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

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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



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 Jürgen L. Müller

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 Sirén

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? Jürgen. L. Müller

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 Köln, 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 Köln, 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-Göttingen, 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 Köln, 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-Göttingen, Germany Maya K. Krischer, University Clinic of Cologne, Department of Child and Adolescent Psychiatry, Robert-Koch-Strasse 10, D-50935 Köln, 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 Köln, 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 Göttingen, Department of Psychiatry and Psychotherapy, Von Siebold Str. 5, D-37075 Göttingen, 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 Köln, Germany Andrew Shiva, 40 Riverside Drive, New York, NY 10023, USA Anna-Leena Sirén, University of Würzburg, Department of Neuro sergery, JosephSchneider Str. 11, 97080 Würzburg, 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 für 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, Kröber & 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., Kröber, 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 für Straftäter in den Vereinigten Staaten und Kanada [Treatment programs for criminal offenders in the United States and Canada]. In H-L. Kröber, D. Dölling, 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, Dissozialität [Psychopathy, Sociopathy and Dissocial Conditions]. Berlin: Springer-Verlag. Saß, H. (1991a). Ein psychopathologisches Referenzsystem zur Beurteilung der Schuldfäligkeit [A psychopathological reference system for the assessment of criminal responsibility]. Forensia, 6, 33–43. Saß, H. (1991b). Forensische Erheblichkeit seelischer Störungen in psychopathologischen Referenzsystem [The forensic relevance of mental disorders in the psychopathological reference system] (pp. 266–81). In H. Schütz, 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.

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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

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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

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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, Müller 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.

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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).


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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 délire [Mania without delirium] Les Monomanies [Monomania] Dégénérés [Degenerates] Delinquente nato [The born criminal] Déséquilibration mentale [Mental instability]

(Pinel, 1809) (Esquirol, 1839) (Morel, 1957) (Lombroso, 1876) (Dupré, 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 délire (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’ (Traité médico-philosophique sur l’aliénation 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

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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 idée 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’ (Traité des dégénéréscences physiques, intellectuelles et morales de l’espéce 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

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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 héréditaires) 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’ (dégénéres supérieurs), 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, Dupré (1925) was the true founder of the concept of mental instability (déséquilibration 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.


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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’ (dégénérés supérieurs) to ‘unbalanced degenerates’ (déséquilibrés dégénérés) and eventually to the constitutionally unstable (déséquilibrés). 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

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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).


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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

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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.


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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

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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 (déséquilibration 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.


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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 Zustände 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’ (Originäre Krankheitszustände) – the group he had earlier called psychopathic states – and psychopathic personalities (Psychopathische Persönlichkeiten). 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 Dupré’s concept of mental instability (déséquilibration mentale), he also paid attention to disharmony of personality traits and abnormal lability of mental stability.

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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 Persönlichkeiten) (first published in 1923), takes root in his earlier studies on The Personality and Fate of Registered Prostitutes (Persönlichkeit 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.


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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

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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 délire as the forerunner of the later term


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‘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

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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,


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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).

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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, Kröber & 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.


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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.

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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 für Studirende und Arzte [Psychiatry. A Textbook for Students and Doctors], 5th edition. Leipzig: Barth. ¨ Kraepelin, E. (1904). Psychiatrie. Ein Lehrbuch für Studirende und Arzte [Psychiatry. A textbook for students and doctors]. Vol. 2, 7th edition. Leipzig: Barth. ¨ Kraepelin, E. (1909–15). Psychiatrie. Ein Lehrbuch für Studirende und Arzte [Psychiatry. A Textbook for Students and Doctors], 8th edition. Leipzig: Barth. Kretschmer, E. (1921): Körperbau 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 Dégénérés (état 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). Traité des Dégénérescences Physiques, Intellectuelles et Morales de l’Espèce Humaine et des Causes qui Produisent ces Variétés Maladive [Treatise on the Physical, Intellectual and Moral Human Degenerates and the Causes which Produce these Various Diseases]. Paris: Baillière. Partridge, G.E. (1930). Current conceptions of psychopathic personality. American Journal of Psychiatry, 10, 53–99. Petrilowitsch, N. (1966). Abnorme Persönlichkeiten [Abnormal Personalities], 3rd edition. Basel: Karger. Pinel, P. (1809). Traité Médico-Philosophique sur L’aliénation 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 Persönlichkeit [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 Persönlichkeitsstörungen [Classification of personality disorders]. Nervenarzt, 56, 193–203. Saß, H. (1987). Psychopathie – Soziopathie – Dissozialität: Zur Differentialtypologie der Persönlichkeitsstörungen [Psychopathy – Sociopathy – Dissociality: The Differential Typology of Personality Disorders]. Berlin: Springer.

