TBI and sensory sensitivity: Translational opportunities

Traumatic brain injury (TBI) is a central nervous system injury that occurs as a result of mechanical force being applied to the body or cranium that is transmitted to the brain and its associated structures.1 Each single event, by definition, occurs in milliseconds and initiates subsequent physiological and cellular processes. The primary injury event directly, possibly irreparably, damages neurological and vascular tissue. It follows that direct damage may go on to trigger subsequent processes of cellular pathophysiology, referred to as the secondary injury cascade.2 This cascade disrupts physiological processes through cerebral edema, ischemia, hypotension, and metabolic challenges.3 - 6 At a cellular level, excitatory amino acids and platelet-activating factors disturb ion channel conductance, ultimately impacting tissue homeostasis and exacerbating metabolic failure.7 These cellular processes are self-perpetuating, often exacerbating damage, whereby pharmacological intervention could improve outcome by controlling damage.2 In the presence or absence of treatment, injury-induced deficits in neurological function (e.g., dizziness, headache, amnesia) likely occur, which can recover, persist, or transition into morbidities over time.