Much of our understanding of the pathophysiology of mild traumatic brain injury (TBI) stems from animal research, which has demonstrated that physiological and metabolic disruption occurs with cerebral concussion and the previously mentioned shear strain. Although knowledge of the neurobiology of concussion is in its infancy, animal models have proven useful in delineating trauma-induced ionic flux, metabolic changes, and disruptions to CBF. Head trauma sufficient to cause concussion triggers changes in intracellular concentration of several ions, including increased potassium and calcium and decreased magnesium, also known as ionic flux. Ionic flux is thought to activate glycolysis (glucose metabolism), which reflects increased energy demands for cell membrane pumps to restore cellular ionic homeostasis. This increased glycolysis has been observed in studies of fluid percussed animals within minutes of injury, with disruption of several metabolic pathways lasting up to 10 days in mature rodent brains. Regions of the brain most prominently affected include the region of the cerebral cortex that is ipsilateral to the injury site and the hippocampus. The pathophysiology and metabolic changes associated with mild TBI are outlined in Table IV.

Ionic flux and metabolic disruption can be conceptualized as an increased "demand" for energy to restore the homeostatic functions of neuronal cells, which places these cells in a vulnerable state. Demand, however, is only part of the issue. Across animal studies of experimental TBI, CBF is reduced by as much as 50% of normal. Therefore, supply of glucose and other cellular energy nutrients required for the restoration of homeostasis can be drastically compromised even in mild head injury. This imbalance of supply and demand is referred to as "uncoupling" and reflects a disruption of the autoregulation of CBF. During changes in cerebral perfusion pressure, cerebral autoregulation serves to maintain constant CBF. Autoregulation in the normal (uninjured) brain is

Table IV

Pathophysiology of Mild Traumatic Brain Injury

Potassium (K+)

Concussion-induced ionic flux Calcium (Ca2 + )

Magnesium (Mg)

Massive increase in extracellular K+ concentration

Caused by sudden intense neuronal discharges

Extracellular K+ surpasses physiological ceiling causing rapid release of neuro-transmitters and additional K+ fluxes

Massive increase in intracellular Ca2 + concentration

Ca2+ plays role in secondary cell death, which alters metabolism

Marked decrease in intracellular Mg

Mg is important to glycolysis and oxidative phosphorylation

Reduced Mg may have implications for cerebral metabolic recovery

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