Cerebral vasospasm is a frequent and severe complication of SAH. Angiographic vasospasm may be seen in 70% of patients and delayed cerebral ischemic deficits are observed in 30% of patients. Since vasodilator drugs cannot reverse cerebral vasospasm, treatment is directed to prevent vasospasm and to prevent or reverse ischemic deficits. The mainstay of treatment of vasospasm is the hypertensive hypervolemia dilution (triple H therapy); the mainstay of prevention is the calcium channel blocker nimodipine. The efficacy of triple H therapy has not been demonstrated in randomized clinical trials, while several randomized trials have demonstrated that nimodipine reduces poor outcome due to vasospasm in all grades of patients. Some randomized, clinical trials are recently performed on the efficacy of rTPA (on the basis of the correlation between the amount of cisternal blood and the incidence and severity of vasospasm) and of tirilazed (on the basis of the role of lipidic peroxidation and free radical generation in the pathogenesis of spasm). Balloon angioplasty and/or super-selective intra-arterial infusion of papaverine can be considered when patient is refractory to medical and pharmacological treatment.