Rugby and CTE (Part 2)

by Ken Quarrie
I am at the point where I think chronic traumatic encephalopathy (CTE) is a term that isn’t very useful, because people are using it to mean very different things. I think “Sport-related neurodegenerative disease” and “Sport-related dementia” might be better. 

Neurosurgeon Discuss Concussion Brain Injury CTE Kids Play Football Risk – Corn Nation

In the above article, I think Dr Samadhani’s comments capture something that is really important – the conflation in the lay understanding of CTE pathology and brain function.In some of the media coverage there almost this “vulture-like” watching for the results of an autopsy, with any behavioural issues or life struggles then attributed to the “CTE” found.

Is CTE a “progressive neurodegenerative disease?” that develops and spreads through the brain after trauma has finished? Or is it a pathology that, once the insult to the brain has “healed” (to the extent it does) pretty much remains inert? (See Iverson et al. 2019) There have been strong claims by some researchers that CTE is a primary, progressive neuropathology, as per Dr Ann McKee’s description here concussionfoundation.org/CTE-resources/…

Case-series studies do not provide a basis for making causal claims. There have been instances in the CTE literature where a discussion point in a paper describing a case-series has subsequently been cited as providing evidence for the assertion in later papers.

Just like epidemiologists are not pathologists, neither are (most) pathologists experts in study design or epidemiology. I think some of the CTE papers might have stated things very differently had they had epidemiologists on board. Or maybe not? 🤷🏻‍♂‍Prof. Goldstein is here discussing the “profound discordance” the issues and difficulties (young people especially) were having prior to their deaths, and the degree of CTE pathology found at post-mortem. videocast.nih.gov/summary.asp?li…
The NIH video cast of the event is worth watching for those with an interest in what is, and is not, known about CTE. Discussions about the importance of Tau versus white matter changes, and much else besides.

Brand & Finkel ⁦‪provide a useful framework for assessing decisions with respect to CTE. I respectfully disagree with *some* of their assertions and conclusions, but agree with much more than I disagree: See Brand & Finkel 2020

People say “you don’t want to be on the wrong side of history with this”. Of course I don’t. No-one looks forward to being judged as having acted unwisely, or not having acted “soon enough” to prevent suspected harms.

I don’t know what the future will hold. To minimise my chances of “being on the wrong side of history” I plan to continue to act according to my best understanding of the evidence, in light of the fact that society’s appetite for, and acceptance of, risk changes over time.

At present I think the risks of developing CTE have:

  • Been exaggerated with respect to likelihood of outcome
  • Simplified (exclusion or disregard of other factors that may be contributing to poor health post-career)
  • There has also been premature linking of clinical conditions with pathology

I have yet to see evidence of “lots” of former players presenting with early onset dementia. I sincerely hope I don’t, but if it occurs I would be driving hard for fundamental changes to the permitted activities in rugby. As I did a generation ago with respect to spinal injuries.

That is not to say that changes in rugby since it became a professional sport might not have increased the risk. Part of a current project in which I am involved is to establish that risk – we are using a similar approach to that used by ⁦‪@WillStewNeuro⁩‬ and colleagues for football.

There is good evidence that rugby, as a sport, has become more “physical” at the elite level of the sport since it became professional. This “old” paper from Will Hopkins and me shows some of the trends early after the introduction of professionalism. (Quarrie and Hopkins 2007). Players got (much) bigger (and faster) , and there were greater numbers of contact situations per match. More recent work by Schoeman et al. (2017) indicates those trends continued, although Tucker et al. (2021) and colleagues have produced a report that suggests that increases in body mass may now have plateaued.
In any case, it is clear that since the sport became professional the average size, strength and speed of players has increased dramatically, as has their exposure to contact and high energy collisions. The effects of this have been well-documented in the extraordinary injury surveillance project run by the RFU. (West et al. 2020). Tackles have been identified as the element of play associated with the greatest injury burden in rugby. “Burden” is defined as incidence multiplied by severity. The research was conducted by people who are interested in rugby.

