Subdural hematoma following traumatic brain injury causes a secondary decline in brain free magnesium concentration

A number of studies have demonstrated that neurologic motor and cognitive d eficits induced by traumatic brain injury (TBI) can be attenuated with admi nistration of magnesium salts, However, many severe traumatic brain injurie s have a significant hematoma that develops subsequent to the primary event s, and it is unclear whether magnesium salts are effective in this situatio n. In the present study, an impact-acceleration rodent model of TBI was use d to produce an injury that causes an extensive subdural hematoma in over 5 0% of injured animals. At 30 min after TBI, rats were randomly administered 250 mu moles/kg intravenous MgSO4 or equal volume saline before being moni tored by magnetic resonance spectroscopy for 8 h to determine brain intrace llular free magnesium concentration. Animals were then assessed for neurolo gic motor deficits over 1 week using a rotarod device, followed by postmort em examination for presence of subdural hematoma. Animals with subdural hem atoma treated with MgSO4 showed no improvement in motor outcome when compar ed to nontreated controls. Animals with no visible subdural hematoma demons trated a significant improvement (p < 0.05 by ANOVA) in rotarod scores with MgSO4 treatment, Brain free magnesium concentration in the magnesium treat ed/hematoma group demonstrated a biphasic decline made up of an immediate i nitial decline, recovery of brain magnesium levels with MgSO4 treatment, an d then a significant second magnesium decline (p < 0.05). Such a secondary decline did not occur in the Mg treated/no hematoma animals. Our results su ggest that development of a subdural hematoma following TBI results in a de cline in brain magnesium, even after bolus administration of magnesium salt s. Such effects of hematoma development will need to be considered in trial s examining efficacy of magnesium salts as an intervention following TBI.