Provided by David Satcher, M.D., Ph.D.
Surgeon General of the United States of America
Chapter 3: Children and Mental Health
Overview of Mental Disorders in Children
Causes
The exact etiology of ADHD is unknown, although
neurotransmitter deficits, genetics, and perinatal complications have been
implicated. In the early post-World War II years, a number of pediatricians,
neurologists, and child psychiatrists noted that brain-damaged children were
often hyperactive (Strauss & Lehtinen, 1947; Eisenberg, 1957; Laufer & Denhoff,
1957). These observations led to the diagnostic concept of“minimal brain damage”
(Wender, 1971), which was thought to be characterized by hyperactivity,
inattention, learning difficulties, and a wide variety of behavior problems.
However, large epidemiological studies (Rutter & Quinton, 1977) of grossly
brain-damaged children with cerebral palsy, epilepsy, and so forth, did not find
an excess of hyperactivity, and more recent imaging studies have found no
evidence of gross brain damage in children with ADHD (Swanson et al., 1998). The
past view that ADHD is a form of minimal brain damage has therefore been
abandoned by experts. Many brain-damaged children are, if anything,
significantly underactive.
In the late 1970s, it was postulated that the core problem in hyperkinetic
children was one of inattention (Douglas & Peters, 1979). This view led, in
1980, to the adoption, in the official DSM-III (American Psychiatric
Association, 1980) nomenclature, of the new diagnostic label attention-deficit
disorder.
Because the symptoms of ADHD respond well to treatment with stimulants, and
because stimulants increase the availability of the neurotransmitter dopamine,
the“dopamine hypothesis” has gained a wide following. The dopamine hypothesis
posits that ADHD is due to inadequate availability of dopamine in the central
nervous system. The neurotransmitter dopamine plays a key role in initiating
purposive movement, increasing motivation and alertness, reducing appetite, and
inducing insomnia, effects that are often seen when a child responds well to
methylphenidate. The dopamine hypothesis has thus driven much of the recent
research into the causes of ADHD.
The fact that ADHD runs in families suggests that inheritance is an important
risk factor. Between 10 and 35 percent of children with ADHD have a first-degree
relative with past or present ADHD. Approximately one-half of parents who had
ADHD have a child with the disorder (Biederman et al., 1995). Over the past
decade, a large number of twin studies have shown that, when ADHD is present in
one twin, it is significantly more likely also to be present in an identical
twin than in a fraternal twin (Goodman & Stevenson, 1989). These findings have
led geneticists to estimate that genes are important in a high proportion of
children with ADHD.
Research to pinpoint abnormal genes is honing in on two genes: a
dopamine-receptor (DRD) gene on chromosome 11 and the dopamine-transporter gene
(DAT1) on chromosome 5 (Cook et al., 1995; Smalley et al., 1998). Several
studies have found evidence that children with ADHD have genetic variations in
one of the dopamine-receptor genes (DRD4), although the largest of these studies
suggests that the presence of such a variation is associated with only a modest
increase in the risk of developing ADHD (Smalley et al., 1998). Several other
studies have found evidence for abnormalities of the dopamine-transporter gene
(DAT1) in children with very severe forms of ADHD (Cook et al., 1995; Gill et
al., 1997; Waldman et al., 1998).
Yet for most children with ADHD, the overall effects of these gene abnormalities
appear small, suggesting that nongenetic factors also are important. Although
none of the many imaging studies have found evidence of gross brain damage, some
investigators have suggested that exposure to toxins, such as lead, or episodes
of oxygen deprivation for the fetus, as may occur during some complications of
pregnancy, may adversely affect dopamine-rich areas of the brain. These theories
support observations that hyperactivity and inattention are more common in
children whose mothers smoked during pregnancy (Nichols & Chen, 1981), in
children who have been exposed to high quantities of lead (Needleman et al.,
1990), and in children who had a lack of oxygen in the neonatal period
(Whittaker et al., 1997).
Some investigators have noted that the parents of hyperactive children are often
overintrusive and overcontrolling (Carlson et al., 1995). It has therefore been
suggested that such parental behavior is another possible risk factor for ADHD.
However, others have noted that, when children are treated with methylphenidate,
there is a reduction in parental negativity and intrusiveness. This suggests
that the observed overintrusive and overcontrolling behavior of the parent is a
response to the child’s behavior rather than the cause (Barkley et al., 1985).
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