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Chronic Traumatic Encephalopathy, also known as CTE, has been a widely used term in today’s society, most importantly in the context of high-impact sports and the military. Research was conducted in 1973 by Corsellis surrounding boxing and repeated head injuries. He referred to it as dementia pugilistica or ‘punch-drunk syndrome’ (Alzheimer’s Association, 2018). Boxers often exhibited cognitive, behavioral, or motor abnormalities. These were well-known to sportswriters and others within the boxing community, and were referred to by a variety of terms, such as “punch drunk,” “goofy,” and “slug-nutty.” These expressions were the source of the term Corsellis used for what we now call CTE (Gavette, 2011). It wasn’t until Dr. Omalu explored the brain of retired Pittsburgh Steeler – Mike Webster, that emphasis on what they referred to as dementia pugilistica amplified. It was at this moment that Dr. Omalu realized the significance of what he had found, and how it could change the lives of many athletes. His research highlighted the fact that not only boxers are affected by this disease.
Dr. Omalu’s findings indicated that CTE has been found in individuals who have experienced head injuries from a range of activities. This includes over 200 cases from football, over 25 cases in the military, over 20 cases in hockey, over 15 cases in boxing, and over 5 cases in rugby, soccer, and pro-wrestling. Cases were also found in less impact sports, albeit significantly less than the other sports (“What Is CTE?” 2018). Many of these cases were highlighted in sports with a high likelihood of sustaining head trauma. Most individuals diagnosed with CTE have suffered hundreds or thousands of head impacts over the course of many years playing contact sports or serving in the military (“What Is CTE?” 2018). A concussion is a mild traumatic brain injury that can be caused by a hard blow to the head. It can cause unconsciousness for 30 minutes or less; some short-term symptoms often appear at the time of the injury, but can develop days or weeks later (Alzheimer’s Association, 2018). However, a single concussion does not put one at risk of CTE; multiple head traumas must occur to be put at risk. Approximately 1.6 to 3.8 million sports-related concussions occur annually in the United States (McKee, 2009). Not everyone who has been concussed will get CTE, as evidenced by the vast disparity between the number of concussions and the number of CTE cases. Since CTE is linked to repeated head trauma, it means that the cells in the brain are under threat every time a blow to the head occurs. Therefore, CTE is a form of a neurodegenerative disease (Gavett, 2011). A neurodegenerative disease is classified by the death or degeneration of nerves in the brain.
How it works
Since CTE affects the brain’s nerves, it is not curable due to the slow regeneration rate of the nervous system. CTE is a neurodegenerative disease marked by the widespread accumulation of the tau protein. The action of these proteins is what separates it from other neurodegenerative diseases (Psychiatry Neuroimaging Laboratory, 2014). However, many neurodegenerative diseases share the same symptoms and pathology, making diagnosis difficult. CTE shares many features with Alzheimer’s disease (AD), progressive supranuclear palsy, post-encephalitic Parkinsonism, and the amyotrophic lateral sclerosis/Parkinson’s-dementia complex of Guam (ALS/PDC) (McKee, 2009). The main comparison is with Alzheimer’s; in fact, Dr. Omula expected Webster’s brain to look like that of an Alzheimer patient because the symptoms were so similar (PBS). These symptoms include memory loss, irritability, outbursts of aggressive or violent behavior, confusion, speech abnormalities, cognitive decline, gait abnormalities, unsteadiness, headaches, slurred speech, and Parkinsonism (McKee, 2009). The intensity of these symptoms can depend on when athletes begin the high-impact sport and the duration of their career. Those who start younger than 12 and have a longer career increase the risk of getting CTE (“What Is CTE?” 2018).
