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Objectives:To test the hypothesis that insular cortical ischaemia is associated with acute hypertension and hyperglycaemia.Methods:From the Canadian Activase for Stroke Effectiveness Study,which included only patients treated with thrombolysis hyperacutely(ie,within 3 h of onset of stroke),966 patients were identified with ischaemia affecting(n = 685),or sparing(n = 281),the insular cortex.Demographic and clinical data,pretreatment indices of blood pressure,blood glucose,atrial fibrillation,and clinical imaging and outcome measures were compared between the two groups.Multivariable linear regression was used to assess predictors of systolic blood pressure and glucose levels before thrombolysis.Results:Pretreatment hypertension(p = 0.009),but not hyperglycaemia(p = 0.32),was predicted by insular ischaemia in univariable linear regression analyses.After adjusting for other factors,however,insular cortical ischaemia was not found to be an independent predictor for acute hypertension or hyperglycaemia.Conclusions:Raised blood pressure or serum glucose levels in hyperacute(< 3 h)cerebral ischaemia is not independently predicted by insular involvement.Several hours are required for sympathetic manifestations of insular ischaemia to evolve.
Objectives: To test the hypothesis that insular cortical ischaemia is associated with acute hypertension and hyperglycaemia. Methods: From the Canadian Activase for Stroke Effectiveness Study, which included only patients treated with thrombolysis hyperacutely (ie, within 3 h of onset of stroke), 966 patients were identified with ischaemia affecting (n = 685), or sparing (n = 281), the insular cortex. Demographic and clinical data, pretreatment indices of blood pressure, blood glucose, atrial fibrillation, and clinical imaging and outcome measures were compared between The two groups. Multivariable linear regression was used to assess predictors of systolic blood pressure and glucose levels before thrombolysis. Results: Pretreatment hypertension (p = 0.009), but not hyperglycaemia (p = 0.32), was predicted by insular ischaemia in univariable linear regression Analyses. After adjusting for other factors, however, insular cortical ischaemia was not found to be an independent predictor for acute hypertension or hy Perglycaemia. Conclusions: Raised blood pressure or serum glucose levels in hyperacute (<3 h) cerebral ischaemia is not independent predicted by insular involvement. Holy compounds are required for sympathetic manifestations of insular ischaemia to evolve.