Effects of Chronic Traumatic Encephalopathy (CTE) on athletes

Effects of Chronic Traumatic Encephalopathy (CTE) on athletes

Chronic Traumatic Encephalopathy (CTE) is classified as a degenerative disease that affects the human brain and it is commonly found if people with a history of repetitive trauma of the mind in particular athletes. The condition includes symptomatic concussions and asymptomatic subconcussive hits to the brain which are often unnoticeable. Since the 1920’s, CTE has been known to affect boxers commonly, and it was initially referred to as “punch drunk syndrome” or dementia pugilistica (Jordan, 2015).

Recently, neuropathologically confirmed CTE has been found in other types of athletes such a football and hockey plays both playing and retired. The disease has also been commonly diagnosed in military veterans with a history of brain trauma with a repetitive pattern of occurrence. The occurrence of CTE is not limited to active professional athletes; it has also been found to occur in retired athletes who did not pursue a career in professional sports after high school or college levels.

A characteristic feature of CTE is that repetitive brain trauma leads to the onset of progressive degeneration of various kinds of cell types in the brain which includes the rapid buildup of an abnormal brain protein called tau.  These degenerative changes in the brain can start showing anywhere from months, years or decades after the most recent incident of brain trauma or the end of active involvement in an athletic career. The kind of brain degeneration associated with the usual symptoms of CTE includes memory loss, impaired judgment, confusion, aggression, impulse control problems, and depression. Furthermore, secondary signs of CTE include Parkinson-like symptoms, suicidal tendencies and ultimately following dementia results.The primary way in which CTE manifests itself includes a reduction in the weight of the brain which is associated with atrophy of the frontal, temporal and medial temporal lobes (Omalu,2014).

Every individual case diagnosed with CTE has one standard feature which is a history of repetitive blows to the head. However, CTE is more common in athletes who play contact sports due to nature of a repetition of hits to the head. The disease has been found in athletes, whose primary source of exposure to head impact is through football tackles, boxing, rugby, soccer, pro wrestling while fewer cases have been identified in individuals who play other forms of contact sports such as baseball and basketball.

It is important to note that being repetitively hit on the head is not the only predisposing factor to the development of CTE. There is some other risk factor that makes some people more prone to developing CTE than others. The age of an individual when they first get exposed to the head impacts is a significant factor which determines the likelihood of developing CTE. Athletes who start playing contact sports at a young age are at a higher risk of developing CTE later in life. Several published research studies on a show that exposure to impact to the head at an age before 12 years is associated with more severe outcomes of the disease than those which start after 12 years.

The length of exposure to the head impacts also determines one’s likelihood of developing CTE. Athletes with longer active careers in sports have a higher risk of developing the disease as compared to those with a shorter career. Furthermore, athletes with longer careers are more likely to create more severe forms of CTE than those with relatively shorter careers. There may be a few other likely risk factors which have not yet been discovered such as possible genetic predisposition which makes some people more susceptible to developing CTE than others. More research needs to be carried out to understand more about the factors associated with developing CTE to know how to prevent, treat and manage the disease.

Pathologically CTE appears in a form that is distinguishable to other forms of diseases caused by an accumulation of tau proteins in the brain such as Alzheimer’s disease. There are four distinct stages of CTE which are correlated with the pathology of tau proteins on the brain tissue. Such neuropathologies range in severity from focal perivascular epicenters of the frontal neocortex to severe tauopathy which affects widespread regions of the brain.

Currently, the only way to diagnose CTE definitively is by direct tissue examination of the brain which includes full autopsy and immunohistochemical which is only possible after death. Due to the absence of in vivo techniques to test for specific biomarkers for CTE, the disease cannot currently be diagnosed in a living individual. Concussions and non-structural injuries of the brain do not result in bleeding, and hence such kinds of trauma cannot be observed on routine neuroimaging tests such CT scans and MRIs (Padalino et al., 2013).

Currently, there is no way of treating or curing CTE. Furthermore, there is no way of preventing it except the avoidance of repetitive head injuries. However, people with potential signs of CTE can benefit from some types of care that are provided for patients who have Alzheimer’s disease  as well as other forms of dementia such a behavioral approaches to managing aggression associated with CTE. Moreover, people in charge of taking care of someone with CTE symptoms can be assisted in their work by being sensitized on what to expect when CTE progresses and by a having a network of support put in place. Such forums are crucial since they encourage sharing of information on different ways of managing CTE for patients at home. Currently, clinical research is being carried out with the aim of discovering how the disease starts and progresses, the risk factors for developing the CTE and how to diagnose the disease can be diagnosed during its formative stages. It is, however, possible to treat the symptoms of the disease such as anxiety and depression individually.

Epidemiological studies suggest that neuropathologically confirmed cases of CTE are more common in athletes whereby 46 (90%) of the 51 cases identified in athletes. Boxers account for 85% of the 39 confirmed cases among athletes. Among the fighters there were varying levels of the pathology of CTE depending on the length of the boxer’s career. The first symptoms of CTE were noticed in athletes whose ages ranged from 25 to 76 years. Individuals suffering from CET who have been reported to experience more behavioral mood symptoms in their lifetime were more likely to have indicative signs of the mild disease as opposed to severe forms. Such symptoms occur in 96% of mild cases as opposed to 89% of acute cases. Individuals with distribution and mild buildup of Tau proteins are more likely to have committed suicide. On the other hand, those with a higher accumulation of the proteins are more likely to have experienced cognitive symptoms of CET such as memory loss.

References

Jordan, B. (2015). Chronic traumatic encephalopathy. Journal of the Neurological Sciences, 357, e502.

Omalu, B. (2014). Chronic traumatic encephalopathy. In Concussion (Vol. 28, pp. 38-49). Karger Publishers.

Yi, J., Padalino, D. J., Chin, L. S., Montenegro, P., & Cantu, R. C. (2013). Chronic traumatic encephalopathy. Current sports medicine reports, 12(1), 28-32.