Occurrence of cerebrovascular accidents has been associated with cocaine abuse. We investigated the relative distribution of cerebral blood flow (CBF) in groups of chronic cocaine users, and of normal controls. Relative CBF was measured using positron emission tomography and 15 oxygen-labelled water. The cocaine users showed areas of deranged CBF as evidenced by patchy regions of defective isotope accumulation throughout their brain. The chronic cocaine users showed decreased relative CBF in the prefrontal cortex when compared with normal subjects. The repeated scans of some cocaine users, after 10 days of cocaine withdrawal, continued to show decreased relative CBF of the prefrontal cortex. We hypothesise that some of the widespread defects in CBF in the cocaine users could reflect the effects of vasospasm in cerebral arteries exposed chronically to the sympathomimetic actions of cocaine.

SDs have been demonstrated recently in patients with acute neuronal injury. Whether treatment with NMDAR antagonists has an effect on this new clinical phenomenon is unclear. 4 -6 In 2 cases with traumatic and spontaneous intracerebral hemorrhage, we show here for the first time in human brain that SDs are indeed blocked by the NMDAR antagonist ketamine. Case PresentationsWe describe 2 patients who underwent emergency craniotomy. In addition to routine monitoring, subdural 6-contact linear electrode strips (Wyler, 5/10 mm platinum; Ad-Tech Medical Instrument Corp, Racine, Wisc) were placed adjacent to the injured cortex in a centrifugal orientation. Details of this procedure have been described previously. 4