Abstract: Nearly four million youth athletes play football in America every year. Recently, evidence has amassed suggesting that a neurodegenerative brain disease called chronic traumatic encephalopathy (CTE) is directly linked to the repetitive concussive and subconcussive injuries that are generated during contact football. This paper investigates the link between CTE and youth football participation, analyzes the policies and laws that govern protection for athletes in Maryland, and questions whether the current legal structure is enough to prevent the development of brain diseases in the nearly thirteen thousand Maryland athletes that engage in youth football. After examining medical research studies, law journals, and other scholarly literature, it was determined that the key to preventing youth head injuries and brain disease in Maryland is through a reform of Maryland’s current concussion laws. Additionally, this work expands the medical and political discussion surrounding youth head injuries by offering recommendations and proposing guidelines for the state of Maryland to consider implementing in pursuit of a safer athletic policy. By altering the existing youth football laws in Maryland, youth athletes will be better protected from brain diseases like CTE in the future.
The surface must be clean, free from anything that will contaminate the work area. A small box is brought into the well-lit room and a chilled brain is removed and placed on the metal table. This brain is measured, weighed, and checked for visual impurities. To the surprise of the surgeons, it is perfectly normal and intact. This is quite intriguing to them, considering the thousands of impacts and damages that brain has sustained the past few years during multiple football seasons in Kansas. They then begin using large knives to slice the brain into long, thin pieces; like a loaf of bread being served at a lunchtime deli. The pieces are carefully placed under a microscope and checked again, this time looking far beyond the surface level, deep into the brain. The second examination confirms what these workers had originally thought, “This brain has been destroyed!” they exclaim, “The only thing holding it together is a glue made from clumped proteins.” Their conclusion becomes a source of finality for the patient’s family. Nathan Stiles died from a brain disease called chronic traumatic encephalopathy, he was seventeen years old (Parks, 2015).
Unfortunately, this story has become a far to common reality for many athletes across the United States. Chronic traumatic encephalopathy, also known as CTE, is a neurodegenerative brain disease resulting from violent and repetitive impacts, crippling football players over time. While football has remained one of America’s most popular sports to watch and to play, the discovery of CTE has caused a major shift in the way football is perceived and approached by players and lawmakers alike. Even parents of young players, including those that are athletically talented, have also begun to reconsider the advantages of the once cherished childhood sport (Zielonka, 2018). Many schools and organizations have adapted to this change, altering game rules, making better equipment, and instituting law policies to combat CTE. However, a growing body of research suggests that treating brain injuries after the fact is not enough to prevent brain diseases like CTE from developing. Instead, medical researchers argue that it is now necessary to create additional legislation that prevents brain injuries at the youth level, along with providing improved, immediate treatment for injured athletes. The state of Maryland is one such example of a governing body that needs to embrace further changes. Having already passed the head injury policy known as the Lystedt Law in 2011, the time has come for Maryland to expand the protections and boundaries that safeguard athletes from CTE by extending the existing legislation in order to create a deeper, broader head injury policy that will prevent youth players from developing this life changing disease later in adulthood (“Maryland Youth Concussion”, 2011).
Football is by far the most dangerous sport in America for an athlete. A breeding ground for injuries, it has the highest injury rate of any sport and it is responsible for the highest concussion rates in youth, collegiate, and professional sports (Moran, 2015). Additionally, it has been consistently responsible for the highest injury rate of all high school sports for the past thirteen years (Kawahara, 2018). While many injuries, such as a broken bone or a torn muscle, can be easily fixed through surgery, the most startling injuries come in the form of traumatic brain injuries (TBI). These are very different from regular injuries because TBI’s cause permanent damage to the structure of the brain while simultaneously interrupting its ability to function properly. The most common TBI in football is the concussion. Concussions are categorized as a mild traumatic brain injury that directly change the neurological functioning of the brain (“What Is a Concussion”, n.d.). They are usually sustained by shaking, whiplashing, or hitting the head in a way that causes the tissue of the brain to stretch beyond its normal capacity. When the brain is stretched, it forces the tissues of the brain to move and change shape, damaging the structural integrity of the tissue in the process. This form of TBI is particularly recognizable because of the noticeable symptoms that are present. While every case is unique, concussions usually impact physical, emotional, cognitive, and other bodily process, such as sleep. For the athlete, concussion symptoms range from headaches and nausea, memory problems and attention issues, depression and anxiety, and an inability to sleep (“What is a concussion?”, n.d.). Considering how the brain literally controls every process in the body, it is logical to have blatant side effects from such a significant injury. Concussions also have the propensity to become specifically lethal when they are sustained in succession, an event is known as “second-impact syndrome” (Miller, 2010). Having two concussions in such a short time-frame can cause the brain to swell within the skull, an event called edema, and will eventually lead to death (Miller, 2010).
While concussions have garnered the most attention surrounding head injuries in football, subconcussive injuries are just as dangerous for the athlete. Subconcussive injuries are microtraumas to the brain tissue that causes damage below the threshold that would normally generate a concussion and destroy brain cells (“Subconcussive Impacts”, 2018). Instead, the subconcussive injury causes substantial damage when sustained in high volumes, such as the many impacts encountered during a football game. As the brain is repeatedly traumatized and impacted, the structure of the brain begins to degrade, and its functions start to become inhibited. In theory, this type of damage is similar to the throwing injuries encountered by baseball pitchers. Every time a pitch is thrown during a game, the ligaments and connective tissue of the pitcher’s arm are slowly stretched and damaged, eventually causing serious injury if not treated with rest and proper recovery (“Subconcussive Impacts”, 2018). So, while one game of high velocity pitching may cause some initial tissue damage, pitching multiple games in a row will present a greater amount of risk. For the football player, sustaining a large amount of hits to the head, even if they do not result in concussions, will result in brain injury over a long-term period of time, just like a baseball pitcher. This sentiment is echoed by professor Lee Goldstein of Boston University who states that “It’s hits to the head, not [just] concussion[s], that cause [traumatic brain disease]” (Barlow, n.d.). However, even though the long-term damage caused by subconcussive injuries is considered more harmful than the effects of a single concussion, the most concerning injuries are caused when concussive and subconcussive injuries are sustained simultaneously. If encountered over a continuous period of time, such a combination will result in brain disease.
Chronic traumatic encephalopathy, commonly known as CTE, has become the most notable and discussed sports-related brain disease associated with playing football. Historically speaking, it was originally identified by pathologist Harrison Martland in the late 1920’s and became known as “punch-drunk syndrome,” an observation made from noticing the neurological effects that punches had on boxers after their fighting careers (Sigurdsson, 2017). In the 1930’s, the disease would become known as dementia pugilistica, a Latin phrase describing the dysfunctional neurological condition experienced by boxers in the later part of their lives (Sigurdsson, 2017).
According to the University of Boston CTE Research Center, CTE is defined as a progressive neurological disease that causes degeneration of brain tissue and a decline in overall brain function. This is because CTE literally causes parts of the brain to rot away over time. The gradual degeneration is the result of an accumulation of a special protein, called tau, that is released after a concussion or subconcussive injury (“The Science of CTE”, 2018). Every part of the brain is comprised of cells called neurons that have specific functions and jobs that coincide with the area of the brain in which they are located. The anatomy of the neuron is also similar for all brain cells and each part of the neuron has specific functions (Robb, n.d.). The neuron is comprised of four main parts: the axon terminal, the axon, the soma (body of the cell), and the dendrites. The axon terminal and the dendrites, which look like clustered tree branches, are located on opposite sides of the neuron and allow the cell to communicate information to other cells by releasing and accepting nerve impulses. The soma facilitates the transfer of information and contains all of the materials that comprise a eukaryotic organism, such as a nucleus and other organelles. The last section of the neuron, the axon, is a thin cord of nerves that connects the soma and dendrites to the axon terminal. The axon also transports information and materials throughout the neuron, holding it together in the process. The axon’s long cord also has smaller cords that are sealed inside it (“The Science of CTE’’, 2018). These smaller cords are covered by the protein tau to provide structure and protect the axon so it can perform its function.
While tau allows the neuron to work properly, it is also the main cause of CTE. As mentioned before, concussions and subconcussive injuries cause the brain to stretch and move within the skull. During such an impact, the axon, the weakest part of the neuron, is the most susceptible to damage and can break apart (“The Science of CTE’’, 2018). This breakage causes the tau protein to become dislodged from the axon’s cord and start to drift into other parts of the neuron. While afloat, the free tau proteins begin to clump together and expand, polluting the other parts of the brain tissue in the process. Most disturbingly, these free bunches of tau will continue to spread without encountering other impacts, sometimes remaining dormant for years after the initial impact (“The Science of CTE’’, 2018). This effect is known as prion spread, where a protein clumps together and expands into other areas, causing decay and damage in the process (“Prion Diseases”, n.d.). As head impacts are repeatedly sustained, and the tau protein is spread, different parts of the brain begin to stop functioning properly due to the pollution. The spreading of tau is so detrimental because it disintegrates the neuron, blocks neural pathways in the brain, and will inhibit the brain’s ability to function properly. Proliferation of tau protein leads to memory problems, emotional changes, and physical handicaps, eventually becoming fatal (“Prion Diseases”, n.d.).
With the brain’s ability to function paralyzed by the proliferation and pollution of the tau protein, many of the body’s normal processes become altered or inhibited. As the tau protein clogs and kills the tissue of the brain, the areas of the brain responsible for specific body functions are destroyed in the process. For example, if the tau protein is spread to the frontal lobe, the part of the brain responsible for controlling decision making and reasoning, it begins to kill the cells within the frontal lobe’s tissue; that portion of the brain will no longer be able to perform its job because the tissue has wasted away. Or, if the hypothalamus is affected, the part of the brain that controls thirst and hunger, a person will not be able to regulate their body’s need for food and water. Because of this, patients with CTE will display a range of physical, emotional, and cognitive symptoms that are caused by the neurodegeneration (“Chronic Traumatic Encephalopathy”, n.d.). Common physical symptoms include persistent headaches, distorted vision, and physical disability, like trouble moving or swallowing. The emotional changes include irritability, anger, impulsive actions, depression, suicidal thoughts, and substance abuse. Lastly, the cognitive symptoms demonstrate an inability to think, memory loss, and speech inhibition. There is also a connection that links this damage to other cognitive disorders such as Parkinson’s disease, Alzheimer's, and dementia (“Chronic Traumatic Encephalopathy (CTE)”, n.d.). These symptoms are just a reflection of the damage and degeneration that has occurred and how the parts of the brain responsible for those processes are no longer in functioning due to the neuropathology.
In football, chronic traumatic encephalopathy has become an epidemic, affecting almost all of those that play on the professional or collegiate level. In a groundbreaking study conducted by Boston University, researchers dissected 202 brains of former football players and analyzed them for signs of CTE. Their study looked at the brains of 111 NFL players, eight Canadian League players, fourteen semi-professional players, fifty-three college players, and fourteen high school players. The results were shocking, finding that over ninety-nine percent of former professional players and ninety-one percent of college players had tested positive for the CTE. They also discovered that twenty-one percent of high school football players has contracted CTE as well. The study also found that all of the brains that did not have CTE present were already beginning to show signs of neurological diseases, like alzheimer’s disease (Moran, 2018). Another study investigating CTE prevalence in football conclude that “96% of deceased former NFL football players showed signs of CTE” and that “79% of all football players tested who played at any level, including some who did not play professionally or collegiately, showed signs of the disease” (Spaude, 2017).
