text:
Principal Attention-Deficit Hyperactivity Disorder: A Handbook for Diagnosis and Treatment
Attention-Deficit Hyperactivity Disorder: A Handbook for Diagnosis and TreatmentRussell A. Barkley
Widely regarded as the standard clinical reference, this volume provides the best current knowledge about attention-deficit/hyperactivity disorder (ADHD) in children, adolescents, and adults. The field's leading authorities address all aspects of assessment, diagnosis, and treatment, including psychological therapies and pharmacotherapy. Core components of ADHD are elucidated. The volume explores the impact of the disorder across a wide range of functional domains--behavior, learning, psychological adjustment, school and vocational outcomes, and health. All chapters conclude with user-friendly Key Clinical Points.
New to This Edition
*Reflects significant advances in research and clinical practice.
*Expanded with many new authors and new topics.
*Chapters on cutting-edge interventions: social skills training, dietary management, executive function training, driving risk interventions, complementary/alternative medicine, and therapies for adults.
*Chapters on the nature of the disorder: neuropsychological aspects, emotional dysregulation, peer relationships, child- and adult-specific domains of impairment, sluggish cognitive tempo, and more.
New to This Edition
*Reflects significant advances in research and clinical practice.
*Expanded with many new authors and new topics.
*Chapters on cutting-edge interventions: social skills training, dietary management, executive function training, driving risk interventions, complementary/alternative medicine, and therapies for adults.
*Chapters on the nature of the disorder: neuropsychological aspects, emotional dysregulation, peer relationships, child- and adult-specific domains of impairment, sluggish cognitive tempo, and more.
Lecture de livre en ligne
You may be interested in
Most frequently terms
adult adhd395
You can write a book review and share your experiences. Other readers will always be interested in your opinion of the books you've read. Whether you've loved the book or not, if you give your honest and detailed thoughts then people will find new books that are right for them.
ebook THE GUILFORD PRESS Attention-Deficit Hyperactivity Disorder Selected Works from Russell A. Barkley For Professionals ADHD and the Nature of Self-Control Russell A. Barkley ADHD in Adults: What the Science Says Russell A. Barkley, Kevin R. Murphy, and Mariellen Fischer Attention-Deficit Hyperactivity Disorder, Third Edition: A Clinical Workbook Russell A. Barkley and Kevin R. Murphy Barkley Adult ADHD Rating Scale–IV (BAARS-IV) Russell A. Barkley Barkley Deficits in Executive Functioning Scale (BDEFS for Adults) Russell A. Barkley Barkley Deficits in Executive Functioning Scale—Children and Adolescents (BDEFS-CA) Russell A. Barkley Barkley Functional Impairment Scale (BFIS for Adults) Russell A. Barkley Barkley Functional Impairment Scale—Children and Adolescents (BFIS-CA) Russell A. Barkley Defiant Children, Third Edition: A Clinician's Manual for Assessment and Parent Training Russell A. Barkley Defiant Teens, Second Edition: A Clinician's Manual for Assessment and Family Intervention Russell A. Barkley and Arthur L. Robin Executive Functions: What They Are, How They Work, and Why They Evolved Russell A. Barkley For General Readers Taking Charge of ADHD, Third Edition: The Complete, Authoritative Guide for Parents Russell A. Barkley Taking Charge of Adult ADHD Russell A. Barkley with Christine M. Benton Your Defiant Child, Second Edition: Eight Steps to Better Behavior Russell A. Barkley and Christine M. Benton Your Defiant Teen, Second Edition: 10 Steps to Resolve Conflict and Rebuild Your Relationship Russell A. Barkley and Arthur L. Robin with Christine M. Benton For mor information, visit www.russellbarkley.org. Attention-Deficit Hyperactivity Disorder A Handbook for Diagnosis and Treatment Fo u r th E d itio n Edited by Russell A. Barkley THE GUILFORD PRESS New York London © 2015 The Guilford Press A Division of Guilford Publications, Inc. 370 Seventh Avenue, Suite 1200, New York, NY 10001 www.guilford.com Paperback edition 2018 All rights reserved No part of this book may be reproduced, translated, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission from the publisher. Printed in the United States of America This book is printed on acid-free paper. Last digit is print number: 9 8 7 6 5 4 3 The authors have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards of practice that are accepted at the time of publication. However, in view of the possibility of human error or changes in behavioral, mental health, or medical sciences, neither the authors, nor the editors and publisher, nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they are not responsible for any errors or omissions or the results obtained from the use of such information. Readers are encouraged to confirm the information contained in this book with other sources. Library of Congress Cataloging-in-Publication Data Attention-deficit hyperactivity disorder : a handbook for diagnosis and treatment.— Fourth edition / edited by Russell A. Barkley. pages cm Includes bibliographical references and index. ISBN 978-1-4625-1772-5 (hardback) ISBN 978-1-4625-3887-4 (paperback) 1. Attention-deficit hyperactivity disorder—Handbooks, manuals, etc. 2. Attentiondeficit hyperactivity disorder—Treatment—Handbooks, manuals, etc. 3. Behavior therapy for children—Handbooks, manuals, etc. I. Barkley, Russell A., 1949– editor of compilation. RJ496.A86A883 2014 618.92′8589—dc23 2014010757 To my grandsons Liam and Craig, for yet another opportunity to experience the joys of childhood About the Editor Russell A. Barkley, PhD, ABPP, ABCN, is Clinical Professor of Psychiatry at the Virginia Treatment Center for Children and Virginia Commonwealth University School of Medicine. Dr. Barkley has worked with children, adolescents, and families since the 1970s and is the author of numerous bestselling books for both professionals and the public, including Taking Charge of ADHD and Your Defiant Child. He has also published six assessment scales and more than 280 scientific articles and book chapters on ADHD, executive functioning, and childhood defiance, and is editor of the newsletter The ADHD Report. A frequent conference presenter and speaker who is widely cited in the national media, Dr. Barkley is past president of the Section on Clinical Child Psychology (the former Division 12) of the American Psychological Association (APA), and of the International Society for Research in Child and Adolescent Psychopathology. He is a recipient of awards from the American Academy of Pediatrics and the APA, among other honors. His website is www.russellbarkley.org. vi Contributors Andrew Adesman, MD, Department of Pediatrics, Hofstra North Shore–Long Island Jewish School of Medicine, Hempstead, New York Stephanie L. Cardoos, MA, Department of Psychology, University of California, Berkeley, Berkeley, California Lenard A. Adler, MD, Departments of Psychiatry and Child and Adolescent Psychiatry, New York University School of Medicine, New York, New York Anil Chacko, PhD, Department of Applied Psychology, Steinhardt School of Culture, Education, and Human Development, New York University, New York, New York Carla C. Allan, PhD, ADHD Specialty Clinic, Children's Mercy Hospital and Clinics, Kansas City, Missouri Alyssa Chimiklis, BA, Department of Psychology, Queens College, City University of New York, New York, New York Samuel Alperin, BS, Hofstra North Shore–Long Island Jewish School of Medicine, Hofstra University, Hempstead, New York Andrea Chronis-Tuscano, PhD, Department of Psychology, University of Maryland, College Park, Maryland Daniel F. Connor, MD, Division of Child and Adolescent Psychiatry, University of Connecticut Medical School and Health Care, Farmington, Connecticut Lindsay Anderson, MA, Department of Psychology, Queens College, City University of New York, New York, New York Melinda Cornwell, BA, Department of Psychology, Queens College, City University of New York, New York, New York L. Eugene Arnold, MD, MEd, Nisonger Center, Ohio State University, Columbus, Ohio Amanda Bader, BA, Department of Education, University of Pennsylvania, Philadelphia, Pennsylvania George J. DuPaul, PhD, Department of Education and Human Services, Lehigh University, Bethlehem, Pennsylvania Russell A. Barkley, PhD, Departments of Psychiatry and Pediatrics, Medical University of South Carolina, Charleston, South Carolina Gregory A. Fabiano, PhD, Department of Counseling, School, and Educational Psychology, University at Buffalo, The State University of New York, Buffalo, New York Joseph Biederman, MD, Department of Psychiatry, Harvard Medical School and Joint Program in Pediatric Psychopharmacology, McLean General Hospital and Massachusetts General Hospital, Boston, Massachusetts Lauren M. Friedman, BA, Department of Psychology, University of Central Florida, Orlando, Florida Michael Gordon, PhD, Department of Psychiatry, State University of New York Upstate Medical University, Syracuse, New York Jennifer Bolden, PhD, Department of Psychology, University of Tennessee, Knoxville, Tennessee vii viii Contributors Bergljot Gyda Gudmundsdottir, MA, Department of Psychology, University of Rhode Island, Kingston, Rhode Island Stephen R. Pliszka, MD, Department of Psychiatry, University of Texas Health Sciences Center, San Antonio, Texas Stephen P. Hinshaw, PhD, Department of Psychology, University of California, Berkeley, Berkeley, California Jefferson B. Prince, MD, Department of Psychiatry, Harvard Medical School and Pediatric Psychopharmacology Clinic, Massachusetts General Hospital, Boston, Massachusetts; Department of Child Psychiatry, MassGeneral for Children at North Shore Medical Center, Salem, Massachusetts Betsy Hoza, PhD, Department of Psychology, University of Vermont, Burlington, Vermont Elizabeth Hurt, PhD, School of Professional Psychology, Wright State University, Dayton, Ohio Charlotte Johnston, PhD, Department of Psychology, University of British Columbia, Vancouver, British Columbia, Canada Laura E. Knouse, PhD, Department of Psychology, University of Richmond, Richmond, Virginia Michael J. Kofler, PhD, Department of Psychology, Florida State University, Tallahassee, Florida Joshua M. Langberg, PhD, Department of Psychology, Virginia Commonwealth University, Richmond, Virginia Lawrence J. Lewandowski, PhD, Department of Psychology, Syracuse University, Syracuse, New York Benjamin J. Lovett, PhD, Department of Psychology, State University of New York Cortland, Cortland, New York Julia D. McQuade, PhD, Department of Psychology, Amherst College, Amherst, Massachusetts Amori Yee Mikami, PhD, Department of Psychology, University of British Columbia, Vancouver, British Columbia, Canada Richard Milich, PhD, Department of Psychology, University of Kentucky, Lexington, Kentucky Kevin R. Murphy, PhD, Adult ADHD Clinic of Central Massachusetts, Northboro, Massachusetts Sarah A. Orban, MS, Department of Psychology, University of Central Florida, Orlando, Florida Elizabeth B. Owens, PhD, Institute of Human Development, University of California, Berkeley, Berkeley, California J. Russell Ramsay, PhD, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania Mark D. Rapport, PhD, Department of Psychology, University of Central Florida, Orlando, Florida Walter Roberts, MS, Department of Psychology, University of Kentucky, Lexington, Kentucky Arthur L. Robin, PhD, Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, and Children's Hospital of Michigan, Detroit, Michigan Nicole K. Schatz, PhD, Department of Counseling, School, and Educational Psychology, University at Buffalo, The State University of New York, Buffalo, New York Cheri J. Shapiro, PhD, Institute for Families in Society and College of Social Work, University of South Carolina, Columbia, South Carolina Bradley H. Smith, PhD, Department of Educational Psychology, College of Education, University of Houston, Houston, Texas Mary V. Solanto, PhD, Department of Psychiatry, New York University School of Medicine, New York, New York Thomas J. Spencer, MD, Department of Psychiatry, Harvard Medical School, and Pediatric Psychopharmacology Clinic, Massachusetts General Hospital, Boston, Massachusetts Jodi Uderman, MA, Department of Psychology, Queens College, City University of New York, New York, New York Lisa L. Weyandt, PhD, Department of Psychology, University of Rhode Island, Kingston, Rhode Island Gina Pera, BS, author and educator, San Francisco, California Timothy E. Wilens, MD, Departments of Child Psychiatry and Pediatric Psychopharmacology, Massachusetts General Hospital, and Department of Psychiatry, Harvard Medical School, Boston, Massachusetts