Lecture 23
Attention-Deficit Hyperactivity Disorder
Lecture Outline
I. Introduction
II. Background
A. Minimal Brain Dysfunction
B. Attention Deficits and Psychosocial Variables
C. DSM-III and III-R
III.Core Features
A. Inattention
B. Impulsiveness
C. Hyperactivity
IV. Etiology
A. Biological Factors
B. Genetics
C. Environmental Factors
D. Psychosocial Factors
V. Course
A. Adolescent outcome
B. Adult outcome
VI. Controversies
VII.Conclusion
-------------------------------------------
I. Introduction
In the last lecture, we discussed the difference between
externalizing and internalizing disorders. In today's lecture we will
examine an example of an externalizing disorder: Attention-deficit
Hyperactivity Disorder (ADHD), or more commonly - "Hyperactivity".
Everybody probably knows at least one child considered to be hyperactive
(Whalen, 1983) - a child who is overly impulsive, has trouble attending
to the task at hand, and in general is exceedingly overactive:
a child in perpetual motion, a child who flits around and blurts
out but doesn't finish assignments or chores, a child with a short
and highly flammable fuse, a child of the present who neither
benefits from the past nor plans for the future (Loney, 1980).
Hyperactivity is the most common problem among school-age children of
normal intelligence, and is the most common problem referred to child
guidance clinics in this country (Barkley, 1981, Sleator, 1982).
Prevalence rates: common, perhaps in as many as 3% of children
(APA, 1987).
Sex Ratio: 6 - 9 times more common in males than females (APA,
1987).
It is also the most widely studied childhood disorder, as well as one of
the most controversial. Debates over diagnosis, etiology, prognosis,
and treatment are common (Barkley, 1981).
II. Background
ADHD has also been called Childhood Hyperactivity, Hyperkinetic
Syndrome, Attention Deficit Disorder, and Minimal Brain Dysfunction to
name but a few of the more common terms.
A. Minimal Brain Dysfunction
Modern, scientific interest in what we now know as ADHD began
in the 1940's with the work by Alfred Strauss and his colleagues
(Schwartz & Johnson, 1985) (although reports about hyperactivity
can be found as early as the 1800's [Barkley, 1981]). In a series
of studies, Strauss isolated a number of characteristics which he
believed could discriminate between groups of mentally retarded
children with and without brain damage. Associated with brain
damage were aggressiveness, impulsivity, distractibility and
hyperactivity. Hyperactivity was seen as the most valid indicator
of brain damage (Schwartz & Johnson, 1985). And so, it became
widely accepted for many years that children with hyperactive
behavior patterns were also brain damaged; the term Minimal Brain
Dysfunction (MBD) was widely used to identify these children.
Problem: Strauss's reasoning was circular! In effect, he was
arguing that hyperactive children were brain damaged because they
were hyperactive (Schwartz & Johnson, 1985).
Future research failed to find the link between hyperactivity
and brain damage. Most children suffering brain damage do not
develop hyperactivity, and it's been estimated that fewer than 5%
of hyperactive children suffer from brain damage (Rutter, 1977).
There was no clear understanding of just what was meant by
MBD; some clinicians insisted that restlessness, distractibility,
impulsivity, and short attention spans were the key, others
insisted it was perceptual/conceptual/learning deficits, and still
others saw aggressiveness as the key ((Schwartz & Johnson, 1985).
B. Attention Deficits and Psychosocial Variables
During the late 60's and early 70's, the focus shifted to the
attentional qualities of the disorder. Virginia Douglas and her
colleagues at McGill University demonstrated the marked attention
deficits seen in these children. Douglas argued that the major
deficit was the inability to "stop, look, and listen" (Douglas,
1972) - ie: to sustain attention and inhibit impulsive responding
(Barkley, 1981).
