CTE in Hockey

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Thursday, April 7 Zoom Speaker Dr Robert A Stern

Concussion Center Speaker Series: Dr. Robert A. Stern, PhD
Chronic Traumatic Encephalopathy (CTE) and the Long-Term Consequences of Sports-Related Repetitive Head Impact Exposure: What We Know Now and What We Need to Know Next

Thursday, April 7
4:00-5:00pm
via Zoom

featuring

Dr. Robert A. Stern, PhD

Professor of Neurology, Neurosurgery, and Anatomy & Neurobiology
Co-Founder and Director of Clinical Research, BU CTE Center
Senior Investigator, BU Alzheimer’s Disease Research Center
Boston University School of Medicine


Dr. Robert Stern will present the neuropathological features of chronic traumatic encephalopathy (CTE), including what is currently known about risk factors for developing CTE, the clinical features associated with CTE, the NINDS Consensus Diagnostic Criteria for Traumatic Encephalopathy Syndrome, and the possible fluid and neuroimaging biomarkers for CTE.

Dr. Robert Stern is a Professor of Neurology, Neurosurgery, and Anatomy & Neurobiology at Boston University (BU) School of Medicine. Dr. Stern has been a clinician, researcher, and lecturer in the area of Alzheimer’s disease and related disorders for over 30 years. From 2010-2019 he was Clinical Core Director of the NIH-funded BU Alzheimer’s Disease Research Center (BU ADRC) and is currently Senior Scientist for the BU ADRC. He oversees several clinical trials for the treatment and prevention of Alzheimer’s and has conducted research on innovative new tests to detect and diagnose the disease. Dr. Stern is an internationally recognized expert on chronic traumatic encephalopathy (CTE) and the long-term effects of repetitive head impacts in athletes. He is Co-Founder and Director of Clinical Research for the BU CTE Center, and he is the lead investigator of a $17 million, 7-year NIH grant for a multi-center study to develop methods of diagnosing CTE during life as well as examining potential risk factors of the disease. Dr. Stern has over 250 publications, is a member of several medical journal editorial boards, and is the co-editor of two textbooks: Sports Neurology (Dr. Brian Hainline, co-editor), part of the Handbook of Clinical Neurology series, and the Oxford Handbook of Adult Cognitive Disorders (Dr. Michael Alosco, co-editor). He is a clinical neuropsychologist and has developed several widely used neuropsychological tests, including the Neuropsychological Assessment Battery (NAB). He is a Fellow of the American Neuropsychiatric Association and the National Academy of Neuropsychology.

To register:
https://umich.zoom.us/webinar/register/ ... DzoVa7uUTQ

For more information: https://concussion.umich.edu/event/conc ... stern-phd/

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Thursday, April 7 Zoom Speaker Dr Robert A Stern

Concussion Center Speaker Series: Dr. Robert A. Stern, PhD
Chronic Traumatic Encephalopathy (CTE) and the Long-Term Consequences of Sports-Related Repetitive Head Impact Exposure: What We Know Now and What We Need to Know Next

Thursday, April 7
4:00-5:00pm
via Zoom

featuring

Dr. Robert A. Stern, PhD

Professor of Neurology, Neurosurgery, and Anatomy & Neurobiology
Co-Founder and Director of Clinical Research, BU CTE Center
Senior Investigator, BU Alzheimer’s Disease Research Center
Boston University School of Medicine


Dr. Robert Stern will present the neuropathological features of chronic traumatic encephalopathy (CTE), including what is currently known about risk factors for developing CTE, the clinical features associated with CTE, the NINDS Consensus Diagnostic Criteria for Traumatic Encephalopathy Syndrome, and the possible fluid and neuroimaging biomarkers for CTE.

Dr. Robert Stern is a Professor of Neurology, Neurosurgery, and Anatomy & Neurobiology at Boston University (BU) School of Medicine. Dr. Stern has been a clinician, researcher, and lecturer in the area of Alzheimer’s disease and related disorders for over 30 years. From 2010-2019 he was Clinical Core Director of the NIH-funded BU Alzheimer’s Disease Research Center (BU ADRC) and is currently Senior Scientist for the BU ADRC. He oversees several clinical trials for the treatment and prevention of Alzheimer’s and has conducted research on innovative new tests to detect and diagnose the disease. Dr. Stern is an internationally recognized expert on chronic traumatic encephalopathy (CTE) and the long-term effects of repetitive head impacts in athletes. He is Co-Founder and Director of Clinical Research for the BU CTE Center, and he is the lead investigator of a $17 million, 7-year NIH grant for a multi-center study to develop methods of diagnosing CTE during life as well as examining potential risk factors of the disease. Dr. Stern has over 250 publications, is a member of several medical journal editorial boards, and is the co-editor of two textbooks: Sports Neurology (Dr. Brian Hainline, co-editor), part of the Handbook of Clinical Neurology series, and the Oxford Handbook of Adult Cognitive Disorders (Dr. Michael Alosco, co-editor). He is a clinical neuropsychologist and has developed several widely used neuropsychological tests, including the Neuropsychological Assessment Battery (NAB). He is a Fellow of the American Neuropsychiatric Association and the National Academy of Neuropsychology.

To register:
https://umich.zoom.us/webinar/register/ ... DzoVa7uUTQ

For more information: https://concussion.umich.edu/event/conc ... stern-phd/

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Does Substance Abuse Cause CTE Pathology? Global Expert Weighs in to Debunk Misguided Theory

As the lead author of the 2nd through 5th Consensus Statement on Concussion in Sport, Dr. Paul McCrory may be the most influential neurologist in sports over the past 20 years. The Statement is famous for both its extraordinary conflicts of interest and for downplaying the link between head impacts and CTE.

The conference that produces updated statements is funded or organized by international sports governing bodies like FIFA and the IOC and 32 of the 36 authors have financial ties to organized sports. Some have suggested that their statement on CTE, "a cause-and-effect relationship has not yet been demonstrated between chronic traumatic encephalopathy and sport related concussion and exposure to contact sports” is critical to successfully defend class-action lawsuits from former athletes. (In contrast, the CDC CTE Fact Sheet says evidence demonstrates a cause-and-effect relationship).

Over the last month, McCrory has had two editorials retracted for plagiarism, faces additional allegations of plagiarism, and is being asked to explain how he treated athletes with concussion symptoms during a time the Medical Board of Australia said he was not allowed perform neurodiagnostic procedures. I also wrote a blog about how he has also misrepresented BU’s research in public talks.

While we’re looking into McCrory’s influence on the global CTE conversation, would you be surprised to learn he is a was also one of the key promoters of the theory that CTE can be caused by the use of opioids? Professional sports organizations embraced it and repeated it because they know their athletes suffer injuries that often require surgery and the use of painkillers. In 2015, McCrory was senior author on an opinion piece that questioned the link between CTE and sports, claiming: “The correlation between opioid abuse and hyperphosphorylated tau deposition is well described, and should be factored as a key variable in any assessment of causation [in CTE].”

We reached out to the world’s expert on how opioids and alcohol impact the brain neuropathologically, and in the following video he debunks McCrory’s nonsensical claim that CTE could be caused by substance abuse. Dr. Gabor Kovacs is an internationally renowned neuropathologist and researcher in the field of neurodegenerative diseases. In 2021, he received the Alfred Meyer Memorial Lecture and Prize from the British Neuropathological Society for his expertise on tau-related conditions. He is currently affiliated with the University of Toronto and the University Health Network (UHN), where he holds numerous roles including consultant Neuropathologist at the Laboratory Medicine Program at the UHN, Principal Investigator at the Tanz Centre for Research in Neurodegenerative Disease, and Senior Scientist at the Krembil Brain Institute.

Does Substance Abuse Cause CTE Pathology? Global Expert Weighs in to Debunk Misguided Theory
Read more: https://concussionfoundation.org/news/b ... ded-theory

Alcoholism, Heroin Abuse, and Repetitive mTBI: What can we see Under the Microscope?
Watch on YouTube: https://www.youtube.com/watch?v=V1z-0ksJ-GI

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8 Major Findings: The risk of additional years of playing ice hockey

Whenever a football player struts in celebration after making another bone-crushing hit, it’s hard not to wonder what the jarring clash of heads did to their brain. Same when watching a soccer defender repeatedly thumping headers upfield or a hockey center skating gingerly away from a bruising body check.

After 15 years of research into the toll of repeated head traumas on the brain, especially among athletes, Boston University’s Chronic Traumatic Encephalopathy (CTE) Center has changed the conversation around contact sports—and shifted the viewing experience for many fans. The center is a national leader in the study of CTE, a progressive degenerative brain disease, and its work—particularly on diagnosing star players like 49er Greg Clark and Canadian Ralph Backstrom—has made news worldwide. CTE has been linked to multiple symptomatic concussions and asymptomatic sub concussive blows to the head; it’s been found in military veterans, as well as former sportspeople.

For those afflicted by CTE, their brain can begin changing—deteriorating, even eventually shrinking—just months after a traumatic knock. For anyone who’s played an impact sport, the list of common symptoms posted on the CTE Center’s website is frightening: memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, suicidality, parkinsonism. The final stage is progressive dementia.

The center is home to the VA-BU-CLF Brain Bank, which holds more than 1,250 brains for study and is billed as “the largest tissue repository in the world focused on traumatic brain injury and CTE.” Thanks to that library, BU researchers have found CTE—which can currently only be diagnosed after death—in more than 90 percent of former NFL players studied and shown CTE risk doubles after just three years of football.

