#1) He's really fuckin STUPID! Because there isn't that much bad luck in the world to keep walking right into one shitty-situation with a woman after another. There comes a point when you might just have to leave it at, go to work. Come home. Go to sleep. Get up. Go to work. Come home. Go to sleep. And steer clear of women for awhile till you get your head screwed on straight. This first option, may just be it. The guys a complete fuckin idiot and needs to just chill out from the dating scene and step away from his fiancee and child because he keeps fuckin up more than anything else.
#2) He's just a straight-up scumbag who likes to beat up women! This is the option that White Americans are gunning for hard! Which? Doesn't surprise me at all. Ray McDonald is making it pretty easy to play into this option too, so. It also means he might also have both this option and #1 as his Final Answer. If this is something he is purposefully doing then he needs to be locked up and he needs to have some immediate psychological counselling. Mind you that all of his previous incidents have ended with HIM BEING CLEARED OF ALL CHARGES. Which only adds to the very last option.
And this LAST ONE? Nooooooooooooooooooooooooooooooooooh, body. Is talking about it. AT ALL. And I'm listening and watching and waiting and then realizing "Heh! Well I know the White-&-White Jewish controlled Media isn't gonna bring this shit up! Because it might cause other Whites to lose billions of dollars, LITERALLY!" AND NO. I AM NOT EXAGGERATING.
#3) Is something that EVERYONE KNOWS ABOUT NOW, but mysteriously nobody White at least wants to bring it up. And that is CTE. What if Ray McDonald is ALREADY SUFFERING FROM CHRONIC TRAUMATIC ENCEPHALOPATHY? CTE is a condition that American Footballers are EXTREMELY VULNERABLE TO. Massive rule-changes have been made over the last 5-years because of this and as more and more information has come out? The White American Football OWNERS!? They think they're SLICK! But they ALREADY KNOW THAT AMERICAN FOOTBALL SHOULD BE SHUT DOWN, IMMEDIATELY. AND PERMANENTLY.
Which means a 9-BILLION DOLLAR REVENUE SHARING INDUSTRY, WOULD BE WIPED OUT OVER NIGHT. And that is a CRITICAL FACT TO REMEMBER PEOPLE.
There are NO TESTS.
There are NO PRELIMINARY WARNINGS.
There is just A PATTERN OF BIZARRE, IRRATIONAL BEHAVIORS.
And then something gives way with that player.
A NUMBER OF HIGH-PROFILE AMERICAN FOOTBALLERS RETIRED LAST YEAR BEFORE THE AGE OF 30, SOME!?
Some were set to make 7 - 9 MILLION DOLLAR DEALS. But decided they'd rather RETIRE OUT OF FEAR OF TURNING INTO SOME CRAZED MONSTER. Or suffering PERMANENT BRAIN INJURIES where the onset of it is only noticeable WHEN YOU HAVE FRIENDS AND FAMILY WHO SEE YOUR PERSONALITY BEGIN TO RANDOMLY, RADICALLY, CHANGE.
Here is information on CTE;
Chronic traumatic encephalopathy (CTE) is a form of encephalopathy that is a progressive degenerative disease, which can currently only be definitively diagnosed postmortem, in individuals with a history of multipleconcussions and other forms of head injury. In March 2014, researchers announced the discovery of an exosome particle created by the brain which has been shown to contain trace proteins indicating the presence of the disease,[1] however, a test is not yet available. The disease was previously called dementia pugilistica (DP), i.e. "punch-drunk", as it was initially found in those with a history of boxing. CTE has been most commonly found in professional athletes participating in American football, ice hockey, professional wrestling and other contact sports who have experienced repetitive brain trauma. It has also been found in soldiers exposed to a blast or a concussive injury,[2] in both cases resulting in characteristic degeneration of brain tissue and the accumulation of tau protein. Individuals with CTE may show symptoms of dementia, such as memory loss,aggression, confusion and depression, which generally appear years or many decades after the trauma.
