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ADHDHistory.ppt

  1. 1. ADHD: Historical Overview FIDGITY PHIL 1845 by German Psychiatrist, Dr. Heinrich Hoffman James H. Johnson, Ph.D University of Florida
  2. 2. ADHD: Not a New Problem <ul><li>Characteristics of this disorder have been recognized for over a century. </li></ul><ul><li>See the Story of Fidgity Phillip </li></ul><ul><li>The disorder has been referred to by a variety of labels over the years; </li></ul><ul><ul><li>Minimal Brain Dysfunction (MBD) </li></ul></ul><ul><ul><li>Hyperkinetic Reaction of Childhood </li></ul></ul><ul><ul><li>Attention Deficit Disorder (ADD) </li></ul></ul><ul><ul><li>Attention Deficit Hyperactivity Disorder (ADHD) </li></ul></ul>
  3. 3. Assumed Core Features <ul><li>Various characteristics have been highlighted as the “core feature” of the disorder. </li></ul><ul><li>These have included: </li></ul><ul><ul><li>Minimal Brain Damage </li></ul></ul><ul><ul><li>Hyperactivity </li></ul></ul><ul><ul><li>Attention Deficits </li></ul></ul><ul><ul><li>Disinhibition of Behavior </li></ul></ul>
  4. 4. The Evolution of ADHD <ul><li>Views of the condition we now refer to as ADHD have evolved over the years. </li></ul><ul><li>Today I would like to briefly walk you through the evolution of this disorder. </li></ul><ul><li>The next few slides list some of the events that have influenced how we view this disorder today. </li></ul><ul><li>This discussion draws heavily on Barkley (1998, 2005). </li></ul>
  5. 5. ADHD: Milestones in the Evolution of the Disorder <ul><li>The Still (1902) Lectures to the Royal College of Physicians </li></ul><ul><li>Encephalitis epidemic of 1917 (Ebaugh 1923) </li></ul><ul><li>Frontal lobe ablation studies with primates (1930’s) </li></ul><ul><li>Beginnings of child psychopharmacology; Amphetamines for treatment – 1930-1940. </li></ul><ul><li>Strauss’ work on Minimal Brain Dysfunction (1940's -1950's) </li></ul><ul><li>MBD becomes Hyperkinetic Disorder (the 1960’s) </li></ul>
  6. 6. ADHD: Evolution of the Disorder (cont.) <ul><li>Hyperkinesis becomes ADD – The decade of the 70’s </li></ul><ul><li>Focus on Dietary Factors – Feingold and the 1970’s </li></ul><ul><li>Studies of pschophysiological responsivity – the 1970’s </li></ul><ul><li>Development of objective diagnostic criteria: DSM III and the recognition of Attention Deficit Disorder – The early 80’s </li></ul>
  7. 7. ADHD: Evolution of the Disorder (cont.) <ul><li>The decade of the 80’s: DSM III & DSM III-R stimulates ADHD research </li></ul><ul><li>Development of new assessment methods </li></ul><ul><li>New treatment methods </li></ul><ul><li>Increased focus on biological factors. </li></ul><ul><li>The 1990’s and beyond: Focus on Neuroimaging, genetics, reevaluation of the DSM system, Evidence Based Practice and Practice Guidelines, etc. </li></ul>
  8. 8. Still (1902): ADHD An Early Case study <ul><li>Perhaps the earliest scientific account of what we today refer to as ADHD was by Still (1902). </li></ul><ul><li>Still was a British Physician who published a series of lectures that he had given to the Royal College of Physicians in London in 1902. </li></ul><ul><li>Here he described 43 children seen in his medical practice who displayed features similar to those we now associate with ADHD. </li></ul>
  9. 9. Still (1902) <ul><li>Still described these children as displaying a range of chronic problems: </li></ul><ul><ul><li>Aggressive, defiant, resistant to discipline. </li></ul></ul><ul><ul><li>Excessively emotional and as showing &quot;little inhibitory volition&quot;. </li></ul></ul><ul><ul><li>The need for immediate gratification seemed to be one of their primary attributes. </li></ul></ul><ul><li>He suggested that these children showed a &quot;major defect in moral control and that most displayed an insensitivity to punishment. </li></ul>
  10. 10. Still (1902) <ul><li>Children in this sample were also said to display major problems with sustained attention. </li></ul><ul><li>The majority were overly active, they tended to be accident prone. </li></ul><ul><li>Most of the children in Still's group developed these problems before age 8. </li></ul><ul><li>The re was a 3 to 1 mail to female sex ratio. </li></ul>
  11. 11. Still (1902) <ul><li>Many of these children displayed minor physical anomalies which he referred to as &quot;stigmata of degeneration&quot;. </li></ul><ul><li>Examples included large head size, malformed palate, and epicanthal folds. </li></ul><ul><li>Alcoholism, criminality and affective disorders were found to be common in biological relatives. </li></ul><ul><li>Some. but not all, had a history of convulsions or other evidence of brain damage. </li></ul><ul><li>Some had tic disorders. </li></ul>
