Brain injuries and concussions are a quickly growing epidemic in athletes who participate in high risk, contact sports according to the website, Head Case. Among these sports, football is at the top of the charts for the number of concussions per year. The Center for Disease Control estimates that football athletes have a 75 percent chance of sustaining a concussion during their career where professional players take 900 to 1,500 impacts to the head every season.
New studies have been released within the last couple of years highlighting the effects that sports like football and other high impact activities have on the brain over a long period of time. Camas High School’s Advanced Sports Medicine Team recently dove into the depths of brain injuries and wrote their own “case studies” to educate the public on the seriousness of these conditions.
The following study was a collaborative project written by Courtney Clemmer, Jax Purwins, Logan Sheline, and Sarah Doyle.
Traumatic brain injuries (TBIs) are classified as acute injuries to the brain occurring after a sudden force or trauma involving the head, neck, or spine. Populations most at risk for TBIs are young children aged 0 to 4, teenagers aged 15 to 24, and the elderly aged 75 and older. Males are 1.5 times more likely to sustain a TBI than females are. Many TBIs occur from common causes including, but not limited to, vehicle-related accidents, violence, sports-related injuries, explosive blasts and other activities. “Motor vehicle–traffic injury is the leading cause of TBI-related death. Rates are highest for adults aged 20 to 24 years,” according to a study conducted between the years 2002 and 2006 by the Center for Disease Control (CDC). It is important for people to understand the severity of TBIs due to the fact that most TBIs diagnosed are caused by accidents that occurred while performing ordinary tasks. Although there are still many unanswered questions surrounding the connection between TBIs and degenerative brain diseases, there is a common hypothesis that repetitive brain traumas can result in conditions such as Chronic Traumatic Encephalopathy (CTE), Alzheimer’s, and epilepsy.
The initial findings of the condition now known as Chronic Traumatic Encephalopathy were discovered in 1928 by American pathologist Harrison Martland. It was discovered by Martland when many of the top boxers in the U.S. began to show symptoms of memory loss, confusion, impaired judgment, aggression, depression, and eventually, dementia. CTE would not become an officially recognized condition for 75 more years. Initially, Martland coined the term “punch drunk syndrome” to explain the symptoms present in these boxers. Along with this term, other popular terms that were used to describe CTE were “cuckoo”, “goofy”, “cutting paper dolls”, and “slug nutty”. CTE mostly affects boxers who are the slugging type or those who were poor boxers that take a lot of hits to the head. Punch drunk syndrome was first seen only in extreme cases because referees and coaches were not aware of the severity of these symptoms. However, as they started noticing the seriousness of the effects and started looking for the symptoms, many more cases began to appear. Another problem with this was that many of the beginning symptoms were easy to keep fighting through. Due to this, many boxers kept fighting to the point where they could not even stand straight anymore. This was how Martland developed his research on CTE that was later taken up by Dr. Bennet Omalu.
Dr. Omalu, doctor and researcher accredited with the discovery of CTE, coined this term after he looked into the brain of football player Mike Webster, immediately observing that there seemed nothing wrong with the surface of the brain. He chose the name stating, “’Chronic’ means long-term, ‘traumatic’ means it is associated with trauma, [and] ‘encephalopathy’ means a bad brain.”’ Upon closer examination of Webster’s brain, it was discovered that the source of Webster’s symptoms was caused by CTE. This was only found after cutting into the deeper tissues of the brain. The brain looked similar to a patient’s brain who had Alzheimer’s, distinguishable only by a couple differences that were significant enough to become a different diagnosis. When a scientist looks into the brains of professional athletes, whether alive or dead, they are looking for specific markers that characteristic of CTE. One symptom that the University of California concluded that links acute neurotrauma and chronic neurodegeneration are “various endoplasmic reticulum stress markers were increased in human chronic traumatic encephalopathy specimens [obtained postmortem from a National Football League player and World Wrestling Entertainment wrestler], and the endoplasmic reticulum stress response was associated with an increase in the tau kinase, glycogen synthase kinase-3 beta.” The tau kinase mentioned is a protein that stabilizes and protects the structure of part of the cell inside the brain, as well as part of the cell’s internal transportation system. The damage from multiple concussions can cause the tau protein to fold and change its shape, which ends with the proteins clumping together. The shape of the protein determines its function, meaning that the changes in shapes will result in the clumps slowly killing the neurons and spreading to other cells.
