ADHD: A HISTORICAL OVERVIEW



ADHD: Introduction and Historical Overview

ADHD is a common neurodevelopmental disorder with a prevalence of 3 to 5 per cent in the elementary school population. It is one of the most common disorders of childhood, accounting for a large number of referrals to child mental health facilities.

While views of what is now called ADHD have evolved over the years, the essential characteristics of this disorder have been recognized for almost a century.

Since this time, the disorder has been referred to by a variety of labels, various characteristics have been highlighted as the essential feature of the disorder, and a number of factors have been highlighted as causal in the development of the disorder.

In this session, we will briefly overview some of the historical milestones and trends in the evolution of this disorder.

EARLY DESCRIPTIONS

Still (1902 described 43 children seen in medical practice who displayed an number of features we now associate with ADHD.

CHARACTERISTICS:

• Children were aggressive, defiant, resistant to discipline, overly emotional and showed "little inhibitory volition".

• Need for immediate gratification was characteristic of most.

• Children displayed major problems with sustained attention

• The majority were overly active and they tended to be prone to accidental injury.

• Some were described as having a "major defect in moral control" and showed an insensitivity to punishment.

• Many displayed minor physical anomalies (large head size, malformed palate, and epicanthal folds) which he referred to as "stigmata of degeneration".

• Some, but not all, had a history of convulsions or documented brain damage.

• Some had tic disorders.

• Family histories of alcoholism, criminality and affective disorders were relatively common.

As a group, most of the children Still described developed these problems before age 8; There was a 3 to 1 sex ratio with more males than females being represented.

Still suggested that the problems in sustained attention and deficits in inhibiting behavior and "moral control" were related and were manifestations of underlying neurological deficiency.

He speculated that these children either had a decreased threshold for inhibition of responding to stimuli or a "cortical disconnection syndrome", "where intellect is disassociated from will" that could be due to some sort of "neuronal cell modification".

Discussion Question:

To what extent was Still's description of these children consistent with what we know about ADHD today?

• Problems of attention, activity and impulsivity.

• Presence of minor physical anomalies.

• Likely neurological involvement.

• Association with tic disorders, oppositional behavior and conduct problems.

• Sex ratio, early age of onset.

In sum, Still's group were similar to children that might be seen as displaying ADHD today, particularly if ADHD children with comorbid conditions were considered.

In addition to Still's early account, others such as Tredgold (1908) also described children who displayed many of the features that are sometimes associated with ADHD today.

EARLY SUGGESTIONS OF BIIOLOGICAL CONTRIBUTIONS TO THE DISORDER

THE ENCEPHALITIS EPIDEMIC OF 1917 - 1918

Many children who were affected by this disease and died.

Others who survived the acute stages of this illness experience major cognitive and behavioral sequelae, including characteristics such as hyperactivity, impulsivity, inattentive and socially disruptive behavior.

Often had memory difficulties as well as other types of cognitive impairments.

Many also displayed features that we would now think of as reflecting oppositional defiant or conduct disordered behavior.

As these characteristics were observed in children who were documented to have neurological disease, it provided early evidence for the notion that behavioral problems of childhood (like those we now associate with ADHD can result f rom neurological impairment.

OTHER EARLY LINKS BETWEEN BRAIN INSULT AND BEHAVIORAL DIFFICULTIES (1930's and 1940's)

Many investigators had an interest in the relationship between "behavioral pathology" and "brain disease."

During this time a range of cognitive and behavioral impairments such as mental retardation, learning problems, and problems with restlessness, hyperactivity and impulsiveness were found to be associated with a childhood history of birth trauma, head injury, viral infections (such as rubella), and exposure to certain types of toxins (e.g., lead).

These findings provided further reason to believe that there might be an association between the disorder we now call ADHD and some sort of brain damage or dysfunction.

FRONTAL LOBE ABLATION STUDIES WITH PRIMATES

Early interest in the possible link between attention deficits, hyperactivity and brain impairment was also sparked by the observed similarity between the behavior of hyperactive children and the behavioral effects resulting from frontal lobe lesions in primates.