  12. 12. Still (1902) <ul><li>Still thought that the major problems in sustained attention and the deficits in inhibitory control and moral control were related and were manifestations of an underlying neurological deficiency. </li></ul><ul><li>He speculated that these children either had an altered threshold for inhibition of responding to stimuli or a &quot; cortical disconnection syndrome&quot;, &quot;where intellect is disassociated from will&quot; and this might be due to some sort of &quot;Neuronal cell modification&quot;. </li></ul>
  13. 13. Still (1902) <ul><li>Aspects of Still's description of these children is supported by what we know about ADHD today. </li></ul><ul><ul><li>Presence of minor physical anomalies. </li></ul></ul><ul><ul><li>Association with heredity or possible neurological involvement. </li></ul></ul><ul><ul><li>Association with Tic Disorders, sex ratio, fairly early age of onset, problems of attention, activity and impulsivity. </li></ul></ul><ul><ul><li>Association with problems of conduct </li></ul></ul><ul><li>Still's group likely included a number of children with comorbid ODD/CD rather than pure cases of ADHD. </li></ul><ul><ul><li>Barkley (2006) </li></ul></ul>
  14. 14. ENCEPHALITIS EPIDEMIC OF 1917 - 1918 <ul><li>In 1917 and 1918 there was a serious outbreak of encephalitis in the United States and Europe. </li></ul><ul><li>Many of the children who were affected by this disease died. </li></ul><ul><li>Many who survived the acute stages of this illness experienced major cognitive and behavioral sequelae. </li></ul>
  15. 15. ENCEPHALITIS EPIDEMIC OF 1917 - 1918 <ul><li>These sequelae were described in a large number of articles that noted the behavioral effects on such children. </li></ul><ul><li>Many of these children displayed behavioral characteristics which are now commonly associated with ADHD. </li></ul><ul><li>They were often seen as hyperactive, impulsive and socially disruptive, with significant attention deficits. </li></ul><ul><li>They also had memory difficulties and other types of cognitive impairment. </li></ul>
  16. 16. ENCEPHALITIS EPIDEMIC <ul><li>Many such children were also described as showing features that we would now think of as reflecting ODD or CD  </li></ul><ul><li>As these characteristics were observed in children who had experienced actual disease-related neurological impairment, it provided early evidence that behavioral problems like those we now associate with ADHD can result from biological causes. </li></ul>
  17. 17. Ebaugh’s 1923 Article <ul><li>An especially influential paper was a publication by Ebaugh (1923 – See Barkley 2007) </li></ul><ul><li>This paper provided additional support for the view that ADHD could arise from acquired brain injury. </li></ul><ul><li>Described 17 child survivors of the encephalitis epidemic. </li></ul><ul><li>He noted that characteristics of such children included impulsiveness, hyperkinesis, inability to concentrate, unruly behavior, school problems, aggressiveness, and failure to respond to discipline. </li></ul>
  18. 18. Ebaugh 1923 <ul><li>Ebaugh believed that ADHD and related problems could arise acutely in normal children following brain injury (10 of his cases) </li></ul><ul><li>They could also represent preexisting problems that were exacerbated by brain injury (7 of his cases) </li></ul><ul><li>In contrast to Still, Ebaugh believed that premorbid unruliness and problem behavior of some of his children resulted from poor parenting. </li></ul><ul><li>It should be noted that the problems in this sample were much more severe that those seen in outpatient ADHD cases, due to the illness </li></ul><ul><li>Impairments in these children likely involved cortical, subcortical, and cerebellar, brain stem, and cranial nerve levels of brain organization (Barkley, 2007). </li></ul>
  19. 19. Ebaugh 1923 <ul><li>Children displayed sleep problems, depression, tic disorders, suicidality, and a range of psychosomatic symptoms </li></ul><ul><li>While this article tells us more about the sequelae of encephalitis in children than those with just ADHD, the similarities are striking. </li></ul><ul><li>As Barkley (2007) has suggested, this is probably due to the involvement of the frontal lobes, basal ganglia and cerebellum in both encephalitis and ADHD. </li></ul><ul><li>This article was a significant early contribution to understanding how ADHD may arise due to the consequence of obvious brain damage. </li></ul>