The research conducted by Boston University, and other institutions, also indicates that the concussive and subconcussive injuries encountered at the youth level directly contribute to developing CTE in the future. According to a study conducted by the National Center for Biotechnical Information, there are nearly four million estimated concussions caused by sporting events every year. For high school football players, concussions account for over 60% of all injuries, football itself being the leading cause of high school concussions (“What Is a Concussion?”, n.d.). Twenty-percent of high school football players will also experience some form of brain injury during the course of a season; a disturbing fact when considering that the players that sustain one concussion are then three times more likely to sustain another (“What Is a Concussion?”, n.d.). Even more concerning, the rates of youth concussions and head injuries are also considered to be largely underestimated, leading experts to believe that children receive brain injuries with a much higher regularity than currently reported (Crisco et. al, 2011). One such NCBI study concluded strongly that, even with a lack of precise concussion data, the large amounts of subconcussive injuries sustained during play will lead to neurological problems and disease over time, and that limiting youth exposure to these injuries is essential for their long-term protection (Crisco et. al, 2011).
Research also indicates that tackling is particularly dangerous for young players. The vast majority of concussions and subconcussive injuries are caused by tackling, hitting into another player, or making direct contact with the head (“Tackling in Youth Football”, 2015). This is understandable when considering the physics behind a head injury. Despite being smaller in stature, younger athletes can still generate enough force to cause acceleration and deceleration in the brain after a collision (McKee et. al, 2009). For example, if a youth player is tackled from the front, their brain will accelerate forward and begin to stretch. Once the brain has moved to the front of the skull, it will then be pulled backwards as it readjusts in the skull. In this way, a direct hit to the head, or a tackle to the ground, creates rapid acceleration, then sudden deceleration; initiating enough force to cause the brain tissue to stretch and, subsequently, create an injury. Another study found that tackling was a leading cause of CTE and other neurological problems, showing that for every year of tackle football played under the age of twelve, CTE symptoms appeared two and a half times earlier (McCarthy, 2018). Tackling at the youth level can also be just as dangerous as it is in higher levels of play. One research study by Virginia Tech focused on seven and eight year-old youth athletes and found that these athletes sustained over one-hundred head injuries while playing, some with impact forces just as strong those seen in college play (Robbins, 2012). The University of Purdue also looked at the danger of youth tackle football, concluding that young athletes can sustain anywhere from 226 to 1,855 head impacts per season (Robbins, 2012). Their study concluded that the weak, under-developed muscles of the athletes, coupled with their incomplete brain development, were both major factors in the incurrence of injury and long-term neurological consequences.
The development of the brain is also a critical factor to consider for youth athletes. Young athlete’s brains are not fully developed at the time of contact play. A study from Boston University states that children under the age of twelve are up to twenty-percent more likely to have cognitive impairments as adults after playing football because of the damage sustained during their youth participation. The study suggests that this is because of how vulnerable the brain is to injury at a young age. “Around age 12, blood flow to the brain increases, and brain structures such as the hippocampus, which is critical for memory, reach their highest volume,” continuing to say that “If you take just the hippocampus, that’s a really important part of your brain. It may be that if you hit your head a lot during this important period, you might have significant memory problems later on.” (Moran, 2015). For the nearly five million youth football players that participate each year on average, 70% of which are under fourteen, playing football presents a serious risk to their long-term health (Moran, 2015). Sustaining such violent injuries at the youth level creates a snowball effect where brain disease will develop more rapidly because of the regular exposure to head impacts over time.
Fortunately, this correlation between head injuries in football and brain disease has not been ignored, rather, it has motivated football leagues, sports associations, and governmental bodies to institute changes, including the state of Maryland. Currently, youth football in Maryland is governed by the policies set forth by the Lystedt Law. This law sets the mandatory procedures that control the management of head injuries and the educational awareness of football related head injuries. The Lystedt Law, originating in Washington state, was proposed in 2009 in response to the severe brain injury, and permanent disability, sustained by a thirteen year-old football player named Zackery Lystedt (Bompadre et. al, 2014). The law has three main stipulations: parents and players must be educated about the risks of concussions, any athlete that is suspected of sustaining a concussion must be removed from play immediately, and that once an athlete is removed from play, they must be cleared to return by a health-care provider before resuming participation (Bompadre et. al, 2014). It was on this basis that Maryland adopted the Lystedt Law, along with its three original stipulations, in 2011 (“Maryland Youth Concussion”, 2011).