With its studies continuing to advance our understanding of the disorder—and potential ways to prevent and diagnose it in the living—here are eight of the biggest CTE discoveries and headlines made by center experts this past year:

1. MRI Could Help Diagnose CTE in the Living

There’s no way to diagnose CTE when someone is alive. A patient and their doctors might make some best guesses—if, say, a former footballer renowned for big tackles is now struggling with confusion and anxiety—but confirmation only comes after death. In December 2021, BU researchers revealed that magnetic resonance imaging (MRI) might have the potential to change that and help spot CTE in the living.

They reviewed MRI images of the brains of 55 men who were diagnosed with CTE postmortem—but who’d been scanned while alive—and spotted shrinkage in the brain that didn’t show up in healthy male controls with normal cognition.

“MRI is commonly used to diagnose progressive brain diseases that are similar to CTE, such as Alzheimer’s disease,” says Michael Alosco, a BU School of Medicine assistant professor of neurology and CTE Center lead investigator. “Findings from this study show us what we can expect to see on MRI in CTE. This is very exciting because it brings us that much closer to detecting CTE in living people.”

A second study of brain scans of former footballers also showed that white matter hyperintensities—a marker of brain injury—could be spotted using MRI.

Researchers are now looking to see whether the patterns they saw in people with CTE “differentiate CTE from Alzheimer’s disease and other causes of dementia,” says Alosco.

2. Memory—but Not Mood—Could Also Hold Clues to Lifetime Diagnosis

Progressive memory loss and issues with executive function, the ability to focus, follow directions, and problem-solve could all be markers that help diagnose CTE in the living. Researchers interviewed family members of 336 brain donors about their loved ones’ cognitive function in life, then evaluated the brains for CTE pathology. They found “progressive memory and executive function symptoms are particularly valuable” for predicting the presence of CTE, says Jesse Mez, a MED associate professor of neurology. Mood and behavior proved less useful.

“Our study provides doctors with information about which symptoms are most predictive of CTE pathology,” says Mez.

3. College Football Players More Likely to Have Brain Disorders

The University of Notre Dame is a college football powerhouse, with 11 national championships and nearly 500 players who went on to the NFL. But a study of former Fighting Irish players who were seniors between 1964 and 1980 found a dark side to that success. The ex-college stars were five times more likely to report cognitive impairment diagnoses than their peers in the general population—and had increased mortality due to degenerative brain disease. They were also two-and-a-half times more likely to report recurrent headaches and 65 percent more likely to have cardiovascular disorders during life.

Although there were some positives for the former players—including lower rates of diabetes and a significantly smaller chance of dying from heart and respiratory disorders—researchers said the negative health consequences were concerning.

“We all loved the game that we played at Notre Dame,” says Rocky Bleier, a former Notre Dame captain and four-time Super Bowl champion with the Pittsburgh Steelers. “We just believe that the health of the game and the health of the players go hand in hand, and hope that the results of this study provide some initial answers and benefits to our teammates, as well as future players and their families at all levels of the sport.”

4. Pro Footballers Have a Greater ALS Risk

Among the other life-altering—and shortening—conditions threatening retired footballers is amyotrophic lateral sclerosis (ALS), a rare progressive neurodegenerative disease that’s also known as Lou Gehrig’s disease. A multi-institution study found NFL athletes are four times more likely to die from ALS than the general population.

According to a press release, the researchers also discovered a link between longer professional careers and increased ALS risk—those who developed the disease played an average of seven seasons, 56 percent longer than matched pro footballers who didn’t. The study included every player who debuted between 1960 and 2019 and played in at least one NFL game—close to 20,000 individuals—with diagnoses drawn from news reports and obituaries. Living players with the disease were also included in the study.

“In our brain bank, we have found a similar relationship between a longer football career and an increased risk of other neurodegenerative diseases,” says Ann McKee, director of the CTE Center. “It has become clear that years of repeated impacts to the head can cause the human brain to break down along many pathways.”

5. A Lot of Bad Stuff Is Going On in the CTE-Hit Brain

Past research on CTE has concentrated on the buildup of abnormal tau—a protein—in the brain’s gray matter. But researchers have also found changes in the white matter, the part of the brain that controls the signals flying up and down the spinal cord. In a study of eight CTE-impacted brains and eight matched control brains, they discovered changes in a type of cell called oligodendrocytes that help neurons speed up their message delivery.

“There is loss of oligodendrocytes and alteration of oligodendrocyte subtypes in CTE that suggest white matter damage is important to the pathogenesis of CTE and might provide new targets for prevention and therapies,” says McKee, who’s also a William Fairfield Warren Distinguished Professor and MED professor of neurology and pathology.

6. Ice Hockey Players Not Immune from CTE Trouble

Although football takes a lot of the CTE headlines, the dangers of ice hockey, with its crunching body checks and board slams, is getting increasing attention. Now, a CTE Center–led study has tied every additional year on the ice to a 23 percent increased chance of having the disorder.

In a study of 74 hockey players—from those who played at the youth level through NHL pros—researchers found more than half had CTE at the time of their death. They also discovered that each additional year of playing was linked to a 15 percent increased chance of someone progressing to the next stage of CTE. The disease has four stages—the final one includes brain shrinkage and associated dementia.

“While the absolute risk for ice hockey players of developing CTE is still unknown, it may be concerning to athletes and their families that we found each year of ice hockey play may increase the odds of developing CTE,” says Mez, who presented the findings in April at the American Academy of Neurology’s annual meeting. “Our research may be useful for them when making informed decisions about play.”

7. Ex-NFL Player Phillip Adams Had Severe CTE When He Killed Six People

In April 2021, officials in York County, South Carolina, were left trying to make sense of the seemingly motiveless killing of a local doctor and five others, including the doctor’s young grandchildren. The county sheriff said they were murdered by Phillip Adams, a former cornerback who’d racked up six seasons in the NFL. Adams had apparently entered the prominent doctor’s home with two pistols, later fleeing to his parents’ home where he took his own life. At the time, his father wondered if years of football—Adams reportedly started playing aged seven—had been a factor in the violent killing spree.

“I can say he’s a good kid—he was a good kid,” Alonzo Adams told local NBC affiliate, WCNC-TV, “and I think the football messed him up.”

After his death, Adams’ brain was donated to the CTE Center. There, researchers found he had stage 2 CTE—which commonly brings symptoms like depression, mood swings, and memory loss—at the time of his death.

“Adams had an extraordinary amount of CTE pathology in the frontal lobe, the area of the brain behind the forehead. Frontal lobe damage is associated with violent, impulsive or explosive behavior, a ‘short fuse,’ and lack of self-control,” says McKee. “His CTE pathology might have contributed to his abnormal behaviors, in addition to other physical, psychiatric, and psychosocial factors. His predominantly frontal lobe CTE pathology, which resulted in atrophy, or shrinkage, of the brain, was similar in severity to Aaron Hernandez.”

8. If You Played Soccer or Football, You Can Participate in BU’s Research—No Brain Donation Necessary

If you played soccer or tackle football—at any level, at any age—you may be eligible to enroll in a new study that aims to examine the risks for developing dementia, cognitive decline, and changes in behavior and mood later in life after playing sports. The Head Impact & Trauma Surveillance Study (HITSS) will include an online annual assessment with questions about sports participation, exposure to head impacts, behavior and mood, and concussion and medical history; it’ll also include memory and cognitive tests. Anyone aged over 40 can sign up online: https://www.hitss.org/

Ambassadors for the study include Super Bowl champion Mike Haynes and World Cup winner Brandi Chastain.

“While there have been significant research advances in recent years, past studies have been limited by focusing solely on former professional tackle football players and/or including only small numbers of male participants,” says Matt Roebuck, HITSS’ recruitment coordinator. “To move the science forward, we are launching a nationwide campaign…to enroll thousands of people who played organized soccer or tackle football at any point in their lives.”

8 Major Findings and Headlines from BU CTE Researchers in the Past Year
Experts have made breakthroughs on diagnosing CTE in the living, and in studying the impact of college football on the brain, pro football’s link to ALS, and the risk of additional years of playing ice hockey
Read more: https://www.bu.edu/articles/2022/8-majo ... last-year/

[goldy313]

Thank you for posting this.

People make their own decisions.

The science is undeniable but science has become debatable. Politics sucks!

Science makes us a top Country. Liberals and Conservatives who ignore science are a bane to us all.

But we still want 9 year olds leading with their heads!

[greybeard58]

"Did you every play football? Or ice hockey?"

Taylor Dever was standing on the side of his dad’s deck taking a photo on his phone, when Tom Dever took a break from a family gathering to come outside.

“I asked him, ‘What’s up?’ and he said, “’See right there? There’s these dudes out there.’”

“Now,” Tom said with a slight tilt of his head. “I’ve got nothing here behind me on the property, but he’s saying he saw guys in camo, either with paintball guns or some kind of weapon or rifles.

“I said, ‘OK, we’re good, Taylor. We’re good. Come inside.’”

But soon again, Taylor was back out on the deck, insisting there were men in the forest behind the home wielding weapons of some sort.

“It got to the point, where he and I went down and walked out back to show him that there was nobody there,” Tom said.

Still, Taylor wasn’t convinced.