  20. 20. Brain Insults & Behavior Difficulties: Other Links <ul><li>By the 1930's and 1940's many investigators had begun to develop an interest in the link between &quot;behavioral pathology&quot; and &quot;brain disease .&quot; </li></ul><ul><li>For example, a range of cognitive and behavioral impairments such as mental retardation, learning problems, and problems with hyperactive/impulsive behavior were found to be related to a history of birth trauma, head injury, viral infections & exposure to toxins. </li></ul>
  21. 21. Brain Insults & Behavior Difficulties: Other Links <ul><li>It is noteworthy that many of these children had clear signs of neurological impairments and a much wider range of problems than are now typically associated with ADHD. </li></ul><ul><li>These sort of findings did, however, suggest to many that the problems exhibited by children with hyperactivity may be associated with some sort of brain damage. </li></ul>
  22. 22. FRONTAL LOBE ABLATION STUDIES <ul><li>Early interest in the possible link between hyperactivity and brain impairment was also sparked by the results of animal studies. </li></ul><ul><li>Of specific interest was the observed similarity between the behavior of hyperactive children and the behavior of primates that had brain lesions. </li></ul>
  23. 23. FRONTAL LOBE ABLATION STUDIES <ul><li>For example, in the 1930's there were a number of Frontal Lobe Ablation Studies of Monkeys which suggested that frontal lobe lesions often result in excessive restlessness, inability to sustain interest in activities, & behavioral disorganization </li></ul><ul><li>This caused investigators to speculate that childhood hyperactivity might result from defects in the area of the frontal lobes. </li></ul><ul><li>Given what we have learned since, this speculation seems not too far off base. </li></ul>
  24. 24. THE CONCEPT OF MBD <ul><li>During the late 1930's and the 1940's it became fashionable to assume that the problems displayed by children like those described here resulted from some sort of neurological impairment or brain injury. </li></ul><ul><li>As has been seen, there was evidence, even at this time, that the development of problems of activity level, attention, impulsivity, and conduct (along with others), CAN result from neurological insult. </li></ul>
  25. 25. THE CONCEPT OF MBD <ul><li>At that time it would have been quite reasonable to assume that childhood problems, like the ones we are talking about here, might have resulted from brain damage in cases where there was a history of trauma or illness that was capable of resulting in some type of neurological impairment. </li></ul><ul><li>However, some working in this area took things a step further, leading to the evolution of the concept of Minimal Brain Damage or Minimal Brain Dysfunction. </li></ul>
  26. 26. THE CONCEPT OF MBD <ul><li>On of the individuals most closely associated with the concept of Minimal Brain Dysfunction was Alfred Strauss . </li></ul><ul><li>In a series of studies, conducted in the 1940's and 1950's, Strauss and his colleagues attempted to isolate characteristics that would discriminate between groups of mentally retarded children with and without documented brain damage. </li></ul>
  27. 27. THE CONCEPT OF MBD <ul><li>These studies suggested a number of psychological and behavioral markers thought to be reliably associated with a history of brain damage. </li></ul><ul><li>Among these were; </li></ul><ul><ul><li>hyperactivity, </li></ul></ul><ul><ul><li>aggressiveness, </li></ul></ul><ul><ul><li>impulsiveness, and distractibility </li></ul></ul><ul><ul><li>along with emotional lability, </li></ul></ul><ul><ul><li>perceptual motor deficits, and </li></ul></ul><ul><ul><li>poor coordination as well as others. </li></ul></ul>
  28. 28. THE CONCEPT OF MBD <ul><li>Finding relationships between a history of brain damage and these sorts of behavioral characteristics, Strauss argued that these markers could be used to infer the presence of brain damage in ambiguous cases, even if there was no clear-cut evidence of neurological impairment . </li></ul><ul><li>Here, hyperactivity was given special status as the most valid indicator of brain damage. </li></ul>
  29. 29. MBD: Or, if you can’t find it is it really there? <ul><li>Characteristics thought to be the result of brain damage were taken to be indicators of brain damage, even in children without evidence of neurological impairment. </li></ul><ul><li>Thus, children were thought to display hyperactivity and other problems as a result of brain damage -- and -- children who were hyperactive were assumed to display brain damage simply as a result of their behavior. </li></ul><ul><li>The circularity of this argument can be readily seen. </li></ul>
