The Effect of Traumatic Brain Injury in Professional Football

The Effect of Traumatic Brain Injury in Professional Football

by Mark Winkel

 

 

Introduction:

In May 2012 at the age of 43, a retired professional football player took his own life. This former San Diego Chargers linebacker, Junior Seau, was one of the best players in the league. However, over time, he began to suffer from wild mood swings, insomnia, and depression. After his tragic death, the family agreed to donate his brain to the National Institute of Health for research. Results of this testing were very recently released in a statement (NIH Statement, 2013):

The official, unanimous diagnosis of Mr. Seau’s brain was a multi-focal taupathy consistent with a diagnosis of chronic traumatic encephalopathy (CTE).

The type of findings seen in Mr. Seau’s brain has been recently reported in autopsies of individuals with exposure to repetitive head injury…including professional athletes who played contact sports…

Now, the family has decided to file a wrongful death suit against the National Football League (NFL) alleging that they failed to disclose the dangers of multiple traumatic brain injury (mTBI). Over the course of his 20 year career, Junior Seau sustained numerous and repetitive head injuries. The American Association of Neurological Surgeons defines mTBI as follows:

A blow or jolt to the head, or a penetrating head injury that disrupts the normal function of the brain. TBI can result when the head suddenly and violently hits an object, or when an object pierces the skull and enters brain tissue. Symptoms of a TBI can be mild, moderate, or severe, depending on the extent of damage to the brain. Mild cases may result in a brief change in mental state or consciousness, while severe cases may result in extended periods of unconsciousness, coma, or even death.

This paper is prepared in a meta-analysis style approach in which an extensive review of the literature was conducted. This literature included peer reviewed journal articles, non-peer reviewed journals and other publications from the popular media. Additionally, congressional testimony and other legal documents such as lawsuits were reviewed. This review was further divided into three subcategories; identified as the science of TBI, the policy, ethics, and conflict between the scientific, sports, and regulatory community, and finally the effects of TBIs in the sport of football.

It seems from 2010 to the present, a major story is breaking almost monthly. Bigger and more important studies are being published which will be further examined in the biology and chemistry section which follows this introduction. In this part of the paper, research on basic brain trauma chemistry and biology from Boston University, Harvard, and University of North Carolina is reviewed and summarized.

The second section of the paper of the paper will examine the ethical, legal, and regulatory issues inherent in the history of how the NFL has handled the TBI epidemic. Much has been published on team physicians and conflicts of interest regarding return to play decisions and this will also be discussed.  Recent developments with law suits from retired players as well as insurance issues are presented. A 2010 congressional hearing on concussion in the NFL is discussed as well as current and future plans for federal legislation.

In the third and last section will focus on how TBIs are greatly affecting the game of football all every level. The NFL and the players are speaking freely about their medical histories and the impact of concussion on their lives. A brief discussion of concussion policy at the high school sports level is included for comparison.

Ultimately, the goal of this paper is to address the following questions:

  • What is a concussion and how does it affect the brain?
  • What are the leading causes of concussion in the NFL?
  • What happened during the last 90 years of the sport’s existence to cause this issue to be so troublesome?
  • What are potential solutions to reduce the number of concussions in professional football?

Professional football is often called America’s favorite sport. Unfortunately, America’s entertainment has come at a great price to the players who have been shown to exhibit significant cognitive illness as a result of their careers. These players choose this career knowing some risk, but not knowing enough. At the 2009 Congressional hearing, in an extremely poignant moment, a congresswoman analogized the NFL’s position on concussion to the tobacco industry’s denial about the link between smoking and lung cancer (Sanchez, 2009).  As the body of scientific evidence continues to grow, denial, even by the NFL may be impossible.

 

The Biology of a Concussion:

To understand the effects of concussion on the brain, it is important to understand some terms of anatomy and physiology of the normal brain. The brain is comprised of  a large group of neurons or nerve cells that are highly organized and differentiated. There are three types of neurons; sensory, motor, and interneurons. Sensory neurons transmit information from the eye or other sensors that detect either internal or external stimuli to the appropriate brain region for processing. For example, the finger touches something hot and the sensory neuron sends the message to the brain to remove the finger from the hot object. The motor neuron transmits the signal from the brain to the muscle cells which causes them to contract. In the example of the hot object, it is the motor neuron that sends the message to the finger to cause muscle contraction which moves the finger from the danger of the hot object. The third category, and the vast majority of neurons are the interneurons which are located only in the brain and act as the local connection within the various regions of the brain.

