Aneurysmal subarachnoid hemorrhage- (aSAH-) associated vasospasm constitutes a clinicopathological entity, in which reversible vasculopathy, impaired autoregulatory function, and hypovolemia take place, and lead to the reduction of cerebral perfusion and finally ischemia. Cerebral vasospasm begins most often on the third day after the ictal event and reaches the maximum on the 5th–7th postictal days. Several therapeutic modalities have been employed for preventing or reversing cerebral vasospasm. Triple “H” therapy, balloon and chemical angioplasty with superselective intra-arterial injection of vasodilators, administration of substances like magnesium sulfate, statins, fasudil hydrochloride, erythropoietin, endothelin-1 antagonists, nitric oxide progenitors, and sildenafil, are some of the therapeutic protocols, which are currently employed for managing patients with aSAH. Intense pathophysiological mechanism research has led to the identification of various mediators of cerebral vasospasm, such as endothelium-derived, vascular smooth muscle-derived, proinflammatory mediators, cytokines and adhesion molecules, stress-induced gene activation, and platelet-derived growth factors. Oral, intravenous, or intra-arterial administration of antagonists of these mediators has been suggested for treating patients suffering a-SAH vasospam. In our current study, we attempt to summate all the available pharmacological treatment modalities for managing vasospasm. 1. Introduction Aneurysmal subarachnoid hemorrhage (aSAH) constitutes a major cause of stroke, as approximately 3–15% of all stroke cases are due to ruptured intracranial aneurysms [1–4]. Data from population-based studies suggest that the incidence rates vary considerably from 6 to 20 per 100,000 population, with the highest rates reported from Japan and Finland [5–8]. Outcome after aSAH depends on several factors, including the severity of the initial event, the peri-ictal medical management, various surgical variables, and the incidence of aSAH-induced complications. Cerebral vasospasm (CV) is the most frequent and troublesome complication after aSAH. Ecker and Riemenschneider [9] and Robertson [10] were the first ones, who pointed out the occurrence of cerebral arterial spasm following aSAH [9, 10]. Later on, Fisher and his colleagues published a synopsis regarding cerebral vasospasm [11]. Vasospasm, as the term implies, constitutes a reduction in the caliber of a vessel. However, in aSAH cases, the occurrence of vasospasm means much more than just narrowing a cerebral vessel lumen, with significant
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