CHRONIC TRAUMATIC ENCEPHALOPATHY AND THE NFL By
NIKKI KASAL JUI MALWANKAR (Editor)
Daniel Te’o-Nesheim, a former University of Washington football player who played for both the Philadelphia Eagles and Tampa Bay Buccaneers, was only thirty years old when he was found dead at a friend’s house in in October 2017 of an apparent overdose. He was later posthumously diagnosed with chronic traumatic encephalopathy, or CTE, a degenerative brain disease linked to repetitive cranial trauma. Prior to his death, Te’o-Nesheim was suffering extensive pain from the injuries caused by half a lifetime of tackle football, including bone spurs, ankle and shoulder surgery, and chronic headaches. As his doctors prescribed ever-increasing amounts of painkillers, he became paranoid and withdrawn – a complete transformation from his friendly, family-oriented personality. He forgot purchases he had made on his credit cards, insisted he was being followed, and made worrisome phone calls to his family from unknown numbers. His sister, Marie, remembers him as distracted, overwhelmed, and dismissive. “It was scary and we tried to reach out, but could not get him to open up,” she confided in a New York Times article in May of this year. Eric Kaufman, Te’o-Nesheim’s former agent, was also among those close to the football player and privy to the direct effect of his downward mental spiral on his career. “Without a doubt in my mind, all of these were early signs of CTE,” says Kaufman. Te’o-Nesheim did apply for “line of duty” benefits given to football players suffering extensive physical injuries early in 2017; however, his request was turned down because his injuries were not considered severe
28 || pulse
enough. Less than a month later, he spent the evening at a friend’s house drinking vodka and talking. After going to sleep in one of the bedrooms for the night, he was found the next morning unresponsive and declared dead of overdose. Te’o-Nesheim had made arrangements to donate his brain to science right before his death; therefore, a subsequent microscopic examination of his frontal lobe revealed a “surprising and disturbing” amount of lesions for “a guy who was just 30,” according to Ann McKee, neuropathologist and expert in degenerative neurological disease at Boston University. Though Te’o-Nesheim’s tragic case was not the most severe manifestation of CTE, it nonetheless was an all-too-common hallmark of one of the most acute yet widely disregarded problems in professional football. CTE is defined by the Concussion Legacy Foundation as “a degenerative brain disease found in athletes, military veterans, and others with a history of repetitive brain trauma.” Football players are particularly affected: in fact, according to a 2018 study from the VA-BU-CLF Brain Bank at Boston University, 94% of college and/or professional football players have been diagnosed with CTE. Its molecular basis is characterized by a protein called tau, which helps to support microtubule networks in neurons in a healthy brain. However, when microtubules break down due to repeated trauma, these tau proteins break free and form clumps in the brain. Eventually, these clumps begin to grow independently in a process called prion spread, at which point they can damage and interfere with regular brain func-