In the late 70's, the focus broadened: research was indicating
that the problems went beyond mere attention deficits. People like
Susan Campbell and Charles Cunningham conducted a number of studies
on parent-child interaction. It was found that the hyperactive
children were noncompliant, attention-seeking and aggressive, and
in need of ongoing supervision; and the mothers were overly
directive, negative, and less responsive to the child in general
(Barkley, 1981). Thus, researchers included social variables into
the increasingly complex picture. Compliance and aggressiveness
gained diagnostic importance.
C. DSM-III and III-R
No one could agree on what the primary features were. In
1980, the American Psychiatric Association entered into the debate.
The DSM-III was published and it defined a disorder termed
Attention Deficit Disorder (ADD), with or without hyperactivity.
It was the consensus of the authors of the manual that attention
deficits, not overactivity, was the key to the disorder.
"Hyperactivity" merely accompanies the disorder as a secondary
symptom, and then in only certain children.
The DSM-III-R has eliminated the category of Attention Deficit
Disorder without hyperactivity, in response to growing research
evidence that ADD rarely occurs without hyperactivity - the DSM-III
diagnosis of ADD without hyperactivity was rarely made (APA, 1987).
The disorder is now termed Attention-deficit Hyperactivity Disorder
(ADHD). It is questionable whether attentional disorders without
hyperactivity should even be considered as a subtype of attention-
deficit disorder. More research is needed on this.
[review DSM-III-R criteria]
Note that this is merely a list of characteristics - no particular
single feature or subset of features is required to make the
diagnosis. Also note that "hyperactivity" is not a necessary
feature for the diagnosis ADHD to be made. It was hoped that such
flexibility and coverage would improve diagnostic reliability. In
addition, these symptoms were selected to better discriminate ADHD
from other childhood disorders such as conduct disorder, with which
there is often significant overlap (Hinshaw, 1987). Nonetheless,
as we have discussed before, constructing a classification scheme
without the guidance of theory is little more than a "shot in the
dark". A mere list of characteristics, with no underlying theory,
is unlikely to ever move us very far in terms of reliability and
validity.
III. Core Features
Even with all the debate concerning the nature of the disorder,
three primary features of ADHD are consistently identified by
researchers.
A. Inattention
Inattentiveness is a key symptom of ADHD. Difficulties in
attention can take various forms (Barkley, 1981; Levine, 1987):
trouble orienting to stimuli
failure to even detect stimuli
respond to the wrong aspects of a stimulus or to an
entirely inappropriate stimulus.
failure to sustain attention to task-relevant stimuli,
while inhibiting responding to nonrelevant stimuli -
they are easily distracted / short attention span
In the home: failure to complete chores, homework, etc, to
listen to directions, to play for prolonged periods without
supervision or attention form others.
At school: problems with attending to the teacher and
completing in-class assignments. The child is often distracted by
other events (what other kids are doing, what's happening outside
the window...). However, they may attend at length to these
nonrelevant stimuli - so the problem is more than just a short
attention span; it often seems to be a problem of allocating the
right amount of time and focus to the appropriate information
(Levine, 1987).
Note: Many children who exhibit deficits in attention alone
do not have ADHD (Garfinkel, 1986). Problems with attention may be
time limited, due to environmental factors (stressors, significant
distractions), physiological variables (fatigue, illness), and mood
(irritability, anger). Attention deficits are also seen in other
disorders such as depression and mental retardation. So, by
itself, attention deficits are not usually sufficient to make the
diagnosis of ADHD (Garfinkel, 1986). They must be part of a larger
clinical picture.
B. Impulsiveness
Impulsivity, or the failure to inhibit responding, has also
been identified as a primary characteristic. This can take various
forms (Barkley, 1981):
o quick responding, with numerous errors
o do not stop to think about consequences of their actions
place themselves in dangerous and risky situations
o fail to fully appreciate all aspect of instructions given
to them
o more likely to respond aggressively (verbally and
physically) when frustrated or emotionally hurt by
others
o do not consider the impact of their actions or statements
on others
Such actions can lead others to see such children as immature
and to their being shunned by others. The impulsive child will
also experience more punishment than normal children.
