title: Molecular signatures of brain injury after intracerebral hemorrhage.
abstract: BACKGROUND
  The mechanisms of cellular death in the tissue surrounding an intracerebral hemorrhage (ICH) are not defined.
  
  
  OBJECTIVE
  To investigate the relationship of markers of excitotoxicity and inflammation to brain injury after ICH.
  
  
  METHODS
  A total of 124 consecutive patients with spontaneous ICH admitted within 24 hours of stroke onset were prospectively investigated. The volumes of the initial ICH, peripheral edema on days 3 to 4, and the residual cavity at 3 months were measured on CT scan. Glutamate, cytokines, and adhesion molecules were measured in blood samples obtained on admission. Stroke severity and neurologic outcome were evaluated with the Canadian Stroke Scale.
  
  
  RESULTS
  Poor neurologic outcome at 3 months (Canadian Stroke Scale < 7) was observed in 53 patients (43%). Stroke severity and glutamate concentrations (by each increment of 10 micromol/L, odds ratio 1.23; 95% CI 1.09 to 1.41), but not the initial volume of ICH, were independent predictors of poor outcome. In the multiple linear regression analyses, tumor necrosis factor-alpha concentration was correlated (r = 0.83, p < 0.0001) with the volume of perihematoma edema, and glutamate concentrations were correlated (r = 0.78, p < 0.0001) with the volume of the residual cavity. These same results were observed when lobar (n = 58) and deep (n = 66) ICH were analyzed separately.
  
  
  CONCLUSIONS
  High plasma levels of proinflammatory molecules within 24 hours of intracerebral hemorrhage onset are correlated with the magnitude of the subsequent perihematoma brain edema, whereas poor neurologic outcome and the volume of the residual cavity are related to increased plasma glutamate concentrations.
authors.affiliation: Department of Neurology, Hospital Clínico Universitario, Santiago de Compostela, Spain. mecasti@usc.es
authors.forename: J
authors.initials: J
authors.lastname: Castillo
authors.forename: A
authors.initials: A
authors.lastname: Dávalos
authors.forename: J
authors.initials: J
authors.lastname: Alvarez-Sabín
authors.forename: J M
authors.initials: JM
authors.lastname: Pumar
authors.forename: R
authors.initials: R
authors.lastname: Leira
authors.forename: Y
authors.initials: Y
authors.lastname: Silva
authors.forename: J
authors.initials: J
authors.lastname: Montaner
authors.forename: C S
authors.initials: CS
authors.lastname: Kase
mesh_terms: D000368:Aged; D015415:Biomarkers; D001930:Brain Injuries / Q000097:blood* / Q000209:etiology / Q000473:pathology; D002543:Cerebral Hemorrhage / Q000097:blood* / Q000150:complications / Q000473:pathology; D015331:Cohort Studies; D016207:Cytokines / Q000097:blood; D005260:Female; D018698:Glutamic Acid / Q000097:blood; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D011446:Prospective Studies; D018709:Statistics, Nonparametric
chemical_list: D015415:Biomarkers; D016207:Cytokines; D018698:Glutamic Acid