And once again, he was soon back on the deck, taking more photos to prove to his dad the men he saw were real.

“‘Look right there! Right there!’ And, obviously, there was no one there,” Tom said. “He’s like ‘You see that tree stump? Just to the right of that. See the guy? See his helmet? Look, you can see his helmet!’

“I thought, ‘Oh my God!’ But, I just wanted to stay calm for him.”

It was in such surreal moments with Taylor that Tom, and the rest of the family, made a point of setting aside the shock of seeing their ‘gentle giant’ struggle. The out-of-character behavior — anger, anxiety, confusion and frustration — grew more frequent and more pronounced. But they often felt helpless in their own struggle to help him find answers, as the doctors also didn’t understand.

“You’d think it would be like ‘OK, I’m having hallucinations, I can’t keep a job, I’m depressed’ … And the doctor would be like, ‘Oh, did you have head trauma? Did you play football? Hockey? Were you in a car accident? Did you play rugby or any from the list of all the other sports that are susceptible to this?’

“But instead it’s like, ‘I played football at Notre Dame and in the NFL.’ And the doctor’s like, ‘Oh, my God, that must have been great! Tell me about that, and how cool that is!’ But they don’t know that you’re there because you have these symptoms, that they’re not equating to CTE. They need to be educated. They need to have a better understanding.”

Helping others better understand CTE and its devastating impact, particularly on football players, is one of the main reasons Tom, Lori and Megan Dever are sharing Taylor’s story.

“(The doctors) hear about these behaviors, but does anybody ask ‘Did you every play football? Or ice hockey?’” Lori said. “It’s just … let’s connect the dots here. But we’re not even close. They don’t understand.

“Looking back on it, no matter how hard he tried, would this still be a struggle for him to function … would he get better?’ How does a person get better? Why do some kids get it and some don’t?”

By educating others about the disease, the Dever family hopes to help other parents make the decision about their own child playing football. They’ve taken comfort in hearing and reading similar stories of other families, knowing they aren’t alone in their struggle to make sense of their child dying young.

And in doing that, 18 months since the shocking death of their 31-year-old son, the Dever family also gets a chance to explain what happened to Taylor.

‘WE’RE NOT ALONE’
That scene on the deck, when Taylor was certain there were men in camouflage behind his dad’s home, came to mind when Tom Dever learned Max Tuerk, another California native, had similar struggles before he died at the age of 26.

Tuerk, a former offensive lineman with USC and the NFL, grew up in Trabuco Canyon where his high school team won a state championship. But after being drafted in 2016 by the San Diego Chargers, Tuerk was out of football two years later. He collapsed and died while on a hike in June 2020, with an autopsy showing he had an enlarged heart, and a study of his brain showing Stage One CTE.

The diagnosis confirmed his family’s suspicion that there was an underlying cause to the anxiety, anger, depression and paranoia he was experiencing — as well as the kind of out-of-character behavior the Dever family saw with their own son.

Tuerk’s father told the L.A. Times that while with the Chargers, Max was visiting in Orange County when his son told him Russians were unloading nuclear weapons at the site of a former nuclear power plant near San Clemente.

“I was scared to death,” Greg Tuerk told the Times. “He became very paranoid. He actually became delusional.”

“That’s what it’s been like talking with these families,” Tom Dever said. “It’s like ‘Oh, my God, he did this? He did that? Taylor did the same thing. Taylor said the same thing.’

“It was not eerie, but comforting because … we’re not alone. It’s helped talking to other families. It’s helped to the point where I want to reach out to other families as soon as I hear. It helps talking.”

The Concussion Legacy Foundation continues to connect families impacted by CTE, continuing its efforts to expand support to all involved. Megan Dever said the foundation’s work to connect parents and siblings of former players who died with CTE could be both eye-opening and life-changing.

Before studying graphic design in college, Megan had studied psychology and considered a career in nursing. Now, after her own experience — and frustration — with the mental health system, she is thinking about becoming a therapist.

“Also, it’s about the awareness of CTE. I’ve talked to so many people who say, ‘What’s that?’” Megan said. “Hopefully, that awareness leads to research, support … everything.

“Just through my own journey of therapy and everything, I think I’d really like to do that. … Taylor always wanted to help people. I don’t know. This has definitely sparked something in me.”

‘THE WORST PART’
Lori Dever said seeing her son’s spiral downward was “the most horrendous thing I’ve ever gone through. … It was like watching him just die in front of you.”

There were several times she grew concerned for his safety, worried his anxious and angry demeanor could lead to confrontations that could result in harm to himself or others. Even though she knew he’d never intentionally hurt anyone, she couldn’t help but be concerned.

“One of the bigger things that I feel bad about was that I was almost feeling a little afraid of him,” Lori said. “I didn’t know if I should hug him or go into the other room. It didn’t seem there was anything I could do, but to encourage him.”

“Somedays it felt like he was 5 years old again, and then there were days when I saw a side of him I’d never seen,” she said. “There was this road rage and these bursts of anger and that wasn’t the gentle giant I knew.”

But, she said, Taylor knew his struggles were real. And it deeply saddened her to see him return to such a realization when he understood he’d overreacted with an angry outburst or became so frustrated losing track of things like his phone, a set of car keys or a padlock to a shed.

“It’s the same situation with Alzheimer’s or dementia,” Lori said. “The worst part of these diseases is when the person is still cognizant enough to realize, ‘I can’t remember your name. What is wrong with me?’ It’s heartbreaking. That’s just the worst part.

“I really do think he tried to be that gentle giant, and tried to be strong. But he told me, ‘Mom, you don’t ever want to know what’s going on in my brain. I can’t figure it out. I just feel so stupid.’”

Because CTE currently cannot be diagnosed until after death, Taylor’s family focused on helping him with the symptoms he was experiencing, including counseling and support for alcohol and substance abuse.

Tom said a doctor told him seizures Taylor was experiencing from time to time — somewhere near a half dozen — toward the end of his life could have been due to alcohol withdrawal.

“I never doubted his self diagnosis (of CTE),” Tom said. “I just felt, OK, you can’t diagnose CTE while alive. Let’s eliminate everything else. My approach was, OK, there’s nothing we can do about that, but let’s not make sure it’s not something else.”

Lori said when she saw Taylor the day before he died, he was working at the local food bank and had a fresh haircut and had shaved his beard.

“He looked great, better than he’d ever looked,” Lori said. “He told me, ’This is cool. I get to go shopping for people in need and put the food in their trunk.’”

Later that day, Lori watched as Taylor searched and searched for a padlock he’d misplaced, growing increasingly frustrated.

“He couldn’t find the padlock that he’d had in his pocket,” she said. “He must have stood there for 5 minutes, looking in his pockets, but he couldn’t find it.”

A short while later, Lori said, she received a final text from Taylor.

“I found the lock and will bring it back over ASAP.”

Taylor Dever died Dec. 7, 2020, at the age of 31.

MOVING FORWARD
“It’s not right,” Tom said. “That’s not the order of life. That’s not how it’s supposed to be.”

Though his family suspected CTE had played a role in his death, it took nearly 18 months to have that confirmed by a post-mortem diagnosis. It’s important to his parents and sister that those who struggled to understand his change in personality and behavior have the full story, particularly now that their suspicions of what happened to Taylor have been confirmed.

And now that they’ve done what Taylor asked, to donate his brain for research, they’re turning their attention to next steps in making a difference in the lives of others dealing with the disease, something they know their son would want them to do.

“Number one, we want the community to know that that wasn’t Taylor,” Tom said. “We want them to know what happened. He didn’t commit suicide. It was an accidental drug interaction. He was suffering from this condition or disease. We want the community to know.

“And then secondly, we want to carry on what really he wanted. And what we want to do in his memory is to carry this forward with the awareness and support to researching this condition.

“It’s like ‘Donate? OK, we did that. Now what do we do, Taylor? Don’t stop there. Keep going.’”

Lori said she wants to set the record straight and also share Taylor’s story so that her son’s legacy is centered around making more people aware of CTE, particularly those expected to provide care to people suffering from it.

“I want to put an end to all the gossip,” she said. “People hear that it was a drug overdose. But it was a drug interaction. And, yes, they were prescribed drugs.

“They would diagnose him with ADHD or something else … he’s this, he’s that. And they’d give him a prescription. … I think that’s such a big problem with these doctors prescribing these medications, because they don’t know what they’re dealing with (when it comes to CTE).”

“They say time heals all wounds,” she said. “I will tell you time does not heal. … I can’t say it will ever go away for mama.”

The Dever family has launched the Taylor’s Tree Foundation (www.TaylorsTree.org), a nonprofit organization dedicated to raising awareness and support for the efforts of the Concussion Legacy Foundation and research into chronic traumatic encephalopathy (CTE) and mental health.

After his death in 2020, Taylor Dever was diagnosed with Stage 2 CTE through a clinical diagnosis by researchers at the Veterans Administration, Boston University, Concussion Legacy Foundation Brain Bank.

“Taylor wanted to change the world,” his family wrote in his legacy story at ConcussionFoundation.org. “He was destined to make an impact. We are carrying on his mission with the formation of Taylor’s Tree, a nonprofit foundation aiming to provide awareness and support for mental health and suspected CTE.”

The first project for the Taylor’s Tree organization is to increase awareness and provide support for the research efforts of those organizations.

“Our legacy, my legacy and everybody who loved him, is to make people more aware,” said Lori Dever, Taylor’s mother. “My son, his legacy will live on and Taylor would want this support and research.”

