July 9, 2021
As has been widely reported, a group of former professional rugby union players (Claimants) have brought a claim against World Rugby, the Rugby Football Union, and the Welsh Rugby Union (Defendants), for causing them to incur chronic traumatic encephalopathy (CTE) and/or early onset dementia (EOD) (the Rugby claim).
The Rugby claim centres on allegations that the Defendants failed to adequately protect the Claimants from the risks of concussion and the risk of repeated concussion causing CTE/EOD. To that extent, the principal cause of action will be in negligence, although there may also be allegations of breach of contract. The Claimants allege that the Defendants owed them each, as individual professional players, a duty to take reasonable care for their safety by establishing and implementing rules and regulations in respect of assessment, diagnosis, and treatment of actual or suspected concussive and sub-concussive injuries during matches and training sessions.
There are a number of significant hurdles which the Rugby claim will have to overcome if it is to succeed. The Claimants will need to establish they were owed a duty of care and that duty was breached. They will need to prove that said breach was causative of their injuries, and that the Defendants had knowledge of the link between concussions and CTE/EOD. There will likely be limitation disputes, and also disputes in respect defences such as volenti non-fit injuria (voluntary assumption of risk). This article focuses on two of those hurdles: knowledge, and causation.
First, it discusses the difficulties the Rugby claim will have in proving the Defendants ought to have had knowledge of the link between CTE/EOD and concussions and taken reasonable steps to allay the risks.
Second, it discusses causation and the important distinction which needs drawing between severe and mild traumatic brain injuries for the purposes of establishing a link with CTE/EOD.
The Claimants must establish the Defendants knew or ought to have known of the risks of concussion and that they failed to take steps to protect the Claimants in light of that knowledge. Therefore the issue of knowledge will inevitably be contentious and will require an in- depth analysis of the medical literature drawing links between concussion and CTE/EOD.
As a matter of fact, there is a substantial body of literature on the long-term effects of head injuries. It begins with Osnato and Giliberti in 1927 who outlined that there is a “strong likelihood that secondary degenerative changes develop” after head injury. In 1928, Martland published a paper in which he considered the concept of being ‘punch drunk’ or “slug nutty”. This was the diagnosis given to the mental and physical states encountered in examination of former boxers. Martland assumed that the condition afflicted at least half of all former fighters, and those most susceptible were the fighters whose fighting style saw them take more blows in order to wear their opponents down.
In 1937, Parker published a paper which concerned the long-term effects of repeated brain injuries to professional boxers. His paper described three cases of chronic disease affecting the nervous system of former professional boxers. Parker described that:
“the clinical picture in each case was very complex and it differed in the once case from the others. The only agreement, however, was in the suggestion of diffuse or scattered lesions of the brain affecting different systems at one and the same time”.
The literature developed around the concept of ‘punch drunk’ throughout the intervening decades, though any more of an exposition of that is unnecessary for the purposes of this article. Lye and Shores then carried out a review in 2000 which suggested that traumatic brain injury was a pathogenic agent in the development of Alzheimer’s disease. Van den Broek highlights that it is now generally accepted that moderate to severe traumatic brain injury (TBI) increases risk of dementia. Concussions are generally understood to be mild TBIs.
This brief description of the literature suggests that this level of knowledge of a link between moderate to severe TBIs and CTE/EOD in clinical psychological circles did not start to become recognised until shortly before the turn of the millennium.
Moreover, the literature on concussions/mild TBIs and CTE/EOD is not nearly so comprehensive. The Consensus Statement on Concussion in Sport in November 2012 concluded that:
“a cause and effect relationship has not yet been demonstrated between CTE and concussions or exposure to contact sports”
In the 2016 Consensus Statement on Concussion in Sport, it was determined that:
“The literature on neurobehavioral sequelae and long-term consequences of exposure to recurrent head trauma is inconsistent. Clinicians need to be mindful of the potential for long-term problems such as cognitive impairment, depression, etc in the management of all athletes. However, there is much more to learn about the potential cause-and-effect relationships of repetitive head-impact exposure and concussions. The potential for developing chronic traumatic encephalopathy (CTE) must be a consideration, as this condition appears to represent a distinct tauopathy with an unknown incidence in athletic populations. A cause-and-effect relationship has not yet been demonstrated between CTE and SRCs or exposure to contact sports. As such, the notion that repeated concussion or sub concussive impacts cause CTE remains unknown.”
