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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.

A 56-year-old male presented with thrombus formation manifesting as cerebral embolic infarction suspected to be caused by hemostasis at the carotid bifurcation, not by the intimal abnormalities or hematological disorders. Thrombus repeatedly and reproducibly appeared at the same area in spite of carotid endarterectomy (CEA). Ultrasonography demonstrated a stenotic lesion of the cervical carotid bifurcation. Medical treatment reduced the stenosis, but the thrombus was repeatedly formed at the same area of the cervical carotid bifurcation. CEA was performed. Histological examination of the specimen found only the underlying thin intima consisting of mild fibrous atheromatic change without ulceration or vascular dissection. Ultrasonography following CEA showed reduced blood flow, indicating hemostasis, and moyamoya appearance in that area. The thrombus had recurred in spite of the medical treatment with anti-platelet agent. This repeated thrombus was gradually dissolved and reduced with anticoagulant therapy. Thrombus causing cerebral embolic stroke and originating at the cervical carotid bifurcation is usually due to the intimal atherosclerotic change such as ulcer formation or vascular dissection. The thrombus in this case was probably formed by hemostasis at the cervical carotid bifurcation and CEA was not effective to prevent recurrence.

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