Neurological Deterioration in Acute Lacunar Infarctions

Abstract

The 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. We 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. Twenty-seven patients (23.9%) had neurological worsening. Plasma concentrations of glutamate (253+/-70 versus 123+/-73 micromol/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 P200 micromol/L and GABA levels 106 had a positive predictive value of 85%. These findings suggest that an imbalance between the glutamate and GABA concentrations may play a role in the pathophysiology of progressing lacunar infarctions.