Chronic Traumatic Encephalopathy

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Chronic traumatic encephalopathy
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Chronic traumatic encephalopathy
From Wikipedia, the free encyclopedia
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 multiple concussions 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),
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.
Repeated concussions and injuries less serious than concussions ("sub-concussions") incurred during the
play of contact sports over a long period have not yet been found to result in CTE. 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]
Contents
1 Epidemiology
2 Pathology
3 Signs and symptoms
4 Prevention
5 Diagnosis
6 History
6.1 American football
6.2 Ice hockey
6.3 Professional wrestling
6.4 Soccer
6.5 Rugby
6.6 Major League Baseball
7 Research
8 Research critique
9 Other athletes diagnosed with CTE
9.1 American football
9.2 Association football
9.3 Canadian football
9.4 Professional wrestling
9.5 Baseball
9.6 Hockey
9.7 Rugby
10 See also
11 References
12 External links
Epidemiology
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
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 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 Gehrigs disease). Progressive muscle weakness and balance and gait problems seem to be
early signs of CTEM.
[7]
Signs and symptoms
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
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
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 functionsa 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 $5000 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
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
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.
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,
[26]
former Houston Oilers and Miami Dolphins linebacker John Grimsley,
[27]
former Tampa Bay Buccaneers
guard Tom McHale,
[28]
former Cincinnati Bengals wide receiver Chris Henry,
[29]
and former Chicago
Bears safety Dave Duerson,
[30]
have all been diagnosed post-mortem with CTE. Other football players
diagnosed with CTE include former Buffalo Bills star running back Cookie Gilchrist
[31]
and Wally
Hilgenberg.,
[32]
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.
[33]
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.
[34]
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.
[35]
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.
[36]
The CSTE found CTE in his brain post-mortem.
[37]
In 2012, retired NFL player Junior Seau committed suicide with a gunshot wound to the chest.
[38]
There
was speculation that he suffered brain damage due to CTE.
[23][39][40][41][42]
Seau's family donated his brain
tissue to the National Institute of Neurological Disorders and Stroke.
[43]
On January 10, 2013, the brain
pathology report was revealed and Seau did have evidence of CTE.
[44]
On July 27, 2012, an autopsy report concluded that the former Atlanta Falcons safety Ray Easterling, who
committed suicide in April 2012, had CTE.
[45][46]
The NFL has taken measures to help prevent CTE. As of July 2011, the NFL has changed its return-to-play
rules. The number of contact practices has been reduced, based on the recent collective bargaining
agreement.
[47]
In 2012, some four thousand former NFL players "joined civil lawsuits against the League, seeking
damages over the Leagues failure to protect players from concussions, according to Judy Battista of the
[New York] Times".
[48]
On August 30, 2013, the NFL reached a $765 million settlement with the former NFL players over the head
injuries.
[49]
The settlement created a $675 million compensation fund from which former NFL players can
collect from 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.
[49]
From the remainder of the settlement, $75 million will be used for medical exams, and $10
million will be used for research and education.
[49]
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".
[50]
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.
[51]
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.
Ice hockey
Athletes from other sports have also been identified as having CTE, such as hockey player Bob Probert.
[52]
Neuropathologists at Boston University diagnosed Reg Fleming as the first hockey player known to have
the disease. This discovery was announced in December 2009, six months after Fleming's death.
[53]
Rick Martin, best known for being part of the Buffalo Sabres' French Connection, was diagnosed with CTE
after his brain was posthumously analyzed.
[54]
Martin was the first documented case of an ice hockey
player not known as an enforcer to have developed CTE; Martin was believed to have developed the
disease primarily as a result of a severe concussion he suffered in 1977 while not wearing a helmet. The
disease was low-grade and asymptomatic in his case, not affecting his cognitive functions. He died of a
heart attack in March 2011 at the age of 59.
