Lucy Ellis

The Effects Of Chronic Traumatic Encephalopathy

Throughout the history of contact sports, there has been a tendency for players to
overlook the serious dangers a concussion can pose. In recent years, medical professionals have
seen that many athletes who have experienced repeated brain trauma eventually develop Chronic
Traumatic Encephalopathy (CTE). This disease causes the degeneration of brain tissue and
buildup of an abnormal protein called Tau (Meehan et al., 2015, p. 2). As the number of athletes
participating in sports involving repeated brain trauma is at an all time high, CTE presents a
crucial public health concern. Recent estimates show between 1.6 and 3.8 million sports-related
concussions in the United States annually, and high school athletes sustain 300,000 concussions
a year (Brain Injury Research Institute [BIRI], n.d). In addition, researchers have concluded that
sports-related head injuries in the United States have reached an epidemic level (The Center for
Disease Control [CDC], 2015). For these reasons, I am interested in the effects of CTE; so that I
may be educated on the dangers that my friends in contact sports may face and be able to help
them.
The neurophysiological and neuropsychiatric changes that the brain faces when one has
CTE are categorized into 3 parts-- cognition, mood, and behavior. Early cognitive symptoms of
CTE include memory and learning impairment. The behavioral changes generally affect one's
impulse control, where individuals have bad tempers and consequences such as outrage. This
aspect goes hand-in-hand with aggressive behavior. Later on, cognitive, mood, and behavioral
changes will worsen, and dementia will begin to present itself. This disease often results in

negative alterations in motor skills; motions carried out when the brain, nervous system, and
muscles work together. (Ellis, 2016) These signs include difficulty with balance, as well as
changes in verbal communication, including the slurring and slowing of speech (Bazarian et al.,
2016, p. 2). In the article titled Chronic traumatic encephalopathy: neurodegeneration following
repetitive

concussive and subconcussive brain trauma, the results of testing a group of players
who were diagnosed with CTE were shared. These players showed signs of a motor neuron
disease that clinically mimics Lou Gehrig's Disease (ALS). These individuals have a very severe
case of CTE, which is marked with muscle weakness, dysphagia, and hyperactive deep tendon
reflexes. Advanced cases of CTE can also be accompanied by severely reduced brain weight;
commonly known as the thinning of the corpus callosum and loss of white matter.
A study that tracked 10 Division III college football players and 5 non-athletes during the
2011-12 season showed that the frequency of brain trauma is connected to damage of white
matter in the brain (Bazarian, p. 3). All subjects underwent diffusion tensor imaging, as well as
physiologic, cognitive, and balance testing during the pre-season, post-season, and after
6-months of no contact sports and rest. Head impact measures were recorded using helmet
accelerometers during football practices, and researchers accounted for the different positions
played to achieve a more accurate reading/representation. Each time, the percentage of whole
brain with significant changes in fractional anisotropy and mean diffusivity from Time 1 to 3
was determined for each subject and correlated to head impacts. Head impacts from the season
measured from 431-1850. None of the athletes actually suffered from a concussion, but the
players still experienced changes in their fractional anisotropy and mean diffusivity. On the
contrary, the 5 non-athletes showed no signs of a concussion and no cerebral white matter

changes in the brain (Ellis, 2016). A single football season full of repeated head injuries and
traumas without any concussions resulted in white matter changes in the brain, due to the
multiple head injuries and continued hits throughout the 6 month off-season. (Bazarian et al.,
2016, p. 1). The deterioration of white matter caused by head trauma, then manifests into
communication difficulties in the brain, in turn causing cognitive damage otherwise known as
CTE. I believe the researchers sample size should have including more players and another
football team in the same division. Although, the conclusions drawn by their research seemed
very accurate and I was shocked that during their 6 month off season with rest, their brains
continued to go through white matter changes.
According to Chronic traumatic encephalopathy and athletes, some athletes exposed to
repetitive brain trauma develop neuropsychological difficulties later on in life (Bazarian, 2016).
The article proposes many hypotheses, one being that, repeated blows lead to shear trauma to
the axons resulting in increased membrane permeability and ion shifts as described by Giza and
Hovda. This, in turn, leads to calcium influx and the subsequent release of caspases and calpains,
triggering Tau phosphorylation and aggregation(Meehan et al ., 2015, p.5). In other words,
these repetitive blows to the head are causing the breakage of axons, increasing the metabolic
rate, nutrient absorption, and toxin elimination in one's brain. The result of this is calcium reflux
and the triggering of Tau protein accumulation to spread (Phillips, n.d, p. 1). When this Tau
spreads in the brain it has many negative effects which start the declination of one's brain
resulting in advanced dementia and in many cases death. It does not surprise me that repetitive
blows to the head shear axons and result in these consequences, I believe there research was
accurate and done concisely.