The tau cell also affects other neurodegenerative diseases, leading many athletes to be diagnosed with other neurodegenerative diseases along with CTE. A literature review published in the British Journal of Sports Medicine found that of “all 158 autopsy cases examined to date for CTE…85 were athletes in a variety of sports examined in the last 10 years of whom 20% had pure CTE; 52% had CTE plus other neuropathology, and about 5% had neuropathological features of CTE without clinical CTE features.” This means that 52 percent of the autopsies that were conducted found that the damage to the brain went farther than just CTE. Other degenerative diseases are potentially found with CTE are Alzheimer’s and epilepsy, both of which can also result from TBIs.
Post-traumatic epilepsy usually has the potential to occur in two out of every ten people who sustain a TBI. Epilepsy is a neurological disorder characterized by sudden episodes of sensory disturbance, loss of consciousness, and/or seizures, that are due to abnormal electrical activity in the brain. Seizures occur when there is an imbalance within neural pathways in the brain, so that neurons “fire off” in an irregular fashion. A neuron (nerve cell) is made up of a cell body and branches called axons and dendrites which join other neurons at connections called synapses. Electrical signals are sent from the cell body along the axon to the synapse. Chemical signals (neurotransmitters) pass across synapses between neurons. Neurotransmitters cross the gap between neurons and attach to points on the adjoining neuron. And it is by these pathways that the millions of neurons within the brain can communicate and function normally. But TBI can disrupt these pathways, therefore leading to epilepsy.
The risk of epilepsy in an individual is often highly affected by family medical history, age, race, and health conditions; the risk is increased by a previous or recent history of a TBI. According to a Danish study conducted in 2009 that aimed to assess the duration at which an individual who sustains a TBI is at increased risk of epilepsy, evaluated a population of 1.6 million Danish citizens who had been diagnosed with a mild or severe TBI from Danish hospitals since 1977 and recorded whether or not they were then diagnosed with epilepsy following the TBI. During the study period, of the 17 thousand people who had an epilepsy diagnoses, 1,017 of them recorded a preceding brain injury. The results of this study concluded that the risk of epilepsy was doubled after mild brain injury and seven times higher after severe brain injury.
Furthermore, this study concluded that TBI was associated with an increased risk of epilepsy in all age groups. Although the risk increased the most with age for mild and severe brain injury and overall was highest among people older than 15 years at the time of injury. In addition, the risk of epilepsy remained at an increased level for more than 10 years after both mild and severe brain injury.
The hippocampus (responsible for memory, emotions, and spatial awareness) and neocortex (involved in sensory perception, commanding movement, spatial awareness, conscious thought, and language) are the most common structures in the brain to be injured by a TBI. Following trauma, the brain undergoes a “self-repair” phase to remodel the synaptic circuit (allows signals in the brain to travel), regain synaptic plasticity (the ability of the brain to change and form new neural pathways), and regrow nervous tissue, blood vessels, and axons (brain cells). While this process is beneficial in many senses, there is a growing theory that some of these same mechanisms are also related to the development of seizures in post-TBI epilepsy. In human and animal models, the presence of seizures following traumatic brain injury has been strongly associated with regrowth of axons and the remodeling of the synaptic circuit in many cases.
However, post-traumatic epilepsy is not extremely common, and about 70 to 80 percent of people who have seizures are helped by medications and can return to their usual activities. Medications often used to control epilepsy are known as antiepileptic drugs (AEDs) and include pharmaceuticals such as phenytoin (Dilantin), levetiracetam (Keppra), and pregabalin (Lyrica). Most AEDs work by either decreasing the number of electrical signals firing in the brain, or inhibiting neurotransmitters from binding to a neuron. Both of these methods help control the amount of electrical activity in the brain and prevent a “storm of electrical activity” that is the mechanism of a seizure.
