Steffen, 1986; Moretti & Odgers, 2006) (nature, target, location of aggression, i.e., likelihood of it being reflected on official records). These findings suggest that while current behavioral descriptors might be relevant to females those traits might be evident only when females demonstrate extreme levels of the characteristics (e.g., PCL-R item 18, juvenile delinquency). Indeed, there is ongoing debate regarding whether antisocial behaviors are core features of the disorder rather than merely secondary features (Cooke & Michie, 2001; Hare, 2003). Experts argue that the weight of the empirical and conceptual evidence is that antisocial behavior is of secondary importance and is not a core part of the disorder (Cooke, Michie & Skeem, 2007; Skeem & Cooke, 2006). It is also possible that those within high-risk contexts may present with features that are indicative of psychopathy, despite the fact that they do not truly possess psychopathic traits. For instance, blunted affect overlaps with the core features of psychopathy, however, this is a response that is often evident in victims of abuse and violence whereby children ‘turn off’ their emotional response as an adaptive coping mechanism (Porter, 1996). It is possible, therefore, that individuals may present as psychopathic on Cooke and Michie’s Factor 2 (affective items) but the traits would not be linked in the same way to the latent construct or have the same etiological origins or treatment implications. In forensic settings we know the rates of victimization are extremely high (and it takes severe forms), this is particularly

WOMEN AND GIRLS WITH PSYCHOPATHIC CHARACTERISTICS

353

true of females; thus, for assessments it may be helpful to be able to distinguish amongst different processes which result in equifinality of expression of symptoms. Other symptom complexes may be affected by gender-linked variations in underlying mechanisms. Forouzan (2003) has conducted some of the only work related to interpersonal symptoms of psychopathy in females. Results of her preliminary qualitative research reflecting clinicians’ evaluations of psychopathy in women provide insights into whether there are gender differences in the core traits of the disorder. She found that most features of (male) psychopathy could be identified in females. The clinicians (N = 25) in her study reported that sexuality in female psychopaths may be used as a means of manipulating others for financial gain. Research on indirect or relational aggression, which is more common than overt forms of aggression among females, suggests that females may manipulate friendships and peers as a vehicle for harming others (Crick & Bigbee, 1998; Paquette & Underwood, 1999). To conclude this section we consider that there are a number of compelling reasons to argue that the nature of, and expression of, psychopathy is likely to vary across gender.

QUESTION II: HOW SHOULD PSYCHOPATHY IN FEMALES BE MEASURED? The assumption underlying current assessment practices for psychopathy among women is that the instruments should function equally well for females and males (Hare, 2003; Webster, 1999); that is, it is assumed that gender plays, at most, a limited role in the expression of the disorder and its relevance to associated antisocial behaviors. Yet, as previously mentioned, research and clinical experience with other PDs (Paris, 1997; Widiger & Spitzer, 1991), as well as temperament and personality (Else-Quest et al., 2006), lead us to anticipate sex-differentiated manifestations of psychopathy. It is no surprise, therefore, that the assessment of psychopathy among women is plagued by incongruent findings (Vitale et al., 2002), ranging from research that supports the application of the PCL-R with women ‘as is’ (Bolt et al., 2004; Hare, 2003) or with minor refinements (Webster, 1999), to results that raise questions as to whether an entirely new measurement framework is required (Forouzan & Cooke, 2005). It should also be noted that there are those who dispute the existence of the construct among women and girls altogether, and hence see no need for the development of this type of assessment tool (Laishes, 2002). Over the last two decades females have become a relevant population in psychopathy research. As a result, we are beginning to learn more about how the psychopathy construct and assessment tools extend into female populations. The following section reviews what is known about the strengths and limitations of the most commonly used measure of psychopathy, the PCL-R (Hare, 1991, 2003), and highlights alternative strategies that have been proposed to incorporate gender into the psychopathy realm.

Mapping the ‘Construct Space’ for Psychopathy The PCL-R (Hare, 1991, 2003) and its derivatives (PCL:SV, Hart et al., 1995; PCL:YV, Forth et al., 2003) have provided a common metric to assess psychopathy and begin isolating the core features of the disorder. Over the last two decades there has been considerable debate

354

VOLUME I: DIAGNOSIS AND TREATMENT

regarding the underlying factor structure of the PCL-R; with the original 2-factor structure giving way to a more differentiated 3-factor structure that excludes the antisocial component (Cooke & Michie, 2001; Jackson et al., 2002). While the debate continues regarding the exact structure of the PCL (three- versus four-factor) and, in particular, whether an antisocial facet is required, in general (Cooke et al., 2005; Cooke, Michie & Skeem, 2007; Hare & Neumann, 2006; Neumann et al., 2006; Skeem & Cooke, 2006; Vitacco, Neumann & Jackson, 2005), or a different factor structure is required for females specifically (Salekin, Rogers & Sewell, 1997), a larger issue has emerged. That is, some experts in the field have adopted the position that a ‘back to basics’ approach is required in order to more fully map the construct space of psychopathy (Cooke et al., 2005). This type of method is advocated as a means of aligning measurement schemes more closely with the original description of psychopathy and incorporating clinical insights. A ‘back to basics approach’ would involve developing and piloting a broader range of items to ensure that the construct space of psychopathy is fully mapped. Advocates of this approach argue that current assessment tools have resulted in a ‘construct drift’ whereby the most commonly used instruments, namely the PCL-R, and the construct of psychopathy have become one and the same. This type of approach is also seen as a means of creating a more dynamic means of assessing psychopathy (read one that will allow for assessments of stability and change across development) and will help to ensure that the core facets of the disorder are included in the assessment criteria. This perspective has been heralded as particularly important, but not uniquely required, for females. Given that the PCL-R originally was developed and calibrated using adult males drawn from forensic samples and, a broader (or unique) pool of items may be needed in order to tap into the core features of psychopathy among women and girls (Cooke et al., 2006; Forouzan & Cooke, 2005). There is a risk, however, that sex-typed criteria might not measure the same construct (Cale & Lilienfeld, 2002b, Schrum & Salekin, 2006; Silverthorn & Frick, 1999). Prior to exploring a ‘back to basics’ approach, it is useful to synthesize what is currently known about the functioning of psychopathy instruments among women and adolescent girls. The following section details the psychometric properties of the PCL family of instruments among females – with a focus on how this knowledge can inform the development of future assessment tools.

Psychometric Properties of the PCL-R within Female Samples In order to understand cross-group equivalence it is necessary to consider both structural and metric equivalence. The first step is to consider whether a coherent syndrome exists (i.e., a pattern of symptoms that cluster together and that can be distinguished from other clusters of symptoms) (e.g., Blashfield & Draguns, 1976; Eysenck, 1970; Kendell, 1989) and demonstrate that this is invariant across groups (e.g., Cooke, Kosson & Michie, 2001). Typically confirmatory factor analysis is used for this task. The second step is to demonstrate that there is metric equivalence. That is, to demonstrate that scores on the test represent the same level on the underlying latent trait being considered; item response methods are typically used for this task (e.g., Cooke & Michie, 1997; Embretson & Reise, 2000). (See Forouzan & Cooke, 2005 for a more complete discussion of these issues.) Studies using confirmatory factor analysis (CFA) to test coherence of psychopathy as a syndrome have produced mixed results. Among adult women, early exploratory factor

WOMEN AND GIRLS WITH PSYCHOPATHIC CHARACTERISTICS

355

analyses of the PCL-R suggested that an alternative structure may be required for women (Salekin, Rogers & Sewell, 1997). However, the Salekin sample was unique in that it comprised female jail inmates (i.e., as opposed to prison inmates), a large proportion of whom were ethnic minorities (44 %), making it difficult to draw direct comparisons with research conducted primarily with Anglo-American Canadian federal inmates (i.e., convicted offenders serving ≥2 years) (Hare, 1991). Subsequent CFA studies have generally supported a similar factor structure among women for both the PCL:SV (Skeem, Mulvey & Grisso, 2003) and PCL-R (Jackson et al., 2002; Warren et al., 2003). Results from nonclinical samples also suggested no clear sex difference on the factor structure of the PCL (Forth et al., 1996; Lilienfeld & Andrews, 1996; Wilson et al., 1999); however, due to small sample sizes and low variances in scores, the ability to test for sex differences across samples in these studies was limited. In sum, the number of factors extracted from this body of work has ranged from a one-factor solution to a four-factor solution, with sample sizes being too small to detect anything but large differences across sex (with the notable exception of Skeem et al., 2003). Similarly, CFA studies testing the factor structure of the PCL:YV across adolescent males and females have produced incongruent findings. Jones and colleagues (2006) reported no gender differences in the factor structure of the PCL:YV and recommending the use of either the four- or three-factor structure for adolescents. Again, the relatively small number of girls (N = 150) compared to boys (N = 508) in this sample, may have limited the ability to detect statistically significant differences across sex. In the PCL:YV manual, Forth and colleagues (2003) merged data from six small unpublished studies of adolescent girls and concluded that the three-factor model represented the best fit to the data; similarly Odgers (2005) found support for the fit of the three-factor model among a sample of incarcerated girls, however, concluded that the model-fit indices fell below absolute standards with exploratory factor analyses converging on a six-factor solution with no discernible factor-loading pattern. In sum, few studies to date have had an adequate number of adolescent girls to test for sex differences in the factor structure of the PCL:YV. The psychometric properties of the PCL-R among women have been assessed using both relative and absolute standards. Relative to men, lower prevalence rates of psychopathy have consistently been documented among women drawn from equivalent settings (Douglas et al., 2005; Forth et al., 1996; Nicholls et al., 2005; Vitale et al., 2002). It is important to note that such comparisons assume that raw scores represent the same level of the underlying latent trait: an assumption that has not been justified empirically, as yet. Cooke (2001) noted that on average, women score 1.8 points lower on the PCL:SV and, thus, recommended that cutoff scores might need to be re-evaluated for application to females. However, they were unable to replicate that finding in unpublished analyses and concluded that clinicians are on safest ground if they refrain from making use of psychopathy assessments numerically but, instead, use them to synthesize and structure clinical decision making (Cooke & Michie, 2006). In order to evaluate whether mean PCL-R scores can be compared across sex, researchers have applied item response theory (IRT), which can be used to test whether the PCL items evidence bias across sex. In one of the largest IRT studies to date, Bolt and colleagues concluded that although the PCL provided slightly more information for adult male (versus female) criminal offenders, it remained an effective instrument based on scalar equivalence across groups (Bolt et al., 2004). This analysis makes strong assumptions about which variables should be the same across gender; such assumptions require strong theoretical justification. To date, there have been only two studies comparing the item

356

VOLUME I: DIAGNOSIS AND TREATMENT

functioning of the PCL:YV across adolescent boys and adolescent girls. Vincent et al. (2006) concluded that gender-related measurement bias, or differential item functioning (DIF), existed for the majority of the PCL:YV items; indicating that boys (N = 615) and girls (N = 390) at the same level of the latent trait would have different PCL:YV total scores. The most marked gender differences were found for the affective component where girls were expected to score 2.5–3 points lower than boys with equivalent levels of the underlying trait. While Schrum and Salekin (2006) reported that the interpersonal (grandiose sense of self-worth, conning and manipulation) and affective components (callousness, lack of empathy) of psychopathy provided the most information based on their IRT analysis. They concluded that gender differences in their sample of adolescent female offenders (N = 123) mirrored what has been found with adults (i.e., girls received lower scores, discriminating items are similar to what has been found with adult males (Hare, 2003) and adolescent males (Cooke & Michie, 1997; Vincent, 2002). They cautioned that some items may be less applicable to girls (e.g., poor anger control, serious violations of conditional release) and that behavioral items in facets 3 (Lifestyle) and 4 (Antisocial) could artificially inflate scores in girls. Further research is required to determine if items function similarly or distinctly across the sexes. In sum, although relative to males, females typically score lower on the PCL, the extent to which scores can be compared across gender is still an open question. While CFA studies have provided some support for structural equivalence across sex, this research also has produced a number of incongruent findings and has been based on relatively small numbers of women and girls. Moreover, differential item functioning of the scale has been observed among women (Bolt et al., 2004), and to a greater extent among adolescent girls (Vincent et al., 2006), indicating that comparing scores across gender is premature. In absolute terms, evaluations of the psychometric properties of the PCL family of instruments among women have also been mixed. On a positive note, the interrater reliability of the PCL-R typically falls within the acceptable boundaries (e.g., Piotrowski et al., 1996; see Nicholls et al., 2005 for a review). Thus, regardless of whether we have adequately mapped the construct, we have evidence that the measure is reliable across raters. Support also has been found for convergent and discriminate validity of the PCL-R among women, for example, Salekin and colleagues (1997) found the expected relationships between psychopathy and staff ratings of violence, verbal aggression, manipulativeness, lack of remorse and noncompliance (Salekin et al., 1997). While other research has documented convergent validity with hypothesized biological and psychological correlates for reviews see Jackson & Richards, in press; Verona & Vitale, 2006). Very few studies have evaluated the psychometric properties of the PCL:YV among adolescent girls. When the PCL:YV manual was published, there were only six studies that included adolescent females, the majority of which did not have adequate power to perform separate analyses by gender (samples ranged from n = 11 to 80). Nonetheless, the PCL:YV was approved for use with adolescent girls, stating that ‘PCL:YV total scores do not appear to be unduly influenced by the youth’s age, ethnicity or gender’ (Forth et al., 2003, p. 51). Since that time, a handful of additional studies have documented further limitations with respect to concurrent validity (Odgers et al., 2005), and a lack of predictive validity among adolescent girls (for a meta-analysis see Edens, Campbell, & Weir, in press). We would argue, at this stage use of the measure with adolescent girls in legal or paralegal settings should be avoided.

WOMEN AND GIRLS WITH PSYCHOPATHIC CHARACTERISTICS

357

Does Being Female Impact the Assessment Context? Understanding how gender matters within forensic assessment and other clinical contexts is not unique to the assessment of psychopathy. Indeed, research has demonstrated that clinicians within civil psychiatric settings, where the base rate of violence is equivalent across men and women, perform poorly when assessing risk for violence among women due to the fact that they underestimate women’s violence potential (Elbogen et al., 2001; Lidz, Mulvey & Gardner, 1993; Skeem et al., 2005). Variability and poor clinical accuracy might reflect method of assessment, record keeping and administration procedures (i.e., what does and does not get asked and recorded), instrument development/composition, and training needs (Grann, 2000; Piotrowski et al., 1996) or a failure to attend to the base rate of aggression in the population of interest. In sum, although there is some evidence that the psychopathy construct can bring added value when applied to females (e.g., predictive value within subpopulations of females discussed below) the extent to which current criteria are optimal for measuring the syndrome in adult women and girls is unknown. Further work is needed to clarify how to ensure the PCL items are maximally sensitive to detect diagnostically unique behavior in females (Grann, 2000; Piotrowski et al., 1996). Widiger and Samuel (2005) proposed that clinicians should approach clinical assessments with structured self-report instruments in combination with structured interviews. Our review of the literature suggests that both self-report assessments and structured interviews will reflect gender differences for assessors attempting to measure psychopathy in females.

Future Directions Given the theoretical concerns and inconsistencies throughout the empirical research, a ‘back to basics’ approach may be required to ensure the content validity of the domain (Messick, 1995) and provide a more gender neutral/sensitive assessment scheme (Forouzan, 2003). For example, this type of approach likely would involve focus groups with clinicians and antisocial females (substance abusers, child abusers, domestic violence perpetrators), systematic reviews of the literature (see Blashfield & Livesley, 1991), prior to developing a measure of the construct. Additionally, given the strong interpersonal nature of the disorder it is important to discover what effect rater gender has on the scores obtained on the PCL-R and related instruments.

QUESTION III: HOW CAN PSYCHOPATHY INFORM FORENSIC ASSESSMENTS WITH FEMALES? As rates of violence and incarceration among females has increased (Snyder & Sickmund, 2006), the question of whether psychopathy may inform decision making within in these contexts has emerged. Although psychopathic traits, in particular the PCL-R-, PCL:SV-, and PCL:YV-defined psychopathy, are unequivocally linked to antisocial and violent behavior in diverse populations (for a review, see Douglas, Vincent & Edens, 2006) vigorous criticisms have been leveled at the application of psychopathy to decision-making regarding liberty

358

VOLUME I: DIAGNOSIS AND TREATMENT

and treatment, generally (Cooke & Michie, 2006; Edens & Petrila, 2006; Gendreau, Goggin & Smith, 2002). More specifically, caution has been recommended in applying the disorder to particular decision-making tasks (e.g., death penalty cases, Edens, Petrila, et al., 2001) and groups (adolescents, Odgers, 2005; Vincent, 2006; women, Vitale & Newman, 2001) for whom critics assert there is insufficient theoretical and empirical evidence amassed to warrant broad clinical applications (see two recent special editions of Behavioral Sciences and the Law, Nicholls & Petrila, 2005; Petrila & Skeem, 2004). In this section, we consider whether psychopathy can be advantageously applied to our understanding of females’ involvement in aggression and crime, treatment responsivity, and institutional adjustment and what evidence there is to validate the assumption that forensic evaluators should be informed by psychopathy when evaluating females.

Why Would We Expect Psychopathy to be Relevant to Future Antisocial Behavior among Females? Psychopathy is Considered to be a Necessary Risk Factor When Assessing Violence and Crime among Men The express purpose of the PCL instruments is to assess psychopathy, not to evaluate risk for violence; however, the strength of the association between psychopathy (most often measured by the PCL instruments) and aggression and criminal offending (Hemphill, Hare & Wong, 1998; Salekin, Rogers & Sewell, 1996; Steadman et al., 2000; also see Gendreau, Goggin & Smith, 2003; Hemphill & Hare, 2004) has led experts to describe the disorder as a fundamental consideration in any violence risk assessment (e.g., Hart, 1998). Psychopathy is increasingly recognized among forensic clinicians and psycho-legal scholars as an ethically and professionally essential consideration in evaluations for placement, sentencing, parole and treatment in diverse populations (Hart, 1998; Ogloff, 2006). Of particular relevance, several scholars have recommended that psychopathy should have a prominent role in violence risk assessments with females (Forth, Kosson & Hare, 2003; Hare, 1991, 2003; Hart, 1997, cited in Nesca et al., 1999; Hart et al., 1995; Webster, 1999); though it must be recognized that others recommend that clinicians should remain cautious in applying existing assessment instruments to females (Odgers et al., 2005; Rogers, 2000; Vitale & Newman, 2001). Moreover, psychopathy is an item found on multiple risk assessment tools (e.g., HCR-20, Webster et al., 1997; VRAG, Quinsey et al., 1998). Conceivably then, it is relevant to consider if and how the construct can inform our understanding of violence and crime committed by females.

Psychopathy is Associated with Diverse Forms of Antisocial Behavior and Translates Well Across Populations This diagnostic category has commanded considerable research and clinical interest because not only do psychopathic individuals commit a disproportionate amount of crime, their offenses are more likely to be of a severe and diverse variety. In addition, these individuals have been found to reoffend more quickly when compared to individuals diagnosed with APD (for a review, see Douglas et al., 2006). Available research suggests that psychopathy is linked to general and violent offending, sexual violence, institutional infractions and poor

WOMEN AND GIRLS WITH PSYCHOPATHIC CHARACTERISTICS

359

treatment outcomes (see Chapter ##, this volume). With regard to women specifically, several recent reviews document the diversity of antisocial behavior characteristic of females with psychopathic characteristics including substance abusers, women from the general population, civil psychiatric settings, forensic hospitals and correctional institutions (Jackson & Richards, in press; Nicholls et al., 2005; Verona & Vitale, 2006). Although these findings look to be generally consistent across time, age, socioeconomic status, culture, country and ethnicity, most of the research has not controlled for rival hypotheses or causal variables and the vast majority has been conducted with males, or very highly selected samples. In addition, there is a risk of tautological reasoning because psychopathy is defined partly in terms of early onset, diverse and pervasive antisocial behaviors and those often are considered as relevant outcome measures, this criticism is not specific to research with females.

Many Risk Factors do not Appear to be Gender-Specific Finally, there is increasing evidence that risk factors for crime and violence are common across gender, culture and diverse populations (e.g., mentally disordered offenders, civil psychiatric patients). Despite widespread consensus that males are responsible for the vast majority of antisocial behavior the question of whether sex differences in the amount of antisocial behavior reflect differences in the correlates and development of antisocial behaviors remains. A growing body of research with adult women suggests that the most robust predictors of violence and crime typically are not gender specific (e.g., Loucks & Zamble, 2000; Webster, 1999; Weizmann-Henelius, 2004) (e.g., antisocial peers, substance abuse, prior antisocial behavior, impulsivity, dysfunctional families of origin and child abuse). Similar assertions have been put forward with regard to adolescents. For instance, Moffit et al. (2001) noted that ‘the extant literature contains very few actual empirical demonstrations of sex differences in the aetiological factors involved with becoming antisocial, in the correlates of antisocial behaviour, or in its long-term consequences’ (p. 5). In the Dunedin Longitudinal Study, Moffit and colleagues (2001) found ‘remarkable’ similarities between risk factors for antisocial behavior in males and females. Importantly, in addition to uncovering evidence of the same risk factors, the size of the effects generally were comparable across the sexes. In short, there is little evidence of replicable gender-specific risk factors, and males and females are vulnerable to the same risk factors, but males appear to be more likely to be exposed to the individual and interpersonal risk factors (Moffit et al., 2001).

Relationship between PCL Scores and Future Antisocial Behavior among Females A few years ago, Vitale and Newman (2001) conducted a review of the literature on psychopathy in women and concluded that ‘if clinicians are using the PCL-R for the sole purpose of predicting specific outcomes for any particular women in these areas [predicting criminal recidivism, predicting institutional violence, planning and implementing treatments and interventions], they would be doing so without empirical evidence of the predictive power of the PCL-R in such domains’ (p. 128). Since that time, results have been somewhat more encouraging for adult women. For example, Richards, Casey and Lucente (2003) found that in comparison to a combination of other variables, psychopathy scores (particularly

360

VOLUME I: DIAGNOSIS AND TREATMENT

the interpersonal and affective features, original Factor 1) were the best predictors of new charges for incarcerated female substance abusers (N = 404) released to the community. In fact, some research suggests that psychopathy, and other risk variables relevant to antisocial behavior in males, might actually be superior predictors of future antisocial behavior in females than in males (Nicholls, Ogloff & Douglas, 2004; Douglas et al., 2005). Although the research corpus is not large, several recent narrative reviews have offered preliminary evidence that the capacity of the PCL instruments to identify women at risk for antisocial behavior, poor treatment outcomes and violent criminal offending is comparable to that with adult men (Nicholls et al., 2005; Jackson & Richards, in press; Verona & Vitale, 2006). That being said, the value of narrative reviews is limited and the field is still lacking a meta-analysis to assess the predictive validity of the PCL with adult women. Moreover, it is not clear whether psychopathy has incremental predictive validity over other less pejorative risk factors, or whether PCL scores remain predictive of future offending among women once other covariates are controlled.

Does the PCL:YV Predict Violence and Crime with Adolescent Females? There are only a handful of studies that have examined the predictive validity of the PCL:YV with girls; with, to our knowledge, no published study to date reporting a relationship between the PCL:YV and future offending (for a meta-analysis see Edens et al., in press). For example, Vincent and colleagues report on a five-year follow-up of incarcerated females and found no relationship with future violence or nonviolent offending (O.R. = 1.1, p = ns). Similarly, Odgers et al. (2005) reported no relationship between PCL:YV scores and offending three months following release, yet, despite the short follow-up period, victimization experiences were predictive of future offending. While these studies have been limited by small sample sizes, short follow-up periods and the use of official offending data only, at this point there is very little reason to suggest that the PCL:YV would be useful for predicting future official offending among females in the juvenile justice system. With that said, the question of whether the PCL:YV predicts more relevant forms of future offending among women, such as aggression within the context of close relationships, has yet to be addressed. The limited body of research available for girls, combined with the lack of developmental fit when extending psychopathy to adolescent populations in general (Vincent, 2006), has lead to the recommendation that the PCL:YV should not be used with adolescent girls for purposes other than research at this time (Odgers et al., 2005). In sum, psychopathy is the preeminent variable in violence risk assessments with men (Steadman et al., 2000) with emerging research linking PCL scores to women’s criminal offending and violence (Nicholls et al., 2005), treatment responsivity (Richards, Casey & Lucente, 2003), and antisocial behaviors in youths (Vincent, 2006). While there is general agreement that the field must be cautious in extending the PCL into female populations given the paucity of empirical data and concerns regarding gender bias, at the same time clinicians have a responsibility to employ the most relevant risk variables in assessing an individual’s risk to others. In particular, efforts to block research are unlikely to be beneficial (Laishes, 2002). Given the track record in male populations, the PCL is a promising candidate that warrants consideration in both research and clinical contexts; however, without full validation within female populations it is premature to make use of something like the

WOMEN AND GIRLS WITH PSYCHOPATHIC CHARACTERISTICS

361

PCL-R/SV numerically with women or girls. With these cautionary notes in mind, it is also the case that the construct of psychopathy holds the potential to aid clinical formulation (i.e., why do these traits, or constellations of traits, increase the likelihood that someone will behave violently in the future?). The relevant interviews provide information that the clinician should be able to combine with other information to develop a defensible formulation. A comprehensive formulation would consider how risk factors interact with each other over time and how they relate to the patient’s circumstances (Hart et al., 2003). Information derived from the PCL-R about an individual’s interpersonal style, emotional experiences and impulsive and reckless behavioral style can be used to inform a risk formulation. Due to the current state of empirical research, however, the focus should be on the psychological processes of the individual rather than on what differentiates individuals from each other (Cooke & Michie, 2006).

CONCLUDING THOUGHTS Although scholarly interest in female psychopathy was slow to emerge in contrast to the lengthy history of study with males, in recent years several pioneering researchers have begun to evaluate the construct and its measurement in women (Salekin et al., 1997; Vitale & Newman, 2001) and a handful of comprehensive reviews on the topic have been published (Cale & Lilienfeld, 2002; Forouzan & Cooke, 2005; Jackson & Richards, 2005; Nicholls et al., 2005; Odgers et al., 2005; Verona & Vitale, 2006). We have departed somewhat from pure empirical terrain and demonstrated the necessity of revisiting the theoretical foundation for the syndrome and the complex meaning of gender and sociocultural contexts for the identification and expression of psychiatric illnesses. In doing so, we have attempted to provide a more nuanced understanding of the meaning of gender for psychopathy. Admittedly, little consensus exists regarding the etiology, expression, assessment, prevention, management and treatment of psychopathy in females; this of courses echoes the position with males. Only a truly integrated theoretical–empirical approach to understanding gender differences and similarities in psychopathic PD will lead to appropriate identification and care. Theoretically informed evaluation would doubtless yield enhanced violence risk assessment accuracy and informed therapeutic interventions. A consideration of the state of the field suggests that psychopathic PD has potentially theoretical and practical relevance to females. Congruent with previous empirical findings (Edens et al., in press; Odgers et al., 2005) and narrative reviews (Nicholls et al., 2005; Vincent, 2006) clinicians, policy-makers and the courts should remain vigilant regarding the limited scientific evidence to date and the negative connotations but should also be mindful of the potential value (Salekin, 2006). Psychopathy remains a controversial construct with potentially far-reaching and extreme negative implications; as such, its application with vulnerable populations is likely to remain under close scrutiny – as it should.

REFERENCES Archer, J. (1991). The influence of testosterone on human aggression. British Journal of Psychology, 82, 1–28. Baron-Cohen, S. (2002). The extreme male brain theory of autism. Trends in Cognitive Science, 6, 248–54.

362

VOLUME I: DIAGNOSIS AND TREATMENT

Bjorklund, P. (2006). No man’s land: gender bias and social constructivism in the diagnosis of borderline personality disorder. Issues in Mental Health Nursing, 27, 3–23. Blackburn, R. (2006). Other theoretical models of psychopathy. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 415–36). New York: Guilford. Blashfield, R.K. & Dragun, J.G. (1976). Evaluative criteria for psychiatric classification. Journal of Abnormal Psychology, 85(2), 140–50. Blashfield, R.K. & Livesley, J.W. (1991) Metaphorical analysis of psychiatric classification as a psychological test. Journal of Abnormal Psychology, 100(3), 262–70. Bolt, D.M., Hare, R.D., Vitale, J.E. & Newman, J.P. (2004). A multigroup item response theory analysis of the Psychopathy Checklist–Revised. Psychological Assessment, 16, 155–68. Book, A.S., Starzyk, K.B. & Quinsey, V.L. (2001). The relationship between testosterone and aggression: a meta-analysis. Aggression and Violent Behavior, 6, 579–99. Cale, E.M. & Lilienfeld, S. (2002a). Histrionic personality disorder and antisocial personality disorder: sex-differentiated manifestations of psychopathy? Journal of Personality Disorders, 16, 52–72. Cale, E.M. & Lilienfeld, S. (2002b). Sex differences in psychopathy and antisocial personality disorder. A review and integration. Clinical Psychology Review, 22, 1179–207. Cale, E.M. & Lilienfeld, S. (2003). What every forensic psychologist should know about psychopathic personality. In W. O’Donohue & E. Levinsky (eds.), Handbook of Forensic Psychology (pp. 395– 428). San Diego, CA: Academic Press. Caspi, A., McClay, J., Moffitt, T.E. et al. (2002). Role of genotype in the cycle of violence in maltreated children. Science, 297, 851–4. Cleckley, H. (1988). Mask of Sanity. 5th edition. Available online at: http://www. cassiopaea.org/cass/sanity 1.PdF. Cooke, D.J. (2001). Psychopathy and antisocial behaviour: clarifying the links. keynote address presented at the International Conference on Violence risk assessment and management: Bringing science and practice closer together. Sundsvall, Sweden, November 28–30. Cooke, D.J., Hart, S.D., Logan, C. & Michie, C. (2006). Evaluating the construct of psychopathic personality disorder: the development of a comprehensive clinical assessment. Invited paper for Journal of Personality Disorders (in preparation). Cooke, D.J., Kosson, D.S. & Michie, C. (2001). Psychopathy and ethnicity: structural, item, and test generalizability of the Psychopathy Checklist–Revised (PCL-R) in Caucasian and AfricanAmerican participants. Psychological Assessment, 13, 531–42. Cooke, D.J. & Michie, C. (1997). An item response theory evaluation of Hare’s Psychopathy Checklist. Psychological Assessment, 9, 2–13. Cooke, D.J. & Michie, C. (1999). Psychopathy across cultures: North America and Scotland compared. Journal of Abnormal Psychology, 108, 55–68. Cooke, D.J. & Michie, C. (2001). Refining the construct of psychopathy: towards a hierarchical model. Psychological Assessment, 13, 171–88. Cooke, D.J. & Michie, C. (2006). The Psychopathy Checklist–Revised and decisions about the single case: limitations of diagnostic precision and predictive utility. Unpublished data. Cooke, D.J., Michie, C., Hart, S.D. & Clark, D. (2005). Assessing psychopathy in the UK: concerns about cross-cultural generalisability. British Journal of Psychiatry, 186, 335–41. Cooke, D.J., Michie, C. & Skeem, J.L. (in press). Understanding the structure of the Psychopathy Checklist-Revised: an exploration of methodological confusion.British Journal of Psychiatry. 190(49), s39–s50. Craig, I.W., Harper, E. & Loat, C. S. (2004). The genetic basis for sex differences in human behavior: role of the sex chromosomes. Annals of Human Genetics, 269–84. Crick, N.R. & Bigbee, M.A. (1998). Relational and overt forms of peer victimization: a multiinformant approach. Journal of Consulting and Clinical Psychology, 66, 337–47. Crick, N.R. & Grotpeter, J.K. (1995). Relational aggression, gender, and social-psychological adjustment. Child Development, 66, 710–22. Douglas, K.S., Strand, S., Belfrage, H. et al. (2005). Reliability and validity evaluation of the Psychopathy Checklist: Screening Version (PCL: SV) in Swedish correctional and forensic psychiatric samples. Assessment, 12, 145–61. Douglas, K.S., Vincent, G. & Edens, J. (2006). Risk for criminal recidivism: the role of psychopathy. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 533–54). New York: Guilford Press.

WOMEN AND GIRLS WITH PSYCHOPATHIC CHARACTERISTICS

363

Draguns, J.G. & Tanka-Matsumi, J. (2003). Assessment of psychopathology across and within cultures: issues and findings. Behavior Research and Therapy, 41, 755–76. Eagly, A.H. & Steffan, V. J. (1986). Gender and aggressive behavior: a meta-analytic review of the social psychological literature. Psychological Bulletin, 100, 309–30. Edens, J.F., Campbell, J.S. & Weir, J.M. (2007). Youth psychopathy and criminal recidivism: a metaanalysis of the Psychopathy Checklist measures. Law and Human Behavior, 31, 53–75. Edens, J.F. & Petrila, J. (2006). Legal and ethical issues in the assessment and treatment of psychopathy. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 573–88). New York: Guilford Press. Edens, J.F., Petrila, J. & Buffington-Vollum, J.K. (2001). Psychopathy and the death penalty: can the psychopathy checklist-revised identify offenders who represent a continuing threat to society? Journal of Psychiatry & Law, 29, 433–481. Edens, J.F., Skeem J.L., Cruise, K.R. & Cauffman, E. (2001). Assessment of juvenile psychopathy and its association with violence: a critical review. Behavioral Sciences and the Law, 19, 53–80. Elbogen, E.B., Williams, A.L., Kim, D. et al. (2001). Gender and perceptions of dangerousness in civil psychiatric patients. Legal and Criminological Psychology, 6, 215–28. Else-Quest, N.M., Hyde, J.S., Goldsmith, H.H. & Van Hulle, C. (2006). Gender differences in temperament: a meta-analysis. Psychological Bulletin, 132, 33–72. Eysenck, H.J. (1970). The classification of depressive illness. British Journal of Psychiatry, 117, 241–50. Embretson, S.E. & Reise, S.P. (2000). Item Response Theory for Psychologists. Mahweh, NJ: Lawrence Erlbaum. Ford, M.R. & Widiger, T.A. (1989). Sex bias in the diagnosis of histrionic and antisocial PDs. Journal of Consulting and Clinical Psychology, 57, 301–5. Forouzan, E. (2003). Psychopathy among women: conceptualization and assessment problems. Paper presented at the Third Annual International Association of Forensic Mental Health Services (IAFMHS) Conference, Miami, FL. Forouzan, E. & Cooke, D.J. (2005). Figuring out la femme fatale: conceptual and assessment issues concerning psychopathy in females. Behavioral Sciences and the Law, 23, 765–78. Forth, A.E., Brown, S.L., Hart, S.D. & Hare, R.D. (1996). The assessment of psychopathy in male and female non-criminals: reliability and validity. Personality and Individual Differences, 20, 531–43. Forth, A., Kosson, D. & Hare, R.D. (2003). The Hare Psychopathy Checklist: Youth Version. Toronto: Multi-Health Systems. Fowles, D.C. & Dindo, L. (2006). A dual deficit model of psychopathy. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 14–34). New York: Guilford Press. Gendreau, P., Goggin, C. & Smith, P. (2002). Is the PCL-R really the unparalleled measure of offender risk? Criminal Justice and Behavior, 29, 397–426. Goldstein, R.B., Powers, S I., McCusker, J. et al. (1996). Gender differences in manifestations of antisocial personality disorder among residential drug abuse treatment clients. Drug and Alcohol Dependence, 41, 35–45. Grann, M. (2000). The PCL-R and gender. European Journal of Psychological Assessment, 16, 147–9. Hare, R.D. (1980). A research scale or the assessment of psychopathy in criminal populations. Personality and Individual Differences, 1, 111–19. Hare, R.D. (1991). The Hare Psychopathy Checklist – Revised. Toronto: Multi-Health Systems. Hare, R.D. (2003). The Hare Psychopathy Checklist – Revised (PCL-R) 2nd edition: Technical Manual. Toronto: Multi-Health Systems. Hare, R.D. & Neumann, C.S. (2006). The PCL-R assessment of psychopathy: development, structural properties and new developments. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 58–90). New York: Guilford Press. Hart, S.D. (1998). The role of psychopathy in assessing risk for violence: conceptual and methodological issues. Legal and Criminological Psychology, 3, 121–37. Hart, S.D., Cox, D.N. & Hare, R.D. (1995). The Hare Psychopathy Checklist: Screening Version (PCL:SV). North Tonawanda, NY: Multi-Health Systems. Hart, S.D., Kropp, P.R. & Laws, D. (2003). The Risk for Sexual Violence Protocol. Vancouver: Mental Health, Law and Policy Institute, Simon Fraser University. Hart, S.D., Watt, K.A. & Vincent, G.M. (2002). Commentary on Seagrave and Grisso: impressions of the state of the art. Law and Human Behavior, 26, 241–5.

364

VOLUME I: DIAGNOSIS AND TREATMENT

Hemphill, J.F. & Hare, R.D. (2004). Some misconceptions about the Hare PCL-R and risk assessment: a reply to Gendreau, Goggin, and Smith. Criminal Justice and Behavior, 31(2), 203–43. Hemphill, J.F., Hare, R.D. & Wong, S. (1998). Psychopathy and recidivism: a review. Legal and Criminological Psychology, 3, 139–70. Jackson, R.L. & Richards, H.J. (in press). Psychopathy in women: a valid construct with clear implications. In H. Herve & J.C. Yuille (eds.), Psychopathy: Theory, Research, and Implications for Society. Jackson, R.L., Rogers, R., Neumann, C. & Lambert, P. (2002). Psychopathy in women: an investigation of its underlying dimensions. Criminal Justice and Behavior, 29, 692–704. Jones, S., Cauffman, E., Miller, J.D. & Mulvey, E. (2006). Investigating different factor structures of the Psychopathy Checklist: Youth Version: Confirmatory factor analytic findings. Psychological Assessment, 18, 33–48. Kendell, R.E. (1989). Clinical validity. Psychological Medicine, 19, 45–55. Kessler, R.C., McGonagle, K.A., Zhao, S. et al. (1994). Lifetime and 12-month prevalence of DSMIII-R psychiatric disorders in the United States, results from the National Comorbidity Survey. Archives of General Psychiatry, 51, 8–19. Laishes. J. (2002). The 2002 Mental Health Strategy for Women Offenders. Retrieved August 18, 2006 from http://www.csc-scc.gc.ca/text/prgrm/fsw/mhealth/8 e.shtml. Lalumiere, M.L., Harris, G.T. & Rice, M.E. (2001). Psychopathy and developmental instability. Evolution and Human Behavior, 22, 75–92. Lidz, C., Mulvey, E. & Gardner, W. (1993). The accuracy of predictions of violence to others. Journal of the American Medical Association, 269, 1007–11. Lilienfeld, S.O. & Andrews, B.P. (1996). Development and preliminary validation of a self-report measure of psychopathic personality traits in noncriminal populations. Journal of Personality Assessment, 66, 488–524 Loucks, A.D. & Zamble, E. (2000). Predictors of criminal behavior and prison misconduct in serious female offenders. Empirical and Applied Criminal Justice Review, 1, 1–47. Marsella, A.J. (1998). Urbanization, mental health, and social deviancy: a review of issues and research. American Psychologist, 53, 621–3. Messick, S. (1995). Validity of psychological assessment: validation of inferences from persons’ responses and performances as scientific inquiry into score meaning. American Psychologist, 50, 741–9. Moffitt, T.E. (2004). Natural histories of delinquency. In E. Wietekamp & H.J. Kerner (eds.), CrossNational Longitudinal Research on Human Development and Criminal Behaviour (pp. 3–61). Dordrecht: Kluwer Academic Press. Moffitt, T.E. (2005). The new look of behavioral genetics in developmental psychopathology: gene– environment interplay in antisocial behaviors. Psychological Bulletin, 131, 533–54. Moffitt, T.E. & Caspi, A. (2001). Childhood predictors differentiate life-course persistent and adolescence-limited antisocial pathways among males and females. Development and Psychopathology, 13, 355–75. Moffitt, T.E., Caspi, A., Rutter, M. & Silva, P.A. (2001). Sex Differences in Antisocial Behaviour: Conduct Disorder, Delinquency, and Violence in the Dunedin Longitudinal Study. New York: Cambridge University Press. Moretti, M.M. & Odgers, C.L. (2006). Preface: sex differences in the functions and precursors of adolescent aggression. Aggressive Behavior, 32, 373–5. Nesca, M., Dalby, J. & Baskerville, S. (1999). Psychological profile of a female psychopath. American Journal of Forensic Psychology, 17, 63–77. Neumann, C.S., Kosson, D.S., Forth, A.E. & Hare, R.D. (2006). Factor structure of the Hare Psychopathy Checklist: Youth Version (PCL: YV) in incarcerated adolescents. Psychological Assessment, 18, 142–54. Nicholls, T.L., Ogloff, J.R.P., Brink, J. & Spidel, A. (2005). Psychopathy in women: a review of its clinical usefulness for assessing risk for aggression and criminality. Behavioral Sciences and the Law, 23, 779–802. Nicholls, T.L., Ogloff, J.R.P. & Douglas, K.S. (2004). Research report – assessing risk for violence among male and female civil psychiatric patients: the HCR-20, PCL: SV, and VSC. Behavioral Sciences and the Law, 22, 127–58.

WOMEN AND GIRLS WITH PSYCHOPATHIC CHARACTERISTICS

365

Nicholls, T.L. & Petrila, J.D. (2005). Gender and psychopathy: an overview of important issues and introduction to the special issue. Behavioral Sciences and the Law, 23, 729–41. Odgers, C.L. (2005). Violence, victimization and psychopathy among female juvenile offenders. Dissertation Abstracts International: Section B: The Sciences and Engineering, 66, 568. Odgers, C.L., Moffit, T.E., Caspi, A. et al. (in press). Female and male antisocial trajectories: from childhood origins to adult outcomes. Development and Psychopathology. Odgers, C.L., Moretti, M.M. & Repucci, N.D. (2005). Examining the science and practice of violence risk assessment with female adolescents. Law and Human Behavior, 29, 7–27. Ogloff, J.R.P. (2006). Psychopathy/antisocial personality disorder conundrum. Australian and New Zealand Journal of Psychiatry, 41, 285–92. Paquette, J.A. & Underwood, M.K. (1999). Young adolescents’ experiences of peer victimization: gender differences in accounts of social and physical aggression. Merrill-Palmer Quarterly, 45, 233–58. Paris, J. (1997). Antisocial and borderline PDs: two separate diagnoses or two aspects of the same psychopathology. Comprehensive Psychiatry, 38, 237–42. Patrick, C.J. (2006). Handbook of Psychopathy. New York: Guilford Press. Patrick, C.J., Verona, E. & Sullivan, E. (2000). Emotion and psychopathy in female offenders. Psychophysiology, 37, S76-S. Petrila, J.D. & Skeem, J.L. (2003). An introduction to the special issues on juvenile psychopathy and some reflections on the current debate.Behavioral Sciences and the Law, 6, 689–94. Pinel, P. (1801). Traite medico-philosophique sur l’alienation mentale. Paris: Richard, Caille & Ravier. Piotrowski, N., Tusel, D., Sees, K. et al., (1996). Psychopathy and antisocial personality disorder in men and women with primary opioid dependence. In D.J. Cooke, A. Forth, J. Newman & R.D. Hare (eds.), Issues in Criminological and Legal Psychology: No. 24, International Perspectives on Psychopathy (pp. 123–6). Leicester, UK: British Psychological Society. Porter, S. (1996). Without conscience or without active conscience? The etiology of psychopathy revisited. Aggression and Violent Behavior, 1, 179–89. Quinsey, V.L., Harris, G.T., Rice, M.E. & Cormier, A.C. (1998). Violent Offenders: Appraising and Managing Risk. Washington, DC: American Psychological Association. Richards, H., Casey, J. & Lucente, S. (2003). Psychopathy and treatment response in incarcerated female substance abusers. Criminal Justice and Behavior, 30, 251–76. Robins, L.N., Tipp, J. & Przybeck, T. (1991). Psychiatric disorders in America. In L.N. Robins & D.A. Regier (eds.), Antisocial Personality Disorder (pp. 258–90). New York: Free Press. Rogers, R. (2000). The uncritical acceptance of risk assessment in forensic practice. Law and Human Behavior, 24, 595–605. Rogers, R., Salekin, R.T., Hill, C. et al. (2000). The Psychopathy Checklist – Screening version: an examination of criteria and subcriteria in three forensic samples. Assessment, 7, 1–15. Rosenblitt, J.C., Soler., H., Johnson, S.E. & Quadagno, D.M. (2001). Sensation seeking and hormones in men and women: exploring the link. Hormones and Behavior, 40, 396–402. Rutherford, M.J., Cacciola, J.S., Alterman, A.I. & McKay, J.R. (1996). Reliability and validity of the Revised Psychopathy Checklist in women methadone patients. Assessment, 3, 145–56. Salekin, R.T. (2006). Psychopathy in children and adolescents: key issues in conceptualization and assessment. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 389–414). New York: Guilford. Salekin, R.T., Rogers, R. & Sewell, K.W. (1996). A review and meta-analysis of the Psychopathy Checklist and Psychopathy Checklist–Revised: predictive validity of dangerousness. Clinical Psychology: Science and Practice, 3, 203–15. Salekin, R.T., Rogers, R., & Sewell, K.T. (1997). Construct validity of psychopathy in a female offender sample: a multitrait-mulitmethod evaluation. Journal of Abnormal Psychology, 106, 576– 85. Schrum, C.L. & Salekin, R.T. (2006). Psychopathy in adolescent female offenders: an item response theory analysis of the Psychopathy Checklist: Youth Version. Behavioral Sciences and the Law, 24, 39–63. Seagrave, D. & Grisso, T. (2002). Adolescent development and the measurement of juvenile psychopathy. Law and Human Behavior, 26, 219–39. Silverthorn, P. & Frick, P.J. (1999). Developmental pathways to antisocial behavior: the delayed-onset pathway in girls. Development and Psychopathology, 11, 101–12.

366

VOLUME I: DIAGNOSIS AND TREATMENT

Silverthorn, P., Frick, P.J. & Reynolds, R. (2001). Timing of onset and correlates of severe conduct problems in adjudicated girls and boys. Journal of Psychopathology and Behavioral Assessment, 23, 171–81. Skeem, J.L. & Cooke, D.J. (2006). Is criminal behavior a central component of psychopathy? Conceptual directions for resolving the debate (Under review). Skeem, J., Schubert, C., Stowman, S. et al., (2005). Gender and risk assessment accuracy: underestimating women’s violence potential. Law and Human Behavior, 29, 173–86. Skeem, J.L., Mulvey, E.P. & Grisso, T. (2003). Applicability of traditional and revised models of psychopathy to the Psychopathy Checklist: Screening Version. Psychological Assessment, 15, 21–55. Snyder, H. N. & Sickmund, M. (2006). Juvenile Offenders and Victims: 2006 National Report. Washington, DC: US Department of Justice, Office of Justice Programs, Office of Juvenile Justice and Delinquency Prevention. Steadman, H.J., Silver, E., Monahan, J. et al. (2000). A classification tree approach to the development of actuarial violence risk assessment tools. Law and Human Behavior, 24, 83–100. Verona, E. & Vitale, J. (2006). Psychopathy in women: assessment, manifestations, and etiology. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 415–36). New York: Guilford. Vincent, G. (2006). Psychopathy and violence risk assessment in youth. Child and Adolescent Psychiatric Clinics of North America, 15, 407–28. Vincent, G. (2002). Investigating the legitimacy of adolescent psychopathy assessment: Contributions of item response theory. Unpublished dissertation, Simon Fraser University. Vincent, G.M., Odgers, C.L., Salekin, R. & Moretti, M.M. (2006, March). Psychopathy in Adolescent Female Offenders: Contributions of Item Response Theory. American Psychology-Law Conference, Tampa, FL. Vitacco, M.J., Neumann, C.S. & Jackson, R.L. (2005). Testing a four-factor model of psychopathy and its association with ethnicity, gender, intelligence, and violence. Journal of Consulting and Clinical Psychology, 73, 466–76. Vitale, J.E. & Newman, J.P. (2001a). Using the Psychopathy Checklist-Revised with female samples: Reliability, validity, and implications for clinical utility. Clinical Psychology: Science and Practice, 8, 117–32. Vitale, J.E. & Newman, J.P. (2001b). Response preservation in psychopathic females. Journal of Abnormal Psychology, 110, 644–7. Vitale, J.E., Smith, S.S., Brinkley, C.A. & Newman, J.P. (2002). The reliability and validity of the Psychopathy Checklist–Revised in a sample of female offenders. Criminal Justice & Behavior, 29, 202–31. Warner, R. (1978). The diagnosis of antisocial and hysterical PDs. Journal of Nervous and Mental Disease, 166, 839–45. Warren, J., Burnette, M.L., South, S.C. et al. (2003). Psychopathy in women. International Journal of Law and Psychiatry, 26, 223–42. Webster, C.D. (1999, December). Risk assessment and risk management with women offenders. Report to the National Parole Board, Ottawa. Webster, C.D., Douglas, K.S., Eaves, D. & Hart, S.D. (1997). HCR-20: Assessing Risk for Violence (Version 2). Vancouver: Mental Health, Law, & Policy Institute, Simon Fraser University. Weizmann-Henelius, G., Viemer¨o, V., & Eronen, M. (2004). Psychological risk markers in violent female behavior. International Journal of Forensic Mental Health, 3, 185–96. Widiger, T.A. & Samuel, D.B. (2005). Evidence-based assessment of PDs. Psychological Assessment, 17, 278–87. Widiger, T.A. & Spitzer, R.L. (1991). Sex bias in the diagnosis of personality disorders: conceptual and methodological issues. Clinical Psychology Review, 11, 1–22. Wilson, D.L., Frick, P.J. & Clements, C.B. (1999). Gender, somatization, and psychopathic traits in a college sample. Journal of Psychopathology and Behavioral Assessment, 21, 221–35. Zagon, I. & Jackson, H. (1994). Construct validity of a psychopathy measure. Personality and Individual Differences, 17, 125–35.

CHAPTER 22

Educational Issues Franz Petermann and Ute Koglin University of Bremmen, Germany

Several longitudinal studies have emphasized the relationship between severe forms of aggressive behavior in childhood and/or adolescence and antisocial personality disorder, sociopathy, violence and/or criminality in adulthood (e.g., Fergussen, Horwood & Ridder, 2005). Educational issues are essential for the etiology and pathogenesis of aggressive behavior. On the one hand, they refer to a child’s learning experiences, which cause or sustain problem behavior, and are experienced within the family context or in school/kindergarten. On the other hand, they refer to the consequences of aggressive antisocial behavior on school achievement and the child’s adaptation to school. A large number of studies have been carried out on aggressive behavior within the school context. This is comprehensible, since aggressive students provoke frequent conflicts with classmates due to their disturbing behavior, intimidate their classmates or instigate others to aggressive antisocial actions. The presence of just one aggressive student can contribute to emotional tensions in class and disturb lessons effectively. Often, the relationship with the teacher is affected as well. Which consequences aggressive behavior has on school success, or which factors favor school failure and aggressive behavior, has been the topic of a number of empirical studies. However, studies which examine academic aspects of aggressive behavior with respect to different forms of aggression or concrete psychopathic behaviors, are lacking. Accordingly the topic can only be approached by taking into account the results on unspecific aggressive behaviors, whereby an attempt is made to discuss these in consideration of the latest results on the developmental psychopathology of psychopathic behavior during childhood and adolescence. After differentiating psychopathic characteristics in children from nonpsychopathic aggressive behaviors, the learning deficits in this group shall be presented. This is followed by an overview of factors, known to influence school success of aggressive children (see Figure 22.1). Comorbid disorders of aggressive behavior, like attention deficit and hyperactivity disorder (ADHD), which can promote school problems and aggressive behaviors, will be examined. In addition, the influence of general intelligence, as well as the family, on the development of aggressive students will be presented. Basically, the social relationships

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

368

VOLUME I: DIAGNOSIS AND TREATMENT

Learning problems (e.g., from specific developmental disorders) Comorbid ADHD Intelligence Family background (e.g., parents’ education, promotion of academic skills by parents) Peer relationships Relationship with the teacher Figure 22.1 Factors which influence the school experiences of aggressive children

with peers and teachers and characteristics of the school itself contribute to the course of aggressive behavior.

PSYCHOPATHY IN CHILDREN AND ADOLESCENTS Aggressive behavior consists of a large number of heterogeneous behaviors which vary with the developmental level and sex of the children (Scheithauer & Petermann, 2002). It can be expressed through injury to persons or animals, damage to things, through stealing of other’s belongings, through the disrespect of societal rules as well as oppositional behavior towards attachment figures like parents or teachers. The expression of aggressive actions ranges from verbal aggression (e.g., verbal abuse, defamation, blackmailing) to physical aggression (e.g., threatening physical violence, beating, kicking) and can be committed individually or in a group. Besides, aggression can be classified according to further dichotomous aspects, for example, hostile (with the intention to harm someone) or instrumental (with the intention to cause harm to a particular person), overt (fights or quarrels) or covert (blackmailing or stealing) and reactive (as reaction to a perceived threat) or proactive (implemented purposely to attend a specific aim) (Vitiello & Stoff, 1997). The diversity of aggressive behaviors results in the fact that conduct disorders, as described by the established ICD-10 (World Health Organization, 1993) or DSM-IV-TR (American Psychiatric Association, 2000) classification systems for children, include children who differ markedly concerning the causes of their common disorder. Aggressive children with psychopathic tendencies constitute a homogeneous group (Blair et al., 2006). According to Hare (1985), psychopathy is characterized by affective interpersonal dysfunctions and impulsive antisocial behavior. The affective interpersonal dysfunctions concern, for example, reduced fearfulness, lack of empathy, superficial charm or an inflated self-esteem. Impulsive antisocial behavior includes little behavioral control, a parasitic lifestyle, irresponsibility or manipulative and fraudulent behaviors. According to Blair, Mitchell and Blair (2005), these affective interpersonal deficits in particular characterize psychopathy and go along with a high rate of antisocial behavior. Additionally, low impulse control or reduced ability to adapt one’s behavior according to the situation (response modulation) leads to aggressive behavior. Aggressive antisocial behaviors can be versatile, whereby the use of planned and purposeful aggressive behavior is particularly noticeable. Reactive aggression can occur additionally as a reaction to a perceived provocation.

EDUCATIONAL ISSUES

369

LEARNING IN PSYCHOPATHIC CHILDREN AND ADOLESCENTS The causes of psychopathy have not been sufficiently clarified. However, explanation attempts particularly refer to impairments regarding the social and moral socialization, resulting from learning deficits. These learning deficits are attributed to genetic factors and the associated dysfunctions in the amygdala and the orbital and ventrolateral frontal cortex (Blair et al., 2006). The dysfunction of the amygdala has been shown to result in reduced fearfulness, that is, particularly with the affective interpersonal impairments of psychopathy. The ability to experience fear is, however, an important prerequisite to learning by avoidance. Avoidance learning includes the anticipation of negative consequences. The anticipation of negative consequences, for example, being scolded by the mother, leads to fear and the desire to avoid the negative consequences. If aggressive behavior is consequently avoided, the fear is reduced. This reduction can be felt physically when, for example, the heart rate drops. Fear reduction is a positive experience and constitutes a negative reinforcement. Therefore, the probability that this behavior will be avoided in future increases. Through avoidance learning, people are able to learn important rules for living together. Children with psychopathic tendencies show reduced fearfulness. This explains why it is difficult for psychopathic children to avoid aggressive behaviors or rule breaking (see Blair et al., 2006). Hence, well-known educational strategies, which usually produce positive developmental results in children, possibly produce lower success with these children (Wootton et al., 1997). An inadequate adjustment to changing social situations is possibly facilitated by the fact that psychopaths are less able to give up well-proven actions. They tend to retain behaviors which formerly yielded positive results longer and continue to practice them even if they no longer lead to the desired outcome or even produce negative consequences. According to Patterson and Newman (1993), this occurs mostly when positive and negative stimuli are present in a situation. This is explained by low impulse control and impaired reaction modulation. Reaction modulation refers to the relatively fast and automatic change in attention from the execution of an action to its evaluation (Newman, Patterson & Kosson, 1987). Attention is directed to the action for a longer time and the evaluation only commences later. This increases the probability of experiencing frustration and consequently aggressive behaviors can occur. These learning peculiarities lead to impairments concerning children’s acquisition of social norms and rules, and make adjustment to changing demands difficult. It is obvious that affected children have substantial difficulties meeting school requirements, have rather negative attitudes toward school and develop school aversion.

LEARNING PROBLEMS IN SCHOOL Children with aggressive antisocial behaviors are often less successful in school and more often affected by developmental disorders like dyslexia, language or speech disorders (Hinshaw, 1992). They show poor school performance and disenrol from school early. Besides, behavior problems of children can contribute to making learning more difficult for them. The disturbing behavior and the amount of time that children cannot take part in

370

VOLUME I: DIAGNOSIS AND TREATMENT

lessons due to a teacher’s disciplinary measures, bar the children from learning. Vice versa, learning problems in children can lead to less success, frustration and self-esteem problems, which in turn provoke disturbing behaviors. Good academic results go along with better self-confidence in children and better school achievement reduces the risk for delinquent behaviors (Caprara et al., 2000). In a study, Fergussen, Horwood and Ridder (2005) have presented results on the consequences of aggressive behavior during middle childhood for early adulthood. These were obtained from data of a birth cohort of boys and girls, which was repeatedly examined over 25 years. Aggressive behavior between the age of seven to nine years goes along with quite a large number of negative developments, like low academic and vocational success, criminality, drug consumption, psychological and partnership problems. Lower academic and vocational success was more probable for aggressive children, if further impairments like lower cognitive abilities and attention problems were present. In general, a dose-dependent effect could be shown: the more intensive the aggressive behavior was during middle childhood, the more grievous were the negative consequences in early adulthood. However, a clear direction of the relationship between aggressive antisocial behavior and academic problems cannot be identified. Probably, a reciprocal relationship exists. Trzesniewski et al. (2006) reported that the connection between low reading skills (as an indicator of school achievement problems) and aggressive antisocial behavior is mostly mediated through family factors. Deficient and inconsistent education is a risk factor for aggressive antisocial behavior and for low reading skills. This parental education supports neither the acquisition of adequate social behaviors nor of academic skills (e.g., they do not provide appropriate material for play). Across the developmental process, aggressive antisocial behaviors and school achievement problems reinforce each other. To which extent these findings can be generalized to children and adolescents with psychopathic characteristics is as yet unclear. Raine et al. (2006) were able to identify a relationship between proactive aggression at the age of seven and psychopathic characteristics at the age of 16. Besides delinquency and serious aggression, the adolescents also showed school aversion and grew up in a family environment with multiple risks, for example, low social status and paternal drug abuse.

ATTENTIONAL PROBLEMS AND ADHD Generally, a high comorbidity between conduct disorder and ADHD can be observed (Loeber et al., 2000; Schachar & Tannock, 1995). The comorbid presence of conduct disorder and ADHD goes along with increasingly stable and more severe antisocial behavior. School achievement problems and lower graduation rate are common negative consequences of ADHD (Biederman et al., 2004). In connection with aggressive behavior, the question arises, whether school achievement problems are caused by comorbid ADHD or by the aggressive behavior itself. From the Developmental Trend Study, Loeber and colleagues (2000) report that the relationship between aggressive behavior and school achievement problems can be explained better through comorbid ADHD. Therefore, school achievement problems of children with conduct disorders possibly result from ADHD and the related impairments of executive functions. The exact relationship between ADHD and psychopathy is still insufficiently researched at present. In the case history of psychopathic adults, ADHD is often found along with

EDUCATIONAL ISSUES

371

a diagnosed conduct disorder. Colledge and Blair (2001) confirm this for children with psychopathic tendencies. They examined the relationship between inattention and impulsivity and psychopathic tendencies in boys with emotional and behavioral problems. They report significant correlations between teacher reporting of inattention, hyperactivity impulsivity and psychopathic tendencies. Following the statistical control for hyperactivity and impulsivity, however, no significant links remained between psychopathic characteristics and the inattentiveness of ADHD. Hence, the link between ADHD and psychopathy is probably due to the general impulsivity common to both disorders and not due to the attentional deficits. Affective interpersonal impairments are thus not connected with attentional deficits. It can be concluded that the feature combining both disorders is impulsivity, which leads to aggressive dissocial behavior (Abramowitz, Kosson & Seidenberg, 2004). It is therefore questionable to what extent school achievement problems and reduced academic success of psychopathic people can be explained through the attentional deficits typical for ADHD.

INTELLIGENCE The intelligence quotient (IQ) has also been considered as an important factor in connection with aggressive behavior and criminality (Fergussen, Horwood & Ridder, 2005). A number of studies show an inverse relation between IQ and aggressive, antisocial and criminal behavior, as well as lower school success. Lower IQ values within the normal range are considered as a risk factor for aggressive behavior and can contribute to behavior problems through a reduced ability to articulate stress or lower self-esteem (Goodman, Simonoff & Stevenson, 1995). According to Moffitt (1993), most aggressive and delinquent adolescents show a lower verbal IQ which is based on neuropsychological impairments. Contrary to this, workaday psychology assumes that psychopaths show higher intelligence (see Blair et al., 2006). This assumption could, for example, mistakenly result from the superficial charm. In studies with adults, no relationships could be identified between affective interpersonal impairments and intelligence (Hare, 2003). From a nonclinical sample of children, Frick et al. (2005) reported that the affective interpersonal impairments are connected with average but somehow lower IQ values compared to normal children. On the other hand, there are the consistent findings that lower intelligence goes along with a higher degree of antisocial behavior. Generally, it is therefore worth questioning to what extent intelligence deficits can be assumed when considering psychopathology as a special form of aggressive antisocial behavior.

FAMILY FACTORS Family factors play an important role in the development and retention of aggressive antisocial behaviors (Loeber et al., 2000; Moffitt et al., 1996). Children with conduct disorders, particularly those who exhibit behavior problems very early in life (early starters), more often grow up within a negative family environment. The parents are often characterized by a low social status, low educational level or suffer from psychological disorders like depression or drug abuse or criminality. The children are exposed to a higher risk for abuse, maltreatment or negligence. The parents’ educational background is poorer and the children

372

VOLUME I: DIAGNOSIS AND TREATMENT

are rarely offered a stimulating learning environment. Furthermore, the parents seldom offer positive role models for their children concerning school work or show appreciation of their school achievements. Children from such families can learn aggressive and antisocial behaviors as survival strategies in the aversive social environment. The parents’ educational behavior plays a decisive role here. The parents do not provide their children with clear rules and do not react consistently to the children’s positive and negative behaviors. Therefore, the children lack orientation to which behaviors are appropriate. Exaggerated strictness up to physical punishment by the parents, as well as lacking interest in the child’s activities outside the family, contribute to a stressful parent–child relationship. Escalation of conflicts is reinforced through coercive interactions (Patterson, Reid & Dishion, 1992), during which the child and the parents blackmail each other through increasingly aggressive and hostile behaviors. Due to this mutual blackmailing, the child learns to use aggressive antisocial behavior as a means to avert demands and assert personal goals. At the same time, parents scarcely offer models for positive social behavior and pay less attention to the positive behaviors of the child. The child thereby systematically learns to use aggressive antisocial behaviors in the interaction with others while positive social behaviors remain underdeveloped. So far, there exist few empirical studies on the effects of family stress and such dysfunctional educational behaviors on the development of children with psychopathic tendencies. It can be assumed, that the parents of these children tend to punish them frequently and more often react negatively to them, because these children rarely respond compliantly to threatened punishment due to their reduced fearfulness. In a review, Dadds and Salmon (2003) discuss the aggressive antisocial behavior of children as a result of the reciprocal influence between children’s insensitivity to punishment and dysfunctional educational behaviors. The child’s insensitivity to punishment, resulting from reduced fearfulness, is described by Kochanska (1997) as a temperamental characteristic. This results in the child reacting less to parents’ emotional expressions like fear or sorrow, which would contribute to behavior regulation in other children. It can be assumed, that the child will react with little agitation and fear to negative feedback from parents. Since mild disciplinary measures cause little unpleasant expectations and feelings in the child, the described cycle, in which the parents react with increasing rejection and severe punishment to the behavior of the child, begins here as well. The low sensitivity to punishment is thus reinforced through the parents’ behavior. On this note, Kochanska (1997) reports from a longitudinal study on five-year-old children, that relatively fearless children develop positively if a secure bond with attachment figures exists and the parents are responsive to the child. Dadds and Salmon (2003) conclude that on the basis of a secure and loving relationship, a child – with his need for reward – can acquire adequate social behaviors through the positive effects of this relationship. The temperament of these children requires very empathetic and loving treatment by parents, so they can develop positively. Lykken (1995) mapped out the interaction of biological and social factors, by emphasizing that children who are difficult to socialize, carry a higher risk of developing aggressive behavior in any family environment, whereas children with easier temperaments carry higher risks only in unfavorable family environments. In an adverse family environment, fearless children probably have the advantage of feeling less threatened and are better protected against the development of fear or depressive disorders (see Blair et al., 2006).

EDUCATIONAL ISSUES

373

RELATIONSHIP WITH PEERS Aggressive antisocial behavior is often associated with peer rejection and the absence or lack of integration into the peer group (Rubin, Bukowski & Parker, 1998). The disrespect of rules, the disruption of playful activities or aggressive assaults make these children and adolescents little valued playmates or group members. On the other hand, aggressive children and adolescents often associate with others displaying the same disruptive behavior. It can be assumed that these friendships are less intensive and supportive because the children lack social skills and negative interactions occur more often (see Bagwell, 2004). From a comparison of aggressive and nonaggressive boys’ friendships in middle childhood, Bagwell and Coie (2004) report that aggressive boys evaluate their friendships equally positive as nonaggressive boys. These self-evaluations, however, are contrary to behavior observation. According to this, nonaggressive boys show more positive engagement and task-related behaviors and there is higher reciprocity between friends. Aggressive boys on the other hand break rules more often and express more negative feelings. It can be assumed, that the children’s problematic behavior is reinforced in such friendships, while adequate social behavior is practiced less. This union of aggressive children can already be observed in kindergarten (Perren & Alsaker, 2006). Aggressive behavior between students influences the classroom atmosphere negatively. In a comparison of classes with different levels of aggression, Klicpera et al. (1995) showed that the solidarity within the class and the relationship between teachers and students is clearly related to the frequency of aggressive behavior. In classes with more aggressive behavior, the students had a more negative attitude towards outsiders and were less ready to offer help in unfair conflicts. The degree to which students experience aggressive behavior in school also influences the frequency of aggressive behaviors. Boxer et al. (2003) report that the observation or experience of aggressive acts can lead to an increase in aggressive behavior among students. In this way, aggressive peers present a model, which leads to the imitation of aggressive behavior by others. Besides aggressive behaviors, students report fewer positive expectations of the future and judge their school to be less safe. So far, no empirical studies on the development of peer-group relationships in children with psychopathic tendencies exist. The affective interpersonal impairments of psychopathic children is expressed through the reduced ability to identify others’ emotions, particularly emotions like sadness and fear (Blair et al., 2001). The reduced ability to recognize or predict others’ emotions is associated with oppositional and aggressive behavior and peer problems in kindergarten (Denham et al., 2002). The ability to react sensitively to others’ emotional expressions is an important prerequisite for empathy, helpful behaviors, as well as the development and management of satisfactory peer relationships. In children with psychopathic tendencies, these difficulties occur early in life and hinder the development of peer relationships. Since the children have difficulties reacting sensitively to others, they are increasingly rejected. Consequently, friendships are rather partnerships of convenience, which serve the achievement of personal advantages and recognition, while lacking a deeper emotional connection. These students presumably have difficulties fitting into the class community, because they are less able to react to emotional stimuli by other students and the teacher for behavior regulation. It is unclear whether a union of these adolescents with other disruptive adolescents leads to a reinforcement of aggressive antisocial behaviors. Vitaro et al. (1997) reported that in severely aggressive antisocial boys, further delinquent behaviors

374

VOLUME I: DIAGNOSIS AND TREATMENT

are not influenced by the friends’ characteristics. The association with deviant peers and future delinquent behaviors result from earlier problem behaviors. Only in moderately aggressive adolescents could an increase in delinquent behavior, through an association with other disruptive adolescents, be observed.

RELATIONSHIP WITH THE TEACHER The teacher is an important attachment figure outside the family and the quality of the relationship with the teacher influences school achievement and social behavior. A good teacher–child relationship can represent a protective factor for children with a high risk of academic problems and externalizing problem behaviors (Pianta, Nimetz & Bennet, 1997). If a close, conflict-free relationship exists between teacher and child and if the teacher has optimistic expectations concerning this student, the student’s school adjustment is improved. Blankemeyer, Flannery and Vazsonyi (2002) reported that aggressive children, who adjust well in school, clearly judge the relationship with their teacher more favorably compared to aggressive children with academic problems. Silver et al. (2005) were able to show that with a close teacher–child relationship, problem behaviors decreased, particularly in children with severe problems. However, more often there exists a stressful and conflicting relationship with aggressive students (Birch & Ladd, 1998). The problematic behavior increases the possibility that no positive relationship can be developed between teacher and student. The teachers’ inability to adequately deal with students’ difficult behaviors and the experience of helplessness, can drive teachers to further reinforce the problematic behavior and react inadequately, for example, with sarcastic comments or belittling of the student in front of others, thereby further damaging the relationship. Students with psychopathic tendencies probably have a particularly high risk for having a bad relationship with the teacher. Insensitivity towards feelings like sadness or fear in others and low sensitivity towards punishment make these children very difficult students. Particularly where no clear behavior rules are provided, it is necessary to regulate individual behaviors according to others’ emotional expressions. With students exhibiting psychopathic tendencies, this hardly seems possible. Fischer and Blair (1998) confirm this by showing that a low ability to differentiate between moral values (based on emotional expression) and conventional rules is related to psychopathy at adolescence. The identification of and adherence to moral values requires emotion knowledge and empathy. The negative interaction style, which children experience with the parents, can easily be transferred to the relationship with the teacher. If teachers achieve no change in the behavior in students by employing the usual educational methods, such as individual expressions of irritation or sadness and mild disciplinary measures, increasingly negative and aggressive interactions will occur here as well.

SUMMARY AND PERSPECTIVE Children with aggressive behaviors often have learning difficulties and less success in school right up to school dropout. At the same time, school is the second sphere besides the parents’ house, where aggressive behaviors present an all-embracing problem. Students’ aggressive

EDUCATIONAL ISSUES

375

behavior not only impairs the development of the child or adolescent concerned, but the psychological health of other students and teachers as well, contributing to a stressful school atmosphere. At present, some proven programs exist, which reduce and prevent these problems within the school context, by strengthening the bond between student, teacher and school, supporting the introduction of clear school and classroom rules, but also by practicing empathic and consistent teaching. The Bullying Prevention Program (BPP) from Olweus (1993) is an example of such a school-based measure to reduce and prevent violence among students, which can be implemented by the teacher. It contains modules that are directed at all the students in one class, as well as elements that specifically target aggressive students and victims. Evaluation studies concerning this program show that it can result in a reduction of aggressive behavior in students. Such interventions are, however, not sufficient for children and adolescents with a stable aggressive behavior and/or psychopathic features. School- or classroom-based interventions probably do not aid them sufficiently in the development of alternative behaviors and critical deficits in social perception, problem solving and empathy cannot be treated. For this purpose, a therapeutic behavior-oriented procedure and the promotion of social problem solving in aggressive children have proven successful (Vitale et al., 2005). An intervention program that targets the social problem solving of aggressive children and the acquisition of socially adequate behavior is described in the Training with Aggressive Children by Petermann and Petermann (2006). This program is composed of combined individual and group trainings with 6- to 12-year-old children and their parents. The superordinate goal of this training is the development of behavioral alternatives to aggressive behaviors. The following are promoted:

r a differentiated perception; r adequate self-assertion; r cooperation and helping behavior; r self-control; and r empathy ability. Within the context of this intervention, the parents’ educational behaviors are promoted, for example, parents’ reaction to children’s misconduct and adequate parental behavior regarding desired behavior of children is discussed, as well as methods like token systems, time out and the management of crisis situations. To what extent the success of these programs can be transferred to subgroups of children and adolescents with psychopathic characteristics is unclear so far. It can be assumed that with these children, an educational behavior, setting clear and precise limits, along with a positive emotional relationship, is supportive both at home and in school. Dadds and Salmon (2003) conclude that an escalation of conflicts through increasing punishment by parents must be avoided and more energy must be invested in the development of a positive parent–child relationship to achieve positive socialization of these children. The same should apply to the teacher–child relationship, so that the child can learn to behave adequately and experience positive feedback in school as well. Thus, the motivation to attend school and to perform well in school can be influenced positively.

376

VOLUME I: DIAGNOSIS AND TREATMENT

REFERENCES Abramowitz, C.S., Kosson, D.S. & Seidenberg, M. (2004). The relationship between childhood Attention Deficit Hyperactivity Disorder and conduct problems and adult psychopathy in male inmates. Personality and Individual Differences, 36, 1031–47. American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders (4th ed. text revision). Washington, DC: American Psychiatric Association. Bagwell, C.L. (2004). Friendships, peer networks, and antisocial behavior. In J.B. Kupersmidt & K.A. Dodge (eds.), Children’s Peer Relations: From Development to Intervention. Decade of Behavior (pp. 37–57). Washington, DC: American Psychological Association. Bagwell, C.L. & Coie, J.D. (2004). The best friendships of aggressive boys. relationship quality, conflict management, and rule-breaking behavior. Journal of Experimental Child Pyschology, 88(1), 5–24. Biederman, J., Monuteaux, M.C., Doyle, A.E. et al. (2004). Impact of executive function deficits and Attention-Deficit/Hyperactivity Disorder (ADHD) on academic outcomes in children. Journal of Consulting and Clinical Psychology, 72, 757–66. Birch, S.H. & Ladd, G.W. (1998). Children’s interpersonal behaviors and the teacher–child relationship. Developmental Psychology, 34, 934–946. Blair, R.J.R., Colledge, E., Murray, L. & Mitchell, D. G. V. (2001). A selective impairment in the processing of sad and fearful expressions in children with psychopathic tendencies. Journal of Abnormal Child Psychology, 29, 491–8. Blair, R.J.R., Mitchell, D. & Blair, K. (2005). The Pyschopath: Emotion and the Brain. Oxford: Blackwell Publishing. Blair, R.J.R., Peschardt, K.S., Budhani, S. et al. (2006). The development of psychopathy. Journal of Child Psychology and Psychiatry, 47, 262–75. Blankemeyer, M., Flannery, D.J. & Vazsonyi, A.T. (2002). The role of aggression and social competence in children’s perceptions of the child–teacher relationship. Psychology in the Schools, 39, 293–304. Boxer, P., Edwards-Leeper, L., Goldstein, S. et al. (2003). Exposure to ‘low-level’ aggression in school: associations with aggressive behavior, future expectations, and perceived safety. Violence and Victims, 18, 691–704. Caprara, G.V., Barbaranelli, C., Pastorelli, C. et al. (2000). Prosocial foundations of children’s academic achievement. Psychological Science, 11(4), 302–6. Colledge, E. & Blair, R.J.R. (2001). The relationship in children between the inattention and impulsivity components of attention deficit and hyperactivity disorder and psychopathic tendencies. Personality and Individual Differences, 30, 1175–87. Dadds, M R. & Salmon, K. (2003). Punishment insensitivity and parenting: temperament and learning as interacting risks for antisocial behavior. Clinical Child and Family Psychological Review, 6, 69–86. Denham, S.A., Caverly, S., Schmidt, M. et al. (2002). Preschool understanding of emotions: contributions to classroom anger and aggression. Journal of Child Psychology and Psychiatry, 43, 901–16. Fergussen, D.M., Horwood, L.J. & Ridder, E. M. (2005). Show me the child at seven II: childhood intelligence and later outcomes in adolescence and young adulthood. Journal of Child Psychology and Psychiatry, 46, 850–8. Fischer, L. & Blair, R.J.R. (1998). Cognitive impairment and its relationship to psychopathic tendencies in children with emotional and behavioral difficulties. Journal of Abnormal Child Psychology, 26, 511–19. Frick, P.J., Lilienfeld, S.O., Ellis, M. et al. (1999). The association between anxiety and psychopathy dimensions in children. Journal of Abnormal Child Psychology, 27, 383–92. Frick, P.J., Stickle, T.R., Dandreaux, D.M. et al. (2005). Callous-unemotional traits in predicting the severity and stability of conduct problems and delinquency. Journal of Abnormal Child Psychology, 33, 471–87. Goodman, R., Simonoff, E. & Stevenson, J. (1995). The impact of child IQ, parent IQ and sibling IQ on child behavioural deviance scores. Journal of Child Psychology and Psychiatry, 36, 409–25.

EDUCATIONAL ISSUES

377

Hare, R.D. (1985). Comparison of procedures for the assessment of psychopathy. Journal of Consulting and Clinical Psychology, 53, 7–16. Hare, R.D. (2003). The Hare Psychopathy Checklist–Revised (PCL-R), 2nd edn. Toronto: Multi Health Systems. Hinshaw, S.P. (1992). Externalizing behavior problems and academic underachievement in childhood and adolescence: causal relationships and underlying mechanisms. Psychological Bulletin, 11, 127–55. Klicpera, C., Gasteiger Klicpera, P, Schabmann, A. et al. (1995). To what extent do school and classspecific factors contribute to aggression in schools? Zeitschrift f¨ur Kinder- und Jurgendpsychiatrie, 23(4), 243–54. Kochanska, G. (1997). Multiple pathways to conscience for children with different temperaments: from toddlerhood to age 5. Developmental Psychology, 33, 228–40. Loeber, R., Green, S.M., Lahey, B.B. et al. (2000). Findings on disruptive behavior disorders from the first decade of the Developmental Trends Study. Clinical Child and Family Psychology Review, 3, 37–60. Lykken, D.T. (1995). The Antisocial Personalities. Hillsdale: Lawrence Erlbaum. Moffitt, T.E. (1993). The neuropsychology of conduct disorder. Development and Psychopathology, 5, 135–51. Moffitt, T.E., Caspi, A., Dickson, N. et al. (1996). Childhood-onset versus adolescent-onset antisocial conduct problems in males: natural history from ages 3 to 18 years. Development and Psychopathology, 8, 399–424. Newman, J.P., Patterson, C.M. & Kosson, D.S. (1987). Response perserveration in psychopaths. Journal of Abnormal Psychology, 96, 145–8. Olweus, D. (1993). Bullying at School: What We Know and What We Can Do. Oxford: Blackwell Patterson, C.M. & Newman, J.P. (1993). Reflectivity and learning from aversive events: toward a psychological mechanism for the syndromes of disinhibition. Psychological Review, 100, 716–36. Patterson, G.R., Reid, J. & Dishion, T.J. (1992). A Social Interactional Approach: Vol. 4. Antisocial Boys. Eugene: Castalia. Perren, S. & Alsaker, F.D. (2006). Social behavior and peer relationships of victims, bully-victims, and bullies in kindergarten. Journal of Child Psychology and Psychiatry, 47, 45–57. Petermann, F. & Petermann, U. (2006). Behavior Therapy with Aggressive Children and Adolescents. New York: Lang. Pianta, R.C., Nimetz, S.L. & Bennett, E. (1997). Mother–child relationships, teacher–child relationships, and school outcomes in preschool and kindergarten. Early Childhood Research Quarterly, 12, 263–80. Raine, A., Dodge, K.A., Loeber, R. et al. (2006). The reactive-proactive aggression questionnaire: differential correlates of reactive and proactive aggression in adolescent boys. Aggressive Behavior, 32, 159–71. Rubin, K.H., Bukowski, W. & Parker, J.G. (1998). Peer interactions, relationships, and groups. In W. Damon & N. Eisenberg (eds.), Handbook of Child Psychology, Vol 3. Social, Emotional, and Personality Development (pp. 619–700). New York: John Wiley & Sons, Inc. Schachar, R. & Tannock, R. (1995). Test of four hypotheses for the comorbidity of attention-deficit hyperactivity disorder and conduct disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 34, 639–48. Scheithauer, H. & Petermann, F. (2002). Aggression. In F. Petermann (ed.), Lehrbuch der Klinischen Kinderpsychologie und –psychotherapie (pp. 187–226). G¨ottingen: Hogrefe. Silver, R.B., Measelle, J.R., Armstrong, J.M. & Essex, M. (2005). Trajectories of classroom externalizing behavior: contributions of child characteristics, family characteristics, and the teacher–child relationship during the school transition, Journal of School Psychology, 43, 39–60. Trzesniewski, K.H., Moffit, T.E., Caspi, A. et al. (2006). Revisiting the association between reading achievement and antisocial behavior: new evidence of an environmental explanation from a twin study. Child Development, 77, 72–88. Vitale, J.E., Newman, J.P., Bates, J.E. et al. (2005). Deficient behavioral inhibition and anomalous selective attention in a community sample of adolescents with psychopathic and low-anxiety traits. Journal of Abnormal Child Psychology, 33, 461–70.

378

VOLUME I: DIAGNOSIS AND TREATMENT

Vitaro, F., Tremblay, R.E., Kerr, M. et al. (1997). Disruptiveness, friends characteristics, and delinquency in early adolescence: a test of two competing models of development. Child Development, 68, 676–89. Vitiello, B. & Stoff, D.M. (1997). Subtypes of aggression and their relevance to child psychiatry. Journal of the Academy of Child and Adolescent Psychiatry, 36(3), 307–15. World Health Organization (1993). Internationale Klassifikation psychischer St¨orungen. ICD-10, Kapitel V (F). Bern: Huber. Wootton, J.M., Frick, P.J., Shelton, K.K. & Silverthorn, P. (1997). Ineffective parenting and childhood conduct problems: the moderating role of callous-unemotional traits. Journal of Consulting and Clinical Psychology, 65, 292–300.

PART IV

Intervention, Treatment and Management

CHAPTER 23

Intervention, Treatment and Management of ADHD Beate Herpertz-Dahlmann, Kerstin Konrad Technical University of Aachen, Germany

Sabine C. Herpertz University of Rostock, Germany

The terminology, classification and symptoms of disorders involving attention deficit, overactivity and impulsivity are outlined in Chapter 12. According to DSM IV there are three subtypes of attention deficit/hyperactivity disorder (ADHD): a predominantly inattentive type; a predominantly hyperactive-impulsive type; and a combined subtype. The treatment strategy of ADHD is multimodal and complex; in most cases there is no single approach (Barkley, 1998). Therapy methods should involve the individual, parents and teachers and depend on the age of the patient (child, adolescent or adult), severity of symptoms and on comorbidity with other psychiatric disorders (Table 23.1). The diagnosis of ADHD is still made on clinical judgment. The diagnostic procedure includes a careful history from birth to the present, the family history, a direct observation of the child in the office and – whenever possible - at school, a psychoeducational assessment including the child’s intelligence and specific learning disabilities and a medical and neurological evaluation. However, neuroimaging methods are unnecessary in selecting treatment strategies for ADHD, because up to now structural and functional brain abnormalities in ADHD are only based on group effects and may not be identified in the individual child. ADHD children are also at high risk to have or develop antisocial behavior (for a review see Chapter 12), substance abuse, anxiety and mood disorders. ADHD is also often associated with tic disorders including Tourette’s syndrome and learning disorders. The comorbid condition of ADHD and conduct disorder (CD), which is an important precursor of adult antisocial personality disorder, particularly benefits from a multidimensional treatment concept comprising medication and psychosocial treatment which is outlined below.

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

382

VOLUME I: DIAGNOSIS AND TREATMENT

Table 23.1 Qualification of evidence of treatment recommendations in ADHD

MPH or AMF ATMX BT MPH + BT Parent training

Level of evidence

Categories of recommendation

I-a I-a I-b I-b III

A A C B B

MPH: methylphenidate; AMF: amphetamine; ATMX: atomoxetine; BT: behavior therapy. Level I-a: evidence obtained from meta-analysis of properly designed randomized controlled trials. Level I-b: evidence obtained from at least one properly designed randomized controlled trial. Level III: evidence obtained from well-designed cohort or case-control studies (US Agency for Health Research and Quality, 1992). Level A: good scientific evidence suggests that the benefits of the clinical service substantially outweighs the potential risks. Level B: at least fair scientific evidence suggests that the benefits of the clinical service outweighs the potential risks. Level C: at least fair scientific evidence suggests that there are benefits provided by this service, but the balance between benefits and risks are too close for making general recommendations (US Preventive Task Force).

MULTIMODAL TREATMENT Pharmacotherapy A large literature documents the beneficial effects of medication, particularly of stimulants (AACAP, 2002) and of antidepressants (Prince, 2006).

PATHOPHYSIOLOGY OF ADHD An emerging amount of literature on neuropsychology and neuroimaging in ADHD suggests a dysfunction of frontostriatal circuits in children with ADHD (Konrad et al., 2006). These brain regions are rich in catecholamines. Catecholamine dysregulation is implicated in the pathogenesis of ADHD, because stimulants and antidepressants directly act on catecholamine metabolism in the brain.

STIMULANTS Stimulant medications are among the first class of compounds to be used in children, adolescents and adults with ADHD. The most important and well-known stimulant is methylphenidate (MPH). Over the last 10 years, there has been an eight-fold increase in the prescription of MPH (AACAP, 2002). The benefits and efficacy of MPH have been demonstrated in more than 150 randomized, controlled trials in school-age children. It has been shown that the administration of stimulant drugs brings about significant improvements in hyperactivity, inattention and impulsivity, as measured by behavioral questionnaires filled out by parents and teachers (Greenhill et al., 2001). In addition, stimulants improve cognitive function on laboratory measures of attention and impulsivity (Kempton et al., 1999).

INTERVENTION, TREATMENT AND MANAGEMENT OF ADHD

383

Stimulants are sympathetic drugs structurally similar to endogenous catecholamines. They are supposed to act on central dopamine and norepinephrine pathways that are important for frontal-lobe function. Among other brain areas the drug acts in the striatum by binding to the dopamine transporter, with a resulting increase of dopamine and norepinephrine in the synaptic cleft. Until recently there were only immediate release (IR) preparations of MPH with a brief duration of action improving attention and hyperactivity for three to five hours after oral administration. These preparations required several doses per day, mostly in the morning and at midday. Today extended release (ER) long-acting forms are available. In most cases they allow for a single dose to be administered in the morning with a peak effect between one to five hours later (Table 23.2). In many children the effect will last for the entire school day. Once-daily dosing is also expected to improve compliance, because many children feel ashamed to take drugs at school. In addition a smooth pharmacokinetic profile of long-acting agents may provide a more consistent medication effect. The most important sustained delivery systems for MPH are OROS-MPH (osmotic exr tended release oral delivery system) and mixed-release MPH. OROS-MPH (Concerta, Johnson & Johnson) acts by an osmotic pump mechanism with an initial release of about 25 % of the dosage. The remainder of the tablet provides a plasma concentration–time profile characterized by an ascending absorption curve and lower peak plasma concentrations with less fluctuation in plasma concentrations than IR-MPH (Patrick et al., 2005). There are other novel forms of mixed-release MPH. One of them offers a 50% ratio of IRr Novartis). The ER preparation is an MPH polymer coated MPH and ER-MPH (Ritalin LA, to offer a four-hour delayed release of MPH. The resultant MPH plasma profile is biphasic and similar to twice-daily IR-MPH (Patrick et al., 2005). More exact pharmacokinetic data on immediate-release MPH, OROS–MPH and mixed-release MPH are shown in Table 23.2. Recent studies have demonstrated that a switch from immediate-release MPH to more extended or mixed forms improves symptom control and compliance (Hoare et al., 2005). Another important psychostimulant to treat ADHD is d-amphetamine, which also enhances dopaminergic and noradrenergic neurotransmission similar to the action of methylphenidate. Another isomer of amphetamine, called l-amphetamine, also releases norepinephrine as well as dopamine. Some children with ADHD may respond better to a mixture of d, l-amphetamine salts than to pure d-amphetamine. In Germany the mixed amphetamine salt prescription is not available, but is often used in the United States. In comparison to IR-methylphenidate, peak behavioral effects of mixed amphetamine salt prescriptions occur later and are more sustained (Pliszca et al., 2000). There is also an extended-release preparation, which contains a half-to-half ratio of immediate-release drug and delayedrelease preparation designed to release mixed amphetamine salts four to six hours after dosing. In general, treatment with mixed amphetamine salts is rather well tolerated and results in significant and persistent improvement of attentional and global functioning. Pemoline is a central nervous system stimulant with a different structure than MPH and amphetamine, which seems to improve central dopaminergic neurotransmission. Its prescription has become rare because there have been hypersensivity reactions involving the liver (see below). Several studies and clinical experience demonstrates that 70–80 % of children profit from treatment with at least one psychostimulant, if the medication is properly titrated (Markowitz, Straughn & Patrick, 2003; MTA Cooperative Group, 1999a). The average effect size for stimulants (0.91 for immediate-release formula and 0.95 for long-acting

0.3–1.0 0.3–1.0a 0.3–1.0a 0.3–1.,0a 0.1–0.5 0.5–2.0

2.5 3.5 ± 0.4 Not known 2.4 5–8 Children: 2–12 Adults: 9–12

30–60

30–60 30–60 30–60 30–60 Differs

T1/2 (h)

Usual absolute (and weight based) dosing range (mg/kg/d)

18–54 10–40 (max. 60) 20–max. 60 5–20 20–100

10–60

Daily dose (mg)

1 1 1 1–3 1

1–3

Number of single doses

a

T1/2 : half-life; IR: immediate release; ER: extended release; MR: mixed release. According to European treatment guidelines there may be a limited number of cases who benefit from higher doses and the maximum for them is 2 mg/kg/day or 108 and 100 mg respectively total daily dose (Banaschewski et al., 2006). b Special conditions of prescription.

Methylphenidate (IR) Methylphenidate (ER, MR) (brand names) R Concerta R Medikinet Retard R LA Ritalin d, l-amphetamine Pemolineb

Generic name

Beginning of clinical efficacy (min)

Table 23.2 Pharmacokinetic properties of stimulant drugs in children and adolescents

INTERVENTION, TREATMENT AND MANAGEMENT OF ADHD

385

preparations) is greater than the average effect for nonstimulants (0.62), although there is great variability (Biederman & Faraone, 2005). In adults the degree of efficacy of MPH is similar to what has been reported for children. In a meta-analysis which included 140 MPH-treated ADHD adults and 113 placebo-treated ADHD adults (Faraone et al., 2004), the mean effect size was 0.9 with even higher effects up to 1.3 when treatment was optimized to high doses, that is, ≥ 0.9 mg/kg/day. According to this study, higher doses are recommended as they led to nearly twice the effect size than lower doses (1.3 vs. 0.7). The medication must be fine-tuned to the needs of the individual patient in regard to the dosages and timing of application, particularly because no parameters have yet been identified that predict optimal performance (Dodson, 2005).

Adverse Effects The most common side effects of stimulants are appetite suppression and sleep disturbance (for a review see Spencer, Biederman & Wilens, 2002). Other less frequent side effects include headache and abdominal pain. In younger children stimulants are more likely to induce depression and anxiety than in older children. A very rare side effect is the exacerbation of psychotic symptoms. Adverse effects of MPH and amphetamine are similar and increase with larger dosage. In spring 2006 the FDA discussed recommending a ‘black-box warning’ that would describe the cardiovascular risks of stimulant drugs. Although a stimulant drug-induced mild increase in heart rate and blood pressure had been recognized for more than 20 years, the committee sought to emphasize more selected and restrictive use, because there is a rapid increase in exposure to ADHD drugs in adults, especially in the United States. According to a report by Nissen (2006), 1.5 million adults take stimulants on a daily basis, with 10 % of users older than 50 years of age. Based on a profound report on the prevalence rates of sudden death associated with ADHD drugs (MPH, amphetamine and atomoxetine) the FDA at last decided not to publish such a warning given the rarity of these adverse events. The background population rates of sudden death appear to be as high as 4.6 per 100,000 persons-year among children and adolescents and about 100 per 100,000 persons-year among adults. Only with small differences between product-specific rates patients taking stimulants or atomoxetine do not seem to have higher rates of sudden death than the general population, in both adults and children (www.fda.gov/ohrms/dockets/ac/06/briefing/20064210b 07 01 safetyreview.pdf). Previous investigations and clinical practice indicated that children with an individual or family history of tics are at greater risk to develop a tic disorder when they are given stimulants. Studies of the past decade have challenged this view (Spencer et al., 1999). There is some evidence that nonstimulants like atomoxetine have less impact on the development of a tic disorder; however, this has to be proven in more extensive studies (McCracken et al., 2003). Probably according to the loss of appetite and weight there is a possible retardation in growth velocity with long-term use. In a recent one to five years long-term study of children with high doses of stimulants (> 2.5 mg MPH/kg/day) showed diminished gains in height after four years of stimulant medication (Charach et al., 2006). However, this dose is extremely high in comparison to that for children treated in Europe. Nevertheless, clinicians are advised to carefully monitor growth in children under stimulant therapy.

386

VOLUME I: DIAGNOSIS AND TREATMENT

Children suspected of stimulant-associated growth deficits should profit from drug holidays or an alternative treatment. Concern has also been raised about an addictive potential of stimulant treatment. However, because of the high effectiveness of stimulant treatment, it does not seem to be ethical to perform long-term placebo-controlled studies; naturalistic observation studies are the only way to solve this issue. Two recent meta-analyses have demonstrated that medication therapy of ADHD had a significant, beneficial effect in reducing the risk for substance abuse by 50 % (Faraone & Wilens, 2003; Wilens et al., 2003). After several months of treatment, pemoline medication was observed to be accompanied by elevations of AST (aspartate aminotransferase) and ALT (alanine aminotransferase). Since the substrate became available in 1975, 15 cases of acute hepatic failure have been reported to the FDA, 12 of which resulted in liver transplantation or death (Prince, 2006). In Germany pemoline may only be prescribed by child and adolescent psychiatrists; in the United States the FDA recommends obtaining liver functions every two weeks. Pemoline is no longer recommended as a stage-three agent in the treatment of ADHD (Pliszka et al., 2006).

COMORBID CONDUCT DISORDER AND/OR AGGRESSION Medication is not a first-line treatment for conduct disorder, but may be helpful when severe impulsivity and aggressive outbursts are present. A combination of behavior therapy including parent training and school-based interventions and of psychostimulants has shown to be effective in targeting antisocial behavior in ADHD (MTA Cooperative Study Group, 1999b). A meta-analysis demonstrated that certain antisocial behavior such as stealing and fighting can be reduced by methylphenidate (Connor, 2002). If the stimulant is not effective enough and the aggressive behavior is dangerous to the patient or others, an atypical antipsychotic may be added to the stimulant. Most randomized controlled trials have used risperidone, which resulted in significant improvements in behavioral disturbances (for a review see Patel et al., 2005; Pliszka et al., 2006). The onset of efficacy was rapid and consistently seen in children of varying ages. However, most of the studies are based on populations with subaverage intelligence or developmental disorders, and long-term effects are unknown. Physicians must be aware of the increased risks of excessive weight gain and metabolic disorders when prescribing antipsychotics. Unfortunately, no head-tohead comparisons are available to suggest whether pharmacological or nonpharmacological treatment is superior in aggressive youths.

NONSTIMULANT MEDICATION For a long time, tricyclic antidepressants were the second choice for treatment of ADHD in childhood. However, sudden unexplained deaths were reported in four children treated with desipramine, although a causal link between desipramine and these deaths could never be established (Biederman et al., 1995). Recently, atomoxetine (ATMX) has been approved by the FDA and the European agencies for treatment of ADHD in children, adolescents and adults; however, in Germany adults may only be medicated with ATMX, when treatment had already begun in adolescence. Similar to the tricyclics, ATMX blocks the norepinephrine reuptake pump on the presynaptic

INTERVENTION, TREATMENT AND MANAGEMENT OF ADHD

387

membrane, thereby increasing norepinephrine concentration in the synaptic cleft. However, in contrast to tricyclics this highly selective norepinephrine reuptake inhibitor has no anticholinergic side effects such as adverse effects on the cardiovascular system (Wernicke et al., 2003). In children and adolescents of lower weight, atomoxetine is initiated at a dose of 0.5 mg/kg and titrated over one to three weeks to a maximum dose of 1.2, in some cases up to 1.8 mg/kg/day (Kratochvil et al., 2003). Older adolescents and adults may start with 40 mg atomoxetine and end up with 80 to 100 mg/day titrated over one to three weeks (Kratochvil et al., 2003). In contrast to psychostimulants ATMX is not a controlled substance. Under the treatment with ATMX, subjects with ADHD have significant reductions in the symptom domains of inattention, hyperactivity and impulsivity. In several studies the effect size for reducing ADHD rating scale scores was about 0.7, in adults 0.4 (Michelson et al., 2003). Although some studies report benefits after one week of treatment, the full benefit of ATMX may take several weeks to become obvious. As there is a severe co-occurrence between ADHD and substance use disorders in young adults, a lack of abuse potential makes atomoxetine an interesting alternative to methylphenidate for patients suffering from the comorbid condition.

Adverse Effects In general ATMX is well tolerated. Side effects that occur more often in ATMX-treated subjects than in subjects receiving placebo, are appetite suppression, somnolence and small increases in heart rate and systolic and diastolic blood pressure. There seems to be no apparent effect on QTc intervals, and special ECG monitoring does not seem to be necessary. Recently the manufacturer of ATMX updated the labeling by adding a bold-face warning about hepatotoxity and suicidality. In two patients (of two million patients already medicated with ATMX) two suffered from severe hepatotoxic effects of the drug which disappeared on discontinuation. A black-box warning about suicidality was added because of increased suicidal ideation and actions (however, no completed suicides) following the inauguration of antidepressant treatment in children and adolescents. Caregivers are asked to closely observe the patient and to communicate concerning behavior to the doctor (Biederman & Faraone, 2005).

Comorbid Conditions Despite isolated case reports that tic severity might worsen under ADHD treatment with atomoxetine (Lee et al., 2004), a larger controlled trial demonstrated that atomoxetine did not exacerbate tic symptoms. Rather, there was some evidence of reduction of tic severity together with a significant reduction of ADHD symptoms (Allen et al., 2005). Patients that suffer from comorbid anxiety disorder also seem to benefit from treatment with atomoxetine. Patients with different forms of anxiety disorders (generalized anxiety disorders, social phobia or separation anxiety disorder) were investigated in a 12-week double-blind placebo-controlled study. At the end of the study atomoxetine demonstrated large effects on ADHD and moderate effects on anxiety symptoms, suggesting that the drug is helpful in the treatment of both conditions (Sumner et al., 2005). However, atomoxetine does not seem to be effective in the treatment of comorbid depression (Bangs et al., 2005).

388

VOLUME I: DIAGNOSIS AND TREATMENT

A case study of four children with nocturnal enuresis and ADHD described resolution of enuresis, but this preliminary finding has to be supported by controlled trials (Shatkin, 2004).

GENERAL RECOMMENDATIONS New pharmacotherapeutic developments have improved treatment for children and adolescents with ADHD: first, extended-release delivery systems for MPH and mixed amphetamine salts (in the United States) make intake for most youngsters easier and less embarrassing by a single dose in the morning. Second, a differently acting agent (ATMX) has been approved for use in this age group and may be helpful for those who do not sufficiently profit from stimulants. NICE (National Institute for Clinical Excellence) guidelines for treatment of ADHD in children and adolescents underline that methylphenidate, atomoxetine and dexamphetamine are all recommended as possible choices. When deciding which to use, doctors should consider the following:

r whether the child or adolescent has other comorbid conditions; r the side effects of each medicine; r factors that might make it difficult for the person to take the medicine at the right time; r the possibility that the medicine may be misused, or passed to another person for misuse; r the individual preference of the child or adolescent and/or their family or carer. Treatment with methylphenidate, atomoxetine or dexamphetamine should only be started after a specialist, who is an expert in ADHD, has thoroughly assessed the child or adolescent and confirmed the diagnosis (http://www.nice.org.uk/page.aspx?o=297171).

BEHAVIORAL THERAPY Behavioral techniques in ADHD can be divided into operant techniques and cognitive behavioral techniques. Operant techniques are very helpful to establish schedules and everyday structure as well as rules and guidelines for general behavior. Parents are advised to apply this technique at home. One of the most promising strategies to reinforce a certain behavior in a child is to increase attention by means of encouragement, praise or activities together. Withdrawing attention may also be a useful tool if the child exhibits problematic behavior. Another important aspect in the treatment of ADHD children is a graduate or stepwise approach. In other words several small steps are needed for the child to reach a certain treatment goal. In the majority of children it is helpful to concentrate first on one problematic situation or behavior and then to incorporate further areas in question. Age-appropriate and appealing incentives or motivational parameters must be provided within a task to reinforce adequate behavior (Barkley, 1990; Quaschner, 2001). Cognitive techniques try to improve self-control and self-management. They aim to enhance self-observation, which may be followed by self-instruction. However, these techniques require a high motivation and introspection capacity on behalf of the patient, which may be difficult for ADHD children, especially for the younger ones (Quaschner, 2001).

INTERVENTION, TREATMENT AND MANAGEMENT OF ADHD

389

Behavioral social skills training can be performed in groups. It is directed at improving understanding of social contexts, for example, to be aware that one’s own behavior will influence the behavior of others. The child is advised to acquire social skills which are lacking or insufficient in his or her behavioral repertoire.

PARENT TRAINING Training programs have been devised to help parents modify their behavior during interactions with their child. This includes establishing rules, reinforcing adaptive behavior (praise, rewards, token economy), making agreements, drawing up behavioral contracts and the use of mild punishment (‘time out’, withdrawal of privileges). Parent training has been used as a technique with children of different ages and a variety of externalizing disorders, including conduct disorders. Success depends on the duration of treatment, adequate comprehension and motivation in the parents, the severity of disturbed family interactions, the family’s socioeconomic status and the social support of the child by individuals outside the family (Herpertz-Dahlmann, 2001). In adults the effects of a specific psychotherapy have not been studied in depth, up to now. Stevenson et al. (2002) found reduced ADHD symptomatology after a cognitive remediation program in a randomized controlled trial of 22 ADHD adults compared to a waiting list control group. Hesslinger and colleagues (2002), from an open pilot study, reported improvement of ADHD severity, depression and personal health status when patients received a treatment program based on the principles of dialectical-behavior treatment and additional cognitive-behavioral treatment strategies. Safren et al. (2005) investigated the effect of cognitive-behavioral therapy in medicated ADHD patients and found a significant benefit from the combined therapy, compared to psychopharmacology alone. Cognitivepsychotherapeutic treatment programs appear to be a feasible, accepted and potentially efficacious treatment approach in adults with ADHD, which particularly focuses on the psychosocial consequences of ADHD.

COMBINED TREATMENT In search of evidence-based treatment recommendations in 1992 the US National Institute of Mental Health and the Department of Education initiated a multicenter randomized clinical trial to compare different strategies. In the Multimodal Treatment Study of Children with ADHD (MTA) more than 500 children with ADHD (combined type), aged 7 to 9.9 years, were assigned to four different treatment modalities for a duration of 14 months: 1. medication management (mostly methylphenidate) without additional psychotherapy; 2. intensive behavioral therapy (including child-focused treatment, parent training and a school-based intervention); 3. a combination of medication and behavior therapy; and 4. standard community care (mostly medication by their own provider). The medication management involved a careful initial titration and monthly assessments followed by dosage adjustments.