Linda J. Pfiffner, PhD, Department of Psychiatry, University of California, San Francisco, San Francisco, California Erik G. Willcutt, PhD, Department of Psychology and Neuroscience, University of Colorado, Boulder, Boulder, Colorado Preface This fourth edition constitutes a nearly complete revision and update of the third edition, comprising at least 80% or more new material, a substantial expansion of topical areas covered on attention-deficit/hyperactivity disorder (ADHD), and at least triple the number of contributors in comparison to the prior edition. While it is essentially a new textbook, like its predecessors, this edition strives to extract from the mine of available scientific literature those nuggets of clinically important information regarding the nature, assessment, diagnosis, and management of ADHD in children, adolescents, and adults. The task of doing so has increased substantially with each new edition given the increasing frequency of journal articles relating to ADHD appearing in the scientific literature, now estimated to be at least 800–1,000 per year, a rate that seems to have doubled in just the past few years owing to a vast increase in the number of international contributors outside of Western Europe and North America. More than 6,000 studies on ADHD have been published since the publication of the 2006 edition of this work. So formidable an undertaking requires the assistance of many more contributors than in prior editions, for it is clear that no single individual can be an expert in all facets of this disorder and its management. To help me with this endeavor, I have invited back many of the principal authors of chapters from the pre- vious edition, along with many new contributors, each expert in the topics contained in their respective chapters. All were charged with incorporating new findings and new conclusions and clinical recommendations from the available research and related publications. I am truly grateful that all agreed to join in this endeavor. In order to draw out the messages essential for clinicians within each chapter, all chapters conclude with a checklist of "Key Clinical Points," most of which I prepared to help the reader quickly summarize the major conclusions and recommendations discussed in that chapter. From time to time, media flare-ups have centered on ADHD, sometimes challenging its very existence. Taken in its totality, this book is a complete refutation of such assertions. It continues to show, as did previous editions, that ADHD is as valid a mental disorder as we are likely to find, with massive evidence from more than 10,000 studies dating back to medical descriptions in 1775. It clearly represents a serious deficiency in one or more psychological adaptations that harm the individuals so afflicted, which is the very definition of a mental disorder. As in previous editions, I once again thank Kitty Moore, Seymour Weingarten, and Robert Matloff at The Guilford Press for supporting this book and providing a home for this and my other books. I also wish ix x Preface to thank Carolyn Graham, Jacquelyn Coggin, and Laura Specht Patchkofsky at Guilford for helping to shepherd this book through the publication process in a professional and expeditious manner. My debt to them and the rest of Guilford's superbly capable staff for having assisted me for more than 33 years of publishing is incalculable, and I express my deep appreciation to all members of the Guilford "family" here. I am also extraordinarily appreciative of my wife, Patricia, who has stood by me for more than 45 years and provided a loving home for me, our two sons, Ken and Steve, now all grown up, and now our two grandsons, to whom this edition is dedicated. All provide me with a profound sense of family and their affection, for which I am exceptionally grateful. In such a home can this type of creative work be accomplished. Russell A. Barkley, PhD Contents Part I. The Nature of ADHD 1. History of ADHD 3 Russell A. Barkley 2. Primary Symptoms, Diagnostic Criteria, Subtyping, and Prevalence of ADHD 51 Walter Roberts, Richard Milich, and Russell A. Barkley 3. Emotional Dysregulation Is a Core Component of ADHD 81 Russell A. Barkley 4. Developmental and Neuropsychological Deficits in Children with ADHD 116 Lisa L. Weyandt and Bergljot Gyda Gudmundsdottir 5. Comorbid Psychiatric Disorders in Children with ADHD 140 Steven R. Pliszka 6. Educational Impairments in Children with ADHD 169 George J. DuPaul and Joshua M. Langberg 7. Families and ADHD 191 Charlotte Johnston and Andrea Chronis‑Tuscano 8. Peer Relationships of Children with ADHD 210 Julia D. McQuade and Betsy Hoza 9. Developmental Progression and Gender Differences among Individuals with ADHD Elizabeth B. Owens, Stephanie L. Cardoos, and Stephen P. Hinshaw xi 223 xii Contents 10. Executive Function Deficits in Adults with ADHD 256 Mary V. Solanto 11. Health Problems and Related Impairments in Children and Adults with ADHD 267 Russell A. Barkley 12. Educational, Occupational, Dating and Marital, and Financial Impairments in Adults with ADHD 314 Russell A. Barkley 13. Comorbid Psychiatric Disorders and Psychological Maladjustment in Adults with ADHD 343 Russell A. Barkley 14. Etiologies of ADHD 356 Russell A. Barkley 15. Theories of ADHD 391 Erik G. Willcutt 16. Executive Functioning and Self‑Regulation Viewed as an Extended Phenotype: Implications of the Theory for ADHD and Its Treatment 405 Russell A. Barkley 17. Concentration Deficit Disorder (Sluggish Cognitive Tempo) 435 Russell A. Barkley Part II. Assessment of ADHD 18. Psychological Assessment of Children with ADHD 455 Russell A. Barkley 19. Psychological Assessment of Adults with ADHD 475 J. Russell Ramsay 20. Diagnosing ADHD in Adults in the Primary Care Setting 501 Lenard A. Adler and Samuel Alperin Part III. Treatment of Children and Adolescents with ADHD 21. Training Parents of Youth with ADHD 513 Anil Chacko, Carla C. Allan, Jodi Uderman, Melinda Cornwell, Lindsay Anderson, and Alyssa Chimiklis 22. Training Families of Adolescents with ADHD Arthur L. Robin 537 Contents 23. Social Skills Training for Youth with ADHD xiii 569 Amori Yee Mikami 24. Treatment of ADHD in School Settings 596 Linda J. Pfiffner and George J. DuPaul 25. Dietary Management of ADHD 630 Elizabeth Hurt and L. Eugene Arnold 26. Executive Function Training for Children with ADHD 641 Mark D. Rapport, Sarah A. Orban, Michael J. Kofler, Lauren M. Friedman, and Jennifer Bolden 27. Stimulant and Nonstimulant Medications for Childhood ADHD 666 Daniel F. Connor 28. Combined Treatments for ADHD 686 Bradley H. Smith and Cheri J. Shapiro 29. Driving Risk Interventions for Teens with ADHD 705 Gregory A. Fabiano and Nicole K. Schatz 30. Complementary and Alternative Medicine for ADHD 728 Amanda Bader and Andrew Adesman Part IV. Treatment of Adults with ADHD 31. Psychological Counseling of Adults with ADHD 741 Kevin R. Murphy 32. Cognitive‑Behavioral Therapies for ADHD 757 Laura E. Knouse 33. Assessment and Management of ADHD in Educational and Workplace Settings in the Context of ADA Accommodations 774 Michael Gordon, Lawrence J. Lewandowski, and Benjamin J. Lovett 34. Counseling Couples Affected by Adult ADHD 795 Gina Pera 35. Pharmacotherapy of ADHD in Adults 826 Jefferson B. Prince, Timothy E. Wilens, Thomas J. Spencer, and Joseph Biederman Author Index 861 Subject Index 883 PA R t i the nature of ADHD ChAPtER 1 History of ADHD russell A. Barkley Attention-deficit/hyperactivity disorder (ADHD) continues to be the current diagnostic label for children and adults presenting with significant problems with attention, and typically with impulsiveness and excessive activity as well. Children and adults with ADHD represent a rather heterogeneous population that displays considerable variation in the degree of members' symptoms, age of onset, cross-situational pervasiveness of those symptoms, and the extent to which other disorders occur in association with ADHD. The disorder represents one of the most common reasons children with behavioral problems are referred to medical and mental health practitioners in the United States and is one of the most prevalent childhood psychiatric disorders. Currently, referrals of adults for ADHD are also increasing at a rapid pace; until the 1990s and even to date, this age group has been a markedly underrecognized and underserved segment of the ADHD population. This chapter presents an overview of ADHD's history—a history that spans more than two centuries in the medical and scientific literature. Whereas the previous edition noted that the medical history of ADHD began with Still's description of childhood cases in 1902, we now know that a number of earlier physicians described such cases dating back to the textbook by Melchior Adam Weikard published in German in 1775 (Barkley & Peters, 2012). This extends the history of ADHD in the medical literature back another 127 years. These new additions to the history of ADHD are described below. But given that the history of ADHD as understood from 1902 through 2006 has changed little since the preceding edition of this text (Barkley, 2006), little has been needed to update those sections of this chapter. In contrast, developments since that previous edition are described at the end of this chapter. In the history of ADHD reside the nascent concepts that serve as the foundation for the current conceptualization of the disorder as largely involving self-regulation and executive functioning, as discussed here by Eric Willcutt (Chapter 15) and myself (Chapter 16). In this history also can be seen the emergence of current notions about its treatment. Such a history remains important for any serious student of ADHD, for it shows that many contemporary themes concerning its nature arose long ago. They have recurred throughout the subsequent history of ADHD to the present as clinicians and scientists strove for a clearer, more accurate understanding of the condition, its comorbid disorders, life course, impairments, and etiologies. Readers are directed to other and earlier sources for additional discussions of the history of this disorder (Accardo & 3 4 I. THE NATURE OF ADHD Blondis, 2000; Goldstein & Goldstein, 1998; Kessler, 1980; Ross & Ross, 1976, 1982; Schachar, 1986; Taylor, 2011; Warnke & Riederer, 2013; Werry, 1992). The Historical Origins of ADHD The Late 1700s One can find literary references to individuals having serious problems with inattention, hyperactivity, and poor impulse control in Shakespeare, who made mention of a malady of attention in King Henry VIII. But as of this writing, the medical history of ADHDlike descriptions traces back nearly 240 years to 1775. This early history has been expertly detailed in several sources (Taylor, 2011; Warnke & Riederer, 2013) but should be amended by more recent discoveries in that history, as discussed below. It now appears that the first description of disorders of attention, at least as of this writing, occurred in the medical textbook by Melchior Adam Weikard in German in 1775 (or perhaps even 1770; see Barkley & Peters, 2012). Initially published anonymously, hence the difficulty with ascertaining the year of its initial publication, the medical textbook by Weikard described adults and children who were inattentive, distractible, lacking in persistence, overactive, and impulsive, which is quite similar to today's description of ADHD. Weikard implied that the disorder could result from poor childrearing but also suggests some biological predispositions as well. For treatment, he recommended sour milk, plant extracts, horseback riding, and even seclusion for severe cases. This textbook would be followed in short order in 1798 with much more detailed descriptions of ADHDlike symptoms in the medical textbook by the Scottish physician Alexander Crichton (see Palmer & Finger, 2001), who may well have studied with Weikard in his medical training. Crichton described two types of attention disorders. The first was a disorder of distractibility, frequent shifting of attention or inconstancy, and lack of persistence or concentration, and aligns more closely with the attention disturbance evident in ADHD. The second was a disorder of diminished power or energy of attention that seems more like the attention problem evident in current descriptions of children and adults with sluggish cognitive tempo (SCT), which is briefly discussed in Chapter 2 on ADHD symptoms and subtypes and far more detailed coverage in Chapter 17, this volume. Crichton had little to say about this second disorder of attention other than it may be associated with debility or torpor of the body that weakens attention and results in individuals who are often characterized as retiring, unsocial, and having few friendships or attachments of any kind; even those few friendships