A study done at UCLA recently overviewed the large cascade of neurological effects of concussions and specifically unveiled the real damage resulting from sustaining multiple concussions in a short period of time.
It all has to do with metabolism, and energy. When the brain sustains a concussion, it falls into an emergency mode, termed hyperglycolysis. Neurons in the brain, and elsewhere in the body are dependent on ion gradients internally and externally to the neuron. When a concussion occurs, membranes of neurons are shaken and broken, leaking ions in and out of the neuron, losing cell-dependent gradients of sodium, potassium, and calcium. Thus, the neuron loses function as membrane pumps fall into overdrive, consuming energy reserves exponentially. This increase in fuel demand results in a metabolic crisis, hyperglycolysis, in which cerebral blood flow isn’t efficient to produce enough energy, and lactate begins to accumulate in the brain. The degree of metabolic crisis comes to define the degree and extent of injury, and shows a mechanism to why the brain is so vulnerable following mild and severe concussions.
With ion concentrations in abnormal numbers in localized regions of the brain, this puts stress on the nervous system, shifting metabolic pathways that initiate long-lasting neuronal harm. This sets the stage for vulnerability for a repeated injury, which is easily applicable to the topic of sports-related concussion today.
After an initial time period of hyperglycolysis and generative damaging free radicals, glucose metabolic rates are impaired from 7 to 10 days in adult animals, and these impairments are correlated to losses in spatial learning. Although this recovery time differs with age, younger animals showing shorter times of impairment (3 days), this comes to show the irreversible damages that occur with second concussions during the period of vulnerability.
It has been clinically understood that the time period of greatest risk associated with concussions comes within the first 10 days of injury. However, researchers measured a metabolite NAA, N-acetylaspartate, in post-concussion humans, relative to normal controls. On average, NAA levels took 30 days to recover, with an exception to patients who sustained a concussion within the 30 days, those subjects didn’t fully recover until 45 days after the initial injury. These studies show the time period of metabolic recovery in the brain, however scientists are yet to correlate NAA levels with symptoms, thus connections between NAA levels and clinical use remain uncertain.
Animal research offered understanding in connecting markers of metabolic stress with losses in cognition. Repeated concussions in adult mice showed degradation of cognition and neuronal injury when incidents were spaced out by 3 to 5 days, and not when injuries were separated by 7 days. In another study involving adult rats, period of glucose metabolism following concussions was correlated with impairments in working memory and generally having the time span of 3 days. When a second injury occurred within this period of metabolic sensitivity, severity of hypometabolism and memory decline was significantly greater. However when the second injury occurred beyond the full metabolic recovery, 5 days, the 2 injuries acted like single, isolated events.
Overall, applications of metabolism-correlated recovery to humans and sports-related concussions are very evident. Indirectly, these studies support clinical procedures to allow recovery for athletes immediately following concussions. It is highly likely that recovery times are longer for humans in contrast to animals, so ultimately further work will decide a specific biomarker for time of recovery for individual patients when relating to traits including cognition, balance and reaction time.
Consequences of Repeated Concussions