390

VOLUME I: DIAGNOSIS AND TREATMENT

The results were surprising: concerning core symptoms of ADHD-like inattention, hyperactivity, impulsivity or overall ADHD symptom ratings, medication management and combined treatment did not differ from each other in any significant way. These two trial arms resulted in a significantly greater improvement than behavior therapy alone or standard community care, although all four groups showed marked reduction in ADHD symptomatology (MTA Cooperative Study Group 1999a,b).

COMORBID DISORDERS There is a high overlap of ADHD with disruptive behavior disorders (for an overview see Chapter 12) and internalizing disorders. According to the nature of the comorbid disorder, different treatment strategies are necessary. In the MTA trial, patients with disruptive disorders like oppositional defiant disorder and conduct disorder (but without anxiety disorder) responded best to interventions that included medication (with or without behavioral therapy) (Jensen et al., 2001), although teachers observed relatively greater benefits in children treated with a combination of behavioral and medication therapy (MTA Cooperative Study Group, 1999b). Patients with internalizing disorders like anxiety and/or depression were likely to respond equally well to behavioral and medication treatment. Children with multiple associated disorders (like those with disruptive and anxiety disorders) profited best from combined treatment. In sum the results of this sophisticated trial demonstrate that a careful assessment of ADHD and its associated disorders is urgently needed for adequate treatment planning.

EVALUATION OF TREATMENT EFFECTS INCLUDING NEUROPSYCHOLOGICAL MEASURES OF INATTENTION AND IMPULSIVITY Until now, the majority of studies have used behavioral indices, such as parent and teacher rating scales or interviews to document treatment effects in ADHD. Only a minority of these studies have utilized objective measures to assess changes of symptoms, such as neuropsychological indices of attention or objective measures of locomotor activity (Denney & Rapport, 2001). Although behavioral ratings from parents and teachers can reliably differentiate between the two symptom domains of inattentiveness and hyperactivity/impulsivity (McBurnett et al., 1999), this approach remains problematic, since behavior which appears ‘inattentive’ may not, per se, necessarily be traceable to dysfunction in attentional processes or their underlying neural networks (Konrad et al., 2006). In addition, it has been demonstrated that stimulant effects on behavior ratings of inattentive symptoms seem to be more closely related to changes of objective measures of motor activity than to objective measures of attention (Konrad et al., 2005). Thus, although symptom scales have been found clinically useful, they suffer from problems of bias and subjectivity. Because they do not provide operational definitions of the specific symptoms of inattention, any one form of behavior (such as being easily distracted by external stimuli) can be misinterpreted as evidence of several different symptoms. For example, children sitting calmly and quietly at

INTERVENTION, TREATMENT AND MANAGEMENT OF ADHD

391

school are rated by their teachers as concentrating better and being less distracted than are fidgeting children. Thus, neuropsychological measures of attention might provide useful indices of treatment outcome. Generally, it has been shown that stimulant medications appear to significantly quicken reaction time (RT) and reduce RT variability. Medication also appears to reduce deficits in inhibition, such as in the Go/NoGo task (see Riccio, Reynolds & Lowe, 2001 for review). While for the reduction in RT and RT variability a linear dose–response relationship has been demonstrated in several studies (e.g., Konrad et al., 2004), there are more conflicting results whether stimulant effects on inhibitory control are better explained by quadratic response curves or not (Bedard et al., 2003; Tannock, Schachar & Logan,, 1995). Recently, Epstein and colleagues (2006) published an evaluation of the MTA study using neuropsychological parameters of inattention as additional outcome measures. Effect sizes for medication were in the moderate to large range with the largest effect sizes observed for RT measures. In summary, examination of standard Conners’ continuous performance test (CPT) outcome measures revealed that medication exerted its effect by making children more accurate in responding, speeding up RTs, and reducing RT variability. Interestingly, correlations between neuropsychological variables and ratings of ADHD behavior were largest for those neuropsychological variables that demonstrated the largest medication effects. In addition, these correlational analyses also revealed that neuropsychological outcomes were more highly correlated with teacher ratings compared to parent ratings. This may attest to a higher level of validity of teacher ratings since they demonstrate a significantly greater relationship to an objective indicator of ADHD behavior than parental ratings.

LONG-TERM TREATMENT OF CHILDREN AND ADOLESCENTS WITH ADHD Only 7% to 50% of subjects with ADHD, depending on the part of the world where they live, are treated with medication or psychosocial strategies. Of those patients with ADHD who are prescribed medication only 18% to 50% are continued with this treatment for some period of time, for example, two to three years (for a review see Hechtman, 2006). In a Canadian study by Miller, Lalonde and McGrail (2004) about 17,000 patients below the age 19 were prescribed MPH. The mean duration of treatment was less than two years. A minority of patients had continuous treatment: most of the children were treated intermittently for a period of less than four months. There are only two controlled multimodal treatment studies in which patients were followed up to two years (Abikoff et al., 2004a,b; Hechtman, Weiss & Perlman, 2004; MTA Cooperative Study Group 1999a, b). In these investigations the efficacy and safety of MPH could be demonstrated: ADHD symptomatology, academic achievement and comorbid oppositional defiant disorder were improved (Abikoff et al., 2004a,b; Jensen et al., 2001). The effect of combined medication and psychosocial treatment was superior to medication alone, not so much for ADHD symptoms, but for social, academic and emotional function. However, no effect of psychosocial treatment was seen 22 months after the treatment had stopped (MTA Cooperative Study Group, 2004a,b). The results of earlier – not controlled – but longer follow-up studies are not very optimistic. Patients who were treated for ADHD for at least three years between ages six and 12

392

VOLUME I: DIAGNOSIS AND TREATMENT

functioned significantly worse than healthy controls in different domains (school, work) and had more personality disorders. In comparison to the unmedicated group they were rather similar. However, they had fewer car accidents and fewer acts of delinquency, better social skills and self-esteem as well as a more positive view of their childhood (Hechtman, Weiss & Perlman, 1984). This study was biased by a rather unbalanced sample size: 104 untreated ADHD probands were compared to only 20 individuals medicated with stimulants. In a four-year longitudinal study the rate of decline in hyperactivity-impulsivity symptoms was independent of the amount and type of treatment received (Hart et al., 1995). In sum up to now there is only limited evidence that treatment with medication or combined multimodal strategies can diminish the risk of criminal behavior or antisocial personality disorder at a later age. However, prospective controlled studies with an adequate design (large enough samples, longer duration of follow-up) are not available. In addition – as ADHD is often a chronic, life-long disorder – studies that investigate the effect of a greater persistence to treatment are missing, while studies with shorter follow-up periods point to a more positive outcome. Moreover, there is some evidence that stimulant treatment has a protective effect concerning substance abuse in adulthood which might also reduce the risk of criminal behavior (Barkley et al., 2003).

CONCLUSION Large numbers of individuals of all ages suffer worldwide from ADHD, a heterogeneous disorder of strong neurobiological origin. Clinicians and researchers are concerned that many of them do not receive appropriate therapy despite the availability of effective treatment strategies. This is especially true for those with comorbid antisocial impairment. Recent consensus recommendations (Pliszka et al., 2006; Kutcher et al., 2004) suggest medication with psychostimulants or atomoxetine aided by psychosocial interventions as the first-line treatment in ADHD patients without comorbidity and for those with comorbid conduct disorder. Careful assessment of diagnosis, social and cognitive factors as well as of potential risks and benefits of pharmacotherapy and psychosocial treatment strategies are an essential preconditon for success. In addition, long-term studies to determine the efficacy of interventions in ADHD are urgently needed.

REFERENCES Abikoff, H., Hechtman, L., Klein, R.G. et al. (2004a). Symptomatic improvement in children with ADHD treated with long-term methylphenidate and multimodal psychosocial treatment. Journal of the American Academy of Child and Adolescent Psychiatry, 43, 802–11. Abikoff, H., Hechtman, L., Klein, R.G. et al. (2004b). Social functioning in children with ADHD treated with long-term methylphenidate and multimodal psychosocial treatment. Journal of the American Academy of Child and Adolescent Psychiatry, 43, 820–9. Allen, A., Kurlan, R., Gilbert, D. et al. (2005). Atomoxetine treatment in children and adolescents with ADHD and comorbid tic disorders. Neurology, 65, 1941–9. American Academy of Child and Adolescent Psychiatry (AACAP) (2002). Practice parameter for the use of stimulant medications in the treatment of children, adolescents, and adults. Journal of the American Academy of Child and Adolescent Psychiatry, 41, 26S–49S.

INTERVENTION, TREATMENT AND MANAGEMENT OF ADHD

393

Banaschewski, T., Coghill, D., Santosh, P. et al. (2006). Long-acting medications for the hyperkinetic disorders. European Child and Adolescent Psychiatry, published online. Bangs, M., Emslie, G., Spencer, T. et al. (2005). A study of atomoxetine in adolescents with ADHD and comorbid depression. Paper presented at 45th Annual Meeting of the New Clinical Drug Evaluation Unit (NCDEU), June 6–9, Boca Raton, FL. Barkley, R.A. (1990). Attention-deficit and hyperactivity disorder. A Handbook for Diagnosis and Treatment. New York: Guildford Press. Barkley, R.A. (1998). Attention-deficit and hyperactivity disorder. A Handbook for Diagnosis and Treatment, second edition. New York: Guilford Press. Barkley, R.A., Fischer, M., Smallish, L. & Fletcher, K. (2003). Does the treatment of attentiondeficit/hyperactivity disorder with stimulants contribute to drug use/abuse? A 13-year prospective study. Pediatrics, 3, 97–109. Bedard, A.C., Ickowicz, A., Logan, G.D. et al. (2003). Selective inhibition in children with attentiondeficit hyperactivity disorder off and on stimulant medication. Journal of Abnormal Child Psychology, 31, 315–27. Biederman, J. & Faraone, S.V. (2005). Attention-deficit hyperactivity disorder. Lancet, 366, 237–48. Biederman, J., Thisted, R., Greenhill, L. & Ryan, N. (1995). Estimation of the association between desipramine and the risk for sudden death in 5- to 14-year old children. Journal of Clinical Psychiatry, 56, 87–93. Charach, A., Figueroa, M., Chen, S. et al. (2006). Stimulant treatment over 5 years: effects on growth. Journal of the American Academy of Child and Adolescent Psychiatry, 45, 415–21. Connor, D., Glatt, S., Lopez, I. et al. (2002). Psychopharmacology and aggression-related behaviors in ADHD. Journal of the American Academy of Child and Adolescent Psychiatry, 41, 253–61. Denney, C. & Rapport, M. (2001). The cognitive pharmacology of stimulants in children with ADHD. In M.V. Solanto, A.F.T. Arnsten & F.X. Castellanos (eds.), Stimulant Drugs and ADHD: Basic and Clinical Neuroscience (pp. 283–302). New York: Oxford University Press. Dodson, W.W. (2005). Pharmacotherapy of adult ADHD. Journal of Clinical Psychology, 61, 589– 606. Epstein, J.N., Conners, C.K., Hervey, A.S. et al. (2006). Assessing medication effects in the MTA study using neuropsychological outcomes. Journal of Child Psychology and Psychiatry, 47, 446–56. Faraone, S.V., Spencer, T., Aleardi, M. et al. (2004). Meta-analysis of the efficacy of methylphenidate for treating adult attention-deficit/hyperactivity disorder. Journal of Clinical Psychopharmacology, 24, 24–9. Faraone, S.V. & Wilens, T. (2003). Does stimulant treatment lead to substance use disorders? Journal of Clinical Psychiatry, 64, 9–13. Greenhill, L., Pliszka, S., Dulcan, M.K. et al. (2001). Practice parameter for the use of stimulant medications in the treatment of children, adolescents, and adults. Journal of the American Academy of Child and Adolescent Psychiatry, 41, 26–49. Hart, E.L., Lahey, B.B., Loeber, R. et al. (1995). Developmental change in attention-deficit hyperactivity disorder in boys: a four-year longitudinal study. Journal of Abnormal Child Psychology, 23, 729–49. Hechtman, L. (2006). Long-term treatment of children and adolescents with attentiondeficit/hyperactivity disorder (ADHD). Current Psychiatry Reports, 8, 398–408. Hechtman, L., Abikoff, H., Klein, R.G. et al. (2004). Academic achievement and emotional status of children with ADHD treated with long-term methylphenidate and multimodal psychosocial treatment. Journal of the American Academy of Child and Adolescent Psychiatry, 43, 812–19. Hechtman, L., Weiss, G. & Perlman, T. (1984). Young adult outcome of hyperactive children who received long-term stimulant treatment. Journal of the American Academy of Child and Adolescent Psychiatry, 23, 261–9. Herpertz-Dahlmann, B. (2001). Conduct disorders, antisocial behaviour, delinquency. In H. Remschmidt (ed.), Psychotherapy with Children and Adolescents (pp. 498–511). Cambridge, UK: Cambridge University Press. Hesslinger, B., Tebartz van Elsst, L., Nyberg, E. et al. (2002). Psychopathy of attention deficit hyperactivity disorder in adults – a pilot study using a structured skills training program. European Archives of Psychiatry and Clinical Neuroscience, 252, 177–84.

394

VOLUME I: DIAGNOSIS AND TREATMENT

Hoare, P., Remschmidt, H., Medori, R. et al. (2005). 12-month efficacy and safety of OROS? MPH in children and adolescents with attention-deficit/hyperactivity disorder switched from MPH. European Child and Adolescent Psychiatry, 14, 305–9. Jensen, P.S., Hinshaw, S.P., Kraemer, H.C. et al. (2001). ADHD comorbidity findings from the MTA study: comparing comorbid subgroups. Journal of the American Academy of Child and Adolescent Psychiatry, 40, 147–58. Kempton, S., Vance, A., Maruff, P. et al. (1999). Executive function and attention-deficit/hyperactivity disorder: stimulant medication and better executive function performance in children. Psychological Medicine, 29, 527–38. Konrad, K., G¨unther, T., Gutenbrunner, M. & Herpertz-Dahlmann, B. (2005). Clinical evaluation of subjective and objective changes in motor activity and attention in children with attentiondeficit/hyperactivity disorder in a double-blind methylphenidate trial. Journal of Child and Adolescent Psychopharmacology, 15, 821–8. Konrad, K., G¨unther, T., Hanisch, C. & Herpertz-Dahlmann, B. (2004). Differential effects of methlyphenidate on attentional functions in children with ADHD. Journal of the American Academy of Child and Adolescent Psychiatry, 43, 191–8. Konrad, K., Neufang, S., Hanisch, C. et al. (2006). Dysfunctional attentional networks in children with attention deficit/hyperactivity disorder (ADHD) – evidence from an event-related fMRI study. Biological Psychiatry, 59, 643–51. Kratochvil, C.J., Vaughan, B.S., Harrington, M.J. & Burke, W.J. (2003). Atomoxetine: a selective noradrenaline reuptake inhibitor for the treatment of attention-deficit/hyperactivity disorder. Expert Opinion on Pharmacotherapy, 4, 1165–74. Kutcher, S., Aman, M., Brooks, S. et al. (2004). International consensus statement on attentiondeficit/hyperactivity disorder (ADHD) and disruptive disorders (DBDs): clinical implications and treatment practice suggestions. European Neuopsychopharmacology, 14, 11–28. Lee, T.S., Lee, T.D., Lombroso, P.J. & King, R.A. (2004). Atomoxetine and tics in ADHD. Journal of the American Academy of Child and Adolescent Psychiatry, 43, 1068–9. Markowitz, J.S., Straughn, A.B. & Patrick, K.S. (2003). Advances in the pharmacotherapy of attentiondeficit-hyperactivity disorder: focus on methylphenidate formulations. Pharmacotherapy, 23, 1282–99. McBurnett, K., Pfiffner, L.J., Willcutt, E. et al. (1999). Experimental cross-validation of DSM-IV types of attention-deficit/hyperactivity disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 38, 17–24. McCracken, J., Biederman, J., Greenhill, L. et al. (2003). Analog classroom assessment of a oncedaily mixed amphetamine formulation, SLI381 (Adderall XR), in children with ADHD. Journal of the American Academy of Child and Adolescent Psychiatry, 42, 673–83. Michelson, D., Adler, L., Spencer, T. et al. (2003). Atomoxetine in adults with ADHD: two randomized placebo-controlled studies. Biological Psychiatry, 53, 112–20. Miller, A.R., Lalonde, C.E. & McGrail, K.M. (2004). Children’s persistence with methylphenidate therapy: a population-based study. Canadian Journal of Psychiatry, 49, 761–8. MTA Cooperative Group (1999a). A 14-month randomized clinical trial of treatment strategies for attention deficit/hyperactivity disorder. Archives of General Psychiatry, 56, 1073–86. MTA Cooperative Group (1999b). Moderators and mediators of treatment response for children with attention deficit/hyperactivity disorder. Archives of General Psychiatry, 56, 1088–96. MTA Cooperative Group (2004a). National Institute of Mental Health multimodal treatment study of ADHD follow-up: 24-month outcomes of treatment strategies for attention-deficit/hyperactivity disorder. Pediatrics, 113, 754–61. MTA Cooperative Group (2004b). National Institute of Mental Health multimodal treatment study of ADHD follow-up: changes in effectiveness and growth after the end of treatment. Pediatrics, 113, 762–9. Nissen, E. (2006). ADHD drugs and cardiovascular risk. New England Journal of Medicine, 354, 1445–8. Patel, N., Crismon, L., Hoagwood, K. & Jensen, P. (2005). Unanswered questions regarding atypical antipsychotic use in aggressive children and adolescents. Journal of Child and Adolescent Psychopharmacology, 15, 270–84.

INTERVENTION, TREATMENT AND MANAGEMENT OF ADHD

395

Patrick, K.S., Gonzalez, M.A., Straughn, A.B. & Markowitz, J.S. (2005). New methylphenidate formulations for the treatment of attention-deficit/hyperactivity disorder. Expert Opinion on Drug Delivery, 2, 121–43. Pliszka, S.R., Crismon, L., Hughes, C. et al. (2006). The Texas children’s medication algorithm project: revision of the algorithm for pharmacotherapy of attention-deficit/hyperactivity disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 45, 642–57. Pliszka, S.R., Browne, R.G., Olvera, R.L. & Wynne, S.K. (2000). A double-blind, placebo-controlled study of Adderall and methylphenidate in the treatment of attention-deficit/hyperactivity disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 39, 619–26. Prince, J.B. (2006). Pharmacotherapy of attention-deficit hyperactivity disorder in children and adolescents: update on new stimulant preparations, atomoxetine, and novel treatments. Child and Adolescent Psychiatric Clinics of North America, 15, 13–50. Quaschner, K. (2001). Hyperkinetic disorders. In H. Remschmidt (ed.), Psychotherapy with Children and Adolescents (pp. 438–56). Cambridge, UK: Cambridge University Press. Riccio, C.A., Reynolds, C.R., Lowe, P. & Moore, J.J. (2002). The continuous performance test: a window on the neural substrates for attention? Archives of Clinical Neuropsychology, 17, 235–72. Safren, S.A., Otto, M.W., Sprich, S. et al. (2005). Cognitive-behavioral therapy for ADHD in medication-treated adults with continued symptoms. Behaviour Research and Therapy, 43, 831– 42. Shatkin, J. (2004). Atomoxetine for the treatment of pediatric nocturnal enuresis. Journal of Child and Adolescent Psychpharmacology, 14, 443–7. Spencer, T., Biederman, J., Coffey, B. et al. (1999). The 4-year course of tic disorders in boys with attention-deficit/hyperactivity disorder. Archives of General Psychiatry, 56, 842–7. Spencer, T., Biederman, J. & Wilens, T. (2002). Attention-deficit/hyperactivity disorder. In S. Kutcher (ed.), Practical Child and Adolescent Psychopharmacology (pp. 230–64). Cambridge, UK: Cambridge University Press. Stevenson, C.S., Whitmont, S., Bornholt, L. et al. (2002). A cognitive remediation programme for adults with attention deficit hyperactivity disorder. Australian and New Zealand Journal of Psychiatry, 36, 610–16. Sumner, C.S., Donnelly, C., Lopez, F.A. et al. (2005). Atomoxetine treatment for pediatric patients with ADHS and comorbid anxiety. Presented at Annual Meeting of the American Psychiatric Association, May 21–6, Atlanta. Tannock, R., Schachar, R. & Logan, G.D. (1995): Methylphenidate and cognitive flexibility: dissociated dose effects in hyperactive children. Journal of Abnormal Child Psychology, 23, 235–66. Wernicke, J.F., Faries, D., Girod, D. et al. (2003). Cardiovascular effects of atomoxetine in children, adolescents, and adults. Drug Safety, 26, 729–70. Wilens, T., Faraone, S.V., Biederman, J. & Gunawardene, S. (2003). Does stimulant therapy of attention deficit hyperactivity disorder beget later substance abuse? Pediatrics, 111, 179–85.

CHAPTER 24

Pharmacotherapy of Clinical Aggression in Individuals with Psychopathic Disorders F. Gerard Moeller and Alan C. Swann University of Texas Health Science Center at Houston, USA

Although there is a large preclinical literature of the neurobiology of aggression, and a number of case reports and unblinded clinical trials of medication for aggression have been published, there has been relatively little controlled research on the pharmacotherapy of aggression in humans. This chapter will present an overview of what is known of the neurobiology of aggression as a basis of pharmacotherapy of aggression in humans, followed by a detailed review of double-blind placebo-controlled pharmacotherapy trials for aggression. Finally, a treatment algorithm for impulsive aggression will be presented as a basis for future work in this area.

NEUROBIOLOGY OF AGGRESSION Aggression is one of the most widely studied animal behaviors. This is partly due to the fact that aggression by its very nature involves an observable act, unlike other behavioral problems such as depression or psychosis. Thus, it is easy to observe the effects of experimental manipulation of aggression in animals. One of the most widely studied experimental manipulations of aggression involves the neurotransmitter serotonin. Serotonin is produced in humans and animals from the essential amino acid tryptophan. It is used in the blood as a signal for clotting. A separate pool of serotonin is produced in the brain for use as a neurotransmitter. Although the neurons that produce serotonin are localized in the midbrain in dorsal and medial raphe nuclei, these neurons project to virtually the entire brain. The fact that serotonin neurons project to diverse brain regions might explain the association between serotonin and a large number of behaviors including sleep, depression, psychosis, appetite and aggression.

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

398

VOLUME I: DIAGNOSIS AND TREATMENT

As reviewed by Olivier and colleagues (1990), many types of animal aggressive behavior, including isolation-induced aggression, muricidal behavior, shock-induced fighting and filicidal behavior are inversely correlated with serotonin activity. Further evidence for a relationship between low serotonin and aggressive behavior comes from pharmacological manipulation studies. The serotonin depleting agent p-chlorophenylalanine (PCPA) and the serotonin neurotoxin 5,7-DHT increase aggression in rats, while this behavior is decreased by the ergot alkaloid dihydroergosine (DHESN) which increases the concentration serotonin in the raphe nuclei. Studies in nonhuman primates find that lower levels of the main breakdown product or metabolite of serotonin, 5-hydroxy-indole-acetic acid (5HIAA) in the spinal fluid are associated with increased aggressive and impulsive behavior (Fairbanks et al., 2001; Mehlman et al., 1994). This nonhuman primate literature is consistent with human studies showing that lower 5HIAA levels in the cerebrospinal fluid (CSF) are associated with aggressive behavior towards self (Asberg, 1997) and others (Brown et al., 1979). Some of the most interesting work studying the relationship between 5HIAA and aggression in humans was done by the late Markku Linnoila. His work showed that lower CSF 5HIAA was not associated with all aggression in humans, but was specifically associated with impulsive aggression (Linnoila et al., 1983). Other evidence links a specific region of the brain, the prefrontal cortex, with impulsive aggression. Clinical work dating back to the nineteenth century showed that injury to the prefrontal cortex was associated with a change in personality, often with aggressive behavior. One of the most famous examples of behavior change after injury to the prefrontal cortex is the case of Phineas Gage. Gage was a railroad engineer who had an iron tamping rod driven through his prefrontal cortex after an explosion. Gage survived the accident with his ability to walk and talk intact, but his personality was radically changed. His physician wrote: His contractors, who regarded him as the most efficient and capable foreman in their employ previous to his injury, considered the change in his mind so marked that they could not give him his place again. He is fitful, irreverent, indulging at times in the grossest profanity (which was not previously his custom), manifesting but little deference for his fellows, impatient of restraint or advice when it conflicts with his desires,. . . In this regard, his mind was radically changed, so decidedly that his friends and acquaintances said he was no longer Gage (Harlow, 1868).

Other recent studies find a link between much more subtle changes in the prefrontal cortex and impulsive and aggressive behavior. New et al. (2002) studied individuals with impulsive aggression using positron emission tomography (PET) scans, finding that impulsive aggressive subjects did not show the same brain activation in the prefrontal cortex after a dose of serotonergic medication compared to individuals without impulsive aggression. Recently our group, using diffusion tensor imaging (DTI), found that impulsivity as measured in the behavioral laboratory was significantly related to alterations in white-matter structures associated with the prefrontal cortex (Moeller et al., 2005). These studies are only a small part of the work showing that the prefrontal cortex is critical for impulse control. Evidence for biologically distinct types of aggressive behavior is consistent with clinical literature showing that pharmacologic treatments for aggressive behavior need to be tailored to the type of aggression. In that regard clinical aggression can be classified as ‘medically’ related aggression, premeditated aggression and impulsive aggression (Barratt & Slaughter, 1998).

PHARMACOTHERAPY OF CLINICAL AGGRESSION

399

Medically related aggression is aggression that is secondary to a psychiatric disorder. An example of this type of aggression would be an aggressive act carried out by an individual due to a psychotic delusion. It is often argued by defense attorneys that their clients commit aggressive acts as a result of a delusion. Aggression secondary to a delusion is an example of medically related aggression. Premeditated aggression is aggression that is committed in order to achieve some desired goal or reward. An example of this type of aggression is slaying a spouse in order to receive insurance money. Impulsive aggression is rapid and unplanned. It is out of proportion to any provocation. Impulsive aggressive acts are not carried out specifically for secondary gain and are carried out without regard for the consequences. An extreme example of an impulsive aggressive act is shooting a man who looked at your girlfriend too long in front of a policeman. This model for aggression works well in many instances. The model has difficulty, however, in determining whether aggression is secondary to another disorder. Even where there is clear evidence for psychosis, it can be difficult to establish with certainty that a specific aggressive act was truly secondary to that psychosis. This becomes even more problematic for aggressive acts in the context of personality or substance use disorders. The diagnostic criteria for intermittent explosive disorder (IED) in the Diagnostic and Statistical Manual for Mental Disorders IV text revision (DSM-IV-TR) (American Psychiatric Association, 2000) provide an excellent example. These criteria require that ‘The aggressive episodes are not better accounted for by another mental disorder (e.g., Antisocial Personality Disorder, Borderline Personality Disorder, a Psychotic Disorder, a Manic Episode, Conduct Disorder, or Attention Deficit Hyperactivity Disorder) and are not due to the direct physiological effect of a substance (e.g. a drug of abuse, a medication) or a general medical condition (e.g., head trauma, Alzheimer’s disease)’. It is therefore difficult or impossible for an individual who meets criteria for any of these conditions to meet strict criteria for IED. However, many individuals with impulsive aggression also meet criteria for another disorder, especially a personality disorder or a substance use disorder (Barratt et al., 1997: Coccaro & Kavoussi, 1997). This association is best understood by realizing that the underlying disorder is not impulsive aggression per se but rather a more general susceptibility to impulsivity. Impulsivity has been defined as a tendency to rapid unplanned responding to internal or external stimuli without regard to the consequences (Moeller et al., 2001). This means that a person who has pathological impulsivity would be prone to act impulsively in a number of areas (e.g., aggression, substance abuse, relationships). Many individuals with antisocial personality disorder or psychopathy have a problem with impulsivity. To the extent that psychopathic individuals have primarily impulsive aggression, they may benefit from pharmacotherapy. Excluding a person from a diagnosis or treatment because of impulsivity in a number of areas can easily deprive from pharmacologic treatment the very person who is most likely to benefit. We propose an alternative approach, combining elements of the categorical treatment model in DSM-IV-TR with a dimensional model based on animal and human studies of the underlying neurobiology of aggression. As shown in the accompanying algorithms, the dimensional aspect of this approach is the determination of whether the individual in question has a preponderance of impulsive or nonimpulsive aggression. If the aggression in question is largely impulsive, the categorical step is to determine whether the individual has any DSM-IV-TR psychiatric disorders that would modify the

400

VOLUME I: DIAGNOSIS AND TREATMENT

medication choice. For instance, a psychostimulant would be contraindicated in an individual with impulsive aggression if that individual also had bipolar disorder; treatment with a stimulant could lead to a manic episode in this person. Evidence to support this approach is shown in the treatment studies described in detail below.

TREATMENT STUDIES Any review of pharmacotherapy for aggression, must address two main issues. First is the specificity of the treatment. As we teach our psychiatry residents, it is not difficult to eliminate any problematic behavior with pharmacotherapy. The difficulty lies in elimination of only that behavior and not all behavior. In emergency room and intensive care settings where aggression can be life threatening, acute pharmacotherapy for aggression requires medication that often causes sedation and thus is not specific in its elimination of aggression. The combination of haloperidol and lorazepam is an example (Garza-Trevino et al., 1989). In addition to the ethical issues concerning the use of chronic sedation to control behavior, nonpsychiatric medical problems, such as aspiration pneumonia and fractures due to falls, are increased in a sedated individual. For these reasons, it is not acceptable to eliminate chronic aggressive behavior by sedation. The second issue in the pharmacotherapy of aggression is the nature of the evidence: especially whether the treatment trial was a double-blind placebo-controlled trial. It is well documented that simply monitoring a behavior can have an effect on that behavior. This is also true of aggression. Thus, without a placebo-controlled comparison group it cannot be determined whether a reduction in aggression after a pharmacotherapy was due to the medication or simply due to monitoring the behavior. There are many unblinded case reports and open-label trials of medication for aggression, but unfortunately the number of placebo-controlled trials is limited.

SPECIFIC MEDICATION TYPES Virtually every class of psychotropic medication has been tried in attempts to reduce aggression, at least in open-label trials. Effectiveness is likely to depend on whether aggressive behavior is impulsive rather than predatory (Barratt, 1993) and on the presence of specific target symptoms or underlying disorders (Campbell & Cueva, 1995). Of the controlled studies, the class of medication that has reported the greatest success in reducing aggression is mood stabilizers/anticonvulsants. We will discuss these two groups as one class of psychotropic medication since they overlap and may well share common mechanisms of action in the treatment of impulsive aggression.

Lithium Lithium has been used in treating impulsive aggression, initially in prison inmates and other institutionalized populations, for nearly 40 years (Sheard, 1971; Wickham & Reed 1987). Lithium is effective in a wide range of animal models for aggression (Sheard, 1975). One of the first placebo-controlled trials of medication for aggression was carried out by Sheard

PHARMACOTHERAPY OF CLINICAL AGGRESSION

401

et al. (1976). In that study, 66 male prisoners in a medium security institution, ranging in age from 16 to 24, were randomized to lithium or placebo in a double-blind fashion for up to three months. These subjects all had histories of chronic impulsive aggressive behavior and were not psychotic, nor had they been treated for a psychiatric disorder. Subjects treated with lithium showed a significant reduction in infractions involving violence. The strengths of this study were its placebo-controlled design and clear treatment outcomes. The main weakness of this study was that some of the reduction in aggression in this age group could have been secondary to treatment of undiagnosed bipolar (manic-depressive) disorder. Nevertheless, this study clearly supports the use of pharmacotherapy in the treatment of impulsive aggression. Since this study, there have been other placebo-controlled trials of lithium for impulsive aggression in children or adolescents with severe conduct disorder (Campbell et al., 1984; Lejoyeux & Ades, 1993; Malone et al., 2000) or mental retardation (Craft et al., 1987; Worrall, Moody & Naylor, 1975). Additionally, there have been an number of positive case series or open-label studies with maternal child abuse (do Prado-Lima et al., 2001), traumatic brain injury (Glenn et al., 1989), and aggressive prisoners (Tupin et al., 1973). Furthermore, there have been very few negative studies (Rifkin et al., 1997; Campbell, Kafantaris & Cueva, 1995). Lithium appears to be most effective in subjects with affective or impulsive aggression, rather than predatory aggression (Malone et al., 1998). Subjects responding to lithium described a subtle but specific improvement in their ability to reflect before acting (Sheard & Marini, 1978). Side effects, most commonly gastrointestinal, tremor, polyuria and sedation, were fairly common and dose related, and tended to occur early in treatment (Silva et al., 1992; Hagino et al., 1995). Unfortunately, lithium has a narrow therapeutic window with a relatively small range between effective and toxic doses, requiring frequent monitoring of blood levels. Malone and colleagues developed a dose-prediction method with the potential of reducing the likelihood of toxic doses (Malone et al., 1995) which may be helpful in this regard. Patients with head trauma or multiple treatments may be at greater risk for neurotoxicity (Worrall, Moody & Naylor, 1975; Glenn et al., 1989). Since lithium is an ion, its chemical structure is simple, and it has no metabolism or protein binding. However, its effects in the brain are complex. Lithium initially enhances, and changes the regulation of, serotonin synthesis and release (Price et al., 1989; Swann et al., 1981; Perez-Crouet et al., 1971), and also acts on the ubiquitous second messenger systems linked to protein kinase C (Lenox & Wang, 2003) and the phosphatidylinositol cycle (Sherman et al., 1986), as well as effects on neuronal membranes (El-Mallakh & Li, 1993). Lithium and valproate may have similar effects on the phosphatidylinositol system, but by different mechanisms (Manji & Lenox, 1999).

Phenytoin Barratt and colleagues (Barratt et al., 1997) compared pharmacological results in premeditated vs. impulsive aggressive acts. Sixty inmates were divided into two groups, based on whether their aggressive acts were primarily premeditated or impulsive. All subjects were then treated with phenytoin (200 mg in the morning and 100 mg in the evening) or placebo in a double-blind crossover design. Aggression was categorized as being primarily impulsive or premeditated using a structured interview. Phenytoin significantly reduced impulsive

402

VOLUME I: DIAGNOSIS AND TREATMENT

aggressive acts but had no effect on premeditated aggression. No significant side effects were noted. The work of the late Ernest Barratt on the pharmacotherapy of impulsive aggression supports the initial work of Sheard and colleagues (1976), in that pharmacotherapy appeared to be effective only in impulsive aggression. A second study in impulsive aggressive outpatients supported these findings. Stanford and colleagues (Stanford et al., 2001) found that phenytoin significantly reduced impulsive aggressive acts compared with placebo. Both studies found that phenytoin but not placebo treatment normalized event-related potentials in impulsive aggressive individuals. This was cited as evidence that the antiaggressive effect of phenytoin may involve improvement in regulation of sensory and early attentional processing (Stanford et al., 2001). More recently, the same research group found that phenytoin, carbamazepine and valproate were similarly effective in a placebo-controlled, parallel groups study of impulsively aggressive men (Stanford et al., 2005). Although phenytoin is primarily used as an anticonvulsant, it is doubtful that the antiaggressive properties of phenytoin can be explained through its anticonvulsant effect. In both the Barratt and Stanford studies, individuals with known histories of seizures were excluded. Further, in both studies the dose and blood level achieved were lower than recommended for treatment of epilepsy.

Valproic Acid Valproic acid in its various preparations was also originally developed as an anticonvulsant. Unlike phenytoin, however, one formulation of valproic acid, divalproex, is also approved by the FDA for the treatment of bipolar disorder (Bowden et al., 1994). It has been used to treat aggressive and impulsive behavior in several contexts (Davis et al., 2000). Stanford and colleagues (2005) reported that effects of valproate, carbamazepine and phenytion were similar in a placebo-controlled, parallel groups trial in men with impulsive aggression. In open-label studies, it appeared to reduce aggression, irritability or impulsivity in violent schizophrenic patients treated with antipsychotics (Afaq et al., 2002), adolescents with disruptive behavior disorders (Donovan et al., 2000), children with autism spectrum disorders (Hollander et al., 2001), elderly patients with dementia (Kunik et al., 1998), adults with intellectual disability and self-injurious behavior (Ruedrich et al., 1999), and aggressive patients with personality disorders who had not responded to fluoxetine (Kavoussi & Coccaro, 1998). The work in disruptive behavior disorders was confirmed by a double-blind, placebo-controlled crossover study, where, in both phases, divalproex was associated with improvement in Overt Aggression Scale (OAS), Symptom Checklist-90 (SCL-90) hostility factor and Clinical Global Impression (CGI) scores (Donovan et al., 2000). Similarly, Steiner et al. (2003) reported that divalproex was effective in reducing aggressive behavior in adolescents incarcerated for violent behavior. In a multicenter double-blind placebocontrolled trial of divalproex for impulsive aggression, 96 cluster B personality disorder subjects, 116 intermittent explosive disorder subjects, and 34 post-traumatic stress disorder subjects were randomized to divalproex or placebo for 12 weeks. Subjects who received divalroex were treated with a mean dose of 1567 mg achieving an average blood level of 64.2 mg/ml (range, 0.0–147 mg/ml). For all groups combined, there was no significant difference in change in impulsive aggression in subjects treated with divalproex compared to subjects treated with placebo. However, in the subjects with cluster B personality disorders, there was a significant reduction in aggression and irritability (Hollander et al., 2003).

PHARMACOTHERAPY OF CLINICAL AGGRESSION

403

Among subjects with borderline personality disorder, there was a significant reduction in aggression in subjects treated with divalproex compared to subjects treated with placebo. Higher baseline aggression as measured by the overt aggression scale and higher baseline impulsivity as measured by the Barratt impulsiveness scale predicted better response to divalproex (Hollander et al., 2005).

Carbamazepine The antiaggressive effects of the anticonvulsant carbamazepine have also been studied in double-blind placebo-controlled trials (Young & Hillbrand, 1994). A placebo-controlled trial found that carbamazepine had similar efficacy to phenytoin and valproate in men with impulsive aggression, but appears to have a slower onset of action (Stanford et al., 2005). Several case series and open-label studies originally suggested that carbamazepine was effective in aggressive patients with head trauma (Azouvi et al., 1999; Chatham-Showalter, 1996), episodic dyscontrol (Lewin & Sumners 1992), and intermittent explosive disorder (Mattes 1990). In a small (n = 4) double-blind, crossover trial, carbamazepine reduced aggressive behavior in patients with frontal lobe dysfunction (Foster, Hillbrand & Chi 1989). In a randomized clinical trial of 51 patients with senile dementia, carbamazepine reduced agitation and aggression significantly more than placebo (Tariot et al., 1998). However, in a six-week randomized clinical trial of subjects with severe conduct disorder, response to carbamazepine did not differ from placebo (Cueva et al., 1996).

Topiramate Recently, three double-blind placebo-controlled trials of topiramate for aggression have been published by the same research group (Nickel et al., 2005a, 2005b, 2005c). In one study 42 male patients with borderline personality disorder randomized to either topiramate up to 250 mg/day or placebo and treated for eight weeks. Aggression was measured using a German version of the State Trait Anger Expression Inventory. This scale has five subscales including State Anger, Trait Anger, Anger Out, Anger In and Anger Control (Nickel et al., 2005a). There was a significant reduction in four of the five subscales in the topiramate-treated group compared to the placebo-treated group, as well as a significant reduction in weight (Nickel et al., 2005a). In another study, 64 female subjects with major depressive disorder were randomized to topiramate up to 200 mg/day or placebo for 10 weeks. That study demonstrated a significant (but modest) reduction in depressive symptoms as measured by the Hamilton Depression Rating Scale and a significant reduction in aggression as measured by the State Trait Anger Expression Inventory. The reduction in aggression correlated with reduction in depression (Nickel et al., 2005b). Lastly, a placebo-controlled trial of topiramate in 29 female patients with borderline personality disorder similarly reported a significant reduction in aggression as measured by the State Trait Anger Expression Inventory in the topiramate-treated subjects (Nickel et al., 2005c). These studies are interesting in light of other studies reporting that topiramate was effective in other disorders of impulse control such as alcohol dependence (Johnson et al., 2003), cocaine dependence (Kampman et al., 2004) and binge eating disorder (McElroy

404

VOLUME I: DIAGNOSIS AND TREATMENT

et al., 2007), highlighting the possibility of a general effect of topiramate on impulse control. However, the aggression studies did not measure overt aggression, and are therefore difficult to compare with other aggression research.

Other Anticonvulsants Not all evidence regarding anticonvulsants in aggressive behavior is positive. Lamotrigine was reported to increase aggressive behavior in intellectually challenged patients with epilepsy (of 19 subjects, one had improved behavior and most of the rest deteriorated) (Beran & Gibson 1998), and in demented patients (Devarajan & Dursun 2000). Gabapentin has been studied in clinical and human laboratory settings. In the human laboratory, gabapentin increased aggressive responding at low and moderate doses and only reduced aggressive responding at the highest dose (800 mg) (Cherek et al., 2004). There was no difference in response between subjects with or without conduct disorder. In 22 patients with dementia, 17 improved with gabapentin (Hawkins et al., 2000). However, there are several reports of increased aggression in patients given gabapentin (Pinninti & Mahajan 2001;Wolf et al., 1995). All are from open-label studies. Still, they suggest that effectiveness of anticonvulsants in treating aggressive behavior may not be a class effect, but may roughly parallel that in mania.

Antidepressants Because of their prominent effects on serotonin, selective serotonin reuptake blockers (SSRIs) and other antidepressants have been used extensively in treatment of aggression and other behavioral disturbances in a variety of contexts including personality disorders, head injury, anxiety or affective disorders, developmental disorders and dementia (Walsh & Dinan, 2001; Hollander, 1999). Recent studies have had mixed results. In open-label and controlled trials, antidepressants reduced anger outbursts in patients with unipolar depression (Fava, 1998). Three weeks’ paroxetine treatment reduced impulsive responding on a test of ability to delay reward in a group of men with conduct disorder; decreased aggressive responding occurred only at the end of the trial (Cherek et al., 2002). There are positive open-label studies or case series for citalopram on impulsive-aggressive behavior in adolescents and children (Armenteros & Lewis, 2002), and assorted antidepressants in dementia following head injury (Kim, Moles & Hawley 2001). A randomized comparison of citalopram, perphenazine and placebo in 85 subjects with behavior disturbances related to dementia found that only citalopram was associated with improvement in agitated aggression and lability tension scales on the Neurobehavioral Rating Scale (Pollock et al., 2002). In a smaller trial of patients with Alzheimer’s disease, there was a trend toward improvement with SSRI compared to placebo (P = 0.08), with better improvement in women, patients with lower baseline aggression scores and patients with larger prolactin responses (Lanctot et al., 2002). Negative behavioral effects have also been attributed to antidepressants, in presumably nonbipolar populations. Without causing hypomanic affect, antidepressants can cause increases in problematic impulsive behavior that appears different from typical impulse control disorders (Ramasubbu, 2004). Increases in violent behavior were reported after fluvoxamine

PHARMACOTHERAPY OF CLINICAL AGGRESSION

405

administration (Okada & Okajima, 2001) and in 9 of 20 patients with mental retardation and epilepsy who were given fluoxetine (Troisi et al., 1995). Behavioral responses to serotoninacting antidepressants may therefore be heterogeneous, depending on subject characteristics, and may also be related to pharmacokinetic effects on other drugs (Okada & Okajima 2001). The occasional occurrence of akisthesia or anxiety may increase susceptibility to negative behavioral responses (Mitchell et al., 1992).

Noradrenergic antagonists Beta-noradrenergic receptor blockers, and alpha-2 noradrenergic agonists like clonidine, which inhibit norepinephrine release, have been used in a wide variety of behavioral disturbances, especially developmental disorders, stress-related disorders and traumatic brain injury, with heterogeneous results. Target behaviors are usually increased arousal, impulsivity and hyperactivity (Donnelly, 2003; Posey & McDougle 2000). A review of beta-blockers found them to be effective for anger outbursts in patients with dementia, attention deficit disorder, personality disorders and post-traumatic stress disorders, but noted that studies were generally small and not rigorously designed (Haspel, 1995). Nadolol was reported to improve extrapyramidal side effects, activation and thought disorder early in the treatment of schizophrenia (Gurguis, Mefford & Uhde, 1991). A comparison between carbamazepine and propranolol in patients with rage outbursts found responses to be similar, with propranolol possibly better in subjects with attention deficit disorders but carbamazepine better in those with intermittent explosive disorder (Mattes, 1990). Where beta-blockers have been most extensively studied is in patients with a history of traumatic brain injury. In a recent review of the literature Fleminger, Greenwood and Oliver (2003) concluded that the beta-blockers have the best evidence for efficacy in reducing aggression in patients with a history of traumatic brain injury. Clonidine has been used to reduce symptoms of hyperarousal and activation in patients with a variety of stress- and trauma-related conditions (Posey & McDougle, 2000; Fava, 1997). It was modestly effective at reducing irritability and hyperactivity in a randomized clinical trial in autistic boys (Jaselskis et al., 1992) and may work synergistically with methylphenidate (Wilens et al., 1999). However, in a randomized comparison of methylphenidate, clonidine and the combination in attention deficit hyperactivity disorder, improvement with the combination was not greater than that with either drug alone (Connor, Barkley & Davis, 2000).

Antipsychotics Antipsychotic treatments are used extensively to treat acute aggression in psychiatric emergency settings. Recent expert consensus guidelines for behavioral emergencies favored identification of specific target symptoms or underlying diagnoses over chemical restraint (Allen et al., 2001). Other than through sedative effects or reduction of overstimulation, there has been little evidence for specific antiaggressive effects of conventional antipsychotic drugs (Fava, 1997). In emergency psychiatric settings, however, antipsychotics with convenient dosage forms, such as oral concentrates, are favored (Allen et al., 2001).

406

VOLUME I: DIAGNOSIS AND TREATMENT

Clozapine appears unusually effective in treating impulsive or aggressive behavior (Fava, 1997). Much of the evidence is from patients with schizophrenia, where clozapine reduced hostility, aggression and related behavioral problems in a variety of settings, regardless of antipsychotic effects (Buckley et al., 1995; Glazer & Dickson 1998; Spivak et al., 1998). In a large mirror design study comparing units of a hospital where clozapine was or was not instituted, clozapine reduced verbal and physical assault, as well as related Brief Psychiatric Rating Scale (BPRS) scores (Rabinowitz, Avnon & Rosenberg, 1996). Clozapine was compared to haloperidol in a six-month open-label study, where it was associated with greater reductions in impulsivity, aggression and suicidal behavior (Spivak et al., 2003). In a retrospective study of 341 patients with schizophrenia, clozapine reduced the incidence of aggressive behavior from 31.4 % to 1.1 % (Volavka, 1999). Clozapine also has been shown to reduce aggressive and/or impulsive behavior in other severely ill patients, including those with developmental disorders and head trauma; use of clozapine also reduced incidents of staff injury (Hector, 1998). In addition to these effects on behavior, clozapine has been shown to reduce suicidal behavior in a variety of severely disturbed patients (Hector, 1998). Clozapine may differ from other second-generation antipsychotics in its effectiveness against impulsivity and aggression (Volavka et al., 2004). Patients with schizophrenia were randomized to receive clozapine, risperidone, olanzapine or haloperidol. With respect to aggression and hostility, all three second-generation drugs were superior to haloperidol. Once dose titration was completed, clozapine was more effective than olanzapine or risperidone. Perhaps most interesting was the relationship between severity of hostility and antipsychotic effectiveness. Clozapine was more effective in patients with high hostility, while olanzapine and risperidone were more effective in patients with low hostility. Another study in assaultive patients with schizophrenia and schizoaffective disorder compared clozapine to olanzapine and haloperidol (Krakowski et al., 2006), again finding that clozapine was superior to the other antipsychotics in reducing aggression. This study found no difference in antipsychotic efficacy between the three medications, lending more evidence that the antiaggressive effects of clozapine are separate from its antipsychotic effects. Unfortunately, due to the risk of potentially life-threatening reduction in white blood cell count, clozapine will probably always be limited to patients who are refractory to other treatments. Risperidone is the most widely studied second-generation antipsychotic for aggression other than clozapine. A meta-analysis of seven randomized clinical trials in schizophrenia found risperidone to reduce hostility and aggression ratings more than conventional antipsychotics (Aleman & Kahn, 2001). Risperidone was associated with greater reductions in disruptive behavior and irritability in ‘disruptive chidren and adolescents with subaverage intelligence’ (Aman et al., 2002) and in children with autism and other severe behavioral problems (McCracken et al., 2002), and dementia (reviewed in Ballard & Waite, 2006). In a mirror study of psychiatric patients (mostly schizophrenia), risperidone was significantly better than the comparison group in reducing time in seclusion but not in reducing restraint incidents (Chengappa et al., 2000). Other open-label studies reported benefit against aggression, irritability or disruptive behavior in antisocial personality disorder (Hirose, 2001) and in children with mood disorders (Schreier, 1998).

PHARMACOTHERAPY OF CLINICAL AGGRESSION

407

Psychostimulants Several psychostimulants are used in the treatment of attention deficit hyperactivity disorder (ADHD), including methylphenidate, dextroamphetamine and amphetamine. As reviewed by Spencer et al. (1996), studies of stimulant treatments have reported improvement in attention and reduction in aggressive symptoms in children and adolescents with ADHD after treatment with stimulants. Other studies show that stimulants decrease aggression in children and adolescents with ADHD and comorbid mental retardation (Pearson et al., 2003) and conduct disorder independent of whether they had comorbid ADHD (Klein et al., 1997). One problem with the use of stimulants in adult forensic populations is the difficulty in determining a diagnosis of ADHD in patients with concomitant substance abuse. Symptoms of inattention and hyperactivity could be secondary to abuse of stimulants and other drugs. One method for clarifying a diagnosis of ADHD in substance-abusing populations was suggested by Levin et al. (1998) requiring a history of ADHD during childhood without remittance of ADHD symptoms since then in addition to current severe ADHD symptoms. The lack of placebo-controlled clinical trials of stimulants for aggression in adult populations in addition to the abuse potential of stimulants limits their usefulness in forensic populations.

TREATMENT ALGORITHM Based on the research described above, it is possible to develop a preliminary algorithm for treating impulsive-aggressive behavior. These guidelines are summarized in Figures 24.1–24.5. Both safety and effectiveness depend on the specific disorder that underlies or contributes to the aggressive behavior, and on the context of the behavior. Other medical conditions, and potential for substance use disorders, also should be taken into account. For psychopathic disorders, misuse of prescribed medication requires monitoring. This misuse can take the form of abuse of prescribed medications that have this potential as well as noncompliance with medications in general. For psychopathic individuals, careful monitoring of medication use is necessary. This monitoring can take the form of regular monitoring of blood levels for medications that have this option (such as lithium and anticonvulsants). Other methods to ensure proper medication use include frequent office visits, prescribing only enough medication to last between visits, and pill counts at office visits.

BASIC TREATMENT PRINCIPLES Some basic principles in applying these algorithms include:

r Be alert for treatable nonpsychiatric medical conditions that may be causes, or effects, of the aggressive behavior.

r Avoid monotherapy or initial therapy with stimulants or antidepressants in patients who have histories of pathological activation, which could be mania.

408

VOLUME I: DIAGNOSIS AND TREATMENT A pattern of aggressive behavior, which causes significant injury to others or destruction of property which is associated with impairment in social or occupational function?

Assess for associated psychiatric or nonpsychiatric medical disorder Assess for impulsive versus nonimpulsive Aggression

Aggressive behavior is primarily impulsive (not performed for secondary gain, not planned, performed in spite of obvious negative consequences for perpetrator)

Aggressive behavior is primarily nonimpulsive (for secondary gain, gang related, performed in way to avoid negative consequences, performed in response to delusions or hallucinations)

See Flowchart B

Treat any psychiatric and nonpsychiatric medical disorders appropriately Aggressive behavior solely associated with psychiatric and nonpsychiatric medical disorder may resolve with appropriate treatment of these disorders Manage aggressive behavior not associated solely associated with psychiatric and nonpsychiatric medical disorder with criminal justice/behavioral interventions

Figure 24.1 Flowchart A

r Avoid monotherapy or initial treatment with medicines that lower the seizure threshold in subjects with the potential for alcohol or sedative withdrawal.

r Monitor the patient’s antiaggressive response, the emergence of any new behaviors or symptoms and the patient’s medical condition.

SUMMARY AND FUTURE DIRECTIONS FOR RESEARCH Aggression is a complex and potentially destructive aspect of behavior common in the psychopathic individual. Its effective management depends on the underlying mechanism. The available literature to date argues that premeditated aggression that is not related to a medical disorder is not amenable to pharmacological treatment. Premeditated aggression related to a nonpsychiatric medical disorder or an Axis I psychiatric disorder, such as aggression based on delusional beliefs, requires treatment of the underlying disorder. In

PHARMACOTHERAPY OF CLINICAL AGGRESSION History of mania, pathological activation or family history of bipolar disorder, Significant head injury, psychosis or ADHD

409

Yes

See Flowchart C No

Significant depressive symptoms?

No

Yes Phenytoin, valproate or lithium Fluoxetine, citalopram or other SSRI

Inadequate response or cannot tolerate due to side effects or contraindications

Inadequate response or cannot tolerate due to side effects or contraindications Risperidone or topiramate Lithium, valproate, or phenytoin

Inadequate response or cannot tolerate due to side effects or contraindications Risperidone topiramate

Figure 24.2 Flowchart B, continued from Flowchart A (Figure 24.1)

some cases, medical disorders predispose to impulsive aggression, requiring treatment for the impulsive aggression to be harmonized with treatment for the medical disorder. This chapter focuses on the treatment of impulsive aggression. Impulsive aggression requires treatment that addresses the underlying mechanism of the impulsivity that is generating the aggressive behavior. While study of the characterization and treatment of aggression is in an early stage, this review summarizes the application of the evidence that is available. Depending on the circumstances, lithium, mood-stabilizing anticonvulsants, antipsychotic drugs, antidepressants, stimulants or other treatments may be effective. Combinations with complementary mechanisms of action may be necessary. Management of the patient’s environment, and behavioral or other measures aimed at improving adaptation and reducing destructive patterns of behavior, are often required for an optimal response to treatment. For the field to advance, further research on the underlying neurobiology and effective treatment for impulsive aggression is needed.

410

VOLUME I: DIAGNOSIS AND TREATMENT

History of frank mania, pathological activation, early onset of depressive disorder or family history of bipolar disorder

No

See Flowchart D

Yes Lithium or valproate based on history of prior treatment response or nonpsychiatric medical contraindications if any

Inadequate response or cannot tolerate due to side effects or contraindications

Risperidone, carbamazepine or topiramate

Figure 24.3 Flowchart C, continued from Flowchart B (Figure 24.2)

Significant psychotic symptoms and impulsive aggression

No

Yes

Risperidone or other newer generation antipsychotic Inadequate response or cannot tolerate due to side effects or contraindications Add lithium, valproate, fluoxetine or carbamazemine

Inadequate response or cannot tolerate due to side effects or contraindications Switch to clozapine bearing in mind risk of agranulocytosis

Figure 24.4 Flowchart D, continued from Flowchart C (Figure 24.3)

See Flowchart E

PHARMACOTHERAPY OF CLINICAL AGGRESSION All of the following are met: (1) DSM-IV criteria for ADHD during childhood (2) Currently has impairing ADHD symptoms (3) ADHD symptoms have not remitted at any period since childhood.

411

No

See Previous Flowcharts

Yes Methylphenidate or amphetamine based on history of prior treatment response or nonpsychiatric medical contraindications if any. Cannot tolerate due to side effects or contraindications Risperidone, divalproex or lithium based on history of prior treatment response or nonpsychiatric medical contraindications if any.

Inadequate response

Clonidine augmentation of psychostimulant if no nonpsychiatric medical contraindications

Figure 24.5 Flowchart E, continued from Flowchart D (Figure 24.4)

With more data it will be possible to design treatment based on science rather than the personal whim of the treating physician.

REFERENCES Afaq, I., Riaz, J., Sedky, K. et al., (2002). Divalproex as a calmative adjunct for aggressive schizophrenic patients. Journal of the Kentucky Medical Association, 100, 17–22. Aleman, A. & Kahn, R.S. (2001). Effects of the atypical antipsychotic risperidone on hostility and aggression in schizophrenia: a meta-analysis of controlled trials. European Neuropsychopharmacology, 11, 289–93. Allen, M.H., Currier, G.W., Hughes, D.H. et al. (2001). The expert consensus guideline series. Treatment of behavioral emergencies. Postgraduate Medicine, 1–88. Aman, M.G., De Smedt, G., Derivan, A. et al. (2002). Double-blind, placebo-controlled study of risperidone for the treatment of disruptive behaviors in children with subaverage intelligence. American Journal of Psychiatry, 159, 1337–46. American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders, fourth edition. Washington, DC, American Psychiatric Association. Armenteros, J.L. & Lewis, J.E. (2002). Citalopram treatment for impulsive aggression in children and adolescents: an open pilot study. Journal of the American Academy of Child and Adolescent Psychiatry, 41, 522–9. Asberg, M. (1997). Neurotransmitters and suicidal behavior. The evidence from cerebrospinal fluid studies. Annals of the New York Academy of Sciences, 836, 158–81. Azouvi, P., Jokic, C., Attal, N. et al. (1999). Carbamazepine in agitation and aggressive behaviour following severe closed-head injury: results of an open trial. Brain Injury, 13, 797–804. Ballard, C. & Waite, J. (2006). The effectiveness of atypical antipsychotics for the treatment of aggression and psychosis in Alzheimer’s disease. Cochrane Database System, 25, CD003476.

412

VOLUME I: DIAGNOSIS AND TREATMENT

Barratt, E.S. (1993). The use of anticonvulsants in aggression and violence. Psychopharmacology Bulletin, 29, 75–81. Barratt, E.S. & Slaughter, L. (1998). Defining, measuring, and predicting impulsive aggression: a heuristic model. Behavioral Sciences and the Law, 16(3), 285–302. Barratt, E.S., Stanford, M.S., Felthous, A.R. & Kent, T.A. (1997). The effects of phenytoin on impulsive and premeditated aggression: a controlled study. Journal of Clinical Psychopharmacology, 17, 341–9. Beran, R.G. & Gibson, R.J. (1998). Aggressive behaviour in intellectually challenged patients with epilepsy treated with lamotrigine. Epilepsia, 39,: 280–2. Bowden, C.L., Brugger, A.M., Swann, A.C. et al. (1994). Efficacy of divalproex vs. lithium and placebo in the treatment of mania. Journal of the American Medical Association, 271, 918–24. Brown, G.L., Goodwin, F.K., Ballenger, J.C. et al. (1979). Aggression in humans correlates with cerebrospinal fluid amine metabolites. Psychiatry Research, 1, 131–9. Buckley, P., Bartell, J., Donenwirth, K. et al. (1995). Violence and schizophrenia: clozapine as a specific antiaggressive agent. Bulletin of the American Academy of Psychiatry and the Law, 23, 607–11. Campbell, M. & Cueva, J.E. (1995). Psychopharmacology in child and adolescent psychiatry: a review of the past seven years. Part II. Journal of the American Academy of Child and Adolescent Psychiatry, 34, 1262–72. Campbell, M., Kafantaris, V. & Cueva, J.E. (1995). An update on the use of lithium carbonate in aggressive children and adolescents with conduct disorder. Psychopharmacology Bulletin, 31, 93–102. Campbell, M., Small, A.M., Green, W.H. et al. (1984). Behavioral efficacy of haloperidol and lithium carbonate. A comparison in hospitalized aggressive children with conduct disorder. Archives of General Psychiatry, 41, 650–6. Chatham-Showalter, P.E. (1996). Carbamazepine for combativeness in acute traumatic brain injury. Journal of Neuropsychiatry and Clinical Neurosciences, 8, 96–9. Chengappa, K.N., Levine, J., Ulrich, R. et al. (2000). Impact of risperidone on seclusion and restraint at a state psychiatric hospital. Canadian Journal of Psychiatry, 45, 827–32. Cherek, D.R., Lane, S.D., Pietras, C.J. & Steinberg, J.L. (2002). Effects of chronic paroxetine administration on measures of aggressive and impulsive responses of adult males with a history of conduct disorder. Psychopharmacology (Berlin), 159, 266–74. Cherek, D.R., Tcheremissine, O.V., Lane, S.D. & Pietras, C.J. (2004). Acute effects of gabapentin on laboratory measures of aggressive and escape responses of adult parolees with and without a history of conduct disorder. Psychopharmacology (Berlin), 171, 405–12. Coccaro, E.F. & Kavoussi, R.J. (1997). Fluoxetine and impulsive aggressive behavior in personalitydisordered subjects. Archives of General Psychiatry, 54(12), 1081–8. Connor, D.F., Barkley, R.A. & Davis, H.T. (2000). A pilot study of methylphenidate, clonidine, or the combination in ADHD comorbid with aggressive oppositional defiant or conduct disorder. Clinical Pediatrics (Philadelphia), 39, 15–25. Craft, M., Ismail, I.A., Krishnamurti, D. et al. (1987). Lithium in the treatment of aggression in mentally handicapped patients. A double-blind trial. British Journal of Psychiatry, 150, 685–9. Cueva, J.E., Overall, J.E., Small, A.M. et al. (1996). Carbamazepine in aggressive children with conduct disorder: a double-blind and placebo-controlled study. Journal of the American Academy of Child and Adolescent Psychiatry, 35, 480–90. Davis, L.L., Ryan, W., Adinoff, B. & Petty, F. (2000). Comprehensive review of the psychiatric uses of valproate. Journal of Clinical Psychopharmacology, 20, 1S–17S. Devarajan, S. & Dursun, S.M. (2000). Aggression in dementia with lamotrigine treatment. American Journal of Psychiatry, 157, 1178. do Prado-Lima, P., Knijnik, L., Juruena, M. Padilla, A. (2001). Lithium reduces maternal child abuse behaviour: a preliminary report. Journal of Clinical Pharmacy and Therapeutics, 26, 279–82. Donnelly, C.L. (2003). Pharmacologic treatment approaches for children and adolescents with posttraumatic stress disorder. Child and Adolescent Psychiatric Clinics of North America, 12: 251–69. Donovan, S.J., Stewart, J.W., Nunes, E.V. et al. (2000). Divalproex treatment for youth with explosive temper and mood lability: a double-blind, placebo-controlled crossover design. American Journal of Psychiatry, 157, 818–20.

PHARMACOTHERAPY OF CLINICAL AGGRESSION

413

El-Mallakh, R.S. & Li, R. (1993). Is the Na+ -K+ -ATPase the link between phosphoinositide metabolism and bipolar disorder? Journal of Neuropsychiatry and Clinical Neuroscience, 5, 361–8. Fairbanks, L.A., Melega, W.P., Jorgensen, M.J. et al. (2001). Social impulsivity inversely associated with CSF 5-HIAA and fluoxetine exposure in vervet monkeys. Neuropsychopharmacology, 24, 370–8. Fava, M. (1997). Psychopharmacologic treatment of pathologic aggression. Psychiatric Clinics of North America, 20, 427–51. Fava, M. (1998). Depression with anger attacks. Journal of Clinical Psychiatry, 59(Supplement 18), 18–22. Fleminger, S., Greenwood, R.J. & Oliver, D.L. (2003). Pharmacological management for agitation and aggression in people with acquired brain injury. Cochrane Database System Review, (1), CD003299. Foster, H.G., Hillbrand, M. & Chi, C.C. (1989). Efficacy of carbamazepine in assaultive patients with frontal lobe dysfunction. Progress in Neuropsychopharmacology and Biological Psychiatry, 13, 865–74. Garza-Trevino, E.S., Hollister, L.E., Overall, J.E. & Alexander, W.F. (1989). Efficacy of combinations of intramuscular antipsychotics and sedative-hypnotics for control of psychotic agitation. American Journal of Psychiatry, 146, 1598–601. Glazer, W.M. & Dickson, R.A. (1998). Clozapine reduces violence and persistent aggression in schizophrenia. Journal of Clinical Psychiatry, 59(Supplement 3), 8–14. Glenn, M.B., Wroblewski, B., Parziale, J. et al. (1989). Lithium carbonate for aggressive behavior or affective instability in ten brain-injured patients. American Journal of Physical and Medical Rehabilitation, 68, 221–6. Gurguis, G.N., Mefford, I.N. & Uhde, T.W. (1991). Hypothalamic-pituitary-adrenocortical activity in panic disorder: relationship to plasma catecholamine metabolites. Biological Psychiatry, 30, 502–6. Hagino, O.R., Weller, E.B., Weller, R.A. et al. (1995). Untoward effects of lithium treatment in children aged four through six years. Journal of the American Academy of Child and Adolescent Psychiatry, 34, 1584–90. Harlow, J.M. (1868). Recovery from the passage of an iron bar through the head. Publications of the Massachusetts Medical Society, 2, 327-347. Haspel, T. (1995). Beta-blockers and the treatment of aggression. The Harvard Review of Psychiatry, 2, 274–81. Hawkins, J.W., Tinklenberg, J.R., Sheikh, J.I. et al. (2000). A retrospective chart review of gabapentin for the treatment of aggressive and agitated behavior in patients with dementias. American Journal of Geriatric Psychiatry, 8, 221–5. Hector, R.I. (1998). The use of clozapine in the treatment of aggressive schizophrenia. Canadian Journal of Psychiatry, 43, 466–72. Hirose, S. (2001). Effective treatment of aggression and impulsivity in antisocial personality disorder with risperidone. Psychiatry and Clinical Neurosciences, 55, 161–2. Hollander, E. (1999). Managing aggressive behavior in patients with obsessive-compulsive disorder and borderline personality disorder. Journal of Clinical Psychiatry, 60(Supplement 15), 38–44. Hollander, E., Dolgoff-Kaspar, R., Cartwright, C. et al. (2001). An open trial of divalproex sodium in autism spectrum disorders. Journal of Clinical Psychiatry, 62, 530–4. Hollander, E., Swann, A.C., Coccaro, E.F. et al. (2005). Impact of trait impulsivity and state aggression on divalproex versus placebo response in borderline personality disorder. American Journal of Psychiatry, 162, 621–4. Hollander, E., Tracy, K.A., Swann, A.C. et al. (2003). Divalproex in the treatment of impulsive aggression: efficacy in cluster B personality disorders. Neuropsychopharmacology, 28, 1186–97. Jaselskis, C.A., Cook, E.H., Jr., Fletcher, K.E. & Leventhal, B.L. (1992). Clonidine treatment of hyperactive and impulsive children with autistic disorder. Journal of Clinical Psychopharmacology, 12, 322–27. Johnson, B.A., Ait-Daoud, N., Bowden, C.L. et al. (2003). Oral topiramate for treatment of alcohol dependence: a randomized controlled trial. Lancet, 17, 1677–85. Kampman, K.M., Pettinati, H., Lynch, K.G. et al. (2004), A pilot trial of topiramate for the treatment of cocaine dependence. Drug and Alcohol Dependence, 75(3), 223–4.

414

VOLUME I: DIAGNOSIS AND TREATMENT

Kavoussi, R.J. & Coccaro, E.F. (1998). Divalproex sodium for impulsive aggressive behavior in patients with personality disorder. Journal of Clinical Psychiatry, 59, 676–80. Kim, K.Y., Moles, J.K. & Hawley, J.M. (2001). Selective serotonin reuptake inhibitors for aggressive behavior in patients with dementia after head injury. Pharmacotherapy, 21, 498–501. Klein, R.G., Abikoff, H,, Klass, E. et al. (1997). Clinical efficacy of methylphenidate in conduct disorder with and without attention deficit hyperactivity disorder. Archives of General Psychiatry, 54(12), 1073–80. Krakowski, M.I., Czobor, P., Citrome, L. et al. (2006). Atypical antipsychotic agents in the treatment of violent patients with schizophrenia and schizoaffective disorder. Archives of General Psychiatry, 63(6), 622–9. Kunik, M.E., Puryear, L., Orengo, C.A. et al. (1998). The efficacy and tolerability of divalproex sodium in elderly demented patients with behavioral disturbances. International Journal of Geriatric Psychiatry, 13, 29–34. Lanctot, K.L., Herrmann, N., van Reekum, R. et al. (2002). Gender, aggression and serotonergic function are associated with response to sertraline for behavioral disturbances in Alzheimer’s disease. International Journal of Geriatric Psychiatry, 17, 531–41. Lejoyeux, M. & Ades, J. (1993). Evaluation of lithium treatment in alcoholism. Alcohol and Alcoholism, 28, 273–9. Lenox, R.H. & Wang, L. (2003). Molecular basis of lithium action: integration of lithium-responsive signaling and gene expression networks. Molecular Psychiatry, 8, 135–44. Levin, F.R., Evans, S.M. & Kleber, H.D. (1998). Prevalence of adult attention-deficit hyperactivity disorder among cocaine abusers seeking treatment. Drug and Alcohol Dependency, 52(1), 15–25. Lewin, J. & Sumners, D. (1992). Successful treatment of episodic dyscontrol with carbamazepine. British Journal of Psychiatry, 161, 261–2. Linnoila, M., Virkkunen, M., Scheinin, M. et al. (1983). Low cerebrospinal fluid 5HIAA differentiates impulsive from nonimpulsive violent behavior. Life Sciences, 32, 2609–14. Malone, R.P., Bennett, D.S., Luebbert, J.F. et al. (1998). Aggression classification and treatment response. Psychopharmacology Bulletin, 34, 41–5. Malone, R.P., Delaney, M.A., Luebbert, J.F. et al. (2000). A double-blind placebo-controlled study of lithium in hospitalized aggressive children and adolescents with conduct disorder. Archives of General Psychiatry, 57, 649–54. Malone, R,P., Delaney, M.A., Luebbert, J.F. et al. (1995). The lithium test dose prediction method in aggressive children. Life Sciences, 31, 379–82. Manji, H.K. & Lenox, R.H. (1999). Protein kinase C signaling in the brain: molecular transduction of mood stabilization in the treatment of manic-depressive illness. Biological Psychiatry, 46, 1328–51. Mattes, J.A. (1990). Comparative effectiveness of carbamazepine and propranolol for rage outbursts. Journal of Neuropsychiatry and Clinical Neurosciences, 2, 159–64. McCracken, J.T., McGough, J., Shah, B. et al. (2002). Risperidone in children with autism and serious behavioral problems. New England Journal of Medicine, 347, 314–21. McElroy, S.L., Hudson, J.I., Capece, J.A. et al. (2007). Topiramate Binge Eating Disorder Research Group. Topiramate for the treatment of binge eating disorder associated with obesity: a placebocontrolled study. Biological Psychiatry, 61, 1039–48. Mehlman, P.T., Higley, J.D., Faucher, I. et al. (1994). Low CSF 5-HIAA concentrations and severe aggression and impaired impulse control in nonhuman primates. American Journal of Psychiatry, 151, 1485–91. Mitchell, W.G., Zhou, Y., Chavez, J.M. & Guzman, B.L. (1992). Reaction time, attention, and impulsivity in epilepsy. Pediatric Neurology, 8, 19–24. Moeller, F.G., Barratt, E.S., Dougherty, D.M. et al. (2001). Psychiatric aspects of impulsivity. American Journal of Psychiatry, 158, 1783–93. Moeller, F.G., Hasan, K.M., Steinberg, J.L. et al. (2005). Reduced anterior corpus callosum white matter integrity is related to increased impulsivity and reduced discriminability in cocaine dependent subjects: diffusion tensor imaging. Neuropsychopharmacology, 30(3), 610–7. New, A.S., Hazlett, E.A., Buchsbaum, M.S. et al. (2002). Blunted prefrontal cortical 18fluorodeoxyglucose positron emission tomography response to meta-chlorophenylpiperazine in impulsive aggression. Archives of General Psychiatry, 59, 621–9.

PHARMACOTHERAPY OF CLINICAL AGGRESSION

415

Nickel, C., Lahmann, C., Tritt, K. et al. (2005a). Topiramate in treatment of depressive and anger symptoms in female depressive patients: a randomized, double-blind, placebo-controlled study. Journal of Affective Disorders, 87(2–3), 243–52. Nickel, M.K., Nickel, C., Kaplan, P. et al. (2005b). Treatment of aggression with topiramate in male borderline patients: a double-blind, placebo-controlled study. Biological Psychiatry, 57(5), 495–9. Nickel, M.K., Nickel, C., Mitterlehner, F.O. et al. (2005c). Topiramate treatment of aggression in female borderline personality disorder patients: a double-blind, placebo-controlled study. Journal of Clinical Psychiatry, 65(11), 1515–9. Okada, F. & Okajima, K. (2001). Violent acts associated with fluvoxamine treatment. Journal of Psychiatry and Neurosciences, 26, 339–40. Olivier, B., Mos, J., Tulp, M. et al. (1990). Serotonergic involvement in aggressive behavior in animals. In H.M. van Praag, R. Plutchik & A. Apter (eds.) Violence and Suicidality (pp. 79–137). London: Brunner/Mazel. Pearson, D.A., Santos, C.W., Roache, J.D. et al. (2003). Treatment effects of methylphenidate on behavioral adjustment in children with mental retardation and ADHD. Jornal of american Academy of Child and Adolescent Psychiatry, 42, 209–16. Perez-Crouet, J., Tagliamonte, A., Tagliamonte, P. & Gessa, G.L. (1971). Stimulation of serotonin synthesis by lithium. Journal of Pharmacology and Experimental Therapeutics, 178, 325–30. Pinninti, N.R. & Mahajan, D.S. (2001). Gabapentin-associated aggression. Journal of Neuropsychiatry and Clinical Neurosciences, 13, 424. Pollock, B.G., Mulsant, B.H., Rosen, J. et al. (2002). Comparison of citalopram, perphenazine, and placebo for the acute treatment of psychosis and behavioral disturbances in hospitalized, demented patients. American Journal of Psychiatry, 159, 460–5. Posey, D.J. & McDougle, C.J. (2000). The pharmacotherapy of target symptoms associated with autistic disorder and other pervasive developmental disorders. The Harvard Review of Psychiatry, 8, 45–63. Price, L.H., Charney, D.S., Delgado, P.L. & Heninger, G.R. (1989). Lithium treatment and serotoninergic function. Neuroendocrine and behavioral responses to intravenous tryptophan in affective disorder. Archives of General Psychiatry, 46, 13–19. Rabinowitz, J., Avnon, M. & Rosenberg, V. (1996). Effect of clozapine on physical and verbal aggression. Schizophrenia Research, 22, 249–55. Ramasubbu, R. (2004). Antidepressant treatment-associated behavioural expression of hypomania: a case series. Progress in Neuropsychopharmacology and Biological Psychiatry, 28, 1201–7. Rifkin, A., Karajgi, B., Dicker, R. et al. (1997). Lithium treatment of conduct disorders in adolescents. American Journal of Psychiatry, 154, 554–5. Ruedrich, S., Swales, T.P., Fossaceca, C. et al. (1999). Effect of divalproex sodium on aggression and self-injurious behaviour in adults with intellectual disability: a retrospective review. Journal of Intellectual Disability Research, 43, 105–11. Schreier, H.A. (1998). Risperidone for young children with mood disorders and aggressive behavior. Journal of Child and Adolescent Psychopharmacology, 8, 49–59. Sheard, M.H. (1971). Effect of lithium on human aggression. Nature, 230, 113–14. Sheard, M.H. (1975). Lithium in the treatment of aggression. Journal of Nervous and Mental Disease, 160, 108–18. Sheard, M.H. & Marini, J.L. (1978). Treatment of human aggressive behavior: four case studies of the effect of lithium. Compr Psychiatry, 19, 37–45. Sheard, M.H., Marini, J.L., Bridges, C.I. & Wagner, E. (1976). The effect of lithium on impulsive aggressive behavior in man. American Journal of Psychiatry, 133, 1409–13. Sherman, W.R., Gish, B.G., Honchar, M.P. & Munsell, L.Y. (1986). Effects of lithium on phosphoinositide metabolism in vivo. Federation Proceedings, 45, 2639–46. Silva, R.R., Campbell, M., Golden, R.R. et al. (1992). Side effects associated with lithium and placebo administration in aggressive children. Psychopharmacology Bulletin, 28, 319–26. Spencer, T., Biederman, J., Wilens, T. et al. (1996). Pharmacotherapy of attention-deficit hyperactivity disorder across the life cycle. Journal of the American Academy of Child and Adolescent Psychiatry, 35, 409–32

416

VOLUME I: DIAGNOSIS AND TREATMENT

Spivak, B., Roitman, S., Vered, Y. et al. (1998). Diminished suicidal and aggressive behavior, high plasma norepinephrine levels, and serum triglyceride levels in chronic neuroleptic-resistant schizophrenic patients maintained on clozapine. Clinical Neuropharmacology, 21, 245–50. Spivak, B., Shabash, E., Sheitman, B. et al. (2003). The effects of clozapine versus haloperidol on measures of impulsive aggression and suicidality in chronic schizophrenia patients: an open, nonrandomized, 6-month study. Journal of Clinical Psychiatry, 64, 755–60. Stanford, M.S., Helfritz, L.E., Conklin, S.M. et al. (2005). A comparison of anticonvulsants in the treatment of impulsive aggression. Experimental and Clinical Psychopharmacology, 13, 72–9. Stanford, M.S., Houston, R.J., Mathias, C.W. et al. (2001). A double-blind placebo-controlled crossover study of phenytoin in individuals with impulsive aggression. Psychiatry Research, 103, 193–203. Steiner H., Petersen, M.L., Saxena, K. et al. (2003). Divalproex sodium for the treatment of conduct disorder: a randomized controlled clinical trial. Journal of Clinical Psychiatry, 64, 1183–91. Swann, A.C., Heninger, G.R., Roth, R.H. & Maas, J.W. (1981). Differential effects of short and long term lithium on tryptophan uptake and serotonergic function in cat brain. Life Sciences, 28, 347–54. Tariot, P.N., Erb, R., Podgorski, C.A. et al. (1998). Efficacy and tolerability of carbamazepine for agitation and aggression in dementia. American Journal of Psychiatry, 155, 54–61. Troisi, A., Vicario, E., Nuccetelli, F. et al. (1995). Effects of fluoxetine on aggressive behavior of adult inpatients with mental retardation and epilepsy. Digestive Diseases and Sciences, 28, 73–6. Tupin, J.P., Smith, D.B., Clanon, T.L. et al. (1973). The long-term use of lithium in aggressive prisoners. Comprehensive Psychiatry, 14, 311–17. Volavka, J. (1999). The effects of clozapine on aggression and substance abuse in schizophrenic patients. Journal of Clinical Psychiatry, 60(Supplement 12), 43–6. Volavka, J., Czobor, P., Nolan, K. et al. (2004). Overt aggression and psychotic symptoms in patients with schizophrenia treated with clozapine, olanzapine, risperidone, or haloperidol. Journal of Clinical Psychopharmacology, 24, 225–8. Walsh, M.T. & Dinan, T.G. (2001). Selective serotonin reuptake inhibitors and violence: a review of the available evidence. Acta Psychiatrica Scandinavica, 104, 84–91. Wickham, E.A. & Reed, J.V. (1987). Lithium for the control of aggressive and self-mutilating behaviour. International Journal of Clinical Psychopharmacology, 2, 181–90. Wilens, T.E., Spencer, T.J., Swanson, J.M. et al. (1999). Combining methylphenidate and clonidine: a clinically sound medication option. Journal of the American Academy of Child and Adolescent Psychiatry, 38, 614–19. Wolf, S.M., Shinnar, S., Kang, H. et al. (1995). Gabapentin toxicity in children manifesting as behavioral changes. Epilepsia, 36, 1203–5. Worrall, E.P., Moody, J.P. & Naylor, G.J. (1975). Lithium in non-manic depressives: antiaggressive effect and red blood cell lithium values. British Journal of Psychiatry, 26, 464–8. Yamamoto, T. & Ueki, S. (1977). Characteristics in aggressive behavior induced by midbrain raphe lesions in rats. Physiology and Behavior, 19, 105–10. Young, J.L. & Hillbrand, M. (1994). Carbamazepine lowers aggression: a review. Bulletin of the American Academy of Psychiatry and the Law, 22, 53–61.

CHAPTER 25

Treatment and Management of Conduct Disorders in Children and Adolescents Manfred Doepfner, Kerstin Adrian and Charlotte Hanisch University of Cologne, Germany

This chapter reviews the state of the art regarding evidence-based treatment for children and adolescents with conduct disorder (CD) and oppositional defiant disorder (ODD). In the first part a short overview over phenomenological, epidemiological and etiological aspects and their implications for different treatment approaches is given. The treatment approaches are classified in parent-focused, school-based, patient-focused and multimodal interventions. These different treatment approaches are described and their empirical evidence is summarized. In the last section, the findings are summarized and discussed with respect to the need of multicomponent and individually tailored intervention.

CONDUCT DISORDER AND OPPOSITIONAL DEFIANT DISORDER – TYPES AND SUBTYPES This chapter focuses on the psychosocial treatment and management of conduct disorder (CD) and oppositional defiant disorder (ODD) in children and adolescents as defined by DSM-IV. Figure 25.1 depicts DSM-IV symptoms of ODD and CD. The most prominent difference between both disorders is that while the essential feature of ODD is a recurrent pattern of negativistic, hostile and defiant behavior towards authorities, children and adolescents with CD are characterized by a recurrent and persistent pattern of behavior that violates the basic rights of others, rules and norms (American Psychiatric Association, 1994; Loeber et al., 2000). Aside from this distinction on the basis of behavior pattern one can think of at least four practical reasons why a distinction between CD and ODD – although rather new and originally not empirically founded – might be useful: first, because the CD diagnosis automatically includes information about treatability and prognosis the clinician might be reluctant to give a young child a diagnosis of CD. Secondly, CD

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

418

VOLUME I: DIAGNOSIS AND TREATMENT

Oppositional defiant disorder A. A pattern of negativistic, hostile and defiant behavior lasting at least six months, during which four (or more) of the following are present: 1. 2. 3. 4. 5. 6. 7. 8.

Often loses temper Often argues with adults Often actively defies or refuses to comply with adults’ requests or rules Often deliberately annoys people Often blames others for his or her mistakes or misbehavior Is often touchy or easily annoyed by others Is often angry and resentful Is often spiteful or vindictive

Conduct disorder 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15.

Often bullies, threatens or intimidates others Often initiates physical fights Has used a weapon Has been physically cruel to people Has been physically cruel to animals Has stolen while confronting a victim Has forced someone into sexual activity Has deliberately engaged in fire setting Has deliberately destroyed others’ property Has broken into someone else’s house, building or car Often lies to con others Has stolen items of nontrivial value without confronting the victim Often stays out late without permission, starting before age 13 Has run away from home overnight at least twice Often truant from school, starting before age 13

Figure 25.1 DSM-IV-TR diagnostic criteria for oppositional defiant disorder and conduct disorder

and ODD might in fact represent distinct entities. They might – thirdly– resemble more or less severe expressions of the same etiology, or fourthly ODD and CD might be distinct but might be etiologically so highly associated that they most often co-occur (Quay, 1999). Most empirical evidence supports the distinction between CD and ODD (Loeber et al., 2000) as well as the distinction between attention deficit hyperactivity disorder (ADHD) and ODD and CD (Hinshaw, 1994; Waldman & Lilienfeld, 1991). It has been argued, however, that further distinction between ODD and CD subtypes is needed to more precisely describe the disorders including their developmental course. These subtypes may also be important in treatment planning. Subtyping has been suggested according to symptom clusters, according to age of onset, or to whether antisocial behavior is committed solitarily or in a group (unsocialized versus socialized) – the latter two distinctions being restricted to subtyping of CD behavior.

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

419

With respect to symptom clusters, it has been argued that covert CD behaviors (e.g., property crimes or status offenses) might resemble a different pattern of behavior than aggressive CD (Loeber et al., 2000). Another differentiation is that of overt disruptive behavior (confrontational, such as fighting) versus covert disruptive behavior (concealing, e.g., theft, opposition or stubbornness; Doepfner & Petermann, 2004; Fergusson, Horwood & Lynskey, 1994). By means of meta-analyses of factor analyses Frick and co-workers (1993) found four symptom clusters of disruptive child behavior: (i) property violations (including stealing, fire setting, vandalism, cruelty to animals and lying); (ii) aggression (spiteful, cruel, blames others, assault, fights, bullies); (iii) status violations (runaway, truancy, swears, breaks rules, substance use); and (iv) oppositional behavior (temper, defies, annoys, stubborn, angry, argues, touchy) (Frick et al., 1993). All of these subtypings or classifications find empirical evidence for boys only. Girls tend to use indirect, verbal and relational aggression rather than physical aggression or overt destructiveness, suggesting the usefulness of distinct diagnostic criteria for both genders (Bj¨orkqvist, Lagerspetz & Kauianen, 1992; Crick & Grotpeter, 1995). DSM-IV suggests subtyping of CD behavior on the basis of an informant’s report on the onset of a single symptom prior to or after age 10. Following this classification Moffitt (1993) proposes a developmental taxonomy of two developmental pathways of CD: childonset (also called early-starter or aggressive-versatile) versus adolescent-onset (also called late-onset or nonaggressive). Lahey and colleagues (1998) have argued that this distinction between early- versus late-onset CD not only reflects the clinical reality more accurately – as they found that boys who meet criteria for CD show fluctuating levels of aggression over time and thus meet criteria of different aggressive subtypes from one assessment to the next – but the distinction also provides extra information on the stability and prognosis of the disorder. That is, early-onset CD has typically met the ODD criteria earlier in childhood, exhibits more physical aggression and due to academic failure and severe peer problems seems to be predictive of adverse consequences in adulthood (Harrington, 2001; Lahey et al., 1998; Moffitt, 1993). In line with this argument, ODD symptoms might be viewed as prodromatal preceding signs of later CD (American Psychiatric Association, 1994). Earlier Jenkins and co-workers offered the differentiation between undersocialized (or solitary) versus socialized (or group) CD behaviors (Hewitt & Jenkins, 1946; Jenkins & Glickman, 1947) by describing whether children or adolescents commit antisocial activities alone or in a group and whether they have social bonds. Due to difficulties in definition, the socialization variable has been dropped from DSM-IV: this distinction is still recognized in the ICD-10 classification, however (American Psychiatric Association, 1994).

DEVELOPMENTAL COURSE Disruptive behavior disorders, or even more general aggression, have been found to represent a highly stable pattern of behavior. Depending on the studied samples, 44–88 % of children who were initially diagnosed persisted with CD three to four years later (Lahey et al., 1995; Offord et al., 1992). The predictive value of the diagnosis is highest in clinic referred samples (Lahey et al., 1995) and in most severely affected children (Cohen, Cohen & Brook, 1993). As stated before the early-onset CD subtype seems to resemble an even

420

VOLUME I: DIAGNOSIS AND TREATMENT

more stable disorder involving high risk of school failure, peer problems, emotional dysregulation, alcohol and drug abuse and adolescent delinquency (Moffitt, 1993). With respect to the predictive value of single symptoms, reports of singular cruelty to people and weapon use respectively showed high correlations with persistent CD (Cohen & Flory, 1998). Persistent physical fighting, proactive or nonimpulsive aggression or the general effects of the emotional component of aggressive behavior have been studied in terms of their predictive utility (see Loeber et al., 2000 for more details). Further, age and gender atypicality of symptoms seem to be predictive of later outcome. For children below 13 years of age, Frick and colleagues (1994) found symptoms of cruelty, running away and breaking into a house to be most predictive for CD. For girls, fighting and cruel behavior were atypical and most likely to predict a later CD diagnosis. A study assessing the stability of aggressive behavior in girls suggests that for girls temporal stability is even higher than for boys between four to five and 10 to 12 years of age (Verhulst & van der Ende, 1991). Despite the lower prevalence rates in girls, once disruptive behavior disorders become apparent in girls they can resemble an even more stable pattern of behavior than in boys.

PREVALENCE Lahey and colleagues reviewed the internationally published data on prevalence rates of disruptive behavior disorders (Lahey et al., 1999). They included 39 population-based studies. Estimated prevalence rates for the various definitions of CD reached 11.9 % for girls and boys combined; the median being about 2.0 %. Boys were three to four times more likely to be diagnosed with CD across ages, after the age of six (Lahey et al., 2000). For ODD the estimates ranged from 0.3–22.5 % with a median about 3.2 %. However, prevalence rates of a specific diagnosis underestimate the extent of the problem, as children or adolescents who do not yet fulfill diagnostic criteria can still show significant impairment and a poor long-term prognosis. A developmental perspective on the epidemiology of CD and ODD has been undertaken by only few studies. Inconsistent results on age-related changes on CD prevalence have been reported in the review by Lahey and colleagues (1999). While one sample from the Ontario Child Health Study found 12–16 year olds to be more frequently diagnosed with CD than 4–11 year olds (Offord et al., 1987), no difference in diagnosis frequency was found between the group of 6–11 versus 12–16 year olds. This inconsistency in findings was evident as well in other studies (Lahey et al., 1999). Reports on age-related changes in dimensional measures of aggression are slightly more consistent, mostly stating age-related decreases in temper tantrums and opposition during preschool years (Hartup, 2005) and reporting age-related increases in nonaggressive delinquent behavior from middle childhood to adolescence. One study suggests a peak in delinquency at 16–17 years and a decline afterwards (Pedersen & Wichstrom, 1995). Some evidence, however, points to age-related declines in aggression during childhood and adolescence (McDermott, 1996). In an attempt to summarize the inconsistent results, Lahey and co-authors (1999) argue that the data point to a decline of aggressive CD behaviors with increasing age, while nonaggressive CD behaviors become more common with increasing age. With respect to ODD, most studies reviewed by Lahey (1999) report no age-related differences in ODD prevalence.

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

421

FACTORS CONTRIBUTING TO PROGNOSIS AND TREATMENT OUTCOME Biological Risk Factors Evidence on the influence of genetic factors on the development of ODD or CD is far from conclusive (Burke, Loeber & Birmaher, 2002). Methodological issues such as the influence of different informants, developmental stages and assessment procedure result in inconsistent findings. Overall, genetic factors seem to play a role in mediating the effect of parental on child behavior (Deater-Deckard, 2000), for example, familial negativity was associated with adolescent antisocial behavior by means of genetic factors (Pike et al., 1996). However, both studies stress that shared environment also mediates the association between child and parental behavior. While it might be difficult to disentangle the effect of genetic factors on more general behaviorally based assessments of antisocial or disruptive behavior, biological factors such as neuroanatomy, neurotransmitters or autonomic underarousal seem to be more clearly associated with CD or ODD symptoms. Low levels of serotonin and its metabolites have been linked to aggression and violence in children, adolescents and young adult males (Clarke, Murphy & Constantino, 1999; Moffitt et al., 1998; Unis et al., 1997). In addition to central serotonin concentrations, cortisol and testosterone levels have been held responsible for mediating disruptive behavior patterns. Salivary cortisol levels were found to be negatively correlated with child ODD (Van Goozen et al., 1998), aggression and with child CD and parent antisocial personality disorder (Vanyukov et al., 1993). Testosterone has been associated with early-onset aggression (Pliszka, 1999). Further biological markers such as skin conductance, startle reflex and heart rate have also been identified to deviate in children and adolescence with ODD and CD. Lower skin conductance levels were found in disruptive boys, higher skin conductance levels being associated with higher anxiety levels (Hastings, Anderson & Kelley, 1996). Lowered heart rate levels were found in ODD boys (Van Goozen et al., 1998) and were predictive of later criminality (Raine, Venables & Williams, 1990). In a study on biological responses to emotionally negative pictures, the startle reflex of CD children deviated from controls (Herpertz et al., 2005). Overall, various biological markers seem to exist that precede or accompany ODD or CD behavioral patterns and suggests a biological basis or at least biological correlates of the disorder. Because temperament is regarded as biologically based, is strongly correlated with disruptive behaviors in early and late childhood (Sanson & Prior, 1999), and is said to mediate the effects of parental and child behavior; early temperamental factors may represent a link between child biological and functional risk factors. Despite the lack of consensus regarding the precise definition of temperament, empirical evidence suggests that early emotional instability actually represents an innate quality that has high predictive value on whether children will exhibit more or less externalizing behavioral problems during childhood (Burke, Loeber & Birmaher, 2002).

Behavioral Risk Factors and Psychological Theories on Etiology Cognitive-behavioral theories indicate that (i) problems with social information processing; (ii) social skill deficits; (iii) lack of impulse control; and (iv) coercive interaction processes may play crucial roles in the development of ODD/CD.

422

VOLUME I: DIAGNOSIS AND TREATMENT

Research on social information processing in youngsters with CD has shown that in ambiguous social situations their cognition is characterized by a hostile attributional bias (Crick & Dodge, 1994). When asked to guess another person’s intention, aggressive children search for fewer cues or facts (Dodge & Newman, 1981). With respect to their competencies in judging social situations, disruptive children have been shown to focus more on aggressive cues and to misattribute hostile intentions to others (Goutz, 1981; Dodge, 1985). They have difficulty solving social problems and respond with less competent strategies to hypothetical conflict situations (Richard & Dodge, 1982; Rubin & Krasnor, 1986). These deficits, especially regarding the perception and interpretation of social situations, contribute to the difficulties CD children have with their parents and peers (Asher & Renshaw, 1981). Deficits in social information processing may cause social skills deficits on a behavioral level. Those children are for instance not able to start a conversation and maintain it; they do not have the skills to ask friends to play with them and what to do if they are rejected in return. Instead they often respond aggressively and will be more often rejected (e.g., Dodge, 1983; Patterson, DeBaryshe & Ramsey, 1989), because disruptive behavior is perceived to be aversive. This rejection by peers persists over time (Coie & Dodge, 1998), which leads to fewer opportunities for practicing social interaction. Being trapped in this vicious cycle, these rejections have negative influences on social adjustment over time, as prospective longitudinal studies and follow-up studies of clinical/high-risk samples indicate (e.g., Ollendick et al., 1992). It is even assumed that these phenomena (i.e., disruptive behavior disorders and low social competencies) are congruent. Findings (Webster-Stratton & Hammond, 1998) show that this is not the case. Twenty-two percent shared variance indicates that there is a relationship but no congruity. These two phenomena are not the ‘opposite sides of the same coin’ (Webster-Stratton & Hammond, 1998). However, 22% shared variance indicates that it is worth emphasizing this matter and implementing treatment that addresses this problem. Some children with ODD/CD do have the cognitive and behavioral social skills necessary for competent social interactions and are able to behave in a socially skillful manner in roleplaying situations. In real life, they nevertheless react aggressively in similar situations. This response pattern may be mediated by problems in behavioral inhibition. Impulsivity and behavioral inhibition deficits seem to resemble a response pattern that is highly associated with the early onset and persistence of ODD or CD symptoms (Lillienfeld & Waldman, 1990; White et al., 1994). Behavioral rather than cognitive inhibition deficits seem to be more relevant (White et al., 1994). All in all Asher and Renshaw (1981) termed this lack of cognitive, social and behavioral skills the child-deficit hypothesis of conduct problem children. Patterson’s coercion hypothesis (Patterson, 1982, Patterson, Reid & Dishion, 1992) examines disruptive behavior problems from a behavioral contingency-based perspective. It describes typical interaction patterns in these families by the following vicious cycle: the child learns to get his own way and escapes parental criticism by escalating his negative behaviors, resulting in aversive parental emotions and reactions. As this cycle of child negative behavior, parental anger and negative discipline progresses, the child not only directly succeeds in avoiding parent demands or criticisms but is also provided with additional modeling of aggression and coercion. The parent on the other hand perceives themselves as incompetent as a parent.

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

423

Comorbidity Conditions comorbid with CD and ODD may resemble different levels of severity of the disorder and generally result in a higher degree of impairment (Petermite, Loney & Roberts, 1995). Comorbid conditions may cause ODD/CD or they may be a consequence of ODD/CD. Most studies of children with ODD report evidence of high rates of comorbidity with CD. However, comorbidity with other disorders is often seen as well. One study found that 14 % of the studied ODD sample was also diagnosed with attention deficit hyperactivity disorder (ADHD), 14 % with an anxiety disorder, and 9 % with depression (Angold & Costello, 1996). In children and adolescents with CD, ADHD is the most frequent comorbid condition, with 35 % of CD children studied in the Ontario Child Health Study (Offord et al., 1987) exhibiting comorbid hyperactivity as opposed to 3 % of those without a CD diagnoses. Although many studies have tried to shed light on the developmental relationship between ADHD and CD, the results remain inconsistent on whether or not ADHD can be regarded a precursor of CD (Loeber et al., 2000). Regardless of whether ADHD precedes or accompanies CD, the relationship between the disorders seems to be based on the hyperactiveimpulsive behavioral pattern and not on the inattention (Babinski, Hartsough & Lambert, 1999). One model of the relation between ADHD and CD has been proposed by Lahey and Loeber (Lahey & Loeber, 1994; Lahey, Waldman & McBurnett, 1999). The authors hypothesize that only those ADHD children who also exhibit symptoms of ODD will develop CD, and a subgroup of these children will later develop antisocial personality disorder (see Figure 25.2). Children and adolescents with CD exhibit an increased risk for comorbid ADHD, anxiety, mood or somatoform disorders, substance abuse, or later antisocial personality disorder (Loeber et al., 2000). The model (Figure 25.2) proposes bidirectional relations between depression and CD and a similar reciprocal relation between substance abuse and CD (Lahey & Loeber, 1994; Lahey, Waldman & McBurnett, 1999). Studies on the temporal relationship between depression and CD yield inconsistent results (Capaldi, 1992): while some argue that CD and its consequences result in depression, others stress that part of lateonset nonaggressive CD is secondary to depression and resembles a distinct form of CD (Masten, 1988). Irrespective of the temporal relationship between both disorders, the high comorbidity rate between depression and CD is of special concern due to the elevated risk for subsequent substance abuse (Buydens-Branchey et al., 1989; Loeber et al., 2000). Again, some authors stress that early-onset CD precedes substance use (Mannuzza et al., 1991), while others point to the fact that early-onset substance abuse predicts later criminality. Increased rates of obsessive-compulsive disorders, mania and schizophrenia have been reported as well (Robins, Tipp & McEvoy, 1991). Low school achievement and school failure is associated with later antisocial behavior, again the temporal causal relationships respectively remaining unsolved (Farrington, 1995; Frick et al., 1991). Comorbid conditions are important to consider with respect to the circumstances for treatment. Children with comorbid anxiety disorder show a better prognosis (Fonagy et al., 2002), those with comorbid substance abuse are harder to motivate or to keep in therapy (Borduin, 1999). In children with ADHD and ODD the pharmacological and the multimodal treatment of ADHD may also result in reduced levels of ODD (Doepfner et al., 2004; Taylor et al., 2004).

424

VOLUME I: DIAGNOSIS AND TREATMENT

Early Childhood

Adolescence

Anxiety

Depression

ODD

CD

ADHD

Somatoform Disorder

Young Adulthood

Substance Use

APD

Figure 25.2 Developmental sequences between disruptive behavior disorders and comorbid conditions. The dotted arrow indicates a relationship in which ADHD serves to hasten and worsen the severity of conduct disorder (CD), but only in the presence of oppositional defiant disorder (ODD). Lines without arrowheads indicate relationships in which the direction is not clear. Antisocial personality disorder (APD) in young adulthood is a primary likely outcome of the disruptive behavior disorders pathway but was not expressly reviewed here. Source: Loeber et al. (2000)

IMPLICATIONS FOR TREATMENT AND OVERVIEW OF TREATMENT APPROACHES As stated above research indicates that the developmental pathway of CD is established during preschool years. Not only do serious conduct problems become more and more resistant to change with increasing age, intervention studies suggest that the younger the child at the time of intervention, the more positive the outcome (Strain et al., 1982). To date approximately 70 % of young conduct problem children do not receive any treatment or are treated with therapy approaches that are not thoroughly empirically validated (Brestan & Eyberg, 1998). Thus, disastrous individual developmental trajectories as well as social and financial costs to society call for effective prevention or treatment programs that identify high-risk populations early in development and provide effective help for caregivers and children (Loeber & Farrington, 2000). Research indicates that serious conduct problems can be identified in children as young as four years of age. Another important factor for intervention programs targeting disruptive preschool children is that school entry is not only an important transition point but also resembles a period of great stress for many children and parents. Early failure of the child due to conduct problems will decrease the probability

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

425

of future success for the child in school, will affect relationships with teachers and peers, and will impair the parents’ attitudes towards their child and school-related topics. Theoretically prevention programs are distinguishable from clinical intervention, in clinical practice the transition from prevention to intervention or therapy is smooth. Depending on the targeted population, prevention programs are further differentiated: indicated prevention programs aim at improving problem behavior in children with prodromal signs or symptoms of a mental disorder in childhood. Selective prevention programs address groups that are – due to social or individual risk factors – at risk of developing externalizing disorders, and universal prevention programs provide support for the general public or an entire population. Psychological theories on etiological factors of ODD either stress child factors, that is, deficits in social information processing, in behavioral social skills or in impulse control; or environmental factors, that is, coercive interaction processes. Interventions therefore focus either on changing child factors by patient-centered treatment or environmental factors (e.g., coercive interaction) by parent-focused or teacher-focused interventions.