For more information, visit https://www.taylorstree.org


‘Time does not heal’: Family talks about next steps in raising awareness about CTE
Read more: https://www.theunion.com/news/time-does ... about-cte/

[goldy313]

Keep up the good work greybeard! It is largely thankless work but work that is important.

[greybeard58]

Breakthrough study reveals repetitive head impacts are a definitive cause of CTE

Sports organizations must acknowledge that head impacts cause CTE to protect children

(Boston) – A new analysis by leading international experts on chronic traumatic encephalopathy (CTE) found conclusive evidence that repetitive head impacts (RHI) cause the degenerative brain disease CTE.

The researchers from Harvard University, Boston University, University of Sydney (Australia), University of Auckland (New Zealand), University of Michigan, University of California-San Francisco, University of Sao Paulo (Brazil), University of Melbourne (Australia), Oxford Brookes University (UK) and the Concussion Legacy Foundation are issuing a global call to action to sports organizations, government officials, and parents to immediately implement CTE prevention and mitigation efforts, especially for children.

The researchers analyzed the data through the “Bradford Hill criteria”, a trusted set of nine benchmarks developed by one of the pioneers of smoking and lung cancer research to gauge the confidence science can place in a causal relationship between an environmental exposure and an adverse health outcome.

Among the revelations in the analysis, the authors discovered that the brain banks of the US Department of Defense, Boston University-US Department of Veterans Affairs, and Mayo Clinic have all published independent studies on distinct populations showing contact sport athletes were at least 68 times more likely to develop CTE than those who did not play contact sports. This incredible strength of association, combined with robust evidence in all nine benchmarks, is conclusive evidence of causation.

“This innovative analysis gives us the highest scientific confidence that repeated head impacts cause CTE,” said study lead author Dr. Chris Nowinski, Concussion Legacy Foundation CEO. “Sport governing bodies should acknowledge that head impacts cause CTE and they should not mislead the public on CTE causation while athletes die, and families are destroyed, by this terrible disease.”

The most studied causes of CTE are contact and collision sports, which include soccer, rugby, boxing, American football, Canadian football, and Australian rules football. The study authors are concerned parents and coaches, who have the most control over whether children are exposed to repetitive head impacts, are not getting the facts from global sports organizations, and are exposing their children to preventable cases of CTE.
While both the United States Centers for Disease Control and Prevention (CDC) and the National Football League (NFL) acknowledge a causal relationship between repetitive head impacts and CTE, global sporting organizations including Fédération Internationale de Football Association (FIFA), World Rugby, International Olympic Committee (IOC), National Hockey League (NHL), Canadian Football League (CFL), National Collegiate Athletic Association (NCAA), Australian Football League (AFL), National Rugby League (NRL) and New Zealand Rugby thus far have refused to publicly acknowledge a causal relationship.

Researchers say it is the duty of these organizations to inform athletes and their families and take appropriate steps toward CTE prevention and mitigation. Many of the organizations, including the NFL, spend millions of dollars a year recruiting athletes, including children, without disclosing the risk of CTE.

“This analysis shows it is time to include repetitive head impacts and CTE among child protection efforts like exposure to lead, mercury, smoking, and sunburns,” said Dr. Adam Finkel, Clinical Professor of Environmental Health Sciences at the University of Michigan School of Public Health and a former Director of Health Standards, US Occupational Safety and Health Administration (OSHA). “Repetitive head impacts and CTE deserve recognition in the global public health discussion of preventable disorders caused by childhood exposures.”

CTE can only be definitively diagnosed through a post-mortem examination of the brain. Scientists don’t yet know how many athletes, military Veterans, and others exposed to head impacts have CTE, but knowing the prevalence of a disease is not required to enact disease prevention efforts, especially as the global scientific community closes in on 1,000 CTE cases diagnosed worldwide in the last decade.

“Even we were surprised by how strong the causal relationship between repetitive head impacts and CTE becomes when the data are analyzed within the appropriate framework and in an unbiased manner,” said study co-senior author Dr. Robert Cantu Concussion Legacy Foundation medical director. “Scientists and policymakers must retire the word association and begin using causation in all forums in an urgent effort to educate the public.”

The authors urge governments to support CTE research and prevention efforts since CTE is associated with developing dementia, which comes with extraordinary healthcare costs.

The research paper, Applying the Bradford Hill Criteria for Causation to Repetitive Head Impacts and Chronic Traumatic Encephalopathy, is published in Frontiers in Neurology, and can be viewed online.

Applying the Bradford Hill Criteria for Causation to Repetitive Head Impacts and Chronic Traumatic Encephalopathy
https://www.frontiersin.org/articles/10 ... 38163/full

Dr. Nowinski and Dr. Finkel answered some of the most frequently asked questions about CTE causation, read their blog here https://concussionfoundation.org/news/b ... -causation

Breakthrough study reveals repetitive head impacts are a definitive cause of CTE
https://concussionfoundation.org/news/p ... -cause-CTE

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New research finds blood tests can predict severe outcomes of brain injury

Simple blood tests taken on the day of a traumatic brain injury (TBI) can predict with fairly high reliability which patients are likely to die and which are likely to survive with severe disability, according to a study published Wednesday in Lancet Neurology.

The rapid assay looks for two protein biomarkers — GFAP, found in glial cells, and UCH-L1, found in neurons. Tests of both biomarkers have been approved by the Food and Drug Administration for their ability to show structural damage to the brain and are used as tools to determine if patients with mild TBI should have costly CT scans.

Now, this paper, by a group of scientists associated with a brain injury research initiative called TRACK-TBI, shows that the assays are not only diagnostic, but also prognostic. Having a strong indication of outcome can shape conversations with families in cases of devastating injury, the researchers said, or contribute to triage decisions and resource allocation in a military setting.

While typical prognostic tests “require an assemblage of some clinical data, some CT imaging data, and some laboratory data,” this test is easy to use and the results are immediate, said Geoffrey Manley, a trauma neurosurgeon at the University of California, San Francisco and senior author on the study.

Firas Kobeissy, an assistant professor in emergency medicine at the University of Florida who is unaffiliated with this research, said that the ability to predict unfavorable outcomes for patients with TBI is a novel and strong finding, though the biomarkers fall short of predicting partial recovery.

Researchers used a rapid portable blood analyzer to look for the biomarkers in samples from 1,500 patients on the day of their traumatic brain injury. Most were injured in traffic accidents or falls. Patients with trauma in addition to a brain injury were excluded.

That could be a limitation. “Without including the polytrauma, you’re excluding a large group of patients that we typically see in the ICU,” said Gretchen Brophy, professor of pharmacotherapy and outcomes science and neurosurgery at Virginia Commonwealth University, who was not involved with this research but serves on the steering committee of TRACK-TBI.

Brophy noted that 30% of the patients in the study reported previous TBI, which might mean there were elevated baseline levels of the protein biomarkers. She also pointed out that secondary injuries can occur while patients are hospitalized and influence biomarker levels. Brophy said it is important for future studies to see if the predictive powers of the biomarkers holds true when patients with more diverse brain injury profiles are included.

The researchers followed the participants for two weeks, three months, and six months to see how they fared. They used the Glasgow Outcome Scale Extended, which is a widely used tool for assessing disability and recovery after a TBI. Patients are assigned a score from 1 — dead — to 8 — fully recovered.

Six months after the initial admission, 7% of the patients had died, 14% had level 2 to 4 injuries, and the rest had incomplete recovery. Researchers found that high initial levels of the biomarkers were associated with death and severe injury — a score of 1-4 — and that the biomarker blood test improved on the most widely validated current prediction tool, the IMPACT prediction model.

The day-of-injury blood tests had a probability of predicting death at six months of 87% for GFAP and 89% for UCH-L1; and a probability of predicting severe disability at the same time point of 86% for both GFAP and UCH-L1. They were significantly less accurate in predicting incomplete recovery compared to complete recovery.

“If these proteins are significantly elevated, we need to share this with families to say that there’s a higher likelihood of incomplete recovery or even death,” Manley said.

But Eric Thelin, an associate professor in experimental neurology at the Karolinska Institute in Stockholm, Sweden, cautions that the tool cannot be applied clinically yet since there might be false positives.

“Right now it’s sort of a guess with brain injuries,” Brophy said. “The biomarkers will help us be a little bit more definitive in speaking with the families of the patients, and also the patients to give them some idea of the recovery from the injury, which we haven’t really been as confident in before.”

While both biomarkers were independently prognostic, they worked best in tandem. The UCH-L1 protein is very rapidly released and cleared from the bloodstream while the GFAP protein peaks a bit later and then sticks around for a while.

“Both of these proteins are highly complementary, in that you’re not going to miss things because you did the test too early, or you’re not going to miss things because you did the test too late,” Manley explains.

Because so-called mild traumatic brain injury has long been considered a one-and-done event as opposed to a potentially chronic illness, a lot of patients with high Glasgow scores at initial evaluation are not given robust follow-up. But Manley says that paradigm is changing and that these blood-based biomarkers could eventually be an effective tool to predict unfavorable outcomes and identify patients who will benefit from follow-up care.

