The Silent Epidemic: Is CTE Changing the Future of Contact Sports?
Dementias are a spectrum of diseases, with diverse causes, some genetic, some unknown, but recent news has highlighted a particular trigger that leads to a form of Dementia known as Chronic traumatic encephalopathy (CTE).
This complex name gives clues as to the underlying cause and effect, whereby repeated traumatic head injury (chronic; traumatic) can lead to sustained damage resulting in brain dysfunction (encephalopathy).
The link between dementia and football (soccer) has gained significant traction in recent years. Notably, five members of England's legendary 1966 World Cup-winning team—Nobby Stiles, Jack Charlton, Martin Peters, Ray Wilson, and Sir Bobby Charlton—developed dementia later in life.
The news of the diagnosis for CTE of prominent Celtic and Burnley footballer Andy Payton has reignited discussions about safety in sports.
Here we delve into cause and effect and explore the possibilities for therapeutic intervention whilst supporting changes to sporting body regulation to avoid traumatic events involving the brain.
The Brain: A complex and delicate organ
The brain is a complex and delicate organ that resides inside a bony skull surrounded by a membrane called the meninges and liquid called cerebrospinal fluid which provide cushioning and protection as well as nutrients. The brain itself contains over 86 billion neurons responsible for thinking, feeling, memory, emotion, action and movement.
These are supported by immune cells called glia which are responsible for maintaining brain health. A blow to the head can result in obvious symptoms of concussion, which usually resolve over time. In the case of a severe blow, the brain may bounce within the skull, resulting in damage to both the side of impact and the opposite side. The brain white matter, which is made up of the elongated axons of neurons along which information flows may be damaged resulting in some acute symptoms.
The body may respond with inflammation around the damaged site which can result in healing but also some unintended consequences of swelling and further damage.
The brain is a complex and delicate organ that resides inside a bony skull surrounded by a membrane called the meninges and liquid called cerebrospinal fluid which provide cushioning and protection as well as nutrients
It is thought that repeated head injury can lead to accumulated damage and that CTE could be the result. Sports bodies have responded with guidance to prevent concussions and to allow sufficient recovery following head injury.
How IS A CTE diagnosed?
CTE was first described by a neurologist Macdonald Critchley in 1949 following previous descriptions of boxing-related dementia, Dementia puglistica. The condition was brought into the spotlight by Dr Bennet Omalu in his work with an American footballer leading to robust discussions between science and sport about cause and effect.
The diagnostic criteria for CTE in still under development, but it can be diagnosed by a combination of assessment of history of repetitive head injury and dementia symptoms, such as memory, coordination, movement problems and severe depression.
However, confirmation is postmortem when protein aggregates can be observed in the brain tissue. These neuronal deposits are made from a protein called tau, which normally supports the architecture of cells but in the case of a group of diseases known as the “tauopathies” aggregates to form fibres that accumulate inside neurons. These fibres are known as amyloid fibres.
Electron microscopy of Tau filaments in postmortem brain tissue (magnification 10,000x).
This process is known as protein misfolding and in the case of CTE, it is thought that the protein misfolding event is triggered by repeated head injury. Pathological protein misfolding is involved in the majority of dementias including Alzheimer’s disease, Parkinson’s and frontotemporal dementia, as well as in some non-brain related diseases such as Diabetes type 2.
Each disease is identified with different protein(s), where Parkinson’s is associated with a protein called alpha-synuclein and Alzheimer’s disease with two proteins, Amyloid-beta and tau.
Research is intense to understand why this protein misfolding and accumulation results in disease and to work towards prevention or removal of the aggregates. For example; recent advances in Alzheimer’s disease treatment have hailed antibody therapies aimed at detecting and removing amyloid-beta aggregates from the brain.
What about Therapy?
Once someone has been diagnosed with CTE, treatment is mainly to help with symptoms, but disease modifying treatments are currently under development.
Exciting new drugs that target tau aggregation and aggregates are being developed and some are nearing the clinic. However, as with all Dementias, early diagnosis is key to effective treatment, since prevention of damage is paramount to prevent brain degeneration. Early diagnostic tools are also being developed, including blood tests to look for specific biomarkers that can assess for the presence of tau and other markers and distinguish from other dementias. Brain imaging using compounds that detect tau in the brain are also being developed so that several tests can be combined to help with a definitive diagnosis.
OUR FINal thoughts
Question: What more could we all do to raise awareness, reduce the risk of CTE in sport, AND protect brain health?
We could start with grassroots youth sport.
Youth Football in the UK
Recent research and policy changes have drawn attention to youth players in football. The Football Association (FA) implemented a phased ban on heading the ball for children under 12 from the 2022/2023 season, reflecting mounting evidence that repetitive head impacts, even those not resulting in diagnosed concussion, may cause longer-term brain changes.
Children are particularly at risk because their skulls are less developed, and they have weaker neck and trunk muscles, making them more susceptible to forces involved in heading.
Moreover, young players often lack proper heading technique, increasing the risk of injury.
This underlines the need for tighter regulation and education around heading and head impacts in youth football.
Youth Rugby in the UK
Rugby poses a higher risk of concussion and head injury than football, with youth rugby showing a significantly higher rate of concussion than any other contact team sport.
Surveillance data from English schools indicate that match injury rates in youth rugby are substantial, with concussion rates highest among older teens, but still significant in younger age groups. Notably, a study examining the brains of former rugby players found CTE pathology in about two-thirds of cases, with a clear link between longer playing careers and higher risk
The majority of rugby-related concussions occur during tackles, and a worrying proportion of concussed players return to play before the minimum recommended recovery period, increasing the risk of further injury and long-term consequences
There is also a lack of independent research and systematic injury tracking in youth rugby, complicating efforts to fully understand and address the problem
What Could Be Done to Mitigate Brain Injuries in Sport?
A multi layered approach is required to reduce the risk of CTE and other brain injuries in youth football and rugby, which includes awareness, education, and action at all levels of sport.
This could include;
Banning or Limiting High-Risk Activities: The ‘phasing out’ of heading in under-12 football is a significant step, aiming to prevent early exposure to repetitive head impacts. Similar calls have been made to limit or ban tackling in school rugby, especially for younger children.
Education and Technique Training: Proper technique training for heading in football and tackling in rugby is crucial. Coaches should be educated to teach safer methods and to recognise and manage head injuries. For example, initial heading training in football can use sponge balls before introducing regulation balls.
Strength and Balance Programmes: Evidence from rugby shows that targeted exercise programmes focusing on neck strength, balance, and movement can reduce concussion rates in youth players.
Strict Concussion Protocols: The UK government has issued new concussion guidelines for grassroots sport, emphasising the principle "if in doubt, sit them out," to ensure that any suspected concussion is managed with caution and that players only return to play after full recovery. These protocols need to be rigorously enforced in both football and rugby.
Monitoring and Research: There is need for further independent research into youth sports injuries and for systematic tracking of head injuries at all levels. This will inform help future policy and help evaluate the effectiveness of preventive measures.
Cultural Change and Support: Governing bodies, clubs, and schools should foster a culture of safety, prioritising player welfare over competitive success. Support systems should be in place for players who sustain brain injuries, including access to medical care and rehabilitation.
