Pathophysiology and treatment of acute ischemic stroke.

Risk factors, pathogenesis, clinical manifestations, diagnosis, and surgical and pharmacological treatment of ischemic stroke are reviewed. Risk factors play an important part in the pathogenesis of ischemic stroke. Knowledge of the complex metabolic and cellular changes that occur during ischemic stroke is rapidly growing. Choosing the correct treatment is dependent upon obtaining a thorough and accurate clinical assessment of the patient. Diagnostic tests help in determining the size, location, etiology, and characteristics of the lesion. Currently no single agent or mode of therapy appears to be most efficacious. Many drugs are still in the human clinical testing stage; promising agents include thrombolytics, low-molecular-weight heparin, and heparinoids. Hemodilution, pentoxifylline, epoprostenol, nimodipine, naloxone, and GM1 therapy have had mixed results in clinical trials, partly because some of these agents were not tested in enough patients to provide an accurate assessment of their efficacy. Atenolol and propranolol are ineffective. Ticlopidine and aspirin decrease the incidence of subsequent stroke but have not been tested in acute ischemic stroke. Heparin may be effective in preventing further cardioembolic stroke or in treating stroke in progress. Nondrug therapies include carotid endarterectomy and surgical decompression for cerebellar stroke. No single agent can be recommended for treatment of ischemic stroke at this time. Promising regimens include ancrod, low-molecular-weight heparin and heparinoids, or thrombolytics.