The nerve cell is very unique in structure from other cells in order to perform the function of transmitting information in the form of chemical signals within the brain and peripheral nervous system (the body outside the brain and brain stem). Below is a drawing of a typical healthy nerve cell and the key components of the cell.

 

The six areas identified in this drawing are significant in understanding how the damage from concussion affects the ability for the cell to function and transmit signals. These six areas are defined as follows:

  1. Cell body- contains the nucleus and other typical parts of the cell
  2. Nodes of Ranier- gaps in the axon which allow the signal to chemically intensify
  3. Axon- extension of the cell that transmits the signal
  4. Dendrite- extension of the cell that receives the signal
  5. Terminal button- areas at the end of the axon where neurotransmitters are located
  6. Myelin sheath- protective coat for the axon and insulation for the electrical signal

The brain is organized into three basic functional regions known as the cerebrum, the cerebellum, and the brain stem. Higher mental processes occur in the cerebrum, such as all voluntary movements and all cognitive functions such as learning, memory, judgment, and perceptions. While there are many distinct regions of the cerebrum (cerebral cortex), only those areas most affected from a brain injury will be described here. The frontal lobe, largest of the brain’s lobes is the easiest to damage by accidental injury due to its size and location. This region controls all executive function, hibition and inhibition, decision making and control of behavior. The corpus callosum is a thick band of white matter located on top of the brain at the junction of the two hemispheres. It contains more than 200 million axons and allows for communication between the two hemispheres. White matter fills the inner layer of the cerebrum and is basically all the axons of the nerve cell bodies in the outer layer also known as the grey matter.

The cerebellum or “little brain” is located beneath the back half of the cerebrum behind the brain stem. It functions to coordinate motion, function, and balance. It provides for judgment in movement such as is required to see a football in mid-air and complete a catch.

The brain stem coordinates the body’s automatic or reflex activities such as breathing, maintaining consciousness or sleep, and regulating heart functions. Located within the brain stem is the thalamus which functions as a switching station for the enormous amount of information arriving into the brain. It essentially sorts information and decides how and where to direct to the appropriate areas of the cerebrum and cerebellum. Below, is a drawing of a typical brain from a side and rear view so that the areas of interest are displayed.

These areas of the brain identified in the drawings are significant in understanding how damage from a concussion affects the ability of the brain regions to perform their functions. These areas are defined as follows:

Rear View

  1. Left Hemisphere- logic, thought, language
  2. Right Hemisphere- intuition, creativity, art and music
  3. Corpus Callosum- transmits information between two hemispheres
  4. Thalmus- switching station for information from body to cerebrum

 

Side View

  1. Frontal Lobe-found in both hemispheres, controls decision making, judgment, etc.
  2. Hypothalmus- in mid brain, controls autonomic functions like breathing
  3. Thalmus- see above
  4. Pituitary Gland-gland that secretes hormones to control homeostasis
  5. Amygdala- in mid brain, controls strong emotions like fear and anger
  6. Hippocampus- controls special awareness, memory and recall

(All drawings are based on information from the FINR (Florida Institute of Neurological Research) Atlas of Brain Anatomy.)

 

Concussion and Traumatic Brain Injury:

The anatomy and physiology of the normal, healthy brain and its components have been described in the previous section. This brain structure is protected by the bony skull and many layers of membranes. Additionally, the brain floats in a fluid within the skull which creates a modest cushion against minor injuries such as a fall or a mild hit to the head.

However, these protective mechanisms have not evolved to guard against injury to the brain from severe blunt force trauma such a bomb blast, a high speed collision, or impact from a contact sport such as American football. In the instance of blunt force, a concussion, a type of mild traumatic brain injury (mTBI) may occur. The American Association of Neurological Surgeons defines concussion or mTBI as:

A blow or jolt to the head, or a penetrating had injury that disrupts the normal function of the brain. TBI can result when the head suddenly and violently hits an object, or when an object pierces the skull and enters brain tissue. Symptoms of a TBI can be mild, moderate, or severe, depending on the extent of damage to the brain. Mild cases may result in a brief change in mental state or consciousness, while severe cases may result in extended periods of unconsciousness, coma, or even death.                                                                            