PARENT-FOCUSED INTERVENTIONS FOR CHILDREN Parent management training (PMT) primarily addresses families with children aged 3 to 12. Compared with other family intervention approaches, this approach has the strongest empirical support (Brestan & Eyberg, 1998; McCart et al., 2006; Serketich & Dumas, 1996). The focus is on parenting, parent–child interaction, enhancement of family relations and parenting skills acquisition. PMT is based on social learning principles and draws from the basic and applied operant conditioning research. Underlying theory assumes that mismanaged contingencies account for a great part of disruptive behavior. Families with conduct problem children typically show ineffective parenting strategies and dysfunctional parent–child interactions that are characterized by the parents’ directly reinforcing deviant behavior, using frequent and ineffective commands, by harsh disciplinary practices, coercion, low parental emotional involvement, and low parental monitoring (Patterson, Reid & Dishion, 1992). Aside from these interaction-based aspects, family characteristics such as marital conflicts, parental stress or parental mental illness, lack of social support and environmental stressors have been found to disrupt parenting behavior and are regarded as parent-related risk factors for the development and maintenance of disruptive behavior problems. WebsterStratton, for example, studied the marital status of 218 families with ODD or CD children and found that 75 % of the sample had been divorced at least once or were living in stressful partnerships, findings that underline the importance of supplying support to the parents. Although many variations of PMT exist, several common characteristics are shared, one of them being that parents are trained to identify, define and observe problem behavior in new ways before a skill training is started. Based on the above outlined social learning, interaction-based model, PMT aims at promoting parent competencies and strengthening parent–child interactions by increasing parents’ positive parenting skills. More specifically, parents are taught to nurture their relationships with their children by engaging in positive child-directed play activities, by concentrating on positive traits and competencies of their child and by paying special attention to their own competencies and successes in parenting. Research indicates that these aspects of positive parenting not only directly influence child

426

VOLUME I: DIAGNOSIS AND TREATMENT

behavior but also affect parents’ sense of competence and self-confidence – which in turn has positive effects on the parents’ attitudes towards their child. Moreover, parents are trained how to effectively communicate commands, how to use prompting and shaping and how to implement positive reinforcement procedures (such as the use of social praise and tokens). Another important topic of PMT is the replacing of harsh discipline strategies such as criticism, emotional or physical violence with positive strategies such as ignoring, or natural and logical consequences. In addition to these parent skill interventions, some programs offer support in dealing with the above-mentioned family risk factors like marital conflicts or parental stress. Because families with conduct disordered children often have problems in meeting confirmed appointments and vary in their pace of learning and using treatment material, some programs favor individual settings. Others use the advantages of a group approach, for example, therapist-led parent group discussions, modeling techniques in the group or social support. Group formats are also more cost-effective. International meta-analyses of treatment studies with PMT report reductions in preand grade-schoolers’ disruptive problem behavior after preventive and therapeutic parentfocused interventions (Brestan & Eyberg, 1998; Greenberg, Domitrovich & Bumbarger 2001; LeMarquand, Tremblay & Vitaro, 2001; McCart et al., 2006; Serketich & Dumas, 1996; Taylor & Biglan, 1998). Overall, effect sizes range from 0.44 to 0.86 depending on time invested, treated population and reported measures (McCart et al., 2006; Serketich & Dumas, 1996). Most programs concentrate on clinic-referred populations, with school-aged samples being studied more often than preschoolers. One prominent example for a parent training program that targets children two to eight years of age is the Incredible Years Program (Webster-Stratton, 1998), which is presented as a group format and includes parent-focused as well as child- and teacher-focused modules. The parent training modules either concentrate on a 26-hour parent skill training (BASIC) or additionally supply support on intra- and interpersonal factors (ADVANCE). Teacherand child-focused modules are under evaluation. In accordance with Bandura’s modeling theory of learning (1977), videotape modeling is used to demonstrate parent–child interactions that promote prosocial behavior and decrease inappropriate behavior. Compared to control groups and other interventions the BASIC program proved to be effective in improving parental attitudes and parent–child interactions, in reducing the frequency of violent discipline strategies and in reducing child conduct problems (Brotman et al., 2005; Drugli & Larsson, 2006; Webster-Stratton, 1988, 1990, 1994; Webster-Stratton, Reid & Hammond, 2004). The Incredible Years Program was also evaluated on selective high-risk samples of low-income single mothers and again produced positive effects on child outcome (Webster-Stratton, 1984). Three-year follow-up data indicated that clinically significant improvements could be maintained by the combined videotape-modeling group-discussion treatment in the BASIC program; single components of the program did not yield comparably positive results (Webster-Stratton, 1990). Adding the ADVANCE modules to the program had an additional positive impact: although both treatment groups (BASIC and ADVANCE) improved significantly with respect to child outcome, parental distress and parent–child interactions, children in the ADVANCE group were more effective in problem solving. Moreover, parents’ communication, problem-solving and collaboration skills improved more in the ADVANCE group, suggesting that adding support in managing personal distress and interpersonal difficulties is a highly promising measure (Webster-Stratton, 1994).

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

427

The Triple P- Positive Parenting Program developed by Sanders and coworkers in Australia is a multilevel, preventively oriented PMT approach (Sanders et al., 2004). Like other PMT strategies, it aims to enhance the knowledge, skills and confidence of parents, by paying special attention to social information processing models which highlight the important role of parental cognitions in the process of parenting (Bandura, 1977, 1989). Triple P incorporates five levels with increasing intensity, addressing parents of children from birth to age 16. Level 1 uses print and electronic media to apply a universal parent information strategy whereas levels 2 and 3 target parents of children with mild to moderate behavioral difficulties including an individually tailored parenting plan to manage a specific behavioral or developmental concern. Level 4 is the Standard Triple P and involves an intensive, broad-focused 10-session parent training program for families with children with severe conduct problems. Level 5, similar to the above-mentioned basic and advanced modules of the Incredible Years Program, adds individual family support for other sources of family distress like marital conflict, parental depression or stress. The various levels of Triple P have been subjected to a wide variety of controlled evaluations (see Sanders, 1999 for a review). Efficacy as well as effectiveness trials have supported the positive effects of the program on parents as well as on children. It proved to be useful in teaching parents to implement behavioral change and positive parenting strategies at home with resultant decrease in child conduct problems (Prinz & Dumas, 2004). After treatment children not only experience fewer problems, but they are more cooperative, get along better with peers, and behave better in school; parents show greater confidence in their parenting ability, have more positive attitudes towards their children, and refrain from abusive parenting practices. Targeting clinically referred cases, Kazdin and co-workers developed and extensively evaluated a treatment program for families with children ages 2 to 13 referred to their outpatient clinic for aggressive and antisocial behavior (see Kazdin, 2003, 2005 for review). The program incorporates individual 12–16 weekly sessions focusing on conveying basic knowledge about parenting, reinforcing principles and interaction principles. Parents are then taught the specific skills on the basis of their individual constellation of problems, taking into account special features of the family situation. The use of the skills at home in relation to their child is practiced by modeling and role-playing techniques. In addition to the PMT modules for parents, children are provided with problem-solving skills training. Both components are fixed and flexible, following a fixed treatment schedule that is adjusted in a flexible way to the needs of the family. Evaluation studies concentrate on the clinical significance of family and child outcome improvements and on identifying moderating factors. Research indicates that this PMT program is capable of reducing antisocial and of increasing prosocial behavior in children between the ages 7 and 13. Effect sizes are reported to be as high as 1.2 (see Kazdin, 2003, 2005 for review). Further, depression and stress can be reduced in parents. Positive treatment effects have been shown to be stable at least beyond one year. Improvements can be attributed to the particular intervention modules (PMT vs. problem-solving skill training) and cannot be explained by nonspecific common treatment factors. Consecutive moderator analysis suggests that treatment outcome is influenced by prior impairment and dysfunction in the child, the parents and the family. The cross-cultural generalizability of PMTs has been documented in several studies. One example is the German Treatment Program for Children with Hyperkinetic and Oppositional Problem Behavior, THOP (Doepfner, Schuermann & Froelich, 2002) and the Prevention Program for Externalizing Problem Behavior, PEP (Plueck et al., 2006), which have been

428

VOLUME I: DIAGNOSIS AND TREATMENT

shown to be effective in school-aged children (Doepfner et al., 2004) and pre-school children (Hanisch et al., under review). Parent management training is a skills training intervention,in which parents are taught to use positive and negative consequences systematically. Another skills training approach used with adolescents is communication training interventions. The Problem Solving Communication Training (PSCT) developed by Robin and Foster (1989) is one example of this kind of intervention. PSCT systematically teaches skills to adolescents and their parents for communicating about issues that cause repeated problems. Later versions incorporated cognitive components and supplemental anger management interventions. PSCT has been shown to produce positive changes in observations of problem-solving skills and reports of conflict at home in small-scale randomized controlled trials (Robin & Foster, 1989, for review).

SCHOOL-BASED INTERVENTIONS School-based interventions for ODD/CD are often conceptualized as preventive interventions. They can be categorized in several ways, for example, by level of preventive intervention (universal vs. indicated prevention), age (children vs. adolescents) and target of interventions. The latter category refers to the categories of Greenberg, Domitrovich and Bumbarger (1999), who make the distinction between: (a) directly targeting aggression and violence; (b) targeting social and affective competence; and (c) targeting the school environment. In this review those programs are considered that show at least promising outcomes according to the Blueprints Model Programs Selection Criteria (Center for the Study and Prevention of Violence, 2002). Programs, which achieve the Blueprint model standard, have to show sustained effects with a strong research design (i.e., experimental design with random assignment or quasi-experimental designs with matched control groups) and multiple site replications. Promising programs must only meet the first criterion. Of the selected programs, two were categorized as a model standard: (i) Promoting Alternative Thinking Strategies (Greenberg & Kusch´e, 1998), which targets social-emotional competence and (ii) the Bullying Prevention Program (Olweus, 1993) which emphasizes interventions in the school environment. Other programs described here are declared as promising, according to the Blueprints Model Programs Selection Criteria.

School-Based Interventions for Children Promoting Alternative Thinking Strategies (PATHS), developed by Greenberg and Kusch´e (1998), is probably one of the best-evaluated programs. As a universal preventive intervention, it is designed to improve social and emotional competence by helping children to identify, understand and self-regulate their emotions. To foster generalization, PATHS also seeks to promote classroom ecology and additionally contains a parental component. Its conceptual framework is the Affective-Behavioral-Cognitive-Dynamic model, ABCD (Greenberg & Kusch´e, 1993), which stresses the developmental integration of affect, behavior and cognitive understanding. The children’s behavior is assumed to be influenced by emotional awareness, affective-cognitive control and social-cognitive understanding. The

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

429

contents of the 131-lesson curriculum are self-control, emotional understanding, positive self-esteem, relationships and interpersonal problem-solving skills, which can be applied from the first to the sixth grade. Numerous randomized controlled studies have been conducted that show robust effects within a variety of populations (for an overview see Greenberg, Domitrovich & Bumbarger, 1999). Children participating in the training show significantly better social problem solving and understanding of emotions at the end of treatment compared to controls. The one-year follow-up showed that the skills were maintained. The studies also showed improvements in self-reported conduct problems, teacher ratings of adaptive behavior, social planning and impulsivity. Compared to the one-year follow-up, two years after the end of treatment, teachers and students reported even fewer conduct problems. The Bullying Prevention Program (BPP; Olweus, 1993) is designed for elementary and middle schools. It aims at reduction and prevention of bullying among school children and the improvement of prosocial behavior. The idea is that a systematically restructured school environment provides fewer opportunities and less reinforcement for bullying. The prerequisites are the awareness and involvement of adults, that is, teachers and parents. At classroom level, rules against bullying are implemented. Classroom meetings are initiated to provide information about bullying and antisocial behavior, to improve adherence to classroom rules, and to learn how to combat bullying. In quasi-experimental designs, BPP is shown to be effective in reducing bullying behavior and antisocial behavior such as vandalism, fighting, theft and truancy. In a first study with a Norwegian population, the effects of reducing bullying were substantial with reduction rates of at least 50 %. Follow-up studies (after 8 and 20 months) show that effects increase after the end of program. These changes were also shown in a variety of cultures, such the United States, England, Germany and in a subsequent study in Norway, but with more modest effects. For a comprehensive overview see Olweus, Limber and Mihalic (1999). Other school-based programs for children were categorized as promising interventions according to the Blueprints Criteria. One of these programs is the Good Behavior Game (GBG; Barrish, Saunders & Wolf, 1969), which promotes prosocial behavior through emphasizing the reinforcement of positive behavior. As a component of the Community Epidemiological Preventive Intervention (CEPI), it is a classroom team-based approach applied to help early elementary students to improve their psychological well-being and social task performance. Teachers divide children into three heterogeneous teams that compete with each other. The team with the lowest rate of rule breaking will be rewarded. Compared to controls, findings indicate significant reductions of aggressive behavior, poor achievement and ‘shy behavior’ (Dolan et al., 1993). These effects were more marked for children with initial high levels of aggressive behavior. The effects that have been found in first and second grades diminished in third and fourth grade, but reappeared in the fifth and were more marked in sixth grade (Kellam et al., 1998). I Can Problem Solve (ICPS; Shure, 1992a,b) originally developed for preschool children and formerly known as Interpersonal Cognitive Problem Solving (Shure, 1997) consists of a structured training in interpersonal cognitive problem-solving skills for preschool and elementary school children. This kind of intervention can be categorized as an one that targets social and affective competence. Changed thinking styles are thought to lead to better social adjustment. Children in the preschool version are trained to generate more solutions to interpersonal problems, consider the consequences of these solutions, and identify cognitions that lead to problems. The issues in the first part of the group sessions are basic

430

VOLUME I: DIAGNOSIS AND TREATMENT

skills, problem-solving language and awareness of emotions. The latter sessions emphasize role-playing and dialoguing to enhance problem-solving skills. For fourth through to sixth graders, the training is augmented with sessions that emphasize the understanding of others’ motives and the implementation of problem-solving steps. Nursery and kindergarten children, who take part in ICPS, show less teacher-reported disruptive classroom behavior and generate more alternative problem-solving skills (Aberson, 1987). A five-year longitudinal study showed improved classroom behavior and problem-solving skills. Positive effects are still found three years after the end of treatment (Shure, 1993). The findings were replicated with fifth graders, who show enhanced ICPS skills and more prosocial behavior (Shure, 1997). Linking the Interests of Families and Teachers (LIFT; Reid et al., 1999) is a multidimensional program that targets first and fifth grade elementary school students and their parents. Besides effective parenting, parents are trained to initiate and maintain contact with teachers, while children obtain classroom-based social and problem-solving skills training. Children also receive an adaptation of the Good Behavior Game as a playground component. In a population-based randomized intervention trial with first and fifth graders, children’s physical aggression on the playground was reduced significantly, with the largest effect size particularly among those who were rated as the most aggressive at pre-test (Reid et al., 1999; Stoolmiller, Eddy & Reid, 2000). As LIFT, the Seattle Social Development Project (SSDP; Hawkins et al., 1992) is a multimodal approach for first to sixth graders, designed to reduce aggression by addressing student, school ecology and family. The teacher component contains three major elements: proactive classroom management, interactive teaching and cooperative learning. First grade students are taught cognitive and social skills, that is, decision making, negotiation and conflict resolution. In the sixth grade, students learn additionally how to resist negative social influences and how to stay out of trouble by generating and suggesting prosocial alternative solutions. Parents get, depending on their personal needs and their child’s grade, training in effective parenting, teaching academic skills and prevention of drug abuse. Evidence for SSDP’s efficacy was shown in longitudinal research conducted by Hawkins and co-workers (Hawkins et al., 1999). Findings of a nonrandomized controlled follow-up study showed significant prevention or reduction in self-reported alcohol abuse, delinquency; less sexual intercourse and fewer sexual partners and decreased pregnancy six years after intervention. In addition to more positive feelings, more commitment to school, improved academic achievement and less maladapted behavior at school were reported.

School-Based Interventions for Adolescents Interventions designed for juveniles are rare. There are no programs that have achieved model standards according to Blueprint Criteria; moreover programs that emphasize social and affective competence are lacking. The School Transitional Environmental Program (STEP; Felner & Adan, 1988) facilitates normative school transitions by enhancing students’ coping strategies, preventing academic failure and school dropout. STEP is based on the Transitional Life Events model, which states that transitional life events place children at risk for maladaptive behavior. Children, assigned to homeroom classes, learn in a more structured and highly supportive environment. Therefore, the teacher’s role is redefined as an administrator and counselor who supervises the child’s behavior, needs and problems.

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

431

The homeroom classes are conceptualized as familiar settings with stable peer groups. In terms of Blueprint Criteria, this program is labeled as promising. Felner and colleagues conducted a series of evaluations and replications (Felner & Adan, 1988; Felner et al., 1993; Felner, Ginter & Primavera, 1982). Compared to controls, students, who participate in STEP, show lower levels of stress and decreased anxiety, depression and delinquency one year after transition. Compared with a more general intervention (i.e., a training in generic copings and problem-solving skills) STEP leads to less academic failure and better social adjustment (Felner et al., 1993). At a four-year follow-up, social and academic adjustments were maintained and rates of school dropout were reduced compared to those of controls (43 % vs. 21 %).

PATIENT-FOCUSED INTERVENTIONS Research indicates that children with ODD-CD have lower social competence. As a consequence, most child-centered interventions primarily focus on the improvement of social competence, using multiple cognitive-behavioral intervention techniques in combination. However, these approaches have limitations: treatments addressing only the child’s problem behavior frequently show only modest effects. Findings of a meta-analysis by Quinn and colleagues (1999), which considered studies on social skills trainings from 1981 to 1994, were almost disillusioning. Global social skills interventions, when used in small groups of children with emotional and behavioral disorders, showed less than substantial changes in prosocial behavior, problem behavior and specific behavior traits (Quinn et al., 1999). Recently, McCart and colleagues (McCart et al., 2006) conducted a meta-analysis of 41 studies on the effects of cognitive-behavioral therapy for antisocial youths and found effect sizes of 0.35 (CI = .25–.47), which are small but substantial according to Cohen’s criteria. When comparisons were made between the PMT and cognitive-behavioral therapy (CBT) studies involving youths in a similar age range (6–12 years), the effect size for PMT (0.45) was significantly higher than the effect size for CBT (0.23). For CBT, there was a positive relationship between age and effect size. The mean effect size of CBT at follow-up (0.31) was in the small range, suggesting that the beneficial effects of CBT tend to be maintained over time. Brestan and Eyberg (1998) characterized some treatments that meet the Chambless criteria of empirically supported treatment (e.g., Lonigan, Elbert & Johnson, 1998) as ‘probably efficacious’. Two of them, Lochman’s Anger Coping Program and Kazdin’s ProblemSolving Skills Training (PSST), will be described in detail as standalone patient-focused treatments. Related research has shown that those patient-focused treatments combined with parent-focused intervention show beneficial effects, that is, effects of clinical relevance are sustained over time (Kazdin, Siegel & Bass, 1992; Lochman & Wells, 2004; Webster-Stratton & Hammond, 1997). These further developments of Anger Coping Program and PSST, including parent-focused components, will be described, although these interventions are multimodal ones. Psychodynamic approaches have not been proven to be effective (Fonagy & Target, 1994). As already noted low social competence is assumed to be one crucial factor for developing disruptive behavior disorders. However, not yet finally answered is the question of what the concept of social competencies itself includes. There is a broad variety of definitions and an ongoing discussion about the concept, for instance, concerning the distinction between

432

VOLUME I: DIAGNOSIS AND TREATMENT

social competencies and social skills (e.g., Kavale, Forness & Walker, 1999). As a consequence of definitional problems, there are difficulties in measurement. Constructs used to assess social competencies can vary from broad measures of social skills through measures of problem behavior to measurements of specific behavior traits (Quinn et al., 1999). The problem of definition and conceptualization also affects the development of effective treatments. First of all, one must consider that socially competent behavior means something completely different in regard to a preschooler in comparison with a young adolescent. Therefore, treatments are developed to address children of different ages. Most of these interventions concern children in elementary school. Few are conceptualized for preschoolers and adolescents. Other factors should probably be considered as well, for example, severity of ODD/CD, the environment children grow up in and the comorbid problems that the children have. Nevertheless, the six-stage model of information processing of children’s social adjustment (Crick & Dodge, 1994) is a model often cited that some interventions use as a conceptual framework (Figure 25.3). Social cognitions, social information processing, for

NICKI R. CRICK AND KENNETH A. DODGE (1994)

5. RESPONSE DECISION • response evaluation • outcome expectations • self-efficacy evaluation • response selection

5. RESPONSE ACCESS OR CONSTRUCTION

5. CLARIFICATION OF GOALS • arousal regulation

DATA BASE • memory store • acquired rules • social schemes • social knowledge

2. INTERPRETATION OF CUES • causal attributions • intent attributions • other interpretative processes - evaluation of goal attainment - evaluation of past performance - self-evaluations -other-evaluations

6. BEHAVIORAL ENACTMENT

PEER EVALUATION AND RESPONSE 1. ENCODING OF CUES (both internal and external)

Figure 25.3 A reformulated social information-processing model of children’s social adjustment

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

433

example, are presumed to be the antecedents for social behavior. Interventions involving cognitions should be more promising than those involving learning behavior. During the first step of Crick and Dodge’s reformulated model, social cues (i.e., internal and external) will be encoded, followed by their interpretation at the second step. Next, at the third step, a goal will be selected or clarified, followed by access of possible responses or construction of a new one at the fourth step. At the fifth step, children choose a response and then finally enact it at the sixth step. Research referring to this model indicates that children with ODD/CD show a wide range of deviant information processing of social cues/social information (Coie & Dodge, 1998; Dodge et al., 2002; Lochman et al., 2006). Compared to nonaggressive peers, aggressive children show distorted information processing during the encoding stage, which is poorer recall of relevant social cues (Dodge, Bates & Pettit, 1990; Lochman & Dodge, 1994; Webster-Stratton & Lindsay, 1999) and selective attention to hostile or aggressive social cues (Dodge, 1986; Gouze, 1987). At the next step of information processing, aggressive preadolescents and adolescents show hostile-biased attribution in peer conflicts (Dodge, Bates & Pettit, 1990; Lochman & Dodge, 1994; Webster-Stratton & Lindsay, 1999). At the fourth step, namely, generating possible responses to a conflict, aggressive children generate fewer solutions (Dodge, 1986; Webster-Stratton & Lindsay, 1999) and their solutions tend to be more aggressive than prosocial (Dodge, 1986; Quiggle et al., 1992; Webster-Stratton & Lindsay, 1999). Differential research indicates that some of these social information-processing distortions are valid for children exhibiting only reactive aggressive behavior (e.g., Dodge & Coie, 1987; Dodge et al., 1990). Children exhibiting proactive aggression show fewer distortions in social information processing. Lochman and Dodge (1994) have not only found a difference in social information processing between aggressive and nonaggressive children, but there are also differences between preadolescents and adolescents as well as between moderately aggressive and severely aggressive children and juveniles. Some of these findings cited above appeared when the children and adolescents showed a severe level of aggression. For instance, only severely violent boys showed poor cue recall, whereas boys with moderate levels of aggression did not (Lochman & Dodge, 1994). The findings concerning Crick and Dodge’s model have some limitations. WebsterStratton and Lindsay (1999) criticize, noting that influences of emotions, perception of other’s attitudes toward oneself and social interactions with parents were not considered. Especially the latter point may be important for the development of social information processing and should be integrated in treatment, as the findings already cited above indicate. Second, all of these studies used artificial situations, so their findings are not yet demonstrated in real-life situations. Third, there is little research that addresses a sample of children aged 4 to 7, because most of the samples consisted of children from 9 to 12; however, Webster-Stratton and Lindsay (1999) confirm the findings for the older sample in a sample of preschool children.

INTERVENTIONS FOR SCHOOL-AGED CHILDREN Numerous anger-control or anger-management programs have been developed that focus the high anger arousal of aggressive children as antecedents of exhibited aggressive behavior (for an overview see Kavale, Forness & Walker, 1999). Techniques applied in

434

VOLUME I: DIAGNOSIS AND TREATMENT

anger-management treatments follow one of two pathways. The first deals with the anger that is already elicited. Techniques, which can be subsumed under this category include, for example, coping statements. The second pathway prevents anger by focusing on deviant cognitive aspects. Lochman’s Anger Coping Program (Lochman, Barry & Pardini, 2003) primarily emphasizes this second pathway. This approach uses Crick and Dodge’s model of social information processing as a framework. The Anger Coping Program emphasizes the distortions and deficiencies in the aggressive child’s social information processing. Eighteen group sessions were originally designed for fourth to sixth grade children with high anger levels. Issues for the group sessions are behavioral and personal goal setting, anger management, self-instruction, perspective taking, accurate emotional awareness and social problem solving. These issues can be implemented in a way that is individually tailored to the group needs. In a preliminary single-group analysis of efficacy with a small sample, teachers reported decreased aggressive behavior (Lochman, Nelson & Sims, 1981). Group effects were shown in a subsequent study (Lochman et al., 1984) that compared the following conditions: (i) anger coping program (AC); (ii) goal setting; (iii) anger coping plus goal setting; and (iv) untreated control. The outcomes in the conditions including the anger coping program were statistically significant, but the effects were only within a moderate range. Children, who have been assigned to the conditions including anger coping, were rated less aggressive at home (parent ratings) and exhibited less disruptive behavior in the classroom (independent raters). Level of self-esteem improved significantly under the anger-coping conditions. Further studies showed greater effects in a prolonged version of the program (Lochman, 1985) but no differences for anger coping with added components, that is, a self-instruction component focusing on academic tasks (Lochman & Curry, 1986) and a teacher consultation component (Lochman et al., 1989). Follow-up studies (Lochman, 1992; Lochman & Lampron, 1988) indicated that the positive effect of the anger coping program on aggressive children diminishes without booster sessions after the end of initial treatment. But there are positive preventive effects on substance abuse among the adolescents who had taken part in the program three years earlier. Lochman, FitzGerald and Whidby (1999) investigated which differential client factors lead to better outcomes. The greatest effects were observed in the sample of children who were extremely poor problem solvers, showed lower perceived level of hostility, were rejected more often by peers, showed an internalized attribution style and had higher levels of anxiety and somatic complaints. The intervention works best for children who understand their behavior as problematic and have the desire to change it. The Coping Power Program (Lochman, Barry & Pardini, 2003) was derived from the anger coping program considering the findings cited above. Outcome effects should be improved and maintained over time by using a multicomponent treatment. Conceptualized as an indicated preventive intervention for at-risk preadolescents, Coping Power contains more sessions and includes a parental component in addition to the child-focused treatment. The parental component addresses dysfunctional parenting practices. In the child-centered component, groups of fourth through sixth grade students (boys and girls) participate in the 33-session program; sessions are primarily applied to the school context but can also be applied to a clinical setting. This program also includes six to eight individualized sessions with the aim of improving rapport and applying individually tailored interventions. The child-focused group sessions include the issues already listed above, as well as the

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

435

development of skills such as advanced emotional awareness skills, relaxation training and enhancing social skills. The parents participate in a 16-session program. The modification of the parenting skills includes topics such as social reinforcement, positive attention, clear house rules and behavioral expectations, monitoring procedures, appropriate and effective discipline strategies, family communication, maintaining positive contact with the school and stress management. Furthermore, the parent’s role in the treatment process is to provide support to their children who are applying prosocial behavior they have learned. An efficacy study (Lochman & Wells, 2004), with a sample of 183 high-risk boys that compared the child component only, child plus parent component and controls, indicated superior effects in the one-year follow-up for the child–parent combination, that is, improvement of parent-rated delinquency and substance use as well as teacher-rated school behavioral improvement. The child-component only condition had a great positive impact on teacher-rated behavioral improvements. Path analyses indicate that these changes were influenced by changes in the primarily distorted and deficient social information processing in this sample (Lochman & Wells, 2002). Comparisons with a normative group demonstrate that these outcomes are clinically significant. The Problem-Solving Skills Training (PSST, Kazdin, 2003) is probably one of the most extensively researched cognitive-behavioral approaches developed for children with ODD/CD. It emphasizes the latter stages (third to sixth step) of the social-information processing model (Figure 25.3), which encompass the generation, evaluation, selection and enactment of solutions for an identified problem. PSST aims at training prosocial problemsolving skills. As in Lochman’s approach, a parental component (parent management training) was developed in addition. PSST is an individual approach, which can be tailored to the needs of the individual child. It consists of 20 sessions with the core interventions of learning and applying a step-by-step problem-solving technique, which is promoted by contingency management, and modeling. The child can apply these steps to problem situations in the therapeutic setting. Afterwards, the child should have practice in real-life situations. The PMT, already described, can be utilized in combination with the PSST. Numerous efficacy studies suggest statistically positive effects of combined PSST and PMT compared to controls on antisocial behavior with more marked effects from the combination of both components (for a comprehensive overview see Kazdin, 2003). In one study, Kazdin, Siegel and Bass (1992) compared the effects of only PSST, with only PMT and the combination of both treatments. They found a reduction of aggressive and antisocial behavior and more exhibited prosocial behavior with the combination of both treatments. These effects were enhanced and more stable under the combined treatment condition as post-treatment and one-year follow-up data suggested. Further studies excluded nonspecific influences unrelated to treatment (Kazdin et al., 1989). These improvements are consistent for diverse settings (i.e., home, school and community) for post-treatment and one-year follow-up as well as for inpatient and outpatient samples. An analysis of moderators has shown several differential effects for subgroups. One of these effects is less therapeutic change for a subgroup of severely deviant children. Reducing parent’s stress level caused by daily hassles promotes the treatment outcomes (e.g., Kazdin, 2003). These outcomes have large mean effect sizes (mean effect size of change > 1.2) (Kazdin & Wassell, 2000) and compared to a normative sample the maladaptive behavior reverts to a normal level, which indicates clinical relevance.

436

VOLUME I: DIAGNOSIS AND TREATMENT

INTERVENTIONS FOR PRESCHOOL CHILDREN AND ADOLESCENTS Interventions for preschool children are rare, not well investigated and usually designed as multimodal interventions. One of them is Dinosaur School (Webster-Stratton & Hammond, 1997), which is a child-focused prevention program using videotape modeling. The parent version of videotape modeling has been showed to be well established by applying the Chambless criteria (Brestan & Eyberg, 1998). The child-centered intervention is a performance-based approach for preschool children, which addresses the issues of social skills problems, perspective taking, social problem solving and feelings of loneliness, stress and anger. Findings indicate that this treatment reduces conduct problems and improves problem solving and conflict management skills significantly compared to a waiting-list control group. These effects can be maintained over time as shown in one-year follow-up (see Webster-Stratton, 2005 for review). Like interventions for preschool children, approaches for adolescents are not well established either. The Anger Control Training (Feindler, Marriott & Iwata, 1984) is assumed to be probably efficacious according to the Chambless criteria but was not further investigated. This school-based group program aims to improve self-control by applying Meichenbaum’s Stress Inoculation Training (1977), which primarily emphasizes cognitive components of anger and improvement in problem-solving skills. The intervention issues are the assessment and analysis of provocation cues and anger responses, the training of alternative responses to external provoking stimuli, and techniques to control one’s own provocative behaviors. Findings have shown that this treatment significantly reduces aggressive and disruptive behavior but also improves problem-solving and social skills, cognitive reflectivity and self-control (Feindler, Marriott & Iwata, 1984). Follow-up data is lacking.

MULTIMODAL INTERVENTIONS FOR ADOLESCENTS The most promising outcomes in treating adolescents with CD/ODD are shown by those programs emphasizing multiple risk factors (Burke, Loeber & Birmaher, 2002). Two programs are outstanding in that context: Multidimensional Treatment Foster Care (MTFC, Chamberlain & Smith, 2003) and Multisystemic Therapy (MST; Henggeler et al., 1998). As a less restrictive form of out-of-home care, several therapeutic foster care models were developed within the last decades, which are also known as therapy foster care, specialist foster care, treatment foster family care, family-based treatment, parent–therapist programs and multidimensional treatment foster care (Hudson, Nutter & Galaway, 1994). As the variety of names indicates, many different concepts have been developed, but they have some characteristics in common. Specially trained foster families provide a high structured environment, as a setting for adolescents to learn more about social and emotional skills. Besides training, the foster parents receive extensive supervision and support from professionals. As an alternative to institutionalization, foster care models are more promising treatments for juveniles who need out-of-home care. Especially serious offenders need rehabilitative services, not limited to incarceration and group care. Both alternatives are supposed to produce negative side- or long-term effects. Incarceration is cost-intensive and leads to higher rates of adult incarceration, whereas group care, as a last step before incarceration, has some unintended negative consequences. Dishion and Andrews (1995)

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

437

corroborated the hypothesis that contact with other troubled adolescents leads to more problematic behaviors. Therapeutic foster care does not include such risk factors and has high ecological validity. The research base is modest and shows rather mixed findings. Sound studies with controlled efficacy trials are rare (e.g., Reddy & Pfeiffer, 1997). As an exception, Chamberlain and colleagues conducted some randomized controlled studies with youths, which show that therapeutic foster care is superior to other out-of-home care in several aspects. This Multidimensional Treatment Foster Care (MTFC; e.g., Chamberlain & Mihalic, 1998; Chamberlain & Smith, 2003) reached in terms of Blueprints Model Programs Selection Criteria (Center for the Study and Prevention of Violence, 2002) model standard. Also proven as cost effective in an analysis of the Washington State Institute for Public Policy (Aos, Barnoski & Lieb, 1998), it is an alternative to group care, residential treatment, incarceration and hospitalization for adolescents who display chronic, delinquent behavior. Based on social learning theory, MTFC aims to reduce antisocial behavior and to promote prosocial behavior. Because adolescent emotions, behavior and attitudes are thought to be influenced substantially by the context in which they live, this multicomponent, multilevel intervention targets all key settings in which the adolescent interact. Changes in teenager behaviors are expected to be more successful, if they occur in a ‘natural’ environment. The foster and biological parents are trained to build a supportive relationship with the teenagers and to use effective parenting principles such as consistent reinforcement, clarification of rules and providing a daily structure. Foster parents receive a pre-service training up to 20 sessions and are provided with ongoing case management that includes individual and group components. The adolescents will not, unlike those in other residential care programs, participate in groups and have exposure to other delinquent peers who could have negative influences on treatment outcome. They receive, if possible, individual therapy to improve problem-solving skills, anger management, educational issues and other individual issues. The average stay of adolescents in their foster families is six months. Meanwhile and in the 12-month aftercare, their biological parents also receive therapeutic support by supervisors. The aim is to return the teenagers to their families. Chamberlain and colleagues found that therapeutic foster care is superior to many other ‘treatments as usual’ placements such as residential treatment centers or homes of relatives (Chamberlain, 1990; Chamberlain & Reid, 1991), standard foster care (Chamberlain & Weinrott, 1990) and community group care (Chamberlain & Reid, 1998). The first studies compared a treatment foster care (TFC) group with severely (Chamberlain, 1990) and disturbed adolescents (Chamberlain & Reid, 1991) to teenagers who received treatment consisting of traditional community placements. The youths of the first study (Chamberlain, 1990) consisted of a sample of 32 youths from 12 through 18 years who were committed to a state training school. Both groups were matched for age, sex and date of commitment. After placement, youths in the TFC group showed less reinstitutionalization. At the oneyear follow-up, the TFC group showed, compared to controls, less incarceration (38 % vs. 88 %), at the two-year follow-up these effects were still significant (43 % vs. 62 %). In the second study (Chamberlain & Reid, 1991), 20 youths from 9 through 18 years in a state mental hospital were randomly assigned to the conditions ‘TFC’ and ‘treatment as usual’. Youths in the ‘TFC’ condition showed higher rates of days placed out of hospital but these findings were not statistically significant. Significantly better results for TFC participants were found in adult reports of child problem behaviors. At the one-year follow-up of a randomized controlled trial (Chamberlain & Reid, 1998) with 79 boys from 12 to 18 years, MTFC was found to show superior outcomes compared to group care (GC). Fewer boys who

438

VOLUME I: DIAGNOSIS AND TREATMENT

participate in MTFC ran away (31 % vs. 58 %), they spent less time incarcerated (means: 53 days for MTFC and 139 for GC), and showed significantly greater decreases in official criminal referral rates (mean decrease 5.9 criminal referrals a year). Those who participated in MTFC completed their placements more often than those assigned to group care (76 % vs. 36 %). Analyses of mediators (Eddy & Chamberlain, 2000) confirmed the impact of two assumptions made by MTFC, which are the role of effective parenting and the influence of deviant peers. Eddy and Chamberlain concluded that a significant part of the influence on youth behavior was mediated by effective parenting and by decreased association with delinquent peers. As a family- and community-based treatment, Multisystemic Therapy (MST; Henggeler et al., 1998) is designed to address multiple problems concerning conduct disorders in youth. Henggeler and Lee (2003) listed three superior aims of MST: (i) to reduce antisocial behavior; (ii) to improve functioning in multiple settings; and (iii) to decrease use of out-of-home placements. Its conceptual framework is based on social-ecological (Bronfenbrenner, 1979) and pragmatic family system theories (Haley, 1976; Minuchin, 1974). MST emphasizes the role of interconnected multiple systems and their influences on adolescents. Clinicians have to consider those systems and their interactions as they include potential risk factors. This focus on intervention is derived from several conceptual assumptions, which are made by MST. Serious clinical problems are presumed to be multidetermined from the reciprocal interplay of individual, family, peer, school and community factors. A further assumption is that improvement of the caregiver’s (a parent or another adult who has an enduring emotional relationship with the adolescent) parenting skills leads to better long-term positive outcomes. Henggeler and colleagues conceptualized MST as an intensive (2 to 15 hours a week), time-limited (3 to 5 months), consumer-friendly treatment with small caseloads. Their concern was to remove the barriers to service access, which lead in traditional mental health programs that address adolescents with CD to high dropout rates. Being implemented in the home, school, neighborhood and community setting, MST is expected to show higher ecological validity and thus better generalization of treatment gains. MST integrates evidence-based practices that include cognitive-behavioral approaches, behavior therapies, behavioral parent training, pragmatic family therapies and pharmacological treatment. To enhance treatment outcomes and fidelity of method, the clinicians are well trained and supervised. Nine treatment principles serve as a practitioner’s guideline for the development and implementation of interventions (Schoenwald & Henggeler, 1999). MST is supposed to be one of the most effective treatments designed for delinquent adolescents (Target & Fonagy, 2005). Extensively tested across problems, therapists and settings, it is effective in decreasing chronic and violent juvenile offending (Borduin et al., 1995; Henggeler et al., 1997; Henggeler, Melton & Smith, 1992), substance abuse (Henggeler et al., 1996), sexual offending (Borduin et al., 1990), psychiatric crises (Henggeler et al., 1999), and for maltreating families (Brunk, Henggeler & Whelan, 1987). The long-term rates of juveniles being rearrested decreased from 25 % to 70 % (Borduin et al., 1995; Henggeler et al., 1997; Henggeler, Melton & Smith, 1992) as well as the long-term rates of days in out-of-home placements (47 % to 64 %). A 10-year follow-up conducted by Schaeffer and Borduin (2005) still indicates promising outcomes. Compared to those who received individual therapy, juvenile offenders, who participated in MST showed still lower recidivism rates (81 % vs. 50 %). MST participants had 54 % lower arrests and 57 % fewer days of confinement in adult detention facilities.

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

439

The lowest rates of reduction are shown in the trial (Henggeler et al., 1997), which examines the influence of treatment fidelity. Compared to the other trials, the quality assurance, which is one of the conceptual assumptions, was low. The high rate of treatment fidelity provided by highly structured training and supervision of the clinicians is probably one crucial factor for MST’s effectiveness, which is unique for treatment programs for adolescents with CD. Analyses of mediators have shown the influence of improved caregivers and family functioning (e.g., Huey et al., 2000). These findings corroborate MST’s assumption of a caregiver as a key factor for positive treatment outcomes. Other findings show that MST outcomes have not been influenced by variables such as case seriousness or demographic characteristics (Henggeler & Lee, 2003). Besides being effective in reducing disruptive behavior, MST is shown to be highly cost effective (Aos et al., 1999). In North America, MST saved overall more than $60,000 per youth in placement, criminal justice and crime victim costs.

NEED OF MULTICOMPONENT AND INDIVIDUALLY TAILORED INTERVENTIONS Treatment of conduct problems in children and adolescents must be based on a comprehensive assessment of the child’s and family’s difficulties which takes into account predisposing, precipitating and sustaining factors with the child, the family and the wider social system. Existing research suggests that efficacious interventions are available for improving oppositional, aggressive and antisocial behavior in children and adolescents. Recent research stresses the idea of individually tailored multicomponent approaches. This supports the assumption that it is not the prototype of aggressive children that needs standard intervention. Every child is assumed to have special deficiencies that should be treated with an appropriate intervention. A heuristic model may help to decide which individually tailored combination of treatment components will be best for the individual child (Doepfner & Petermann, 2004; Goertz-Dorten & Doepfner, in press). In children with oppositional defiant disorders whose problems are confined to the home, parenting problems are often observed and parent management training is the treatment of choice. In children with oppositional and aggressive behavior at preschool or school, school-based interventions are indicated. Child-focused interventions also have to be tailored according to the individual factors contributing to the maintenance of the conduct problems. Distortions in social information processing and problem solving should be treated by problem-solving training, which aims to improve social problem solving. Children and adolescents with high impulsivity and behavioral inhibition deficits may benefit from anger control training that aims to reduce arousal and anger in real-life settings. Findings indicate that anger is more likely related to reactive aggression (Hubbard et al., 2002). Patients with social skills deficits on a behavioral level may need to be trained in socially skilful behavior for different social situations. Some of the multicomponent interventions described here are increasingly being applied and researched in real-world service delivery settings. For example, many mental health treatment provider organizations have adopted MST throughout the United States, based on findings of considerable cost savings relative to alternative juvenile justice approaches (Aos et al., 1999). A growing literature suggests that, if carefully implemented with attention to adherence, supervision and therapist requirements, multicomponent interventions can produce positive results in real-world settings (Schoenwald et al., 2003). However, engaging

440

VOLUME I: DIAGNOSIS AND TREATMENT

and motivating the patients and the family members to participate in treatment is crucial for these approaches, according to their developers (e.g., Sexton & Alexander, 2003). Additional therapeutic skills required for these complex interventions to work need to be more fully established, although faithful adherence to treatment guidelines appears to be a prerequisite for achieving positive outcomes (Henggeler et al., 1997).

REFERENCES Aberson, B. (1987). I Can Problem Solve (ICPS): a cognitive training program for kindergarten children. Report to the Bureau of Education, Dade County. Florida: Dade County Public Schools. American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV). Washington, DC: American Psychiatric Association. Angold, A. & Costello, E.J. (1996). Toward establishing an empirical basis for the diagnosis of oppositional defiant disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 35, 1205–12. Aos, S., Barnoski, R. & Lieb, R. (1998). Watching the Bottom Line: Cost-Effective Interventions for Reducing Crime in Washington. Olympia: Washington State Institute for Public Policy. Aos, S., Phipps, P., Barnoski, R. & Lieb, R. (1999). The Comparative Costs and Benefits of Programs to Reduce Crime: A Review of National Research Findings with Implications for Washington State, Version 3.0. Olympia: Washington State Institute for Public Policy. Asher, S.R. & Renshaw, P.D. (1981). Children without friends: social knowledge and social skill training. In S.R. Asher & S.H. Goodman (eds.), Children Without Friends: Social Knowledge and Social Skill Training (pp. 273–96). Cambridge: Cambridge University Press. Babinski, L.M., Hartsough, C.S. & Lambert, N.M. (1999). Childhood conduct problems, hyperactivity-impulsivity, and inattention as predictors of adult criminal activity. Journal of Child Psychology and Psychiatry, 40, 347–55. Bandura, A. (1977). Self-efficacy: toward a unifying theory of behavioral change. Psychological Review, 84, 191–215. Bandura, A. (1989). Regulation of cognitive processes through perceived self-efficacy. Developmental Psychology, 25, 729–35. Barrish, H.H., Saunders, M. & Wolf, M.M. (1969). Good behavior game: effects of individual contingencies for group consequences on disruptive behavior in a classroom. Journal of Applied Behavior Analysis, 2,119–24. Bj¨orkqvist, K., Lagerspetz, K.M.J. & Kauianen, A. (1992). Do girls manipulate and boys fight? Developmental trends in regard to direct and indirect aggression. Aggressive Behaviour, 18, 117– 28. Borduin, C.M. (1999). Multisystemic treatment of criminality and violence in adolescents. Journal of the Academy for Child and Adolescent Psychiatry, 38, 242–9. Borduin, C.M., Henggeler, S.W., Blaske, D.M. & Stein, R. (1990). Multisystemic treatment of adolescent sexual offenders. International Journal of Offender Therapy and Comparative Criminology, 35, 105–14. Borduin, C.M., Mann, B.J., Cone, L.T. et al. (1995). Multisystemic treatment of serious juvenile offenders: Long-term prevention of criminality and violence. Journal of Consulting and Clinical Psychology, 63, 569–78. Brestan, E.V. & Eyberg, S.M. (1998). Effective psychosocial treatments of conduct-disordered children and adolescents: 29 years, 82 studies, and 5,272 kids. Journal of Clinical Child Psychology, 27, 180–9. Bronfenbrenner, U. (1979). The Ecology of Human Development: Experiments by Design and Nature. Cambridge, MA: Harvard University Press. Brotman, L.M., Gouley, K.K., Chesir-Teran, D. et al. (2005). Prevention for preschoolers at high risk for conduct problems: immediate outcomes on parenting practices and social competence. Journal of Child and Adolescent Psychology, 34, 724–34.

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

441

Brunk, M., Henggeler, S.W. & Whelan, J.P. (1987). A comparison of multisystemic therapy and parent training in the brief treatment of child abuse and neglect. Journal of Consulting and Clinical Psychology, 55, 311–18. Burke, J.D., Loeber, R. & Birmaher, B. (2002). Oppositional defiant disorder and conduct disorder: a review of the past 10 years, part 2. Journal of the American Academy of Child and Adolescent Psychiatry, 41, 1275–93. Buydens-Branchey, L., Branchey, M. H., Noumair, D. & Lieber, C. S. (1989). Age of alcoholism onset. II. Relationship to susceptibility to serotonin precursor availability. Archives of General Psychiatry, 46, 231–6. Capaldi, D.M. (1992). The co-occurence of conduct problems and depressive symptoms in early adolescent boys, II: a 2-year follow-up at grade 8. Development and Psychopathology, 4, 125–44. Center for the Study and Prevention of Violence (2002). Blueprints for Violence Prevention. Boulder, CO: Center for the Study and Prevention of Violence, Institute of Behavioral Sciences, University of Colorado at Boulder. Chamberlain, P. (1990). Teaching and Supporting Families: A Model of Reunification of Children with their Families. Grant No. 90CW0994, Administration for Children, Youth, and Families, Child Welfare Services, Human Development Services, Department of Health and Human Services. Chamberlain, P. & Mihalic, S.F. (1998). Multidimensional treatment foster care. In D.S. Elliott (ed.), Book Eight: Blueprints for Violence Prevention. Boulder: Institute of Behavioral Science, University of Colorado at Boulder. Chamberlain, P. & Reid, J.B. (1991). Using a specialized foster care community treatment model for children and adolescents leaving the state mental hospital. Journal of Community Psychology, 19, 266–76. Chamberlain, P. & Reid, J.B. (1998). Comparison of two community alternatives to incarceration for chronic juvenile offenders. Journal of Consulting and Clinical Psychology, 66, 624–33. Chamberlain, P. & Smith, D.K. (2003). Antisocial behavior in children and adolescents. In A.E. Kazdin & J.R. Weisz (eds.), Evidence-Based Psychotherapies for Children and Adolescents (pp. 282–300). New York: Guilford Press. Chamberlain, P. & Weinrott, M. (1990). Specialized foster care: treating seriously emotionally disturbed children. Child Today, 19, 24–7. Clarke, R.A., Murphy, D.L. & Constantino, J.N. (1999). Serotonin and externalizing behavior in young children. Psychiatry Research, 86, 29–40. Cohen, P., Cohen, J. & Brook, J. (1993). An epidemiological study of disorder in late childhood and adolescence, II: persistence of disorders. Journal of Child Psychology and Psychiatry, 34, 869–77. Cohen, P. & Flory, M. (1998). Issues in the disruptive behaviour disorders: attention deficit disorder without hyperactivity and the differential validity of oppositional defiant and conduct disorders. In T.A. Widiger, A.J. Frances, H.A. Pincus et al. (eds.), DSM-IV Sourcebook (Vol. 4). Washington, DC: American Psychiatric Press. Coie, J.D. & Dodge, K.A. (1998). Aggression and antisocial behavior. In W. Damon (series ed.) & N. Eisenberg (vol. ed.), Handbook of Child Psychology, Vol. 3: Social, Emotional, and Personality Development (5th edition, pp. 779–862). New York: John Wiley & Sons, Inc. Crick, N.R. & Dodge, K.A. (1994). A review and reformulation of social information- processing mechanisms in children’s social adjustment. Psychological Bulletin, 115, 74–101. Crick, N.R. & Grotpeter, J.K. (1995). Relational aggression, gender, and social psychological adjustment. Child Development, 66, 710–22. Deater-Deckard, K. (2000). Parenting and child behavioral adjustment in early childhood: a quantitative genetic approach to studying family processes. Child Development, 71, 468–84. Dishion, T.J. & Andrews, D.W. (1995). Preventing escalation in problem behaviors with high-risk young adolescents: immediate and 1-year outcomes. Journal of Consulting and Clinical Psychology, 63, 538–48. Dodge, K.A. (1983). Behavioral antecedents of peer social status. Child Development, 54, 1386–99. Dodge, K.A. (1985). Attributional bias in aggressive children In P.C. Kendall (ed.), Advances in Cognitive-Behavioral Research and Therapy (pp. 73–110). San Diego: Academic Press. Dodge, K.A. (1986). Social information processing variables in the development of aggression and altruism in children. In C. Zahn-Waxler, M. Cummings, & M. Radke-Yarrow (eds.), The

442

VOLUME I: DIAGNOSIS AND TREATMENT

Development of Altruism and Aggression: Social and Biological Origins (pp. 280–302). New York: Cambridge University Press. Dodge, K.A., Bates, J.E. & Pettit, G.S. (1990). Mechanisms in the cycle of violence. Science, 250, 1678–83. Dodge, K.A. & Coie, J.D. (1987). Social information-processing factors in reactive and proactive aggression in children’s peer groups. Journal of Personality and Social Psychology, 53, 1146–58. Dodge, K.A., Laird, R., Lochman, J.E. et al. (2002). Multidimensional latent-construct analysis of children’s social information processing patterns: Correlations with aggressive behavior problems. Psychological Assessment, 14, 60–73. Dodge, K.A. & Newman, J.P. (1981). Biased decision-making processes in aggressive boys. Journal of Abnormal Psychology, 90, 375–9. Dodge, K.A., Price, J.M., Bachorowski, J. & Newman, J. M. (1990). Hostile attributional biases in severely aggressive adolescents. Journal of Abnormal Psychology, 99, 385–92. Doepfner, M., Breuer, D., Sch¨urmann, S. et al. (2004). Effectiveness of an adaptive multimodal treatment in children with attention deficit hyperactivity disorder – global outcome. European Child & Adolescent Psychiatry, 13(Supplement 1), I/117–I/129. Doepfner, M. & Petermann, F. (2004) Leitlinien zur Diagnostik und Psychotherapie von aggressivdissozialen St¨orungen im Kindes- und Jugendalter: ein evidenzbasierter Diskussionsvorschlag. Kindheit und Entwicklung, 13, 9–112. Doepfner, M., Schuermann, S. & Froelich, J. (2002). Therapieprogramm f¨ur Kinder mit hyperkinetischem und oppositionellem Problemverhalten (THOP). (3. Aufl.). Weinheim: Beltz, Psychologie Verlags Union. Dolan, L.J., Kellam, S.G., Brown, C.H. et al. (1993). The short-term impact of two classroom-based preventive interventions on aggressive and shy behaviors and poor achievement. Journal of Applied Developmental Psychology, 14, 317–45. Drugli, M.B. & Larsson, B. (2006). Children aged 4–8 years treated with parent training and child therapy because of conduct problems: generalisation effects to day-care and school settings. European Child & Adolescent Psychiatry, online 13. April 2006. Eddy, J.M. & Chamberlain, P. (2000). Family management and deviant peer association as mediators of the impact of treatment condition on youth antisocial behavior. Journal of Consulting and Clinical Psychology, 68, 857–63. Farrington, D.P. (1995). The development of offending and antisocial behaviour from childhood: key findings from the Cambridge study in delinquent development. Journal of Child Psychology and Psychiatry, 36, 929–64. Feindler, E.L., Marriott, S.A. & Iwata, M. (1984). Group anger control training for junior high school delinquents. Cognitive Therapy and Research, 8, 299–311. Felner, R.D. & Adan, A.M. (1988). The School Transitional Environment Project: an ecological intervention and evaluation. In R.H. Price, E.L. Cowen, R.P. Lorion & J. Ramos-McKay (eds.), 14 Ounces of Prevention: A Casebook for Practitioners (pp. 111–22). Washington, DC: American Psychological Association. Felner, R.D., Brand, S., Adan, A.M. et al. (1993). Restructuring the ecology of the school as an approach to prevention during school transitions: longitudinal follow-ups and extensions of the school transitional environment project (STEP). Prevention in Human Services, 10, 103–36. Felner, R.D., Ginter, M. & Primavera, J. (1982). Primary prevention during school transitions: social support and environmental structure. American Journal of Community Psychology, 10, 277–90. Fergusson, D., Horwood, L.J. & Lynskey, M.T. (1994). Structure of DSM-III-R criteria for disruptive childhood behaviours: confirmatory factor model. Journal of the American Academy of Child and Adolescent Psychiatry, 33, 1145–57. Fonagy, P. & Target, M. (1994). The efficacy of psychoanalysis for children with disruptive disorders. Journal of the American Academy of Child and Adolescent Psychiatry, 33, 45–55. Fonagy, P., Target, M., Cottrell, D. et al. (2002). What Works for Whom? A Critical Review of Treatments for Children and Adolescents. New York: Guilford Press. Frick, P.J., Kamphaus, R.W., Lahey, B.B. et al. (1991). Academic underachievement and the disruptive behavior disorders. Journal of Consulting and Clinical Psychology, 59, 289–94.

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

443

Frick, P.J., Lahey, B.B., Applegate, B. et al. (1994). DSM-IV field trials for the disruptive behavior disorders: symptom utility estimates. Journal of the American Academy of Child and Adolescent Psychiatry, 33, 529–39. Frick, P.J., Lahey, B.B., Loeber, R. et al. (1993). Oppositional defiant disorder and conduct disorder: a meta-analytic review of factor analyses and cross-validation in a clinical sample. Clinical Psychological Review, 13, 319–40. Goertz-Dorten, A. & Doepfner, M. (in press). Therapieprogramm fuer Kinder mit aggressivem Verhalten (THAV). G¨ottingen: Hogrefe. Goutz, K. (1981). Children’s initial aggression level and the effectiveness of intervention strategies in moderating television effects of aggression. Journal of Abnormal Child Psychology, 15, 181–97. Gouze, K.R. (1987). Attention and social problem solving as correlates of aggression in preschool males. Journal of Abnormal Child Psychology, 15, 181–97. Greenberg, M.T., Domitrovich, C. & Bumbarger, B. (1999). Preventing Mental Disorders in SchoolAge Children: A Review of the Effectiveness of Prevention Programs. University Park, PA: Pennsylvania State University, Prevention Research Center for the Promotion of Human Development. Greenberg, M.T., Domitrovich, C. & Bumbarger B. (2001). The prevention of mental disorders in school-aged children: current state of the field. Prevention & Treatment, 4, 1–39. Greenberg, M.T. & Kusch´e, C.A. (1993). Promoting Social and Emotional Development in Deaf Children: The PATHS Project. Seattle, WA: University of Washington Press. Greenberg, M.T. & Kusch´e, C.A. (1998). Preventive interventions for school-aged deaf children: the PATHS curriculum. Journal of Deaf Studies and Deaf Education, 3, 49– 63. Haley, J. (1976). Problem Solving Therapy. San Francisco: Jossey-Bass. Hanisch, C., Freund-Braier, I., Meyer, N. et al. (under review). Effects of the indicated Prevention Programme for Externalizing Problem Behaviour on child symptoms, parenting, and parental quality of life. Hastings, T.L., Anderson, S.J. & Kelley, M.L. (1996). Gender differences in coping and daily stress in conduct-disordered and non-conduct-disordered adolescents. Journal of Psychopathology and Behavioural Assessments, 18, 213–26. Harrington, R. (2001). Childhood depression and conduct disorder: different routes to the same outcome? Archives of General Psychiatry, 58, 237–8. Hartup, W.W. (2005). The development of aggression. In R.E. Tremblay, W.W. Hartup & J. Archer (Eds.), Developmental Origins of Aggression. New York: Guilford Press. Hawkins, J.D., Catalano, R.F., Kosterman, R. et al. (1999). Preventing adolescent health-risk behaviors by strengthening protection during childhood. Archives of Pediatrics and Adolescent Medicine, 153, 226–34. Hawkins, J. D., Catalano, R. ., Morrison, D. et al. (1992). The Seattle Social Development Project: effects of the first four years on protective factors and problem behaviors. In J. McCord & R. Tremblay (eds.) The Prevention of Antisocial Behavior in Children (pp. 139–61). New York: Guilford Press. Henggeler, S. & Lee, T. (2003). Multisystemic treatments of serious clinical problems. In A.E. Kazdin & J.R. Weisz (Eds.), Evidence-Based Psychotherapies for Children and Adolescents (pp. 301–21). New York: Guilford Press. Henggeler, S.W., Melton, G.B., Brondino, M.J. et al. (1997). Multisystemic therapy with violent and chronic juvenile offenders and their families: the role of treatment fidelity in successful dissemination. Journal of Consulting and Clinical Psychology, 65, 821– 33. Henggeler, S., Melton, G. & Smith, L.A. (1992). Family preservation using multisystemic therapy: an effective alternative to incarcerating serious juvenile offenders. Journal of Consulting and Clinical Psychology, 60, 953–61. Henggeler, S.W., Pickrel, S.G., Brondino, M.J. & Crouch, J.L. (1996). Eliminating (almost) treatment dropout of substance abusing or dependent delinquents through home-based multisystemic therapy. American Journal of Psychiatry, 153, 427–8. Henggeler, S.W., Rowland, M.R., Randall, J. et al. (1999). Home-based multisystemic therapy as an alternative to the hospitalization of youth in psychiatric crisis: clinical outcomes. Journal of the American Academy of Child and Adolescent Psychiatry, 38, 1331–9.

444

VOLUME I: DIAGNOSIS AND TREATMENT

Henggeler, S.W., Schoenwald, S.K., Borduin, C.M. et al. (1998). Multisystemic Treatment of Antisocial Behavior in Children and Adolescents. New York: Guilford Press. Herpertz, S., Mueller, B., Ounaibi, M. et al. (2005). Response to emotional stimuli in boys with conduct disorder. American Journal of Psychiatry, 162, 1100–7. Hewitt, L.E. & Jenkins, R.L. (1946). Fundamental Patterns of Maladjustment: The Dynamics of their Origin. Springfield, IL: Thomas. Hinshaw, S.P. (1994). Conduct disorder in childhood: conceptualization, diagnosis, comorbidity, and risk status for antisocial functioning in adulthood. In D.C. Fowles, P. Sutker & S.H. Goodman (eds.), Progress in Experimental Personality and Psychopathology Research (pp. 3–44). New York: Springer. Hubbard, J.A., Smithmyer, C.M., Ramsden, S.R. et al. (2002). Observational, physiological, and self-report measures of children’s anger: relations to reactive versus proactive aggression. Child Development, 73, 1101–18. Hudson, J., Nutter, R.W. & Galaway, B. (1994). Treatment foster family care: development and current status. Community Alternatives: International Journal of Family Care, 6, 1–24. Huey, S.J., Henggeler, S.W., Brondino, M.J. & Pickrel, S.G. (2000). Mechanisms of change in multisystemic therapy: reducing delinquent behavior through therapist adherence and improved family and peer functioning. Journal of Consulting and Clinical Psychology, 68, 451–67. Jenkins, R.L. & Glickman, S. (1947). Patterns of personality organization among delinquents. Nervous Child, 6, 329–39. Kavale, K.A., Forness, S.R. & Walker, H.M. (1999). Interventions for oppositional defiant disorder and conduct disorder in schools. In H.C. Quay & A.E. Hogan (eds.), Handbook of Disruptive Behavior Disorders (pp. 441–54). New York: Kluwer. Kazdin, A.E. (2003). Problem-solving skills training and parent management training for conduct disorder. In A.E. Kazdin & J.R. Weisz (eds.), Evidence-Based Psychotherapies for Children and Adolescents (pp. 241–62). New York: Guilford Press. Kazdin, A.E. (2005). Problem solving and parent management in treating aggressive and antisocial behavior. In E.D. Hibbs & P.S. Jensen (eds.), Psychosocial Treatments for Child and Adolescent Disorders: Empirically Based Strategies for Clinical Practice (2nd edition; pp. 377–408). Washington, DC: American Psychological Association. Kazdin, A.E., Bass, D., Siegel, T.C. & Thomas, C. (1989). Cognitive-behavioral treatment and relationship therapy in the treatment of children referred for antisocial behavior. Journal of Consulting and Clinical Psychology, 57, 522–35. Kazdin, A.E., Siegel, T.C. & Bass, D. (1992). Cognitive problem-solving skills training and parent management training in the treatment of antisocial behavior in children. Journal of Consulting and Clinical Psychology, 60, 733–47. Kazdin, A.E. & Wassell, G. (2000). Therapeutic changes in children, parents, and families resulting from treatment of children with conduct problems. Journal of the American Academy of Child and Adolescent Psychiatry, 39, 414–20. Kellam, S.G., Mayer, L.S., Rebok, G.W. & Hawkins, W.E. (1998). Effects of improving achievement on aggressive behavior and of improving aggressive behavior on achievement through two preventive interventions: an investigation of causal paths. In B.P. Dohrenwend (ed.), Adversity, Stress, and Psychopathology (pp. 486–505). New York: Oxford University Press. Lahey, B.B. & Loeber, R. (1994). Framework for a developmental model of oppositional defiant disorder and conduct disorder. In D.K. Routh (ed.), Disruptive Behavior Disorders in Childhood (pp. 139–80). New York: Plenum. Lahey, B.B., Loeber, R., Hart, E.L. et al. (1995). Four-year longitudinal study of conduct disorder in boys: patterns and predictors of persistence Journal of Abnormal Psychology, 104, 83–93. Lahey, B.B., Loeber, R., Quay, H.C. et al. (1998). Validity of DSM-IV subtypes of conduct disorder on age of onset. Journal of the American Academy of Child and Adolescent Psychiatry, 37, 435–42. Lahey, B.B., Miller, T.L., Gordon, R.A. & Riley, A.W. (1999). Developmental epidemiology of the disruptive behavior disorders. In H.C. Quay & A.E. Hogan (eds.), Handbook of Disruptive Behavior Disorders (pp. 23–48). New York: Kluwer. Lahey, B.B., Schwab-Stone, M., Goodman, S.H. et al. (2000). Age and gender differences in oppositional behavior and conduct problems: a cross-sectional household study of middle childhood and adolescence Journal of Abnormal Psychology, 109, 589–601.

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

445

Lahey, B.B., Waldman, I.D. & McBurnett, K. (1999b). The development of antisocial behavior: an integrative causal model. Journal of Child Psychology and Psychiatry, 40, 669–82. LeMarquand, D., Tremblay, R.E. & Vitaro, F. (2001). The prevention of conduct disorder: a review of successful and unsuccessful experiments. In J. Hill & B. Maughan (eds.), Conduct Disorders in Childhood and Adolescence (pp. 449–77). Cambridge: Cambridge University Press. Lillienfeld, S.O. & Waldman, I. (1990). The relation between childhood attention deficit hyperactivity disorders and adult antisocial behavior reexamined: the problem of heterogeneity. Clinical Psychology Review, 10, 669–725. Lochman, J.E. (1985). Effects of different treatment lengths in cognitive-behavioral interventions with aggressive boys. Child Psychiatry and Human Development, 16, 45–56. Lochman, J.E. (1992). Cognitive-behavioral interventions with aggressive boys: three-year follow-up and preventive effects. Journal of Consulting and Clinical Psychology, 60, 426–32. Lochman, J.E., Barry, T.D. & Pardini, D.A. (2003). Anger control training for aggressive youth. In A.E. Kazdin & J.R. Weisz (eds.), Evidence-Based Psychotherapies for Children and Adolescents (pp. 263–81). New York: Guilford Press. Lochman, J.E., Burch, P.P., Curry, J.F. & Lampron, L.B. (1984). Treatment and generalization effects of cognitive-behavioral and goal setting interventions with aggressive boys. Journal of Consulting and Clinical Psychology, 52, 915–16. Lochman, J.E. & Curry, J.F. (1986). Effects of social problem-solving training and selfinstruction training with aggressive boys. Journal of Clinical Child Psychology, 63, 549– 59. Lochman, J.E. & Dodge, K.A. (1994). Social-cognitive processes of severely violent, moderately aggressive, and nonaggressive boys. Journal of Consulting and Clinical Psychology, 62, 366–74. Lochman, J. E., FitzGerald, D. P & Whidby, J. M. (1999). Anger management with aggressive children. In C. Schaefer (ed.), Short-Term Psychotherapy Groups for Children (pp. 301–49). Northvale, NJ: Jason Aronson. Lochman, J.E. & Lampron, L.B. (1988). Cognitive behavioral intervention for aggressive boys: seven month follow-up effects. Journal of Child and Adolescent Psychotherapy, 5, 15–23. Lochman, J.E., Lampron, L.B., Gemmer, T.C. et al. (1989). Teacher consultation and cognitivebehavioral interventions with aggressive boys. Psychology in the Schools, 26, 179–88. Lochman, J.E., Nelson, W.M. & Sims, J.P. (1981). A cognitive behavioral program for use with aggressive children. Journal of Clinical Child Psychology, 10, 146–8. Lochman, J.E., Powell, N.R., Whidby, J.M. & FitzGerald, D.P. (2006). Aggressive children: cognitivebehavioral assessment and treatment. In P.C. Kendall (ed.), Child and Adolescent Therapy: Cognitive-Behavioral Procedures (3rdedition, pp. 33–81). New York: Guilford Press. Lochman, J.E. & Wells, K.C. (2002). Contextual social cognitive mediators and child outcome: a test of the theoretical model in the Coping Power Program. Development and Psychopathology, 14, 945–67. Lochman, J.E. & Wells, K.C. (2004). The Coping Power program for preadolescent aggressive boys and their parents: outcome effects at the one-year follow-up. Journal of Consulting and Clinical Psychology, 72, 571–8. Loeber, R., Burke, J., Lahey, B.B. et al. (2000). Oppositional defiant and conduct disorder: a review of the past 10 years, part I. Journal of the American Academy of Child and Adolescent Psychiatry, 39, 1468–81. Loeber, R. & Farrington, D. P. (2000). Young children who commit crime: epidemiology, developmental origins, risk factors, early interventions, and policy implications. Development and Psychopathology, 12, 737–62. Lonigan, C.J., Elbert, J.C. & Johnson, S.B. (1998). Empirically supported psychological interventions for children: an overview. Journal of Clinical Child Psychology, 27, 138–45. Mannuzza, S., Klein, R.G., Bonagura, N. et al. (1991). Hyperactive boys almost grown up. V. Replication of psychiatric status. Archives of General Psychiatry, 48, 77–83. Masten, A.S. (1988). Toward a developmental psychopathology of early adolescence. In M.D. Levine & E.R. McArney (eds.), Early Adolescent Transitions (pp. 261–78). Lexington: Heath. McCart, M.R., Priester, P.E., Davies, W.H. & Azen, R. (2006). Differential effectiveness of behavioral parent-training and cognitive-behavioral therapy for antisocial youth: a meta-analysis. Journal of Abnormal Child Psychology, 34, 525–41.

446

VOLUME I: DIAGNOSIS AND TREATMENT

McDermott, P.A. (1996). A nationwide study of developmental and gender prevalence for psychopathology in childhood and adolescence. Journal of Abnormal Child Psychology, 24(1), 53–66. Meichenbaum, D.H. (1977). Cognitive Behavior Modification. An Integrative Approach. New York: Plenum Press. Minuchin, S. (1974). Families and Family Therapy. Cambridge, MA: Harvard University Press. Moffitt, T.E. (1993). Adolescent-limited and life-course-persistent antisocial behavior: a developmental taxonomy. Psychological Review, 100, 674–701. Moffitt, T.E., Brammer, G., Caspi, A. et al. (1998). Whole blood serotonin relates to violence in an epidemiolocal study. Biological Psychiatry, 43, 446–57. Offord, D. R., Boyle, M. H., Racine, Y. A., Fleming, J.E. et al. (1992). Outcome, prognosis, and risk in a longitudinal follow-up study. Journal of the American Academy of Child and Adolescent Psychiatry, 31, 916–22. Offord, D. R., Boyle, M. H., Szatmari, P. et al. (1987). Ontario Child Health Study, II: six-month prevalence of disorder and rates of service utilization. Archives of General Psychiatry, 44, 832–6. Ollendick, T.H., Weist, M.D., Borden, M.C. & Greene, R.W. (1992). Sociometric status and academic, behavioral, and psychological adjustment: a five-year longitudinal study. Journal of Consulting and Clinical Psychology, 60, 80–7. Olweus, D. (1993). Bullying at School: What We Know and What We Can Do. Oxford: Blackwell. Olweus, D., Limber, S. & Mihalic, S.F. (1999). Blueprints for Violence Prevention, Book Nine: Bullying Prevention Program. Boulder, CO: Center for the Study and Prevention of Violence. Patterson, G.R. (1982). Coercive Family Process. Eugene, OR: Castalia. Patterson, G.R., DeBaryshe, B.D. & Ramsey, E. (1989). A developmental perspective on antisocial behavior. American Psychologist, 44, 329–35. Patterson, G.R., Reid, M.J. & Dishion, T. (1992). Antisocial Boys: A Social Interactional Approach (Vol. 4). Eugene, OR: Castalia. Pedersen, W. & Wichstrom, L. (1995). Patterns of delinquency in Norwegian adolescents. British Journal of Criminology, 35, 543–62. Petermite, C.E., Loney, J. & Roberts, M.A. (1995). External validation of oppositional disorder and attention deficit disorder with hyperactivity. Journal of Abnormal Psychology, 23, 453–71. Pike, A., McGuire, S., Hetherington, E.M. et al. (1996). Family environment and adolescent depressive symptoms and antisocial behavior: a multivariate genetic analysis. Developmental Psychology, 32, 590–603. Pliszka, S.R. (1999). The psychobiology of oppositional defiant disorder and conduct disorder. In H.C. Quay & A.E. Hogan (eds.), Handbook of Disruptive Behavior Disorders (pp. 371–95). New York: Kluwer. Plueck, J., Wieczorrek, E., Wolff Metternich, T. & Doepfner, M. (2006). Pr¨aventionsprogramm f¨ur Expansives Problemverhalten (PEP). Ein Manual f¨ur Eltern- und Erziehergruppen. Goettingen: Hogrefe. Prinz, R.J. & Dumas, J.E. (2004). Prevention of oppositional defiant disorder and conduct disorder in children and adolescents. In P.M. Barrett & T.H. Ollendick (2004) Handbook of Interventions that Work with Children and Adolescents (pp. 475–88). New York: John Wiley & Sons, Inc. Quay, H.C. (1999). Classification of the disruptive behavior disorders. In H.C. Quay & A.E. Hogan (eds.), Handbook of Disruptive Behavior Disorders (pp. 3–21). New York: Kluwer. Quiggle, N.L., Garber, J., Panak, W.F. & Dodge, K.A. (1992). Social information processing in aggressive and depressed children. Child Development, 63, 1305–20. Quinn, M.M., Kavale, K.A., Mathur, S.R. et al. (1999). A meta-analysis of social skill interventions for students with emotional or behavioral disorders. Journal of Emotional and Behavioral Disorders, 7, 54–64. Raine, A., Venables, P.H. & Williams, M. (1990). Relationships between central and autonomic measures of arousal at age 15 years and criminality at age 24 years. Archives of General Psychiatry, 47, 1060–4. Reddy, L.A. & Pfeiffer, S.I. (1997). Effectiveness of treatment foster care with children and adolescents: a review of outcome studies. Journal of the American Academy of Child and Adolescent Psychiatry, 36, 581–8.

CONDUCT DISORDERS IN CHILDREN AND ADOLESCENTS

447

Reid, J.B., Eddy, J.M., Fetrow, R.A. & Stoolmiller, M. (1999). Description and immediate impacts of a preventive intervention for conduct problems. American Journal of Community Psychology, 27, 483–517. Richard, B.A. & Dodge, K.A. (1982). Social maladjustment and problem solving in school-aged children. Journal of Consulting and Clinical Psychology, 50, 226–33. Robin, A.L. & Foster, S. (1989). Negotiating Parent–Adolescent Conflict. New York: Guilford Press. Robins, L.N., Tipp, J. & McEvoy, L. (1991). Antisocial personality. In L.N. Robins & D. Regier (eds.), Psychiatric Disorders in America (pp. 258–90). New York: Free Press. Rubin, K.H. & Krasnor, L. (1986). Social-cognitive and social behavioral perspectives on problem solving. In M. Perlmutter (ed.), The Minnesota Symposia on Child Psychology, Vol. 18: Cognitive Perspectives on Children’s Social and Behavioral Development (pp. 1–18). Hillsdale, NJ: Erlbaum. Sanders, M.R. (1999). Triple P-Positive Parenting Program: towards an empirically validated multilevel parenting and family support strategy for the prevention of behavior and emotional problems in children. Clinical Child and Family Psychology Review, 2, 71–90. Sanders, M.R., Markie-Dadds, C., Turner, K.M.T. & Ralph, A. (2004). Using the Triple P system of intervention to prevent behavioural problems in children and adolescents. In P. Barrett & T.H. Ollendick (eds.), Handbook of Interventions that Work with Children and Adolescents: Prevention and Treatment (pp. 489–516). Chichester, UK: John Wiley & Sons, Ltd. Sanson, A. & Prior, M. (1999). Temperament and behavioral precursors to oppositional defiant disorder and conduct disorder. In H.C. Quay & A.E. Hogan (eds.), Handbook of Disruptive Behavior Disorders (pp. 397–417). New York: Kluwer. Schaeffer, C.M & Borduin, C.M. (2005). Long-term follow-up to a randomized clinical trial of multisystemic therapy with serious and violent juvenile offenders. Journal of Consulting and Clinical Psychology, 73, 445–53. Schoenwald, S.K. & Henggeler, S.W. (1999). Treatment of oppositional defiant disorder and conduct disorder in home and community settings. In H.C. Quay & A.E. Hogan (eds.), Handbook of Disruptive Behavior Disorders (pp. 475–493). New York: Kluwer. Schoenwald, S.K., Sheidow, A.S., Letourneau, E.J. & Liao, J. G. (2003). Transportability of multisystemic therapy: evidence for multi-level influences. Mental Health Research, 5, 223–39. Serketich, W.J. & Dumas, J.E. (1996). The effectiveness of behavioral parent training to modify antisocial behavior in children: A meta-analysis. Behavior Therapy, 27, 171–86. Sexton, T.L. & Alexander, J.F. (2003). Functional family therapy: a mature clinical model for working with at-risk adolescents and their families. In T.L. Sexton, G.R. Weeks & M.S. Robbins (eds.), Handbook of Family Therapy: The Science and Practice of Working with Families and Couples (pp. 323–48). New York: Brunner-Routledge. Shure, M.B. (1992a). I Can Problem Solve (ICPS): An Interpersonal Cognitive Problem-Solving Program: Kindergarten/Primary Grades. Champaign, IL: Research Press. Shure, M.B. (1992b). I Can Problem Solve (ICPS): An Interpersonal Cognitive Problem-Solving Program: Kindergarten/Primary Grades. Champaign, IL: Research Press. Shure, M.B. (1993).Interpersonal Problem-Solving and Prevention: A Five Year Longitudinal Study – Kindergarten through Grade 4. (Research and training final report, No. MH-40801). Washington, DC: National Institute of Mental Health. Shure, M.B. (1997). Interpersonal cognitive problem solving: Primary prevention of early high-risk behaviors in the preschool and primary years. In G.W. Albee & T.P. Gulotta (eds.), Primary Prevention Works (pp. 167–88). Thousand Oaks, CA: Sage. Stoolmiller, M., Eddy, J.M. & Reid, J.B. (2000). Detecting and describing preventive intervention effects in a universal school-based randomised trial targeting delinquent and violent behavior. Journal of Consulting and Clinical Psychology, 68, 296–306. Strain, P.S., Steel, P., Ellis, T. & Timm, M.A. (1982). Long-term effects of oppositional child treatment with mothers as therapists and therapist’s trainers. Journal of Applied Behavior Analysis, 15, 163–9. Target, M. & Fonagy, P. (2005). The psychological treatment of child and adolescent psychiatric disorders. In A. Roth & P. Fonagy (eds.), What Works for Whom? A Critical Review of Psychotherapy and Research (2nd edition, pp. 385–424). New York: Guilford Press. Taylor, E., Doepfner, M., Sergeant, J. et al. (2004). Clinical guidelines for hyperkinetic disorder – first upgrade. European Child & Adolescent Psychiatry, 13(Supplement 1), I/7–I/30.

448

VOLUME I: DIAGNOSIS AND TREATMENT

Taylor, T.K. & Biglan, A. (1998). Behavioural family interventions for improving child-rearing: a review of the literature for clinicians and policy makers. Clinical Child and Family Psychology Review, 1, 41–60. Unis, A.S., Cook, E.H., Vincent, J.G. et al. (1997). Platelet serotonin measures in adolescents with conduct disorder. Biological Psychiatry, 43, 531–9. Van Goozen, S.H.M., Matthy, W., Cohen-Kettenis, P.T. et al. (1998). Salivary cortisol and cardiovascular activity during stress in oppositional-defiant disorder boys and normal controls. Biological Psychiatry, 43, 531–9. Vanyukov, M.M., Moss, H.B., Plial, J.A. et al. (1993). Antisocial symptoms in preadolescent boys and in their parents: associations with cortisol. Psychiatry Research, 46, 9–17. Verhulst, F.C. & van der Ende, J. (1991). Four-year follow-up of teacher reported problem behaviours. Psychological Medicine, 21, 965–77. Waldman, I. D. & Lilienfeld, S. O. (1991). Diagnostic efficiency of symptoms for oppositional defiant disorder and attention-deficit hyperactivity disorder Journal of Clinical and Consulting Psychology, 59, 732–8. Webster-Stratton, C. (1984). A randomized trial of two parent training programs for families with conduct-disordered children. Journal of Clinical and Consulting Psychology, 52, 666–78. Webster-Stratton, C. (1988). Self-administered videotape therapy for families with conduct-problem children: Comparison with two cost-effective treatments and a control group. Journal of Consulting and Clinical Psychology, 56, 558–66. Webster-Stratton, C. (1990). Long-term follow-up of families with young conduct problem children: from preschool to grade school. Journal of Clinical Child Psychology, 19, 144–9. Webster-Stratton, C. (1994). Advancing videotape parent training: a comparison study. Journal of Consulting and Clinical Psychology, 62, 583–93. Webster-Stratton, C. (1998). Preventing conduct problems in Head Start children strengthening parenting competencies. Journal of Consulting and Clinical Psychology, 66, 715–30. Webster-Stratton, C. (2005). Early intervention with videotape modeling: programs for families and children with oppositional defiant disorder or conduct disorder. In E.D. Hibbs & P.S. Jensen (eds.), Psychosocial Treatments for Child and Adolescent Disorders: Empirically Based Strategies for Clinical Practice (2nd ediion; pp. 435–74). Washington, DC: American Psychological Association. Webster-Stratton, C. & Hammond, M. (1997). Treating children with early-onset conduct problems: a comparison of child and parent training interventions. Journal of Consulting and Clinical Psychology, 65, 93–109. Webster-Stratton, C. & Hammond, M. (1998). Conduct problems and level social competence in Head Start children: prevalence, pervasiveness and associated risk factors. Clinical Child and Family Psychology Review, 1, 101–24. Webster-Stratton, C. & Lindsay, D.W. (1999). Social competence and conduct problems: issues in assessment. Journal of Clinical Child Psychology, 28, 25–43. Webster-Stratton, C., Reid, M.J. & Hammond, M. (2004). Treating children with early-onset conduct problems: intervention outcomes for parent, child, and teacher training. Journal of Clinical Child and Adolescent Psychology, 33, 105–24. White, J. L., Moffitt, T.E., Caspi, A. et al. (1994). Measuring impulsivity and examining its relationship to delinquency. Journal of Abnormal Psychology, 103, 192–205.

CHAPTER 26

Psychotherapy of Psychopathic Disorders Gill McGauley, Gwen Adshead Broadmoor Hospital, London, UK

and Sameer P. Sarkar Broadmoor Hospital

In 1992 Cope (1992) surveyed all forensic psychiatrists working across the range of forensic settings in England, Scotland and Wales. Using three clinical vignettes, Cope asked the psychiatrists about how to treat psychopathic disorder: one psychiatrist’s answer to the question about how to treat three psychopaths was ‘God knows . . . God might know . . . not even God knows’. We cite this bleakly humorous response because it encapsulates the sense of therapeutic pessimism many clinicians feel in relation to treating psychopathic disorder. In this chapter we will review the evidence for this pessimism. We will adopt a broad concept of psychopathic disorder in order to facilitate a wider discussion about psychotherapeutic interventions and management for this group. We discuss the complexities of providing treatment in these cases, including the impact this patient group can have on staff and secure institutions. We will conclude by offering our own view of the question posed by Cope.

CONCEPTS AND CONTEXT In the UK and Europe forensic psychiatry has two practical applications: the interface between psychiatry and the law and the treatment of mentally disordered offenders. In the UK, forensic psychiatric practice has emphasized treatment (Gunn, 2004), beginning with the treatment of mentally disordered prisoners and more recently providing alternative secure treatment settings for prisoners and those diverted from the criminal justice system (Forshaw & Rollin, 1990). In the United States forensic psychiatry traditionally consisted only of medico-legal practice and it is only comparatively recently that the remit of forensic psychiatry has widened to include a therapeutic arm. Changes in the organization for the accreditation and assessment of both the competencies of forensic psychiatrists and the The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

450

VOLUME I: DIAGNOSIS AND TREATMENT

standards of their training programs, brought the treatment of people detained in secure hospitals and correctional facilities into mainstream US forensic psychiatry (Prosono, 2003; Rosner, 2006). Forensic psychiatrists in both the US and Europe can therefore expect to be involved in planning treatment programs for mentally disordered offenders, either within secure psychiatric facilities or within prisons. The concept of ‘psychopathic disorder’ has a long and complicated history and clinical tradition (see Chapter 1 in book) and could be described as the first recognized personality disorder (Trull & Durrett, 2005). Historically, the concept derived from the work of Pinel, and others, who reported the existence of individuals whose mental disorder consisted largely of impulsive violence and bizarre or persistent rule breaking in the presence of clear consciousness and the absence of psychotic symptoms (Millon, Simonsen & Birket-Smith, 2003). Over 30 years ago Lewis (1974) described what he referred to as ‘the elusive category of psychopathic disorder’ as follows: ‘The diagnostic groupings of psychiatry seldom have sharp and definite limits. Some are worse than others in this respect. Worst of all is psychopathic personality, with its wavering confines’. Wavering or not, psychiatrists are still expected to manage and treat criminal psychopaths because of the intensity of the legal, clinical and social concern they generate (Ogloff, Wong & Greenwood, 1990). For philosophers of psychiatry (and therapists), there has been considerable debate about whether psychopathic disorder counts as a medical condition at all. The conceptual difficulty lies in how to make a diagnosis of a medical disorder, when the main symptom is social rule breaking and the ‘patient’ does not seem to suffer (Field, 1976). This has led some authors to suggest that the whole concept of psychopathic disorder is moral condemnation in disguise (Blackburn, 1988; Gunn, 2003). Any ‘treatment’ therefore is better understood as moral re-education and is the province of schools, the law or the religious. This concern about therapy as moral imperialism made some of the early psychiatrists uneasy about providing treatment for psychopathically disordered individuals. There was also concern that potential patients did not want treatment, or as they were incarcerated, psychological therapy for involuntary patients was impossible. Psychologists and psychotherapists have also been confused by the tendency for different jurisdictions and practitioners to use apparently similar concepts in different ways; for example, the US concept of ‘psychopathy’, as described by Cleckley (1941) and elaborated by Hare (2003) bears little relationship to the UK concept of ‘psychopathic disorder’, which is a legal construct in mental health law. Under UK law, an individual must be shown to be suffering from one of four categories of mental disorder before they can be legally detained. Those detained under the category of psychopathic disorder are deemed to be ‘seriously irresponsible or abnormally aggressive’, and they are often referred to as ‘psychopaths’, although their scores on the Hare Psychopathy Checklist-Revised (PCL-R) are typically below the clinical cut-off (Hare, 1991) . Neither Hare ‘psychopathy’ nor UK ‘psychopathic disorder’ are synonymous with the DSM-IV-TR (American Psychiatric Association, 2000) diagnosis of antisocial personality disorder (APD) or the ICD diagnosis of dissocial personality disorder (DPD; World Health Organization, 1993). Although they overlap symptomatically, compared with psychopathy, the broader category of APD emphasizes antisocial and criminal behaviors rather than personality traits. For the purposes of this chapter, we will take ‘psychopathic disorders’ to comprise APD and the concept of psychopathy, as defined by Hare. Additionally, as categorical personality disorder diagnoses are heterogeneous at the severe end of the personality

PSYCHOTHERAPY OF PSYCHOPATHIC DISORDERS

451

disorder spectrum, we would expect most patients to exhibit comorbidity across DSM diagnoses and clusters. Given the level of confusion involving the conceptual and ethical issues as well as the behavioral characteristics associated with psychopathy, it is perhaps not surprising that psychologists and psychotherapists have been reluctant to involve themselves in providing therapy for this patient group. This is especially so, given that these are people who are likely to be involuntarily detained, committed to antisocial and rule breaking behavior (Blackburn, 1988) and do not fit easily into the traditional medical patient role, let alone the traditional psychotherapy patient role. Consequently, they are more problematic to manage than other offenders, irrespective of whether they are in or outside institutions. It is also not surprising that research programs have been difficult to implement, leading to a lack of high-quality evidence about treatment efficacy, which has contributed to the view that psychopathy and APD are ‘untreatable’.

PREVALENCE AND PSYCHOPATHOLOGY Forensic psychiatrists working therapeutically in prisons or secure settings are likely to have many patients with APD. Studies of prisoners in the US and the UK indicate that APD is present in 40–70 % (Fazel & Danesh, 2002; Grimshaw et al., 2006). This figure for APD, may be compared to US prevalence rates for psychopathy of 15–20 % (as defined by the PCL-R; Hare, 2003) and UK prevalence rates of 30 % in prison populations (Cooke & Michie, 1999). Similar rates have been reported in high secure psychiatric settings (Hogue et al., 2007). Care needs to be taken comparing prevalence rates as Cooke and colleagues (2005) report that the same level of psychopathy was associated with lower PCL-R scores in the UK. APD diagnoses and symptoms correlate more with PCL-R factor 2 rather than factor 1, confirming that the overlap is accounted for by socially deviant behaviors and that the affective and interpersonal symptoms distinguish psychopathic from APD individuals (Trull & Durrett, 2005). In secure psychiatric settings, APD is frequently comorbid with Axis I conditions such as affective and psychotic disorders, as well as other Axis II disorders, such as borderline personality disorder (BPD) and narcissistic personality disorder. In one study of mentally disordered offenders in a high secure hospital, the prevalence of personality disorder was 75 % and most patients suffered from at least two personality disorders, mainly APD and BPD (Blackburn et al., 2003). This is also true for female offenders, although the prevalence of APD is somewhat less and the prevalence of BPD somewhat more (Coid et al., 2000).

THERAPEUTIC APPROACHES FOR PSYCHOPATHIC DISORDERS The nature of the psychopathology of psychopathic disorders is crucial for determining therapeutic objectives. The purpose of offering treatment to patients with APD or psychopathy is two-fold: to reduce risk and where possible to promote and restore mental health. However, it is precisely those aspects of psychopathology that make these patients dangerous that also make them difficult to engage in treatment. Psychopathic patients lack empathy and sympathy for others’ distress; a key symptomatic feature of psychopathy is contempt for weakness or distress. Such patients are therefore unlikely to have much

452

VOLUME I: DIAGNOSIS AND TREATMENT

sympathy or interest in their own neediness and distress, capacities that are often crucial for therapeutic engagement. It is precisely this lack of sympathy for distress and inability to take their emotional and mental life seriously that is the therapeutic challenge in this population.

EARLY THERAPEUTIC TREATMENT STUDIES WITH PSYCHOPATHS In his classic study The Mask of Sanity, Cleckley expressed doubt about how best to treat psychopathic patients and flagged up their resistance to treatment as a feature of their psychopathology (Cleckley, 1941). As in other conditions, there were early individual case reports of therapeutic success. Freud (1916) suggested that criminality arose from an unconscious sense of oedipal guilt and psychiatrists using an analytic approach based their treatment accordingly. However, it is likely that the most disturbed individuals were not offered treatment; Cleckley’s own sample were generally nonviolent offenders and therapeutic interventions were rarely offered to such men in prisons, a notable exception being the therapeutic regime at Grendon prison in the UK, which will be discussed later. There was early interest in group approaches to therapy, expressed first by Foulkes (1948). In an article discussing the possible treatment of antisocial patients, Foulkes suggested that in a group such patients might ‘collectively form a norm from which they individually deviate’. By forming a group norm, they might be able to regain the capacity to be part of a social group and internalize group rules as others do. This concept along with other key underlying principles was integrated into therapeutic community approaches to treating psychopathic and personality-disordered offenders. The democratic style therapeutic community (TC) had its origins in the changes that occurred in UK psychiatric hospitals post World War II. They represented a move away from an authoritarian doctor–patient model of treatment to a more democratic style (Jones, 1952). Designed as cohesive communities whose members, staff and patients have an active involvement in the decision making and running of the community. Main suggested (1983) that it is the culture, rather than organizational structure, which is distinctive and that democratic TCs operate within a ‘culture of enquiry’ – into personal, interpersonal and intersystem problems. Indeed, Dolan and Coid’s 1993 review of treatments for individuals with psychopathic disorder and APD (Dolan & Coid, 1993) concluded that, ‘studies of TC treatment have shown the most promising results of any form of treatment for psychopathy in terms of psychological and behavioral changes during treatment, reduction of violent incidents in treatment settings, significant improvements following treatment in life history variables (e.g., recidivism, rehospitalization) and psychological states. In some cases these changes have been maintained at follow-up’. However, they cautioned that owing to the lack of scientific rigor of reviewed studies little could be definitively concluded regarding the effectiveness of TC treatment. With respect to cognitive behavioral therapy (CBT) and dynamic psychotherapy approaches, Dolan and Coid found only a few studies that evaluated the use of psychodynamic psychotherapy and CBT alone with psychopaths independent of other treatment modalities and that there was only limited evidence for the long-term effectiveness of these therapies for treating psychopathic disorder. Overall Dolan and Coid

PSYCHOTHERAPY OF PSYCHOPATHIC DISORDERS

453

concluded that the jury was ‘still out’ as there was no convincing evidence that psychopaths could or could not be successfully treated and suggested that the then prevailing therapeutic pessimism for this group was not entirely justified. The beginning of this more optimistic period was dented by the publication of a series of articles in the early 1990s assessing the impact of group interventions in therapeutic community settings on behavioral change and recidivism rate of ‘criminal psychopaths’ (Harris, Rice & Cormier, 1991, 1994; Ogloff, Wong & Greenwood, 1990). Ogloff and colleagues reported that psychopaths stayed in treatment for a shorter time period and had a poorer treatment response, compared to nonpsychopaths. However, Harris, Rice and Cormier (1994) had perhaps the greatest impact. They reported that, although the program was effective in reducing violent recidivism in nonpsychopaths, the inverse was true for psychopaths, so that psychopaths were actually made worse by group psychotherapeutic approaches. The influence of these studies was profound and few treatment studies of psychological therapies were published for some time; despite concerns that the Harris and Rice studies related to an institution that did not fit the generally accepted criteria for a TC because its program was strongly hierarchical and incorporated unusual treatment interventions such as ‘nude marathon therapy’ (Warren, 1995). The notion of the ‘untreatable psychopath’ took hold and influenced not only treatment services but also the development of mental health legislation (Peay, 1988).

RECENT THERAPEUTIC TREATMENT STUDIES WITH PSYCHOPATHS The last few years have seen a more systematic integration of the literature with respect to assessing the effectiveness of psychological therapies in treating personality disorder including psychopathy. At least four systematic reviews (Dolan & Anderson, 2003; Duggan et al., 2006; Salekin, 2002; Warren et al., 2003), two of which included meta-analysis (Duggan et al., 2006; Salekin, 2002) have been published. Salekin specifically addresses treatment of psychopathy while the other three consider psychological (and pharmacological) treatments of personality disorder in general. After reviewing 42 treatment studies, Salekin (2002) reported that there is little scientific basis for concluding that psychopathy is untreatable and suggests that the previous therapeutic pessimism is both unwarranted and premature, because some psychopathic traits such as lying, remorse, lack of empathy and interpersonal dysfunctional relationships may in fact be amenable to treatment. The urgent question then is: Which traits might be amenable to change and how to reliably monitor these in incarcerated populations (Hobson, Shine & Roberts, 2000)? Recent research suggests that the more deviant individuals are interpersonally, the more likely they are to reoffend (Glover et al., 2002). Similarly, the presence of comorbid APD traits leads to worse outcomes for patients with BPD. However, the presence of some comorbid conditions may improve treatment outcomes: Hobson and colleagues (2000) found that PCL-R factor 1 items such as glibness and superficial charm, grandiose sense of self-worth and a failure to take responsibility showed the highest correlations with negative behaviors in the Grendon prison TC program. However, the presence of some comorbid conditions may improve treatment outcomes; Woody et al. (1985), in opiate-addicted APD patients, found that although APD alone is a negative predictor of psychotherapy outcome, the presence of depression improved outcome.

454

VOLUME I: DIAGNOSIS AND TREATMENT

The Warren and Duggan reviews adopted similar methodological approaches using a hierarchy of evidence following Khan (Khan, ter Riet & Glanville, 2001), which gave the greatest weight to well-designed and reported randomized control trials (RCTs) meeting the Cochrane criteria (Bero & Rennie 1995). The conclusions of both reviews were broadly similar, namely that the evidence base for psychological treatment interventions in people with APD is weak. Duggan et al. (2005) were only able to identify one RCT which met inclusion criteria. This outpatient study was a preliminary report involving a small number of patients who met research criteria for both APD and opiate dependence (Brooner et al., 1998). Patients received a counseling and contingency management behavioral intervention, but unfortunately poor reporting of results meant that the main outcome data could not be reported on. The majority of the other studies reviewed (14 out of 20) were noncontrolled cohort or case series studies. Duggan and colleagues stress the importance of conducting further treatment trials, and the need to fund properly designed and powered randomized trials of psychological treatment intervention in those with APD if the evidence base is to be strengthened. A particular difficulty revealed by the reviews is how to define a study population. Should studies include individuals who are implicitly likely to have a personality disorder but where personality disorder has not been specifically diagnosed? Both reviews adopted the approach of excluding treatment studies for ‘offenders’, or those referred to as having ‘dangerous, violent or antisocial’ behaviors, unless they included consideration of the personality disorder status of the participants. The Warren and Duggan reviews therefore do not include evaluative research on sex offender treatment programs (SOTPs), or the prison-based reasoning and rehabilitation programs. The SOTPs introduced into both prison and subsequently forensic psychiatric settings often included individuals with psychopathy or APD (Seto & Barbaree, 1999; see also Part II in this book). These programs are cognitively based and usually include interventions, such as enhanced thinking skills (ETS), aimed at increasing victim empathy. How effective these programs are is unclear, as the evidence has not been systematically examined; the best evidence suggests that men who complete these programs have lower recidivism rates, but treatment engagement is not a certain predictor. All the reviews have struggled with the inherent difficulties in examining this literature; for example, the different conceptualizations of psychopathy, as many studies in Salekin’s review employed the older Cleckley concept of psychopathy rather than the contemporary Hare model. Other problems include the diverse range of treatment interventions used, wide variation in defining and measuring ‘outcome’ and contingent on this difficulty, the extensive range of outcome measures used, that is, addressing improvement in aberrant behavior, change in personality structure, symptomatic improvement or decrease in recidivism. There are continuing concerns that some forms of psychological therapy make psychopathic traits worse. The Rice study (Rice, Harris & Cormier, 1992) concluded that psychopaths simply exploited the trust and vulnerability of others, learning in fact to be ‘better’ psychopaths (although the recidivism data, based presumably on apprehended criminality, rather contradicts this). There have been similar concerns that sex offenders with APD who attend therapeutic programs might simply learn better ways to groom or otherwise exploit potential victims. D’Silva, Duggan and McCarthy (2004) examined the research evidence that high PCL-R scoring psychopaths were untreatable and may even be made worse by treatment. They reviewed 10 studies in detail, finding that although four studies suggested that psychopaths have a negative response to treatment, another four suggested

PSYCHOTHERAPY OF PSYCHOPATHIC DISORDERS

455

the opposite. Additionally, Lees’s systematic review (Lees, Manning & Rawlings, 1999) of outcome research of TCs’ effectiveness in treating people with personality disorders in secure, nonsecure psychiatric and other settings, generally found therapeutic communities to be beneficial for personality disorder, although specific effects for specific patient groups remain unclear. Unfortunately, none of the randomized trials were conducted on personality-disordered offenders. A key issue seems to be the effect of voluntariness. Most current therapeutic programs for APD, either in prison or secure psychiatric settings, offer a highly structured groupwork program, consisting of cognitive and psychoeducational interventions to participants who volunteer for therapy. Gordon and Wong (2000) describe the Violence Reduction Programme for men with personality disorder who can choose to opt out at any time, or who can be expelled from the program if they do not participate. In the UK, a modified democratic style therapeutic community for male offenders with APD has been running for over 40 years in Her Majesty’s Prison Grendon (Cullen, 1994). Participation is voluntary and typically the inmates have been convicted of serious offenses (often violent and/or sexual as opposed to property offenses). There is some evidence (Marshall, 1997; Taylor, 2000) that the Grendon program reduces recidivism rates, contrary to the findings of Rice (Rice, Harris & Cormier, 1992). Taylor (2000) conducted a continuation of the four-year follow-up cohort study reported by Marshall in 1997. These studies followed 700 patients over seven years admitted to Grendon between 1984 and 1989 and compared them to 142 prisoners on a waiting list for Grendon and some 1400 prisoners from a general prison population. Marshall found that the admitted group were significantly less likely to reoffend than the waiting list group ( p < 0.1). However, the significance of the result was slightly reduced once the difference in criminal histories between the groups had been accounted for. Another finding was that Grendon may have a specific impact on sexual or violent offenders, particularly repeat sexual offenders or older violent offenders. While Taylor generally found these effects to be replicated after seven years, the rates of reoffending were insignificant at the 10 % level. Although after seven years the rates of reconviction specifically for violent offenses did show a significant difference at the 10 % level by length of stay, the numbers in these groups were small. People who had convictions on two or more occasions were more likely to reoffend in the waiting list group than people admitted to Grendon with a similar history. The authors conclude that Grendon appears to select people who have a high risk of reoffending, possibly due to their personality disorders. For those who stayed for at least 18 months, life sentence prisoners and repeat sexual offenders there was a treatment effect. However, there was no treatment effect for those who stayed for under a year. The 1990s saw increasing political concern about public protection from mentally disordered offenders, particularly focusing on those with personality disorder. In Canada, Wong and Gordon began to develop treatment programs for offenders. The Violence Reduction Programme’s objectives (Wong & Gordon, 1994) are to reduce the frequency and intensity of aggressive behaviors, decrease or eliminate antisocial beliefs and attitudes that support aggression and violence and to teach interpersonal skills that aim to reduce recidivism. It is based on three elements: a highly structured therapeutic program; trained and support staff who can deliver treatment faithfully; and an intervention based on cognitive behavioral and social learning principles. The cognitive intervention incorporates a relapse prevention model, although the program is sufficiently flexible to incorporate other treatment interventions. The program is

456

VOLUME I: DIAGNOSIS AND TREATMENT

delivered in three phases, usually in groups. Phase one focuses on enhancing the person’s understanding of the origins and maintenance of aggressive behaviors, identifying treatment targets and building the therapeutic alliance. Phase two concentrates on skill acquisition to restructure negative thoughts and behaviors that culminate in aggression and violence, while phase three focuses on relapse prevention. Treatment change is assessed using the Violence Risk Scale (VRS: Wong & Gordon, 1994) which uses an adapted version of Prochaska and DiClemente’s stages of change model for addictive behavior (1986). The model postulates that individuals modify problem behaviors by moving through a series of stages: the precontemplation, preparation, action and maintenance stages all correspond to improvement made by the patient. Successful treatment completion often involves the person completing most or all of the stages a number of times. In the UK, the Home Office and Department of Health produced a joint policy initiative to provide services for individuals whose personality disorder was both severe and gave rise to dangerous behavior (dangerous severe personality disorder (DSPD): Home Office & Department of Health, 1999). DSPD is not a clinical diagnosis, but refers to a category of offenders who are thought to be potentially most at risk of causing harm to others. The category has subsequently been refined to include those suffering from two or more DSM personality disorder diagnoses and who have a PCL-R score of over 25 and where there is a functional link between the personality disorder and the offending behavior. This initiative proposed a new legal measure to detain such individuals, which gave rise to intense debate within UK psychiatric opinion; with some suggesting that controlling dangerous behavior by patients was a proper role for psychiatry (Maden & Tyrer, 2003); others taking a different view (Moran 2002; Sarkar, 2002). Although new and specific legislation for this group of offenders was not eventually enacted, new secure treatment facilities for this group have been developed, based in both prisons and high secure hospitals. Treatment regimes are based largely on CBT and modified CBT approaches, such as Gordon and Wong’s VRP and the cognitive interpersonal model as described by Young (2003). These units and their treatment programs are still in their infancy, and the results of their evaluation are awaited over the next few years.

WHAT’S THE PROBLEM? THE EXTERNAL AND INTERNAL WORLD OF THE PSYCHOPATH A crucial problem in psychopathological terms has been how to move from crude behavioral based diagnoses to a formulation based on psychological experience. There needs to be a way to distinguish the deviant rule breaking of APD and psychopathy from ‘ordinary’ criminality. Cooke and colleagues (2005) report that the most discriminating symptoms (as rated using the PCL-R) are deficient affective experience, followed by symptoms of deceptive interpersonal style. Impulsive and irresponsible behavioral style was the least discriminating, for both the UK and North American populations. This finding suggests that clinicians need to focus on affective experience and regulation, not simply on behavioral control. Cleckley’s original description suggested that psychopaths suffer from a problem in emotional recognition; or, that emotionally, they ‘know the words but not the music’ (Johns & Quay, 1962). Decades later his suggestion finds empirical support from the work of neuropsychologists and neurologists. These researchers and others have found that some

PSYCHOTHERAPY OF PSYCHOPATHIC DISORDERS

457

psychopaths have reduced affective responses to others’ distress. Blair (2003) reports that psychopaths not only fail to respond to emotional distress in others, they also do not recognize it, even though they have good theory of mind skills. These findings suggest that psychopaths have either learnt to depress or repress their emotional responses to distress; or they never acquired a capacity to be distressed effectively. The capacity to manage distress is crucially linked to early attachment histories, and there is evidence that many psychopaths employ cognitive representational models of attachment that are based on the dismissing of the need to depend on others, or any admission of weakness or distress (Frodi et al., 2001). Several studies of criminal populations have showed a similar dismissing pattern of attachment, although these were not specifically psychopathic populations (Adshead, 2002). It may also be that dismissing attachment representations are a proxy for lack of empathy, which is clearly a feature of psychopathy. In terms of psychological experience, we suspect that because most patients with severe psychopathic disorders have narcissistic disorders, they have a rudimentary or highly fragile sense of self, which is easily overwhelmed by feelings of anxiety (Akhtar & Thomson, 1982; Stucke & Sporer, 2002). A dismissing or repressor coping style may not be sufficient to contain anxiety, which will then give rise to hostility, rage and a wish to hurt. Interpersonal encounters with others are likely to generate anxiety (both conscious and unconscious) because other people are unpredictable and uncontrollable. Psychopathic individuals are therefore likely to experience others as a source of threat who need either to be neutralized or taught a savage lesson. Given the above, it would seem that any treatment approach has to address:

r psychopathic affective detachment; r a tendency to dysregulated negative affective responses; and r dysregulated affective and arousal responses to the perception of distress in others (including hostile and contemptuous responses to distress);

r disorganized behavioral responses to their own or others distress. This approach might be seen as taking a mentalizing approach to the development of a capacity for empathy and the cognitive and affective distortions inherent in the psychopath’s lack of empathy. Mentalization is a term coined by Bateman and Fonagy (2004) to describe the ability to implicitly and explicitly interpret the actions of both oneself and others as meaningful. Interpretation implies the understanding of intentional mental states, that is, the feelings, beliefs, thoughts, desires, intentions and needs of oneself and others. The acquisition of the capacity to mentalize is seen as a developmental process and as such encompasses a variety of neurobiological, psychosocial and interpersonal factors known to be relevant to the development of psychopathy and APD. Bateman and Fonagy, hypothesizing that personality disordered individuals lack the capacity to mentalize, have devised a therapeutic program for BPD, using Mentalization Based Treatment (MBT). Like CBT and its derivative therapies such as Diatectic Behavioral Therapy (DBT, Linehan, Armstrong & Suarez, 1991) MBT was developed and researched for the treatment of BPD (Bateman & Fonagy, 1999, 2004, 2006). However, there is emerging evidence that it is applicable and effective in patients with APD (Bateman & Fonagy, personal communication). In the external world, psychopaths are seen both to lack interest in the distress or weakness of others and to be equally unmoved by their own distressing experiences. However,

458

VOLUME I: DIAGNOSIS AND TREATMENT

this account of affective alienation is not the whole story. There are clearly psychopaths who are positively excited and aroused by the distress or vulnerability of others and/or respond to distress in others with feelings of contempt and hostility. Such an attitude to vulnerability has been described by Meloy as being in ‘predator mode’ (Meloy, 2006). Such psychopathic individuals may have such low thresholds for threat perception that they are always on the offensive; in their internal world, they perceive themselves always at risk and will be keen to exploit any potential weakness in those they see as enemies. Without a secure model of trusting relationships, most other people will be seen either as enemies or victims.

