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Sports-Related Head Injuries: Concussions and Chronic Traumatic Encephalopathy

By: Anna Christou

While participating in sports improves physical activity and hones skills, such as teamwork, discipline, and hard work, playing contact sports, especially football and wrestling, can come at a cost—an increased risk of head injuries that can have long-lasting effects. According to the Brigham Health Hub, for people between ages 15 and 24, participation in sports is the second most common cause of head injuries, after motor vehicle accidents. In particular, the two most common head disorders that result from sports are concussions and chronic traumatic encephalopathy (CTE). Although doctors initially thought that CTE arose exclusively from concussions, a recent study found that hits to the head can cause CTE, even in the absence of a concussion. This study revealed that taking steps to reduce head trauma in sports is crucial, and merely treating concussions when they arise is not necessarily the most effective way to prevent the long-term cognitive deficits of head trauma.

Concussions affect a large number of athletes every year, with 1.6 to 3.8 million sports-related concussions occurring annually in the United States, according to a study published in Translational Research in Traumatic Brain Injury.

What-is-concussion-illustration

Normally, the brain is cushioned by cerebrospinal fluid, a substance with a gelatin-like consistency that protects the structure of the brain from the everyday movements that cause the brain to bump against the skull. However, a violent collision or rapid acceleration of the head, such as that caused by a hit during sports, is no match for cerebrospinal fluid. Head trauma of this degree can cause the brain to collide forcefully against the walls of the skull, often resulting in brain hemorrhaging, headaches, ringing in the ears, confusion, fatigue, and a temporary loss of consciousness. These symptoms result from a variety of changes to the brain on the cellular and molecular level, that are catalyzed by the trauma. Specifically, the impact disrupts cell membranes in the brain, leading to the release of ions and neurotransmitters that promote the excessive firing of neurons. As a result, the brain attempts to increase the production of energy in order to meet the metabolic demand caused by this increased firing. This produces lactic acid, a byproduct of energy production, which leads to excess acidity in the brain, disrupts the normal functioning of the brain, and leads to cognitive deficits. Also, inflammation from the trauma may cause axons—projections from nerve cells that are involved in the conduction of nerve impulses—to lose shape and degrade.

Recovery is very slow in the injured brain, since energy production is impaired and blood flow is reduced, impeding the flow of oxygen and nutrients that are necessary for the healing process. As a result, concussions, especially severe ones, can leave people with symptoms for weeks or even months, during which they cannot participate in physical activity, view screens, or be exposed to bright lights. In addition to these relatively short-term effects, the National Center for Health Research has stated that concussions can have long-term effects, such as a heightened risk of neurodegenerative diseases, including Alzheimer’s Disease, Parkinson’s Disease, and CTE, due to the permanent damage to the brain during the injury.

CTE, according to the National Center for Health Research, is a brain disorder that results from repeated head injuries and results in symptoms such as memory loss, impaired judgement, and depression. In essence, repeated hits to the head injure nerve cells in the brain, which conduct electrical impulses and are necessary for communication between brain cells. Consequently,  areas of the brain atrophy, specifically the frontal cortex, which is involved in motor movements and executive functions, and the temporal lobe, which is involved in language processing. The hippocampus and amygdala, both sections of the brain that are involved in the production of memories, may also degrade. This very serious disorder affects many athletes, especially those who participate in contact sports. For example, a study published in the Journal of the American Medical Association analyzed the brains of 202 deceased football players and found that 110 of them had CTE.

Concussions and CTE have similar symptoms, but little is known about the relation between the two disorders: though repeated hits to the head can cause both concussions and CTE, not everyone who has a concussion necessarily develops CTE. Therefore, to further examine the links between head injuries, concussions, and CTE, researchers at Boston University studied brain injuries in humans and mice, and published a paper with their findings earlier this year in Brain: A Journal of Neurology. They first examined post-mortem brains of teenage athletes who had suffered head injuries and found evidence of brain damage, as compared to the brains of teenage athletes who had not had recent head injuries. For example, the brains of the athletes who had suffered from head injuries contained damage to small blood vessels and neuro-inflammation, which are symptoms of concussions. In a few cases, the researchers also detected changes to the Tau protein, an indication of CTE. Tau is a protein that stabilizes neurons, but if it is phosphorylated—a phosphate molecule is added—its function changes, and it is no longer able to effectively stabilize neurons. This results in brain degradation, because the neurons are not stabilized and the Tau proteins even accumulate into clumps that infect brain regions. High levels of phosphorylated Tau proteins are linked to both concussions and CTE, but the Tau proteins in the case of CTE accumulate and spread in a distinctive pattern that allows CTE to be identified.

Although the findings from the human study further elucidated the pathology of concussions and CTE, it is difficult to study to what extent head injuries such as concussions cause CTE, evident in post-mortem brains. Therefore, the researchers designed a mouse model of head injury, subjecting mice to unilateral impact, trauma that accelerates the head without deforming the skull. As a result, they found evidence of concussion-like symptoms very shortly following the injury. Specifically, the mice that underwent the trauma showed lower performance on the administered tests, which included beam-walking and other balance tests, suggesting that they had experienced neurobehavioral deficits as a result of the trauma. In addition to these acute concussion-like symptoms, the researchers found that many of the mice that underwent the trauma had brains that showed evidence of CTE, such as damaged blood vessels and injury to the blood-brain barrier, which is a network of blood vessels that keeps harmful substances from reaching the brain. Notably, researchers also discovered that although the concussion symptoms eventually resolved themselves, the long-term impairments in brain structure, such as inflammation, damaged Tau protein, and disruption of the blood-brain barrier, persisted. Mice that did not undergo any trauma did not show any cognitive deficits, such as CTE. These findings made clear that hits to the head can result in long-term brain damage, such as symptoms of CTE; however, not every concussion is necessarily followed by CTE. Moreover, in this study, the existence or severity of concussion symptoms was not correlated with these long-term symptoms. However, in the group of mice that did experience head trauma, CTE could still result even without symptoms of concussion. This finding does not detract from the severity of concussions but, rather, suggests that long-term deficits, including CTE, can be caused by hits to the head even in the absence of a concussion. Consequently, it is important to generally reduce head impact and hits in sports—not just try to relieve concussions when they arise.

Organizers of some sports teams have, to an extent, heeded advice from research findings such as that described above, and accordingly modified the rules to make playing safer. For example, the National Football League (NFL) moved the line at which players take kickoffs to shorten the distance over which opposing teams run towards each other, consequently lowering the speed upon impact. Also, the NFL recently implemented the crown-of-the-helmet rule, which penalizes football players who contact another player with the top of their helmet; hits between helmets cause the most injury and are closest to the brain. However, these rules to make play safer have been met with resistance from some players and coaches. For example, although some players have said that the issue of injuries should be addressed with safer rules, other players have remarked that playing in a violent way is part of football and that these rules will eventually take away from the essence of the sport.

Studies such as the ones described in this article raise awareness about the importance of preventing and properly treating head trauma, especially that which results from sports, rather than allowing violent hits and then treating concussions that arise. Even though a large number of athletes are affected by injuries, many continue to play without receiving adequate rest, and the persistence in associating football with violence has made hits so ingrained in the sport that implementing rules to ensure safety is difficult. However, if sports officials continue to ignore scientific evidence and recommendations regarding the dangers of head trauma, increasing numbers of athletes will suffer from long-term neural deficits that extend beyond the field.

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