• Takeo Murahashi, Kenji Kamiyama, Keiji Hara, Mitsunori Ozaki, Masaaki Mikamoto, Yusuke Nakagaki, Yoichi Nakagaki, and Hirohiko Nakamura.
• Department of Neurosurgery, Nakamura Memorial Hospital, South-1 West-14, Chuo-ku, Sapporo-city, Hokkaido 060-8570, Japan.
• No Shinkei Geka. 2013 May 1; 41 (5): 393-400.

AbstractDelayed ischemic deficit following subarachnoid hemorrhage(SAH)is a major source of morbidity and mortality after rupture of an intracranial aneurysm. Once symptomatic cerebral vasospasm has occured, available treatments do not provide good outcomes for all patients. Symptomatic vasospasm results in serious sequelae for 10-15% of patients and the etiology and pathogenesis remain unclear. Cilostazol is a specific inhibitor of cAMP(cyclic adenosine monophosphate)phosphodiesterase, and is used for treating ischemic symptoms of peripheral vascular disease. Cilostazol has various actions, such as inhibiting vascular smooth muscle proliferation, and increasing nitric oxide(NO)levels derived from endothelial cells. The present study included 81 patients with SAH caused by ruptured cerebral aneurysms treated in two hospitals between June, 2008 and September, 2009. All patients were treated with clipping surgery, and were classified into two groups: 25 patients who received cilostazol from postoperative day 1 to 14 or 28; and 56 control patients. Clinical symptoms due to cerebral vasospasm and frequency of severe spasm were compared between each of the groups. The frequencies of severe spasm appearing on angiography(age>65)and symptomatic cerebral vasospasm were lower in the cilostazol group than in controls. These findings suggest that cilostazol may prevent symptomatic cerebral vasospasm after subarachnoid hemorrhage.

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