Cerebral Vasospasm Following Subarachnoid Hemorrhage M. Akif Topcuoglu, MD Johnny C. Pryor, MD * Christopher S. Ogilvy, MD † J. Philip Kistler, MD Address Stroke Service, Department of Neurology and Interventional Neuroradiology and Neurosurgery, * Neurovascular Surgery, † Massachusetts General Hospital, 55 Fruit Street, VBK 802, Boston, MA 02114, USA. E-mail: pkistler@partners.org Current Treatment Options in Cardiovascular Medicine 2002, 4:373–384 Current Science Inc. ISSN 1092-8464 Copyright © 2002 by Current Science Inc. Introduction The presence of cerebral vasospasm (VSP) has been corre- lated with a 1.5- to threefold increase in mortality and morbidity in the first 2 weeks after subarachnoid hemor- rhage (SAH) from aneurysm rupture [1]. This exceeds that of surgical and endovascular morbidity as well as re- rupture, hydrocephalus, systemic or central nervous system infections, and metabolic complications. Despite many years of extensive research, the underlying molecular mechanism of VSP after SAH has not completely been elucidated. Two contemporary theories are still suggested. The first suggests that morphologic changes or dysfunction of the endothelial and vascular smooth muscle cells (VSMCs) are thought to be at the core. The second suggests that exposure to the blood breakdown products including potassium, oxyhemoglobin, and bilirubin in addition to a variety of paracrine mediators, eg, eicosanoids, free radicals, inflammatory and a vasoactive substance, eg, nitric oxide (NO) and endothelin (ET), initiate vasocon- striction. The spasm in turn stimulates endothelial and VSMC proliferation [2]. Studies performed at our institution in the early 1980s suggest a close relationship between the extent and location of subarachnoid blood noted on CT scan and the severity and location of VSP of the basal arteries Opinion statement Cerebral vasospasm and related ischemic stroke continue to be significant complicating factors in the course of many patients with subarachnoid hemorrhage from berry aneurysm rupture. The risk of this well-recognized but poorly understood complication can be estimated on the basis of patient medical history, neurologic examination, and head CT findings. Every patient with possible risk needs specialized neurologic intensive care unit care after aneurysm obliteration. Surgical and pharmacologic wash-out of subarachnoid blood around the basal arteries, proper management of intracranial pressure and fluid status, hyponatremia, hypomagnesemia, and fever, as well as use of calcium channel blockers, have been considered helpful in patient management prior to and with the symptomatic vasospasm development. Transcranial Doppler (TCD) ultrasound is important in detecting vasospasm before the patient suffers ischemic neurologic deficit or infarct. Elevated TCD velocities often initiate the use of triple-H (HHH: hypertension, hemo- dilution, and hypervolemia) therapy and subsequently guide it. Up to the end of the first 3 weeks after subarachnoid hemorrhage and aneurysm obliteration, development of any focal neurologic deficit or mental deterioration, unless convincingly proven otherwise, is assumed to be from cerebral vasospasm. When a hemodynamically significant vasospasm in the arterial segments of clinical concern is suggested, emergency cerebral angiography with balloon dilatation angioplasty or intra-arterial infusion of vasodilating agents may be helpful in relieving ischemic symptoms.