Cilostazol is an antiplatelet aggregation inhibitor drug associated with increased cerebral blood flow and inflammation suppression. This study evaluated administration of cilostazol to prevent cerebral vasospasm following subarachnoid hemorrhage (SAH) in 50 patients treated surgically from December 2004 to November 2006. All patients, excluding those with Hunt and Kosnik grade 5 or who had undergone late surgery, were classified into two groups: 26 patients who received 200 mg/day cilostazol from postoperative day 1 to day 14 and 24 control patients. The frequency and the degree of cerebral vasospasm, occurrence of ischemic lesion, and clinical symptoms due to vasospasm were compared between the two groups. The appearance of severe vasospasm on angiography, persistent symptomatic spasm, and new cerebral infarction due to vasospasm demonstrated by neuroimaging were apparently lower in the cilostazol group than in the control group, suggesting that cilostazol may significantly suppress cerebral vasospasm following SAH.

Abrupt normalization of cerebral blood flow (CBF) after surgical procedures to improve excessive cerebral hypoperfusion can cause irreversible brain parenchymal damage. Such hyperperfusion, which is caused by inflow at normal blood pressure into maximally dilated fine vessels, is an important complication following carotid endarterectomy (CEA). Strict control of blood pressure in the perioperative period can prevent this complication except in a few patients, who have severe cerebral hypoperfusion and poor cerebrovascular reserve due to extremely severe stenosis of the ipsilateral or the bilateral carotid arteries, for which CEA is indicated. The requirement for improved CBF and the risk of postoperative hyperperfusion conflict in the pathogenesis of these patients. We tried to prevent abrupt improvement in perfusion by attempting gradual restoration of CBF. Superficial temporal arterymiddle cerebral artery anastomosis was first performed to improve the poor cerebrovascular reserve by allowing insufficient blood flow. A few weeks later, CEA was performed to completely restore CBF. This surgical approach obtained good results without postoperative problems in four patients. The indications of this surgical management and efficacy of stepwise restoration of CBF to prevent postoperative hyperperfusion depend on careful preoperative evaluation of perfusion studies.

Carotid artery restenosis is a serious complication following carotid endarterectomy (CEA), so preventative management of the risk factors is important. The present study investigated the potential of cilostazol, a mediator of vascular stabilization as well as inhibitor of platelet aggregation, to suppress restenosis on the ipsilateral carotid artery and new plaque development on the contralateral carotid artery. Eighty-two patients treated by CEA were divided into two groups according to the postoperative antiplatelet aggregation drugs into the cilostazol and other groups. Patients were periodically examined for recurrence of the plaque on the ipsilateral side, development of plaque on the contralateral side, and the bilateral intermedia thicknesses measured by ultrasonographic examination for up to 6 years. Restenosis and development of the contralateral plaque were not detected in any patients in the cilostazol group, whereas such changes were found in seven patients in the other group. Cilostazol might be effective to inhibit the growth mechanism of plaque.

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EC-IC bypass surgery to prevent cerebral ischemia must be performed carefully and safely. We apply several techniques and devices to reduce the operative risk as much as possible by: