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 Awad, I. A. Articles by Magdinec, M. Search for Related Content PubMed PubMed Citation Articles by Awad, I. A. Articles by Magdinec, M. Pubmed/NCBI databases Medline Plus Health Information Brain Diseases Carotid Artery Disease MRI Scans

Stroke, Vol 24, 1339-1346, Copyright © 1993 by American Heart Association

ARTICLES

Pathogenesis of subcortical hyperintense lesions on magnetic resonance imaging of the brain. Observations in patients undergoing controlled therapeutic internal carotid artery occlusion

IA Awad, T Masaryk and M Magdinec
Section of Cerebrovascular Surgery, Cleveland Clinic Foundation, Ohio.

BACKGROUND AND PURPOSE: Factors associated with the pathogenesis of subcortical hyperintense lesions on magnetic resonance imaging of the brain are not known. We describe four cases of de novo genesis of subcortical hyperintense lesions in patients undergoing controlled therapeutic internal carotid artery occlusion, and we speculate on associated pathophysiological mechanisms. METHODS: Twelve consecutive patients underwent controlled therapeutic internal carotid artery occlusion for symptomatic giant cerebral aneurysm using the detachable balloon technique under full anticoagulation. Preocclusion (within 2 weeks) and postocclusion (within 6 weeks) magnetic resonance imaging of the brain was performed in eight cases and evaluated for preexisting and new appearance of subcortical hyperintense lesions. RESULTS: There were four instances of de novo genesis of subcortical hyperintense lesions after carotid occlusion. New subcortical hyperintense lesions were ipsilateral to carotid occlusion in every instance and in two cases were associated with ipsilateral hemispheric ischemic symptoms despite anticoagulant therapy. In one instance, there were transient hemispheric symptoms without the appearance of new subcortical hyperintense lesions. Age, vascular risk factors, and preexisting subcortical hyperintense lesions did not appear to predispose patients to de novo genesis of new hyperintensities. CONCLUSIONS: This is the first documentation of de novo genesis of subcortical hyperintense lesions in a controlled setting of hemodynamic ischemic insult. Symptomatic and asymptomatic lesions can be detected in this setting. Anticoagulation does not appear to provide protection from this phenomenon. Careful prospective studies are required to further evaluate risk factors and possible clinical consequences associated with the genesis of new subcortical hyperintense lesions.

This article has been cited by other articles:

				D. M. Moody, C. R. Thore, J. A. Anstrom, V. R. Challa, C. D. Langefeld, and W. R. Brown Quantification of Afferent Vessels Shows Reduced Brain Vascular Density in Subjects with Leukoaraiosis Radiology, December 1, 2004; 233(3): 883 - 890. [Abstract] [Full Text] [PDF]

				L. Pantoni and J. H. Garcia Pathogenesis of Leukoaraiosis : A Review Stroke, March 1, 1997; 28(3): 652 - 659. [Abstract] [Full Text]

				H. Wakita, H. Tomimoto, I. Akiguchi, and J. Kimura Protective Effect of Cyclosporin A on White Matter Changes in the Rat Brain After Chronic Cerebral Hypoperfusion Stroke, August 1, 1995; 26(8): 1415 - 1422. [Abstract] [Full Text]