In the 1930's Frontal Lobe Ablation Studies of Monkeys suggested that frontal lobe lesions often result in excessive restlessness, poor ability to sustain interest in activities, and disorganization in behavior.

This resulted in early speculation that hyperactivity in children might result from pathological defects in the area of the frontal lobes.

THE CONCEPT OF MINIMAL BRAIN DYSFUNCTION

During the late 1940's and 50's it was commonly assumed that the problems displayed by children like those considered here were the result of some sort of neurological impairment or brain injury.

Indeed, there was evidence, by this time, that the development of behavioral problems of activity level, attention, impulsivity, and conduct (along with others), CAN result from neurological difficulties.

There was no real problem in assuming that behavioral problems, like the ones considered here, may be the result of brain damage in cases where there is a clear history of trauma or illness that could cause in neurological impairment.

However, some working in this area took things a step further, by making the assumption that behaviors known to result from brain damage can serve as indicators of brain damage where the cause of the child's behavior problems have not been documented.

Evolution of the MBD Concept

In a series of studies, in the 1940's and 1950's, Alfred Strauss and his colleagues attempted to isolate characteristics that would discriminate between groups of mentally retarded children with and without a history of documented brain damage.

These studies suggested a number of psychological and behavioral markers to be reliably associated with a history of brain damage, including:

• Hyperactivity

• Aggressiveness

• Impulsivity

• Distractibility

• Emotional liability

• Perceptual motor deficits

• Poor coordination, etc.

Finding relationships between a history of brain damage and these sorts of behavioral characteristics, Strauss argued that these behavioral markers could be used to infer the presence of brain damage in ambiguous cases, even when there was no documented evidence of neurological impairment.

Hyperactivity was given special status as the most valid indicator of brain damage.

Children were thought to display behavioral problems such as hyperactivity as a result of brain damage -- and -- children who were hyperactive were assumed to display brain damage because of the behaviors they displayed.

The circularity of this argument can be readily seen.

The use of the term "Minimal" in Minimal Brain Dysfunction, related to the assumption that degree of brain damage can exist along a continuum and that 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 definitive neurological signs.

This notion of Minimal Brain Dysfunction flourished in the 1950's.

Corollaries of the MBD Concept

In addition to Strauss's role in the development of the concept of MBD, he also provided recommendations regarding the education of children with the disorder.

Strauss assumed children with this disorder to be over stimulated, due to their neurological difficulties which made it impossible to filter out extraneous stimuli.

This over stimulation was seen as contributing to the child's attention and activity-level problems.

As a result, Strauss suggested an educational environment where the child would be placed in small classes with the learning environment being specially designed to reduce excessive stimulation that could interfere with learning.

Behavioral difficulties of the MBD child were assumed to be helped by a "stimulus reduced" environment and made worse by an environment characterized by heightened levels of stimulation.

In the 1960's these sorts of educational suggestions were applied in the classroom by Cruikshank, without finding a great deal of support for the stimulus reduction hypothesis.

BEGINNINGS OF CHILD PSYCHOPHARMACOLOGY

Developing interest in child psychopharmacology appeared in the late 1930's and the early 1940's when studies began to suggest that amphetamines were useful in reducing disruptive behavior and in improving academic performance.

Studies suggested that such medication helped at least half of the treated children.

MBD BECOMES THE HYPERACTIVE CHILD SYNDROME

By the early 1960's investigators began to seriously question the circular reasoning associated with the concept of MBD.

And, they began to question the notion of a unitary concept of brain damage which suggested a specific constellation of symptoms resulting from brain damage.

As a result, the focus on the concept of MBD diminished greatly, with this change in focus being accompanied by an increased interest in more specific problems such as learning disabilities, language disorders, mental retardation, and hyperactivity, rather than more general conditions such as the “Brain Damage Child”).

Consistent with this tendency to become more specific in focus, many clinicians came to focus on what, by this time, was becoming known as the Hyperactive Child Syndrome.

Chess (1960) , in a seminal article, argued that the primary defining feature of this disorder was an excessively heightened activity level.

"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."

In this paper she 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.

While the focus was on hyperactivity, Stress 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.

