Glutamate Is a Marker for Cerebral Ischemia in Cortical but Not Deep Infarcts

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Abstract
We analyzed glutamate levels in cerebrospinal fluid (CSF) with respect to cerebral infarct topography in 67 patients with cortical infarcts and 78 with deep infarcts of less than 24 h duration. Infarct volume and topography were determined on repeated cerebral CT performed between 4 and 7 days after admission. Stroke severity was evaluated by the Canadian Stroke Scale (CSS) at 48 h after inclusion. Glutamate concentration in CSF was 8.4 ± 4.9 µmol/l in patients with cortical infarcts and 6.5 ± 5.2 µmol/l in patients with deep infarcts (p = 0.028). In cortical infarcts, glutamate levels correlated with the CSS score (Spearman coefficient –0.601, p < 0.001) and with the infarct volume (Spearman coefficient 0.671, p < 0.001). In the logistic regression analysis, glutamate was an independent predictor for stroke severity (high: CSS score < 5; low: CSS score ≧ 5) after controlling for age, inclusion delay, body temperature, glucose levels and fibrinogen (odds ratio = 1.3; 95% confidence interval= 1.07–1.67). Glutamate was not related significantly with the severity and size of deep cerebral infarcts. Early neurological deterioration was more frequent in cortical infarcts than in deep infarcts (43 vs. 19%, p < 0.001), and was independently related to glutamate levels in CSF. These results suggest that drugs that inhibit or antagonize glutamate may be useful particularly in cortical infarcts.

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