Brain Advance Access originally published online on September 10, 2007
Brain 2007 130(12):e86; doi:10.1093/brain/awm159
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Reply: Hyperglycaemia and the outcome of stroke
Department of Neurology, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands
Correspondence to: J. De Keyser E-mail: j.h.a.de.keyser{at}neuro.umcg.nl
Sir, we thank Dr Metso and Dr Murros for their interest and valuable comments on our study. Our study explored the effect of blood glucose levels in two different types of ischaemic stroke, and was not intended to guide acute stroke therapy. Whatever the underlying mechanism (stress or other causes) there is substantial evidence that hyperglycaemia in acute non-lacunar ischaemic stroke is associated with a worse clinical outcome. By using magnetic resonance imaging and spectroscopy, Parsons and colleagues nicely showed that hyperglycaemia in acute non-lacunar stroke leads to increased lactate production in the penumbra and adversely affects clinical outcome (Parsons et al., 2002
). These data are in agreement with several observations made in animal models of stroke (Anderson et al., 1999; Li et al., 2000; Lin et al., 1998; Prado et al., 1988). We demonstrated that the effect of hyperglycaemia is different in patients with lacunar ischaemic stroke.
In the GIST-UK trial (Gray et al., 2007), both non-lacunar and lacunar strokes (representing approximately one in five of the included patients) were treated in the same manner. Whether this affected study results is unlikely, because the investigators performed a post-hoc analysis on stroke subtypes. However, a beneficial effect in non-lacunar stroke may have been missed because the median onset to treatment time was approximately 13 h, and only 8 of the 933 patients were treated within 3 h. Thus, for most patients, this late start of treatment may have been insufficient to prevent hyperglycaemia-induced irreversible damage in the penumbra. We propose that ongoing and future trials aimed at controlling glucose levels in acute ischaemic stroke should differentiate between strokes subtypes and start sooner after symptom onset.
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Anderson RE, Tan WK, Martin HS, Meyer FB. Effects of glucose and PaO2 modulation on cortical intracellular acidosis, NADH redox state, and infarction in the ischemic penumbra. Stroke (1999) 30:160–70.
Gray CS, Hildreth AJ, Sandercock PA, et al. Glucose-potassium-insulin infusions in the management of post-stroke hyperglycaemia: the UK Glucose Insulin in Stroke Trial (GIST-UK). Lancet Neurol (2007) 6:397–406.[CrossRef][Web of Science][Medline]
Li PA, Shuaib A, Miyashita H, He QP, Siesjo BK, Warner DS. Hyperglycemia enhances extracellular glutamate accumulation in rats subjected to forebrain ischemia. Stroke (2000) 31:183–92.
Lin B, Ginsberg MD, Busto R. Hyperglycemic exacerbation of neuronal damage following forebrain ischemia: microglial, astrocytic and endothelial alterations. Acta Neuropathol (1998) 96:610–20.[CrossRef][Medline]
Parsons MW, Barber PA, Desmond PM, et al. Acute hyperglycemia adversely affects stroke outcome: a magnetic resonance imaging and spectroscopy study. Ann Neurol (2002) 52:20–8.[CrossRef][Web of Science][Medline]
Prado R, Ginsberg MD, Dietrich WD, Watson BD, Busto R. Hyperglycemia increases infarct size in collaterally perfused but not end-arterial vascular territories. J Cereb Blood Flow Metab (1988) 8:186–92.[Web of Science][Medline]
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