Magnesium Deficiency Exacerbates and Pretreatment Improves Outcome Following Traumatic Brain Injury in Rats: 31P Magnetic Resonance Spectroscopy and Behavioral Studies

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Abstract
The biochemical mechanisms mediating delayed or secondary tissue injury after central nervous system trauma remain speculative. We have demonstrated previously that traumatic brain injury in rats causes a rapid decline in tissue intracellular free magnesium [Mg]f and total magnesium [Mg]t concentrations, which were significantly correlated with injury severity. In order to examine the relationship between magnesium and traumatic brain injury, we assessed whether (1) magnesium deficiency exacerbates or (2) magnesium treatment improves posttraumatic outcome following fluid–percussion brain injury (2.0–2.4 atm) in rats. Animals placed on magnesium-deficient diet for 14 days showed a 15% decrease in brain [Mg]f as measured by phosphorus (31P) magnetic resonance spectroscopy (MRS). Magnesium deficiency significantly exacerbated neurologic dysfunction and increased mortality following injury when compared to normally fed saline-treated controls. Conversely, pretreatment with magnesium sulfate (0.1 mEq) 15 min before brain injury prevented the fall in [Mg]f observed by 31P MRS in saline-treated animals and significantly improved both cellular bioenergetic state and chronic posttraumatic neurologic outcome. These combined observations suggest that alterations in brain [Mg]f after trauma may play a role in the pathophysiology of traumatic brain injury.