Effect of magnesium given 1 hour after head trauma on brain edema and neurological outcome

Zeev Feldman, Boris Gurevitch, Alan A. Artru, Arieh Oppenheim, Esther Shohami, Eli Reichenthal, Yoram Shapira

    Research output: Contribution to journalArticlepeer-review

    114 Scopus citations


    Excitatory amino acids (EAA), mainly glutamate and aspartate, are released in excessive amounts from terminals of ischemic or traumatically injured neurons. These excessive levels of EAAs initiate a cascade of events believed to lead to secondary delayed damage to the surrounding brain. The N-methyl- D-aspartate receptor antagonists MK-801 and ketamine are reported to suppress excessive EAA release and to attenuate the development of focal brain edema following neuronal injury. Magnesium is also reported to work at the postsynaptic receptor to reduce the neurotoxic effect of glutamate. The present study was undertaken to examine the effect of postinjury treatment with Mg++ on brain edema and neurological outcome after traumatic brain injury. Sixty-nine rats that survived halothane anesthesia and closed head trauma (CHT) were randomly assigned to one of seven experimental groups: sham, CHT, and CHT with administration of Mg++ 1 hour postinjury. At 48 hours, brain tissue Mg++ concentration (calculated from optical density using a standard curve) was significantly increased compared to baseline levels (10.06 ± 2.44 mg/g vs. 6.83 ± 0.81 mg/g, p < 0.01 calculated by one- way analysis of variance). Also at 48 hours postinjury, brain tissue specific gravity in the contused hemisphere of Mg++ treated rats was significantly greater than that in the contused hemisphere of untreated rats, indicating attenuation of brain edema formation by Mg++. The neurological severity score (NSS) of rots treated with Mg++ improved significantly at both 18 and 48 hours, compared to baseline values obtained 1 hour after CHT but prior to administration of Mg++ (11.2 ± 2.5 vs. 15.2 ± 4.1, p = 0.03; and 12.3 ± 6.1 vs. 17.3 ± 3.6, p = 0.004, respectively). In the untreated groups, the NSS at 18 and 48 hours was not significantly different from baseline values (that is, no neurological improvement). The present study indicates that postinjury treatment with Mg++ attenuates brain edema formation and improves neurological outcome after experimental CHT.

    Original languageEnglish
    Pages (from-to)131-137
    Number of pages7
    JournalJournal of Neurosurgery
    Issue number1
    StatePublished - 1 Jan 1996


    • brain edema
    • head injury
    • magnesium
    • neurological outcome
    • rat

    ASJC Scopus subject areas

    • Surgery
    • Clinical Neurology


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