PITFALLS AND PROBLEMS IN TREATMENT Irrespective of treatment modality, be it individual or group, psychodynamic adapted therapies like MBT, CBT and its derivatives such as the VRP and DBT, or TC based therapeutic regimes; working therapeutically with psychopathic individuals raises common difficulties for the therapist, treating team and detaining institution or system. Some of these have already been touched on throughout the chapter, but below we present some of the main problems together with some practical guidelines. Schematically we have divided them into knowledge and experientially based difficulties. However, there is one major consideration that spans both areas: working therapeutically with individuals with psychopathic disorders presents a risk to the therapist and other professionals, which must continually be assessed and managed. Teamwork and supervision are essential.

Knowledge Base: Complexity and Responsiveness First, it is necessary to assess severity of the psychopathy or APD, the extent of psychopathic traits and the existence of comorbid conditions. It has often been suggested that a mild degree of psychopathy, especially if balanced by intelligence and social advantage, may not be a handicap in some sorts of society, or at some times in a society’s history. It may well be that it is only the most severe degrees of psychopathy, without any resilience or compensatory traits, that result in criminal and antisocial behaviors that are seen so often in custodial or secure treatment settings. When assessing individuals with psychopathic disorders for treatment, it will be crucial to assess for psychological strengths as well as weakness, and to assess comorbidity. If, as Salekin’s meta-analysis suggests, psychopathic disorders are more treatable than first thought, this may be because there are degrees of severity of psychopathy, which are influenced positively and negatively by a variety of individual risk and resilience factors. Here, therapists face the problem of the lack of diagnostic clarity described above and also a lack of an evidence base. Tyrer et al. (2005) reviewed the reliability of the PCL-R (Hare, 1991) the Historical Clinical Risk-20 (HCR-20; Douglas & Webster, 1999) and the International Personality Disorder Examination (IPDE; Loranger et al., 1994) and concluded that the intraclass correlation levels are too low to rely only on these measures alone for assessment. None of these measures adequately assess deficient affective capacity in terms of affective responding, capacity for detachment or lack of empathy), which Cooke identifies as the main discriminator and obvious treatment focus. In terms of targeting

PSYCHOTHERAPY OF PSYCHOPATHIC DISORDERS

459

patients who will benefit most, it seems likely that individuals with very high psychopathy scores (appropriately adjusted for context; Cooke et al., 2005) benefit least from treatment interventions. However, it is not clear what to make of those who score in the middle range for psychopathy; or whether in fact it is a particular type of factor 1 profile that makes treatment ineffective. Second, as suggested above, APD and psychopathy often coexist with other DSM personality disorders and Axis 1 conditions, which need to be assessed as they impact on treatment engagement and response. Although there is no gold standard of assessment for APD, a comprehensive assessment should include consideration of both Axis I and II psychopathology, using a combination of clinical judgment and standardized structured or semi-structured instruments. Our clinical experience is that psychotic disorders are not uncommon in this group; consistent with studies of the comorbidity of Axis and Axis II disorders by Oldham et al. (1995), Blackburn et al. (2003) and Mueser et al. (2006). Although brief psychotic episodes are diagnostic in BPD, they have not been thought to be a feature of APD or narcissistic personality disorder. However, our clinical experience is that many people with psychopathic disorders have degrees of cognitive distortion that are almost indistinguishable from psychotic thought disorder. The pervasive depression or repression of affective experience impairs reality testing as much as other types of perceptual abnormality. Other types of impaired reality testing, such as dissociation, derealization and depersonalization are also common in this group and should be the subject of enquiry. Such individuals may benefit from low doses of antipsychotic medication, especially if they become more disturbed in the initial stages of therapy. With respect to discrete groups, there are particular problems in the treatment of psychopathic women and younger adults. In relation to women, highly psychopathic women are the minority, and psychopathic traits are usually comorbid with BPD and major affective disorder. However, psychopathy in women may be hidden by gender stereotypes like charm or apparent vulnerability associated with previous trauma; it is important that psychopathic women are not excluded from suitable treatment interventions, none of which have been evaluated in women because highly antisocial women are rare. In relation to younger adults and adolescents, the problem is one of diagnosis, and the fact that antisocial personality traits may still be emerging. Theoretically, this should mean that younger psychopathic patients are more open to treatment, as their cognitive and affective capacities are more plastic. There is however lack of evidence to support this at present and more importantly a lack of therapeutic resources with which such hypotheses could be tested.

Experiential: Staff and Institution Individuals with psychopathic disorders are demanding to work with for a number of reasons. First, they do not easily accept the traditional sick role as described by Parsons (1951), let alone that of a traditional psychotherapy patient (Norton & McGauley 1998): they do not request help easily and are not grateful for help given. Those patients whose psychopathic disorder is largely a defense against early childhood trauma may find it impossible to trust the therapist and may act in ways that provoke rejection by the therapist and the cessation of therapy. By definition, these are people who do not have the cognitive and affective capacity to manage negative affects psychologically;

460

VOLUME I: DIAGNOSIS AND TREATMENT

they are forced to manage their emotions somatically in the external world by acting them out. Whatever the pathology, no normal degree of interpersonal trust can be assumed by the therapist. Such patients take much longer to engage in therapy than others, and a therapeutic alliance cannot be assumed too early. Psychopathic individuals who have spent a lifetime avoiding interpersonal relating, and the normally distressing affects that go with them are likely to find the process of therapy difficult as they begin to experience affects of shame or anxiety. Feelings of shame and humiliation, especially when ‘made public’ to the therapist, can by projective processes, lead to the patient feeling that their therapist’s aim is to sadistically exploit and humiliate them further. The emotional histories of individuals with psychopathic disorder often reveal that the moment when they have experienced most shame and humiliation is the moment when violence has broken through (Gilligan, 2002). The potential replication of these moments in the therapeutic situation, if not anticipated and contained, exposes the therapist to the risk of their patient acting out aggressively. A detailed relationship history of both friendships and intimate partnerships, which can be checked using corroborative data, should elicit information about stability of attachments and histories of exploitation. Attitudes to vulnerability in others and the self may also be informative. The key issues in assessment are coherence and consistency of the personal narrative, as well as awareness of inconsistency: an individual who claims to have a close relationship with his mother, but who then reveals that he hardly talks to her and is not aware of the discrepancy, is describing a personal relationship in a highly incoherent way which suggests that their interpersonal relating capacity is disorganized.

Problems in Therapy The unempathic and contemptuous attitudes of these individuals result in care-eliciting behaviors which alienate staff and add to therapeutic pessimism. They may be hostile or deceptive, which then angers and antagonizes staff. The patient may spend time attempting to con or exploit the therapist, especially by the use of intellectualization of distress or problems. At one level, this might be seen as just another way of exploiting others; deceptiveness is innate and widespread in nonhuman primates and emerges early in humans as a behavioral strategy, usually to avoid conflict. Use of deception as a predatory strategy requires further study to determine the underlying beliefs and attitudes of those who use it; not least because deception makes human communication and relationships difficult, and tends to increase the social isolation of psychopaths. Alternatively, psychopathic patients may use superficial charm to engage staff and deceive them into collusion with some form of rule-breaking behavior. Patients with a high degree of narcissism may find it intolerable that the therapist is in a position of power and control over them and sabotage the therapy by attempting a type of friendship with the therapist. All staff are susceptible to being made to feel potent or kind or simply appreciated, especially in institutions which are traditionally careless of staff needs, like custodial or secure treatment settings. Staff may simply be frightened of such individuals, knowing that these are people who are prepared to hurt others who oppose them. This can lead to rule-breaking behaviors being ignored because staff fear getting into conflict with such individuals. Information from staff is therefore a crucial part of assessment.

PSYCHOTHERAPY OF PSYCHOPATHIC DISORDERS

461

People with psychopathic disorders typically use immature psychological defenses against negative affects, such as projection and somatization and do not appear to have access to more mature defenses, such as humor or hope (Vaillant, 1975). The therapist is therefore likely to be on the receiving end of projected affects of helplessness, hopelessness and powerless to act. It is not unusual for therapists to find themselves feeling like potential victims in the therapeutic space, and any sense of fear in the room should not be taken lightly. In response to such projections, therapists may defend themselves with countering affects of rage, competitiveness and revenge. They may enact these feelings within institutions by supporting punitive measures against the patient, or withdrawing therapy at crucial moments. Therapists may resonate with patients’ grandiosity and find themselves attempting to be more psychopathic than the patient; to beat him or her at his own game. Therapists working with such patients need to be at ease with their own vulnerability and neediness and also need to be prepared to be conned by the patient, and still survive. It is vital that therapists do not consciously or unconsciously collude with the attitude that being vulnerable or mistaken is contemptible. It is perhaps obvious that supervision is essential; therapists need to be aware of the need to protect themselves. The difficulty of individual work with severely personality disordered patients has led to renewed interest in group therapy for this client group. Bateman and Fonagy (2004) suggest that group work may be optimal for patients with poor affect regulation, because it is less arousing, and offers more opportunities for understanding other minds. In group therapy it is more possible for the therapists to observe the dynamics of the interpersonal and not be so caught up in them; it is also harder for psychopathic patients to con each other. Although working with a co-therapist may be complicated by the patients trying to play each against the other, ultimately co-therapists can support each other and reduce the competition for dominance that is a characteristic of APD groups.

PROBLEMS IN THE ENVIRONMENT As described above, psychopathic patients have profound effects on staff and the institutions in which they reside. In part this is because most psychopathic patients or clients are detained in long-stay residential institutions where they make up the majority of the social group. It is unusual in human social groups to have such large concentrations of antisocial people living together in groups, and there are inevitable tensions and conflicts between antisocial individuals, who are ill equipped to deal with them. Staff may feel at a disadvantage, because they are in a minority, although they clearly have more power than the patients at one level. Professional boundary violations are the commonest type of problem faced by institutions dealing with psychopathic disorders. In the UK one secure psychiatric service dealing with psychopathic patients became involved in two forms of boundary violations: first, the physical abuse of patients; second, collusion with patients in dealing pornography and the exploitation of the vulnerable (Blom-Cooper et al., 1992; Fallon et al., 1999). In the first sort of boundary violation, staff became identified with the perpetrator/predator aspect of their patients and enacted their own fear and wish for revenge on the patients. In the second, staff presumably identified with trusting victims who could be conned; they may also have felt powerless to resist their patients’ manipulations. These extreme examples are a potent reminder that even experienced institutions can become involved in extensive and

462

VOLUME I: DIAGNOSIS AND TREATMENT

systematic boundary violations. Hinshelwood (1993) and Sarkar (2005) have described the dynamics of working as therapists with antisocial patients detained in secure institutions. There is also a problem that psychopathic patients may ‘play the system’ by making complaints about treatment and therapists that derail the therapeutic process. Further, they may deceive managers of services, who are separated from the clinical milieu, by appearing to be ‘well’ and ‘no management problem’; whereas in fact their attitudes to staff and fellow patients are still highly psychopathic. This is yet another example of how clinical teams can become split in this work. At present, best practice suggest that any treatment offered should be embedded in a multidisciplinary approach, with a focus on containment of antisocial behaviors, promotion of prosocial attitudes and the maintenance of professional boundaries. This means that staff support and supervision is essential. Working with such patients will always be difficult and to some extent the problems are part of the therapeutic process. They may be a demonstration of what we think of as the 3D model; deficit, disability and damage and as such will inevitably occur within the therapeutic process. As the neuropsychiatric/genetic damage done to the brain leads to cognitive and affective deficits, which result in severe interpersonal disabilities. Therapists need a set of skills and techniques that preserve their capacity to think and feel in the face of pervasive antisocial attitudes. Therapists need to be trained and experienced before such work can be started, and therapists also need to be able to provide and receive supervision. Antisocial patients can easily deceive and con therapists and staff, opportunities for reflection on one’s work with other professionals is essential to allow the therapist to maintain reality testing. Therapists may usefully consult with teams managing these patients; to help reduce splits.

Recommendations for Therapists Gabbard (1994) provided six recommendations for the therapist working with APD patients, which were further expanded by Cordess et al. (2005). In Figure 26.1, we add our further adaptations and additions. It will be seen straight away that these are a tall order; and most therapists are likely to gain these competencies slowly over time and with experience. It is also noteworthy that the word ‘should’ appears often in the list; which indicates how much of an ethical flavor there is to the work with APD. Treating psychopaths is about dealing with boundary violations, and the recommendations listed highlight the most vulnerable areas.

FURTHER QUESTIONS It is a truism to say that more research is necessary but in relation to the question, ‘How do we treat psychopaths?’ it is obvious that more information is needed. We are still not able to be clear about what is ‘wrong’ with psychopathic men and women and so not clear whether the treatment tools we have at our disposal are effective. There are huge questions to be answered about how best to deal with comorbid conditions; whether gender really makes a difference to psychopathology, and what would count as a successful treatment outcome. Finally, there is a question of whether there really are people who are not and will

PSYCHOTHERAPY OF PSYCHOPATHIC DISORDERS

463

1. They should try to be incorruptible, stable and persistent in the face of failure; as attacks on thinking and the work are the norm and things will go wrong. 2. They should be honest dealing and speaking. 3. They should be willing to pay attention to and interpret the patient’s denial or minimizations (and other psychological defense mechanisms). 4. They should help patients link their actions with their emotional states. 5. They should name and explore behaviors that occur in the here and now. 6. They should monitor their counter-transference; always asking ‘What am I not thinking about?’ 7. They should avoid excessive expectations of improvement; appropriate therapeutic hope needs to be discerned and worked on. 8. They must make and maintain working relationships with other colleagues managing the patient, to avoid dangerous splitting; especially when there are disagreements between the therapist and team, or the therapy is marginalized. 9. Supervision is essential, even for the most senior staff. 10. It is useful to retain a developmental perspective to help understand why the patient is alienated and alienating. We favor a 3D model, understanding APD in terms of deficits, disability and damage (see text).

Figure 26.1 Recommendations for the therapist who wishes to work with APD (Gabbard, 1994; Cordess et al., 2005)

never be responsive to therapy. Presumably, there are such people, but we do not know their characteristics, nor is it clear what the social response to them should be.

REFERENCES Adshead, G. (2002). Three degrees of security: attachment and forensic institutions. Criminal Behaviour and Mental Health, 12(Supplement 2), 31–45. Akhtar, S. & Thomson, J.A. (1982) Overview: narcissistic personality disorder. American Journal of Psychiatry, 139, 12–20. American Psychiatric Association. (2000). Diagnostic and Statistical Manual of Mental Disorders, 4th edition, text revision. Washington, DC: American Psychiatric Association. Bateman, A. & Fonagy, P. (1999). The effectiveness of partial hospitalisation in the treatment of borderline personality disorder- a randomised controlled trial. American Journal of Psychiatry, 156, 1563–9. Bateman, A. & Fonagy, P. (2004). Psychotherapy for Borderline Personality Disorder: Mentalization Based Treatment. Oxford: Oxford University Press. Bero, L. & Rennie, D. (1995). The Cochrane Collaboration: preparing, maintaining and disseminating systematic reviews of the effects of healthcare. Journal of the American Medical Association, 274, 1935–8. Blackburn, R. (1988). On moral judgements and personality disorder. The myth of psychopathic disorder revisited. British Journal of Psychiatry, 153, 505–12. Blackburn, R., Logan, C., Donnelly, J. & Renwick, S. (2003). Personality disorders, psychopathy and other mental disorders: co-morbidity among patients in English and Scottish high security hospitals. Journal of Forensic Psychiatry and Psychology, 14, 111–37. Blair, R.J. (2003). The neurobiological basis of psychopathy. British Journal of Psychiatry, 182, 5–7. Blom-Cooper, L., Brown, M., Dolan, R. & Murphy, E. (1992). Report of the Inquiry of Complaints into Ashworth Hospital. London: HMSO. Brooner, R.K., Kidorf, M., King, V.I. & Stoller, K. (1998). Preliminary evidence of good treatment response in antisocial drug abusers. Drug and Alcohol Dependence, 49, 249–60. Cleckley, H. (1941). The Mask of Sanity (1st edition). St Louis: Mosby.

464

VOLUME I: DIAGNOSIS AND TREATMENT

Coid, J., Kahtan, N., Gault, S. & Jarman, B. (2000). Women admitted to secure forensic psychiatric services. II: Identification of categories using cluster analysis. Journal of Forensic Psychiatry, 11, 296–315. Cordess, C., Davidson, K., Morris, M. & Norton, K. (2005). Cluster B antisocial personality disorders. In J. Holmes, J. Beck & G. Gabbard (eds.), Oxford Textbook of Psychotherapy (pp. 269–78). Oxford: Oxford University Press. Cooke, D. & Michie, C. (1999). Psychopathy across cultures: Scotland and North America compared. Journal of Abnormal Psychology, 108, 58–68. Cooke, D., Michie, C., Hart, S. & Clark, D. (2005). Assessing psychopathy in the UK: concerns about cross-cultural generalisability. British Journal of Psychiatry, 186, 335–41. Cope, R. (1992). A survey of forensic psychiatrists’ views on psychopathic disorder. Journal of Forensic Psychiatry, 4(2), 215–28. Cullen, E.C. (1994). Grendon: a therapeutic prison that works. Therapeutic Communities, 15, 301–11. D’Silva, K., Duggan, C. & McCarthy, L. (2004). Does treatment really make psychopaths worse? A review of the evidence. Journal of Personality Disorders, 18(2), 163–77. Dolan, B. & Coid, J. (1993). Summary of findings and recommendations for future research, Chapter 12. In B. Dolan & J. Coid (eds.), Psychopathic and Antisocial Personality Disorders: Treatment and Research Issues. London: Gaskell. Dolan, M.C. & Anderson, I.M. (2003). The relationship between serotonergic function and the Psychopathy Checklist: Screening Version. Journal of Psychopharmacology, 17(2), 216–22. Douglas, K.S. & Webster, C.D. (1999). The HCR-20 risk assessment – concurrent validity in a sample of incarcerated offenders. Criminal Justice and Behavior, 26, 3–19. Duggan, C., Adams, A., McCarthy, L. et al. (2005). Systematic Review of the Effectiveness of Pharmacological and Psychological Treatments for those with Personality Disorder. Commissioned by Forensic Mental Health Research and Development, Draft Version 2005. Fallon, P., Bluglass, R., Edwards, B. & Daniels, G. (1999). Report of the Inquiry into the Personality Disorder Unit at Ashworth Special Hospital. Volumes 1 & 2. London: HMSO. Fazel, S. & Danesh, J. (2002). Serious mental disorder in 230000 prisoners: a systematic review of 62 surveys. Lancet, 359, 545–50. Field, D. (1976). The social definition of illness. In D. Tuckett (ed.), Introduction to Medical Sociology (pp. 334–66). London: Tavistock. Fonagy, P. & Bateman, A. (2006). Progress in the treatment of borderline personality disorder. British Journal of Psychiatry, 188, 1–3. Forshaw, D. & Rollin, H. (1990). The history of forensic psychiatry in England. In P. Bowden & R. Bluglass (eds.), Principles and Practice of Forensic Psychiatry (pp. 61–102). London: Churchill Livingstone. Foulkes, S. (1948). Introduction to Group Analytic Psychotherapy. Reprinted 1983. London: Karnac. Freud, S. (1916). Some Character Types Met in Psychoanalysis. Standard Edition, 14. London: Hogarth. Frodi, A., Dernevik, M., Sepa, A., Philipson, J. & Bragesio, M. (2001). Current attachment representations of incarcerated offenders varying in degree of psychopathy. Attachment and Human Development, 3, 269–83 Gabbard, G. (1994). Psychodynamic Psychotherapy in Clinical Practice. Washington, DC: American Psychiatric Press. Gilligan, J. (2002). Violence: Reflections on our Deadliest Epidemic. London: Jessica Kingsley. Glover, A.J., Nicholson, D.E., Hemmati, T. et al. (2002). A comparison of predictors of general and violent recidivism among high-risk federal offenders. Criminal Justice and Behavior, 29, 235–49. Gordon, A. & Wong, S. (2000). The Violence Reduction Programme: Facilitators Manual. Sasketoon, Saskatchewan. Canada: Regional Psychiatric Centre. Grimshaw, T., Alwin, N., Blackburn, R. & Davidson, M. (2006). Understanding Personality Disorder: A Professional Practice Board Report: Report 36. London: British Psychological Society. Gunn, J. (2003). Psychopathy: an elusive concept with moral overtones. In T. Millon, E. Simonsen, M. Birket-Smith & R. Davis (eds.). Psychopathy (pp. 32–9). New York: Guilford Press. Gunn, J. (2004). Introduction: what is forensic psychiatry? Criminal Behavior and Mental Health, 4, S1–S5 . Hare, R.D. (1991). The Hare Psychopathy Checklist-Revised. Toronto: Multi-Health Systems.

PSYCHOTHERAPY OF PSYCHOPATHIC DISORDERS

465

Hare, R.D. (2003). The Hare Psychopathy Checklist-Revised (PCL-R), 2nd edition. Tonawanda: Multi-Health Systems. Harris, G,T., Rice, M.E. & Cormier, C.A. (1991). Psychopathy and violent recidivism. Law and Human Behavior, 15(6), 625–37. Harris, G,T., Rice, M.E. & Cormier, C.A. (1994). Psychopaths: is a therapeutic community therapeutic? Therapeutic Communities, 15(4), 283–99. Hinshelwood, R. (1993). Locked in role: a psychotherapist within the social defence system of a prison. Journal of Forensic Psychiatry, 4, 427–40. Hobson, J., Shine, J. & Roberts, R. (2000). How do psychopaths behave in a prison therapeutic community? Psychology, Crime and the Law, 6, 139–54. Hogue, T., Mooney, E., Johnston, S. et al. (2007). The Applicability of Personality Disorder and Risk Assessment Measures in a Sample of Intellectually Disabled Offenders (RDS/01/247). London: HMSO. Home Office & Department of Health (1999). Managing Dangerous People with Severe Personality Disorder. London: HMSO Johns, J.H. & Quay, H.C. (1962). The effect of social reward on verbal conditioning in psychopathic and neurotic military officers. Journal of Consulting and Clinical Psychology, 26, 217–20. Jones, M. (1952). A Study of Therapeutic Communities. London: Tavistock. Khan, K.S., ter Riet, G. & Glanville, J. (eds.) (2001). Undertaking Systematic Reviews of Effectiveness: CRD Guidelines for Those Carrying Out or Commissioning Reviews. CRD Report 4 (2nd edition). University of York: NHS Centre for Reviews and Dissemination. Lewis, A. (1974). Psychopathic personality: a most elusive category. Psychological Medicine, 4, 133–40. Lees, J., Manning, N. & Rawlings, B. (1999). Therapeutic Effectiveness. A Systematic International Review of Therapeutic Community Treatment for People with Personality Disorders and Mentally Disordered Offenders. CRD Report 17. University of York: NHS Centre for Reviews and Dissemination. Linehan, M., Armstrong, H.E. & Suarez, A. (1991). Cognitive behavioral treatment of chronically suicidal patients. Archives of General Psychiatry, 48, 1060–4. Loranger, A.W., Sartorious, N., Andreoli, A. et al. (1994). The International Personality Disorder Examination: the WHO/ADAMHA international pilot study of personality disorders. Archives of General Psychiatry, 51, 215–14. Maden, T. & Tyrer, P. (2003). Dangerous and severe personality disorders: a new personality concept from the United Kingdom. Journal of Personality Disorders, 17(6), 489–96. Main, T.F. (1983). The concept of the therapeutic community: its variations and vicissitudes. In M. Pines (ed.). The Evolution of Group Analysis. London: Routledge and Kegan Paul. Marshall, P. (1997). A Reconviction Study of HMP Grendon Therapeutic Community. No 53. London: Home Office Research and Statistics Directorate. Meloy, J.R. (2006). Empirical basis and forensic application of affective and predatory violence. Australia and New Zealand Journal of Psychiatry, 40, 539–42. Millon, T., Simonsen, E. & Birket-Smith, M. (2003). Historical conceptions of psychopathy in the US and Europe. In T. Millon, E. Simonsen, M. Birket-Smith & R. Davis (eds.). Psychopathy (pp. 3–31). New York: Guilford Press. Moran, P. (2002). Dangerous severe personality disorder-bad tidings from the UK. International Journal of Social Psychiatry, 48(1), 6–10. Mueser, K., Crocker, A., Frisman, L. et al. (2006). Conduct disorder and antisocial personality disorder in persons with severe psychiatric and substance use disorders. Schizophrenia Bulletin, 4, 626–36. Norton, K. & McGauley, G.A. (1998). The counselling transaction. In K. Norton & G.A. McGauley (eds.), Counselling Difficult Clients (pp. 1–15). London: Sage. Oldham, J.M., Skodol, A.E., Kellman, H.D. et al. (1995). Comorbidity of axis I and axis II disorders. American Journal of Psychiatry, 152, 571–8. Ogloff, J.R.P., Wong, S. & Greenwood, A. (1990). Treating criminal psychopaths in a therapeutic community program. Behavioral Sciences and the Law, 8, 181–90. Parsons, T. (1951). The Social System. Glencoe: Free Press.

466

VOLUME I: DIAGNOSIS AND TREATMENT

Peay, J. (1988). Offenders suffering from psychopathic disorder: the rise and demise of a consultation document. British Journal of Criminology, 67–81. Prochaska, J. & DiClementi, C. (1986). The transtheoretical approach: crossing traditional boundaries of therapy. In J. Norcross (ed.). Handbook of Eclectic Therapy (pp. 163–20). New York: Brunner Mazel. Prosono, M. (2003). History of forensic psychiatry. In R. Rosner (ed.), Principles and Practice of Forensic Psychiatry, 2nd edition (pp. 14–30). London: Hodder Arnold. Rice, M.E., Harris, G.T. & Cormier, C.A. (1992). An evaluation of a maximum secure therapeutic community for psychopaths and other mentally disordered offenders. Law and Human Behavior, 16, 399–412. Rosner, R. (2006). Introduction. In C. Newith, C. Meux & P.J. Taylor (eds.), Personality Disorder in Serious Offending. Hospital Treatment Models (pp. xii–xv). London: Hodder Arnold. Salekin, R.S. (2002). Psychopathy and therapeutic pessimism. Clinical lore or clinical reality? Clinical Psychology Review, 22, 79–112. Sarkar, S.P. (2002). A British psychiatrist objects to the dangerous and severe personality disorder proposals. (Editorial). Journal of the American Academy of Psychiatry and the Law, 30, 6–9. Sarkar, S.P. (2005). The other 23 hours: special problems of psychotherapy in a ‘special’ hospital. Psychoanalytic Psychotherapy, 19, 4–16. Seto, M. & Barbaree, H. (1999). Psychopathy, treatment behaviour and sex offender recidivism. Journal of Interpersonal Violence, 14, 1235–48. Stucke, T.S. & Sporer, S.L. (2002). When grandiose self-image is threatened: narcissism and selfconcept clarity as predictors of negative emotions and aggression following ego-threat. Journal of Personality, 70, 509–32. Taylor, R. (2000). A Seven Year Reconviction Study of HMP Grendon Therapeutic Community. London: Home Office Research, Development and Statistics Directorate. Tyrer, P., Cooper, S., Seivewright, H. et al. (2005). Temporal reliability of psychological assessments for patients in a special hospital with severe personality disorder: a preliminary note. Criminal Behavior and Mental Health, 15, 87–92. Trull, T.J. & Durrett, C.A. (2005). Categorical and dimensional models of personality disorder. Annual Review Clinical Psychology, 1, 355–80. Vaillant, G. (1975). Sociopathy as a human process: a viewpoint. Archives of General Psychiatry, 32, 178–83. Warren, F. (1995). What do we mean by a therapeutic community for offenders? International Journal of Therapeutic Communities, 15(4), 312–18. Warren, F., McGauley, G.A., Norton, K., Dolan, B., Preedy-Fayers, K., Pickering, A. & Geddes, J.R. (2003) Review of treatments for severe personality disorder. Online report 30/03. http://www.homeoffice.gov.uk/rds/pdfs?/rdsolr3003.pdf London: Home Office. World Health Organization (1993). International Classification of Diseases Version 10. Geneva: World Health Organization. Woody, G.E., McLellan, T., Luborsky, L. & O’Brien, C.P. (1985). Sociopathy and psychotherapy outcome. Archives of General Psychiatry, 42, 1081–6. Wong, S. & Gordon, A. (2004). The Violence Risk Scale. Sasketoon, Saskatchewan. Canada: Regional Psychiatric Centre. Young, R.M. (2003). Cognitive architectures need compliancy, not universality. Behavioral and Brain Sciences, 26(5), 628.

CHAPTER 27

Comprehensive Outpatient Treatment and Management Andreas Hill, Peer Briken and Wolfgang Berner University Medical Center Hamburg-Eppendorf, Germany

Following a time of therapeutic pessimism, recent decades have at least demonstrated some effectiveness in treating offenders. A positive effect was confirmed especially for community-related approaches. According to results of some investigators, psychopathic patients appear as likely as nonpsychopathic patients to benefit from treatment, other authors are more skeptical. This chapter describes outpatient treatment, management and supervision programs for psychopathy (e.g., forensic outpatient clinics, probation and parole programs), including special problems and interventions in substance abusers and sexual offenders with psychopathy. Pharmacological studies directed at the treatment of psychopathy (e.g., atypical antipsychotics, mood stabilizers, selective serotonin reuptake inhibitors, omega fatty acids) and psychotherapeutic approaches especially cognitive-behavioral therapy, are reviewed. Psychopathic traits are discussed that can lead to therapeutic pessimism or false optimism. Risk assessment and monitoring will be described especially on the basis of currently used risk assessment instruments. This chapter focuses on the assessment, treatment and monitoring of adult, male criminal offenders with psychopathic symptoms in outpatient and community settings, in contrast to institutionalized inpatient settings, such as prisons and forensic or other psychiatric hospitals. Although special treatment programs have been developed – mainly for institutionalized offenders – the literature on intervention studies with sufficient methodological rigor is still scarce, even more so for outpatient or community settings. Therefore most evidence and conclusions for outpatient treatment of psychopathic individuals have to be deduced from general findings on psychopathy, typically investigated in prison or forensic mental hospital samples. Outpatient treatment and supervision for offenders can be administered in two different situations: either instead of incarceration or inpatient care, or as aftercare following release from a prison or forensic mental hospital. Typically more serious offenders had been incarcerated for some time and received some sort of treatment in a prison or forensic hospital, before they are released into the community and aftercare.

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

468

VOLUME I: DIAGNOSIS AND TREATMENT

First the literature on treatment studies on psychopathic offenders will be reviewed focusing on the available relevant information for outpatient/community settings. This review will also include literature on antisocial (DSM-IV-TR, American Psychiatric Association, 2000) and dissocial (ICD-10, World Health Organization, 2005) personality disorder, since one can expect a considerable overlap of these disorders with psychopathy in the narrower sense as defined by Cleckley (1941) or Hare (1991) (for discussion of the different concepts of psychopathy as well as of antisocial/dissocial personality disorder see Chapter 1, pp 9–30). Based on a review of empirical studies, assessment, psychotherapeutic and pharmacological treatment and monitoring of psychopathic offenders in ambulatory settings will be outlined. Special characteristics and needs of psychopathic individuals with comorbid substance abuse as well as psychopathic sexual offenders will also be addressed. The specific characteristics and needs of child and adolescent individuals with psychopathic traits, female psychopaths as well as so-called successful, noncriminal psychopaths are not addressed: no published data or programs could be found on female and noncriminal psychopaths in outpatient settings, whereas assessment and treatment of adolescent psychopathic offenders is covered elsewhere in this book (Chapter 25, pp 417–448). Epidemiological data suggest that psychopathy is relevant not only for inpatient care in prisons and forensic psychiatric hospitals. Since data on prevalence rates of psychopathy in the general population are missing, we have to refer to studies on conduct disorder (CD) and antisocial personality disorder (APD): CD is found in 6–16 % of males and 2–9 % of females under the age of 18 years, with much higher rates in child and adolescent clinics (33– 50 %) (American Psychiatric Association, 2000; Gacono et al., 2001). APD community base rates are approximately 3 % for men and 1 % for women (American Psychiatric Association, 2000); in forensic and correctional settings rates commonly exceed 50 % (Gacono et al., 2001). Aging effects and burn-out of psychopathic traits and behavior need to be considered in the outpatient management of psychopathic and antisocial individuals. Generally an attenuation of psychopathic characteristics has been observed with the aging of these individuals. Improvements are largely due to reductions in their impulsivity and unstable, criminal lifestyle, that is, PCL-R factor 2 (Black et al., 1996; Douglas, Vincent & Edens, 2006; Harpur & Hare, 1994; for a review on longitudinal studies on APD see Paris, 2003).

REVIEW OF RECIDIVISM AND TREATMENT STUDIES The pessimistic view on the treatability and positive development of individuals with psychopathic disorders – that is, psychopathy (as defined by Cleckley or Hare) or antisocial or dissocial personality disorder – is supported by an abundance of empirical data about the predictive value of psychopathic symptoms for criminal recidivism (compare Chapter 3, pp 41–67; Douglas, Vincent & Edens, 2006; Gendreau, Goggin & Smith, 2002; Gendreau, Little & Goggin, 1996; Hare et al., 2000; Hemphill, Hare & Wong, 1998; Salekin, Rogers & Sewell, 1996). Focusing on offenders after release into the community, Hemphill, Hare and Wong (1998) obtained weighted correlations regarding the PCL-R total score of .27 for violent recidivism (total n = 1374), .23 for sexual recidvism (total n = 178) and .27 for general recidivism (total n = 1275). Differentiating between PCL-R factor 1 (affectiveinterpersonal core features) and factor 2 (impulsive antisocial behavior), Walters (2003) computed higher predictive correlations of factor 2 for violent (r = .26) as well as for

OUTPATIENT TREATMENT AND MANAGEMENT

469

general recidivism (r = .32) than for factor 1 (r = .18 for violent, r = .15 for general recidivism), whereas Hemphill, Hare and Wong (1998) had also found higher predictive power of factor 2 regarding general recidivism, but no differences between the two PCL-R factors in the prediction of violent recidivism. Recidivism as well as epidemiological studies suggest that impulsive antisocial behavior (factor 2 of the PCL-R) is more relevant for criminal recidivism and also less stable over time. This has to been taken into account as well in the treatment and management of psychopathic individuals in outpatient settings. In contrast to the almost overwhelming evidence that psychopathy is a risk factor for criminal recidivism, well-controlled intervention studies on the treatment of psychopathic offenders are scarce (for reviews see Hare et al., 2000; Hemphill & Hart, 2002; L¨osel, 1998; Salekin, 2002; Skeem, Monahan & Mulvey, 2002). In a study by Hare et al. (2000) offenders in the high PCL-R group (PCL-R total score ≥ 25) were as likely as those in the low PCL-R group (PCL-R total score < 25) to attend a treatment program, but were less likely to complete educational and vocational programs or to work in prison. Of those 278 offenders who were released into the community significantly more offenders in the high PCL-R group (n = 55) than and in the low PCL-R group (n = 223) were reconvicted for any offense (82 % vs. 40 %, p < .001) as well as for violent offenses (38 % vs. 3 %, p < .001). In both groups participation in a treatment program – mainly short-term programs involving anger management and social skills training – showed little effect on reconviction rates. However, when dichotomizing into offenders with high and low PCL-R factor 1 scores (cutoff = 9), in the high factor 1 group those who had participated in at least one treatment program were reconvicted for any offense more often than those without treatment (86 % vs. 59 %, p < .01), whereas no differences between the treatment and no-treatment groups were found in offenders with low factor 1 scores (general reconviction rate about 30 % in both subgroups). In addition, educational or vocational training programs had no effect on reconviction rates in the high PCL-R total score group (82 % in offenders who had participated vs. 80 % in those who had not). Again factor 1 characteristics are important predictors of treatment success; whereas among those with high factor 1 scores those with training recidivated more often than those without any training (ca. 80 % vs. 60 %), some positive effect of educational or vocational training could be found among those with low factor 1 scores (ca. 20 % vs. 50 % reconviction rate). It appears that offenders with high scores on PCL-R factor 1 may learn better to manipulate and deceive others and that they may be more capable ‘of convincing therapists and staff that they made good progress when in fact they have not’ (Hare et al., 2000, p. 638). These negative findings regarding treatment effect in psychopathic offenders confirm the frequently cited study of Rice, Harris and Cormier (1992) wherein treatment was associated with lower violent recidivism rates in nonpsychopathic offenders, but higher violent recidivism in psychopathic offenders (PCL-R total score ≥ 25). According to the authors psychopathic offenders used their increased knowledge and skills regarding feelings of others, taking others’ perspective, using emotional language, behaving in socially skilled ways, and delaying gratification to manipulate and exploit others – therapists as well as future victims. Also other studies on therapeutic community programs revealed less motivation, less improvement and poorer adjustment to the treatment program in psychopathic offenders (Hobson, Shine & Roberts, 2000; Ogloff, Wong & Greenwood, 1990; for a review see Harris & Rice, 2006).

470

VOLUME I: DIAGNOSIS AND TREATMENT

The skeptical view on the effect of cognitive-behavioral therapy is also confirmed by a treatment study on sexual offenders in Canada who completed a highly structured, groupbased cognitive-behavioral program that targeted deviant sexual preferences as well as antisocial attitudes (Seto & Barbaree, 1999). Although offenders with high PCL-R scores were rated as having shown the most improvement in conduct during treatment sessions, quality of homework and therapists’ ratings of motivation and change, they reoffended more often than offenders with low PCL-R scores, particularly with violent offenses. Those offenders who scored high in psychopathy and better in ‘treatment behavior’ were more than five times more likely to seriously reoffend than those in the other three groups combined. In an extended follow-up of the same sample, psychopathy continued to be a significant predictor of recidivism, but treatment behavior was no longer related to recidivism (Barbaree, 2005). The therapeutic pessimism that was fuelled by these studies has been challenged by Salekin’s meta-analysis (2002) of 42 studies on the treatment of psychopathy including single-case studies. Salekin calculated an overall proportion of successful intervention of 6 0%, when case studies were dropped from the analysis. For combinations of group and individual psychotherapy the proportion of improved patients rose to 81 %. Inclusion of family members in treatment programs resulted in an improvement rate of 75 %, and intensive individual psychotherapy – on average four sessions per week for at least one year – improved as much as 91 % of the patients. Control groups (from eight studies, total n = 287) showed an improvement rate of 20 % (80 %, CI = 18–29 %), the proportion that has to be subtracted from all reported improvement rates. Comparing different types of therapeutic programs, most successful programs appeared to be eclectic methods that combined cognitive-behavioral and insight-orientated approaches, pharmacotherapy, cognitive-behavioral therapy and psychoanalytic therapy, whereas again little effect could be demonstrated for therapeutic communities. Duration of psychotherapy was an important moderating factor: the average improvement rate for programs lasting less than six months was 61 %, but 91 % for those lasting more than one year. No information was given about the settings for the programs (e.g., inpatient or outpatient), but most therapies seemed to have been delivered in inpatient facilities, either in prisons or psychiatric hospitals. However, this meta-analysis has been criticized for various methodological reasons (Harris & Rice, 2006): Only four of the reviewed studies employed the PCL-R; only eight studies included control groups; less than a fifth of the studies assessed outcome in terms of criminal behavior, whereas treatment success was mostly (>70 %) based on the therapists’ impression which has been shown in the previously cited studies to be an unreliable predictor of criminal recidivism. In searching for outpatient treatment programs for psychopathic offenders, one should not dismiss promising results of multisystemic therapy (MST) for juvenile delinquents. Although this approach has not been evaluated for psychopathic adults, it has been shown to be highly effective in reducing violent and other serious criminal behavior in randomized controlled trials even after four years follow-up (Borduin et al., 1995; for review see Brown, Borduin & Henggeler, 2001; Harris & Rice, 2006). Multisystemic therapy is based on a social–ecological theory of behavior, viewing the child and family’s friends, school, work, neighborhood and community as interconnected systems with dynamic and reciprocal influences on the behavior of family members. MST is directed to address and modify different systems relevant for developing and sustaining delinquent behavior, such as dysfunctional families, ineffective schools and antisocial peers. It is an intensive, but also

OUTPATIENT TREATMENT AND MANAGEMENT

471

very individualized and flexible treatment program that includes building skills (also for parents); monitoring and consequent feedback for both adolescents and parents; positive reinforcement; promoting behaviors incompatible with antisocial conduct; emphasizing specific, observable, active behaviors; and ensuring therapeutic integrity and adherence. MST is usually delivered in the family’s home, and not in secluded institutions. The MST therapists must be capable of applying a range of empirically based therapeutic approaches such as structural family therapy or cognitive-behavioral therapy. Therapists work in teams of three, the typical MST caseload is four to six families per therapist, the team being available to clients round-the-clock seven days per week.

COMORBIDITY If psychopathy and psychopathic traits are difficult to alter, it is even more important to address comorbid disorders and problems that are relevant for criminal behavior, particularly for outpatient therapy and monitoring. For a more detailed review of comorbidity in psychopathic patients see Chapters 15, pp 252–274. First of all it is important to diagnose comorbid disorders, such as substance abuse and dependency, pathological gambling and other impulse control disorders, paraphilias, other personality disorders (e.g., borderline or sadistic personality disorder), or intellectual impairment. Comorbid disorders such as anxiety disorders and depression are not always risk factors, and can actually be favorable predictors of treatment success in psychopathic and antisocial offenders (Gacono et al., 2001). The presence of depressive or anxious symptoms probably reflect a capacity to feel guilt (super-ego functioning) or anxiety in dangerous situations, which may act as protective factors against criminal and sensation seeking behavior. Special problems arising from substance abuse and sexual deviancy are addressed later in this chapter. In addition, somatic diseases resulting from substance abuse (e.g., liver failure, cancer), sexually transmitted diseases (e.g., HIV, syphilis, hepatitis), brain damage resulting from head injuries or other consequences of risk taking behavior typical in psychopathic patients should not been overlooked. Such diseases can function as stress factors, impair the patient’s psychosocial functioning as well as present risks to partners and potential victims.

DIAGNOSTIC ASSESSMENT In designing an adequate outpatient treatment and management plan for individual patients, comprehensive assessment is an important prerequisite (see Chapter 2, pp 33–40). Foremost psychopathy must be diagnosed reliably, and individual characteristics should be assessed, since different expressions and subtypes of psychopathy have been shown to carry specific risks and implications for treatment (e.g., those psychopaths with high PCL-R factor 1 or factor 2 scores). For comprehensive personality assessment structured instruments should be used such as the Structured Clinical Interview for DSM-IV (part 2: personality disorders; SKID-II; First et al., 1997), the Minnesota Multiphasic Personality Inventory 2 Antisocial Practices Scale (MMPI-2, Butcher et al., 1990), the Levenson Primary and Secondary Psychopathy Scale (LPSP, Levenson, Kiehl & Fitzpatrick, 1995), or the revised version of the Psychopathic Personality Inventory (PPI-R, Lilienfeld & Andrews, 1996). However, in forensic assessments of offenders one must always keep in mind the possibilities

472

VOLUME I: DIAGNOSIS AND TREATMENT

of distortion, deception and denial, particularly with self-report instruments; this problem is even more pronounced in psychopathic offenders for whom manipulation is a key personality trait. This problem has been addressed in several publications that attempted to identify interview techniques and instruments for avoiding dangerous pitfalls (Lilienfeld & Fowler, 2006; Rogers & Cruise, 2000; Vitacco & Rogers, 2005; Vrij, 2000). Although psychodynamic projective tests have been criticized on various methodological grounds, in psychopathic offenders they have the advantage that their content is less evident and directed and therefore might be more difficult to be manipulated. Researchers such as Reid Meloy and Carl Gacono have emphasized that Rorschach testing (Exner, 1986, 1991) is ideally suited for contributing to the assessment of psychopathy and antisocial personality disorder, avoiding the face validity of other self-report measures, although Rorschach results can be invalidated by psychopathic individuals who sufficiently constrict their response frequency (for a review see Gacono, Meloy & Heaven, 1994; Meloy & Gacono, 2000). Information on the individual’s psychopathology and psychodynamics may also provide useful information for the outpatient management of psychopathic offenders. Diagnosis of psychopathy and a comprehensive assessment of personality and other psychopathology must always include objective, external judgment (as in the PCL-R, or the SKID-II). This implies that assessment also has to be based on collateral information from: 1. extensive file investigations (court and hospital files as well as other health and social care files); and 2. third parties, such as healthcare providers (e.g., psychiatrists, psychologists, general practitioners), social workers, probation officers and parole supervisors, staff from former residential institutions/homes, spouses and other family members, colleagues and employers, sometimes also fellow patients, prisoners or friends). In addition to a complete psychiatric and somatic clinical interview and assessment, a standardized measure of intelligence, such as the Wechsler Adult Intelligence Scale (WAIS-III, Wechsler, 1997) should be performed, if abnormal low or high intelligence is suspected clinically, since this is important to tailor adequate treatment and supervision and to estimate deceptive and manipulative capacities. If medical history (e.g., head injuries, seizures, meningitis or encephalitis) or medical examination hint to any neuropsychological impairments further neurological workup is warranted, including EEG, cranial CT scan, MRI, fMRI, PET or SPECT (see Chapter 4, pp 69–81, Chapter 10, pp 171–185, Chapter 11, 187–198 for functional and/or anatomical brain abnormalities in psychopathic individuals, for a review see also Blair, 2006; Habermeyer & Herpertz, 2006; Raine & Yang, 2006; Rogers, 2006). If irritability or sexual aggressiveness is a prominent feature in the psychopathic individual medical workup should include thyroid function, hypothalamus–pituitary–adrenal axis function (HPA axis) and testosterone. Future developments in the genetics of aggression, antisocial behavior and psychopathy might yield results relevant for subtyping, risk assessment, treatment and management of psychopathic offenders (see Chapter 9, pp 149–169, further reviews in Minzenberg & Siever, 2006; Waldman & Rhee, 2006). An algorithm for outpatient assessment of psychopathic offenders is outlined in Figure 27.1.

OUTPATIENT TREATMENT AND MANAGEMENT

473

1. Comprehensive, careful general psychiatric, somatic and forensic/criminal history. 2. General physical and neurological examination. ↓ 3. External information – with written informed consent – from: – criminal and other official files – parole or probation officers etc. – previous healthcare providers – relatives, employers, friends and other significant third persons. ↓ 4. Preliminary diagnoses of psychiatric and somatic disorders. Look out for comorbidity (especially substance disorders, personality disorders, impulse control disorders, paraphilias, brain abnormalities, sexually transmitted diseases, hepatitis). ↓ 5. Standardized, operationalized assessment of psychopathic personality (PCL-R, including factor 1 and factor 2 subscores). 6. Standardized, operationalized assessment of other personality disorders (e.g., SCID-II). Do not rely on self-report measures alone! ↓ 7. If hints from the clinical history or examination are present: – for intellectual disabilities: formal testing of intelligence (e.g., HAWIE) – for neurological abnormalities: brain imaging (MRT, cranial CT scan), EEG – for offenders with high irritability: tests of thyroid function and HPA axis – for alcohol disorders: blood tests (MCV, liver function parameter, CDT), blood/breath alcohol test – other substance disorders: blood and/or urine screening for illegal drugs/medications; for intravenous drug use: hepatitis, HIV – for paraphilias and sexual offenders: blood tests (testosterone, luteinizing hormone (LH), follicle stimulating hormone (FSH)) – for other somatic disorders: special assessments (e.g., blood tests). 8. Optional: if experienced psychological assessment with projective tests is available, Rorschach testing can be helpful. ↓ 9. Standardized, operationalized criminal risk assessment (using instruments such as the HCR-20, VRAG, LSI-R for violent offenders, SVR-20, Static-99, Static-2002, SORAG for sexual offenders).

Figure 27.1 Algorithm for outpatient assessment of psychopathic offenders

RISK ASSESSMENT Initial as well as continuous assessment should include some form of structured risk assessment. Although psychopathy itself has been demonstrated to be one eminent predictive factor for future criminal behavior, other risk factors in psychopathic individuals should not been underestimated, more so, since psychopathy itself is difficult to modify, whereas other criminogenic factors might be more easily altered. It is beyond the scope of this chapter to review all the criminal risk assessment instruments that have been developed over the last two decades (see Douglas, Vincent & Edens, 2006; Nedopil, 2005). However, some of the most used and evaluated instruments will be briefly introduced to show the main topics and problems that have to be addressed in risk assessment and management. Static or

474

VOLUME I: DIAGNOSIS AND TREATMENT

actuarial risk factors have been differentiated from more dynamic factors. Risk assessment instruments have been designed for specific offender or offense types, for example, violent or sexual offenses, juvenile offenders. Most risk assessment instruments include the PCL-R score or other measures of antisocial disposition as one risk factor. The Violence Risk Appraisal Guide (VRAG, Harris, Rice & Quinsey, 1993) focuses on static variables with the PCL-R total score as the most prominent single risk factor, but includes general social variables (elementary school problems, not being raised with both biological parents, never married), diagnostic features (any personality disorder, alcohol problems, schizophrenia), criminal history (previous nonviolent offenses, age the time of the violent offense, failure on prior conditional release) as well as victim-related criteria (e.g., degree of injury, female victim). Age, schizophrenia, female victim and degree of physical injury are negatively correlated with violent recidivism. The revised version of the Level of Service Inventory (LSI-R, Andrews & Bonta, 1995) with 54 items covers 10 different areas (criminal history, school and employment, finances, intimate partnership and family, housing, leisure activities, friends and peers, alcohol and drugs, psychological problems, general attitudes). The HCR-20 (Historical Clinical Risk, Webster et al., 1997) also combines static and dynamic risk factors. The historical factors are mainly static (previous violence, young age at first violent incident, prior supervision failure, relationship instability, employment problems, early maladjustment, substance use problems, major mental illness, psychopathy, any personality disorder), whereas the clinical factors (lack of insight, negative attitudes, active symptoms of major mental illness, impulsivity and unresponsiveness to treatment) as well as risk factors regarding the future social environment (impractical plans, exposure to destabilizing influences, lack of personal support, noncompliance with remediation, stressors) can be modified by therapeutic, social or supervisory interventions. This instrument as most others has been criticized for not including protective factors. Recently, a specific algorithm and risk assessment technique for the conditional release of insanity acquittees has been published. A follow-up study showed that male patients with moderate symptoms and low PCL-R scores were associated with recommendation for release (McDermott & Thompson, 2006). Urbaniok (2004) has developed a computerized, very comprehensive, perhaps somewhat redundant instrument in German to assess risk as well as treatability and therapeutic progress (Forensisches Operationalisiertes Therapie-Risiko-Evaluations-System, FOTRES, Forensic Operationalized Therapy-Risk-Evaluation System) that can be applied for different offense types separately. The more than 300 variables cover structural recidivism risk favoring static factors (general antisocial personality dispositions; specific problems relevant to delinquency such as other personality problems, deviant sexuality, or substance abuse; and detailed analysis of the index offense), treatability (general possibilities, actual resources), dynamic risk reduction (treatment progress), current situational risk factors as well as addressing a single dominant risk factor. In addition to these risk factors for general or violent delinquency, the specific risk assessment instruments for sexual offenders include items on sexual deviancy (i.e., paraphilias or sexual preference disorders), previous sexual offenses, analysis of the index offenses and victim characteristics. The most widely used instruments are the Sex Offender Risk Appraisal Guide (SORAG, Rice & Harris, 1997), the Static-99 and Static-2002 (Hanson & Thornton, 1999), and the Sexual Violence Risk 20 (SVR-20, Boer et al., 1997) (for reviews see Nedopil, 2005; Prentky & Burgess, 2000).

OUTPATIENT TREATMENT AND MANAGEMENT

475

In recent years risk assessment has been used to guide and enhance treatment and monitoring. This is an important advance for evidence-based, safe therapy. The FOTRES (Urbaniok, 2004) has been specifically developed to apply adequate treatment, the HCR-20 (Webster et al., 1997) has been supplemented by the HCR-20 Violence Risk Management Companion Guide (Douglas et al., 2001). The SONAR (Hanson & Harris, 2000) has been specifically developed to assess treatment needs in sexual offenders.

TREATMENT AND MONITORING Since sound empirical data on the efficacy of interventions in psychopathic patients in outpatient as well as inpatient or prison settings are scarce, one must search for promising components of treatment programs for patients with antisocial traits and offenders in general (for reviews and selected studies on outpatient programs see Ashford, Sales & LeCroy, 2001; Heilbrun & Peters, 2000; Huchzermeier & Aldenhoff, 2002; Knecht et al., 1996; Lamb & Weinberger, 2001; M¨uller-Isberner, 1996; M¨uller-Isberner, Eucker & Herpertz, 2003; Roskes et al., 2005; for juvenile offenders: Brown, Borduin & Henggeler, 2001). Meta-analyses of correctional outpatient treatment programs with criminal offenders (most of whom were juveniles) revealed mean effect sizes between .13 and .35. Longer lasting, more intensive programs, risk-tailored interventions and probational supervision programs (compared to probation orders alone) appear to be related to lower recidivism rates (Lau, 2003). For the smaller number of studies on forensic psychiatric outpatients, similar findings were reported: mandatory treatment, higher frequency and longer duration of treatment, an active approach (e.g., visiting noncompliant patients at home), group interventions, regular medication checks and regular urine drug monitoring were more effective in reducing criminal recidivism (review in Lau, 2003). Psychopathic personality characteristics have a deep impact on the therapeutic relationship between therapists and psychopathic patients. Since psychopathic patients have a diminished capacity to form meaningful interpersonal relationships, although they can effectively mimic such a capacity, interventions relying on a close therapeutic alliance between patient and therapist are likely to fail (Serin & Preston, 2001). Forming a deeper therapeutic alliance is also impeded by prominent defense mechanisms of psychopathic offenders, such as projection, splitting, denial and externalization/acting out. Typical patterns of resistance on the side of the patient and counter-transference reactions on the therapist’s can result (Figure 27.2; Gacono et al., 2001; Meloy, 1988). Deception and an illusionary treatment alliance are serious risks in the treatment of these patients, more so as mental health workers may often be ‘benign narcissists’, nurturing their self-esteem by helping others. Manipulation by psychopathic offenders can involve and endanger the staff: in a group of psychopathic patients who malingered an insanity defense, 39 % had been sexually involved with or married to female staff (Gacono et al., 1995). To avoid splitting in teams, informed staff communication, unified team member confrontations of the patient’s behavior, the use of structure with immediate consequences for antisocial attitudes and behaviors, and respect for staff–patient boundaries are means of securing the therapeutic process with psychopathic offenders (Gacono et al., 2001). Although it should be clear that psychopathic patients need skilled, experienced therapists, due to counter-transference reactions, commodity in clinical practice and limited resources, these difficult and not very rewarding patients are often treated by younger,

476

VOLUME I: DIAGNOSIS AND TREATMENT

Resistance and transference (on the patient’s side)

r Manipulative cycling r Deceptive practice r Malignant pseudo-identification r Sadistic control

Counter-transference (on the therapist’s side) Therapeutic nihilism Illusionary treatment alliance Fear of assault or harm Denial and deception Helplessness and guilt Devaluation and loss of professional identity Hatred and wish to destroy Assumption of psychological complexity.

Figure 27.2 Typical problems of resistance, transference and counter-transference between therapists and antisocial patients (adapted from Gacono et al., 2001; Meloy, 1988)

inexperienced therapists (Gacono et al., 2001; Rauchfleisch, 1999). For any therapist qualified supervision is essential for treating psychopathic and antisocial individuals. When treating psychopathic patients, one must handle a paradox: a good (in well-defined limits), trustful and accepting relationship between therapist and patient – as a precondition in any psychotherapy – must always be balanced by a certain amount of control and distrust, taking seriously psychopathic traits and behavior. This should be discussed with the patient openly and at the beginning of any treatment. In addition to problems for the therapist, negative effects that psychopathic individuals have on other patients have to be considered. For example, therapeutic alliance and atmosphere in group psychotherapy with offenders can be threatened by the presence of only one highly psychopathic individual, even more so if he or she scintillates the typical superficial charm that conceals the detrimental aims and personality traits. Group therapy is also problematic in homogeneous groups with exclusively psychopathic offenders. Such groups not only place an almost intolerable burden on the therapists, but also run the risk that harmful alliances develop among the patients enhancing antisocial and criminal cognitions and behavior. Hemphill and Hart (2002) have pointed out that beside well-known treatment-related motivational deficits (e.g., lack of insight, distress, attachment, trust, honesty, responsibility and impulse control), psychopathic offenders also show four strengths related to therapeutic processes: 1. Status orientation: psychopathic offenders have a strong need to feel superior to other people. Therefore they are likely to experience discomfort when they are denied status or feelings of superiority, not when affection or approval is withheld. 2. Strong desire for and tolerance of novelty: it is rather easy to convince psychopathic offenders to try something new (like a new job, new peer relationship, new way of

OUTPATIENT TREATMENT AND MANAGEMENT

477

thinking, new activities), although they experience difficulties or distress in maintaining behavioral change. 3. Good interpersonal skills: besides their lack of attachment, warmth, empathy and deep relationships, many psychopathic offenders can be articulate, engaging, charming and persuasive. 4. Desire to be in control: psychopathic offenders generally have good capacities to be active and autonomous, to be in control, rather than to be passive and to take directions. 5. Treatment targets for outpatient and inpatient psychopathic offenders can be divided into those directed towards problematic personality features, and those directed to other criminal risk factors (Figure 27.3). Addressing the latter is of high importance, since psychopathy itself is difficult to treat. Although PCL-R factor 1 traits are particularly difficult to improve and PCL-R factor 2 characteristics are more relevant for criminal recidivism, attempts to alter the former symptoms should not be disregarded altogether. If empathy for previous or potential future victims is difficult to attain and may yield the risk of increasing manipulative capacities in psychopathic offenders, enhancing awareness of negative consequences of criminal behavior for the patient himself or his family could be more successful. This is also true for manipulative, deceptive and other problematic personality traits. Treatment modalities also depend on the level of antisociality or psychopathy. According to Gacono et al. (2001) for most nonsexual offending patients with antisocial traits in the mild range (PCL-R total score < 19) treatment of one to two years might be sufficient to achieve relevant changes, those in the moderate range (PCL-R score = 20–27, which parenthetically seems to be an arbitrary range) need a highly structured treatment and supervision regimen lasting two to five years, whereas for those with fully developed psychopathy (PCL-R score ≥ 30) no effective treatment is available at the moment. Motivating the unmotivated is a difficult task. Elements of motivational interviewing (Miller & Rollnick, 1991) found to be effective in various problematic behaviors such A. Modification of problematic personality traits r Lack of deep affection, attachment and empathy r Deception and manipulation r Impulsivity and instability r Lack of responsibility r Lack of discipline r Lack of insight into problematic attitudes and behavior r Deficits in learning from experience B. Modification of other criminal risk factors Housing problems Employment problems Antisocial peers Other stressful living situations Procriminal attitudes Substance abuse Comorbid major mental illnesses Comorbid paraphilias

Figure 27.3 Treatment targets in psychopathic offenders

478

VOLUME I: DIAGNOSIS AND TREATMENT

as smoking, alcohol or drug abuse – have been transferred to the treatment of criminal offenders (Mann, Ginsburg & Weekes, 2002; McMurran, 2002). According to Hemphill and Hart (2002) the following measures can enhance motivation and enable treatment success in psychopathic offenders: 1. Treatment motivation should be formally assessed, including examination of purported reasons to enter treatment, participation in and benefit derived from previous treatment programs, and current commitment to change. Offenders who are unmotivated for treatment might first participate in a group designed to facilitate motivation, enhance readiness to change, and recognize problematic personal behaviors. Only reasonably motivated individuals should be considered for more intensive therapy. 2. Criminal lifestyle has to be highlighted as low status. Psychopathic offenders should be supported to capitalize on their strengths to achieve higher status via socially legitimate means. This enhancement of prosocial behavior can include selection of jobs that demand persuasive capacities and desire for excitement and novelty seeking. 3. Psychopathic offenders should be helped to understand the rationale behind psychological intervention, by providing concrete examples. It should be kept in mind that antisocial personality disorders are associated with higher performance than verbal IQs. 4. Personal contributions of the offender to his problems have to be explored, including careful considerations of the events and behaviors (including use of alcohol and illegal drugs) that lead to antisocial and criminal behavior, that is, analysis of the ‘offense scenario’ or ‘offense cycle’ that has been frequently employed for sexual offenders (Berner et al., 2004; Berner & Briken, 2007). Psychopathic offenders may find interventions that emphasize personal control and self-management skills to be particularly empowering. 5. A positive therapeutic alliance should be established by emphasizing the therapist’s role as treatment facilitator, helping the psychopathic offenders to maximize their potential while remaining free of criminal activities. Therapists should be forthright and honest, informing and obtaining consent to consult collateral information, but avoiding an overly dominant position. 6. Self-sufficiency should be emphasized to counter the ‘parasitic lifestyle’ (PCL-R item 9) of psychopathic individuals. Again their strengths should be used to find prosocial ways to financially support themselves and to reduce problems with family, friends, relatives, social services and employers. 7. Managing antisocial behaviors should be the main focus of treatment rather than changing personality characteristics. 8. Teaching strategies to change behaviors should focus on the impulsivity (i.e., acting before thinking) of psychopathic offenders. This includes planning ahead by formulating short- and long-term goals, identifying and selecting realistic ways of achieving these goals, and continuously monitoring the success of the behavioral plan. Learning to routinely pause and reflect upon one’s own behavior is an important part in reducing impulsivity. 9. Focusing on cognitive strengths rather than on affective deficits appears more fruitful since psychopathic offenders are unlikely to benefit from programs aimed at reducing intra-psychic turmoil and developing self-esteem, empathy and conscience. 10. Strategies to maintain behavioral changes are particularly important after release into the community. The offenders have to be constantly aware that they are highly

OUTPATIENT TREATMENT AND MANAGEMENT

479

vulnerable to relapse, they must implement newly acquired skills and sustain efforts to avoid relapse. Relapse prevention plans, often applied with sexual offenders (Pithers, 1990, 1991), should be an integral part also in the treatment of psychopathic offenders. Abstaining from antisocial peers and environments is an important goal in relapse prevention. However, one has to expect that lapses and relapses are often the rule and not the exception in psychopathic offenders.

Cognitive-behavioral therapies (CBT) have been shown to improve interpersonal functioning, self-esteem, anger management and to decrease anxiety and disciplinary actions with incarcerated offenders (Morgan & Flora, 2002) as well as to reduce criminal recidivism (for meta-analyses see Landenberger & Lipsey, 2005; Pearson et al., 2002; Wilson, Bouffard & MacKenzie, 2005). Cognitive-behavioral programs were more effective in reducing recidivism than purely behavioral ones with a mean recidivism reduction of about 30 % (Pearson et al., 2002). In another meta-analysis (Wilson, Bouffard & MacKenzie, 2005) representative CBT programs showed recidivism reductions of 20–30 % compared to control groups. Larger reductions in recidivism were found in higher risk offenders, high-quality treatment implementation, and a CBT program that included anger control, interpersonal problem solving, but not victim impact or behavior modification components (Landenberger & Lipsey, 2005). One form of CBT, dialectical behavior therapy (DBT, Linehan, 1987, 1993), has been developed and shown to be effective in outpatient settings specifically for borderline personality disorder. DBT has been modified for, applied and evaluated in institutionalized forensic populations, particularly for female and juvenile offenders (Berzins & Trestman, 2004; McCann & Ball, 2000; Sly & Taylor, 2003; Washington State Institute for Public Policy, 2006). Empirical evidence for its efficacy in offenders is still not sufficient, but DBT appears to be a promising treatment modality for forensic patients and also psychopathic offenders, since: (a) they often share common features with borderline personality disorder (e.g., poor impulse control, violent aggression); (b) DBT offers a comprehensive cognitivebehavioral treatment that is highly structured with a clear behavioral hierarchy; (c) DBT is targeted towards aggressive behaviors; and (d) DBT addresses explicitly staff burnout, a common problem in offender therapy, more so with psychopathic individuals (Berzins & Trestman, 2004). In an adaptation of DBT for a forensic population, McCann and Ball (2000) added components to address the emotional insensitivity of patients with antisocial personality disorder (emotional attachment, empathy and mindfulness of consequences to others), a skills training in ‘Random Acts of Kindness’, a module on ‘Crime Review’ and ‘Myths about Interpersonal Effectiveness’. In the ‘Crime Review’ patients learn what led up to their crimes (comprehensive chain analysis of the crime using police reports), practice taking the place of their victim and develop a relapse prevention plan that includes specific DBT skills. Particular attention is directed towards violent, therapy-interfering and unit-destructive behaviors. As a consequence of deficits in conscience and super-ego functions, psychopathic patients may need long-term, even lifelong supervision, monitoring and control in delinquency relevant areas (Ashford, Sales & LeCroy, 2001; Harris & Rice, 2006). However, it should be kept in mind that psychopathic offenders fail more often to complete parole than nonpsychopathic offenders (Hart, Kropp & Hare, 1988; Salekin, Rogers & Sewell, 1996; Serin & Amos, 1995).

480

VOLUME I: DIAGNOSIS AND TREATMENT

For the aftercare of offenders with special needs, Ashford, Sales and LeCroy (2001) have emphasized a shift from treatment and rehabilitation to monitoring and control. To ascertain adequate, continuous delivery and integration of different interventions, some sort of case management should be implemented, also to avoid manipulation and playing off different agents against each other. For psychopathic offenders classical case management, serving as a sort of brokerage and on demand, is probably insufficient, and some sort of assertive community treatment (ACT), such as intensive parole supervision (IPS) and intensive aftercare programs (IAP), should be implemented to ensure that the individual will be actively approached, rather than expected to come to all appointments. Assertive community treatment has been shown to be more effective in offenders with serious mental impairments, not only to prevent hospitalization, but also to reduce contacts with the police (Ashford, Sales and LeCroy, 2001; Bond et al., 1990). However, among 200 psychiatric patients leaving jails, Solomon and Draine (1995) did not find the psychosocial and clinical outcome differences between those assigned to an ACT, to a forensic specialist case manager or to a usual community mental health center. Contrary to expectations more offenders under case management returned to jail during follow-up. This result could also be interpreted as a – positive – effect of tighter control in regard to treatment noncompliance under case management supervision leading to revocation of parole (Ashford, Sales & LeCroy, 2001). In another study offenders were randomly assigned to either intensive supervision programs (ISPs), probation, parole or prison: offenders in ISPs had slightly higher arrests (37 %) than controls (33 %), however, significant reductions in rearrests were detected for those offenders who participated in treatment programs in addition to supervision alone (Cullen, Wright & Applegate, 1996). In California and Texas, ISP participants who were in treatment showed a 10 to 20 % decrease in criminal recidivism (Petersilia & Turner, 1993, cited by Ashford, Sales & LeCroy, 2001). Again intensity and comprehensiveness of interventions is a key issue for safe management of offenders, and control alone appears to be insufficient. Rauchfleisch – from a psychoanalytical perspective – advised that the psychotherapist him- or herself should take up the function of a case manager in antisocial patients, to avoid splitting and to address directly typical antisocial tendencies of acting out internal conflicts in the external world and social environment (Rauchfleisch, 1999, pp. 106–29). However, in most programs the therapist is not the person responsible for legal supervision and probation control. But regular, closed and – in situations of threatening risk – immediate communication of all professionals involved in the treatment, management and supervision of the psychopathic individual must be secured. Part of intensive case management in the community is to ensure adequate housing, diet (see below) and employment for the offender (Ashord, Sales & LeCroy, 2001; Heilbrun & Peters, 2000; Lamb & Weinberger, 2001). Supported housing might be necessary for some psychopathic individuals (such as transitional halfway houses, long-term group residences, cooperative apartments, lodge programs, work camps, or board and care homes). However, psychopathic offenders normally do not need the degree of support as other, more mentally disturbed offender groups, and their inclination to exploit others has to be guarded against. Close cooperation with different professional groups (psychiatrists, psychologists, other mental and physical health workers, probation and parole officers, police, attorneys, judges) and other third persons (spouses, partners, relatives, employers, colleagues, friends, neighbors) is necessary. These other third persons might be contacted either by the therapist or the supervising professional or both. The limits of confidentiality by the therapists (not only to avert immediate risks for potential victims) have to be made clear from the very beginning:

OUTPATIENT TREATMENT AND MANAGEMENT

481

who will inform whom, when and about what? A well-structured treatment plan should be developed initially and made transparent to the patient and the involve third parties as necessary. According to our experience the therapist should regularly contact the probation officer personally (e.g., by telephone) to exchange information about possible problems as well as progress, if possible without revealing personal, intimate details about the patient. Written reports about serious events – e.g., undermining the maintenance of treatment or carrying risk for criminal behavior – should be sent to the parole officer and other legal supervisors. Written, informed consent about this exchange of information should be obtained from the patient in advance. However, Douglas et al. (2001) have stressed that in some offenders control that is too strict and narrowing control can lead to withdrawal, anger and eventually aggression, and overprotection may impede the development of self-responsibility. Supervision includes monitoring for abstinence or moderate consumption of alcohol and other psychotropic substances (urine, blood, hair analyses) and compliance with medication (Douglas et al., 2001). Access to firearms and other dangerous weapons should be forbidden and controlled in psychopathic (as well as other criminal offenders) to reduce the risk of serious harm. Stronger legal restrictions for access to such weapons would be an effective preventive measure to reduce the effects of violence, for example, in countries with lax regulations such as the United States. As part of relapse prevention plans, risky situations and environments, such as quarters or locations with high criminal activity in general or play and school grounds for sexual child abusers, should be identified with the psychopathic offender and avoided. Electronic monitoring (electronic ankles or chains, linked to GPS systems) are increasingly used in Europe and North America as a new mode of sanction and supervision for less dangerous offenders, but also for sexual offenders (e.g., for monitoring home arrest, Albrecht, 2006). The future could also see attempts to use these techniques to monitor dangerous and psychopathic offenders in the community, for example, monitoring adherence to parole and probation conditions (such as avoiding areas with a high criminal infrastructure, or former or potential victims’ homes). However, electronic monitoring has not yet been shown to reduce recidivism in released offenders (Bonta, Wallace-Capretta & Rooney, 2000). Public announcement of dangerous offenders, especially sexual offenders, has been propagated and implemented particularly in the United States and Great Britain. Potential gains in the prevention or early detection of criminal behavior should be balanced not only against the human rights of the offenders, but also against possible risks for the public. To date, few research studies about community notification have been conducted. Such studies have not been able to conclude that community notification reduces recidivism or enhances community safety (Association for the Treatment of Sexual Abusers, ATSA, 2005). However, public denunciation can easily result in stress, hostility and open violence (up to lynching) against the offenders – a sort of modern witch-hunt – and hereby carrying the risk for aggressive and violent reactions as well as flight into illegality and criminal underground. This critical view of public notification does not imply that in single cases specific persons at risk (e.g., previous victims, witnesses) could not be notified on the release of a dangerous offender and precautions undertaken. In the psychotherapy and management of psychopathic offenders the therapist must continuously balance the need to establishing clear and controllable rules to limit manipulation and corruption of the therapeutic process on the one hand, with the risk of overcontrolling and ‘incapacitating’ the patient and thereby driving him away on the other hand. The same tightrope walk is necessary to give the patient the support and help that he needs, and to

482

VOLUME I: DIAGNOSIS AND TREATMENT

motivate him to take responsibility for his life and accept the consequences for inadequate behavior. Be aware that the narcissistic characteristics of psychopathic individuals often lure them – and sometimes the therapist – into unrealistic ideas about their own capacities and possibilities, for example, achieving high professional positions without having adequate education. For these difficult therapeutic tasks, no clear guidelines and recipes can be given, however, longstanding therapeutic and forensic experience as well as regular supervision by experienced colleagues are helpful. An algorithm for outpatient treatment and monitoring of psychopathic offenders is outlined in Figure 27.4.

PHARMACOTHERAPY Pharmacological therapy in psychopathic individuals should principally be similar in inpatient and outpatient settings. However, pharmacological control and reduction of impulsivity and noncompliance with medication might be of particular relevance in outpatient management. For a more extensive review of the pharmacotherapy of psychopathy see Chapter 24, pp 397–416 (for further reviews: Minzenberg & Siever, 2006; Volavka, 2002; Volavka & Citrome, 2000). Also in neuropharmacology more is known and can be done about the neurotransmitter and neurohormonal functions of impulsivity and aggression (related to PCL-R factor 2) than about the affective-interpersonal characteristics of psychopathy (PCL-R factor 1). As a general rule psychopharmacology should target specific symptoms rather than diagnostic entities. Selective serotonin-reuptake inhibitors (e.g., sertraline, fluoxetine, citalopram) are not only effective in reducing irritability, impulsivity, aggression and antisocial behavior (Minzenberg & Siever, 2006), but have also been shown to normalize recognition of facial expressions of fear (Harmer et al., 2003) and to improve sexual symptoms in patients with paraphilias and sexual compulsivity/addiction (Berner et al., 2004; Hill et al., 2003). Since the 1970s lithium has been shown to be effective in reducing violence in nonpsychotic, chronic impulsive aggressive offenders as well as children and adolescents (Minzenberg & Siever, 2006; Sheard et al., 1976). Other mood stabilizers, valproate and phenytoin, have been found to be effective in decreasing irritability and aggression in Cluster B personality disorders (Hollander et al., 2003; Lindenmayer & Kotsaftis, 2000; Minzenberg & Siever, 2006), whereas evidence of anti-aggressive effects of carbamazepine is weaker (Volavka, 2002; Volavka & Citrome, 2000). Increased dopamine function is associated with aggressive, impulsive and noveltyseeking behavior as well as PCL-R factor 2 scores. Dopamine antagonists, typical (especially haloperidol) as well as atypical antipsychotics (especially clozapine, risperidone, quetiapine), have been shown to reduce hostility and aggressive behavior in many psychiatric disorders, particularly in psychoses (Briken et al., 2002; Minzenberg & Siever, 2006; Volavka, 2002; Volavka & Citrome, 2000). However, antipsychotics have rarely been evaluated for antisocial disorders: in one randomized, double-blind placebo-controlled study, risperidone improved aggression in boys with conduct disorder (Findling et al., 2000). Since patients with attention deficit hyperactivity disorders (ADHD) are more likely to develop antisocial personality disorder, those adult psychopathic patients with comorbid ADHD should be treated with psychostimulants (Habermeyer & Herpertz, 2006); the risk of substance abuse and dependence has to be considered.

OUTPATIENT TREATMENT AND MANAGEMENT

483

1. Form a therapeutic alliance between therapist and patient/offender. Highlight advantages and disadvantages for the patient in participating treatment. Express self-confident authority without being too dominant. Be vigilant for idealizing as well as negative counter-transferences and burnout! 2. Assess treatment motivation (intrinsic and extrinsic). ↓ 3. Optional: unmotivated offenders might first need to participate in a group to enhance motivation (according to principles of motivational interviewing, Miller & Rollnick, 1991). ↓ 4. Explain rational of psychotherapeutic intervention to the patient. 5. Make clear the formal setting of treatment and monitoring. Set rules for communication and investigation with third parties (transparency). 6. Formulate rules and possible, realistic sanctions and consequences for breaking these rules by the offender. ↓ 7. Treatment is generally multimodal and should be well structured. 8. Identify main treatment and monitoring targets, focusing on changing antisocial behavior (including impulsivity) rather than personality characteristics, and on cognitive strengths than on affective deficits. 9. Differentiate between short- and long-term goals. Integrity of the therapeutic setting, avoidance of criminal behavior and antecedents (especially alcohol and drug abuse) need to have top priority. 10. Support responsibility and self-sufficiency of the offender, without supporting unrealistic expectations and plans due to the offender’s narcissistic traits. 11. Treatment techniques are mainly cognitive-behavioral therapies (including modified dialectic behavioral treatment). Psychodynamic oriented programs need to focus on super-ego deficits, guard external reality, and address primitive defense mechanisms such as splitting, projection and denial. 12. Analyses of offence scenario/offense cycle and relapse prevention plans should also be part of outpatient therapy. ↓ 13. If impulsivity (PCL-R factor 1) is a major problem, consider psychopharmacological treatment (SSRI, mood stabilizers, neuroleptics). 14. Watch and explain the need for balanced diet, including omega-6 and omega-3 essential fatty acids, consider nutritional supplements. 15. Identify need for and implement supplementary treatment: – for substance disorder: counseling or therapy, self-help group; control of abstinence by regular monitoring (blood/urine/breath tests); consider anticraving medication. In case of relapse: do not hesitate to start inpatient detoxification and in- or outpatient rehabilitation programs. – for ADHD: consider psychostimulant medication – for paraphilias or sexual offenders: consider SSRI or antiandrogen medication and special treatment programs. – if other comorbid disorders are present: treatment as necessary, including psychopharmacotherapy. ↓ 16. Psychotherapy should be supplemented by closed supervision and monitoring for antisocial behavior and antecedents. Supervision and monitoring is often not executed by the therapist, but a probation or parole officer. Regular exchange of information between these professional groups must be secured. 17. The therapist and/or supervisor should regularly keep in contact with relatives, spouses, employers or other relevant third persons – always according to informed consent with the patient/offender. 18. The therapist’s and supervisor’s approach to the patient/offender must be active, especially if risk situations develop. 19. Monitoring should include continuous risk assessment, particularly for dynamic risk factors. ↓ 20. Hospitalization should be implemented in case of acute symptoms with immediate risk of harm to self and others (acute suicidality, severe depression, life-threatening acute intoxication, acute violence against others, uncontrollable paraphilic impulses, acute psychotic symptoms or other dangerous destabilizing crises) and for detoxification in substance abuse or dependency.

Figure 27.4 Algorithm for outpatient treatment and monitoring of psychopathic offenders

484

VOLUME I: DIAGNOSIS AND TREATMENT

Although benzodiazepines are commonly used in the short-term management of aggression, the effectiveness of their long-term application has not been demonstrated and carries the risk of abuse and dependency as well as paradoxical, aggressive reactions (Volavka & Citrome, 2000). Therefore, benzodiazepines should be avoided in the outpatient treatment of psychopathic patients. Also for beta-adrenergic blocking agents (e.g., propanolol, nadolol) there is only limited evidence for positive effect in aggressive patients with schizophrenia and organic brain disease (Volvaka, 2002; Volavka & Citrome, 2000). Testosterone has been clearly linked to aggressive behavior, hostility, sensation seeking and extraversion in nonclinical samples; to aggression, violence, PCL-R factor 2 scores and even criminal recidivism in general forensic populations (Minzenberg & Siever, 2006), as well as to violent sexual offenses (Briken, Hill & Berner, 2003; Giotakos et al., 2003; Hill et al., 2003). In one study in a community sample of adult male plasma, estradiol was related to the capacity to negotiate emotionally, whereas plasma testosterone was associated with physical assault and injury scales, suggesting that estradiol might mitigate adverse interpersonal effect of testosterone (Eriksson et al., 2003). Nevertheless, antiandrogen medications have been applied and evaluated almost exclusively in sexual offenders (see below). Lower cholesterol levels are associated with increased risks of nonillness deaths (due to suicide, violence or accident) and with aggression, violence and antisocial personality disorder. These effects of low serum cholesterol appear to be mediated by decreased central serotonergic function (Minzenberg & Siever, 2006). The results of low cholesterol might also be linked to the functions of essential fatty acids. Omega-6 and omega-3 essential fatty acids have been found to be deficient among violent offenders (Corrigan et al., 1994). In a randomized double-blind, placebo-controlled study on incarcerated offenders nutritional supplementation of vitamins, minerals and omega-6/omega-3 essential fatty acids led to a significant 37 % decrease in serious intramural incidents (including violence) in the index group compared to a statistically insignificant decrease of 10 % in the placebo group (Gesch et al., 2002). Dietary interventions including education and nutritional supplements should be considered in antisocial behaviors and might be even more important in offenders in the community where generally no attention is paid to their diet. An early study conducted in the community claimed that dietary education proved more effective at reducing recidivism than conventional probation programs (Schauss, 1978). Such interventions might be easier to implement in the outpatient treatment of psychopathic offenders, since they do not have negative side effects and are likely to be perceived as beneficial care and improvement of quality of life rather than as control and restriction. For the outpatient treatment of psychopathic offenders, monitoring compliance with medication is a key issue and is often complicated by substance abuse (Volvaka, 2000). Intake of medication under direct supervision, for example, by a ambulatory health worker, intramuscular or subcutaneous application of depot medications (available for risperidone and antiandrogen medications) and regular monitoring of blood levels can be helpful to improve compliance.

SUBSTANCE ABUSE High comorbidity rates between antisocial personality disorder or psychopathy and substance abuse and dependence – regarding alcohol as well as illegal drugs – are a

OUTPATIENT TREATMENT AND MANAGEMENT

485

well-established fact and might be explained by some common etiological pathways (weak behavioral inhibition system, affective/cognitive dysregulation, externalizing vulnerability factor) and genetic influences (Krueger et al., 2002; Taylor & Lang, 2006; see Chapter 9, pp 149–169). In forensic samples substance abuse (especially illegal drug abuse) is more closely related to the impulsive, antisocial lifestyle (PCL-R factor 2) than to the affectiveinterpersonal component (PCL-R factor 1), and higher correlations are found for psychopathy with illegal drug abuse than with alcoholism (Hemphill, Hart & Hare, 1994; Taylor & Lang, 2006). The comorbidity of substance abuse and psychopathy has profound impact on the course of both disorders, treatment outcome and supervision. Psychopathic offenders with substance abuse recidivated more often after release than those without such comorbid disorders (Taylor & Lang, 2006). Substance abuse was an important predictor for lack of improvement in the long-term follow-up study by Black et al. (1996): None of the men with APD who were alcoholic at the time of the follow-up investigation had shown remission of their personality disorder. Specific strategies to treat this difficult comorbidity have been described in detail elsewhere (McNeece, Springer & Arnold, 2001; Wanberg & Milkman, 1998). Brain damage and mental deficits as sequels of long-standing alcohol or drug abuse have to be taken into account also in outpatient management of psychopathic offenders. Motivational interviewing can be applied to enhance willingness to change substance abuse as well as antisocial behavior, as has been discussed earlier. Premature termination of inpatient as well as outpatient substance abuse treatment is a special problem in psychopathic subjects. Incentives for meeting clinical goals can be valuable in outpatient treatment of psychopathic offenders: for example, a reduction in the required number of community service hours or the required number of visits with the probation officer can be offered, if a client is providing clean urine samples and is compliant with treatment (Rutherford, Alterman & Cacciola, 2000). Also teaching alternative ways to be stimulated is an important means to reduce substance abuse in this patient group. Information about and encouragement of safer sex and safer use of syringes, if abstinence from intravenous drug use cannot be achieved, are other important means to reduce risk for the psychopathic individual as well as for others. Some authors have favored outpatient treatment for offenders with substance abuse rather than inpatient treatment, because of lower cost, direct transfer of behavioral changes into the normal environment, as well as less stigma and disruption of normal life. Community treatment of psychopathic individuals include participation in self-help groups (such as Alcoholics Anonymous or Narcotics Anonymous), however, the risk of manipulating and negatively influencing other group members or the group as a whole must always be kept in mind. Of course in cases of active substance abuse or dependency early and firm interventions, such as inpatient detoxification or in- or outpatient rehabilitations programs have to be considered. Effective medications in reducing substance abuse, craving or negative consequences of substance abuse include opioidergic substances (methadone, levo-alpha-acetylmethadol, naltrexone, buprenorphine), disulfiram and acamprosate, but no specific findings in relation to antisocial personality disorders or psychopathy have been published (McNeece, Springer & Arnold, 2001; Minzenberg & Siever, 2006). Also acupuncture has been proposed as useful treatment for substance abuse in offenders (McNeece, Springer & Arnold, 2001). Whether harm reduction related to substance abuse is a useful goal in psychopathic offenders remains an open question; given psychopaths’ tendencies to use plausible excuses to justify their problematic behavior, harm reduction strategies carry the risk of offering

486

VOLUME I: DIAGNOSIS AND TREATMENT

welcomed arguments for not trying to abstain or reduce substance abuse. Monitoring for abstinence or moderate consumption of alcohol and other psychotropic substances (urine, blood, hair analyses of alcohol and/or drugs, liver enzymes, mean corpuscular volume (MCV), carbohydrate deficient transferring (CDT)) and compliance with medication are important, not only to reduce relapse rates, but also to reduce criminal recidivism (Douglas et al., 2001; McNeece, Springer & Arnold, 2001).

SEXUAL OFFENDERS The outpatient treatment of sexual offenders with comorbid psychopathy is a particularly difficult field. Again empirical data are scarce. As mentioned psychopathy is related to sexual recidivism after release from prison or forensic hospitals into the community (see Barbaree, 2005; Hanson & Bussi`ere, 1998; Hanson & Morton-Bourgon, 2005; Hare et al., 2000; Hemphill, Hare & Wong,1998; Knight & Guay, 2006; Looman et al., 2005; Seto & Barbaree, 1999; Seto & Lalumi`ere, 2000). The association between psychopathy and sexual offending has been explained by the disinhibitory tendencies and empathy deficits in psychopathic individuals as well as by evolutionary models of sexual violence (for a review see Knight & Guay, 2006). Rapists generally score higher than child molesters on the PCL-R (Seto & Barbaree, 1999; Seto & Lalumi`ere, 2000). It is evident that the combination of sexual deviance and antisociality or psychopathy increases also the risk for sexual coercion and sexual recidivism (Hill et al., 2006; Rice & Harris, 1997; Seto & Lalumi`ere, 2000). Decisions on which individual sexual offender should be released into the community should be based on thorough risk assessment procedures. The combination of a current paraphilia (particularly pedophila or sexual sadism) and high scores in the PCL-R (> 25) should be regarded as a warning signal, that should not be overlooked, particularly in offenders with high capacities of persuasiveness and superficial charm (remember the above-cited study by Seto & Barbaree, 1999). At least particular precautions regarding post-release treatment and supervision have to be instituted. Regarding treatment modalities for sexual offenders with psychopathy, again empirical intervention studies are missing for outpatient as well as institutionalized settings. However, treatment of sexual offenders in general has been shown to be effective (Berner et al., 2006; Hall, 1995; Hanson & Bussi`ere, 1998; Hill, Briken & Kraus, 2004; L¨osel & Schmucker, 2005). Effect sizes for reducing recidivism rates were higher for outpatient treatment (.30) than for treatment in prisons or forensic hospitals (.10), however this effect is likely due to selection bias with the less dangerous offenders being treated in ambulatory settings (Hall, 1995). In meta-analysis behavioral and cognitive-behavioral therapies have been shown to be more effective than insight-oriented programs (L¨osel & Schmucker, 2005). However, looking more closely at the recent developments in cognitive-behavioral therapies of sexual offenders, one has to acknowledge a tacit integration of psychodynamic concepts and techniques, that is, emphasis on attachment, early childhood experiences, therapist–patient alliance, transference and counter-transference processes, as well as group interactions (Berner & Briken, 2005; Berner, Briken & Hill, 2006; Berner et al., 2004; Marshall et al., 1999). Analyzing the offense cycle or crime scenario and developing relapse prevention are important components of most recent cognitive-behavioral as well as psychodynamic programs. Although group settings are preferred – not only for economical reasons – in most

OUTPATIENT TREATMENT AND MANAGEMENT

487

institutionalized as well as ambulatory settings, a caveat applies to group psychotherapy with psychopathic sexual offenders. The disruptive and manipulative behavior of psychopathic offenders in group psychotherapy also has to be observed when working with sexual offenders. If a highly psychopathic sexual offender can be effectively treated at all in an outpatient facility, this should probably be done in individual treatment by an experienced therapist within a larger institution, and not in private practice. In general, outpatient treatment should follow an inpatient treatment program and secure the maintenance and control of previous treatment progresses. Monitoring should again focus also on dynamic risk factors for reoffending, such as unrealistic plans with impulsive changes of employment, housing or partner, abuse of psychotropic substances or noncompliance with medication. Pharmacological treatment plays an increasingly important role in sexual offenders (for reviews see Berner, Hill & Briken, 2006; Briken, Hill & Berner, 2003; Bradford, 2001; Hill et al., 2003). Selective serotonin reuptake inhibitors (SSRIs) have been shown to reduce sexual fantasies, desire, masturbation and sexually deviant behavior in patients with various paraphilias. In one controlled study the combination of SSRI with psychotherapy was more effective than psychotherapy alone (Bradford & Greenberg, 1996). However, these studies often relied on rather small samples, short follow-up periods; they were not placebo-controlled or double-blind and did not assess criminal recidivism as an outcome variable. SSRIs show relatively few and mild side effects and are often well tolerated by sexual offenders even on a long-term basis. Antiandrogen treatments are used particularly in dangerous sexual offenders with sexual deviance and/or psychopathic traits. Surgical castration has been shown to substantially reduce recidivism rates of sex offenders (Hansen, 1991; Langel¨uddeke, 1963; St¨urup, 1972; Wille & Beier, 1989). Since surgical castration is irreversible and poses many ethical problems, it has been restricted to individual cases that are severe, and otherwise treatment resistant, after trials of pharmacological antihormonal treatment with cyproterone acetat (CPA) and medroxyprogestoerone acetate (MPA) that have been associated with reduced criminal recidivism. Controlled, double-blind studies showed reduction of sexual desire, arousability and behavior in paraphilic patients and sex offenders (Bradford & Pawlak, 1993). CPA and MPA can be given orally or as intramuscular depot injections. Luteinizing hormone-releasing hormone agonists (LHRHs) that are administered intramuscularly or subcutaneously have been shown to be effective in the treatment of paraphilic offenders, also in outpatient settings, although placebo-controlled, double-blind studies are missing and difficult to conduct in forensic samples (Briken, Nika & Berner, 2001; R¨osler & Witztum, 1998; for a review see Briken, Hill & Berner, 2003). Hansen and Lykke-Olesen (1997) treated recidivistic dangerous sex offenders – all showed dissocial personality structures and some sadistic sexual fantasies – with a combination of triptorelin and CPA (both administered by depot). They used the combination with CPA to block the androgen receptors, thus ensuring against illegal procurement of anabolic steroids. The authors reported that offenders were often able to talk about their sadistic fantasies after they disappeared in the course of treatment, confirming our experiences in clinical practice. However, all antiandrogen treatments carry the risk of severe side effects, such as thromboembolism, osteoporosis, diabetes, hypertension and adipositas. Liver dysfunctions are mainly seen in CPA and MPA, renal dysfunctions and the very rare phenomenon of pituitary apoplexia only in LHRH agonists, whereas surgical castration (orchiectomy) is supposed to carry a smaller risk for diabetes and gall stones than MPA. As far as possible, antihormonal treatment should be

488

VOLUME I: DIAGNOSIS AND TREATMENT

started about 6 to 12 months before release from prison or forensic hospital to guard against and treat possible negative psychological reactions, for example, narcissistic crises with depression, frustration, anger, including attempts to counterbalance destabilized male identity (‘chemical castration’) with aggressive sexual behavior. When antihormonal medication is initiated during outpatient treatment, a safe environment should be available, if possible in a general psychiatric hospital. Combination of SSRIs with antiandrogen treatment has also been proposed. A preliminary algorithm for the pharmacological treatment of paraphilias and sexual offenders (Berner et al., 2004) advised SSRI treatment as a first line for mild and less dangerous cases (hands-off offenses), particularly if additional symptoms like anxiety, social phobia, depression, severe feelings of guilt, obsessions and compulsions are present. If there is insufficient improvement and a moderate to high risk for ‘hands-on’ offenses (e.g., in impulsive, aggressive and psychopathic patients, pedophila and sexual sadism), CPA or MPA should be given. Taking into account the as yet relatively small data base and short clinical experience with LHRH agonists in paraphilic patients as well as the lack of an official approval for these indications by the health authorities, CPA treatment (or MPA in the USA) still has to be considered as the first line of antihormonal medication. If (a) pre-existent hepatocellular damage is seen as a contraindication for CPA or MPA treatment, (b) liver dysfunction develops during treatment, or (c) CPA/MPA does not improve symptoms, LHRH agonist should be considered. Intramuscular application of antiandrogen medication should be used, especially in cases with unreliable compliance in medication, that is, outpatient treatment of psychopathic offenders. Some LHRH agonists can be administered subcutaneously every three months, an important advantage over CPA (intramuscular injections every 10–14 days) especially in long-term treatment. The combination of an antiandrogen agent with an SSRI should be considered in patients with insufficient improvement from CPA, MPA or an LHRH agonist alone. In psychopathic patients with unreliable treatment compliance, one has to be vigilant for the possibility that the patient could attempt to counter the effects of the antihormonal treatment (e.g., by secret self-application of testosterone). Even if monitored by regular blood tests, this form of noncompliance may still pose a problem for antihormonal treatment. A combination of LHRH agonists and CPA could be a possible option for these patients (Hansen & Lykke-Olesen, 1997).

HOSPITALIZATION As for other outpatients hospitalization should be considered for psychopathic patients, if acute symptoms with risk of harm to self and others develop, such as acute suicidality, severe depression (which is rather rare in psychopathy), life-threatening acute intoxication, acute or threatened violence against others, uncontrollable paraphilic impulses in comorbid paraphilias, acute psychotic symptoms or in individual cases as a preventive measure in other high-risk situations for severe criminal recidivism (e.g., destabilization due to loss of housing, partner, employment). Of course, involuntary hospitalization must follow the jurisdictional, regulatory laws. In addition hospitalization is advised for the initiation of medications with severe side effects (e.g., antiandrogens) and for safe detoxification in

OUTPATIENT TREATMENT AND MANAGEMENT

489

substance dependence. Duration of hospitalization should be kept to a minimum to prevent disruptive and manipulative behavior on the ward.

CONCLUSIONS For outpatient settings only few empirical data are available on diagnostic features, risk assessment and the effects of psychotherapeutic, pharmacological and sociotherapeutic interventions in psychopathic and antisocial individuals. On the basis of this limited evidence and recommendations by experienced practitioners, a few basic guidelines can be formulated: 1. Psychopathic individuals with high PCL-R factor 1 scores are more difficult to treat than those with high PCL-R factor 2 scores. 2. Structured risk assessment should be performed at the beginning and at regular intervals. 3. Be familiar with psychopathic symptoms and be vigilant for the manipulative, deceitful, charming and persuasive characteristics of psychopathy! 4. Treatment should be carried out in an institutional ambulatory setting (not in private practice because of security reasons) easy access to a variety of other services, including emergency and inpatient treatment, and supervision for therapists. 5. Treatment should be multimodal, often combining medication with psychotherapy. 6. Psychotherapy should be direct, well-structured and transparent. A respectful therapeutic alliance should be developed. The therapist should be experienced and express a self-confident authority without being overbearing. Be vigilant for negative and idealizing counter-transferences, as well as burnout. Do not get too involved, but do not give up hope, either! 7. An active approach is needed (including visits at home), particularly in noncompliant clients. 8. Psychotherapy should be behavior-oriented and risk tailored, address criminogenic targets and include detailed offense-cycle analysis and relapse prevention. 9. Treatment response and outcome should be monitored on the basis of observable behavior, not just of self-reports and subjective impression. 10. The most frequently used and evaluated medications include atypical antipsychotics, SSRIs, mood stabilizers and (in sexual offenders) antiandrogens. Depot medications and plasma level monitoring should be applied to ensure compliance. 11. Substance abuse has to be treated and monitored thoroughly, as well as paraphilias and other comorbid disorders. 12. Close and long-term supervision, controlling and monitoring is necessary, including monitoring medication, monitoring for alcohol and drug consumption, access to firearms and other dangerous weapons as well as avoidance of criminogenic environments. 13. Collaboration with and collateral information from other professionals, relatives, employers and friends is crucial. 14. Treatment and supervision of psychopathic patients is not a stable endeavor, but constantly up and down: crises requiring intensive treatment are followed by more stable phases with fewer strains on the therapist.

490

VOLUME I: DIAGNOSIS AND TREATMENT

REFERENCES American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders (4th edition, text revision). Washington, DC: American Psychiatric Association. Andrews, D.A. & Bonta, J.L. (1995). LSI-R: The Level of Service Inventory – Revised. Niagara Falls, Toronto: Multi-Health Systems. Ashford, J.B., Sales, B.D. & LeCroy, C.W. (2001). Aftercare and recidivism prevention. In J.B. Ashford, B.D. Sales & W.H. Reid (eds.), Treating Adult and Juvenile Offenders with Special Needs (pp. 373–400). Washington, DC: American Psychological Association. Association for the Treatment of Sexual Abusers (ATSA) (2005). The Registration and Community Notification of Adult Sexual Offenders. http://www.atsa.com/ppnotify.html. Barbaree, H.E. (2005) Psychopathy, treatment behavior, and recidivism. Journal of Interpersonal Violence, 9, 1115–31. ¨ Berner, W. & Briken, P. (2007). St¨orung der Sexualpr¨aferenz (Paraphilie) – Diagnostik, Atiologie, Epidemiologie, Behandlung und pr¨aventive Aspekte. Bundesgesundheitsblatt, 50, 33–43. Berzins L.G. & Trestman, R.L. (2004). The development and implementation of dialectical behavior therapy in forensic settings. International Journal of Forensic Mental Health, 3, 93–103. Black, D.W., Baumgard C.H., Bell, S.E. & Kao, C. (1996). Death rates in 71 men with antisocial personality disorder: a comparison with general population mortality. Psychosomatics, 37, 131–6. Blair, R.J.R. (2006). Subcortical brain systems in psychopathy: the amygdala and associated structures. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 296–312). New York: Guilford Press. Boer, D.P., Hart, S.D., Kropp, P.R. & Webster, C.D. (1997). Manual for the Sexual Violence Risk. Burnaby, Canada: Simon Fraser University. Bond, G.R., Witheridge, T.F., Fincin, J. et al. (1990). Assertive community treatment for frequent users of psychiatric hospitals in a large city: a controlled study. American Journal of Community Psychology, 18, 865–91. Bonta, J., Wallace-Capretta, S. & Rooney, J. (2000). A quasi-experimental evaluation of an intensive rehabilitation supervision program. Criminal Justice and Behavior, 27, 312–29. Borduin, C.M., Mann, B.J., Cone, L.T. et al. (1995). Multisystemic treatment of serious juvenile offenders: long-term prevention of criminality and violence. Journal of Consulting and Clinical Psychology, 63, 569–78. Borduin, C.M., Schaeffer, C.M., Ronis, M. & Scott, T. (2003). Multisystemic treatment of serious behaviour in adolescents. In C.A. Essau (ed.), Conduct and Oppositional Defiant Disorders: Epidemiology, Risk Factors and Treatment (pp. 299–318). Mahwah, NJ: Erlbaum. Bradford, J.M.W. (2001). The neurobiology, neuropharmacology, and pharmacological treatment of the paraphilias and compulsive sexual behavior. Canadian Journal of Psychiatry, 46, 26–33. Bradford, J.M.W. & Greenberg, D.M. (1996). Pharmacological treatment of deviant sexual behavior. Annual Review of Sex Research, 7, 283–306. Bradford, J.M.W. & Pawlak, A. (1993). Double-blind placebo crossover study of cyproterone acetate in the treatment of the paraphilias. Archives of Sexual Behavior, 22, 383–402. Briken, P., Hill, A. & Berner, W. (2003). Pharmacotherapy of paraphilias with long-acting agonists of luteinizing hormone-releasing hormone: a systematic review. Journal of Clinical Psychiatry, 64, 890–7. Briken, P., Nika, E. & Berner, W. (2001). Treatment of paraphilia with luteinizing hormone-releasing. hormone agonists. Journal of Sex and Marital Therapy, 27, 45–55. Briken, P., Nika, E., Krausz, M. & Naber, D. (2002). Atypische Neuroleptika in der Behandlung von Aggressivit¨at und Feindseligkeit bei schizophrenen Patienten. Fortschritte der Neurologie – Psychiatrie, 70, 139–44. Butcher, J.N., Graham, J.R., Williams, C.L. & Ben-Porath, Y. (1990). Development and Use of the MMPI-2 Content Scales. Minnneapolis: University of Minnesota Press. Cleckley, H. (1941). The Mask of Sanity. St. Louis, MO: Mosby. Corrigan, F.M., Gray, R., Strathdee, A. et al. (1994). Fatty acid analysis of blood from violent offenders. Journal of Forensic Psychiatry, 5, 83–92.

