Traumatic injury to the central nervous system (CNS) is a leading cause of morbidity and mortality, and represents a significant public health issue. Despite intensive research, no effective neuroprotective therapy exists, and survivors of CNS injury, including traumatic brain injury (TBI) and spinal cord injury (SCI), can be left with severe disabilities that require long-term rehabilitation. Much of the damage that occurs after TBI and SCI develops over time with the primary injury initiating a secondary injury cascade made up of deleterious biochemical and pathophysiological reactions. This delayed development of secondary injury provides a vital opportunity for therapeutic intervention and considerable effort is currently being directed toward identifying these injury factors and developing interventions that may potentially prevent their actions. Magnesium (Mg2+) decline has been identified as playing a key role in the secondary injury process, in part because of its central role in the regulation of a large number of known injury factors and that its decline is associated with the development of motor and cognitive deficits. Mg2+ administration has been extensively investigated both preclinically in TBI and SCI and clinically as a neuroprotectant in TBI with varied success. This chapter focuses on the role of Mg2+ in TBI and SCI pathophysiology, with particular emphasis on Mg2+ as a potential therapeutic agent.
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