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Published on: September 11, 2017
Molecular signatures of brain injury after intracerebral hemorrhage
J Castillo1, A Dávalos, J Alvarez-Sabín
1Department of Neurology, Hospital Clínico Universitario, Santiago de Compostela, Spain. mecasti@usc.es
Insights
Markers of inflammation and excitotoxicity are linked to brain damage after intracerebral hemorrhage (ICH). High glutamate levels predict poor outcomes, while inflammatory molecules correlate with brain edema following ICH.
Area of Science:
- Neuroscience
- Neurology
- Pathophysiology
Background:
- Mechanisms of cell death in the brain tissue surrounding intracerebral hemorrhage (ICH) remain undefined.
- Understanding these mechanisms is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the relationship between markers of excitotoxicity and inflammation and brain injury following ICH.
- To identify predictors of poor neurologic outcome in ICH patients.
Main Methods:
- Prospective investigation of 124 patients with spontaneous ICH within 24 hours of onset.
- Measurement of ICH volumes, edema, and residual cavity using CT scans.
- Assay of plasma glutamate, cytokines, and adhesion molecules; evaluation of stroke severity and outcome using the Canadian Stroke Scale.
Main Results:
- Glutamate concentrations and stroke severity independently predicted poor neurologic outcome (Canadian Stroke Scale < 7).
- Tumor necrosis factor-alpha correlated with perihematoma edema volume (r = 0.83, p < 0.0001).
- Glutamate concentrations correlated with residual cavity volume (r = 0.78, p < 0.0001).
Conclusions:
- High plasma levels of proinflammatory molecules within 24 hours of ICH correlate with the magnitude of subsequent brain edema.
- Poor neurologic outcome and residual cavity volume are related to increased plasma glutamate concentrations.
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.
