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
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