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Title: ADHD: Historical Overview


1
ADHD Historical Overview
  • FIDGITY PHIL 1845 by German Psychiatrist, Dr.
    Heinrich Hoffman
  • James H. Johnson, Ph.D
  • University of Florida

2
ADHD Not a New Problem
  • Characteristics of this disorder have been
    recognized for over a century.
  • See the Story of Fidgity Phillip
  • The disorder has been referred to by a variety of
    labels over the years
  • Minimal Brain Dysfunction (MBD)
  • Hyperkinetic Reaction of Childhood
  • Attention Deficit Disorder (ADD)
  • Attention Deficit Hyperactivity Disorder (ADHD)

3
Assumed Core Features
  • Various characteristics have been highlighted as
    the core feature of the disorder.
  • These have included
  • Minimal Brain Damage
  • Hyperactivity
  • Attention Deficits
  • Disinhibition of Behavior

4
The Evolution of ADHD
  • Views of the condition we now refer to as ADHD
    have evolved over the years.
  • Today I would like to briefly walk you through
    the evolution of this disorder.
  • The next few slides list some of the events that
    have influenced how we view this disorder today.
  • This discussion draws heavily on Barkley (1998,
    2005).

5
ADHD Milestones in the Evolution of the Disorder
  • The Still (1902) Lectures to the Royal College of
    Physicians
  • Encephalitis epidemic of 1917 (Ebaugh 1923)
  • Frontal lobe ablation studies with primates
    (1930s)
  • Beginnings of child psychopharmacology
    Amphetamines for treatment 1930-1940.
  • Strauss work on Minimal Brain Dysfunction
    (1940's -1950's)
  • MBD becomes Hyperkinetic Disorder (the 1960s)

6
ADHD Evolution of the Disorder (cont.)
  • Hyperkinesis becomes ADD The decade of the 70s
  • Focus on Dietary Factors Feingold and the
    1970s
  • Studies of pschophysiological responsivity the
    1970s
  • Development of objective diagnostic criteria DSM
    III and the recognition of Attention Deficit
    Disorder The early 80s

7
ADHD Evolution of the Disorder (cont.)
  • The decade of the 80s DSM III DSM III-R
    stimulates ADHD research
  • Development of new assessment methods
  • New treatment methods
  • Increased focus on biological factors.
  • The 1990s and beyond Focus on Neuroimaging,
    genetics, reevaluation of the DSM system,
    Evidence Based Practice and Practice Guidelines,
    etc.

8
Still (1902) ADHD An Early Case study
  • Perhaps the earliest scientific account of what
    we today refer to as ADHD was by Still (1902).
  • 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.
  • Here he described 43 children seen in his medical
    practice who displayed features similar to those
    we now associate with ADHD.

9
Still (1902)
  • Still described these children as displaying a
    range of chronic problems
  • Aggressive, defiant, resistant to discipline.
  • Excessively emotional and as showing "little
    inhibitory volition".
  • The need for immediate gratification seemed to be
    one of their primary attributes.
  • He suggested that these children showed a "major
    defect in moral control and that most displayed
    an insensitivity to punishment.

10
Still (1902)
  • Children in this sample were also said to
    display major problems with sustained attention.
  • The majority were overly active, they tended to
    be accident prone.
  • Most of the children in Still's group developed
    these problems before age 8.
  • There was a 3 to 1 mail to female sex ratio.

11
Still (1902)
  • Many of these children displayed minor physical
    anomalies which he referred to as "stigmata of
    degeneration".
  • Examples included large head size, malformed
    palate, and epicanthal folds.
  • Alcoholism, criminality and affective disorders
    were found to be common in biological relatives.
  • Some. but not all, had a history of convulsions
    or other evidence of brain damage.
  • Some had tic disorders.

12
Still (1902)
  • 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.
  • He speculated that these children either had an
    altered threshold for inhibition of responding to
    stimuli or a "cortical disconnection syndrome",
    "where intellect is disassociated from will" and
    this might be due to some sort of "Neuronal cell
    modification".

