OBJECTIVE: To examine whether the maintenance of elevated magnesium serum 
concentrations by intravenous administration of magnesium sulfate can reduce the 
occurrence of cerebral ischemic events after aneurysmal subarachnoid hemorrhage.
DESIGN: Prospective, randomized, placebo-controlled study.
SETTING: Neurosurgical intensive care unit of a University hospital.
INTERVENTIONS: One hundred ten patients were randomized to receive intravenous 
magnesium sulfate or to serve as controls. Magnesium treatment was started with 
a bolus of 16 mmol, followed by continuous infusion of 8 mmol/hr. Serum 
concentrations were measured every 8 hrs, and infusion rates were adjusted to 
maintain target levels of 2.0-2.5 mmol/L. Intravenous administration was 
continued for 10 days or until signs of vasospasm had resolved. Thereafter, 
magnesium was administered orally and tapered over 12 days.
MEASUREMENTS AND MAIN RESULTS: Delayed ischemic infarction (primary end point) 
was assessed by analyzing serial computed tomography scans. Transcranial Doppler 
sonography and digital subtraction angiography were used to detect vasospasm. 
Delayed ischemic neurologic deficit was determined by continuous detailed 
neurologic examinations; clinical outcome after 6 months was assessed using the 
Glasgow outcome scale. Good outcome was defined as Glasgow outcome scale score 4 
and 5.The incidence of delayed ischemic infarction was significantly lower in 
magnesium-treated patients (22% vs. 51%; p = .002); 34 of 54 magnesium patients 
and 27 of 53 control patients reached good outcome (p = .209). Delayed ischemic 
neurologic deficit was nonsignificantly reduced (9 of 54 vs. 15 of 53 patients; 
p = .149) and transcranial Doppler-detected/angiographic vasospasm was 
significantly reduced in the magnesium group (36 of 54 vs. 45 of 53 patients; p 
= .028). Fewer patients with signs of vasospasm had delayed cerebral infarction.
CONCLUSION: These data indicate that high-dose intravenous magnesium can reduce 
cerebral ischemic events after aneurysmal subarachnoid hemorrhage by attenuating 
vasospasm and increasing the ischemic tolerance during critical hypoperfusion.