The knowledge around brain injuries is improving – but there is still much to learn. Michael Aylwin reports
The science of brain injuries in rugby
A sport’s relationship with science is troubling at the best of times. Science starts by fuelling performance, which makes many feel uneasy anyway, but in collision sports the implications of improved performance are profound for player welfare. Then science steps in to lay out before sport in gory detail the damage it is doing to itself. The final twist in the relationship is when science presents itself as sport’s only hope for salvation.
Rugby finds itself somewhere between the last two stages of this pas de deux. The effects of full-time professionalism and improved techniques in the, well, science of preparation have exposed players to ever-escalating levels of repetitive “insult”, as the scientists like to term traumatic events of even the mildest nature. This seems to be resulting in that other recent finding of science – that players are suffering the symptoms of dementia at uncommonly early ages.
What is beyond doubt, statistically, is that this is no coincidence, but science has not quite mapped the process through from start to finish. As this is achieved, solutions may or may not present themselves, or possibly even cures, but for now the challenge is just to work out what is going on.
The key areas of study are what is happening to players’ brains at the point of insult (ie, on the pitch and training paddock), what happens afterwards and how it is that some of them end up with neurodegenerative conditions.
In practical terms, this would translate into a consistent technology by which we might measure the injection of energy into players’ brains in live situations, another for detecting the resultant injuries and their severity, and finally a technology to confirm pathology in those who develop dementia.
Although the symptoms of dementia are clear, the diagnosis of certain types can be ascertained only post-mortem. In the case of athletes in collision sports, the prime suspect is chronic traumatic encephalopathy (CTE).
This is characterised by accumulations of a noxious version of the protein ‘tau’ in particular corners of the cerebral cortex called sulci. Unfortunately, their presence can be confirmed only by dissection of the brain. There are hopes of a method of diagnosis ante-mortem in the not-too-distant future, but for now technologies in the other two areas are closer to hand.
Measuring the intensity of collisions in a rugby match has been a goal for some years now. The difficulty is isolating the acceleration of the skull – or the energy injected into the brain, which is the root cause of the problems. Sensors in the back of shirts have been tried, but those end up measuring no more than the acceleration of the fabric. Likewise, the patches on the side of the head we have seen used by Saracens, and currently Newcastle, tend to measure the slippage of the skin as much as the shaking of the brain.
Because it is fixed to the skull, mouthguard technology has emerged as the best hope – and that only recently. These days science can cram a lot of tech into a regular-sized gumshield.
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Alas, the introduction of this technology across the Gallagher Premiership has been delayed, but Harlequins have been using it and attribute much of last season’s success to the insights they gathered.
One of them, incidentally, is that blows to the body account for significantly more of the cumulative transfer of energy to the skull than do direct blows to the head. If people think that cutting out the odd high tackle will solve rugby’s problems, they are likely to be confounded.
Either way, an accurate, real-time anatomisation of the forces a player’s brain is exposed to seems nigh. An accurate method of brain-injury detection is not far off either. Already, it is technically possible to detect the telltale signals – or biomarkers – that give notice of a distressed brain. The challenges are two-fold: to render tests for them practical at pitch-side and to decide on the point at which we deem an injury too severe.
Currently, rugby’s concussion protocols are more or less openly scorned by the neurological community, as is the notion of concussion itself, which is just an arbitrary collection of superficial symptoms. All people’s brains, however, object to being shaken too much. Science is searching for a method that will identify which players have taken too much, regardless of how many fingers they think they can see.
Most tests involve time and heavy-duty specialist equipment in a clinic, which is why there was some excitement in March when researchers at the University of Birmingham announced, with the RFU sitting proudly alongside, they had found a saliva test for microRNAs, a very sensitive biomarker released at the point of injury.
They hope the test might be available at pitch-side in three to five years. The trouble with this study is that it used as its standard the very HIA it is trying to transcend. As in a blind tasting, they tried to identify, with some success (the clearest being achieved 36-48 hours after injury), the saliva of players who had failed their HIA.
Other scientists are sceptical that biomarkers from an event in the brain can be picked up in a distant ‘ultra-filtrate’ like spit, which is not quite the same as saliva.
“The way you standardise salivary secretions,” says Dr Lee Goldstein of the CTE Center at Boston University, “is by cannulation of your salivary gland with a glass pipette. And let me tell you, people will not be lining up for that. It would be a toss-up whether I’d rather have my fingernails pulled off with pliers.”
Other biomarkers are being found in blood tests, but these tend to be heavier proteins, such as tau, which mean a certain level of damage has already occurred. They also tend to appear some time after the event that triggers them.
Some time later again, in what we must hope will remain a minority of players exposed to such injuries repeatedly, the symptoms of dementia creep in. The researchers at Boston have studied the brains post-mortem of more former collision-sport athletes than anywhere else. CTE is found in most of the brains of those who reported symptoms in life.
If only we could confirm the disease in those living, we might be able to chart the path from injury to pathology more precisely. In November, the CTE Center produced a paper that found a hopeful correlation between certain markers on the brain scans of former athletes who were later confirmed as suffering from CTE. The ubiquitous refrain of “more research required” applies here, but this seems another step towards understanding.
But how much understanding do we need of what seems already fairly clear? This is where science is far less squeamish than sport in calling out the obvious.
Goldstein is in no doubt about what collision sports need, and the technology is already there. His team have recruited scanning technology traditionally used for tumours, called dynamic contrast enhanced MRI, for detecting localised disruptions of the blood brain barrier, which regulates the passage of nutrients into the nervous system. He favours a course of preventative action, and his recommendations are stark and prohibitive.
“You don’t need a pitch-side test, and you don’t need diagnoses,” says Goldstein. “I would want to know who’s at risk before they even go on the pitch. If someone is carrying this marker at the beginning of the season, they shouldn’t play that season. It’s that simple.”
Rugby’s nightmare would be to discover in some sort of mass testing programme that there are players everywhere with such leaky vessels in their brains. This is not indicative of CTE, but it is serving notice that a process is under way that could lead to it.
“We know what the drivers are now,” says Goldstein. “We see CTE in and around the vessels, where the stress (in a shaking brain) is concentrated – at the base of the sulci. So if you have leaky vessels there, you are, in effect, developing CTE. That doesn’t mean you’re going to get CTE, but you have a pathophysiological marker that is driving the process.
“It is not normal, it is not good for your brain, and it puts you at elevated risk for CTE. You don’t really want to diagnose CTE after it’s in place; you want to identify people who are at risk.”
That relationship between sport and science remains agonisingly poised. We can rest assured science will sooner or later unravel the processes that lead from brain injury to dementia, but that may yet spell disaster for sports like rugby, if the injuries and the worst of their consequences are already as entrenched as some fear they may be.
The next twist might be for science to present sport with a cure for these ailments. Goldstein is hopeful of progress on that front. CTE is what is known as a primary tauopathy, a lot less complicated than diseases such as Alzheimer’s, where other proteins gather to corrupt the circuitry. There are multiple antibody treatments against tau that are in development.
But he warns they will be expensive and that cannulation of the salivary glands with a glass pipette would seem like a tickle with a feather compared to the deployment of immuno-therapeutics into the brain.
Far better to prevent the diseasing process in the first place. Whether science ends up saving rugby or closing it down altogether remains, it seems, in the balance.
This article originally appeared in the February 2022 edition of Rugby World.
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