Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease characterized by the accumulation of hyperphosphorylated tau (p-tau) in the brain. Most documented cases have occurred in athletes with mild repetitive head impacts (RHI) over an extended period. Evidence indicates that repetitive concussive and subconcussive blows to the head cause CTE. Chronic traumatic encephalopathy: A paradigm in search of evidence? Rudy J Castellani New insights into the long-term effects of mild brain injury Charlotte Ridler Nature Reviews Neurology volume 13, page195 (2017) Concussion, microvascular injury, and early tauopathy in young athletes after impact head injury and an impact concussion mouse model - Brain, Volume 141, Issue 2, February 2018 Clinical subtypes of chronic traumatic encephalopathy: literature review and proposed research diagnostic criteria for traumatic encephalopathy syndrome - Alzheimers Res Ther. 2014; 6(5): 68. Published online 2014 Sep 24. Effects of Subconcussive Head Trauma on the Default Mode Network of the Brain - J Neurotrauma. 2014 Dec 1; 31(23): 1907–1913. Understanding the Consequences of Repetitive Subconcussive Head Impacts in Sport: Brain Changes and Dampened Motor Control Are Seen After Boxing Practice - ORIGINAL RESEARCH article Front. Hum. Neurosci., 10 September 2019 In particular, it is associated with contact sports such as boxing, American football, Australian rules football, wrestling, mixed martial arts, ice hockey, rugby, and association football. In association football, whether this is just associated with prolific headers or other injuries is unclear as of 2017.
What is CTE?
CTE is described as p-tau accumulation in the superior frontal gyrus, entorhinal cortex, parahippocampal gyrus, insula, temporal pole, amygdala, and hippocampus of the brain, and more simply, a neurodegenerative disease linked to repeated trauma to the head. The factors thought to influence CTE development and progression are age at first Traumatic Brain Injury (TBI) exposure, duration between injuries, cognitive reserve, genetic predisposition, and chronic systemic inflammation, like obesity.
CTE is often associated with multiple neuropsychiatric signs and symptoms. Symptoms of CTE range from paranoia, depression, childish behavior, anxiety, memory loss, poor judgment, anger, irritability, apathy, confusion, and poor concentration. Neurobehavioral changes may occur at any time during the development of CTE. CTE patients can also exhibit behaviors like hyperorality and hypersexuality.
Athletes with CTE had more ventricular dilatation, cavum septi pellucidi, thalamic notching, and perivascular pigment-laden macrophages in the frontal white matter than those without CTE. Cognitive and neurobehavioral symptoms were frequent among the brains of the deceased athletes, with suicide being the most common cause of death, followed by unintentional overdose.
CTE Cases Most documented cases of chronic traumatic encephalopathy have occurred in many athletes involved in contact sports such as boxing, American football, professional wrestling, ice hockey, mixed martial arts, rugby, and soccer. Other risk factors include being in the military, prior domestic violence, and repeated banging of the head. The exact amount of trauma required for the condition to occur is unknown. Below is a list of notable cases of CTE in sports.
American football
The study of CTE's relationship with American football began in 2002. Since then, hundreds of players have been diagnosed posthumously with CTE, including a number of players who committed suicide. CTE has affected not only professional football players, but also athletes who played only in college or in high school.
In 2005, Bennet Omalu, a forensic pathologist and neuropathologist in Pittsburgh, Pennsylvania, found CTE in the brains of Mike Webster, Terry Long, Andre Waters, Justin Strzelczyk, and Tom McHale. Omalu, initially a medical examiner, then associate adjunct professor in California, was a co-founder of the Brain Injury Research Institute and reportedly in 2012 participated in the autopsy of Junior Seau. Omalu's participation was halted during the autopsy after Seau's son Tyler Seau, under pressure from the NFL, revoked previously provided oral permission. Tyler had received telephone calls from NFL management denouncing Omalu's professional ethics, qualifications, and motivation when the league asked him to revoke Dr. Omalu's research.
Research into football players with CTE has continued with neuropathologist Ann McKee of Boston University's CTE Center, who diagnosed the bodies of twelve former professional American football players with CTE postmortem between 2008 and 2010. An autopsy McKee conducted in 2010 on the brain of Owen Thomas, a 21-year-old junior lineman at the University of Pennsylvania who died of suicide, showed early stages of CTE, making him the second youngest person at the time to be diagnosed with the condition. Thomas was also the second amateur football player diagnosed with CTE. (Mike Borich, who died at 42, had been the first such player diagnosed with CTE, also by McKee.)Staff. "First former college football player diagnosed with CTE: Former Brigham Young University Football Coach Died at 42", Center for the Study of Traumatic Encephalopathy, October 22, 2009. Accessed October 19, 2010. The doctors who performed the autopsy indicated that they found no causal connection between Thomas's early-stage CTE and his suicide. There was no indication that Thomas missed playing time due to concussions; however, as a player who played hard and "loved to hit people," Thomas may have played through concussions and received thousands of subconcussive impacts on the brain.Schwarz, Alan. "Suicide Reveals Signs of a Disease Seen in N.F.L.", The New York Times, September 13, 2010. Accessed September 14, 2010.