In response to this force, the brain may smash against the front of the skull and cause damage to the frontal cortex (reference diagram 3). Sometimes, the impact is so severe, that the force can cause the brain to bounce of the front and back of the skull, also damaging the rear areas of the brain (reference diagram 2). Moreover, the neurons, especially the long axons (reference diagram 1), can stretch, tear, or tangle as a result of TBI. If an axon tears or tangles, the transmission of the message (the electrical signal) to the next nerve cell may be interrupted. As these axons are damaged, the nerve cell also disintegrates, and ultimately the cell will die. As the neuron disintegrates, it can also lead to the release of abnormal amounts of neurotransmitters. Neurotransmitters are the chemicals that are released from the terminal buttons at the ends of the axon (reference diagram 1), and help transmit the electrical signal to the next neuron. Release of abnormal levels of neurotransmitters can also damage the nerve cell and ultimately cause cell death. The research into the effects of damage to axons as well as other brain tissues will be detailed in a later subsection.

In the event of a traumatic brain injury, changes occur in the brain and its components that can be either temporary or permanent. Most sports related concussions are minor and the brain recovers within a few days to a month. In these cases, the brain can be bruised and tissues may stretch or even tear. However, sometimes a concussion is severe, or there can be instances of repeat concussion, and the damage sustained to the brain is very different. This damage can be long-lasting, progressive and permanent. Changes in the brain can lead to disease with a wide range of biological changes and clinical symptoms. In the example of sports related injuries, a player could experience hundreds of mTBI hits in a single season (Guskiewicz, 2003). Dr. Kevin Guskiewicz, professor of sports science at Univ. of North Carolina, at Chapel Hill has spent his career studying the relationship between concussion and clinical measures primarily in college football players. In a study reported in the February 2011 issue of National Geographic, Guskiewicz describes the season of one player, a defensive end, who experienced 537 hits to the head. Of those, 417 had a magnitude of 10g or more force, and two resulted in concussion. To put this in perspective, 10g of force represents enough force to knock down a human body with an average weight of 140 pounds. As the report states, “ While magnitude matters, the biggest hits aren’t necessarily the most damaging.” For this player, the two concussions did not result from the hardest hits. The following drawing, taken from the National Geographic article, portrays the magnitude and frequency of hits to this player.

 

Chronic Traumatic Encephalopathy:

From concussion and injury, repeat brain trauma can lead to disease. Since the 1920’s and the sport of boxing, it has been known that repeat trauma can cause progressive neurological deterioration known in the past as dementia pugilistica or punch drunk. Today, this same disease is known as chronic traumatic encephalopathy (CTE). Professor Ann McKee of Boston University defines CTE as:

…progressive neurological deterioration associated with repetitive brain trauma. Clinically, CTE is associated with memory disturbances, behavior and personality changes, parkinsonism, and gait abnormalities. CTE is characterized by atrophy of the cerebral hemispheres…extensive tau-immunoreactive neurofibrillary tangles…(McKee 2009).

CTE is a progressive taupathy with very distinct clinical and pathological features. Taupathy is defined as broad class of many neurological diseases where excess amounts of tau proteins accumulate in the spaces between the neurons and interfere with normal activity. Tau proteins are normally found within the cell body and are used to stabilize the microtubules which are the “skeletal” structure of the nerve cell body. They also serve the function of guiding nutrients from the cell body to the axon. In damaged cells, tau is changed chemically ad rather than provide structure, they become tangled (neurofibrillary tangles) and cannot provide structure. So, the microtubules fall apart, and nutrients are no longer transported to the axon and ultimately the cell dies. As the disease progresses clumps of proteins, known as amyloid plaques (see drawing below) form. Rather than normal elimination from the cell, these clumps accumulate between nerve cells and form hard plaques. The other distinction in the pathology of CTE is the presence of neurofibrilliary tangles. These tangles are aggregates of hyperphosphorylated tau protein which are twisted threads of proteins found inside the nerve cell body (reference drawing).

brain matter cannabis

Although CTE was historically associated with boxing, it has been evident that other sports such as American football, hockey, and wrestling, or blasts from military roadside bombs are also causative. Most sports related head injury is minor and recovery from concussion is complete within a few days or weeks. Some, however, will progress to long-lasting CTE. In spite of all the research in the last decades, it is still not known how severe or recurrent the injury must be to initiate CTE (McKee, 2009). From studies of post-mortem brains of NFL players, CTE has been characterized clinically and microscopically. From her research, McKee has characterized CTE into four stages progressing in signs and symptoms from mild to severe. The clinical assessments and pathological findings which define each stage are summarized in the following table.

