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.