Eighteen hyperactive clinical responders to methylphenidate were taken off medication and tested in two sessions during which they received an acute dose of methylphenidate and placebo in counterbalanced order. Seventeen normal boys of comparable age were tested without drugs. For both samples, evoked potentials were recorded during a Continuous Performance Test. Normal children made fewer errors of commission and omission and displayed faster reaction times than hyperactives tested under placebo. In addition, under active attention, the late positive component (LPC) of placebo‐treated hyperactive boys' evoked responses exhibited smaller amplitude than normal controls'. Methylphenidate increased the amplitude of hyperactive patients' LPC and generally ameliorated their performance, especially commission errors and reaction times. The results confirmed previous findings of attentional disturbance in hyperactivity and normalization by methylphenidate of these patients' performance and electrophysiological activity during sustained attention.

Evoked potentials during the × and B‐X versions of the Continuous Performance Test (CPT) were evaluated in 29 hyperactive children after ingestion of placebo or methylphenidate (0.3 mg/Kg). Twenty‐one age matched normal children were also assessed twice but without any drugs. In both tests, placebo‐treated hyperactives made more omission and commission errors and displayed smaller late positive components (LPC) of the evoked response to salient experimental cues. Methylphenidate ameliorated hyperactives’ performance in both tasks and enlarged their LPCs in CPT‐X. Several of these drug effects and diagnostic differences were absent for older hyperactive subjects, probably because some of the procedures were too easy for them. For younger patients the present tasks were sufficiently challenging, and the results reflect normalization of their deficits in sustained attention.

Twenty‐two normal young men received a counterbalanced and double blind administration of 20 mg methylphenidate and placebo. Two tasks were administered in counterbalanced order: an uninterrupted 45‐min vigilance test and a paired‐associates learning test. As previously reported, under placebo, accuracy and speed decreased monotonically over the course of the vigil. This degradation of performance was significantly reduced by the stimulant drug. Event‐related potentials (ERPs) were derived for correctly detected targets and nontargets. The most salient pharmacologic effects involved a late positive wave (P464) identified as P3b. Methylphenidate reversed or reduced the decrease in amplitude and increase in latency of P464 present over phases of the placebo session. The results suggest that the stimulant‐induced improvement in performance may be mediated by enhancement of evaluation processes. In the paired‐associates test there were no pharmacologic effects. Instead there was an unexpected, pronounced improvement in learning in the second session, irrespective of the substance administered. However, the ERP evoked by the “stimulus” cue of each pair was systematically related to the achievement of learning criteria. A late positive was identified as P3b (P555) increased significantly in amplitude following the attainment of learning. There were no amplitude changes among ERPs evoked in the early post‐criterion, late post‐criterion, or overlearning “phases.” Nor were there amplitude changes between early and late pre‐criterion categories. Thus, ERP amplitude displayed a binary association with the achievement of learning.

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