Chronic Traumatic Encephalopathy Jenna Cottet Athletic Health Care Ms. Maull Chronic Traumatic Encephalopathy First described in the year 1928 (McKee 2010), Chronic Traumatic Encephalopathy is a progressive neurodegenerative disease that has been found to be the cause of retired NFL linebacker Junior Seau’s suicide. The disease deteriorated his brain and hindered his ability to think logically. Seau is not the only retired NFL player found to have had CTE through autopsy following their death. Mike Webster was the first football player found to have CTE, when scientists found the characteristic buildup of the tau protein in his brain.
Another significant find in CTE affected brains such as his includes the shrinkage of the hippocampus, the part of the brain responsible for memory and thinking processes. The disease was originally noticed in boxers, first being called “punch drunk. ” These boxers were described as exhibiting “cuckoo” and “goofy” characteristics. The observation in boxers led to a term meaning dementia of a fighter – “dementia pugilistica” which was later renamed its current name, Chronic Traumatic Encephalopathy, in the 1960s (Saulle 2012).
It’s been confirmed that the cause of CTE is repetitive head trauma but it is unclear whether or not it can be brought on by a single mTBI (minor Traumatic Brain Injury) or if it can only be caused by recurrent blows to the head. The obvious group with the highest risk for CTE development is athletes, who are involved in contact sports such as football, boxing, and martial arts, but they aren’t alone. Other groups at risk for the disease include military veterans, epileptics, and victims of domestic abuse. As of today, there is no definitive diagnosis, other than postmortem autopsy, for Chronic Traumatic Encephalopathy.
It is difficult due to the lack of consensus among doctors and scientists about the criteria of diagnosis and the void of clinicopathologic correlation studies. The similarity between CTE and other brain diseases also make differential diagnosis tough. Diseases like AD (Alzheimer’s disease) and FTD (frontotemporal dementia) share similar symptoms and just as CTE, come from a history of head trauma. Age can dismiss Alzheimer’s from a patient’s diagnostic options but it cannot help in differentiating between CTE and FTD (Saulle 2012).
It is, however, possible to distinguish postconcussive syndrome from CTE. PCS symptoms usually improve within a year, so if they do not subside, the patient is logically considered to have CTE, but still not definitively. Due to the inability to definitively diagnose Chronic Traumatic Encephalopathy, treatment methodologies are nonexistent. Prevention is purely the only form of treatment as of now and even just that is very difficult. In football, those hard hits the players perform are not only a simple aspect of the game, but they are a huge part of the sport’s identity.
It would require a collective effort on behalf of the administrators, coaches, players, referees, team physicians, and even the fans who watch the games. Policies, techniques, player’s understanding of potential dangers of downplaying injuries, rules, playing environment, return-to-play criteria, protective equipment and so much more would need to be improved in order for prevention to be effective. Boston University is extensively working to change the fact that there is no definitive diagnosis for CTE.
One research program called LEGEND, Longitudinal Examination to Gather Evidence of Neurodegenerative Disease, has participants both with and without a history of concussions, take interviews over the phone as well as yearly questionnaires online. These individuals also have to opportunity to provide a saliva sample in order for BU to use it in genetic testing. The university also has a study called DETECT, Diagnosing and Evaluating Traumatic Encephalopathy Using Clinical Tests, which was the first research project on CTE ever funded by the NIH (National Institutes of Health).
It is stated on their Center for the Study of Traumatic Encephalopathy website that this study’s ultimate goal is to develop methods of diagnosing the disease during life through the use of a variety of tests, including MRIs, MRSs, blood tests, and measures of the proteins in spinal fluid. The participants, who are planned to include 150 former NFL players ages forty to sixty-nine and 50 same-age athletes who played non-contact sports, will also undergo neurological, psychiatric, and cognitive assessments, as well as genetic testing.
In conclusion, I think it’s safe to say that there is no question that repetitive head trauma can cause permanent brain damage. Despite the NFL’s attempts to hide these facts from the public, it is now a known fact that football players are an approximate nineteen times more likely to have a memory disease than men of the same age who have not played any contact sport. Boston University and, I’m sure, other organizations will continue to conduct experiments and studies in order to find every clinical answer we are currently missing.
In time, we will know how to definitively diagnose, treat, and prevent Chronic Traumatic Encephalopathy. Until then, I believe the only option we have is to prevent concussions with safer play and better equipment, and also to attempt to stop the progressing of damage after a player’s mTBI by following return-to-play procedures more accurately.