Subarachnoid hemorrhage caused by a ruptured aneurysm accounts for only 5% of strokes, but occurs at a fairly young age and carries a worse prognosis. Delayed cerebral ischemia is an important cause of death and dependence after aneurysmal SAH. The current mainstay of preventing delayed cerebral ischemia is nimodipine and maintenance of normovolemia, but even with this strategy delayed cerebral ischemia occurs in a considerable proportion of patients. Magnesium is an inexpensive, easily available neuroprotective agent that reduces cerebral vasospasm and infarct volume after experimental subarachnoid hemorrhage. In a meta-analysis of all randomized clinical trials, magnesium shows a tendency to reduce the occurrence of delayed cerebral ischemia and poor outcome after subarachnoid hemorrhage, but the question if magnesium is advantageous in subarachnoid hemorrhage patients is still in abeyance. Currently a large phase III trial aiming for 1200 patients is being conducted that will hopefully provide definite evidence whether magnesium treatment is beneficial in subarachnoid hemorrhage patients.
Subarachnoid hemorrhage (SAH) caused by a ruptured aneurysm accounts for only 5% of strokes, but occurs at a fairly young age and carries a worse prognosis than other types of stroke (van Gijn et al, 2007). The cardinal feature is a history of unusually severe headache that started suddenly, but patients frequent deteriorate into unconsciousness shortly after onset.
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