NFL Acknowledges Football, Brain Damage Link

Mounting evidence shows connection between contact sports and dementia.

On March 14, 2016 the National Football League’s (NFL) top health and safety executive, Jeff Miller acknowledged there is a direct link between playing football and degenerative brain disorders such as chronic traumatic encephalopathy (CTE).

While speaking in front of a Congressional Committee roundtable discussion on concussions, he was asked by Representative Jan Schakowsky if “there is a link between football and degenerative brain disorders like C.T.E.”  Miller’s response was “The answer to that is certainly, yes.”

Mr. Miller acknowledged that research completed by Dr. Ann McKee and other leading neurologists and researchers contributed to establishing the connection between playing American football, and developing CTE.

Dr. McKee works out of Boston University where she serves as co-director of the Center for the Study of Traumatic Encephalopathy. She has published over 60 studies on this and related neurologic issues, and has received numerous awards for her groundbreaking research. Her work focuses primarily on athletes such as professional football players, and members of the military exposed to repeated traumas in the field.

How Common Is It in Football?

Recent findings from a number of research studies on CTE show that a significant number of professional football players may be at different stages of CTE related brain degeneration. One study out of Boston University found CTE in 96% of the former NFL players’ brains, which were examined.

The players whose brains were studied, had demonstrated signs of possible CTE prior to their deaths.

Traumatic encephalopathy has also been found in individuals who only played high school or college football.  Early signs and symptoms have been noted in players who only played the sport for a few years.

What Are the Signs and Symptoms of CTE?

Chronic Traumatic Encephalopathy results in gradual, but progressive changes in many of the brain’s functions. The ability to access and use memories, and the ability to think critically both decline. The likelihood of developing depression and emotional instability goes up, and suicidal behavior is also more common.

Some have reported concerning behavioral changes such as aggression and poor impulse control. Symptoms that mimic those of Parkinson’s disease such as tremors and movement impairments may develop. Finally, dementia sets in.

According to researchers, the behavioral and cognitive changes that develop as a result of CTE progress through four stages.

Stage 1: at an early stage, insomnia, headaches and nausea are common. One’s ability to pay attention, and concentrate on specific tasks goes down. It’s easier to get distracted.  

Stage 2: at this stage, emotions become involved. Depression develops and there may be explosive outbursts. Short term memory is affected, so learning new skills or tasks becomes more difficult.

This can develop at an age much younger than most people begin to have short term memory problems.

Stage 3: the brain’s ability to perform complex tasks degenerates. Complex tasks that are lost include making decisions that require understanding several key issues or influencers, and understanding the long term consequences of one’s choices. Mutli-tasking becomes difficult if not impossible.

Stage 4: at this final stage there is complete dementia. It interferes with the ability to take care of one’s basic needs, recognize family and friends. This becomes a contributor to early death.

How Is it Diagnosed?

Chronic traumatic encephalopathy is difficult to diagnose until permanent, irreversible damage has occurred. CTE involves changes to the structure of nerve cells, and the total brain mass.

According to the Centers for Disease Control, damage may not show up on objective tests such as CT scans or MRIs for years. This is because visible changes such as reduced brain size and enlargement of the natural spaces within the brain (called ventricles) only show up in the later stages of the disease.

One of the most important physiologic changes that happens to the brain occurs at the microscopic level of the nerve cell. The cellular changes can only be studied once a person suspected of having CTE, has died.

At that point an autopsy can be performed during which thin slices of brain tissue are collected and examined under a powerful microscope. Under the microscope, permanent brain cell damage caused by “Tau proteins” comes into view. These changes are unique to CTE and not found in the same configuration as other dementias such as Alzheimer’s disease. Many NFL players have agreed to donate their brains to research after they die, so this phenomenon can be better understood.

What Are Tau Proteins?

Tau proteins serve an important role in brain cells. They line up along the inside of a brain cell and provide stabilizing support. However, when the brain begins to deteriorate as a result of repeated head trauma, tau proteins start building up in abnormal ways. Tau proteins form tangles that have been described as appearing like squiggly clumps of yarn.

Tau protein tangles are found in a number of degenerative brain diseases, but the manner in which they cluster around the brain in CTE is unique. This is how researchers know that the tau protein buildup isn’t due to a different type of degenerative brain disease, but is actually caused by the multiple head traumas experienced while playing contact sports such as football.

Tau Tangles and Brain Cell Dysfunction?

When the tau proteins are no longer stabilizing the cell, and instead creating tangles, then the cell loses its ability to effectively send chemical signals.  This is a critical change. In order for the brain to function effectively, it has to be able to send electrical impulses down the length of a nerve cell. These impulses, or signals, then pass that message along to the next cell, until the message reaches its intended destination and causes the desired response.

If tau protein tangles build up in the cells, then the message can no longer get through. The brain has lost its ability communicate and direct the complex functions required for normal life. This is when we see the signs and symptoms of chronic traumatic encephalopathy emerge, from forgetfulness, to emotional changes, to a complete loss of comprehending and interacting with the world.

Why Don’t Helmets Prevent CTE?