 

Four Stages of CTE
 

Stage I

 

 

Clinical Observations

Headaches

Loss of attention

Short term memory problems

Pathology

Some tau protein

Some tangles in cortex

 

Stage 2

 

 

Some depression

Mood swings

Explosivity

More tau in cortex

tangles in more brain regions

Changes to amygdala

Cerebral atrophy

Stage 3

 

 

 

Executive function disorder

Aggression

Cognitive impairment

 

Lower brain weight

Thinning of corpus callosum

Widespread tangles in all brain

Macroscopic changes

Stage 4

 

 

 

All above observations

Severe gait changes

Suicidal tendencies

Large decrease in brain weight

Atrophy of white matter

Severe tau protein and tangles

 

 

 

The figure below shows the differences in the brains from a normal, healthy volunteer and five living NFL players who have reported various clinical observations. This work represents the recent research from the team of Small and Gary at UCLA which was recently published in the American Journal of Geriatric Psychiatry (Small, 2013).

 

Relationship Between TBI and CTE:

From the information presented in the previous sections, it is evident that there is a relationship between TBI and CTE. A review of the literature reveals a tremendous increase in peer reviewed studies beginning around 2000. In 2005, Dr. Omalu, at the University of Pittsburg first reported the discovery of extensive evidence of tangles and plaques in a brain donated by an NFL player who died suddenly 12 years after retirement from the game. This case woke up the sports world and called for more studies to establish a relationship between TBI and CTE (Omalu, 2005).

As interest in this area began to grow, researchers at Boston University reviewed the literature and found three documented cases of CTE in professional athletes. From interviews with the families of the deceased athletes, a clinical history of signs and symptoms of CTE were established. In a landmark 2009 paper, Ann McKee of Boston University reported that these clinical symptoms were definitely linked to the classical pathology of CTE (McKee, 2009). She was also able to establish, the disease can progress even decades after retirement from active sports.

In 2012, The largest and most definitive study to date was again conducted by Ann McKee’s team at Boston. In this study, the physiological and clinical effects of repetitive brain injury (especially in professional football) and the link to CTE was evaluated. Because Boston University works cooperatively with a local VA hospital, which had established a brain bank, many donations of injured brains had been received over the years. As a result, McKee was able to study samples from 85 brains and examine them for evidence of CTE. Once again, the clinical history was established through interviews with the families of the deceased. The neuropathology examination was conducted using tissue samples from the brain bank. The results conclusively linked CTE to a history of repeat head trauma in 63% of the cases (McKee, 2012). While this study was the most extensive evaluation to date, it was limited in that it did not compare samples of CTE from the general population, where there could also be a history of neurological problems.

Then, On January 10, 2013, the National Institute of Health (NIH) released a statement about the deceased San Diego linebacker, Junior Seau whose brain had been donated to research by the family. The official, unanimous diagnosis of Mr. Seau’s brain was “multi-focal taupathy consistent with a diagnosis of chronic traumatic encephalopathy.” (NIH Statement, 2013). The report cautioned that CTE research is still in the early stages, and there is still no way to perform evaluations in a living person. Furthermore, there is still a lack of understanding, who is at risk, or how much trauma to put players at risk for CTE.

In February, 2013, just one month after NIH released its statement. Gary Small from UCLA published a small study, of just five subjects who are living retired NFL players. Using PET scanning with a special dye, they were able to see tau deposits and other evidence of CTE in the brains of these players (Small, 2013). Obviously, this work needs to be expanded in a larger scale, but it may offer a means to identify CTE in its early stages in living athletes. This could potentially allow clinicians to develop strategies and interventions to protect those players with early symptoms.

Finally and very recently published was some interesting research from the Institute of Molecular Biology in Vienna Austria. In the September 2013 issue of Nature, Knoblich and team published their work on growing “mini brains” from human stem cells (Knoblich, 2013). While this work does not directly relate to CTE or TBI in professional football players, this could become a model for studying the roots of human neurological disease.