Identifying that some aspect of an activity is the “most dangerous” does not necessarily imply that it must be removed. This is where comparative risks (across other activities/at different levels of the same activity) need to be considered.

For what it is worth, I suspect that in cohorts of former high-level rugby players sequelae from musculoskeletal injuries (for example, osteoarthritis) will result in greater DALYs than will cognitive or psychological issues.

As ⁦‪@WillStewNeuro⁩‬ has said elsewhere, we need to understand both absolute and relative risk to keep things in context. A large increase in relative risk on a very “vanishing small” base rate still yields a very low rate.

Re-highlighting this important paper from the Lancet last year. It suggests that across the population, traumatic brain injury (across the entire spectrum of severity) accounts for about 3% of the modifiable life risks for the development of dementia. (Livingston et al. 2020)

Heavy alcohol use, which has been (at least historically) a feature of involvement with participating in New Zealand rugby from the teenage years on, features as a risk. The lack of solid science to date around causal relationships between head injury and CTE is highlighted. (Livingston et al. 2020)

The lack of solid science to date around causal relationships between head injury and CTE is highlighted.

“The term chronic traumatic encephalopathy describes sports head injury, which is not yet fully characterised and covers a broad range of neuropathologies and outcomes, with current views largely conjecture.” (Livingston et al. 2020)

This statement on the strength of the evidence stands in stark contrast to the claims made by various policy advocates and what seems to be widely believed in the media.

There is an entire body of work underpinning public health interventions in sport – we aren’t just “making this up as we go along”. See, for example:health.gov.on.ca/en/pro/program…

Many changes to rugby have been made as a result of that work. RugbySmart, BokSmart and other injury prevention programmes have been widely recognised within the sports science/ sports medicine communities as having had positive effects on the risks of injuries. Like many areas of science where the evidence is equivocal, debates often get heated. When the science is settled, there is little to argue about.
I think people’s values and biases (and *everyone* has them, including me) play a part in how they interpret the evidence. I am happy to engage in good faith on the issues, but will ignore trolls who imply that I am a “shill” or “CTE denier”. I, having had multiple concussions during my rugby playing days, plus depression, would qualify as “possible CTE”. Have I got CTE pathology in my brain? Who knows? If I do, what relation does it bear to my current state? Again, who knows?!!
The “Traumatic Encephalopathy Syndrome” first proposed by Montenigro et al. (2014) is remarkable in the breadth of conditions it encompasses, and the lack of specificity it entails. With respect to sports people going through tough times following their retirement – this is real, and well-recognised across a range of sports (contact and non-contact). But for former collision sports players these issues *do not necessarily mean* that they have “CTE” and have a one-way ticket to dementia. There are lots of very worried people who have conditions that are iatrogenic. Again, this doesn’t mean that for some the brain injuries they sustained during their sport didn’t contribute to what they are now experiencing, and for some their brain injuries were probably the major contributor.

Ken Quarrie is the Chief Scientist for NZ Rugby. All views expressed are his own, and do not necessarily represent the position of his employer. The above article was compiled, with permission, from a thread of tweets by @KenQuarrie. For more on the topic, you can follow Ken at @KenQuarrie. You can also view Ken’s publications here – Ken’s Google Scholar Profile. 

Rugby and CTE

By Ken Quarrie 

I have been seeing claims that some people are “sowing doubt” with respect to CTE (Chronic Traumatic Encephalopathy) and are thus acting like tobacco companies did with respect to heart diseases and lung cancer. I want to make a few comments about this. Before I get to the CTE issue, it is worthwhile that I put some background about me on the record, so that people are able to judge whether I am likely to have biases that might sway me to one position or another.