13
Still (1902)
  • Aspects of Still's description of these children
    is supported by what we know about ADHD today.
  • Presence of minor physical anomalies.
  • Association with heredity or possible
    neurological involvement.
  • Association with Tic Disorders, sex ratio, fairly
    early age of onset, problems of attention,
    activity and impulsivity.
  • Association with problems of conduct
  • Still's group likely included a number of
    children with comorbid ODD/CD rather than pure
    cases of ADHD.
  • Barkley (2006)

14
ENCEPHALITIS EPIDEMIC OF 1917 - 1918
  • In 1917 and 1918 there was a serious outbreak of
    encephalitis in the United States and Europe.
  • Many of the children who were affected by this
    disease died.
  • Many who survived the acute stages of this
    illness experienced major cognitive and
    behavioral sequelae.

15
ENCEPHALITIS EPIDEMICOF 1917 - 1918
  • These sequelae were described in a large number
    of articles that noted the behavioral effects on
    such children.
  • Many of these children displayed behavioral
    characteristics which are now commonly associated
    with ADHD.
  • They were often seen as hyperactive, impulsive
    and socially disruptive, with significant
    attention deficits.
  • They also had memory difficulties and other types
    of cognitive impairment.

16
ENCEPHALITIS EPIDEMIC
  • Many such children were also described as showing
    features that we would now think of as reflecting
    ODD or CD 
  • 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.

17
Ebaughs 1923 Article
  • An especially influential paper was a publication
    by Ebaugh (1923 See Barkley 2007)
  • This paper provided additional support for the
    view that ADHD could arise from acquired brain
    injury.
  • Described 17 child survivors of the encephalitis
    epidemic.
  • He noted that characteristics of such children
    included impulsiveness, hyperkinesis, inability
    to concentrate, unruly behavior, school problems,
    aggressiveness, and failure to respond to
    discipline.

18
Ebaugh 1923
  • Ebaugh believed that ADHD and related problems
    could arise acutely in normal children following
    brain injury (10 of his cases)
  • They could also represent preexisting problems
    that were exacerbated by brain injury (7 of his
    cases)
  • In contrast to Still, Ebaugh believed that
    premorbid unruliness and problem behavior of some
    of his children resulted from poor parenting.
  • 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
  • Impairments in these children likely involved
    cortical, subcortical, and cerebellar, brain
    stem, and cranial nerve levels of brain
    organization (Barkley, 2007).

19
Ebaugh 1923
  • Children displayed sleep problems, depression,
    tic disorders, suicidality, and a range of
    psychosomatic symptoms
  • While this article tells us more about the
    sequelae of encephalitis in children than those
    with just ADHD, the similarities are striking.
  • 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.
  • This article was a significant early contribution
    to understanding how ADHD may arise due to the
    consequence of obvious brain damage.

20
Brain Insults Behavior Difficulties Other
Links
  • By the 1930's and 1940's many investigators had
    begun to develop an interest in the link between
    "behavioral pathology" and "brain disease."
  • 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.

21
Brain Insults Behavior Difficulties Other Links
  • 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.
  • 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.

22
FRONTAL LOBE ABLATION STUDIES
  • Early interest in the possible link between
    hyperactivity and brain impairment was also
    sparked by the results of animal studies.
  • Of specific interest was the observed similarity
    between the behavior of hyperactive children and
    the behavior of primates that had brain lesions.

23
FRONTAL LOBE ABLATION STUDIES
  • 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
  • This caused investigators to speculate that
    childhood hyperactivity might result from defects
    in the area of the frontal lobes.
  • Given what we have learned since, this
    speculation seems not too far off base.

24
THE CONCEPT OF MBD
  • 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.
  • 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.

25
THE CONCEPT OF MBD
  • 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.
  • 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.

26
THE CONCEPT OF MBD
  • On of the individuals most closely associated
    with the concept of Minimal Brain Dysfunction was
    Alfred Strauss .
  • 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.

27
THE CONCEPT OF MBD
  • These studies suggested a number of psychological
    and behavioral markers thought to be reliably
    associated with a history of brain damage.
  • Among these were
  • hyperactivity,
  • aggressiveness,
  • impulsiveness, and distractibility
  • along with emotional lability,
  • perceptual motor deficits, and
  • poor coordination as well as others.

28
THE CONCEPT OF MBD
  • 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.
  • Here, hyperactivity was given special status as
    the most valid indicator of brain damage.

29
MBD Or, if you cant find it is it really there?
  • 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.
  • 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.
  • The circularity of this argument can be readily
    seen.

30
The Notion of Minimal Brain Dysfunction
  • The descriptor "Minimal" in Minimal Brain
    Dysfunction, related to the assumption that brain
    damage can be seen as existing on a continuum.
  • 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.
  • This concept of Mimimal Brain Dysfunction
    flourished in the 1950's.