CTE is a progressive degenerative disease of the brain found in people with a history of repetitive brain trauma, including symptomatic concussions as well as sub-concussive hits to the head that do not cause symptoms. In the case of blast injury, a single exposure to a blast and the subsequent violent movement of the head in the blast wind can cause the condition.[2]
Epidemiology[edit]
CTE is a neurological degenerative disease found in individuals who have been subjected to repetitive traumatic brain injuries[3] by way of the acceleration of the head on impact and the subsequent damage to axons. While repetitive brain trauma is thought to be necessary to cause CTE, it is not sufficient, meaning that not everyone exposed to repetitive brain trauma will get the disease. Other risk factors are possible but have not yet been reported, due to the donated brains in the brain bank at the Boston University School of Medicine and elsewhere, which consists mostly of the brains of athletes with a history of professional participation in contact sports.[4] Professional level athletes are the largest demographic to suffer from CTE due to frequent concussions from play in contact-sport. These contact-sports include American football, ice hockey, rugby, boxing, and wrestling.[5] Other individuals that have been diagnosed with CTE were involved in military service, had a previous history of chronic seizures, victims of domestic abuse, and or were involved in activities resulting in repetitive head collisions.[6] Reports of CTE have steadily increased in younger athletes, most likely due to increased awareness of the issue and perhaps due in part to athletes becoming bigger and stronger producing greater magnitudes of force in collision.[5]
Pathology[edit]
The primary physical manifestations of CTE include a reduction in brain weight, associated with atrophy of the frontal and temporal cortices and medial temporal lobe. The lateral ventricles and the third ventricle are often enlarged, with rare instances of dilation of the fourth ventricle.[7] Other physical manifestations of CTE include anterior cavum septi pellucidi and posterior fenestrations, pallor of the substantia nigra and locus ceruleus, and atrophy of the olfactory bulbs, thalamus, mammillary bodies, brainstem and cerebellum.[8]As CTE progresses, there may be marked atrophy of the hippocampus, entorhinal cortex, and amygdala.[3]
On a microscopic scale the pathology includes neuronal loss, tau deposition, TAR DNA-binding Protein 43 (TDP 43)[9] beta-amyloid deposition, white matter changes, and other abnormalities. The tau deposition occurs as dense neurofibrillary tangles (NFT), neurites, and glial tangles, which are made up of astrocytes and other glial cells[7] Beta-amyloid deposition is a relatively uncommon feature of CTE.
A small group of individuals with CTE have chronic traumatic encephalomyopathy (CTEM), characterized by motor neuron disease symptoms and mimics Amyotrophic Lateral Sclerosis (ALS) (known in the United States as Lou Gehrig’s disease). Progressive muscle weakness and balance and gait problems seem to be early signs of CTEM.[7]
Signs and symptoms[edit]
Other than repeated brain trauma, the risk factors for CTE remain unknown.[7] So far, CTE can only be diagnosed posthumously. Research studies are looking into possible genetic, exposure level, and other risk factors.
Researchers who conducted a CTE pilot study at UCLA described the findings as a significant step toward being able to diagnose CTE, in living patients.[10]
Research performed at the Cleveland Clinic and at the University of Rochester[11] has shown that in addition to concussions, sub-concussive head hits also produce measurable changes in athletes' MRI. Bazarian (University of Rochester) demonstrated persistent changes in white matter properties in athletes who did not experience a concussion during a season but had several blows to the head. This finding is consistent with the hypothesis that a number of sub-concussive events may be as damaging as a frank concussion. The MRI changes reported in this study were causally related to the presence in serum of players of auto-antibodies against the brain protein S100B. The sequence of events proposed by Janigro at the Cleveland Clinic links sub-concussion to leakage of the blood-brain barrier, extravasation of brain S100B in blood,[12] activation of an immune response due to antigen unmasking and production of auto-antiboides. These auto-antibodies maybe pathogenic as shown for example in epileptic human brain.[13] The link between S100B auto-antibodies and CTE needs experimental confirmation; however, antibodies against S100B or other brain protein have been found in patients affected by Alzheimer's disease.