The basic anatomy of neurons consists of the cell body, the axon, and the dendrites. There are also microtubules scattered throughout the neuron which help protect it and maintain its structure. The axon is the neuron’s weakest point; therefore, when someone sustains a concussion, these axons tend to get damaged or break. However, microtubules, although smaller and weaker than the axons, can be destroyed by just a minor head injury, even though the axons may not be affected (“The Science of CTE”, 2018). A protein called tau, associated with these microtubules, helps hold them together by adhering to the outside. In a healthy brain, one that hasn’t been damaged due to repetitive head trauma, this protein supports the microtubules, aiding cell function and ensuring the normal functioning of the brain. However, in a brain with CTE, this protein actually impairs the brain’s functionality and gradually deteriorates it (“The Science of CTE”, 2018). Because of repetitive head trauma, the tau protein changes its shape through phosphorylation and eventually clumps together, making brains with CTE unique compared to other normal or neurodegenerative brains. Brains that test positive for CTE exhibit a unique pattern of tau accumulation and clumping which results in the destruction of the cortex (“The Science of CTE”, 2018). These proteins scatter and clump at a slow rate, leading scientists to believe this to be the reason for the late onset of symptoms. It takes a considerable amount of time for these slow-moving clumps to infect enough brain tissue to alter brain function (“The Science of CTE”, 2018).
An exact diagnosis for CTE has not been found, but there are many ways that scientists believe CTE is different from other neurodegenerative diseases. A definitive diagnosis can only be made through an autopsy after death. Because of this, CTE can only be partially diagnosed based on the symptoms shown (Alzheimer’s Association, 2018). CTE symptoms often manifest around the age of 40 (“Frequently Asked Questions”). Due to the slow onset of symptoms, CTE has been seen in people as young as 17. However, since symptoms do not occur until years after the repetitive head injuries, it is impossible to tell a 17-year-old they have CTE (“What Is CTE?”, 2018). CTE is often associated with symptoms related to memory disturbances, behavioral and personality changes, Parkinsonism, and speech and gait abnormalities. Digging deeper, Dr. Ann McKee categorized the symptoms into three stages based on their invasiveness. The first stage consists of affective disturbances and psychotic symptoms. The second stage is a little more specific and consists of memory loss, erratic behavior, and early Parkinson’s disease symptoms. The last stage, being the most invasive, comprises cognitive dysfunction that can lead to symptoms related to dementia and Parkinson’s disease; speech abnormalities can also occur (McKee, 2009). Although these symptoms can be monitored, CTE can only be definitively detected after death in an autopsy.
To perform a test for CTE, doctors who specialize in brain diseases slice brain tissue and use special chemicals to make the tau clumps visible (“What Is CTE?” 2018). Doctors have found many characteristics in the brains of those with CTE that aren’t limited to just the clumping of the tau protein. These neuropathic findings include a reduction in brain weight, enlargement of the lateral and third ventricles, thinning of the corpus callosum, caving of septum pellucidum, and scarring and neuronal loss of the cerebellar tonsils. In CTE, the buildup of the tau protein often looks like a cluster of plaque that is spread throughout the cortex of the brain due to the buildup of neurons in the gray matter of the cortex (McKee, 2009). Just like any other disease, CTE varies in severity. Based on these findings in the autopsies performed, Dr. Ann McKee was able to separate the progression of the disease into different stages. There are four different stages. The first stage, one that hasn’t progressed very far, is when a few clumps of tau proteins are found in the cortex of the brain. The second stage involves more clumps present and not just in the cortex but in the cortical sulci. Here, the clumps are starting to spread and migrate. In the third stage, Dr. McKee started to see the clumps blend into one large bundle and the hippocampus and amygdala were starting to get overcome by the protein. The hippocampus and the amygdala are associated with memory and emotions which is why many people with CTE show symptoms of cognitive dysfunction. The final and more invasive stage consists of dense protein bundles covering the whole cortex of the brain and even invading the spinal cord. This leads to the symptoms of Parkinson’s Disease because those affected start to lose function of their bodies (McKee, 2015). Many of these stages involve the emotional and visceral area of the brain, explaining the symptoms many people with CTE may experience, such as emotional lability and aggressive or violent outbursts (McKee, 2009). However, these outbursts are inexplicable when they happen due to the fact that CTE cannot be diagnosed in a living person.