31
Correlates of MBD
  • Along with Strauss's impact on the developing
    concept of MBD, he also provided recommendations
    regarding the education of children with this
    disorder.
  • One had to do with the view that children with
    this disorder were over stimulated.
  • This was thought to be due to their neurological
    difficulties which made it impossible to filter
    out extraneous stimuli.
  • This increased stimulation was seen as
    contributing to the child's attention and
    activity-level problems.

32
MBD Over Stimulation
  • 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.
  • Teachers would wear no jewelry or brightly
    colored clothing, there would be few pictures on
    the walls, etc.
  • This represented the beginnings of a stimulus
    reduction model of ADDH.
  • In the 1960's these sorts of educational
    suggestions were applied in the classroom by
    Cruikshank.

33
The Beginnings of Child Psychopharmacology
  • 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.
  • Early observations suggested that such medication
    helped at least half of the treated children.
  • Obviously interest in the role of medication in
    the treatment of children has continued to this
    day.

34
Questioning the Notion of MBD
  • By the early 1960's investigators began to
    seriously question the circular reasoning
    associated with the concept of minimal brain
    dysfunction.
  • 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.

35
The Demise of MBD
  • This resulted in less of a focus on the issues of
    "minimal brain damaged" and an increased focus on
    more homogeneous groupings of child problems.
  • Here, there was increased interest in more
    specific problems such as learning disabilities,
    language disorders, mental retardation, and
    problems such as hyperactivity.

36
Focus on Hyperactivity
  • As a result, many investigators became interested
    in what came to be referred to as the
    Hyperkinetic Child Syndrome or the Hyperactive
    Child Syndrome.
  • 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 childs excessive activity level.

37
The Hyperactive Child Syndrome
  • 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."
  • 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.

38
The Hyperactive Child Syndrome
  • 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.
  • The core symptom, however, was thought to be
    hyperactivity

39
The Hyperactive Child Syndrome
  • 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.
  • 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

40
The Hyperactive Child Syndrome
  • For those working with children with this
    disorder, it was often assumed that hyperactivity
    represented a brain-dysfunction syndrome.
  • Assumptions regarding causality were, however,
    usually presented in terms of the involvement of
    brain mechanisms rather than in terms of frank
    brain damage.

41
Hyperkinetic Reaction of Childhood
  • The disorder was seen has having a relatively
    homogeneous set of symptoms, most notably
    excessive activity level.
  • 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).
  • Treatment was through stimulation medication and
    psychotherapy along with stimulus reduced
    educational environments.

42
THE 70'S - ATTENTION TO ATTENTION DEFICITS
  • 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.
  • 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.

43
The Focus on Attention
  • 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.
  • 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.

44
The Focus on Attention
  • 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.
  • 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.

45
The Focus on Attention
  • 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.
  • 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.

46
Focus on Dietary Factors
  • The 1970's also witnessed much attention being
    given to the role of dietary factors in
    hyperkinetic behavior.
  • The assumption was that allergic or toxic
    reactions to food additives such as dyes,
    preservatives, and salicylates caused hyperactive
    behavior.
  • This view, developed and popularized by Benjamin
    Feingold, claimed that over half of children with
    hyperactivity had problems because of diet
    related issues.

47
Focus on Dietary Factors
  • It was suggested that treatment should involve
    buying or making foods without dyes, preservative
    or salicylates.
  • This view became so widespread that organized
    parent groups which promoted this Feingold diet
    were organized in most states.
  • 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.

48
Focus on Dietary Factors
  • Indeed, substances associated with the Feingold
    diet have been found to have little or no effect
    on child behavior.
  • The more recent view, that refined sugar is the
    culprit in hyperactivity, has also failed to
    receive empirical support.
  • 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.

49
PSYCHOPHYSIOLOGICAL RESPONSIVITY
  • An additional fruitful area of investigation in
    the 1970's involved studies of the
    psychophysiological responsivity of hyperactive
    children.
  • 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.

50
PSYCHOPHYSIOLOGICAL RESPONSIVITY
  • These study often were designed to test the
    notions of cortical overstimulation that were
    first advanced in the 1950's.
  • 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.
  • The basic assumption was they hyperactive
    children were over. rather than under stimulated.

