Sports. The centre of social mobility, from protecting yourself as a leather sphere darts at you to getting armoured up ready for war only to get yet another ball to the other side of the pitch. On paper they seem to be only for the brave, but sports are celebrated all around the world bringing all types of personalities together. Nevertheless, there is a danger which cannot be ignored.
Chronic Traumatic Encephalopathy (CTE), a neurodegenerative disease thought to be linked to a history of successive blows to the head, such as those you may see on a rugby or an American football field. This disease was first seen in literature as ‘punch drunk’ often spotlighting the boxing population. But it was later found that the disease affects a much larger and diverse group of individuals with one thing in common: repeated mild traumatic brain injury (mTBI). Traumatic brain injury (TBI) is a significant public health issue. Approximately 1.5 million TBIs occur in the US per annum, with total medical costs going up to $40.6 billion a year. However there has been a large shift in focus on mTBI due to their nature consisting of long term and often fatal consequences. Over 60 million youth and adolescents participate in organised sports each year, with a growth of 16 million from 1997 to 2008. Hence the growing concern in public health, and significant scientific interest in the long-term effects of mTBIs and thus CTE, due to the recent deaths of several high-profile cases. Health sensor data indicate that football players on average experience more than 1000 hits to the head over a season. This relative exposure has resulted in subtle cognitive, mood, and behavioural changes often made apparent in later stages of life and over time progressing to dementia. Epidemiological studies indicate that professional football players are at least 4x more likely to develop memory impairment or dementia and at least 3x greater risk of dying from neurodegenerative disease. To date, all cases of neuropathologically confirmed CTE have a history of repetitive mTBI. Due to the long-term nature of the disease, investigation have usually involved post-mortem neuropathological assessment (ex vivo diagnostic) with retrospective clinical interviews (to calendar behavioural changes). Hence the severity of the symptoms are not directly proportional nor can give an arbitrary value on the force of the strikes but lies in how the brain responds to it, being different for everyone.
The brain consists of 60% soft fatty tissue and 40% of water, proteins, carbohydrates, salts and so on. This matter is called either grey or white matter. It is surrounded by many membranes and the skull itself to protect this delicate vital organ. But a sudden jolt can make the brain shift and hit against the protective layer, one can visualise this with an egg being placed in a fluid filled container.
If you look at the brain's tissue it is not uniform (image right), it is made out of a network of around 90 billion neurons; these relay signals through their long axons which are used to communicate algorithms throughout the brain (like a biological computer). This delicate structure will make them stretch and tear as the brain is impacted. That not only disrupts their ability to communicate but as destroyed axons begin to degenerate, they also release toxins causing the death of other neurons too. This combination of events causes a concussion. The damage can manifest in many different ways including blackout, headache, blurry vision, balance problems, altered mood and behaviour, problems with memory, thinking, and sleeping, and the onset of anxiety and depression. However, for most it is not a worry as a majority of concussions fully heal within a week or so. Sometimes, victims of concussion can experience something called post-concussion syndrome, or PCS. People with PCS may experience constant headaches, learning difficulties, and behavioural symptoms that last for months or years after the injury. Trying to play through a concussion, even for only a few minutes, or returning to sports too soon after a concussion, makes it more likely to develop PCS. In some cases, a concussion can be hard to diagnose because the symptoms unfold slowly over time. That's often true of sub concussive impacts (or mTBIs) which result from lower impact jolts to the head than those that cause concussions. This category of injury doesn't cause noticeable symptoms right away but can lead to severe degenerative brain diseases over time.
This then eventually links to CTE, since these people experience a big personality change and memory loss even leading to dementia. This all happens due to the protein called Tau. It supports the microtubules in our axons and so the damage of these tubes causes Tau to dislodge and clump together. These clumps will interrupt the communication signal in our brain and break down those connections. Clumps cause more clumps and spread throughout the brain even after hits have stopped.
Data shows that well over half of NFL player concussions go untreated and unreported, by oversight or otherwise. You see our brains are not built to withhold that many repeated impacts; it is not adapted to do so. If you look at the structure of the skull of the Wood-Pecker, it has a massive spiral absorption mechanism. The human anatomy is not constructed to withstand such blows.
CTE is so degenerative that it can lead to suicidal thoughts - executive dysfunction (a behavioural symptom that disrupts a person's ability to manage their own thoughts, emotions, and actions). A human being will get concussed at 60 Gs, common head-to-head contact on a football field is 100 Gs. This way of play and structure will be calling for damage.
Mike Webster was an American football center, meaning he was subjected to possibly the most amount of physical trauma on the pitch. The repeated sub-concussive blows to the head built up in every single play of every single game and every practice. From when he was a little boy up until he was a college graduate, an 18-year professional career by the calculation of Dr Bennet Omalu, Mike Webster sustained more than 70 thousand blows to the head. All of this triggered a cascading series of neurological events which unleashed killer protein Tau upon Mike Webster and all those affected by mTBIs. These clumps began within his brain and slowly developed, spreading outward.
In conclusion, we can see that college and professional football players experience more problems with executive function in everyday activity than that of an average person of their age. The symptoms appear to worsen over time usually in the 4th or 5th decade of life. Due to the diseases’ unprecedented nature of being different for each individual, there has been lots of contrast between results and no clear linear pattern has been identified as of yet. Even with this knowledge the media has a tendency to over exaggerate the extent of these findings, often painting a picture around individual cases rather than looking at it as a whole. Some data also shows that not all football players experience executive dysfunction. CTE is very difficult to treat and diagnose, most of which at the post-mortem; the development of an in-vivo diagnostic tool is a much needed and pressing issue for many researchers. In order to avoid unnecessary anxiety for individuals and their relatives who have had a history of mTBIs, the media and the scientific community need to properly address the gaps in the knowledge of CTE.