Read the full transcript of Brain expert Dr Emer MacSweeney’s talk titled “CTE: The Silent Killer In Contact Sports” at TEDxAthens 2022 conference.
Listen to the audio version here:
TRANSCRIPT:
The Impact of Contact Sports on Brain Health
DR EMER MACSWEENEY: Sport challenges and changes society unlike anything else. It is a culturally powerful, multibillion commercial industry that transforms lives, businesses, and nations. And whilst life comes with risk, contact sport heightens those risks, thrillingly so. But the early development of dementia, due to a condition known as CTE, almost unique to contact sports, is now the most feared risk for millions of amateur and professional athletes across the globe.
Despite the 2013 landmark multimillion NFL settlement for retired American football players with brain injury and the 2015 Will Smith movie “Concussion,” the fear and reality of dementia in contact sports is still not widely known. It is not adequately addressed, and it is not going away. We rely on experts to identify and explain these risks, but many have downplayed the reality. Consequently, too many players, coaches, parents, and fans remain unaware of what is now known. Let me share with you what we do understand today about brain injury and dementia in contact sports.
The History of CTE
The relationship between dementia and repetitive brain injury was known by the ancient Greeks. And a hundred years ago, the condition “punch drunk” was formally recognized as a complication of boxing. In 1940, the term chronic traumatic encephalopathy or CTE was introduced to describe a combination of symptoms including mood changes, memory loss, disturbance in thinking, leading eventually to dementia and arising from repetitive impact to the head. But medical scientists were not really able to progress their understanding of these symptoms until 2002 when Mike Webster, a brilliant athlete honored by the NFL Hall of Fame, died aged 50.
From his early forties, Webster’s behavior became increasingly strange. He became lethargic and angry. He threatened to kill strangers. When his teeth fell out, he stopped them back in with superglue, and he zapped himself with a taser gun to try to help him sleep. His cognition and his memory became increasingly worse, and he died with severe dementia.
The Discovery of Tau Protein
Doctor Bennet Omalu examined Webster’s brain. At first glance, there was no evidence of any brain injury. But when he looked inside his brain, he found an abnormal version of a protein called tau in regions of Webster’s brain responsible for mood, memory, and intellectual function. And this abnormal form of tau protein was identical to the tau protein that had been found in boxers who had died with dementia.
Doctor Omalu then searched and found the same protein in other contact sports players who had died with dementia at an early age. And somehow, in each case, the normal healthy tau protein, which is designed to protect the brain cells, had changed into this new harmful version capable of spreading through the brain relentlessly killing more and more brain cells.
Given the similarity between this abnormal tau protein and the abnormal protein found in Alzheimer’s disease and other dementias, scientists realized that this disease, CTE, in Webster’s brain was progressive and, like Alzheimer’s, had most likely started many years before Webster developed even his first symptoms.
This same year, 2002, Jeff Astle, a famous English soccer player, died with severe dementia aged 59. Examination of his brain confirmed CTE. An intense debate linking heading of the ball in soccer to CTE commenced. Over the next decade, it was wrongly assumed that CTE was a very rare condition affecting only professional boxers, American football players, ice hockey and soccer players and that it started late in the player’s career.
The Tragic Case of Zach Easter
Then in 2015, a very significant event occurred. Zac Easter suspected he had CTE. Zac had started playing American football at 8, but by 11th grade, he started to complain of headaches. Shortly after, problems with his memory, then slurred speech, mood swings, and depression. He developed dependency upon drugs to try to manage his declining brain function.
Zac stopped playing contact sports at 18. Then at age 24, Zac wrote a suicide note to his parents explaining that he wanted his brain to be examined after his death to help future players. Then Zac shot himself in the chest. Doctor Omalu examined Zac’s brain, and he found advanced CTE. This tragic event prompted new questions. How early does CTE actually develop, and why? And why does it affect some but not all players?
Recent Discoveries in CTE Research
In 2020, answers started to emerge. Doctor Ann McKee, director of Boston University’s Brain Bank, confirmed a strong positive link between the cumulative dose of head impact in contact sports and the subsequent development in life of problems with extreme behavior, memory loss, and other cognitive symptoms. And players with confirmed CTE after life were ten times more likely to have played American football for more than 14.5 years. And for every additional year played, the odds of having CTE after life increased by 30%.
Separately, studies found children who started playing American football under the age of 12 grew up to have worse thinking and learning ability than their peers who started playing after their 12th birthday. And this is not too surprising as a critical and dynamic period of brain development occurs between the ages of 9 and 11.
The Role of Subconcussive Impacts
The next critical discovery was possibly the least expected. That is that the risk and severity of CTE is not caused primarily by the single big hit concussions but by multiple smaller subconcussive impacts to the head and body. And 20% of people diagnosed with CTE after life had never had a single recorded concussion. Failure to grasp this critical discovery is too common, and it presents a huge issue in understanding how we tackle CTE.
So it is crucial to understand the difference between a concussion and a subconcussion.
A concussion occurs when the force of impact to the brain is sufficient to cause an acute brain injury with symptoms: headache, brain fog, irritability, slowed reaction time. Quite different from a subconcussion, a lower force of impact, which damages brain cell function but does not cause any symptoms. So these impacts go largely unnoticed.
And the force to the brain to cause a concussion is about two to four times greater than a subconcussion, but subconcussions are more than 500 times more frequent. Whilst a single concussion is never a good idea and can be life-changing, so too are multiple repetitive subconcussions.
