(Stroke. 2001;32:1154.)
© 2001 American Heart Association, Inc.
Original Contributions |
From the Section of Neurology, Hospital Universitari Doctor Josep Trueta, Girona, Spain (J.S., M.C., A.D.), and Service of Neurology (J.C., R.L.) and Neuroradiology (J.M.P.), Hospital Clínico Universitario, Santiago de Compostela, Spain.
Background and PurposeThe mechanisms involved in the neurological deterioration of acute lacunar strokes are unknown. Although accumulating evidence suggests that glutamate release plays a role in the progression of territorial infarctions, it remains to be established whether excitotoxicity also participates in lacunar stroke progression. We investigated whether excitatory and inhibitory amino acid concentrations in blood predict subsequent progressive motor deficits in lacunar infarctions.
MethodsWe studied 113
consecutive patients with lacunar infarct, defined by clinical and
computed tomography/magnetic resonance imaging criteria, within the
first 24 hours after stroke onset. Neurological deterioration was
defined as a decrease of
1 points in the motor items of the Canadian
Stroke Scale in the first 48 hours after admission. Glutamate, glycine,
and GABA were determined by high-performance liquid
chromatography in plasma samples obtained on admission.
Predictive values, sensitivity, specificity, and accuracy of specific
glutamate and GABA concentrations and glutamatexglycine/GABA
index for progression of lacunar stroke were
calculated.
ResultsTwenty-seven patients (23.9%) had neurological worsening. Plasma concentrations of glutamate (253±70 versus 123±73 µmol/L, mean±SD) were higher and those of GABA (140±63 versus 411±97 nmol/L) were lower in the progressing group than in the nonprogressing group (both P<0.001). Glutamate concentrations >200 µmol/L and GABA levels <240 nmol/L had a positive predictive value for neurological deterioration of 67% and 84%, respectively. A excitotoxic index >106 had a positive predictive value of 85%.
ConclusionsThese findings suggest that an imbalance between the glutamate and GABA concentrations may play a role in the pathophysiology of progressing lacunar infarctions.
Key Words: excitotoxicity GABA glutamates lacunar infarction stroke, acute
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