Chronic traumatic encephalopathy (CTE) is a
neurodegenerative disorder thought to be related with a past of recurring head
collisions could occur through sports which involves contact or military
combat. CTE was first initiated in the term as “punch drunk” in the early 1900s
because of its connection with boxing. In fact, most of their research was
mostly based on boxing population. Although, the disease is discovered in a
more distinct group of individuals that has a past of recurring head collisions
incorporating a range of contact sport players, military veterans, and domestic
abuse victims. In CTE, repeated brain trauma build up an abnormal protein called
Tau. It is an affluence which functions to alleviate cellular structure in the neurons,
which later may trigger major intervention with the purpose of the neurons. These
abnormal proteins spot can affect months, years or even sometimes decades after
the last time trauma or end of the active involvement of sports.
CTE was first noticed in 1928, after Dr. Harrison Martland described
it as “punch drunk syndrome”. Over the next 6 decades many researchers have
reported similar findings in boxers and as well in the victims of head trauma,
but not even 50 cases were confirmed. Pathologist Bennet Omalu broadcasted
primary evidence of CTE in an American Football Player in 2005. He found CTE in
brain of Mike Webster, who played for Pittsburg Steelers as a safety position. “Since
Webster’s death in 2002, many more NFL players: Seau, Frank Gifford, John
Mackey and Kenny Stabler were spotted with CTE afterwards their deaths”.
The CTE has been spotted in 110 of 111 earlier NFL players
whose brains were offered for research, according to an updated study “CTE
diagnosed in 99% of former NFL players studied by researchers” (CNN 2012). So
if we take that percentage on Current NFL players who are active on roster the
count will be 1679 out of 1696 have a possible of chance of getting CTE in near
future or have it already. Also, CTE was spotted in 87% of 202 former football
players (see appendix A) with high school, college, NFL, Canadian Football
League and semipro, study done by Boston University. Though research had
implied that concussions were one of the likely causes of CTE, new statistics advocates
that “minor head trauma that occurs regularly in football may pose”(NY
Times 2012) a superior risk than the rare violent collision. It also shows that
40 percent of the tests were positive sign of CTE was done on offensive or
defensive linemen, who are the mostly subject of vicious collisions on almost
every play in a football game. As we see the CTE has appeared to grow more a person who played the sport.
Those who played in High school were also involved in the
study, tend to have minor disease of CTE. Although players who played for
college, semi-professional and professional players had major disease of CTE. Researchers
classify that performance and reasoning problems were mutual among the players
which diagnosed from mild to severe CTE. Those players with severe CTE, 85% shows
signs of dementia. They were also likely to have issues in brain areas
associated with miserable symptoms, impulsivity and anxiety. More than 90% had cognitive
symptoms, as of like issues with memory, decision-making function and
The latest CTE fallouts, yet, are not as affected as the
headlines would lead you to believe. In fact, we are no improved up-to-date
today than we were yesterday or past years. All those brains evaluated in the
Boston University study were not randomly selected. Relatively, family members
of the deceased or mentioned by medical examiners, had somewhat reason that
doctors might find sign of injury. They have stated from all the football player,
who plays for NFL 1 out 10 have tolerance to CTE.
What might be the corresponding
lower bound? As the New York Times points out, the BU sample
represents about one-tenth of the former NFL players who’ve died since the
study began. If we assume that every other player in that group had a healthy
brain, the total prevalence for CTE would be in the vicinity of 9 percent. From
this we can conclude that the true rate of the disease is somewhere between 9
and 99 percent.
Let’s visualize that the occurrence of CTE in the NFL is
somewhere between the 9-to-99-percent range that McKee has stated above. We
will adopt that more than half of all players who retired from football —54
percent—anchorage some mark of football-related injury to their brains. What
does those mean to upcoming new players? If it’s true that more than half of
NFL retirees have CTE, and 90% of men with that disorder have signs during the
time they were still playing. So in that sense the numbers don’t add up. It
either propose that CTE is not as extensive as we imagined or that the signs of
CTE are not as severe as we’ve imagined. At least, we established that 99
percent of football players with brains injury are likely to stand the signs of
Evidently, CTE research is in its beginning, and years of study
are likely needed to change the view point. CTE can be spotted premature in its
progression by operating a mixture of medical instruments and biomarkers. It is
unidentified whether a lone blow to the head is enough to begin the metabolic gush
that leads the solid and neuro pathological alterations feature of CTE. Hence,
the apparent way to avoid CTE is to avoid yourself from recurring head injuries.