OUTPATIENT TREATMENT AND MANAGEMENT

491

Cullen, F.T., Wright, J.P. & Applegate, B.K. (1996). Control in the community: the limits of reform. In A.T. Harland (ed.) Choosing Correctional Options That Work: Defining the Demand and Evaluating the Supply (pp. 69–116). Thousand Oaks, CA: Sage. Douglas, K., Vincent, G.M. & Edens, J. (2006). Risk for criminal recidivism: the role of psychopathy. In C. Patrick (ed.), Handbook of Psychopathy (pp. 533–54). New York: Guilford Press. Douglas, K.S., Webster, C.D., Hart, S.D. et al. (2001). HCR-20 – Violence Risk Management Companion Guide. Barnaby: Simon Fraser University, Mental Health, Law, and Policy Institute. Eriksson, C.J.P., Pahlaen, B., Ssarkola, T. & Seppa, K. (2003). Oestradiol and human male alcoholrelated aggression. Alcohol and Alcoholism, 38, 589–96. Exner, J. (1986). The Rorschach: A Comprehensive System: Volume 1. Basic Foundations (2nd edition). New York: John Wiley & Sons, Inc. Exner, J. (1991). The Rorschach: A Comprehensive System: Volume 2. Interpretation (2nd edition). New York: John Wiley & Sons, Inc. Findling, R.L., McNamara, N.K., Branicky, L.A. et al. (2000). A double-blind pilot study of risperidone in the treatment of conduct disorder. Journal of the Academy of Child and Adolescent Psychiatry, 39, 509–16. First, M.B., Spitzer, R.L., Gibbon, M. et al. (1997). User’s Guide for the Structured Clinical Interview for DSM-IV Axis II Personality Disorders: SCID-II. Washington, DC: American Psychiatric Association. Gacono, C.B., Meloy, J.R. & Heaven, T. (1994). The Rorschach Assessement of Aggressive and Psychopathic Personalities. Hillsdale, NJ: Erlbaum. Gacono, C.B., Meloy, J.R., Sheppard, K. et al. (1995). A clinical investigation of malingering and psychopathy in hospitalized insanity acquittes. Bulletin of the American Academy of Psychiatry and the Law, 23, 387–97. Gacono, C.B., Nieberding, R.J., Owen, A. et al. (2001). Treating conduct disorder, antisocial, and psychopathic personalities. In J.B. Ashford, B.D. Sales & W.H. Reid (eds.), Treating Adult and Juvenile Offenders with Special Needs (pp. 99–129). Washington, DC: American Psychological Association. Gendreau, P., Goggin, C. & Smith, P. (2002). Is the PCL-R really the ‘unparalled’ measure of offender risk? A lesson in knowledge cumulation. Criminal Justice and Behavior, 29, 397–426. Gendreau, P., Little, T. & Goggin, C. (1996). A meta-analysis of the predictors of adult offender recidivism: what works! Criminology, 34, 575–07. Gesch, C.B., Hammond, S.M., Hampson, S.E. et al. (2002). Influence of supplementary vitamins, minerals and essential fatty acids on the antisocial behaviour of young adult prisoners. British Journal of Psychiatry, 181, 22–8. Giotakos, O., Markianos, M., Vaidakis, N. & Christodoulou, G.N. (2003). Aggression, impulsivity, plasma sex hormones, and biogenic amine turnover in a forensic population of rapists. Journal of Sex and Marital Therapy, 29, 215–25. Habermeyer, E. & Herpertz, S.C. (2006). Dissoziale Pers¨onlichkeitsst¨orung. Der Nervenarzt, 77, 605–15. Hall, G.C.N. (1995). Sexual offender recidivism revisited. A meta-analysis of recent treatment studies. Journal of Consulting and Clinical Psychology, 63, 802–9. Hansen, H. & Lykke-Olesen, L. (1997). Treatment of dangerous sexual offenders in Denmark. Journal of Forensic Psychiatry, 8, 195–9. Hanson, R.K. & Bussi`ere, M.T. (1998). Predicting relapse: a meta-analysis of sexual offender recidivism studies. Journal of Consulting and Clinical Psychology, 66, 348–62. Hanson, R.K. & Harris, A.J.R. (2000). Where should we intervene? Dynamic predictors of sexual offense recidivism. Criminal Justice and Behavior, 27, 6–35. Hanson, R.K. & Morton-Bourgon, K.E. (2005). The characteristics of persistent sexual offenders: A meta-analysis of recidivism studies. Journal of Consulting and Clinical Psychology, 73, 1154–63. Hanson, R.K. & Thornton, D. (1999). Static 99: Improving Actuarial Risk Assessment for Sex Offenders. Ottawa: Department of the Solicitor General of Canada. Hanson, R.K. & Thornton, D. (2003). Notes on the Development of Static-2002. Ottawa: Department of the Solicitor General of Canada.

492

VOLUME I: DIAGNOSIS AND TREATMENT

Hare, R.D. (1991). The Hare Psychopathy Checklist-Revised. Toronto: Multi-Health Systems. Hare, R.D., Clark, D., Grann, M. & Thornton, D. (2000). Psychopathy and the predictive validity of the PCL-R: an international perspective. Behavioral Science and the Law, 18, 623–45. Harmer, C.J., Bhagwagar, Z., Perret, D.I. et al. (2003). Acute SSRI administration affects the processing of social cues in healthy volunteers. Neuropsychopharmacology, 28, 148–52. Harpur, T.J. & Hare, R.D. (1994). Assessment of psychopathy as a function of age. Journal of Abnormal Psychology, 103, 604–9. Harris, G.T., Rice, M.E. & Quinsey, V.L. (1993). Violent recidivism of mentally disordered offenders: The development of a statistical prediction instrument. Criminal Justice and Behavior, 20, 315–35. Hart, S.D., Kropp, P.R. & Hare, R.D. (1988). Performance of male psychopaths following conditional release from prison. Journal of Consulting and Clinical Psychology, 56, 227–32. Heilbrun, K. & Peters, L. (2000). The efficacy and effectiveness of community treatment programmes in preventing crime and violence among those with severe mental illness in the community. In S. Hodgins (ed.), Violence Among the Mentally III (pp. 341–57). Dordrecht: Kluwer. Hemphill, J.F., Hare, R.D. & Wong, S. (1998). Psychopathy and recidivism: a review. Legal and Criminological Psychology, 3, 141–72. Hemphill, J.F. & Hart, S.D. (2002). Motivating the unmotivated: psychopathy, treatment, and change. In M. McMurran (ed.), Motivating Offenders to Change (pp. 193–219). Chichester: John Wiley & Sons, Ltd. Hemphill, J.F., Hart, S.D. & Hare, R.D. (1994). Psychopathy and substance use. Journal of Personality Disorders, 8, 169–80. Hill, A., Briken, P., Kraus, C. et al. (2003). Differential pharmacological treatment of paraphilias and sex offenders. International Journal of Offender Therapy and Comparative Criminology, 47, 407–21. Hobson, J., Shine, J. & Roberts, R. (2000). How do psychopaths behave in a prison therapeutic community? Psychology, Crime and the Law, 6, 139–54. Hollander, E., Tracy, K.A., Swann, A.C. et al. (2003). Divalproex in the treatment of impulsive aggression: efficacy in cluster B personality disorders. Neuropsychopharmacology, 28, 1186–97. Huchzermeier, C. & Aldenhoff, J.B. (2002). Zum gegenw¨artigen Stand der Forensischen Psychotherapie in Deutschland (Current standing of forensic psychotherapy in Germany). Fortschritte der Neurologie, Psychiatrie, 70(7), 374–84. Knecht, G., Schanda, H., Berner, W. et al. (1996). Outpatient treatment of mentally disordered offenders in Austria. International Journal of Law and Psychiatry, 19, 87–91. Knight, R.A. & Guay, J.P. (2006). The role of psychopathy in sexual offenders against women. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 521–32). New York: Guilford Press. Krueger, R.F., Hicks, B., Patrick, C.J. et al. (2002). Etiologic connections among substance dependence, antisocial behavior, and personality: modelling the externalizing spectrum. Journal of Abnormal Psychology, 111, 411–24. Lamb, H.R. & Weinberger, L.E. (2001). Adult offenders and community settings: Some case examples. In J.B. Ashford, B.D. Sales & W.H. Reid (eds.), Treating Adult and Juvenile Offenders with Special Needs (pp. 465–78). Washington, DC: American Psychological Association. New Directions for Mental Health Services (pp. 29–49). San Francisco: Jossey-Bass. Landenberger, N.A. & Lipsey, M.W. (2005). The positive effects of cognitive-behavioral programs for offenders: a meta-analysis of factors associated with effective treatment. Journal of Experimental Criminology, 1, 451–76. Lau, S. (2003). Wirkt ambulante Kriminaltherapie? Psychiatrische Praxis, 30, 119–26. Levenson, M.R., Kiehl, K.A. & Fitzpatrick, C.M. (1995). Assessing psychopathic attributes in a noninstitutionalized population. Journal of Personality and Social Psychology, 68, 151–8. Lilienfeld, S.O. & Andrews, B.P. (1996). Development and preliminary validation of a self report measure of psychopathic personality traits in noncriminal populations. Journal of Personality Assessment, 66, 488–524. Lilienfeld, S.O., & Fowler, K.A. (2006). The self-report assessment of psychopathy: promises, problems, and solutions. In C. Patrick (ed.), Handbook of Psychopathy (pp. 107–32). New York: Guilford Press. Linehan, M.M. (1987). Dialectical behavior therapy for borderline personality disorder. Bulletin of the Menninger Clinic, 51, 261–76.

OUTPATIENT TREATMENT AND MANAGEMENT

493

Linehan, M.M. (1993). Cognitive-Behavioral Treatment of Borderline Personality Disorder. New York: Guildford Press. Looman, J., Dickie, I. & Abracen, J. (2005). Responsivity issues in the treatment of sexual offenders. Trauma, Violence, and Abuse, 6(4), 330–53. L¨osel, F. & Schmucker, M. (2005). The effectiveness of treatment for sexual offenders: a comprehensive meta-analysis. Journal of Experimental Criminology, 1, 117–46. Mann, R.E., Ginsburg, J.I.D. & Weekes, J.R. (2002). Motivational interviewing with offenders. In M. McMurran (ed.), Motivating Offenders to Change (pp. 87–102). Chichester: John Wiley Sons, Ltd. Marshall, W.L., Anderson, D. & Fernandez, Y. (1999). Cognitive Behavioural Treatment of Sexual Offenders. Chichester: Wiley. McDermott, B.E. & Thompson, J.W. (2006). The review panel process: an algorithm for the conditional release of insanity acquittees. International Journal of Law and Psychiatry, 29, 101–11. McMurran, M. (2002) Alcohol and crime: a paper for the Alcohol Concern Research Forum, http://www.alcoholconcern.org.uk/doc/618. McNeece, C.A., Springer, D.W. & Arnold, E.M. (2001). Treating substance abuse disorders. In J.B. Ashford, B.D. Sales & W.H. Reid (eds.), Treating Adult and Juvenile Offenders with Special Needs (pp. 131–69). Washington, DC: American Psychological Association. Meloy, J.R. (1988). The Psychopathic Mind: Origins, Dynamics, and Treatment. Northvale, NJ: Aronson Inc. Meloy, J.R. & Gacono, C.B. (2000). Assessing psychopathy: psychological testing and report writing. In C.B. Gacono (ed.), The Clinical and Forensic Assessment of Psychopathy. A Practitioner’s Guide (pp. 231–49). Mahwah, NJ: Erlbaum. Miller, W.R. & Rollnick, S. (eds.) (1991). Motivational Interviewing. Preparing People to Change Addictive Behavior. New York: Guildford Press. Minzenberg M.J. & Siever L.J. (2006). Neurochemistry and pharmacology of psychopathy and related disorders. In C.J. Patrick (Ed.), Handbook of Psychopathy (pp. 251–77). New York: Guilford Press. M¨uller-Isberner, J.R. (1996). Forensic psychiatric aftercare following hospital order treatment. International Journal of Law and Psychiatry, 19(1), 81–6. M¨uller-Isberner, R., Eucker, S. & Herpertz, S.C. (2003). Dissoziale Pers¨onlichkeitsst¨orung. In S.C. Herpertz & H. Saß (eds.), Pers¨onlichkeitsst¨orungen (pp. 71–84). Stuttgart: Thieme. Nedopil, N. (2005). Prognosen in der Forensischen Psychiatrie. Ein Handbuch f¨ur die Praxis. Lengerich: Pabst. Ogloff, J.R.P., Wong, S. & Greenwood, A. (1990). Treating criminal psychopaths in a therapeutic community program. Behavioral Sciences and the Law, 8, 181–90. Paris, J. (2003). Personality Disorders Over Time: Precursors, Course, and Outcome. Washington DC: American Psychiatric Association. Pearson, F.S., Lipton, D.S., Cleland, C.M. & Yee, D.S. (2002). The effects of behavioral/cognitive– behavioral programs on recidivism. Crime and Delinquency, 48, 476–96. Petersilia, J. & Turner, S. (1993). Evaluating intensive supervision probation/parole: results of a nationwide experiment. In Research in Brief. Washington, DC: National Institute of Justice. Pithers, W.D. (1990). Relapse prevention with sexual aggressors: a method for maintaining therapeutic gain and enhancing external supervision. In W.W. Marshall, D.R. Laws & H.E. Barbara (eds.), Handbook of Sexual Assault: Issues, Theories and Treatment Of Offenders (pp. 343–61). New York: Plenum. Pithers, W.D. (1991). Relapse with sexual aggressors. Forum on Corrections Research, 3, 20–4. Prentky, R.A. & Burgess, A.W. (2000). Forensic Management of Sexual Offenders. New York: Kluwer Academic/Plenum. Raine, A. &Yang, Y. (2006). Neural foundations to moral reasoning and antisocial behavior. Social Cognitive and Affective Neuroscience, 1(3), 203–13. Rauchfleisch, U. (1999). Außenseiter der Gesellschaft. G¨ottingen: Vandenhoeck & Ruprecht. Rice, M.E. & Harris, G. (1997). Cross validation and extension of the Violence Risk Appraisal Guide for child molesters and rapists. Law and Human Behavior, 21, 231–41. Rice, M.E., Harris, G. & Cormier, C. (1992). An evaluation of a maximum security therapeutic community for psychopaths and other mentally disordered offenders. Law and Human Behavior, 16, 399–412.

494

VOLUME I: DIAGNOSIS AND TREATMENT

R¨osler, A., & Witztum, E. (1998). Treatment of men with paraphilia with a long-acting analogue of gonadotropin-releasing hormone. New England Journal Medicine, 338, 416–22. Rogers, R.D. (2006). The functional architecture of the frontal lobes: implications for research with psychopathic offenders. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 313–33). New York: Guilford Press. Rogers, R. & Cruise, K.R. (2000). Malingering and deception among psychopaths. In C.B. Gacono (ed.), The Clinical and Forensic Assessment of Psychopathy. A Practitioner’s Guide (pp. 269–84). Mahwah, NJ: Erlbaum. Roskes E., Cooksey, C., Feldman, R. et al. (2005). Assessment of malingering in correctional settings. In C.L. Scott & J.B. Gerbasi (eds.) Handbook of Correctional Mental Health (pp. 229–58). Washington: Amercian Psychiatric Association. Rutherford, M.J., Alterman, A.I. & Cacciola, J.S. (2000). Psychopathy and substance abuse: a bad mix. In C.B. Gacono (ed.), The Clinical and Forensic Assessment of Psychopathy. A Practitioner’s Guide (pp. 351–68). Mahwah, NJ: Erlbaum. Salekin, R.T. (2002). Psychopathy and therapeutic pessimism: clinical lore or clinical reality? Clinical Psychology Review, 22, 79–112. Salekin, R.T., Rogers, R. & Sewell, K.W. (1996). A review and meta-analysis of the Psychopathic Checklist-Revised: predictive validity of dangerousness. Clinical Psychology: Science and Practice, 3, 203–15. Schauss, A.G. (1978). Differential outcomes among probationers comparing orthomolecular approaches to conventional casework/counselling. Journal of Orthomolecular Psychiatry, 8, 158–68. Serin, R.C. & Amos, N.L. (1995). The role of psychopathy in the assessment of dangerousness. International Journal of Psychiatry and the Law, 18, 231–8. Seto, M.C. & Barbaree, H.E. (1999). Psychopathy, treatment behavior, and sex offender recidivism. Journal of Interpersonal Violence, 14, 1235–48. Seto, M.C. & Lalumi`ere, M.L. (2000). Psychopathy and sexual agrression. In C.B. Gacono (ed.), The Clinical and Forensic Assessment of Psychopathy. A Practitioner’s Guide (pp. 333–50). Mahwah, NJ: Erlbaum. Sheard, M.H., Marini, J.L., Bridges, C.I. & Wagner, E. (1976). The effect of lithium on impulsive aggressive behavior in man. American Journal of Psychiatry, 133, 1409–13. Skeem, J.L., Monahan, J. & Mulvey, E.P. (2002). Psychopathy, treatment involvement, and subsequent violence among civil psychiatric patients. Law and Human Behavior, 26, 577–603. Sly, A. & Taylor, K. (2003). Preliminary Evaluation of Dialectical Behaviour Therapy within a Women’s Structured Living Environment. Correctional Service Canada. Solomon, P. & Draine, J. (1995). One-year outcomes of a randomized trial of case managment with seriously mentally ill clients leaving jail. Evaluation Review, 19, 256–73. St¨urup, G.K. (1972). Castration. The total treatment. In H.L.P. Resnik & M.E. Wolfgang (eds.), Sexual Behaviors. Social, Clinical and Legal Aspects (pp. 361–82). Boston: Little Brown. Taylor, J. & Lang, A. (2006). Psychopathy and substance use disorders. In C. Patrick (ed.), Handbook of Psychopathy. New York: Guilford Press. Urbaniok, F. (2004). FOTRES: Forensisch operationalisiertes Therapie-Risiko-Evaluations-System. Oberhofen am Thunsee: Zytglogge Verlag. Vitacco, M.J. & Rogers, R. (2005). Assessment of malingering in correctional settings. In C.L. Scott & J.B. Gerbasi (eds.), Handbook of Correctional Mental Health (pp. 133–54). Washington: Amercian Psychiatric Association. Volavka, J. (2002). Neurobiology of Violence. Washington, DC: American Psychiatric Association. Volavka, J. & Citrome, L. (2000). Pharmacological interventions for preventing violence among the mentally ill with co-occurring personality disorders. In S. Hodgins (ed.), Violence among the Mentally Ill (pp. 193–203). Dordrecht: Kluwer. Vrij, A. (2000). Detecting Lies and Deceit: The Psychology of Lying and the Implication for Professional Practice. Chichester: John Wiley & Sons, Ltd. Waldman, I.D. & Rhee, S.H. (2006). Genetic and environmental influences on psychopathy and antisocial behavior. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 205–28). New York: Guilford Press.

OUTPATIENT TREATMENT AND MANAGEMENT

495

Walters, G.D. (2003). Predicting criminal justice outcomes with the psychopathy checklist and lifestyle criminality screening form: a meta-analytic comparison. Behavioral Sciences and the Law, 21, 89–102. Wanberg, K.W. & Milkman, H.B. (1998). Criminal Conduct and Substance Abuse Treatment: Strategies for Self-Improvement And Change. Thousand Oaks, CA: Sage. Washington State Institute for Public Policy (2006). Recidivism Findings for the Juvenile Rehabilitation Administration’s Dialectical Behaviour Therapy Program: Final Report. Olympia, WA. Webster, C.D., Douglas, K.S., Eaves, D. & Hart, S. (1997). The HCR-20 Scheme: the Assessment of Dangerous and Risk (2nd edition). Vancouver: Simon Fraser University and Forensic Psychiatric Services Commission of British Columbia. Wille, R. & Beier, K.M. (1989). Castration in Germany. Annals of Sex Research, 2, 103–33. Wilson, D.B., Bouffard, L.A. & MacKenzie, D.L. (2005). A quantitative review of structured, grouporiented, cognitive-behavioral programs for offenders. Journal of Criminal Justice and Behavior, 32, 172–204. World Health Organization (2005). ICD 10. International Statistical Classification of Diseases and Related Health Problems: 10th Revision, 2nd edition. Geneva: World Health Organization.

CHAPTER 28

Antisocial Disorders and Domestic Violence: Treatment Considerations L. Kevin Hamberger Medical College of Wisconsin, USA

and Jennifer Langhinrichsen-Rohling University of South Alabama, USA

Domestic violence is a serious problem that has profound effects on the victim, the perpetrator, other family members and society. It also constitutes a health, social and economic burden for US citizens as efforts to prevent, intervene or cope with the consequences of domestic violence have impacted our healthcare system, law enforcement and criminal justice systems, and the business sector. Consequently, domestic violence has been the focus of study by professionals from a variety of scholarly disciplines, including psychologists, sociologists, criminologists, nurses, physicians, lawyers, economists and anthropologists. One finding that has repeatedly emerged is that there is a subgroup of domestic violence perpetrators who exhibit characteristics of antisocial personality disorder (e.g., Hamberger et al., 1996; Holtzworth-Munroe & Stuart, 1994). Therefore, in this chapter, our focus will be to describe research that has been conducted on the role of antisocial spectrum disorders in the expression of domestic violence, the dynamics of the domestically violent relationship, and then describe current treatment approaches that may have particular promise when applied to domestic violence perpetrators who have antisocial tendencies. In the current chapter, we use the term domestic violence to refer to an ongoing and intentional pattern of physical and psychological abuse occurring between intimate partners. This particular term was chosen for a number of reasons: (i) it has historically been used to refer to a husband’s or male partner’s violence against his female partner rather than referring to both men’s and women’s partner abuse; (ii) it has been broadly defined to include acts of psychological as well as physical aggression; (iii) it is typically thought to occur with some frequency in the relationship; (iv) it is expected to be perpetrated intentionally in order to The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

498

VOLUME I: DIAGNOSIS AND TREATMENT

assert control in an intimate relationship; and (v) it has been associated with a characteristic set of relationship dynamics. It has become evident that batterers form a heterogeneous, rather than a homogeneous group (e.g., Dixon & Browne, 2003; Langhinrichsen-Rohling, 2005; Lohr et al., 2005). Consequently, initial comparisons of domestically violent to nonviolent men may eventually prove themselves overly simplistic. Nonetheless, within the past several years, researchers have effectively used these types of comparative studies both to qualitatively (e.g., Holtzworth-Munroe et al., 1997; Holtzworth-Munroe, Smutzler & Bates, 1997; Schumacher et al., 2001) and quantitatively (e.g., Stith et al., 2004) determine risk factors for perpetrating domestic violence. For example, the Stith et al. (2004) meta-analysis compiled data generated from 85 studies to determine which risk factors are most associated with the perpetration of intimate partner physical abuse. Large effect sizes were obtained for five risk factors. Physical abuse perpetration was associated with perpetrating emotional abuse, forcing a partner to have sex, illicit drug use, attitudes condoning marital violence and lack of marital satisfaction. Moderate effect sizes were obtained for another set of risk factors which included having a traditional sex-role ideology, high levels of anger/hostility, a history of partner abuse and greater levels of alcohol use, depression and career/life stress. Relatively weak, but still significant, risk factors for perpetration included jealousy, younger age, lower levels of education and lack of employment or reduced income. Each of these identified risk factors has implications for batterer treatment, prevention efforts and public policy. Current theory asserts that batterer treatment efficacy will also improve, if specific treatment components are targeted to particular subtypes of domestically violent men (e.g., Cavanaugh & Gelles, 2005; Langhinrichsen-Rohling, 2005). There may also be different developmental pathways that lead to the expression of various types of aggression (i.e., authority conflict, overt aggression and covert aggression; Loeber & Loeber, 1998). Particular prevention strategies may best diminish specific types of violence in certain types of perpetrators. Relevant to the current chapter, one of the key distinctions among batterers may be the presence or absence of certain types of Axis II psychopathology or personality characteristics. Specifically, there is consensus that it is important to assess for the occurrence of antisocial personality disorder (e.g., Beasley & Stoltenberg, 1992; Langhinrichsen-Rohling, Huss & Rohling, 2006; Remington et al., 1999) and perhaps, psychopathy, in batterers (e.g., Cornell et al., 1996; Huss & Langhinrichsen-Rohling, 2000; Lynam, 2004). There is less consensus, however, about which other forms of Axis II psychopathology may potentiate the perpetration of domestic violence, although several scholars have indicated that characteristics of borderline personality disorder are also relevant (e.g., Dutton & Starzomski, 1997; Edwards et al., 2003; Hamberger & Hastings, 1988; Holtzworth-Munroe, Stuart & Hutchinson, 1997; Saunders, 2004). The centrality of determining whether the batterer has co-occurring personality disturbance was supported by data published by Dutton and colleagues in 1997. They found that batterers with elevated scores on measures of antisocial, borderline and avoidant personality disorder had the highest rates of post-treatment recidivism (Dutton et al., 1997). Likewise, a study by Hamberger and colleagues found that higher scores on the borderline-dysphoric factor of the MCMI-I were related to late treatment drop-out (Hamberger, Lohr & Gottlieb, 2000).

ANTISOCIAL DISORDERS AND DOMESTIC VIOLENCE

499

While reviews substantiate that personality disturbance is related to treatment efficacy and completion (Daly & Pelowski, 2000), there is continued debate about which personality aspects are central to assess. There is also little consensus about how many meaningful subtypes of batterers exist. Researchers generally find between two and four distinct subgroups of batterers. Two subgroup proponents have included animal as well as human researchers such as Gottman and colleagues (1995) who differentiated between Type I and Type II batterers. A recent review by Weinshenker and Siegel (2002) concluded that human aggression can best be understood dichotomously – as either containing affective or predatory characteristics. Affective aggression is typically carried out defensively and impulsively whereas predatory aggression is carried out offensively as part of a planned attack. Other similar terms that have been used to describe the aggression dichotomy are impulsive/reactive versus premeditated, predatory, instrumental or proactive (Chase, O’Leary & Heyman, 2001; Cornell et al., 1996; McEllistrem, 2004). In 1995, Johnson proposed a second two-group typology that has become widely known. Johnson distinguished between men who were engaging in common couple violence and men who were engaged in patriarchal terrorism. This latter group of perpetrators was expected to have significant characteristics of antisocial personality disorder and, perhaps, psychopathy; whereas the violence of men perpetrating common couple violence was expected to be better understood in terms of dyadic or relationship factors (Holtzworth-Munroe & Meehan, 2004). Holtzworth-Munroe and Stuart (1994) advanced the most noteworthy three-group typology. Holtzworth-Munroe and Stuart delineated their three-group model after reviewing at least 15 preceding batterer typologies. They theorized that domestically violent men could be differentiated across three dimensions: (i) the severity and frequency of their violence; (ii) the generality of their violence; and (iii) the personality characteristics of the batterer. Using these dimensions, they described three subtypes of batterers. The family-only batterer is expected to engage in less severe and frequent domestic violence compared to the other subtypes. He is unlikely to be violent with strangers and he suffers from few, if any, personality disorders or disturbances. His violence is thought to be situational in nature or related to dyadic factors. In contrast, the dysphoric/borderline batterer is thought to engage in more frequent and severe domestic violence. He exhibits significant symptoms of dysregulated affect, such as impulsivity, jealousy and depression, and he perpetrates some violence outside the home. In contrast, the generally violent/antisocial batterer is expected to engage in frequent and severe domestic violence. He is the most likely to exhibit characteristics of antisocial personality disorder which would include criminal behavior, arrests and increased substance abuse. He also perpetrates the highest level of violence against nonfamily members. Despite the theoretical elegance of Holtzworth-Munroe and Stuart’s three-subtype solution, empirical efforts to validate this typology have met with only partial success. For example, Holtzworth-Monroe and colleagues own attempt to empirically replicate their theory resulted in four, rather than the hypothesized three, batterer subgroups. In support of their theory, three of the obtained subgroups were as predicted: family only, generally violent/antisocial, and borderline/dysphoric. However, a fourth subgroup emerged. They named this group low-level antisocial (Holtzworth-Monroe et al., 2000). Likewise, a separate replication attempt by Delsol, Margolin and John in 2003 resulted in the expected

500

VOLUME I: DIAGNOSIS AND TREATMENT

three groups. However, contrary to theory, these authors indicated that they could not find meaningful empirical discriminations between the generally violent/antisocial batterers and the borderline/dysphoric batterers. Instead, they recommended identifying a generally violent/psychologically distressed group and a family-only violent group of perpetrators. Meanwhile, a replication by Waltz et al. (2000) did result in three discernible groups. However, they reported that, contrary to theory, personality characteristics did not distinguish between the generally violent/antisocial and the borderline/dysphoric batterers. Some four-batterer subgroup solutions have been derived via an examination of empirical data (e.g., Holtzworth-Munroe et al., 2000). Other researchers have created typologies that are more complex by integrating dimensions from disparate research areas. For example, Monson and Langhinrichsen-Rohling (1998) integrated findings from the domestic violence literature with those obtained from the sexual aggression literature in order to derive a fourgroup integrated typology of perpetrators. They then collected empirical data that partially confirmed the utility of their integrated typology solution (Monson & LanghinrichsenRohling, 2002). Clearly continued work is needed to determine the most relevant number of batterer subtypes. Greater consensus is also needed on which dimensions are essential for distinguishing among domestically violent men. However, there does seem to be consensus that antisocial personality features are directly related to the etiology or perpetration of domestic violence for some batterers.

DYNAMICS OF DOMESTIC VIOLENCE By definition, the domestically violent perpetrator intentionally inflicts assaultive behavior upon their intimate partner. This behavior then functions to control the victim through the induction of fear. Typically, the victim attempts to avoid or end the violence by changing her behavior. When this happens, the perpetrator’s assaultive behavior gets reinforced both by his experience of tension reduction and by his attainment of behavioral compliance by the victim. The specific type of assaultive behavior (sexual, physical or psychological) that he used is unimportant as long as it results in victim fear, behavioral compliance and tension reduction for the perpetrator. Within most domestically violent relationships, one member of the dyad then holds a disproportionate degree of power over the fearful victim. Within this culture, the fearful victim is typically a woman; however, this is not always the case. Moreover, as reviewed above, research suggests that acts of violence can occur at the hands of several different kinds of perpetrators and the etiology and relationship dynamics associated with the violence may differ accordingly. However, most investigators in the field agree that men who have antisocial tendencies perpetrate a significant proportion of domestic violence. The relationship dynamics described within this chapter are particularly relevant for the male antisocial perpetrator who is violent within a heterosexual relationship. The power imbalance and fear induction wielded by the domestically violent antisocial perpetrator can affect virtually every aspect of the abusive relationship. The antisocial perpetrator has the ability to isolate his victim from outside sources of support and feedback. The social control he exerts can also extend to relationships with helping professionals such as healthcare providers. The antisocial abuser often accompanies his victim to her healthcare appointments. He might even speak for her or provide her with ‘scripts’ of acceptable and

ANTISOCIAL DISORDERS AND DOMESTIC VIOLENCE

501

unacceptable issues to discuss in these situations. These perpetrators can even interfere with the relationships between victims and their spiritual teachers and leaders (Miles, 2000). Hence, even if a clergy person is educated about domestic violence issues, he or she may be prevented from providing ministerial assistance to the victim by the dynamics of the abusive relationship she is involved in. The abuser can also control relationship resources such as money and property. Even if the victim has a job, the perpetrator may compel her to turn her income over, so that he may have almost complete say over the distribution of assets. Furthermore, although the victim may take great pains to comply with the rules laid down by the perpetrator, these rules can change unpredictably, which can further destabilize decision making by the victim and lead to excessive or incapacitating levels of self-doubt. Anger is also a part of the violent relationship (Norlander & Eckhardt, 2005). Research indicates that both victims and perpetrators in violent relationships show increased anger and belligerence compared to nonviolent couples. Types of anger and hostility exhibited by couples experiencing domestic violence include blame, dismissal, belligerence and contempt (Burman, John & Margolin, 1992; Burman, Margolin & John, 1993; Margolin, Burman & John, 1989). Such negative communication behaviors are often reciprocal (Cordova et al., 1993), with women engaging in such behaviors as frequently as men (Holtzworth-Munroe, Smutzler & Stuart, 1998; Jacobson et al., 1994). Hence, it is inaccurate to characterize violent relationships as consisting of an active abuser and a passive victim. Rather, it appears that the perpetrator and victim are both active in dealing with the issue of abuse, as many victims respond with anger, indignation and even violence (Hamberger & Guse, 2002). Despite the apparent symmetry of negative emotions and behaviors between victims and perpetrators of domestic violence, fear of partner’s violence appears to be gender asymmetric. This highlights the unequal power dynamics that are often present in these relationships. In keeping with this assertion, Jacobson and colleagues (1994) demonstrated that the primary predictors of both men’s and women’s violence within a relationship were their partner’s use of violence and emotional abuse. However, across both violent and nonviolent arguments, Jacobson et al. (1994) found that men were more abusive than women, and that men were generally not fearful during such arguments, whereas women were. Furthermore, Jacobson et al. (1994), as well as Dobash et al. (1998) found that once a man began abusive behavior against his female partner, no behavior on her part could end the violence. Rather, it ended when he decided to end it. This pattern did not hold for women’s violence. As a pattern that occurs over time, another important dynamic of domestic violence is the victim’s sense of entrapment. To the casual, uninformed observer, it would appear that a victim could easily end the violence she is experiencing by leaving the abusive relationship. However, victims do not easily leave such relationships, and violence and abuse can go on for years. There are many reasons why it is so difficult for victims to extricate themselves from an abusive, controlling relationship. These include fear of injury or death if they leave, fear of inability to survive independently, and often, fear of loss of family ties and relationships if the relationship is severed. Concerns about economic survival, as well as ambivalence about taking children away from the abusive parent or fear of losing custody of children to the abusive parent can also contribute to the victim’s sense of entrapment. Lack of community, religious or societal support for leaving an abusive relationship and living independently are other factors that may interfere with a victim’s efforts to leave a violent relationship. The woman may also have limited access to friends and family who

502

VOLUME I: DIAGNOSIS AND TREATMENT

could assist her in leaving, because of her ongoing isolation by the abuser. Isolation may also result in her having limited knowledge of community resources that could assist her in making the transition to a violence-free life. Further, the intimate nature of the relationship in which the abuse and violence is occurring creates another dynamic that can facilitate feelings of entrapment. Victims self-report that love is one of the reasons that they are staying with their domestically violent partner (Langhinrichsen-Rohling et al., 1998). Feelings of love for, and loyalty to the perpetrator, combined with the intermittent occurrence of violence may create a dynamic of traumatic bonding, as described by Dutton and Painter (1993). Specifically, the cyclical pattern of violence coupled with expressions of love and affection at other times may actually increase the victim’s dependence on the perpetrator, which would make escape efforts less likely. As described so eloquently by a survivor to one of the authors (LKH) during a violence assessment of her antisocial, abusive partner: ‘He treats me with abuse and disrespect 75 % of the time. The other 25 % of the time he treats me like his princess. I live for that 25 %’.

TREATMENT CONSIDERATIONS WITH ANTISOCIAL BATTERERS A great deal has been written on treatment of male batterers. Although many different treatment models exist (e.g., see Aldarando & Mederos, 2002; Dutton & Sonkin, 2003), across models, some important commonalities are believed necessary for effective batterer treatment. For example, the primary goal of batterer treatment is to end intimate partner violence and increase safety of the victim. Although most early research on treatment outcome focused primarily on the cessation of physical violence (e.g., Hamberger & Hastings, 1990), more recent research has also included reductions in psychological abuse and changes in the victim’s perceptions of danger and her sense of fear (e.g., Gondolf, 1999). Secondly, most models of batterer treatment stress the importance of holding the perpetrator solely accountable for his actions. Thus, the abuser is viewed as responsible for committing acts of abuse and coercion. He is also responsible for developing and implementing nonabusive relationship behaviors, even during times of intense relationship conflict. There are several strategies for imposing such responsibility and accountability on the batterer/client. Some of these strategies emerge directly from the treatment setting. Other accountability strategies come out of the treatment system, and still others are imposed by the criminal justice and community corrections systems that may be supervising the perpetrator’s involvement in treatment. Although there is some literature on the role and impact of these various systems in holding perpetrators accountable, we are also guided in the following discussion by our clinical experience.

Criminal Justice and Community Corrections Intuitively, the criminal justice and community correction systems appear to be logical arbiters of community norms for perpetrator accountability. The abuser is arrested, goes through the court process, and is placed on probation, which is typically supervised by a community corrections officer. The arrest, prosecution and court finding of guilt all

ANTISOCIAL DISORDERS AND DOMESTIC VIOLENCE

503

constitute strong messages of responsibility and accountability, as does the mandated referral for abuse abatement counseling. Regular probation supervision, including checking up on the abuser’s involvement in counseling also communicates accountability. If the abuser fails to attend counseling sessions at the required frequency, or attends but does not cooperate or comply with other aspects of the counseling program, the probation officer is expected to learn about these infractions and then to impose sanctions against the abuser. Such sanctions can range from issuing a caution or a warning that future infractions will be met with more severe consequences, to the delivery of consequences such as being placed in jail for a few days, to revocation of probation and imposition of a full jail sentence. Because antisocial batterers are characterized by rule violations, absence of remorse, lack of concern for the rights of others and impulsivity, the criminal justice and community corrections systems seem ideally suited to monitor and enforce accountability for this subgroup of batterers. By imposition of clear expectations for counseling and other rules of conduct, these systems can provide the guidance necessary to position such perpetrators to learn nonviolent, prosocial skills, if not attitudes and beliefs about relationships, power and domestic violence. They can stipulate the number and type of counseling sessions the client will receive. They can provide clear expectations for attendance and compliance, as well as articulate the consequences for failure. They can also deliver the necessary consequences. Relatively few studies have evaluated the effectiveness of criminal justice and community corrections interventions on cessation of violence. Most such studies have combined criminal justice, corrections and treatment effects in such a manner as to make it difficult to identify the independent contributions of each component. Nevertheless, a number of studies have evaluated the impact of court mandating and system responsiveness on batterer treatment participation. One way this has been done is to evaluate court mandate (versus voluntary referral) as a predictor of treatment completion. In general, results of such studies have been inconsistent (Daly & Pelowski, 2000). For example, Hamberger and Hastings (1989) reported that court-ordered men were more likely to complete a treatment program. However, Saunders and Parker (1989) found that court order for treatment was related to treatment completion only for young, lower educated men. Non-court-ordered status was related to completion among older, more educated men. Rosenbaum, Gearan and Ondovic (2001) found that court mandate for treatment was related to significantly higher completion rates for a treatment program consisting of 20 sessions. However, court mandate did not affect completion for shorter program lengths of 10 and 7 sessions. Rosenbaum et al. (2001) also observed that recidivism was lowest for men who were court ordered to treatment and who also completed treatment. Specifically, treatment completion was related to lower recidivism for court-ordered men but not for self-referred men. In 2000, Gondolf described a court review process that was related to improved attendance compliance and treatment completion. The offender was required to attend court proceedings for compliance review initially following arrest, at 30 days to verify treatment participation and at 90 days to verify treatment completion. Failure to appear or evidence of reoffense resulted in issuance of a warrant, then arrest and, in most cases, incarceration. Over a three-year study period, completion of the intake evaluation improved from 64 % to 90 %, and counseling completion rates improved from 48 % to 65 %. Further, compared to longer treatment programs that provided more comprehensive services, the court review program, combined with 12 weeks of treatment, resulted in comparable treatment outcome in terms of recidivism and female partner safety estimates (Gondolf, 1999).

504

VOLUME I: DIAGNOSIS AND TREATMENT

Very few studies have evaluated the impact of prosecution on recidivism. As an exception, Ford and Regoli (1993) described the Indianapolis Domestic Violence Prosecution Experiment. Briefly summarized, police either arrested perpetrators on the scene or the victim filed a complaint personally in the prosecutor’s office. In both conditions, victims were told that they could not drop charges. Within the victim-initiated arrest condition, batterers were assigned to one of four experimental options – pre-trial diversion and counseling; prosecution to conviction with probation and counseling; prosecution to conviction and presumptive sentencing; or the woman being allowed to drop charges. Results of case tracking from six months before the index offense, through the prosecution process to six months post-case settlement revealed a 50 % reduction in assault rate. The condition in which victims were allowed to drop charges was related to the lowest recidivism rates. Reduction of violence recidivism rates was comparable between the other three experimental interventions. Of note, however, across all interventions, approximately 20 % of offenders repeated their domestic violence even while the index case was still before the court. The results of this series of studies suggest that the criminal justice and community corrections systems play important roles in facilitating behavior change in domestic violence perpetrators. As pointed out by Ford and Regoli (1993) and Gondolf (1998), such systems exert their most powerful effects through the consistency and immediacy of their responses to violations of orders and stipulated expectations. Hence, these systems must be responsive to reports of perpetrator noncompliance with counseling programs and other provisions of probation or deferred prosecution agreements. Warrants need to be served in a timely manner, court processes must move perpetrators through the system and into corrections and counseling quickly. Those who violate counseling program agreements and rules must be swiftly returned to probation officers and judges. Relevant counseling programs and agencies must provide timely reports of compliance to supervising probation officers and the courts. Such interagency communication and cooperation is required to facilitate perpetrator program involvement, and to uniformly give the message that perpetrators are accountable for all their actions. Little research has been conducted on whether subtypes of domestic violence perpetrators are differentially sensitive to involvement in the criminal justice system. Theoretically, however, antisocial men may be the least likely to voluntarily enter treatment for domestic violence and the most likely to figure out ways to manipulate the system without complying with and benefiting from the treatment program. Thus, we would suggest that active and immediate communication between treatment providers and the representatives of the criminal justice system would be particularly important for this type of batterer. There is also relatively little research focusing on what type of treatment works best with antisocial batterers. However, one related study did compare two types of treatment approaches: structured, cognitive behavioral versus process psychodynamic. Results indicated that batterers with antisocial characteristics had lower recidivism rates if they participated in cognitive-behavioral treatment than if they participated in process psychodynamic treatment (Saunders, 1996). Structured, cognitive-behavioral treatment may be well suited for treating antisocial batterers for two reasons. First, the skills training emphasis of cognitive-behavioral treatment is a good match for the action-oriented style of many antisocial clients. Second, the structure which is typical of cognitive-behavioral approaches may facilitate increased focus and accountability among antisocial clients, while simultaneously decreasing the likelihood of these perpetrators manipulating or gaining control of the therapy process.

ANTISOCIAL DISORDERS AND DOMESTIC VIOLENCE

505

A number of articles and chapters have been written that generally describe cognitive-behavioral treatment for domestic violence (e.g., Hamberger, 1996, 1997, 2002; Hamberger & Barnett, 1995; Murphy & Eckhardt, 2005). The interested reader should consult those resources for in-depth description and discussion of the treatment components associated with this therapeutic strategy. In this chapter, we will provide an overview of key assessment, treatment and policy and procedure components that are likely to be helpful for the professional who is working with antisocial batterers.

Assessment Components Cognitive-behavioral assessment aims to identify intervention targets that have functional significance. Hence, the focus is on specific behaviors, attitudes and thought processes that can be identified for intervention. For example, a typical domestic violence assessment seeks to identify whether the batterer has antisocial tendencies. These include problems with authority, which is determined through an assessment of the perpetrators’ educational, work and military history (including questions relating to job turnover, conflicts with supervisors, disciplinary problems and reasons for quitting). This type of assessment might also illuminate the degree to which the batterer is impulsive and the extent to which he tends to be dominating or controlling. For example, antisocial batterers frequently report dropping out of school due to boredom, and further describe a history that includes numerous episodes of fighting with classmates, as well as high levels of involvement in deviant activities such as drug dealing. With regard to work history, antisocial batterers are likely to report a pattern of job instability. They often relate their employment changes to working for a series of less intelligent bosses, to their frequent conflicts with unreasonable coworkers and/or to their boredom with the routine. Assessment of legal problems and problems with drug and alcohol abuse also provide further insights into the impulsivity that is characteristic of the antisocial batterer. A good assessment can also demonstrate that the batterer has a history of failing to learn from previous negative experiences. Hamberger et al. (1996) found that antisocial/narcissistic batterers had higher annual rates of arrest for both violent crime and for nonviolent, actingout crimes, as compared to nonpathological batterers. Involvement in acting-out crimes has been shown to predict premature dropout from batterer treatment (Hamberger & Hastings, 1989). Alcohol- and drug-related crimes have been found to predict recidivism following treatment (Hamberger & Hastings, 1990). Thus, assessment of drug and alcohol abuse problems is extremely important for determining additional treatment needs, as well as to determine each batterer’s actuarial risk of reoffending. Some researchers (e.g., Saunders, 1992) have reported that antisocial batterers also typically report histories of severe abuse as children. Therefore, it is important to assess the client’s history of abuse victimization. This component of the assessment should include an evaluation of the client’s history of having witnessed parental violence and criminality. Such information is important in helping conceptualize the batterer’s learning history for domestic violence perpetration. Antisocial batterers have also been shown to be more generally violent (i.e., commit violence against persons other than the intimate partner) than other types of abusive men (Hamberger et al., 1996; Saunders, 1992). Therefore, it is important to evaluate the breadth and extent of the client’s extrafamilial violence perpetration, as well as their violence against

506

VOLUME I: DIAGNOSIS AND TREATMENT

prior intimate partners. This information can be used to determine if there is an overall pattern of disregarding the rights of others, in conjunction with a general lack of empathy, and an ongoing desire to exploit and control others. A standard cognitive-behavioral assessment also seeks to uncover the specific thought processes that both underlie and guide the batterer’s behavior. A number of studies have attempted to identify the thought patterns and beliefs of abusive men using paper and pencil measures of broad attitudes. A comprehensive review by Murphy and Eckhardt (2005) suggests that such an approach to cognitive assessment is not particularly revealing. Instead, tools that measure specific attitudes related to domestic violence, such as attitudes toward violence against women or beliefs about the blameworthiness of the partner for the violence seem to hold greater promise for identifying key cognitive intervention targets. Another approach to cognitive assessment is to identify real-time appraisal and interpretational thoughts that may be related to increased arousal and justification for use of violence. This approach is called ‘articulated thoughts in simulated situations’ (Murphy & Eckhardt, 2005). Using such an approach, the assessor and client can develop realistic scenarios involving the client and his partner. The evaluator describes the scenario in detail and the client is instructed to monitor his thoughts as the scenario unfolds. At various points during the scenario description, the therapist stops and asks the client to verbalize his actual thoughts during the scenario description. The process repeats itself until the scenario is complete. Multiple scenarios can be developed and used for the cognitive evaluation. Assessment of the articulated thoughts seeks to identify themes related to blameworthiness, dehumanization of the partner, justification for violence and self-instructions for use of violence. Eckhardt, Barbour and Davison (1998) observed that, while violent and distressed, nonviolent men did not differ on paper and pencil measures of irrational beliefs, martially violent men expressed articulated thoughts that were significantly different than the nonviolent men. In particular, violent men expressed more demeaning thoughts, absolute rule making, jumping to conclusions and black–white thinking. Because of the interpersonal nature of domestic violence, many treatment programs include a component on responsible assertive behavior (e.g., Hamberger, 2002). The research literature on assertive deficits among male batterers, particularly antisocial batterers, is somewhat sparse, and there is little guidance on how to assess assertiveness before treatment. A number of paper and pencil measures of assertiveness exist, and such an approach appears to validly differentiate batterers from nonviolent men (Maiuro, Cahn & Vitaliano, 1986). As with attitudes and beliefs, however, other researchers have found that a more direct assessment of assertiveness deficits related to spouse-specific situations may hold greater promise in differentiating violent from nonviolent men (O’Leary & Curley, 1986; Rosenbaum & O’Leary, 1981). More recent behavioral assessments of assertiveness deficits among domestic violence perpetrators have also shown that, compared to nonviolent men, batterers have more difficulty expressing their feelings. They are also more likely to engage in verbal insult, anger and belligerent expression in their attempt to ‘win’ the argument (Barbour et al., 1998; Eckhardt, Jamison & Watts, 2001). Further, abusive men show such deficits even when instructed to give their best effort in a situation (Holtzworth-Munroe & Anglin, 1991). Clinically, a practical way to assess assertiveness is to use paper and pencil measures of spouse-specific assertiveness, while simultaneously observing how the client responds to conflict situations occurring in the clinical setting (e.g., negotiating the treatment plan,

ANTISOCIAL DISORDERS AND DOMESTIC VIOLENCE

507

adhering to policies and procedures and expected rules of conduct while participating in the treatment program). Pretreatment assessment should also include review of all police reports and criminal complaints related to the index offense. Batterers typically deny or minimize the extent of their violence. Police reports often contain details of the actual events as recounted by the victim and other witnesses. Police reports usually contain descriptions of the victim’s emotional state as well as graphic descriptions of injuries. These data can be shared with the perpetrator/client to address discrepancies with his self-report and to confront any denial or lack of responsibility he exhibits. Another very important part of pretreatment assessment of the antisocial batterer is collecting independent information from the partner or victim via a collateral interview. Male batterers are known to minimize or deny the extent and impact of their violent and abusive behaviors (Dutton & Hemphill, 1992). Given that antisocial batterers, in particular, lack empathy for their victims, they are not likely to report the full impact of their violence. Thus, it is essential to gather the victim’s perspective. The independent collateral interview provides an opportunity to accomplish several goals. First, important information about the abusive client can be gathered that he might otherwise not have disclosed. Second, the provider can communicate important information to the victim about the treatment program, both identifying its strengths and giving her a realistic sense of its limitations. Third, the treatment provider can educate the victim with community resource and safety planning information. Because of the intrusiveness of antisocial batterers, it is important to see the victim/partner alone and not disclose information she has provided to the perpetrator without her consent. While there may be times she requests that information be dispersed, it should not be done unless an extensive discussion has occurred with her about the potential costs as well as benefits for doing so. In all, the pretreatment assessment typically requires between three and six hours. This includes between one and three hours for the direct evaluation of the batterer/client, one hour for review of official records such as police reports and criminal complaint, and one hour for the independent, partner collateral interview. Additional time will be required to administer and score the paper and pencil measures of attitudes, coping styles, psychopathology, alcohol and drug abuse, and other assessed variables.

Treatment Planning and Treatment Orientation Following assessment, the therapist will need to meet with the perpetrator/client to discuss key assessment findings, to suggest an overall case conceptualization, and to integrate the findings into specific treatment recommendations. Case conceptualization is an important part of the intervention process because it allows for the continued development of a therapeutic alliance. The alliance-building process began during assessment with the therapist providing a warm, accepting environment wherein, in collaboration with the client, information important to the therapy process was gathered. During case conceptualization, the therapist provides a mostly accurate summary of how the client was perceived. This provides an opportunity to further connect with the client because the therapist ‘understands’. Integrating the case conceptualization into a comprehensive treatment plan (e.g., one that identifies specific targets and goals) then offers the client a sense of hope that change is possible, and the client’s life can improve. This further enhances the therapeutic alliance.

508

VOLUME I: DIAGNOSIS AND TREATMENT

Of course, with antisocial batterers, such alliance building is complicated by the frequent tendency of such clients to remain detached from others in their world, to view the therapist as another object to be manipulated, and to consider treatment as another set of ‘hoops’ they need to jump through to keep the system off their back. Therefore, during this stage of the intervention, it is particularly necessary to help the antisocial client self-identify how treatment participation might help him achieve his goals of improved relationship and social functioning. Another key aspect of the feedback and treatment planning session is a discussion of the policies and procedures related to treatment. This discussion provides the structure that may be so important for holding all batterers, but particularly those with antisocial tendencies, accountable for their actions. Because antisocial batterers tend to be exploitive and unconcerned about the rules or other’s rights, it is essential that expectations and policies related to treatment participation be presented in clear and unambiguous language. For example, it is insufficient to tell an antisocial batterer that he may not miss ‘too many’ sessions. Rather, he should be told that he may not miss more than two sessions without consequences. Likewise, discussion of consequences for failure to comply must also be clear and unambiguous. Using the missed session example, it would not be sufficient to say that he ‘could face consequences’ if he misses three sessions. Rather he needs to be told that if he misses three sessions, he ‘will be suspended from further treatment participation’ and that his ‘probation agent will be notified of the suspension and the reasons for it’. In a related manner, the therapist should inform the client of the relevant communication and feedback loops related to his treatment. Therefore, he should be informed that the referral source (probation agent, supervising court official) will be informed periodically of his progress in treatment. He should also be told that such communication will include not only his attendance to treatment but also his compliance, or lack thereof. With respect to partner contacts, it is appropriate to inform the client that the therapist will initiate contact with her to evaluate her safety as it relates to his treatment involvement. However, it is also important to inform him that such contacts are confidential and he will not have access to the information she provides to the therapist. Such feedback loops are crucial to the treatment process. Without such structure, the treatment provider is subject to greater manipulation by the antisocial batterer. A brief case example with an antisocial batterer illustrates the importance of clearly communicating policies and procedures to the batterer while maintaining open communication with the referral source. Joe (not his real name) was a 24-year-old man with a lengthy record of assault and other crimes. He was referred through the courts for abuse abatement treatment. Joe went through the assessment and orientation procedures as described above, which included receiving specific information related to attendance and consequences for failure to do so. After a number of sessions in which he participated adequately, but in a somewhat detached manner, he began to miss sessions. Following his third missed session, the court was notified of his suspension from treatment. When Joe showed up for the next available session, the therapist spoke to him apart from the rest of the group. At this time, Joe was informed of his suspension, and he was told that the court was notified. Although the therapist was prepared for an angry, manipulative outburst, Joe sat down, looked away and said ‘Oh, yeah, I remember you telling me that. The judge is gonna be mad’. He then left without incident, and following his appearance before the judge, where he had to account for his absences and experience sanctions, Joe was allowed to return to treatment.

ANTISOCIAL DISORDERS AND DOMESTIC VIOLENCE

509

In addition to verbally explaining the rules, policies and procedures, it is helpful to provide each client with a written version. That way, when a client is in violation and he challenges whether the rule exists, he can be asked to pull out his copy of the policies and procedures for reference. This strategy has cut short many potential arguments or conflicts over what may or may not have been said several weeks ago at the orientation session.

Program Content Ideally, program content emerges from the assessment. In general, batterer treatment program content from a cognitive-behavioral perspective consists of three major content areas and three primary philosophical underpinnings. Philosophically, the following tenets guide all aspects of treatment decision making. First, abusive violence has a function. The immediate function, based on many clinical interviews, is tension relief. The batterer gets upset with his partner for some imagined or real indiscretion and, as he attempts to control her, he experiences increased and escalating aversive arousal. His outburst of aggressive behavior reduces the tension and is negatively reinforced. A more obvious, but also more distal function of abusive behavior is control of the partner. The batterer uses force and gets his way, if only temporarily. Thus, treatment is seen as part of a broader effort within society to change the functional value of abusive behavior and learn new, more prosocial behaviors. A related, second philosophical tenet of cognitive-behavior treatment for domestic violence is that violent behavior is, for the most part, learned. Sources of learning are varied and include societal messages and violence-laden images, gender-based socialization, witnessing parental role models, and even trial and error learning of the value of aggression to reduce tension and take control. From a treatment perspective, if violent behavior can be learned, so can nonviolent and nonabusive behaviors. The challenge to the therapist is to help the client appreciate the greater value in using nonviolent, nonabusive and respectful relationship behaviors, rather than violence, even if he does not always get his way. The third philosophical tenet is that responsibility for the violence, for ending it and for learning new, nonabusive behaviors rests entirely with the batterer. The cognitive-behavioral model lends itself neatly to the latter conceptualization in that every aspect of the therapy process is aimed at helping the client see and understand his self-defeating behaviors and his underlying thought processes. Such appreciation requires the client to acknowledge that his thoughts and actions are no one else’s but his own, and therefore, no one else but him can change them. Learning new behaviors requires the client to engage in self-monitoring, observing, practicing new skills and then applying these skills directly to his particular life situation. With regard to particular skills, one of the most important components might be teaching batterers to engage in responsible and assertive behavior. As pointed out by Murphy and Eckhardt (2005), several studies of the interpersonal interactions between abusive men and their partners suggest a male-demand/female-withdrawal pattern. Within the context of an abusive relationship, the man’s demands are typically experienced by his partner as oppressive, threatening and disrespectful. Abusive men need to learn to actively listen to their partner’s communications without feeling inadequate, to make requests rather than issue commands, and to express empathy or see the situation from their partner’s perspective. They also need to learn to express feelings other than anger and sexual arousal, to give and receive negative feedback without being attacking or defensive, and to have the skills

510

VOLUME I: DIAGNOSIS AND TREATMENT

to resolve conflict without threats, intimidation or escalating. Each area of assertiveness is presented as a skill that the batterer needs to do for himself but which can also benefit his intimate relationships. Each batterer has a right to express himself, but a corresponding responsibility to acknowledge his partner’s right to respond in her own way. Thus, skill rehearsal of assertive techniques focuses on his own expressions and not on his partner’s presumed responses. This way, even if his partner does not respond as he imagined, the batterer can still feel good about himself as long as he was appropriate in his assertiveness. The biggest therapeutic challenge to teaching assertive behaviors to antisocial batterers is the potential that these men will misuse these skills to order to manipulate others. While there is no way for a therapist to guarantee that the antisocial batterer (or any batterer for that matter) will not exploit learned assertive skills, there are some things that can be done proactively. First, from the outset of assertiveness training, it is important to emphasize the primacy of both party’s rights in a relationship. Second, at every training session, it is necessary to reinforce the idea that assertive expressions are not about getting another person to do what one wants. Instead, assertiveness is about communicating clearly and respectfully to another about one’s own viewpoint, desires and expectations. Finally, though an improved relationship cannot be guaranteed by assertive behavior, the therapist and client can discuss the potential benefits of responsible assertive behavior for any type of relationship (intimate, business or social). Since the abusive client, like most other people, ultimately desires improved relationships, he learns that, in the long run (though sometimes even immediately), responsible assertive behavior can lead to more rewarding relationship outcomes than manipulation or intimidation. A second area of cognitive-behavioral treatment focuses on the thought processes that underlie violent and abusive behaviors. Through didactic discussion, the client can be shown that his beliefs, attitudes, labels and attributions are related to his abusive behaviors, both distally and in the immediate situation. Through this process, the client comes to see how he sets himself up for anger and abusive behavior by how he thinks about particular situations and what he tells himself to do in response. To further reinforce the lessons from didactic discussion, the client is also taught to self-monitor his thoughts in situations wherein he feels angry or is upset with his partner. His specific thoughts are then examined with the therapist to further consolidate the functional relationship between having these thoughts and subsequently experiencing particular feelings and engaging in specific actions. The selfdefeating and filtering nature of the batterer’s particular thought processes are identified and discussed. The possibility of looking at the situation differently, in ways that do not lead to aversive emotional arousal or abusive behavior is also explored. Once the client understands the relationship between attitudes, beliefs, labels, attributions, self-instructions and feelings and behaviors, he is helped to develop alternative attitudes, thoughts and self-instructions that do not lead to abusive and violent behaviors. Methods similar to those outlined by Murphy and Eckhardt (2005), Hamberger (2002) and Beck, Freeman and Associates (1990) for cognitive intervention are used. In particular, for each self-defeating thought the client identifies, he is encouraged to develop three alternative, problem-solving ways of looking at the problematic situation. Typical beliefs and attitudes expressed by antisocial batterers center around the importance of being tough and the weakness of feelings, the disregard for rules of convention and pride in the ability to circumvent them, the belief that immediate gratification of his needs is of paramount importance regardless of the cost to others, and the utilitarian value of others as means to facilitate self-gratification, with the corresponding lack of appreciation

ANTISOCIAL DISORDERS AND DOMESTIC VIOLENCE

511

for the intrinsic value of others as persons. Antisocial batterers typically view other people (including their therapists) either as obstacles to their self-gratification or as tools to be used to meet their needs. Hence, typical situational self-talk related to others includes covert name calling and other dehumanizing statements, with a concomitant focus on the batterer’s own needs and how he might get them gratified, regardless of cost. Typical difficulties encountered by abusive clients with cognitive interventions include troubles identifying alternative ways of thinking about a particular situation. Clients are sometimes deeply invested in a particular set of beliefs and attitudes, and simply accept them as right and true. The challenge for the therapist is to help the client consider alternatives without alienating him through heavy-handed demands that the client change. One such strategy is to have the client consider ‘hypothetical’ alternatives without automatically accepting them. Another approach is to encourage the client to visualize how his life might be different, both positive and negative, if he gave up his cherished beliefs and adopted new ones. A third strategy is to encourage the client to consider how he can live a violence and abuse-free life, even if he does not fully surrender and change his prized self-defeating attitudes, beliefs and attributional processes. A third major component of abuse abatement treatment is relaxation training. This is done to teach the client body control and to provide an alternative way to reduce aversive arousal. Abusive clients often spontaneously describe the intense aversive arousal they experience in situations, prior to engaging in abusive behavior. Although no research has examined the experience of antisocial batterers, our clinical experience is that many antisocial batterers describe a feeling of tension relief following a violent outburst. Hence, relaxation is offered as an alternative, self-control method for reducing aversive arousal and experiencing tension relief without the use of abusive and violent behavior. Relaxation training is also consistent with the philosophical tenet that the abuser, alone, is responsible for his actions and for changing them. If he is aversively aroused, he can take charge of his body and the situation by using his relaxation skills to modify and reduce his arousal. Hamberger (2002) advocates using a fairly brief (10-minute) exercise, as clients usually will not take the time to practice daily with longer regimens. Relaxation is presented as an active, applied coping skill that the client can implement in any situation immediately upon noticing physical cues of aversive arousal. It is important to stress to clients that implementing relaxation may not always reduce arousal to comfortable levels. Rather, the appropriate goal of relaxation is to short-circuit the escalation of aversive arousal, level it out and then reduce it. Within the sessions, any experience of the leveling out of aversive arousal, as well as any reports of even slight reductions in negative arousal, are interpreted as positive examples of taking control.

Treatment Outcome Many studies have evaluated the effectiveness of treatment with partner abusive men. Most of the research in this area has been quasi-experimental with vague or limited measures and weak methodologies (Davis & Taylor, 1999; Hamberger & Hastings, 1993). A recent meta-analysis of treatment outcomes showed an overall effect size of .18, suggesting a fairly weak impact of abuser treatment (Babcock, Green & Robie, 2004). Overall, then, batterer treatment by itself appears to have limited impact. Recent research by Gondolf and Jones (2001) indicates that batterer treatment can result in 44 % to 64 % violence reduction

512

VOLUME I: DIAGNOSIS AND TREATMENT

following treatment completion. However, random assignment, controlled experimental designs have not shown treatment to be greatly more effective than intense supervision (Dunford, 2000). Research focused on the outcome of treatment with antisocial batterers is still in its infancy. In an early study of physical violence recidivism, Hamberger and Hastings (1990) hypothesized that batterers with antisocial/narcissistic personality styles would show higher recidivism rates following treatment completion than those without. Results showed that narcissistic-antisocial personality style was significantly associated with recidivism status, however, it only accounted for about 18 % of the variance. Gondolf (1999), however, reported that neither antisocial nor narcissistic personality styles were related to recidivism in his multisite treatment outcome study. Finally, as noted above, Saunders (1996) reported that antisocial batterers had lower recidivism rates in a structured, cognitive-behavioral treatment than in a less structured, psychodynamic process group intervention.

Future Research Treatment outcomes might improve if batterer treatment is more individualized (Murphy & Eckhardt, 2005). For example, most batterers have awareness of some of the risk factors for their perpetration. These factors might comprise the initial intervention targets while the therapist uses motivational interviewing strategies to increase awareness about other important targets for change (such as attitudes that promote the acceptance of violence, rigid gender-stereotypical beliefs, antisocial characteristics). Preliminary work shows that use of motivational strategies does increase session attendance, particularly among batterers who are members of minority ethnic groups (Taft et al., 1999). There is consensus that there are at least two subtypes of batterers, one of whom exhibits significant levels of antisocial personality disturbance (Lynam, 2004; Saunders, 2004). These individuals are likely to need specific intervention strategies that reduce the likelihood of successful manipulation of the legal or therapeutic system. As reviewed above, consistency, clear communication and cohesion among the various components of the treatment team will also be crucial components of treatment. This subtype of batterer is also more likely to have comorbid alcohol and substance abuse disorders (Remington et al., 1999) and greater use of alcohol is associated with increased abusiveness (Margolin, John & Foo, 1998). Continued research is needed about how to integrate domestic violence and substance abuse treatments in the most efficacious manner. Antisocial batterers are also particularly likely to have significant deficits in experiencing empathy for any other person’s position (Covell, Huss & Langhinrichsen-Rohling, 2007). This should be a specific focus of treatment. Moreover, since there is not clear evidence of differences between generally violent/antisocial and borderline/dysphoric subgroups of batterers, it may be that issues relating to rejection, jealousy, abandonment and lack of control in vulnerable and intimate relationships are concerns for the majority of batterers with personality disturbances. These concerns may well arise from unstable and difficult childhoods which may, in turn, have resulted in violence becoming a highly available option in situations of interpersonal instability (Langhinrichsen-Rohling, Hankla & Stormberg, 2004). The degree to which clinicians in various settings can accurately determine batterer subtypes is equivocal (e.g., Langhinrichsen-Rohling, Huss & Ramsey, 2000; Lohr et al., 2005).

ANTISOCIAL DISORDERS AND DOMESTIC VIOLENCE

513

Efforts are needed to determine the minimum number of clinically relevant batterer subgroups as well as a reliable, valid and cost-efficient strategy with which to make subtyping decisions. This is a necessary first step toward providing more batterer-specific, efficacious interventions, particularly for men who exhibit characteristics of antisocial personality disorder.

SUMMARY AND CONCLUSIONS Men who batter their partners comprise a heterogeneous group, and research has identified between two and four distinct subtypes of perpetrators based on personality style and violence perpetration pattern. One significant and consistently identified subtype is men who exhibit antisocial personality characteristics. Such characteristics include lack of empathy, sense of entitlement, difficulty learning from experience, defiance and difficulty following conventional rules and expectations, manipulativeness and consistent violation of the rights of others. Antisocial batterers do not typically confine their use of violence to their intimate relationships. Rather, they tend to be generally violent, both within their families and intimate relationships, and with nonfamily members. Within the context of interpartner violence (IPV), antisocial batterers have consistently been found to commit the most frequent and severe levels of violence. Further, the partner violence of antisocial men is typically instrumental and predatory in nature, with its primary motivation being to dominate and control. Dynamically, antisocial batterers control through the induction of fear and isolation of their partners. Although antisocial batterers exhibit high levels of anger, such anger tends, clinically, to be instrumental, as well. That is, antisocial batterers use their anger much as a tool to further dominate and control their partners. Thus, with antisocial batterers, the violence and abusive behaviors are not so much ‘loss of control’ as the imposition of control through use of anger expression and violent behaviors. The characteristics and dynamics of IPV perpetrated by antisocial batterers leads to a number of implications for their treatment in an effort to end such behaviors. In particular, because antisocial batterers can be so manipulative and dismissive of conventional rules and expectations, it is extremely important for all involved in the treatment process to be in agreement about the policies, procedures, goals and expectations of the antisocial client and to communicate such information to the client in clear, unambiguous ways. It is also essential to hold the perpetrator totally and completely responsible and accountable for his violent and abusive behavior, and for ending it. In addition, achieving the above objectives requires close collaboration between the treatment provider and the criminal justice referral source. From a treatment perspective, it is important to conduct thorough, multidimensional assessment prior to treatment. Such assessment includes psychological functioning, alcohol and drug abuse history. In addition, it is important to assess the client’s legal and criminal justice history, social and family history and violence history, not only in the present relationship, but also more generally. It is also important, whenever possible, to conduct an independent, collateral interview with the victim. Such an interview provides a richer picture of the abuse and violence that is occurring in the relationship. It also offers the opportunity for the provider to impart important information about community support resources and treatment limitations to the victim/partner.

514

VOLUME I: DIAGNOSIS AND TREATMENT

Treatment proceeds best with development of a positive working alliance and helping the client to appreciate that ending violent and abusive behavior is in his best interests, both from a social and a legal perspective. Research suggests that antisocial batterers respond best to therapy that is structured and skills or action oriented. Thus, a cognitive-behavioral approach that incorporates responsible assertive communication skills training, cognitive restructuring and relaxation for arousal management may be well suited to working with antisocial batterers. Unfortunately, we know little about treatment effectiveness with antisocial batterers. Contradictory findings have been reported about the extent to which antisocial/narcissistic personality characteristics predict post-treatment recidivism. Thus, more research is needed to determine the most effective courses of treatment with antisocial batterers. We have suggested that one useful approach might be to develop more individual treatment approaches with antisocial batterers in order to develop more reflexive and effective methodologies. In addition, because of the high correlation of alcohol and drug problems within this treatment population, research is needed to guide us in the most effective ways to integrate alcohol and drug treatment with abuse abatement treatment. Antisocial IPV perpetrators constitute a very difficult treatment population. Effective intervention requires a coordinated and collaborative effort between law enforcement, criminal justice and batterer treatment providers. Much more work remains to be done to identify effective and lasting intervention and treatment approaches with this subgroup of batterers.

REFERENCES Aldarando, E. & Mederos, F. (eds.) (2002). Programs for Men Who Batter: Intervention and Prevention Strategies in a Diverse Society. Kingston, NJ: Civic Research Institute. Babcock, J.C., Green, C.E. & Robie, C. (2004). Does batterers’ treatment work? A meta-analytic review of domestic violence treatment. Clinical Psychology Review, 23, 1023–153. Barbour, K.A., Eckhardt, C.I., Davison, G.C. & Kassinove, H. (1998). The experience and expression of anger in martially violent and martially discordant-nonviolent men. Behavior Therapy, 29, 173–91. Beasley, R. & Stoltenberg, C.D. (1992). Personality characteristics of male spouse abusers. Professional Psychology, 23, 310–17. Beck, A.T., Freeman, A. & Associates. (1990). Cognitive Therapy of Personality Disorders. New York: Guilford Press. Burman, B., John, R.S. & Margolin, G. (1992). Observed patterns of conflict in violent, nonviolent, and nondistressed couples. Behavioral Assessment, 14, 15–37. Burman, B., Margolin, G. & John, R.S. (1993). America’s angriest home videos: behavioral contingencies observed in home reenactments of marital conflict. Journal of Consulting and Clinical Psychology, 61, 28–39. Cavanaugh, M.M. & Gelles, R.J. (2005). The utility of male domestic violence offenders typologies: New directions for research, policy, and practice. Journal of Interpersonal Violence, 20, 155–66. Chase, K.A., O’Leary, K.D. & Heyman, R.E. (2001). Categorizing partner-violent men within the reactive-proactive typology model. Journal of Consulting and Clinical Psychology, 69, 567–72. Cordova, J.V., Jacobson, N.S., Gottman, J.M. et al. (1993). Negative reciprocity and communication in couples with a violent husband. Journal of Abnormal Psychology, 102, 559–64. Cornell, D.G., Warren, J., Hawk, G. et al. (1996). Psychopathy in instrumental and reactive violent offenders. Journal of Consulting and Clinical Psychology, 64, 783–90. Covell, C.N., Huss, M.T. & Langhinrichsen-Rohling, J. (2007). Empathic deficits among male batterers: a multidimensional approach. Journal of Family Violence, 22, 165–74. Daly, J.E. & Pelowski, S. (2000). Predictors of dropout among men who batter: a review of studies with implications for research and practice. Violence and Victims, 15, 137–60.

ANTISOCIAL DISORDERS AND DOMESTIC VIOLENCE

515

Davis, R.C. & Taylor, B.G. (1999). Does batterer treatment reduce violence? A synthesis of the literature. Women and Criminal Justice, 10, 69–93. Delsol, C., Margolin, G. & John, R.S. (2003). A typology of martially violent men and correlates of violence in a community sample. Journal of Marriage and Family, 65, 635–51. Dixon, L. & Browne, K. (2003). The heterogeneity of spouse abuse: a review. Aggression and Violent Behavior, 8, 107–30. Dobash, R.P., Dobash, R.E., Cavanagh, K. & Lewis, R. (1998). Separate and intersecting realities: a comparison of men’s and women’s accounts of violence against women. Violence Against Women, 4, 382–414. Dunford, F.W. (2000). The San Diego Navy experiment: an assessment of interventions for men who assault their wives. Journal of Consulting and Clinical Psychology, 68, 468–76. Dutton, D.G., Bonarchuck, M., Kropp, R. et al. (1997). Client personality disorders affecting wife assault post-treatment recidivism. Violence and Victims, 12, 37–50. Dutton, D.G. & Hemphill, K.J. (1992). Patterns of socially desirable responding among perpetrators and victims of wife assault. Violence and Victims, 7, 29–39. Dutton, D.G. & Painter, S.L. (1993). Emotional attachments in abusive relationships: a test of traumatic bonding theory. Violence and Victims, 8, 105–20. Dutton, D.G. & Sonkin, D.J. (eds.) (2003). Intimate Violence: Contemporary Treatment Innovations. Binghamton, NY: The Haworth Press. Dutton, D.G. & Starzomski, A.J. (1997). Personality predictors of the Minnesota Power and Control Wheel. Journal of Interpersonal Violence, 12(1), 70–82. Eckhardt, C.I., Barbour, K.A. & Davison, G.C. (1998). Articulated thoughts of martially violent and nonviolent men during anger arousal. Journal of Consulting and Clinical Psychology, 66, 259–69. Eckhardt, C.I., Jamison, T.R. & Watts, K. (2001). Anger experience and expression among male dating violence perpetrators during anger arousal. Journal of Interpersonal Violence, 17, 1102–114. Edwards, D.W., Scott, C.L., Yarvis, R.M. et al. (2003). Impulsiveness, impulsive aggression, personality disorder, and spousal violence. Violence and Victims, 18, 3–14. Ford, D.A. & Regoli, M.J. (1993). The criminal prosecution of wife assaulters: process, problems, and effects. In N.Z. Hilton (ed.), Legal Responses to Wife Assault: Current Trends and Evaluation (pp. 127–64). Newbury Park, CA: Sage. Gondolf, E.W. (1998). Do batterer programs work? A 15 month follow-up of multi-site evaluation. Domestic Violence Report, 3, 65–6, 78–9. Gondolf, E.W. (1999). A comparison of reassault rates in four batterer programs: do court referral, program length and services matter? Journal of Interpersonal Violence, 14, 41–61. Gondolf, E.W. (2000). Mandatory court review and batterer program compliance. Journal of Interpersonal Violence, 15, 428–37. Gondolf, E.W. & Jones, A.S. (2001). The program effect of batterer programs in three cities. Violence and Victims, 16, 693–704. Gottman, J.M., Jacobson, N.S., Rushe, R.H. et al. (1995). The relationship between heart rate reactivity, emotionally aggressive behavior, and general violence in batterers. Journal of Family Violence, 9, 227–48. Hamberger, L.K. (1996). Group treatment of men who batter their female partners. In Session, 2, 49–62. Hamberger, L.K. (1997). Cognitive-behavioral treatment of men who batter their partners. Cognitive and Behavioral Practice, 4, 147–69. Hamberger, L.K. (2002). The Men’s Group Program: a community-based, cognitive-behavioral, profeminist intervention program. In E. Aldarondo & F. Mederos (eds.), Batterer Intervention Programs: A Handbook for Clinicians, Practitioners, and Advocate (Chapter 7). Kingston, NJ: Civic Research Institute. Hamberger, L.K. & Barnett, O.W. (1995). Assessment and treatment of men who batter. Innovations in Clinical Practice, 14, 31–54. Hamberger, L.K. & Guse, C. (2002). Men’s and women’s use of partner violence in clinical samples. Violence Against Women, 8, 1301–30. Hamberger, L.K. & Hastings, J.E. (1988). Characteristics of male spouse abusers consistent with personality disorders. Hospital and Community Psychiatry, 39, 763–70.

516

VOLUME I: DIAGNOSIS AND TREATMENT

Hamberger, L.K. & Hastings, J.E. (1989). Counseling male spouse abusers: characteristics of treatment completers and dropouts. Violence and Victims, 4, 275–86. Hamberger, L.K. & Hastings, J.E. (1990). Recidivism following spouse abuse abatement counseling: treatment program implications. Violence and Victims, 5, 157–69. Hamberger, L.K. & Hastings, J.E. (1993). Court-mandated treatment for men who batter their partners: issues, controversies, and outcomes. In N.Z. Hilton (ed.), Legal Responses to Wife Assault: Current Trends and Evaluation (pp. 188–229). Newbury Park, CA: Sage. Hamberger, L.K., Lohr, J.M., Bonge, D. & Tolin, D.F. (1996). A large sample empirical typology of male spouse abusers and its relationship to dimensions of abuse. Violence and Victims, 11, 277–92. Hamberger, L.K., Lohr, J.M. & Gottlieb, M. (2000). Predictors of treatment dropout from a spouse abuse abatement program. Behavior Modification, 24, 528–52. Holtzworth-Munroe, A. & Anglin, K. (1991). The competency of responses given by maritally violent versus nonviolent men to problematic marital situations. Violence and Victims, 6, 257–69. Holtzworth-Munroe, A., Bates, L., Smutzler, N. & Sandin, E. (1997). A brief review of the research on husband violence: Part I: maritally violent versus nonviolent men. Aggression and Violent Behavior, 2(1), 65–99. Holtzworth-Munroe, A. & Meehan, J.C. (2004). Typologies of men who are martially violent: scientific and clinical implications. Journal of Interpersonal Violence, 19, 1369–89. Holtzworth-Munroe, A., Meehan, J.C., Herron, K. et al. (2000). Testing the Holtzworth-Munroe and Stuart (1994) batterer typology. Journal of Consulting and Clinical Psychology, 68, 1000–19. Holtzworth-Munroe, A., Smutzler, N. & Bates, L. (1997). A brief review of the research on husband violence: Part III: sociodemographic factors, relationship factors, and differing consequences of husband and wife violence. Aggression and Violent Behavior, 2, 285–307. Holtzworth-Munroe, A., Smutzler, N. & Stuart, G.L. (1998). Demand and withdraw communication among couples experiencing husband violence. Journal of Consulting and Clinical Psychology, 66, 731–43. Holtzworth-Munroe, A. & Stuart, G.L. (1994). Typologies of male batterers: Three subtypes and the differences among them. Psychological Bulletin, 116, 476–97. Holtzworth-Munroe, A., Stuart, G.L. & Hutchinson, G. (1997). Violent versus nonviolent husbands: differences in attachment patterns, dependency, and jealousy. Journal of Family Psychology, 11, 314–31. Huss, M.T. & Langhinrichsen-Rohling, J. (2000). Identification of the psychopathic batterer: the clinical, legal, and policy implications. Aggression and Violent Behavior, 5, 403–22. Jacobson, N.S., Gottman, J.M., Waltz, J. et al. (1994). Affect, verbal content, and psychophysiology in arguments of couples with a violent husband. Journal of Consulting and Clinical Psychology, 62, 982–8. Johnson, M.P. (1995). Patriarchal terrorism and common couple violence: two forms of violence against women. Journal of Marriage and the Family, 57, 283–94. Langhinrichsen-Rohling, J. (2005). Top 10 greatest ‘Hits’: important findings and future directions for intimate partner violence research. Journal of Interpersonal Violence, 20, 108–18. Langhinrichsen-Rohling, J., Hankla, M. & Stormberg, C.D. (2004). The relationship behavior networks of young adults: a test of the intergenerational transmission of violence hypothesis. Journal of Family Violence, 19, 139–51. Langhinrichsen-Rohling, J., Huss, M.T. & Ramsey, S. (2000). The clinical utility of batterer typologies. Journal of Family Violence, 15(1), 37–53. Langhinrichsen-Rohling, J., Huss, M.T. & Rohling, M. (2006). Aggressive behavior. In M. Herson (ed.), Cliniician’s Handbook of Adult Behavioral Assessment (pp. 371–400). New York: Elsevier. Langhinrichsen-Rohling, J., Schlee, K., Monson, C. et al. (1998). What’s love got to do with it?: Perceptions of marital positivity in H-to-W aggressive, distressed, and happy marriages. Journal of Family Violence, 13, 127–42. Loeber, R. & Loeber, M.S. (1998). Development of juvenile aggression and violence. American Psychologist, 53, 242–59. Lohr, J., Bonge, D., Witte, T. et al. (2005). Clinical utility of batterer typologies: another look. Journal of Family Violence, 20, 253–8. Lynam, D.R. (2004). Looking earlier in the life course for the GVA: comment on Holtzworth-Munroe and Meehan. Journal of Interpersonal Violence, 19, 1401–4.

ANTISOCIAL DISORDERS AND DOMESTIC VIOLENCE

517

Maiuro, R., Cahn, T. & Vitaliano, P.P. (1986). Assertiveness deficits and hostility in domestically violent men. Violence and Victims, 1, 279–89. Margolin, G., John, R.S. & Foo, L. (1998). Interactive and unique risk factors for husbands’ emotional and physical abuse of their wives. Journal of Family Violence, 13, 315–44. Margolin, G., Burman, B. & John, R.S. (1989). Home observations of married couples reenacting naturalistic conflicts. Behavioral Assessment, 11, 101–18. McEllistrem, J.E. (2004). Affective and predatory violence: a bimodal classification system of human aggression and violence. Aggression and Violent Behavior, 10, 1–30. Miles, A. (2000). Domestic Violence: What Every Pastor Needs to Know. Minneapolis, MN: Augsburg Fortress. Monson, C.M. & Langhinrichsen-Rohling, J. (1998). Sexual and nonsexual marital aggression: legal considerations, epidemiology, and an integrated typology of perpetrators. Aggression and Violent Behavior, 3, 369–89. Monson, C.M. & Langhinrichsen-Rohling, J. (2002). Sexual and nonsexual dating violence perpetrators: testing an integrated perpetrator typology. Violence and Victims, 17, 403–28. Murphy, C.M. & Eckhardt, C.I. (2005). Treating the Abusive Partner: An Individualized CognitiveBehavioral Approach. New York: Guilford Press. Norlander, B. & Eckhardt, C. (2005). Anger, hostility, and male perpetrators of intimate partner violence: A meta-analytic review. Clinical Psychology Review, 25, 119–52. O’Leary, K.D. & Curley, A. (1986). Assertion and family violence: correlates of spouse abuse. Journal of Marriage and Family Therapy, 12, 281–9. Remington, N., Murphy, C., Scott, E. & Simoneti, S. (1999, November). Relationship and behavioral characteristics associated with antisocial personality disorder among domestic violence perpetrators. Paper presented at the annual meeting of the association for advancement of behavior therapy, Toronto, Canada. Rosenbaum, A., Gearan, P.J. & Ondovic, C. (2001). Completion and recidivism among court- and selfreferred batterers in a psychoeducational group treatment program: implications for interventions and public policy. Journal of Aggression, Maltreatment and Trauma, 5, 199–220. Rosenbaum, A. & O’Leary, K.D. (1981). Marital violence: characteristics of abusive couples. Journal of Consulting and Clinical Psychology, 49, 63–76. Saunders, D.G. (1992). A typology of men who batter: three types derived from cluster analysis. American Journal of Orthopsychiatry, 62, 264–75. Saunders, D.G. (1996). Feminist-cognitive behavioral and process-psychodynamic treatments for men who batter: interactions of abuser traits and treatment model. Violence and Victims, 11, 393–414. Saunders, D.G. (2004). The place of a typology of men who are ‘maritally’ violent within a nested ecological model: a response to Holtzworth-Munroe and Meehan. Journal of Interpersonal Violence, 19, 1390–5. Saunders, D.G. & Parker, J. (1989). Legal sanctions and treatment follow-through among men who batter: A multivariate analysis. Social Work Research and Abstracts, 23, 21–9. Schumacher, J.A., Feldbau-Kohn, S., Smith-Slep, A.M. & Heyman, R.E. (2001). Risk factors for male-to-female partner physical abuse. Aggression and Violent Behavior, 6, 281–352. Stith, S.M., Smith, D.B., Penn, C.E. et al. (2004). Intimate partner physical abuse perpetration and victimization risk factors: a meta-analytic review. Aggression and Violent Behavior, 10, 65–98. Taft, C.T., Murphy, C.M., Elliot, J.D. & Morrel, T. (1999, November). Enhancing session attendance in group treatment for domestic abuse perpetrators. Paper presented at the 33rd Annual Convention of the Association for Advancement of Behavior Therapy, Toronto, Canada. Waltz, J., Babcock, J.C., Jacobson, N.S. & Gottman, J.M. (2000). Testing a typology of batterers. Journal of Counseling and Clinical Psychology, 68, 658–69. Weinshenker, N.J. & Siegel, A. (2002). Bimodal classification of aggression: Affective defense and predatory attack. Aggression and Violent Behavior, 7, 237–50.

CHAPTER 29

Workplace Violence Goes Beyond Psychopathology Michael H. Corcoran Henley-Putnam University, USA

The primary motivational factors for workplace violence are still often felt to be connected to retribution by disgruntled employees who have psychological issues (after all, it’s not normal to hurt others), or the criminal element from outside the workplace where no one in the workplace has direct control over their actions. Couple this with the adage coined by a colleague of mine, ‘The odds of you being a victim of workplace violence is about as great as being bitten by a shark while swimming in the ocean, and then when you get to shore you are struck by lightning’. Is it any wonder that little empirical data has been collected in this total area of violence? In June of 2003, the Department of Health and Human Resources report from the National Institute for Occupational Safety and Health (NIOSH), Centers for Disease Control and Prevention (CDC) stated that fairly detailed information has been described on fatal workplace violence; but much less is known about the circumstances and the risk factors for nonfatal workplace violence and almost no empirical knowledge exists about what has been implemented and what impact such strategies may have (Bartenfeld, 2003). What we can say is the obvious – for someone to commit a violent act there is a stronger likelihood that there is some psychopathology going on . . . whether it’s in the workplace or not. Additionally, because of new laws, corporate security managers, human resource managers, even school principals are faced with determining the potential of violence within their environments and they are looking to the mental health and law enforcement professions for guidance. However, the first major difficulty is that workplace violence by today’s conception covers more ground than simply dealing with a violent act that occurs within the workplace. The very definition varies depending upon which expert is consulted or which regulatory agency is asked. The general understanding of the definition is: workplace violence is generally considered to be any violence or threat of violence against workers on the job or away from the work site. Acts of concern can range from verbal threats to homicides, from disruptive behaviors such as interference with or obstruction of organizational functions, to behaviors that endanger the health or safety of others, including: shouting, use of profanity, waving of arms or fists or verbal abuse. Threatening acts can extend from physical actions short of personal contact to implicit threats. Violent job site

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

520

VOLUME I: DIAGNOSIS AND TREATMENT

behaviors can include physical assaults, other acts people would believe to be potentially violent, or specific threats to inflict physical harm. It is easy to see the all encompassing possibilities within workplace violence when trying to identify those who may become workplace violence perpetrators and then to define ways of dealing with the potential perpetrator. Thus workplace violence is more than simply shooting an employee. It can include threatening someone, harassing them (including sexually), stalking behavior and even intimidation (in Europe the more common terms include mobbing and/or bullying). With this in mind, it logically appears to be an overwhelming task to narrow the focus down to one common identifiable feature (psychopathological or otherwise) which will allow anyone to identify a potential workplace violence perpetrator as well as determine a common or consistent methodology of treatment. Just as it has been found with so many areas in dealing with human beings, a multidisciplinary approach seems to be necessary as humans are simply too convoluted. This author’s own doctoral research project, when trying to find a single modality of alleviating stress, proved the multidisciplinary approach was always more successful – both in identifying the way someone perceived stress as well as designing a stress alleviation process. While a clinician in a cancer clinic, this author consistently discovered that just as there was no one common cure even for the same types of cancer, helping patients understand and cope with their ailment via one methodology of treatment was also impossible since individuals perceive things differently and responded to treatment differently. . . so the multidisciplinary approach was the only responsible tactic of therapy – both physically and mentally.

PSYCHOPATHOLOGY IN THE WORKPLACE There have been many studies conducted in confined and controlled settings such as mental health facilities and jails that have shown a large population of those who commit a violent act have one diagnosis or another. Of course these are more controlled environments which help the collection of data. But these populations can hardly be compared to working on an assembly line or trying to sell a product to a customer. However, does one setting or another really have that much influence on the issue of a potentially violent act over another? Let us first examine what facts have been presented to distinguish and define the perpetrator of workplace violence. One of the better studies in this area is the 1999 study conducted by Theodore B. Feldman and Phillip W. Johnson, examining 255 incidents of workplace violence across the United States. It was exhaustive research involving examining newspaper accounts, personal contact with local law enforcement, the organizations involved, family, friends, victims, witnesses and even the perpetrators where possible. The study also included clinical interviews as well as psychological testing when possible. The results, while surprising in some categories, help shed light on other important considerations when dealing with ‘predicting’ the potential for workplace violence. No surprise was the fact that the largest category, almost 29 % of all the incidents, was committed by criminals and thus came from outside the work environment. The next category was the disgruntled employee and this accounted for approximately 19 %. No surprise again was that the overwhelming majority of acts were committed by males (96 %). The mean age in this study was approximately 30 years. For this section of the chapter, the revealing component of this study deals with the psychopathology levels of these perpetrators, starting with the fact that 89 % of the subjects

WORKPLACE VIOLENCE

521

studied had psychiatric diagnoses. The most common diagnosis was that of the antisocial personality (21 %), followed closely by depression (19 %) and then dropping down to the borderline personality disorder (13 %). Placing the diagnoses into revealing groups established that 41 % of the perpetrators had personality disorders, 21 % had affective disorders, 14 % had substance abuse disorders and 10 % had psychotic disorders. From this research the authors suggest that the recommendations for better background investigations – or banning assault weapons – would have little to do with stopping the majority of criminals who commit a workplace violent act with a handgun. On the other hand, they point to the revealing and surprising information that the psychological profile of the workplace violent perpetrator is much more convoluted than some of the earlier studies suggested. Those studies resulted in the assumption that the most likely perpetrator demonstrated paranoia, often delusional behavior as well as poor interpersonal skills, had few friends and demonstrated poor work performance. They point to the ‘narcissistic injury’ research which has uncovered a more comprehensive psychopathology element that may explain the more prevalent violent actions of those in the workplace. The cautionary note here, as with many similar studies, is the attempt to narrow the focus to the issues of the psychopathology of the potential perpetrator to identify their risk of violence within the workplace. It appears everyone is looking for that one identifiable personality disorder, that one instrument of prediction, that one clinically validated personality that will determine the likelihood of violent behavior. Other areas of concern are sometimes mentioned as in this case (e.g., race, gender, age, drug abuse, weapon availability), but the emphasis is on the identification of psychopathology. Now if a worker makes a threat against a supervisor this cannot be dismissed. Yet statistical formulas are of minimal value due to the infrequency of the act of violence supplying sufficient base rates for actuarial findings. A clinical approach is limited if there is no mental disorder, and even if testing and clinical interviews are administered and revealing, the relationship of the disorder to the potential target limits the relevancy of the findings.

OTHER DEFINING RESEARCH There is research that points to the behavioral approach to make this determination, defining clearly established actions and conduct to determine the likelihood of violent behavior. The literature is full of information establishing that similar behavior is the strongest prediction of future behavior. As recently as August 2006 at the Annual Association of Threat Assessment Professionals Conference, Michael G. Gelles said that when he deals with these issues of potentially violent individuals, whether it’s in the workplace or not, he is more concerned about the behavior, past and present, than the specific psychopathology of the individual (Gelles & Palarea, 2006). The caution here is the driving factor. To expedite a resolve, clinicians are often called upon to assess a situation ‘on the run’. An individual has already committed a violent act and is not available for obtaining clinical information. The immediacy of the situation dictates that the clinician finds a quicker way of prediction – hence it is easy to forsake those methodologies which may include additionally supportive or divergent information. Added to the question is the consideration of genetics contributing to this formula – are the biological predispositions so strong that they cause the violent behavior? Literature abounds with newly discovered elements of examining violence from a complex biological perspective. It is suggested by such authors as Debra Niehoff (1999) that by understanding

522

VOLUME I: DIAGNOSIS AND TREATMENT

human biology we can control violence, and some of these matters are addressed in other chapters of this text. There is the occupational psychologist/psychiatrist who not only wants to consider behavioral analysis of individual relationships and dynamics between individuals, groups and organizations (Tosi, Mero & Rizzo, 2000, pp. 1–29), but also personality theories, individual neurobiological operations as well as broader organizational development and change perspectives (Perrott, 2000). Finally, there are the ‘big picture’ psychiatric researchers who feel it is mostly due to a massive society issue which has increased the predilection of individuals to respond violently to problems and frustrations, that is, the media, movies, neglected and brutalized children, for example, Paul J. Fink, quoted by Grinfield (2000).

STALKING BEHAVIOR Stalkers and stalking in the workplace is also a genuine concern to the issue of violence, and in this twenty-first century, stalking via cyberspace must also be included. While definitions of stalking vary depending if you are a clinician or approaching the act from the legal perspective, suffice to say it is certainly a form of unwelcome and repetitive harassing or threatening behavior towards an individual. It can be in many forms: letters, emails, repetitive phone calls and/or voicemails, or the more common forms of always seeming to show up where the victim frequents, leaving messages or objects on the victim’s property and/or persistently vandalizing the victim’s property. The consistent psychopathology discovered and explained of these perpetrators by numerous researchers over the years (Davis, 2001; Meloy, 1994, 1997, 1998; Mullen & Pathe, 1994; White & Cawood, 1998; Zona, Sharma & Lane, 1993) has proven useful in predicting certain stalking behaviors (even identifying them for us). But there can still be no narrowing of focus to one psychological profile of a stalker as the variables of characteristics, relationships between subjects and the very environments themselves all played roles in the predictive outcome. This clearly demonstrates how one cannot preclude psychopathology from the mix or predictors, nor can one ever expect to deal with and explain or foresee potentially violent events by limiting the focus on the psychiatric disorders of the subject of concern. The difficulty with stalking, especially within the workplace, is that it often presents a more difficult situation to control as it frequently involves one who is completely removed from any controls from within the organization, and the likelihood is that the ‘stalker’ is simply not going to go away either on their own or because they are prompted – even after being arrested. Hence, with the regulatory pressures of providing for a safe work environment, stalkers within the workplace setting, even though most do not commit violent acts, must be considered potentially dangerous until a proper assessment can be obtained from an experienced professional.

BULLYING (MOBBING) ‘New evidence has been emerging of the impact and harm caused by non-physical violence, often referred to as psychological violence. . . . It is often considered to include bullying, mobbing, coercion, verbal abuse and sexual harassment. . . . the cumulative impact on the recipients results in very serious consequences’ (Chappell & di Martino, 2006, p. 17).

WORKPLACE VIOLENCE

523

What is this workplace bullying, and is mobbing essentially the same thing? It has been shown to be associated with higher turnover, decreased productivity and higher absenteeism within organizations. For the individual victim of bullying, the studies show a higher incidence of psychosomatic symptoms, physical illnesses and lower levels of job satisfaction. Because of this there have been many studies (mostly outside the United States) to try to define the mechanisms involved in this problem as well as identify personality traits and organizational factors that contribute to the problem. The easiest definition to explain the occurrence of bullying is: the repeated and persistent negative acts towards one or more individuals which involve a perceived power imbalance and creates a hostile work environment. Mobbing is often used when this situation involves several subjects ‘ganging up’ on another individual to obtain the same results, although ‘bullying’ is more of a UK, Ireland and Australia term while Germany prefers to use ‘mobbing’. All countries seem to interchange the term and have amassed such descriptive terms as ‘workplace incivility’, ‘victimization’ and ‘workplace aggression’. Bullying is often a difficult problem to identify within the workplace because of the numerous and often petty kind of negative behaviors that encompass bullying. The victim may experience isolation or the ‘silent treatment’. Coworkers or a supervisor may be overly critical of the individual, discounting ideas and suggestions. They may simply be staring at the individual, or be talking about the person as if they were not present and then speak in a demeaning or humiliating manner about the person. Hence, it is often suggested that the victim should ‘toughen up’ as this sounds more like the schoolyard antics all have lived through at one time or another. The major differences between bullying and other potential workplace violence situations are several: (i) it always involves individuals inside the organization; (ii) it is repeated, persistent and continuous; (iii) it has more to do with the subjective perception of the victim; (iv) not all acts of bullying can actually be identified as negative per se (e.g., not being asked to join coworkers for lunch; given a seemingly difficult deadline to meet); and (v) it invariably involves a power imbalance, that is, the target is the prolonged victim of so much negativity, they begin to feel inferior and see no way to defend themselves. Many researchers have attempted to explain this issue by identifying personalities and/or the psychopathology of both the perpetrators and the victims (Coyne, Seigne & Randall, 2000). Many others have chosen to look at the deficiencies or problems within the organization (Einarsen & Skogstad, 1996). What is being realized from all this research is that it is actually the interaction of the individuals involved and their situational factors that really defines the potentials for this problem as well as suggests the potentials for alleviation (Neuman & Baron, 1998).

AND WHAT OF THE TOOLS OF MEASUREMENT? There is now an abundance of research trying to define all of these issues to substantiate the validity in determining potentials of violence, especially establishing the individual’s psychopathology, as well as substantiating the stronger likelihood of recidivism. While bits and pieces of several assessment instruments have proven useful, the studies to date appear to favor the PCL-R (Psychopathy Checklist-Revised). Unfortunately this alone has raised some controversial issues which should be considered by anyone relying on this particular instrument to ‘label’ someone for any ‘adversarial proceeding’.

524

VOLUME I: DIAGNOSIS AND TREATMENT

While it seems adequate to suggest the PCL-R is a tremendously successful research tool, translating this data into clinical validity appears questionable. The creator of this instrument himself has said, ‘In cases where the assessments are likely to have a serious impact on an individual or a decision, I strongly recommend that at least two independent ratings be obtained and averaged’ (Hare, 1998, p. 113). The obvious question in any legal proceeding would then be who selects the independent raters, to what degree have they been trained to utilize this instrument, how can you determine their level of competence, and what level of information did they use to determine a sufficient data base? These questions were proposed by a recent paper (Campbell, (in press), p. 3) where the author goes on to say, ‘There is no available data demonstrating that averaging the PCL-R scores, obtained from defense and prosecution evaluators, is a valid procedure.’ The problem is not the scores of the clinical testing failing to predict an individual’s potential towards violence, nor is it trying to distinguish the psychopath from the nonpsychopathic personality as other articles in this text will substantiate – including the use of the PCL-R. The problem is simply the narrowness of the focus – trying to obtain that one measurement instrument that will ultimately be predictive and valid and then trying to place it into areas of assessment, especially as it relates to specific targeted violence. Additionally, the abandonment of the risk assessment instruments is not the answer as it can help in evaluating the contribution of psychopathology in the workplace. But what also must be taken into account are the interactions of the behaviors of all parties involved – within the specific environment of these interactions. This includes the organization itself, as well as needing to define the circumstantial behaviors within these confines. All this must then be related to the evaluation process and to this end determine if someone is at risk of committing a violent act towards a specific person(s) within a specific environment. This is the only narrowing of focus that should be addressed within the context of a threat assessment to determine the potential of violence in the workplace – does this person present a level of potential for violence toward that person within this environment?

THIS ‘HOLISTIC’ APPROACH An entirely different approach to this issue is thus an important consideration for it is important to have a set of investigative and operational activities designed to identify, assess and manage persons who may pose a threat of violence to identifiable targets (Fein, Vossekuil & Holden, 1995). This fact-based method of evaluation has been developed, refined and utilized by the United States Secret Service to protect its charges. Although the data to distinguish this approach was gathered by studying those who attacked or attempted to attack public officials (Fein & Vossekuil, 1999), a similar approach in the workplace makes the evaluation of the actual risk of violence towards a specific target more meaningful. By moving away from concerns of psychopathology alone and focusing on how the person of concern is processing his or her ideas as well as looking at past behaviors, indicators of a greater (or lesser) risk of targeted violence are more identifiable. This also precludes the attempt of trying to develop the ‘profile’ of the workplace violent perpetrator as to date the individuals who have committed such violent acts fit no such profile as there have always been ‘exceptions’. This ‘Secret Service’ process involves several critical steps towards the determination of the potential of violence by an individual. These are contained and covered in

WORKPLACE VIOLENCE

525

their ‘10-question survey’ which is available on their web site (http://www.secretservice. gov/ntac.shtml#programs) and virtually being reprinted in a variety of texts these days. But note that the issues to determine the potential for violence revolve around the expansion of looking at the narrowing interactions of the subject of concern, the potential victim(s) and their involvement within a specific environment. It is this type of action which has led many to question the success of this process; for individuals interviewed by the Secret Service have committed violent acts after the agency had deemed them ‘not a threat at this time’. However, the real success comes about from their effectively maintaining their charge – they have identified those individuals who are potential threats to their protectees when and if their protectee and the questioned subject are in the same environment. This process, as outlined and used by this author, includes the following four steps.

Subject Behavior and Cognitive Processing The first step requires looking at the potential volatile person’s behavior and thinking process. What kinds of behavior has the individual demonstrated in the past? How have they handled stressful situations in the past? What have been their responses and what have they stated to others that would give insight as to how they were processing these issues? Equally important, has the subject indicated one set of actions but demonstrated another? (‘If I have to work overtime again, I’m going to quit’, has been heard a dozen times from Bob – but he never has quit and he continues to work overtime.) Are they willing to accept responsibility for their own actions or do they blame others or situations for their problems? Are they impulsive, deceptive, secretive, manipulative, obsessive, callous, egotistical, etc. – these are many of the behavioral character traits that should be assessed in order to evaluate the persons probable thought process and behavior – and yes, their psychopathology.

Past Behaviors Related to the Specific Environment The second step in this process requires determining how the interaction of the individual’s past situations that led to a volatile reaction occurred. Hence this becomes an environmental concern as much as an internal processing issue. Because of this consideration, it would be impractical at best to consider all the environments that this individual may interact in. This might be compared to the situational aspect of removing the violent criminal from his/her living environment, placing the subject in a controlled environment where ‘rehabilitation’ appears to occur, yet discovering once released from this ‘controlled’ environment the recidivism rate in the same or similar violent crime seems disproportionately high. The question seems not if they would be violent again, but when were they more likely to act out violently again?

Relationship Between Subject and Victim(s) The third step in this process involves assessing the current situation that the subject is in and how the potential victim is connected. In the workplace, let’s take the example of the potential perpetrator of violence who seems to get upset every time he has been asked

526

VOLUME I: DIAGNOSIS AND TREATMENT

to go to the supervisor’s office. When he has been asked to go to the supervisor’s office, if the potential victim is the supervisor, then this third step is waving its flag. Thus it is important to realize another element in this overall assessment process. The potential for violence is also connected to the number of times the ‘provocation’ is presented. (In the study by Feldman and Johnson referred to in the beginning of this chapter this was what they referred to as ‘precipitant’ behavior – either the perpetrator acted spontaneously or the ‘anger’ built up over time. In 251 out of 252 cases, they determined warning signals were seen (built up over time) and either ignored or attempts to mitigate the anger were unsuccessful.) If the potential perpetrator is never called to the supervisor’s office again to talk to this specific supervisor, isn’t the potential for violence lessened? Thus this concept of a ‘build up’ of behaviors leading to the eventual acting out of a violent act becomes an important consideration.

Subject’s Relationship to Violence The last step of this assessment process involves questioning the subject’s relationship with violence as well as their ability to carry out their ‘threat’. For example, while the actual act of violence may not have been carried out (actually shooting someone), has the individual been talking about doing this as well as recently joining an ‘extremist’ group, and is now reading a ‘Guns & Ammo’ type magazine during their break at work? Additionally, what is known of their capability? If someone says they want to shoot someone and they have no access to or knowledge of a weapon, does this tend to lessen the overall concern? Questions concerning their outside interests and hobbies become relevant. This again helps to broaden the focus of the causes. Yet the application is to only apply these causes to the narrowness of this specific environment and its interaction between potential victim and perpetrator. To further illustrate the point, the fact that someone owns a gun and enjoys target shooting is hardly reason enough to suggest they are going to shoot their supervisor after just being overheard saying something like, ‘If he tells me that one more time, I’m going to shoot him’. This statement coupled with the target shooting is cause for concern and should be assessed. However, ‘People make threats for a variety of reasons: to intimidate, to coerce, to express anger, to bring attention to themselves, to get help, to force a change in their circumstances, to warn before they act, to be stopped’ (Fein & Vossekuil, 1999, p. 330). Further evidence of such a statement being of limited value comes from the research of Dietz and Martell (1989, pp. 166–7): ‘We have disproved the myth that threats and threateners are the only communications or people of concern. The most common assumption in all quarters – laymen, mental health professionals, law enforcement professionals and lawmakers – is that threats foretell more dangerous behavior, but that other odd communications do not. This is a groundless assumption and the source of more misguided policy and decision making than any other error in this field.’

