Magnesium in ischemic stroke and subarachnoid hemorrhage

Abstract

There is considerable evidence confirming the important physiological role of magnesium in the central nervous system. Although advances have been made over the past 3 decades, understanding of its precise role remains incomplete. It has been observed in several animal and human studies that serum depletion occurs after stroke and that this correlates with worse functional outcomes. Compelled by the unrelenting impetus to add to the limited options of stroke treatment strategies, a potential neuroprotective effect of magnesium was promptly suggested. It is close to an ideal therapeutic agent being inexpensive, conveniently administered, has a well-documented safety profile, and is widely available. There is also convincing evidence from preclinical animal models that systemically administered magnesium could reduce infarct volumes and attenuate functional deficit. Unfortunately, a series of clinical stroke trials designed to determine its effectiveness have yielded inconsistent results. Here, a review on the role of magnesium in ischemic stroke and subarachnoid hemorrhage, current evidence on its efficacy, and possible explanations for the failure to translate such encouraging laboratory findings in the clinical setting is delivered. To conclude, it is believed that magnesium therapy in combination with other pharmacological and physiological interventions aimed at regulating these pathways could be an effective neuroprotective regimen for stroke.