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(Stroke. 2004;35:363.)
© 2004 American Heart Association, Inc.
Advances in Stroke 2003 |
From the Department of Neurology (P.J.L., R.O.R), Helsinki University Central Hospital; and Neurosciences Programme (P.J.L.), Biomedicum Helsinki, Helsinki, Finland.
Correspondence to P.J. Lindsberg, Neurosciences Programme, Biomedicum Helsinki, PO Box 700, FIN 00029 HUS, Helsinki, Finland. E-mail perttu.lindsberg@hus.fi
Key Words: Advances in Stroke hyperglycemia stroke, acute
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Elevated blood glucose is common in the early phase of stroke. The prevalence of hyperglycemia, defined as blood glucose level >6.0 mmol/L (108 mg/dL), has been observed in two thirds of all ischemic stroke subtypes on admission and in at least 50% in each subtype including lacunar strokes.1 Extensive experimental evidence in stroke models supports that hyperglycemia has adverse effects on tissue outcome, and an association between blood glucose and functional outcome has been found in an increasing number of clinical studies. Although no interventional stroke studies have addressed the acute reversal of hyperglycemia, active lowering of elevated blood glucose by rapidly acting insulin is recommended in most published guidelines, even in nondiabetic patients (European Stroke Initiative [EUSI] guidelines >10 mmol/L, American Stroke Association [ASA] guidelines >300 mg/dL).2
Causes of Acute Hyperglycemia
Although up to one third of acute stroke patients have either diagnosed or newly diagnosed diabetes, probably a major proportion of patients have stress hyperglycemia mediated partly by the release of cortisol and norepinephrine. It is also a manifestation of relative insulin deficiency, which is associated with increased lipolysis. Even in nondiabetic patients, stress hyperglycemia may be a marker of deficient glucose regulation in individuals with insulin resistance and developing diabetes mellitus.
How Elevated Glucose Injures the Ischemic Brain
By provoking anaerobic metabolism, lactic acidosis, and free radical production, hyperglycemia may exert direct membrane lipid peroxidation and cell lysis in metabolically challenged tissue. Moderately and severely increased blood glucose has been found to further the metabolic state and mitochondrial function in the area of ischemic penumbra.3 Insulin resistance is
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