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  Vol. 56 No. 11, November 1999 TABLE OF CONTENTS
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Strategic Location of Large-Vessel Atherothrombotic Cerebral Vascular Disease

Arch Neurol. 1999;56:1329-1330.

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

STROKE IS A heterogeneous disorder. Ischemic stroke, as identified in the National Institutes of Health Stroke Data Bank,1 can be classified into 3 basic pathologic stroke subtypes.2-5 They include embolic, accounting for 60% of all ischemic strokes; small-vessel lacunar, accounting for 25%; and large-vessel atherothrombotic, accounting for 15%. Large-vessel atherothrombotic stroke, or transient ischemic attack (TIA), is caused by either hemodynamic "low-flow" ischemia or "artery-to-artery" embolism, in which there is an interplay between local and systemic hemostatic mechanisms6-8 and the atheromatous plaque, similar to the interplay in atherothrombotic coronary artery disease. Vascular-bed–specific hemostasis6 may play a role in thrombosis of the intracranial and extracranial vessels; however, in embolic stroke, it operates only at the site of thrombus formation (ie, the heart or aortic arch). Therefore, it becomes important to think about large-vessel atherothrombotic disease leading to TIA or stroke as occurring at strategically important loci,2-5 just as in the coronary . . . [Full Text of this Article]


RELATED ARTICLE

Bilateral Intracranial Vertebral Artery Disease in the New England Medical Center Posterior Circulation Registry
Hyun-Kil Shin, Kyung-Moo Yoo, Hui Meng Chang, and Louis R. Caplan
Arch Neurol. 1999;56(11):1353-1358.
ABSTRACT | FULL TEXT  


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Carotid Endarterectomy Revisited
Kistler and Furie
NEJM 2000;342:1743-1745.
FULL TEXT  





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