Evaluation and diagnosis of attention deficit hyperactivity disorder in children
INTRODUCTION — Attention-deficit/hyperactivity disorder (AD/HD) is a condition that manifests in early childhood with symptoms of inattention, hyperactivity, and impulsivity. The symptoms affect cognitive, academic, behavioral, emotional, and social functioning [
1-3], and persist into adulthood in as many as 70 percent of cases [
4-7]. (
See "Adult attention deficit hyperactivity disorder").
PATHOGENESIS — The pathophysiologic basis of AD/HD is not definitively clear and there are many competing theories. The first major hypothesis involves a genetic imbalance in catecholamine metabolism in the cerebral cortex. This hypothesis is based upon structural and functional brain imaging, animal studies, and the response to drugs with noradrenergic activity (eg,
methylphenidate, a stimulant used to treat AD/HD). (
See "Pharmacotherapy for attention deficit hyperactivity disorder in children and adolescents").
Structural brain imaging in children with and without AD/HD demonstrates significant differences. Those with AD/HD have reversed or absent asymmetry of the caudate nucleus, smaller cerebral and cerebellar volume, smaller posterior corpus callosum regions, and increased gray matter in the posterior temporal and inferior parietal cortices [18-27].
Functional brain imaging reveals that children with AD/HD have reduced global activation and reduced local activation in the area of the basal ganglia and anterior frontal lobe [28-31]. The administration of methylphenidate affects activation in these areas. However, the effect varies depending upon the area and whether the child has AD/HD [32]. These findings support the hypothesis that AD/HD is characterized by atypical frontal-striatal function and that methylphenidate affects striatal activation differently in AD/HD than in healthy children.
Bronnen
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