seldom were of a durable nature. He argued that the faculty of attention can become sufficiently weakened that it may leave an individual insensible to external objects or to impressions that ordinarily would awaken social feelings. The 1800s In 1809, John Haslam described what may have been a case of ADHD in a 10-year-old boy who was uncontrollable, impulsive, and "a creature of volition and the terror of the family" (p. 199). Three years later, the famous American physician Benjamin Rush (1812) discussed three cases involving "the total perversion of moral faculties" (p. 359), which included the inability to focus attention. In the mid-1800s, the German pediatrician Heinrich Hoffman (1865) published a book of poems about psychological conditions of children based on observations from his clinical practice. He described both a very impulsive fidgety child he called "Fidgety Phil" and a very inattentive, daydreamy child he called "Johnny Head-in-Air" (see Stewart, 1970). Two years thereafter in England, Henry Maudsley (1867) published a report about a child who was driven by impulsiveness and was also quite destructive. In 1899, the Scottish psychiatrist, Thomas Clouston discussed cases of impulsive children who had learning problems. Much later in the United States, William James (1890/1950) noted in his Principles of Psychology a normal variant of character that he called the "explosive will," which may resemble the difficulties experienced by those who today are described as having ADHD. In France the concept of ADHD may have originated in 1845 in the description of children and adults with attention problems by Jean-Etienne Dominique Esquirol, who believed that the insane no longer "enjoy the faculty of fixing, and directing their attention" (p. 28). Or perhaps the French history of ADHD began in the notion of "mental instability" that appears in the French medical literature in the 1885–1895 period under the leadership of Désiré-Magloire Bourneville (1885, 1895; see Bader & Hidjikhani, in press) at the Hospital Bicêtre in Paris. He observed children and adolescents who had been labeled "abnormal" and placed in medical and educational institutions, many 1. History of ADHD of whom were characterized by attention and other behavioral problems. Charles Baker, a student of Bourneville, wrote a clinical description of hyperactive and impulsive symptoms in 4 children in his 1892 thesis, according to Bourneville (1895). Attention problems were also mentioned in one case in this work. The Period 1900 to 1959 Still's Description in 1902 In the earlier editions of this text, credit for authoring the first medical description of cases resembling ADHD was awarded to George Still in 1902, owing to the lack of information on the earlier works of Weikard and Crichton. While this no longer remains the case, having been ousted from this credit by the discovery of Weikard's description noted earlier, Still did provide probably the most detailed account of the symptoms of these cases and the largest sample of such cases to that time. For these reasons, his observations deserve some recognition here. In a series of three published lectures to the Royal College of Physicians in 1902, Still described 43 children in his clinical practice who had serious problems with sustained attention; he agreed with William James (1890/1950) that such attention may be an important element in the "moral control of behavior." Most were also quite overactive. Many were often aggressive, defiant, resistant to discipline, and excessively emotional or "passionate." These children showed little "inhibitory volition" over their behavior, and they also manifested "lawlessness," spitefulness, cruelty, and dishonesty. Still proposed that the immediate gratification of the self was the "keynote" quality of these children, among other attributes. Passion (or heightened emotionality) was the most commonly observed attribute and the most noteworthy. Still noted further that such children had an insensitivity to punishment, for they would be punished (even physically) yet engage in the same infraction within a matter of hours. Still believed that these children displayed a major "defect in moral control" over their behavior; a defect that was relatively chronic in most cases. He believed that in some cases, these children had acquired the defect secondary to an acute brain disease, and it might remit on recovery from the disease. He noted a higher risk for criminal acts in later development in some, though not all, of the chronic cases. Although this defect could be associated with intellectual retardation, as 5 it was in 23 of the cases, it could also arise in children of near-normal intelligence, as it seemed to do in the remaining 20. To Still (1902), the moral control of behavior meant "the control of action in conformity with the idea of the good of all" (p. 1008). Moral control was thought to arise out of a cognitive or conscious comparison of the individual's volitional activity with that of the good of all—a comparison he termed "moral consciousness." For purposes that will become evident later, it is important to realize here that to make such a comparison inherently involves the capacity to understand the consequences of one's actions over time and to hold in mind forms of information about oneself and one's actions, along with information on their context. Those forms of information involve the action being proposed by the individual, the context, and the moral principle or rule against which it must be compared. This notion may link Still's views with the contemporary concepts of self-awareness, working memory, and rule-governed behavior discussed later in this text. Still did not specifically identify these inherent aspects of the comparative process, but they are clearly implied in the manner in which he used the term "conscious" in describing this process. He stipulated that this process of comparison of proposed action to a rule concerning the greater good involved the critical element of the conscious or cognitive relation of individuals to their environment, or "self-awareness." Intellect was recognized as playing a part in moral consciousness, but equally or more important was the notion of volition or will. The latter is where Still believed the impairment arose in many of those with defective moral control who suffered no intellectual delay. Volition was viewed as being primarily inhibitory in nature, that a stimulus to act must be overpowered by the stimulus of the idea of the greater good of all. Still concluded that a defect in moral control could arise as a function of three distinct impairments: "(1) defect of cognitive relation to the environment; (2) defect of moral consciousness; and (3) defect in inhibitory volition" (p. 1011). He placed these impairments in a hierarchical relation to each other in the order shown, arguing that impairments at a lower level would affect those levels above it and ultimately the moral control of behavior. Much as researchers do today, Still noted a greater proportion of males than females (3:1) in his sample, and he observed that the disorder appeared to arise in most cases before 8 years of age (typically in early childhood). Many of Still's cases displayed a 6 I. THE NATURE OF ADHD proneness to accidental injuries—an observation corroborated by numerous subsequent studies reviewed in a later chapter. And Still saw these youngsters as posing an increased threat to the safety of other children because of their aggressive or violent behavior. Alcoholism, criminality, and affective disorders such as depression and suicide were noted to be more common among their biological relatives—an observation once again buttressed by numerous studies published in recent years. Some of the children displayed a history of significant brain damage or convulsions, whereas others did not. A few had associated tic disorders, or "microkinesia"; this was perhaps the first time tic disorders and ADHD were noted to be comorbid conditions. We now recognize that while 10–15% of children with ADHD may manifest some form of tic disorder, as many as 50–70% of children with tic disorders and Tourette syndrome may have ADHD (Simpson, Jung, & Murphy, 2011). Although many of Still's subjects were reported to have a chaotic family life, others came from households that provided a seemingly adequate upbringing. In fact, Still believed that when poor childrearing was clearly involved, the children should be exempt from the category of lack of moral control; he reserved it instead only for children who displayed a morbid (organic) failure of moral control despite adequate training. He proposed a biological predisposition to this behavioral condition that was probably hereditary in some children but the result of pre- or postnatal injury in others. In keeping with the theorizing of James (1890/1950), Still hypothesized that the deficits in inhibitory volition, moral control, and sustained attention were causally related to each other and to the same underlying neurological deficiency. He cautiously speculated on the possibility of either a decreased threshold for inhibition of responding to stimuli or a cortical disconnection syndrome, in which intellect was dissociated from "will" in a manner that might be due to neuronal cell modification. Any biologically compromising event that could cause significant brain damage ("cell modification") and retardation could, he conjectured, in its milder forms lead only to this defective moral control. Also in England, Alfred Tredgold (1908) described children of low intelligence having abnormal behavior and limited powers of attention, impulse control, and willpower. He extended Still's theories and observations that early brain damage might present as behavioral and learning problems in later childhood. Fore- shadowing current views of treatment, both Still (1902) and Tredgold found that temporary improvements in conduct might be achieved by alterations in the environment or by medications, but they stressed the relative permanence of the defect even in these cases. They emphasized the need for special educational environments for these children. We see here the origins of many later and even current notions about children with ADHD and oppositional defiant disorder (ODD), although it would take almost 70 years to return to many of them—owing in part to the ascendance in the interim of psychoanalytic, psychodynamic, and behavioral views that overemphasized childrearing as largely causing such behavioral disorders in children. The children described by Still and Tredgold would probably now be diagnosed as having not only ADHD but also ODD or conduct disorder (CD), and most likely a learning disability as well (see Chapters 5 and 6). Around this same time, in Spain, the physician Rodriguez-Lafora (1917) wrote about his interests in childhood mental illness and described a group of children having psychopathic constitutions, a subset of which he called the "unstables." His description of them matches closely the modern view of ADHD (Bauermeister & Barkley, 2010), including inconstancy of attention, excessive activity, and impulsive behavior, as does his observation that such children get carried away by their adventurous temperament. The Influence of the Encephalitis Epidemic The history of interest in ADHD in North America can be traced to the outbreak of an encephalitis epidemic in 1917–1918, when clinicians were presented with a number of children who survived this brain infection but were left with significant behavioral and cognitive sequelae (Cantwell, 1981; Kessler, 1980; Stewart, 1970). Numerous articles that reported these sequelae (Ebaugh, 1923; Strecker & Ebaugh, 1924; Stryker, 1925) included many of the characteristics we now incorporate into the concept of ADHD. Such children were described as being impulsive and having impaired attention and regulation of activity, as well as impairments in other cognitive abilities, including memory; they were often noted to be socially disruptive as well. Symptoms of what is now called ODD, as well as delinquency and CD, also arose in some cases. "Postencephalitic behavior disorder," as it was called, was clearly the result of brain damage. The large number of affected 1. History of ADHD children resulted in significant professional and educational interest in this behavioral disorder. Its severity was such that many children were recommended for care and education outside the home and away from normal educational facilities. Despite a rather pessimistic view of the prognosis of these children, some facilities reported significant success in their treatment with simple behavior modification programs and increased supervision (Bender, 1942; Bond & Appel, 1931). The Origins of a Brain Damage