New research finds blood tests can predict severe outcomes of brain injury
Read more: https://www.statnews.com/2022/08/10/blo ... -outcomes/

Prognostic value of day-of-injury plasma GFAP and UCH-L1 concentrations for predicting functional recovery after traumatic brain injury in patients from the US TRACK-TBI cohort: an observational cohort study
Read the study: https://www.thelancet.com/journals/lane ... 3/fulltext

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Did scientific misconduct alter concussion care? CTE Denier has 9 more papers retracted

The British Journal of Sports Medicine (BJSM), a BMJ publication, is retracting nine more non-research articles authored by former editor-in chief and concussion researcher Paul McCrory, MBBS, PhD, of the Florey Institute of Neuroscience and Mental Health in Melbourne, Australia.

Expressions of concern will be placed on another 38 articles published in BMJ journals on which McCrory is the only author, noted Helen Macdonald, MBBS, MSc, of BMJ Publishing, and Jonathan Drezner, MD, of the University of Washington in Seattle, and co-authors in the BJSM.

The decision follows an internal investigation by BMJ's research integrity team and Drezner, who is the current editor-in-chief of the BJSM. It was prompted by allegations about publication misconduct made by researcher Nick Brown, PhD.

McCrory edited the BJSM from 2001 to 2008, during which time he published at least 164 articles in BMJ journals.

Earlier this year, an article by McCrory was retracted in the BJSM, prompted by concerns that it shared similarities with one that another author had written for Physics World.

Plagiarism may not be the most serious breach that might concern BJSM readers, observed Stephen Casper, PhD, of Clarkson University in Potsdam, New York, and Adam Finkel, ScD, of the University of Michigan in Ann Arbor, in an accompanying editorial.

Misquotation may be worse, they noted. In a 2001 article, "McCrory fundamentally changed a quote from sports medicine pioneer Thorndike [Augustus Thorndike, MD], in an egregious warping of Thorndike's published words," Casper and Finkel wrote.

"In a 1952 New England Journal of Medicine article, Thorndike had written unequivocally that patients with cerebral concussion that has recurred more than three times or with more than momentary loss of consciousness at any one time should not be exposed to further body-contact trauma,'" they noted.

"However, in his editorial, McCrory purported to 'quote' Thorndike's 1952 article as having advised that after 'three concussions, which involved loss of consciousness for any period of time, the athlete should be removed from contact sports for the remainder of the season,'" changing and weakening Thorndike's recommendation in two different ways, Casper and Finkel pointed out.

In his career, McCrory led several iterations of consensus statements on concussion in sports, which were published in BJSM.

"While those statements were said to be informed by systematic reviews (some of which McCrory was part of or led) and include many co-authors who also contributed to the consensus guidelines, readers may question how McCrory's misquotation or the possible mindset it reveals on his part, especially when considered together with McCrory's plagiarism and the possibility of other misrepresentations, may have altered the interpretation of concussion science and thus shaped the content of consensus statements on concussion," Casper and Finkel wrote.

Questions about McCrory's actions go beyond published work, noted Chris Nowinski, PhD, of the Concussion Legacy Foundation in Boston.

"We are only beginning to understand the implications of Paul McCrory's serial scientific misconduct," Nowinski told MedPage Today.

"In my mind, the serial plagiarism and duplicate publications are dwarfed by the fact that he has repeatedly misrepresented the work of others in public scientific forums, both regarding historical concussion care guidelines in a medical journal and chronic traumatic encephalopathy [CTE] research in a public lecture," Nowinski observed.

"That is what we know he was willing to misrepresent publicly. Who knows what he said in private meetings, but I suspect it has played a role in global sports' past and current hostile resistance to conservative concussion care and acceptance that CTE is caused by contact sports," he added.

The nine retractions all concern opinion pieces, commentaries, and editorials on which McCrory is the only author. They include five cases of plagiarism and three of redundant publication. The other retracted article is the one in which McCrory quoted Thorndike.

After a review of the 2016 concussion consensus statement, the BMJ research integrity team concluded it had "no concerns about plagiarism," and considered that "the question of the extent of McCrory's contribution to, and influence on, the five versions of the consensus statement is a matter within the purview of the scientific committee appointed by the Concussion in Sport Group (CISG)."

After plagiarism allegations first surfaced, McCrory resigned his leadership position in the CISG and stepped down from his role as a member of the Scientific Committee of the International Consensus Conference on Concussion in Sport, Macdonald and co-authors noted.

"The scientific record relies on trust, and BMJ's trust in McCrory's work -- specifically the articles that he has published as a single author -- is broken," they wrote.

"We will investigate any new allegations that we receive about McCrory's work in BMJ journals," they added. "We ask other publishers and his institution to do the same."

Concussion Expert's Papers Retracted — Did misquotations alter concussion science and care?
Read more: https://www.medpagetoday.com/neurology/ ... uma/101152

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Thursday, October 27th Sixth Annual CTE Virtual Conference

6th Annual: Chronic Traumatic Encephalopathy
Save the Date: 1-Day Virtual Event
Thursday, October 27th, 2022
10:00 AM - 5:30 PM ET

The annual CTE Conference is back! This virtual course will feature an opportunity for all of our participants to learn about all aspects of CTE, including its pathology, pathophysiology, genetics, biomarkers, imaging, clinical syndromes, and clinical criteria.

Speakers:
Ann McKee, MD
Director of BU CTE

Kate Turk, MD
Course Director

Robert Stern, PhD
Director of Clinical Research

Jesse Mez, MD, MS
Clinical Care Leader

Michael Alosco, PhD
Clinical Care Co-Leader

Lee E. Goldstein, MD, PhD
Biomedical Engineering and Biomarker Care Co-Leader

Eric Reiman, MD
Executive Director, Banner Alzheimer’s Institute

Breton M Asken, PhD, ATC
Assistant Professor, University of Florida

More conference info:
https://www.cteconference.com

Free registration at:
https://bostonu.zoom.us/webinar/registe ... Em931OIR4w

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On anniversary of his death, wife of former NHLer Marek Svatos says he had CTE
Marek Svatos, who played parts of eight NHL seasons and skated for Slovakia in the 2006 Olympics in Torino, had the degenerative brain disease chronic traumatic encephalopathy (CTE) at the time of his death in 2016.
By Rick Westhead

Marek Svatos, who played parts of eight NHL seasons and skated for Slovakia in the 2006 Olympics in Torino, had the degenerative brain disease chronic traumatic encephalopathy (CTE) at the time of his death in 2016.

Svatos’ wife, Diana, confirmed his posthumous diagnosis in a series of recent interviews with TSN. Diana – who said the date of her husband’s death has been misreported on the Internet – wanted to speak publicly about Svatos’ life and death because she says it was more complicated than media reports have portrayed.


Svatos died Nov. 4, 2016, at the age of 34 in his home in Lone Tree, Colo. A coroner reported Svatos had codeine, morphine and anti-anxiety medication in his system when he died, The Denver Post reported at the time. His official cause of death was an accidental overdose, Diana said.

Diana shared how her husband suffered through at least a half-dozen documented concussions and at least as many surgeries during his NHL career, after being drafted by Colorado in the seventh round of the 2001 entry draft.

“I wanted to get my kids to a good place before talking about this, but I want people to know that Marek was a good person who loved his family and made decisions because of CTE, not because he was a bad person,” Diana said. “I don’t know how many times I heard him say ‘the lights went out’ after he had had a concussion. I heard it enough times to remember that phrase.”

Diana and met Svatos in 2004 during his NHL rookie season in Denver and married in 2007.

“Marek was never comfortable being the center of attention,” Diana said. “He hated the spotlight. If he had a great game, he’d basically beg the media to interview anybody else but him. He was the kind of guy who loved to laugh and loved to play a practical joke, usually on me. He would say goodbye and leave the house to go to the rink for practice, then drive around the block and park before coming back inside to try to scare me to death. He was always observing, always with his signature mischievous smirk on his face.”

After donating her husband’s brain to researchers at Boston University days after his death, Diana was provided with a three-page pathology report on Nov. 12, 2017, that showed Marek had Stage 2 CTE. (There are four stages.)

“One of the main reasons I want to tell this story now is I want to help other NHL families."
“Although Stage 2 is considered to be a mild form of CTE, it is often characterized by striking mood and behavioral changes, and sometimes memory loss,” Boston University neuropathologist Dr. Ann McKee wrote in an email to TSN. “Mr. Svatos suffered from severe depression and memory loss that began at age 25 and worsened over time...”

Svatos’ posthumous diagnosis of CTE is noteworthy because he was known as a scorer and playmaker. A winger, his career high for penalty minutes in a season was 60.

Researchers believe CTE not only comes from concussions that might be suffered during a fight on the ice, but also from the repeated blows to the head and jarring bodychecks that occur routinely during a game.

CTE can only be diagnosed posthumously. The degenerative brain disease is linked to symptoms like personality changes, memory loss and impulsive outbursts. It has been discovered in athletes, military veterans, and others with a history of repeated hits to the head.

Diana said the CTE diagnosis has helped her to understand some of her husband’s behavior's. She said he would become easily agitated and forgetful.

“I’m not talking about forgetting to take out the garbage,” she said. “I’m talking about having a conversation with him and him coming back five seconds later saying, ‘What were we talking about?’ That would happen three times in a row. It was to the extreme.”

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“He had concussions and all of this pain and everything kind of all fell perfectly together in a horrible storm for him.”
At the same time as he navigated symptoms connected to repeated brain trauma, Svatos formed an addiction to the Oxycodone he was given by both team and independent doctors to help him recover from a string of injuries, his wife said.