Because of the way football is played, athletes are at increased risk of developing both sudden and long term brain damage. According to a study published in 2011, it is estimated that “athletes at certain positions (eg, linemen) may sustain up to 1400 impacts per season, and high school players who play both offense and defense potentially sustain closer to 2000 impacts.”

 These traumas do not have to be powerful enough to knock someone out. A mild head butt with symptoms such as confusion, dizziness or wooziness means that the brain’s normal processing has been momentarily interrupted. As the impacts happen over and over again, brain cells and blood vessels develop microscopic tears, protein breakdown and possible leakage of cellular chemicals. This in turn leads to brain swelling and sometimes even cellular death.

Research shows that modern helmets do not protect the brain from these types of blows. While helmets help prevent skull fractures and reduce the likelihood of brain bruising from direct, linear blows, they do not protect against rotational injuries. Rotational injuries impact from the side, and are a major contributor to bruising and shearing of brain cells.

The brain itself is surrounded by, and technically floats in, cerebrospinal fluid.  Even if the initial shock of a head butt during game play  is absorbed by the helmet, the brain is still jarred inside the skull. The force of the impact causes the brain to bounce and twist against the inside of the skull.

No matter what type of helmet is worn, the rapid acceleration and deceleration of the brain cannot be stopped. The same mechanisms are at play during car accidents or with shaken baby syndrome. The skull itself doesn’t have to physically strike another surface for the brain to suffer damage, because the rapid movement of the entire head is what’s traumatizing the brain and damaging cells.

This is why helmets do not prevent chronic traumatic encephalopathy.

Is it More Dangerous for Kids?

According to a 2009 Institute of Medicine report, high school players experience concussions at almost twice the rate of professional football players.

Young brains are at particular risk of damage for a variety of reasons. For one thing, the body is still growing and the brain is learning new ways to manipulate complex information. This is one of the most important times in life to ensure the brain has every opportunity to grow and develop to its full potential. Repeated mild head trauma is concerning.

Younger brains are also at risk of something called Second Impact Syndrome, or SIS. SIS has been noted to happen more often in juveniles who play American Football. Sudden impact syndrome develops when a player who has just experienced a mild blow to the head, receives a second blow to the head before the symptoms from the first impact have cleared up.

For example, if a player hits his or her head, feels a bit woozy and dizzy, but gets back into the game and gets another strong head butt, s/he is at increased risk of developing SIS.

SIS causes blood vessels to become engorged with blood. This leads swelling throughout the brain and which can sometimes get so severe that it leads to death. According to the data, it is most common in male athletes around 17 years of age.

So What Now?

Chronic Traumatic Encephalopathy isn’t a brain disease that kills on the field. But it is a disease that has serious, life-long implications for those affected, and can kill slowly.  Many experts are researching how to make the sport safer for players of all ages.

According to one study co-authored by Dr. McKee, “by instituting and following proper guidelines for return to play after a concussion or mild traumatic brain injury, it is possible that the frequency of sports-related CTE could be dramatically reduced.” Many of these trials are still in their infancy, and there is more to learn about CTE and the effects of contact sports on the brain.  

Sources:

Ann C. McKee,  Robert C. Cantu, MD, Christopher J. Nowinski, Tessa Hedley-Whyte, MD, Brandon E. Gavett, PhD, Andrew E. Budson, MDVeronica E. Santini, MD, Hyo-Soon Lee, MD,1 Caroline A. Kubilus, and Robert A. Stern, PhD (2009) Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy following Repetitive Head Injury J Neuropathol Exp Neurol  doi:  10.1097/NEN.0b013e3181a9d503

ChroAnn C. McKee, MD, Robert C. Cantu, MD, Christopher J. Nowinski, ABTessa Hedley-Whyte, MD, Brandon E. Gavett, PhD, Andrew E. Budson, MD, Veronica E. Santini, MD,1 Hyo-Soon Lee, MD, Caroline A. Kubilus, and Robert A. Stern, PhD Ann McKee MD (2016) Boston University Chronic Traumatic Encephalopathy Center; Retrieved from http://www.bu.edu/cte/about/leadership/ann-mckee-md/

IOM (2009) Sports related concussions in youth. Retrieved from https://www.ninds.nih.gov/research/tbi/sports_concussion_report.pdf

Mori et al., 2006 Acute hemispheric swelling associated with thin subdural hematomas: pathophysiology of repetitive head injury in sports Brain Edema XIII, Springer (2006), pp. 40–43

Stern RA, Riley DO, Daneshvar DH, Nowinski CJ, Cantu RC, McKee AC (2011) Long-term consequences of repetitive brain trauma: chronic traumatic encephalopathy. doi: 10.1016/j.pmrj.2011.08.008.

Stern, R. A., Riley, D. O., Daneshvar, D. H., Nowinski, C. J., Cantu, R. C., & McKee, A. C. (2011). Future trend: Long-term Consequences of Repetitive Brain Trauma: Chronic Traumatic Encephalopathy. Pm&R, 3(Supplement 2), S460-S467. doi:10.1016/j.pmrj.2011.08.008

Stein TD, Alvarez VE, McKee AC. (2014) Chronic traumatic encephalopathy: a spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel  Alzheimers Res Ther. 2014 Jan 15;6(1):4. doi: 10.1186/alzrt234. eCollection

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