Syndrome This association of a brain disease with behavioral pathology apparently led early investigators to study other, potential causes of brain injury in children and their behavioral manifestations, including birth trauma (Shirley, 1939); other infections besides encephalitis, such as measles (Meyer & Byers, 1952); lead toxicity (Byers & Lord, 1943); epilepsy (Levin, 1938); and head injury (Blau, 1936; Werner & Strauss, 1941). All were studied in children and found to be associated with numerous cognitive and behavioral impairments, including the triad of ADHD symptoms noted earlier. Other terms introduced during this era for children displaying these behavioral characteristics were "organic driveness" (Kahn & Cohen, 1934) and "restlessness" syndrome (Childers, 1935; Levin, 1938). Many of the children seen in these samples also had mental retardation or more serious behavioral disorders than what is today called ADHD. It would take investigators several decades to attempt to parse out the separate contributions of intellectual delay, learning disabilities, or other neuropsychological deficits from those of behavioral deficits in the maladjustment of these children. Even so, scientists at this time would discover that activity level was often inversely related to intelligence in children, increasing as intelligence declined in a sample—a finding supported in many subsequent studies (Rutter, 1989). It should also be noted that a large number of children in these older studies did in fact have brain damage or signs of such damage (epilepsy, hemiplegias, etc.). Notable during this era was also recognition of the striking similarity between hyperactivity in children and the behavioral sequelae of frontal lobe lesions in primates (Blau, 1936; Levin, 1938). Frontal lobe ablation studies of monkeys had been done more than 60 years earlier (Ferrier, 1876), and the lesions were known to result in excessive restlessness, poor ability 7 to sustain interest in activities, aimless wandering, and excessive appetite, among other behavioral changes. Several investigators, such as Levin (1938), used these similarities to postulate that severe restlessness in children might well be the result of pathological defects in the forebrain structures, although gross evidence of such was not always apparent in many of these children. Later, investigators (e.g., Barkley, 1997a; Chelune, Ferguson, Koon, & Dickey, 1986; Lou, Henriksen, & Bruhn, 1984; Lou, Henriksen, Bruhn, Borner, & Nielsen, 1989; Mattes, 1980) would return to this notion, but with greater evidence to substantiate their claims. Milder forms of hyperactivity, in contrast, were attributed in this era to psychological causes, such as "spoiled" child-rearing practices or delinquent family environments. This idea that poor or disrupted parenting causes ADHD would also be resurrected in the 1970s, and it continues even today among many laypeople and critics of ADHD. Over the next decade, it became fashionable to consider most children hospitalized in psychiatric facilities with this symptom picture to have suffered from some type of brain damage (e.g., encephalitis or prenatal– perinatal trauma), whether or not there was evidence of such in the clinical history of the case. The concept of the "brain-injured child" was born in this era (Strauss & Lehtinen, 1947) and applied to children with these behavioral characteristics, many of whom had insufficient or no evidence of brain pathology. In fact, Strauss and Lehtinen argued that the psychological disturbances alone were de facto evidence of brain injury as the etiology. Owing in part to the absence of such evidence of brain damage, this term would later evolve into the concept of "minimal brain damage" and eventually "minimal brain dysfunction" (MBD) by the 1950s and 1960s. Even so, a few early investigators, such as Childers (1935), would raise serious questions about the notion of brain damage in these children when no historical documentation of damage existed. Substantial recommendations for educating these "brain-damaged" children were made in the earlier text by Tredgold (1908) and later in the classic text on special education by Strauss and Lehtinen (1947), which served as a forerunner to special educational services adopted much later in U.S. public schools. These recommendations included placing these children in smaller, more carefully regulated classrooms and reducing the amount of distracting stimulation in the environment. Strikingly austere classrooms were developed, 8 I. THE NATURE OF ADHD in which teachers avoided wearing jewelry or brightly colored clothing, and few pictures adorned the walls so as not to interfere unnecessarily with the education of these highly distractible students. Although the population served by the Pennsylvania center in which Strauss, Werner, and Lehtinen worked principally contained children with mental retardation, the work of Cruickshank and his students (Dolphin & Cruickshank, 1951a, 1951b, 1951c) later extended these neuropsychological findings to children with cerebral palsy but near-normal or normal intelligence. This extension resulted in the extrapolation of the educational recommendations of Strauss to children without mental retardation who manifested behavioral or perceptual disturbances (Cruickshank & Dolphin, 1951; Strauss & Lehtinen, 1947). Echoes of these recommendations are still commonplace today in most educational plans for children with ADHD or learning disabilities, despite the utter lack of scientific support for their efficacy (Kessler, 1980; Routh, 1978; Zentall, 1985). These classrooms are historically significant because they were predecessors as well as instigators of the types of educational resources that would be incorporated into the initial Education for All Handicapped Children Act of 1975 (Public Law 94-142) mandating the special education of children with learning disabilities and behavioral disorders, and its later reauthorization, the Individuals with Disabilities Education Act of 1990 (IDEA; Public Law 101-476). The Beginnings of Child Psychopharmacology for ADHD Another significant series of articles on the treatment of hyperactive children appeared from 1937 to 1941. They marked the beginnings of medication therapy (particularly stimulants) for behaviorally disordered children in particular, as well as the field of child psychopharmacology in general (Bradley, 1937; Bradley & Bowen, 1940; Molitch & Eccles, 1937). Initiated originally to treat the headaches that resulted from conducting pneumoencephalograms during research studies of these disruptive youth, the administration of amphetamine resulted in a noticeable improvement in their behavioral problems and academic performance. Later studies would also confirm such a positive drug response in half or more of hyperactive hospitalized children (Laufer, Denhoff, & Solomons, 1957). As a result, by the 1970s, stimulant medications were gradually becoming the treatment of choice for the behavioral symptoms now associated with ADHD. And so they remain today (see Chapter 27). The Emergence of a Hyperkinetic Impulse Syndrome In the 1950s, researchers began a number of investigations into the neurological mechanisms underlying these behavioral symptoms, the most famous of which was probably that by Laufer and colleagues (1957). These writers referred to children with ADHD as having "hyperkinetic impulse disorder," and reasoned that the central nervous system (CNS) deficit occurred in the thalamic area. Here, poor filtering of stimulation occurred, allowing an excess of stimulation to reach the brain. The evidence was based on a study of the effects of the "photo-Metrozol" method, in which the drug metronidazole (Metrozol) is administered while flashes of light are presented to a child. The amount of drug required to induce a muscle jerk of the forearms, along with a spike wave pattern on the electroencephalogram (EEG), serves as the measure of interest. Laufer and colleagues found that inpatient children with hyperactivity required less Metrozol than those without hyperactivity to induce this pattern of response. This finding suggested that the hyperactive children had a lower threshold for stimulation, possibly in the thalamic area. No attempts to replicate this study have been done, and it is unlikely that such research would pass today's standards of ethical conduct in research required by institutional review boards on research with human subjects. Nevertheless, it remains a milestone in the history of the disorder for its delineation of a more specific mechanism that might give rise to hyperactivity (low cortical thresholds or overstimulation). Others at the time also conjectured that the existence of an imbalance between cortical and subcortical areas caused diminished control of subcortical areas responsible for sensory filtering that permitted excess stimulation to reach the cortex (Knobel, Wolman, & Mason, 1959). By the end of this era, it seemed well accepted that hyperactivity was a brain damage syndrome, even when evidence of damage was lacking. The disorder was thought to be best treated through educational classrooms characterized by reduced stimulation or through residential centers. Its prognosis was considered fair to poor. The possibility that a relatively new class of medications, the stimulants, might hold promise for its treatment was beginning to be appreciated. 1. History of ADHD The Period 1960 to 1969 The Decline of MBD and the Rise of Hyperactivity In the late 1950s and early 1960s, critical reviews began to question the concept of a unitary syndrome of brain damage in children. They also pointed out the logical fallacy that if brain damage resulted in some of these behavioral symptoms, these symptoms could be pathognomonic of brain damage without any other corroborating evidence of CNS lesions. Chief among these critical reviews were those of Birch (1964), Herbert (1964), and Rapin (1964), who questioned the validity of applying the concept of brain damage to children who had only equivocal signs of neurological involvement, not necessarily damage. A plethora of research followed on children with MBD (see Rie & Rie, 1980, for reviews); in addition, a task force by the National Institute of Neurological Diseases and Blindness (Clements, 1966) recognized at least 99 symptoms for this disorder. The concept of MBD would die a slow death as it eventually was recognized to be vague, overinclusive, of little or no prescriptive value, and without much neurological evidence (Kirk, 1963). Its remaining value was its emphasis on neurological mechanisms over the often excessive, pedantic, and convoluted environmental mechanisms proposed at that time— particularly those etiological hypotheses stemming from psychoanalytical theory, which blamed parental and family factors entirely for these problems (Hertzig, Bortner, & Birch, 1969; Kessler, 1980; Taylor, 1983). The term "MBD" would eventually be replaced by more specific labels applying to somewhat more homogeneous cognitive, learning, and behavioral disorders, such as "dyslexia," "language disorders," "learning disabilities," and "hyperactivity." These new labels were based on children's observable and descriptive deficits rather than on some underlying, unobservable etiological mechanism in the brain. The Hyperactivity Syndrome As dissatisfaction with the term "MBD" was occurring, clinical investigators shifted their emphasis to the behavioral symptom thought to most characterize the disorder—that of hyperactivity. And so the concept of a hyperactivity syndrome arose, described in the classic articles by Laufer and Denhoff (1957), Chess (1960), and other reports of this era (Burks, 1960; Ounsted, 1955; Prechtl & Stemmer, 1962). Chess defined "hy- 9 peractivity" as follows: "The hyperactive child is one who carries out activities at a higher than normal rate of speed than the average child, or who is constantly in motion, or both" (p. 2379). Chess's article was historically significant for several reasons: (1) It emphasized activity as the defining feature of the disorder rather than speculation about underlying neurological causes, as other scientists of the time would also do; (2) it stressed the need to consider objective evidence of the symptom beyond the subjective reports of parents or teachers; (3) it took the blame for the child's problems away from the parents; and (4) it separated the syndrome of hyperactivity from the concept of a brain damage syndrome. Other scientists of this era would emphasize similar points (Werry & Sprague, 1970). Hyperactivity would now be recognized as a behavioral syndrome that could not only arise from organic pathology but also occur in its absence. Even so, it would continue to be viewed as the result of some biological difficulty rather than as being due solely to environmental causes. Chess (1960) described the characteristics of 36 children diagnosed with "physiological hyperactivity" from a total of 881 children seen in a private practice. The ratio of males to females was approximately 4:1, and many children were referred prior to 6 years of age, intimating a relatively earlier age of onset than that for other childhood behavioral disorders. Educational difficulties were common in this group, particularly scholastic underachievement, and many displayed oppositional defiant behavior and poor peer relationships. Impulsive and aggressive behaviors, as well as poor attention span, were commonly associated characteristics. Chess believed that the hyperactivity could also be associated with mental retardation, organic brain damage, or serious mental illness (e.g., schizophrenia). Similar findings in later research would lead others to question the specificity and hence the utility of this symptom for the diagnosis of ADHD (Douglas, 1972). As with many of today's prescriptions, a multimodal treatment approach incorporating parent counseling, behavior modification, psychotherapy, medication, and special education was recommended. Unlike Still (1902), Chess and others writing in this era stressed the relatively benign nature of hyperactivity's symptoms and claimed that in most cases they resolved by puberty (Laufer & Denhoff, 1957; Solomons, 1965). Here, then, were the beginnings of a belief that would be widely held among clinicians well into the 1980s—that hyperactivity (ADHD) was outgrown by adolescence. 