The consensus statements make clear that they are not intended as clinical practice guidelines or legal standards of care, but that they are a guide which is consistent with the reasonable practice of a healthcare professional. Both aforementioned consensus statements were published in the British Journal of Sports Medicine. The 2012 statement listed 54 contributors, and the 2016 statement listed 46 contributors. These statements do not represent a fringe outlying body of thought. They serve to evidence the fact that whilst there may be a vein of literature highlighting the risks of CTE/EOD from moderate to severe TBIs, the literature remains far from united for mild TBIs.
Arguments about the adequacy of the concussion protocols in light of what the Defendants knew or ought to have known need setting in their context. It is very difficult to state definitively that the Defendants ought to have known about the causative link between concussion and CTE/EOD because as late as 2016, the causative link was and is not consensus scientific opinion.
The issue of knowledge also speaks to the fundamental difference between the Rugby claim, and the 2013 claim brought by former American football players against the National Football League in America for CTE/EOD. In the NFL claim, the principle allegation was that the NFL had knowledge about the effects of mild TBI and its links with CTE/EOD but had taken steps to cover it up. The Rugby claim does not, in its current form, appear to allege malign intent or any kind of cover up on the part of the Defendants. The Rugby claim is concerned with the adequacy of the protections put in place by the Defendants in light of the knowledge which they had available to them at the time.
If the Rugby claim were to succeed in demonstrating that the Defendants knew, or ought to have known of the risks of concussion, causation should and will be strongly contested. As above, the link between mild TBI and CTE/EOD “remains controversial” and whilst there may be studies which are suggestive of a link “this finding will require replication before it can be widely accepted.”
Causation will therefore become an issue of epidemiological evidence, as the court is confronted with a claimed cause and an observed effect. The Bradford Hill criteria are the principles typically used to assess the link between cause A and effect B based on epidemiological (medical) evidence. These criteria first emerged in Sir Austin Bradford Hill’s seminal 1965 paper: “The Environment and Disease: Association or Causation?”. It should be noted that these are not an unbending set of requirements for establishing causation, but they are accepted to be indicative. Therefore, it is worth considering the Claimants’ position against those criteria which may prove most difficult for the Claimants’ case, those being: strength of association, consistency, specificity, temporality, and biological gradient.
Assessing strength of association in the Rugby claim will turn on the ability to discount correlations and data variability. This will require painstaking cross examination of each of the Claimants as to the number of concussions they likely incurred over their professional careers, and the difficult task of discounting any other more severe head injuries that individual may have incurred outside of rugby.
Consistency stresses the importance of repetitive findings because “a single study, no matter how statistically sound, cannot be relied upon to prove causation due to ever-present threats to internal validity.” As above, Van Den Broek is clear that suggestions of a link between concussion and CTE/EOD have yet to be replicated across multiple studies. This will present a difficulty for the Claimants in proving consistency.
The principle of specificity contends that causal associations are stronger where exposure causes a specific effect without another probable explanation. This is a more compelling point when a specific agent can be properly and precisely explained as the cause of the effect. There may be scientific literature which links concussions/mild TBIs with EOD/CTE but, as above, the link remains controversial.
Temporality has been described as “inarguable” to causal inference. That’s to say that onset must be preceded by exposure such that a temporal progression is discernible from one to the other. Again this is difficult for the Claimants. The temporal field of exposure preceding onset is so vast, and includes all instances of TBI incurred during each Claimant’s lifetime. This will make isolating the temporal progression from, what will be argued is, tortious TBI to the onset of EOD/CTE near impossible.
Biological gradient is concerned with the relationship between dose and response; the more exposure, the greater the incidence. This issue will turn on expert evidence. It’s likely that any relationship between dose and relationship which the Claimants point to will be non-linear due to individual susceptibility to EOD/CTE. It is further difficult to see how the Claimants could establish a lower dose threshold on the basis of the current state of knowledge. Simply, any relationship which the Claimant point to between dose and response will be embedded with caveats and easily confounded.
Amidst the media speculation about the veracity of the allegations likely to form the basis of the Rugby claim, the fact remains that the Claimants have a very difficult case to make out. In short, they will need to demonstrate that:
i. concussions/mild TBIs can cause EOD/CTE
ii. concussions did so in the case of the Claimants in the group whilst under the care of the Defendants
iii. the Defendants knew or ought to have known of the potential for (i) to cause (ii)
iv. the Defendants’ processes failed to take appropriate steps to protect the Claimants in light of that knowledge.
The Claimants will find themselves under the weight of a significant evidential burden, with no obvious route to discharging it.