Chronic traumatic encephalopathy (CTE) is aneurodegenerative disorder thought to be related with a past of recurring headcollisions could occur through sports which involves contact or militarycombat. CTE was first initiated in the term as “punch drunk” in the early 1900sbecause of its connection with boxing. In fact, most of their research wasmostly based on boxing population. Although, the disease is discovered in amore distinct group of individuals that has a past of recurring head collisionsincorporating a range of contact sport players, military veterans, and domesticabuse victims. In CTE, repeated brain trauma build up an abnormal protein calledTau. 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. Theseabnormal proteins spot can affect months, years or even sometimes decades afterthe last time trauma or end of the active involvement of sports.
CTE was first noticed in 1928, after Dr. Harrison Martland describedit as “punch drunk syndrome”. Over the next 6 decades many researchers havereported similar findings in boxers and as well in the victims of head trauma,but not even 50 cases were confirmed. Pathologist Bennet Omalu broadcastedprimary evidence of CTE in an American Football Player in 2005. He found CTE inbrain of Mike Webster, who played for Pittsburg Steelers as a safety position. “SinceWebster’s death in 2002, many more NFL players: Seau, Frank Gifford, JohnMackey and Kenny Stabler were spotted with CTE afterwards their deaths”. The CTE has been spotted in 110 of 111 earlier NFL playerswhose brains were offered for research, according to an updated study “CTEdiagnosed in 99% of former NFL players studied by researchers” (CNN 2012). Soif we take that percentage on Current NFL players who are active on roster thecount will be 1679 out of 1696 have a possible of chance of getting CTE in nearfuture or have it already.
Also, CTE was spotted in 87% of 202 former footballplayers (see appendix A) with high school, college, NFL, Canadian FootballLeague and semipro, study done by Boston University. Though research hadimplied that concussions were one of the likely causes of CTE, new statistics advocatesthat “minor head trauma that occurs regularly in football may pose”(NYTimes 2012) a superior risk than the rare violent collision. It also shows that40 percent of the tests were positive sign of CTE was done on offensive ordefensive linemen, who are the mostly subject of vicious collisions on almostevery 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 thestudy, tend to have minor disease of CTE. Although players who played forcollege, semi-professional and professional players had major disease of CTE.
Researchersclassify that performance and reasoning problems were mutual among the playerswhich diagnosed from mild to severe CTE. Those players with severe CTE, 85% showssigns of dementia. They were also likely to have issues in brain areasassociated with miserable symptoms, impulsivity and anxiety. More than 90% had cognitivesymptoms, as of like issues with memory, decision-making function andattention.
The latest CTE fallouts, yet, are not as affected as theheadlines would lead you to believe. In fact, we are no improved up-to-datetoday than we were yesterday or past years. All those brains evaluated in theBoston University study were not randomly selected.
Relatively, family membersof the deceased or mentioned by medical examiners, had somewhat reason thatdoctors 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 correspondinglower bound? As the New York Times points out, the BU samplerepresents about one-tenth of the former NFL players who’ve died since thestudy began.
If we assume that every other player in that group had a healthybrain, the total prevalence for CTE would be in the vicinity of 9 percent. Fromthis we can conclude that the true rate of the disease is somewhere between 9and 99 percent. Let’s visualize that the occurrence of CTE in the NFL issomewhere between the 9-to-99-percent range that McKee has stated above. Wewill adopt that more than half of all players who retired from football —54percent—anchorage some mark of football-related injury to their brains.
Whatdoes those mean to upcoming new players? If it’s true that more than half ofNFL retirees have CTE, and 90% of men with that disorder have signs during thetime they were still playing. So in that sense the numbers don’t add up. Iteither propose that CTE is not as extensive as we imagined or that the signs ofCTE are not as severe as we’ve imagined.
At least, we established that 99percent of football players with brains injury are likely to stand the signs ofCTE. Evidently, CTE research is in its beginning, and years of studyare likely needed to change the view point. CTE can be spotted premature in itsprogression by operating a mixture of medical instruments and biomarkers. It isunidentified whether a lone blow to the head is enough to begin the metabolic gushthat 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 factorfor developing CTE, Accurate concussion evaluation and controlling may be vitalfor avoiding long-term effects. Though, new approaches to shrink the number andrelentlessness of head trauma are probable, such as reducing tackle practices, applyingrules of play which could reduce the chance of continual head trauma.
BU researchers say they have discovered CTE in more than100 former NFL players, a handful of whom have committed suicide. Medicalexaminers delivered Hernandez’s brain, weighing 1,573 grams, to BU’s labs inApril. From the outside, it looked like a typical brain — no lesions, nobruises, no abnormalities. When researches sliced the brain into sections, theydiscovered startling damage. Symptoms could be examined physically, since it shows nosigns that something is going on in the brain. Although I am even X-ray andother advanced technology could not spot the CTE otherwise it would made lifeso easier for doctors to diagnosed in patients.
The time at which a player undergoeshis or her head injuries may also affect future CTE risk. As a youth the brainmay be more defenseless to damage, but enlarged elasticity of the young brainmay be able to reimburse for certain troubles such as interactive dysfunction.Possibly, healthiness and medical issues that are absent or present throughoutthis experimental step may impact the degree of neurodegeneration. Genetic differences might work as a critical function in regulatingthe relations between head trauma, disordered reasoning and performance, and neuropathologicalchanges. “Unusual genes thought to impact CTE possibility is the apolipoproteinE (APOE) gene.
