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The Growing Concern of CTE in Contact Sports

Annabella Diakité-Ritzau
Every fall season, all 32 teams in the National Football League (NFL) release their official roster of 53 players, starting an electric period of time where Superbowl Champion predictions, rookie news, and the most surprising trades and signings often make the headlines. Yet, news of how one in three NFL players believe they have a Chronic Traumatic Encephalopathy (Grashow et al., 2023), or how 345 out of 376 ex-NFL players were found to have a CTE (Mckee, 2023), often yields the media spotlight to predictions for NFL team of the week. 

Chronic traumatic encephalopathy is a brain disorder associated with repeated blows to the head. CTE was first studied in boxers and initially referred to as the “Punch-Drunk Syndrome” by forensic pathologist Harrison Stanford Martland. The development of symptoms in CTE are understood to occur in four stages (Fesharaki-Zadeh, 2019). First, an individual will experience symptoms of disorientation, dizziness, and headaches. This progresses to second stage symptoms where behaviors like memory loss, impulsive actions, and lack of good judgment start to manifest. Unfortunately, CTEs can progress further to a third and even fourth stage where symptoms such as depression,  suicidal ideation and paranoia are common. Also, as a result of the repeated hits to the head, those with a suspected CTE in the fourth stage often experience the symptoms of memory loss, dyskinesia, involuntary muscle movements, and Parkinsonism, where symptoms include: Bradykinesia (slowness of movement), and rigidity (stiffness) .

But the human skull is not weak—in fact, one research suggests that it could take up to 5,400 newtons ,1200 lbs or 544kg,  (Matsui et al, 1975) to crush a skull. So even if the heaviest ever NFL player Aaron Gibson (410lbs) tackled his opponent with all his weight, his opponent's skull still may not be crushed. Of course there are caveats like the location of the fracture in the skull (like  the occipital bone is thicker than the frontal bone), or at what frequency the collision occurred or the age of the individual’s skull being crushed. But, while on average it takes between 1,100 to 1600 newtons of force ,247 lbs or 112 to 360 lbs or 163kg, (Furkan, 2025) to have a skull fracture, NFL and rugby players still have the added layers of protection, like helmets and scrum caps,. So how does the repeated blows to such an athlete's head result in dire consequences?

This is because CTEs are classified as tauopathies (Asken et al., 2017), a class of neurodegenerative diseases typically associated with Alzheimer’s disease. A key characteristic of tauopathies is the aggregation of abnormal tau proteins, a group of proteins that stabilize microtubules in neurons and therefore support the crucial transport of molecules within the neuron. In a brain with a suspected CTE,  the progression of the four stages can be associated with tau pathology, where the hyperphosphorylation of tau proteins causes them to form insoluble aggregates called neurofibrillary tangles. These insoluble clumps of protein crowd up the intracellular space, disrupting the propagation of action potentials down axons and impairing communication between neurons. This is a critical part of how Alzheimer’s patients can lose many cognitive functions and have damaged brains (Goedert et al ., 2017). A key neuropathological distinction between a CTE and Alzheimer’s is the reduction of brain mass. In Chronic Traumatic Encephalopathies, atrophy is more localized to the frontal and temporal cortices and medial temporal lobe (Mckee et al., 2010). These are areas that are responsible for the acquisition and retrieval of memory, speech ( frontal lobe), and language comprehension (temporal lobe). CTEs also lacked a distinct atrophy found in the cerebral cortical ( outer layer of the brain) that is commonly found in Alzheimer’s (Turner et al, 2016).Further hits to the brain can leave marks of atrophy in the amygdala (which plays a role in emotional processing) and hippocampus (which plays a large role in converting short term memories into long term memories). In spite of this, CTEs cannot be diagnosed while a person is alive. Due to the lack of biomarkers ( a measurable substance like blood glucose levels or a biological process like the frequency of blood pressure) that can show us what is happening in the brain and the fact that concussions are non-structural injuries that do not result in brain bleeds, a CTE diagnosis cannot be definitely made while the patient is alive.Its overlapping symptoms with Alzheimer’s and Parkinson’s also make it harder to give a comprehensive diagnosis of whether an individual is suspected to have a CTE or has Alzheimer’s or Parkinson’s. Instead, microscopic examination of tau proteins is needed—something which can only be done postmortem. So, because we cannot currently diagnose a living person with a CTE, this article wishes to understand  what preventative measures could be suggested to reduce the chances of athletes developing CTEs? 

A huge problem that arises from this question is that contact sports such as American football, boxing, and mixed martial arts (MMA) are extremely profitable and can also transform the lives of many aspiring athletes. For example, let’s take a look at accomplished athletes like Muhammed Ali, who was nicknamed “The Greatest” and  known for his significant contributions to the world of boxing. However,  by 1984, Ali was diagnosed with Parkinson’s. It’s estimated that Ali was exposed to an estimated 200,000 hits to his head (Eig, 2018.) .Furthermore, when considering  the salaries of NFL players like Dak Prescott who signed a contract with the Dallas Cowboys worth 231 millions dollars or Travis Kelce (of the Kansas City Chiefs) who earns an annual salary of 17 million dollars  it’s easy to see how the benefits of fame and money can often outweigh the cost of potentially developing a CTE. This presents an ongoing conflict. Sporting organizations must answer the question of whether they implement changes to their sport that risk a loss in viewership but prevent the potential development of neurodegenerative disorders in athletes, or continue this current model which continually sees more and more professional athletes speak out about neurocognitive issues. 