In sports where frequent hits to the head are inescapable and is a risk factor
for developing CTE, Accurate concussion evaluation and controlling may be vital
for avoiding long-term effects. Though, new approaches to shrink the number and
relentlessness of head trauma are probable, such as reducing tackle practices, applying
rules of play which could reduce the chance of continual head trauma.
BU researchers say they have discovered CTE in more than
100 former NFL players, a handful of whom have committed suicide. Medical
examiners delivered Hernandez’s brain, weighing 1,573 grams, to BU’s labs in
April. From the outside, it looked like a typical brain — no lesions, no
bruises, no abnormalities. When researches sliced the brain into sections, they
discovered startling damage.
Symptoms could be examined physically, since it shows no
signs that something is going on in the brain. Although I am even X-ray and
other advanced technology could not spot the CTE otherwise it would made life
so easier for doctors to diagnosed in patients. The time at which a player undergoes
his or her head injuries may also affect future CTE risk. As a youth the brain
may be more defenseless to damage, but enlarged elasticity of the young brain
may be able to reimburse for certain troubles such as interactive dysfunction.
Possibly, healthiness and medical issues that are absent or present throughout
this experimental step may impact the degree of neurodegeneration.
Genetic differences might work as a critical function in regulating
the relations between head trauma, disordered reasoning and performance, and neuropathological
changes. “Unusual genes thought to impact CTE possibility is the apolipoprotein
E (APOE) gene. The APOE ?4 allele, important in the genetics of AD, may also
increase the risk of CTE”.(cited). Founded
on chromosomal examination managed in combination with neuropathological studies
of people with a past of recurrent brain injuries, roughly 57 percent of people
with neuropathological were confirmed with CTE possessed at least one APOE gene.
Doctors and examiners are only starting to comprehend various
characteristics of CTE. Additional time and study is required. For that purpose,
it has not yet been touched on the symptoms of CTE. Nevertheless, based on current
information, the signs of CTE could occasionally be alike to individuals of
other disorders that engage considerable loss of brain cells. Researcher have
made 4 stages of symptoms on based of their research so far are as following:
Stage 1: Mild headaches, attention and concentrating
problems. Internally in brain very tiny spots of “tau” has starting to build up
in the frontal lobe.
Stage 2: Short term memory loss, depression and mood swing.
Internally tau has starting to slowly affect nerve cells in the frontal lobe.
Stage 3: Aggression, behavioral impairing, memory loss and
confusion. Internally tau has now reached to amygdala and hippocampus of
frontal lobe which cause the things that I stated before.
Stage 4: Severe memory loss, dementia and cognitive
disorder. Internally tau has now mostly killed the nerve cells and now brain is
Presently, CTE can be identified merely after an individual
has deceased, because a study of the individual’s brain is necessary to perform
the diagnosis. It is difficult to know the particular signs of the disorder. Lately,
however, experts are trying to discover a new sign for CTE that could
aid experts analyze the disorder while an individual is still alive.
Dr. Bennett Omalu a
neurologist who did his most of his education in Nigeria. In 2002 he was going
through Mike Webster’s brain cell slide in Pittsburg, Pennsylvania. Suddenly he
found very unusual evidence that should not be found in a 50-year-old man or
any normal brain, after testing he discovered it was CTE. He later published
his findings on the brain so people and officials could get to know what
happens when players get hit to head, but NFL and other neurosurgeons related
to league told him to retract his paper. Shortly after release of report ,
another Steeler’s player committed suicide by drinking anti-freeze. Dr. Omalu
aslo tested his brain and find the same findings he did in Webster’s brain. So
now his research had begun to attract attention of public. This was the case
that turned table of how parents perceive football for their children’s future.