C. Hyperactivity
Overactivity has also been identified as a key feature of
ADHD. The typically picture of such a child is "long on motility
and short on restraint" (Loney, 1980); in other words, always on
the move, with no apparent regard to rules, directions, or the
like. It is thus not surprising that ADHD is often first
identified upon the child's entrance to school. It is here that
hyperactivity (as well inattentiveness, and impulsivity) is
directly incompatible with the structure and goals of the
classroom.
There is some debate, however, over the significance of
excesses in motor behavior. Studies that have actually measured
rates of motor activity have found that ADHD children are not
necessarily more active than other children, certainly not in all
situations. Hyperactivity seems to be most often a problem when
the child is in a restrictive environment where concentration is
required (eg: a classroom!). Novel or unfamiliar situations seem
to elicit the hyperactive behaviors as well (Barkley, 1981).
These, then are the core features: Inattentiveness, Impulsivity, and
Hyperactivity. The picture is far from clear, however. These
characteristics don't always "hang together" - they often fail to
correlate with one another (Barkley, 1981). So, it is a question
whether or not ADHD represents a single, unified disorder. More likely,
ADHD comprises a quite heterogenous group of children, with varying
constellations of the above symptoms.
IV. Etiology
Numerous etiological factors have been identified over the years.
Research often produces conflicting findings. Most researchers view
ADHD as the final common result of a variety of etiologies - again we
are faced with the unlikely prospects of finding a "Unitary
explanation".
A. Biological factors
As we've already noted, ADHD was once thought to be the result
of brain damage. Much research has been conducted to find specific
organic or neurological factors that could account for ADHD. The
"jury is still out", although a number of factors have been
hypothesized:
1. Prefrontal cortex abnormalities: This part of the brain
plays an important role in inhibiting, modulating, planning,
and regulating complex behavior, such as planning for the
future and following instructions. People with damage to this
part of the brain often exhibit ADHD-like symptoms
(inattentive, easily distracted, impulsive, restless, etc).
It has thus been hypothesized that ADHD may be caused by
abnormalities in this part of the brain (Barkley, 1981).
Nevertheless, there is presently no clear direct evidence to
support this hypothesis.
2. Neurotransmitter abnormalities: It is known that many (60-
90% [Schwartz & Johnson, 1985]) ADHD children respond to
stimulants with reduced ADHD symptoms, a seemingly paradoxical
effect. The behavior most improved: attention. For a number
of years it was thought that this effect indicated abnormal
biochemical processes, especially deficiencies of the
neurotransmitters norepinephrine and dopamine (Barkley, 1981).
More recent research, however, has shown that ADHD children do
not respond differently to stimulant drugs than "normal"
children: Stimulants increase attention and concentration for
both groups (Schwartz & Johnson, 1985, Yellin, 1986)). There
is nothing "paradoxical" about the effects of these drugs:
they have the same effects on nonADHD children. This does not
necessarily mean neurotransmitters are not etiologically
important, only that their importance must be more complex
than a simple deficiency model.
3. Neurological Immaturity: An alternative hypothesis is that
maturation of central nervous system structures is delayed,
rather than actually damaged (Barkley, 1981). Observations of
ADHD children make this hypothesis appealing - the children do
seem to be acting in immature ways. Some studies of brain
activity (especially CNS structures underlying attention and
response inhibition) also suggest immature processes. For
example, as many as 50% of ADHD children show underaroused EEG
(a recording of brain waves) patterns suggestive of cortical
immaturity (Barkley, 1981). Nevertheless, the support for
this hypothesis is still very far from conclusive.
4. Other signs: Abnormalities have been found in EEG
patterns, Event-related potentials, particularly the P300, and
skin conductance (Yellin, 1986). In addition, drugs that
reduce ADHD symptoms (Ritalin) also normalize the abnormal
P300 patterns. These findings all point to deficits in
arousal and orienting, in processing information from the
environment, or in other words: deficits in "arousal" and
"attention". Because ADHD children appear to have a lower
than normal state of arousal, some researchers have
hypothesized that the children are therefore engaging in extra
activity in order to increase their level of stimulation
(Schwartz & Johnson, 1985). This could also be why stimulant
drugs are effective - they provide the needed stimulation.