The institution of the law lead to some important findings regarding youth head injuries and their prevalence. One NCBI study, investigating the concussion diagnosis of over four thousand high school football players, found that only 66% of athletes realized that they had sustained a concussion during play and that only 43% of players reported it to their coaches or trainers (Bompadre et. al, 2014). The researchers also found that the implementation of the Lystedt Law lead to an increase in concussion diagnosis in youth players. Their study concluded the following:
Before passage of the Lystedt law, rates of documented concussions were 11.5% (48 of 419) of total injuries (2008–2009). After the Lystedt law went into effect, rates of concussion increased to 19.7% (114 of 579) and 21.0% (111 of 529) in subsequent years. Gessel et al reported a concussion rate of 8.9% in high school athletes during the years 2005–2006, and Marar et al observed a concussion rate of 13.2% from data collected in 2008–2010 (Bompadre et. al, 2014).
Additionally, these data findings have encouraged the narrative that youth football does contribute to the development of brain disease through the large accumulation of concussive and subconcussive injuries and that the genuine need for the Lystedt Law, and its safeguards, were strongly substantiated. As it stands now, all fifty states, including Maryland, have accepted some form of the Lystedt Law as a means of protecting their athletes during play. However, while the legislation put forth by the Lystedt Law makes an honorable attempt to address the risks associated with football at the youth level, it does not produce a tangible solution that dictates and oversees injury prevention and long-term injury management for youth athletes. Specifically, it does not require Maryland to mandate strict regulations on how injury prevention is handled, who it is handled by, and it does not propose a set of guidelines––such as a concussion protocol––for teams to implement so they can effectively protect their players.
In order to create a deeper, broader policy that can prevent future CTE in youth players, the state of Maryland must expand the guidelines of the Lystedt Law by implementing a series of changes that add context and structure to the existing legislation. This new law will have to function as a set of living guidelines that instruct football institutions while providing best practices. A possible template may have been provided by the University of Marquette’s Law School. In a 2017 review of a case surrounding one Mr. Daniel Bukal and the state of Illinois, Mr. Bukal claimed that he suffered from the long-term effects of football related brain damage and that Illinois was responsible for damages because of a lack of mandated protocols (Spaude, 2017). In his accusation, Mr. Bukal suggested several potential implementations that would correct the lack of specific guidelines. He argued for “concussion protocols for youth athletes at both practices and games,” “preseason baseline testing,” “a program for concussion tracking and reporting,” a mandate for medical professionals to be present during games and practices, and for an education and training program to be created for athletic trainers (Spaude, 2017). These demands offered by the law review provides a solid template for Maryland use when addressing the youth concussion imperative.
For Maryland, the implementation of similar guidelines and practices will be necessary in order to create a long-term solution to youth brain disease. Firstly, Maryland should incorporate a more effective concussion awareness initiative into their Lystedt Law. Since the medical community has established the connection between football, long-term brain disease, and youth head injuries, it is important to market football as a sport that directly causes brain disease. The current law is quite ambiguous when describing the dangers of playing youth football; having a stronger stance, one that blatantly states the known risks, will influence the choice to participate more than it does now. This addition should follow the same structure as the The Family Smoking Prevention and Tobacco Control Act that was passed by the Obama administration. This act placed limitations on how tobacco companies advertised smoking and tobacco products, provided stronger, more poignant warning labels, and prevented companies from selling “reduced risk” products to consumers (“Compliance, Enforcement & Training”, n.d.). Just as hospital admissions rates and statistics for certain diseases decreased with the implementation of this act, so will the percentage of athletes that ignorantly participate in contact football without understanding the long-term risks (“Smoking & Tobacco Use,” 2016). Another alteration should include the addition of baseline testing prior to the beginning and at the end of each season. The Center for Disease Control describes baseline testing as “a pre-season exam conducted by a trained health care professional [that] assess[es] an athlete’s balance and brain function.” Additionally, a medical professional will test for concussion symptoms or signs that the athlete is not functioning at an effective cognitive or physical level (“FAQs about Baseline Testing,” 2015). Having each athlete undergo baseline testing will allow a medical team to determine whether an athlete is fit to play and will also create a reference point for the medical team to use if an injury is suspected. This test will provide a literal baseline of health for every athlete before and after a season of football.