[55]
Also within a few months in 2011, the deaths of three hockey "enforcers"Derek Boogaard from a
combination of too many painkillers and alcohol, Rick Rypien, an apparent suicide, and Wade Belak, who,
like Rypien, had reportedly suffered from depression; and all with a record of fighting, blows to the head
and concussionsled to more concerns about CTE. Boogaard's brain was examined by BUSM, which in
October 2011 determined the presence of CTE.
[56]
One National Hockey League player known in part for
leading "the thump parade", Shawn Thornton of the Boston Bruins, mulled over the "tragic coincidence" of
the three recent league deaths and agreed that their deaths were due to the same cause, yet still defended the
role of fighting on the rink.
[57]
Professional wrestling
In 2007, neuropathologists from the Sports Legacy Institute (an organization co-founded by Christopher
Nowinski, himself a former professional wrestler) examined the brain of Chris Benoit, a professional
wrestler with the WWE, who had apparently killed his wife and son before committing suicide. The suicide
and double murder were originally attributed to anabolic steroid abuse, but a brain biopsy confirmed
pathognomonic CTE tissue changes: large aggregations of tau protein as manifested by neurofibrillary
tangles and neuropil threads, which cause neurodegeneration.
[58][59]
In 2009, Bennet Omalu discovered CTE in recently retired wrestler Andrew "Test" Martin, who died at age
33 from an accidental medicine overdose.
[60]
Soccer
In 2012, Patrick Grange a semi-pro soccer player, was diagnosed in an autopsy with Stage 2 CTE with
motor neuron disease. "The fact that Patrick Grange was a prolific header is important," Christopher
Nowinski, co-founder of the Sports Legacy Institute, said in an e-mail. "We need a larger discussion around
at what age we introduce headers, and how we set limits to exposure once it is introduced."
[61]
Grange
played soccer at high school; college at Illinois-Chicago and New Mexico; in the Premier Development
League; for Albuquerque Asylum and Chicago Fire Premier. He died of ALS at age 29 in 2012 with a
posthumous diagnosis of CTE.
[62]
Rugby
Researchers found Australian rugby union player Barry "Tizza" Taylor died in 2013 of complications of
severe CTE with dementia at age 77. Taylor played for 19 years in amateur and senior leagues before
becoming a coach.
[61]
In 2013, Dr Willie Stewart, Consultant Neuropathologist at the Institute of Neurological Sciences at the
Southern General Hospital in Glasgow, identified CTE in the brain of a former amateur rugby player in his
50s which is believed to be the first confirmed case of early onset dementia caused by CTE in a rugby
player.
[63]
Major League Baseball
In 2012, Ryan Freel testing of his brain tissue after his death found that he had Stage 2 CTE, Freel has the
distinction of being the first Major League Baseball player to be diagnosed with chronic traumatic
encephalopathy.
[64]
Research
In 2008, the CSTE at Boston University at the BU School of Medicine started the CSTE brain bank at the
Bedford VA Hospital to analyze the effects of CTE and other neurodegenerative diseases on the brain and
spinal cord of athletes, military veterans, and civilians
[9]
To date the CSTE Brain Bank is the largest CTE
tissue repository in the world.
[7]
On December 21, 2009, the National Football League Players Association
announced that it would collaborate with the CSTE at the Boston University School of Medicine to support
the Center's study of repetitive brain trauma in athletes.
[65]
Additionally, in 2010 the National Football
League gave the CSTE a $1 million gift with no strings attached.
[66][67]
In 2008, twelve living athletes
(active and retired), including hockey players Pat LaFontaine and Noah Welch as well as former NFL star
Ted Johnson, committed to donate their brains to CSTE after their deaths.
[22][68]
In 2009, NFL Pro Bowlers
Matt Birk, Lofa Tatupu, and Sean Morey pledged to donate their brains to the CSTE.