Scientists are looking into research that will allow doctors to diagnose living people. However, there isn’t one definite test yet that will show a positive result for tau protein buildup. Scientists are currently experimenting with PET scans and fluid-based biomarkers. A PET scan involves the use of a low-level radioactive tracer that is injected into a vein. The scanner is then able to trace the route of the tracer throughout the brain. Researchers are continually working to develop PET markers to detect tau abnormalities associated with CTE that are the most cost-effective (Mayo Clinic, 2016). There have been reports about a tracer called FDDNP. This tracer is radioactive and has the capability to bind with the abnormal proteins in the brain. Subsequently, it appears in neural PET scans (Goldman, 2018). However, there is no research showing that there has been a positive test in a living person post this finding. Research also supports the idea of fluid-based biomarkers. This method allows scientists to detect proteins present in the blood at low levels. The objective of this test is to locate the abnormal tau protein in the blood that could then lead to CTE. Typically, these biomarkers can’t cross the blood-brain barrier. However, due to repetitive damage to the brain from ongoing trauma, the blood-brain barrier is weakened (“The Science of CTE”, 2018). Researchers also propose that there might be a genetic component to this disease. As it is seen in research that not every person with repetitive head traumas or concussions develop CTE, it suggests that there might be an underlying genetic factor. Dr. Ann McKee conducted ApoE genotyping, a gene found in many cases of CTE. Some cases carried just one allele and another was homozygous. She concluded that 15% of the population has this gene and may be at greater risk for CTE if multiple head traumas have occurred (McKee, 2009). There is no definite link between genetics and CTE as of now, but with further research, the relationship can possibly be discovered.
Just like many other neurodegenerative diseases, CTE has no cure, and treating the actual disease is challenging. The only treatment at this moment involves trying to lessen the intensity of some of the symptoms. These symptoms include depression and anxiety, which are easily diagnosed by a doctor and then treated with medication (“Frequently Asked Questions”). Since CTE is closely related to Alzheimer’s disease, people with this brain disease may benefit from using the same care provided to Alzheimer’s patients. Much of this care focuses on helping these patients cope with the changes in behavior and managing their anger (Alzheimer’s Association, 2018). CTE can only be diagnosed after death, so it is difficult to treat a disease that we know so little about. A more effective way to combat this disease is to find better preventative strategies.
Prevention is one of the first and most important steps that need to be taken to control the number of people dying from CTE. It is difficult to avoid a concussion or minor head trauma without completely eliminating the sport or cause of these traumas. There have been a number of rule changes due to the increased research on the negative impacts of repetitive head traumas. However, concussions will always be an ongoing injury that require close monitoring. Therefore, the proper care and management of mild traumatic brain injuries, in general, and particularly in sports, will help reduce the number of CTE cases (McKee, 2009). Generally, athletes can return to play within a week of the initial impact. However, studies show that complete recovery from a concussion may take at least 4 to 6 weeks. This period of recovery helps prevent the chance of reinjury because a second concussion within this time period often occurs more frequently as the brain is in a weakened state. Additionally, introducing children to high impact sports at an older age can decrease brain damage. Children below the age of 12 are more susceptible to concussions, and since their brains are not fully developed, they can sustain more damage than older children (“What is CTE?” 2018).
In conclusion, only recently has CTE become a topic of discussion in relation to football and many other high-impact sports. Dr. Omula was a key factor in changing the perspective on what used to be called dementia pugilistica. He knew that his findings would change the way football is played and how even a simple concussion could be regarded as a more serious injury. Research has improved ever since Dr. Omula’s discovery in Mike Webster’s brain, but it is challenging to research and fund a disease that isn’t known until a post-mortem autopsy is performed. Since the discovery and further research into CTE, many friends and family members who have lost their loved ones to this disease now have some of their questions answered. Many people previously thought these retired players were merely depressed or had PTSD but, with today’s research, we know this isn’t the case. These athletes were suffering far more, but no one could see that. As research continues to advance, improvements in the treatment of head injuries are increasing worldwide, and hopefully, the number of CTE cases will decline. The most challenging aspect is that these improvements will not be noticeable for another decade due to the slow onset of the disease and the fact that it can only be identified after death.
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