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Intracerebral and subarachnoid hemorrhages (ICH and SAH, respectively) are associated with activation of microglia and growing evidence suggest that inflammation is the key contributor of secondary brain injury induced by ICH or SAH (108, 109)

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Clinical studies examining changes in autoregulation after pediatric TBI have shown that the prevalence of impaired autoregulation increases with injury severity (Vavilala et al., 2004)