B. Genetics
Studies have found a higher incidence of ADHD in the
biological relatives of hyperactive children than in the population
at large. This seems to be true even with ADHD children who are
adopted. Similarly, there is a high concordance rate for twins
(when one twin has ADHD, the other has a higher than average chance
of also having ADHD) (Barkley, 1981; Schwartz & Johnson, 1985).
These studies all suggest a genetic component to the disorder,
although how general and how significant the genetic contribution
is remains to be determined.
C. Environmental Factors
Various toxins and allergy-producing substances in the
environment have been identified as possibly relevant to the
etiology of ADHD.
1. Lead Poisoning: Lead is found in many substances: paint,
automobile fumes (although this is decreasing as unleaded fuel
becomes more the standard). A number of studies during the
70's noted an elevated level of lead in the blood of ADHD
children. 30 -35% of children with elevated blood lead levels
were also hyperactive. So, there does seem to be a connection
between lead and at least on symptom of ADHD: hyperactivity
(Barkley, 1981: Schwartz & Johnson, 1985).
2. Food Additives and Refined Sugars: For awhile there was a
lot of talk about food additives (eg: artificial food
colorings and flavorings) and refined sugars as being a cause
of ADHD. The interest in this hypothesis was spurred on by
the publication of the popular book Why Your Child is
Hyperactive, by Feingold, in 1975. While still quite popular
as an explanation of the disorder, there is actually very
little scientific evidence to support this hypothesis
(Barkley, 1981).
3. Other Factors: Various other environmental factors have
been suggested, including low-level X-rays emitted by
fluorescent lights, maternal smoking during pregnancy, and
maternal alcohol consumption during pregnancy. These factors
have failed to gain any clear cut support, however (Barkley,
1981).
D. Psychosocial Factors
Some researchers have claimed that hyperactivity is the result
of poor parenting skills: inconsistent rules, over-reliance on
punishment, excessive and ill-timed commands. Indeed, treatment
programs which teach parents more effective parenting skills have
had significant success. Nevertheless, it is not at all clear that
these psychosocial factors are the cause of ADHD. For example:
such a model fails to explain why ADHD symptoms often occur at a
very early age; or why the symptoms are consistent across
situations (home, school, play) and thus different forms of child
management. In addition, inconsistent or chaotic rules, excessive
punishment, and the like are possibly a result of ADHD. There is a
concern that parents are being blamed for something that is not
their fault (Barkley, 1981). Nevertheless, it is safe to say that
for some of these children, parenting styles can have an important
influence on maintaining or even aggravating the ADHD symptoms
(Wicks-Nelson & Israel, 1984).
V. Course
Relatively few studies have examined the course of ADHD: What
happens to the child as s/he grows up. Clinical lore often suggests
that the symptoms fade away. The studies that have been conducted do
not, however, support this conclusion (Lambert, 1988; Schwartz &
Johnson, 1985; Weiss & Hechtman, 1986).
A. Adolescent outcome
Most studies indicate the core features persist; however, they
are frequently no longer the most obvious complaint. Instead, the
following become salient:
poor school performance
social deviancy
relationship difficulties with peers and adults
delinquency
low self-esteem
significant under-achievement
nervousness, restlessness
aggressive/easily angered
alcohol/drug use or abuse
There is also some indication that a significant percentage of
ADHD adolescents (about 25%) have a history of antisocial behavior.
It has been suggested that adults with Antisocial Personality
Disorder may have been hyperactive as children.
B. Adult outcome
As many as 1/3 to 1/2 of hyperactive children continue to be
troubled by symptoms of ADHD in adulthood. Continued problems seem
particularly likely if antisocial behavior and drug use/abuse was
present in their childhood/adolescence. Adulthood problems
include:
20% or more have Antisocial Personality Disorder
low self-esteem
impaired social skills
inferior work status (held jobs for a shorter duration, laid
off/quit more frequently, inferior work performance)
VI. Controversies
The topic of ADHD is fraught with controversies. The major
treatment of the disorder is with stimulant drugs, such as Ritalin. It
is estimated that 60 - 90% respond favorably to these drugs (Schwartz &
Johnson, 1985). But there has been concern that these drugs are being
administered merely to keep children quite and to facilitate classroom
management, and that hyperactivity is simply a myth constructed to
justify this control: the natural vigor of youth is being denied.