By the mid to late 1960's the focus of attention was clearly on hyperactive children (or hyperkinesis) rather than on those presumed to be brain damaged, minimally or otherwise.

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.

Hyperkinetic Reaction of Childhood was seen has having:

• a relatively homogeneous set of symptoms, most notably excessive activity level.

• a relatively benign course and to often be outgrown by puberty (which we now know is not the case).

• Treatment was through stimulation medication and psychotherapy along with stimulus reduced educational environments.

THE DECADE OF THE 70'S - TRANSITION FROM HYPERKINESIS TO ATTENTION DEFICIT DISORDER

By the early to mid 1970's the concept of the hyperkinetic child syndrome was being broadened to include what investigators thought were associated characteristics such as impulsivity, low frustration tolerance, and attentiond difficulties.

While the focus of research interest had moved from a focus on brain damage to a focus on hyperactivity or hyperkinesis, this view began to change, in large part due to the work of McGill psychologist Virginia Douglas.

In 1972, Douglas, in her Presidential address to the Canadian Psychological Association, argued that deficits in sustained attention and impulse control were more likely to account for the difficulties seen in these children than just hyperactivity.

Here she cited findings from her research suggesting that hyperactive children show some of their greatest deficits on tasks like the Continuous Performance Test which assess characteristics such as vigilance, sustained attention and impulsivity.

She noted that a primary characteristic of this disorder was the extreme degree of variability in the task performance of such children on measures 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.

An additional argument for attentional problems being highlighted was that problems with attention and concentration seem to continue even into later life, while problems with activity level often decline as the child gets older.

Douglas's work on attentional processes, and the results of other research which stimulated by her work, appear to have been the primary reason for the later renaming of this disorder as Attention Deficit Disorder when the DSM III was published in 1980.

THE ROLE OF DIETARY FACTORS

In addition to the focus on attentional problems of hyperkinetic children, the 1970's witnessed much attention being directed toward the role of dietary factors as they relate to hyperkinetic behavior.

The assumption here 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 developed their problems because of diet related issues.

Suggested treatment was to involve buying or making foods that did not contain dyes, preservative or salicylates.

This focus on dietary factors as the cause of this disorder became so widespread that organized parent groups promoting the Feingold diet were organized in most states.

Despite the popularity, research designed to investigate the role of such dietary factors in the development or reduction of hyperactive behavior have generally not been supportive of this hypothesis.

The more recent view, that refined sugar is the culprit in hyperactivity, has also failed to receive significant empirical support.

While there may possibly be a very small number of children who's hyperactive behavior may be effected by some elements of their diet (and this is not even well documented), dietary factors are unlikely to be contributors to behavioral problems in children in the vast majority of instances.

STUDIES OF PSYCHOPHYSIOLOGICAL RESPONSIVITY IN HYPERACTIVE CHILDREN

An additional fruitful area of investigation in the 1970's involved studies to assess the pschophysiological responsiveness of hyperactive children.

These studies used measures such as GSR's, heart rate, EEG responses, and evoked potentials to assess hyperactive children.

Many of these studies were designed to test the notions of cortical over-stimulation, first advanced in the 1950's, that because children with MBD were not able to filter out stimuli they were over stimulated.

While many studies in this area were methodologically flawed, results of these investigations tended to provide more support for the notion that hyperactive children showed underreactive as opposed to overreactive electrophysiological responses to simulation.

They often tended to show lower amplitude responses to new stimulation and tended to habituate more rapidly to new stimulation than did normal children.

In some instances, this under reactivity or apparent underarousability to new stimuli appeared to be normalized by stimulant drugs.

This line of research seemed to argue against the notion of an over stimulated cerebral cortex as a cause of hyperactivity in children. In fact, it seems that the opposite may be the case; If anything, these children may be under aroused or underarousable in response to environmental stimulation.

By the mid-1970's such findings were cited as arguments for an "optimal stimulation view of hyperactivity" which 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.

THE 1980'S AND THE FORMAL ADVENT OF ATTENTION DEFICIT DISORDER (ADD)

In part, based on the research findings of Virgina Douglas, her colleagues, and those who had follow her research leads the focus in the late 1970's and early 1980's had shifted from hyperactivity to attention deficits.

