ABSTRACT
TBI, whether an open-(such as a penetration wound) or closed-head injury (such as acceleration/deceleration of the brain), is characterized by both primary and secondary injuries. Primary injuries may include diffuse axonal injury and direct vascular disruption. These phenomena lead to secondary injuries such as metabolic disturbances, edema, and dysfunctional autoregulation of CBF (reviewed in Betrus, 2013). Arguably, these secondary injuries contribute most to the ensuing pathotrajectory of TBI and present the most complex challenges for attempting to mitigate suffering
associated with brain injury. For instance, lack of proper oxygen and metabolite delivery to the brain can lead to longterm alterations in membrane permeability, improper release of excitatory neurotransmitters (Bullock et al., 1998), and ion imbalances that ultimately cause axon degeneration (Bullock et al., 1998; Tekkok et al., 2007).
