The data on contact sport, concussion and CTE is convincing. But not conclusive

The International Sport Concussion Conference was held in Melbourne earlier this week, in the days preceding the first regular-season NFL game played on Australian soil.

During Tuesday’s session, research figures from the Australian Sports Brain Bank were presented. Of the first 150 brains of participants in contact sport examined by the bank, 51 belonged to men who had a reported history of playing rugby league. Thirty-one of those 51 carried the pathological signature of chronic traumatic encephalopathy (CTE).

Rugby league players both amateur and professional; men who died in their 20s, 30s and 40s. Among them Paul Green, an NRL premiership-winning coach who died by suicide at 49, and the Manly Sea Eagles player Keith Titmuss, who was 20 when he collapsed after a training session and died of heat stroke. Rightly, those numbers can’t be ignored and are cause for concern, if not alarm.

Temper your musings, however. The findings of the NSW Deputy State Coroner, handed down in 2024, were that Titmuss died of exertional heat stroke. He might have had CTE pathology at the time of his death, but it says nothing about why he died.

The finding is invoked as a marker of exposure and a portent, which isn’t an illegitimate scientific use. But it’s not a finding that he died of CTE, or that the pathology affected his function, or that it would have. He is, strictly, a case of dying with. Like the 102-year-old man who dies with prostate cancer, but not because of it.

Repeated blows to the head appear to cause this CTE pathology. In brain banks replete with the brains of people who weren’t former collision and combat sport participants, the pathology is rarer. A study conducted a little over a decade ago by the Mayo Clinic detected CTE pathology in 21 of 66 former contact sport athletes and in none of 198 people who’d never participated in those activities. But those are small sample sizes.

So this isn’t the data of coincidence. The families donating these brains of their deceased loved ones aren’t hysterics. But we must be careful with what the data shows.

By definition, a “concussion” is a mild traumatic brain injury caused through the violent ping-ponging of the brain inside the skull. No sport has its history and existence more intertwined with brain injury than American football.

More than a decade ago, more than 4500 former NFL players and their families sued the NFL, on the case theory that the NFL had, for decades, been aware players were being exposed to an unacceptable risk of repeated concussions and connected traumatic and degenerative brain conditions by playing gridiron within the rules set by the NFL.

The plaintiffs further contended that, despite the game’s governing minds being armed with that knowledge, the NFL knowingly failed to take the necessary and appropriate steps to shield them from harm, in turn exposing the players to the possible onset of CTE manifesting in memory loss, depression, early onset dementia and a propensity to suicide.

To put the quantum of plaintiffs into some semblance of context, (very) roughly 20,000 men played in the NFL between 1967 and 2014. In an unsophisticated way, that in turn illustrates that over 22 per cent of players suffered significant enough damage to qualify to join in legal proceedings.

The class action was settled for a ten-figure sum and no admissions of liability, but an agreement laced with tacit recognition and responsibility which spared the players from shifting the incredibly difficult burden of proving the causal links between their professional football careers and the catastrophic afflictions with which they were left.

Risks associated with brain trauma represent an existential risk to collision and combat sports. Such matters must be treated with utmost seriousness. But care also must be taken when determining what it really means if of 150 brains analysed, the reported instances of CTE were discovered.

What proportion of people might die with CTE pathology present, but not of any condition the pathology leads to? If 100,000 brains were donated and analysed post-mortem, what would the incidence of CTE pathology be in females who died when aged 70 or older, who seldom ever bought a ticket to Kogarah’s Jubilee Oval let alone played the game on the hallowed ground?

What of the recreational rugby league player who also had an unhealthy thirst0 for the Nectar of the Gods and pub fights during the “Kebab Hours” of a weekend morning? Which are the predominant causative factors for any CTE pathology identified once his brain is sliced into slivers?

The conflation between identifiable and abnormal accumulation of tau protein around the blood vessels in particular parts of the brain – which is the defining pathological hallmark of CTE – is a hypothesis and inferred based on studies involving older donors over time. That pattern is consistent with progression; it is equally consistent with survivorship or with age-related tauopathy occurring alongside a static traumatic brain lesion.

Second, the conflation between the brain disease and the manifestation of traumatic encephalopathy syndrome, which is the clinical construct of CTE. In a 2014 study published in The Journal of the Alzheimer’s Association, a study of 336 donated brains from people exposed to repetitive head impacts from contact sports, military service, or physical violence in their lifetime concluded that while 97 per cent were clinically diagnosed with the syndrome based on exhibited symptomology, the brain pathology was only present in one-fifth of those cases.

The third issue is that 31 of 51 is a proportion of donors, not of players. Families donate their loved one’s brain to research for an important and valid reason, and the reasons are not randomly distributed. A family whose father died after a decade of decline is likelier to seek an answer than one whose father died with his faculties intact.

The proportion of CTE in a brain bank equals population prevalence only to the extent that a proper and statistically reliable number of brains are donated, from people from all walks of life. In a paper published in the British Medical Journal the week before last, the authors identified every former NFL player who died between 2008 and 2021, being a total of 1712 men, and determined that 338 had donated their brains. Of that cohort, 315 had a diagnosis of CTE. The remaining 1400-odd weren’t examined.

Nothing here denies that repetitive head impact causes CTE pathology. The burden of persuasion on that point has shifted to those who would deny it.

What’s denied is that current evidence licenses the further steps that public discussion and litigation take for granted – that the brain lesion is the disease; that the disease is the syndrome; that the donors are the players, and that a man found with protein build-up in a specific part of his brain died because of it.

Each matter is an inference, and each is under-determined. Sixty-one per cent of 51 is a number that demands further study and research. It’s not yet a number that decides an argument of existential relevance.

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