Neurology 2002;58:624-629
© 2002 American Academy of Neurology
Molecular signatures of brain injury after intracerebral hemorrhage
J. Castillo, MD;,
A. Dávalos, MD;,
J. Álvarez–Sabín, MD;,
J. M. Pumar, MD;,
R. Leira, MD;,
Y. Silva, MD;,
J. Montaner, MD; and
C.S. Kase, MD
From the Departments of Neurology (Drs. Castillo and Leira) and Neuroradiology (Dr. Pumar), Hospital Clínico Universitario, Santiago de Compostela; Section of Neurology (Drs. Dávalos and Silva), Hospital Universitari Doctor Josep Trueta, Girona; Department of Neurology (Drs. Álvarez-Sabín and Montaner), Hospital Universitari Vall d’Hebrón, Barcelona, Spain; and Department of Neurology (Dr. Kase), Boston Medical Center, Boston, MA.
Address correspondence and reprint requests to Prof. José Castillo, Servicio de Neurología, Hospital Clínico Universitario, 15706 Santiago de Compostela, Spain; e-mail: mecasti{at}usc.es
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 µmol/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- 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.
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