Earlier this year, Aaron Hernandez, an American football player, killed himself in his cell after being tried for a double murder. He was a rising football star when his legal issues first became public and many lamented how this put an end to what could have been an extraordinary career. Hernandez’s family decided to donate his brain to the CTE research center in Boston, with the intention to discover whether the athlete was affected by this neurological condition.
Although I have heard about Chronic traumatic encephalopathy before, it wasn’t until I read the news on Aaron Hernandez that I decided to delve into it. CTE is barely mentioned outside of the United States and I think that European sports authorities should be aware of the problem of repeated head trauma in players.
The consequences of repeated brain trauma amongst boxers are well documented. Dementia pugilistica -a subtype of CTE- has been studied since the late 1920s. Repeated head injuries in boxers can cause a pattern of neurodegeneration that produces dementia-like symptoms; cognitive and motor impairment, as well as mood and personality changes, which range in severity.
For many years, it was thought to only affect boxers, leading some medical professionals to ask for a ban on the sport. It is a recent discovery that repeated mild traumatic brain injuries increase the risk of neurodegenerative disease in athletes who play contact sports.
Although most research has been carried out in the context of American football, it is important to note that there are cases of CTE in many other sports; hockey, rugby, baseball, martial arts, soccer and motocross (BMX), as well as in people with military service.
Chronic traumatic encephalopathy usually manifests itself after about a decade of repeated injuries. Considering that many athletes begin their sports practice early on (ages 12 to 18), first-stage symptoms can be observed in young players in their early twenties . Nevertheless, problems usually begin later in life.
CTE shouldn’t be confused with a post-concussion syndrome where symptoms are present shortly after a concussion but eventually go away. CTE consists in a progressive degeneration of the cortex and neuronal loss that, once it has been triggered, won’t stop in the individual’s lifetime. It has many similarities with Alzheimer’s and Parkinson’s disease, but in the case of CTE, we do know it has a clear environmental cause.
The diagnosis can only be confirmed post-mortem, once brain material is available to be examined. The research center I mentioned at the beginning of the article has examined the brain tissue of 94 former NFL players that presented symptoms and has concluded that 90 of them suffered from CTE.  Some of them had committed suicide at an early age, just like Aaron Hernandez did.
So, what can be done about this?
Since CTE is caused by recurrent concussions, the only way to prevent it, it’s by reducing the amount of exposure to head trauma. Unfortunately, that’s not an easy task. Sports-specific helmets seem to reduce injury in some sports. It is important to pay attention to the design and materials of the helmet as well as to make sure that it is replaced once it has taken a big hit.
Another very important factor is the “Return-to-play” criteria after a head injury. Studies suggest that a head injury should require at least 4 to 6 weeks of recovery time to avoid re-injury. Sadly, in some cases, these guidelines are not strictly enforced.
Lastly, athletes would benefit from some sports rules changes as well as from severe penalization for intentional hits to the head.