Dad’s love of rugby led to CTE – players should know the risks
The consequences of getting CTE are brutal. Players at all levels need to know what the researchers are finding, writes Geoff Cooper.
My father didn’t intend to die doing what he loved. Fifty-seven years of playing rugby gave Geoffrey Joseph Cooper friends and fitness. But it also gave him chronic traumatic encephalopathy (CTE): a form of dementia caused by numerous small, undetected knocks to the head.
His diagnosis follows Māori All Black Billy Guyton, who was the first professional athlete to be diagnosed postmortem in New Zealand, just three weeks ago.
My dad loved rugby. The tactical gamesmanship, the big hits, the camaraderie. He likened it to a physical game of chess and the bigger the bruises, the better. His first rugby photos start at age 7 and by the time the boots were hung up, he had played for 12 clubs across three continents.
He was not an All Black. He did not play Super Rugby. His grubber kicks didn’t always go where they should. Instead, he was the quintessential weekend warrior; deeply devoted. The first to shake hands with any opponent and an embodiment of grassroots rugby.
But, as the games added up, so too did the knocks. Each hit exerted a force on his brain: impossible to detect in real time. But the blows compounded, one after the other. “Small”, of course, is a deceptive term. The G-force of these tackles has been measured just below that of a car crash at 50kph. For most of us, we’d be unlucky to have one in a lifetime. But for those playing contact sport, it’s a weekly or even daily occurrence. Carl Hayman, the former All Black with suspected CTE, estimates he took 150,000 such head knocks over his career.
As he said in his book, Head On: “The doctor told me he wouldn’t expect to see a scan like this for a 70-year-old, let alone someone not yet in his mid-forties.”
The human skull is not designed for such trauma. It cannot prevent the brain from striking up against the interior. These movements stretch and break brain tissue, triggering a chain of events that can ultimately interfere with normal brain activities. We’re only now beginning to understand the full extent of what this “interference” means.
My father was the chief executive of the Waikato Dairy Co-operative and assistant director-general of the former DSIR. But by his late 50s, those small knocks gradually transitioned him to a new place. Not a physical move, but a psychological one.
For those living in dementia, it is a place where time loses its regularity. Where days become a meander. For Dad, this meant leaving the boardroom and becoming a “citizen of the wind”. Sometimes completely out of touch. Caught in between two worlds. The Spanish have a saying for this, ni de aquí, ni de allá – not from here, not from there.
That is dementia; a slow, irreversible process that slowly strips away layers of our self. It is associated with memory loss, impulsive behaviour, depression and suicidal thoughts.
Families watch helplessly as rudimentary tasks become hard, if not impossible. By 2050, 170,000 New Zealanders will live with the disease, impacting 10% of people over 65. For those living with CTE dementia, it is a journey that typically starts much earlier in life.
We know more about the causes of CTE than ever before. In a seminal 2023 study of 631 donated brains from NFL athletes in the US, 71% had CTE. The severity of the diagnosis was determined by career longevity and the number of small knocks.
Of course, many questions remain. We still don’t know at what force an impact is detrimental; what is the prevalence of CTE; or how to diagnose CTE before death. These are the questions that Dr Helen Murray and Dr Maurice Curtis grapple with daily at the Centre for Brain Research at the University of Auckland.
It’s a confronting issue for a country that identifies so strongly with high impact sport. Nothing is more unifying than the All Blacks romping to victory against an old foe; or the sight of Warriors skipper Tohu Harris stopping an offensive play dead in its tracks.
But we need to confront the evidence before us. Identifiable concussions are not predictive of CTE. What matters is the quantity and force of small knocks – or “sub-concussive trauma”. Targeting concussion recovery is therefore inadequate. Instead, efforts to reduce contact are needed, for instance by eliminating full contact trainings, shortening seasons or delaying the age at which contact is introduced.
These efforts cannot solely target elite athletes either, since they comprise such a small proportion of all players. Weekend warriors, like Dad, and the children coming through in age grades, are just as important. But information is painfully slow to trickle down.
Players and parents need information to make their own judgments. It’s hard to make definitive conclusions about risk – what we should and shouldn’t do.
But there are things we know: CTE is a real thing. It occurs from years of small, undetectable head knocks.
The risks increase with the number and force of hits. And the consequences of getting CTE are brutal. Players at all levels need to know what the researchers are finding.
These efforts cannot solely target elite athletes either, since they comprise such a small proportion of all players. Weekend warriors, like Dad, and the children coming through in age grades, are just as important.