In acute stroke, chemical neuroprotection is an important strategy aimed at limiting the biochemical cascade of events induced by cerebral ischemia which lead to secondary neuronal damage. Among multiple pharmaceutical interventions tried magnesium (Mg++), which is a physiological voltage-dependent N-metyl-D-aspartate (NMDA) antagonist, has demonstrated promising results. As opposed to other antiglutamate agents, Mg++ has limited adverse effects, is widely available, easy to administer, and has good penetrability in the central nervous system (CNS). Mg++ is involved in the pathogenesis of an expanding array of clinical conditions via vascular and cellular effects. Experimental stroke models and pilot clinical studies have provided encouraging data regarding the neuroprotective role of Mg++ in acute ischemic stroke. Observations from subarachnoid hemorrhage (SAH) animal models have suggested that Mg++ might have a neuroprotective effect directed against the ischemic injury which accompanies cerebral vasospasm. Large randomized, double blind clinical studies assessing Mg++ efficacy in stroke are already in progress. Magnesium sulfate is also under active investigation as a neuroprotective agent in SAH.