Cerebral vasospasm after subarachnoid hemorrhage.

PURPOSE OF REVIEW

To summarize new pathophysiologic insights and recent advances in the diagnosis and treatment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

RECENT FINDINGS

Important, newly recognized mediators of cerebral arterial spasm after subarachnoid hemorrhage include superoxide free radicals, ferrous hemoglobin (which acts as a nitric oxide scavenger), endothelins, protein kinase C, and rho kinase. Microvascular dysfunction and autoregulatory failure also has been an area of increasing research focus in recent years. New diagnostic modalities include measures of cerebral blood flow such as single-photon emission computed tomography and perfusion computed tomography, magnetic resonance imaging, intracranial brain oxygen tension probes, and jugular venous oxygen saturation monitors. Proton magnetic resonance spectroscopy and microdialysis can detect tissue biochemical abnormalities, but these techniques have not found their way into routine clinical practice as of yet. In addition to nimodipine and hypertensive hypervolemic therapy, promising new treatments for vasospasm or its ischemic complications include magnesium sulfate, fasudil hydrochloride, tirilazad mesylate, erythropoietin, and induced hypothermia. Balloon angioplasty has emerged as the primary weapon for treating medically refractory ischemia from vasospasm and in many centers is being used as a first-line treatment or even prophylactically.

SUMMARY

The neurointensive care management of vasospasm after subarachnoid hemorrhage has evolved significantly over the past 10 years, with many new diagnostic modalities and promising treatments now available. Clinical trials are needed to evaluate the efficacy of these new techniques and to further define the optimal management of this often devastating complication.