While adding additional educational warnings and pre-season medical tactics are both important parts of this proposed update, serious steps must be taken regarding injury protocol management as well. One of the most glaring shortcomings of the Lystedt Law is that it lacks a standardized protocol for teams to follow. A concussion protocol can be defined as a “set of policies, tools, and assessments for caring for a concussion” (“Concussion Protocol 101 Guide,” n.d.). A protocol should deploy a team of at least three professionals that work together in unison to provide optimal care and supervision for the athlete; the three being an injury manager, an athletic trainer, and a rehabilitation professional, such as a therapist (“Concussion Protocol 101 Guide,” n.d.). The manager, a medical professional trained in neurological injuries, will monitor players for signs of concussions and symptoms of injury, diagnose injuries, and will be in charge of the healthcare team, the athletic trainer will conduct evaluations on players suspected of injuries, and the therapist will administer long and short-term treatment to injured athletes (“Concussion Protocol 101 Guide,” n.d.). Additionally, the law must incorporate a set of rigid guidelines to govern the actions of this medical team. An effective template should include a basic concussion definition along with essential head injury information, baseline testing procedures, standards by which athletes are removed from play, head injury assessment standards, professional evaluation guides, average timelines for safe return, and an academic reintegration timeline (“Concussion Protocol 101 Guide,” n.d.). The need for this group of medical professionals, and a protocol to guide them, cannot be understated because they are directly responsible for detecting injuries and conducting treatment for athletes during games and practices. Since the Lystedt Law does not require such a healthcare team, or a standard set of regulations, a “padded” version of the law needs to make their medical presence and a protocol mandatory.
Most importantly, an updated version of the Lystedt Law must address the dangers of subconcussive injuries, and their damaging long-term effects, by implementing an age requirement for tackle football. Currently, the Lystedt Law does not have a tackling restriction, nor does any state that has passed a variation of it. As discussed previously, the most detrimental form of brain injury to sustain in high volume is the subconcussive injury. While a competent medical staff, an effective head injury protocol, pre-season tests, and strong warning labels all contribute to identifying and managing concussions, none of these changes propose an actionable solution to the long-term threat of subconcussive injuries or the overall prevention of concussions for a youth player. With this in mind, it is necessary to withhold tackling until a later age. After analyzing the body of literature presented by medical researchers, it appears that the most acceptable age for contact play is fifteen as it is past the point of critical development. As mentioned before, the brain undergoes serious developmental growth and change during the period of childhood and adolescence, causing consistent head injuries to create extremely impactful damage. By limiting tackling to over fifteen, Maryland’s youth athletes would be able to avoid the primary source of all concussive and subconcussive injuries––impacts sustained from tackling. This change would allow the athlete more time for uninterrupted brain development, it would allow for most of the danger surrounding youth football to be circumnavigated, and it would let the athlete make a far more conscious, informed decision as to whether they would want to pursue an athletic career in football and accept its potential consequences at a later age.
Finally, setting the tackling age limit at fifteen would also allow for an updated Lystedt Law to be considered more seriously and potentially passed without unnecessary legal hardship. Other states, namely California, have struggled to pass legislation banning tackling for youth players as many parents have protested such changes despite evidence of long-term damage (Kawahara, 2018). It is completely unrealistic to ban tackling limits until an age of consent, which ideally would be eighteen. Major sports associations, such as the NFL, NCAA, and many high school football associations, would strongly protest to the limitations placed on their future prospects. Such an implementation would also affect chances at collegiate scholarships and would impact funding for school programs––so much of which is derived from athletics, specifically football. Another argument can be made that withholding the age of tackling play for too long will create a situation where players are put at risk for head injuries due to their inexperience––an assertion that would have to be seriously considered. However, Maryland has already adopted legislation banning heading in soccer games for players under eleven years old (Barker et. al, 2018). Having existing legislation such as this may open a forum to discuss why the state would protect athletes from the long-term dangers of one sport while simultaneously neglecting the players of another.
