This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Svensson, L. G. Articles by Levien, L. J. Search for Related Content PubMed PubMed Citation Articles by Svensson, L. G. Articles by Levien, L. J.

Stroke, Vol 17, 1198-1202, Copyright © 1986 by American Heart Association

ARTICLES

Influence of anatomic origin on intracranial distribution of micro- emboli in the baboon

LG Svensson, MF Robinson, J Esser, VU Fritz and LJ Levien

The purpose of this study was to investigate whether the anatomic origin of micro-emboli influences their intracranial distribution. In twenty-two baboons, we examined the distribution of 99-Technetium labelled albumin aggregates (5 to 40 microns in size) after injection into the circulation at the left atrium (LA), carotid trifurcation (CA), and anterior and posterior common carotid artery (CCI). In a further subgroup, the emboli were introduced at the carotid trifurcation with the contralateral carotid artery ligated (CA + L). The results of this study demonstrated that aggregates introduced at the carotid artery lodged preferentially in the ophthalmic (p = 0.032) and middle cerebral artery territories (p = 0.016). If the contralateral common carotid artery was ligated, however, more aggregates were found in the ipsi- and contralateral anterior cerebral artery territories (p = 0.01, p = 0.003). Aggregates introduced into the cardiac circulation were equally distributed throughout the brain. This experimental model determined patterns of flow that might be analogous to the human situation where unilateral or bilateral carotid stenosis or stenosis with contralateral occlusion has occurred or embolus from cardiac source has occurred. The results do not imply that the 40 micron microaggregates do cause TIA. These experimental findings support clinical observations that cardiac lesions may cause transient ischemic attacks (TIA) anywhere in the brain. In contrast, those of carotid artery origin cause predominantly middle cerebral or ophthalmic artery territory TIAs unless the contralateral carotid artery is severely stenosed or occluded.

This article has been cited by other articles:

				D. Bushi, Y. Grad, S. Einav, O. Yodfat, B. Nishri, and D. Tanne Hemodynamic Evaluation of Embolic Trajectory in an Arterial Bifurcation: An In-Vitro Experimental Model Stroke, December 1, 2005; 36(12): 2696 - 2700. [Abstract] [Full Text] [PDF]