Introduction 

Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disease caused by repeated head trauma, which involves both symptomatic concussive and non-concussive hits. There are growing concerns over the prevalence of CTE in contact sports; CTE has been most diagnosed in athletes who participate in contact and collision sports, including American football, rugby, boxing, MMA, and wrestling. As the effects of CTE can be detrimental, it is important for athletes and sports organisations to understand the risk of repetitive head injury, and to advocate safe practice.¹

What is CTE?

Cause and risk factors 

CTE is a progressive neurodegenerative disorder whose underlying pathophysiology is still unknown. CTE can be characterised by an accumulation of hyperphosphorylated tau proteins deposited as neurofibrillary tangles which interfere with the brain’s neuronal function.

There is a positive correlation between the number of head injuries and the amount of tau deposition in the brain. Studies have shown that the TDP-43 protein is also present in 80% of CTE cases. Postmortem studies of CTE patients revealed altered brain anatomy, mostly including enlargement of the frontal and temporal horns of the lateral ventricles.² 

The biggest risk factor is a history of repetitive head injury, with all cases of neuropathologically confirmed CTE reporting incidences. Currently, there is no other confirmed non-genetic risk factor. CTE and Alzheimer’s disease (AD) share similar neuropathological features; hyperphosphorylated tau.

The apolipoprotein E (ApoE) e4 allele is a recognised genetic risk factor for AD, and it is thus speculated that the ApoE-e4 allele increases the chance of CTE.³ Research on CTE, is still limited. Not everyone who has experienced repeated brain injury or concussion will develop CTE, nor does the possession of the ApoE-e4 allele necessarily result in CTE. 

Symptoms 

The clinical symptoms typically present years after the initial brain injury, with symptomatic presentation appearing sooner if exposed to repeated head trauma. 

CTE can affect patients via three domains: behavioural/psychiatric, cognitive, and motor. Clinical symptoms of CTE present in stages:

• stage I is typically asymptomatic with the occasional affective disturbances
• stage II symptoms include social and motor instability
• stage III involves general cognitive dysfunction
• stage IV presents with severe symptoms including language deficits, psychotic symptoms, and motor deficits

Common symptoms include memory loss, impaired judgement, confusion, parkinsonism, and depression. Symptoms can be attributed to altered brain structures, for example, changes to the structure of the hippocampus or the amygdala can limit decision-making skills and the ability to regulate emotions.⁴ It is important to note that having some of these symptoms does not guarantee CTE, as its diagnosis can only be made post-mortem. A lot of these symptoms overlap with other neurodegenerative diseases. 

The connection between contact sports and CTE

History

There has always been a strong connection between sports-related brain injuries and CTE, the first clinical description of CTE was coined “punch drunk syndrome” in the 1920s to describe the effects of repetitive head trauma in boxers.⁵ In the past “sports-related traumatic brain injury” (TBI) and CTE were used interchangeably, however, the latter gained popularity after the 1940s due to an increased understanding of induced neurodegenerative diseases. 

Research evidence

Researchers at Boston University revealed in a study that 345 out of 376 (91.7%) former NFL players were diagnosed with CTE, highlighting the prevalence of CTE in high-contact sports.⁶ In a 2023 study where 631 postmortem brains of ex-football players were studied, it was found that 163 had low-stage CTE, while 288 had high-stage CTE. Only 28% of samples had no evidence of CTE. 

The number of years playing football and the amount of exposure to head injury also affected the severity of CTE, every additional year playing football increased the chance of CTE diagnosis by 15%. Analysis suggests that repetitive mild traumatic head injuries were major drivers of CTE rather than acute symptomatic concussion.

Although the detrimental effects of repeated TBI are acknowledged, there is still scepticism on where there is a confirmed link between sports concussions and CTE.⁷

Notable cases

The first major league baseball player to be diagnosed with CTE is Ryan Freel, resultants of several concussions during his career. In 2012, Freel committed suicide, at the time of death, he was suffering from stage II CTE.