Football is both America’s game and one of the most influential sports in the world. However, the state of head injuries, and their long-term effects, in American football presents an epidemic that demands an impactful solution. As the medical community continues to affirm the position that youth football in particular is detrimental to long-term health and brain function, it is now necessary for governing bodies to implement enduring change. The institution of advertising restrictions and mandatory baseline testing, along with the creation of a head injury protocol and a tackling restriction for young players, are all vital changes that must be generated by an update to the current Maryland legislature. By padding the Lystedt Law through the proposed changes suggested in this work, Maryland will be able to safeguard vulnerable youth athletes, impact the long-term health and safety of football players, and will be able to create a long-term solution to athletic brain disease.
Amanda Robb. “What Is A Cell Body?– Definition, Function & Types .” Study.com, Study.com, Retrieved December 10, 2018, from study.com/academy/lesson/what-is-a-cell-body-definition-function-types.html.
Barker, Jeff, and Erin Cox. “Maryland Bill Would Bar Tackle Football for Kids on Public Fieldsuntil High School.” Baltimore Sun, 30 June 2019, https://www.baltimoresun.com/politics/bs-md-football-safety-legislation-20180206-story.html.
Barlow, Rich. “BU-Led Study May Explain CTE without Concussions.” Family and Medical Leave Act (FMLA) | Human Resources, Retrieved December 10, 2018, from www.bu.edu/research/articles/bu-led-study-may-explain-cte-without-concussions/.
Bompadre, V., Jinguji, T. M., Yanez, N. D., Satchell, E. K., Gilbert, K., Burton, M., Conrad, E. U., … Herring, S. A. (2014). Washington State's Lystedt law in concussion documentation in Seattle public high schools. Journal of athletic training, 49(4), 486-92. Retrieved December 10, 2018.
Bryan, Mersine A., et al. “Sports- and Recreation-Related Concussions in US Youth.” American Academy of Pediatrics, Retrieved July 1, 2016, from pediatrics.aappublications.org/content/138/1/e20154635.
Center for Tobacco Products. “Compliance, Enforcement & Training - Family Smoking Prevention and Tobacco Control Act - An Overview.” U S Food and Drug Administration Home Page, Center for Drug Evaluation and Research. Retrieved December 10, 2018, from www.fda.gov/tobaccoproducts/guidancecomplianceregulatoryinformation/ucm246129.htm.
“Concussion Protocol 101 Guide - What to Do with Potential Concussions in Your Organization.” Concussion Care Resources. Retrieved December 10, 2018, from concussioncareresources.com/concussion-protocol-101-guide/
“Chronic Traumatic Encephalopathy.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 20 Apr. 2016. Retrieved December 10, 2018, from www.mayoclinic.org/diseases-conditions/chronic-traumatic-encephalopathy/symptoms-causes/syc-20370921).
“Chronic Traumatic Encephalopathy (CTE).” Alzheimer's Association. Retrieved December 10, 2018, from www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/chronic-traumatic-encephalopathy-(cte).
Council On Sports Medicine And Fitness. “Tackling in Youth Football.” American Academy of Pediatrics, 1 Nov. 2015. Retrieved December 10, 2018, from pediatrics.aappublications.org/content/136/5/e1419.
Crisco, J. J., & Greenwald, R. M. (2011). Let's get the head further out of the game: a proposal for reducing brain injuries in helmeted contact sports. Current sports medicine reports, 10(1), 7-9. Retrieved December 10, 2018.
“FAQs about Baseline Testing.” Centers for Disease Control and Prevention, 16 Feb. 2015. Retrieved December 10, 2018, from www.cdc.gov/headsup/basics/baseline_testing.html.