Unraveling the nature of hyperactivity in children with attention-deficit/hyperactivity disorder

Seated hyperactivity is a defining feature of the combined and predominantly hyperactive-impulsive subtypes of attention-deficit/hyperactivity disorder (ADHD), but its underlying nature is unknown.

To determine whether hyperactivity is a consequence of an impaired ability to inhibit activity to low levels or to maintain positional stability.

Case-control study.

Academic research center and school.

Sixty-two boys 9 to 12 years of age (of 73 screened), recruited from the community by advertisement, who met DSM-IV criteria for ADHD combined subtype on structured interview. Sixty-two controls were selected by matching for age and sex from a community sample of 1168 subjects in 3 participating school districts. Pupils with Conners' Teacher Rating Scores Revised within +/-1 SD of the mean for age were eligible for randomized matching. Intervention Infrared motion analysis of head-marker movements (50 Hz) during performance of a 15-minute cognitive control task. Subjects with ADHD were tested at least 18 hours following their last dose of methylphenidate and again 120 minutes after a 0.4-mg/kg probe dose.

Inhibitory control (spike and basal amplitude) and head-marker stability (approximate entropy, Lyapunov, and spectral exponents).

Inhibitory control measures were 2-fold higher in subjects with ADHD (d' = 0.63-0.95). Group differences in head-marker stability were even greater (d' = 2.20-4.71; receiver operating characteristic area = 0.956-1.0). Methylphenidate restored inhibitory ability to control levels but only partially corrected stability deficits, which still distinguished subjects with ADHD from controls (receiver operating characteristic area = 0.722-0.995).

Children with ADHD have a deficient ability to inhibit activity to low levels and unstable control of head-marker position characterized by deterministic chaos (sensitivity to initial conditions). These deficits differed in degree of correctability by methylphenidate, suggesting that they may be mediated by different neural circuits (eg, corticostriatal vs cerebrovestibular).