  30. 30. The Notion of “Minimal” Brain Dysfunction <ul><li>The descriptor &quot;Minimal&quot; in Minimal Brain Dysfunction, related to the assumption that brain damage can be seen as existing on a continuum. </li></ul><ul><li>That is one that can have mild or minimal brain damage or dysfunction which is reflected primarily in its impact on the organization behavior, rather than in any sort of hard neurological signs. </li></ul><ul><li>This concept of Mimimal Brain Dysfunction flourished in the 1950's. </li></ul>
  31. 31. Correlates of MBD <ul><li>Along with Strauss's impact on the developing concept of MBD, he also provided recommendations regarding the education of children with this disorder. </li></ul><ul><li>One had to do with the view that children with this disorder were over stimulated. </li></ul><ul><li>This was thought to be due to their neurological difficulties which made it impossible to filter out extraneous stimuli. </li></ul><ul><li>This increased stimulation was seen as contributing to the child's attention and activity-level problems. </li></ul>
  32. 32. MBD & Over Stimulation <ul><li>Strauss suggested the importance of an educational environment where the child would be placed in small classes and where stimulation which could be distracting to the child was removed. </li></ul><ul><li>Teachers would wear no jewelry or brightly colored clothing, there would be few pictures on the walls, etc. </li></ul><ul><li>This represented the beginnings of a stimulus reduction model of ADDH. </li></ul><ul><li>In the 1960's these sorts of educational suggestions were applied in the classroom by Cruikshank. </li></ul>
  33. 33. The Beginnings of Child Psychopharmacology <ul><li>Interest in child psychopharmacology appeared in the late 1930's and early 1940's when studies began to suggest that amphetamines were useful in reducing disruptive behavior and in improving academic performance. </li></ul><ul><li>Early observations suggested that such medication helped at least half of the treated children . </li></ul><ul><li>Obviously interest in the role of medication in the treatment of children has continued to this day. </li></ul>
  34. 34. Questioning the Notion of MBD <ul><li>By the early 1960's investigators began to seriously question the circular reasoning associated with the concept of minimal brain dysfunction. </li></ul><ul><li>And they began to questioned the notion of a unitary concept of brain damage which suggested a specific constellation of symptoms, resulting from brain damage. </li></ul>
  35. 35. The Demise of MBD <ul><li>This resulted in less of a focus on the issues of &quot;minimal brain damaged&quot; and an increased focus on more homogeneous groupings of child problems. </li></ul><ul><li>Here, there was increased interest in more specific problems such as learning disabilities, language disorders, mental retardation, and problems such as hyperactivity . </li></ul>
  36. 36. Focus on Hyperactivity <ul><li>As a result, many investigators became interested in what came to be referred to as the Hyperkinetic Child Syndrome or the Hyperactive Child Syndrome . </li></ul><ul><li>The emphasis on hyperkinesis was highlighted in a seminal article by Stella Chess (1960) where the core symptom of this disorder was described in terms of the child’s excessive activity level. </li></ul>
  37. 37. The Hyperactive Child Syndrome <ul><li>Here, the hyperactive child was described as 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.&quot; </li></ul><ul><li>In this paper Chess stressed the need to consider objective evidence of the symptoms, apart from parent and teacher report, and to separate the Hyperactive Child Syndrome from the notion of the Brain Damaged Child. </li></ul>
  38. 38. The Hyperactive Child Syndrome <ul><li>Chess noted that children with this disorder did often have an array of difficulties such as educational problems, oppositional behavior, peer problems, & attentional difficulties, which could contribute to their difficulties. </li></ul><ul><li>The core symptom, however, was thought to be hyperactivity </li></ul>
  39. 39. The Hyperactive Child Syndrome <ul><li>By the mid to late 1960's the focus of attention was clearly on HYPERACTIVE CHILDREN rather than on those presumed to be BRAIN DAMAGED. </li></ul><ul><li>Here it can be noted that in 1969 DSM II , published by the American Psychiatric Association, included the category HYPERKINETIC REACTION OF CHILDHOOD , which provided for a diagnosis of those children now referred to as ADHD </li></ul>
  40. 40. The Hyperactive Child Syndrome <ul><li>For those working with children with this disorder, it was often assumed that hyperactivity represented a brain-dysfunction syndrome. </li></ul><ul><li>Assumptions regarding causality were, however, usually presented in terms of the involvement of brain mechanisms rather than in terms of frank brain damage. </li></ul>
