An overview of pharmacotherapy for cerebral vasospasm and delayed cerebral ischemia after subarachnoid hemorrhage.

Survival from aneurysmal subarachnoid hemorrhage has increased in the past few decades. However, functional outcome after subarachnoid hemorrhage is still suboptimal. Delayed cerebral ischemia (DCI) is one of the major causes of morbidity. Mechanisms underlying vasospasm and DCI after aneurysmal subarachnoid hemorrhage and pharmacological treatment are summarized in this review. Oral nimodine, an L-type dihydropyridine calcium channel blocker, is the only FDA-approved drug for the prevention and treatment of neurological deficits after aneurysmal subarachnoid hemorrhage. Fasudil, a potent Rho-kinase inhibitor, has also been shown to improve the clinical outcome and has been approved in some countries for use in patients with aneurysmal subarachnoid hemorrhage. Although other drugs, including nicardipine, cilostazol, statins, clazosentan, magnesium and heparin, have been expected to have beneficial effects on DCI, there has been no convincing evidence supporting the routine use of those drugs in patients with aneurysmal subarachnoid hemorrhage in clinical practice. Further elucidation of the mechanisms underlying DCI and the development of effective therapeutic strategies for DCI, including combination therapy, are necessary to further improve the functional outcome and mortality after subarachnoid hemorrhage.