This article contains subject matter some readers may find distressing. If you or someone you know needs help with mental health, contact Lifeline on 13 11 14 and Beyond Blue on 1300 224 636. Red Nose Australia provides 24/7 bereavement and counselling services for those affected by the loss of a child on 1300 308 307.
Chronic Traumatic Encephalopathy – or CTE – is a neurodegenerative disorder that is gaining increasing attention in light of high-profile cases being diagnosed among former athletes.
Neurodegenerative diseases are a range of issues that result in the break down of neurons (brain cells), often due to genetic or environmental factors, but sometimes with no known cause.
In July, the late Heather Anderson became the first former female athlete diagnosed with CTE after an autopsy showed she suffered from mild symptoms.
Anderson played in the inaugural season of the semi-professional Australian Football League women’s competition and was a medic in the Army.
Footballers – of all codes – are among the highest-profile cases. That’s because CTE is linked with concussion, head injury and repeated head impact.
CTE is similar to other neurodegenerative disorders like Alzheimer’s disease, but the disease is in focus because current and former professional athletes are increasingly concerned neurological and cognitive symptoms they are experiencing are signifying they have the disease. This has led to class actions in Australia and around the world. There are also concerns among amateur athletes about the long-term risks of sport participation.
However, neuroscientists around the world have studied the impact of mild traumatic brain injury (mTBI) in a range of settings – not just pro sportspeople. Motor accident victims, military personnel and domestic violence victims are among those who may suffer from mTBI.
But working out whether a person has CTE is not a straightforward matter.
CTE, and its connection to Alzheimer’s and other neurodegenerative diseases
CTE is associated with abnormal accumulations of a protein – called tau – dislodged from structural microtubules connected to brain cells.
These tau proteins hold together delicate transportation structures within brain cells, called microtubules. When these structures break down, the tau protein can misfold, clump together and spread throughout the brain.
This is similar in some respects to neurodegenerative disorders like Alzheimer’s, though CTE begins in specific regions and progresses in its own unique pattern.
Associate Professor Michael Buckland, founder of the Australian Sports Brain Bank and co-director of the Multiple Sclerosis Australia Brain Bank, based at Sydney University says the tau is actually a normal cellular protein.
“It’s found in most, if not all, neurons of the brain, and it serves to stabilise their long projections… called axons,” Buckland says.
“The tau stabilises the microtubules to give structural integrity to that axon, that nerve fibre. In CTE, as in Alzheimer’s disease, the tau takes on an abnormal shape, gets abnormally modified chemically … and it tends to move out of the axons clump in the nerve cell body.
“Particularly in the brain, a lot of the neurodegenerative diseases, underlying them is the abnormal accumulation of these abnormally folded proteins that tend to clump together, much like a blood clot, and can be very hard to disentangle.”
We can’t diagnose it with current technology
While current medical imaging technology – such as MRI and CT scans – can produce pictures of the human body at very high resolution, the changes observed in the brains of those with CTE are so small that the brain itself needs to be accessed.
In brain banks overseen by Buckland, a segment of brain tissue about the size of a large postage stamp is extracted, and then cut into thin slithers of cells that are five micrometres wide.
If you took a piece of cotton wool and removed a single fibre, it’s half that width – incredibly precise.
But for obvious reasons, performing such an analysis on a living person is simply not possible; which is why brain banks often rely on families of deceased persons donating their brains for post-mortem study.
How prevalent is it?
It’s difficult to say how many people have CTE.
A 2022 study by the Australian Sports Brain Bank found all bar one brain studied in its first three years had signs of CTE.
This small sample of brains was predominantly obtained from ex-pro footballers (Aussie Rules, Rugby and soccer).
The ASBB also confirmed the first case of CTE in a woman in the brain of Heather Anderson. There is also evidence female athletes may be more susceptible to problems like CTE than their male counterparts.
“We will at some point see more cases of CTE in female athletes, not just in professional sports, but also at club levels as well,” says Latrobe University neuroscientist Professor Alan Pearce.
- Account for about 4 in 5 intracranial injuries in sport
- Resulted in 3,100 hospitalisations nationwide in 2020-21 from sport activities alone.
- Of these, 7 in 10 admissions were males.
- 1 in 6 were cyclists.
What if you’re not concussed?
Concern is moving away solely from concussion – although that’s still an important focus – towards sub-concussive impacts.
Increasingly, neuroscientists are worried that drawn-out exposure to repeated, mild brain impacts increase the risk of CTE. These sub-concussive impacts build up over time and exposure – force and frequency, according to new research from Boston University and Harvard Medical School.
This means people involved in activities over many years and are exposed to force that causes the brain to ‘rattle’ against the inside of the skull may be at increased risk of developing neurodegenerative issues.
Studies out of Sweden and the UK suggest top-level soccer players – but not necessarily goalkeepers – have a significantly higher risk of developing neurological disease in later life; the inference being that in-field players ‘heading’ the ball subject themselves to repeated head impacts throughout the course of their playing careers, although more research is required in this field.
Clinicians rely on symptoms to make a provisional diagnosis
While a CTE diagnosis can only be confirmed by a microscopic examination of a deceased person’s brain, some neurologists do study and diagnose Traumatic Encephalopathy Syndrome based on a careful study of patient symptoms – effectively a provisional CTE diagnosis.
Dr Rowena Mobbs is a neurologist at Macquarie University Hospital who sees new patients with suspected CTE every week.
“It’s like any subtype of dementia, be it Alzheimer’s disease, or frontotemporal dementia, Lewy body disease,” Mobbs says.
“All I can do is really collect my information and those pieces of the jigsaw puzzle, knowing that I’m missing a few, but get a likelihood over 90% that somebody has that condition to attain a provisional diagnosis.
“The data would dictate that you need at least five years of exposure [to head impacts], probably 11, probably at least a couple at the higher levels [of sport] to really start talking a risk of CTE. So the first step is to really categorize patients into that exposure.”
Can it be prevented? What about helmets?
Wearing a hard helmet in sport can help protect the head from moderate and severe traumatic brain injury by dissipating impact force on the head.
For example, a helmet on a cyclist might help spread the force from a crash while also lessening the suddenness of the impact on the brain. This could result in less severe trauma to the head.
As for soft helmets associated with footballers in rugby and Aussie Rules, the Queensland Brain Institute points out there’s little evidence to suggest these protect against brain injury. In its public advice, the US-based Centers for Disease Control and Prevention says “While there is no concussion-proof helmet, a helmet can help protect … from a serious brain or head injury”.
What is clear from neuroscientists both in Australia and globally is the desire to see governing bodies – and potentially governments – invest time and funding to build an understanding of the risks of participating in sport and develop appropriate protocols to limit head impact.
Recently, Concussion Legacy and Boston University released a new set of prevention protocols it recommends to reduce long-term risk exposure to CTE.
“We need to think about how we train our athletes,” Pearce says.
“We should not just focus purely on the physicality, but perhaps coaching and training our athletes smarter, not harder. This means working on skills and strategies, training drills that are the most physical need to be programmed the least.
“We need to discuss the issue of modifying sports for children and young adolescents. Having full contact sports from five or six years of age needs to be reconsidered. It’s not about concussion – as any kid can be concussed – but [Anderson’s] case study shows that those who participate in full contact sports from a young age are at greater risk.”