J Castillo1, A Dávalos, J Naveiro, M Noya. 1. Department of Neurology, Hospital General de Galicia, Clínico Universitario, Santiago de Compostela, Spain.
Abstract
BACKGROUND AND PURPOSE: The participation of excitatory amino acids (EAAs) in the pathogenesis of ischemic neuronal lesion has been experimentally demonstrated, but clinical experience is scarce. Our objective was to examine EAA levels during the acute phase of cerebral infarction in relation to infarct size and intensity of neurological deficit. METHODS: Using high-performance liquid chromatography, we determined the glutamate, aspartate, taurine, and glycine concentrations in the plasma and cerebrospinal fluid (CSF) of 128 patients with ischemic cerebral infarction confirmed by CT and 43 control subjects. Blood and CSF samples were obtained on admission within the first 24 hours from symptom onset. The severity of the neurological deficit was assessed with the Canadian Stroke Scale immediately after these tests and at 48 hours after inclusion in the study. Infarct volume was determined in a second CT performed between the 4th and 7th day after the patient's inclusion. RESULTS: The concentration of plasmatic glutamate was 121.39 +/- 80.89 mumol/L in the control group and 163.71 +/- 103.13 mumol/L in the patient group (P = .015); in CSF it was 3.46 +/- 1.20 mumol/L in control subjects and 6.55 +/- 4.65 mumol/L in patients (P < .0001). The concentration of glycine in plasma was 158.02 +/- 32.15 mumol/L in control subjects and 189.37 +/- 74.04 mumol/L in patients (P = .007); in CSF it was 6.18 +/- 2.28 mumol/L in control subjects and 11.23 +/- 6.96 mumol/L in patients (P < .0001). The concentrations of glutamate in plasma and in CSF were significantly higher in patients with large cerebral infarcts and in those with cortical infarcts. Levels of glutamate and glycine in plasma and CSF were significantly higher in patients with a higher degree of neurological deficit. CONCLUSIONS: Our results support the excitotoxic activity of glutamate and glycine in patients with cerebral infarction.
BACKGROUND AND PURPOSE: The participation of excitatory amino acids (EAAs) in the pathogenesis of ischemic neuronal lesion has been experimentally demonstrated, but clinical experience is scarce. Our objective was to examine EAA levels during the acute phase of cerebral infarction in relation to infarct size and intensity of neurological deficit. METHODS: Using high-performance liquid chromatography, we determined the glutamate, aspartate, taurine, and glycine concentrations in the plasma and cerebrospinal fluid (CSF) of 128 patients with ischemic cerebral infarction confirmed by CT and 43 control subjects. Blood and CSF samples were obtained on admission within the first 24 hours from symptom onset. The severity of the neurological deficit was assessed with the Canadian Stroke Scale immediately after these tests and at 48 hours after inclusion in the study. Infarct volume was determined in a second CT performed between the 4th and 7th day after the patient's inclusion. RESULTS: The concentration of plasmatic glutamate was 121.39 +/- 80.89 mumol/L in the control group and 163.71 +/- 103.13 mumol/L in the patient group (P = .015); in CSF it was 3.46 +/- 1.20 mumol/L in control subjects and 6.55 +/- 4.65 mumol/L in patients (P < .0001). The concentration of glycine in plasma was 158.02 +/- 32.15 mumol/L in control subjects and 189.37 +/- 74.04 mumol/L in patients (P = .007); in CSF it was 6.18 +/- 2.28 mumol/L in control subjects and 11.23 +/- 6.96 mumol/L in patients (P < .0001). The concentrations of glutamate in plasma and in CSF were significantly higher in patients with large cerebral infarcts and in those with cortical infarcts. Levels of glutamate and glycine in plasma and CSF were significantly higher in patients with a higher degree of neurological deficit. CONCLUSIONS: Our results support the excitotoxic activity of glutamate and glycine in patients with cerebral infarction.
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