Recently, there has been a lot of media attention given to the
Church of Scientology's national campaign against ADHD and Ritalin
treatments. This campaign, under the Church's Citizen's Commission on
Human Rights (CCHR) has claimed that Ritalin commonly leads children to
suicide, murder, seizures and brain damage, addiction, and permanent
emotional disturbance. Such a highly visible and emotional campaign is
disturbing to many because it is based on little firm scientific data.
In well controlled studies, side effects, in fact, appear to be quite
limited.
For example (Barkley, 1988) (See Handout 23-1):
82 ADHD children (ages 5 to 16) underwent an objective double
blind, placebo controlled evaluation of two doses of Ritalin (0.3 and
0.5 mg/kg twice daily). Results:
None of the severe side effects claimed by CCHR occurred.
Of the side effects that did occur (see handout), many also
occurred in the placebo group as well. What this suggests is that
many of the supposed side effects of Ritalin may in fact be pre-
existing behavioral or emotional problems. It seems likely that
such problems could be mistaken for Ritalin side effects.
most common side effects: decreases in appetite, insomnia,
stomachaches and headaches - all of which were rated as quite mild
(form 0 to 3 on a 9 point scale).
other side effects: 10% developed mild nervous tics
one child developed mild psychotic symptoms
These symptoms, however, disappeared shortly after medication was
stopped.
In response to the medication, 87% of the 82 children displayed
improvements in school behavior and performance.
In short: Even when significant side effects occur, they are
transient, abating within hours after stopping medication. For the
majority of children, improvements occurred.
While the CCHR campaign is provocative and has a certain simplistic
appeal, such a hypothesis is not supported by the available data, and it
hardly accounts for the numerous physical, behavioral, cognitive and
social impairments that these children suffer (Barkley, 1981).
However...one real problem here is that there are no clear norms
concerning what is appropriate in childhood behavior. How active does
one have to be to be considered hyperactive? Without such norms, how
can we be certain that we are not also, inadvertently, medicating normal
children? [Again, we are confronted with the ever-present question:
What is it that we mean by "normal" and "abnormal"?].
VII. Conclusion
Today we have looked at an example externalizing disorder:
Attention deficit Hyperactivity Disorder. If you are left with the
feeling that there are more questions than answers about this disorder,
you are correct. We have yet to pin-down exactly what ADHD is, what
causes it, let alone how to treat it. Yet it remains a phenomenon of
real concern to teachers and parents, and it is frequently seen in child
guidance clinics and pediatricians' offices. Handout 23-1
Percentage of 82 ADHD Children Experiencing Each Side Effect of
Ritalin at Two Dose Levels (0.3 and 0.5 mg/kg twice daily)
Possible Placebo Low Dose Moderate Dose
Side Effect % Sev.* % Sev. % Sev.
Decreased Appetite 15 0.4 52 1.8 56 2.6
Insomnia 40 1.5 62 2.7 68 3.1
Stomachaches 18 0.5 39 1.0 35 1.5
Headaches 11 0.3 26 0.6 21 0.8
Prone to Crying 49 1.8 59 2.3 54 2.0
Tics/Nervous Movements 18 0.7 18 0.9 28 1.2
Nailbiting 22 1.1 26 1.1 29 1.3
Talks Excessively 16 0.4 20 0.6 22 0.9
Irritable 72 3.2 65 2.6 66 2.7
Sadness 43 1.6 48 1.9 41 1.8
Stares Excessively 40 1.3 38 1.2 38 1.0
*Sev. = Mean Severity Rating of this side effect using a scale
from 0 (not at all) to 9 (severe).
(Barkley, 1988)