51
PSYCHOPHYSIOLOGICAL RESPONSIVITY
  • 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.
  • They tended to show lower amplitude responses to
    new stimulation and tended to habituate more
    rapidly than did normal children.
  • This underreactivity/underarousability, to
    stimuli appeared to be normalized by stimulant
    drugs in some cases.

52
PSYCHOPHYSIOLOGICAL RESPONSIVITY
  • Thus, this line of research seemed to argue
    strongly against the notion of an overstimulated
    cerebral cortext as a cause of hyperactivity in
    children.
  • In fact, it seems that perhaps the opposite of
    this is more likely the case.
  • 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.

53
The Concept of Optional Stimulation
  • By the mid-1970's such findings were cited as
    arguments for an "optimal stimulation view of
    hyperactivity.
  • 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.

54
The Early 80'S and The Advent of ADD
  • In 1980 the American Psychiatric Association
    published its Third Edition of the Diagnostic and
    Statistical Manual of Mental Disorders.
  • 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

55
DSM III Focus on ADD
  • 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.
  • 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.

56
DSM III Focus on ADD
  • The treatment of this disorder in DSM III was
    noteworthy for several reasons
  • The renaming of the disorder
  • The focus on inattention and impulsivity as
    defining features
  • The development of more objective diagnostic
    criteria
  • The presentation of numerical cutoff scores for
    symptoms
  • Age of onset criteria
  • Criteria for duration of condition
  • Exclusionary criteria

57
DSM III and ADD
  • Most notable in these DSM III criteria, however,
    was the creation of ADD Subtypes.
  • Here, basic symptoms of the disorder were grouped
    into three classes.
  • 1.     Symptoms of Inattention
  • 2.     Symptoms of Impulsivity
  • 3.     Symptoms of Hyperactivity
  • Based on the constellation of symptoms displayed
    children were to be diagnosed as having ADD
    either with or without hyperactivity.

58
DSM III and ADD
  • Children displaying ADD without hyperactivity met
    diagnostic criteria for symptoms of inattention
    and impulsivity but not hyperactivity.
  • Children diagnosed as ADD with hyperactivity met
    criteria for inattention, impulsivity and
    hyperactivity.
  • 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.

59
DSM III and ADD
  • 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).
  • 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.

60
DSM III-R AN Example of Inattention and
Impulsivity
  • 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.
  • These changes appear to reflect a lack of
    attention to the developing research literature
    and an impulsive approach to publishing activity.

61
The Nature of DSM III-R
  • 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.
  • ADD - without hyperactivity was no longer
    recognized as a distinct subtype of ADD and was
    relegated to the category of UNDIFFERENTIATED
    ADD.
  • The revision contained in DSM III-R were
    significant on several counts.

62
The Nature of DSM III-R
  • 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.
  • 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.

63
The Nature of DSM III-R
  • 3. The need to establish that symptoms are
    developmentally inappropriate for the child's
    mental age was stressed more emphatically.
  • 4. The coexistence of affective disorders with
    ADHD no longer excluded the diagnosis of ADHD.
  • 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

64
The Nature of DSM III-R
  • 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.
  • 7. Criteria for severity were also included which
    were ranked from mild to moderate to severe.
  • It is noteworthy that a number of these changes
    were reversed with the publication of DSM IV.

65
Etiological Research of the 1980s
  • In the 1980s 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 -
  •  studies on cerebral blood flow  
  • studies designed to documented possible
    neurotransmitter deficiencies involvingdopamine
    and norepinephrine

66
Decade of Neuroimaging and Genetics The 1990s
  • Newer imaging techniques employed in the 1990's
    added to this body of literature linking ADHD
    with abnormalities in brain functioning.
  • These involved PET scans, MRI and fMRI
    methodologies.
  • In the 1990s 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.

67
Other Developments of the 1990
  • Development of new drugs to treat ADHD (Adderall,
    other sustained release stimulant medications)
  • First long term multimodal treatment study
    related to effectiveness of stimulant drugs and
    psychosocial treatments.
  • Developing of DSM IV
  • Consensus conference on ADHD.

68
The New Millennium
  • Here we will wait another year to see what will
    be all of the advances of the 2000s.
  • A couple that are noteworthy are the the
    development of Straterra.
  • This is the first effective medication for ADHD
    that is not a controlled substance and that
    targets a neurotransmitter other than dopamine.

69
The New Millennium
  • Another is the Daytrana Patch, a drug delivery
    system for children not good with pills.
  • . . . ?
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