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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 Persönlichkeitsvarianten 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 für 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). Studienerüfer Persönlichkeit eingeschriebener Prostitutierten. Springer: Berlin. Schneider, K. (1950). Die psychopathischen Persönlichkeiten [The Psychopathic Personalities], 9th edition. Wien: Deuticke. (1st edn.1923, Thieme, Leipzig). Schultz, J.H. (1928). Die konstitutionelle Nervosität [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. Württemb. Medizinvereins, 10, 17. Ziehen, T.H. (1905, 1907, 1908, 1912). Zur Lehre von den psychopathischen Konstitutionen [The Doctrine of the Psychopathic Constitutions]. Charité-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


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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

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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

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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.


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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

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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.


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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. Möller, 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 für 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 – Dissozialität: zur Differentialtypologie der Persönlichkeitsstörungen [Psychopathy – Sociopathy – Dissociality: The Differential Typology of Personality Disorders]. Berlin: Springer. Saß, H. & Hoff, P. (2003). Deskriptiv-psychopathologische Befunderhebung. In H.J. Möller, 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.

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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; Hervé, 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.

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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; Hervé & 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

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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; Hervé & 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

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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.


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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

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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


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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; Hervé, 2007b; O’Toole, 2007).

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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; Hervé &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


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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).

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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


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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.

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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


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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

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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; Tengström et al., 2004; Tengström et al., 2000; Tengström 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);


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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 (Sjöstedt & L˚angström, 2002); violent recidivism by Belgium prison inmates and forensic psychiatric patients (Pham et al., 2005); violent recidivism by Swedish violent offenders (Tengström, 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.

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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


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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).

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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. Lösel (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.


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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.

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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


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(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

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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

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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.


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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

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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


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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

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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


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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

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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.

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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).


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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

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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

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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.


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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.

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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-


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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).

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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


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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

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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.


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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

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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


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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.

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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,


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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

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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).

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

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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 (Hervé, 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).


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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.

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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

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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.

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EXECUTIVE FUNCTION AND RESPONSE MODULATION

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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.

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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)


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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, Lösel 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.

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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


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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.

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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.

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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

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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

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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


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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).

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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


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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).

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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


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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.

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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


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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.

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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.


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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

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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


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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

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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.


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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


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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 (Tengström 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

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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; Tengström 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

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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 (Tengström 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 (Tengström 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

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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 (Tengström 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.

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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 (Lösel, 1998). What was really evaluated was a therapeutic community in which group treatment in the form of marathon sessions and

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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

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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 & Pfäfflin, 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

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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.

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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.


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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

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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)

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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


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

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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


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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

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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).


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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

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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).


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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

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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


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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

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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).


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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.

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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.

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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


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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

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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

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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, Müller 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,


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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).

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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 (Müller 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


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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 (Müller 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

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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 (Müller 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; Müller 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


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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

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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.


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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

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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.

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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.

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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).

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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).

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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.

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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

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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.

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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

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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

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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

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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.

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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.


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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

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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

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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).


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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

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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.


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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,

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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,


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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).

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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


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(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

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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.


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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).