 

Policy and Ethics Related Issues for TBI in Football:

There is an extensive history of concern about the long term impact of repeat trauma to the head. As early as 1928, the Journal of the American Medical Association reported abnormalities in boxers who remained in the sport for several years. Nine years later in 1937, the American Football Coaches Association (precursor to the NFL) made a first statement about their sport by urging players to leave the game in the event of a concussion to receive personal attention. In the intervening decades from the 1930’s to the 1960’s, only a handful of official comments or recommendations came from the scientific community about repeat concussion in football and boxing. Then, beginning in early 1960’s, the scientific community began reporting on findings of encephalopathy in brain tissue of boxers who had exhibited signs of Parkinson’s disease. Encephalopathy, now known as chronic traumatic encephalopathy, was defined as “a progressive degenerative disease associated with multiple concussions and other forms of head injury” (Critchley, 1949, 1957).

The NFL remained largely silent until 1994 when they formed a committee (mild Traumatic Brain Injury Committee, MTBIC) to study the effects of mTBI on NFL players. By then, the research community had conducted studies on college players and reported findings of brain damage. In the next ten years, the MTBI produced absolutely nothing about TBI, except to ask for a retraction of an important study by Dr. Omalu who was the first to examine a deceased player’s brain and find evidence of CTE ( Omalu, 2002). Even more astonishing was a published statement one year later in which the committee released their first findings which declared that “concussion had no long negative health consequences” (MTBI Committee, 2003).

During the decade from 2000-2010, two or three major announcements of new research a year were published by the medical community, as the evidence continued to mount about the clear correlation of repeat concussion and CTE. By the latter part of the decade, Boston University published findings from the post mortem brain autopsies of two more players and found massive evidence of CTE (McKee, 2008).

In response, the NFL continued to deny the mounting evidence and issued statements of denial and outright rejection of the medical community’s findings. For example, in 2004, the NFL made a statement that there was no risk of repeated concussions in players with previous concussions and the 7-10  day post-concussion rest period was not necessary (MTBI Committee, 2004). Later on that year, in a second statement, the committee also released their own research showing no signs of decreased brain function in 655 tested players (Neurology, 2004).

Then, in late 2009, the U.S. House of Representatives convened a hearing on the subject and testimony was heard from both the research community and the NFL. The  NFL commissioner, Roger Goodall, acknowledged the unique position of influence that the NFL had in the football community and promised that the NFL would “act in the best interest” (Goodall, 2009 Congressional Testimony) of all children, college, and professional athletes who played football. Dr Casson, co-chair of the MTBI committee testified that “there is not enough valid, reliable, or objective evidence at present to determine whether or not repeat head impacts in professional football result in long term brain damage” (Casson, 2009 Congressional Testimony). During that same hearing, Dr. Omalu, a leading researcher, stated that “we have known about concussions and the effect of concussions in football for over a century” (Omalu, 2009 Congressional Testimony).

Shortly after this hearing concluded, Dr. Casson and his co-chair, Dr. Viano resigned under pressure from allegations that there was inherent conflicts of interest and that the work by the MTBI committee was “infected” (Omalu) and there was no science in their long term study. They were replaced by Dr. H. Hunt Batjer and Dr. Richard G. Ellenbogen, both neurological surgeons. Unsurprisingly, it took all of one month for the NFL, in part due to the advice of the committee, to at lat acknowledge that concussions lead to long term problems and that playing football can lead to TBI. The NFL followed this announcement up with stricter guidelines for return-to-play situations, “…stating that any player that exhibits symptoms of a concussion should not return to play on the same day.” (Ezell.)

With this long overdue acknowledgment from the NFL, the next step became what do to about this issue that you are finally admitting exists. The most important step would be to put money into research for the top neurological scientists in the nation to study the problem and try to find potential solutions. Despite the fact that the NFL is an $8 billion per year industry, the NFL took their typical route in taking action by starting slow and progressing over time. It started in January 2010  with $1 million given to Dr. McKee, who was designated the “preferred brain bank of the NFL.” (Ezell.) This was followed by a $30 million grant to the NIH for research into TBI. The most recent example showed the NFL’s most committed statement to date as they donated $100 million to the Harvard Medical School to research the health of football players, in particular relating to brain injuries. While the league was finally investing in the safety of current and future players in the NFL, it took even longer for the NFL to assist those most in need; the retired players suffering from decades of ignorance and bludgeoning.

