Last month, a Victorian coroner discovered that AFL veteran Danny Frawley, who committed suicide in 2019, suffered from a poorly understood degenerative brain disease that resulted in repeated blows to the head.
The disease, chronic traumatic encephalopathy (CTE), can only be diagnosed post mortem – and occurs almost exclusively in retired professional contact athletes, especially boxers and soccer players.
It presents as a form of dementia with marked changes in behavior and mood.
Beloved AFL player, coach and commentator Danny Frawley struggled with his mental health in later years. Maybe CTE was to blame. Photo: Getty
Coroner Paresa Spanos revealed that an autopsy of Frawley’s brain found he had a low CTE – and that it was “difficult to assess the CTE’s contribution to personality, behavior, cognitive deficits, or emotions over the course of a lifetime.”
However, the coroner noted that CTE was a potential contributing factor to the depression Frawley suffered in the years before his death – and recommended encouraging AFL footballers to donate their brains to science to advance CTE research.
Former Richmond player Shane Tuck was knocked out by Lucas Miller at the Melbourne Convention and Exhibition Center on November 11, 2015. CTE is almost entirely limited to boxers and soccer players. Photo: Getty
Frawley – popular player, coach and commentator – died at the age of 56.
In January an autopsy found that Richmond veteran and boxer Shane Tuck, who took his own life last year, had suffered from severe CTE. Tuck is also said to have struggled with his sanity.
Neuropathologist Michael Buckland reportedly described it as “the worst case I’ve seen”. Tuck was 38 when he died.
Last year, an autopsy revealed that soccer legend Graham “Polly” Farmer had CTE. And in 2019, two former rugby professional players who were not identified were found to have died of the disease.
How many soccer players are incubating or suffering from the disease? What can be done to prevent this from happening?
Is it a rare disease – or is it rarely diagnosed?
Associate Professor Michael Buckland is Director of Neuropathology at Royal Prince Alfred Hospital, Director of the Molecular Neuropathology Program at the Brain & Mind Research Institute, and Co-Director of the Australia Brain Bank for Multiple Sclerosis Research. He is also the executive director of Sports Brain Bank.
Professor Buckland said the incidence of CTE in Australia is unknown – and studies done overseas are still crude calculations.
In the wider population, he said, “the risk is almost zero”
As illustrated here, the damage to a brain from CTE is significant and ultimately catastrophic. Image: Ema Osavkov
He said it was “difficult to get really narrow incidence numbers as these can only be diagnosed post mortem at this time”.
And people who are motivated to donate their brains to the brain bank do so when they or their family think something is wrong.
“So there is a selection bias in the brain bank cohorts,” he said.
Otherwise, it’s complicated because “technically every neurodegenerative disease requires post-mortem confirmation, but mostly not these days,” he said.
“If you get a diagnosis from a qualified neurologist, 80 to 90 percent of the time in the general population it will be correct.”
However, if you take out those who have repeatedly knocked on the heads, then turn to athletes. “Half of those diagnoses would turn out to be CTE if you looked at them under a microscope.”
Professor Buckland cited a study in the UK that looked at the death certificates of football players in the Scottish League: 7,500 of them over a long period of time.
The researchers also looked at a control population, people with a profile similar to the soccer players, except that they were not contact sports professionals.
“They found that the Alzheimer’s rate, which is listed on the death certificate, was three to four times higher than the general population,” said Dr. Buckland. “So many of these may be CTE, but we don’t have enough data to be definitive on anything.”
He said, “I’ve seen estimates of 1 percent and estimates of 20 percent.”
The best estimate seems to come from the Boston Brain Bank.
And helmets are not protection
In 2017, US neuropathologists examined the brains of 202 deceased former soccer players. Given that these brains were donated because there was a suspicion that something was wrong, the results were astounding. CTE was found in the following:
- Three out of 14 men (21 percent) who played grid iron in high school
- 48 out of 53 (91 percent) college players
- 9 out of 14 semi-professional players (64 percent)
- 7 out of 8 Canadian Football League (88 percent)
- 110 out of 111 National Football League players (99 percent).