Clinical symptoms of CTE are only beginning to be understood. They are thought to include changes in mood (i.e. depression, suicidality, apathy, anxiety), cognition (i.e. memory loss, executive dysfunction), behavior (short fuse, aggression), and in some cases motor disturbance (i.e. difficulty with balance and gait). While the pathology of CTE has been broken up into stages,[9] the clinical symptoms and clinical progression of CTE are not yet fully understood.
Prevention[edit]
No agreement has been reached about how much or little head trauma is needed for CTE to develop, or the overarching mechanism of injury.[4] Recently, investigators demonstrated that immobilizing the head during a blast exposure prevented the learning and memory deficits associated with CTE that occurred when the head was not immobilized. This research, represents the first case series of postmortem brains from U.S. military personnel who were exposed to a blast and/or a concussive injury.[2] However, the protein tau which binds microtubules of brain axons, was found to have an elastic limit which is speed dependent; when breached, the microtubles become undone and cause brain swellings due to backups of information transport.[14]
Diagnosis[edit]
The lack of in-vivo techniques to show distinct biomarkers for CTE is the reason CTE cannot be diagnosed during lifetime. The only known diagnosis for CTE occurs by studying the brain tissue after death. Concussions are non-structural injuries and do not result in brain bleeding, which is why most concussions cannot be seen on routine neuroimaging tests such as CT or MRI.[15] Acute concussion symptoms (those that occur shortly after an injury) should not be confused with CTE. Differentiating between prolonged post-concussion syndrome (PCS, where symptoms begin shortly after a concussion and last for weeks, months, and sometimes even years) and CTE symptoms can be difficult. Research studies are currently examining whether neuroimaging can detect subtle changes in axonal integrity and structural lesions that can occur in CTE.[3] Recently, more progress in in-vivo diagnostic techniques for CTE has been made, using DTI, fMRI, MRI, and MRS imaging; however, more research needs to be done before any such techniques can be validated.[7]
Positron Emission Tomography(PET) using a newly developed radiopharmaceutical [18F]FDDNP is being investigated as a tool to allow in-vivo diagnosis of CTE.[16] In late 2013, breaking research was completed by the University of California Los Angeles in which for the first time ever, Chronic Traumatic Encephalopathy was found in living-retired National Football League players. Prior to this breakthrough study conducted by UCLA, Chronic Traumatic Encephalopathy could only be found posthumously through autopsies of diseased athletes, however, this study found the brain disease in numerous living athletes. The scan lit up for tau in all five former players, according to the study. The protein was concentrated in areas that control memory, emotions and other functions—a pattern consistent with the distribution of tau in CTE brains that have been studied following autopsy, according to the researchers. A small study of 5 patients has been reported to show accumulation of tau protein in the brains of suspected CTE patients seen on PET scan.[17] This finding is also noted in a number of other dementing disorders such as Alzheimer's disease, Pick's disease, progressive supranuclear palsy, corticobasal degeneration and familial frontotemporal dementia and Parkinsonism linked to chromosome abnormality.[18] At the current time PET scanning is not widely used in screening because of the high cost of the study (estimated to be $5,000 USD).[19]
A putative biomarker for CTE is the presence in serum of auto-antibodies against the brain. These may enter the brain by means of a disrupted blood-brain barrier, and attack neuronal cells which are normally protected from an immune onslaught.[20] Given the large numbers of neurons present in the brain, and considering the poor penetration of antibodies across a normal blood-brain barrier, there is an extended period of time between the initial events (head hits) and the development of any signs or symptoms. Nevertheless, autoimmune changes in blood of players may consist the earliest measurable event predicting CTE.