DISCUSSION One cannot simply overlook the psychopathology of the individual and how that affects the overall assessment process. Certainly it must be readily agreed that many of the four points

WORKPLACE VIOLENCE

527

addressed in the above process are revealing or at least probative of those very issues. But how can the threat of violence actually be labeled specifically within the parameters of an environment via determining psychopathology alone? The issue is not the exclusion of how mental illness enters into the consideration, for in the Secret Service research of all persons known to have attacked a public figure in the United States since 1949 (Fein et al., 1995) almost all had psychological problems and the same was true in the workplace violence research done by Feldman and colleagues (1999). The question becomes one of relating the psychopathology findings to the degree of risk of a specific target of violence, especially when, as in the Secret Service study, all perpetrators were able to think clearly enough to plan and organize their attack. While there may seem to be no psychological instrument that consistently and reliably predicts violent behavior for all assessment settings, appropriate psychological testing can prove valuable in determining potential attributes or characteristic behaviors that are known precursors of violence. The question becomes (mostly due to liability issues) what are the most important considerations in making these types of assessments that are available today? Since the US Secret Service is the only long-term standing agency to be directly responsible for preventing targeted violence (many others are now doing similar processes with the new laws involving stalking and terrorism), their format and research to date appears to provide a more viable alternative to addressing the issues. When it comes to assessing potentials for violence, the methodology for resolve must be a multidisciplinary approach because the subjects of concern are complex and uncertain human beings. A workplace violence assessment must be viewed as a dynamic process, not a static one. It is an ongoing process which must not only include an individual’s potential towards violence, but also the relationship of the individuals involved as well as the environment in which they are involved. Additionally, what is the organization going to do about it once it is discovered? How is the organization moving forward to lessen its liability, to mitigate its accountability as well as acknowledge its responsibility to its employees because of what it knew, or ‘reasonably’ should have known? If the narrowness of the focus of the assessment process looks primarily at the psychopathological aspects of a subject, then what of the laws that require the organization to make ‘reasonable accommodations’ for an individual who is found to have a mental disorder? By focusing on this alone, it can be argued that the organization is providing the very defense for the subject who may in fact present a potential danger to the organization – or at least some of its members. For unless the organization can substantiate that the person represents a significant risk of harm to themselves and/or others within that environment, or that they truly cannot do the job, they cannot do anything more than provide that person with another place to work within that organization if all they discover is a degree of mental illness.

CONCLUSION The circumstances and targets of workplace violence vary widely as do the motivations of the perpetrators. Also, because of the low number of violent occurrences, predictability by any means is limited. Additionally, there is little research on either the criminal offender or the mentally ill and how these populations generally develop within the workplace. Therefore the issue of understanding and dealing with workplace violence is not the simplistic

528

VOLUME I: DIAGNOSIS AND TREATMENT

narrowing of focus of either the psychopathology or the behavior of the individual – and if researchers continue to focus on these areas alone they will never develop the needed answers to this problem. Instead, research needs to broaden its focus on the concepts of looking at the individuals involved, their total relationships to one another and to their environment, and then determine how to best narrow the end focus to establish a more definitive potential of violence between defined subjects within a defined environment. The fact-finding methodology promoted by the Secret Service at least prevents the influence of relying on ‘profiling’ or looking for the ‘right signs’. Further, it provides a definitive focus on an individual’s way of thinking, how he or she is processing the information, his or her exhibited patterns of behavior and thus to a certain extent, just what direction he or she is moving towards a violent act. . . or not. This format should progress with existing risk assessment tools as research further studies and determines appropriate methodologies for assessments.

REFERENCES Bartenfeld, T.A. (2003). Proposed Data Collection Submitted for Public Comment and Recommendations. Department of Health and Human Services, Center for Disease Control and Recommendation, Federal Register, 68(107), p. 33494. Campbell, T.W. (in press). The validity of the Psychopathy Checklist-Revised in adversarial proceedings. Journal of Forensic Psychology Practice. Chappell, D. & di Martino, V. (2006). Violence at Work, third edition. Geneva: International Labour Office. Coyne, I., Seigne, S. & Randall, P. (2000). Predicting workplace victim status from personality. European Journal of Work and Organizational Psychology, 9(3), 335–49. Davis, J.A. (2001). Stalking Crimes and Victim Protection. New York: CRC Press. Dietz, P. & Martell, D. (1989). Mentally Disordered Offenders in Pursuit of Celebrities and Politicians. Final Report. Washington, DC: National Institute of Justice. Einarsen, S. & Skogstad, A. (1996). Bullying at work: epidemiological findings in public and private organizations. European Journal of Work and Organizational Psychology, 5(2), 185–201. Fein, R.A. & Vossekuil, B. (1998). Protective Intelligence and Threat Assessment Investigations: A Guide for State and Local Law Enforcement Officials. July, NCJ 170612. Washington, DC: US Department of Justice, Office of Justice Programs, National Institute of Justice. Fein, R.A. & Vossekuil, B. (1999). Assassination in the United States: an operational study of recent assassins, attackers, and near-lethal approachers. Journal of Forensic Science, 44(2), 321–33. Fein, R.A., Vossekuil, B. & Holden, G.A. (1995). Threat Assessment: An Approach to Prevent Targeted Violence. NIJ Research in Action. September. Feldman, T. & Johnson, P. (1999). Workplace violence: a new form of lethal aggression. In H. Hall (ed.), Lethal Violence, Pacific Institute for the Study of Conflict and Aggression. New York: CRC Press. Gelles, M.G. & Palarea, R.E. (2006). Critical Construct of the Behavioral Based Threat Assessment. Presented at the annual Association of Threat Assessment Professionals Conference, Anaheim, California. Grinfield, M. (2000). An interview with Paul J. Fink, M.D. In ‘The big picture, averting the course of violence’. Psychiatric Times, 17(1), www.psychiatrictimes.com/article/ showArticle.jhtml?articleId=186700084 . Hare, R.D. (1998). The Hare PCL-R: some issues concerning its use and misuse. Legal and Criminological Psychology, 3, 99–119. Lipman, I.A. (1999). The Lipman Report: Workplace Violence. Memphis: Guardsmark, Inc. Meloy, J.R. (1994). The Psychopathic Mind: Origins, Dynamics and Treatments. Northvale, NJ: Jason Aronson.

WORKPLACE VIOLENCE

529

Meloy, J.R. (1998). The Psychology of Stalking: Clinical and Forensic Perspectives. San Diego: Academic Press Meloy, J.R. (1997). Violent Attachments. Northvale, NJ: Jason Aronson. Mullen, P.E. & Pathe, M. (1994). Stalking and the pathologies of love. Australian and New Zealand Journal of Psychiatry, 28, 469–77. Neuman, J.H. & Baron, R.A. (1998). Workplace violence and workplace aggression: evidence concerning specific forms, potential causes, and preferred targets. Journal of Management, 24(3), 391–419. Niehoff, D. (1999). The Biology of Violence. New York: Free Press. Perrott, L. (2000). Psychiatrist in corporate boardroom. Psychiatric Times, 17(10), www.psychiatrictimes.com/p001055.html . Tosi, H.L., Mero, N.P. & Rizzo, J.R. (2000) Managing Organizational Behavior, fourth edition. Malden, MA: Blackwell. White, S.G. & Cawood, J.S. (1998). Threat management of stalking cases. In J.R. Meloy (ed.), The Psychology of Stalking: Clinical and Forensic Perspectives (pp. 295–315). San Diego: Academic Press. Zona, M.A., Sharma, K.K. & Lane, J. (1993). A comparative study of erotomanic and obsessional subjects in forensic sample. Journal of Forensic Science, 38, 894–903.

CHAPTER 30

Addressing the Associated Conditions of Drug and Alcohol Abuse Falk Kiefer and Karl Mann Central Institute of Mental Health (CIMH), University of Heidelberg, Germany

Antisocial disorders including conduct disorder (CD), oppositional defiant disorder (ODD) and antisocial personality disorder (APD) are frequently associated with substance use disorders, especially alcohol abuse (Hesselbrock, Hesselbrock & Stabenau, 1985; Lewis & Bucholz, 1991). The evaluation of inpatient alcoholic treatment programs indicates that approximately 15 % of male alcoholics and 5 % of female alcoholics have primary antisocial personalities with secondary alcoholism (Goodwin & Guze, 1994). CD, ODD and APD interact with pathogenesis and clinical course of addictive disorders. Subjects with APD were shown to have an earlier age of onset of first intoxication, problem drinking and alcohol dependence (Cadoret, Troughton & Widmer, 1984; Hesselbrock, Hesselbrock & Stabenau, 1985; Hesselbrock, Hesselbrock & Workman-Daniels, 1986; Rounsaville et al., 1987). In these comorbid patients, the course of alcohol dependence was noted to be more severe including more alcohol-related arrests, occupational and social consequences of drinking. Furthermore, it was reported that these subjects are at an increased risk for higher average daily alcohol consumption and concomitant substance use disorders (Cadoret, Troughton & Widmer, 1984). The development of an alcohol use disorder in adolescence may be an indicator of other problems: adolescents with alcohol use disorders have high rates of comorbid psychopathology; especially those interfering with social functioning (e.g., CD, APD) and disorders that cause severe depression or increased anxiety (Bukstein, Brent & Kaminer, 1989; Clark & Neighbors, 1996). Understanding the effects of comorbid psychopathology on the development and course of alcohol use disorders may enhance preventive and treatment interventions for adolescents with alcohol use disorders.

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

532

VOLUME I: DIAGNOSIS AND TREATMENT

EPIDEMIOLOGY Up to 80 % of adolescents with an alcohol use disorder present also some kind of psychopathological disturbance (Rohde, Lewinsohn & Seeley, 1996). Among a group of alcohol-dependent adolescents receiving alcohol dependence therapy, 89 % also fulfilled the diagnostic criteria of a CD, a major depressive disorder, or both (Clark et al., 1997). Adolescent males with substance use disorders and male adults who developed substance use disorders as adolescents were shown to have higher rates of disruptive behavior disorders and major depression as well as more rapid progression from first use to substance dependence compared with men who developed substance use disorders as adults (Clark, Kirisci & Tarter, 1998). Subjects with APD were shown to have an increased risk for higher average daily alcohol consumption and concomitant substance use disorders compared with non-APD subjects (Cadoret, Troughton & Widmer, 1984; O’Boyle & Barratt, 1993). The ECA study (Epidemiologic Catchment Area Program; Regier et al., 1990) – an investigation on dual diagnosis accomplished in the 1980s – showed that the lifetime prevalence of psychological diseases of the US-American population is 22.5 %, that of alcohol use disorders 13.5 %, and that of drug use disorders 6.1 %. Twenty-nine percent of individuals who suffer from mental disorders also experienced a substance use disorder. Hence, the probability of developing a comorbid addictive disorder additionally is increased by 2.7 times compared to the general population. Only 16.2 % suffered exclusively from a mental disorder. On the other hand, among patients with alcohol use disorder 45 % developed a secondary mental disorder and/or addiction. Also the results of the NCS study (National Comorbidity Survey; Kessler & Merikangas, 2004), with representative population samples from several western countries, showed an important correlation between mental health and substance use disorders. In this survey, the probability of developing a substance use disorder was increased by 2.3 with concurrent mental disorders. Fifty percent of people suffering from a mental health disorder developed a substance use disorder, too (one-year prevalence: 14.7 %). In comparison with data gained in the 1980s, the prevalence rates of single mental health disorders as well as of dual diagnoses seems to have increased considerably in the 1990s. Regarding borderline personality disorder, the prevalence of comorbidity with substance use disorder is considerable. Clinical studies showed prevalence rates of both borderline personality disorders combined with alcohol abuse of about 49 % as well as prevalence rates of personality disorders combined with drug abuse of about 38 % (Moggi & Donati, 2004). Conversely, comorbidity of borderline personality disorder was found in 14.3 % of patients with an alcohol use disorder; in 16.8 % of patients with cocaine dependence and 18.5 % of patients with an opiate use disorder (Moggi & Donati, 2004).

ETIOPATHOGENESIS AND DIAGNOSTIC DIFFERENTIATION Three main theories have been proposed to explain the co-occurrence of antisocial disorders and substance use disorders. The first suggests that the presence of psychopathology increases the adolescent’s risk of developing a substance abuse (Zucker, 1986). Second and

DRUG AND ALCOHOL ABUSE

533

conversely, substance use disorders may influence the development of psychopathology through social, psychological and neurobiological disturbance (Martin & Bates, 1998). The third theory claims that psychopathology and substance use disorders may be linked indirectly by shared risk factors. Hence, the development of both antisocial behaviors and substance use disorders can be explained by the combination of environmental, including parental and socioeconomic factors, family as well as individual characteristics, which may increase the adolescent’s vulnerability to these problems. Therefore substance abuse can be conceived as one component of a multitude of deviant behaviors resulting from common risk factors. Affecting the severity and outcome of a substance use disorder as well as the coexistent deviant social behavior, these shared risk factors may act either independently or synergistically. Several longterm studies of adolescents and young adults supported this theory (Donovan & Jessor, 1985). On the other hand, the fact that APD and substance abuse often co-occur and share common symptoms has raised questions about the genotypic–phenotypic heterogeneity and overlap of these two disorders. Some researchers distinguish between alcoholic sociopaths and sociopathic alcoholics (Rada, 1978) and point to important differences in the onset and development of antisocial behavior and alcoholism. Schuckit and colleagues established the primary versus secondary classification of comorbid conditions in alcohol use disorders (Schuckit & Irwin, 1989). In this concept, it is hypothesized that there is a distinction between alcohol use disorders occurring independent of pre-existing psychiatric disorders, that is, primary alcohol use disorders, and those occurring as a consequence of another major psychiatric disorder, that is, secondary alcohol use disorders. Results from cross-sectional studies indicate that mainly two personality characteristics are related to alcohol consumption: (i) impulsivity/novelty seeking and (ii) neuroticisms/negative emotionality. The latter reflects consequences of alcohol consumption (neuroticism/negative emotionality) at least to a certain extent. Frequent use of alcohol enhances the risk of developing depressive or anxiety symptoms through, for example neurophysiological processes. The first personality characteristic is consistent with results from longitudinal section studies suggesting that antisocial behavior and hyperactivity are related to later excessive alcohol use (Robins, 1966). Negative affectivity turned out to be less important in these studies. Findings from cross-sectional studies led researchers to the conclusion that there are mainly two types of alcoholism. Babor and colleagues (1992) and Cloninger and colleagues (1981) are the leading representatives. The latter (Cloninger, Bohman & Sigvardsson, 1981) proposed two potential subtypes of alcohol use disorder based on the Stockholm Adoption Study: type 1 (low novelty seeking/high harm avoidance) or ‘milieu-limited’ alcoholism is associated with adult onset and low criminality. It is found in both female and male offspring of alcohol-dependent biological parents and is influenced by postnatal environmental effects in the adoptive family. In contrast, type 2 (high novelty seeking/low harm avoidance) or ‘male-limited’ alcoholism is thought to have an early onset and is usually associated with antisocial traits. Severe, recurrent alcohol dependence and delinquency often begins during adolescence. It is suggested that type 2 alcoholism is genetically transmitted primarily from father to son showing little environmental influence. Anthenelli et al. (1994) reported a prevalence rate of 73 % between type 2 alcohol-dependent subjects and APD.

534

VOLUME I: DIAGNOSIS AND TREATMENT

Schuckit and Irwin (1989) suggested that Cloninger’s type 2 alcoholism (impulsivity/ novelty seeking) might represent a separate and independent diagnostic entity, which is characterized mainly by APD and not alcohol dependence itself, challenging the validity of Cloninger’s typology because type-2 alcoholism rather seems to be an artifact of comorbid APD. Thus, alcohol abuse or dependence might be a frequent but secondary phenomenon occurring in the course of APD. Schuckit and Irwin (1989) concluded that the premorbid course of APD is unique compared to alcohol-dependent subjects without comorbid conditions. All in all, with type I alcoholism reflecting alcohol sequels and type II being an artifact of comorbid APD, the validity of such typologies is rather controversial. Furthermore, the authors argued that the prognosis of patients with comorbid APD is less favorable not only due to alcohol-related problems but also because of their increased likelihood of having an additional substance use disorder and showing violent and criminal behavior. Finally, APD itself may be genetically influenced by factors different from those of alcohol dependence. Generally, genuine personality measures such as extraversion, neuroticism or novelty seeking had only minimal effects on later alcohol consumption. More important factors could be measures like the affiliation with deviant groups or poor school achievement as proximal risk factors. Sher and Trull (1994) revealed that deviance proneness is an important factor in the transmission of alcohol problems. The authors conclude that childhood temperament traits of impulsivity and disinhibition, accompanied by ineffectual parental control, will lead to deficits in socialization, associated with a range of problem behaviors such as poor academic performance, school failure, delinquent behaviors, deviant peers, and – last but not least – alcohol/substance abuse.

CRIMINOLOGICAL ASPECTS OF DRUG AND ALCOHOL ABUSE There is a strong association between criminality and alcohol use disorders (Collins, 1982; Guze, Goodwin & Crane, 1969) and other types of substance abuse (Fry, 1985; Nurco et al., 1985). Significantly higher prevalence rates of alcohol use disorders and drug abuse are found in offenders with APD (Collins, Schlenger & Jordan, 1988; Lewis, Cloninger & Pais, 1983). Collins and colleagues found that 71.3 % of detained offenders with APD showed a lifetime diagnosis of alcohol abuse or dependence compared with 40.2 % of the non-APD offenders. The risk of developing a drug use disorder was also increased among APD offenders (28.3 %) than among non-APD offenders (10.4 %). Hence, detainees with a lifetime APD diagnosis clearly had higher co-occurrences of lifetime alcohol and drug disorders. Also in detained adult offenders, the comorbidity of personality disorder and substance abuse is high. Patients with personality disorder are more likely than patients without a personality disorder to have a diagnosis of alcoholism or drug disorder, to abuse specific drugs (alcohol, amphetamines, barbiturates and opoids) and to use multiple drugs (Smith & Newman, 1990). While personality disorder has been extensively researched among adult offenders, surprisingly little research has focused on adolescent offenders. The incidence of personality disorder in detained adolescent male offenders is estimated at 34 % (Forth, Kosson & Hare, 1996; Hemphill, Hart & Hare, 1994), while its comorbidity with substance abuse is unknown.

DRUG AND ALCOHOL ABUSE

535

Alcohol drinking by the offender, the victim or both often precedes violent events, including murders. Criminals who use illegal drugs commit robberies and assaults more frequently than do nonuser criminals, and they commit them especially frequently during periods of heavy drug use. In a study of New York City murders in 1988, researchers classified more than half of the homicides (53 %) as drug-related: 39 % in the course of drug distribution, 8 % through pharmacological effects on the offender, 2 % while the offender was obtaining money to buy drugs and 4 % through more than one of these links (Goldstein et al., 1989). Whereas alcohol consumption commonly seems to increase aggressive behaviors, amphetamines, cocaine, LSD and phencyclidine (PCP) can reach to violent outbursts in certain vulnerable individuals by inducing psychosis-like symptoms. Pre-existing psychosis especially appears to account for occasional violent outbursts by people who are under influence of amphetamines or hallucinogens, in particular PCP. While these drugs are well known to cause disorganized, bizarre behavior, they trigger violence in only a few people who are not also psychotic. However, it has to be kept in mind that illegal drugs and violence are also linked by drug marketing: disputes among rival distributors, arguments and robberies involving buyers and sellers, and property crimes committed to raise drug money. Research on humans and many animal species suggests that there are several neurobehavioral links between violence and psychoactive substances. Use of psychoactive substances during pregnancy affects fetal development and causes learning and communication problems that, in turn, increase the risk of early grade school failure, a well-documented precursor of violent behavior. Marijuana and opiates temporarily inhibit violent behavior, but withdrawal from opiate addiction tends to exaggerate both aggressive and defensive responses to provocations. Evidence from research on animals and humans indicates that patterns of substance abuse and aggressive behavior reinforce each other. Patterns of aggressive behavior and substance abuse often become intertwined starting in childhood. Early childhood aggression is a predictor of later heavy drinking, and the combination is associated with an above-average risk of adult violent behavior, especially among those who also abuse other psychoactive drugs.

TREATMENT COURSE AND PROGNOSIS Inadequate treatment of patients with dual diagnoses often leads to an unfavorable course of the disease with alternating phases of improvement and deterioration. In delivering care to patients with primary APD and secondary alcoholism it is necessary to recognize the high rates of concomitant drug abuse and the elevated risk for the commission of serious crimes by these individuals (Liskow et al., 1990; Randolph & Yates, 1993). In alcohol rehabilitation programs, the APD subject is more likely to manipulate other patients against staff and is less likely to complete the program. APD individuals frequently require a large amount of staff time, the result of which is that some programs choose to limit the number of APD individuals allowed to participate within a particular group. However, due to disruptive behaviors and lack of cooperation resulting from the APD, in some cases a single patient may also interfere with the safe and effective treatment of other patients to an extent that a hospitalized treatment can hardly be accounted. While a hospital should do what it can to treat such a patient, no hospital should place other patients, physicians or hospital staff in a potentially dangerous or harmful situation.

536

VOLUME I: DIAGNOSIS AND TREATMENT

Moreover, with more care being offered, problems often arise with noncompliance, lateness, missed appointments, abuse of medications and abuse of hospital staff. Treatment course and prognosis of patients with dual diagnoses depend significantly on the severity of the two disturbances; however, treatment strategies focusing on behavior change are successful for adolescents with co-occurring alcohol use disorder and sociopathic disorder. Those strategies include family interventions, contingency management programs (which offer incentives, such as retail items or special privileges, along with social reinforcement to encourage proper behavior), and social skills training (Bukstein, 1995). There is an exigent need of more intensive treatment strategies for adolescents with serious conduct and alcohol-related problems. In this context, the so-called multisystemic treatment (MST) developed by Henggeler and colleagues (1998) has shown to be efficacious. MST is an intensive multidimensional approach which combines family, peer, school and community interventions with individual treatment to aim at multiple risk factors and problems. Treatment sessions are carried out at the patient’s home and at appropriate times, which again result in fewer missed appointments and more intensive family involvement in treatment (Henggeler et al., 1996). Family interventions are designed to enhance effective education and poor family cohesion by using strategies from multiple theoretical bases. Parents are instructed to supervise their child’s relationships with peers and to support improved school achievement. Individual interventions with the adolescent tend to skills training and behavior change.MST has been evaluated in controlled trials and has shown to be effective in reducing antisocial behaviors, substance-related arrests and substance use (Henggeler et al., 1998). Moggi and Donati (1999) contributed a framework for integrated treatment of persons with co-occurring mental disorders and substance use problems. Research showed that an accurate and individualized view of the patient’s problems and individualized treatment planning is associated with better outcomes (Grawe, 1998). A key factor in successful treatment is a precise understanding of the specific interactions between substance use disorders and mental disorders. Basic principles of intervention according to Grawe (1998) are, for example, problem updating, clarification perspective, problem solving and resource updating. A first step to identify adequate treatment goals are diagnostic issues and treatment allocation. Consequently, the authors suggested the following classification:

r Type 1: severe substance use disorder (including polysubstance use) and severe psychopathological burden (e.g., schizophrenia, severe depressive episodes, antisocial or borderline personality disorders) → inpatient integrated treatment r Type 2: mild substance use disorder and severe psychopathological burden (e.g., schizophrenia, severe depressive episodes, antisocial or borderline personality disorders) → inpatient treatment with the focus on the mental disorder r Type 3: substance use disorder (including polysubstance use) and mild psychopathological burden (e.g., anxiety disorders, mild/moderate depression) → inpatient treatment with the focus on the substance use disorder r Type 4: mild substance use disorder and mild psychopathological burden (e.g., specific phobias, mild depression) → outpatient integrated treatment

DRUG AND ALCOHOL ABUSE

537

On the basis of previous conceptualizations (Osher & Kofoed, 1989), four treatment phases have been postulated: 1. Enhancing insight and therapeutic alliance through diagnostic issues, problem and resource updating, sharing of information on co-occurring disorders (COD) and treatment principles. 2. Enhancing motivation for change by executing principles of motivational interviewing (Miller & Rollnick, 2002). Both substance use disorder and mental disorders should be considered. 3. Behavioral experiential change by applying evidence-based treatment strategies (i.e., on personality disorder and substance use disorder). Although treatment for substance use disorder and mental disorder should begin simultaneously, abstinence is a precondition. 4. Relapse prevention and health promotion by learning skills for relapse prevention and self-management as well as elements of a healthy and satisfying lifestyle to stabilize patients and to enable them to live in a self-determined fashion. This strategy has proven to be successful. Multi-center evaluation studies have revealed better results for this method compared to traditional treatment without COD orientation (one-year follow-up: abstinence: 40.9 % vs. 32.6 %; no psychiatric symptoms: 71.4 % vs. 64.5 %, respectively) (Moggi et al., 1990, 1999). Treatment approaches focusing on behavior change should additionally include pharmacotherapy for adolescents with conduct disorder and alcohol use disorders. Impulsivity, aggression or anxiety is often shown by adolescents with conduct disorder; all of which may be improved by pharmacotherapeutic treatment. Hence, the prevalent comorbidity of conduct disorder with ADHD suggests that medication with a stimulant for these adolescents could be effective. However, as discussed earlier, the use of stimulants like methylphenidate or dextroamphetamine (Klein et al., 1997) can be problematic due to the risk of abuse and illegal sale and should be prescribed to ADHD children only under serious clinical implications. In a large, well-characterized sample of pediatrically and psychiatrically referred ADHD and non-ADHD youth, pharmacotherapy for ADHD did not predict an increased risk for substance use disorder. This study found instead that subjects with ADHD who did not receive pharmacologic treatment were at a significantly increased risk for substance use disorder suggesting that pharmacotherapy may protect children with ADHD from this risk (Goldman et al., 1998; Spencer et al., 1996; Wilens & Biedermann, 1992). If substance abuse has led to physical dependence, detoxification often is the first necessary step into treatment. When patients experience withdrawal symptoms, they are directly confronted with the negative effects of drug consumption. During this time, they can be motivated for further treatment. If detoxification is accompanied by a treatment program that includes motivational sessions to encourage abstinence, psychosocial counseling and additive therapies such as the teaching of coping strategies, social skills training or creative work can be labeled a ‘qualified detoxification program’ (Mann & Mundle, 1996). In Germany, five studies showed that 3–8 weeks of qualified detoxification successfully motivated patients for abstinence. About 50 % of the patients who were available for followup after 6–28 months were abstinent (Mann & Stetter, 2002). Even if all patients who were not available for follow-up are counted as relapsers, the abstinence rate was still impressive

538

VOLUME I: DIAGNOSIS AND TREATMENT

and ranged from 46 % at six months after detoxification (Stetter & Mann, 1997) to 32 % when patients were assessed 28 months after termination of the qualified detoxification program (Bauer & Hasen¨ohrl, 2000). In the hospital, patients should be motivated to acknowledge their alcohol-related problems. They should be encouraged to choose help from a number of options provided by the professional team. Successful referral is usually improved if patients contact self-help groups or counseling centers while they are still on the ward. A core element of all qualified detoxification programs is the cooperation with self-help groups, such as ‘Alcoholics Anonymous’, and with the counseling centers that are often provided by the city government or by the churches. In a modern disease management concept, hospital detoxification is seen as just one step in a chain of events to stabilize alcohol abstinence. Qualified detoxification is not only successful in promoting abstinence and referring patients to further treatment, it also significantly reduces health costs due to a marked reduction in alcohol-related health costs (Driessen et al., 1999). However, an alcohol rehabilitation program will not significantly change the APD itself. The philosophy of treatment is that a sober APD individual is less likely to get into trouble and more likely to be able to adjust well to life situations than a drinking APD individual (Schuckit, 1995). After detoxification, some patients need further treatment by means of regular consultations with a psychiatrist or psychologist, especially if mood or anxiety disorders persist. Furthermore, due to the prolonged recovery of some monoaminergic systems and the interaction with negative mood states (Heinz et al., 1998), some patients need adequate psychiatric outpatient treatment after the cessation of acute withdrawal symptoms. It has been shown repeatedly that pharmacological treatment for example with acamprosate or naltrexone is efficacious in the reduction of craving and risk of relapse in abstinent alcohol-dependent patients (Kiefer et al., 2003; Spanagel & Mann, 2005). For illegal drugs too, pharmacological therapies that reduce drug craving may lower the demand that supports violent drug markets. For decades, methadone and related chemicals have been used to reduce craving for heroin. There is no analog to methadone for treating addiction to cocaine in powdered or smokable form. However, using animals as test subjects, researchers have identified the receptors for certain subtypes of two brain chemicals, dopamine and norepinephrine, as promising sites to begin developing such medications.

REFERENCES Anthenelli, R.M., Smith, T.L., Irwin, M.R. & Schuckit, M.A. (1994). A comparative study of criteria for subgrouping alcoholics: the primary/secondary diagnostic scheme versus variations of the type 1/type 2 criteria. American Journal of Psychiatry, 151, 1468–74. Babor, T.F., Hofmann, M., DelBoca, F.K. et al. (1992). Types of alcoholism. I. Evidence for an empirical derived typology based on indicators of vulnerability and severity. Archives of General Psychiatry, 49, 861–8. Bauer, I. & Hasen¨ohrl, G. (2000). Therapieerfolg Alkoholabh¨angiger nach qualifizierter Entzugsbehandlung und konventioneller Entgiftung (vergleichende 28-Monats-Katamnese). Sucht, 46, 250–9. Bukstein, O.G. (1995). Adolescent Substance Abuse: Assessment, Prevention, and Treatment. New York: John Wiley and Sons, Inc. Bukstein, O.G., Brent, D.A. & Kaminer, Y. (1989). Comorbidity of substance abuse and other psychiatric disorders in adolescents. American Journal of Psychiatry, 146, 1131–41.

DRUG AND ALCOHOL ABUSE

539

Cadoret, R., Troughton, E. & Widmer, R. (1984). Clinical differences between antisocial and primary alcoholics. Comprehensive Psychiatry, 25, 1–8. Clark, D.B. & Neighbors, B. (1996). Adolescent substance abuse and internalizing disorders. Child and Adolescent Psychiatric Clinics of North America, 5(1), 45–57. Clark, D.B., Pollock, N., Bukstein, O.G. et al. (1997). Gender and comorbid psychopathology in adolescents with alcohol dependence. Journal of the American Academy of Child and Adolescent Psychiatry, 36, 1195–203. Clark, D.B., Kirisci, L. & Tarter, R.E. (1998) Adolescent versus adult onset and the development of substance use disorders in males. Drug and Alcohol Dependence, 49, 115–21. Cloninger, C.R., Bohman, M. & Sigvardsson, S. (1981). Inheritance of alcohol abuse. Cross-fostering analysis of adopted men. Archives of General Psychiatry, 38, 861–68. Collins, J.J. (ed.) (1982). Drinking and Crime: Perspectives on the Relationships Between Alcohol Consumption and Criminal Behavior. London: Tavistock. Collins, J.J., Schlenger, W.E. & Jordan, B.K. (1988). Antisocial personality and substance abuse disorders. Bulletin of the American Academy of Psychiatry and the Law, 16, 187–98. Donovan, J.E. & Jessor, R. (1985). Structure of problem behavior in adolescence and young adulthood. Journal of Consulting and Clinical Psychology, 53, 890–904. Driessen M., Veltrup, C., Junghanns, K. et al. (1999). Kosten-Nutzen-Analyse klinisch-evaluierter Behandlungsprogramme. Erweiterte Entzugs-therapie bei Alkoholabh¨angigkeit. Der Nervenarzt, 70(5), 463–70. Forth, A.E., Kosson, D.S. & Hare, R.D. (1996). The Hare Psychopathy Checklist: Youth Version (Unpublished manuscript). Ottawa: Carleton University. Fry, L.J. (1985). Drug abuse and crime in a Swedish birth cohort. British Journal of Criminology, 25, 46–59. Goldman, L., Genel, M., Bezman, R. & Slanetz, P. (1998). Diagnosis and treatment of attentiondeficit/hyperactivity disorder in children and adolescents. Journal of the American Medical Association, 279, 1100–7. Goldstein, P.J., Brownstein, H.H., Ryan, P.J. & Bellucci, P.A. (1988). Crack and homicide in New York City, 1988: a conceptually based event analysis, Contemporary Drug Problems, 16, 651–87. Goodwin, D.W. & Guze, S.B. (1994). Psychiatric Diagnosis (5th edition). New York: Oxford University Press. Grawe, K. (1998). Psychologische Therapie (Psychological therapy). G¨ottingen, Germany: Hogrefe – Verlag f¨ur Psychologie. Guze, S.B., Goodwin, D.W. & Crane, J.B. (1969). Criminality and psychiatric disorders. Archives of General Psychiatry, 20, 583–91. Heinz, A., Ragan, P., Jones, D.W. et al. (1998). Reduced central serotonin transporters in alcoholism. American Journal of Psychiatry, 155(11), 1544–9. Hemphill, J.F., Hart, S.D. & Hare, R.D. (1994). Psychopathy and substance use. Journal of Personality Disorders, 8, 176–80. Henggeler, S.W., Pickrel, S.G., Brondino, M.J. & Crouch, J.L. (1996). Eliminating (almost) treatment dropout of substance abusing or dependent delinquents through home-based multisystemic therapy. American Journal of Psychiatry, 153, 427–28. Henggeler, S.W., Pickrel, S.G. & Brondino, M.J. (1999). Multisystemic treatment of substanceabusing and dependent delinquents: outcomes, treatment fidelity, and transportability. Mental Health Services Research, 1, 171–84. Henggeler, S.W., Schoenwald, S.K., Borduin, C.M. et al. (1998). Multisystemic Treatment of Antisocial Behavior in Children and Adolescents. New York: Guilford Press. Hesselbrock, V.M., Hesselbrock, M.N. & Stabenau, J.R. (1985). Alcoholism in men patients subtyped by family history and antisocial personality. Journal of Studies on Alcohol, 46, 59–64. Hesselbrock, V.M., Hesselbrock, M.N. & Workman-Daniels, K.L. (1986). Effect of major depression and antisocial personality on alcoholism: course and motivational patterns. Journal of Studies on Alcohol, 47, 207–12. Kessler, R.C. & Merikangas, K.R. (2004). The National Comorbidity Survey Replication (NCSR): background and aims. International Journal of Methods in Psychiatric Research, 13(2), 60–8.

540

VOLUME I: DIAGNOSIS AND TREATMENT

Kiefer, F., Jahn, H., Tarnaske, T. et al. (2003). Comparing and combining naltrexone and acamprosate in relapse prevention of alcoholism: a double-blind, placebo-controlled study. Archives of General Psychiatry, 60(1), 92–9. Klein, R.G., Abikoff, H., Klass, E. et al. (1997). Clinical efficacy of methylphenidate in conduct disorder with and without attention deficit hyperactivity disorder. Archives of General Psychiatry, 54, 1073–80. Lewis, C.E. & Bucholz, K.K. (1991). Alcoholism, antisocial behavior and family history. British Journal of Addiction, 86, 177–94. Lewis, C.E., Cloninger, C.R. & Pais, J. (1983). Alcoholism, antisocial personality and drug use in a criminal population. Alcohol and Alcoholism, 18, 53–60. Liskow, B., Powell, B.J., Nickel, E.J. & Penick, E. (1990). Diagnostic subgroups of antisocial alcoholics: outcome at 1 year. Comprehensive Psychiatry, 31(6), 549–56. Mann, K. & Mundle, G. (1996). Die Behandlung von Alkoholabh¨angigen. Klinikarzt, 7+8(25), 203–7. Mann, K. & Stetter, F. (2002). Die qualifizierte Entzugsbehandlung von Alkoholab-h¨angigen: Entwicklung und Evaluation. In K. Mann (ed.), Neue Therapieans¨atze Bei Alkoholab-h¨angigkeit (pp. 59–72). Lengerich: Pabst. Martin, C.S. & Bates, M.E. (1998). Psychological and psychiatric consequences of alcohol. In R.E. Tarter, P.J. Ott & R.T. Ammerman (eds.), Handbook of Substance Abuse: Neurobehavioral Pharmacology. New York: Plenum Press. Miller, W.R. & Rollnick, S. (2002). Motivational Interviewing, 2nd edition. New York: Guilford Press. Moggi, F. & Donati R. (2004). Psychische St¨orungen und Sucht: Doppeldiagnosen. Hogrefe, Verl. f¨ur Psychologie. Fortschritte der Psychotherapie. Moggi, F., Ouimette, P.C., Finney, J.W. & Moos, R.H. (1990). Effectiveness of treatment for substance abuse and dependence for dual diagnosis patients. Journal of Studies on Alcohol, 60, 856–66. Moggi, F., Ouimette, P.C., Moos, R.H. & Finney, J.W. (1999). Dual diagnosis patients in substance abuse treatment. Relationship of general coping and substance-specific coping to one-year outcomes. Addiction, 94, 1805–16. Nurco, D.N., Ball, J.C., Shaffer, J.W. & Hanlon, T.E. (1985). The criminality of narcotic addicts. Journal of Nervous and Mental Disease, 173, 94–102. O’Boyle, M. & Barratt, E.S. (1993). Impulsivity and DSM-III-R personality disorders. Personality and Individual Differences, 14, 609–11. Osher, F.C. & Kofoed, L.L. (1989). Treatment of patients with psychiatric and psychoactive substance abuse disorders. Hospital and Community Psychiatry, 40, 1025–30. Rada, T.T. (1978). Sociopathy and alcohol abuse. In W.H. Reid (ed.), The Psychopath: A Comprehensive Study of Antisocial Disorders and Behaviors. New York: Brunner/Mazel. Randolph, M.J. & Yates, W.R. (1993). Antisocial personality disorder in alcohol- and drug-dependent individuals. American Journal on Addictions, 2, 9–17. Regier, D.A., Farmer M.E., Rae, D.S. et al. (1990). Comorbidity of mental disorders with alcohol and other drug abuse. Results from the Epidemiologic Catchment Area (ECA) Study. Journal of the American Medical Association, 264(19), 2511–18. Robins, L.N. (1966). Deviant Children Grown Up. Baltimore: Williams & Wilkins. Rohde, P., Lewinsohn, P.M. & Seeley, J.R. (1996). Psychiatric comorbidity with problematic alcohol use in high school students. Journal of the American Academy of Child and Adolescent Psychiatry, 35, 101–9. Rounsaville, B.J., Dolinsky, Z.S., Babor, T. F. & Meyer, R.E. (1987). Psychopathology as a predictor of treatment outcome in alcoholics. Archives of General Psychiatry, 44, 505–13. Schuckit, M.A. (1985). The clinical implications of primary diagnostic groups among alcoholics. Archives of General Psychiatry, 42, 1043–9. Schuckit, M.A. (1995). Drug and Alcohol Abuse: A Clinical Guide to Diagnosis and Treatment (4th edition). New York: Plenum. Schuckit, M.A. & Irwin, M. (1989). An analysis of the clinical relevance of type 1 and type 2 alcoholics. British Journal of Addiction, 84, 869–76. Sher, K.J. & Trull, T.J. (1994). Personality and disinhibition psychopathology: alcoholism and antisocial personality disorder. Journal of Abnormal Psychology, 103, 92–102. Smith, S.S. & Newman, J.P. (1990). Alcohol and drug abuse-dependence disorders in psychopathic and nonpsychopathic criminal offenders. Journal of Abnormal Psychology, 99, 430–9.

DRUG AND ALCOHOL ABUSE

541

Spanagel, R. & Mann, K. (2005). Drugs for Relapse Prevention of Alcoholism. Berlin: Birkh¨auser. Spencer, T.J., Biederman, J., Wilens, T. et al. (1996). Pharmacotherapy of ADHD across the life cycle: a literature review. Journal of the American Academy of Child and Adolescent Psychiatry, 35, 409–32. Stetter, F. & Mann, K. (1997). Zum Krankheitsverlauf Alkoholabh¨angiger nach einer station¨aren Entgiftungs- und Motivationsbehandlung. Der Nervenarzt, 68(7), 574–81. Wilens, T. & Biederman, J. (1992). The stimulants. In D. Schaffer (ed.), Psychiatric Clinics of North America (pp. 191–222). Philadelphia, PA: W.B. Saunders. Zucker, R.A. (1986). The four alcoholisms: a developmental account of the etiologic process. In P.C. Rivers (ed.), Alcohol and Addictive Behavior. Lincoln: University of Nebraska Press.

CHAPTER 31

Experiential and Community Treatment of Adult Antisocial Syndromes Stephen A. Thorne Austin, Texas

and William H. Reid University of Texas Health Science Center at San Antonio, USA

ANTISOCIAL PERSONALITY AND PSYCHOPATHY The various definitions and distinctions among psychopathy, antisocial personality, other disorders that are associated with antisocial behaviors and simple antisocial behavior found without significant psychiatric diagnosis have been discussed elsewhere in this book. Those distinctions are not merely academic; they are crucial for accurate assessment, understanding of the origins of antisocial behavior, developing treatment or management approaches with the best potential for usefulness, and separating situations in which clinically feasible approaches may be useful from those in which social control and protection of potential victims are the only reasonable approaches. Traditional medical and psychosocial treatment approaches almost never work unless the source of antisocial behavior lies largely within one of the psychiatric or neurological conditions with which we have had treatment success (such as an ictal focus, bipolar disorder or some forms of substance abuse). Antisocial behavior whose origins lie in psychological factors such as self-esteem may also be more amenable to treatment. Occasionally, individualized clinical or socioclinical activities focusing on antisocial cognitions and activities can change behavior, even, albeit rarely, the psyche. Sometimes therapeutic pessimism, even nihilism, is a reasonable stance for the clinician. This chapter will cautiously explore some of those approaches with, we hope, neither undue optimism nor knee-jerk nihilism. This chapter does not address juvenile antisocial behavior, or conditions such as conduct disorder. We will not dwell on mixed syndromes such as mood disorders with antisocial behavior, criminality associated solely with drug addiction, or violence which is a result

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

544

VOLUME I: DIAGNOSIS AND TREATMENT

of explosive dyscontrol. In those cases, treatment of the comorbid disorder is primary, and often (but not always) substantially alters the antisocial behavior. Neither will we focus on the ‘career criminal,’ whose antisocial behavior has a businesslike purpose. Such people may be confused with psychopaths; however, their behavior is often more accurately described as a socially aberrant lifestyle than psychopathy. For purposes of this chapter, we will also separate the DSM/ICD concept of ‘antisocial personality’ (ASP) from the deeper, less behavioral or empirical concept of psychopathy envisioned by Cleckley, Hare, Karpman and others (Cleckley, 1976; Hare, 1991; Karpman, 1948; Reid, 1978). Though the constructs of ASP and psychopathy both involve a lack of remorse and the presence of various socially deviant behaviors, diagnostic criteria for ASP place a greater emphasis on overt (and more objective) delinquent and criminal behaviors, and less of an emphasis on relevant interpersonal and affective factors (Hare, 2003) that may, in part, explain such behaviors. Many people with violent or criminal lifestyles meet criteria for ASP but do not fulfill most US definitions of ‘psychopathy’, such as that represented in the various iterations of Hare’s Psychopathy Checklist (PCL) (Hare, 1991, 2003) or Cleckley’s 16 Mask of Sanity factors (Cleckley, 1976). In his groundbreaking work on psychopathy, Cleckley differentiated between ‘ordinary’ or ‘typical’ antisocial behavior and those socially deviant acts indicative of psychopaths. Hare (2003) has also stated that psychopathy (as measured by the PCL-R) and ASP ‘may share some diagnostic features but this does not mean they measure the same traditional construct’ (p. 6). More recently, Hare and Neumann (2006) estimated that the prevalence of ASP in forensic settings is ‘two or three times higher than the prevalence of psychopathy, as measured by the PCL-R’ (p. 61), and that the majority of those individuals displaying significant psychopathic tendencies meet ASP criteria, though most individuals diagnosed with ASP are not viewed as prototypical psychopaths. In addition, while the majority of incarcerated individuals with ASP have not engaged in homicidal behavior or extreme violence (Rogers & Shuman, 2005), those individuals classified as psychopaths are generally considered to represent a higher risk for dangerous and violent behavior. It is the opinion of the authors that the apparent differences between ASP and the current conceptualization of psychopathy would make it appropriate to address persons with ASP and true psychopaths in separate chapters on treatment. As such, the primary focus of the current chapter will be to address factors relating to the treatment of those individuals constituting the largest percentage of adult criminal offenders; namely those who display a history of overt delinquent and criminal behavior in the absence of true psychopathy. Even though ASP is considered a personality disorder, some clinicians believe those who barely meet the criteria, for example, by virtue of static (historical) factors that may not represent their current conditions, may be amenable to change. Nevertheless, amenability to change is not the same as likelihood of change, nor does it take into account the availability and accessibility of competent treatment programs.

HISTORICAL PERSPECTIVE In North America, early non-hospital treatments were largely either punitive or religion based. People who would likely meet diagnostic criteria for psychopathy or a similar syndrome were not generally viewed by courts as ‘mentally ill’ until the early twentieth century (Pinel’s manie sans delire (1800–01) and Prichard’s ‘moral insanity’ (1835) notwithstanding). If and when criminals with characterologic antisocial syndromes (not necessarily meeting today’s diagnostic criteria) were not simply incarcerated or otherwise punished, it was common to steep transgressors in a strict regimen of rules, self-denial, biblical

ADULT ANTISOCIAL SYNDROMES

545

principles, and hard work. Anecdotes of success were common, but there is really no data with which to measure accurately the effects of such efforts. For the better part of the twentieth century the guiding social (if not always correctional or judicial) principle behind treatment for antisocial adults was that they could, and should, be rehabilitated and/or reformed. Many treatment and rehabilitation programs were created between 1960 and 2000 (some drawing on earlier models), some with very positive outcome data. Their methods and outcomes are chronicled in books and articles of their eras, as well as numerous edited reviews (Ashford, Sales & Reid, 2001; Matthews & Reid, 1981; Millon et al., 1998; Reid, 1981; Reid & Solomon, 1981; Reid et al., 1986; St¨urup, 1964, 1968; Tyce, Olson & Amdahl, 1980; Wolman, 1987). One key to success (and portent of failure if it is not heeded) has been to accurately characterize or diagnose the source of the participant’s/patient’s antisocial behavior (e.g., lack of social education and experience, major mental illness, substance abuse or addiction, intellectual deficiency, non-antisocial personality disorder, antisocial personality). Programs that limited themselves to those groups and tailored their approaches appropriately tended to increase personal and social success and decrease recidivism. True antisocial personality (as well as psychopathy), unfortunately, continued to be an outlier, frustrating efforts at changing them and, when such persons were included in broader programs, interfering with efforts to help those who had a better prognosis. Almost all the programs developed between 1950 and the present have come and gone regardless of their success, with comparable or better programs only occasionally taking their places. Some of their loss of popularity may be related to the whims of media popularity or the ‘fad’ nature of some approaches. Some can be blamed on the public’s frustration when viewing all antisocial behavior as lumped into the ‘antisocial personality’ or ‘psychopath’ realm. The bigger problem, however, was (and is) that no treatment or program offers a panacea satisfying all of society’s priorities: community protection, psychological change, political expediency and lower public cost. A wave of pessimism took hold during the 1970s with Robert Martinson’s essay, ‘What Works? Questions and Answers about Prison Reform’ (Martinson, 1974). Martinson supported and reflected a ‘nothing works’ doctrine, concluding that treatment programs ‘had no appreciable effect on recidivism’. His essay, though at odds with previous findings and not universally accepted at the time, had a profound influence on both political policy and clinical opinion for a good portion of the next two decades. As Andrews and colleagues (Andrews, Zinger et al., 1990) opined in their frequently cited 1990 meta-analysis, the ‘nothing works’ doctrine offered by Martinson appeared to satisfy ‘conservative political reactions to the apparent disorder of the 1960s, liberal sorrow over perceived failures of the Great Society, and the ideological persuasions of those academicians whose social visions of deviance asserted that only radical social change could have an impact on crime’ (pp. 371–2). While a detailed critique of Martinson’s analysis and conclusions lies beyond the scope of this chapter, more recent studies (Andrews, Zinger et al., 1990; Lowenkamp & Latessa, 2004, 2005) have (if nothing else) cast doubt upon the validity of his conclusions and has helped foster a renewed sense of optimism regarding the potential efficacy of ‘appropriate’ treatment programs for antisocial adults and criminal offenders.

CURRENT TASKS AND GOALS OF TREATMENT Any discussion regarding the treatment of antisocial adults must first acknowledge that there are numerous potential reasons for providing treatment, and a variety of treatment objectives

546

VOLUME I: DIAGNOSIS AND TREATMENT

may be desirable. Although the interpersonal, social and economic costs associated with antisocial behaviors (and those who display them) are rarely a source of disagreement, legal and political goals and the clinical objectives for developing treatment programs for such behaviors may not be one and the same. While policy makers and/or court officials often view treatment efficacy in terms of secure containment, deterrence, reduced correctional costs, relief of chronic prison overcrowding and/or lower recidivism rates, mental health professionals may (for better or worse) tend to see therapeutic success as more individual and humanistic. Within both perspectives, however, at least one primary treatment objective is, at the core, to change the thoughts, behaviors and predispositions that lead offenders/patients to violate society’s norms and expectations, and that increase their likelihood of recidivism. The goal of decreased antisocial and criminal recidivism is shared by a majority of policy makers and clinicians, but the means by which this goal is pursued is at the heart of a larger philosophical divide. There are those who fall generally on the side of containment and ‘rehabilitation’ by way of incarceration. Others often argue that treatment (as contrasted with simple incarceration) will yield greater value to society. Lurigio notes, ‘The battles are as pitched as ever with little hope for rapprochement between factions that believe in harsher restrictions and (those) that advocate better treatments as the keys to alleviating American’s crime problem’ (2005, p. 259). Where one falls in this debate will likely not change as a result of this chapter; however, if we are to assume that various analyses and reviews of outcome data are accurate (Andrews, Zinger et al., 1990; Lowenkamp & Latessa, 2004, 2005; Lowenkamp, Latessa & Holsinger, 2006), we should at least have some sense of optimism that appropriate treatment procedures can reduce criminal and antisocial behavior for at least some people. Although confidence regarding the potential efficacy of treatment programs for some antisocial adults indeed seems warranted, our aforementioned quest to avoid both undue optimism and nihilism requires acknowledging that treatment of this population frequently does not yield the desired results (Kempinen & Kurlychek, 2003; Martinson, 1974; Poole & Slavick, 1995;). In addition, risk to the public must often dictate the site of treatment (that is, a controlled rather than uncontrolled setting). Thus some ‘helping’ professionals’ well-meaning treatment preferences (such as to avoid incarceration or hospitalization) may, for some perpetrators, contradict society’s best interests. The interests of courts and society (not to mention the reputations of mental health professions) are hardly served if offenders are indiscriminately sent to any available treatment program. Both outcome hopes and funding limitations dictate careful assessment of treatment needs and priorities, as well as honest assessment of the likelihood of success. Mental health professionals can best serve both their own professions and their communities generally by providing empirically supported data to courts and other social decision makers with respect to who may be the most appropriate candidates for different kinds of therapeutic intervention, as well as, perhaps, who may not benefit from available treatments and be more appropriate for incarceration alone. One should note that those professionals or teams who offer opinions on this topic, which can easily affect evaluees’ lives in irrevocable ways, should be mature and forensically experienced. Rogers and Webster (1989) emphasized the importance of basing treatment recommendations on a sound understanding of the relevant research. The authors wrote that mental health professionals too often focus on an individual’s psychological needs and, as a result, are more likely to recommend treatment services for offenders ‘with even the slightest prospect for change’ (p. 22). Such a focus on what they perceived as personality and emotional traits with little relevance to treatment amenability and future recidivism led Rogers and Webster to

ADULT ANTISOCIAL SYNDROMES

547

argue that treatment recommendations resulting from such assessment approaches are generally not evidence based and are ‘too often offered blithely without sufficient consideration of treatment goals, availability of resources, and the likely outcome’ (p. 22). Latessa, Cullen and Gendreau (2002) refer less kindly to this tendency, calling it ‘professional quackery’. It seems very likely that treatment techniques and programs lacking in empirical support and administered to individuals whose needs are resistant to change have, at least in part, contributed to the longevity of the ‘nothing works’ doctrine. The past two decades have brought not only a significant increase in criminological research, but also a renewed sense of optimism that antisocial behavior can be reduced through therapeutic means. Frequently cited literature reviews and meta-analyses have indicated that effective treatment strategies appropriately matched with the individual offender’s needs can lead to significant reductions in criminal recidivism for certain individuals (Andrews, Bonta & Hoge, 1990; Andrews, Zinger et al., 1990). In addition, Doris MacKenzie, as part of a larger report to the United States Congress, stated that ‘the important issue is not whether something works but what works for whom’ (1997). The consideration of treatment as a viable strategy when allocating limited resources and providing for the safety and well being of the public is further strengthened when one notes that the primary alternatives, incarceration and intensive supervision or monitoring, have not consistently shown effectiveness in reducing recidivism (Andrews, Zinger et al., 1990; Byrne & Taxman, 2005; MacKenzie, 2005; Palmer, 1975; Sherman, 2000). As Sherman (2000) argued, ‘It requires massively pessimistic assumptions to predict that incarceration will win out over more theoretically powerful alternatives for changing the lives of all but the most serious offenders’ (p. 301). Any discussion or consideration of ‘what works’ in the treatment of adult offenders should incorporate a holistic assessment of empirically supported principles rather than a focus on a particular treatment program whose facets may be genuinely unique (e.g., assessment, admission, staff qualifications and credentials, implementation, integrity, aftercare availability). Andrews, Bonta and Hoge (1990) initially suggested this notion in their original work on the four principles of classification for effective rehabilitation. In recognizing the relevance of an offender’s recidivism risk, his criminogenic needs and the ability of available treatment programs to serve an individual’s needs and abilities when designing and implementing effective correctional treatment programming, the authors suggested that these principles ‘provide reasonable guides to service and research in rehabilitation’, and that future emphasis be placed on ‘creating broad setting and program conditions that support the efforts of rehabilitation professionals’ (p. 45). Over a decade later, Latessa (2004) offered similar support for this argument: ‘What Works’ is not a program or an intervention, but a body of knowledge that has been conducted by numerous scholars in North America and Europe. Also referred to as evidence-based practice, the What Works movement demonstrates empirically that theoretically sound well-designed programs that meet certain conditions can appreciably reduce recidivism rates for offenders (p. 170).

The important principles of risk, need and responsivity have been studied and discussed by numerous authors, with the continued goal of offering guidance and empirical support to the assignment of treatment resources to offenders (Gendreau, Little & Goggin, 1996; Lowenkamp & Latessa, 2005; Lurigo, 2005). In general, these principles call for basing treatment recommendations on the ability of a program to match an offender’s needs, learning style and level of risk. The risk principle, in particular, has offered promise in its clarity

548

VOLUME I: DIAGNOSIS AND TREATMENT

of the extent to which treatment effectiveness is in large part predicated on a program’s ability to assess an individual’s relevant pretreatment characteristics, use empirically supported methods of assessing risk and match them to the appropriate treatment program. Both the underlying beliefs and goals of the risk principle are succinctly summarized by Lurigo (2005): Offenders are different from one another. They require services to help them desist from crime. Varying interventions and supervisory strategies are more effective with some offenders than with others. Correctional resources are limited and must therefore be used wisely and efficiently. Hence, offenders should be placed in specific programs that pointedly address their particular configuration of criminal propensities, problems, skills, aptitudes, and readiness for change, and make the best use of treatment dollars. This goal is easy to state but not so easy to accomplish (p. 260).

Support for the risk principle can be found in a variety of studies that suggest that high-risk offenders placed in appropriate treatment programs tend to display greater treatment effects than those with perceived lower level needs (Andrews, Bonta & Hoge, 1990; Lowenkamp & Latessa, 2005; Lowenkamp et al., 2006; MacKenzie, 2005; MacKenzie & Souryal, 1994). Additional support can be derived from mounting evidence that low- and low-to-moderaterisk offenders actually show higher levels of recidivism following residential or community treatment than high-risk participants (Lowenkamp & Latessa, 2004, 2005; Lowenkamp et al., 2006). While the relevance of the risk principle in matching offenders to appropriate treatment strategies has increased, it has also become ‘increasingly clear that the mere process of assessing offenders will not increase effectiveness’ (Lowenkamp & Latessa, 2004, p. 245). In addition to the assessment of various pre-service characteristics, Andrews, Bonta and Hoge (1990) theorized that appropriate and effective treatment must address dynamic and criminogenic variables. ‘Dynamic’ (as contrasted with ‘static’) variables are those that can be changed and are thus amenable to intervention. While some static variables (e.g., juvenile history of antisocial behavior, gender, race, age) are commonly associated with criminal recidivism (and thus may be actuarially relevant to prognosis and treatment choice), they have little therapeutic utility, since they cannot be altered by treatment. ‘Criminogenic’ variables, on the other hand, are dynamic factors thought to be associated with an individual’s criminal behavior. Andrews, Bonta and Hoge (1990) emphasized the importance of differentiating between criminogenic and noncriminogenic needs when attempting to identify the causal factors in antisocial behavior, with the ultimate goal of changing such thought patterns, choices and behaviors. Until recently, the various psychological and/or emotional symptoms displayed by offenders were viewed as having equal significance in treatments designed to reduce or eliminate antisocial behavior (Bonta & Cormier, 1999). Andrews and his colleagues (1990), however, emphasized that not all potential treatment needs are criminogenic; that is they are not all related to criminal behavior. Rather, they argued, an individual may have psychiatric symptoms that have little, if any, association with past or future antisocial behavior. They labeled these conditions and treatment needs noncriminogenic and asserted that their treatment offers little toward the overall goal of reduced recidivism. Andrews et al. believe that the focus of treatment should be on the individual’s criminogenic needs, those that in some way can be shown to be related to his or her criminal behavior. Their opinions, while gaining in empirical support, ‘are in stark contrast to the practices of many therapists and programs that give priority to lowering offenders’ anxiety level and raising their self-esteem’

ADULT ANTISOCIAL SYNDROMES

549

(Gendreau, Little & Goggin, 1996, p. 577). Any focus on noncriminogenic issues such as self-esteem or overall mental functioning would be unlikely to elicit significant reductions in recidivism, and thus be a misuse of treatment resources (Andrews, Bonta & Hoge, 1990; Gendreau, Little & Goggin, 1996; Latessa, 2004; Latessa et al., 2002; MacKenzie, 2005). Availability of treatment strategies and modalities for selected offenders and their needs is a logical extension of the concepts of risk and need. As indicated previously, a discussion of ‘what works’ among treatment strategies should focus on empirically supported principles rather than solely on a particular (often unique) program. Good treatment programs are generally assumed to be multimodal and tailored to the client’s criminogenic needs. They incorporate cognitive and behavioral techniques, social learning techniques and various modeling principles (Andrews, Zinger et al., 1990; Bonta & Cormier, 1999; Latessa, 2004; Latessa et al., 2002; MacKenzie, 2000, 2005). Those approaches frequently viewed as not ‘appropriate’ and unresponsive to the criminogenic needs of offenders include several individual psychotherapy approaches (e.g., psychodynamic, client-centered, insight-oriented) as well those that emphasize a military model or fear of punishment (Andrews, Bonta & Hoge, 1990; Andrews, Zinger et al., 1990; Bonta & Cormier, 1999; Latessa, 2004; Latessa et al., 2002; MacKenzie, 2005; MacKenzie & Souryal, 1994). A frequently cited meta-analytic review of 80 studies of correctional treatment interventions (involving both juveniles and adults, from the 1950s through the 1980s) appears to confirm the assumption that appropriate treatment is more effective in reducing recidivism than criminal sanctions without rehabilitative services (Andrews, Zinger et al., 1990). In addition, programs whose components matched the authors’ criteria (targeting high-risk offenders, addressing appropriate criminogenic needs and incorporating cognitive or behavioral principles matching a client’s needs and learning abilities) had better results than those that did not (described by the authors as not ‘appropriate’). The former group of programs reduced recidivism by approximately 50 %. The authors also noted that ‘the major source of variation in effects on recidivism was the extent to which service was appropriate according to the principles of risk, need and responsivity’ (p. 384). They further supported employing behavioral principles when treating offenders, noting that 95 % of the behavioral treatments reviewed qualified as ‘appropriate’, and 70 % of those deemed appropriate were behavioral. The authors offered the increasingly popular mantra that ‘the effectiveness of correctional treatment is dependent upon what is delivered to whom in particular settings’ (p. 372).

EXPERIENTIAL PROGRAMS Much of the research on experiential treatment programs for antisocial personality centers on ‘shock incarceration’ or ‘boot camp’ programs. Adult boot camp programs began in 1983 as an alternative to incarceration, though they were initially more similar to a military boot camp than to a treatment program (MacKenzie, 1994; MacKenzie & Souryal, 1994; Osler, 1991; Zhang, 1998). Their rise in popularity appears to have been the result of a variety of social, economic and political factors, and is seen as satisfying society’s need/desire for those who commit crimes to be punished while at the same time also providing an environment in which they may obtain the skills to avoid their past mistakes. Attempts to evaluate the effectiveness of such programs have yielded mixed results. Several authors have noted that boot camps do not show consistent long-term reductions in recidivism (Burns & Gennaro, 1995; Kempinen & Kurlycheck, 2003; Latessa et al., 2002;

550

VOLUME I: DIAGNOSIS AND TREATMENT

MacKenzie, 1994; MacKenzie et al., 1995; MacKenzie & Souryal, 1994; Poole & Slavick, 1995; Sechrest, 1989; Stinchcomb & Terry, 2001; Tonry, 1997). MacKenzie and Souryal (1994) summarized their findings regarding the effectiveness of adult boot camp programs with the following: Based on the totality of the evidence, boot camp programs did not reduce offender recidivism. By and large, the recidivism rate of boot camp graduates did not differ from the rates of comparison samples of similarly situated inmates who had served a longer term of incarceration in a conventional prison. When differences in recidivism rates appeared to favor samples of boot camp graduates, their superior performance could not be attributed to the effect of the program (p. 47).

Reviews of state-based adult boot camp programs have also concluded that participants do not generally display significantly lower levels of recidivism than offenders who received probation or incarceration. Specifically, analysis of 1996 and 1997 data from the Pennsylvania Motivational Boot Camp Program showed (after controlling for other variables) no significant differences between adult graduates of a six-month boot camp program and a comparison group of adult offenders released from state prison in either new crimes or technical violations (Kempinen & Kurlychek, 2003). In addition, a 1995 study assessing the effectiveness of Alabama boot camp programs for adult offenders indicated that, compared to groups of offenders on probation and offenders released from prison, boot camp participants tended to have the highest rate of new offenses. The differences among the groups were not considered clinically significant (Burns & Vito, 1995). The authors of both the Pennsylvania and Alabama studies did report that money was saved and prison overcrowding relieved by the shock incarceration programs. Others have also suggested that boot camp programs can reduce costs and relieve prison crowding (Burns & Gennaro, 1995; MacKenzie, 1994; Poole & Slavick, 1995). Some studies have also indicated positive attitudinal change among program participants, though it should be noted that those changes were not necessarily shown to be related to subsequent reductions in recidivism (Burton et al., 1993; MacKenzie, 1994). While many studies of boot camp programs have evaluated state-run programs, one review of a 90-day county-operated program also found no significant differences in recidivism between program graduates and those in a comparison group who had received jail time, probation or some form of community control (Stinchcomb & Terry, 2001). A closer analysis of the literature about the effectiveness and cost-effectiveness of boot camp programs suggests that client variables are not the only important source of outcome findings. A large portion can be accounted for by important differences in the implementation of treatment principles (Kempinen & Kurlychek, 2003; MacKenzie & Souryal, 1994; Poole & Slavick, 1995). After acknowledging an overall lack of success in reducing recidivism, MacKenzie and Souryal’s frequently cited review of eight states’ boot camp programs (in Florida, Georgia, Illinois, Louisiana, New York, Oklahoma, South Carolina and Texas) illustrated a great deal of variation among them. The estimated recidivism rates for program graduates ranged from 23 % to 63 % for rearrests, 1.3 % to 13 % for revocations resulting from a new offense, and 2.1 % to 14.5 % for technical violations (1994). Further analysis of the treatment data revealed that the three programs with the lowest recidivism figures (Illinois, New York and Louisiana) were those that were longer, devoted the most time to therapy-related programming (more than three hours a day), had high dismissal rates and selected offenders who volunteered and who were otherwise prison bound (MacKenzie, 1994).

ADULT ANTISOCIAL SYNDROMES

551

COMMUNITY PROGRAMS Overcrowded prisons and the economic strains of the correctional system have led to a variety of programs that seek a balance between rehabilitation and incapacitation (Lurigio, 2005; Martin, Lurigio & Olson, 2003; Tonry, 1997). These alternatives have frequently been described as ‘intermediate’ sanctions, as they were originally conceptualized ‘as punishments located on a continuum between prison and probation and were supposed to be more intrusive and burdensome than standard probation’ (Tonry, 1997, p. xii). Since their emergence (in the United States) in the mid-1980s, a variety of intermediate sanctions have been tried as correctional systems experiment with intensive supervision, community treatment, house arrest, electronic monitoring and day reporting to lower recidivism rates, reduce prison/jail overcrowding and decrease corrections costs. These sanctions can be characterized as either ‘front end’ or ‘back end’, with participants entering before trial or as a condition of probation, parole or early release (Martin, Lurigio & Olson, 2003; Tonry, 1997). All such sanctions appear to increase access to treatment, but early outcome analysis of intermediate sanctions such as halfway houses, residential programming and day reporting centers indicates that many do not reliably reduce recidivism (MacKenzie, 1997; MacKenzie, 2000; Tonry, 1997). Like research on adult boot camp programs, increased focus on intermediate sanctions involving community-based treatment reveals considerable variability in design, implementation and efficacy. Christopher Lowenkamp and Edward Latessa have led several University of Cincinnati researchers to publish studies of the utilization of evidence-based programming in community-operated treatment facilities. With this increased scrutiny and focus, evidence is emerging that community-based treatment programs that incorporate empirically supported assessment and treatment techniques can have some success in reducing criminal recidivism. One large-scale analysis and review of community-based residential treatment programs in Ohio suggests that using the risk principle to match offenders to appropriate treatment programs increases the likelihood of positive outcome in high-risk offenders (Lowenkamp & Latessa, 2005). A review of the study’s methodology indicates that an offender’s risk level was determined ‘based on a review of important risk predictors and existing risk assessment instruments’. These factors included predominantly static and behavioral factors and were devoid of any interpersonal or affective factors, thus making it difficult to determine the extent to which the high-risk offenders may have displayed psychopathic characteristics. As such, the author’s conclusions and recommendations concerning high-risk offenders should not be confused with the higher risk level generally associated with psychopaths. The authors analyzed data from 53 community programs treating over 7000 adult offenders released from a state institution, placed on parole or some other form of post-release supervision, and placed in either a halfway house or a community correctional facility. Offenders from the experimental group were compared to nearly 6000 offenders under parole/post-release control (who were not placed in any type of residential treatment) from Ohio correctional institutions. The authors concluded that a majority of the studied programs were associated with reduced recidivism among participants. They further noted that the offender risk level accounted for significant differences in program effectiveness. Twenty-four of the 36 programs assessed had no positive impact on low-risk offenders, with the low-risk sample as a whole showing a 4 % increase in recidivism. ‘Low/moderate’ offenders showed a slight increase

552

VOLUME I: DIAGNOSIS AND TREATMENT

(1 %) in recidivism, with half the programs having either no effect or a negative effect on recidivism. Nearly 70 % of ‘moderate’ offenders in the studied programs, however, reflected a positive impact on recidivism, with the entire sample of moderate offenders yielding a 3 % reduction in recidivism. The high-risk offenders participating in community-based treatment had significant reductions in both magnitude and frequency of recidivism compared to the comparison group. Twenty-seven of the 38 observed programs lowered recidivism rates for high-risk offenders. Lowenkamp and Latessa concluded that ‘low-risk offenders should be excluded, as a general rule, from residential programs’ and that ‘corrections agencies should target mostly high-risk offenders for placement in residential programs’ (p. 284). Once again, however, keep in mind that subjects in Lowenkamp and Latessa’s studies were not assessed for psychopathy. Given what is known about the increased levels of violent behavior among psychopaths, as well as the dearth of established and effective treatment options for psychopaths, it would seem premature (if not unwise) to conclude that available treatment resources should be disproportionately weighted toward the treatment of psychopaths. A more recent analysis of Ohio data from 97 correctional programs (13,676 offenders) consisting of halfway houses, community-based correctional facilities, residential programs and intensive supervised probation showed somewhat similar results (Lowenkamp et al., 2006). Individuals in the experimental groups were matched to parolees and other individuals under post-release control. Results indicated that treatment participants showed a small, but significant, increase in recidivism compared to the comparison group, but that both residential and nonresidential programs that did not treat high-risk offenders demonstrated increased rates of recidivism. The authors concluded that placing lower risk offenders in treatment programs can actually lead to increases in recidivism rates, that residential programs were ‘far more effective’ at reducing recidivism than were nonresidential programs, and that those programs described as cognitive-behavioral or behavioral in nature were more effective than those that relied on other treatment modalities. Longer programs appeared to be more effective than shorter ones. Day reporting centers (DRCs) are another intermediate sanction developed to provide increased supervision and access to treatment options in lieu of incarceration. Research assessing their effectiveness in reducing recidivism is limited. Martin et al. (2003) published what they described as the first long-term outcome study of DRCs in the United States. In it, the authors assessed recidivism rates of approximately 1400 clients admitted to the Cook County Day Reporting Center (CCDRC) during 1995. Although lacking random assignment, the study compared recidivism rates of offenders who had been in the program for at least 70 days with those of individuals who had been in the program fewer than 10 days. Members of the latter group were not classified as treatment ‘dropouts’, as the group consisted of offenders who had left within the first 10 days ‘for reasons other than their performance in the program’ (the majority had either made bail or their charges had been dismissed). Participants were followed for 12 months after release. The authors concluded that members of the experimental group had significantly lower rates of rearrest and reincarceration than did controls; however, the one-year rearrest and reincarceration rates for both the treatment and control group were substantial. About 50 % of those in the experimental group were rearrested within 12 months compared with 75 % of controls.

ADULT ANTISOCIAL SYNDROMES

553

CONCLUSIONS We have discussed programs that change the antisocial behaviors of selected perpetrators. The concern remains, however, that once comorbid psychiatric, neurological and substance use disorders have been stripped away from the concept of truly characterologic syndromes, such as antisocial personality and its subset psychopathy, psychiatry and psychology remain challenged by our inability to create consistently positive and sustained treatment effects. Rather than succumb entirely to our nihilistic tendencies, it seems reasonable to argue that a doctrine of ‘nothing works’ currently lacks empirical support and likely serves only to deter clinicians and researchers from continued progress in matching appropriate candidates to well-designed and implemented treatment programs. While the debate about effectiveness of adult treatment programs continues, there appears to be increasing recognition that programs incorporating evidence-based principles can yield positive results. As Andrews, Zinger and colleagues surmised, ‘At least some service programs are working with at least some offenders under some circumstances’ (1990, p. 374). Gacono et al. (2001) more recently concluded that ‘when posed as a yes–no dichotomy, questions concerning treatment amenability cannot be answered’ (p. 120). The appropriate question is thus not whether or not treatment should be pursued, but rather how can one effectively match the problems and needs of individual clients to appropriate and available treatment programs so that reductions in recidivism can be achieved. Many years ago, one of the authors met with Dr. Georg St¨urup, retired superintendent of Herstedvester Institution and a tireless worker to change severely antisocial people, in his Randers, Denmark, home. Bent with age and knowing that his decades of work ‘treating the untreatable’ were over, he said, in effect, ‘Don’t forget these people. They have no one, yet they are people. They are desperately lacking and in terrible pain. Those who understand this are so rare; you must not turn your back on them.’ Those who labor in these fields have our admiration, along with our hope that their work someday will bear lasting fruit.

REFERENCES Andrews, D.A., Bonta, J. & Hoge, R.D. (1990). Classification for effective rehabilitation: rediscovering psychology. Criminal Justice and Behavior, 17(1), 19–52. Andrews, D.A., Zinger, I.Z., Hoge, R.D. et al. (1990). Does correctional treatment work? A clinically relevant and psychologically informed meta-analysis. Criminology, 28(3), 369–404. Ashford, J.B., Sales, B.D. & Reid, W.H. (eds.) (2001). Treating Adult and Juvenile Offenders with Special Needs. Washington, DC: American Psychological Association. Bonta, J. & Cormier, R.B. (1999). Corrections research in Canada: impressive progress and promising prospects. Canadian Journal of Criminology, 41, 235–47. Burns, J.C. & Gennaro, F.V. (1995). An impact analysis of the Alabama Boot Camp Program. Federal Probation, 59, 63–7. Burns, J.C. & Vito, G.F. (1995). An impact analysis of the Alabama Boot Camp Program. Federal Probation, 59(1), 63–7. Burton, V.S., Marquart, J.W., Cuvelier, S.J. & Alarid, L.F. (1993). A study of attitudinal change among boot camp participants. Federal Probation, 57(3), 46–52. Byrne, J.M. & Taxman, F.S. (2005). Crime (control) is a choice: divergent perspectives on the role of treatment in the adult corrections system. Criminology and Public Policy, 4(2), 291–310.

554

VOLUME I: DIAGNOSIS AND TREATMENT

Cleckley, H. (1976). The Mask of Sanity, 5th edition (pp. 337–64). St. Louis, IL: Mosby. Gacono, C.B., Nieberding, R.J., Owen, A. et al. (2001). Treating conduct disorder, antisocial, and psychopathic personalities. In J.B. Ashford, B.D. Sales & W.H. Reid (eds.), Treating Adult and Juvenile Offenders with Special Needs (pp. 99–129). Washington, DC: American Psychological Association. Gendreau, P., Little, T. & Goggin, C. (1996). A meta-analysis of the predictors of adult recidivism: what works! Criminology, 34(4), 575–607. Hare, R.D. (1991). The Hare Psychopathy Checklist-Revised. New York: Multi-Health Systems. Hare, R.D. (2003). The Hare Psychopathy Checklist-Revised, 2nd edition. New York: Multi-Health Systems. Hare, R.D. & Neumann, C.S. (2006). The PCL-R assessment of psychopathy: development, structural properties, and new directions. In C.J. Patrick (ed.), Handbook of Psychopathy (pp. 58–88). New York: Guilford Press. Karpman, B. (1948). The myth of the psychopathic personality. American Journal of Psychiatry, 104(3), 523–34. Kempinen, C.A. & Kurlychek, M.C. (2003). An outcome evaluation of Pennsylvania’s boot camp: does rehabilitative programming within a disciplinary setting reduce recidivism. Crime and Delinquency, 49(4), 581–602. Latessa, E.J. (2004). From theory to practice: what works in reducing recidivism. State of Crime and Justice in Ohio, 170–1. Latessa, E.T., Cullen, F.T. & Gendreau, P. (2002). Beyond correctional quackery: professionalism and the possibility of effective treatment. Federal Probation, 66(2), 43–9. Lowenkamp, C.T. & Latessa, E.J. (2004). Residential community corrections and the risk principle: Lessons learned in Ohio.In Ohio Corrections Research Compendium, Volume II, Columbus, Ohio: Ohio Department of Rehabilitation and Correction. Lowenkamp, C.T. & Latessa, E.J. (2005). Increasing the effectiveness of correctional programming through the risk principle: identifying offenders for residential placement. Criminology and Public Policy, 4(2), 263–90. Lowenkamp, C.T., Latessa, E.J. & Holsinger, A.M. (2006). The risk principle in action: what have we learned from 13,676 offenders and 97 correctional programs. Crime and Delinquency, 51(1), 1–17. Lurigio, A.J. (2005). Taking stock of community corrections programs. Criminology and Public Policy, 4(2), 259–62. MacKenzie, D.L. (1994). Results of a multisite study of boot camp prisons. Federal Probation, 58(2), 60–6. MacKenzie, D.L. (1997). Criminal justice and crime prevention.In Preventing Crime: What Works, What Doesn’t, What’s Promising: A Report to the United States Congress. Washington, DC: US Department of Justice, Office of Justice Programs, National Institute of Justice. MacKenzie, D.L. (2000). Evidence-based corrections: identifying what works. Crime and Delinquency, 46(4), 457–71. MacKenzie, D.L. (2005). The importance of using scientific evidence to make decisions about correctional programming. Criminology and Public Policy, 4(2), 249–57. MacKenzie, D.L., Brame, R., McDowall, D. & Souryal, C. (1995). Boot camp prisons and recidivism in eight states. Criminology, 33(3), 327–57. MacKenzie, D.L. & Souryal, C. (1994). Multisite Evaluation of Shock Incarceration. Washington, DC: US Department of Justice, National Institute of Justice. Martin, C., Lurigio, A.J. & Olson, D.E. (2003). An examination of rearrests and reincarcerations among discharged day reporting centers. Federal Probation, 67(1), 24–30. Martinson, R. (1974). What works? Questions and answers about prison reform. The Public Interest, 35, 22–54. Matthews, W.M. & Reid, W.H. (1981). A wilderness experience treatment program for offenders. In W.H. Reid (ed.), The Treatment of Antisocial Syndromes. New York: Van Nostrand Reinhold. Millon, T., Simonsen, E., Birket-Smith, M. & Davis, R.D. (Eds.) (1998). Psychopathy: Antisocial, Criminal and Violent Behavior. New York: Guilford Press. Osler, M.W. (1991). Shock incarceration: Hare realities and real possibilities. Federal Probation, 55(1), 34–42.

ADULT ANTISOCIAL SYNDROMES

555

Palmer, T. (1975). Martinson revisited. Journal of Research in Crime and Delinquency, 12, 133–52. Pinel, P. (1800–1). Traite Medico-Philosophique sur l’Alienation Mentale: Mentale ou la Manie. Paris: Richard, Caille & Ravier (English translation by D.D. Davis, London: Cadell & Davies, 1806). Poole, C. & Slavick, P. (1995). Boot camps: A Washington State Update and Overview of National Findings. Olympia, Washington: Washington State Institute for Public Policy. Prichard, J.C. (1835). A Treatise on Insanity and Other Disorders Affecting the Mind. London: Sherwood, Gilbert & Piper. Reid, W.H. (1978). The sadness of the psychopath. In W.H. Reid (ed.), The Psychopath: A Comprehensive Study of Antisocial Disorders and Behaviors (pp. 7–21). New York: Brunner/Mazel. Reid, W.H. (ed.) (1981). The Treatment of Antisocial Syndromes. New York: Van Nostrand Reinhold. Reid, W.H., Dorr, D., Walker, J.I. & Bonner, J.W. III (1986). Unmasking the Psychopath: Antisocial Personality and Related Syndromes. New York: W.W. Norton. Reid, W.H. & Solomon, G.F. (1981). Community-based offender programs. In W.H. Reid (ed.), The Treatment of Antisocial Syndromes. New York: Van Nostrand Reinhold. Rogers, R. & Shuman, D.W. (2005). Fundamentals of Forensic Practice: Mental Health and Criminal Law. New York: Springer. Rogers, R. & Webster, C.D. (1989). Assessing treatability in mentally disordered offenders. Law and Human Behavior, 13(1), 19–29. Sechrest, D.K. (1989). Prison ‘boot camps’ do not measure up. Federal Probation, 53(3), 15–20. Sherman, L.W. (2000). Reducing incarceration rates: the promise of experimental criminology. Crime and Delinquency, 46(3), 299–314. Stinchcomb, J.B. & Terry, W.C. III (2001). Predicting the likelihood of rearrest among shock incarceration graduates: moving beyond another nail in the boot camp coffin. Crime and Delinquency, 47(2), 221–42. St¨urup, G.K. (1964). Treatment of chronic criminals. Bulletin of the Menninger Clinic, 28, 229–43. Tonry, M. (1997). Intermediate Sanctions in Sentencing Guidelines. Washington, DC: US Department of Justice, National Institute of Justice. Tyce, F.A., Olson, R.O. & Amdahl, R. (1980). P.O.R.T. of Olmsted County, Minnesota. In J. Masserman (ed.), Current Psychiatric Therapies. New York: Grune & Stratton. Wolman, B.B. (1987). The Sociopathic Personality. New York: Brunner/Mazel. Zhang, S.X. (1998). In search of hopeful glimpses: a critique of research strategies in current boot camp evaluations. Crime and Delinquency, 44(2), 314–34.

CHAPTER 32

Legal, Medical and Social Impediments to Better Psychopaths: How Best to Deal with Persons with Psychopathic Disorders? Jurgen. ¨ L. Muller ¨ ¨ Georg August University of Gottingen, Germany

PRELIMINARY REMARKS AND INTENTION These people don’t fit into prisons or into mental institutions. In prisons they’re seen as sick, in hospitals they are troublemakers who cause so many problems (Dr. Pierre Gang´e, Canadian Psychiatric Association, in Davis-Baron, 1995).

The title of this chapter challenges the author and affronts the readers. Do we really have laws or in a broader sense do we have frameworks that have been established in order to protect society and in order to prevent crimes that lead to the opposite effect? Why do we have these frameworks? Is anyone to blame for that? If we do have such laws and rules, what are they? And if we do know that they are misleading, why don’t we modify or abolish them? Legal and medical impediments seem to be an issue that should be easy to understand. For example, if there are high relapse rates due to legal or medical interventions. But who defines the outcome criteria for the legal or medical intention that leads to the distinct ‘impediment’? Is the intention to provide treatment for persons with psychopathic disorders a so-called legal impediment since we are unable to cure psychopaths and to protect society by treating psychopaths? Therapy might be the wrong approach for persons who are bad and evil and who frequently relapse, as is indicated by the inclusion criteria themselves. If we agree that these people need treatment, we encourage the opinion that they are insane as well and unable to account for their crimes. Victims emphasize that true crime prevention should be lifetime detention if not an even worse penalty. For some of them, the intention The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

558

VOLUME I: DIAGNOSIS AND TREATMENT

to prevent further crimes by treating psychopaths is the real legal impediment to protecting society. If we don’t want to agree with this, we have to define what can be done with psychopaths from a medical or psychological point of view, and how legal interventions interfere with this intention. We have to be aware that therapeutic decision trees are not the right outcome criteria for legal interventions pursuing quite other interests. We have to understand the legal intentions behind a certain law. Thus, in discussing this topic seriously, we have to become ‘multi’professionals. This chapter deals with different approaches from heterogeneous professional disciplines with overlapping interests. The impact of this interchange will be addressed in the following chapter. The author of this chapter is a medical doctor, with special education in psychiatry and in particular in forensic psychiatry charged with forensic consultations as well as with treatments. This is the professional background of the author of this chapter and the perspective articulated in it. He is occupied with problems caused by different professions that interfere with his psychiatric self-concept. Consequently, other points of view, in particular from legal, political, educational and philosophical standpoints have necessarily been neglected. Furthermore, the author is educated in and occupied with the legal as well as with the forensic psychiatric situation in Europe, in particular in Germany. Although a comparison of political, medical and forensic systems all over the world will have been excluded, this is not the intention of this chapter. The author takes an approach that is much more basic: everyone who is occupied with forensic psychiatry regarding expert consultations as well as treatments, must deal with diagnosis, behavior, aspects of treatment and prognosis and relapse rates in persons with psychopathy. He has to handle these persons and his duty is necessarily embedded in a sociopolitical context that is dominated by safety concerns. If he wants to treat psychopaths and be responsible for their conditional release, he must justify his thinking and hope that the legal circumstances enable him to do his work. If this context is not helpful, he has a practical problem with legal impediments interfering with his work. The practical contact and the experience of professionals in the mental health system with persons experiencing the clinical syndrome of psychopathy is the theme of this chapter. Experiences that have occurred with different legal interventions, political procedures and their interference with the medical health system are discussed. The articulated experiences and misgivings are so far solitary, but they are embedded in a broader, perhaps worldwide context since the conditions of the German forensic situation are similar to most other countries. Thus, most other legal systems are confronted with the same problems brought about by a group of persons for whom no legal system and no social system is designed.

BETWEEN POLITICS, PSYCHIATRY AND PENOLOGY The administrative officers of penal institutions attempt to have such individuals transferred to mental hospitals because they believe them to be mentally ill. Knowing how little they can do for them and what difficult problems they are, the superintendents of mental hospitals attempt to get rid of them as soon as possible and transfer them back to prison as ‘not psychotic’. ‘Pushed from prison to hospital and back again, wanted in neither, the psychopathic delinquent is essentially the orphan of both penology and psychiatry’ (Thompson, in Cleckley, 1951).

LEGAL, MEDICAL AND SOCIAL IMPEDIMENTS

559

Since early clinical descriptions of psychopathy, the interaction between penal institutions, psychiatric wards and psychopaths have been difficult. Medical, legal and social concepts are formulated in a specific way. Medical institutions developed specific treatment concepts that usually were not made for treating psychopaths. According to Harvey Cleckley, psychopaths don’t fit very well with an existing concept. They are not insane in a medical sense, consequently there is no established treatment to change their behavior. On the other hand, they are far from being socially intact, as many of them fail to be able to integrate in society (Cleckley, 1951). In addition, psychopaths fail to accept any help and they do not benefit from punishment that is intended to encourage them to change their lives accordingly. Finally, their treatment outcome is poor, since their character features can be described using a checklist that has been established to predict further criminal behavior: being a psychopath means to be a high-risk person for relapses (Hare et al., 2000; Hemphill, Hare & Wong, 1998). From a point of view that focuses on the safety of society, the last point is most striking. In order to predict criminal prognosis and to protect society from further crimes, assessment scales have been established that identify psychopaths as high-risk individuals. In mentally ill persons, treatment programs have been used in order to change criminal behavior and to reduce relapse rates, but no therapeutic approach currently established has convincingly shown evidence of effectiveness in psychopaths. In contrast, some studies even showed the opposite effect (Rice, Harris & Cormier, 1992; Seto & Barbaree, 1999). So, it is doubted whether treatment approaches using medical or psychological concepts can contribute to changing dangerous psychopaths. This is in line with early clinical descriptions by Emil Kraepelin and Kurt Schneider, who attributed a negative prognosis to psychopaths who have been described as selfish, unable to learn from punishment and unable to change their behavior (Kraepelin, 1909–15; Schneider, 1948). Thus, it was doubted that ‘psychopaths’ could benefit from psychiatric treatment or psychotherapy intended to change their behavior. In the 1990s, several investigations showed that psychopaths did not benefit from therapy: therapy was found to worsen psychopaths, making them more dangerous and worsening their prognosis, as was pronounced by Rice, Harris and Cormier (1992) and by Seto and Barbaree (1999). This result challenged the purpose of therapy in forensic inpatients in toto. In discussions of the implications for society of these striking results, every point of view has been articulated: treatment must be improved, research encouraged and prognoses improved on the one hand yet preventive detention must be considered on the other hand. Scientists required wellperformed studies, politicians appealed for higher safety standards, searching for the right combination of punishment, detention and therapy. They postulated a long-lasting change in psychopaths towards nonviolent and noncriminal behavior. A new strategy was sought that would be embedded in a safety oriented, restrictive political background with limited financial resources. This is the background for ‘legal impediments to treatment’ and the discussions on how best to deal with psychopaths. To discuss this issue, many topics must be addressed regarding the legal and moral conditions for punishment and rehabilitation, regarding risk assessment and treatment outcome studies in psychopathy. According to our legal system, criminals including psychopathic criminals must be punished for their crimes and serve their sentences. Psychopaths have been found to be unable to change their behavior through punishment. After release, psychopaths are still at high risk for relapsing (Hemphill, Hare & Wong, 1998; Salekin, Rogers & Sewell, 1996). If psychopaths are still dangerous and likely to

560

VOLUME I: DIAGNOSIS AND TREATMENT

commit further crimes, can they ever be released from prison? Yes, one would like to answer, if they have been examined and their criminal prognosis is good. But how far can we trust our assessments? In public opinion, the false negatives of our assessments are much too high, but the rate of false positives is even higher. In spite of progress in the scientific assessment of prognosis, predicting the future of criminal inmates is still difficult. Currently, checklists addressing psychopathic symptoms are used to examine noncriminal, so-called successful or community psychopaths (Vitale et al., 2005; Yang et al., 2005). The emotional core feature, measured by the emotional detachment scale of the PCL-R, helps to qualify noncriminal subjects as psychopaths (Hare, 1999). What should be done if an expert determines that a person is at high risk for criminal or dangerous behavior, but the person has not yet committed a crime? Can crimes, relapses and dangerous behavior be predicted with a sufficient probability using current methods? Otherwise, do we have the right to impose preventive detention on many harmless people in order to protect society from a few dangerous individuals? This question must be addressed by authors in various forensic fields because psychopathy has been established as an ideal example for discussing central forensic issues. Foremost because of their dangerousness and poor treatment outcome.

PREVENTIVE DETENTION FOR ALL PSYCHOPATHS? HOW TO PROTECT SOCIETY FROM HIGH RISK PERSONS? Never have western and industrialized societies been safer than today. In spite of increased safety standards, the desire to avoid harm and danger has rarely been greater. Considering criminals and the management of violent and criminal behavior, the standards in predicting relapses and risk assessment have never been higher. Nevertheless, the public interest in avoiding any theoretical danger counterbalances low relapse rates and therapeutic approaches to treatment. In particular, sexual offenders and psychopaths are of special interest. Psychopathy has been associated with relapses and failure during probation, since development of the diagnostic tool for psychopaths, the Psychopathy Checklist-Revised version, has become a widely used tool for risk assessment. High scores on the PCL-R describe a person who is both psychopathic and has a high risk of relapse at the same time. What does it mean, if a high scorer has a three to fivefold risk of relapse in a distinct period of time? Taking care of high-risk persons is challenging, because risk assessment interacts with treatment strategies. Psychopaths, who have served their prison sentence, still may be dangerous. How should high-risk persons who have served their sentence be dealt with? Different legal procedures have been initiated in order to protect society from more or less dangerous persons. Legal rights have been jeopardized in the name of safety. In Germany, potentially dangerous persons who have served their prison sentence for a specific crime have been admitted to a psychiatric ward in order to prevent further crimes, in spite of not having had an earlier diagnosis of severe psychiatric disorder. According to this intention, fully responsible persons have been regarded as inherent safety risks after their release from prison. These healthy (sane) persons were considered in legal terms to be potentially dangerous criminals. In Germany, persons who are dangerous due to a severe psychiatric condition that is severe enough to interfere with criminal responsibility can be admitted to a psychiatric facility to prevent crime by curing the psychiatric condition and reintegrating these patients into society. Regarding persons with a personality disorder

LEGAL, MEDICAL AND SOCIAL IMPEDIMENTS

561

such as psychopathy, recidivistic and dangerous behavior are inherent. Conventionally, psychopathic disorders are not considered disturbed enough to have their legal responsibility compromised. Nevertheless, relapse rates are high among criminal psychopaths and they are often still dangerous after having served their time in detention. With consideration of the ‘References to the Execution of the Bavarian Law of Confinement’ (Hinweise zum Vollzug des Bayerischen Unterbringungsgesetzes, 2000), the Bavarian Ministry of Labor, Social and Family Affairs, Health and Women (Bayerisches Staatsministerium f¨ur Arbeit und Sozialordnung, Familie, Frauen und Gesundheit) tried to block this perceived security leak by broadening the definition of mental illness and the indications for treatment of the ‘Bavarian Law of Confinement’ extensively (for an overview see M¨uller, 2004; M¨uller, Klein & Cording 2002). This change in interpreting the Bavarian Law of Confinement was criticized by the heads of psychiatric facilities because it broadened commitment power of the government in favor of general security at the expense of mentally ill members in the community, psychiatric institutions and psychiatry in general. The heads of psychiatric hospital wards argued that dangerous persons are admitted to psychiatric wards for safety reasons, but without any psychiatric illness of required severity. Abuse of psychiatry and of the law of confinement was feared. According to the intention of the ‘References to the Execution of the Bavarian Law of Confinement’, nearly everybody with a disorder according to the International Classification of Diseases (ICD-10; Dilling, Mombour & Schmidt, 1993) or the Diagnostic and Statistical Manual of Psychiatric Disorders (DSM-IV, American Psychiatric Association, 2000) could have been admitted to a psychiatric ward by force if at any time in the future any misdemeanor or any offense is anticipated. Consistent with the ‘References to the Execution of the Bavarian Law of Confinement’, every smoker who commits a traffic offense in the future could be admitted to a psychiatric service because a diagnosis could be made (nicotine dependency: DSM-IV 305.1) and the possibility of crime is feared. According to this approach, in the name of safety, any stability of the law and any predictability of legal decisions would be abandoned. In line with the modified ‘References to the Execution of the Bavarian Law of Confinement’, several criminal persons who were considered to be dangerous and who had been serving their sentence were admitted to an inpatient psychiatry service for an undetermined time. This provoked opposition, bringing this legal approach from the Bavarian Ministry to higher courts. The controversial legal position between psychiatrists and the Ministry was illustrated by a subject whom the court sentenced as fully responsible. In this subject, the need for preventive detention as explained by Section 66 in the German Penal Code (Sicherungsverwahrung) had been explicitly denied during the trial. After being released from prison, the person had been hospitalized on the basis of the Bavarian Confinement Law in order to protect society. Experts argued that even if the subject has several diagnoses according to ICD-10 or DSM-IV, none of them were of sufficient severity to compromise his legal responsibility that is required for a person to be admitted to a psychiatric department according to the ‘Bavarian Law of Confinement.’ Since this subject did not suffer from a psychiatric illness with the required severity, he could not be accommodated in a psychiatric department even if he were still dangerous and relapses were feared. Both criteria were not denied by the experts. The arguments from the experts were considered by the court. The subject had to be released from the psychiatric department. The department in charge of this affair filed an objection, the subject has since been rearrested and readmitted to a psychiatric ward pending a decision of the Bavarian Supreme Court. In the end, the release of the subject was

562

VOLUME I: DIAGNOSIS AND TREATMENT

ordered by the Bavarian Supreme Court, after the arguments of the experts were accepted (M¨uller, 2004; M¨uller, Klein & Cording, 2002). This case report and the report about the important amendment that broadened the definitions of illness had led to the release of the subject from the psychiatric hospital despite his potential dangerousness. The interpretation of the Law of Confinement had been rejected by the judgment of the Bavarian Supreme Court. Nevertheless, the fundamental social problem remained unsolved. How should dangerous persons be dealt with? After this judgment, a Bavarian bill for a national law that would regulate preventive detention was submitted, but rejected as well: preventive detention must be addressed as a nationwide affair; it is not allowed to be enacted by an individual federal state. As a result, the German Department of Justice submitted a bill addressing preventive detention that was adopted by the German parliament in 2004. Today, dangerous persons can be admitted to prison for preventive detention in Germany, if several other conditions are fulfilled (M¨uller, 2004; M¨uller, Klein & Cording, 2002).

ARE PSYCHOPATHS AMENABLE TO CHANGE? Earlier well-known psychiatrists pronounced a skeptical attitude regarding treatment effects in psychopathy (Witter, 1970). Unlike most other offenders, psychopaths suffer little personal distress, see little wrong in their attitudes and behavior, and seek treatment only when it is in their best interests to do so, such as when applying for probation or parole. It is therefore not surprising that they derive little benefit from traditional treatment programs, particularly from those which are aimed at the development of empathy, conscience and interpersonal skills (Hare, 1999). Psychopaths are assumed to be unresponsive to treatment for a host of reasons, not least of which is their lack of motivation to change. They lack empathy, and they have a rock-solid personality structure that is extremely resistant to outside influence (Hare, according to Davis-Baron, 1995). Consistent with pessimistic treatment outcome studies, social pressure is growing to keep violent offenders locked up. Krueger, an incarcerated psychopath, argues that ‘the system’ hasn’t tried hard enough to cure him, that governments have silently decided that psychopaths are simply evil and cannot be cured and see no point in wasting taxpayers’ dollars. ‘But before you lock the barn doors and throw away the key, I think you have to give that person assistance to help understand his or her own ways to go wrong’. Contrary to Krueger, most researchers favor the point of view that the ‘system’ has tried (but might have failed) to treat psychopaths. Despite decades of energy and effort, psychiatrists, psychologists and other professionals have been unable to find medication, treatment or a form of therapy that has any positive effect on the behavior of criminal psychopaths. Some treatment programs have actually made them worse (Davis-Baron, 1995). Fulfilling the criteria of the PCL-R, psychopathy has been found to be a significant predictor of violent recidivism (Hemphill, Hare & Wong, 1998; Rogers et al., 1995). The rate of violent recidivism among psychopathic sex offenders is high, with 90 % violently reoffending within seven years (Rice & Harris, 1997). Psychopathic offenders reoffend violently about four times more frequently than nonpsychopathic offenders (Hemphill, Hare & Wong, 1998). In absolute terms reviews estimate that about 50 % to 70 % of psychopathic offenders will violently recidivate (Hemphill, Hare & Wong, 1998; Salekin, Rogers & Sewell, 1996). While most research has been conducted with American, male

LEGAL, MEDICAL AND SOCIAL IMPEDIMENTS

563

populations, recent research suggests that the findings can be generalized (Grann et al., 1999; Hare et al., 2000) and can be applied to female offender populations (Salekin, Rogers & Sewell 1997; Rogers, Ustad & Salekin 1998). Thus, a psychopathic offender presents a strong and continuing danger to society, since the PCL-R is regarded by some as the best predictor of violent recidivism (Hemphill, Hare & Wong, 1998; Salekin, Rogers & Sewell, 1996; although see Gendreau, Goggin & Smith 2002). Regular outcome criteria or official records used in follow-ups of criminal behavior probably underestimate the risk, because individuals might have successfully evaded arrest for violent crimes or might have moved to another jurisdiction. Some of the data presented also do not take into account psychopathic offenders who recidivate nonviolently but, nonetheless, violate the welfare and rights of others.

DOES THERAPY MAKE SENSE? One of the world’s best-known treatment efforts began at the Oak Ridge Hospital, which is a maximum-security forensic psychiatric facility in Ontario, Canada, in the mid-1960s when a program of intensive group therapy for psychopaths was developed under Elliott Barker. Almost 20 years after its demise, the program is still considered among the most intensive programs for psychopathic patients ever undertaken. Participants were involved in intensive group therapy for up to 80 hours a week, with very little diversion. They could be ordered to participate. Once in a program, patients who refused to talk in detail about their offenses could be sent to a disciplinary program until they fulfilled program requirements (Davis-Baron, 1995). For psychopaths the program failed. Of the study subjects, one-third were psychopaths who had spent at least two years in the program. The results were not only disappointing but also startling. While nonpsychopathic participants did better upon release than their peers who had also been imprisoned, the psychopaths who spent time in the treatment program did worse than psychopaths who went to prison and never underwent treatment (Davis-Baron, 1995). Psychopaths actually used the program to develop their skills at manipulating people. They mastered the language of healing therapy, learning which patient responses signaled positive changes. They learned better than their nonpsychopathic peers what they were supposed to say, how they were supposed to feel and how they were supposed to act in order to show marked improvement. Some actually referred to treatment programs like Oak Ridge as ‘finishing schools’ (Hare, according to Davis-Baron, 1995). The outcomes of several studies on treatment effects in psychopathy are discouraging, because they suggest that treatment might make psychopaths more dangerous and raise the question whether psychopaths can worsen through therapy. There are some overviews and meta-analyses of the treatment effects on psychopathy (D’Silva, Duggan & McCarthy, 2004). In this chapter, only several are listed. Rice, Harris and Cormier (1992) reported on the 10-year recidivism rates of violent offenders treated in a maximum-security psychiatric hospital. They retrospectively scored the PCL-R from the institutional files of patients of a maximum security psychiatric facility. Psychopaths were defined by a PCL-R score of 25 or higher and nonpsychopaths by a score of below 25. Inpatients treated in a therapeutic community were compared with matched participants sampled from a correctional setting. Comparing the groups overall, there were no differences in recidivism. The violent recidivism rate of nonpsychopaths who had been

564

VOLUME I: DIAGNOSIS AND TREATMENT

treated in an intensive and lengthy therapeutic community program was lower than that of a matched group of untreated patients. However, the violent recidivism rate of treated psychopaths was actually higher than that of untreated psychopaths. Separating the groups into psychopathic and nonpsychopathic subgroups, treated psychopaths were more likely to reoffend than untreated psychopaths, whereas treated nonpsychopaths were less likely to reoffend than untreated nonpsychopaths. This study has been criticized because it was based on a retrospective evaluation with a particular population of mentally disordered offenders. And with an unusually complex and controversial treatment program that included nude ‘encounter sessions’ and ingestion of LSD. In 1999, Seto and Barbaree reported that adult male sex offenders who scored higher on psychopathy and exhibited improved behavior in treatment were almost four times more likely to commit a new serious offense than other offenders once released (Seto & Barbaree, 1999). These data came from a follow-up study of 224 sex offenders who were treated in a prison-based program. ‘Treatment behavior’ had been scored according to the offender’s attendance, level of participation, interactions with other group members, quality of homework assignments, and therapist ratings of motivation for treatment and treatment progress. In contrast to the hypothesis, good treatment behavior was not associated with less recidivism. Instead, it was associated with greater recidivism, especially among individuals who scored higher on psychopathy. Men scoring 15 or higher on the PCL-R and who behaved better in treatment were more likely to commit a new offense of some kind than other offenders, and almost four times as likely to commit a new serious offense (Seto & Barbaree, 1999). In a follow-up study, Barbaree (2005) re-examined this sample using more complete recidivism data from a national police database. Although psychopathy continued to be a significant predictor of general and serious recidivism, treatment behavior was no longer related to either general or serious recidivism, and there was no statistically significant interaction between psychopathy and treatment behavior: additional analyses ruled out the possibility that the differences between studies could be accounted for by the different average lengths of follow-up. A direct comparison of the two data sources showed that differences in recidivism between subgroups were reduced by using the more complete recidivism data (Barbaree, 2005). Consistent with this, Looman et al. (2005) attempted but failed to replicate the Seto and Barbaree (1999) finding in a sample of convicted sex offenders treated at a correctional psychiatric center. Using a PCL-R cutoff score of 25 to identify psychopaths, psychopathy was significantly related to serious recidivism, but offenders who performed well in treatment did not significantly differ from those who did less well in terms of their rates of serious recidivism during the follow-up period (Looman et al., 2005).

