In times of fear and uncertainty, people’s instinct is to look to those who know better. These days politicians, in the west at least, tend not to satisfy that yearning, but science remains sacrosanct. To science we might turn for reassurance.
Rugby is looking for reassurance more keenly than ever now that cases of dementia are being diagnosed in former professional players under the age of 45. In the ever-escalating crisis of head injury that all collision sports – and even some contact sports – are facing, the urgency of appeals to the men in white coats intensifies with the collisions.
Science is not immune to the corrupting exigencies of politics. In neuroscience, the subject matter remains sufficiently mysterious and uncharted as to create all manner of doubts and conflicts of opinion, as will no doubt play out in the months and years to come during the legal action set to be taken against rugby’s governing bodies by afflicted players such as the England Rugby World Cup-winner, Steve Thompson and former Wales intermational Alix Popham. Trying to pick out consensus even among the finest minds in this field is not straightforward – and that is before considering the bewildering concepts and terminology involved in the discussion.
Terminology is important, it turns out. One term with which everyone in sport is familiar is that of “concussion”. There are some in neuroscience who wish for the word to be expunged from the record. Others recognise the strides that have been made in concussion awareness and fear that to discredit the notion would be to regress in that area.
The problem is that what we have come to label as concussion is a side-effect of a more profound series of chemical reactions in the brain, most of which have no perceptible symptoms at all. “Concussion is a syndrome, not a disease,” says Dr Lee Goldstein of the Chronic Traumatic Encephalopathy (CTE) Center at Boston University. “It’s a collection of signs and symptoms, and its definition varies from group to group from year to year.”
The scientists at the CTE Center have examined more brains, approaching a thousand, in search of CTE than anyone else. They are both the field’s leading experts and, by extension with so contentious a topic, the butt of its most heated denials.
The alarming implication of their work, from rugby’s perspective, is the need to shift the focus away from concussion, just as the sport was getting to grips with it, and towards the notion of brain injury. This is essentially the triggering of adverse chemical reactions in the brain by a traumatic event, however mild, and is much harder to detect. Indeed, concussion is little more than an indicator of the more severe examples. Although, even there, some are more prone to concussive symptoms than others.
It looks as if CTE is becoming an outcome, unfortunately, of playing rugby, as well as American football
“Concussion itself is not the driver,” says Goldstein. “There’s no relationship between the disease CTE and concussion, even if we could decide on a definition of concussion. But we do see a very strong relationship with total cumulative years of exposure. So that suggests, not that the concussive hits are good, but that they’re a much smaller contributor to the disease than the cumulative sub-concussive hits.”
This is the nub of the problem for a sport like rugby. Concussion protocols must be maintained and improved at all costs, but how much of a difference will they make if concussive events represent a small proportion of the injuries that contribute to neurological degeneration? The neurologists call it cumulative dose, a kind of points system, where some blows (including those recognised as “concussive”) might register more than others, which might be barely noticed even by the player. But they all add up.
“As a medical student I was taught about pack years,” says Dr Michael Buckland, founding director of the Australian Sports Brain Bank. “You look at smoking risk in pack years – a packet a day for how many years – and it’s the same concept of cumulative exposure.”
It almost goes without saying that the understanding of this process is ongoing and at almost every turn disputed, but the defining characteristic of CTE is sufficient amounts of tau protein in particular corners of the brain. Tau is in all of our brains, but over time it becomes dislodged from its proper place, which is as a kind of scaffolding to support nerve fibres, and can morph into a floating menace, which gathers in clumps and disrupts connections. As we age, this process occurs naturally, but there is a specific signature of these deposits by which diagnoses of CTE can be confirmed post-mortem. And there are hundreds of different types of tau, some benign, some pathological.
The relationship with blows to the head occurs via disruption of what is known as the blood-brain barrier, which sieves the blood to allow certain nutrients to pass into the nervous system. When the blood-brain barrier becomes disrupted by a shaking of the brain, it starts to leak, which causes inflammation, which can lead via several other processes to the loosening of tau.
“You set up this cascade of chemical reactions,” says Dr Emer MacSweeney of Re:Cognition Health, a brain clinic in Harley Street. “And they never quite have time to dampen down. Then you bang your head again, and it doesn’t dampen down, and then you bang it again ���”
If the brain was given the chance to recover from each injury, the risk would be dramatically reduced. This notion is enshrined in the return-to-play protocols of any sport, but they are necessarily applied only to those injuries that are recognisable as concussive. The target for science now is a means of detecting the ones that are not. The problem for rugby could be the sheer frequency of those revealed by any change in the technology.
“It looks as if CTE is becoming an outcome, unfortunately, of playing rugby, as well as American football,” says Dr Ann McKee of the CTE Center. “We have a limited number of rugby players [at the Boston brain bank]. We don’t know the prevalence. But from my point of view they look identical, the absolute changes in the brain, to the ones we’ve seen in American football. There was no difference in the pathology. These cases of early dementia are not a surprise.”
Not a surprise, but still, for all the horror of the cases emerging now (and there will be more), surely or, hopefully, a minority. What is it that leaves some vulnerable to this process and others not?
“That’s something of a mystery,” concedes Goldstein. “It’s very likely partly due to genotypic determinants, but we just don’t have enough data on that. There’s going to be some people who will never get it, just as there are some who can smoke five packs a day for 20 years and they’re fine. There’s the cumulative factor, there’s the repetitive factor, and then there’s the luck of the draw. If you get hit repetitively in the same spot …”
Goldstein is optimistic about the prospects of identifying CTE ante-mortem and even for future treatment. CTE is what they call a primary tauopathy, much simpler than, for example, Alzheimer’s Disease. He hopes for real progress on these fronts in the next few years. Already, there are technologies to detect breaches in the blood-brain barrier. Dynamic contrasted-enhanced (DCE) scans, normally deployed to detect tumours, are now being deployed to this effect.
Rugby’s future will be determined by the science, and the science on this is far from finished. The more consensus can be favoured over politics and argument, the more that process might be accelerated.
“What I’d like to see is a lot more collaboration,” says Professor Damian Bailey of the University of South Wales, “joining forces across the globe. It requires funding councils to provide the opportunities that biomedical specialists can chase after.
“It requires government, it requires journalists, it requires a team effort to raise awareness. It’s a call to arms.”