On top of the neuropsychiatric and neuropsychological damages of CTE, neurologists

have found that the age of individuals at the time of being exposed to contact sports can put
players at a higher risk for developing CTE and progressive dementia. According to a study done
by the Mayo Clinic, CTE was found in the brains of a third of the men who played amateur
contact sports in their youth. But no sign of the disease was found in the brains of those who
never played contact sports at a young age (Preidt, 2015, p. 2). This is why youth should not
participate in contact sports because the traumatic brain injuries are a significant cause of death.
Generally, there are four stages of CTE: in the first, no symptoms are evident, but spots
of Tau build up primarily around the frontal lobe (Baugh, 2012, p.2). The proteins form
around the brain's blood vessels, halting normal functions and eventually killing the nerve cells.
In stage two, symptoms begin to manifest depression, rage, and impulsivity rise as Tau affects
the brains superior frontal lobes. The third stage is characterized by the spread of Tau to the
temporal lobe and the development of memory loss and confusion. The disease then spreads, and
begins to affect the amygdala the decision-making area of the brain, and the hippocampus,
which impairs emotions and memories. In the final stage, CTE presents itself as advanced
dementia. Tau deposits have spread all over the brain, killing the nerve cells and shrinking the
brain by half of its size. This can be caused by the thinning of the corpus callosum, making the
brain severely underweight. Because the brain is deformed, cognitive functions are very limited
at this stage (Ellis, 2016). In addition to the accumulation of Tau protein, a large concentration of
TAR DNA-Binding Protein 43 a protein often found in excess in patients with ALS builds
up in the brain and contributes to advanced dementia. (Baugh, 2012, p.3)

As of now, only men's brains have been donated to brain banks to study the effects of
repetitive hits to the head. This is a major problem for researchers, because women do get
concussions at higher rates than men in numerous sports and may suffer more severe symptoms.
Furthermore, evidence has shown that if brain trauma differs significantly between men and
women, that they might benefit from gender specific treatments. In the article Womens Brains
Needed for Concussion Research, the author proclaims, Many studies show the female brain
does appear to react differently when concussed. Female rats behave differently than males, and
there are biological differences, toofemales have cycling hormones, higher rates of blood flow
through their brains, less myelin sheathing around nerve fibers, and more migraine headaches.
All those factors might affect concussion response (McFarling, 2016, p.2 ). With that being
said, men and women could respond differently to the way medical professionals treat them for
repeated blows to the head, or for CTE. Researchers are in need to study women's brain to
ascertain whether women and men will benefit from gender specific treatments.
Although the long term effects of repeated brain trauma are finally coming to light, there
are still speculations and unknowns. Unfortunately, neurologists cannot diagnose CTE until post
mortem by dissecting the brain and taking biopsies at brain banks. However, Boston University
has plans to find the underlying disease mechanisms and try to work on the ability to diagnose
someone during life, not after death, The ultimate goal of this study is to develop methods of
diagnosing CTE during life through the use of a variety of tests, including MRI scans (such as
diffusion tensor imaging), MRS scans (also known as a virtual biopsy), blood tests, and
measures of proteins in spinal fluid. Participants will also undergo neurological, psychiatric, and
cognitive assessments, as well as genetic testing, (Baugh, 2012, p.8). With that said, developing

these biomarkers for detection would be extremely advantageous for future patients who have
symptoms of CTE.
Chronic Traumatic Encephalopathy negatively affects many athletes who play contact
sports by degenerating their brain and eventually leading to death. It is extremely important to be
educated on CTE because of the many people affected by head trauma. I plan on educating
players about the risks of contact sports and how it can potentially affect their life in the long
run. From reading these research articles I believe stricter actions must be put into place to
prevent repeated blows to the head, because many players do not know the extent of the dangers
that a head trauma injury can pose. Are the risks of contact sports worth it? The answer is up to
you.

References
Baugh, C. M., Stamm, J. M., Riley, D. O., Gavett, B. E., Shenton, M. E., Lin, A., . . . Stern, R. A.
(2012). Chronic traumatic encephalopathy: Neurodegeneration following repetitive
concussive and subconcussive brain trauma. Brain Imaging and Behavior, 6(2), 244-254.
doi:10.1007/s11682-012-9164-5
Bazarian, J. J., Zhu, T., Zhong, J., Janigro, D., Rozen, E., Roberts, A., . . . Blackman, E. G.
(2014). Persistent, Long-term Cerebral White Matter Changes after Sports-Related
Repetitive Head Impacts. PLoS ONE, 9(4). doi:10.1371/journal.pone.0094734
Brain Injury Basics. (2015, February 16). Retrieved from
https://www.cdc.gov/headsup/basics/index.html
McFarling, U. L., & S. (2016, November 21). Women's Brains Needed for Concussion
Research. Retrieved from
https://www.scientificamerican.com/article/women-rsquo-s-brains-needed-for-concussion
-research/
Meehan, W., Mannix, R., Zafonte, R., & Pascual-Leone, A. (2015). Chronic traumatic
encephalopathy and athletes: Table. Neurology, 85(17), 1504-1511.
doi:10.1212/wnl.0000000000001893
Philips, R. M. (n.d.). What is the permeability of the cell membrane? Retrieved from
http://book.bionumbers.org/what-is-the-permeability-of-the-cell-membrane/

Preidt, R. (2015, December 03). Youth Contact Sports May Raise CTE Risk. Retrieved
from WEBMD,
http://www.webmd.com/brain/news/20151203/playing-contact-sports-in-youth-may-raise
-risk-for-degenerative-brain-disease#1
What is a Concussion? (n.d.). Retrieved from
http://www.protectthebrain.org/Brain-Injury-Research/What-is-a-Concussion-.aspx