The Vulnerability of Young Brains
And how resilient is the brain to these lesser impacts? Well, in 2016, the Wake Forest report shed some light on the danger of subconcussions by demonstrating evidence of structural brain injury in a group of 8 to 12-year-olds playing American football for just one season. Whilst no child received a concussive impact, each child received an average of about 200 subconcussions. And the higher the cumulative dose of subconcussive impact, the greater the degree of structural brain injury.
Remember Zac, started playing American football at 8, developed symptoms of CTE by 11. Now compare the number of subconcussive impacts with NFL players who receive in one season between 1,000 and 1,500 subconcussive impacts. And in rugby union and rugby league, this number is significantly higher.
This frequency of subconcussive hits explains why CTE is ten times more common in rugby and American football players and symptoms begin in their thirties to forties compared to soccer players where CTE begins in their fifties or later. And whilst the intense focus on dementia in soccer has been related to heading the ball, it is not widely known that only 13% of all subconcussions in soccer are actually due to head-to-ball impact. So CTE in football or soccer is so much more than heading the ball.
Women in Contact Sports
Now what about women in sport? Almost no women’s brains have been studied until two years ago when superb athlete and Aussie rules football player, Jacinda Barclay, took her own life aged 29 after short intense mental illness. Her parents donated her brain to sports injury research.
Jacinda’s brain demonstrated a degenerative disease known to be associated with the development of mental illness and suicide. And whilst not CTE, the degenerative changes were attributed 100% to the multiple head impacts. And the same degenerative disease has been found in other players, some of whom have played only one season of contact sports. Jacinda had only one reported serious concussion during her career.
So given the significant increase in the participation of girls and women in contact sports, they too now face a very real and serious risk of CTE.
The Mechanism of CTE
So why is CTE primarily the result of numerous unnoticed minor head impacts? The brain is the most sophisticated and complex thing on the planet, and it has, of course, evolved self-protective mechanisms to respond effectively to one or two impacts. But when the brain is subjected to multiple impacts, especially the dangerous rotational forces from angled hits, the brain rotates inside the skull and eventually the delicate nerves and tiny blood vessels are torn.
A protective structure, the blood-brain barrier, is disrupted, and the normal protective neurochemical response to a single impact is massively exaggerated. This triggers a huge inflammatory harmful response, which instead of protecting, it damages the brain cells and leads eventually to the accumulation of abnormal tau protein.
The Global CTE Iceberg
We are at the tip of a global CTE iceberg, and three critical areas of focus are required: brain protection, CTE diagnosis in life, and treatment.
Brain Protection
Firstly, brain protection for every player. We need effective interventions to reduce the number and force of both concussions and subconcussions. Instrumented mouth guards identify concussions and detect silent concussions. Whilst removing a player from the pitch with a concussion is accepted practice now, removing a player with a cumulative dose of subconcussions is unlikely to be popular or even practical when the player has no symptoms. And whilst collecting the data is important, the threshold dose to direct removal of a player with subconcussions is not yet known.
Immediate on-pitch sideline assessment, eye movements, saliva tests, and others may facilitate identification of a concussion but are irrelevant to subconcussions. Changes in the rules and style of play are also underway but controversial, dependent upon compliance and monitoring, unpopular with fans, and not working for subconcussions.
Protective headwear sounds like an obvious solution. Ironically, the hard helmet increases rotational forces to the brain by permitting greater impact as the skull is protected from fractures, but the brain is not protected and receives the full force of the impact. Effective brain as opposed to skull protection is desperately needed.
A new product, Reason Halos, entered the market earlier this year. Reason Halos is the only legal CE marked protective headband in the UK and Europe, and it is designed specifically to decrease by at least 60% all rotational forces to the brain. Often, it is the simple but fit-for-purpose items like seatbelts that make the most sense and hopefully a big difference.
Diagnosis
Secondly, diagnosis. The mantra that CTE can’t be diagnosed in life with meaningful clinical accuracy is simply no longer true. Our team at Re:Cognition Health and King’s College London have demonstrated evidence of brain injury consistent with CTE in one of the biggest groups of retired contact sports players globally using our novel sophisticated MRI DTI sequences. For these individuals with CTE, the diagnosis is instantly life-changing. Our discovery, however, is groundbreaking. It now creates the possibility to provide potential treatments for CTE.
Future Treatments
Which takes me to future treatments. Given the billions already invested to develop new treatments to remove abnormal tau protein in Alzheimer’s and other dementias, surely, we can use some of these potential treatments for CTE too. At Re:Cognition Health, we are starting to do exactly this under special early access drug license. We will provide HMTM, a potential new treatment for Alzheimer’s, to a number of the ex-professional contact sports players in whom we have confirmed evidence of brain damage consistent with CTE. HMTM was developed by Professor Claude Wischik, cofounder of TauRx Therapeutics.
Our objective for the first time ever is now to try to halt or at least slow progression of CTE symptoms.
Conclusion
We cannot escape that CTE is a complex global political scientific challenge, which is just about to be understood in sport and probably should no longer be considered as a great unknown. And by focusing on brain protection, CTE diagnosis in life, and treatment, we will change the future. And if this TED Talk has caused one parent, one coach, or one player to think differently about how they protect their brain in contact sports, it will have served its purpose. Thank you.