“He formed a habit,” Diana said. “He had concussions and all of this pain and everything kind of all fell perfectly together in a horrible storm for him.”

Diana said a few months before his death, Svatos shared with her that he had used heroin to try to mute his pain and that he had tried to take his own life. Svatos went to rehab three times to try to break his dependence.


“He didn’t choose to do this to himself or to his family and people need to know that. They need to know his full story,” Diana said. “One of the main reasons I want to tell this story now is I want to help other NHL families.

“I’m saying this from a place of love, but the league can do more for players during and after their careers. When guys go to rehab, the league can follow up with them and with their wives to see how things are going. And they can still try to do a better job helping players be prepared for what happens after their hockey careers. These guys train their whole life to be a pro hockey player, then it’s over, and then they and their families start to have problems. Being honest about how big a problem this is would be a good first step by the NHL.”

Svatos also played for Slovakia in world junior tournaments in 2000 and 2002 and played in the 2010 world championships. He scored 100 goals and had 72 assists in 344 NHL games. He played with the Avalanche, Nashville Predators and Ottawa Senators before finishing his pro career in Slovakia.

Of the 14 former NHL players whose brains have been studied by researchers, 13 have been found to have had CTE.

“I don’t know how many times I heard him say ‘the lights went out’ after he had had a concussion. I heard it enough times to remember that phrase.”
McKee, director of Boston University’s CTE Center, said she is currently examining the brains of other former NHL players and will have more updates to share publicly about the prevalence of CTE in hockey players within about six months.

NHL players diagnosed with CTE include Ralph Backstrom, Stan Mikita, Steve Montador, Todd Ewen, Bob Probert, and Rick Martin. Former Toronto Maple Leaf Kurt Walker is the only former NHL player who tested negative.

If CTE can eventually be diagnosed in living patients, researchers would be able to begin medical trials to learn whether certain drugs are effective at slowing or stopping the damage caused by the disease.

The NHL has not publicly acknowledged a link between head injuries sustained while playing hockey and long-term cognitive disorders. A league spokesperson did not respond to a request for comment.

The NHL in November of 2018 announced an $18.9 million (U.S.) settlement with 318 former players who joined a lawsuit accusing the league of downplaying the long-term dangers of repeated brain trauma.
https://www.tsn.ca/on-anniversary-of-hi ... -1.1873252

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Chronic Traumatic Encephalopathy Isn’t New
• ESSAYS
By Stephen T Casper10/21/2021
In 1928 a forensic examiner named Harrison Martland published a famous paper in the Journal of the American Medical Association. It was titled “Punch Drunk.” It is often said to have introduced medical readers to an occupational disease caused by recurrent hits to the head.
Called now chronic traumatic encephalopathy or CTE, “punch drunk,” Martland said, originated in boxing slang. In his hands, it evolved into a clinical entity.

In the history of concussion research since Martland published his classic studies, many authorities have fixated their interests on the fact that Martland was reporting an occupational disease in boxers.
In fact, Martland’s study was more ambitious than that. He was directing attention to the way that boxers could reveal pathologies from even mild hits to the head in anyone who had been hit in the head, even once, but especially if the hits were repeated.

As an historian of neurology writing a book on the history of modern violence and brain trauma, I am frequently fascinated by journalism and scientific writing that treats the head impact medical problem in sports as a new topic, one just now emerging. It is an old problem.

Researchers and journalists today rightly look towards new trends in science, medicine, and engineering. From that viewpoint, 1928 certainly does seem a long time ago. Yet, I think one of the reasons that Harrison Martland’s 1928 study so often surprises people when they first encounter it is the shock that this scientific concern about recurrent head impacts dates to so long ago.
In fact, the documentary evidence for that knowledge from the past is far wider and deeper than is today widely appreciated.

The results of Martland’s research had first been reported in a 1927 paper read at the American Neurological Association meeting in Atlantic City, New Jersey. Martland and his collaborator Christopher Beling reported on a series of 309 autopsies of traumatic brain injury. The report included a clinical description of a man named H. D.

A shipping clerk and boxer, H. D. was all of 22 years of age. H.D. had received “many blows on the head and face while boxing.” He had also been hit on the head with a blackjack. Nine months after the blow with the blackjack, H. D. had begun to show signs of disease. He had, Martland and Beling said, a post-traumatic parkinsonian syndrome.

H.D. had been committed to hospital “after several attempts at suicide”. There Martland said he was “irritable, depressed at times, emotionally unstable, and impulsive”. H. D. fit the profile of what Martland would argue a year later in his 1928 paper was the consequence of recurrent concussions. H.D. was punch drunk.

Documents from collegiate sports authorities also illustrate how common knowledge about these problems was in the past. (In the spirit of full disclosure, I am retained as a testifying expert witness in cases pending against the NCAA and other organizations.)

During the course of the famous concussion lawsuit against the National Football League, a copy of the National Collegiate Athletic Association Medical Handbook for Schools and Colleges turned up. It was published in 1933. Public copies exist at the New York Academy of Medicine among other libraries.
The authors of the 1933 NCAA medical handbook were Edgar Fauver, August Thorndike, and Joseph Raycroft. These were pioneers of sports medicine, and Thorndike would become especially illustrious.
The NCAA appointed these physicians in 1933 to “study and report on the general subjects of training and medical supervision of athletic squads.” In the manual, the doctors wrote “there is definitely a condition described as ‘punch drunk’ and often recurrent concussion cases in football and boxing demonstrate this.”

Documentary evidence of this kind was fairly common, and I have located many compelling examples.
As part of my research, I often scour e-Bay for hardcopy versions of old magazines and periodicals for my growing personal archives on violence and brain injury. One document I recently purchased on eBay was The Official 1944 Boxing Guide of the National Collegiate Athletic Association.
In this guide, Alfred Griess, then team doctor at Penn State College, took up the question of whether boxing opponents were right.

Griess wrote that “punch drunk” was not common among amateur boxers. He observed, however, that “cases had been cited to occur among wrestlers, professional football players, victims of automobile or industrial accidents, etc.” He also said, “This pathetic condition may occur in any activity which causes jarring of the brain.”

Similarly, I recently located an undated faculty report (from before 1950) of the development of intercollegiate boxing at the University of Illinois. That document included the results of a survey of neurologists and psychiatrists, with 46 responding.

When university faculty asked neurologists and psychiatrists “can repeated blows on the head over a period of two to four years cause a gradual change in mental pattern, etc., of the individual?,” 76% of the respondents then asked said “yes.”

As these early examples (all appeared before 1950) show so well, doctors and sporting authorities understood in those days that repeated blows to the head are dangerous and sometimes caused clinically observable illness.

Since 1950 reference materials, medical textbooks, dictionaries, and even diagnostic manuals have defined and described occupational illness resulting from violence to the head. For all of that, sports players and coaches have struggled to appreciate the risks of recurrent head impact violence. Denial starts at that level.

A 1985 textbook entitled Principles of Sports Medicine by W. N. Scott, B. Nisonson, and J. A. Nicholas is one example. It describes a community college coach glibly unaware that one of his players was showing severe deterioration from cumulative concussion as well as early clinical hallmarks of becoming “punch-drunk.” It is easy to speculate that the brain-injured player was even less aware of these facts.

Some players probably did wonder if they were merely disposable bodies and brains, although it is hard to find such recognition recorded in primary sources.
In an astonishing profile by Alex Poinsett that appeared in Ebony Magazine in 1964 of American footballer and fullback Jim Brown, described as football’s mightiest player, Brown recalled one time when he had a significant cerebral concussion resulting in amnesia at the sideline.
His coach, Brown said, seemed to think he was faking and wanted him to get back into the game. To Brown it was clear that the coach “didn’t seem to care if you lived or died, so long as you played.”
Is the elite game so different today?

Since the NFL Concussion Settlement in 2013, it has become common for doctors and psychologists to clarify strenuously that the occupational diseases resulting from careers of recurrent head injury exposure can only be diagnosed post-mortem. I sometimes speculate about whether there is a cultural and historical relationship between those denials and the way the settlement sits as a background feature to all investigations and policy discussions about brain injury and head impact.
Meanwhile, it is not uncommon to find seminars and publications for clinicians that argue that research on chronic traumatic encephalopathy remains in its infancy. It should not be lost on us that there is a deep irony in that observation. Scientists obviously know far more today about CTE then Martland and Beling did in 1927. Yet where Martland and Beling could clinically characterize their patient H.D. without debate, today some doctors appear unable to do so for their patients with similar life histories.
What has happened in the intervening years since 1928 is a longer and complex story about a struggle for truth. Sadly, that struggle for truth has not come with warnings. There is no reason those warnings cannot be given today.

If CTE research is truly in its infancy, then there is reason enough to use prevention as a means of making sure it never grows up.

Image credit: Joseph Vogel. “Football.” Smithsonian American Art Museum, Gift of Audrey McMahon.
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https://blog.lareviewofbooks.org/essays ... -isnt-new/

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Review strengthens evidence that repetitive head impacts can cause CTE

Summary
Over 600 CTE cases have been published in the literature from multiple international research groups. And of those over 600 cases, 97 percent have confirmed exposure to RHI, primarily through contact and collision sports. CTE has been diagnosed in amateur and professional athletes, including athletes from American, Canadian, and Australian football, rugby union, rugby league, soccer, ice hockey, bull-riding, wrestling, mixed-martial arts, and boxing.