[69]
In 2010, 20 more
NFL players and former players pledged to join the CSTE Brain Donation Registry, including Chicago
Bears linebacker Hunter Hillenmeyer, Hall of Famer Mike Haynes, Pro Bowlers Zach Thomas, Kyle
Turley, and Conrad Dobler, Super Bowl Champion Don Hasselbeck and former pro players Lew Carpenter,
and Todd Hendricks . In 2010, Professional Wrestlers Mick Foley and Matt Morgan also agreed to donate
their brains upon their deaths. Also in 2010, MLS soccer player Taylor Twellman, who had to retire from
the New England Revolution because of post-concussion symptoms, agreed to donate his brain upon his
death. As of 2010, the CSTE Brain Donation Registry consists of over 250 current and former athletes.
[70]
In 2011, former North Queensland Cowboys player Shaun Valentine became the first rugby player to agree
to donate his brain upon his death, in response to recent concerns about the effects of concussions on Rugby
League players, who do not use helmets. Also in 2011, boxer Micky Ward, whose career inspired the film
The Fighter, agreed to donate his brain upon his death.
In related research, the Center for the Study of Retired Athletes, which is part of the Department of
Exercise and Sport Science at the University of North Carolina at Chapel Hill, is conducting research
funded by National Football League Charities to "study former football players, a population with a high
prevalence of exposure to prior Mild Traumatic Brain Injury (MTBI) and sub-concussive impacts, in order
to investigate the association between increased football exposure and recurrent MTBI and
neurodegenerative disorders such as cognitive impairment and Alzheimers disease (AD)".
[71]
In February 2011, Dave Duerson committed suicide,
[42]
leaving text messages to loved ones asking that his
brain be donated to research for CTE.
[72]
The family got in touch with representatives of the Boston
University center studying the condition, said Robert Stern, a co-director of the research group. Stern said
Duerson's was the first time he was aware of that such a request had been left by a suicide potentially linked
to CTE.
[73]
Stern and his colleagues found high levels of the protein tau in Duerson's brain. These elevated
levels, which were abnormally clumped and pooled along the brain sulci,
[9]
are indicative of CTE.
[30]
In July 2010, NHL enforcer Bob Probert died of heart failure. Before his death, he asked his wife to donate
his brain to CTE research because it was noticed that Probert experienced a mental decline in his 40s. In
March 2011, researchers at Boston University concluded that Probert had CTE upon analysis of the brain
tissue he donated. He is the second NHL player from the program at the Center for the Study of Traumatic
Encephalopathy to be diagnosed with CTE postmortem.
[74]
BUSM has also found indications of links between Amyotrophic lateral sclerosis (ALS) and CTE in
athletes who have participated in contact sports. Tissue for the study was donated by twelve athletes and
their families to the CSTE Brain Bank at the Bedford, Massachusetts VA Medical Center.
[75]
Researchers at the Cleveland Clinic have shown auto-antibodies directed against the brain of players who
experience a large number of head hits but no concussions, suggesting that even sub-concussive episodes
may be damaging to the brain.
[11]
In 2013, President Barack Obama announced the creation of the Chronic Effects of Neurotrauma
Consortium or CENC, a federally funded research project devised to address the long-term effects of mild
traumatic brain injury in military service personnel (SMs) and Veterans.
[76][77][78]
After a competitive
application process, a consortium led by Virginia Commonwealth University prevailed and was announced
as the recipient of the award by President Obama on August 20, 2013.
[79][80][81][82][83][84]
At the time of
the award, this was the single largest grant ever awarded to Virginia Commonwealth University.
[81]
Nearly
20% of the more than 2.5 million U.S. Service Members (SMs) deployed since 2003 to Operation Enduring
Freedom (OEF) and Operation Iraqi Freedom (OIF) have sustained at least one traumatic brain injury
(TBI), predominantly mild TBI (mTBI),
[85][86]
and almost 8% of all OEF/OIF Veterans demonstrate
persistent post-TBI symptoms more than six months post-injury.
[87][88]
Unlike those head injuries incurred
in most sporting events, recent military head injuries are most often the result of blast wave exposure.
