title: Insular cortical ischemia is independently associated with acute stress hyperglycemia.
abstract: OBJECTIVE
  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 (HbA1c), 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.
authors.affiliation: Department of Neurology, Royal Melbourne Hospital, University of Melbourne, Parkville, Victoria, Australia.
authors.forename: Louise E
authors.initials: LE
authors.lastname: Allport
authors.forename: Ken S
authors.initials: KS
authors.lastname: Butcher
authors.forename: Tracey A
authors.initials: TA
authors.lastname: Baird
authors.forename: Lachlan
authors.initials: L
authors.lastname: MacGregor
authors.forename: Patricia M
authors.initials: PM
authors.lastname: Desmond
authors.forename: Brian M
authors.initials: BM
authors.lastname: Tress
authors.forename: Peter
authors.initials: P
authors.lastname: Colman
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Davis
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001786:Blood Glucose / Q000378:metabolism; D002545:Brain Ischemia / Q000097:blood* / Q000150:complications* / Q000473:pathology; D038524:Diffusion Magnetic Resonance Imaging; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology*; D020243:Infarction, Anterior Cerebral Artery / Q000097:blood / Q000150:complications / Q000473:pathology; D008875:Middle Aged
chemical_list: D001786:Blood Glucose; D006442:Glycated Hemoglobin