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Editorial
April 4, 2001

Neuroprotection in Acute Ischemic Stroke

Author Affiliations

Author Affiliation: Weill Medical College of Cornell University, New York Presbyterian Hospital, New York, NY.

JAMA. 2001;285(13):1760-1761. doi:10.1001/jama.285.13.1760

In acute stroke resulting from cerebral arterial thrombosis or embolism, damage to brain tissue is initiated by tissue anoxemia with depletion of tissue energy supplies. A cascade of neurotoxicity follows, with the release of glycine, glutamate, free radicals, nitric oxide, and other mediators of cell death. For some patients with acute stroke, blood flow may be restored with agents such as recombinant tissue-type plasminogen activator (rt-PA),1,2 prourokinase,3 or ancrod.4 Unfortunately, no pharmacologic agent has yet shown efficacy in arresting the human brain's ischemic cascade once it starts to spread. Indeed, De Keyser et al5 reviewed the stroke literature describing 22 completed phase 3 trials of neuroprotective pharmacologic drugs, all of which failed.

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