  41. 41. Hyperkinetic Reaction of Childhood <ul><li>The disorder was seen has having a relatively homogeneous set of symptoms, most notably excessive activity level. </li></ul><ul><li>It was thought to have a relatively benign course and to often be outgrown by puberty (which we now know to be inaccurate in most cases). </li></ul><ul><li>Treatment was through stimulation medication and psychotherapy along with stimulus reduced educational environments. </li></ul>
  42. 42. THE 70'S - ATTENTION TO ATTENTION DEFICITS <ul><li>By the early to mid 1970's the concept of the hyperkinetic child syndrome was broadened to include associated characteristics such as impulsivity, low frustration tolerance, and attentional difficulties. </li></ul><ul><li>While the focus of research interest had moved from a focus on brain damage to a focus on hyperactivity this was to change, in large part due to the work of McGill psychologist Virginia Douglas. </li></ul>
  43. 43. The Focus on Attention <ul><li>In 1972, Virgina Douglas gave her Presidential address to the Canadian Psychological Association in which she argued that deficits in sustained attention and impulse control were most likely the core symptoms of this disorder, rather than hyperactivity. </li></ul><ul><li>Here she cited a her own work which suggested that hyperactive children have some of their greatest difficulties on tasks like the Continuous Performance Test which assess vigilance, sustained attention and impulsivity. </li></ul>
  44. 44. The Focus on Attention <ul><li>She noted that a primary characteristic of this disorder was the extreme degree of variability in the task performance of such children, specifically as it related to issues of attention. </li></ul><ul><li>She presented research to suggest that the degree of attentional control demonstrated by such children varied with reinforcement schedules (with attention being better under conditions of continuous reinforcement) and exceptionally poor under very thin schedules of partial reinforcement. </li></ul>
  45. 45. The Focus on Attention <ul><li>An additional argument for attentional problems being the core deficit was that problems with attention and concentration seem to continue even into later life, while problems with activity level often diminish significantly as the child gets older. </li></ul><ul><li>Douglas's work, and the results of other research stimulated by her work on attention, appear to have been the primary reason for the renaming this disorder as Attention Deficit Disorder when DSM III was published in 1980 . </li></ul>
  46. 46. Focus on Dietary Factors <ul><li>The 1970's also witnessed much attention being given to the role of dietary factors in hyperkinetic behavior. </li></ul><ul><li>The assumption was that allergic or toxic reactions to food additives such as dyes, preservatives, and salicylates caused hyperactive behavior. </li></ul><ul><li>This view, developed and popularized by Benjamin Feingold, claimed that over half of children with hyperactivity had problems because of diet related issues. </li></ul>
  47. 47. Focus on Dietary Factors <ul><li>It was suggested that treatment should involve buying or making foods without dyes, preservative or salicylates. </li></ul><ul><li>This view became so widespread that organized parent groups which promoted this Feingold diet were organized in most states. </li></ul><ul><li>Despite the popularity of the Feingold approach, research designed to investigate the role of these sorts of dietary factors in the development of hyperactive behavior were not supportive of this hypothesis. </li></ul>
  48. 48. Focus on Dietary Factors <ul><li>Indeed, substances associated with the Feingold diet have been found to have little or no effect on child behavior. </li></ul><ul><li>The more recent view, that refined sugar is the culprit in hyperactivity, has also failed to receive empirical support. </li></ul><ul><li>While there may be a very small number of children who's hyperactive behavior is affected by some elements of their diet (and this is not even well documented), dietary factors are unlikely to be contributors to the behavior of most hyperactive children. </li></ul>
  49. 49. PSYCHOPHYSIOLOGICAL RESPONSIVITY <ul><li>An additional fruitful area of investigation in the 1970's involved studies of the psychophysiological responsivity of hyperactive children. </li></ul><ul><li>Here a large number of studies were conducted which sought to measure variables such as GSR's, heart rate, EEG responses, evoked potentials, and other aspects of the psychophysiological responsivity of hyperactive children. </li></ul>