Indeed, in 1980 when DSM III was published the disorder we are dealing with was renamed. Hyperkinetic Disorder of Childhood was replaced with Attention Deficit Disorder.

DEVELOPMENT OF DSM III

In 1980 the American Psychiatric Association published its Third Edition of the Diagnostic and Statistical Manual of Mental Disorders.

Compared with the earlier diagnostic criteria for Hyperkinetic Reaction of Childhood (DSM II), the treatment of this category in DSM III was radically changed.

In DSM III the disorder was renamed Attention Deficit Disorder (ADD), so as to highlight the presumed central role of attentional difficulties (and to some extent impulsivity) in this condition.

Again, this change probably had a lot to do with research conducted by Virginia Douglas which highlighted the role of deficits in attention and impulse control in children with this disorder.

The treatment of this disorder in DSM III was noteworthy on several counts, including

1. the renaming of the disorder

2. the focus on inattention and impulsivity as defining features

3. the development of more objective diagnostic criteria

4. the presentation of numerical cutoff scores for symptoms

5. age of onset criteria

6. criteria for duration of condition

7. exclusionary criteria for diagnosis

DSM III criteria, not only departed from those of DSM II, but also differed dramatically from ICD-9 criteria which had been published by the World Health Organization in 1978.

Here, ICD-9 emphasized “extreme and pervasive hyperactivity” as the defining features of the disorder rather than problem of inattention and impulsivity highlighted in DSM III.

Also notable in the DSM III criteria 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 could be diagnosed as having ADD, with or without hyperactivity.

Children displaying ADD without hyperactivity met diagnostic criteria for symptoms of inattention and impulsivity but not hyperactivity.

Children displaying ADD with hyperactivity met diagnostic criteria for symptoms of inattention, impulsivity and hyperactivity.

While there was little in the way of firm research support for these subtypes at the time DSM III appeared subsequent research, stimulated by the development of these new criteria, seemed to suggest that children displaying ADD with and without hyperactivity did differ in terms of major domains of adjustment.

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 be less aggressive than those diagnosed as having ADD (With Hyperactivity).

While studies in the mid 1980's were just beginning to highlight major differences between these ADD subtypes, and provide useful information regarding children with ADD diagnoses, the American Psychiatric Association saw fit to make further major changes in these diagnostic criteria only seven years later in 1987.

These changes were presented in DSM III-R, and seemed to represent evidence of both inattention (to research developing findings) and impulsivity (making changes before it was determine that they were warranted) on the part of the psychiatric APA.

DSM III – R: ATTENTION DEFICIT DISORDER (ADD) BECOMES AD/HD

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 DSM III-R revisions were significant on several counts.

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 listing of diagnostic criteria was 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.

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 AD/HD, which was seen as a category in need of more extensive research.

6. ADHD was now classified along with two other behavioral disorders (Oppositional Defiant Disorder and Conduct Disorder) in a super ordinate category known as Disruptive Behavior Disorders, because of their substantial overlap or comorbidity in clinic-referred samples.

7. Criteria for severity were also included which were ranked from mild to moderate to severe.

ADHD AS A MOTIVATIONAL DEFICIT DISORDER

Barkley, in reviewing the history of this disorder, has suggested that one of the most profound developments of the late 1980's was the somewhat radical view that Attention Deficit Hyperactive Disorder was not really a disorder of attention at all, but rather a disorder characterized by motivation deficits.

Here more detailed investigations of attentional processes suggested that, if attention is conceptualized as involving the perception, of stimuli, the filtering of stimuli or the processing of information, no evidence of such deficits are to be found in children with ADHD.

Further, a sizeable number of fairly rigorous studies have suggested that, while problems with attention are found in some circumstances, they are not found in others.

For example, children with ADHD may perform well on attentional tasks, under conditions of continuous reinforcement, but display performances suggestive of attentional difficulties when tested under thin schedules of reinforcement.

Other studies have suggested that even the type of instructions given to children with ADHD in experiments often determine whether they do or do not show attentional problems.