After that another big time case was ken Stabler’s, he was quarterback
for Oakland Raiders for few season. He was the first quarterback that diagnosed
with CTE. “Dr. Ann McKee, a professor of neurology and pathology at Boston
University, said that after examining Stabler’s brain, it was clear he suffered
from Stage 3 CTE and that the disease was widespread throughout his brain”.
provided extra safety from blows than any other
football players. Even offensive line’s one of the main purpose is to shield
the quarterback. Very known leagues like the N.F.L. have extraordinary rules to
discourage hard hits to players in the most essential position on the turf. But
Stabler’s diagnosis added that no spot in football, except maybe kicker, is safe
from progressive brain injury connected to blows to the head, both physical and
mental. In fact, see Appendix B to see that research shows even place-kicker
have diagnosed with CTE. “On some days,
when he wasn’t feeling extremely bad, things were kind of normal, but on other
days it was intense. I think Kenny’s head rattled for about 10 years.” His
partner said that cancer may have took his body but his mind was a downward
spiral for almost last 15- 20 years. And last 10 years were the hardest days
for both of us.
Most Recent and severe case of CTE has been found in Aaron
Hernandez brain after he committed suicide in April of 2017.Until killing of Lloyd
in 2013 he was a superstar for patriots. Scientist said it was the most severe stage 3
CTE they have ever seen at this age. He was convicted of multiple killings in
2013, researchers did not connect that with CTE, although symptoms like aggression
and confusion could have been associated with his doings. He been in off field
trouble since college day, with drugs and shady friends. For the first five
weeks of 2017 ratings and views of games were down significantly. Awareness of
CTE is spreading.
So for, the medical diagnosis of CTE is challenging since
there are no specific investigating standards or significant. The various analysis
of CTE will frequently end up in dementia. Adult individuals with memorial struggles
may show to have CTE neuropathological. Hence, exclusive of neuropathological validation,
a medical analysis of CTE cannot be finished with a excessive mark of sureness.
Additionally, the medical analysis of CTE could be confused by alcohol or other
drug misuse. A sum of individuals with neuropathological definite CTE are supposed
to have advanced complications with drug misuse as result of disorder. Nevertheless,
it can be tough to resolve whether the drug misuse troubles are origin of
symptoms. John Urschel a Baltimore Raven offensive lineman who retired in 2016
while he had a huge contract waiting, same with Aaron lynch 49ers linebacker
retired after rookie year. Both said family is important than to play football
and get CTE. Also they both mentioned it would be great if they find a way to
diagnose it while they have CTE. There are minor success in diagnosing CTE in a
living person but no sure evidence has been stated.
CTE is just like stale food, there is no way you can turn it
to eatable. As in CTE, it is an advanced degenerative brain disease that no
treatment will make you any healthier. Most of the brain disease is incurable and
CTE is one of them. Even though many scientist is working on the cure and
hoping for a breakthrough.
For prevention there is no treatment as I stated above.
However, you may prevent it from happening to you by cutting back on contact
sports. Also CTE mostly associated with concussion you may take care after you
have your first concussion or even before that. Helmets have been very useful
to reduce the brain injury but not just thoroughly. Also players should not
abuse alcohol and drug use, since the studies have shown it affects CTE to
develop. Coaches and players should understand the guidelines of the concussion
protocol and always keep player’s safety first because after few years they
need to live a normal life and by taking preventive steps it may help them in
future to live a disease free life.
CTE is a neurodegenerative disease that happens late in the
lives of few people amongst a past of recurring head trauma. The accurate affiliation
among recurring minor traumatic brain damage and with or without suggestive
concussion with CTE is not totally well-defined. CTE has been testified in connection
with the player of American football, hockey, soccer, wrestling. CTE often shows
up in mid-life and creates medical signs of disorderly, depression, and memory
loss. Now, neuropathological analysis of brain tissue is the merely way to identify
CTE, while concentrated research powers are proceeding to pinpoint device to identify
the disorder and display its development, and to improve treatments to slow or converse
its progress. The exact variables allied to head neuropathology, trauma, and
clinical presentation of CTE that remain unanswered.