In abstinent cocaine dependent patients, cortical blood flow was reduced, frontal EEG beta power was asymmetric and cognitive deficits were observed. These alterations persist and may be related to residual neurological damage produced by prolonged exposure to cocaine. Cocaine use in relatively young individuals has, also, resulted in subarachnoid hemorrhage, seizures and stroke. In addition to its neuroprotective effects in subarachnoid hemorrhage, nimodipine improves cognitive performance in young, old and brain-damaged animals. The pharmacological properties of nimodipine may protect the cocaine abuser in treatment from the adverse cerebrovascular effects of cocaine while relieving the cognitive deficits observed in abstinence. However, little is known about nimodipine in drug abusers. This study investigates the subjective, cardiovascular and CNS effect of nimodipine in drug users. The CNS measures included resting EEG, sensory and cognitive evoked potentials and cognitive task performance. Single (0, 30 and 60) and three daily doses (O to 180 mg at 4 hour intervals) of nimodipine and/or placebo were administered in double blind cross over experimental design. Seven subjects were tested this year to complete the planned total of 14 subjects. The subjective and cardiovascular effects of single and multiple daily doses of nimodipine in this population were minimal. Nimodipine did not lower the seizure threshold as judged by EEG photic driving procedures. Nimodipine, however, did reduce the frontal EEG beta asymmetry and prevent the reduction in P300 amplitude in two cognitive tasks. The P300 brain potential is an index of a stimulus evaluation and the ability to update working memory. The P300 and frontal beta is abnormal in cocaine dependent individuals. Thus nimodipine may be useful in the treatment of cocaine dependence.
