Serum Magnesium Levels May Play Role in Traumatic Brain Injury Outcome

Close to 1.5 million cases of traumatic brain injury (TBI) occur in the United States every year. Approximately 5.3 million people live with a disability caused by TBI in the United States alone, and an additional 60,000 people die annually from TBI. Brain injury is the ultimate cause of death in 40 percent of all fatal trauma cases. Annual direct and indirect TBI costs are estimated at $56 billion. In comparison, a manned space mission to Mars has been estimated to cost $12 billion.

During the past two decades, medical research has demonstrated that all brain injury does not occur at the time of the initial trauma. Instead, the area of injured brain evolves after the impact over the ensuing hours and days. This type of additional damage is referred to as secondary injury. The damage to the neurons caused at the initial impact cannot be repaired with medical science’s current knowledge about brain regeneration; however, emerging evidence indicates that secondary injury is preventable.

Animals models of severe brain injury have demonstrated that serum magnesium concentration affects various secondary injury factors, including neurotoxicity, oxidative stress, protein synthesis and energy metabolism. Presumably, this effect is related to magnesium's role as a competitive antagonist for calcium-binding sites. This study was designed to assess the relationship between initial serum magnesium levels (and subsequent replacement) to neurological outcome following severe TBI.

The initial serum magnesium levels were assessed in 83 severe TBI patients admitted to the University of Pittsburgh Brain Trauma Research Center. The results of this study, The Role of Serum Magnesium Levels in Severe Traumatic Brain Injury Outcome, will be presented by Martina Stippler, MD, 3:15 to 3:30 p.m. on Monday, April 24, 2006, during the 74th Annual Meeting of the American Association of Neurological Surgeons in San Francisco. Co-authors are Ava Puccio RN, MSN, Michael Fischer BS, C. Edward Dixon, PhD, and Kevin Walter MD.

The analysis of the data on the 83 patients indicated that 35 had normal serum magnesium levels on arrival, while 48 had low magnesium levels (<1.3 mg/dl). The two groups were identical with regard to presenting Glasgow Coma Scale (GCS) score, age, and other known prognostic factors. Using multivariate analysis (binary logistic regression), the authors demonstrated that patients presenting with low serum magnesium levels had a significantly worse outcome as measured by the Glasgow Outcome Scale (GOS) at six months (p = 0.012).

“The simplest interpretation of this data would support replenishing serum magnesium levels as soon as possible in TBI patients. However, the utility of this approach needs to be proven,” stated Dr. Stippler. It is possible that serum magnesium levels are depressed as a result of the trauma itself, implying that low magnesium levels equate to a more severe injury than would be assumed based on the remainder of the clinical and radiographic findings. “We will continue to assess the promising potential of these findings at the University of Pittsburgh Brain Trauma Research Center,” concluded Dr. Stippler.