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CHAPTER 13

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

Anna-Leena Sirén ¨ 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.

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- 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

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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


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

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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

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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; Sirén 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

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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)

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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

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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 (Sirén 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, Sirén & Ehrenreich, 2004; Sirén 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; Sirén 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 (Sirén 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).

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VOLUME I: DIAGNOSIS AND TREATMENT p 1.2) (Kazdin & Wassell, 2000) and compared to a normative sample the maladaptive behavior reverts to a normal level, which indicates clinical relevance.

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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)

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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

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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.


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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

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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).

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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.

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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

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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

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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


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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.

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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


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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

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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


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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,

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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


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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;

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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.


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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

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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


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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.

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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.


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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

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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; Lösel, 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).

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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


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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

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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.


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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

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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).


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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; Müller-Isberner, 1996; Müller-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,

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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


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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

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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


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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).

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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:


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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

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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.


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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

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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


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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

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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 & Bussière, 1998; Hanson & Morton-Bourgon, 2005; Hare et al., 2000; Hemphill, Hare & Wong,1998; Knight & Guay, 2006; Looman et al., 2005; Seto & Barbaree, 1999; Seto & Lalumière, 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 & Lalumière, 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 & Lalumière, 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 & Bussière, 1998; Hill, Briken & Kraus, 2004; Lösel & 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 (Lösel & 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


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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; Langelüddeke, 1963; Stürup, 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; Rösler & 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

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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


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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.

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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.

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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).

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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

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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


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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

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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


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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).

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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.


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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

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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,


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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.

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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.


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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

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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


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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

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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).


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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.

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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.

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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


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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

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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

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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).

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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’.

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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

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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

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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

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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

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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.

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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.


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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

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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.

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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.


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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.

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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


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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

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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 & Hasenöhrl, 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.

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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 Alkoholabhängigen. Klinikarzt, 7+8(25), 203–7. Mann, K. & Stetter, F. (2002). Die qualifizierte Entzugsbehandlung von Alkoholab-hängigen: Entwicklung und Evaluation. In K. Mann (ed.), Neue Therapieansätze Bei Alkoholab-hängigkeit (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 Störungen und Sucht: Doppeldiagnosen. Hogrefe, Verl. für 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.


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Spanagel, R. & Mann, K. (2005). Drugs for Relapse Prevention of Alcoholism. Berlin: Birkhäuser. 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 Alkoholabhängiger nach einer stationären 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


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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

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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; Stürup, 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

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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


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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

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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’


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(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;

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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).


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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

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(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.


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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 Stürup, 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.

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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. Stürup, 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 Gangé, 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.

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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

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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

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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


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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 für 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 Müller, 2004; Müller, 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

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ordered by the Bavarian Supreme Court, after the arguments of the experts were accepted (Müller, 2004; Müller, 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 (Müller, 2004; Müller, 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


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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

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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


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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.

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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.


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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

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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


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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

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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.


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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 Störungen 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 für 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. Müller, J.L. (2004). Vom BayUnterbrG zum Bay. StrUBG: Rückfallprävention zwischen staatlichem Sicherheitsanspruch, Selbstverständnis psychiatrischer Kliniken und individuellen Freiheit¨ srechten. In G. Hajak & J.L. Müller (eds.), Uber die Zerbrechlichkeit der Willensbestimmung (pp. 55–78). Berlin: Springer. Müller, J.L., Klein, H.E. & Cording, C. (2002). Missbrauch der Psychiatrie? Konflikte zwischen staatlichem Sicherheitsanspruch und dem Selbstverständnis 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.

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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 délire 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.


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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

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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)

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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


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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 (Müller 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.

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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


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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 & Gächter, 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.

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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? (Kröber & Lau, 2000). So far this question can be answered


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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.

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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. Müller-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 Dupré, 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 Gangé, 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 idée 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 Müller, Jürgen 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 Sirén, 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)

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1

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Figure 10.3

Figure 12.1

6 0 Time [scans]

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