The Neurometabolic Cascade of Concussion.

TLDR

The pathophysiologic cascade after concussion involves abrupt neuronal depolarization, excitatory neurotransmitter release, ionic shifts, altered glucose metabolism, cerebral blood flow changes, and axonal dysfunction, which correlate with postconcussion vulnerability and neurobehavioral deficits and are well characterized in animals but only emerging in humans. This review aims to relate these neurometabolic changes to sports‑related clinical issues and to inform improved concussion‑management guidelines as the functional significance and duration of these derangements become clearer. The authors synthesized over 100 basic‑science and clinical articles relevant to concussive brain injury, postinjury pathophysiology, and functional recovery. Concussion produces cerebral dysfunction lasting days in animals and weeks in humans, with significant glucose‑metabolism alterations detectable even in patients with normal Glasgow Coma Scores, underscoring the need for detailed clinical assessment.

Abstract

OBJECTIVE: To review the underlying pathophysiologic processes of concussive brain injury and relate these neurometabolic changes to clinical sports-related issues such as injury to the developing brain, overuse injury, and repeated concussion. DATA SOURCES: Over 100 articles from both basic science and clinical medical literature selected for relevance to concussive brain injury, postinjury pathophysiology, and recovery of function. DATA SYNTHESIS: The primary elements of the pathophysiologic cascade following concussive brain injury include abrupt neuronal depolarization, release of excitatory neurotransmitters, ionic shifts, changes in glucose metabolism, altered cerebral blood flow, and impaired axonal function. These alterations can be correlated with periods of postconcussion vulnerability and with neurobehavioral abnormalities. While the time course of these changes is well understood in experimental animal models, it is only beginning to be characterized following human concussion. CONCLUSIONS/RECOMMENDATIONS: Following concussion, cerebral pathophysiology can be adversely affected for days in animals and weeks in humans. Significant changes in cerebral glucose metabolism can exist even in head-injured patients with normal Glasgow Coma Scores, underscoring the need for in-depth clinical assessment in an effort to uncover neurocognitive correlates of altered cerebral physiology. Improved guidelines for clinical management of concussion may be formulated as the functional significance and duration of these postinjury neurometabolic derangements are better delineated.