| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on June 22, 2006
From Division of Clinical Neurosciences, University of Glasgow, Institute of Neurological Sciences, Southern General Hospital, Glasgow, Scotland, UK. * To whom correspondence should be addressed. E-mail: k.muir{at}clinmed.gla.ac.uk.
Background and Purpose--Insular cortex ischemia is proposed to mediate a sympathetic stimulus that leads to acute hyperglycemia after stroke. Methods--We retrospectively analyzed insular perfusion on perfusion CT (median 180 minutes after onset) in 35 patients. Results--We found no association of hypoperfusion (relative cerebral blood flow <0.51) with early (<6 hours) or delayed (<72 hours) hyperglycemia, or hemispheric lateralization. Conclusions--Insular cortex hypoperfusion <6 hours after stroke onset was not associated with hyperglycemia.
Accepted on September 18, 2006
Insular Cortex Hypoperfusion and Acute Phase Blood Glucose After Stroke. A CT Perfusion Study
Fiona C. Moreton BSc;
This article has been cited by other articles:
![]() |
M. T. McCormick, K. W. Muir, C. S. Gray, and M. R. Walters Management of Hyperglycemia in Acute Stroke: How, When, and for Whom? Stroke, July 1, 2008; 39(7): 2177 - 2185. [Full Text] [PDF] |
||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2006 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |