GLUTAMATE IS A MARKER FOR CEREBRAL-ISCHEMIA IN CORTICAL BUT NOT DEEP INFARCTS

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 a nd topography were determined on repeated cerebral CT performed betwee n 4 and 7 days after admission. Stroke severity was evaluated by the C anadian Stroke Scale (CSS) at 48 h after inclusion. Glutamate concentr ation in CSF was 8.4 +/- 4.9 mu mol/l in patients with cortical infarc ts and 6.5 +/- 5.2 mu mol/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 an alysis, glutamate was an independent predictor for stroke severity (hi gh: CSS score < 5; low: CSS score greater than or equal to 5) after co ntrolling for age, inclusion delay, body temperature, glucose levels a nd 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 fre quent in cortical infarcts than in deep infarcts (43 vs. 19%, p < 0.00 1), and was independently related to glutamate levels in CSF. These re sults suggest that drugs that inhibit or antagonize glutamate may be u seful particularly in cortical infarcts.