  50. 50. PSYCHOPHYSIOLOGICAL RESPONSIVITY <ul><li>These study often were designed to test the notions of cortical overstimulation that were first advanced in the 1950's. </li></ul><ul><li>Here it was suggested that because of brain damage, children were not able to filter out stimuli and that because of this they became overly stimulated and thus inattentive and hyperactive. </li></ul><ul><li>The basic assumption was they hyperactive children were over. rather than under stimulated. </li></ul>
  51. 51. PSYCHOPHYSIOLOGICAL RESPONSIVITY <ul><li>Taken together, results of these studies tended to provide support for the notion that hyperactive children showed underreactive as opposed to overreactive responses to simulation. </li></ul><ul><li>They tended to show lower amplitude responses to new stimulation and tended to habituate more rapidly than did normal children. </li></ul><ul><li>This underreactivity/underarousability, to stimuli appeared to be normalized by stimulant drugs in some cases. </li></ul>
  52. 52. PSYCHOPHYSIOLOGICAL RESPONSIVITY <ul><li>Thus, this line of research seemed to argue strongly against the notion of an overstimulated cerebral cortext as a cause of hyperactivity in children. </li></ul><ul><li>In fact, it seems that perhaps the opposite of this is more likely the case. </li></ul><ul><li>That is hyperactive children may benefit from stimulation less than normal children and may be if anything under aroused or underarousable in response to environmental stimulation. </li></ul>
  53. 53. The Concept of Optional Stimulation <ul><li>By the mid-1970's such findings were cited as arguments for an &quot;optimal stimulation view of hyperactivity“. </li></ul><ul><li>This view holds that such children display less that optimal levels of stimulation and that their increased activity level and apparent distractibility can be seen as attempts to increase stimulation to some more optimal level. </li></ul>
  54. 54. The Early 80'S and The Advent of ADD <ul><li>In 1980 the American Psychiatric Association published its Third Edition of the Diagnostic and Statistical Manual of Mental Disorders. </li></ul><ul><li>Compared with the diagnostic criteria for Hyperkinetic Reaction of Chldhood included in DSM II, the treatment of this disorder in DSM III was radically changed </li></ul>
  55. 55. DSM III: Focus on ADD <ul><li>In DSM III the disorder was renamed: Attention Deficit Disorder or ADD , so as to highlight the presumed central role of attentional difficulties and impulsivity in this condition. </li></ul><ul><li>Again, this change probably had much to do with research conducted by Virginia Douglas which highlighted deficits in attention and impulse control displayed by children with this disorder. </li></ul>
  56. 56. DSM III: Focus on ADD <ul><li>The treatment of this disorder in DSM III was noteworthy for several reasons: </li></ul><ul><ul><li>The renaming of the disorder </li></ul></ul><ul><ul><li>The focus on inattention and impulsivity as defining features </li></ul></ul><ul><ul><li>The development of more objective diagnostic criteria </li></ul></ul><ul><ul><li>The presentation of numerical cutoff scores for symptoms </li></ul></ul><ul><ul><li>Age of onset criteria </li></ul></ul><ul><ul><li>Criteria for duration of condition </li></ul></ul><ul><ul><li>Exclusionary criteria </li></ul></ul>
  57. 57. DSM III and ADD <ul><li>Most notable in these DSM III criteria, however, was the creation of ADD Subtypes. </li></ul><ul><li>Here, basic symptoms of the disorder were grouped into three classes. </li></ul><ul><li>1.      Symptoms of Inattention </li></ul><ul><li>2.      Symptoms of Impulsivity </li></ul><ul><li>3.      Symptoms of Hyperactivity </li></ul><ul><li>Based on the constellation of symptoms displayed children were to be diagnosed as having ADD either with or without hyperactivity. </li></ul>
  58. 58. DSM III and ADD <ul><li>Children displaying ADD without hyperactivity met diagnostic criteria for symptoms of inattention and impulsivity but not hyperactivity. </li></ul><ul><li>Children diagnosed as ADD with hyperactivity met criteria for inattention, impulsivity and hyperactivity. </li></ul><ul><li>While there was little research support for these subtypes when DSM III first appeared, later research did suggest that children displaying ADD with and without hyperactivity did differ in terms of major domains of adjustment. </li></ul>
  59. 59. DSM III and ADD <ul><li>This research seemed to suggest that children diagnosed with ADD (Without Hyperactivity) were characterized as more hypoactive and lethargic, with tendencies toward daydreaming, and as more likely to have learning disabilities or other academic problems and less likely to be aggressive than those displaying ADD (With Hyperactivity). </li></ul><ul><li>In general, DSM III represented a major advance in classification and serve as a major impetus to research on ADD and other forms of child psychopathology. </li></ul>
