Chronic Traumatic Encephalopathy: Science, Hollywood, and the Media

It is difficult these days to read or watch anything about contact sports, in particular the NFL, without hearing at least peripherally about chronic traumatic encephalopathy (CTE). The movie “Concussion”, starring Will Smith, brought the issue more into the mainstream as well. Unfortunately, much of what is reported in the media often makes it appear as though the science of CTE is completely settled, and that nearly everyone who plays football (or any contact sport) will end up having CTE, and may even die as a result. There have been more than a few physicians who have tried to correct misconceptions regarding CTE, urging people to allow science or research to try to make definitive cause-effect relationships; but at times, they are made out to be apologists for big money sports teams and leagues. So in this article, we will take a brief look at the current science of CTE, and clear up some current misconceptions while at the same time not minimizing the potential long-term effects of repetitive head trauma.

CTE is defined as progressive neurodegeneration associated with repetitive head trauma and the deposition of tau protein in the brain.(1) Anatomically, or neuropathologically, it is characterized by atrophy of parts of the brain, including the cerebral hemispheres, medial temporal lobe, thalamus, mammillary bodies, and brainstem. Clinically, CTE is associated with memory disturbance, behavioral and personality changes, parkinsonian type changes, and speech and gait abnormalities.(1) The key word in the definitions is “associated.” It is a hypothesis that repetitive contact to the head in sports (whether diagnosed as concussions or not) causes CTE; the direct cause and effect relationship has not been established. True cause and effect is different than an association, even a “strong association.” In the opening abstract of their influential paper “Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy following Repetitive Head Injury”, the authors even point out that repetitive brain trauma ASSOCIATED with boxing MAY produce a progressive neurological deterioration.....”(1) This association has been known since the 1920s. CTE as an entity, however, was first defined in 1949. Dr. Bennet Omalu, the protagonist in the movie “Concussion,” is credited with first finding CTE in a former NFL player in 2002.

Confusion often arises when CTE is discussed in the news and sports media. CTE is often portrayed as a disease with a welldefined pathophysiologic process as a result of concussive and subconcussive blows. So if a player has sustained a concussion(s), he/she will get CTE, or at least have a high chance of it. However, as stated above, this is actually a proposed hypothesis. It has not yet been proven that a concussion, or concussive injury, starts that process. For instance, recently researchers with the Krembil Neuroscience Centre’s Canadian Concussion Centre analyzed the brain of former NHL player Todd Ewen, who had suffered multiple concussions during his playing career. He suffered from depression, memory loss, chronic body pain, and other illnesses. According to his wife, Ewen was convinced that he suffered from CTE. Tragically, he committed suicide. However, the Canadian researchers found no evidence of CTE in his brain during an autopsy. As neuropathologist Dr. Lili-Naz Hazrati stated: “Our findings continue to show that concussions can affect the brain in different ways. This underlines the need to not only continue this research (into CTE), but also be cautious about drawing definitive conclusions about CTE until we have more data.” (3) In other words, not every athlete who sustains a concussion will develop CTE.

Adding further complexity to the issue is the fact that there are many factors which play a role in tau protein deposition in the brain, including genetic mutations, drugs, normal aging, environmental factors, and postmortem brain processing and toxins. It is very difficult to control for all of these factors or to completely eliminate them from playing a role in autopsy findings suggesting CTE. Despite what recent publicity suggests regarding high profile athletes who have committed suicide and/ or battled severe depression (which some intimate is due to CTE), the all cause mortality and suicide rates in former NFL players are actually considerably lower than the general population. What percent of those in the general population who ostensibly have not undergone trauma to the head but who suffer from symptoms similar to those of CTE also have Tau protein? To be clear, this is not to say that in the future a direct causative link will not be found, or that there is not an association between repeated brain injury/concussions and CTE in some athletes, only that more research needs to be done, a fact that all parties involved should agree upon.

At the current time, CTE can only be diagnosed with a postmortem autopsy. There are ongoing studies that are looking at various methods to detect CTE in living patients; for instance, researchers at UCLA are using positron emission tomography (PET) with a specific chemical marker called FDDNP to look for abnormal brain proteins associated with CTE. Recently, these researchers reported that changes in a PET scan of former NFL player Fred McNeill while he was still living seemed to correlate with his autopsy findings that showed evidence of CTE. Perhaps this is a breakthrough into anatomically diagnosing CTE in a living person. A confounding factor, though, is that Mr. McNeill was diagnosed with ALS in 2014. Certainly this needs to be taken into account in the research findings.

The sports medicine community continues to devote a lot of time and resources into reducing the risk for concussions in contact sports, and into preventing athletes from returning too soon from a head injury or concussion. Safer return-to-play protocols have been developed, and consensus statements are examined and updated regularly adding new recommendations based on new research. The non- medical community including parents, school officials, state high school athletic associations, professional sports leagues, etc. are all more educated on the harm of playing through concussive symptoms. I don’t think it is a stretch to say that the culture has changed; the days of playing “with your bell rung” or of “toughing out that dizziness and headache” are, and should be, ending. Concrete steps have been taken to protect athletes, and as research advances, more will be taken. There may be a time in the future when we discover a gene that will inform us of a player’s risk for CTE, and thus he/she can make an educated decision about his/her future in a contact sport. Until that time, we should encourage current concussion safeguards, and educate those involved in athletic endeavors on the importance of recognizing and removing from activity those athletes that demonstrate signs or symptoms of a concussion. If an athlete is shown to have suffered a concussion, the focus should be on protecting them from further injury until they have completely recovered.

In summary, we know that CTE is a tauopathy of unknown incidence in the athletic population. There appears to be an association between some athletes with repetitive head trauma and symptoms of CTE, but a direct cause and effect relationship has not been demonstrated. “We do not know if Tau protein is a biomarker and a problem, or just a pathologic finding on autopsy unrelated to symptoms of CTE. We also do not know if individuals who have never sustained a concussion, but have other issues such as chronic pain, anabolic steroid or other drug abuse have tau deposition in brain areas considered unique to CTE. “ (3) Does Tau protein cause symptoms? Why does there appear to be a strong association between Tau protein and CTE in some athletes, but not in others? These questions are being researched, and as a sports medicine community, it is important to support those studying these questions in the interest of keeping the athletes we care for safe. It is also incumbent upon the sports medicine community to continue to accurately educate people on where we are in this process.

  1. McKee AC, et al. Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury. J Neuropathol Exp Neurol. 2009 Jul:68(7):709-35.
  3. centre_releases_ewen_brain_autopsy_results.aspx