CONFLICTING OUTCOME STUDIES Prominent and influential authorities in the field have combined studies by Seto and Barbaree (1999) and the studies by Rice and colleagues (1992) to argue that treatment for psychopathic sex offenders is harmful (Barbaree, 2005; Harris, Rice & Cormier, 2005; Looman et al., 2005). The striking effect of these studies might be explained by the problem that authors as well as authorities may have been unaware of the more ominous possibility that

LEGAL, MEDICAL AND SOCIAL IMPEDIMENTS

565

treatment could cause harm. If either of their explanations received empirical support, this finding would have serious implications. Sex offender evaluations are routinely conducted by psychologists and psychiatrists to inform courts in sexually violent predator applications (enacted 1990, Rogers & Jackson, 2005). Such proceedings have direct and considerable effects on the long-term detention or liberty of the individuals involved. The ‘treatment causes harm hypothesis’ and subsequent inferences place all treated persons who rated above a certain PCL-R score, in a serious double bind: any evidence that they exhibit treatment compliance and success can be interpreted as indicating increased risk for serious reoffense, and if the ‘treatment-causes-harm’ hypothesis is eventually supported by further empirical data, psychopathic sex offenders might reasonably be prevented from having psychological treatment. The potential impact of the ‘treatment-causes-harm’ hypothesis on current practice in the field and on individual offenders is profound. In contrast to this discouraging perspective, the majority of treatment outcome studies on psychopaths, however, emphasizes that there is no conclusive evidence that psychopaths are untreatable or that their behavior cannot be modified (D’Silva, Duggan & McCarthy, 2004; Looman et al., 2005) In contrast to the ‘treatment-causes-harm’ protagonists, other authors failed to show a relationship between treatment behavior and recidivism. For example, Quinsey, Khanna and Malcolm (1998) found that clinician ratings of treatment gain were unrelated to recidivism among 193 sex offenders treated at a correctional psychiatric center, even though the treated sex offenders showed significant improvements on within-treatment measures. In addition, the follow-up study by Barbaree and colleagues could not support the evidence from his earlier study (Barbaree, 2005). Accordingly, Looman and colleagues also failed to replicate the earlier Seto and Barbaree (1999) finding in a sample of convicted sex offenders with a PCL-R score above 25. This is consistent with findings of other researchers who did not focus on ‘psychopathy’ in particular when they examined the relationship between sex offender treatment behavior and recidivism. Marques and colleagues reported that sex offenders who participated in an institutional treatment program and obtained good post-treatment scores (on phallometrically measured sexual arousal, self-reported attitudes and beliefs about sexual offending, and ratings of their relapse prevention assignments) were less likely to reoffend than those who did not obtain positive post-treatment scores (Marques et al., 2005). In a study on the efficacy of the California treatment program, Marques and colleagues (2005) reported that treatment participants who had been judged to have ‘gotten it’ in terms of their understanding of the principles of relapse prevention, had recidivism rates below 10 %, whereas their treatment counterparts who had not ‘gotten it’ had recidivism rates in excess of 50 % (Marques et al., 2005). Thus, recent findings are more optimistic than the earlier ones reporting on treatment effects in psychopathy. Given these contradictory results, the relationship between treatment behavior and recidivism among sex offenders and psychopaths deserves further investigation. Major methodological weaknesses in the relevant literature, including inadequate assessment procedures, poorly defined treatments, lack of post-treatment follow-up and lack of adequate controls or comparison groups, make it difficult to be certain that nothing works. Psychopathy is described using different scales and assessing different symptoms. Treatment settings as well as follow-up periods and outcome criteria are heterogeneous making clear perspectives impossible. Well-conceptualized study protocols, including sufficiently well-defined participants and clearly defined outcome criteria, are required to answer scientifically whether trying to treat and change psychopaths is a promising approach.

566

VOLUME I: DIAGNOSIS AND TREATMENT

ARE PSYCHOPATHS IRRESPONSIBLE? Recent neurophysiological data link core syndromes of psychopathic behavior to distinct brain regions and neural networks that are critically out of balance in psychopathy (Sommer et al., 2006). This raises the question whether changes in the neurobiology make psychopaths irresponsible for their doings. If psychopaths commit their crimes because of neurobiological impairments and if psychopaths relapse because they are unable to learn from punishment, it has been discussed whether they can be punished for their crimes. Theories on the purposes and justifications of punishment may be divided into the retributive and the utilitarian. Utilitarian theories fundamentally look forward and focus on the beneficial consequences for society and the individual that may be brought about by punishment. Retributive or just desert theories are fundamentally backward looking and focus on the agent and on his relation to the wrongful act. Punishment has a retributive function. Findings of criminal responsibility and subsequent punishment serve to express the community’s moral condemnation of the offense and the offender. They aim to restore the balance of rights disturbed by the crime and to deliver justice to both victim and offender. Since punishment should be morally deserved, it is necessary that the offender meets the conditions of moral responsibility. In psychiatric history, psychopaths have been considered responsible for their doings. According to the German forensic psychiatrist Hermann Witter, the term psychopathy is misleading since psychopathy implicates a kind of illness whereas psychopaths just keep on acting in a wrongful way (Witter, 1970). The only way to change their behavior is to have them face the consequences of their wrongful acts. Consistent with forensic psychiatric tradition, it would be wrong to assess psychopaths as insane and irresponsible. Since psychopaths continue to commit crimes and cause harm, they have to be punished to prevent further crimes and to ensure that crimes will be prosecuted. Regarding the backward-looking retributive purpose, punishing psychopaths might help to restore law and morals, even if punishment does not prevent further offenses. Regarding the forward-looking, primarily utilitarian function, which kind of punishment or treatment is necessary to prevent crimes and to protect the community must be considered. According to this, therapy has to change their behavior and to solidify this change in behavior for the future. Only reforming an offender will effectively prevent future criminal acts. It does not make sense to convict a mentally insane offender to restore the law.

LEGAL IMPEDIMENTS Legal impediments to treatment apply governmental interventions that might not be helpful in psychopathy. To address this question, positive data from research as well as less empirically based clinical impressions have to be considered. Different aspects are important: (i) How should the courts treat persons with psychopathy according to the inclusion criteria of insanity and culpability? (ii) What is the benefit of putting psychopaths in prison? (iii) How can psychopathic behavior be improved by means of therapy? (iv) What can be done to reduce the risk of reoffending? (v) What has to be avoided? (vi) What must be done in the future? Based upon scientific approaches to the concerns outlined above, influencing factors can be addressed from a meta-perspective required in this chapter.

LEGAL, MEDICAL AND SOCIAL IMPEDIMENTS

567

How Should the Courts Treat Persons with Psychopathy According to the Inclusion Criteria Regarding Insanity and Culpability? One of the most fundamental principles for changing psychopathic behavior is to encourage people to be responsible for their own doings. If psychopaths are convicted for their crimes, they must face punishment as a consequence. Therefore, punishment is the first step in changing behavior. If one has done wrong, society reacts by convicting and punishing. One must face the consequences. Facing the consequences can be considered as the first step in behavioral therapy. Therefore, agreeing with the hypothesis that psychopaths can be held accountable for their acts is important to help them change their behavior according to the consequences of their wrongful acts. Not to punish for crimes would only encourage further crimes by the absence of negative consequences.

What is the Benefit of Putting Psychopaths in Prison? If psychopaths are convicted for their crimes, they must face punishment as a consequence and as a first step to changing their behavior. This consequence can be considered as the first step in behavioral therapy. During imprisonment, daily routine with duties and work helps to accustom the prisoners to a daily structure that is otherwise lacking for most of them. Simultaneously, confronting and encouraging them to deal with their own behavior should prepare them for the next step to change their behavior, namely treatment. This next step in therapy is difficult, time consuming, requiring adequate programs and well-trained staff to avoid disheartening experiences with the penal system. Some of these experiences are described by Hare: Some form of group therapy is an important part of most prison programs but it doesn’t work for psychopaths because they tend to dominate group sessions, impose their views on others and ensure that discussion is diverted away from them. They generally don’t seek help on their own and once in therapy often do little more than go through the motions. They are incapable of the emotional intimacy and deep searching for which most therapist strive (Hare, in Davis-Baron, 1995).

With respect to this impairment, the treatment of psychopaths should focus on changing their behavior, not on developing emotional skills such as empathy. The most important aim of imprisonment regarding psychopaths is to confront them with the consequences of their crimes, to accustom them to following a daily routine, regular duty and work and to encourage them to reflect upon their criminal careers. The next step is to maintain the achieved progress in a more open setting, for example, in a special therapeutic facility connecting prison with post-prison settings or forensic psychiatric wards. Thus, during imprisonment, one has to pave the way to reintegrate this person into society by the use of special treatment concepts.

How Can Psychopathic Behavior be Changed by Means of Therapy? The finding that a treatment program increased the risk for violence was striking, because the benefit of therapeutic options is generally doubted. Moreover, it can be argued that some

568

VOLUME I: DIAGNOSIS AND TREATMENT

kinds of therapy might favor further psychopathic behavior by helping them to develop better ways of manipulating, deceiving and finally relapsing. The majority of treatment outcome studies on psychopaths emphasize that there is no conclusive evidence that psychopaths are untreatable or that their behavior cannot be modified. More recent studies are methodologically improved regarding inclusion criteria, follow-up period and outcome criteria. Even if they fail to show clearly that specific therapeutic strategies can change psychopathic behavior substantially or cure psychopathy, they show no worsened relapse rates through therapy. Most studies have major methodological weaknesses, including inadequate assessment procedures, poorly defined treatment settings, lack of post-treatment follow-ups and lack of adequate controls or comparison groups, making it difficult to compare and discuss their results. Since changing psychopathic behavior is the only way to protect society from relapsing offenders, society must work harder to manage the problem. Model-treatment programs must be developed that aim at improving the post-treatment behavior of psychopaths although it appears to be impossible to cure them. In addition, a model is required to identify the triggers that precede their violent and criminal behavior.

What Can be Done to Reduce the Risk of Relapse? One early but important aim of imprisonment as well as the first step to treatment is to confront criminal psychopaths with the consequences of their crimes and to have them face the consequences. Knowing that to commit a crime will be followed by a definite consequence; they will take the consequences into account. They must critically deal with their behavior. Based upon this, therapy must guide them to follow a daily routine consistent with society’s laws. Consequently, advances that are achieved have to be maintained in opened settings. Accordingly, treatment should guide convicted psychopaths and from a time-intensive period towards increasing degrees of freedom and personal responsibility. Even after conditional release, they should remain in contact with special therapeutic facilities connected with the prison or with a forensic psychiatric ward. Thus, temporary and limited detention in a prison might have to be replaced by a risk-dependent and rehabilitation-based program for resocialization. This approach would interfere with personal rights, because predictability of legal decisions and the distinct punishment for a certain crime is replaced by an outcome and prognosis-based rehabilitation program. This raises the question: How certain are our diagnoses and risk predictions? How strong does the diagnosis ‘psychopathy’ correlate with danger to society? Strong enough to warrant detention by reason of self-defense? Regarding the uncertainty of legal prognosis and risk assessment, it must be discussed which level of risk and which crime is to be feared and should justify this infringement on personal rights.

What is Better to be Avoided? Some well-intended positions are adverse for treatment effects and even worse for the safety of society: other treatment approaches, as the one outlined above, might be helpful but have been rejected. In Germany, so-called therapeutic wards were asked for and with good arguments. They were, however, never established. These wards should be built for criminals who have a high risk for relapse and a poor prognosis and who have been found responsible for their acts, thus precluding admission to a forensic psychiatric facility. Wards

LEGAL, MEDICAL AND SOCIAL IMPEDIMENTS

569

like this have to have special rehabilitation and reintegration programs. Their residents must remain in this long-term unit until they can be released conditionally with a more favorable prognosis. Rehabilitation programs on social therapeutic wards would make sense, since a special program to reintegrate them into society and to prevent further crimes would have been conceptualized and realized there. Nevertheless, these wards have never been established in a noteworthy sense, at least in Germany. Criminals who are dangerous to society are being put in prison, perhaps for the purpose of preventive detention. In spite of imprisoned criminals having been found fully responsible and considered to be mentally sane, specific programs to change their attitudes and behavior through well-trained and educated persons are necessary. Since, at least in Germany, these possibilities are lacking, one must look for treatment opportunities elsewhere. Regarding preventive detention, German lawyers try to place them in psychiatric facilities. According to German law, a criminal who has been remanded for preventive detention for a felony can petition for transfer to a psychiatric facility, if therapy and rehabilitation are more easily performed there. Because treatment facilities in prison are missing, it is easy to argue that the inmate must be transferred to a psychiatric ward for therapy. It is very easy, too, to argue that psychiatric facilities are better at treatment than prisons which have been designed to prevent crimes by punishment. To be transferred to psychiatry, the prisoners must be found to have a psychiatric disorder that can be improved through treatment. Under this condition, the judge must decide whether the prisoner should be transferred to psychiatric treatment. The lawyer for the criminal will continue to insist on this transfer, since this is the first step to freedom for his client. Nevertheless, the transfer will raise many problems for the institution as well as for other psychiatric inpatients. Regularly, sane but dangerous criminals are not disabled, compared to psychotic patients with schizophrenia. Those, however, are the persons for whom psychiatric facilities have been designed. Criminals, including psychopaths do not have very much difficulty in coping with treatment requirements. After a more or less short time, they will plead for relief. It must be feared that they will gain relief that is not consistent with their risk assessment, because they progressed through the psychotic rehabilitation program for psychotic patients. Summarizing, the right to receive therapy in a therapeutic setting, although adequate opportunities for them are lacking in prison, will help dangerous persons to gain release without adequate rehabilitation.

What Has to be Done? Most of the requirements have been addressed before. Persons with psychopathy usually are not admitted to a psychiatric facility since normally they are regarded as legally responsible for their crimes. Imprisonment restores the law by punishment. Prisons have not been conceptualized for purposes of relapse prevention through treatment or rehabilitation. Specialized units for the rehabilitation of dangerous criminals are required but have not been established, at least not in Germany. These units are necessary to rehabilitate dangerous criminals in order to reduce the risk for further crimes. In order to rehabilitate dangerous persons, these units should provide specific programs as described above. Relapse-prevention techniques should integrate elements of the available cognitive-behavioral correctional programs. The program should be less concerned with developing empathy and conscience or affecting changes in personality than with convincing participants that they alone are

570

VOLUME I: DIAGNOSIS AND TREATMENT

responsible for their behavior and that they can learn more prosocial ways of using their strengths and abilities to satisfy their needs and wants. It would involve controlling and supervising them at an institution following their release into the community. For scientific reasons, an experimental design would permit empirical evaluation of special treatment settings and intervention modules. This would be helpful to attain scientific data on relapse prevention and treatment effects of different settings. Having achieved and established a well-conceptualized study protocol, stringent safeguards for maintaining the integrity of the program are required (Hare, 1999). Correctional programs are constantly in danger of erosion because of changing institutional priorities, community concerns and political pressures. Earlier, Robert Hare summarized the requirements: there has to be a program for psychopaths that is firmly grounded in theory, research and correctional experience, and that is carefully run and evaluated’. I think he is right.

SUMMARY Psychopathic disorders are not considered to be mental illnesses. People with such disorders do not qualify for existing inpatient or outpatient treatment. Conventionally, most psychopaths are considered to be responsible for their criminal acts. Since they do not benefit from punishment and have a high relapse rate, psychopaths are transferred to forensic facilities. Psychopathic individuals have the cognitive capacity to make rational and informed treatment decisions. Therefore, they do not qualify for court-ordered involuntary treatment, even when dangerous. Although the risk of future dangerousness is statistically elevated in psychopathy, the risk typically is not imminent, further disqualifying the individual from emergency, involuntary measures. Afflicted individuals commit criminal acts without the presence of mental illness: they are more apt to be prosecuted and sent to prison than admitted to a treatment setting and if already in a treatment setting further criminal activity can result in prosecution and transfer to prison and away from the treatment setting. More and more mental health codes are designed to protect the rights of the mentally ill and address the mentally ill person’s lack of control. Restraints, seclusion, restrictive and intrusive measures must be avoided. However, those with psychopathic disorders are also capable of planned aggression. Therefore, it can be more dangerous to attempt treatment of the psychopathic individual in a treatment setting, resulting in increased pressure to discharge, transfer, prosecute or in some other way get rid of the psychopathic ‘trouble maker’. So far, there is no well-designed study that proves that psychopaths become more dangerous through therapy. Neither has the opposite been convincingly shown yet. Special facilities are required that help to release psychopaths into individually designed settings. The outcome of this approach has to be evaluated scientifically.

REFERENCES American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders (4th edition, text revision). Washington, DC: American Psychiatric Association. Barbaree, H.E. (2005). Psychopathy, treatment behavior, and recidivism: an extended follow-up of Seto and Barbaree. Journal of Interpersonal Violence, 20, 1115–31. Cleckley, H. (1988). The Mask of Sanity, fifth edition. Augusta, Georgia: Mosby Co.

LEGAL, MEDICAL AND SOCIAL IMPEDIMENTS

571

Davis-Barron, S. (1995). Psychopathic patients pose dilemma for physicians and society. Canadien Medical Association Journal, 152, 1314–17. Dilling, H., Mombour, W. & Schmidt, M.H. (1993). International Klassifikation psychischer St¨orungen ICD-10, 2. Huber. D’Silva, K., Duggan, C. & McCarthy, L. (2004). Does treatment really make psychopaths worse? A review of the evidence. Journal of Personality Disorders, 18, 163–77. Gendreau, P., Goggin, C. & Smith, P. (2002). Is the PCL-R really the ‘unparalleled’ measure of offender risk? A lesson in knowledge cumulation. Criminal Justice and Behavior, 29( 4), 397–426. Grann, M., Langstrom, N., Tengstrom, A. & Stalenheim, E.G. (1998). Reliability of file-based retrospective ratings of psychopathy with the PCL-R. Journal of Personality Assessment, 70, 416–26. Grann, M., Langstrom, N. Tengstrom, A. & Kullgren, G. (1999). Psychopathy (PCL-R) predicts violent recidivism among criminal offenders with personality disorders in Sweden. Law and Human Behavior, 23, 205–17. Hare, R.D. (1998). Psychopathy, affect, and behavior. In D. Cooke, A. Forth & R. Hare (eds.), Psychopathy: Theory, Research, and Implications for Society (pp. 105–37). Dordrecht: Kluwer. Hare, R.D. (1999). Psychopathy as a risk factor for violence. Psychiatric Quarterly, 70, 181–97. Hare, R.D., Clark, D., Grann, M. & Thornton, D. (2000). Psychopathy and the predictive validity of the PCL-R: an international perspective. Behavoral Science and the Law, 18, 623–45. Harris, G.T., Rice, M.E. & Cormier, C.A. (2002). Prospective replication of the Violence Risk Appraisal Guide in predicting violent recidivism among forensic patients. Law and Human Behavior, 26, 377–94. Hemphill, J.F., Hare, R.D. & Wong, S. (1998). Psychopathy and recidivism: a review. Legal and Criminological Psychology, 3, 139–70. ¨ Kraepelin, E. (1909–15). Psychiatrie. Ein Lehrbuch f¨ur Studierende und Arzte (8th edition). Leipzig: Ambosius Barth. Looman, J., Abracen, J. Serin, R. & Marquis, P. (2005). Psychopathy, treatment change, and recidivism in high-risk, high-need sexual offenders. Journal of Interpersonal Violence, 20, 549–68. Marques, J.K., Wiederanders, M., Day, D.M. et al. (2005). Effects of a relapse prevention program on sexual recidivism: final results from California’s sex offender treatment and evaluation project (SOTEP). Sexual Abuse, 17, 79–107. M¨uller, J.L. (2004). Vom BayUnterbrG zum Bay. StrUBG: R¨uckfallpr¨avention zwischen staatlichem Sicherheitsanspruch, Selbstverst¨andnis psychiatrischer Kliniken und individuellen Freiheit¨ srechten. In G. Hajak & J.L. M¨uller (eds.), Uber die Zerbrechlichkeit der Willensbestimmung (pp. 55–78). Berlin: Springer. M¨uller, J.L., Klein, H.E. & Cording, C. (2002). Missbrauch der Psychiatrie? Konflikte zwischen staatlichem Sicherheitsanspruch und dem Selbstverst¨andnis psychiatrischer Kliniken. Psychiatrische Praxis, 28, 416–20. Quinsey, V.L., Khanna, A. & Malcolm, P.B. (1998). A retrospective evaluation of the Regional Treatment Centre Sex Offender Treatment Program. Journal of Interpersonal Violence, 13, 621–44. Rice, M.E. & Harris, G.T. (1997). Cross validation and extension of the Violence Risk Appraisal Guide for child molesters and rapists. Law and Human Behavior, 21, 231–41. Rice, M.E., Harris, G.T. & Cormier, C.A. (1992). An evaluation of a maximum-security therapeutic community for psychopaths and other mentally disordered offenders. Law and Human Behavior, 16, 399–412. Rogers, R., Sewell, K.W., Ross, M. et al. (1995). Determination of dangerousness in forensic patients: an archival study. Journal of Forensic Science, 40(1), 74–7. Rogers, R., Ustad, K.L. & Salekin, R.T. (1998). Convergent validity of the personality assessment inventory: a study of emergency referrals in a correctional setting. Assessment, 5, 3–12. Rogers, R. & Jackson, R.L. (2005) Sexually violent predators: the risky enterprise of risk assessment. Journal of the American Academy of Psychiatry and the Law, 33(4), 523–8. Salekin, R.T., Rogers, R. & Sewell, K.W. (1996). A review and meta-analysis of the Psychopathy Checklist and the Psychopathy Checklist-Revised: predictive validity of dangerousness. Clinical Psychology: Science and Practice, 3, 203–15.

572

VOLUME I: DIAGNOSIS AND TREATMENT

Salekin, R.T., Rogers, R. & Sewell, K.W. (1997). Construct validity of psychopathy in a female offender sample: a multitrait-multimethod evaluation. Journal of Abnormal Psychology, 106, 576–85. Schneider, K. (1948). Klinische Psychopathologie. Stuttgart: Thieme. Seto, M. & Barbaree H.E. (1999). Psychopathy, treatment behavior, and sex offender recidivism. Interpersonal Violence, 14, 1235–48. Sommer, M., Hajak, G., Dohnel, K. et al. (2006). Integration of emotion and cognition in patients with psychopathy. Progress in Brain Research, 156C, 457–66. Vitale, J.E., Newman, J.P., Bates, J.E. et al. (2005). Deficient behavioral inhibition and anomalous selective attention in a community sample of adolescents with psychopathic traits and low-anxiety traits. Journal of Abnormal Child Psychology, 33(4), 461–70. Witter, H. (1970). Grundriß der gerichtlichen Psychologie und Psychiatrie. Heidelberg: Springer. Yang, Y., Raine, A., Lencz, T. et al. (2005) Volume reduction in prefrontal gray matter in unsuccessful criminal psychopaths. Biological Psychiatry, 15(10), 1103–8.

CHAPTER 33

Social Policy Considerations on Psychopathic Disorders Harald Dreßing, Hans Joachim Salize and Peter Gass University of Heidelberg, Germany

In all societies there is a large body of people who are incapable of meeting social norms and leading normal lives. It is estimated that psychopaths are responsible for more than 50 % of serious crimes (Hare, 1993). Psychopathic behavior causes great distress and represents a major challenge for policy, the criminal justice system and the mental health system. Psychopaths demonstrate a pattern of offending that is more persistent, severe and violent than that of other criminals and they tend to recidivate more quickly and frequently than nonpsychopathic offenders (Serin & Amos, 1995). The core behavioral problems of psychopathy seem to be as old as mankind. Scientific interest in this issue can be traced back to the beginning of thenineteenth century. Pinel already addressed it by using the term manie sans d´elire to describe a behavior that includes complete remorselessness (Werlinger, 1978). Shortly afterwards, the English psychiatrist J.C. Prichard (1837) described a syndrome in which the ‘moral and active principles of the mind are strongly perverted or depraved’. For this syndrome he coined the term ‘moral insanity’. The modern concept of psychopathy was put forward by Cleckley in his work The Mask of Sanity (1941) in which he described the psychopath as an intelligent person who is characterized by a poverty of emotions, lack of shame and remorse, superficial charm, as well as manipulative and irresponsible behavior. Partly based on Cleckley’s observations, Hare (1991) developed the Psychopathy Checklist refining the construct of psychopathy into a distinct personality disorder. Hare proposed several items that fall into two clusters: one cluster reflects core interpersonal and affective characteristics; while the other cluster consists of items that reflect a socially deviant lifestyle. The much broader concept of the antisocial personality disorder (APD) of the DSM IV (American Psychiatric Association, 1994) focuses on behavioral items that mirror persistent violations of social norms. Although there is some evidence that it seems to be easier to agree on behavioral items than on personality traits and therefore the reliability of the diagnosis of APD might be better, it has to be stressed that the predictive power of the APD concept concerning the probability of reoffending is much lower than the concept of psychopathy. Therefore the following considerations will primarily focus on core psychopathy and not on APD.

The International Handbook of Psychopathic Disorders and the Law. Edited by Alan R. Felthous and Henning Saß. C 2007 John Wiley & Sons, Ltd.

574

VOLUME I: DIAGNOSIS AND TREATMENT

However, it is worth noting, that the diagnostic entities often are used interchangeably even in scientific research. This must be kept in mind, when empirical studies on the effectiveness of psychotherapy and psychosocial rehabilitation and their implications on social policy considerations are discussed in this chapter, because intervention studies often do not explicitly focus on psychopathy, and the underlying study samples frequently consist of offenders with mixed diagnoses. Contrary to intervention studies, most neurobiological research on psychopathy focuses on probands with a clear diagnosis of psychopathy according to the Hare criteria. Therefore these research findings are of special interest and it has to be discussed whether neurobiological alterations in psychopathic individuals should mitigate criminal responsibility and change the way to deal with psychopaths. A core question is whether modern neurobiological research indicates that there should be more therapy and social rehabilitation than punishment and imprisonment for the psychopaths. This discussion has also to consider general developments in the attitudes of societies towards the placement and treatment of mentally ill offenders. There seems to be a trend for persons with mental disorders to be increasingly perceived as violent and threatening by major sectors of society including politicians, and for public safety to become the central focus. The implications of this development on social policy considerations concerning psychopaths are evident, and of whether civil commitment laws and forensic legislation mirror this development must be discussed. The question may not be whether to treat, incarcerate or punish the psychopaths is the best way to deal with them but which combinations of approaches are more likely to achieve the maximum benefit for both the psychopathic individual and society.

SOCIAL POLICY CONSIDERATIONS IN THE CONTEXT OF LEGAL REGULATIONS A fundamental question regarding the therapy of psychopaths is whether one considers persons with this diagnosis as ‘bad’ or ‘mad’. Punishment and retribution would be the adequate way to deal with psychopathic individuals if one assumes that they are ‘bad persons’ with morally despicable behavior, for which they are to be held responsible. Following this assumption, considerations regarding therapeutic efforts or social rehabilitation would actually be unnecessary. If one assumes that psychopathy is a mental illness, retribution and punishment might not play a role and the therapeutic efforts would have be the complete center of attention. Although this dichotomy is based more on social prejudices than on scientific evidence, it seems obvious that the first assumption – psychopaths are ‘bad persons’– dominates social policy considerations, because the statement of Cleckley from the year 1941 is still valid, when he wrote: ‘It is only in exceptional instances that the therapist can get his hands on the patient, and even then he has little more opportunity to take useful measures than would a surgeon called upon to remove the gallbladder of a jackrabbit in the full flight. Our medical, legal and social concepts are so formulated and our institutions so devised that it is usually impossible to bring the psychopath into the range of treatment’ (Cleckley, 1988). This basic assumption leads to the fact that most jurisdictions consider psychopathy to be an aggravating rather than a mitigating factor in determining criminal responsibility. In

SOCIAL POLICY CONSIDERATIONS

575

some US states an offender convicted of first-degree murder and diagnosed as a psychopath is likely to receive the death penalty on the grounds that psychopaths are cold-blooded, remorseless, untreatable and almost certain to reoffend (Hare, 1993). A European study that aimed at gathering and analyzing information about the similarities and differences in legislation on the placement and treatment of mentally disordered offenders across 15 EU member states revealed that the basic terminology for addressing the mental condition of the persons concerned varies widely in the laws of member states. In this study only legal regulations relevant for decisions on the assessment and placement of mentally ill or disordered offenders were studied (Salize & Dressing, 2005a). Legal regulations referring to civil commitment were scrutinized in another EU study (Dressing & Salize, 2004). The legal terminology for describing the mental state of offenders in relevant legislation within the member states is outlined in Table 33.1. No member states provide all-embracing forensic legislation in a clearly demarcated code or statute, but rather member states provide a variety of codes, laws or acts regulating the many different aspects of forensic cases (e.g., criminal responsibility, rules for detention or treatment of mentally ill offenders, trial or discharge procedures). In consequence, the following overview does not cover all possible regulations, but describes the most significant forensic laws or codes as selected by the contributing national experts. The terms or descriptions are particularly nonspecific, widely varied and, from a professional psychiatric point of view, in large part antiquated. With the exception of England, psychopathic disorder is not mentioned in the legal descriptions of the EU member states. Although psychopathy must be considered as a relevant and common disorder in the context of assessment and placement of criminal offenders, the respective legal regulations in EU member states do not explicitly address this diagnostic category. This omission may lead to ambiguous consideration of psychopathic disorders in the routine care of forensic psychiatry. This assumption is confirmed by an analysis of mental disorders covered by forensic legislation as established in routine care that was also carried out in the context of the above-mentioned European study (Salize & Dressing, 2005a). The results of the analysis of disorders that are considered as relevant disorders for the assessment and placement of mentally disordered offenders in routine care are presented in Table 33.2. The national experts were asked to refer to ICD 10. Results according to DSM IV were not scrutinized. Although many diagnoses can be transferred from ICD 10 to DSM IV some significant differences between the diagnostic systems must be considered. Typical pitfalls in the discussed context are the different concepts of the antisocial personality disorder of the DSM IV and the dissocial personality disorder of ICD 10. While the DSM IV applies a broad concept of this personality disorder that focuses on behavioral items, the ICD 10 applies a much narrower concept of the dissocial personality disorder that comprises typical cognitive and affective personality traits. In the vast majority of EU member states, personality disorders are considered as diagnostic entities that may have an effect on the assessment of criminal responsibility and the placement of an offender. According to the statements of collaborating national experts in this study, the diagnostic entity of personality disorders may also comprise psychopathy and dissocial personality disorder. However, as clear legal regulations are lacking in most EU member states, the consequences of the diagnosis of psychopathy or dissocial personality disorder are ambiguous and may lead to an assumption of either full criminal responsibility or diminished criminal responsibility of a psychopathic offender. Therefore the decision on the placement of the respective offender is also ambiguous and psychopathic offenders may be admitted to a forensic psychiatric hospital or sentenced to a prison.

Table 33.1 Legal terminology for describing the mental state in criminal law statutes concerning mentally disordered defendants* EU member state

Legal terminology

Austria

Mental illness Mental deficiency Profound impairment of consciousness Other abnormal mental conditions Mental abnormality of higher degree Mental deficiency or mental retardation Severe mental unbalance Insanity Mental illness State equal to mental illness Moderate to profound mental retardation Mild mental retardation Inadequate development, impairment or disturbance of mental abilities Mental disorder, which is defined as any of the following: – mental illness (not defined) – mental impairment (when treatment is likely to alleviate or prevent deterioration) – severe mental impairment (when treatment is likely to alleviate or prevent deterioration) – psychopathic disorder (when treatment is likely to alleviate or prevent deterioration) – other disability of mind State of lunacy, senile lack of understanding, alike similar condition (penal law) Mentally ill (mental health act) Mental disorder suppressing discernment or control of action Mental disorder Severe disorder of consciousness Severe mental abnormality Intellectual disability Morbid perturbation of intellectual functions or perturbation of consciousness Mental illness Mental handicap Dementia or any disease of the mind Mental flaw Mental inferiority Insanity Mental disorder suppressing discernment or control of one’s actions Mental disorder impairing discernment or control of one’s actions Power or irresistible restraint Severe psychiatric disorder endangering oneself or others Developmental deficiencies Pathological mental disturbance Psychic abnormality Anomaly Psychological alteration Intoxication Perceptual disturbance Serious mental disorder Mental disorder Severe personality disorders

Belgium Denmark

England and Wales

Finland France Germany

Greece Ireland Italy Luxembourg

The Netherlands Portugal Spain

Sweden

*Please note that these terms are translated from the original language into English by collaborating experts for the purpose of this study and therefore cannot be considered as official.

x x x x x x x x x* x x x x x x x x x x x

x x* x*

x x x In part* x

F1 Substance abuse disorders x x x x x x x x x* x x x x x x

F2 Schizo-phrenia

x x x* x x x x x x

x x x x x

F3 Affective, mood disorders

x x x x x

x x x

x* x x In part*

F4 Neurotic, stress related & somatoform disorders

x x x x* x*

x x* x

x* x x In part*

F6 Personality disorders

x x x* x x x x x

x x x* x* x

F7 Mental retardation

∗

Austria: F4, F6 only in severe cases, status for F60.2 (dissocial personality) unknown. England and Wales: F1.3, F1.4, F1.5, F1.6, parts of F1.7 are included; F1.2 are specifically excluded among F4: F42 and other items are covered, although very rarely encountered. F6 covered explicitly by law, although including only F60, F61, F62 and F69, all other items of the F6-block are not. F7 covered explicitly by law. ∗ Denmark: F7 explicitly covered by law. France: F1, F4, F6 specifically excluded by law, status for F3 and F7 unknown. ∗ Greece: F1 explicitly covered by law, status for F60.2 (dissocial personality disorder) and F65 (disorder of sexual preference) unknown. ∗ Ireland: F1: intoxication explicitly excluded by law, F0, F2, F3, F7 covered by law. ∗ Italy: F1 explicitly excluded by law. ∗ Spain: status for F60.2 (dissocial personality disorder) unknown. ∗ Sweden: F6 covered by law definition.

∗

Austria Belgium Denmark England and Wales Finland France Germany Greece Ireland Italy Luxembourg The Netherlands Portugal Spain Sweden

F0 Organic mental disorders

Table 33.2 Mental disorders covered by criminal law statutes concerning mentally disordered defendants* (as established in routine care)

578

VOLUME I: DIAGNOSIS AND TREATMENT

Both legal regulations and routine care in EU member states must be considered as unsatisfactory as far as offenders with the diagnosis of psychopathy are concerned. Treatment as well as incarceration and punishment seem to be options that are applied without clear guidance by legal regulations. In the opinion of the authors, social policy should begin to consider the ambiguity of this situation which seems to be unfair towards the psychopaths and to increase the threat to the general public. Although social policy considerations on psychopathy must be based on current legislation, there should be some ideas that go beyond the present legal situation. However, these ideas should be strongly influenced by the increasing scientific knowledge on psychopathy and not by prejudices or ideology. In this context studies on therapeutic efforts and neurobiology of psychopathy are of particular interest. In the following sections some of these research findings will be briefly outlined. Based on these empirical results some ideas for social policy will be derived.

SOCIAL POLICY CONSIDERATIONS IN THE CONTEXT OF TREATMENT OUTCOME STUDIES The severely decreased capability or incapacity to benefit from experience is an essential item for the diagnosis of psychopathy. Therefore, the description of psychopathy itself offers a strong hint that psychopaths are difficult to treat or even untreatable, because the effect of psychotherapy is based on learning and integration of new cognitive and emotional experiences. Cleckley, an outstanding expert and enthusiastic advocate of therapy, expressed his pessimism about the effectiveness of the treatment of psychopaths when he wrote: I have now, after more than three decades, had the opportunity to observe a considerable number of patients who, through commitment or the threat of losing their probation status or by other means, were kept under treatment not only for many months but for years. The therapeutic failure in all such patients observed leads me to feel that we do not at present have any kind of psychotherapy that can be relied upon to change the psychopath fundamentally (p. 439).

Although many years have passed since, current empirical evidence on the effectiveness of treatment of psychopaths is still consistent with Cleckley’s statement. A large number of studies on the effectiveness of therapy have been published, but the quality of many studies seems to be questionable. Particularly the diagnostic criteria for psychopathy, diagnostic reliability, adequate description of the treatment program, appropriateness of treatment evaluation, inclusion of follow-up period and the use of a control group are important but often neglected quality criteria. As a result of a meta-analysis of 75 studies, Wong (2000) concluded that, ‘ . . . an appropriately designed and implemented treatment programme for the Cleckley-type psychopath has yet to be carried out’ (p. 440). Social policy considerations should take into account the empirical evidence of treatment outcome studies. Since ineffective treatment of psychopaths is very costly, a minimum demand would be to consider the above-mentioned quality criteria for treatment studies. However, the neglect of empirical evidence by social policy suggests not only a waste of economic resources but also risks for public safety. An intensive therapeutic community treatment program for mentally disordered offenders, including psychopaths, suggested that treated psychopathic individuals might be even more dangerous than untreated psychopathic

SOCIAL POLICY CONSIDERATIONS

579

patients (Harris, Rice & Cormier, 1991). There is also a large body of sex offenders with the diagnosis of psychopathy (Borchard, Gnoth & Schulz, 2003). A treatment study of sex offenders revealed that treated sex offenders with a high PCL score had a four times higher risk for recidivism than those who did not receive any specific therapy (Barbaree, 2005). These empirical results of treatment outcome studies should be mirrored by social policy actions. Treatment programs that reflect such poor results should not longer be funded. However, punishment and incarceration also showed no corrective or prophylactic effects on the antisocial tendencies of the psychopaths. Therefore, the alternative for social policy considerations is not to replace treatment efforts with more punishment, because this approach is confronted with the same core problem of psychopaths that renders psychotherapeutic efforts at least up to now ineffective: the psychopath is unable to learn by experience. An urgent demand for social policy is to invest the savings from termination of inadequate treatment programs into innovative, clearly designed and controlled treatment studies. These approaches should also reflect recent results of neurobiological research on psychopathy that will be discussed in the next section. Although evidence has not yet established the treatability of psychopathic disorders, there is some hope that appropriate treatment may improve prognosis. Clearly designed treatment programs do not target the core psychopathic features, such as lack of capacity for empathy, grandiosity, egocentricity or shallow emotions, but try to change antisocial behavior, such as impulsivity, stimulation seeking and irresponsibility (Hare, 2002; Wong, 2000). So far, outcome data from programs specifically designed for psychopaths have not been published.

SOCIAL POLICY CONSIDERATIONS IN THE CONTEXT OF NEUROBIOLOGICAL RESEARCH ON PSYCHOPATHY There is evidence that early prefrontal cortex lesions may cause impaired social behavior, insensitivity to future consequences of decisions, defective autonomic responses to punishment contingencies and failure to respond to behavioral interventions despite normal basic cognitive abilities. Therefore, it has been hypothesized that early-onset prefrontal damage may result in a syndrome resembling psychopathy (Anderson et al., 1999). Psychophysiological data support the hypothesis that psychopaths are characterized by a pronounced lack of fear in response to aversive events and a general deficit in processing affective information (Herpertz et al., 2001). Functional neuroimaging offers the chance to investigate brain circuits that may play a role in the manifestation of criminal psychopathy in more detail. In an fMRI study psychopaths displayed no significant activity in the limbic–prefrontal circuit during an aversive differential Pavlovian delay-conditioning paradigm (Birbaumer et al., 2005). In another fMRI study psychopaths showed increased activation of right prefrontal regions and amygdala, in response to negative contents (M¨uller et al., 2003). There is also evidence that gene–environment interactions may have a significant influence on the manifestation of antisocial behavior (Caspi, McClay & Moffit, 2002). Although the neurobiological underpinning of psychopathy is not understood so far in its entire complexity, neurobiological research offers promising hypotheses. At the present state of knowledge, the etiology of psychopathy may best be explained by a combination of genetic, neurological and environmental factors.

580

VOLUME I: DIAGNOSIS AND TREATMENT

Contrary to the above-cited treatment outcome studies, the samples studied in neurobiological investigations are carefully diagnosed and fairly homogeneous. Actually these carefully arranged samples provide opportunity for more sophisticated intervention strategies. Social policy and research funding should focus on innovative research strategies that are engaged in the combination of basic neurobiological studies and intervention studies on psychopathy. However, such a combination of neurobiological basic research and treatment outcome studies has not yet been carried out. Such innovative research strategies would offer the possibility of studying treatment effects based on clearly defined hypotheses. Neurobiological research data suggest altered neural activation patterns in psychopathy that is also considered to be relevant for delinquent behavior. It can be hypothesized that successful intervention strategies could change the altered neural activation patterns in psychopathy. The inclusion of basic neurobiological research in intervention studies is overdue. On the one hand the validity of hypotheses based on neurobiological data must be investigated. It would be of utmost interest if neurobiological substrates of recidivism could be identified and understood, and alterations by therapy could be monitored directly via functional imaging. On the other hand, it must be stressed that previously published treatment outcome studies offering multimodal treatment approaches and focusing on recidivism, have so far yielded only disappointing results. Social policy should stress the possibilities of research that combines neurobiological research and intervention strategies in clearly defined samples of persons with psychopathy. Studies should be based on clearly formulated hypotheses and outcome criteria should consist of both the modifications of postulated significant neural activation patterns and recidivism rates.

SOCIAL POLICY CONSIDERATIONS IN THE CONTEXT OF LEGISLATION ON COMPULSORY OUTPATIENT TREATMENT Deinstitutionalization and community-based care have increasingly stimulated the debate on changing the locus of involuntary treatment of mentally ill patients from mental hospitals to open community settings (Salize & Dressing, 2005b). There is controversy as to whether compulsory outpatient treatment improves clinical outcome and social functioning. In a meta-analysis of randomized controlled clinical trials, compulsory community treatment was not superior to standard care with respect to health service use, clinical outcome and social functioning. There were also no significant effects of compulsory outpatient treatment with respect to the prevention of arrest (Kisely, Xiao & Preston, 2004). Studies on compulsory outpatient treatment have focused on patients with severe mental illness, and randomized controlled studies have excluded patients with primary diagnosis of personality disorder (Swartz et al., 1999). Nevertheless, it can be hypothesized that the study samples include a proportion of patients with comorbid antisocial personality disorders and even some patients with more or less severe forms of psychopathy, hence comorbidity is significant (Falck et al., 2004, Marmorstein, 2006). However, studies on compulsory outpatient treatment did not scrutinize the effects of compulsory outpatient treatment on patients with comorbid psychopathic personality disorder. Outpatient treatment of psychopaths has a longstanding history (Lion, 2001) and at least psychopaths or people with antisocial personality disorder and comorbid severe mental illness are sometimes ordered by judges or other decision makers in the legal system to comply with treatment. Therefore, it is remarkable

SOCIAL POLICY CONSIDERATIONS

581

that scientific research on the effectiveness of the legal instrument of compulsory outpatient treatment concerning patients with severe mental disorders and comorbid psychopathic personality disorder is scarce. Given the fact that the diagnosis of psychopathy is not a dichotomous decision and features of psychopathy are occurring on a continuous dimension, it can be hypothesized that the severity of psychopathy influences the effectiveness of coercive treatment in the community. Therefore, it would be of utmost interest to study the effects of compulsory outpatient treatment, taking into account the dimensional criteria of psychopathy. Social policy should facilitate such studies instead of fostering magic expectations that sometimes surround the treatment of psychopaths.

IMPLICATIONS FOR THE CRIMINAL JUSTICE SYSTEM AND THE MENTAL HEALTH SYSTEM The idea that offenders suffering from a mental disorder must primarily be considered as ill and should therefore be exempted from punishment is of considerable antiquity and can be traced back to ancient Greek and Roman sources. It is grounded in the concept that mentally sane human beings have a free will and are able to differentiate between right and wrong. Due to this concept, a mentally sane person who commits a crime has chosen to violate the law and is, therefore, subject to punishment (Salize & Dressing, 2005a). Punishment is a deeply rooted human trait and represents an important element in maintaining the stability of human societies. Moreover, punishment seems to be a key force in the establishment of human cooperation (Fehr & G¨achter, 2002). Punishment may be justified either by the idea of retribution or by the assumption of future beneficial effects of this procedure (Greene & Cohen, 2004). The principle of retribution is based on the idea that punishment is aimed at giving the offender what he deserves based on his actions in the past. However, the prerequisite for retribution is that we are dealing with a mentally sane offender who possesses a free will and has chosen to violate the law. As indicated above, there is increasing evidence that the peculiarities of psychopaths concerning their cognitive style, emotional reactions and impulsiveness are caused by neurobiological dysfunctions. Despite the lack of a gross neuropathological damage in the prefrontal cortex of psychopaths, there seems to be a significant variation in the biological function of this brain area that renders the individual organically incapable of appropriately regulating his behavior (Sapolsky, 2004). This may lead to the assumption that psychopaths or even persons with antisocial personality disorder should be considered to be substantially impaired in their accountability and criminal responsibility. In this context punishment of these persons that is based on the libertarian conception of free will and retributivist thinking cannot be considered to be an appropriate approach. However, punishment of psychopaths can also be justified by anticipated beneficial effects of this procedure. Such beneficial effects of punishment may be expected for both the society and the psychopath himself. Prevention of future offenses through the deterrent effect of punishment and protection of the society while the psychopath is incarcerated could be beneficial effects of punishment concerning the society. With regard to the psychopath himself, punishment could be justified by the idea of rehabilitation and reintegration. However, the above-mentioned results of neurobiological research on psychopaths and the results of treatment outcome studies also challenge these justifications of punishment.

582

VOLUME I: DIAGNOSIS AND TREATMENT

First of all, it must be remembered that a key symptom of psychopathy is that afflicted persons do not learn from experience and do not anticipate the consequences of their behavior. As a consequence the hypothesized beneficial effect of punishment in terms of primary deterrence with regard to the psychopath himself must be questioned. However, secondary deterrence with regard to the rest of the society is a worthy goal of punishment of psychopathic offenders. The importance of secondary deterrence is that nonpsychopathic members of society may learn not to violate the laws through the offender’s example and punishment. The results of the treatment outcome studies also undermine the idea that punishment of psychopaths may be justified, if it is aimed at rehabilitation and reintegration. So far empirical evidence does not support the hypothesis that psychopathy significantly improves with any form of treatment. Following this line of argument, the only but strong justification of punishment is the protection of society by the containment of these persons. It is no question that violent and aggressive behavior of psychopaths requires forceful interventions. However, it should be possible to reach this aim without blaming these persons by retributivist thinking. If most of the justifications for the punishment of psychopaths do not stand up to scientific evidence, the question arises, why the idea of punishment plays such an important role in the management of psychopaths. There is some evidence that common moral intuitions that govern our way of dealing with psychopaths and the impulse to exact punishment are driven by phylogenetically old mechanisms (Greene & Cohen, 2004; Sanfey et al., 2003). Cognitive neuroscience is challenging the approaches to criminal responsibility and punishment of psychopaths (Goodenough, 2004). Many types of behavior formerly considered as voluntary wrongdoing are now classed as disease. We stand at the beginning of an era that will probably see enormous growth in our knowledge of the neurobiological correlates of normal and socially deviant human behavior. Functional brain abnormalities and genes that alone or in combination with environmental influences put persons at high risk to develop psychopathic behavior will probably be identified. So far it is too early to give a final answer how society and the criminal justice system should respond to the ethical dilemmas that will arise from this knowledge (Appelbaum, 2005). However, an intensive dialogue between neuroscientists, representatives of the legal profession, politicians, philosophers and other significant stakeholders is overdue. One could argue that there is increasing evidence that psychopathy is a neurobiologically based mental disorder that reduces the capacity for self-control. In this line of argumentation one could postulate, that these people should not be punished and the sentence should be mitigated. However, we must keep in mind that psychopathy currently must be considered as not treatable and that psychopaths are more likely than other people to reoffend. This may lead to the assumption that psychopaths should not be punished but preventive and indefinite detention would be the correct way to handle them. Although many decades have passed since Cleckley published the first edition of his book The Mask of Sanity in 1941, the following statement by him, still seems to provide a very modern answer to this dilemma: ‘Despite traditional concepts and confusions, can we not conceive of a defect that seriously incapacitates and calls for restraining measures, without assuming that this defect necessarily absolves the subject from culpability and penalties of the law?’ (Cleckley, 1988, pp. 423–4). If protection of society by containment of these persons is the only effective intervention so far, the question arises where this custody should take place and how long it should last. Should persons with an antisocial personality disorder or with psychopathy be sent to prison or to a hospital? (Kr¨ober & Lau, 2000). So far this question can be answered

SOCIAL POLICY CONSIDERATIONS

583

only from a utilitarian point of view. Nevertheless, the way we deal with psychopaths today seems to be inefficient. Due to insufficient awareness of this problem, insufficient training in the diagnosis of psychopathy, ambiguous legal regulations and disappointment and frustration that may occur in the treatment of psychopaths, these persons are sometimes treated in psychiatric hospitals, sometimes in forensic facilities or they are arrested in prisons. Actually nobody really feels responsible for them and caretakers often are happy, if they can transfer a psychopath to another institution that is allegedly equipped with a better treatment concept. However, most often these actions are not based on scientific evidence and honesty but caused by feelings of helplessness, powerlessness and sometimes even of anxiety. To proceed in the management of psychopaths, it would be necessary to move this issue into the center of social policy considerations. The different professions that are responsible for the management of psychopaths must build up a network cooperation. Empirical scientific research on psychopathy should be the basis of all actions to be taken in the future. Although disappointment and frustration may occur in the engagement with psychopaths, therapeutic nihilism is not an adequate answer. On the one hand, early interventions during childhood, when the first symptoms of antisocial behavior occur, could be a promising method. On the other hand, antisocial and psychopathic personality features can be conceptualized on a continuum from the most severe to the least severe form of these disorders. This continuum is mirrored by different scores on the Hare Psychopathy Checklist. Different severities of the disorder require different ways to deal with the problem. Treatment can proceed when the presence of psychopathy is measurably mild to moderate and a genuine motivation for treatment exists. If this is not the case, risk management should be the primary task (Meloy, 2001). Even if no really adequate therapeutic method becomes available in the near future, it must be kept in mind that medical doctors had and have to deal with other mentally and organically ill patients long before adequate treatment possibilities were found. It could be a significant duty of social policy to design and implement special facilities for persons with severe core psychopathy, besides general and forensic psychiatric hospitals and besides the prison system. These facilities should not become places of hopelessness and frustration, but institutions aimed at improvement in control and adjustment as well as scientific progress in the understanding and therapy of this disorder. Social policy must consider the large spectrum of psychopathic disorders, and therefore complex and sophisticated answers are necessary. It is noteworthy, that not all psychopaths commit an offense, that the quality of offenses committed by psychopaths comprises a large spectrum – from violent offences to white collar offences like embezzlement – and that social integration of psychopaths may range from marriage and employment to socially disintegrated criminality. Although it is obvious that psychopaths who are invested in society are deterred from punishment more than those who are socially disintegrated, the consequence of social policy cannot be to abstain from punishment of the most violent psychopathic offender. It would be very unfair to punish only those with the greatest likelihood of benefiting. Preventive detention could be an option for psychopaths with a criminal career, progressive relapse rate of typical offences (e.g., assault, rape), external attribution of guilt, egosyntonic delinquency and integration into a criminal subculture (Habermeyer & Saß, 2004). In most cases some combination of treatment and punishment seems to be the best way, since this combination seems to be more effective than either approach alone.

584

VOLUME I: DIAGNOSIS AND TREATMENT

REFERENCES American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders, fourth edition. Washington, DC: American Psychiatric Association. Anderson, S.W., Bechara, A., Damasco, H. et al. (1999). Impairment of social and moral behavior related to early damage in human prefrontal cortex. Nature Neuroscience, 2, 1032–7. Appelbaum, P.S. (2005). Psychiatry: behavioral genetics and the punishment of crime. Psychiatric Services, 56, 25–7. Barbaree, H.E. (2005). Psychopathy, treatment behaviour, and recidivism: an extended follow-up of Seto and Barbaree. Journal of Interpersonal Violence, 20, 1115–31. Birbaumer, N., Veit, R., Lotze, M. et al. (2005). Deficient fear conditioning in psychopathy. Archives of General Psychiatry, 62, 799–805. Borchard, B., Gnoth, A. & Schulz, W. (2003). Pers¨onlichkeitsst¨orungen und ‘psychopathy’ bei Sexualstraft¨atern im Maßregelvollzug. Psychiatrische Praxis, 30, 133–8. Caspi, A., Mc Clay, J. & Moffit, T.E. (2002). Role of genotype in the cycle of violence by maltreated children. Science, 297, 851–4. Cleckley, H.C. (1988). The Mask of Sanity, fifth edition: Private printing for non-profit educational use. Copyright E.S. Cleckley. Augusta, Georgia. http://www.cassiopaea.org/. Dressing, H. & Salize, H.J. (2004). Zwangsunterbringung und Zwangsbehandlung psychisch Kranker: Gesetzgebung und Praxis in den Mitgliedsl¨andern der Europ¨aischen Union. Bonn: Psychiatrie Verlag. Falck, R.S., Wang, J., Siegal, H.A. & Carlson, R.G. (2004). The prevalence of psychiatric disorder among a community sample of crack cocaine users: an exploratory study with practical implications. Journal of Nervous and Mental Disease, 192, 503–7. Fehr, E. & G¨achter, S. (2002). Altruistic punishment in humans. Nature, 415, 137–40. Goodenough, O.R. (2004). Responsibility and punishment: whose mind? A response. Philosophical Transactions of the Royal Society London, 359, 1805–9. Greene, J. & Cohen, J. (2004). For the law, neuroscience changes nothing and everything. Philosophical Transactions of the Royal Society London, 359, 1775–85. Habermeyer, E. & Saß, H. (2004). Maßregel der Sicherungsverwahrung nach §66 StGB. Grundlagen und Differenzialindikation gegen¨uber der Maßregel gem¨aß §63 StGB. Der Nervenarzt, 75, 1061–7. Hare, R.D. (1991). The Hare Psychopathy Checklist-Revised. Toronto: Multi-Health Systems. Hare, R.D. (1993). Without Conscience: The Disturbing World of the Psychopaths Among Us. New York: Simon and Schuster. Hare, R.D. (2002). Psychopathy and risk for recidivism and violence. In N. Gray, J. Laing & L. Noaks (eds.), Criminal Justice, Mental Health, and the Politics of Risk. London: Cavendish. Harris, G.T., Rice, M.E. & Cormier, C.A. (1991). Psychopathy and violent recidivism. Law and Human Behavior, 15, 625–37. Herpertz, S.C., Werth, U., Lukas, G. et al. (2001). Emotion in criminal offenders with psychopathy and borderline personality disorder. Archives of General Psychiatry, 58, 737–45. Kisely, S., Xiao, J. & Preston, N. (2004). Impact of compulsory community treatment on admission rates: survival analysis using linked mental health offender databases. British Journal of Psychiatry, 184, 432–8. Kr¨ober, H.L. & Lau, S. (2000). Bad or mad? Personality disorders and legal responsibility. The German situation. Behavioral Sciences and the Law, 18, 679–90. Lion, J.R. (2001). Outpatient treatment of psychopaths. In J.R. Meloy (ed.), The Mark of Cain. Hillsdale, NJ: The Analytic Press. Marmorstein, N.R. (2006). Adult antisocial behavior without conduct disorder: demographic characteristics and risk for coocurring psychopathology. Canadian Journal of Psychiatry, 51, 226–33. Meloy, R. (2001). Introduction to section II. In R. Meloy (ed.), The Mark of Cain. Hillsdale, NJ: The Analytic Press. M¨uller, J., Sommer, M., Wagner, V. et al. (2003). Abnormalities in emotion processing within cortical and subcortical regions in criminal psychopaths: evidence from a functional magnetic resonance imaging study using pictures with emotional content. Biological Psychiatry, 15, 152–62.

SOCIAL POLICY CONSIDERATIONS

585

Prichard, J.C. (1837). A Treatise on Insanity and Other Disorders Affecting the Mind. Philadelphia: Haswell, Barrington & Haswell. Salize, H.J. & Dressing, H. (2005a). Placement and Treatment of Mentally Disordered Offenders – Legislation and Practice in the European Union. Lengerich: Pabst Science. Salize, H.J. & Dressing, H. (2005b). Coercion, involuntary treatment and quality of mental health care: is there any link? Current Opinion in Psychiatry, 18, 576–84. Sanfey, A.G., Rilling, J.K., Aronson, J.A. et al. (2003). The neural basis of economic decision-making in the ultimatum game. Science, 300, 1755–8. Sapolsky, R.M. (2004). The frontal cortex and the criminal justice system. Philosophical Transactions of the Royal Society London, 359, 1787–96. Serin, R.C. & Amos, N.L. (1995). The role of psychopathy in the assessment of dangerousness. International Journal of Law and Psychiatry, 18, 231–8. Swartz, M.S., Swanson, J.W., Wagner, H.R. et al. (1999). Can involuntary outpatient commitment reduce hospital recidivism? Findings from a randomized trial with severely mentally ill individuals. American Journal of Psychiatry, 156, 1968–75. Werlinger, H. (1978). Psychopathy: A History of the Concepts. Stockholm: Almquist & Wiksell International. Wong, S. (2000). Psychopathic offenders. In S. Hodgins & R. M¨uller-Isberner (eds.), Violence, Crime and Mentally Disordered Offenders. Chichester, UK: John Wiley & Sons, Ltd.

Index ABCD see Affective-Behavioral-CognitiveDynamic model abnormal brain functions 42–3, 208–11, 582–3 see also brain . . . abnormal personality disorders see also antisocial . . . ; dissocial . . . ; psychopathic . . . conceptual history 1–5, 9–30, 83–6, 135–6, 150–1, 172–3, 276, 281, 450–3, 558–60, 573–4 differentiation scheme 26–7 abusive tendencies, psychopathic disorders 2, 4 acamprosate 485, 538 ACC see anterior cingulate cortex accountability strategies, domestic violence 502–14 acquired psychopathy see also brain trauma; psychopathic disorders assessments 244, 245–8 concepts 69, 73–4, 111, 237–48, 264–5 manifestations 242–3 nature 238–40 pathogenesis 240–2 prognosis 244–5 acquired sociopaths 73–4, 111, 242–3, 533 see also sociopathy ACT see assertive community treatment activation patterns, neuroimaging perspectives 173–4, 181–2 activity programs 4, 124 activity therapists, short-term risk of violence 124–32 activity–passivity orientations, personality dimension 24 actuarial instruments 54, 124–5, 137–8 see also Psychopathy Checklist-Revised acupuncture 485 addictions 25, 71, 149, 153, 157–9, 251–2, 267–9, 386, 484–6, 531–8 see also alcohol; substance abuse genetics 149, 153, 157–9, 251–2, 267–8 stimulant drugs 386

ADHD see attention deficit hyperactivity disorder adolescent-limited offenders, antisocial behavior 202–3 adolescent-onset type, antisocial behavior 200–11, 419–20 adolescents see also children alcohol/substance abuse 531–8 CD 150–64, 188, 189–90, 199–211, 251–2, 265–7, 281, 291–8, 337–8, 349–50, 368–75, 381–2, 417–40, 531–8 multimodal CD interventions 436–40 school-based CD interventions 430–1 adoptive studies, genetics 152–3 Adrian, Kerstin 417–48 Adshead, Gwen 449–66 ADVANCE program 426 Advanced Study Institute (ASI) 50 adverse effects 385–7, 388, 409–11 affect, modulation of affect 342–3 affective items, PCL-R 37, 44–58, 71, 84–5, 93–5, 106, 113, 319–31, 335, 355–61, 456–7, 468–73, 477–89 Affective-Behavioral-Cognitive-Dynamic model (ABCD) 428–9 affectiveness disorders see also mood disorders APD 251–2, 257–9 brain trauma 220 comorbid disorders 157–8, 251–2, 257–9, 267–8 conceptual development 10–12, 19, 22–3, 83–6 country comparisons 575–8 gender issues 257–9 statistics 257–9 substance abuse 257–9, 267–8 violence 120–1, 257–9, 497–514 aftercare plans 130–1 age factors APD 35, 150–1, 153–5, 164, 205 brain trauma 219–21

588 aggression 4, 14–15, 35–8, 41, 43–59, 69–78, 88–9, 93–5, 104–5, 107–13, 117–32, 150–64, 181–2, 193, 200–11, 298, 335, 343, 367–75, 397–411, 417–40, 472–3, 482–4 see also anger; violence alcohol 117–18, 119, 120, 121–2, 126, 127–8, 253–4, 257–9, 260–1, 323–4, 534–8 anger-control/management programs 433–5 anticonvulsants 400–4, 407 antidepressants 404–5 antipsychotics 405–7, 409–11, 481–4 benzodiazepines 484 brain imaging research 69–78, 93–5, 105–9, 112, 398–9 brain trauma 228, 398–9 carbamazepine 403, 410–11 catecholamines 161–4, 382–6 CD 200–11, 265–7, 368–75, 417–40, 531–8 clozapine 406, 410–11, 482 definitions 155, 368, 399–400 domestic violence 497–514 dopamine 161–4, 204–6, 297–8, 383–6, 482–4 double-blind placebo-controlled trials 397–411 genetics 153, 154–5, 251–2, 267–8, 297–8 impulsive aggression 398–411 lithium 400–1, 407, 409–11, 482–4 medically related aggression 398–411 noradrenergic antagonists 405–6, 484 Overt Aggression Scale 127 pharmacotherapy 4, 118, 181, 397–411, 482–4, 537–8 phenytoin 401–2, 409–11, 482 premeditated aggression 193, 398–411 psychoanalytic view 343, 457–8 rewards 107 risperidone 406, 409–11, 482 schools 367–75 serotonin 159–61, 205–6, 397–411, 421 specific medication types 400–7 stimulants 407, 482–4, 537–8 substance abuse 117–18, 120–3, 126, 127, 253–4, 257–9, 260–1, 534–8 testosterone 163, 350, 421, 472–3, 484 topiramate 403–4, 410–11 treatment 397–411, 433–40, 482–4 treatment algorithm 407–11 types 398–411 valproic acid 402–3, 409, 482 agitation, brain trauma 228–9 agranulocytosis 410–11 agreeableness, concepts 24 Ahmed, A.G. 275–90 AIDS 124, 269, 471

INDEX akathisia 119–20 alcohol 71–6, 117–18, 119, 120–2, 126–8, 149, 153, 157–9, 176–7, 206–7, 219–21, 228–9, 253–4, 257–61, 282–9, 307–14, 471–5, 484–6, 505–6, 514, 531–8 see also addictions; substance abuse ADHD risk factors 206–7, 537–8 APD 253–4, 257–61, 484–6, 531–8 behavioral therapy 536–8 brain 71, 73, 76, 121, 176–7, 219–21, 228–9, 485 children 265–7, 307–14, 531–8 cocaine 122 cognitive effects 127 comorbid disorders 149, 153, 157–9, 176–7, 253–4, 257–61, 265–8, 282–9, 484–6, 531–8 concepts 149, 153, 157–9, 176–7, 253–4, 257–61, 265–8, 282–9, 484–6, 531–8 CP 307–14 criminality 534–5 depression 531–8 detoxification programs 537–8 domestic violence 505–6, 514 effects 117–18, 119, 120, 121–2, 127–8, 176–7, 206–7, 253–4, 257–61, 282–9, 471–5, 484–6, 531–8 epidemiology 532 etiology 532–4 fetal alcohol syndrome 206–7 genetics 149, 153, 157–9, 267–8, 533–4 impulsivity 533–4 inhibitions 121, 127, 282, 484–6 intelligence levels 127 neuroticism 533–4 paraphilias 282–9 personality types 533–4 pharmacotherapy 537–8 prenatal/postnatal risk factors 206–7, 210, 535 prognosis 535–8 rehabilitation programs 485, 535–6 risk factors 206–7, 210, 532–4 schizophrenia 253–4, 259–61, 536 sociopathy 533 somatic diseases 471–5 statistics 531–5 treatment 484–6, 531, 535–8 treatment phases 537–8 types 1&2 alcoholism 533–4 violence 117–18, 119, 120, 121–2, 126, 127–8, 253–4, 257–9, 260–1, 323–4, 534–8 withdrawal 121, 126, 537–8 Alcoholics Anonymous 485 Alexander, F. 15–16

INDEX Alfred P.Murrah Federal Building, Oklahoma City 230 algorithms 407–11, 472–3, 482–3, 488 alpha-adrenergic drugs 227–8 Alzheimer’s disease 229–30, 244 American Medical Association 248 American Psychiatric Association 16, 24–5, 84–6, 118–23, 150–1, 237–9, 276, 282, 368, 399, 417, 450, 468, 561, 573–4 see also Diagnostic and Statistical Manual of Mental Disorders AMF see amfetamine amfetamine (AMF) 122, 127, 161, 407, 535 see also stimulants ADHD treatment 382–6, 411 adverse effects 385–6 violence 122, 127, 161, 535 amnesia, brain trauma 228–9 aMRI see anatomical magnetic resonance imaging amygdala 69–70, 75–8, 93–5, 105–9, 113, 150, 159, 162–4, 173–5, 180–2, 189, 192, 195, 209–11, 227–8, 369, 579–80 see also autonomic responses brain trauma 227–8 EDA 189, 192 anabolic steroids, violence 123 anatomical magnetic resonance imaging (aMRI) 69–76 Andersen et al 37 Andrews et al 219 anethopaths, concepts 10, 16, 18 anger 4, 14–15, 35–8, 41, 43–59, 69–78, 88–9, 93–5, 104–13, 117–32, 193, 338, 433–6, 501–2 see also aggression; emotions; violence CD programs 433–5 domestic violence dynamic 501–2 emotion recognition 105–7 Anger Control Training 436 Anger Coping Program 434–5 anger-control/management programs, CD 433–5 Anglo-American concepts see also Great Britain; North America psychopathic disorders 9–10, 13–18, 21–2, 24–5, 26–7, 41–2, 172, 450–3, 573–4 animals, cruelty to animals/other children 202–3, 342 Annual Association of Threat Assessment Professionals Conference 521 ANS see autonomic nervous system anterior cingulate cortex (ACC) 69–70, 77–8, 89–95, 105–9, 110–13, 189, 208–11 antiandrogen medications, sexual offenders 484, 487–8 anticonvulsants, aggression 400–4, 407

589 antidepressants see also SSRIs ADHD treatment 382, 386–7 adverse effects 387 aggression 404–5 antipsychotics, aggression 405–7, 409–11, 481–4 antisocial behavior see also conduct disorder ADHD 199–211, 265–7, 307–8, 367–71, 381–92, 482, 537–8 adolescent-limited offenders 202–3 adolescent-onset type 200–11, 419–20 alcoholic parents 206–7, 533–4 assessments 199–202 childhood trauma 207 childhood-onset type 200–11, 419–20 concepts 26, 33–8, 41, 87, 103–4, 107–13, 135–43, 149–64, 199–211, 265–8, 321–31, 417–40 CP 306–14, 321–31, 372 definitions 200–1, 251–2, 268, 368 domestic violence 497–514 early-starter pathway 202–3 etiology 203–11, 484–6 families 206–7, 210, 291–8, 312–31, 367–8, 371–5, 533–4 females 347–61 genetics 149–64, 204–6, 210–11, 251–2, 267–8, 297–8 late-starter pathway 202–3 life-course persistent (LCP) offenders 202–3, 351 maladaptive types of character 34 mental disorders 33–4, 87 neurocognitive impairment 207–10 prenatal/postnatal risk factors 205–7, 210 rewards 107 smoking parents 206–7, 210, 326–7 symptomatology 202–3 types 200–1 antisocial items, PCL-R 37, 44–58, 84–95, 319–31, 335, 355–61, 468–89 antisocial personality disorder (APD) 1–5, 16, 25–7, 33–8, 49–50, 69–78, 84–95, 103, 110–12, 117–32, 149–64, 201–2, 251–69, 319–31, 336, 358–61, 367–75, 423–4, 453–5, 468, 497–514, 521, 531–8, 573–4 see also dissocial personality disorder; sociopathy affectiveness disorders 251–2, 257–9 age factors 35, 150–1, 153–5, 164, 205 alcohol 253–4, 257–61, 484–6, 531–8 anxiety 251–2, 261–2, 390 assessments 33–8, 49–50, 84–95, 103, 110–12, 358–61, 531–8, 573–4

590 antisocial personality disorder (Cont.) brain imaging research 2, 69–78 categorical approaches 34–8 CD 150–4, 201–2, 251–2, 265–7, 281, 381–2, 423–4 comorbid disorders 251–69, 423–4, 453–5, 531–8 concepts 16, 25–7, 33–8, 49–50, 84–95, 103, 110–12, 201–2, 251–69, 336, 349–50, 423–4, 453–5, 468, 497–514, 521, 573–4 criteria 17, 25–6, 35–8, 49–50, 84–95, 103, 118, 150–1, 172, 237–8, 251–2, 268, 291, 319–31, 468–71, 562–3, 573–4 differentiation scheme 27 dimensional approach 34–8, 399–400 domestic violence 497–514 DSM-IV/DSM-IV-TR diagnostic criteria 35–6, 49–50, 84–8, 128, 150–1, 172, 199–204, 224, 237–8, 248, 251–2, 368, 399, 450, 459, 468, 561, 573–4 early predictors 17, 35–8, 151, 154–5, 188, 189, 210–11, 265–7, 291–8, 319–31, 342–3, 560, 562–4, 583 emotions 104–5 etiology 34–8, 149–64, 484–6 features 14, 17, 25–6, 35–8, 49–50, 84–95, 104–5, 118, 150–1, 172–3, 237–8, 251–2, 268, 291, 319–31, 353–61, 468–71, 562–3, 573–4 gender issues 3, 35–6, 42–3, 47–8, 103–4, 150–1, 153, 155–7, 162–4, 188, 201–3, 205–6, 257–9, 260–1, 347–61, 459 genetics 149–64, 193, 251–2, 267–8, 297–8 imprisoned offenders 1–2, 35 neurobiologies 159–64, 171–82, 203–11 political issues 33–8 prenatal/postnatal risk factors 205–7, 210 psychiatric assessments 33–8 psychopathy overlap 49–50, 83–95, 110–12, 150–1, 172, 251–69, 281, 451, 459, 468, 573–4 psychophysiological correlates 83–95, 210–11, 382 PTSD 262 schizophrenia 251–7, 259–61 standardization of nomenclature 24–6, 172, 251–2 statistics 201–2, 349–50, 451, 468, 532, 573–4 substance abuse 251–2, 259–61, 267–9, 298, 371–2, 484–6, 531–8 violence 117–32, 150–64, 252–9, 267–8 workplace violence 521–8 Antisocial Process Screening Device (APSD) 43, 52 antisocial reaction, concepts 25–6

INDEX anxiety 76–8, 88–9, 94, 105–13, 121, 153, 157–8, 227–8, 251–2, 261–2, 306–14, 336, 337–43, 387–90, 423–4, 457–8, 531–8 see also fear; mood . . . APD 251–2, 261–2 comorbid disorders 251–2, 261–2, 387–90, 423–4, 471, 531–8 concepts 337–43, 387–90, 423–4 CP 306–14 definitions 337 evolutionary basis 337–8 suicide 261 treatment 387–90 APD see antisocial personality disorder apolipoprotein E 226–7, 244–5 appearance of the patient, violence risks 126 APSD see Antisocial Process Screening Device area under the curve (AUC) 54–5 Armed Forces, US 24 arrogance 42, 71–2, 84–8, 93–5, 106, 319–31, 335, 453–9, 468–73, 477–89, 573–4 ‘articulated thoughts in simulated situations’, domestic violence 506 ASI see Advanced Study Institute asocial disorder 26 Asperger’s syndrome 266 assertive community treatment (ACT) 480 see also intensive . . . assertiveness deficits, domestic violence 506–10, 514 assessments see also Diagnostic . . . ; International . . . ; Psychopathy Checklist . . . acquired psychopathy 244, 245–8 actuarial methods 54, 124–5, 137–8 ADHD 200–1, 381–2 antisocial behavior 199–202 APD 33–8, 49–50, 84–95, 103, 110–12, 358–61, 531–8, 573–4 brain imaging research 2, 69–78, 89–95, 105–13, 173, 208–11, 246–8, 337–8, 369, 398–9, 472–3, 579–80 brain trauma 221–3, 244, 245–8, 398–9 CD 200–1, 417–21, 531–8 country comparisons 46–7, 48, 54–6, 137–43, 575–8 domestic violence 497–8, 505–14 females 347–61, 459 historical background 37, 41–3, 573–4 lifetime detention 557–8, 560–70, 582–3 neuroimaging perspectives 182, 246–8, 335, 381–2, 472–3, 579–80 outpatient treatment 471–5, 536–7 psychiatric assessments 2, 33–40 psychological assessments 2, 34–8, 41–59

INDEX psychopathic disorders 2, 23, 33–8, 41–59, 69–78, 83–95, 103–13, 172–3, 237–8, 245–8, 319–31, 348–61, 471–82, 531–8, 557–70, 573–4 psychophysiological correlates 83–95, 105–13, 210–11 risk assessments 2, 33–4, 48, 53–8, 117, 124–32, 135–43, 206–7, 210, 319–31, 347–61, 421–3, 473–5, 532–4, 557–70, 578–83 risks of diagnosis 2, 33–4, 117, 129–32, 135–43, 252, 352–3, 458–61 self-report measures 48–9, 52–3 structured clinical assessments 36–7, 54–6, 471–5 violence risks 124–32, 137–43, 358–61, 523–7 workplace violence 523–7 assimilation processes 339–40 associative learning, deficits 105, 107–9, 174–5, 194, 369–70, 559–60, 578–9 asthenic psychopaths 21, 22 athletic body types 20 atomoxetine (ATMX) ADHD treatment 382, 386–8 adverse effects 387 attachment concepts 336–43, 457 see also dismissive individuals attention deficit hyperactivity disorder (ADHD) 3–4, 106, 149, 157–8, 190, 195, 199–211, 265–7, 307–8, 367–71, 381–92, 423–4, 537–8 adult treatments 385, 386–7 alcoholic parents 206–7 AMF treatment 382–6 antisocial behavior 199–211, 265–7, 307–8, 367–71, 381–2, 537–8 anxiety 387–90 assessment 200–1, 381–2 ATMX treatment 382–5, 386–8 behavioral therapy 382, 388–90 CD 200–6, 209–11, 265–7, 370–1, 381–2, 386, 418–19, 423–4, 537–8 childhood trauma 207 combined treatments 389–90 comorbid disorders 157–8, 199, 203–4, 206, 209–11, 265–7, 367–71, 381–2, 386–90, 407, 423–4, 482–4, 537–8 concepts 199–211, 307–8, 367–71, 381–92, 407, 423–4, 537–8 CP 307–8 criminality 199–211 definition 200–1, 381–2 depression 387–90 epidemiology 201–2 evaluation of treatment effects 390–1

591 families 204–6, 389–92 general treatment recommendations 388 genetics 204–7, 210–11 intelligence levels 207 long-term treatment 391–2 MPH treatment 382–5, 388, 389–90 multimodal treatment 381–2, 389–90 neurocognitive impairment 207–10 neuroimaging perspectives 208–11, 381–2 neurophysiological defects 3, 173, 207–11 neuropsychological treatment measures 390–1 nonstimulant medication 386–8, 389–90, 392 parent training 389–92 pemoline 383–6 prenatal/postnatal risk factors 205–7, 210 psychopathic disorders 3, 106, 149, 157–8, 190, 199–211, 265–7, 370–1 psychophysiological correlates 210–11 smoking parents 206–7, 210 statistics 201–2 stimulants 382–6, 388, 389–90, 392, 407, 411, 482–4, 537–8 temperament 203–4 treatment 4, 211, 381–92, 407, 482–4, 537–8 types 200–11, 370–1, 381–2 attention shifting, executive functions 110–11, 240–1, 246–8 attentional processes, cognitive correlates 110–11, 112–13 AUC see area under the curve auditory cortex 74–5 auditory hallucinations see also hallucinations dangers 128 Australia 264, 295, 427–8 Austria 263, 312, 576–7 autism, genetics 153 autonomic functions concepts 87–95, 104–13, 174–5, 187–96, 210–11, 241–2, 337–53, 579–80 HR 91–3, 106, 188–96, 210–11, 337–8 autonomic measures, impulsivity 91–3 autonomic nervous system (ANS) 91–3, 187–96, 241–2 autonomic psychophysiological techniques 87–95, 210–11 autonomic responses see also amygdala; electrodermal activity; heart rate; prefrontal cortex concepts 104–13, 174–5, 187–96, 210–11, 241–2, 337–43, 579–80 emotions 104–13, 174–5, 579–80 available means, violence risks 126–7 aversive conditioning 108–9, 337–43 avoidant personality disorder 498–9

592 ‘back to basics’ approach 354, 357 Barker, Elliot 563 Barona Index 246–7 Barrash et al 239–40 Barratt, Ernest S. 83–101 BAS see behavioral approach system basal forebrain 179–80 basal ganglia 73 BASIC program 426 batterers see domestic violence Baumrind, Diana 304 Bavarian Law of Confinement 561–2 Bazarian et al 222 behavioral approach system (BAS) 37–8, 107–9 behavioral controls 44, 47–58, 73–8, 110–12, 179–82, 204–5, 368–75, 456–7 see also self-control behavioral inhibition system (BIS) 37–8, 107–9, 484–6 behavioral risk factors, CD 421–3 behavioral social skills training 389 behavioral therapy see also self-control ADHD 382, 388–90 alcohol/substance abuse 536–8 CBT 388–9, 431–3, 452–3, 456–8, 470, 479–80, 504–14 cognitive technique 388–9 concepts 388–9, 431–3, 536–8, 559–60 operant technique 388–9 Belgium 55, 312–13, 576–7 benign narcissists, clinicians 475–6 benzodiazepines 484 Berner, Wolfgang 467–95 Bernstein et al 110 beta-blockers 405, 484 see also noradrenergic antagonists biofeedback approaches, treatment 181–2 biological epoch, psychiatric research 11, 25, 34, 42–3 bipolar disorder 220, 257–9, 265–7, 400, 402–3 see also depression; mania brain trauma 220 comorbid disorders 257–9, 265–7, 400 Birnbaum, K. 10, 19, 21, 23 BIS see behavioral inhibition system Blair, R.J.R. 42–3, 104–5, 108, 113, 368–72, 457 blame 17, 36–8, 84–5, 93–5 Bleuler, E. 10, 20 Blueprints Model Programs Selection Criteria 428, 431 body types, personality links 10, 20 Bonferroni correction 177 Book et al 41

INDEX borderline personality disorder 118, 128, 295–6, 339, 341, 351, 403, 451, 457–9, 471, 479, 498–9, 521, 532, 536–8 domestic violence 498–9 substance abuse 532, 536–8 violence 118, 128, 498–9 workplace violence 521 boredom 47–58, 84–5, 88–93 see also need for stimulation born criminals, French concepts 10, 12 Bowlby, John 336, 337–8 BPP see Bullying Prevention Program Bradford, John M.W. 275–90 brain see also brain trauma abnormal brain functions 42–3, 208–11, 582–3 activation patterns 173–4, 181–2 alcohol 71, 73, 76, 121, 176–7, 219–21, 228–9, 485 damage 69, 71–2, 73–8, 105–12, 120–1, 123, 176–82, 194–5, 217–31, 237–48, 264–5 infections 244 serotonin 159–61, 181–2, 205–6, 397–411, 421 volume losses 71–2, 73–8, 176–82, 195, 208–10, 225–7, 398–9 brain imaging research see also neuroimaging perspectives ACC 69–70, 77–8, 89–95, 105–9, 110–13, 162–4, 173–82, 189, 208–11 aggression 69–78, 93–5, 105–9, 112, 398–9 alcohol 71, 73, 76, 176–7 amygdala 69–70, 75–8, 93–5, 105–9, 113, 150, 159, 162–4, 173–5, 180–2, 192, 195, 209–11, 227–8, 369, 579–80 assessments 2, 69–78, 89–95, 105–13, 173, 208–11, 246–8, 369, 472–3, 579–80 concepts 68–78, 89–95, 105–13, 173–82, 246–8, 337–8, 398–9, 472–3, 579–80 corpus callosum 69–70, 77–8, 177–9, 337–8 DLPFC 70–8, 110–12, 175–80, 208–11, 243 hippocampus 69–70, 75–8, 93–5, 107–8, 113, 173, 177–9, 181, 225, 227–8 impulse disorders 69–78, 89–93 medial temporal structures 70, 75–8 murderers 76, 77–8 OFC 70–8, 108–13, 173, 175–9, 181–2, 238–48, 369 PCC 74, 77–8 PFC 69–78, 91–5, 108–12, 159, 162–4, 173–5, 179–82, 189, 194–6, 208–11, 237–48, 264–5, 297–8, 398–9, 579–80, 581 psychopathic disorders 2, 69–78, 89–95, 105–13, 162–4, 173–82, 398–9, 472–3, 579–80

INDEX superior temporal cortex 70, 74–8, 113, 176–9 temporal cortex 69–78, 93–5, 173–9, 180–2, 207–10, 229 VLPFC 70–8, 108–9, 111–12, 369 VMPFC 70–8, 111–12, 175–9, 189, 237–48 volume losses 71–2, 73–8, 176–82, 195, 208–10, 225–7, 398–9 Brain Injury Association of America 217–18 brain trauma 69, 71–2, 73–8, 105–12, 120–1, 123, 176–82, 194–5, 217–31, 237–48, 264–5, 398–9 see also neurotrauma; psychotrauma affectiveness disorders 220 age factors 219–21 aggression 228, 398–9 agitation 228–9 alcohol 121, 176–7, 219–21, 228–9 Alzheimer’s disease 229–30, 244 amnesia 228–9 amygdala 227–8 apolipoprotein E 226–7, 244–5 assessments 221–3, 244, 245–8, 398–9 atrophy 225–7 bipolar disorder 220 causes 220–2, 264–5 children 219–20, 225–7, 230–1 cognitive effects 223–31, 240–8 cognitive function assessment 246–8 comorbid disorders 220–1, 230, 262, 264–5 concepts 217–31, 237–48, 398–9 consequences 225–7, 228–31, 237–48, 264–5 definition 217 degenerative diseases 229–30, 244–5 delayed consequences 228–9 depression 221, 228–30 DSM-IV-TR criteria 238–40, 248 early consequences 228 environmental issues 226–8 epidemiology 217–21, 244 families 219–21 gender issues 219–21 genes 222–8 genetics 219–21 Glasgow Coma Scale 221–3, 244, 245 Glasgow Outcome Scale 221–3, 244 inattention symptoms 228–9, 240–2, 246–8 intelligence levels 244, 246–8 late consequences 229–30, 244–5 lawsuits 248 long-term outcomes 225–7, 238, 244–5 malinger tendencies 246 molecular pathogenesis 222–8, 240–2 motor skills/spatial skills 244 negative modifiers 219–21 occupational/social functioning 230–1 overview flowchart 217–18

593 Parkinson’s disease 229–30, 244 Phineas Gage 69, 237–40, 398 pituitary dysfunction 227 preinjury mental abilities 246–7 prior history-related risk factors 219–21 psychopathic disorders 69, 71–2, 73–8, 105–12, 120–1, 123, 176–82, 194–5, 229–31, 237–48, 398–9 PTSD 157, 181–2, 218–31, 244–5, 262, 265–7 responses 221–3, 244–5 risk factors 217–21 schizophrenia 220, 229–30 severity rating 221–3, 244–8 social knowledge 240–8 socioeconomic costs 219–21, 230–1 statistics 217–21, 244 suicide 228–9 treatment 227–8, 244 violence 220–31, 264–5, 398–9 Briken, Peer 467–95 Brodmann area 70 Buckley, Peter F. 251–74 Bulgaria CP 312 PCL-R 48 bullying 200–11, 375, 418–40, 522–3 see also conduct disorder definition 523 workplace violence 522–3 Bullying Prevention Program (BPP) 375, 429–30 Bundy, Ted 338 buprenorphine 485 burnout problems, clinicians 479 Buros Institute Mental Measurement Yearbooks 43 Cacioppo, J.T. 189 callousness 14, 21, 36–8, 41–3, 84–5, 93–5, 103, 172, 238–48, 319–31, 337–43, 356–60 concepts 84–5, 93–5 psychophysiological correlates 93–5 Cambridge Study in Delinquent Development 320–31 Campbell, C. 181 Canada homicidal sex offenders 263–4 Oak Ridge Hospital 563 prisoners 37, 140–1, 281, 284–5, 557, 559, 563 cannabis 259–61, 266, 267, 535 see also substance abuse carbamazepine, aggression 403, 410–11 case conceptualization, domestic violence 507–9

594 castration, surgical castration 487–8 catecholamines, genetics 161–4, 382–6 categorical approaches, APD 34–8 Category Test 242 CATIE see Clinical Antipsychotic Trials of Intervention Effectiveness CBT see cognitive-behavioral therapy CD see conduct disorder Centers for Disease Control and Prevention (CDC) 519 CEPI see Community Epidemiological Preventive Intervention CFA see confirmatory factor analysis change sensitivities, PCL-R critique 142–3 character neurosis, concepts 15–16, 34 charm 17, 42, 44, 47–58, 84–8, 103, 172, 276, 281, 368, 453–5, 477–8, 573–4 see also glibness child abuse 42, 293–8, 304–5, 322–31, 401, 486–8, 505–6 see also pedophiles child-deficit hypothesis, CD 422 child-to-parent violence, CP 311–14 childhood-onset type, antisocial behavior 200–11, 419–20 children see also families ADHD 3–4, 106, 149, 157–8, 190, 195, 199–211, 265–7, 307–8, 367–71, 381–92, 423–4, 482, 537–8 alcohol 265–7, 307–14, 531–8 alcoholic parents 206–7, 533–4 APSD 52 biological features as vulnerability/protective factors 297–8 brain trauma 219–20, 225–7, 230–1 CD 150–64, 188, 189–90, 199–211, 251–2, 265–7, 281, 291–8, 336–8, 349–50, 368–75, 381–2, 417–40, 531–8 comorbid disorders 251–2, 265–9, 423–4, 531–8 CP 303–14, 321–31, 372 cruelty to animals/other children 202–3, 342 dating violence 311 depression 265–7, 292–3, 306–14, 371–2, 423–4, 531–8 discipline 162, 303–14, 321–31, 372, 425–7 genetics 297–8 HR 188 inhalants 123 maltreated children 42–3, 162–4, 204–6, 207, 276–89, 291–8, 321–31, 338–9, 341–3, 401, 438–9 maternal rejection 162, 292–6, 322, 336–43 narcissism 342–3

INDEX neglect 162, 292–6, 322–31 parent–child interaction 293, 324–31, 336–43, 371–2, 425–40 PCL:YV 43, 50–2, 295–7, 348–60 pedophiles 262–4, 276–89, 294–8, 323–4, 486–9 peer affiliations 292–3, 307, 327–31, 367–8, 373–4 prenatal/postnatal risk factors 205–7, 210, 535 psychopathic disorders 17, 19, 23–6, 37–8, 42–3, 50–2, 84, 135–6, 143, 149–64, 188–90, 196, 200–3, 251–2, 265–9, 291–8, 303–14, 319–31, 342–3, 347–61, 367–75, 583 PTSD 265–7, 294–5 schizophrenia 254, 267 schools 328, 367–75 smoking parents 206–7, 210, 326–7 substance abuse 265–7, 292–3, 371–2, 438–9, 531–8 traumas 162–4, 204–6, 207, 276–89, 291–8, 324–31 trust issues 294 verbal interactions 311–12 violence 42–3, 162–4, 204–6, 207, 220–31, 276–89, 291–8, 303–14, 323–31, 367–75, 438–9 China, CP 308–9 cholesterol levels 484 citalopram 409–11, 482 civil psychiatric patients, PCL-R 55, 84 Cleckley, H. 10, 17, 25, 35, 42, 83, 84–6, 93, 103, 107, 135, 172, 174–5, 200–1, 237–9, 276, 281, 347, 450, 452, 454, 456–7, 468, 558–9, 573–4, 578–9, 582–3 Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) 253 clinicians benign narcissists 475–6 burnout problems 479 hospitals 128, 129–32, 488–9, 536–7, 557–70 intraspecies predators 53, 339–43, 460 lawsuits 117, 129–32 recommendations 462–3 short-term risk of violence 124–32, 460, 475–7 therapeutic relationships 475–7, 535–6 trained staff 461–2, 475–7 treatment impediments 558–70 trust issues 459–60 written evidence 131–2 clonidine 405 see also noradrenergic antagonists Cloninger, C.R. 24, 205, 533–4

INDEX clozapine see also antipsychotics aggression 406, 410–11, 482 CNV see contingent negative variation cocaine see also substance abuse alcohol 122 effects 122, 127, 161, 257–61, 269, 535, 538 treatment outcomes 269, 538 violence 122, 127, 161, 257–9, 535 withdrawal 122, 538 coercion hypothesis, CD 422 cognitive correlates ADHD 207–10 associative learning 105, 107–9, 174–5, 194, 369–70, 559–60, 578–9 attentional processes 110–11, 112–13 CD 207–10 components 103–4 concepts 103–13, 175–6, 240–2 definition 103–4 emotions 104–13, 175–6 executive functions 72–8, 93–5, 110–12, 175–6, 208–10, 240–1, 246–8 language processing 106–7, 110–11, 112–13, 207–10, 244, 246–8 learning 104–13, 174–6, 194, 241–2, 267–8, 369–70, 559–60 orienting issues 112–13, 189, 190 Pavlovian/instrumental conditioning 107–9, 579 risky decisions 111–13, 175, 242–3 somatic markers 111–13, 240–2 cognitive development, CP 311–14 cognitive effects alcohol 127 brain trauma 223–31, 240–8 cognitive empathy, concepts 104–5 cognitive processing defects 42–3, 71–8, 103–13, 175–6, 207–10, 240–8 workplace violence 525 cognitive-behavioral correctional programs 58 cognitive-behavioral therapy (CBT) 388–9, 431–3, 452–3, 456–8, 470, 479–80, 504–14 see also behavioral therapy CD 431–3 concepts 388–9, 452–3, 456–8, 470, 479–80, 504–7 critique 470 domestic violence 504–14 cognitive/emotional processing defects 42–3, 71–8, 103–13, 175–6, 207–10, 240–8 collaborations, solutions 1–2 combat, PTSD 220–1, 262 combined treatments, ADHD 389–90

595 communication training interventions 428, 508–14 Community Epidemiological Preventive Intervention (CEPI) 429–30 community treatment see also outpatient treatment concepts 543–55 psychopathic disorders 4, 180, 467–89, 543–55, 557–70, 580–3 comorbid disorders ADHD 157–8, 199, 203–4, 206, 209–11, 265–7, 367–71, 381–2, 386–90, 407, 423–4, 482–4, 537–8 adults 251–65 affectiveness disorders 157–8, 251–2, 257–9, 267–8 alcohol 149, 153, 157–9, 176–7, 253–4, 257–61, 265–8, 282–9, 484–6, 531–8 anxiety 251–2, 261–2, 387–90, 423–4, 471, 531–8 APD 251–69, 423–4, 453–5, 531–8 bipolar disorder 257–9, 265–7, 400 brain trauma 220–1, 230, 262, 264–5 CD 423–4, 531–8 children 251–2, 265–9, 423–4, 531–8 concepts 157–8, 203–4, 206, 209–11, 220–1, 230, 251–69, 471, 580–1 critique 268–9 depression 157–8, 221, 230, 257–9, 265–8, 292–3, 387–90, 423–4, 453–5, 471, 531–8 etiology 251–69, 532–4 genetics 149, 157–64, 251–2, 267–8 mood disorders 157–8, 251–2, 257–9, 264 paraphilias 262–4, 282–3, 288–9, 471, 486–9 pedophiles 262–4, 282–3, 486–9 psychopathic disorders 3–4, 36–8, 48, 117–32, 149, 157–64, 203–4, 209–11, 251–69, 453–5, 471, 484–6, 531–8, 580–1 PTSD 220–1, 230, 262, 265–7 schizophrenia 251–7, 259–64, 536 sexual offenders 262–4, 282–3, 471, 486–9 substance abuse 3–4, 35, 36–8, 117–18, 120–3, 126, 127, 149, 157–8, 251–2, 253–69, 282–3, 298, 471, 484–6, 531–8 treatment implications 268–9, 471 complexity issues, psychiatric assessments 34, 458–9 compulsory outpatient treatment, social policies 580–3 computerized tomography (CT) 246, 472–3 COMT, genetics 163–4, 205–6, 267 conceptual history paraphilias 275–6 psychopathic disorders 2, 9–30, 83–6, 135–6, 150–1, 172–3, 276, 281, 450–3, 558–60, 573–4

596 conditioned stimuli (CS) 94, 108–9 conduct disorder (CD) 150–64, 188, 189–90, 199–211, 251–2, 265–7, 281, 291–8, 337–8, 349–50, 368–75, 381–2, 417–40 see also antisocial behavior; oppositional defiant disorder ADHD 200–6, 209–11, 381–2, 386, 418–19, 423–4, 537–8 anger-control/management programs 433–5 APD 150–4, 201–2, 251–2, 259–61, 265–7, 281, 381–2, 423–4 assessments 200–1, 417–21, 531–8 behavioral risk factors 421–3 CBT 431–3 child-deficit hypothesis 422 childhood trauma 207 coercion hypothesis 422 comorbid disorders 423–4, 531–8 concepts 199–211, 251–2, 259–61, 336–7, 386, 417–40, 468 definitions 150–1, 200–1, 251–2, 268, 368, 417–18 depression 423–4 developmental course 418–20 epidemiology 201–2, 419–20, 468 etiology 421–5 families 204–6, 291–8, 371–5, 417, 425–40 foster care models 436–9 genetics 204–7, 210–11, 251–2, 267–8, 421–2 individually-tailored multicomponent interventions 439–40 intelligence levels 207, 367–8, 371 marital conflicts 425 MST 436–9, 470–1, 536–7 multicomponent interventions 439–40 multimodal interventions 417, 436–40 neurocognitive impairment 207–10 neuroimaging perspectives 208–11 parent-focused interventions 417, 425–40 patient-focused interventions 417, 425, 431–40 preschool-children interventions 436 psychophysiological correlates 210–11 school-aged children interventions 433–5 school-based interventions 417, 428–40 SCR 189–90, 210–11, 337–8 social information processing 422, 427, 431–40 social skills deficits 422, 431–40 statistics 201–2, 419–20, 468 treatment 417–40, 482 treatment overview 424–5 types 200–1, 417–19

INDEX confidentiality issues domestic violence 507 outpatient treatment 480–1 confirmatory factor analysis (CFA) 354–60 conning 44, 47–58, 84–8, 150–64, 172, 356–60, 453–5 conscience 341–3 conscientiousness, concepts 24 constitution doctrine, concepts 12, 14–15, 18 constitutional inferiority, concepts 15, 21 constitutions see also genetics psychopathic disorders 10, 12, 14–15, 18, 19 contingency management programs 536 contingent negative variation (CNV) 91–3, 94, 192–3 continuous performance test (CPT) 391 Controlled Oral Word Association Test 110 conventions 41–3, 72–3, 85–95, 150–64, 374, 513 Cooke, D.J. 37, 84–94, 319, 347–66, 456–9 Cope, R. 449 Copenhagen study 325–6 Coping Power Program 434–5 coping strategies 434–5, 537–8 coprophilia 277 see also paraphilias Corcoran, Michael H. 519–29 Cordess, C. 462–3 corporal punishment (CP) see also discipline anxiety 306–14 child behavior problems 312–14, 321–2, 372 child-to-parent violence 311–14 clinical populations 307–8 cognitive development 311–14 concepts 303–14, 321–31, 372 cultural issues 305, 308–9, 312–13 dating violence 311–12 definition 304–5 depression 306–14 gender issues 306–7 legal status 312–14 longitudinal studies 309–12, 321–2 meta-analysis 306 myths 305 pre-existing behavior problems 309–12 psychopathic disorders 305–14, 321–2, 372 research 306–7, 321–2 statistics 305–14, 321–2 types 303–5, 306 corpus callosum 69–70, 77–8, 177–9, 337–8 correctional programs see also criminal justice system; prisoners limitations 4–5

INDEX costs psychopathic disorders 1–2, 4, 22, 43, 117–32, 135–6, 331, 343, 455–6, 557–70, 573–83 society 1–2, 4, 22, 43, 117–32, 135–6, 331, 343, 455–6, 557–70, 573–83 counseling programs, domestic violence 503–5, 508 CP see corporal punishment CPA see cyproteroneacetat CPT see continuous performance test Craft, M. 14 creative psychopathic condition 14, 20 Creutzfeldt–Jakob disease 244 Crick, Nicki R. 432–3 criminal justice system see also correctional programs; prisoners APD 33–8 critique 557–70, 574–83 domestic violence 502–5, 508–9, 514 impediments 557–70 lifetime detention 557–8, 560–70, 582–3 psychopathic disorders 3, 41–59, 95, 135–43, 502–5, 508–9, 514, 557–70, 574–83 purposes 3–4, 557–70 rehabilitation purpose 3, 4, 142–3, 557–70, 574–83 risks of diagnosis 2, 33–4, 117, 129–32, 135–43, 252 criminal responsibility 14, 180–1, 566–70, 574–83 criminal versatility 44–58 criminality ADHD 199–211 alcohol 534–5 families 293, 325–6, 371–2 females 357–61 hard core of offenders 1, 27, 150, 559–70 PCL-R 53–9, 86–8, 135–43, 172, 255, 263–4, 319–31, 450–1, 468–71, 560 psychopathic disorders 1–2, 4, 14, 17, 19, 26–7, 37–8, 41–59, 86–95, 135–43, 150–64, 172, 180–2, 202, 253–4, 255–6, 265, 283–9, 319–31, 454–63, 468–71, 474–5, 477, 557–83 recidivism tendencies 1–2, 4, 14, 37–8, 41–59, 135–43, 255–6, 265, 283–9, 454–63, 468–71, 474–5, 477, 486–9, 503–5, 512, 514, 558–70, 573–83 schizophrenia 252–7, 259–64, 575–8 substance abuse 3–4, 253–4, 360, 534–5, 575–8 criteria see also features

597 APD 17, 25–6, 35–8, 49–50, 84–95, 103, 118, 150–1, 172, 237–8, 251–2, 268, 291, 319–31, 468–71, 562–3, 573–4 psychopathic disorders 17–21, 35–8, 41–58, 84–95, 103, 135–6, 142, 150–1, 172, 237–8, 251–2, 268, 276, 281, 291, 319–31, 335, 353–61, 468–71, 562–3, 573–4 Croatia 312 cruelty to animals/other children 202–3, 342 CS see conditioned stimuli CT see computerized tomography cues, social information processing 432–3 culpability criteria, legal and forensic impediments 566–70, 574–83 cultural issues discipline 305, 308–9, 312–13, 427–8 PCL-R scores 139–40 psychopathic disorders 48, 139–40, 351–2 cut scores, PCL-R 46, 140, 172, 468–71, 477–82, 563–5 cyclical pattern, domestic violence 502 cyproteroneacetat (CPA) 487–8 Cyprus 312 DA see dopamine Damasio et al 238–42 dangerous severe personality disorder (DSPD) 456 Darwin, Charles 12 dating violence, CP 311–12 DBT see dialectical-behavior treatment death penalty 139, 143, 358, 575 deception 78, 84–8, 150–64, 200–11, 456–7, 475–6 see also lying decision making 72–8, 111–13, 175–82, 240–8 see also executive functions emotions 241–8 gut feelings 73 risky decisions 111–13, 175, 242–3 defensive responses amygdala 69–70, 75–8, 93–5, 105–9, 113, 150, 159, 162–4, 173–5, 192, 195, 209–11 electrophysiology 190–6 eyeblink reflex 190–2, 195–6 deficient affective experience, three-factor model 84–5, 93–5, 319–31, 335, 468–73, 477–89 deficient violence inhibition mechanism, concepts 104–5 degenerates French concepts 10, 11–13, 19, 21, 22–3 German concepts 10, 19, 34 degenerative diseases see also neurological disorders brain trauma 229–30, 244–5

598 delinquents 19, 25, 35, 37, 44, 47–58, 137–43, 150–64, 203–11, 291–8, 320–31, 438–9, 470–1, 583 delusions cocaine 122 schizophrenia 119–20, 128, 129–31, 253–7 violence 119–20, 122, 124, 127, 129–31, 253–7, 399 withdrawal symptoms 121–2, 127 dementia 10, 17, 124, 405 demographic characteristics, violence risks 129, 328 denial of treatment 140–3, 557–70 Denmark 254, 312, 336–7, 576–7 Department of Health 389–90, 519 depression 19, 20, 120–2, 153, 157–8, 204, 221, 228–31, 257–9, 265–8, 292–3, 306–14, 371–2, 387–8, 404–6, 409–11, 423–4, 453–5, 521, 531–8 see also bipolar disorder; mood disorders ADHD 387–90 alcohol 531–8 brain trauma 221, 228–31 CD 423–4 children 265–7, 292–3, 306–14, 371–2, 423–4, 531–8 comorbid disorders 157–8, 221, 230, 257–9, 265–8, 292–3, 387–90, 423–4, 453–5, 471, 531–8 concepts 120–2, 157–8, 221, 228–30, 257–9, 265–8, 292–3, 387–90, 404–6, 409–11, 423–4 CP 306–14 depressed mothers 292–3, 326–7, 328–31, 371–2 gender issues 257–9 genetics 267–8 psychosis 121 PTSD 221, 228–31 rTMS 182 SSRIs 159, 181, 404–5, 409 statistics 257–9, 266–8 substance abuse 257–9, 531–8 treatment 159, 181–2, 390, 404–6 violence 120–1, 257–9 withdrawal symptoms 121–2, 537–8 workplace violence 521 desipramine 386 detachment concepts 336–43 detention see also prison . . . lifetime detention 557–8, 560–70, 582–3 detoxification programs, alcohol/substance abuse 537–8 Developmental Trend Study 370

INDEX dextroamphetamine 407 see also stimulants diagnosis see also assessments risks of diagnosis 2, 33–4, 117, 129–32, 135–43, 252, 458–61 Diagnostic and Statistical Manual of Mental Disorders (DSM) background 25–6, 35–6, 49–50, 84–8, 150–1, 237–8, 251–2, 275–6, 399, 417–19, 459 critique 35–6, 49–50, 84–8, 150–1, 251–2 DSM-I 24–5, 85–6, 275–6 DSM-II 25, 86, 275–6 DSM-III 16, 25–6, 50, 84–8, 150, 263, 266, 275–6, 282 DSM-III-R/DSM-IV 16, 50, 84–8, 128, 150–1, 172, 240, 263, 266, 275–6, 282, 468 DSM-IV 1, 16, 17, 21, 26–7, 35–6, 49–50, 84–8, 128, 150–1, 172, 199–204, 224, 237–8, 251–2, 268, 275–6, 281–2, 381, 411, 417–19, 468, 561, 573–8 DSM-IV-TR 238–40, 248, 251–2, 268, 275–6, 368, 399, 417–19, 450–1, 468, 561 PCL-R 49–50, 84–8, 281 diagnostic terms 2 dialectical-behavior treatment (DBT) 389, 479–80 see also cognitive-behavioral therapy dietary interventions 484 dimensional approach APD 34–8, 399–400 psychopathic disorders 2, 399–400 dimensional models, personality 24–5, 37 dimethyltryptamine (DMT) 122–3 diminished criminal responsibility 14, 566–70, 574–83 Dinosaur School 436 disasters, PTSD 220–31 discharge planning, violence risks 130–1 discipline see also corporal punishment; parents Baumrind parenting styles 304 concepts 162, 303–14, 321–31, 372, 425–7 cultural issues 305, 308–9, 312–13, 427–8 definitions 303–4 legal status 312–14 pre-existing behavior problems 309–12 types 303–4, 425–7 disgust see also emotions emotion recognition 105–7 dismissive individuals see also attachment concepts concepts 336–43, 457–8 disorders see mental disorders disorganization problems 72

INDEX dissocial behavior, concepts 26 dissocial personality disorder see also antisocial personality disorder concepts 9–10, 14, 16, 17, 18, 21, 25–6, 35–8, 49–50, 84–95, 450–1, 468, 487–8, 575–8 differentiation scheme 26–7 dissocial reaction 25–6 early predictors 17, 35–8 features 14, 17, 25–6, 35–8, 49–50, 84–95, 172–3, 575–8 ICD-10 diagnostic criteria 36, 49–50, 84–8, 172, 201, 368, 450–1, 468, 561, 575–8 primary features 14, 36–8 psychopathy 14, 16, 18, 49–50, 84–95 psychophysiological correlates 83–95 secondary features 14, 36–8 dissocial reaction 25–6 disulfiram 485 divalproex 402–3, 411 see also valproic acid dizygotic twins (DZ), genetics 152–3, 156, 193, 210–11 DLPFC see dorsolateral prefrontal cortex DMPFC see dorsomedial prefrontal cortex DMT see dimethyltryptamine Dodge, Kenneth A. 432–3 Doepfner, Manfred 417–48 domestic violence 497–514 accountability strategies 502–14 alcohol 505–6, 514 anger dynamic 501–2 antisocial batterers 499–514 ‘articulated thoughts in simulated situations’ 506 assertiveness deficits 506–10, 514 assessment components 497–8, 505–14 case conceptualization 507–9 CBT treatment approach 504–14 concepts 497–514 confidentiality issues 507 counseling programs 503–5, 508 criminal justice system 502–5, 508–9, 514 cyclical pattern 502 definition 497–8 dynamics 500–2 dysphoric/borderline batterers 499–500, 512–13 emotions 501–14 empathy 509–10, 512–13 entrapment dynamic 501–2 extrafamilial violence 505–6 feedback loops 508–11 future research 512–13 gender issues 500–1 healthcare appointments 500–1 histories of abuse 505–6

599 job instability 505–6 love dynamic 502 philosophical aspects of treatment 509 power dynamic 500–1 pretreatment assessments 505–7, 513 program content 509–11 recidivism tendencies 503–5, 512, 514 relaxation training 511, 514 risk factors 498–9 skills 509–11, 514 statistics 511–12 substance abuse 505–6, 514 subtypes 499–502, 512–14 thought processes 510–11 treatment 497–8, 502–14 treatment outcome 511–12 treatment planning/orientation 507–9 victim interviews 507, 513 written rules/policies/procedures 509, 513 dominance-submission paradigm, psychopathic disorders 339–43 dopamine (DA) 161–4, 204–6, 297–8, 383–6, 482–4, 538 dorsal system 94–5 dorsolateral prefrontal cortex (DLPFC) 70–8, 110–12, 175–80, 208–11, 243 dorsomedial prefrontal cortex (DMPFC) 72–8 Dot-Counting Test 246 Douglas, Emily M. 303–17 Down’s syndrome 123 DPD see dissocial personality disorder DreBing, Harald 573–85 dropout rates, treatment 141–2, 269, 505–6 DSM see Diagnostic and Statistical Manual of Mental Disorders DSPD see dangerous severe personality disorder Ducci, Francesca 149–69 Dunedin study 211, 327, 359 Dupr´e, E. 10, 12, 19 duration considerations, treatment 470, 477–82 dyslexia 369–70 dysphoric/borderline batterers, domestic violence 499–500, 512–13 dysthymia 228–9 early-starter pathway, antisocial behavior 202–3 Eastman, N. 181 ECA see Epidemiologic Catchment Area Program eccentrics 19 EDA see electrodermal activity educational issues 3, 11, 328, 367–75 see also schools comorbid ADHD 367–8, 370–1 concepts 328, 367–75 disruptive aggressive students 367–8

600 educational issues (Cont.) family background 367–8, 371–2 intelligence levels 367–8, 371 interventions 375 learning problems 367–8, 369–70 peer affiliations 367–8, 373–4 psychopathic disorders 3, 11, 328, 367–75 teachers 367–75 EEG see electroencephalogram EF see executive functions EFEC see event–feature–emotion complex ego 15–16, 17, 22, 36–8, 88, 135–6, 335, 339–43, 579, 583 egocentricity 17, 22, 36–8, 88, 135–6, 335, 579, 583 see also narcissism Ehrenreich, Hannelore 217–36 electrocortical psychophysiological techniques 87–95, 188–96 electrodermal activity (EDA) 87–8, 91–5, 106–9, 188–96, 210–11 see also autonomic . . . ; electrophysiology; skin conductance . . . amygdala 189, 192 changes 190–2 concepts 188–96, 210–11 emotions 191 hypothalamus 189 measurement method 188–9 orienting stimuli 189, 190 resting parameters 189–90 startle responses 188–96, 579–80 electroencephalogram (EEG) 75, 89–93, 106, 108, 158, 192–6, 337–8, 472–3 concepts 192–6, 337–8, 472–3 potentials 192–6, 472–3 sensation-seeking behavior 89–93, 192–6, 337–8 electronic monitoring 481 electrophysiology abnormalities theories 193–6 concepts 187–96 EDA 87–8, 106–9, 188–96 EEG potentials 192–6, 337–8, 472–3 eyeblink reflex 190–2, 195–6 fearlessness 194–6 future prospects 195–6 gender issues 196 HR 91–3, 106, 188–96, 210–11, 337–8 psychopathic disorders 3, 187–96 Elsne, Klaus 135–46 emotions see also anger; disgust; fear; joy; sadness; surprise autonomic responses 104–13, 174–5, 241–2, 579–80

INDEX CD interventions 428–40 CNV 94, 192–3 cognitive correlates 104–13, 175–6 cognitive/emotional processing defects 42–3, 71–8, 103–13, 175–6, 207–10, 240–8, 456–7 decision making 241–8 domestic violence 501–14 EDA 94, 191 empathy 14, 36–58, 73–8, 84–8, 93–5, 103–13, 135–6, 142, 172, 174–9, 239–40, 356–60, 368, 451–2, 456–9, 477–82, 509–10, 512–13, 562–3, 579 ERP 94, 113, 192–3 facial expressions 105–7, 192–3, 256–7, 349–50, 482 imagery 106–7, 191–3 mental diseases 10–11, 93–5, 175–6 perception processes 93–4 psychopathic disorders 4, 10–11, 13, 17, 21, 22, 35–8, 42–3, 53–9, 69–78, 84–5, 93–5, 103–13, 142, 172–6, 194, 240–8, 281, 294–8, 319–31, 335, 456–7 psychopharmacological agents 4, 118, 181 psychophysiological correlates 93–5, 105– 13 recognition abilities 105–13, 192–3, 456–7 resources 175–6 responses 71, 105–13, 174–6, 456–7, 579–80 shallow affect 44, 47–58, 73–8, 84–5, 93–5, 103, 135–6, 172, 297–8, 319–31, 579 spoken words 106–7 startle potentiation 94, 106–7, 174–5, 189–96, 579–80 empathy 14, 36–58, 73–8, 84–8, 93–5, 103–13, 135–6, 142, 172, 174–9, 239–40, 356–60, 368, 451–2, 456–9, 477–82, 509–10, 512–13, 562–3, 579 concepts 104–13, 142, 174–6, 178–9, 368, 451–2, 456–9, 477–82, 509–10, 512–13, 562–3, 579 domestic violence 509–10 emotions 14, 36–58, 73–8, 84–8, 93–5, 103–13, 135–6, 142, 172, 174–9, 239–40, 356–60, 368, 451–2, 456–9, 477–82, 509–10, 512–13, 562–3, 579 theory of mind 104–5, 349–50, 457–8 types 104–5 EMV see eyes, motor, verbal assessment endogenous psychosis see also psychosis personality disorders 22–6 endophenotypes 158, 210–11 enhanced thinking skills (ETS) 454 entrapment dynamic, domestic violence 501–2 enuresis 388

INDEX environmental issues brain trauma 226–8 genetics 152–3, 158, 159–64, 193, 196, 204–5, 210–11, 251–2, 267–8, 297–8, 338–40 psychopathic disorders 3, 42–3, 107–8, 129, 150, 152–5, 158–64, 193, 196, 204–5, 251–2, 267–8, 291–8, 338–40, 461–2, 481 violence risks 129 workplace violence 525–6 Epidemiologic Catchment Area Program (ECA) 532 epilepsy 10, 13–14 erogenous areas, infantile psychological development 15–16, 23–4 erotomania 11 ERP see event-related potential error-related negativity (Ne/ERN) 91–3 Esquirol, E. 10, 11, 13 ethnic issues, psychopathic disorders 48 etiology 2–3, 11–18, 34–8, 42–3, 117–32, 149–64, 187–96, 199–211, 217–31, 237–48, 251–69, 275–89, 298, 319–31, 367–75, 484–6, 532–4, 579–80 ADHD role 199–211 alcohol/substance abuse 532–4 antisocial behavior 203–11, 484–6 APD 34–8, 117–32, 484–6 brain trauma 217–31, 237–48 CD 421–5 comorbid disorders 251–69, 532–4 educational issues 3, 11, 328, 367–75 electrophysiology 187–96 genetics 2–3, 11, 12, 18–19, 22–3, 34–8, 42–3, 149–64, 251–2, 267–8, 579–80 impulse disorders 4 paraphilias 262–4, 275–89, 486–8 psychoanalytic view 15–16, 23–4, 335–43, 456–8 psychopathic disorders 2–3, 11–18, 34–8, 42–3, 117–32, 149–64, 203–11, 237–48, 251–69, 298, 319–31, 335–43, 484–6, 579–80 ETS see enhanced thinking skills Europe see also individual countries brain trauma 218–19 country comparisons 575–8 legal and forensic practice 575–8 PCL-R scores 46–7, 54–5, 137, 139–40, 451 event–feature–emotion complex (EFEC) 179 event-related potential (ERP) 90–1, 94, 113, 158, 192–3 excessive talking, ADHD 201 executive functions 72–8, 93–5, 110–12, 142, 150–1, 175–6, 208–10, 240–1, 246–8

601 see also cognitive correlates; goals; planning; self-control attention shifting 110–11, 240–1, 246–8 exhibitionism 229, 276–81, 287–9 see also paraphilias experiential issues psychopathic disorders 3, 42–3, 458, 459–63, 543–55 treatment 458, 459–63, 543–55 explosive disorder 21, 119, 128, 399 externalizing concepts 149, 157–64, 349–50, 485 extraversion, concepts 24–5, 89, 107–8, 338, 534 eyeblink reflex, electrophysiology 190–2, 195–6 eyes, motor, verbal assessment (EMV) 245 eyes test, theory of mind 104 Eysenck, H.J. 24, 37, 89, 92, 107 Eysenck, M.W. 37, 92 Eysenck Personality Questionnaire 240 facial expressions, emotion recognition 105–7, 192–3, 256–7, 349–50, 482 fact-based method of evaluation, workplace violence 524–5 factor structure psychological disorders 37, 44–5, 47–8, 50–2, 71–2, 84–5, 103–7, 172–4, 285–8, 319–31, 354–61 violence risks 124–9 the Fall 12 families see also parents ADHD 204–6, 389–92 antisocial behavior 206–7, 210, 291–8, 312–31, 367–8, 371–5, 533–4 brain trauma 219–21 CD 200–1, 204–6, 291–8, 371–5, 417, 421, 425–40 concepts 291–8, 324–31, 367–8, 371–5 criminality 293, 325–6, 371–5 depressed mothers 292–3, 326–7, 328–31, 371–2 disrupted families 324–5, 328–31 domestic violence 497–514 educational issues 367–8, 371–2 imprisoned parents 293, 325–6, 328–31 intra/extrafamilial factors 291, 292–3, 324–31, 371–2 large families 325, 328–9 maternal rejection 162, 292–6, 322, 336–43 parent–child interaction 293, 324–31, 336–43, 371–2, 425–40 psychopathic disorders 3, 42–3, 155–64, 204–6, 291–8, 321–31, 338–9, 371–2 single-parent families 324–31

602 families (Cont.) socioeconomic characteristics 291–8, 326–31, 371–2 teenage pregnancies 326 traumas 162–4, 204–6, 207, 276–89, 291–8, 324–31 treatment successes 470 trust issues 294 fanatics 21 Farrington, David P. 319–34 FDA 385–7, 402 fear 76–8, 94, 104–13, 174–5, 191–2, 227–8, 337–43 see also anxiety; emotions concepts 337–43 definition 337 emotion recognition 105–7 fearlessness 38, 76–8, 94, 150–64, 174–5, 191–2, 194–6, 368–9, 372–5, 579–80 see also low arousal electrophysiology 194–6 features see also criteria paraphilias 275–81 psychopathic disorders 14, 17–21, 35–8, 41–58, 84–95, 103, 118, 135–6, 143, 150–1, 172–3, 237–8, 251–2, 268, 276, 281, 291, 319–31, 353–61, 468–71, 476–7, 562–3 feedback loops, domestic violence 508–11 Feldman, Theodore B. 520–7 Felthous, Alan R. 1–5, 9–30 females see also gender issues assessment biases 349–50, 355–7 assessments 347–61, 459 ‘back to basics’ approach 354, 357 concepts 347–61, 459 criminality 357–61 domestic violence 497–514 future antisocial behavior 357–61 measurement considerations 353–7 misdiagnosis risks 352–3 PCL-R scores 348–9, 353–61 personality features 348–53 prisoners 357–61 psychometric PCL-R properties 354–6 psychopathic disorders 3, 35–6, 150–1, 155–6, 162–3, 347–61, 459 relative-to-males PCL scores 356 researchers 347–61 risk assessments 347–61 statistics 349–50 fetal alcohol syndrome 206–7 fetishism 276–89 see also paraphilias; transvestic . . .

