Stroke is a clinical syndrome typified by sudden onset of focal or global loss of cerebral function of presumed vascular origin which lasts for more than 24 hours or leads to death. Cerebral infarction accounts for 80% of strokes and may be due to large vessel disease, small vessel disease, or cardioembolism. Rarer causes include coagulopathy, vasculitis, and endocarditis. Fifteen percent of strokes are due to primary intracranial hemorrhage and 5% are due to subarachnoid hemorrhage.
A complex, coordinated, and interrelated cascade of molecular events follows brain ischemia and infarction. Ischemia is defined as a reduction in blood flow sufficient to cause an alteration of normal cellular function; hypoxia is defined as a reduction of tissue oxygen to levels insufficient to maintain homeostasis. Initial events after ischemia result in necrosis of core infarcted tissue with reduced blood flow, maintained metabolism, and reduced function of adjacent penumbra tissue. After disruption of adenosine 5′-triphosphate (ATP) generation and the Na+/K+ transporter, cellular depolarization allows Ca2+ influx, resulting in activation of the intrinsic apoptosis pathway and cell death. Glutamate accumulation in the extracellular space results in activation of N-methyl-d-aspartate (NMDA), a-amino-3-hydroxy-5-methyl-4-isoxazole propionate(AMPA), and kainate glutamate receptors, which mediate Ca2+ influx.

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