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  • Ovid Technologies (Wolters Kluwer Health)  (3)
  • 1
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. 8 ( 2004-08), p. 1886-1891
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 1467823-8
    Location Call Number Limitation Availability
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  • 2
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 34, No. 9 ( 2003-09), p. 2208-2214
    Abstract: Background and Purpose— Hyperglycemia at the time of ischemic stroke is associated with increased mortality and morbidity. Animal studies suggest that infarct expansion may be responsible. The influence of persisting hyperglycemia after stroke has not previously been examined. We measured the blood glucose profile after acute ischemic stroke and correlated it with infarct volume changes using T2- and diffusion-weighted MRI. Methods— We recruited 25 subjects within 24 hours of ischemic stroke symptoms. Continuous glucose monitoring was performed with a glucose monitoring device (CGMS), and 4-hour capillary glucose levels (BGL) were measured for 72 hours after admission. MRI and clinical assessments were performed at acute (median, 15 hours), subacute (median, 5 days), and outcome (median, 85 days) time points. Results— Mean CGMS glucose and mean BGL glucose correlated with infarct volume change between acute and subacute diffusion-weighted MRI ( r ≥0.60, P 〈 0.01), acute and outcome MRI ( r =0.56, P =0.01), outcome National Institutes of Health Stroke Scale (NIHSS; r ≥0.53, P 〈 0.02), and outcome modified Rankin Scale (mRS; r ≥0.53, P =0.02). Acute and final infarct volume change and outcome NIHSS and mRS were significantly higher in patients with mean CGMS or mean BGL glucose ≥7 mmol/L. Multiple regression analysis indicated that both mean CGMS and BGL glucose levels ≥7 mmol/L were independently associated with increased final infarct volume change. Conclusions— Persistent hyperglycemia on serial glucose monitoring is an independent determinant of infarct expansion and is associated with worse functional outcome. There is an urgent need to study normalization of blood glucose after stroke.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
    detail.hit.zdb_id: 1467823-8
    Location Call Number Limitation Availability
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  • 3
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 1992
    In:  Obstetrical & Gynecological Survey Vol. 47, No. 1 ( 1992-01), p. 60-61
    In: Obstetrical & Gynecological Survey, Ovid Technologies (Wolters Kluwer Health), Vol. 47, No. 1 ( 1992-01), p. 60-61
    Type of Medium: Online Resource
    ISSN: 0029-7828
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1992
    detail.hit.zdb_id: 2043471-6
    Location Call Number Limitation Availability
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