Such changes in brain structure could be responsible for certain symptoms such as visual disturbances, but other sets of symptoms, especially those of a psychological nature, are more likely to be caused by reversible pathophysiological changes in cellular function that occur after concussion, such as alterations in neurons biochemistry. These reversible changes could also explain why dysfunction is frequently temporary. A task force of head injury experts called the Concussion In Sport Group met in 2001 and decided that "concussion may result in neuropathological changes but the acute clinical symptoms largely reflect a functional disturbance rather than structural injury. "Using animal studies, the pathology of a concussion seems to start with mechanical shearing and stretching forces disrupting the cell membrane of nerve cells through "mechanoporation". This results in potassium outflow from within the cell into the extracellular space with the subsequent release of excitatory neurotransmitters including glutamate which leads to enhanced potassium extrusion, in turn resulting in sustained depolarization, impaired nerve activity and potential nerve damage. Human studies have failed to identify changes in glutamate concentration immediately post-mTBI, though disruptions have been seen 3 days to 2 weeks post-injury. In an effort to restore ion balance, the sodium-potassium ion pumps increase activity, which results in excessive ATP (adenosine triphosphate) consumption and glucose utilization, quickly depleting glucose stores within the cells. Simultaneously, inefficient oxidative metabolism leads to anaerobic metabolism of glucose and increased lactate accumulation. There is a resultant local acidosis in the brain and increased cell membrane permeability, leading to local swelling.
As of 2007, studies with athletes have shown that the amount of force and the location of the impact are not necessarily correlated with the severity of the concussion or its symptoms, and have called into question the threshold for concussion previously thought to exist at around 70–75 g.The parts of the brain most affected by rotational forces are the midbrain and diencephalon. It is thought that the forces from the injury disrupt the normal cellular activities in the reticular activating system located in these areas and that this disruption produces the loss of consciousness often seen in concussion. Other areas of the brain that may be affected include the upper part of the brain stem, the fornix, the corpus callosum, the temporal lobe, and the frontal lobe. Angular accelerations of 4600, 5900, or 7900 rad/s2 are estimated to have 25, 50, or 80% risk of mTBI respectively. Pathophysiology
In both animals and humans, mTBI can alter the brains physiology for hours to years, setting into motion a variety of pathological events. As one example, in animal models, after an initial increase in glucose metabolism, there is a subsequent reduced metabolic state which may persist for up to four weeks after injury.