Magnesium in acute brain injury

Abstract

Acute injury to the central nervous system, such as stroke and traumatic brain injury (TBI), is a leading cause of morbidity and mortality, and represents a significant public health issue worldwide. Despite extensive pre-clinical investigation, few therapeutic treatment options are available to patients meaning that severe disability and requirement of long-term rehabilitation are common outcomes. The majority of the damage that occurs following stroke and TBI is initiated by the primary injury and develops over time. Such secondary injury encompasses a number of damaging biochemical and pathophysiological events. However, the delayed nature of such injury provides an opportunity for therapeutic intervention. Indeed, magnesium decline has been identified as a key secondary injury process, one that is associated with significant functional impairment. Magnesium administration has been extensively evaluated in both experimental and clinical stroke and TBI with varied success. This chapter focuses on the role of magnesium in TBI and stroke pathophysiology, with particular emphasis on magnesium as a potential therapeutic agent.