PATHOPHYSIOLOGY AND TREATMENT OF ACUTE ISCHEMIC STROKE

Citation
Sj. Rogers et Dg. Sherman, PATHOPHYSIOLOGY AND TREATMENT OF ACUTE ISCHEMIC STROKE, Clinical pharmacy, 12(5), 1993, pp. 359-376
Citations number
NO
Journal title
ISSN journal
02782677
Volume
12
Issue
5
Year of publication
1993
Pages
359 - 376
Database
ISI
SICI code
0278-2677(1993)12:5<359:PATOAI>2.0.ZU;2-I
Abstract
Risk factors, pathogenesis, clinical manifestations, diagnosis, and su rgical and pharmacological treatment of ischemic stroke are reviewed. Risk factors play an important part in the pathogenesis of ischemic st roke. Knowledge of the complex metabolic and cellular changes that occ ur during ischemic stroke is rapidly growing. Choosing the correct tre atment is dependent upon obtaining a thorough and accurate clinical as sessment 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 d rugs are still in the human clinical testing stage; promising agents i nclude thrombolytics, low-molecular-weight heparin, and heparinoids. H emodilution, pentoxifylline, epoprostenol, nimodipine, naloxone, and G M1 therapy have had mixed results in clinical trials, partly because s ome of these agents were not tested in enough patients to provide an a ccurate assessment of their efficacy. Atenolol and propranolol are ine ffective. 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 treatin g 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. Promisi ng regimens include ancrod, low-molecular-weight heparin and heparinoi ds, or thrombolytics.