According to studies performed on animals (which are not always applicable to humans), large numbers of neurons can die during this period in response to slight, normally innocuous changes in blood flow. Concussion involves diffuse (as opposed to focal) brain injury, meaning that the dysfunction occurs over a widespread area of the brain rather than in a particular spot. It is thought to be a milder type of diffuse axonal injury, because axons may be injured to a minor extent due to stretching. Animal studies in which rodents were concussed have revealed lifelong neuropathological consequences such as ongoing axonal degeneration and neuroinflammation in subcortical white matter tracts. Axonal damage has been found in the brains of concussion sufferers who died from other causes, but inadequate blood flow to the brain due to other injuries may have contributed. Findings from a study of the brains of deceased NFL athletes who received concussions suggest that lasting damage is done by such injuries. This damage, the severity of which increases with the cumulative number of concussions sustained, can lead to a variety of other health issues. The debate over whether concussion is a functional or structural phenomenon is ongoing. Structural damage has been found in the mildly traumatically injured brains of animals, but it is not clear whether these findings would apply to humans. 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.