Abstract
Secondary injury after traumatic brain injury proceeds through several partly independent mechanisms, of which neuroinflammation [1], oxidative stress [2] and disruption of the blood-brain barrier with endothelial dysfunction [3] are the best characterised. Genetic association studies in this field are usually organised one gene against one outcome, most often mortality or a dichotomised functional score. Whether the biochemical pathway to which a gene belongs predicts the type of complication that develops, and not merely its likelihood, has rarely been tested directly.
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