ADHD: An Historical Overview

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Transcript ADHD: An Historical Overview

ADHD: Historical
Overview
FIDGITY PHIL 1845 by German Psychiatrist, Dr. Heinrich Hoffman
James H. Johnson, Ph.D
University of Florida
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;
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Minimal Brain Dysfunction (MBD)
Hyperkinetic Reaction of Childhood
Attention Deficit Disorder (ADD)
Attention Deficit Hyperactivity Disorder
(ADHD)
Assumed Core
Features
• Various characteristics have
been highlighted as the “core
feature” of the disorder.
• These have included:
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Minimal Brain Damage
Hyperactivity
Attention Deficits
Disinhibition of Behavior
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).
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 (1930’s)
• Beginnings of child
psychopharmacology;
Amphetamines for treatment – 19301940.
• Strauss’ work on Minimal Brain
Dysfunction (1940's -1950's)
• MBD becomes Hyperkinetic Disorder
(the 1960’s)
ADHD: Evolution of the
Disorder (cont.)
• Hyperkinesis becomes ADD – The
decade of the 70’s
• Focus on Dietary Factors – Feingold
and the 1970’s
• Studies of pschophysiological
responsivity – the 1970’s
• Development of objective diagnostic
criteria: DSM III and the recognition
of Attention Deficit Disorder – The
early 80’s
ADHD: Evolution of the
Disorder (cont.)
• The decade of the 80’s: DSM III & DSM
III-R stimulates ADHD research
• Development of new assessment
methods
• New treatment methods
• Increased focus on biological factors.
• The 1990’s and beyond: Focus on
Neuroimaging, genetics, reevaluation of
the DSM system, Evidence Based
Practice and Practice Guidelines, etc.
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.
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.
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.
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.
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".
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)
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.
ENCEPHALITIS EPIDEMIC
OF 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.
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.
Ebaugh’s 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.
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).
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.
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.
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.
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.
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.
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.
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.
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.
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;
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hyperactivity,
aggressiveness,
impulsiveness, and distractibility
along with emotional lability,
perceptual motor deficits, and
poor coordination as well as others.
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.
MBD: Or, if you can’t 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.
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.
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.
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.
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.
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.
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.
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 child’s
excessive activity level.
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.
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
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
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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
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.
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
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.
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.
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.
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.
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.
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.
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
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.
Etiological Research of
the 1980’s
• 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 – studies on cerebral blood flow
– studies designed to documented
possible neurotransmitter deficiencies
involvingdopamine and norepinephrine
Decade of Neuroimaging
and Genetics: The 1990’s
• 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 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.
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.
The New Millennium
• Here we will wait another year to
see what will be all of the
advances of the 2000’s.
• 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.
The New Millennium
• Another is the Daytrana
Patch, a drug delivery
system for children not
good with pills.
• ...?