Cerebral vasospasm and delayed cerebral ischemia remain an unsolved problem in 
patients with aneurysmal subarachnoid hemorrhage (SAH). In theory, high-dose 
magnesium sulfate (MgSO(4)) therapy offers vascular and neuroprotective benefits 
and is therefore currently under evaluation. The intensity of the inflammatory 
response after SAH is associated with the outcome. The aim of the current study 
was to evaluate a possible link between the inflammatory response and MgSO(4) 
therapy, since magnesium (Mg(2+)) has anti-inflammatory properties. In 15 
patients with SAH, inflammatory cytokine levels in the cerebrospinal fluid (CSF) 
and peripheral blood were determined daily using an enzyme-linked immunosorbent 
assay between day 4 and day 12. Eight patients were treated with standard 
therapy alone (group 1) and seven patients were treated with an additional, 
high-dose of MgSO(4) (group 2). Serum Mg(2+) levels in group 2 were 
significantly higher compared to group 1: 1.48 ± 0.04 mmol/L versus 0.90 ± 0.01 
mmol/L, ρ<0.001. Interleukin-6 (IL-6) in the CSF was significantly lower in 
group 2 compared to group 1: 6680 ± 989 vs.11079 ± 1277 pg/mL, ρ = 0.021. A 
trend towards lower systemic IL-6 levels was found in group 2: 58 ± 7 versus 104 
± 21 pg/mL, ρ = 0.052. Systemic IL-1β levels were significantly lower in group 
2: 0.66 ± 0.11 and 0.15 ± 0.01 pg/mL (ρ<0.001), while the CSF levels did not 
differ. Tumor necrosis factor-α levels did not differ between the two groups. 
Although there were more patients with favorable outcome in group 2, the 
difference was not statistically significant. This was probably due to the small 
sample size. The results indicate a suppression of inflammatory cytokine 
release, in particular IL-6, in patients treated with high-dose MgSO(4). These 
results call for further studies of the effect of Mg(2+) on the inflammatory 
signaling pathway with regard to delayed cerebral ischemia following SAH.