Antithrombotic Therapy for Cerebrovascular Disorders: Features of the stroke

Antithrombotic Therapy for Cerebrovascular Disorders: Features of the strokeIndividual neurologic features of the stroke are neither sensitive nor specific in determining mechanism. Abrupt onset of the maximal neurologic deficit has been reported in 25-80% of patients with potential cardioembolic sources and in 14-55% of other etiologies for ischemic stroke. Seizures and undue headache do not distinguish cardioembolic strokes from other types. TIAs preceding stroke occur in 1113% of cardioembolic strokes; only about 3% of cardioembolic stroke patients have prior or concurrent systemic embolism. In short, recent studies have challenged traditional ideas about the predictive value of neurologic features for embolic stroke.

Most cardioembolic strokes involve the cortex of the cerebral hemispheres and are frequent causes of isolated branch artery syndromes. Most (75%) patients with isolated Wernickes aphasia are found to have presumed cardioembolic stroke. Global aphasia without hemiparesis and posterior cerebral artery syndromes are most often cardioembolic. Subcortical infarctions have been reported in 16-22% of presumed cardioembolic strokes.” While most subcortical infarctions associated with presumed cardioembolic strokes are large (1.5 cm), suggesting obstruction of more than 1 adjacent penetrating artery (eg, “lagoon-ar” stroke), small subcortial infarctions in the distribution of a single penetrating artery (lacunar stroke) has been reported.

Amaurosis fugax (transient monocular blindness) is not uncommonly associated with cardioembolism, particularly with heart diseases causing small emboli.
The iack of specificity of neurologic features may largely be due to overlap between emboli from cardiac sources and “local” artery-to-artery embolism from proximal arterial sources.* It is unclear and controversial how frequently local arteriogenic embolism accounts for stroke in patients with proximal cerebrovascular atherosclerosis. It is likely that the size and composition of arteriogenic emboli differ from cardiogenic emboli, although emboli in the latter group are not uniform. Small emboli syndromes appear to be particularly common with mitral valve prolapse, infective endocarditis, calcific aortic stenosis, and anticoagulated prosthetic cardiac valves. The similarity of many clinical features in strokes due to arteriogenic vs cardiogenic emboli is easy to conceptualize. The average size of the embolic fragment varies with the cardioembolic source.