History[edit]
CTE was first noticed as a “peculiar condition” casually referred to as a “punch-drunk” syndrome in boxers and prizefighters before the 1930s. It was recognized as affecting individuals who took considerable blows to the head, but was believed to be confined to boxers and not other athletes.[21] In 2008, the Sports Legacy Institute joined with the Boston University School of Medicine (BUSM) to form the Center for the Study of Traumatic Encephalopathy (CSTE).[22] Brain Injury Research Institute (BIRI) also studies the impact of concussions.[23][24]
American football[edit]
Main article: Concussions in American football
Between 2008 and 2010, the bodies of twelve former professional American football players underwent postmortem evaluations for CTE, and all of them showed evidence of the disease, indicating a conservatively estimated prevalence rate of 3.7% among professional football players if no other players who died during this period had CTE.[25]
Bennet Omalu, a forensic pathologist and neuropathologist in Pittsburgh, Pennsylvania found CTE in the brains of Mike Webster, Terry Long, Andre Waters, Justin Strzelczyk and Tom McHale.[24] Omalu, in 2012 a medical examiner and associate adjunct professor in California, was a co-founder of BIRI[24] and reportedly in 2012 participated in the autopsy of Junior Seau.[23] Omalu's participation was halted during the autopsy after Junior Seau's son revoked previously provided oral permission after he received telephone calls from NFL management denouncing Omalu's professional ethics, qualifications, and motivation.
On December 1, 2012, Kansas City Chiefs linebacker Jovan Belcher killed his girlfriend and drove to Arrowhead Stadium and killed himself in front of then GM Scott Pioli and then head coach Romeo Crennel. A year later, a family lawyer filed a wrongful death lawsuit, on behalf of Belcher's minor daughter, against the Chiefs alleging the team deliberately ignored warning signs of CTE, possibly leading to his suicide. The lawyer also hired a medical examiner to examine Belcher's brain for signs of CTE. On September 29, 2014, it was confirmed that he suffered from CTE.[26]
As of December 2012, thirty-three former National Football League (NFL) players have been diagnosed post-mortem with CTE. Former Detroit Lions lineman and eight-time Pro Bowler Lou Creekmur,[27] former Houston Oilers and Miami Dolphins linebacker John Grimsley,[28] former Tampa Bay Buccaneers guard Tom McHale,[29] former Cincinnati Bengals wide receiver Chris Henry,[30] and former Chicago Bears safety Dave Duerson,[31] have all been diagnosed post-mortem with CTE. Other football players diagnosed with CTE include former Buffalo Bills star running back Cookie Gilchrist[32] and Wally Hilgenberg.,[33] among others.
An autopsy conducted in 2010 on the brain of Owen Thomas, a 21-year-old junior lineman at the University of Pennsylvania who committed suicide, showed early stages of CTE, making him the second youngest person to be diagnosed with the condition. Thomas was the second amateur football player diagnosed with CTE, after Mike Borich, who died at 42.[34] The doctors who performed the autopsy indicated that they found no causal connection between the nascent CTE and Thomas's suicide. There were no records of Thomas missing any playing time due to concussion, but as a player who played hard and "loved to hit people," Thomas may have played through concussions and received thousands of subconcussive impacts on the brain.[35]
In October 2010, 17-year-old Nathan Stiles died hours after his high school homecoming football game, where he took a hit that would be the final straw in a series of subconcussive and concussive blows to the head for the highschooler. The CSTE diagnosed him with CTE, making him the youngest reported CTE case to date.[36]
In July, 2011, Colt tight end John Mackey died after several years of deepening symptoms of frontotemporal dementia. BUSM was reported to be planning to examine his brain for signs of CTE.[37] The CSTE found CTE in his brain post-mortem.[38]
In 2012, retired NFL player Junior Seau committed suicide with a gunshot wound to the chest.[39] There was speculation that he suffered brain damage due to CTE.[23][40][41][42][43] Seau's family donated his brain tissue to the National Institute of Neurological Disorders and Stroke.[44] On January 10, 2013, the brain pathology report was revealed and Seau did have evidence of CTE.[45]
