Cerebral vasospasm （CVS） may cause cerebral vasoconstriction and thus disrupt the complex vascular regulatory system. CVS is one of the leading causes of disability and death after subarachnoid hemorrhage， as well as a driving factor for delayed cerebral ischemia and neurological deficits. At present， there are few treatment options for CVS in clinical practice. Drug therapies mainly include induced blood pressure elevation， calcium channel blockers， vasodilators， phosphodiesterase inhibitors， statins， antispasmodic drugs， erythropoiesis-stimulating agents， and endothelin-receptor antagonists， and non-pharmacological therapies include intravascular intervention with vasodilators and mechanical angioplasty. The pathogenesis of CVS remains unknown at present， and there is still a lack of effective therapies for CVS. With the deep understanding of the potential pathogenesis of CVS， it may be possible to find good therapeutic targets. Neuroinflammation and microthrombosis are new mechanisms that contribute to vasospasm and delayed cerebral ischemia after subarachnoid hemorrhage. Up to now， the most promising therapeutic approach is to modulate nitric oxide or endothelin pathways and benefit from the effect of inhibiting spasm. Further studies are being conducted for calcium channel blockers to better understand their mechanisms of action in vasospasm. Nimodipine can cause vasodilation in patients with subarachnoid hemorrhage， improve neurological symptoms， and prevent delayed cerebral ischemia to a certain degree， but it has little effect on mortality after subarachnoid hemorrhage. Therefore， multimodal combination therapy targeting different mechanisms may be a better option. This article reviews the therapies for CVS in recent years. ［Journal of International Neurology and Neurosurgery, 2023, 50(3): 60-65］