The most notable case of CTE in sports is American football player, Aaron Hernandez, who suffered the most severe case of CTE ever discovered in a person. Scientists discovered stage 3 CTE postmortem at the age of 27, which had never been seen in a person younger than 46.

This discovery highlighted the silent and ongoing crisis of repeated head injuries in sports and raised awareness of the risk of CTE. Hernandez’s case also provides evidence for ApoE-e4 as a risk factor, researchers postulated that the severity of CTE in his brain was partly due to genetic factors.⁸

Prevention and safety measures

Currently, there are no recognised treatments for CTE, and the only method of diagnosis is post-mortem brain analysis, emphasising the significance of prevention and safety measures in sports. Protocols, protective headgear, and rule changes are enforced to minimise the number of head traumas and concussions. 

Safety protocol

Safety protocols consist of CTE prevention during practise and the game itself; aiming to reduce the number of head impacts and reducing the strength of head impacts. Athletes should reduce or replace practise drills that result in head trauma, as well as focus on techniques that involve tackling or blocking.

This technique can also reduce the strength of impact on the head. Rules changes to the game can help reduce the amount of hits athletes face, for example, in baseball, a new rule in 2013 outlawed collision at the home plate.

NHL games were notorious for on-ice fighting, however governing bodies started implementing misconduct rules and penalties for those who participate to minimise health risks. The NFL has reduced the number of kickoff returns by moving up the kickoff line to reduce the strength of head injury, and implementing penalty hits to the back of the head to defenceless players.⁹

Protective headgear and technology

For contact sports, protective headgear should always be worn for games and practise. Wearing a helmet can prevent head injuries and concussions. Evidence also suggests that wearing an ill-fitting and improper helmet at the time of head injury results in more severe and longer-lasting symptoms.

Technological advancements to headgear can further protect athletes, sensors on the helmet can record the strength of impact and the number of head hits per game. If records go over the safety threshold, the athlete would be advised to retire from the game.

Rule changes

New return to play (RTP) guidelines have been developed to determine when athletes are allowed to return to playing their respective sports. RTP guidelines are based on the severity of concussion, and the number of concussions occurring in one sports season.

For example, a grade I concussion requires the athlete to be asymptomatic for a minimum of one week before returning to play, whereas a grade III concussion requires one month. An athlete’s second grade I concussion requires two weeks symptom-free, while a second grade II concussion results in a terminated season for the athlete. 

Controversy

The connection between sports and CTE is still a cause for controversy; many are still sceptical about the link between concussion and brain disease, as shown at the International Consensus Conference in Sports. To completely prevent CTE in sports, sports governing bodies and associations must recognise the dangers of repeated head injuries, and implement standardised safety protocols in their respective sport.¹⁰

Treatment 

The distinctive tauopathy of CTE can only be determined postmortem, therefore diagnosis of CTE can be challenging. Without proper diagnosis, putting patients on a treatment plan can be difficult. Currently, there is no specific treatment available, emphasising the importance of prevention and safety protocol. Supportive therapies can be used to help cope with the disorder, for example, motor therapy and cognitive rehabilitation therapy. There is a high suicidality rate among athletes with CTE, antidepressants/anxiolytics may be prescribed to manage the psychiatric symptoms of CTE.¹¹

Summary

CTE is a neurodegenerative disease caused by repetitive head trauma leading to cognitive, motor, and psychiatric deficits. The disorder is most common in athletes who play contact sports, prevalence within the sports community and its potentially debilitating effects call for preventive action and emphasise the importance of prioritising safety in contact sports.

Future medical advancements for CTE includes innovations in diagnosis and the introduction of treatments that cure CTE on a neuropathological basis, for example, drugs that target tau phosphorylation for acetylation. In the meantime, sports organisations and governing bodies are responsible for educating athletes on the risk of repetitive minor head injuries, and ensuring informed consent.

Preventive measures must be implemented to minimise the risk of CTE development, this includes establishing safety protocol, wearing a helmet, and making rule changes when an athlete’s safety is compromised.