Review ArticlesNeurobiology of attention-deficit hyperactivity disorder
Introduction
Attention-deficit hyperactivity disorder (ADHD) is an early-onset, clinically heterogeneous disorder of inattention, hyperactivity, and impulsivity. Its impact on society is enormous in terms of its financial cost, stress to families, adverse academic and vocational outcomes, and negative effects on self-esteem. In this article we provide an overview of what is known about the neurobiology of ADHD by examining studies of genetics, environmental adversity, neuropsychology, neuroimaging, and neuropharmacology.
Section snippets
Family, twin, adoption, and segregation analysis studies
As we have reviewed in detail elsewhere, family studies derived from clinically referred samples consistently support the assertion that ADHD runs in families Faraone and Biederman 1994a, Faraone and Biederman 1994b. There is agreement on this point between early studies of hyperactivity and subsequent studies of DSM-III attention deficit disorder (ADD) and DSM-IV ADHD. These studies find the parents of ADHD children to have a 2- to 8-fold increase in the risk for ADHD. Thus, they confirm the
Environmental risk and protective factors for ADHD
Numerous aspects of the biological and psychosocial environment have been examined as potential risk or protective factors for ADHD. Although several factors have been implicated in the etiology of the disorder, none has emerged as a necessary and sufficient cause that can account for most cases of ADHD.
ADHD and the brain
Satterfield and Dawson (1971) were among the first to propose that ADHD symptoms were caused by frontolimbic dysfunction. They suggested that weak frontal cortical inhibitory control over limbic functions might lead to ADHD. The success of stimulant medications, and animal models implicating dopamine pathways were taken as support for this model. A review of the neurological literature (Mattes 1980) articulating the similarities between adult patients with frontal lobe damage and children with
Summary and conclusions
Few would argue with the idea that ADHD is a disorder of the brain that has multiple causes: genes, biological adversity, and psychosocial adversity. But the details of how these components combine to cause ADHD are unknown. Moreover, the available data provide support for the etiologic and pathophysiologic heterogeneity of the disorder. We are not likely to find a necessary and sufficient cause that explains a substantial fraction of ADHD cases. Instead, the challenge for future research is to
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