  60. 60. DSM III-R: AN Example of Inattention and Impulsivity <ul><li>Despite the fact that DSM III served to stimulate research in the area of ADD and that basic distinctions between ADD subtypes were receiving support by research findings, major changes were made in DSM III-R which was published in 1987. </li></ul><ul><li>These changes appear to reflect a lack of attention to the developing research literature and an impulsive approach to publishing activity. </li></ul>
  61. 61. The Nature of DSM III-R <ul><li>The changes seen in DSM III-R provided for only the diagnosis of ADD with Hyperactivity and the name was changed to Attention Deficit Hyperactivity Disorder. </li></ul><ul><li>ADD - without hyperactivity was no longer recognized as a distinct subtype of ADD and was relegated to the category of UNDIFFERENTIATED ADD. </li></ul><ul><li>The revision contained in DSM III-R were significant on several counts. </li></ul>
  62. 62. The Nature of DSM III-R <ul><li>1.   A single item list of symptoms and a single cutoff score replaced the three separate lists (inattention, impulsivity and hyperactivity) and cutoff scores of DSM III. </li></ul><ul><li>2.   The item list was now based more on empirically derived dimension of child behavior from behavior rating scales and the items and cutoff scores underwent a large field trial to determine their discriminating power to distinguish ADHD from other disorders and normal children. </li></ul>
  63. 63. The Nature of DSM III-R <ul><li>3.   The need to establish that symptoms are developmentally inappropriate for the child's mental age was stressed more emphatically. </li></ul><ul><li>4.   The coexistence of affective disorders with ADHD no longer excluded the diagnosis of ADHD. </li></ul><ul><li>5. The subtype of ADHD without hyperactivity was removed as a subtype and relegated to a vaguely defined category, Undifferentiated ADD, which was seen as a category in need of more extensive research </li></ul>
  64. 64. The Nature of DSM III-R <ul><li>6.   ADHD was now classified along with two other behavioral disorders (Oppositional Defiant Disorder and Conduct Disorder) in a supraordinate category known as Disruptive Behavior Disorders, because of their substantial overlap or comorbidity in clinic-referred populations of children. </li></ul><ul><li>7. Criteria for severity were also included which were ranked from mild to moderate to severe. </li></ul><ul><li>It is noteworthy that a number of these changes were reversed with the publication of DSM IV. </li></ul>
  65. 65. Etiological Research of the 1980’s <ul><li>In the 1980’s there were increasingly attempts to use sophisticated medical approaches to obtain information regarding the etiology of this disorder - in particular the role of brain functioning. These included - </li></ul><ul><ul><li>  studies on cerebral blood flow   </li></ul></ul><ul><ul><li>studies designed to documented possible neurotransmitter deficiencies involvingdopamine and norepinephrine </li></ul></ul>
  66. 66. Decade of Neuroimaging and Genetics: The 1990’s <ul><li>Newer imaging techniques employed in the 1990's added to this body of literature linking ADHD with abnormalities in brain functioning. </li></ul><ul><li>These involved PET scans, MRI and fMRI methodologies. </li></ul><ul><li>In the 1990’s there was also increased attention paid to the genetics of ADHD and expanded work in the area of molecular genetics which focused on findings specific genetic markers for ADHD. </li></ul>
  67. 67. Other Developments of the 1990 <ul><li>Development of new drugs to treat ADHD (Adderall, other sustained release stimulant medications) </li></ul><ul><li>First long term multimodal treatment study related to effectiveness of stimulant drugs and psychosocial treatments. </li></ul><ul><li>Developing of DSM IV </li></ul><ul><li>Consensus conference on ADHD. </li></ul>
  68. 68. The New Millennium <ul><li>Here we will wait another year to see what will be all of the advances of the 2000’s. </li></ul><ul><li>A couple that are noteworthy are the the development of Straterra. </li></ul><ul><li>This is the first effective medication for ADHD that is not a controlled substance and that targets a neurotransmitter other than dopamine. </li></ul>
  69. 69. The New Millennium <ul><li>Another is the Daytrana Patch, a drug delivery system for children not good with pills. </li></ul><ul><li>. . . ? </li></ul>

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