As of 2016, 5.3 million Americans have been diagnosed with Alzheimer’s disease, according to the Alzheimer’s Association. Due to the recent technological revolution, the capacity for knowledge is now increasing allowing for further information in the medical field; one of these cases being Alzheimer’s. The disease was first recognized in 1906 by Dr. Alois Alzheimer in a case of extreme psychological and neurological disturbances; however, this disease unnamed, the patient showed symptoms of profound memory loss and a groundless suspicion of her family. In her autopsy, Dr. Alzheimer found her brain to be dramatically shrunk and showing unusual deposits around the nerve cells. Then named, in 1910 by a co-worker, as Alzheimer’s disease, the disease increasingly became more understood. Scientists, believing aging to be the only cause, conducted research under this assumption only to be finding how certain symptoms occurred but not finding a cause. It was not until the 1990s that treatments were finally developed to decrease the rate of decay in the brain. In 1993, researchers found that genetics might increase risks for said disease. Recently in 2013, the International Genomics of Alzheimer’s Project (IGAP) gathered hundreds of researchers under a common umbrella of information to identify any genetic variations linked to an increased risk of developing Alzheimer’s. Twenty different variations were discovered.
Over 110 years after the first recognition of Alzheimer’s disease, there is still no cure, and very few treatments exist. These treatments alter cognitive and behavioral aspects of the patient to work around areas of the brain that have died. Hypothetically, prevention is the most recommended treatment for a patient, but with Alzheimer’s having no known cause, not attaining Alzheimer’s is only a coin flip chance. However, medication to prevent this disease is only on the horizon of science and is not even an improbability.
In recent years, traumatic brain injuries have gained significant attention in comparison to 30 years ago when it was only compared to that of a bruise that someone would receive on their arm. In today’s time it is now seen as a significant injury and now has major recognition in the medical field. Due to the relation of a TBI and Alzheimer’s in the brain, it has been considered that Alzheimer’s might not be a disease but a condition that is a result of underlying issues and/or causes; like that of an impact to the head.
While the future of Alzheimer’s disease is unknown, it is naive to believe that it is not a single disease that is a result of age, but instead a result of an external cause that can be prevented and potentially abolished.
References:
“Chronic Traumatic Encephalopathy (CTE) in a National Football League Player: Case Report and Emerging Medicolegal Practice Questions.” – Omalu. N.p., n.d. Web. 31 Oct. 2016. Website
Corps, Daniel T., Thor D. Stein, Philip H. Montenigro, and Robert A. Stern. “Chronic Traumatic Encephalopathy: Historical Origins and Perspectives.” Research Gate. N.p., Jan. 2015. Web. Oct. 27. Website
“CTE: Discovery of a New Disease.” PBS. PBS, n.d. Web. 31 Oct. 2016.
Gardner, Andrew, Grant L. Iverson, and Paul McCroy. “Chronic Traumatic Encephalopathy in Sport: A Systematic Review.” ProQuest. N.p., Jan. 2014. Web. 31 Oct. 2016.
Health & Medicine Week. “Neurotrauma; New Neurotrauma Findings from University of California Described (Endoplasmic Reticulum Stress Implicated in Chronic Traumatic Encephalopathy).” ProQuest. N.p., 25 Mar. 2015. Web. 21 Oct. 2016.
Hunt, Robert F., Jeffery A. Boychuk, and Bret N. Smith. “Neural Circuit Mechanisms of Post–traumatic Epilepsy.” Frontiers in Cellular Neuroscience. Frontiers Media S.A., 2013. Web. 28 Oct. 2016.
Schachter, Steven C., MD, Patricia O. Schafer, RN, MN, and Joseph I. Sirven, MD. “Who Gets Epilepsy?” Epilepsy Foundation. N.p., July 2013. Web. 26 Oct. 2016.
The Royal Children’s Hospital Melbourne. “The Royal Children’s Hospital Melbourne.” Neurology: Antiepileptic Medications. N.p., n.d. Web. 30 Oct. 2016.
“What Is CTE?” Concussion Legacy Foundation. N.p., 27 July 2016. Web. 31 Oct. 2016.
