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Ischemic stroke has numerous causes. Cerebral infarction may result from large artery atherosclerosis, cardiac embolism, small artery lipohyalinosis, cryptogenic embolism, or, more rarely, from other diverse conditions such as arterial dissection, infective endocarditis, and sickle cell disease.2 Arterial occlusion is the cause of at least 80% of acute cerebral infarctions.3,4

Decreased cerebral blood flow, resulting from acute arterial occlusion, reduces oxygen and glucose delivery to brain tissue with subsequent lactic acid production, blood-brain barrier breakdown, inflammation, sodium and calcium pump dysfunction, glutamate release, intracellular calcium influx, free-radical generation, and finally membrane and nucleic acid breakdown and cell death.5 The degree of cerebral blood flow reduction following arterial occlusion is not uniform. Tissue at the

Acute Ischemic Stroke: An Evidence-based Approach, Edited by David M. Greer. Copyright © 2007 John Wiley & Sons, Inc.

center of the zone of hypoperfusion is typically exposed to lower blood flow than tissue at the periphery. Animal studies suggest that brain tissue with cerebral blood flow <8-10mL/100g/min will almost certainly not survive, while brain tissue with cerebral blood flow 18-20 mL/100 g/min is nonfunctional, but may recover if perfusion is re-established.6 This forms the basis of the concept of the ischemic ''penumbra''— viable but dysfunctional brain tissue, often surrounding a zone of irreversible damage that is destined for infarction in the absence of perfusion.6 Restoration of blood flow to the penumbra is the goal of thrombolytic therapy.7-9 As time passes, more and more of the hypoperfusion zone goes on to infarction, and the relative size of the penumbra decreases.10 Late reperfusion, in contrast to early reperfusion, may be associated with reperfusion injury and hemorrhagic transformation of the infarction, with worse outcomes than those observed in the absence of reperfusion.11

Preclinical studies have suggested that early thrombolysis, within 3.5 hours of arterial occlusion, resulted in neurological improvement with an acceptable risk of secondary central nervous system hemorrhage.3,12-21

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