10 I. THE NATURE OF ADHD Also noteworthy in this era was the definition of hyperactivity given in the official diagnostic nomenclature at the time, the second edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-II; American Psychiatric Association, 1968). It employed only a single sentence describing the hyperkinetic reaction of childhood disorder and, following the lead of Chess (1960), stressed the view that the disorder was developmentally benign: "The disorder is characterized by overactivity, restlessness, distractibility, and short attention span, especially in young children; the behavior usually diminishes by adolescence" (p. 50). Europe and North America Diverge in Viewpoints It is likely that during this period (or even earlier), the perspective on hyperactivity in North America began to diverge from that in Europe, particularly Great Britain. In North America, hyperactivity would become a behavioral syndrome recognized chiefly by greater- than-normal levels of activity; would be viewed as a relatively common disturbance of childhood; would not necessarily be associated with demonstrable brain pathology or mental retardation; and would be regarded as more of an extreme degree in the normal variation of temperament in children. In Great Britain, the earlier and narrower view of a brain damage syndrome would continue into the 1970s: Hyperactivity or hyperkinesis was seen as an extreme state of excessive activity of an almost driven quality; was viewed as highly uncommon; and was usually thought to occur in conjunction with other signs of brain damage (e.g., epilepsy, hemiplegias, or mental retardation) or a clearer history of brain insult (e.g., trauma or infection) (Taylor, 1988). The divergence in views would lead to large discrepancies between North American and European estimations of the prevalence of the disorder, their diagnostic criteria, and their preferred treatment modalities. A rapprochement between these views would not occur until well into the 1980s (Rutter, 1988, 1989; Taylor, 1986, 1988). The Prevailing View by 1969 As Ross and Ross (1976) noted in their exhaustive and scholarly review of the era, the perspective on hyperactivity in the 1960s was that it remained a brain dysfunction syndrome, although of a milder magnitude than previously believed. The disorder was no longer ascribed to brain damage; instead, a focus on brain mechanisms prevailed. The disorder was also viewed as having a predominant and relatively homogeneous set of symptoms, chief among which was excessive activity level or hyperactivity. Its prognosis was now felt to be relatively benign because it was believed to be often outgrown by puberty. The recommended treatments now consisted of short- term treatment with stimulant medication and psychotherapy, in addition to the minimum-stimulation types of classrooms recommended in earlier years. The Period 1970 to 1979 Research in the 1970s took a quantum leap forward, with more than 2,000 published studies by the time the decade ended (Weiss & Hechtman, 1979). Numerous clinical and scientific textbooks (Cantwell, 1975; Safer & Allen, 1976; Trites, 1979; Wender, 1971) appeared, along with a most thorough and scholarly review of the literature by Ross and Ross (1976). Special journal issues were devoted to the topic (Barkley, 1978; Douglas, 1976), along with numerous scientific gatherings (Knights & Bakker, 1976, 1980). Clearly, hyperactivity had become a subject that attracted serious professional, scientific, and popular attention. By the early 1970s, the defining features of hyperactivity or hyperkinesis were broadened to include what investigators previously felt to be only associated characteristics, including impulsivity, short attention span, low frustration tolerance, distractibility, and aggressiveness (Marwitt & Stenner, 1972; Safer & Allen, 1976). Others (Wender, 1971, 1973) persisted with the excessively inclusive concept of MBD, in which even more features (e.g., motor clumsiness, cognitive impairments, and parent–child conflict) were viewed as hallmarks of the syndrome, and in which hyperactivity was unnecessary for the diagnosis. As noted earlier, the diagnostic term "MBD" would fade from clinical and scientific usage by the end of this decade—the result in no small part of the scholarly tome by Rie and Rie (1980) and critical reviews by Rutter (1977, 1982). These writings emphasized the lack of evidence for such a broad syndrome. The symptoms were not well defined, did not correlate significantly among themselves, had no well-specified etiology, and displayed no common course and outcome. The heterogeneity of the disorder was overwhelming, and more than a few commentators took note of the apparent hypocrisy in defin- 1. History of ADHD ing an MBD syndrome with the statement that there was often little or no evidence of neurological abnormality (Wender, 1971). Moreover, even in cases of well- established cerebral damage, the behavioral sequelae were not uniform across cases, and hyperactivity was seen in only a minority of individuals. Hence, contrary to 25 years of theorizing to this point, hyperactivity was not a common sequela of brain damage; children with true brain damage did not display a uniform pattern of behavioral deficits; and children with hyperactivity rarely had substantiated evidence of neurological damage (Rutter, 1989). Wender's Theory of MBD This decade was notable for two different models of the nature of ADHD (see also Barkley, 1998): Wender's theory of MBD (outlined here) and Douglas's model of attention and impulse control in hyperactive children (discussed in a later section). At the start of the decade, Wender (1971) described the essential psychological characteristics of children with MBD as comprising six clusters of symptoms: problems in (1) motor behavior, (2) attentional and perceptual–cognitive functioning, (3) learning, (4) impulse control, (5) interpersonal relations, and (6) emotion. Many of the characteristics first reported by Still (1902) were echoed by Wender (1971) within these six domains of functioning. 1. Within the realm of motor behavior, the essential features were noted to be hyperactivity and poor motor coordination. Excessive speech, colic, and sleeping difficulties were thought to be related to the hyperactivity. Foreshadowing the later official designation of a group of children with attentional problems but without hyperactivity (American Psychiatric Association, 1980), Wender (1971) expressed the opinion that some of these children who were hypoactive and listless still demonstrated attention disturbances. Such cases might now be considered to have the predominantly inattentive type of ADHD. He argued that they should be viewed as having this syndrome because of their manifestation of many of the other difficulties thought to characterize it. 2. Short attention span and poor concentration were described as the most striking deficits in the domain of attention and perceptual–cognitive functioning. Distractibility and daydreaming were also included with these attention disturbances, as was poor organization of ideas or percepts. 11 3. Learning difficulties were another domain of dysfunction, with most of these children observed to be doing poorly in their academic performance. A large percentage were described as having specific difficulties with learning to read, with handwriting, and with reading comprehension and arithmetic. 4. Impulse control problems, or a decreased ability to inhibit behavior, were identified as a characteristic of most children with MBD. Within this general category, Wender (1971) included low frustration tolerance; an inability to delay gratification; antisocial behavior; lack of planning, forethought, or judgment; and poor sphincter control, leading to enuresis and encopresis. Disorderliness or lack of organization and recklessness (particularly with regard to bodily safety) were also listed within this domain of dysfunction. 5. In the area of interpersonal relations, Wender (1971) singled out the unresponsiveness of these children to social demands as the most serious. Extraversion, excessive independence, obstinence, stubbornness, negativism, disobedience, noncompliance, sassiness, and imperviousness to discipline were some of the characteristics that instantiated the problem with interpersonal relations. 6. Finally, within the domain of emotional difficulties, Wender (1971) included increased lability of mood, altered reactivity, increased anger, aggressiveness, and temper outbursts, as well as dysphoria. The dysphoria of these children involved the specific difficulties of anhedonia, depression, low self-esteem, and anxiety. A diminished sensitivity to both pain and punishment was also felt to typify this area of dysfunction in children with MBD. All these symptoms bear a striking resemblance to the case descriptions that Still (1902) had provided in lectures to support his contention that a defect in moral control and volitional inhibition could exist in children apart from intellectual delay. Wender (1971) theorized that these six domains of dysfunction could be best accounted for by three primary deficits: (1) a decreased experience of pleasure and pain, (2) a generally high and poorly modulated level of activation, and (3) extraversion. A consequence of the first deficit was that children with MBD would prove less sensitive to both reward and punishment, making them less susceptible to social influence. The generally high and poorly modulated level of activation was thought to be an aspect of poor inhibition. Hyperactivity, of course, was the consummate demon- 12 I. THE NATURE OF ADHD stration of this high level of activation. The problems with poor sustained attention and distractibility were conjectured to be secondary aspects of high activation. Emotional overreactivity, low frustration tolerance, quickness to anger, and temper outbursts resulted from the poor modulation of activation. These three primary deficits, then, created a cascade of effects into the larger social ecology of these children, resulting in numerous interpersonal problems and academic performance difficulties. Like Still (1902), Wender (1971) gave a prominent role to the construct of poor inhibition. He believed that it explained the activation difficulties and the attention problems stemming from them, as well as the excessive emotionality, the low frustration tolerance, and the hot-temperedness of these children. It is therefore quite puzzling why deficient inhibition was not made a primary symptom in this theory, in place of high activation and poor modulation of activation. Unlike Still (1902), who attempted to devise a theory, however, Wender (1971) did not say much about normal developmental processes with respect to the three primary areas of deficit, and therefore did not clarify more precisely what might be going awry in them to give rise to these characteristics of MBD. The exception was his discussion of a diminished sensitivity to the reasonably well-understood processes of reinforcement and punishment. A higher-than-normal threshold for pleasure and pain, as noted earlier, was thought to create these insensitivities to behavioral consequences. From a present-day