Concussions have become a hot topic in sports. Athletes in sports like football and hockey are getting bigger along with their hits. This has made concussions more prevalent and an issue that arises is the time period an athlete should sit out before returning from a concussion. The answer to this can be found in the mechanism and neurometabolic cascades of a concussion.
A concussion is a type of traumatic brain injury caused by a blow to the head or any motion that causes the brain to shake within the skull. After this happens, an abrupt indiscriminant release of neurotransmitters and a rapid flow of ions occur. This disrupts the membrane potential in the neurons that plays a very large role in cell signaling. To restore the natural membrane potential to carry on with normal cell signaling, the sodium-potassium pump must work extra hard. To do this, the cell requires a large increase in ATP and a large jump in glycolysis to produce the ATP. This hypermetabolism soon leads to hypometabolism as glucose supplies in the brain run low. During this time, an increase of calcium ions and a decrease on magnesium ions appears in the neurons along with a increase of lactate from the spike in glycolysis. The increase of calcium ions can lead to free radical productions, cytoskeletal reorganization, and activation of apoptotic genetic signals. A decrease in magnesium ions may lead to neuronal dysfunction via multiple mechanisms because of magnesium’s important role as a cofactor in glycolysis.
This cascade resulting from a concussion leaves many areas of vulnerability for a second injury. During the time of hyperglycolysis, the cell is trying to rebuild the membrane potential that was disrupted by the initial concussion. If a second concussion occurs during this time, all the work that the sodium-potassium pump as done will be wiped away. But this time the cell won’t have enough glucose to power the action of the sodium-potassium pump because most of it was used up from the first injury. A similar result will happen if the second injury occurred during the period of hypoglycolysis. Another area of vulnerability is during the period of increase intracellular calcium. Calcium levels may impair mitochondrial metabolism and reduce to the production of ATP. But if an injury happens, the cell won’t be able to go into hyperglycolysis to reinstate the membrane potential because of this reduction in the ability to produce ATP in the mitochondria. Also, another increase of intracellular calcium can lead to cell death by activating proteases that promote apoptosis. The period of higher concentrations of calcium lasts for 2 to 4 days. Similar side affects can occur from the decreased concentration of magnesium. Since magnesium plays a crucial role in the process of glycolysis, so if another injury occurs, it will again decrease the concentration of magnesium inside the cell and inhibit glycolysis, which is highly needed.
The cascades that arise from concussions have dramatic affects of everyday processes that take place in the brain. Membrane potentials are disrupted which inhibits normal cell signals. Glycolysis is a very important process that is disrupted after a concussion as it goes into overdrive to drive the sodium-potassium pump and reinstate the membrane potential. Adding a second injury to a concussion during the recovery period can be detrimental to a brain because of how the brain recovers from the first concussion. The second injury will setback all the work the brain has done to heal from the first injury but the same resources are not as readily available.
Effect of Double Concussions
