CTE in sport – what are the risks?

CTE stands for chronic traumatic encephalopathy

CTE is a neurodegenerative disease that is most often found in people who have been exposed to repeated knocks to the head, such as boxers and football players earlier in their life. These knocks to the head can be relatively mild, such as concussions, and do not need to include loss of consciousness. CTE can only be definitively diagnosed by sectioning and viewing the brains of people who have died.

In the brains of most people with CTE, there are distinctive patterns of deposits of a particular protein called hyper phosphorylated tau as well as other pathological proteins. These proteins are also found in other forms of neurodegeneration such as Alzheimer’s Disease, but the pattern and extent of distribution of these proteins are distinctive in CTE. The clinical symptoms of CTE are variable and have included reports of lack of emotional control and suicide, as well as debilitating dementia and problems with motor function.

CTE was initially described as dementia pugilistica or ‘punch drunk’ disease in boxers in the first half of the twentieth century. Since then, American football players and athletes in martial arts, ice hockey and other sports have been diagnosed with CTE. Understandably, there is widespread and increasing concern about the long-term effects of multiple impacts to the head, such as are experienced in contact sports. The Australian context has been emphasised recently with the establishment of the Australian Sports Brain Bank, which continues to analyse the brains of Australian sports players after their deaths, including rugby league players and Australian Football legend Polly Farmer; and diagnosed them with CTE.

It is difficult to get a clear idea of how widespread CTE is in the Australian population. CTE neuropathology has been found in the brains of contact sport athletes with repetitive concussive and subconcussive head injuries, in military veterans with combat-related blast exposure, and in long-term survivors of a single more severe TBI. While most people with CTE have a history of these kinds of injuries, a subset is notable for the absence of prior concussion, and it is possible that repeated knocks to the head, even in the absence of frank concussion, may lead to brain pathologies associated with CTE.

The situation is complicated because studies rely on brain banks where people donate their brains for study. People may be more likely to donate their brains if they suspect they have a problem. Therefore the studies are not necessarily well controlled by the inclusion of people with a similar history of concussions but no long-term symptoms. There have also been numerous reports on findings from a single person, known as case reports. While interesting, these studies lack good controls and findings are not able to be extrapolated to the wider population. This potentially biased sampling may lead to an over-estimation of the incidence of CTE in contact sport athletes.

Therefore, it is important not to over-emphasise the problem of CTE. Surveys show that retired professional American football players have lower standard mortality rates and lower risk of suicide than the general population. Sport brings important benefits to health and wellbeing and risks of CTE are relatively low and balanced by the benefits of improved fitness, weight control and quality of life.

However, given that CTE occurs predominantly in people with a history of repeated concussion, it is sensible to reduce the likelihood of repeated concussions to lower one’s risk. Even though one may no longer be experiencing symptoms from a concussion, changes to the brain continue. Experiencing a second concussion close to the first, while brain metabolism and cellular changes are likely to be continuing, increases the risk of prolonged symptoms.

There is a long latency period between blows to the head and development of symptoms consistent with CTE. This means that athletes may continue to expose themselves to additional concussions and thereby exacerbate the damaging processes that lead to CTE. Repeated subconcussive impacts may also lead to similar brain changes, although this is much less studied.

Current helmets do not reduce the impact of the brain on the inside of the skull that occurs with concussion and probably subconcussive impacts, and will not influence the rotational forces that act on the brain. To reduce the incidence of CTE, it is necessary to protect the brain by reducing the likelihood of repeated concussions. The enjoyment of contact sports can hopefully be compatible with continued efforts to adjust rules to minimise risks of repeated concussions.

Recent changes to the rules for soccer heading in the UK in children are testament to community concern and the possibilities of future CTE. Given the critical developmental brain changes occurring in adolescents, it is sensible to limit possible damage, at least until more studies have been conducted to enable an evidenced base decision about headers in soccer and other sports where subconcussive impacts occur.


Author: Melinda Fitzgerald: Professor of Neurotrauma, Curtin University and the Perron Institute for Neurological and Translational Science, and CEO Connectivity.