OBJECTIVE: Based on preclinical investigations, magnesium sulfate (MgSO4) has 
gained interest as a neuroprotective agent. However, the ability of peripherally 
administered MgSO4 to penetrate the blood-brain barrier is limited in normal 
brain. The current study measured the passage of intravenously administered Mg 
into cerebrospinal fluid in patients with brain injury requiring ventricular 
drainage.
DESIGN: A prospective evaluation of the cerebrospinal fluid total and ionized 
magnesium concentration, [Mg], during sustained hypermagnesemia was performed.
SETTING: Neurosciences intensive care unit at a major teaching institution.
PATIENTS: Thirty patients with acute brain injury secondary to subarachnoid 
hemorrhage, traumatic brain injury, primary intracerebral hemorrhage, subdural 
hematoma, brain tumor, central nervous system infection, or ischemic stroke were 
studied.
INTERVENTIONS: Patients underwent 24 hrs of induced hypermagnesemia during which 
total and ionized cerebrospinal fluid [Mg] was measured. Serum [Mg] was adjusted 
to 2.1-2.5 mmol/L. Cerebrospinal fluid [Mg] was measured at baseline, at 12 and 
24 hrs after onset of infusion, and at 12 hrs following infusion termination.
MEASUREMENTS AND MAIN RESULTS: At baseline, total (1.25 +/- 0.14 mmol/L) and 
ionized (0.80 +/- 0.10 mmol/L) cerebrospinal fluid [Mg] was greater than serum 
total (0.92 +/- 0.18 mmol/L) and ionized (0.63 +/- 0.07 mmol/L) [Mg] (p < .05). 
Total (1.43 +/- 0.13 mmol/L) and ionized (0.89 +/- 0.12 mmol/L) cerebrospinal 
fluid [Mg] was maximally increased by 15% and 11% relative to baseline, 
respectively, during induced hypermagnesemia (p < .05).
CONCLUSIONS: Hypermagnesemia produced only marginal increases in total and 
ionized cerebrospinal fluid [Mg]. Regulation of cerebrospinal fluid [Mg] is 
largely maintained following acute brain injury and limits the brain 
bioavailability of MgSO4.