These factors caused some investigators to suggest that ADHD may arise out of an insensitivity to consequences, reinforcement, punishment, or both.

Thus, it might be argued that, the problems of children with ADHD may result from a deficit in responding to behavioral consequences rather than attention deficits per se.

Regarding the Motivation Deficit Explanation, Barkley (1998) has suggested that the appeal of this model has come from several sources.

1. Its greater explanatory value in accounting for findings of variability in attention in ADHD resulting from situational factors.

2. Its consistency with neuroanatomical studies suggesting decreased activation of brain reward centers and their cortical-limbic regulating circuits.

3. Its consistency with studies of the functions of dopamine pathways in regulating locomotor behavior and incentive or operant learning.

He goes on to suggest that any attempts at theory construction will need to incorporate some components and processes that deal with issues of motivation or effort.

THE DEVELOPMENT OF ASSESSMENT AND THERAPY APPROACHES IN THE 1980's.

The 1980's saw the development of numerous approaches useful in the assessment of AHDD as well as treatment approaches thought to be applicable to this population.

Included here are measures such as the CBCL, the ADHD Rating Scale, the Child Attention Profile, and the ACTeRS. Also introduced at this time were computerized versions of the Continuous Performance Test by Gordon and Conners. Additionally, the 80's saw the development of several behavioral observation approaches specifically designed to assess the behavior of children with ADHD in both the classroom and clinic.

The 80's also saw the introduction of cognitive behavioral approaches being applied to children with ADHD. While this approach initially showed promise in several case studies and in studies dealing with children from non clinical populations, research with clinical cases has been more disappointing. While having been shown to result in some improvement of children’s behavior on laboratory tasks, such approaches have not been routinely shown to result in clinically significant changes in children with ADHD.

Work in the area of parent oriented approaches to behavior management with ADHD children flourished during this period as did approaches to teaching social skills to children with this disorder.

During this time there were also advances in the use of medications, in that medications other than stimulants began to be used with children with ADHD. Of special note was the enhanced use of trycyclic antidepressants with ADHD children displaying evidence of anxiety and/or depression and the use of the antihypertensive drug such as clonidine in the treatment of ADHD children, particularly those with very high levels of impulsive and aggressive behavior.

ETIOLOGICAL RESEARCH IN THE 1980's

In the 1980’s there were attempts to use increasingly sophisticated medical approaches to investigate etiological factors related to this disorder. In particular, the focus was on the role of brain functioning.

During this time there were studies on cerebral blood flow which suggested patterns of underactivity in the prefrontal areas of the brain and their connections to the limbic system.

Other studies documented deficiencies in the neurotransmitters dopamine and norepinephrine in children with ADHD.

Here, it is noteworthy that the patterns of underactivity found in the studies of cerebral blood flow were in the same areas were dopamine and norepinephrine are most importantly involved in brain functioning.

THE DECADE OF NEUROIMAGING, GENETICS, THE REEVALUATION OF DSM CRITERIA, MULTIMODAL STUDIES AND CONSENSUS CONFERENCES - THE 1990'S (Considered in more detail under Etiology).

Researchers have long suspected that ADHD was associated in some way with abnormalities or delays in brain functioning.

This view had previously been supported by the result of neuropsychological studies showing deficits in the performance of ADHD children on tests presumed to assess frontal lobe or executive functions.

Earlier psychophysiological research had also tentatively suggested brain underactivity, particularly in the area of the frontal lobes.

Newer imaging techniques employed in the 1990's added to this body of literature linking ADHD with abnormalities in brain functioning.

Examples include Pet Scan studies conducted by Alan Zametkin and his colleagues at NIMH.

Here, Zametkin studied 25 adults with a childhood history of ADHD and who also had a child with ADHD.

He used PET scans to study areas of reduced brain metabolic activity in these individuals with ADHD, comparing them to control subjects.

Results suggested significantly reduced brain activity in adults with ADHD relative to controls, primarily in the frontal and striatal regions.

Although these results were not with ADHD children, these findings seem to support the notion of reduced brain activity, particularly in the frontal regions in the brain.

