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(Stroke. 2004;35:1886.)
© 2004 American Heart Association, Inc.

Original Contributions

Insular Cortical Ischemia Is Independently Associated With Acute Stress Hyperglycemia

Louise E. Allport, BMed, FRACP; Ken S. Butcher, MD, PhD, FRCP(C); Tracey A. Baird, MRCP; Lachlan MacGregor, MBBS, MmedSc; Patricia M. Desmond, MD, FRACR; Brian M. Tress, MD, FRACR; Peter Colman, MD, FRACP Stephen M. Davis, MD, FRCP, FRACP

From the Departments of Neurology (L.E.A., K.S.B., T.A.B., S.M.D.), Clinical Epidemiology (L.M.), Radiology (P.M.D., B.M.T.), and Diabetes and Endocrinology (P.C.), Royal Melbourne Hospital, University of Melbourne, Parkville, Victoria, Australia.

Correspondence to Dr Stephen M. Davis, Director of Neurology, Royal Melbourne Hospital, Parkville, Victoria 3050, Australia. E-mail stephen.davis{at}mh.org.au

Background and Purpose— Acute poststroke hyperglycemia has been associated with larger infarct volumes and a cortical location, regardless of diabetes status. Stress hyperglycemia has been attributed to activation of the hypothalamic-pituitary-adrenal axis but never a specific cortical location. We tested the hypothesis that damage to the insular cortex, a site with autonomic connectivity, results in hyperglycemia reflecting sympathoadrenal dysregulation.

Methods— Diffusion-weighted MRI, glycosylated hemoglobin (HbA_1c), and blood glucose measurements were obtained in 31 patients within 24 hours of ischemic stroke onset. Acute diffusion-weighted imaging (DWI) lesion volumes were measured, and involvement of the insular cortex was assessed on T2-weighted images.

Results— Median admission glucose was significantly higher in patients with insular cortical ischemia (8.6 mmol/L; n=14) compared with those without (6.5 mmol/L; n=17; P=0.006). Multivariate linear regression demonstrated that insular cortical ischemia was a significant independent predictor of glucose level (P=0.001), as was pre-existing diabetes mellitus (P=0.008). After controlling for the effect of insular cortical ischemia, DWI lesion volume was not associated with higher glucose levels (P=0.849). There was no association between HbA_1c and glucose level (P=0.737).

Conclusions— Despite the small sample size, insular cortical ischemia appeared to be associated with the production of poststroke hyperglycemia. This relationship is independent of pre-existing glycemic status and infarct volume. Neuroendocrine dysregulation after insular ischemia may be 1 aspect of a more generalized acute stress response. Future studies of poststroke hyperglycemia should account for the effect of insular cortical ischemia.

Key Words: glucose • hyperglycemia • stroke, acute • magnetic resonance imaging, diffusion-weighted

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