perspective, Wender (1971) is also unclear about a number of issues. For instance, how would the three primary deficits account for the difficulties with motor coordination that occurred alongside hyperactivity in his category of motor control problems? It is doubtful that the high level of activation that was said to cause the hyperactivity would also cause these motor deficits. Nor is it clear just how the academic achievement deficits in reading, math, and handwriting could arise from the three primary deficits in the model. It is also unclear why the construct of extraversion needed to be proposed at all, if what Wender meant by it was reduced social inhibition. This model might be just as parsimoniously explained by the deficit in behavioral inhibition already posited. And the meaning of the term "activation" as used by Wender is not very clearly specified. Did it refer to excessive behavior, in which case hyperactivity would have sufficed? Or did it refer to level of CNS arousal, in which case ample subsequent evidence has not found this to be the case (Hastings & Barkley, 1978; Rosenthal & Allen, 1978)? To his credit, Wender recognized the abstract nature of the term "activation" as he employed it in this theory but retained it because he felt it could be used to incorporate both hyperactivity and hypoactivity in children. It is never made clear just how this could be the case, however. Finally, Wender failed to distinguish symptoms from their consequences (impairments). The former would be the behavioral manifestations directly associated with or stemming from the disorder itself, such as impulsiveness, inattention, distractibility, and hyperactivity. The latter would be the effects of these behaviors on the social environment, such as interpersonal conflict within the family, poor educational performance, peer rejection, and accident proneness, to name just a few. From the advantage of hindsight and subsequent research over the decades since the formulation of this theory, it is also evident that Wender (1971) was combining the symptoms of ODD (and even CD) with those of ADHD to form a single disorder. Still (1902) did very much the same thing. This was understandable given that clinic-referred cases were the starting point for both theories, and many clinic-referred cases are comorbid for both disorders (ADHD and ODD). However, sufficient accumulated evidence has subsequently shown that ADHD and ODD are not the same disorder (August & Stewart, 1983; Hinshaw, 1987; Stewart, deBlois, & Cummings, 1980). The Emergence of a Central Place for Attention Deficits At this time, disenchantment developed over the exclusive focus on hyperactivity as the sine qua non of this disorder (Werry & Sprague, 1970). Significant at this historical juncture would be the article based on the presidential address of Virginia Douglas (1972) to the Canadian Psychological Association. She argued that deficits in sustained attention and impulse control were more likely than just hyperactivity to account for the difficulties seen in these children. These other symptoms were also seen as the major areas on which the stimulant medications used to treat the disorder had their impact. Douglas's article was historically significant in other ways as well. Her extensive and thorough battery of objective measures of various behavioral and cognitive domains, heretofore unused in research on ADHD, allowed her to rule in or out 1. History of ADHD various characteristics felt to be typical for these children in earlier clinical and scientific lore. For instance, Douglas found that hyperactive children did not necessarily and uniformly have more reading or other learning disabilities than other children, did not perseverate on concept-learning tasks, did not manifest auditory or right–left discrimination problems, and had no difficulties with short-term memory. Most important, she and Susan Campbell (1973) demonstrated that children with hyperactivity were not always more distractible than children without it, and that the sustained attention problems could emerge in conditions in which no significant distractions existed. The McGill University research team headed by Douglas repeatedly demonstrated that hyperactive children had some of their greatest difficulties on tasks assessing vigilance or sustained attention, such as the continuous- performance test (CPT). These findings would be repeatedly reconfirmed over the next 30 years of research using CPTs (Corkum & Siegel, 1993; Frazier, Demareem, & Youngstrom, 2004). Variations of this test would eventually be standardized and commercially marketed for diagnosis of the disorder (Conners, 1995; Gordon, 1983; Greenberg & Waldman, 1992). Douglas (1972) remarked on the extreme degree of variability demonstrated during task performances by these children—a characteristic that would later be advanced as one of the defining features of the disorder. The McGill team (Freibergs, 1965; Freibergs & Douglas, 1969; Parry & Douglas, 1976) also found that hyperactive children could perform at normal or near-normal levels of sustained attention under conditions of continuous and immediate reinforcement, but that their performance deteriorated dramatically when partial reinforcement was introduced, particularly at schedules below 50% reinforcement. Campbell, Douglas, and Morgenstern (1971) further demonstrated substantial problems with impulse control and field dependence in the cognitive styles of hyperactive children. Like Still (1902), roughly 70 years earlier, Douglas commented on the probable association between deficits in attention–impulse control and deficiencies in moral development that were plaguing her subjects, particularly in their adolescent years. The research of the McGill team showed dramatic improvements in these attention deficiencies during stimulant medication treatment, as did the research at other laboratories at the time (Conners & Rothschild, 1968; Sprague, Barnes, & Werry, 1970). Finally, of substantial significance were the observations of Douglas's colleague, Gabrielle Weiss, from 13 her follow-up studies (see Weiss & Hechtman, 1986) that although the hyperactivity of these children often diminished by adolescence, their problems with poor sustained attention and impulsivity persisted. This persistence of the disabilities and the risk for greater academic and social maladjustment would be identified by other research teams from their own follow-up investigations (Mendelson, Johnson, & Stewart, 1971), and would be better substantiated by more rigorous studies in the next two decades (see Barkley, Fischer, Edelbrock, & Smallish, 1990; Barkley, Fischer, Smallish, & Fletcher, 2002; Gittelman, Mannuzza, Shenker, & Bonagura, 1985). Douglas's Model of Attention Deficits Douglas (1980a, 1980b, 1983; Douglas & Peters, 1979) later elaborated, refined, and further substantiated her model of hyperactivity, which culminated in the view that four major deficits could account for symptoms of ADHD: (1) the investment, organization, and maintenance of attention and effort; (2) the inhibition of impulsive responding; (3) the modulation of arousal levels to meet situational demands; and (4) an unusually strong inclination to seek immediate reinforcement. This perspective initiated or guided a substantial amount of research over the next 15 years, including my own early studies (Barkley, 1977, 1989b; Barkley & Ullman, 1975). It constituted a model as close to a scientific paradigm as the field of hyperactivity was likely to have in its history to that point. Yet over the next 10 years results that emerged were somewhat at odds with this perspective. Scientists began seriously to question both the adequacy of an attention model in accounting for the varied behavioral deficits seen in children with ADHD and the effects of stimulant medications on them (Barkley, 1981, 1984; Draeger, Prior, & Sanson, 1986; Haenlein & Caul, 1987; van der Meere & Sergeant, 1988a, 1988b). Also deserving of mention is that such a description of deficiencies constitutes a pattern and not a theory, given that it stipulates no conditional relations among its parts or how they orchestrate to create the problems seen in the disorder. That is, it makes no testable or falsifiable predictions apart from those contained in the pattern so described. Douglas's article and the subsequent research published by her team were so influential that they were probably the major reasons the disorder was renamed attention deficit disorder (ADD) in 1980 with the publication of DSM-III (American Psychiatric Associa- 14 I. THE NATURE OF ADHD tion, 1980). In this revised official taxonomy, deficits in sustained attention and impulse control were formally recognized as being of greater significance in the diagnosis than hyperactivity. The shift to attention deficits rather than hyperactivity as the major difficulty of these children was useful, at least for a time, because of the growing evidence (1) that hyperactivity was not specific to this particular condition but could be noted in other psychiatric disorders (anxiety, mania, autism, etc.); (2) that there was no clear delineation between "normal" and "abnormal" levels of activity; (3) that activity was in fact a multidimensional construct; and (4) that the symptoms of hyperactivity were quite situational in nature in many children (Rutter, 1989). But this approach corrected the problem of definition for little more than a decade before these same concerns were also raised about the construct of attention (multidimensional, situationally variable, etc.). Yet some research would show that at least deficits in vigilance or sustained attention could be used to discriminate this disorder from other psychiatric disorders (Werry, 1988). Other Developments of the Era A number of other historical developments during this period deserve mention. The Rise of Medication Therapy The first of these developments was the rapidly increasing use of stimulant medication with school-age hyperactive children. This use was no doubt spawned by the significant increase in research showing that stimulants often had dramatic effects on these children's hyperactive and inattentive behavior. A second development was the use of much more rigorous scientific methodology in drug studies, due in large measure to the early studies by C. Keith Conners (then working with Leon Eisenberg at Harvard University), and somewhat later to the research of Robert Sprague at the University of Illinois, Virginia Douglas at McGill University, and John Werry in New Zealand. This body of literature became voluminous (see Barkley, 1977; Ross & Ross, 1976), with more than 120 studies published through 1976 and more than twice this number by 1995 (Swanson, McBurnett, Christian, & Wigal, 1995), making this treatment approach the most well-studied therapy in child psychiatry. Despite the proven efficacy of stimulant medication, public and professional misgivings about its increasing- ly widespread use with children emerged. For example, one news account (Maynard, 1970) reported that in Omaha, Nebraska, as much as 5–10% of the children in grade schools were receiving behavior- modifying drugs. This estimate of drug treatment would later be shown to be grossly exaggerated, as much as 10-fold, due to a misplaced decimal point in the story. And this would certainly not be the last instance of the mass media's penchant for hyperbole, sensation, and scandal in their accounts of stimulant medication treatments for ADHD—a penchant that seems only to have increased over subsequent years. Yet the public interest that was generated by the initial reports led to a congressional review of the use of psychotropic medications for schoolchildren. At this same time, the claim was being advanced that hyperactivity was a "myth" arising from intolerant teachers and parents, and an inadequate educational system (Conrad, 1975; Schrag & Divoky, 1975). Environment as Etiology Almost simultaneous with this backlash against "drugging" schoolchildren for behavior problems was another significant development in that decade: a growing belief that hyperactivity was a result of environmental causes. It is not just coincidental that this development occurred at the same time that the United States was experiencing a popular interest in natural foods, health consciousness, the extension of life expectancy via environmental manipulations, psychoanalytic theory, and behaviorism. An extremely popular view was that allergic or toxic reactions to food additives, such as dyes, preservatives, and salicylates (Feingold, 1975), caused hyperactive behavior. It was claimed that more than half of all hyperactive children had developed their difficulties because of diet. Effective treatment could be had if families of these children would buy or make foods that did not contain the offending substances. This view became so widespread that organized parent groups or "Feingold associations," comprised mainly of parents advocating Feingold's diet, were established in almost every U.S. state, and legislation was introduced (although not passed) in California requiring that all school cafeteria foods be prepared without these substances. A sizable number of research investigations was undertaken (see Conners, 1980, for a review), the more rigorous of which found these substances to have little, if any, effect on children's behavior. A National Advisory Committee on Hyperkinesis and Food Addi- 1. History of ADHD tives (1980) that was convened to review this literature concluded more strongly than Conners that the available evidence clearly refuted Feingold's claims. Nevertheless, it would be more than 10 years before this notion receded in popularity, to be replaced by the equally unsupported hypothesis that refined sugar was more to blame for hyperactivity than were food additives (for reviews, see Milich, Wolraich, & Lindgren, 1986; Wolraich, Wilson, & White, 1995). The emphasis on environmental causes, however, spread to include possible sources other than diet. Block (1977) advanced the rather vague notion that technological development and more rapid cultural change would result in an increasing societal "tempo," causing growing excitation or environmental stimulation. This excitation or stimulation would interact with a predisposition in some children toward hyperactivity, making it manifest. It was felt that this theory explained the apparently increasing incidence of hyperactivity in developed cultures. Ross and Ross (1982) provided an excellent critique of the theory and concluded that there was insufficient evidence in support of it and some that would contradict it. Little evidence suggested that hyperactivity incidence was increasing, though its identification among children may well have been. Nor was there evidence that its prevalence varied as a function of societal development. Instead, Ross and Ross proposed that cultural effects on hyperactivity have more to do with whether important institutions of enculturation are consistent or inconsistent in the demands made and standards set for child behavior and development. These cultural views were said to determine the threshold for deviance that will be tolerated in children, as well as to exaggerate a predisposition to hyperactivity in some children. Consistent cultures will have fewer children diagnosed with hyperactivity, as they minimize individual differences among children and provide clear and consistent expectations and consequences for behavior that conforms to the expected norms. Inconsistent cultures, by contrast, will have more children diagnosed with hyperactivity, as they maximize or stress individual differences and provide ambiguous expectations and consequences to children regarding appropriate conduct. This intriguing hypothesis remains unstudied. However, on these grounds, an equally compelling case could be made for the opposite effects of cultural influences: In highly consistent, highly conforming cultures, hyperactive behavior may be considerably more obvious in children as they are unable to conform to these societal expec- 15 tations, whereas inconsistent and low-conforming cultures may tolerate deviant behavior to a greater degree as part of the wider range of behavioral expression they encourage. A different environmental view—that poor childrearing generally and poor child behavior management specifically lead to hyperactivity—was advanced by schools of psychology/psychiatry at diametrically opposite poles. Both psychoanalysts (Bettelheim, 1973; Harticollis, 1968) and behaviorists (Willis & Lovaas, 1977) promulgated this view, though for very different reasons. The psychoanalysts claimed that parents lacking tolerance for negative or hyperactive temperament in their infants would react with excessively negative, demanding parental responses, giving rise to clinical levels of hyperactivity. The behaviorists stressed poor conditioning of children to stimulus control by commands and instructions that would give rise to noncompliant and hyperactive behavior. Both groups singled out mothers as especially etiologically important in this causal connection, and both could derive some support from studies that found negative mother–child interactions in the preschool years to be associated with the continuation of hyperactivity into the late childhood (Campbell, 1987) and adolescent (Barkley, Fischer, et al., 1990) years. However, such correlational data cannot prove a cause. They do not prove that poor childrearing or negative parent–child interactions cause hyperactivity; they only show that such factors are associated with its persistence. It could just as easily be that the severity of hyperactivity elicits greater maternal negative reactions, and that this severity is related to persistence of the disorder over time. Supporting this interpretation are the studies of stimulant drug effects on the interactions of mothers and their hyperactive children, which show that mothers' negative and directive behavior is greatly reduced when stimulant medication is used to reduce the hyperactivity in their children (Barkley, 1989b; Barkley & Cunningham, 1979; Barkley, Karlsson, Pollard, & Murphy, 1985; Danforth, Barkley, & Stokes, 1991). Moreover, follow-up studies show that the degree of hyperactivity in childhood is predictive of its own persistence into later childhood and adolescence, apart from its association with maternal behavior (Barkley, Fischer, et al., 1990; Campbell & Ewing, 1990). And given the dramatic hereditary contribution to ADHD, it is also just as likely that the more negative, impulsive, emotional, and inattentive behavior of mothers with their hyperactive children stems in 16 I. THE NATURE OF ADHD part from the mothers' own ADHD—a factor that has never been taken into account in the analysis of such data or in interpreting findings in this area. Nevertheless, family context would still prove to be important in predicting the outcome of hyperactive children, even though the mechanism of its action was not yet specified (Weiss & Hechtman, 1986). Parent training in child behavior management, furthermore, would be increasingly recommended as an important therapy in its own right (Dubey & Kaufman, 1978; Pelham, 1977), despite a paucity of studies concerning its actual efficacy at the time (Barkley, 1989c). The Passage of Public Law 94‑142 Another highly significant development was the passage of Public Law 94-142 in 1975, mandating special educational services for children with physical, learning, and behavioral disabilities, in addition to those services already available for mental retardation (see Henker & Whalen, 1980, for a review of the legal precedents leading up to this law). Although many of its recommendations were foreshadowed by Section 504 of the Rehabilitation Act of 1973 (Public Law 93-112), the financial incentives for the states associated with the adoption of Public Law 94-142 probably encouraged its immediate and widespread implementation by them all. Programs for learning disabilities, behavioral– emotional disturbance, language disorders, physical handicaps, and motor disabilities, among others, were now required to be provided to all eligible children in all public schools in the United States. The full impact of these widely available educational treatment programs for hyperactive children has not yet been completely appreciated, for several reasons. First, hyperactivity, by itself, was overlooked in the initial criteria set forth for behavioral and learning disabilities warranting eligibility for these special classes. Children with such disabilities typically also had to have another condition, such as a learning disability, language delay, or emotional disorder, to receive exceptional educational services. The effects of special educational resources on the outcome of hyperactivity are difficult to assess given this confounding of multiple disorders. It was only after the passage of IDEA in 1990 (and a subsequent 1991 memorandum) that the U.S. Department of Education and its Office of Special Education chose to reinterpret these regulations, thereby allowing children with ADHD to receive special educational services for ADHD per se under the "Other Health Impaired" category of IDEA. Second, the mandated services had been in existence for only a little more than a decade when the long-term outcome studies begun in the late 1970s began to be reported. Those studies (e.g., Barkley, Fischer, et al., 1990) suggested that over 35% of children with ADHD received some type of special educational placement. Although the availability of these services seems to have reduced the percentage of children with ADHD retained in grade for their academic problems, compared to earlier follow-up studies, the rates of school suspensions and expulsions did not decline appreciably from pre-1977 rates. A more careful analysis of the effects of Public Law 94-142, and especially of its more recent reauthorization as the IDEA, is in order before its efficacy for children with ADHD can be judged. The Rise of Behavior Modification This growing emphasis on educational intervention for children with behavioral and learning disorders was accompanied by a plethora of research on the use of behavior modification techniques in the management of disruptive classroom behavior, particularly as an alternative to stimulant medication (Allyon, Layman, & Kandel, 1975; O'Leary, Pelham, Rosenbaum, & Price, 1976). Supported in large part by their successful use for children with mental retardation, behavioral technologies were now being extended to myriad childhood disorders—not only as potential treatments of symptoms but also as theoretical statements of their origins. Although the studies demonstrated considerable efficacy of these techniques in the management of inattentive and hyperactive behavior, they were not found to achieve the same degree of behavioral improvement as the stimulants (Gittelman-Klein et al., 1976), and so did not replace them as a treatment of choice. Nevertheless, opinion was growing that the stimulant drugs should never be used as a sole intervention, but should be combined with parent training and behavioral interventions in the classroom to provide the most comprehensive management approach for the disorder. Developments in Assessment Another hallmark of this era was the widespread adoption of the parent and teacher rating scales developed by C. Keith Conners (1969) for the assessment of symptoms of hyperactivity, particularly during trials on stimulant medication. For at least 20 years, these simply constructed ratings of behavioral items would be the "gold standard" for rating children's hyperac- 1. History of ADHD tivity for both research purposes and treatment with medication. The scales would also come to be used for monitoring treatment responses during clinical trials. Large- scale normative data were collected, particularly for the teacher scale, and epidemiological studies throughout the world relied on both scales for assessing the prevalence of hyperactivity in their populations. Their use moved the practice of diagnosis and the assessment of treatment effects from that of clinical impression alone to one in which at least some structured, semi-objective, and quantitative measure of behavioral deviance was employed. These scales would later be criticized for their confounding of hyperactivity with aggression. This confounding called into question whether the findings of research that relied on the scales were the result of oppositional, defiant, and hostile (aggressive) features of the population or of their hyperactivity (Ullmann, Sleator, & Sprague, 1984). Nevertheless, the widespread adoption of these rating scales in this era marks a historical turning point toward the use of quantitative assessment methods that can be empirically tested and assist in determining developmental patterns and deviance from norms. Also significant during this decade was the effort to study the social-ecological impact of hyperactive– inattentive behavior. This line of research set about evaluating the effects on family interactions produced by a child with hyperactivity. Originally initiated by Campbell (1973, 1975), this line of inquiry dominated my own research over the next decade (Barkley & Cunningham, 1979; Cunningham & Barkley, 1978, 1979; Danforth et al., 1991), particularly evaluations of the effects of stimulant medication on these social exchanges. These studies showed that children with hyperactivity were much less compliant and more oppositional during parent–child exchanges than