In conclusion, there appears to be strong evidence from these studies supporting the existence of a postcocaine abuse syndrome. The general hypothesis stated that cocaine-dependent patients would exhibit impaired performance on tests of motor system functioning. It was further hypothesized that these impairments would be more severe and persistent than impairments in other areas. These hypotheses were confirmed. Cocaine-dependent, patients were found to exhibit a statistically significant resting hand tremor, which did not remit despite 3 months of verified abstinence. In contrast, alcohol-dependent patients exhibited an enhanced action tremor and enhanced body sway that remitted after 1 week. Cocaine-dependent, but not alcohol-dependent, patients also exhibited slower reaction times than controls during a protracted vigilance tasks and during simpler tasks requiring visual or auditory divided attention. The reaction time slowing was substantial (approximately 50 to 75 ms), task independent, and, like resting tremor, did not remit after 3 months of abstinence. The demonstration of smooth pursuit eye movement irregularities in the cocaine-dependent group further reinforced the motor system hypothesis. During visual tracking of an oscillating pendulum, the tracking accuracy of cocaine-dependent patients was superior to that of controls at all three time points. Studies that have administered acute amphetamine to normal, nondrug-dependent individuals have reported a similar finding. Collectively, these findings suggest that chronic cocaine use may induce a hyperexcitability of the smooth pursuit eye movement control system, which persists into abstinence. Evidence for EEG abnormalities among recovering cocaine-dependent patients was provided by a variety of experiments. In a new and ongoing experiment, cocaine-dependent patients exhibit reduced P300b ERPs to rare stimuli, which they must acknowledge with a motor response. Evidence for a nonmotor CNS dysfunction was provided by examining EEG responses to a simple flickering light. However, the nature of the dysfunction was complex. EEG responses to square wave modulated light revealed diminished reactivity among both cocaine-dependent and alcohol-dependent patients at all three time points. In contrast, EEG responses to sine wave modulated light revealed enhanced reactivity among the cocaine-dependent patients only. The coexistence of diminished or enhanced EEG reactivity and diminished or enhanced motor system functioning implies that cocaine dependence can simultaneously depress and enhance different aspects of brain function in the same individual. The diversity of cocaine's EEG and psychomotor effects may have an analog in demonstrations of the simultaneous development of sensitization and tolerance among animals chronically exposed to cocaine.