Neuroprotection of Acute Ischemic Stroke: Where are We?

Abstract

Neuroprotective treatments for acute ischemic stroke are targeted at the large array of cellular biochemical and metabolic disturbances that occur after focal brain ischemia to prevent the evolution of injury toward irreversibility. Enhanced comprehension about the pathophysiology of focal brain ischemia has expanded the number of neuroprotective modalities under development and identification of the most likely target for these therapies. Many of the neuroprotective interventions are targeted at reducing calcium influx into ischemic cells and the downstream consequences of excessive intracellular calcium. Other neuroprotective strategies include: free radical scavengers, hyperpolarization of resting transmembrane potentials, and inhibition of the inflammatory response and growth factors. Some interventions potentially may enhance recovery and have neuroprotective effects (i.e., basic fibroblast growth factor [bFGF] and citicoline). Despite the lack of proven clinical efficacy with any neuroprotective intervention, the future will hopefully yield convincing evidence that neuroprotection can be effective and then be ultimately combined with thrombolysis to maximize improvement after ischemic stroke.