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

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dc.contributor.authorHeath, D.
dc.contributor.authorVink, R.
dc.date.issued2001
dc.descriptionCopyright © 2001 Mary Ann Liebert, Inc.
dc.description.abstractA number of studies have demonstrated that neurologic motor and cognitive deficits induced by traumatic brain injury (TBI) can be attenuated with administration of magnesium salts. However, many severe traumatic brain injuries have a significant hematoma that develops subsequent to the primary events, and it is unclear whether magnesium salts are effective in this situation. In the present study, an impact-acceleration rodent model of TBI was used to produce an injury that causes an extensive subdural hematoma in over 50% of injured animals. At 30 min after TBI, rats were randomly administered 250 µmoles/kg intravenous MgSO4 or equal volume saline before being monitored by magnetic resonance spectroscopy for 8 h to determine brain intracellular free magnesium concentration. Animals were then assessed for neurologic motor deficits over 1 week using a rotarod device, followed by postmortem examination for presence of subdural hematoma. Animals with subdural hematoma treated with MgSO4 showed no improvement in motor outcome when compared to nontreated controls. Animals with no visible subdural hematoma demonstrated a significant improvement (p < 0.05 by ANOVA) in rotarod scores with MgSO4 treatment. Brain free magnesium concentration in the magnesium treated/hematoma group demonstrated a biphasic decline made up of an immediate initial decline, recovery of brain magnesium levels with MgSO4 treatment, and 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 suggest that development of a subdural hematoma following TBI results in a decline in brain magnesium, even after bolus administration of magnesium salts. Such effects of hematoma development will need to be considered in trials examining efficacy of magnesium salts as an intervention following TBI.
dc.description.statementofresponsibilityDeanne L. Heath, Robert Vink
dc.identifier.citationJournal of Neurotrauma, 2001; 18(4):465-469
dc.identifier.doi10.1089/089771501750171074
dc.identifier.issn0897-7151
dc.identifier.issn1557-9042
dc.identifier.orcidVink, R. [0000-0002-4885-0667]
dc.identifier.urihttp://hdl.handle.net/2440/38761
dc.language.isoen
dc.publisherMary Ann Liebert Inc Publ
dc.source.urihttps://doi.org/10.1089/089771501750171074
dc.subjectBrain
dc.subjectAnimals
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectBrain Injuries
dc.subjectHematoma, Subdural
dc.subjectWounds, Nonpenetrating
dc.subjectMagnesium
dc.subjectMagnesium Sulfate
dc.subjectMotor Activity
dc.subjectOsmolar Concentration
dc.subjectMale
dc.titleSubdural hematoma following traumatic brain injury causes a secondary decline in brain free magnesium concentration
dc.typeJournal article
pubs.publication-statusPublished

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