Preventive measures have been increasing in recent years as seen by the latest move by the NFL with the the launch of Guardian Caps, a soft shelled pad worn over football helmets made to absorb at least 10% of the force from each hit. While the introduction is relatively recent and Guardian Caps have faced resistance from players due to their bulky aesthetic, they are certainly a step in the right direction. In other sport domains like MMA, suggestions have been made like allowing more stoppage time when a component is knocked down, and better training for referees to spot whether a fighter has suffered a concussion. Unfortunately concussions are not immediately obvious and symptoms can develop gradually. While referees can look for signs of brain injuries in knockouts or stop fights when a fighter has lost consciousness, there are still cases like Prichard Colón where after his match with Terrel Williams in which he received multiple hits to the back of his head without any immediate intervention, Colón had collapsed after the match and had a brain hemorrhage which saw him in a coma for 221 days. 
​
When answering the question of what preventative measures could be suggested to reduce the chances of athletes developing CTEs? Theoretically, the answer would be to find a solution to detect CTEs in living persons. This would transform the world of  brain imaging and potentially aid sport neurologists in their assessment of athletes but also help athletes understand the biological cause of their symptoms. But realistically, until more research is conducted to find this solution, better regulations in sports are needed. Perhaps instead of 2 minute timeouts in the NFL, it could be 5-10 minutes to allow a more thorough examination by an onsite neurologist. Furthermore, by bringing more awareness to this situation and having more documentaries like the League of Denial: The NFL’s Concussion Crisis or Unforgotten: The Story of Paul Pender, a greater understanding of CTE’s can occur and this could allow for more scientific innovations like the guardian caps. Therefore, every fall season where news of the most surprising trades, predictions or rookie news are released, individuals can also see just as much news  about the latest innovations or concepts discovered to tackle this ongoing battle against CTEs, or what regulations institutions like the NFL or NCAA have put in place to keep protecting the health of their players.

About the Author
Annabella Diakité-Ritzau​ ('28) is a freshman at Harvard College intending to concentrate in cognitive neuroscience and evolutionary psychology.

References
  • Grashow, R., Terry, D. P., Iverson, G. L., DiGregorio, H., Dairi, I., Brown, C., Atkeson, P. S., Whittington, A. J., Reese, L., Kim, J. H., Konstantinides, N., Taylor, H. A., Speizer, F. E., Daneshvar, D. H., Zafonte, R. D., Weisskopf, M. G., & Baggish, A. L. (2024). Perceived Chronic Traumatic Encephalopathy and Suicidality in Former Professional Football Players. JAMA Neurology. https://doi.org/10.1001/jamaneurol.2024.3083
  • McKee, A. (2023, February 6). Researchers Find CTE in 345 of 376 Former NFL Players Studied | Chobanian & Avedisian School of Medicine. Www.bumc.bu.edu. https://www.bumc.bu.edu/camed/2023/02/06/researchers-find-cte-in-345-of-376-former-nfl-players-studied/
  • Fesharaki-Zadeh, A. (2019). Chronic Traumatic Encephalopathy: A Brief Overview. Frontiers in Neurology, 10(713). https://doi.org/10.3389/fneur.2019.00713
  • T, Matsui, et al. “[Experimental Studies of Skull Fracture in the Temporal Region (Author’s Transl)].” No Shinkei Geka. Neurological Surgery, 1 Feb. 1975, pubmed.ncbi.nlm.nih.gov/1238919/.
  • Furkan. “Skull Fracture Threshold: How Much Force It Takes.” Acibadem Health Point - ACIBADEM Hospitals - Acibadem Health Group, 16 Sept. 2024, www.acibademhealthpoint.com/skull-fracture-threshold-how-much-force-it-takes/. Accessed 11 Feb. 2025.
  • Asken, B. M., Sullan, M. J., DeKosky, S. T., Jaffee, M. S., & Bauer, R. M. (2017). Research Gaps and Controversies in Chronic Traumatic Encephalopathy. JAMA Neurology, 74(10), 1255. https://doi.org/10.1001/jamaneurol.2017.2396
  • ‌Goedert, M., & Spillantini, M. G. (2017). Propagation of Tau aggregates. Molecular Brain, 10(1). https://doi.org/10.1186/s13041-017-0298-7
  • McKee, A. C., Cantu, R. C., Nowinski, C. J., Hedley-Whyte, E. T., Gavett, B. E., Budson, A. E., Santini, V. E., Lee, H.-S., Kubilus, C. A., & Stern, R. A. (2009). Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy After Repetitive Head Injury. Journal of Neuropathology & Experimental Neurology, 68(7), 709–735. https://doi.org/10.1097/nen.0b013e3181a9d503‌
  • Turner, Ryan C., et al. “Alzheimer’s Disease and Chronic Traumatic Encephalopathy: Distinct but Possibly Overlapping Disease Entities.” Brain Injury, vol. 30, no. 11, 2016, pp. 1279–1292, pubmed.ncbi.nlm.nih.gov/27715315/, https://doi.org/10.1080/02699052.2016.1193631.
  • Eig, J. (2018). ALI : a life. Simon & Schuster Ltd
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