INDEX fight/flight responses 88, 107–8 Fink, Paul J. 522 Finland 312, 324, 576–7 Firestone, Philip 275–90 First et al 36 five-factor personality model 24 Flor, Herta 103–16 flowing interviews 34 fluoxetine 409–11, 482 fMRI see functional magnetic resonance imaging fMRT, treatment technique 181–2 forensic concepts, psychopathic disorders 42–59, 357–61, 449–63, 557–70 Forensic Operationalized Therapy-Risk-Evaluation System (FOTRES) 474–5 forensic psychiatry 449–63, 557–70 foster care models, CD 436–9 FOTRES see Forensic Operationalized Therapy-Risk-Evaluation System Foulkes, S. 452 Fozdar, Manish A. 237–50 freedom of will 180–1, 581–3 French concepts legal terminology 576–7 psychopathic disorders 9–13, 18, 21–3, 576–7 Freud, S. 15–16, 23–4, 335, 337, 339, 452 froteurism 276–89 see also paraphilias functional magnetic resonance imaging (fMRI) 69–76, 162–3, 175–6, 178–9, 181–2, 209–11, 246, 472–3, 579 gabapentin 404 Gabbard, G. 462–3 Gage, Phineas 69, 237–40, 398 gambling task 111, 243 Gang´e, Pierre 557 gangs, institutional problems 56 Gass, Peter 573–85 GBG see Good Behavior Game GCS see Glasgow Coma Scale Gelles, Michael G. 521 gender issues see also females APD 3, 35–6, 42–3, 47–8, 103–4, 150–1, 153, 155–7, 162–4, 188, 201–3, 205–6, 257–9, 260–1, 347–61, 459 assessment biases 349–50, 355–7 ‘back to basics’ approach 354, 357 brain trauma 219–21 CP 306–7 criminality 357–61 depression 257–9, 292–3 domestic violence 500–1

INDEX electrophysiology 196 misdiagnosis risks 352–3 PCL-R scores 348–9, 353–61 personality features 348–53 prisoners 357–61 psychometric PCL-R properties 354–6 psychopathic disorders 3, 35–6, 42–3, 47–8, 103–4, 150–1, 153, 155–7, 162–4, 188, 201–3, 205–6, 257–9, 260–1, 347–61, 459, 462 PTSD 220–1 qualitative/quantitative differences 156 researchers 347–61 sociocultural determinants 351–2 statistics 349–50 substance abuse 260–1 Genesis 11–12 genetics see also constitutions addictions 149, 153, 157–9, 251–2, 267–8 ADHD 204–7, 210–11 adoptive studies 152–3 aggression 153, 154–5, 251–2, 267–8, 297–8, 397–411 alcohol 149, 153, 157–9, 267–8, 533–4 amygdala 69–70, 75–8, 93–5, 105–9, 113, 150, 159, 162–4, 173–5, 180–2, 189, 192, 195, 209–11, 227–8, 369, 579–80 antisocial behavior 149–64, 204–6, 251–2, 267–8, 297–8 brain trauma 219–21, 222–8 catecholamines 161–4, 382–6 CD 204–7, 210–11, 251–2, 267–8, 421 children 297–8 comorbid disorders 149, 157–64, 251–2, 267–8 COMT 163–4, 205–6, 267–8 concepts 149–64, 193, 204–6, 222–8, 251–2, 267–8, 297–8, 579–80 definitions 149–51 depression 267–8 dizygotic twins (DZ) 152–3, 156, 193, 210–11 environmental issues 152–3, 158, 159–64, 193, 196, 204–5, 210–11, 251–2, 267–8, 297–8, 338–40 intermediate phenotypes 158 MAOA 161–4, 205–6, 297–8 monozygotic twins (MZ) 152–3, 193, 210–11 neurobiologies 159–64 PFC 69–78, 91–5, 108–12, 159, 162–4, 173–5, 179–82, 189, 194–6, 208–11, 237–48, 264–5, 297–8, 398–9, 579–80, 581 psychiatric disorders 152–3

603 psychopathic disorders 2–3, 11, 12, 18–19, 22–3, 34–8, 42–3, 149–64, 173, 193, 204–6, 210–11, 251–2, 267–8, 297–8, 579–80 schizophrenia 153, 267 serotonin 159–61, 205–6, 397–411, 421 twin data 152–64, 193, 210–11 Germany 9–10, 12, 18–23, 34–5, 48, 54–5, 137, 172, 312, 386–7, 427–9, 557–70, 576–7 Bavarian Law of Confinement 561–2 BPP 429 detoxification programs 537–8 forensic psychiatry 557–70 legal terminology 576–7 PCL-R 48, 54–5, 137 Penal Code 561–2 PMTs 427–8 psychopathic disorders 9–10, 12, 18–23, 34–5, 48, 54–5, 172, 557–70, 576–7 treatment impediments 557–70 girls see also children; females PCL-R scores 348–9, 353–61 PCL:YV predictions 360–1 psychopathic disorders 347–61 Glasgow Coma Scale (GCS), brain trauma 221–3, 244, 245 Glasgow Outcome Scale, brain trauma 221–3, 244 glibness 44, 47–58, 84–8, 172, 453–5 see also charm glucocorticoid levels 297 goals see also motivation deficits lack of goals 41, 44, 47–58, 84–5, 88–93, 110–12, 142, 242–8, 281, 477–82 Goldman, David 149–69 Good Behavior Game (GBG) 429 good home backgrounds, psychopathic disorders 338 Grafman, J. 241 Granacher, Robert P. 237–50 grandiosity 42, 44, 47–58, 84–8, 112, 135–6, 172, 339–43, 356–60, 453–5, 457–8, 579 components 340 concepts 340–3, 579 omnipotent fantasy 340 Gray, J.A. 37–8 gray matter volumes 71–2, 73–8, 177–9, 195, 208–10, 225–7, 350, 398–9 see also brain . . . Great Britain see also Anglo-American concepts; United Kingdom conceptual history 10, 13–14, 18, 450–3, 573–4

604 Great Britain (Cont.) legal terminology 575–7 Mental Health Act 14 PCL-R scores 46–7, 54–5, 139–40, 450, 451 personality disorders 136 prisoners 37, 281 Greece 576–7 Grendon prison 452–5 Griesinger, W. 11, 18, 22–3, 34 group results, PCL-R 137–9 group therapy 57–8, 461, 476–7, 486–8, 567 guilt 14, 17, 35–8, 41–2, 44, 47–58, 78, 84–5, 93–5, 103, 118, 135–6, 172, 319–31, 460 see also remorse gut feelings, decision making 73 hallucinations schizophrenia 119–20, 128 withdrawal symptoms 121–2, 127 hallucinogens effects 122–3, 127, 535 violence 122–3, 127, 535 haloperidol 482 Halstead–Reitan Test Battery 247 Hamberger, L. Kevin 497–517 Hanisch, Charlotte 417–48 hard core of offenders, criminality 1, 27, 150, 559–70 Hare, R.D. 26–7, 35–7, 41–67, 83–5, 103–13, 135–6, 172, 174–5, 193, 237–9, 276, 281, 320, 337, 347, 352, 368, 450, 468–9, 524, 562, 567, 570, 573–5, 583 Harlow, John 238 harm-avoidance personality dimension 24, 38 harsh discipline 162 Hart, S.D. 320 Hawaii 329 HAWIE 473 HCR-20: Assessing Risk for Violence 54, 458–9, 473–5 HD see hyperkinetic disorder healthcare appointments, domestic violence 500–1 heart rate (HR) see also autonomic . . . children 188 concepts 91–3, 106, 188–96, 337–8 impulsivity 91–3, 106 psychopathic disorders 91–3, 106, 188–96, 337–8 responses 188 resting heart rate 91–3, 106, 188, 210–11, 337–8 hebephiles 282 see also pedophiles Henderson, D. 10, 14

INDEX hepatitis 471 heroin 257–61, 269, 538 see also opioids; substance abuse Herpertz, Sabine C. 33–40, 187–98, 199–216, 381–95 Herpetz-Dahlmann, Beate 199–211, 381–95 high daring, risk factors 328–31 Hill, Andreas 467–95 hippocampus 69–70, 75–8, 93–5, 107–8, 113, 173, 177–9, 181, 225, 227–8 history assessments 37, 41–3, 573–4 psychopathic disorders 2, 9–30, 41–3, 83–6, 135–6, 150–1, 172–3, 450–1 HIV 124, 269, 471 Hoff, Paul 33–40 ‘holistic’ approach, workplace violence 524–7 homicide see also murderers APD comorbid disorders 255–6, 262–3 grandiose self-structure 340–1 paraphilias 263–4, 287–9 pedophiles 263–4, 287–9 sexual offenders 263–4, 287–9 substance abuse 535 homovanillic acid (HVA) 161 hormones 163, 350–1, 482–4, 487–8 hospitals critique 4–5, 557–70, 582–3 limitations 4–5 outpatient treatment 488–9, 536–7, 557–70 politics 558–70, 582–3 prisoners 4–5, 557–70, 582–3 violence risks 128, 129–32, 488–9 Houston, Rebecca J. 83–101 HPA see hypothalamic–pituitary–adrenal axis HR see heart rate HTR1B 159–60 HTT see hydroxytryptamin transporter human rights 348–9 Hungary 312 HVA see homovanillic acid hydroxytryptamin transporter (HTT) 160–1 see also serotonin hyperactivity/impulsivity symptoms, ADHD 200–11, 370–1, 381–92 hyperarousal 294 hyperkinetic disorder (HD) 201, 206 hyperthymic psychopathic constitutions 19, 21 hypoarousal 297–8, 336–43 hypothalamic–pituitary–adrenal axis (HPA) 159, 227–8, 350–1, 472–3 hypothalamus 159, 179–80, 189, 227–8, 350–1, 472–3 hypoxia-ischemia 244 hysterical psychopathic constitutions 19

INDEX I Can Problem Solve (ICPS) 429–30 IAP see intensive aftercare programs ICD see International Classification of Mental Disorders Iceland 312 ICPS see I Can Problem Solve id 341 idea of continuum, concepts 22–4 id´ee fixe 11 identifications, internalization concepts 339–43 idiopathic/symptomatic forms, psychopathic disorders 16, 17–18 IED see intermittent explosive disorder IES see integrated emotion systems model imagery, emotional responding 106–7, 191–3, 456–7 impulse disorders 14, 35–8, 41–3, 44, 47–58, 69–78, 84–5, 87–93, 112, 118–32 brain imaging research 69–78, 89–93 etiology 4 impulsive aggression 398–411 see also aggression impulsive and irresponsible behavioral style, three-factor model 84–5, 88–95, 319–31, 468–73, 477, 482–9 impulsivity 14, 35–58, 69–78, 84–5, 87–95, 112, 118–32, 135–6, 142, 150–64, 181–2, 192–6, 267–9, 281, 297–8, 319–31, 349–50, 368–75, 390–1, 397–411, 422–40, 468–71, 482–4, 533–4, 579 see also irresponsibility; sensation-seeking behavior ADHD 200–11, 390–1 alcohol consumption 533–4 ANS index 91–3 autonomic measures 91–3 CNV 91–3, 192–3 concepts 85, 88–93, 112, 118, 135–6, 181–2, 193, 267–9, 281, 297–8, 349–50, 390–1, 397–411, 482–4, 533–4, 579 EDA 91–3 EEG 89–93 ERP 90–1, 113, 192–3 HR 91–3, 106 P3 results 90–3 psychophysiological correlates 88–93, 112, 267, 533–4 serotonin 159–64, 397–411, 421 treatment 390–1, 397–411, 482–4, 579 inadequate psychopathic condition 14 inattention symptoms ADHD 200–11, 370–1, 381–92 brain trauma 228–9, 240–2, 246–8 incapacity for love 17 incest 263–4, 282, 283–4 see also paraphilias

605 incorporation processes, internalization concepts 339–43 India, CP 309 Indianapolis Domestic Violence Prosecution Experiment 504 individually-tailored multicomponent CD interventions 439–40 infantile psychological development 15–16, 23–4 inferiority, constitutional inferiority 15, 21 information processing, concepts 72–8, 103–13, 174–6, 422, 427, 431–40 inhalants, violence 123 inhibitions 37–8, 53–9, 71–8, 104–5, 107–13, 121, 127, 208–10, 282, 484–6 alcohol 121, 127, 282, 484–6 BIS 37–8, 107–9, 484–6 insanity legal and forensic impediments 566–7 moral insanity 10, 11, 12, 13–14, 17, 22, 573–4 insecure psychopaths 21 insight-oriented programs 57 insincerity 17, 35–8, 41, 44–58, 281 see also lying insomnia, withdrawal symptoms 121–3 institutional problems 56, 140–3, 461–2, 557–70, 583 impediments 557–70 PCL-R 56, 140–3 social groups 461–2, 476–7 treatment 461–2, 557–70, 583 insula 93, 113 integrated approaches, psychopathic disorders 3 integrated emotion systems model (IES) 108–9 the intellect, mental diseases 10–11, 13–14, 17, 20, 22, 37, 103–4 intelligence levels ADHD 207 alcohol 127 brain trauma 244, 246–8 CD 207, 367–8, 371 educational issues 367–8, 371 psychopathic disorders 103–4, 207–8, 328–31, 367–8, 371, 473–5, 478 intensive aftercare programs (IAP) 480 intensive parole supervision (IPS) 480 intent, violence risks 126, 560 interclass correlation (ICC), PCL-R 45–6 interdisciplinary collaborations 1–2 intermediate phenotypes, genetics 158 intermittent explosive disorder (IED) concepts 119, 128, 399 violence 119, 128, 399 internalization failures, psychoanalytic view 338–43, 456–8

606 International Classification of Mental Disorders (ICD) background 26, 36–7, 49–50, 84–8, 172, 199–201, 276, 368, 450–1, 561 critique 36–7, 49–50, 84–8 ICD-10 21, 26, 35–6, 49–50, 84–8, 172, 193, 201, 206, 276, 368, 450–1, 468, 561, 575–8 PCL-R 49–50 international collaborations 1–2 International Personality Disorder Examination (IPDE) 36–7, 458–9 interpersonal items, PCL-R 37, 44–58, 77–8, 84–8, 106, 113, 319–31, 335, 355–61, 453–5, 468–73, 477–89, 573–4 interpersonal violence, PTSD 220–31 interventions 3–5, 375, 381–92, 417–40, 467–89 see also treatment ADHD 381–92 CD 417–40 educational issues 375 prevention programs 425 psychopathic disorders 3–5, 375, 467–89 social policies 573–83 interviews 34, 36–7, 44–5, 50–2, 471–2, 507, 513 domestic violence 507, 513 motivational interviewing 485, 537–8 PCL-R 44–5, 50–2, 240 intraspecies predators 53, 339–43, 460 introjections, internalization concepts 339–43 Iowa gambling task 111, 243 IPDE see International Personality Disorder Examination IPS see intensive parole supervision IR-MPH 383 Ireland 576–7 irresponsibility 14–15, 35–8, 41–3, 44, 47–58, 71–8, 84–5, 88–95, 135–6, 150–64, 179–82, 193, 319–31, 453–5, 566–70, 573–4, 579 see also impulsivity neuroimaging perspectives 180–1 irritability 150–64, 472–3 IRT see item response theory Israel 312 Italy, CP 309, 312–13 item response theory (IRT) 46–8, 356 Janzarik, W. 23 Japan, PCL-R 48 job instability, domestic violence 505–6 Johnson, Phillip W. 520 joy 105–7 see also emotions

INDEX Karpman, B. 10, 16, 86 Kelsey, R.M. 87–8 Kendler et al 157–8 Kenya, CP 309 Kerr et al 38 Kessler et al 221 Kiefer, Falk 531–41 Kiehl, K.A. 110–13 kleptomania 11 Koch, J.L.A. 10, 18, 21 Koglin, Ute 367–78 Konrad, Kerstin 199–211, 381–95 Korea, PCL-R 48 Kraepelin, E. 10, 19, 20, 21, 22–3, 33, 172, 559 Krampe, Henning 217–36 Kretschmer, E. 10, 20, 23 Krischer, Maya K. 291–302 label problems, psychopaths 142–3 lack of goals 41, 44, 47–58, 84–5, 88–93, 110–12, 142, 242–8, 281, 477–82 lamotrigine 404 Langhinrichsen-Rohling, Jennifer 497–517 language processing 75–8, 106–7, 110–11, 112–13, 207–10, 244, 246–8 large families 325, 328–9 late-starter pathway, antisocial behavior 202–3 Latvia 312 lawsuits, brain trauma 248 lawsuits against clinicians discharge planning 130–1 violent patients 117, 129–32 LCP see life-course persistent offenders learning 14–17, 36–8, 71, 77–8, 84–5, 93–5, 104–13, 159, 174–6, 194, 241–2, 244, 267–8, 281, 319–31, 337–43, 367–8, 369–70, 559–60, 578–9, 582–3 see also punishment associative learning deficits 105, 107–9, 174–5, 369–70, 559–60, 578–9 concepts 104–13, 174–6, 194, 241–2, 244, 267–8, 367–8, 369–70, 559–60, 578–9, 582–3 conditioning 94, 107–9 educational issues 367–8, 369–70 from experience 14–17, 36–8, 77–8, 84–5, 93–5, 107–9, 174–6, 194, 281, 319–31, 337–43, 369, 559–60, 578–9, 582–3 learning stimulus–response/reward associations 71, 107–9, 174–5, 369–70, 578–9 legal and forensic practice see also criminal justice system country comparisons 575–8 Europe 575–8 PCL-R 136–43, 357–61, 583

INDEX social policies 574–8 treatment impediments 557–70 legal responsibilities 14, 180–1, 566–70, 574–83 legal status, CP 312–14 legislation 1–2 Lehmkuhl, Gerd 291–302 leptosomic body types 20 Level of Service Inventory (LSI-R) 473–5 levels, psychopathic disorders 477–82, 583 Levenson Primary and Secondary Psychopathy Scale (LPSP) 471–2 Leygraf, Nobert 135–46 LHRHs see luteinizing hormone-releasing hormone agonists life-course persistent (LCP) offenders, antisocial behavior 202–3, 351 life-threatening events, PTSD 220–31 lifestyle items, PCL-R 37, 44–58, 84–5, 88–93, 468–73, 485–6 lifetime detention 557–8, 560–70, 582–3 LIFT see Linking the Interests of Families and Teachers limbic system 42–3, 69–70, 75–8, 92–5, 113, 150, 159–64, 179–82, 209–11 Lindsley, David 89 lingual gyrus 77–8 Linking the Interests of Families and Teachers (LIFT) 430 lithium, aggression 400–1, 407, 409–11, 482–4 Lombroso, C. 10, 12 long-term outcomes, brain trauma 225–7, 238, 244–5 long-term treatment, ADHD 391–2 Loranger et al 36 love delusional disorder 120 domestic violence 502 incapacity for love 17 low arousal 24, 38, 41, 44, 47–58, 88–95, 192–6, 210–11, 336–43 see also fearlessness LPSP see Levenson Primary and Secondary Psychopathy Scale LSD see lysergic acid diethylamide LSI-R see Level of Service Inventory Luria–Nebraska Neuropsychological Battery for Adults 247 luteinizing hormone-releasing hormone agonists (LHRHs) 487–8 Luxembourg 576–7 lying 17, 19, 35–8, 41, 44, 47–58, 72–8, 84–8, 117–18, 135–6, 150–64, 172, 200–11, 281, 453–5 see also insincerity brain image research 72–8 lysergic acid diethylamide (LSD) 122–3, 535

607 McArthur Community Violence interview 253 McArthur Competence Assessment Tool 248 MacArthur Study of Mental Disorder and Violence 50, 55 McGauley, Gill 449–66 Magnan, M. 12, 13 magnetic resonance imaging (MRI) 246, 472–3 maladaptive types of character, antisocial behavior 34 malinger tendencies, brain trauma 246 malnutrition, prenatal/postnatal risk factors 207, 210 maltreated children 162–4, 204–6, 207, 276–89, 291–8, 321–31, 338–9, 341–3, 401, 438–9 management see also treatment ADHD 381–92 CD 417–40 outpatients 4, 467–89 psychopathic disorders 1–2, 3–5, 467–89, 583 mania 10–11, 15, 22–3, 120–1, 151, 252, 257–9, 409–11 see also mood disorders conceptual development 10–11, 22–3 definition 120 mania without delirium 10–11, 22–3 moral mania 15 violence 120–1, 257–9 mania without delirium, French concepts 10–11, 22–3 manic-depressive diseases 19 manipulative behavior 44, 47–58, 84–8, 103, 135–6, 150–64, 172, 356–60, 368, 453–5, 472, 477–82, 513, 535–6, 563–4, 573–4 Mann, Karl 531–41 Mann, Thomas 103 MAOA see monoamine oxidase marital conflicts, CD 425 The Mask of Sanity (Cleckley) 452, 573–4, 582–3 mass murders 128, 340–1 MAST see Michigan Alcohol Screening Test masturbation 278–89 see also paraphilias maternal rejection 162, 292–6, 322, 336–43 Maudsley, H. 14 Mauritius 337 MBT see mentalization based treatment MCMI see Millon Clinical Multiaxial Inventory MDS see multidimensional scaling medial prefrontal cortex (MPFC) 74–8, 176–9 medial temporal structures 70, 75–8 medical disorders, violence 124 medical impediments, treatment 557–70 medical model, concepts 34–8

608 medically related aggression 398–411 see also aggression medroxyprogestoerone acetate (MPA) 487–8 Meloy, J.Reid 335–46 memory concepts 104–13, 207–10, 227–8, 229, 240–8 working memory 229, 240–8 mental diseases 10–11, 13–14, 17, 20, 22–6, 93–5, 575–8 mental disorders see also individual disorders antisocial behavior 33–4, 87 country comparisons 575–8 legal terminology 575–8 sociocultural determinants 351–2 standardization of nomenclature 24–6, 142–3, 172, 251–2 violence 117–32 mental health 22–6, 135–46, 306–14, 581–3 Mental Health Act, Great Britain 14 mental hospitals see hospitals mental illnesses, treatment options 3 mental instability, French concepts 10, 12, 19 mental retardation 120, 123–4, 266–7, 575–7 mentalization based treatment (MBT) 457–8 mentalizing 75, 104–5, 336–7, 349–50, 457–8 mescaline 122–3 methadone 260–1, 485, 538 methylphenidate (MPH) 382–6, 388, 389–90, 407, 411 see also stimulants ADHD treatment 382–5, 388, 389–90, 411 adverse effects 385–6 Meyer, Adolph 25 Meyer, Alford 15 Michie, C. 84–94 Michigan Alcohol Screening Test (MAST) 283–6 mild punishment 389 see also punishment milestones in history, psychopathic disorders 9–21, 41–2 militaristic themes, paranoid personality disorder 118–19 Millon Clinical Multiaxial Inventory (MCMI) 350, 498–9 Millon, T. 24 the mind of the psychopath 335–43 see also psychoanalytic view Minnesota Multiphasic Personality Inventory (MMPI) 240, 247, 262, 338, 350, 471–2 Minnesota Supreme Court 137–8 mismatch negativity (MMN) 90–1 MMN see mismatch negativity MMPI see Minnesota Multiphasic Personality Inventory (MMPI)

INDEX mobbing see also bullying workplace violence 522–3 modulation, responses 110–12, 175–6, 181–2, 195, 369 modulation of affect 342–3 Moeller, F.Gerard 397–416 molecular pathogenesis, brain trauma 222–8, 240–2 Moll et al 179 monoamine neurotransmitter genes 159–64 monoamine oxidase (MAOA) 161–4, 205–6, 297–8 monomania, French concepts 10, 11 monozygotic twins (MZ), genetics 152–3, 193, 210–11 mood disorders 10–12, 19, 22–3, 83–6, 120–1, 157–8, 251–2, 257–9, 264, 400 see also affectiveness disorders; depression; mania comorbid disorders 157–8, 251–2, 257–9, 264 conceptual development 10–12, 19, 22–3, 83–6 violence 120–1, 257–9 moral, definitions 13 moral alienation of the mind 15 moral cognition 179–82, 242 moral emotion 179–82 moral faculties, perversions 15 moral insanity concepts 10, 11, 12, 13–14, 17, 22, 573–4 definition 13, 573 moral mania, concepts 15 moral reasoning 74–8, 173–5, 179–82, 242 moral shock 13–14 Morel, B.A. 10, 11–13 motivation deficits 17, 44, 47–58, 84–5, 88–93, 142, 179–82, 281, 477–82 see also goals enhancement measures 478–9 outpatient treatment 477–82 motivational interviewing 485, 537–8 motor empathy, concepts 104–5 motor skills, brain trauma 244 motor-neuron disease 244 MPA see medroxyprogestoerone acetate MPFC see medial prefrontal cortex MPH see methylphenidate MRI see magnetic resonance imaging MST see Multisystemic Therapy MTA see Multimodal Treatment Study of Children with ADHD MTFC see Multidimensional Treatment Foster Care M¨uller, J¨urgen L. 4, 171–85, 557–70 multicomponent interventions, CD 439–40

INDEX multidimensional scaling (MDS) 47–8 Multidimensional Treatment Foster Care (MTFC) 436–8 multimodal treatment 381–2, 389–90, 417, 436–40, 520, 580 ADHD 381–2, 389–90 CD 417, 436–40 workplace violence 520 Multimodal Treatment Study of Children with ADHD (MTA) 389–90 Multisystemic Therapy (MST) 436–9, 470–1, 536–7 murderers APD comorbid disorders 255–6, 262–3 brain imaging research 76, 77–8 grandiose self-structure 340–1 lawsuits against clinicians 129–30 mass murders 128, 340–1 Musil 9 N300 192 nadolol 484 naltrexone 485, 538 narcissism 52, 84–8, 118, 128, 335, 340, 342–3, 351, 457–60, 475–6, 482, 505–6, 512 see also charm; deception; grandiosity; manipulative . . . benign narcissists 475–6 children 342–3 concepts 84–8, 128, 335, 340, 342–3, 457–60, 475–6, 482, 505–6 fight/flight responses 88 PEP 87–8 psychophysiological correlates 87–8 SCR 87–8 violence 118, 128, 335, 457–60, 505–6 Narcissistic Personality Inventory (NPI) 87–8 Narcotics Anonymous 485 National Adult Reading Test 247 National Epidemiological Survey on Alcohol and Related Conditions 150 National Family Violence Survey 307 National Institute for Clinical Excellence (NICE) 388 National Institute of Mental Health 253, 389–90 National Institute for Occupational Safety and Health (NIOSH) 519 National Longitudinal Survey of Youth 309–11, 327–8 National Youth Victimization Prevention Study 306–7 NCS study 532 NE see norepinephrine Ne/ERN see error-related negativity necrophilia 277 see also paraphilias

609 need for stimulation 24, 38, 41, 44, 47–58, 84–5, 88–93, 193–6 see also sensation-seeking . . . neighborhood factors see demographic characteristics NEPSY 247 nervous constitution, concepts 18 Netherlands legal terminology 576–7 PCL-R scores 48, 54–5, 140 Neufeld, Kylie 41 Neumann, C.S. 41–51 neurasthenic psychopathic constitutions 19 neurobiologies 159–64, 171–82, 203–11, 338–9, 397–411, 574, 579–83 genetics 159–64, 180–2 irresponsibility 180–1, 579–83 psychopathic disorders 159–64, 171–82, 203–11, 338–9, 397–411, 579–83 social policies 579–83 neurocognitive impairment, ADHD/CD 207–10 neuroendocrine alterations, PTSD 227–8 neuroimaging perspectives see also brain imaging research activation patterns 173–4, 181–2 ADHD 208–11, 381–2 assessments 182, 246–8, 335, 381–2, 472–3, 579–80 CD 208–11 concepts 171–82, 227–8, 246–8, 335, 472–3, 579–80 critique 182 findings and methods 173–4 future prospects 181–2 irresponsibility 180–1 methods 173–4, 176–82, 246–8 morality and responsibility issues 179–80 psychopathic disorders 3, 69–78, 87, 171–82, 472–3, 579–80 real-time fMRT 181–2 right superior temporal gyrus 176–82 rTMS 182 samples 171–4 templates 173–4 test issues 174–5 treatment possibilities 181–2 neuroleptic drugs 181–2 neurological disorders 124, 244–5, 457 see also degenerative diseases neurophysiological defects 3, 12, 42–3, 173, 207–11 neuropsychological findings 34, 173–6, 246–8, 371, 390–1, 457 neuroscience 171–82 irresponsibility issues 180–1 penal laws 180–2

610 neurosis character neurosis 15–16, 34 concepts 15–16, 17–18, 22 psychopathic disorders 15, 17–18, 22 neuroticism alcohol 533–4 concepts 24–5, 37, 533–4, 575–8 country comparisons 575–8 neurotransmitters 159–64, 397–411, 482–4 see also serotonin neurotrauma 69, 71–2, 73–8, 105–12, 120–1, 123, 176–82, 194–5, 217–31, 237–48, 264–5, 398–9 see also brain trauma assessments 221–3, 244, 245–8, 398–9 causes 221–2 concepts 217–31, 237–48, 398–9 consequences 225–7, 228–31, 237–48, 264–5 definition 217 falls 221–2 molecular pathogenesis 222–8, 240–2 Phineas Gage 69, 237–40, 398 psychopathic disorders 69, 71–2, 73–8, 105–12, 120–1, 123, 176–82, 194–5, 229–31, 237–48, 264–5, 398–9 risk factors 218–21 sports 222 traffic accidents 221–2, 225 New York Academy of Medicine 24 New Zealand 327 NICE see National Institute for Clinical Excellence Nichita, Elena Carmen 251–74 Nicholls, Tonia L. 347–66 nicotine 206–7, 210 see also smoking Niehoff, Debra 521–2 NIMH Epidemiological Catchment Area project 202 NIOSH see National Institute for Occupational Safety and Health nocturnal enuresis 388 nomenclature, standardization 24–6, 142–3, 172, 251–2 noncompliance with treatment, violence risks 129 nonstimulant medication, ADHD treatment 382–8, 389–90, 392 noradrenaline levels 297–8 noradrenergic antagonists, aggression 405–6, 484 norepinephrine (NE) 161–4, 205–6, 227–8, 383–7, 538 North America see also Anglo-American concepts; Canada; United States

INDEX conceptual history 10, 15–18, 24–5, 41–2, 450–1 PCL-R scores 46–8, 54–6, 139–40, 451 Norway BPP 429 CP 312 PCL-R 48 Nottingham survey 322 novelty-seeking personality dimension 24, 38, 41, 44, 47–58, 88–95, 192–6, 337–8, 349–50, 482, 533–4, 579 see also impulsivity; sensation-seeking . . . NPI see Narcissistic Personality Inventory nurses, short-term risk of violence 124–32, 475–7 Oak Ridge Hospital, Canada 563 object permanence, concepts 336 object relations, psychoanalytic view 336–43 object representation, concepts 336 obsessive psychopathic constitutions 19 occupational/social functioning, brain trauma 230–1 ODD see oppositional defiant disorder Odgers, Candice L. 347–66 oedipal guilt 452 OFC see orbitofrontal cortex offenders, hard core of offenders 1, 27, 150, 559–70 Oklahoma Estimate 247 omega-6/omega-3 essential fatty acids 484 omnipotent fantasy, grandiose self 340–1 openness, concepts 24 operant behavioral technique see also behavioral therapy concepts 388–9 opioids 257–61, 269, 453, 485, 535 see also heroin; substance abuse oppositional defiant disorder (ODD) see also conduct disorder concepts 200–11, 265–7, 417–40, 531 definition 417–19 treatment 417–40 orbicularis oculi 191–2 orbitofrontal cortex (OFC) 70–8, 108–13, 173, 175–9, 181–2, 238–48, 369 SSRIs 181 Oregon Youth Study 327–8 orienting issues, cognitive correlates 112–13, 189, 190 Original Sin 12 origins, psychopathic disorders 2–3 OROS-MPH 383 outpatient treatment 4, 467–89, 536–7, 557–70, 580–3 see also community treatment; treatment

INDEX ACT 480 algorithms 472–3, 482–3, 488 assessment algorithm 472–3 assessments 471–5, 536–7 CBT 479–80 compulsory outpatient treatment 580–3 concepts 4, 467–89, 536–7, 557–70, 580–3 confidentiality issues 480–1 DBT 479–80 hospitals 488–9, 536–7, 557–70 monitoring issues 475–82 motivation enhancement measures 478–9 pharmacotherapy 482–9, 537–8 psychopathic disorders 4, 467–89, 557–70 risk assessments 473–5, 557–70 sexual offenders 470–5, 478–81, 484, 486–9 situations 467–8 studies 468–71 substance abuse 484–6, 536–7 therapeutic relationships 475–7, 535–6 treatment algorithm 482–3 Overt Aggression Scale 127 overview 1–5 P300 amplitude 90–3, 158, 164, 192–3 Paced Auditory Serial Attention Task (PASAT) 91–3 panic disorder 153, 228–30, 260 paralimbic system 42–3, 113, 174–5, 179–82 paranoia, violence 118–19, 124, 128 paranoid ideation, substance abuse 122 paranoid personality disorder concepts 118–19, 128 militaristic themes 118–19 violence 118–19, 128 paranoid psychopathic constitutions 19 paranoid schizophrenia 10 paraphilias 4, 262–4, 275–89, 294–5, 323–31, 474–5, 486–9 see also pedophiles; sexual . . . alcohol 282–9 arrests 279 characteristics 276–80 comorbid disorders 262–4, 282–3, 288–9, 471, 486–9 concepts 262–4, 275–89, 486–9 conceptual history 275–6 course 279 definitions 275–6 fantasies/urges 277 features 275–81 homicide 263–4, 287–9 masturbation 278 multiple paraphilias 282–3 onset 279 personality disorders 275–6

611 pharmacological treatment 288–9 psychopathic disorders 4, 262–4, 275, 282–9, 486–9 rape 282, 286–9, 486–8 recidivism tendencies 279–89, 486–8, 562–5, 579 serotonin 288–9 sexual activity with object of fantasy 278 SSRIs 288–9, 482, 487–8 statistics 262–4, 282–3 substance abuse 282–3 surgical castration 487–8 treatment 288–9, 438–9, 454–5, 470–5, 478–81, 484, 486–9 types 276–81 use of force 279 parasitic lifestyle 44, 47–58, 84–5, 88–93, 478–9 parent management training (PMT) 425–40 parental discipline see discipline parents 3, 155, 162, 204–6, 291–8, 303–14, 321–31, 336–43, 371–5, 389–92, 417, 425–40 see also families ADHD training 389 antisocial behavior 291–8, 321–31, 371–5 attachment concepts 336–43, 457 Baumrind parenting styles 304 CD training 417, 425–40 CP 303–14, 321–31, 372 depressed mothers 292–3, 326–7, 328–31, 371–2 dispositional factors 292–3 grandiose self-structure 340–1 imprisoned parents 293, 325–6, 328–31 intra/extrafamilial factors 291, 292–3, 324–31, 371–5 maternal rejection 162, 292–6, 322, 336–43 parent–child interaction 293, 324–31, 336–43, 371–2, 425–40 positive parenting programs 425–8 prenatal/postnatal risk factors 205–7, 210, 535 psychopathic disorders 3, 42–3, 155–64, 204–6, 291–8 single-parent families 324–31 smoking 206–7, 210, 326–7 socioeconomic characteristics 291–8, 326–31, 371–2 substance abuse 292–3, 326–7, 371–2 teenage pregnancies 326 training programs 389, 425–40 traumas 162–4, 204–6, 207, 276–89, 291–8, 324–31 warmth factors 322 parietal cortex 72

612 Parkinson’s disease 229–30, 244 Partridge, G.E. 10, 15–16, 35 PASAT see Paced Auditory Serial Attention Task past history, violence risks 127, 525–6 pathological synergy, comorbid disorders 3 PATHS see Promoting Alternative Thinking Strategies patient-focused interventions, CD 417, 425, 431–40 Pavlovian/instrumental conditioning, cognitive correlates 107–9, 579 PCC see posterior cingulate cortex PCL-R see Psychopathy Checklist-Revised PCL:SV see Psychopathy Checklist: Screening Version PCL:YV see Psychopathy Checklist: Youth Version PCP see phencyclidine PCR see polymerase chain reaction Peabody Picture Vocabulary Test 311–12 pedophiles 262–4, 276–89, 294–8, 323–4, 486–9 see also paraphilias; sexual offenders comorbid disorders 262–4, 282–3, 486–9 homicide 263–4, 287–9 psychopathic disorders 262–4 recidivism tendencies 279–89, 486–8 peer affiliations children 292–3, 307, 327–31, 367–8, 373–4 educational issues 367–8, 373–4 rejections 327–8, 373–4 pemoline ADHD treatment 383–6 adverse effects 386 penal laws see also criminal justice system neuroscience 180–2 PEP see pre-ejection period perception processes concepts 93–4, 103–13 emotions 93–4 personality 20, 24–5, 37, 203–4 alcohol consumption 533–4 body types 10, 20 dimensional models 24–5, 37 Personality Assessment Inventory 247 personality disorders 1–5, 9–30, 34–8, 83–6, 87, 117–32, 136, 150–64, 172, 275–6, 348–61, 456, 497–514, 575–8 see also individual disorders conceptual development 1–5, 9–30, 40–3, 83–6, 172, 275–6, 450–3 country comparisons 575–8 domestic violence 497–514 DSPD 456

INDEX gender issues 348–61 milestones in history 9–21 paraphilias 275–6 psychopathic disorders 26–7, 87, 172 psychosis 22–6, 37, 119–21, 128 sociological aspects 10, 16, 17, 19–20, 21–2, 34–8, 351–2 standardization of nomenclature 24–6, 172, 251–2 statistics 201–2, 257–9, 262–4, 266–8, 282–3, 349–50, 419–20, 451, 468, 532, 562–3, 573–4 violence 117–32 workplace violence 520–1 personality traits, gender issues 349–50 PET see positron emission tomography Petermann, Franz 367–78 PFC see prefrontal cortex pharmacotherapy 4, 118, 382–92, 397–411, 482–9, 537–8 ADHD 382–92 aggression 4, 118, 181, 397–411, 482–4, 537–8 alcohol/substance abuse 537–8 concepts 4, 118, 382–92, 397–411, 482–9, 537–8 double-blind placebo-controlled trials 397–411 outpatient treatment 482–9, 537–8 sexual offenders 288–9, 482, 484, 487–8 phencyclidine (PCP) 122–3, 127, 535 phenytoin, aggression 401–2, 409–11, 482 Philippines, CP 309 philosophical aspects of treatment, domestic violence 509 philosophy 11–12, 509 Pick’s disease 244 Pinel, P. 10–11, 13, 18, 450 Pittsburgh Youth Study 325–9 pituitary dysfunction, brain trauma 227 planning 72–8, 84–5, 88–93, 110–12, 150–64, 193 see also executive functions PLC-R see Psychopathy Checklist-Revised pleasure–pain orientations, personality dimension 24, 37–8 PMT see parent management training political issues 33–8, 557–70 polymerase chain reaction (PCR) 222–4 polymorphic degeneration see also genetics concepts 12–13, 22–3 Porteus maze task 111–12 Portland Digit Recognition Test 246 Portugal CP 313

INDEX legal terminology 576–7 PCL-R 48 positive parenting programs 425–8 positron emission tomography (PET) 69–76, 175–6, 246, 398–9, 472–3 post-traumatic stress disorder (PTSD) 157, 181–2, 218–31, 244–5, 262, 265–7, 294–5 see also brain trauma; psychotrauma APD 262 causes 220–2 children 265–7, 294–5 combat 220–1, 262 comorbid disorders 220–1, 230, 262, 265–7 concepts 220–31, 244–5, 265–7, 294–5 consequences 228–31, 244–5 depression 221, 228–31 diagnosis criteria 224 disasters 220–31 DSM-IV criteria 224 epidemiology 220–1, 262, 265–7 gender issues 220–1 interpersonal violence 220–31 life-threatening events 220–31 molecular pathogenesis 227–8 occupational/social functioning 230–1 rape 220–2 remission 221 sexual molestation 220–2 socioeconomic costs 230–1 treatment 227–8 posterior cingulate cortex (PCC) 74, 77–8 postnatal risk factors, ADHD/APD 205–7 poverty 129 power dynamic bullying 523 domestic violence 500–1 PPI-R see Psychopathic Personality Inventory practice effects, psychological test instruments 246–8 pre-ejection period (PEP) 87–8 predator part-object 41, 53–8, 339–43 predatory behavior 41, 53–8, 339–43 predictions early predictors 17, 35–8, 151, 154–5, 189, 210–11, 265–7, 291–8, 319–31, 342–3, 560, 562–4, 583 PCL-R predictions 37, 42–59, 137–43, 319–31, 357–61, 468–71, 560, 562–5, 583 prefrontal cortex (PFC) 69–78, 91–5, 108–12, 159, 162–4, 173–5, 179–82, 189, 194–6, 208–11, 237–48, 264–5, 297–8, 383, 398–9, 579–81 see also autonomic responses

613 acquired psychopathy 237–48, 264–5 concepts 69–78, 91–5, 108–12, 159, 162–4, 173–5, 179–82, 189, 194–6, 208–11, 237–48, 297–8, 398–9, 579–81 functional domains 240 late-maturity effects 195 preinjury mental abilities, brain trauma 246–7 premeditated aggression 193, 398–411 see also aggression prenatal/postnatal risk factors, ADHD/APD 205–7, 210, 535 preoedipal theory 341–3 presence of violent ideation, risk assessments 126 pretreatment assessments, domestic violence 505–7, 513 prey–predator dynamic 41, 53–8, 339–43, 460–1 Prichard, J.C. 10, 13–14, 18, 573 prison dilemma 180 prisoners see also correctional programs APD 1–2, 35, 255–6, 257–9 benefits of imprisonment 567–70, 581–3 comorbid disorders 255–69 critique 557–70, 574–83 females 357–61 hospitals 4–5, 557–70, 582–3 imprisoned parents 293, 325–6, 328–31 lifetime detention 557–8, 560–70, 582–3 politics 558–70 psychopathic disorders 1–2, 35, 37, 53–9, 135–43, 150, 255–9, 281, 449–63, 467, 557–70, 574–83 substance abuse 3–4, 257–9, 360 treatment 4–5, 140–3, 449–63, 557–70 Problem Solving Communication Training (PSCT) 428 Problem-Solving Skills Training (PSST) 435 profit from experience 14–15, 17, 36–8, 77–8, 84–5, 93–5, 107–9, 174–6, 194, 281, 319–31, 337–43, 369, 559–60, 578–9, 582–3 progressive degeneration, concepts 12–13 projections 461 promiscuity 41, 47–58 see also sexual relationships Promoting Alternative Thinking Strategies (PATHS) 428–9 propranolol 228, 484 provocation issues, workplace violence 525–6 PSCT see Problem Solving Communication Training pseudopsychopathic features 239 PSST see Problem-Solving Skills Training

614 psychiatric assessments 2, 33–40, 152–3, 557–70 APD 33–8 complexity factors 34, 458–9 concepts 33–40 violence 117–32 psychiatric concepts 2, 9–10, 22–4 psychiatric disorders, genetics 152–3 psychiatrists benign narcissists 475–6 short-term risk of violence 124–32, 475–7 psychoactive substances see also alcohol; substance abuse effects 121–3, 126, 161, 535–8 violence 121–3, 126, 127, 535–8 psychoanalytic view affects 342–3, 456–8 aggression 343, 457–8 anxiety levels 337–43, 457–8 attachment concepts 336–43, 457 concepts 335–43, 456–8 dismissive individuals 336–43, 457–8 grandiose self 340–1, 457–8 internalization failures 338–43, 456–8 low arousal 336, 337–43 object relations 336–43 omnipotent fantasy 340 psychopathic disorders 15–16, 23–4, 335–43, 456–8 superego 16, 339–43, 479–80 psychological assessments 2, 34–8, 41–59, 246–8 concepts 41–59 instruments 41–59 psychopathic disorders 2, 34–8, 41–59 test instruments 246–8 psychologists benign narcissists 475–6 short-term risk of violence 124–32, 460, 475–7 psychopathic disorders 1–5, 9–30, 33–40, 41–67, 69–78, 83–95, 103–13, 135–6, 149–64, 200–1, 237–48, 291–8, 319–31, 335–43, 347–61, 531–8, 557–70 abusive tendencies 2, 4 acquired psychopathy 69, 73–4, 111, 237–48, 264–5 ADHD 3–4, 106, 149, 157–8, 190, 199–211, 265–7, 370–1 age factors 35, 150–1, 153–5, 164, 205 alcohol/substance abuse 531–8 Anglo-American concepts 9–10, 13–18, 21–2, 24–5, 26–7, 41–2, 172, 450–3, 573–4 APD overlap 49–50, 83–95, 110–12, 150–1, 172, 251–69, 281, 451, 459, 468, 573–4

INDEX assessments 2, 23, 33–8, 41–59, 69–78, 83–95, 103–13, 172–3, 237–8, 245–8, 319–31, 348–61, 471–82, 531–8, 557–70, 573–4 body types 10, 20 brain imaging research 2, 69–78, 89–95, 105–13, 162–4, 173–82, 398–9, 472–3, 579–80 brain trauma 69, 71–2, 73–8, 105–12, 120–1, 123, 176–82, 194–5, 229–31, 237–48, 398–9 children 17, 19, 23–6, 37–8, 42–3, 50–2, 84, 135–6, 143, 149–64, 188–90, 196, 200–3, 251–2, 265–9, 291–8, 303–14, 319–31, 342–3, 347–61, 367–75, 583 cognitive correlates 103–13, 175–6, 207–10 cognitive/emotional processing defects 42–3, 71–8, 103–13, 175–6, 207–10 community treatment 4, 180, 467–89, 543–55, 557–70, 580–3 comorbid disorders 3–4, 36–8, 48, 117–32, 149, 157–64, 203–4, 209–11, 251–69, 453–5, 471, 484–6, 531–8, 580–1 conceptual history 2, 9–30, 41–3, 83–6, 135–6, 150–1, 172–3, 276, 281, 450–3, 558–60, 573–4 constitutions 10, 12, 14–15, 18, 19 costs 1–2, 4, 22, 43, 117–32, 135–6, 331, 343, 455–6, 557–70, 573–83 country comparisons 575–8 CP 305–14, 321–31, 372 criminal justice system 3, 41–59, 95, 135–43, 502–5, 508–9, 514, 557–70, 574–83 criminality 1–2, 4, 14, 17, 19, 26–7, 37–8, 41–59, 86–95, 135–43, 150–64, 172, 180–2, 202, 253–4, 255–6, 265, 283–9, 319–31, 454–63, 468–71, 474–5, 477, 557–83 criteria 17–21, 35–8, 41–58, 84–95, 103, 118, 135–6, 142, 150–1, 172, 237–8, 251–2, 268, 276, 281, 291, 319–31, 335, 353–61, 468–71, 562–3, 573–4 cultural issues 48, 139–40, 351–2 definitions 2, 14, 17, 41–59, 103, 135–6, 149–51, 171–3, 200–1, 237–8, 251–2, 268, 276, 281, 291, 335, 368, 450–1, 566, 573–8 degenerates 10, 11–13, 19, 21, 22–3, 34 denial of treatment 140–3, 557–70 differentiation scheme 26–7 dimensional approach 2, 399–400 dissocial personality disorders overlap 14, 16, 18, 49–50, 84–95, 172, 281, 451, 468 dominance-submission paradigm 339–43 early predictors 17, 35–8, 42–3, 53–8, 151, 154–5, 188, 189, 210–11, 265–7, 291–8, 319–31, 342–3, 560, 562–4, 583

INDEX educational issues 3, 11, 328, 367–75 electrophysiology 3, 187–96 emotions 4, 10–11, 13, 17, 21, 22, 35–8, 42–3, 53–9, 69–78, 84–5, 93–5, 103–13, 142, 172–6, 194, 240–8, 281, 294–8, 319–31, 335, 456–7 environmental issues 3, 42–3, 107–8, 129, 150, 152–5, 158–64, 193, 196, 204–5, 251–2, 267–8, 291–8, 338–40, 461–2, 481 etiology 2–3, 11–18, 34–8, 42–3, 117–32, 149–64, 203–11, 237–48, 251–69, 298, 319–31, 335–43, 484–6, 579–80 experiential issues 3, 42–3, 458, 459–63, 543–55 factor structure 37, 44–5, 47–8, 50–2, 71–2, 84–5, 103–7, 172–4, 285–8, 319–31, 354–61, 451, 468–89 families 3, 42–3, 155–64, 204–6, 291–8, 321–31, 338–9, 371–2 features 14, 17–21, 35–8, 41–58, 84–95, 103, 118, 135–6, 142, 150–1, 172–3, 237–8, 251–2, 268, 276, 281, 291, 319–31, 353–61, 468–71, 476–7, 562–3 females 3, 35–6, 150–1, 155–6, 162–3, 347–61, 459 forensic concepts 42–59, 357–61, 449–63, 557–70 French concepts 9–13, 18, 21–3, 576–7 gender issues 3, 35–6, 42–3, 47–8, 103–4, 150–1, 153, 155–7, 162–4, 188, 201–3, 205–6, 257–9, 260–1, 347–61, 459, 462 genetics 2–3, 11, 12, 18–19, 22–3, 34–8, 42–3, 149–64, 173, 193, 204–6, 210–11, 251–2, 267–8, 297–8, 579–80 German concepts 9–10, 12, 18–23, 34–5, 48, 54–5, 172, 576–7 good home backgrounds 338 gray matter volumes 71–2, 73–8, 177–9, 195, 208–10, 350, 398–9 history 2, 9–30, 41–3, 83–6, 135–6, 150–1, 172–3, 276, 281, 450–3, 558–60, 573–4 HR 91–3, 106, 188–96, 210–11, 337–8 idiopathic/symptomatic forms 16, 17–18 infantile psychological development 15–16, 23–4 integrated approaches 3 intelligence levels 103–4, 207–8, 328–31, 367–8, 371, 473–5, 478 intraspecies predators 53, 339–43, 460 labels 142–3 learning 14–15, 17, 36–8, 71, 77–8, 84–5, 93–5, 104–13, 174–6, 194, 241–2, 267–8, 281, 319–31, 369–70, 559–60, 578–9, 582–3 levels 477–82, 583

615 lifetime detention 557–8, 560–70, 582–3 milestones in history 9–21, 41–2 neurobiologies 159–64, 171–82, 203–11, 338–9, 397–411, 574, 579–83 neuroimaging perspectives 3, 69–78, 87, 171–82, 335, 472–3, 579–80 neurophysiological defects 3, 12, 42–3, 173, 207–11 neurosis contrasts 15, 17–18, 22 origins 2–3 outpatient treatment 4, 467–89, 557–70, 580–3 paraphilias 4, 262–4, 275, 282–9, 486–9 pedophiles 262–4, 276–89, 323–4, 486–9 personality disorders 26–7, 87, 172 pharmacotherapy 4, 118, 397–411, 482–9 politics 558–70 prey–predator dynamic 41, 53–8, 339–43, 460–1 primary features 14, 36–8, 89, 579 prisoners 1–2, 35, 37, 53–9, 135–43, 150, 255–9, 281, 449–63, 467, 557–70, 574–83 psychiatric assessments 2, 33–40 psychoanalytic view 15–16, 23–4, 335–43, 456–8 psychological assessments 2, 34–8, 41–59 psychopathology 451–2 psychophysiological correlates 83–95, 105–13, 158, 196, 210–11 psychosis 14, 17, 20–1, 22–6, 35–8, 55, 119–21, 128, 252–7 psychotherapy 4–5, 181–2, 449–63, 467–89, 565–70 public policies 1–2, 5, 557–70, 575–83 recidivism tendencies 1–2, 4, 14, 37–8, 41–59, 135–43, 255–6, 265, 281–9, 454–63, 468–71, 474–5, 477, 486–9, 558–70, 573–83 risk assessments 2, 33–4, 48, 53–8, 117, 124–32, 135–43, 319–31, 347–61, 421–3, 473–5, 557–70, 578–83 risks of diagnosis 2, 33–4, 117, 129–32, 135–43, 252, 352–3, 458–61 SCR 87–8, 106–9, 188–96, 210–11, 337–43 secondary features 14, 36–8, 89 semantic dementia 10, 17 social aspects 1–2, 5, 19–20, 21–2, 34–8, 42–3, 104–5, 179–82, 240–8, 291–8, 319–31, 351–2, 557–70, 573–83 social policies 1–2, 5, 557–70, 573–83 social-judgement concepts 19–20 sociopathy 10, 16, 17, 34, 35, 86, 111–12 standardization of nomenclature 24–6, 135, 142–3, 172, 251–2 strengths 476–7 taxonomical approach 2, 34, 42–3

616 psychopathic disorders (Cont.) treatability concerns 3, 449–63, 468–71, 477, 535–6, 558–70, 574–83 treatment 3–5, 33–8, 57–9, 140–3, 268–9, 397–411, 449–63, 557–70, 573–83 ‘treatment causes harm’ hypothesis 563–70, 578–9 value-free judgments 20–1, 22 victims 117–32, 135–6, 343, 497–514, 522–3, 525–7, 557–70 violence 2, 4, 35–8, 41, 43–59, 69–78, 103–5, 117–32, 137–43, 150–64, 252–9, 267–8, 343 word tests 106–7, 110–11 workplace violence 4, 119, 129–30, 257–9, 519–28 psychopathic inferiorities, concepts 18, 21 psychopathic personalities, concepts 19–21, 23–4, 471–2 Psychopathic Personality Inventory (PPI-R) 471–2 psychopathic states, concepts 10, 14 psychopathology, psychopathic disorders 451–2 Psychopathy Checklist: Screening Version (PCL:SV) 43, 48, 50–2, 55–6, 320–31, 347–61 Psychopathy Checklist: Youth Version (PCL:YV) 43, 50–2, 295–7, 348–60 Psychopathy Checklist-Revised (PCL-R) 37–59, 71–2, 84–5, 103–6, 135–43, 171–5, 237–8, 240, 255, 263–4, 276, 281–9, 295–7, 319–31, 335, 338, 347–61, 450–1, 468–81, 523–4, 562–3, 573–4, 583 administration 44–5 assessment structure 44–5, 47–8, 106, 135–43, 354–61, 468–81, 583 background 37–8, 42–59, 71–2, 84–5, 135–43, 171–5, 237–8, 240, 276, 281–9, 295–7, 319–31, 335, 347–61, 450–1, 468–81, 523–4, 562–3, 573–4, 583 civil psychiatric patients 55, 84 collateral information 45, 50–2 country comparisons 46–7, 48, 54–6, 137–43 criminality 53–9, 86–8, 135–43, 172, 255, 263–4, 319–31, 450–1, 468–71, 560 critique 37, 43–4, 45–6, 48–52, 56–9, 84–8, 135–43, 171–5, 276, 281, 353–61, 523–4, 562–3, 583 cultural aspects 139–40 cut scores 46, 140, 172, 468–71, 477–82, 563–5, 583 death penalty 139, 143, 358 derivative measures 50–3 DSM-IV 49–50, 84–8, 281

INDEX factor structure 37, 44–5, 47–8, 50–2, 71–2, 84–5, 103–7, 172–4, 285–8, 319–31, 335, 354–61, 451, 468–89 females 353–61 gender issues 347–61 generalizability issues 48, 59, 84–5 gray matter volumes 71–2 group results 137–9 historical background 43–4, 276, 281, 573–4 ICD-10 49–50, 84–8 institutional problems 56, 140–3 interclass correlation (ICC) 45–6 intercultural aspects 139–40 interviews 44–5, 50–2 IRT analysis 46–8, 356 items 37, 44–5, 171–5, 319–31, 335, 355–61, 468–73, 477–89 legal and forensic practice 136–43, 357–61, 583 misuse issues 45, 135–43 other measures 48–53 paraphilias 281–9 predictive potency 37, 42–59, 137–43, 357–61, 468–71, 474–5, 560, 562–4, 583 reliability issues 45–6, 135–43, 281, 458–9, 560, 562–5 risk assessments 48, 53–8, 135–43, 319–31, 474–81, 523–4, 560, 583 risks of diagnosis 135–43 ROC analyses 54–5 Second Edition 43, 45 self-report measures 48–9, 52–3 sensitivity to change 142–3 sexual violence 54, 56–8 treatment 57–9, 140–3, 468–71, 474–81, 583 validity issues 48, 135–43 Psychopathy Screening Device 84 psychopharmacological agents 4, 118, 181–2, 211, 228, 288–9, 381–92, 397–411, 467–89 see also pharmacotherapy ADHD 211 brain activation patterns 181–2 critique 181–2, 288–9, 482–4 emotions 4, 118, 181 psychotrauma 228 violence 4, 118, 181, 397–411, 482–4 psychophysiological correlates 83–95, 105–13, 158, 187, 196, 210–11, 382 ADHD 210–11, 382 callousness 93–5 CD 210–11 concepts 83–95, 105–13, 158, 187, 196, 210–11 emotions 93–5, 105–13 impulsivity 88–93, 112, 267, 533–4 narcissism 87–8

INDEX prevention implications 196 psychopathic disorders 83–95, 105–13, 158, 196, 210–11 sensation-seeking behavior 88–93, 192–6, 337–8, 349–50, 533–4 psychosis 14, 17, 20–1, 22–6, 35–8, 55, 119–21, 128, 129–31, 252–7, 399 see also schizophrenia antipsychotics 405–7, 409–11 definition 128 depression 121 noncompliance with treatment 129 personality disorders 22–6, 37, 119–21, 128 psychopathic disorders 14, 17, 20–1, 22–6, 35–8, 55, 119–21, 128, 252–7 violence 119–21, 128, 219–31, 252–7, 399 psychotherapy 4–5, 181–2, 228, 449–64, 467–89, 565–70, 574–83 duration considerations 470, 477–82 early therapeutic treatment studies 452–3 institutional problems 461–2, 583 problems 458–64, 565–70 psychopathic disorders 4–5, 181–2, 449–63, 467–89, 565–70 psychotrauma 228 recent therapeutic treatment studies 453–6 recommendations 462–3, 569–70 trained staff 461–2, 475–7 ‘treatment causes harm’ hypothesis 563–70, 578–9 psychoticism, concepts 24–5 psychotrauma see also brain trauma; post-traumatic stress disorder amygdala 227–8 concepts 217–31 consequences 228–31 definition 217 hippocampus 227–8 molecular pathogenesis 227–8 psychopharmacological agents 228 psychotherapy 228 risk factors 218–21 treatment 227–8 PTSD see post-traumatic stress disorder public announcements, sexual offenders 481 public policies 1–2, 5, 557–70, 575–83 punishment 77–8, 107–9, 139, 174–6, 194, 303–14, 321–31, 337–43, 389, 557–70, 574–83 see also corporal punishment; learning from experience; prisoners benefits of imprisonment 567–70, 581–3 death penalty 139, 143, 358, 575 lifetime detention 557–8, 560–70, 582–3 mild punishment 389

617 retributive theories 566, 581–3 treatment 557–70, 574–83 utilitarian theories 566, 581–3 pyknic body types 20 qualified detoxification programs, alcohol/substance abuse 537–8 qualitative/quantitative differences, gender issues 156 questionnaires 36–7 racism, paranoid personality disorder 118–19 Raine, Adrian 38, 69–81, 176–7, 187–9, 190, 193–6, 337 randomized control trials (RCTs) 454 rape 220–2, 262–3, 282, 286–9, 486–8 see also sexual offenders paraphilias 282, 286–9, 486–8 Ray, I. 15 RCTs see randomized control trials reaction times (RT), ADHD treatment 391 reading problems 207–8, 247 real-time fMRT, treatment 181–2 reasoning, moral reasoning 74–8, 173–5, 179–82, 242 receiver operating characteristic (ROC) 54–5 recidivism tendencies domestic violence 503–5, 512, 514 paraphilias 279–89, 486–8, 562–5, 579 psychopathic disorders 1–2, 4, 14, 37–8, 41–59, 135–43, 255–6, 265, 281–9, 454–63, 468–71, 474–5, 477, 486–9, 558–70, 573–83 sexual offenders 279–89, 486–8, 562–5, 579 recklessness 35–8 recognition abilities, emotions 105–13, 192–3, 456–7 reformulated model, social information processing 432–3 rehabilitation purpose, criminal justice system 3, 4, 142–3, 557–70, 574–83 Reich, W. 15 Reid, William H. 4, 543–55 relapse-prevention programs 58, 455–6, 478–81, 486–9, 537–8, 557–70 relaxation training, domestic violence 511, 514 reliability, PCL-R 45–6, 135–43, 281, 458–9, 560, 562–5 religion 11–12, 340 remorse 14, 17, 35–8, 41–3, 44, 47–58, 78, 84–5, 93–5, 118, 128, 135–6, 150–64, 172, 281, 319–31, 337–43, 460, 573–4 see also guilt repetitive transcranial magnetic stimulation (rTMS) 182 residential and activity programs 4

618 resources, emotions 175–6 responses brain trauma 221–3, 244–5 emotional responding 71, 105–13, 174–6, 456–7, 579–80 HR 188, 210–11, 337–8 modulation 110–12, 175–6, 181–2, 195, 369 resting heart rate 91–3, 106, 188–96, 210–11, 337–8 see also heart rate retributive theories, punishment 566, 581–3 retrospective studies 319–20 revenge 118 revocation conditional release 44–58 reward-dependence personality dimension 24, 37–8 rewards aggression 107 BAS 37–8, 107–9 learning stimulus–response/reward associations 71, 107–9, 174–5, 369–70, 578–9 Rey 15-item Figure Memory Test 246 Rice, M.E. 140–1, 454, 559 right superior temporal gyrus 176–82 rights of other people 4, 41, 43, 150–1, 269, 451–2, 455–6, 506, 562–70 risk assessments 2, 33–4, 48, 53–8, 117, 124–32, 135–43, 206–7, 210, 319–31, 347–61, 421–3, 473–81, 523–4, 532–4, 557–70, 578–83 alcohol 206–7, 210, 532–4 appearance of the patient 126 auditory hallucinations 128 available means 126–7 demographic characteristics 129, 328 discharge planning 130–1 females 347–61 history 127, 505–6, 525–6 hospitals 128, 129–32, 488–9, 536–7, 557–70, 582–3 intent 126, 560 lawsuits against clinicians 117, 129–32 noncompliance with treatment 129 outpatient treatment 473–5, 557–70 PCL-R 48, 53–8, 135–43, 319–31, 474–81, 523–4, 560, 583 presence of violent ideation 126 psychopathic disorders 2, 33–4, 48, 53–8, 117, 124–32, 135–43, 319–31, 347–61, 473–5, 557–70, 578–83 sexual offenders 54–5, 474–5 violence 117, 124–32, 137–43, 252–9, 319–31, 357–61, 473–5, 560–70, 578–83 workplace violence 520–4 written evidence 131–2

INDEX risk factors, brain trauma 217–21 risk/needs/responsivity treatment principles 58, 458–9 risks of diagnosis PCL-R 135–43 psychopathic disorders 2, 33–4, 117, 129–32, 135–43, 252, 352–3, 458–61 risky decisions, cognitive correlates 111–13, 175, 242–3 risperidone see also antipsychotics aggression 406, 409–11, 482 Robins, L.N. 17, 25–6 ROC see receiver operating characteristic Rochester Youth Development Study 328 Romania 312 RT see reaction times rTMS see repetitive transcranial magnetic stimulation rules 41–3, 72–3, 85–95, 103, 135–6, 150–64, 200–11, 369, 373–4, 460–1, 513 see also legal . . . Rush, B. 10, 15, 18 Russia, PCL-R 48 SaB, Henning 1–5, 9–30, 34 sadism 263–4, 276–89, 341–2, 471, 486–8 sadistic personality disorder 263–4, 471 sadness 105–13, 179–80 see also emotions emotion recognition 105–7 St Louis survey 325 Salekin, R.T. 355–6, 361, 453, 458, 470 Salize, Hans Joachim 573–85 Sarkar, Sameer P. 4, 449–66 schizoid personality disorder 20, 23, 190, 255, 295–6, 351 schizophrenia 10, 20, 23, 35–6, 55, 119–20, 128, 129–30, 151, 153, 204–6, 220, 229–30, 251–7, 259–64, 474, 484, 536, 575–8 see also psychosis akathisia 119–20 alcohol 253–4, 259–61, 536 APD 251–7 brain trauma 220, 229–30 children 254, 267 comorbid disorders 251–7, 259–64, 536 concepts 119–20, 128, 251–7, 259–64 criminality 252–7, 575–8 definition 128 delusions 119–20, 128, 129–31, 253–7 genetics 153, 267 hallucinations 119–20, 128 noncompliance with treatment 129 sexual disturbances 262–3

INDEX substance abuse 253–4, 259–61, 536 violence 119–20, 128, 129–30, 252–7, 262–3, 267 Schneider, K. 10, 19, 20–1, 22–3, 34, 559–60 School Transitional Environmental Program (STEP) 430 schools 328, 367–75, 417, 428–40 see also educational issues ADHD 381–92 aggression 367–75 CD interventions 417, 428–40 comorbid ADHD 367–8, 370–1 disruptive aggressive students 367–8 family background 367–8, 371–2 intelligence levels 367–8, 371 interventions 375 learning problems 367–8, 369–70 peer affiliations 367–8, 373–4 teachers 367–75 SCID-II 471–3 SCR see skin conductance response screening questionnaires 36–7 Seattle Social Development Project (SSDP) 430 SEC see structured-event complex Secret Service, US 524–7 self-assertive psychopaths 21 self-control 110–12, 368–75, 388–9, 582–3 see also behavioral controls; executive functions self-esteem 118, 368, 475–9 self–other orientations, personality dimension 24 self-report measures, concepts 48–9, 52–3 self-structures, grandiose self 340–3 selfishness 36–8, 204–5, 559–60 SEM see standard error of measurement semantic dementia, concepts 10, 17 semantic mismatch 113, 179–80 semi-structured interviews 36–7, 44–5, 50–2, 240 sensation-seeking behavior 24, 38, 41, 44, 47–58, 88–95, 192–6, 337–8, 349–50, 482, 533–4, 579 see also impulsivity; novelty-seeking . . . concepts 88–95, 337–8, 349–50, 482, 579 EEG 89–93, 192–6, 337–8 ERP 90–1, 192–3 psychophysiological correlates 88–93, 192–6, 337–8, 349–50, 533–4 sensitivity to change, PCL-R critique 142–3 septal nuclei 179–80 septohippocampal system 107–8 serotonin genetics 159–61, 181–2, 205–6, 397–411, 421 paraphilias 288–9

619 SSRIs 159, 181, 288–9, 404–5, 409, 482–4, 487–8 stress resiliency 159–64, 205–6 sertraline 482 Sevecke, Kathrin 291–302 Sex Offender Risk Appraisal Guide (SORAG) 54–5, 473–5 sexism, paranoid personality disorder 118–19 sexual abuse 54, 56–8, 141, 162, 191–2, 220–2, 229, 262–4, 275–89, 293–8, 323–31, 438–9, 454–5, 470–5, 478–81, 484, 486–9, 562–5, 579 sexual deviations 4, 25, 56–8, 141, 180, 262–4, 275–89, 323–31, 474–5 see also paraphilias sexual masochism 276–89 see also paraphilias sexual molestation 220–2, 262–4, 276–89, 294–5 see also paraphilias; pedophiles sexual offenders 54, 56–8, 141, 191–2, 220–1, 229, 262–4, 275–89, 323–31, 438–9, 454–5, 470–5, 478–81, 484, 486–9, 562–5, 579 see also paraphilias antiandrogen medications 484, 487–8 APD 262–4 comorbid disorders 262–4, 282–3, 471, 486–9 concepts 282–9, 323–4, 438–9, 454–5, 470–5, 478–81, 486–9, 579 CPA 487–8 electronic monitoring 481 homicide 263–4, 287–9 LHRHs 487–8 MPA 487–8 MST 438–9 outpatient treatment 470–5, 478–81, 484, 486–9 pharmacotherapy 288–9, 482, 484, 487–8 public announcements 481 recidivism tendencies 279–89, 486–8, 562–5, 579 risk assessments 54–5, 474–5 SSRIs 288–9, 482, 487–8 statistics 262–4, 323–4, 562–3 surgical castration 487–8 treatment 288–9, 438–9, 454–5, 470–5, 478–81, 484, 486–9 unreported offences 284 sexual paraphilias see paraphilias sexual relationships 17, 23–5, 47–58, 179–80, 269 sexual sadism 263–4, 276–89, 486–8 see also paraphilias

620 sexual violence 54, 56–8, 141, 220–1, 229, 263–4, 276–89, 293–5, 323–4, 472–3, 486–9 see also sexual abuse Sexual Violence Risk-20 (SVR-20) 54, 473, 474–5 sexually transmitted diseases 124, 269, 471 Sexually Violent Predator Acts 135–6 shallow affect 44, 47–58, 73–8, 84–5, 93–5, 103, 135–6, 172, 297–8, 319–31, 579 shame 17, 281, 460, 573–4 see also remorse Shiva, Andrew 335–46 Simon paradigm 176 single photon emission computerized tomography (SPECT) 69–76, 93–4, 181–2, 246, 472–3 single-parent families 324–31 Sir´en, Anna-Leena 217–36 skin conductance response (SCR) 87–8, 106–9, 188–96, 210–11, 337–43 see also electrodermal activity CD 189–90, 210–11, 337–8 concepts 87–8, 106–9, 188–96, 210–11, 337 smoking, prenatal/postnatal risk factors 206–7, 210, 326–7 social aspects brain trauma 219–21, 240–8 Cambridge Study in Delinquent Development 320–31 concepts 1–2, 5, 240–8, 319–31, 557–70, 573–83 lifetime detention 557–8, 560–70, 582–3 longitudinal surveys 319–31 Nottingham survey 322 psychopathic disorders 1–2, 5, 19–20, 21–2, 34–8, 42–3, 104–5, 179–82, 240–8, 291–8, 319–31, 351–2, 557–70, 573–83 social distress cues 104–5, 456–7 social impediments, treatment 557–70 social information processing CD 422, 427, 431–40 reformulated model 432–3 social knowledge, brain trauma 240–8 social misconduct 33–4 social policies 1–2, 5, 557–70, 573–83 compulsory outpatient treatment 580–3 concepts 573–83 country comparisons 575–8 interventions 573–83 legal regulations 574–8 neurobiologies 579–83 special facilities 583 treatment outcome studies 578–9 social skills 422, 431–40, 537–8

INDEX social workers, short-term risk of violence 124–32 social-judgement concepts, psychopathic disorders 19–20 society costs 1–2, 4, 22, 43, 117–32, 135–6, 331, 343, 455–6, 557–70, 573–83 lifetime detention 557–8, 560–70, 582–3 rights of other people 4, 41, 43, 150–1, 269, 451–2, 455–6, 506, 562–70 workplace violence 522 sociocultural determinants, mental disorders 351–2 socioeconomic characteristics brain damage 219–21 families 291–8, 326–31, 371–2 violence risks 129, 150, 326–31 socioeconomic costs, brain trauma 219–21, 230–1 sociological aspects, personality disorders 10, 16, 17, 19–20, 21–2, 34–8, 351–2 sociopathy see also antisocial personality disorder acquired sociopaths 73–4, 111, 242–3, 533 alcohol 533 concepts 10, 16, 17, 26, 34, 35, 86, 111–12, 367–75, 533 definition 16 psychopathic disorders 10, 16, 17, 34, 35, 86, 111–12 sociotherapeutic interventions 467–89 somatic diseases 471–5 somatic markers 34, 111–13, 240–2 see also autonomic . . . cognitive correlates 111–13, 240–2 somatization 461 SONAR 475 see also sexual offenders SORAG see Sex Offender Risk Appraisal Guide Spain legal terminology 576–7 PCL-R 48 spanking 303–5, 306–14 see also discipline spatial ability 77–8, 244 SPECT see single photon emission computerized tomography spoken words, emotions 106–7 sports, neurotrauma 222 SSDP see Seattle Social Development Project SSRIs 159, 181, 288–9, 404–5, 409, 482–4, 487–8 see also antidepressants effects 159, 181, 288–9, 482–4, 487–8 OFC 181 paraphilias 288–9, 482, 487–8

INDEX stalking behavior, workplace violence 522 standard error of measurement (SEM) 46 standardization of nomenclature, mental disorders 24–6, 135, 142–3, 172, 251–2 Stanford, Matthew S. 83–101 startle potentiation 94, 106–7, 174–5, 189–96, 579–80 states, traits 23 Static-99 473–5 see also sexual offenders Static-2002 473–5 STEP see School Transitional Environmental Program stimulants addictive potential 386 ADHD treatment 382–6, 388, 389–90, 392, 407, 411, 482–4, 537–8 adverse effects 385–6, 388 aggression 407, 537–8 treatment 382–6, 388, 389–90, 392, 407, 411, 482–4, 537–8 Stith et al 498 Stockholm study 327–8 Straus, Murray A. 303–17 strengths, psychopaths 476–7 stress exposure 162, 205–6, 227–8, 297–8, 575–8 see also post-traumatic stress disorder MAOA genotype 162, 205–6, 297–8 stress resiliency, serotonin 159–64, 205–6 Stroop test 110–11 structural–dynamic concept 23, 473–5 structural–social concepts 33–4 structured clinical assessments 36–7, 54–6, 471–5 Structured Clinical Interview for Mental Disorders II 36–7, 471–2 structured interviews 34, 36–7, 44–5, 50–2, 471–2 structured-event complex (SEC) 241–2 substance abuse 3–4, 35–8, 117–18, 120–3, 126, 127, 149, 157–8, 204, 251–2, 253–64, 267–9, 282–3, 298, 360, 371–2, 438–9, 484–6, 505–6, 514, 531–8, 575–8 see also addictions; alcohol affectiveness disorders 257–9, 267–8 APD 251–2, 253–4, 259–61, 267–9, 298, 484–6 behavioral therapy 536–8 borderline personality disorder 532, 536–8 children 265–7, 292–3, 371–2, 438–9 comorbid disorders 3–4, 35, 36–8, 117–18, 120–3, 126, 127, 149, 157–8, 253–69, 282–3, 298, 471, 484–6, 531–8

621 concepts 3–4, 35, 36–8, 117–18, 120–3, 126, 127, 149, 157–8, 253–69, 282–3, 298, 471, 484–6, 531–8 criminality 3–4, 253–4, 360, 534–5, 575–8 depression 257–9, 531–8 detoxification programs 537–8 domestic violence 505–6, 514 epidemiology 532 etiology 532–4 homicide 535 MST 438–9 outpatient treatment 484–6, 536–7 paranoid ideation 122 paraphilias 282–3 parents 292–3, 326–7, 371–2 pharmacotherapy 537–8 prisoners 3–4, 257–9, 360 schizophrenia 253–4, 259–61, 536 somatic diseases 471–5 statistics 257–61, 268–9, 531–5 suicide 157 treatment 438–9, 484–6, 531, 535–8 treatment phases 537–8 violence 117–18, 120–3, 126, 127, 253–4, 257–9, 260–1, 534–8 withdrawal 121–3, 126, 537–8 suicide 118, 121, 125, 128, 130–1, 149, 157, 159–61, 163–4, 228–9, 261–2, 307–14 anxiety 261 brain trauma 228–9 catecholamines 161 CP 307–14 dopamine 163–4 serotonin 159–61 substance abuse 157 superego 16, 339–43, 479–80 superficial charm 17, 42, 44–68, 84–8, 103, 172, 276, 281, 368, 453–5, 477–8, 573–4 superior temporal cortex 70, 74–8, 113, 176–9 surgical castration 487–8 surprise see also emotions emotion recognition 105–7 SVR-20 see Sexual Violence Risk-20 Swann, Alan C. 397–416 Sweden childhood comorbid disorders 266 CP 312–13 legal terminology 576–7 PCL-R 48, 55 prisoners 37 Switzerland 136, 296 symptomatic forms, psychopathic disorders 16, 17–18 syphilis 471

622 Tardiff, Kenneth 117–33 targets, treatment 477–82 taxonomical approach, psychopathic disorders 2, 34, 42–3 TC see therapeutic community teachers 367–75, 417, 428–40 see also schools CD interventions 417, 428–40 teenage pregnancies 326 telephone scatologia 277 see also paraphilias temperament, ADHD 203–4 templates, neuroimaging perspectives 173–4 temporal cortex 69–78, 93–5, 173–9, 180–2, 207–10, 229 temporal lobe abnormalities 74–8, 113, 180–2 Test of Memory Malingering 246 Test of Social Intelligence (TSI) 243 testosterone 163, 350, 421, 472–3, 484 Texan death row inmates 139 thalamus 75–8 theory of mind (mentalizing) 75, 104–5, 336–7, 349–50, 457–8 concepts 75, 104–5, 349–50, 457–8 eyes test 104 therapeutic community (TC) 452–3, 458 therapeutic relationships, outpatient treatment 475–7, 535–6 therapeutic wards 568–9 Thorne, Stephen A. 4, 543–55 threats 76–8, 104–13, 191–2, 457–8 three-factor models 24, 37, 84–8, 93–5, 103–7, 172–3, 319–31, 335, 354–61, 453–9, 468–73, 477–89 thyroid 472–3 tic syndromes 381, 385–6, 387–8 see also Tourette’s syndrome tinnitus 182 topiramate, aggression 403–4, 410–11 Tourette’s syndrome 381 see also tic syndromes TPH see tryptophan hydroxylase traffic accidents, neurotrauma 221–2, 225 training programs communication training interventions 428, 508–14 parents 389, 425–40 relaxation training 511, 514 social skills 537–8 staff 58, 461–3, 475–7 traits, states 23 Tranel, D. 241–3 transference concepts 338–43 transvestic fetishism 276–89 see also fetishism; paraphilias

INDEX traumas, children 23–4, 162–4, 204–6, 207, 276–89, 291–8, 324–31 treatability concerns, psychopathic disorders 3, 449–63, 468–71, 477, 535–6, 558–70, 574–83 treatment ACT 480 ADHD 4, 211, 381–92, 407, 482–4, 537–8 aggression 397–411, 433–40, 482–4 alcohol 484–6, 531, 535–8 algorithms 407–11, 482–3, 488 anticonvulsants 400–4, 407 antidepressants 382, 386–7, 404–5 antipsychotics 405–7, 409–11 anxiety 387–8, 390 approaches 1–2, 557–70, 579 behavioral therapy 388–90, 431–3, 536–8, 559–60 biofeedback approaches 181–2 brain trauma 227–8, 244 CBT 388–9, 431–3, 452–3, 456–8, 470, 479–80, 504–14 CD 417–40, 482 combined treatments 389–90 community treatment 4, 180, 467–89, 543–55, 557–70, 580–3 comorbidity implications 268–9, 471 compulsory outpatient treatment 580–3 country comparisons 575–8 critique 57–9, 140–3, 181–2, 268–9, 449–63, 467–89, 557–70, 574–83 dangers 454–5, 557–70 DBT 389, 479–80 denial of treatment 140–3, 557–70 depression 159, 181–2, 390, 404–6 dietary interventions 484 domestic violence 497–8, 502–14 dropout rates 141–2, 269, 505–6 duration considerations 470, 477–82 early therapeutic treatment studies 452–3 experiential treatment 458, 459–63, 543–55 family members 470 fMRT 181–2 group therapy 57–8, 461, 476–7, 486–8, 567 impediments 557–70 impulsivity 390–1, 397–411, 482–4, 579 institutional problems 461–2, 557–70, 583 knowledge-based problems 458–63 legal impediments 557–70 lifetime detention 557–8, 560–70, 582–3 long-term ADHD treatment 391–2 MBT 457–8 medical impediments 557–70 motivation enhancement measures 478–9 MST 436–9, 470–1, 536–7

INDEX multimodal treatment 381–2, 389–90, 417, 436–40, 520, 580 neuroimaging perspectives 181–2 noncompliance with treatment 129, 141–2 noradrenergic antagonists 405–6, 484 Oak Ridge Hospital 563 omega-6/omega-3 essential fatty acids 484 outcomes 269, 470, 511–12, 538, 559–70, 574–83 outpatient treatment 4, 467–89, 536–7, 557–70, 580–3 paraphilias 288–9 PCL-R 57–9, 140–3, 468–71, 474–81, 583 pharmacotherapy 4, 118, 382–92, 397–411, 482–9, 537–8 prisoners 4–5, 140–3, 449–63, 557–70 problems 458–63, 557–70 psychopathic disorders 3–5, 33–8, 57–9, 140–3, 268–9, 397–411, 449–63, 557–70, 573–83 psychopharmacological agents 4, 118, 181–2, 211, 288–9, 381–92, 397–411, 482–9 psychotherapy 4–5, 181–2, 449–63, 467–89, 565–70 public policies 1–2, 5, 557–70, 575–83 punishment 557–70, 574–83 real-time fMRT 181–2 reasons 451–2, 557–70, 579–83 recent therapeutic treatment studies 453–6 relapse-prevention programs 58, 455–6, 478–81, 486–9, 537–8, 557–70 rTMS 182 sexual offenders 288–9, 438–9, 454–5, 470–5, 478–81, 484, 486–9 social impediments 557–70 social policies 1–2, 5, 557–70, 573–83 stimulants 382–6, 388, 389–90, 392, 407, 411, 482–4, 537–8 substance abuse 438–9, 484–6, 531, 535–8 targets 477–82 TC 452–3, 458 trained staff 58, 461–3, 475–7 VRP 455–6, 458 workplace violence 519–28 ‘treatment causes harm’ hypothesis 563–70, 578–9 tricyclic antidepressants 386–7 Triple P Positive Parenting Program 427–8 trust issues children 294 clinicians 459–60 tryptophan hydroxylase (TPH) 160–4, 397–411 see also serotonin TSI see Test of Social Intelligence twin data, genetics 152–64, 193, 210–11 two-factor four-facet model 103–7, 354

623 Ukraine 312 ultimatum game 180 unitary psychosis, concepts 22–3 United Kingdom (UK) 46–7, 54–5, 136, 139–40, 305, 449–51, 456–7, 575–7 see also Anglo-American concepts; Great Britain BPP 429 CP 305 forensic psychiatry 449–50 legal terminology 575–7 PCL-R scores 46–7, 54–5, 139–40, 450, 451 United Nations Committee on the Rights of the Child 313 United States (US) 3–4, 24–6, 111, 135–6, 139–43, 150, 164, 201–2, 217–18, 230–1, 238–43, 251–69, 283–6, 305–31, 429, 449–51, 524–5, 575 see also Anglo-American concepts; North America BPP 429 brain trauma 217–18, 230–1 CP 305–14 death penalty 139–43, 575 domestic violence 497–514 forensic psychiatry 449–50 Secret Service 524–7 standardization of nomenclature 24–6 substance abuse 3–4 workplace violence 524–5 University of Iowa 111, 238–43 unreliability 17, 281 utilitarian theories, punishment 566, 581–3 validity issues, PCL-R 48, 135–43 valproic acid, aggression 402–3, 409, 482 value-free judgments, psychopathic disorders 20–1, 22 Van Goozen et al 192 variable number of tandem repeat (VNTR) 161–2, 204 ventral striatum 93–4, 180–2 ventrolateral prefrontal cortex (VLPFC) 70–8, 108–9, 111–12, 369 ventromedial prefrontal cortex (VMPFC) 70–8, 111–12, 175–9, 189, 237–48 acquired psychopathy 237–48 decision making 240–3 functions 240–2 gambling task 111, 243–4 somatic markers 111–13, 240–2 ventromedial space-occupying masses 244 verbal interactions, children 311–12 Veterans Administration nomenclature 24–5 VETR see Vietnam Twin Registry study

624 victims 117–32, 135–6, 343, 497–514, 522–3, 525–7, 557–70 Victoria Symptom Validity Test 246 Vietnam Twin Registry study (VETR) 154 violence 2, 4, 35–8, 41, 43–59, 69–78, 103–5, 117–32, 137–43, 150–64, 252–9, 260–1, 267–8, 293–5, 303–14, 323–31, 343, 398–9, 438–9, 472–3, 534–8 see also aggression; sexual . . . affectiveness disorders 120–1, 257–9, 497–514 alcohol 117–18, 119, 120, 121–2, 126, 127–8, 253–4, 257–9, 260–1, 323–4, 534–8 amfetamine 122, 127, 161, 535 anabolic steroids 123 APD 117–32, 252–9, 267–8 appearance of the patient 126 assessment of short-term risks 124–32, 460 auditory hallucinations 128 available means 126–7 borderline personality disorder 118, 128, 498–9 brain imaging research 69–78, 105–9 brain trauma 220–31, 264–5, 398–9 child-to-parent violence 311–14 children 42–3, 162–4, 204–6, 207, 220–31, 276–89, 291–8, 303–14, 323–31, 367–75, 438–9 cocaine 122, 127, 161, 257–9, 535 concepts 117–32, 252–9, 343 CP 303–14, 321–31, 372 deficient violence inhibition mechanism 104–5 delusions 119–20, 122, 124, 127, 129–31, 253–7, 399 dementia 124 demographic characteristics 129, 328 depression 120–1, 257–9 domestic violence 497–514 factors of risk 125–9 hallucinogens 122–3, 127, 535 history 127, 505–6, 525–6 hospitals 128, 129–32, 488–9 inhalants 123 intent 126, 560 intermittent explosive disorder 119, 128, 399 lawsuits against clinicians 117, 129–32 mania 120–1, 257–9 medical disorders 124 mental disorders 117–32 mental retardation 120, 123–4, 266–7 mood disorders 120–1, 257–9 MST 438–9, 470–1 narcissistic personality disorder 118, 128, 335, 457–60, 505–6, 512 neurological disorders 124

INDEX noncompliance with treatment 129 paranoia 118–19, 124, 128 PCP 122–3, 127, 535 presence of violent ideation 126 psychoactive substances 121–3, 126, 127, 535–8 psychopathic disorders 2, 4, 35–8, 41, 43–59, 69–78, 103–5, 117–32, 252–9, 267–8, 343, 357–61 psychopharmacological agents 4, 118, 181, 397–411, 482–4 psychosis 119–21, 128, 129–31, 252–7, 399 PTSD 220–31, 294–5 risk assessments 117, 124–32, 137–43, 252–9, 319–31, 357–61, 473–5, 560–70, 578–83 schizophrenia 119–20, 128, 129–30, 252–7, 262–3, 267 socioeconomic characteristics 129, 150, 326–31 substance abuse 117–18, 120–3, 126, 127, 253–4, 257–9, 260–1, 534–8 types 117–32, 343 victims 117–32, 135–6, 343, 497–514, 522–3, 525–7 workplace violence 4, 119, 129–30, 257–9, 519–28 written evidence 131–2 Violence Reduction Programme (VRP) 455–6, 458 Violent Risk Appraisal Guide (VRAG) 54–5, 473–5 violent/antisocial batterers, domestic violence 499–500 VLPFC see ventrolateral prefrontal cortex VMPFC see ventromedial prefrontal cortex VNTR see variable number of tandem repeat volume losses, brain 71–2, 73–8, 176–82, 195, 208–10, 225–7, 398–9 voxel-based morphometry 177–8 voyeurism 276–89 see also paraphilias VRAG see Violent Risk Appraisal Guide VRP see Violence Reduction Programme warmth factors, parents 322 weak-willed psychopaths 21, 22 weapons, workplace violence 526 Weber, Max 24 Wechsler Tests 247 Wernicke’s area 74–5 West, Donald 331 Wide Range Achievement Test 247 Widinger, T.A. 24, 49 Wilson’s Formula 247

INDEX Wisconsin Card Sorting Test 110, 241, 242 withdrawal 121–3, 126, 537–8 alcohol 121, 126, 537–8 cocaine 122, 538 Witter, Hermann 566 Wolfgang, Martin 1 women see also females psychopathic disorders 3, 35–6, 150–1, 155–6, 162–3, 347–61, 459 Wong et al. 58 word tests 106–7, 110–11 working memory, concepts 229, 240–8 workplace violence 4, 119, 129–30, 257–9, 519–28 see also violence assessments 523–7 behavioral approach 521–2, 525–6 bullying 522–3 cognitive processing 525 concepts 519–28 definition 519–20 environmental issues 525–6 fact-based method of evaluation 524–5 ‘holistic’ approach 524–7 multidisciplinary treatment approach 520 past behaviors 525–6 Index compiled by Terry Halliday.

625 PCL-R measures 523–4 perpetrator types 520–1 personality disorders 520–1 provocation issues 525–6 psychopathic disorders 4, 119, 129–30, 257–9, 519–28 research 520–2 risk assessments 520–4 society issues 522 stalking behavior 522 statistics 520–1 treatment 519–28 US Secret Service 524–7 victims 522–3, 525–7 weapons 526 World Health Organization 26, 84, 368 see also International Classification of Mental Disorders written evidence, violence risks 131–2 X chromosone 350 Yale Family Study 157 Yang, Yaling 69–81 Zeller, A. 22–3 Ziehen, T.H. 10, 19

(A) 9 46

10

45

11

44

47

(B) 9 10

12 11

Figure 4.1

tMRI response (% BOLD signal)

2

1

0

–1

–2

–6

Figure 10.3

Figure 12.1

6 0 Time [scans]

12