When NFL brain-recorded deaths were compared to all former NFL player deaths that occurred “over a period of eight to 12 years,” it found that “around 10 percent of American professional footballers had a CTE.”
These results are suggestive rather than conclusive. “You really are back from the envelope calculations,” said Professor Buckland.
Thousands of small blows to the head
There are two types of injuries that occur. One is the classic back-and-forth motion of the brain you see in car accidents – where the brain travels until it collides with the skull.
But rotational injuries can be worse than going back and forth, said Professor Buckland.
Here the head turns to one side and “stretches and tears” the brain.
Two types of impact damage the brain. The classic front-to-back movement in car accidents. But more damaging is rotary tapping, which is where the brain spins and tears. Image: Ema Osavkov
These are predominantly subconcussive hits from duels and falls.
Associate Professor Alan Pearce is a neurophysiologist from La Trobe University with a research focus on exercise-related concussions. He is a colleague of Michael Buckland: Dr. Pearce manages the Victorian arm of the Australian Sports Brain Bank, launched in December.
He told The New Daily that experiments with sensors have shown that footballers receive around 50 of these head blows per contact training session per game. These sensors, accelerometers, have a threshold of 10G – which means they won’t fire for shocks less than ten times the force of gravity.
“If you multiply that over every contact training session and game that has been played over many years, that’s thousands of accumulated blows to the head,” said Dr. Pearce.
What happens to these brains?
Professor Buckland said the “typical scenario” is that the player withdraws from contact sports with no symptoms and experiences a “latency period” that can last several to many years.
Older retired players with CTE then suffer from Alzheimer’s-like dementia, “but with stronger changes in behavior than in a normal Alzheimer’s case”.
Others simply present themselves with “more florid behaviors”.
CTE is a progressive disease. Like Alzheimer’s, it is characterized by an accumulation of the abnormal tau protein in the brain. Image: Ema Osavkov
Some of the symptoms associated with CTE are memory and thinking problems, confusion, personality changes, and erratic behavior, including aggression, depression, and thoughts of suicide.
CTE is a progressive disease characterized by the build-up of the abnormal tau protein, which is also found in Alzheimer’s patients.
What is the mechanism that links multiple bruises to progressive brain disease? “Nobody really knows,” said Professor Buckland. “The seeds are sown through a period of repeated head butts.”
In some people, like Tuck, the disease worsens “like a bushfire” fairly quickly.
In other cases, “it smoulders for years. And some may have normal lives and end up with dew buildup. “
If there is a silver lining here, then CTE is “the only neurodegenerative disease where we have a strong association between exposure to something and a later life disease.”
And because the tau protein accumulates in Alzheimer’s disease and also in frontal-temporal dementia, “it can give us insights into what is going on in other neurodegenerative diseases.”
What do the soccer codes do to prevent CTE?
The AFL has changed its return-to-play policy to exclude affected players with obvious symptoms from playing for 12 days.
“This is good for concussion management,” said Professor Buckland. “Whether it is enough is an open question.”
But it’s not about all of those little accumulating shocks.
Should professional careers have a fixed duration?
“It’s a way of doing it,” he said.
While not a fan of “regulation”, he has suggested that consideration should be given to a minimum age for children starting contact sports.
He points out that footballers who started playing before age 12 tend to have a worse CTE than those who start later.
He has also suggested that changing the structure of training could help reduce subconcussive exposure.
“The American Players Association has come together and set limits for extensive contact training,” he said. “If you reduce full contact in workouts, you may be reducing your lifetime exposure by half.
“Without making any changes to the game, it seems like a smart thing to do. I’m not an expert on the game and how to train for it, but it seems to work in America. “
Professor Alan Pearce is blunt in his assessment of where things could go if serious changes are not made.
“CTE could prove to be an existential threat to professional sport.”