These data suggest that a single concussion is associated with behavioral dysfunction and subcellular alterations that may contribute to a transiently vulnerable state during which a second concussion within 3 to 5 days can lead to exacerbated and more prolonged axonal damage and greater behavioral dysfunction.
Abnormalities in blood coagulation, although quite common after traumatic brain injury (TBI), are of unknown significance. The authors review the clinical and pathophysiological features of this phenomenon and emphasize its origin in disseminated intravascular coagulation. This connection provides a possible explanation for much of the cerebral ischemia that accompanies TBI, namely intravascular microthrombosis. The authors' own research findings support this contention and suggest possible therapeutic avenues. A number of compelling studies demonstrate that DIC is a common and important consequence of TBI. In particular, posttraumatic coagulopathy appears to be linked to secondary cerebral injury. Although the extent of this process has yet to be elucidated fully, coagulation abnormalities are evident soon after trauma. This allows early identification of patients likely to suffer secondary complications and provides an opportunity to evaluate promising agents that may mitigate posttraumatic DIC and related pathologies in these patients. This is an area deserving of more intensive research.
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