I was brought up in New Zealand, in a family where rugby was *very* important. Dad played rep rugby for Wanganui and Waikato, and was an All Blacks triallist. As a kid I was a fan and obsessively read books about rugby and the All Blacks. I played the sport from childhood until my late 20’s. I had some really enjoyable times along the way. I also sustained (at least) five concussions. I was immersed in the Otago Uni/Dunedin rugby heavy drinking culture.

I found that as I got older there were fewer aspects of the “rugby” culture with which I identified – @XTOTL captures some of that here: https://www.rnz.co.nz/news/the-wireless/374305/the-pencilsword-in-the-bin. I also had a good friend injured at the age of 15 in a scrum. He has been in a wheelchair since 1984.

As well as rugby, as a kid I loved science. I have managed to combine those two loves into a career. I wouldn’t call myself a rugby “fan” anymore. I am a rugby scientist, and it helps to have a little distance from your object of study. Nevertheless, I still work for NZ Rugby (conflict of interest klaxons!). Having worked on independent research studies examining risks for injury in the 1990’s, I took a role with NZ Rugby in 2000 as their first “Injury Prevention Manager”. I realised that, as a scientist, my employment represented a conflict of interest, but I believed I could have a greater impact on improving player safety and welfare from within rugby than from the outside.

I have been adamant with NZ Rugby and World Rugby that I must be allowed to conduct research without interference about what I can study, how I can analyse it, and what I can say about it. A look at my research outputs will reveal an eclectic mix of rugby studies. So when people “poison the well” by implying that any research funded by or conducted by sports organisations must necessarily be “suspect” I feel personally attacked. Doing good science is what I care about.

Doing good science is what I care about.

From a personal level, the welfare of players has, and does, take precedence for me over considerations of “tradition” or “maintaining the essence of the game”. But managing risks does not imply “eliminating all risks”. Reasonable people can look at an issue and disagree about it.

So – the “tobacco company line”. Tobacco companies systematically downplayed the risks of their products, and attempted to “sow doubt” in the public mind. How is the CTE/concussion debate different? A key difference is that, despite there having been strong claims made about what causes CTE, how it develops, and what clinical outcomes it leads to, the reality is that the science of CTE is very young. There really *is* a lot of doubt about a number of the issues!

The issues include whether CTE is, as has been claimed by some, a primary, progressive neurodegenerative disease. Questions remain about the cause(s) of the pathology. Questions remain about the “pathognomonic lesion” – i.e. what distinguishes CTE from other pathologies. Questions remain about the prevalence of the pathology. MAJOR questions remain about the relationship between having CTE pathology in the brain and any given clinical outcome. Do I think brain injuries are bad for health? Yes, undoubtably. I also think that the public perception of the strength of the evidence, and the prevalence of CTE as a public health issue doesn’t match the scientific understanding of it *at this point*.

So to accuse “rugby” as having acted like tobacco companies to sow doubt about CTE is simply a smear, and a lazy and demonstrably false one at that.

If former rugby players are struggling – for whatever reason – my heart is with them. I pledge to do my best to understand more about the long term health outcomes of playing rugby, so that people can better understand the risks and make informed choices about play. People involved in rugby, like Colin Fuller, @Sharief_H, @drkeithstokes, @drsimonkemp, @mattjcrossie, @Scienceofsport and yours truly and many others have identified and documented risks in rugby via research studies and injury surveillance. Many changes to rugby have been made as a result of that work. RugbySmart, BokSmart and other injury prevention programmes have been widely recognised within the sports science/sports medicine communities as having had positive effects on the risks of injuries. Likewise, the @NZRugbyFound has done great work on tertiary prevention. So to accuse “rugby” as having acted like tobacco companies to sow doubt about CTE is simply a smear, and a lazy and demonstrably false one at that.

Ken Quarrie is the Chief Scientist for NZ Rugby. All views expressed are his own, and do not necessarily represent the position of his employer. The above article was compiled, with permission, from a thread of tweets by @KenQuarrie. For more on the topic, you can follow Ken at @KenQuarrie. You can also view Ken’s publications here – Ken’s Google Scholar Profile.