Chronic Traumatic Encephalopathy (CTE)

Chronic Traumatic Encephalopathy (CTE)

Chronic Traumatic Encephalopathy is a disease that is currently gaining popularity in the medical field. Could sport be the primary cause of CTE? Are football players more exposed to the development of CTE than the general population?

Introduction

Chronic Traumatic Encephalopathy (CTE) is a degenerative neurological disease that has been known to cause cognitional, behavioral, motor skills, and mood changes or deficits among the victims. Repetitive or continuous head or brain injuries or trauma has been known to be the most factor that causes the disease. This medical term, CTE, is becoming familiar in medicine due to its direct relationship with head impacts. In the world of sport, especially boxing, rugby, and football, head impacts that cause brain trauma for the players happens more often in the field. Most researchers and medical practitioners look at CTE from the perspective of head impacts and not from the epidemiological perspective. CTE has been found in 80 to 98% of football players linked to repeated head injuries when autopsied. This paper gives an analysis of Chronic Traumatic Encephalopathy (CTE).

The long-term effects of Chronic Traumatic Encephalopathy have just recently gained the attention of the public. However, the impact of continuous brain trauma was first explained by Martland in the late 1920s. Martland described that after repetitive blows to the head amongst the boxers, they tend to display punch-drunk syndrome. Later in the years, this condition among the boxers got referred to as dementia pugilistica. This medical term was used to describe the behavior that boxers tend to show over a continuous boxing career. Today, all these behaviors and syndromes from boxing players and other victims of continuous brain injuries are referred to as Chronic Traumatic Encephalopathy. CTE today describes all those behaviors that occur due to continuous or single and severe head trauma. Accumulation of these injuries leads to progressive brain neurodegeneration.

The exact transition from concussion to CTE is yet to get established among medical professionals. It is, however, believed that concussions transition to CTE when the victim continues to get brain injuries in short intervals. These continuous brain injuries lead to the development of metabolic abnormalities and disturbances in the human cytoskeletal. CTE causes a protein cell in the brain known as ‘tau” to build up ion some areas of the brain. The buildup of tau in some areas of the human brain causes problems for the victim. The result of the buildup of the protein is the development of higher levels of depression than before amongst the victims. The buildup of the protein also leads to memory problems for the victim. Another effect of the build-up of the protein in the human brain is the onset of poor control of impulses amongst the victims.

In America, the victims of CTE have been mostly football players and military men. Studies to the disease have established that neurotrauma and CTE are common among the players of the American Football (NFL). A group in 2005 first described CTE in a series of reports that were purely based on autopsies on the brains of deceased players (Omalu et al.). Considering a large number of players who engage in sports like football in America, the issue of CTE should be a health concern that needs the attention of the public, clinicians, and scientists.

Risk factors for CTE in the NFL players

The way American Football is played exposes the players involved in repetitive head trauma that forces the brains of the players to experience forces of instant acceleration and deceleration. These instant forces bring forth brain injuries to the players (Aldag et al.). These injuries on the players of American Football can show in the form of concussions, sub-concussions, or even loss of consciousness at that moment (Stein et al.). These players with concussions and sub-concussions are normally treated in the field, and in a short time, the players are back in the field. There is a possibility that these players get another concussion in the field due to the nature of the game. Over a long period of time, the poorly managed brain injuries amongst the players, together with the inadequacy in the recovery time, exposes the players to other chronic inflammatory processes. These inflammatory processes that develop in the brains of the players at the beginning of CTE (McKee et al.).

Works like those of Guskiewicz shows that 61% of NFL players experience at least one concussion in their entire career (Guskiewicz et al.). Many others experience minor head injuries that do not manifest as concussion or sub-concussion. It is possible that a severe brain injury with the absence of concussion could also lead to the development of CTE (Tagge et al.). This is because a player could get knocked in the head severely in their careers. This leads to severe brain injuries. As mentioned earlier, the continuous brain trauma with poor management and inadequate recovery time leads to a build-up of tau protein in some parts of the human brain. The buildup of tau in some parts of the brain interferes with the brain’s white matter tracts. The interference of these white matter tracts leads to the development of abnormalities in signaling and communication (Alosco et al.).

From the current studies done on CTE, it is clear that the primary risk factor for the onset of CTE amongst the victims is repetitive brain trauma. The literature suggests that multiple concussions and brain injuries are a risk factor for numerous cognitive neurodegenerations. These injuries and concussions might also have serious effects on the mental health of some of the victims. These mental health issues, and especially cognitive neurodegeneration, expose the victims to the development of CTE later in their lives (Guskiewicz et al.).

A single blow to the head that causes concussion could have no serious impacts to the brain that could lead to CTE. Individuals who experience single brain trauma could fully recover and not get exposed to CTE (Stein et al.). However, three or more concussions or brain traumas for an individual is correlated to a higher percentage of prolonged symptoms. Again, although the development of CTE has been associated with multiple and repetitive brain injuries or concussions, there is a possibility that individuals exposed to repetitive concussions or brain injury fail to become victims of CTE. The current literature available on the development of CTE is not clear on the magnitude of brain trauma, frequency of concussions, and the duration necessary for the development of CTE among individuals.