On May 2, 2012, retired twelve-time Pro Bowler Junior Seau died of suicide from a gunshot wound to the chest. There was speculation that he had brain damage due to CTE.Smith, Michael David, "Boston researchers request Junior Seau's brain". NBC Sports Pro Football Talk, May 3, 2012. Retrieved 2012-05-03. Seau's family donated his brain tissue to the National Institute of Neurological Disorders and Stroke. On January 10, 2013, the brain pathology report was released, and Seau's brain showed evidence of CTE. Seven months after Seau's death, on December 1, 2012, Kansas City Chiefs linebacker Jovan Belcher killed his girlfriend, then drove to Arrowhead Stadium and killed himself in front of then-GM Scott Pioli and then-head coach Romeo Crennel. A year later, on behalf of Belcher's minor daughter, a family lawyer filed a wrongful-death lawsuit against the Chiefs, alleging that the team deliberately ignored warning signs of CTE, possibly leading to Belcher's suicide. The lawyer also hired a medical examiner to examine Belcher's brain for signs of CTE. On September 29, 2014, it was confirmed that he had CTE. Coverage of Belcher's murder-suicide, combined with the suicide of Junior Seau, drew national attention to CTE and its effects on the brains of football players.
In September 2015, researchers with the United States Department of Veterans Affairs and Boston University announced that they had identified CTE in 96 percent of National Football League players that they had examined and in 79 percent of all football players. By November 2016, 90 of 94 former NFL players had been posthumously diagnosed with CTE by McKee. Professional players diagnosed included eight-time Pro Bowler Lou Creekmur,Case Study: Lou Creekmur, Center for the Study of Traumatic Encephalopathy. Accessed August 17, 2010. Cookie GilchristGaughan, Mark (November 6, 2011). Gilchrist had severe damage to brain . The Buffalo News. Retrieved November 6, 2011. and Wally Hilgenberg.
In March 2016, former NFL running back Kevin Turner, who played for the New England Patriots and Philadelphia Eagles, died at age 46. Earlier, in 2010, he had been diagnosed with amyotrophic lateral sclerosis (ALS). But after his death, his brain was donated to Boston University Brain CTE Center, which diagnosed Turner with a severe case of CTE and stated that it was CTE, not ALS, that had killed him. However, there has been research into the connections of both CTE and ALS.
In April 2017, former New England Patriots tight end Aaron Hernandez died by suicide in prison at age 27. On September 21, 2017, an autopsy report from Boston University identified Stage 3 CTE in Hernandez's brain. Until Hernandez's autopsy, researchers had never seen Stage 3 CTE in a brain younger than 46 years old.Aaron Hernandez suffered from most severe CTE ever found in a person his age Adam Kilgore, The Washington Post, November 9, 2017
The Journal of the American Medical Association released an updated study in July 2017 reporting that out of 111 brains of deceased former NFL players studied, 110 (99%) had CTE. This also led to players retiring very early in their careers. As of December 2018, 87% of the 202 American football players' brains that have been donated to Boston University tested positive for CTE.
O. J. Simpson was suspected of having chronic traumatic encephalopathy before his death in 2024. After his death, Scientists had requested for Simpson's brain to be studied for signs of CTE, but the Simpson estate refused, who announced that his whole body will be cremated instead.
A recent 2024 study focusing on the quantitative characteristics of the brain in American Football players have identified structural brain differences in former American football players when compared to same-age men without a history of traumatic brain injury (TBI) or participation in sports. Former football players showed a minimization in the vivo cortical thickness and decreased cortical/subcortical volumes across brain regions.
The regions exhibiting reduced volume in former players included the superior frontal gyrus, entorhinal cortex, parahippocampal gyrus, insula, temporal pole, amygdala, and hippocampus. The study indicated that former professional players showed reduced volume in six regions: the entorhinal cortex, parahippocampal gyrus, insula, superior frontal gyrus, amygdala, and hippocampus. In contrast, unexposed former collegiate players showed reduced volume in only three regions: the superior frontal gyrus, amygdala, and hippocampus. These findings suggest that the intensity of exposure to football may be associated with alterations in brain structure.
League updates
In the early 20th century, a growing concern for the rising number of serious injuries and fatalities in football prompted calls for reform. In 1905, President Theodore Roosevelt held a meeting with representatives from Ivy League institutions to address the safety issues in college football. As a result, a series of rule changes were implemented to reduce dangerous collisions, legalize the forward pass, and grant officials greater authority to intervene in cases of injury. These safety reforms also led to the establishment of the Intercollegiate Athletic Association of the United States, which was later renamed the National Collegiate Athletic Association.
In 1939, the NCAA made it mandatory to wear helmets in college games. Before the instatement of this policy, it was optional to wear helmets, which usually meant the field was split half and half in terms of helmet or no helmet. This policy was instated due to concerns about safety and protection.
In 1964, the NCAA produced a policy that required football players to wear mouthguards during play. The mouthguard works to not only protect the teeth but also to prevent concussions by absorbing impact forces instead of letting force travel to the base of the skull and then consequently to the brain.