children without it, and that their mothers were more directive, commanding, and negative than mothers of nonhyperactive children. These difficulties would increase substantially when the situation changed from free-play to task-oriented demands. Studies also demonstrated that stimulant medication resulted in significant improvements in child compliance and decreases in maternal control and directiveness. Simultaneously, Humphries, Kinsbourne, and Swanson (1978) reported similar effects of stimulant medication, all of which suggested that much of parents' controlling and negative behavior toward hyperactive children was the result rather than the cause of the children's poor self-control and inattention. At the same time, Carol Whalen and Barbara Henker at the University of California–Irvine 17 demonstrated similar interaction conflicts between hyperactive children and their teachers and peers, as well as similar effects of stimulant medication on these social interactions (Whalen & Henker, 1980; Whalen, Henker, & Dotemoto, 1980). This line of research would increase substantially in the next decade, and would be expanded by Charles Cunningham and others to include studies of peer interactions and the effects of stimulants on them (Cunningham, Siegel, & Offord, 1985). A Focus on Psychophysiology The decade of the 1970s was also noteworthy for a marked increase in the number of research studies on the psychophysiology of hyperactivity in children. There were numerous published studies measuring galvanic skin response, heart rate acceleration and deceleration, various parameters of the EEG, electropupillography, averaged evoked responses, and other aspects of electrophysiology. Many researchers were investigating the evidence for theories of over- or underarousal of the CNS in hyperactivity—theories that grew out of the speculations in the 1950s on cortical overstimulation and the ideas of both Wender (1971) and Douglas (1972; both discussed earlier) regarding abnormal arousal in the disorder. Most of these studies were seriously methodologically flawed, difficult to interpret, and often contradictory in their findings. Two influential reviews at the time (Hastings & Barkley, 1978; Rosenthal & Allen, 1978) were highly critical of most investigations but concluded that if there was any consistency across findings, it might be that hyperactive children showed a sluggish or underreactive electrophysiological response to stimulation. These reviews laid to rest the belief in an overstimulated cerebral cortex as the cause of the symptoms in hyperactivity, but they did little to suggest a specific neurophysiological mechanism for the observed underreactivity. Further advances in the contributions of psychophysiology to understanding hyperactivity would await further refinements in instrumentation and in definition and diagnosis of the disorder, along with advances in computer-assisted analysis of electrophysiological measures. An Emerging Interest in Adult MBD or Hyperactivity Finally, the 1970s should be credited with the emergence of clinical and research interests in the existence of MBD or hyperactivity in adult clinical patients. Ini- 18 I. THE NATURE OF ADHD tial interest in adult MBD can be traced to the latter part of the 1960s, seemingly arising as a result of two events. The first of these was the publication of several early follow-up studies demonstrating persistence of symptoms of hyperactivity or MBD into adulthood in many cases (Mendelson et al., 1971; Menkes, Rowe, & Menkes, 1967). The second was the publication by Harticollis (1968) of the results of neuropsychological and psychiatric assessments of 15 adolescent and young adult patients (ages 15–25) seen at the Menninger Clinic. The neuropsychological performance of these patients suggested evidence of moderate brain damage. Their behavioral profile suggested many of the symptoms that Still (1902) initially identified in the children he studied, particularly impulsiveness, overactivity, concreteness, mood lability, and proneness to aggressive behavior and depression. Some of the patients appeared to have demonstrated this behavior uniformly since childhood. Using psychoanalytic theory, Harticollis speculated that this condition arose from an early and possibly congenital defect in the ego apparatus, in interaction with busy, action-oriented, successful parents. The following year, Quitkin and Klein (1969) reported on two behavioral syndromes in adults that might be related to MBD. The authors studied 105 patients at the Hillside Hospital in Glen Oaks, New York, for behavioral signs of "organicity" (brain damage); behavioral syndromes that might be considered neurological "soft signs" of CNS impairment; and any EEG findings, psychological testing results, or aspects of clinical presentation and history that might differentiate these patients from patients with other types of adult psychopathology. From the initial group of 105 patients, the authors selected those having a childhood history that suggested CNS damage, including early hyperactive and impulsive behavior. These subjects were further sorted into three groups based on current behavioral profiles: those having socially awkward and withdrawn behavior (n = 12), those having impulsive and destructive behavior (n = 19), and a "borderline" group that did not fit neatly into these other two groups (n = 11). The results indicated that nearly twice as many of the patients in these three "organic" groups as those in the control group had EEG abnormalities and impairments on psychological testing indicating organicity. Furthermore, early history of hyperactive– impulsive–inattentive behavior was highly predictive of placement in the adult impulsive–destructive group, implying a persistent course of this behavioral pattern from childhood to adulthood. Of the 19 patients in the impulsive–destructive group, 17 had received clinical diagnoses of character disorders (primarily emotionally unstable types), as compared to only five patients in the socially awkward group (who received diagnoses of the schizoid and passive–dependent types). The results were interpreted as being in conflict with the beliefs widely held at the time that hyperactive– impulsive behavior tends to wane in adolescence. Instead, the authors argued that some of these children continued into young adulthood with this specific behavioral syndrome. Quitkin and Klein (1969) also took issue with Harticollis's (1968) psychoanalytic hypothesis that demanding and perfectionistic childrearing by parents caused or contributed to this syndrome given that their impulsive–destructive patients did not uniformly experience such an upbringing. In keeping with Still's (1902) original belief that family environment could not account for this syndrome, these authors hypothesized "that such parents would intensify the difficulty, but are not necessary to the formation of the impulsive–destructive syndrome" (Quitkin & Klein, 1969, p. 140) and that the "illness shaping role of the psycho-social environment may have been over- emphasized by other authors" (p. 141). Treatment with a well-structured set of demands and educational procedures, as well as with phenothiazine medication, was thought to be indicated. Later in this decade, Morrison and Minkoff (1975) similarly argued that explosive personality disorder or episodic dyscontrol syndrome in adulthood might well be the adult sequel to the hyperactivity syndrome in childhood. They also suggested that antidepressant medications might be useful in their management; this echoed a suggestion made earlier by Huessy (1974) in a letter to the editor of a journal that both antidepressants and stimulants might be the most useful medications for the treatment of adults with hyperkinesis or MBD. But the first truly scientific evaluation of the efficacy of stimulants for adults with MBD must be credited to Wood, Reimherr, Wender, and Johnson (1976), who used a double-blind, placebo-controlled method to assess response to methylphenidate in 11 of 15 adults with MBD, followed by an open trial of pemoline (another stimulant) and the antidepressants imipramine and amitriptyline. The authors found that eight of the 11 individuals tested on methylphenidate had a favorable response, whereas 10 of the 15 individuals tested in the open trial showed a positive response to either the stimulants or the antidepressants. Others in the 1970s and into the 1980s would also make the case for the existence of an adult equivalent of childhood hyperki- 1. History of ADHD nesis or MBD and the efficacy of using stimulants and antidepressants for its management (Gomez, Janowsky, Zetin, Huey, & Clopton, 1981; Mann & Greenspan, 1976; Packer, 1978; Pontius, 1973; Rybak, 1977; Shelley & Riester, 1972). Yet not until the 1990s would both the lay public and the professional field of adult psychiatry seriously begin to recognize the adult equivalent of childhood ADHD on a more widespread basis and to recommend stimulant or antidepressant treatment in these cases (Spencer et al., 1995; Wender, 1995) and even then the view was not without its critics (Shaffer, 1994). The work of Pontius (1973) in this decade is historically notable for her proposition that many cases of MBD in adults demonstrating hyperactive and impulsive behavior may arise from frontal lobe and caudate dysfunction. Such dysfunction would lead to "an inability to construct plans of action ahead of the act, to sketch out a goal of action, to keep it in mind for some time (as an overriding idea) and to follow it through in actions under the constructive guidance of such planning" (p. 286). Moreover, if adult MBD arises from dysfunction in this frontal–caudate network, it should also be associated with an inability "to re-program an ongoing activity and to shift within principles of action whenever necessary" (p. 286, original emphasis). Pontius went on to show that, indeed, adults with MBD demonstrated deficits indicative of dysfunction in this brain network. Such observations would prove quite prophetic over 20 years later, when research demonstrated reduced size in the prefrontal–caudate network in children with ADHD (Castellanos et al., 1996; Filipek et al., 1997), and when ADHD theorists argued that the neuropsychological deficits associated with it involved the executive functions, such as planning; and the control of behavior by mentally represented information, rule- governed behavior, and response fluency and flexibility; among other deficits (Barkley, 1997a, 1997c). The Prevailing View by 1979 The 1970s closed with the prevailing view that hyperactivity was not the only or most important behavioral deficit seen in hyperactive children, and that poor attention span and impulse control were equally (if not more) important in explaining their problems. Brain damage was relegated to an extremely minor role as a cause of the disorder, at least in the realm of childhood hyperactivity or MBD; however, other brain mechanisms, such as under-arousal or under-reactivity, brain 19 neurotransmitter deficiencies (Wender, 1971), or neurological immaturity (Kinsbourne, 1977), were viewed as promising. Greater speculation about potential environmental causes or irritants emerged, particularly diet and childrearing. Thus, the most frequently recommended therapies for hyperactivity were not only stimulant medication but also widely available special education programs, classroom behavior modification, dietary management, and parent training in child management skills. A greater appreciation for the effects of hyperactive children on their immediate social ecology, and for the impact of stimulant medication in altering these social conflicts, was beginning to emerge. However, the sizable discrepancy between North American and European views of the disorder remained: North American professionals continued to recognize the disorder as more common, in need of medication, and more likely to be an attention deficit, while those in Europe continued to view it as uncommon, defined by severe overactivity, and associated with brain damage. Those children in North America diagnosed as having hyperactivity or attention deficits would in Europe likely be diagnosed as having CD and be treated with psychotherapy, family therapy, and parent training in child management. Medication would be disparaged and little used. Nevertheless, the view that attention deficits were as important in the disorder as hyperactivity was beginning to make its way into European taxonomies (e.g., the International Classification of Diseases, ninth revision [ICD-9]; World Health Organization, 1978). Finally, in the 1970s there was some recognition that there were adult equivalents of childhood hyperactivity or MBD, that they might be indicative of frontal–caudate dysfunction, and