Endovascular Management of Cerebral Vasospasm Ben McGuinness, MBChB, FRANZCR a , Dheeraj Gandhi, MBBS, MD a,b, * Cerebral vasospasm causes significant morbidity and mortality in patients with subarachnoid hemorrhage (SAH). The management of these patients is challenging and requires the multidisci- plinary input of intensive care, neurosurgical, and endovascular specialists. Angiographic vaso- spasm occurs in approximately 70% of all aneurysmal SAH, but clinical neurological mani- festations occur in only one third of these cases. 1 Up to 15% of patients surviving the initial subarachnoid hemorrhage will suffer stroke or death as a result of vasospasm. 2,3 Vasospasm rarely occurs before day 4; it tends to peak at day 7, and it may last up to 2 weeks after the initial hemorrhage. Most cases of vasospasm can be managed medically. Medical strategies for treating vaso- spasm include hemodynamic augmentation to improve cerebral perfusion pressure and medical therapy to prevent or reduce cerebral vasospasm. A combination of volume expansion, hemodilution, and induced hypertension (Triple H therapy) has been used extensively, but its value has not been tested rigorously. 4 Currently, oral nimodipine is recommended for patients with aneurysmal SAH. Other, newer agents being evaluated include albumin, statins, magnesium sulphate infusion, and clazosentan (endothelin-1 antagonist). 4 Detailed discussion of medical therapy is beyond the scope of this article. Instead, it will focus on the endovascular therapy of vasospasm and the role of radiological imaging in the appropriate selection of patients who are likely to benefit from this form of treatment. The clinical diagnosis of vasospasm often is based on detailed neurologic examination. The monitoring of patients at risk for clinical vaso- spasm requires constant neurological examination by intensive care specialists and the decision making of an experienced, multidisciplinary physi- cian team. The diagnosis of symptomatic vaso- spasm requires identification of new focal motor deficits or sudden changes in mental status in at- risk patients. These new deficits should not be easily attributed to other causes such as develop- ment of hydrocephalus, systemic infection, seizures, or ongoing delirium. Although clinical examination is very useful, it is not always reliable. A significant proportion of patients with SAH may be neurologically impaired or comatose at base- line. In such patients, a meaningful neurological examination may not be obtainable. IMAGING ASSESSMENT Diagnostic imaging assessment of a patient with SAH in the vasospasm window serves many functions. These include ruling out other a Division of Interventional Neuroradiology, Department of Radiology, Johns Hopkins Hospital, 600 North Wolfe Street, Nelson B-100, Baltimore, MD 21287, USA b Division of Interventional Neuroradiology, Department of Neurology and Neurosurgery, Johns Hopkins Hospital, 600 North Wolfe Street, B100, Baltimore, MD 21287, USA * Corresponding author. Division of Interventional Neuroradiology, Department of Neurology and Neurosur- gery, Johns Hopkins Hospital, 600 North Wolfe Street, B100, Baltimore, MD 21287. E-mail address: dgandhi2@jhmi.edu KEYWORDS  Vasospasm  Endovascular  Angioplasty  Interventional  Subarachnoid hemorrhage  Angiography Neurosurg Clin N Am 21 (2010) 281–290 doi:10.1016/j.nec.2009.10.007 1042-3680/10/$ – see front matter ª 2010 Elsevier Inc. All rights reserved. neurosurgery.theclinics.com