In a note that police found in his wallet, the gunman who killed four people in New York on Monday claimed he had chronic traumatic encephalopathy (CTE) — a result of playing [American] football in high school.CTE is a degenerative brain disease linked to repeated brain trauma. It can lead to debilitating symptoms such as depression, memory loss, aggression, impared judgment, erratic behaviour, suicidal tendencies, anxiety, and dizziness.The disease is most commonly diagnosed among athletes, especially those in contact sports, and has been referred to in recent years as a “silent epidemic” because it often goes undiagnosed and its causes are underplayed.Accumulated traumaCTE is not caused by a single blow to the head — rather, it is the result of the accumulation of years of concussive and sub-concussive impacts that lead to noticeable and progressively debilitating symptoms over time. (Concussions cause the brain to move rapidly within the skull, potentially stretching and damaging brain cells.)The “repeated blows to the head… injure the brain’s cells and blood vessels, [creating] areas of microscopic bleeding and abnormal protein deposits called tangles, which kill brain cells”, says an article on the website of the Harvard Medical School.Researchers have estimated that around 17% of people with years of repetitive concussions or sub-concussive incidents will develop CTE, the article says. The disease can only be definitively diagnosed after death, during autopsy.‘Punch drunk’ in boxingGreek physician-philosopher Hippocrates (460-377 BCE) described commotio celebri — ‘commotion of the brain’ — as a vigorous shake or blow to the head that caused temporary loss of speech, hearing, and sight.Story continues below this adIn the 16th century, the Italian physician Jacopo Berengario da Carpi proposed that this ‘brain commotion’ was caused by the brain getting ‘bruised’ after hitting the skull.While da Carpi’s understanding of what we now refer to as a concussion was largely accurate, scientists remained unsure until the early 20th century whether such injuries had any long-term impacts.Then, in 1927, neuropsychiatrists Michael Osnato and Vincent Giliberti published a paper in the Journal of the American Medical Association (JAMA) that stated that a concussion was not a “transient state” — it could lead to “structural cerebral injury”, causing significant “secondary degenerative changes”.Harrison Martland, a forensic pathologist and boxing enthusiast, immediately linked these findings to the antics of many popular boxers at the time. “Fans called them “cuckoo”, “goofy”, or “slug nutty”, and people enjoyed screaming at them as they staggered around the ring like intoxicated fools,” an article in The Atlantic said.Story continues below this adMartland coined the term “punch drunk” to describe this disease that afflicted pugilists. “Punch drunk most often affects fighters of the slugging type…who are usually poor boxers and who take considerable head punishment, seeking only to land a knockout blow,” he wrote in his 1928 submission to JAMA.Martland’s claims would be clinically proven in 1973, when neuropathologist J A N Corsellis cracked open the skulls of 15 former boxers and studied their brains under a microscope. In his paper, ‘The Aftermath of Boxing’, published in Psychological Medicine, Corsellis provided detailed descriptions of damage to the brain tissue of the deceased boxers, and coined the term “dementia pugilistica” to refer to the disease.The Webster caseBut there was still not much mainstream conversation about CTE. Also, the condition was framed as being explicitly boxing-specific. It was not until the 2000s that the scale of the problem began to be understood.A pivotal moment in this story was the death — and subsequent diagnosis — of the legendary Pittsburgh Steelers centre Mike Webster in 2002. Webster died after a heart attack, but he had displayed years of erratic behaviour after his retirement from pro football.Story continues below this ad“One day he peed in the oven… He would walk up to strangers and rant. “Kill ’em! I’m gonna kill ’em!… His teeth started falling out. He got Super Glue, squirted each fallen tooth, and tried to stick them back in…,” The Atlantic article said. When pathologist Bennet Omalu examined Webster’s brain under a microscope, his findings echoed those of Corsellis some 30 years back.The Webster case triggered a lot of CTE research, and eventually led to the National Football League (NFL) acknowledging the link between football and the disease. As research expanded beyond traditional combat sports like boxing, researchers found that even seemingly minor hits had major long-term repercussions.“When you expose your head to long-force trauma with or without a helmet, with or without symptoms, there is a significant risk of permanent brain damage 40 years later,” Omalu told the BBC in 2015.No silver bulletGrowing awareness of CTE has led to many reforms in sport. NFL rules have been modified to better protect players from head trauma, England’s Football Association (FA) has banned youth players from deliberately heading the ball, and cricket has introduced the concept of a “concussion substitute”.Story continues below this adBased on our current understanding, however, the risks of CTE can at best be mitigated, not eliminated. Over the past couple of decades, researchers have experimented with all kinds of equipment from helmets to mouthguards to mitigate the risk of CTE among players. Research has looked at woodpeckers, birds that drill into trees without getting concussions.There is currently no treatment or cure for CTE. Athletes in certain sports remain at high risk. In 2023, Boston University’s CTE Center studied 376 former NFL players, and diagnosed as many as 345 with CTE.