Neural substrates of impaired sensorimotor timing in adult attention-deficit/hyperactivity disorder.

نویسندگان

  • Eve M Valera
  • Rebecca M C Spencer
  • Thomas A Zeffiro
  • Nikos Makris
  • Thomas J Spencer
  • Stephen V Faraone
  • Joseph Biederman
  • Larry J Seidman
چکیده

BACKGROUND Timing abilities are critical to the successful management of everyday activities and personal safety, and timing abnormalities have been argued to be fundamental to impulsiveness, a core symptom of attention-deficit/hyperactivity disorder (ADHD). Despite substantial evidence of timing deficits in ADHD youth, only two studies have explicitly examined timing in ADHD adults and only at the suprasecond time scale. Also, the neural substrates of these deficits are largely unknown for both youth and adults with ADHD. The present study examined subsecond sensorimotor timing and its neural substrates in ADHD adults. METHODS Using functional magnetic resonance imaging, we examined paced and unpaced finger tapping in a sample of 20 unmedicated adults with ADHD and 19 control subjects comparable on age, sex, and estimated IQ. The blood oxygenation level-dependent contrast response was used to estimate task-related neural activity. RESULTS Behavioral data showed no between-group differences in mean tapping rates but greater within-subject variability in tap-to-tap intervals for ADHD adults relative to control subjects. Importantly, ADHD adults had greater clock rather than motor variability, consistent with a central timing locus for the atypical movements. The imaging results demonstrated that, relative to control subjects, ADHD adults showed less activity in a number of regions associated with sensorimotor timing, including prefrontal and precentral gyri, basal ganglia, cerebellum, inferior parietal lobule, superior temporal gyri, and insula. CONCLUSIONS Our findings show that subsecond timing abnormalities in ADHD youth persist into adulthood and suggest that abnormalities in the temporal structure of behavior observed in ADHD adults result from atypical function of corticocerebellar and corticostriatal timing systems.

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عنوان ژورنال:
  • Biological psychiatry

دوره 68 4  شماره 

صفحات  -

تاریخ انتشار 2010