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.
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.
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…
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.