Recent evidence pointing to a disturbance of function of the striatum in attention deficit hyperactivity disorder (ADHD) is reviwed from the Department of Pediatric Neurology, The John F Kennedy Institute Glostrup, Denmark. Concomitant involvement of the cingulo-striato-thalamo-cortical loop which subserves awareness results in impulsivity, inattention and hyperactivity. Perinatal hypoxic-ischemic encephalopathy, common in prematurity, a known antecedent of ADHD, results in release of excitatory amino acids, especially glutamate, which cause neuronal swelling and cell death. The anatomy of the striatum, with its convergent glutaminergic afferent synaptic transmission from the cortex, contributes to its vulnerability in ischemia-induced glutamate release. The increased survival of premature infants has led to a higher incidence of ADHD in this patient group. [1]

COMMENT. ADHD is a heterogeneous disorder with a number of presumed etiologic factors. This author emphasizes the role of prematurity and hypoxic-ischemic events in damage to the striatum and its connections in the pathophysiology of ADHD. Several studies are cited showing up to one third of premature infants with birthweight <1500 gm have ADHD when examined at 5 to 7 years.