During the past 17 years, there has been a remarkable increase in scientific research concerning chronic traumatic encephalopathy (CTE) with researchers at the BU CTE Center at the forefront. While some sports organizations like the National Hockey League and World Rugby still claim their sports do not cause CTE, a new review of the evidence by the world's leading CTE expert strengthens the case that repetitive head impact (RHI) exposure is the chief risk factor for the condition.

CTE became national news in the United States in 2007, but it wasn't until 2016 that the National Institute of Neurological Disorders and Stroke/National Institute of Biomedical Imaging and Bioengineering (NINDS-NIBIB) criteria for the neuropathological diagnosis of CTE were published, and they were refined in 2021. Rare, isolated case studies reporting aberrant findings or using non-accepted diagnostic criteria have been disproportionately emphasized to cast doubt on the connection between RHI and CTE.

In a review article in the journal Acta Neuropathologica, Ann McKee, MD, chief of neuropathology at VA Boston Healthcare System and director of the BU CTE Center, stresses that now over 600 CTE cases have been published in the literature from multiple international research groups. And of those over 600 cases, 97 percent have confirmed exposure to RHI, primarily through contact and collision sports. CTE has been diagnosed in amateur and professional athletes, including athletes from American, Canadian, and Australian football, rugby union, rugby league, soccer, ice hockey, bull-riding, wrestling, mixed-martial arts, and boxing.

What's more, 82 percent (14 of the 17) of the purported CTE cases that occurred in the absence of RHI, where up-to-date criteria were used, the study authors disclosed that families were never asked what sports the decedent played.

According to the researchers, despite global efforts to find CTE in the absence of contact sport participation or RHI exposure, it appears to be extraordinarily rare, if it exists at all. "In studies of community brain banks, CTE has been seen in 0 to 3 percent of cases, and where the information is available, positive cases were exposed to brain injuries or RHI. In contrast, CTE is the most common neurodegenerative disease diagnosis in contact and collision sport athletes in brain banks around the world. A strong dose response relationship is perhaps the strongest evidence that RHI is causing CTE in athletes," she added.

"The review presents the timeline for the development of neuropathological criteria for the diagnosis of CTE which was begun nearly 100 years ago by pathologist Harrison Martland who introduced the term "punch-drunk" to describe a neurological condition in prizefighters," explained McKee, corresponding author of the study. The review chronologically describes the multiple studies conducted by independent, international groups investigating different populations that found CTE pathology in individuals with a history of RHI from various sources.”

CTE is characterized by a distinctive molecular structural configuration of p-tau fibrils that is unlike the changes observed with aging, Alzheimer's disease, or any other diseases caused by tau protein.
Funding for this research was provided by the National Institute of Neurological Disorders and Stroke (U54NS115266; R01NS119651; U01 NS 086659), National Institute on Aging (P30AG13846; U19AG06875; R01AG062348; RF1AG057902; K01AG070326), Department of Veterans Affairs (101BX002466, 101BX004613, BX004349), the Nick and Lynn Buoniconti Foundation, Andlinger Foundation, National Football League (NFL) and World Wrestling Entertainment (WWE) through unrestricted gifts, the Mac Parkman Foundation, and the National Operating Committee on Safety for Sports Equipment (NOCSEA).

Review strengthens evidence that repetitive head impacts can cause CTE
Read more: https://www.sciencedaily.com/releases/2 ... 115511.htm

Summary
CTE is a distinctive pathology characterized by neuronal p-tau aggregates that are focal, perivascular, and cortical in mild disease in young individuals and widespread and diffuse in severe disease and in older individuals. CTE tau consists of a distinctive molecular structural configuration of p-tau fibrils that is unlike the changes observed with aging, Alzheimer's disease, or any other tauopathy. Since the publication of NINDS–NIBIB criteria for the neuropathological diagnosis of CTE in 2016 and refined criteria in 2021, multiple studies conducted by independent, international groups investigating different populations have found CTE pathology in individuals with a history of RHI from various sources. Conversely, studies involving large community populations and brain banks have found CTE pathology to be rare or absent (0–2.8%). Multiple experimental models have demonstrated that tissue strain and physical deformation is greatest in the perivascular and sulcal depth regions after head impact injury, accurately predicting the location of p-tau deposits. In addition, there is a robust dose–response relationship between CTE and years of American football play. The preponderance of the evidence suggests a high likelihood of a causal relationship between RHI and CTE, a conclusion that is strengthened by the absence of any evidence for plausible alternative hypotheses. There is no other common variable, aside than RHI, that explains why so many contact sports players worldwide, playing diverse sports, have been diagnosed with CTE, while individuals without RHI exposure have not [91]. Nevertheless, there remain areas of uncertainty in CTE and topics that require future investigation. These include better distinction of mild CTE pathology from the changes of ARTAG and better detection of CTE pathology in the presence of a co-existing tauopathy such as AD. In addition, although dementia correlates with severity of p-tau pathology in CTE and CTE stage, the clinical symptoms associated with CTE pathology, or TES, especially the mood and behavioral symptoms, need better specificity, especially in mild stages of disease. To improve detection and diagnosis of the clinical syndrome of TES, prospective, longitudinal studies of individuals at risk for CTE are needed, along with robust fluid and imaging biomarker studies, and analysis of other pathologies known to occur in CTE, including neuroinflammation, small vessel changes, and white matter degeneration.

Chronic traumatic encephalopathy (CTE): criteria for neuropathological diagnosis and relationship to repetitive head impacts
Read the entire Acta Neuropathologica article: https://link.springer.com/article/10.10 ... 23-02540-w

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Irv Cross’ widow opens up about late husband’s health following CTE diagnosis
Eric Chaloux KSTP
Updated: March 2, 2023 - 7:14 PM
Published: March 2, 2023 - 5:24 PM
Family, faith and football were important pieces of the late Irv Cross’ life.
The family of Irv Cross announced this week that Boston University CTE Center researchers diagnosed him with stage 4 chronic traumatic encephalopathy (CTE).
He died two years ago at the age of 81.

“It’s sad that CTE made him into a person he wasn’t,” said Liz Cross, Irv’s widow. “He was strong and athletic and upbeat and happy and loved life, loved god, loved his family. He just became somebody else.”
Liz Cross said her husband, who was diagnosed with mild cognitive dementia in 2018, often sat in a chair and grimaced from headaches that weren’t going away.

The former NFL defensive back became the first Black man to work full-time as a sports analyst on national television for CBS Sports’ NFL Today in the 1970s.

Back in 2018, Irv Cross sat down with 5 EYEWITNESS NEWS reporter Eric Chaloux when he announced he would donate his brain to science after his death.
“Like so many retired pro football players, I’ve had some issues with my nervous system, my brain,” he said in that interview.
Irv Cross opened up about trying to find help while battling mild cognitive dementia. The former NFL star with the Philadelphia Eagles also championed trying to have kids not play tackle football until they were 14.
“We’re all on earth for a purpose. Your challenge is to find out what our purpose in life is all about,” Irv Cross said.
He wanted to make sure others don’t suffer, which is why he chose to donate.
“He was just a sweet thoughtful guy. He was really a treasure,” said Dr. Chris Nowinski, Concussion Legacy Foundation CEO, who knew Cross.

The Concussion Legacy Foundation is connected to the Boston University CTE Center researchers who are studying Cross’ brain.

5 EYEWITNESS NEWS is one of only a few news outlets in the world granted access to the Boston University facility.

Researchers say CTE is a progressive degenerative disease that has been found in people who have a history of repetitive head impacts. It’s believed the trauma triggers a degeneration of brain tissue, leading to symptoms that could include memory loss, confusion and impulse control problems.
Nowinski hopes Irv Cross’ donation gets researchers closer to being able to detect CTE while someone’s still alive and figure out a treatment.

“We need to get more scientists working on this so we have cures in the future for the next generation who follow Irv,” Nowinski said. “Irv has given so much back and is helping us understand how we can eventually treat and stop this disease.”
The Associated Press contributed to report.

https://kstp.com/kstp-news/top-news/irv ... diagnosis/

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Montador lawsuit brings NHL's 'absurd' stance on CTE to light once again
Ex-NHLer Steve Montador's father alleges the NHL has profited off violence while not properly advising players of the risks of repeated brain injuries.