Explosive munitions, predominantly improvised explosive device (IEDs), have caused the overwhelming
majority of these identified cases. The incidence is likely even significantly higher than reported, as many
mTBIs may go unrecognized during and even after deployment because of more visible concomitant
injuries capturing greater attention, clinicians limited awareness of the often subtle initial findings, and
patients reduced subjective awareness related to cognitive deficits in the acute period.
[89]
The mission of
the CENC is to fill the gaps in knowledge about the basic science of mild TBI (also termed concussion), to
determine its effects on late-life outcomes and neurodegeneration, to identify service members most
susceptible to these effects, and to identify the most effective treatment strategies.
[79][80][81][90]
The CENC
is a multi-center collaboration linking premiere basic science, translational, and clinical neuroscience
researchers from the DoD, VA, academic universities, and private research institutes to effectively address
the scientific, diagnostic, and therapeutic ramifications of mild TBI and its long-term
effects.
[81][82][83][84][91]
The CENC serves as the comprehensive research network for DoD and VA that
focuses on the long-term effects of combat-related and military-relevant TBI.
[84]
The CENC is designed to
conduct research that provides clinically relevant answers and interventions for current service members
and Veterans and to develop the long-term solutions to the chronic effects of TBI. The CENC is identifying
and characterizing the anatomic, molecular, and physiological mechanisms of chronic injury from TBI and
potential neurodegeneration, investigating the relationship of comorbidities (psychological, neurological,
sensory, motor, pain, cognitive, neuroendocrine) of trauma and combat-exposure to TBI with
neurodegeneration, and assessing the efficacy of existing and novel treatment and rehabilitation strategies
for chronic effects and neurodegeneration following TBI.
[90]
The project principal investigator for the
CENC is David Cifu, Chairman and Herman J. Flax professor
[92]
of the Department of Physical Medicine
and Rehabilitation (PM&R) at Virginia Commonwealth University (VCU) in Richmond, Virginia, Staff
Physiatrist at the Hunter Holmes McGuire Veterans Administration Medical Center (HHM-VAMC),
[93]
Founding Director of the VCU-Center for Rehabilitation Science and Engineering
[94]
and National Director
of PM&R Services in the Department of Veterans Affairs' Veterans Health Administration.
[80][81][82][95][96]
Project co-principal investigators are Ramon Diaz-Arrastia, Professor of Neurology, Uniformed Services
University of the Health Sciences, and Director of Clinical Research at the Center for Neuroscience and
Regenerative Medicine (CNRM),
[84]
and Rick L. Williams, statistician at RTI International and a Fellow of
the American Statistical Association.
[91]
Research critique
Some researchers advise caution when interpreting currently available data. There are no published
epidemiological, cross-sectional or prospective studies relating to chronic traumatic encephalopathy. The
current studies are primarily case reports and pathological case series. These types of studies may lack
controls for observer bias, causality, or other risk factors. The existing literature is unable to account for
changes caused by other factors such as aging, psychiatric or mental health illness, alcohol/drug use or
coexisting dementia of other causes.
The hypothesis that repeated concussion or subconcussive impacts cause CTE remains unproven.
Confirmation is needed by prospective longitudinal studies utilizing standard scientific method.
[97]
Other athletes diagnosed with CTE
American football
Association football
Jeff Astle
[98]
Canadian football
Bobby Kuntz
Jay Roberts
Cookie Gilchrist
[99]
Professional wrestling
Chris Benoit
Andrew "Test" Martin
Baseball
Ryan Freel
[100]
Hockey
Reg Fleming
Rick Martin
Bob Probert
Derek Boogaard
Rugby
Barry Taylor
See also
League of Denial
List of NFL players with chronic traumatic encephalopathy
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Retrieved from "http://en.wikipedia.org/w/index.php?
title=Chronic_traumatic_encephalopathy&oldid=626792524"
Categories: Motor neurone disease Neurotrauma Sports controversies Overuse injuries
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