 

The Players and the Game:

In an article written in 2006 by Dr. Elliot Pellman and Dr. David Viano about the NFL’s recent findings regarding TBI in the sport, they did research  to try and uncover where the most troublesome aspects for the game were involved. The following table shows their statistics:

The breakdown shows a clear issue with those that are being tackled during the course of the game. The two most concerning common collisions include the Quarterback being sacked and the Wide Receiver/Defensive Secondary interactions. Combined  with the shared philosophical standpoint of NFL owners concerned about protecting their most valuable assets (Quarterbacks and Wide Receivers are the 2 highest paid positions in the game), this data helped to send a message to the league that there had to be major changes to the game.  Since that time the NFL has started to adopt and enforce new rules to the game. Players are being flagged, fined, and potentially suspended for any blow to the head made by any player. According to the NFL Rules, Article 9 Section B Sub-section 1-2

(b) Prohibited contact against a player who is in a defenseless posture is:

(1) Forcibly hitting the defenseless player’s head or neck area with the helmet, facemask, forearm, or shoulder, regardless of whether the defensive player also uses his arms to tackle the defenseless player by encircling or grasping him; and

(2) Lowering the head and making forcible contact with the top/crown or forehead/”hairline” parts of the helmet against any part of the defenseless player’s body.

(http://www.nfl.com/static/content/public/image/rulebook/pdfs/15_Rule12_Player_Conduct.pdf)

These rules, adopted in 2010, have created something of a controversy throughout the NFL. While offensive players feel grateful for the inferred protection from the officials in the game, the defensive players are not as thrilled to the changes. Many players and fans feel that these rules have watered the game down and taken away the fans enjoyment of hard hitting and action. However, the NFL has decided to take a stand and commit to the safer tackling techniques that they have preached of late. The fact of the matter is that players in the NFL realized that the modern day helmets are capable of being used as a weapon. The NFL originally used leather helmets in its founding days, and over time the material for the helmet has become sturdier to protect the players better. As a cruel twist of fate, defensive players started to lower their head and use the top of the helmet or “crown” to deliver the blow to opposing players knowing that the hard substance of the helmet is capable of providing more pressure than any human body part. As a response to this new strategy, offensive ball carriers were being taught to lower their head at the point of impact in order to try and negate the materialistic advantage. The result of this thinking has caused helmet to helmet contact to become a common occurrence in most every NFL game played. The force that is created by this type of collision is more than enough to cause TBIs as was discussed previously.

Another controversial decision by the NFL involves the kickoff, or the part of the game when one team kicks the ball to the other team. This action involves 22 of the finest athletes in the world running at each other at full sprint and colliding. Prior to the 2011 season, the NFL made a rule change to have the kick off  moved 5 yards forward to induce an increased number of touchbacks, which results in the kickoff play basically being nullified. The following table is a compilation of statistics regarding kickoffs and how they are related to TBI over the last decade:

(http://www.footballoutsiders.com/stat-analysis/2013/nfls-battle-concussions-and-severe-injuries)

The two rows highlighted in green are the years in which the new rules have been adopted. As you can see, there was a significant change in the number of kickoffs that were returned over the last 2 years. As expected, the total number of concussions during this time also shows a dramatic decrease. However, it is very interesting to note the last column, in that almost 2% of kickoffs returned resulted in a player receiving a TBI during the play. The kickoff returner is typically a very specifically skilled player, many of which make a living only performing this function. Naturally these players (as well as the teams who employ the best returners) were unhappy with their limited opportunities to perform their job function that earns them a place on the roster. While sympathy for these parties would be a natural emotion, the data clearly shows that the kickoff is far too dangerous of a play to be performed on a regular basis. In fact, there are many people, including New York Giants owner John Mara who feels that kickoffs should be eliminated from the game altogether. According to an ESPN article, Mara was quoted as saying

“…the problem is that the concussions come from everywhere — from the wedge, from the crossing blocks where a guy goes from one side of the field to another, from a full-speed collision between a return guy and a tackler. So there’s no one thing that you can do. It’s something that we’ll continue to watch as closely as possible.” (Chadiha)

While this sentiment is still unpopular by the majority of decision makers to eliminate this potentially exciting aspect of the game, it remains clear that the subject should constantly be scrutinized and inspected.

