Insular cortical ischemia is independently associated with acute stress hyperglycemia

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 HbA1c 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.