Other researcher such as Hynd and his colleagues employed MRI methodology to assess total brain volume as well as specific regions in the anterior and posterior brain.

Children with ADHD were found to have abnormally smaller anterior cortical regions, especially on the right side, and they lacked the normal right-left frontal asymmetry.

They also found that both the anterior and posterior portions of the corpus callosum were smaller in children with ADHD.

Other MRI studies with larger samples of ADHD children have documented significantly smaller right prefrontal lobe and striatal regions in children with ADHD.

Other investigators have found other types of neurological abnormalities.

In discussing these findings Barkley (1998) has indicated:

"Despite some inconsistencies across studies, most have implicated the prefrontal-striatal network as being smaller in children with ADHD, with the right prefrontal region being smaller than the left. Such studies have placed on a considerably firmer foundation the view that ADHD does, indeed, involve impairments in the development of the brain, particularly in the preforntal-striatal regions and that the origin of these differences from normal are likely to have occurred in embryological development (p. 36)."

It would be of interest to determine the extent to which these types of brain abnormalities are correlated with the more obvious minor physical anomalies, which are thought to have originated in embryological development, and which are found with greater frequency in boys with ADHD.

STUDIES OF GENETICS

Family Aggregation Studies

Studies dating as far back as the 1970's indicated that children with hyperactivity or ADHD tend to have parents with a greater frequency of ADHD and other psychiatric disorders.

In adoption studies have also suggested, that for hyperactive children or children with ADHD, there are higher rates of hyperactivity in biological than adoptive parents.

In the 1990's there were numerous other studies which have provided more convincing information regarding the possible genetic contribution to ADHD.

For example, studies by Biederman and his colleagues have found that between 10 and 35% of the immediate family members of children with ADHD display this disorder.

Risk for siblings of children with ADHD is approximately 32%.

Other studies by Biederman have suggested that, if a parent has ADHD, the risk to the offspring is approximately 57%.

Thus, family aggregation studies find that ADHD clusters among biological relatives of children or adults with this disorder. This strongly implies a hereditary bases for this condition.

Twin Studies

Large scale twin studies in the 90's have been quite consistent in the findings of a high heritability for this trait or for a clinical diagnosis of ADHD.

For example, Gilger et al (1992) found that if one twin was diagnosed with ADHD, the concordance for the disorder was 81% in monozygotic twins and 29% in dizygotic twins.

In a summary of the results of twin studies that dealt with symptoms of ADHD, Stevenson (1994) concluded that the average heritability is .80 for symptoms of this disorder.

Other studies are consistent in suggesting that the majority of variance (70-90%) in the trait of hyperactivity-impulsivity is due to genetic factors (averaging around 80%).

Molecular Genetics Studies

In the 1990's there were also studies which used molecular genetic techniques to analyze DNA taken from children with ADHD and members of their families.

Consistent with the goals of the human genome project, the attempt was to identify genes that may be related to this disorder.

The initial focus of this research was on the dopamine type2 gene which has been found to be associated with alcoholism, Tourette's syndrome, and ADHD.

More recently a dopamine transporter gene has been implicated in ADHD.

Another gene related to dopamine, the D4RD (repeater gene) has more recently been found to be overrepresented in children with ADHD.

While in its early stages in investigations of ADHD, such molecular genetic research holds promise for the development of genetic tests for ADHD and perhaps for identifying subtypes of this disorder.

ADHD IN ADULTS

While we will leave discussion of ADHD in older individuals for another time (Dr. Dede will discuss this as a guest speaker later in the term), suffice it to say that the 1990's has been a time where serious clinical and research attention has been devoted to looking at this disorder in adults.

OTHER DEVELOPMENTS IN THE 1990'S

(considered in more detail in later sessions)

• Development of DSM IV

• 1998 ADHD Consensus Conference (NIMH).

• NIMH Multisite study of ADHD which focused on various combinations of treatment (psychopharmacological, psychosocial, combined) for various types of ADHD.

• Development of new stimulant drugs (e.g., Concerta, Adderal)

• Declining use of other stimulant drugs (e.g., Cylert).

END CLASS ONE

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