From the study of former NFL players, dysfunctions in the neurological and psychiatric behavior of individuals have been associated with the age of first exposure to football (Alosco et al.). The period between childhood and towards the end of adolescence is an important period for an individual. This is the period where there is massive development and maturation of the neurological system (Lebel et al.). Between the age of 9 and 12, gray and white matter and neurological development in an individual are at the peak. This is also the period where an individual is most exposed to severe damages to the brain. If an individual at this age is exposed to numerous concussions, there is a high chance that the individual will develop CTE later in life.

The American Football system involves training the players at the age of 10 to 16. The tackling football involved in the American football exposes NFL players to the development of CTE early ion their lives. It is at this age when the brain cells, white and gray matter, are rapidly developing. This makes the brain equally vulnerable to injuries at this period (Lebel et al.). Some research, however, explains that the neuroplasticity of the brain compensates for the behavioral problems associated with head trauma (Stein and Jeremy).

CTE Epidemiology

The exact facts on the epidemiology of CTE require further studies. The inadequate studies on CTE epidemiology are due to the nature of the development of CTE. The history of CTE has been studied and concluded using various athletes and their athletic histories in the past. The sample used for the studies is, therefore, biased. The various studies and research done on CTE have been based on athletes’ samples only. The studies have not been done on other members of the society, the non-athletes. The study of the subject has, therefore, been limited by the lack of a control group. The epidemiology of CTE has also not been clearly defined due to the fact that CTE can not be diagnosed on a live subject (Tetor). Numerous studies were done on athletes; however, they show some unequivocal findings.

Mez et al. (Mez et al.) carried out the largest CTE case analysis that involved 202 deceased ex-football players. This case analysis showed that there was a presence of CTE in 86% of the players. Of the 86% of the deceased ex-football players, 99% were former NFL players (Mez et al.). The analysis also showed that the magnitude at which the players played football was correlational to the level of play. Those deceased ex0-football players who played at high school level showed mild CTE development. The most severe CTE was evident amongst the players who played in the NFL. This means that the level or period of exposure to brain injuries was associated with the severity of the CTE developed amongst the victims. The high-school level players were exposed to brain injuries for a short period of time. The high-school level players also probably experienced mild knocks due to the age of the players. This explains the mild development of CTE amongst the ex-footballers at the high-school level.

The players who played in the NFL showed severe levels of CTE. This is because these players were exposed to brain traumas for prolonged periods. These players were also exposed to serious or strong head and brain injuries considering their age and strength. This means that the severity and the level of exposure to head and brain trauma are correlational to the severity of the CTE developed.

Another study conducted on a sample of 1721 cases of sports athletes, there was a 32% case of CTE presence in sports athletes. There were no cases of CTE for patients who had no history of brain trauma in the control group (Bieniek et al.). This means that contact sport is the major cause of the development of CTE. Contact sport is a risk factor that leads to the development of CTE amongst the athletes. However, the exact occurrence or development of CTE is not known, but it might be related to the age of first exposure to contact sport, duration of play, the position of play, and even the type of sport. Further studies need to be done on the possibility of possible risk factors of genetics. This needs a comparison of individuals with repetitive head trauma history and healthy controls.

Symptoms of CTE

The symptoms associated with CTE do not show immediately. The symptoms of CTE begin during the individual’s midlife, probably years after the brain injuries occurred. Among 51 CTE confirmed occurrences, the mean of the occurrence of the CTE symptoms is around 43 years of age after the initial head trauma. The age, however, ranges from 25 to 76 years of age (McKee et al.). Another study of the confirmed cases of CTE and the victim’s history show that individuals take an average of 15 years before the first symptoms of CTE occur (stein et al.). From these studies, it is clear that the symptoms of CTE do not appear immediately after the first brain trauma. The symptoms might take years before they begin to show. This means that CTE develops for a long period. The disease takes a long time before the effects kick in for the victims.

The symptoms of CTE include memory loss and confusion developed from the buildup of the tau protein in the human brain. The symptoms that follow are irritability, aggression, and suicidal thoughts. The victims also begin to show signs of depression and mood fluctuations (Mez et al.). At the onset of these symptoms, the victim might begin to show changes in behavior. These symptoms are normally accompanied by substance abuse and a high case of suicides amongst the victims (McKee et al.). As the disease advances in development, the victim continues to show more symptoms, for example, disrupted motor functions of the individual.

Chronic Traumatic Encephalopathy (CTE) at the moment can not get diagnosed when the victim is alive. Diagnosis can only be made during the neuropathological examination of a deceased victim. There is also no clear procedure for the treatment of CTE due to the lack of diagnosis. Concussions and head injury patients should manage the injuries and have an adequate recovery time, especially for the athletes.

Conclusion

From the analysis of the existing literature on CTE, it is clear that the disease is common among the athletes. Different studies done on the NFL players showed that most of the ex-American Football players had CTE. The risk factor associated with CTE is exposure to contact sport. The risk factor is continuous brain injuries, sub-concussions, and concussions. NFL players are, therefore, more exposed to CTE compared to other American citizens. From the study, it can also be concluded that diagnosing CTE during life is difficult. This should be a concern for the public, clinicians, and scientists. This is because a significant size of the population all over the world are involved in a contact sport. This part of the population is at a high risk of CTE exposure. For them to get help, research should be done on an efficient way to diagnose and treat CTE.

Works cited

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