 

Conclusion: Retired Veterans

There was a great travesty during the 1970s/1980s in that veterans of the wars in Vietnam and Korea were treated in an inhumane way. Many were chastised by people who were against the war in the first place for taking part in it. Others were blatantly ignored despite the fact that they were injured or needed assistance in being assimilated into American society. The result of which caused an entire population of heroes struggling through the rest of their lives, when instead they should have been glorified for the sacrifices they made.

Similarly, the retired veterans of the NFL have been ignored, dismissed, and disenfranchised by the very foundation that they helped create and flourish. Before the sport became so popular that the minimum wage for the NFL is still in the top 1% for household income, there were decades of football players that competed with reckless abandon, but were paid as common laborers. After years of physical damage, these players were then denied retirement disability help from the NFL for decades as the league refused to admit something that is just common sense; playing football is a major risk for permanent brain damage. These players are the reason the league became so popular as their effort, determination, and sacrifice paved the way for quite possibly the most exorbitant entertainment franchise in the history. Yet while they are dealing with debilitating diseases like CTE and dementia, the NFL refused to take any responsibility.

Finally, after decades of attempts to get some reconciliation, the retired players received a small recompense for their turmoil In August of 2013, there was a significant victory to those who had previously been ignored, dismissed, and abused.

“The NFL has reached a $765 million deal with a group of more than 4,500 former players – one third of all former NFL athletes – in a lawsuit that claims the NFL hid the dangers of the sport” (Sneed.)

While many players have already died and many others are too far beyond the ability to repair, this was at last a way for players to get compensation and hopefully will help them live with the permanent scars that are not visible to the naked eye.

 

AGRiMED Perspective

AGRiMED advocates for access to “safer” medical treatment for professional sports players through the use of cannabis to treat chronic pain.

 

 

 

 

 

 

 

 

 

This Capstone was written with the sad memory of those football players suffering through this terrible epidemic, and for those that have died in their struggles. Therefore, I dedicate this paper to those players whose lives were lost in the process of this struggle:

Cookie Gilchrist

Dave Duerson

Eric Pelly

John Grimsley

John Mackey

Junior Seau

Lou Creekmur

Mike Borich

Mike Webster

Nathan Stiles

Ollie Matson

Owen Thomas

Ray Easterling

Ron Perryman

And for the countless others who are fighting to live a normal life with the brain damage they suffered in the process to entertain us.

 

 

Bibliography:

Chadiha, Jeffri. (Aug. 2012) 10 Steps to Make the Game safer. ESPN. ESPN Internet Ventures, 30. Web. 18 Nov. 2013.

Department of Health and Human Services. National Institute of Health. (January 10, 2013)  NIH Statement on Junior Seau. Washington,.

Ezell, Lauren. (2013) Timeline: The NFL’s Concussion Crisis. PBS. PBS, 8 Oct. 2013. Web. 18 Nov. 2013.

Guskiewicz, K. (2003) Cumulative Effects Associated With Recurrent Concussion in Collegiate Football Players. JAMA.; 19: 2549-2554.

Kacsmar, Scott. (2013, August) Football Outsiders. Football Outsiders Everything. USA Today, 16. Web. 18 Nov. 2013.

Knoblich, J. (2013)  Cerebral Organoids Model Human Brain Development and Microencephaly. Nature. 501: 373-379.

McKee, A. (2009) Chronic Traumatic Encephalopathy in Athletes: Progressive Taupathy After Repetitive Head Injury. Journal of Neuropathology and Experimental Neurology. 68: 709-735.

McKee, A. (2012) The Spectrum of Disease in Chronic Traumatic Encephalopathy. Brain, A Journal of Neurology. 1-22.

NFL Official Playing Rules. (2013).  www.NFL.com.

Omalu, B. (2005) Chronic Traumatic Encephalopathy in a National Football League Player. Neurosurgery. 57: 128-134.

Pellman, E. , & Viano, D. (2006). Concussion in professional football: Summary of the research conducted by the national football league’s committee on mild traumatic brain injury. Neurosurgical FOCUS, 21(4), 1-10.

Shyr, L (2011, February). Lasting Impact. National Geographic, 2,28-30.

Small, G. (2013) PET Scanning of Brain Tau in Retired National Football Players: Preliminary Findings. Am. J. Geriatric Psychiatry.; 21: 138-144.

Sneed, T. (2013). Nfl, players reach $765 million deal concerning brain damage accusations. U.S. News & World Report, 1.

 

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