Concussion (latin concussio or concutere): ‘‘to strike together’’ or ‘‘to shake violently’’

NO doubt you have become aware of the growing media interest regarding the long term effect of concussion sustained during sport.

In fact, sports-related concussion has become big news for both front and back pages, none more so than the campaign being waged by the Sydney Morning Herald, particularly in relation to concussion injuries sustained by first-grade players in the National Rugby League.

The story that has gained increasing media attention may perhaps be best exemplified by the Hollywood blockbuster that starred Will Smith, Concussion. The key message to date has been that concussion causes chronic traumatic encephalopathy (CTE), associated with mood disturbance and potentially suicidal behaviour. And perhaps seemingly as alarming, particularly for parents of budding footballers, CTE may also result from standard practices, such as heading the ball in soccer, leading to an increased risk of dementia.

As a result, in tandem with this expanding media coverage, national and international sporting organisations have been considering the way forward, particularly in relation to guidelines, position statements and best practice recommendations.

Of particular local interest in Australia, participation sports such as rugby league, Australian rules and rugby union have some of the highest rates of head injury in team sports worldwide, with an incidence of up to 10 concussive injuries per 1000 player hours, equating to five injuries per team per season. In America, up to 4 million sports-related concussions occur annually, although this may be an underestimate, as many concussions do not come to medical attention. This has the potential to represent a significant public health issue.

While concern for premature return-to-play risk has traditionally been the focus for sports-related concussion, there has been a growing concern for potential long term cumulative impairments resulting from multiple concussions over an athlete’s career, for both professionals and amateurs, particularly in relation to the development of Alzheimer’s dementia, Parkinson’s disease and motor neurone disease later in life.

So, what is the real story and where is the science?

Mainstream understanding seems to derive from the life story of an American footballer, “Iron” Mike Webster. In addition to the movie portrayal of Webster in Concussion, there was a narrative that he had been addicted to opiates and amphetamines after his playing career; had been convicted for forging prescriptions; had other substance misuse problems, including performance enhancing drugs while playing; and had subsequent alcohol problems on retirement (here, and here). This narrative was combined with a possible family history of psychiatric disease. Webster’s personal history had played out in the context of sport at the time, with doping stories around professional athletes in official files and media outlets.

Regardless of Webster’s clinical history, it was reported at autopsy that he had evidence of CTE with diffuse amyloid plaques, sparse neurofibrillary tangles and tau-positive neuritic threads in neocortical areas. From this, the pathologists highlighted the potential long term neurodegenerative outcomes in retired professional league players who experienced repeated brain injury. The link between traumatic brain injury and neurodegeneration has developed from such origins, although perhaps the story is not so straightforward.

Recent opportunistic cohort studies in professional hockey players and international rugby players, the latter studied up to 20 years after retirement, have not identified significant effects of concussion (here, and here). It is understandable that authors in the field remain cautious and that more long term data will be required before definitive judgement can be reached.

By analogy, I recall data projections for the number of potential patients who would develop “mad cow disease” when I was working as a postdoctoral neurologist in the UK, ranging up to many millions. Over more recent years, those estimates reduced dramatically when science caught up with the reality and the disease process itself was defined, including potential genetic risk factors that were required to develop it.

It is clear that the field of sports-related concussion needs a major injection of scientific rigour and indeed evidence. While waiting for science to catch up, what should we do?

At the outset, we need to better identify and define the process of concussive injury. To cloud the area, many players have reported that despite brief losses of consciousness, changes in mental state, and visual and auditory hallucinations that persisted throughout parts or the totality of games, they appeared normal to their teammates and training staff. There also remains the conflict of under-reporting and I am aware, firsthand, of player and coach concerns that reporting a concussion will likely result in loss of playing time.

Separately, in spite of recent advances in brain imaging, long term cognitive outcomes remain poorly understood. As the physical, cognitive and emotional consequences of concussion gain wider public attention, our incomplete knowledge of how to prevent, diagnose and treat such injuries endangers the health of competitive football players, with particular emphasis on their brain health.

In 2010, the National Football League (NFL) created the Head, Neck and Spine Committee, which established a protocol for the diagnosis and management of on-field concussion that called for uniform and regimented changes to management. First, it mandated the use of the NFL’s Sideline Concussion Assessment Tool on the day of the injury. In 2014, the committee provided a formal set of recommendations to instruct and educate team physicians on how to reintroduce a player back into full activity, although there remains no evidence on the effect of return-to-play guidelines on prognosis.

The mechanisms underlying concussion remain poorly understood, with current consensus that the injury reflects physiological disturbance, including neurochemical and metabolic changes and, potentially, changes in gene expression, rather than structural injury to the brain. Common acute symptoms include headache, dizziness, nausea, confusion, memory impairment, imbalance and behavioural changes. These symptoms will usually resolve in most athletes within a week.

Recovery and post-concussion syndrome remain similarly poorly defined and understood. There remains no gold standard measure of brain disturbance and recovery following concussion in sport. Instead, clinicians rely on clinical judgement. There needs to be improved knowledge of risk exposures that may lead to preventive approaches, including changes in competition rules.

Perhaps most critically, the potential effects of multiple concussions remain a source of controversy. Most studies are retrospective and rely on self-reported concussion history. There is a need for properly designed, longitudinal studies that use multiple control groups, including non-contact athletes and uninjured impact sport athletes. Irrespective of the process of concussion, perhaps more time should be devoted to targeting those well defined risks, including the return of high performance athletes into mainstream society, for their life after fame. Many elite athletes have been forced to leave education early and are not trained to deal with the after-effects of their successful careers.

Until this and the process of head trauma, concussion and the pathophysiology of neurodegeneration and dementia are fully understood, we would be well advised to mind the gap between media hearsay and scientific fact.

Professor Matthew Kiernan is the Bushell Chair of Neurology at the University of Sydney, and President of the Australian and New Zealand Association of Neurologists.

 

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One thought on “Mind the gap: sport, concussion and dementia

  1. Dr Roslyn Carbon says:

    Dear Professor Kiernan,
    thank you for your article on concussion and risk of subsequent dementia. My reading of your paper is that you consider the association unproven and without evidence. However I am concerned that your statement:
    ‘The key message to date has been that concussion causes chronic traumatic encephalopathy (CTE), associated with mood disturbance and potentially suicidal behaviour’ is not suitably denied and is the kind of rhetoric which is repeated by the press and even our own profession.
    It would be very helpful if someone of your standing in the profession was able to more clearly articulate the present evidence gap, and that the current influence of the press (as well as some members of our own profession) is unhelpful in guiding clinical practice and the sensible management of the sporting environment.
    Dr Roslyn Carbon
    Combat Sports Commission (WA)

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