ABSTRACT
Traumatic brain injury triggers a complex and interwoven sequence of ionic and metabolic events from which damaged cells may eventually recover or, in certain circumstances, degenerate and die. Brain concussion triggers a multi-layered neurometabolic cascade of physiologic changes that has important implications for cerebral vulnerability, cell death, plasticity and persistent neurocognitive deficits. Concussive brain injury has been shown to elicit a neurometabolic cascade of acute ionic changes, metabolic perturbations and axonal dysfunction. Children and adults respond to brain injury differently, with children seemingly more vulnerable to cerebral swelling and subdural hematomas after mild injury. Athletic brain injury is of particular concern in children, who tend to participate in sports putting them at risk for head trauma and in whom neurological development is ongoing. Developmental deficits after childhood brain trauma are difficult to assess due to variations in injury severity, location, and disruption of normal childhood activities resulting from hospitalization and corresponding rehabilitation.
