Stroke investigators have made great progress in defining the neurochemical consequences of brain ischemia, as well as providing a scientific foundation for the medical and surgical therapies of secondary stroke prevention. Nevertheless, it is striking that relatively little is known of the initiating process of the clinical event constituting stroke. This process, lacking precise characterization, is typically referred to as ’hypoperfusion’ or ’embolization’. Current neurodiagnostic technology has blurred, rather than clarified, this distinction. An example of this phenomenon comes from the landmark North American Symptomatic Carotid Endarterectomy Trial, in which the efficacy of surgical removal of symptomatic carotid plaques appeared to be directly related to the degree of hemodynamic compromise produced by these lesions (NASCET Collaborators 1991). Yet angiography performed in the first hours after stroke commonly shows possible embolic occlusion distal to carotid stenosis (del Zoppo et al. 1992).
KeywordsAspirin Heparin Warfarin Prostaglandin Neurol
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