What to Know About C.T.E. in Football (2023)

Chronic traumatic encephalopathy, or C.T.E., has affected boxers since the 1920s, but it surged into the national consciousness in 2007, when The New York Times reported that Andre Waters sustained brain damage from playing football, which led to his depression and ultimate death by suicide.

The degenerative brain disease associated with repeated blows to the head has been found in the brains of more than 320 former N.F.L. players, Waters the third but whose death brought the condition into the mainstream. The group includes at least 24 players who died in their 20s and 30s, according to Dr. Ann McKee, a neuropathologist and the director of the C.T.E. Center at Boston University.

Junior Seau, 43, Waters, 44, and Dave Duerson, 50, were all found to have C.T.E. after their deaths by suicide, as were Jovan Belcher, 25, a linebacker for the Kansas City Chiefs who killed his girlfriend before shooting himself in 2012; Aaron Hernandez, 27, a former New England Patriots tight end who died by suicide after being convicted of a 2013 murder; and Phillip Adams, 32, an N.F.L. defensive back who shot and killed six people in April 2021 before dying by suicide.

Vincent Jackson, a longtime receiver with the San Diego Chargers and Tampa Bay Buccaneers who was found dead in February 2021, was determined to have had a mild form of C.T.E. Demaryius Thomas, a former receiver for the Denver Broncos, was diagnosed with it after his death in December 2021.

Here’s what to know about C.T.E.

What is C.T.E.?

C.T.E., which can be diagnosed only posthumously, has been linked to a host of symptoms, including memory loss, depression, aggressive behavior and, sometimes, suicidal thoughts. It is a progressive disease, and the symptoms can arise long after the hits to the head have ceased.

Although the condition has come to be most often associated with football players, C.T.E. has been found in the brains of boxers, hockey players, soccer players, a bobsledder, and other athletes.

Doctors at the C.T.E. Center have found the disease in more than 90 percent of the brains of N.F.L. players that they have examined, and many more brains are waiting to be diagnosed.

Do concussions cause C.T.E.?

Diagnosed concussions are not reliable indicators of C.T.E. About 20 percent of people found to have C.T.E. never had a diagnosed concussion, according to doctors at the C.T.E. Center at Boston University, who analyzed Jackson’s brain.

More predictive, studies have shown, are the smaller, repeated blows to the head that do not cause symptoms, known as subconcussive hits. The severity of C.T.E., studies have shown, is exacerbated by the length of a football player’s career.

What does C.T.E. look like in the brain?

In the brains of people with C.T.E., a naturally occurring protein, known as tau, builds up over time in certain patterns. The clumps of tau strangle brain cells, diminishing their ability to function before killing them entirely. C.T.E. often affects the dorsolateral frontal cortex, an area critical for cognition and executive function, including working memory, planning and abstract reasoning.

What are the stages of C.T.E.?

Dr. McKee developed a staging system, ranging from mild (stage 1) to most severe (stage 4), to codify the pathology of C.T.E. Although general trends exist, there isn’t a clear delineation of symptoms within those stages, said Chris Nowinski, the co-founder and chief executive of the Concussion Legacy Foundation.

“The brain is 86 billion neurons,” Nowinski said in a telephone interview. “We’re talking about somewhat microscopic lesions here and there. The location of the lesions and how your brain is wired will probably have more of an impact than the staging. A lesion that’s a millimeter in the other direction could be the difference between normal behavior and impaired behavior.”

Stage 1 is the earliest sign of C.T.E. The lesions are found primarily in the frontal lobe, and symptoms often include slight memory loss. In Stage 2, the lesions spread to the adjacent cortex, continuing their assault on memory. Frontal lobe damage, Nowinski said, is well-known to be associated with concentration, cognition and impulse control issues. The examination of Adams’s brain, which was found to have Stage 2, indicated an abnormally severe diagnosis for a person in his 30s, akin to that found in Hernandez, whom McKee diagnosed with Stage 3, in which the lesions have taken over the medial temporal lobe, affecting the hippocampus and amygdala, and causing impulsive, violent reactions; paranoia; and the erosion of memory.

In Stage 4, when the C.T.E. has spread to multiple parts of the brain, Nowinski said, the vast majority of people have been clinically diagnosed with dementia. He said that 13 years tends to elapse between stages and that people over 60 with C.T.E. almost always are found to have Stage 3 or 4.

What has been C.T.E.’s impact on the N.F.L.?

The Hall of Fame center Mike Webster was the first N.F.L. player found to have had C.T.E., with the result published in a scientific journal three years after his death in 2002. More than 320 former players, including Ken Stabler and Frank Gifford, who have been posthumously diagnosed with C.T.E. Researchers at Boston University announced in a 2019 study that tackle football players doubled their risk of developing the worst forms of C.T.E. for each 5.3 years they played.

For many years, the N.F.L. denied any connection between long-term brain damage and blows to the head until confronted with overwhelming scientific evidence. After a class-action lawsuit brought by former players surfaced, the league agreed to a roughly $1 billion settlement; the N.F.L. has since agreed to stop using race-based methods in evaluating dementia claims that denied benefits worth potentially hundreds of thousands of dollars to Black players.

In 2016, a league official, speaking in Congress, acknowledged for the first time a connection between the disease and football.

In response to the rising prevalence of C.T.E., the N.F.L. has developed intensive protocols for players who have, or show signs of, a head injury. The league installed a head-injury spotter in the press boxes of all games; doctors and neuro-trauma specialists on the sideline; and experts in neuro-cognitive testing in the locker room. The league has also strengthened rules against hitting quarterbacks and players who lower their helmets to initiate contact.

The N.F.L. has invested hundreds of millions of dollars in helmet and concussion research, and even staged a $3 million grant competition intended to improve helmet performance and safety. According to the league, 99.9 percent of players wore what it considered a “top-performing helmet” last season, and it is hoped that position-specific helmets will be introduced soon.

The increased awareness of head injuries has prompted some players to willingly remove themselves from games and others, such as the former linebackers A.J. Tarpley and Chris Borland, to retire, citing safety concerns.

Can C.T.E. be treated?

There is no known cure for C.T.E., and since it cannot be accurately identified within the brains of people who are living, the disease itself cannot be treated. But medication and certain therapies can help manage symptoms and regulate moods and behavior. And researchers are developing blood biomarkers and PET scans that they hope can be used to identify the disease in players while they’re alive.