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Concussion-Cerebral Pathophysiology of Concussion

Concussion injuries are thought to result from diffuse axonal injuries caused by rapid acceleration/deceleration of the head, which results in stretching of nerve fibers. During the past decade, significant insight has been gained regarding the pathophysiology of concussion. The postconcussive defects clearly do not occur with significant anatomic perturbation and do appear to resolve over time.

This has led to the concept that MTBI results in temporary neuronal dysfunction rather than cell death. However, whereas brain cells are not irreversibly destroyed by MTBI, neural cells remain in a vulnerable state before recovery. The neurometabolic events after experimental concussive brain injury have been elucidated, yielding insight concerning the etiology of postconcussive symptomatology and vulnerability.

Experimental animal models have demonstrated metabolic dysfunction to be the key physiological event after a concussive event. Disorganized release of neurotransmitters results in poorly regulated neuronal depolarizations and abnormal ionic shifts. The altered cellular physiology causes a hypermetabolism of glucose and a “cellular energy crisis” that is exacerbated by a decrease in cerebral blow flow.

This cellular energy crisis is thought to cause the increased vulnerability to a second concussive event. After the initial period of hypermetabolic glucose consumption, the concussed brain is thought to enter a period of depressed metabolism that may impair posttraumatic neural connectivity, leading to lasting changes in cognitive potential.

Cerebral metabolic function can be adversely affected for days in animals, but the time course appears to be significantly longer in humans .As the clinical significance and duration of the neurometabolic events after MTBI are defined further, more appropriate guidelines for return to play will be established.

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