Mapping attention-deficit/hyperactivity disorder from childhood to adolescence--no neurophysiologic evidence for a developmental lag of attention but some for inhibition.

BACKGROUND The role of a developmental lag for deficits of higher brain functions in attention-deficit/hyperactivity disorder (ADHD) has not yet been tested in longitudinal studies. We examined the development of neurophysiological markers of attention (Cue P300; contingent negative variation [CNV]) and inhibition (NoGo P300) in ADHD and control groups from childhood to adolescence for support of the developmental lag hypothesis of ADHD. METHODS ADHD (n = 28/3 girls) and control (n = 22/5 girls) subjects were assessed at baseline (Time 1; ADHD age 10.8 +/- 1.8 years, controls 10.4 +/- 1.1 years) and at two follow-up examinations (Time 2 after 1.2 years, Time 3 after 2.5 years). Event-related potential maps were recorded during a cued Continuous Performance Test (CPT) at all assessments and analyzed using scalp and source (sLORETA) measures. RESULTS CPT performance showed common effects of ADHD and younger age, consistent with (but not specific to) developmental lag. The NoGo P300 developed earlier and became stronger in control subjects than in the ADHD group, again consistent with an initial developmental lag. In contrast, the attenuation of the Cue P300 and the CNV with ADHD at all assessments was opposite to the enhancement with younger age and thus inconsistent with developmental lag. The sLORETA source localization also differed between ADHD and developmental effects. CONCLUSIONS These results provide strong evidence for multiple and persistent neural processing deficits in ADHD. They do not support the developmental lag hypothesis for attentional dysfunction in ADHD despite partial evidence that developmental lag contributes to inhibitory brain dysfunction during early adolescence.