On July 27, 2012, an autopsy report concluded that the former Atlanta Falcons safety Ray Easterling, who committed suicide in April 2012, had CTE.[46][47]
The NFL has taken measures to help prevent CTE. As of July 2011, the NFL has changed its return-to-play rules.[citation needed] The number of contact practices has been reduced, based on the recent collective bargaining agreement.[48]
In 2012, some four thousand former NFL players "joined civil lawsuits against the League, seeking damages over the League’s failure to protect players from concussions, according to Judy Battista of the [New York] Times".[49]
On August 30, 2013, the NFL reached a $765 million settlement with the former NFL players over the head injuries.[50] The settlement created a $675 million compensation fund from which former NFL players can collect depending on the extent of their conditions. Severe conditions such as Lou Gehrig's disease and postmortem diagnosed chronic traumatic encephalopathy would be entitled to payouts as high as $5 million.[50] From the remainder of the settlement, $75 million will be used for medical exams, and $10 million will be used for research and education.[50] However, in January, 2014, U.S. District Judge Anita B. Brody refused to accept the agreed settlement because "the money wouldn't adequately compensate the nearly 20,000 men not named in the suit".[51]
Bernie Kosar, who sustained several concussions during his twelve-year NFL career and has shown symptoms of CTE, has submitted himself to an experimental treatment program led by Rick Sponaugle of Florida that has alleviated many of his symptoms. The program, the details of which are proprietary, involves increasing blood flow to damaged portions of the brain. He has spoken out in public about his successes with the treatment in the hopes that others who suffer from the disease can find relief and avoid the fates of Duerson and Seau, both of whom were personal friends of Kosar's.[52] The efficacy of Sponaugle's treatment has not been validated through any published clinical trials or other validated scientific process, nor has this treatment been supported by any reputable medical group conducting research into CTE.
Early retirements[edit]
In the 2015 off-season, a number of NFL players retired early with concussion- and other health-risk as express or possible motive. The youngest, in March, Chris Borland, 24, would have been entering his second year in the league after a third-round draft out ofUniversity of Wisconsin and a "stellar" rookie season with the San Francisco 49ers.[53] Explaining his decision to ESPN, Borland said "I just honestly want to do what's best for my health. ... From what I've researched and what I've experienced, I don't think it's worth the risk."[54]
ESPN noted that four of the retirees—Borland, Willis, Locker and Worilds—were under 30 years of age and that Borland had replaced Willis during the season due to a Willis toe injury and had been expected to replace him in the coming year. It also recounted Borland's course of decision from a possible concussion he "played through" in training camp as he was trying to make the team to the post-season decision. He said in making his decision he'd "read about Mike Webster and Dave Duerson and Ray Easterling"—two of them suicides, all, per ESPN, "diagnosed with the devastating brain disease chronic traumatic encephalopathy, or CTE, after their deaths"—and he had talked to "prominent concussion researchers and former players" after the season.[54]
To IGNORE HOW DANGEROUS AND UNPREDICTABLE CTE IS, only shows where a person or peoples PRIORITIES ARE OR AREN'T. Me personally, I LOVE AMERICAN FOOTBALL. But I love human life more. No sport is worth peoples lives and especially NOT FOR MONEY. Here is the article and note the bizarre ending where McDonald VIOLATES the restraining order, then CALMLY GOES TO A SANDWICH SHOP. Where he then surrenders to police WITHOUT INCIDENT. This Blackman needs counselling and a full psychological evaluation to see where his head is at AND WHY. Otherwise this will not only end BADLY, but something tells me some family member will request a CTE-evaluation once he is dead and they will find that he has CTE. Something that EVERY SPORTS JOURNALIST SHOULD ALREADY BE LOOKING AT AS A POSSIBLE REASON BEHIND HIS BIZARRE BEHAVIOR;
Ray McDonald gets arrested for second time in three days
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