title: Neurological deterioration in acute lacunar infarctions: the role of excitatory and inhibitory neurotransmitters.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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 P<0.001). Glutamate concentrations >200 micromol/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%.
  
  
  CONCLUSIONS
  These findings suggest that an imbalance between the glutamate and GABA concentrations may play a role in the pathophysiology of progressing lacunar infarctions.
authors.affiliation: Section of Neurology, Hospital Universitari Doctor Josep Trueta, Girona, Spain.
authors.forename: J
authors.initials: J
authors.lastname: Serena
authors.forename: R
authors.initials: R
authors.lastname: Leira
authors.forename: J
authors.initials: J
authors.lastname: Castillo
authors.forename: J M
authors.initials: JM
authors.lastname: Pumar
authors.forename: M
authors.initials: M
authors.lastname: Castellanos
authors.forename: A
authors.initials: A
authors.lastname: Dávalos
mesh_terms: D000208:Acute Disease; D000368:Aged; D020520:Brain Infarction / Q000097:blood / Q000175:diagnosis* / Q000503:physiopathology*; D018450:Disease Progression; D005260:Female; D018698:Glutamic Acid / Q000097:blood; D005998:Glycine / Q000097:blood; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D018377:Neurotransmitter Agents / Q000097:blood*; D011237:Predictive Value of Tests; D011379:Prognosis; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D014057:Tomography, X-Ray Computed; D005680:gamma-Aminobutyric Acid / Q000097:blood
chemical_list: D018377:Neurotransmitter Agents; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D005998:Glycine