The APOE ?4 allele, important in the genetics of AD, may alsoincrease the risk of CTE”.(cited). Foundedon chromosomal examination managed in combination with neuropathological studiesof people with a past of recurrent brain injuries, roughly 57 percent of peoplewith neuropathological were confirmed with CTE possessed at least one APOE gene. Doctors and examiners are only starting to comprehend variouscharacteristics 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 currentinformation, the signs of CTE could occasionally be alike to individuals ofother disorders that engage considerable loss of brain cells. Researcher havemade 4 stages of symptoms on based of their research so far are as following:Stage 1: Mild headaches, attention and concentratingproblems. Internally in brain very tiny spots of “tau” has starting to build upin 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 andconfusion.
Internally tau has now reached to amygdala and hippocampus offrontal lobe which cause the things that I stated before.Stage 4: Severe memory loss, dementia and cognitivedisorder. Internally tau has now mostly killed the nerve cells and now brain isdistorted. Presently, CTE can be identified merely after an individualhas deceased, because a study of the individual’s brain is necessary to performthe 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 couldaid experts analyze the disorder while an individual is still alive. Dr.
Bennett Omalu aneurologist who did his most of his education in Nigeria. In 2002 he was goingthrough Mike Webster’s brain cell slide in Pittsburg, Pennsylvania. Suddenly hefound very unusual evidence that should not be found in a 50-year-old man orany normal brain, after testing he discovered it was CTE. He later publishedhis findings on the brain so people and officials could get to know whathappens when players get hit to head, but NFL and other neurosurgeons relatedto league told him to retract his paper. Shortly after release of report ,another Steeler’s player committed suicide by drinking anti-freeze.
Dr. Omaluaslo tested his brain and find the same findings he did in Webster’s brain. Sonow his research had begun to attract attention of public. This was the casethat turned table of how parents perceive football for their children’s future. After that another big time case was ken Stabler’s, he was quarterbackfor Oakland Raiders for few season. He was the first quarterback that diagnosedwith CTE. “Dr.
Ann McKee, a professor of neurology and pathology at BostonUniversity, said that after examining Stabler’s brain, it was clear he sufferedfrom Stage 3 CTE and that the disease was widespread throughout his brain”. Quarterbacks areprovided extra safety from blows than any other football players. Even offensive line’s one of the main purpose is to shieldthe quarterback. Very known leagues like the N.F.L. have extraordinary rules todiscourage hard hits to players in the most essential position on the turf.
ButStabler’s diagnosis added that no spot in football, except maybe kicker, is safefrom progressive brain injury connected to blows to the head, both physical andmental. In fact, see Appendix B to see that research shows even place-kickerhave diagnosed with CTE. “On some days,when he wasn’t feeling extremely bad, things were kind of normal, but on otherdays it was intense. I think Kenny’s head rattled for about 10 years.” Hispartner said that cancer may have took his body but his mind was a downwardspiral for almost last 15- 20 years. And last 10 years were the hardest daysfor both of us.
Most Recent and severe case of CTE has been found in AaronHernandez brain after he committed suicide in April of 2017.Until killing of Lloydin 2013 he was a superstar for patriots. Scientist said it was the most severe stage 3CTE they have ever seen at this age. He was convicted of multiple killings in2013, researchers did not connect that with CTE, although symptoms like aggressionand confusion could have been associated with his doings.
He been in off fieldtrouble since college day, with drugs and shady friends. For the first fiveweeks of 2017 ratings and views of games were down significantly. Awareness ofCTE is spreading. So for, the medical diagnosis of CTE is challenging sincethere are no specific investigating standards or significant. The various analysisof CTE will frequently end up in dementia. Adult individuals with memorial strugglesmay 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 otherdrug misuse.
A sum of individuals with neuropathological definite CTE are supposedto have advanced complications with drug misuse as result of disorder. Nevertheless,it can be tough to resolve whether the drug misuse troubles are origin ofsymptoms. John Urschel a Baltimore Raven offensive lineman who retired in 2016while he had a huge contract waiting, same with Aaron lynch 49ers linebackerretired after rookie year. Both said family is important than to play footballand get CTE.
Also they both mentioned it would be great if they find a way todiagnose it while they have CTE. There are minor success in diagnosing CTE in aliving person but no sure evidence has been stated. CTE is just like stale food, there is no way you can turn itto eatable. As in CTE, it is an advanced degenerative brain disease that notreatment will make you any healthier. Most of the brain disease is incurable andCTE is one of them. Even though many scientist is working on the cure andhoping 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 contactsports.
Also CTE mostly associated with concussion you may take care after youhave your first concussion or even before that. Helmets have been very usefulto reduce the brain injury but not just thoroughly. Also players should notabuse alcohol and drug use, since the studies have shown it affects CTE todevelop. Coaches and players should understand the guidelines of the concussionprotocol and always keep player’s safety first because after few years theyneed to live a normal life and by taking preventive steps it may help them infuture to live a disease free life. CTE is a neurodegenerative disease that happens late in thelives of few people amongst a past of recurring head trauma.
The accurate affiliationamong recurring minor traumatic brain damage and with or without suggestiveconcussion with CTE is not totally well-defined. CTE has been testified in connectionwith the player of American football, hockey, soccer, wrestling. CTE often showsup in mid-life and creates medical signs of disorderly, depression, and memoryloss. Now, neuropathological analysis of brain tissue is the merely way to identifyCTE, while concentrated research powers are proceeding to pinpoint device to identifythe disorder and display its development, and to improve treatments to slow or converseits progress. The exact variables allied to head neuropathology, trauma, andclinical presentation of CTE that remain unanswered.