Neurologic deficits evident when patients initially awaken from surgery are generally due to intraoperative embolization or inadequate cerebral protection in patients with marginal cerebral perfusion; neurologic deficits occurring in the immediate postoperative period are usually related to acute carotid occlusion or embolization. However, in a small subset of patients, transient postoperative neurologic dysfunction seems to be related to a syndrome of cerebral hyperperfusion rather than a lack of adequate cerebral blood flow. This study describes the courses of 10 patients with classic findings of cerebral hyperperfusion syndrome. Typically, this syndrome occurred in patients with longstanding severe chronic cerebral ischemia and occurred after correction of a very high-grade carotid stenosis. Intraoperatively, there was often a dramatic increase in xenon-labeled cerebral blood flows, with postocclusion flows sometimes attaining three to four times baseline levels. Postoperatively, the patients initially did well. However, over the next several days, many of them began to complain of unilateral headache on the operated side and subsequently had seizures. Electroencephalography obtained during this period uniformly revealed periodic lateralizing epileptiform discharges on the side of the brain ipsilateral to the endarterectomy. Although neurologic dysfunction fully resolved in all of the patients in this group, it is possible that intracerebral hemorrhage may occur in some patients with hyperperfusion syndrome. The pathophysiology of this syndrome is believed to be related to preoperative loss of cerebral autoregulatory mechanisms caused by chronic cerebral ischemia.