Last month, a Victorian coroner found that AFL veteran Danny Frawley – who took his own life in 2019 – was suffering from a little-understood degenerative brain disease linked to repeated blows to the head.
The disease, chronic traumatic encephalopathy (CTE), can only be diagnosed post-mortem – and is almost exclusively found in retired professional contact sports people, notably boxers and footballers.
It presents as a form of dementia with marked changes in behaviour and mood.
Coroner Paresa Spanos revealed that a post-mortem analysis of Frawley’s brain found he had low-stage CTE – and noted that it was “difficult to evaluate the contribution of CTE to personality, behaviours, any cognitive deficits, or emotion over a lifetime.”
However, the coroner found that CTE was a potential contributor to the depression that Frawley suffered in the years preceding his death – and recommended that AFL footballers be encouraged to donate their brains to science to further CTE research.
Frawley – popular player, coach and commentator – died at the age of 56.
In January, a post-mortem found that Richmond veteran and boxer Shane Tuck – who took his own life last year – had suffered from severe CTE. Tuck was also said to have struggled with his mental health.
Neuropathologist Michael Buckland reportedly described it as “the worst case I’ve seen so far”. Tuck was 38 when he died.
Last year, a post-mortem revealed that football legend Graham “Polly” Farmer suffered with CTE. And in 2019 two former professional rugby league players, not identified, were found to have died with the disease.
So how many footballers are incubating or suffering with the disease? What can be done to prevent it?
Is it a rare disease – or just rarely diagnosed?
Associate Professor Michael Buckland is the Head of the Department of Neuropathology at Royal Prince Alfred Hospital, Head of the Molecular Neuropathology Program at the Brain & Mind Research Institute, and Co-Director of the Multiple Sclerosis Research Australia Brain Bank. He is also the Executive Director of the Sports Brain Bank.
Professor Buckland said the incidence of CTE in Australia is unknown – and studies done overseas still amount to rough calculations.
In the wider population, he said, “the risk is almost zero”
He said it was “hard to get really tight incidence figures, because at the moment it can only be diagnosed at post-mortem.”
And people who are motivated to donate their brains to the brain bank do so if they or their family think that something is wrong.
“So there’s a selection bias in the brain bank cohorts,” he said.
Otherwise, it’s complicated because “technically, any neurodegenerative disease requires post-mortem confirmation, but mostly these days that doesn’t happen,” he said.
“If you get a diagnosis from a qualified neurologist, 80 to 90 per cent of the time it’s correct in the general population.”
But if you took out those who have had repetitive knocks to the heads, contact sports athletes, “half of those diagnoses would turn out to be CTE if you looked at them under the microscope.”
Professor Buckland cited a study in the UK which looked at the death certificates of soccer players in the Scottish league: 7500 of them over a large period of time.
The researchers also looked at a control population, people of a similar profile to the soccer players, except they weren’t contact-sports professionals.
“They found the rate of Alzheimer’s being listed on the death certificate was three to fours times higher than the general population,” Dr Buckland said. “So many of those may be CTE, but we don’t have enough data to be definitive about anything.”
He said: “I’ve seen estimates of 1 per cent, and estimates of 20 per cent.”
The best guesstimate appears to come from the Boston Brain Bank.
And helmets are no protection
In 2017, US neuropathologists examined the brains of 202 deceased former football players. Keeping in mind that these brains were donated because of a suspicion that something was wrong, the results were startling. CTE was found in the following:
- Three out of 14 men (21 per cent) who’d played grid iron at high school
- 48 of 53 (91 per cent) college players
- 9 of 14 semiprofessional players (64 per cent)
- 7 of 8 Canadian Football League (88 per cent)
- 110 of 111 National Football League players (99 per cent).
When the NFL deaths recorded in the brain were compared to all ex-NFL player deaths that had occurred “over an eight to 12-year period” it worked out that “around 10 per cent in professional American footballers had CTE.”
These results are more suggestive than conclusive. “They’re back of the envelope calculations really,” Professor Buckland said.
Thousands of little knocks to the head
There are two kinds of injuries that occur. One is the classic back-and-forth movement of the brain that you see in car accidents – where the brain keeps travelling until it collides with the skull.
But rotational injuries may be worse than back and forth, Professor Buckland said.
This is where the head rotates to the side, “stretching and tearing” the brain.
These are predominately sub-concussive knocks from tackles and falls.
Associate Professor Alan Pearce is a La Trobe University neurophysiologist with a primary research focus on sports-related concussion. He’s a colleague of Michael Buckland: Dr Pearce manages the Victorian arm (launched in December) of the Australian Sports Brain Bank.
He told The New Daily that experiments with sensors have shown that footballers receive about 50 of these knocks to the head per contact training session, and per game. These sensors, accelerometers, have a threshold of 10G – meaning they’re not triggered for knocks of less than 10 times the force of gravity.
“When you multiply that over every contact training session and every match played over many years, that’s thousands of accumulated knocks to the head,” Dr Pearce said.
What happens to these brains?
Professor Buckland said the “typical scenario” is the player retires from contact sport with no symptoms, lives through a “latency period” that can last several to many years.
Older retired players with CTE then present with an Alzheimer’s-like dementia “but with more pronounced behavioural changes than a standard Alzheimer’s case.”
Others simply present with “more florid behaviours.”
Some of the symptoms associated with CTE include memory and thinking problems, confusion, personality changes and erratic behaviour including aggression, depression and suicidal thinking.
CTE is a progressive disease, characterised by a build-up of the abnormal tau protein that’s also found in Alzheimer’s patients.
What’s the mechanism that links multiple bruising to a progressive brain disease? “No one really knows,” said Professor Buckland. “The seeds are sown through a period of repetitive head knocks.”
In some people, like Tuck, the disease takes off pretty quickly “like a bushfire.”
In others, “it smoulders along for years. And some may have a normal life and experience a tau accumulation at the end.”
If there’s any silver lining here, it’s that CTE “is the only neuro-degenerative disease where we have a strong association between an exposure to something and later life disease.”
And because the tau protein builds up in Alzheimer’s disease and also frontal-temporal dementia, “it may give us insights into what’s going on in other neurodegenerative diseases.”
What are the football codes doing to prevent CTE?
The AFL has changed their return-to-play policies such that concussed players showing obvious symptoms are sat out from the game for 12 days.
“That’s good for concussion management,” said Professor Buckland. “Whether it’s enough is an open question.”
But it doesn’t address all those little accumulating knocks.
Should professional careers have a fixed term?
“It’s one way to do it,” he said.
While he’s not a fan of “prescriptive measures,” he has suggested that putting a minimum age on children starting a contact sport needs to be considered.
He points out that footballers who began playing before the age of 12 tend to end up with worse CTE than those who start later.
He’s also suggested that changing the way training is structured could help reduce sub-concussive exposure.
“The American Players Association got together and demanded limits to full contact training,” he said. “If you reduce full contact in training sessions, you potentially reduce by half your life-long exposure.
“Without making any changes to the game, that seems to be a smart thing to do. I’m not an expert in the game, and how you train for it, but it seems to be working in America.”
Professor Alan Pearce is blunt in his assessment of where things may go if serious change isn’t implemented.
“CTE could prove to be an existential threat to professional sport.”
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