Delayed ischemic neurological deficit or clinical vasospasm remained a major cause for delayed neurological morbidity and mortality for patients with aneurysmal subarachnoid hemorrhage (SAH). Magnesium is a cerebral vasodilator. In experimental model of drug or SAH-induced vasospasm, magnesium blocks voltage-dependent calcium channels and reverses cerebral vasoconstriction. Furthermore, its antagonistic action on N-methyl-D-aspartate receptor in the brain prevents glutamate stimulation and decreases calcium influx during ischemic injury. Clinically, the protective effect of magnesium has also been found useful in women with preeclampsia, a condition thought to be due to cerebral vasospasm. Initial experimental result in human was found to safe and effective as compared to historical data. In our pilot study, 60 patients were randomly allocated to receive either magnesium sulfate infusion 80 mmol/day or saline infusion for 14 days. The incidence of symptomatic vasospasm decreased from 13/30(43

作者：George Kwok Chu, Wong；Matthew Tai Vai, Chan；Tony, Gin；Wai Sang, Poon

来源：Acta neurochirurgica. Supplement 2011 年 110卷 Pt 2期