Has Gary Bettman made hockey better?
JULIAN MCKENZIE: I said
my thing was to name one

Ian Kennedy
·Writer
Sun, March 12, 2023 at 9:02 p.m. CDT·8 min read
In this article:
NHL commissioner Gary Bettman has repeatedly denied the link between brain injuries and CTE, or chronic traumatic encephalopathy, a degenerative brain disease caused by repeated head trauma.
“The science regarding C.T.E., including on the asserted ‘link’ to concussions that you reference, remains nascent, particularly with respect to what causes C.T.E. and whether it can be diagnosed by specific clinical symptoms,” Bettman wrote in response to questioning from a U.S. senator back in 2016. “The relationship between concussions and the asserted clinical symptoms of C.T.E. remains unknown.”
As recently as 2019, Bettman continued this denial and dismissed the links between head trauma suffered in hockey and CTE. Bettman’s stance on brain injuries has continued to be a concern among past players, including former NHL defenseman Chris Therien who told Yahoo Sports in 2022 that “Gary Bettman denies that concussions are almost real,”
It’s a clear contradiction to the NHL’s recent stance, while arguing Steve Montador, a 14-year NHL veteran with six NHL clubs, knew the risks of CTE and brain injuries, which eventually played a role in his death. Montador’s father is currently embattled in a wrongful death lawsuit in an Illinois state court against the NHL related to the passing of his son in 2015.
“During his life, Montador struggled with substance abuse, depression, anxiety, insomnia and strained/abusive personal relationships,” the NHL wrote in new court filings this week. “Despite being repeatedly made aware of and informed about potential long-term risks of head injuries, including CTE, by numerous individuals as detailed above, Montador continued to play in the NHL for years.”
The league added:
“Montador was told by multiple specialists that he should stop playing hockey due to his concussion history but ignored these medical professionals and continued his career, suffering additional head injuries,” the NHL continued. “Montador also expressly told Blackhawks’ medical personnel that he assumed the risk of continuing to play hockey at the professional level.”
While mentioning their league, and the continuation of Montador’s injury struggles, the NHL also asserted that “None of these injuries can possibly be attributed to his play in the NHL.” The league asserts Montador, who fought 69 times in his NHL career, and amassed 807 penalty minutes in 571 games, suffered his brain injuries playing in other leagues.

Will NHL commissioner Gary Bettman's legacy be tarnished by any of this? (Getty)

Although the comments were criticized by many, according to leading brain injury and chronic traumatic encephalopathy (CTE) specialist Dr. Chris Nowinski, the founding CEO of the Concussion Legacy Foundation, the comments themselves are not more dangerous than the NHL’s refusal to acknowledge CTE.
“Ever since CTE became a topic of discussion in 2007, the NHL has claimed that there’s no proof their game causes CTE,” Dr. Nowinski told Yahoo Sports. “To still be saying that in 2023 is absurd.”
Research has shown the link between repetitive brain trauma and CTE, particularly as it relates to impact sports like hockey and football. Despite the overwhelming evidence of a recent study conducted by 14 leading experts in the field, the NHL said they will not change their stance based on a single study. “A single medical article does not determine our view on these issues,” Bill Daly, the league’s deputy commissioner, told The Toronto Star. “We rely on the consensus opinion of medical experts to guide us.”
As Dr. Nowinski says, the court filings in Steve Montador’s case show the NHL knows their own statements are false.
“[CTE] is caused by repetitive traumatic brain injuries,” said Dr. Nowinski. “This court filing shows that even the NHL doesn’t believe their own story. That they claim that Steve Montador was informed about CTE risk by the NHLPA at the same time they were telling players there was no risk, I’m just in shock. I think of it as a window into what [the NHL] actually believes, but I also feel great sympathy for Steve Montador, at that time in his life he’s being told by the league that orchestrates the game he played that he’s not at risk for CTE.”
As Dr. Nowinski stated, youth are taught to look up to leagues like the NHL and NFL, and trust these institutions as groups “who were trying to do the right thing or had some moral authority.” In the case of Steve Montador, who passed away at age 35 in 2015, only four days prior to the birth of his son, Dr. Nowinski says Montador could have believed the NHL was working in his best interest, despite the evidence.
“It wouldn’t surprise me if Steve believed the NHL…it’s bizarre, but it’s another sign that the NHL, when they talk about their game not causing CTE, they know it’s not true, but they’re saying that to protect their assets at the expense of the players’ health and the entire hockey community’s health.”
“They will say anything if they think it will protect their assets,” Dr. Nowinski continued. “They’ll say it doesn’t cause CTE to prevent future lawsuits, but for current lawsuits they’ll say you were informed about the risk by someone else and you should have believed them over us; that’s what’s happening here.”
In 2018, the NHL was forced to pay $18.9 million to settle a class action lawsuit by more than 100 ex-NHL players who accused the NHL of "failing to better prevent head trauma or warn players of risks while promoting violent play that led to their injuries.”
In the case of Steve Montador, his mental state was documented to be deteriorating in the weeks and months prior to his death. As evidenced from scientific studies involving football players who have suffered concussions and traumatic brain injuries, the ability to manage interactions with others, and “more-frequent problems with executive function in everyday activities” are common features of those suffering with CTE.

Steve Montador died in 2015 after a lengthy, concussion-filled NHL career.
While no one is arguing Steve Montador was unable to make his own decisions, or assume the risk as the NHL states, the link between executive functioning, decision making, risk taking behavior, and harm has been documented in individuals who have suffered concussions and other traumatic brain injuries. As Dr. Nowinski says, while it’s clear that people should not be driving, or “making difficult decisions, life decisions” in the days following a concussion, at some point the brain recovers. When those injuries become repetitive, however, many of these functions become permanently impaired.
“The more brain injuries you've had, people sometimes trend toward taking riskier and riskier behaviors,” Dr. Nowinski said. “Your ability to gauge risk can become impaired.”
Dr. Nowinski explained that science is not at a point where people in their 30s, as Montador was at the time of his death, who suffer from CTE, can’t make good decisions, but there are examples of this occurring. One example, as noted by Dr. Nowinski, is that of former NFL player Phillip Adams, who suffered from CTE at the time he killed six strangers before taking his own life at age 32. As Dr. Ann McKee who examined Adams’ brain said, his football participation “definitely ... gave rise” to his CTE diagnosis and that Adams suffered from an impairment due to those injuries.
“There were inklings that he was developing clear behavioral and cognitive issues,” McKee told ESPN in 2021. “I don't think he snapped. It appeared to be a cumulative progressive impairment. He was getting increasingly paranoid, he was having increasing difficulties with his memory, and he was very likely having more and more impulsive behaviors. ... It may not have been recognized, but I doubt that this was entirely out of the blue.”
The deterioration of Adams’ mind is not unrecognizable to those closest to Montador. As former NHLer and Montador’s friend Dan Carcillo stated, “Over the years, I saw that deterioration of [Montador’s] mind, and he must have felt that as well. Just recently going home to Mississauga and to his home and seeing the number of sets of keys he had for the same lock kind of tells you the story of what was going on in his head and his memory loss and his mental state.”
While Dr. Nowinski was not ready to assert Montador suffered similar impairments to Adams, he believes the impacts of CTE and brain injuries on decision-making is definitely a point to consider.
“I don’t have any evidence to say this is necessarily the case here, to say he couldn’t accept the risk,” Dr. Nowinski said of the Montador case. “But in the big picture, it’s a question we can and should ask and try to understand better, how judgment becomes impaired with early CTE and the more brain injuries you have.”
“If players have had a ton of concussions, and may be self-medicating because of those concussions, and they may have a degenerative brain disease in process in their brain, will they be making good decisions? The answer is, they’ll be making worse decisions than they used to.”
A wrongful death lawsuit filed by Montador’s father Paul was recently transferred from U.S. federal court to an Illinois state court. First filed against the NHL in 2015 following his son’s death, the lawsuit contends Montador suffered at least 11 undocumented concussions while playing in the NHL, including four in 2012. The case is ongoing.

https://ca.sports.yahoo.com/news/nhl-co ... 52778.html

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NHL commissioner disputes link between hockey and CTE brain disease
Updated April 19, 20237:49 AM ET
Heard on Morning Edition
By

H.J. Mai

6-Minute Listen
Download
Transcript

For hockey fans, it's the best time of the year – the start of the Stanley Cup playoffs. But the physical aspect of playing the game has led to increased concerns about potential links between hockey and chronic traumatic encephalopathy (CTE). National Hockey League (NHL) Commissioner Gary Bettman says he remains unconvinced that there are any connections between the degenerative brain disease and playing NHL hockey.

"We listen to the medical opinions on CTE, and I don't believe there has been any documented study that suggests that elements of our game result in CTE. There have been isolated cases of players who have played the game [who] have had CTE. But it doesn't mean that it necessarily came from playing in the NHL," Bettman told NPR's A Martinez on Morning Edition.

Preliminary findings of a study conducted by Boston University (BU) appear to contradict Bettman's assertion. Researchers found that each additional year of playing hockey may increase a person's chance of developing CTE by about 23%.

"In football, we've shown this really robust relationship between years of football play and risk for CTE. We wanted to take the same approach for hockey and our numbers are now such that we can start to make estimates about the relationship between years of hockey play and risk for CTE," Jesse Mez, associate professor of neurology at the BU School of Medicine and a BU CTE Center investigator, tells NPR.


The study looked at the brains of 74 people, ranging in age from 13 to 91, who played hockey at various levels from youth hockey to professional sport. Nearly half of the individuals, 46%, also participated in other contact sports such as football. All of them donated their brains to research after their deaths. The researchers found that among 74 donors, 40 of them, or 54%, had developed CTE.

The researchers note that more research is needed, as the study may not represent the general population of hockey players. After years of denial, in 2016 the National Football League acknowledged a link between CTE and playing football and last year revised its concussion protocols once again.

During a sometimes-heated exchange with NPR's A Martinez, Bettman dismissed any comparison between football and hockey. "The two are not comparable in terms of the amount of contact," he says.

Both football and hockey, however, are among the contact sports with some of the highest concussion rates.

"It should be in the NHL's purview to try to reduce head impact, so I don't think it's useful to make statements that there seems to be no relationship [between hockey and CTE]. I think there should be a desire to help to address the health and safety of players," Mez says.

Several NHL players who were diagnosed with CTE after their deaths were "enforcers" whose unofficial role is to protect the team's top players. This can include aggressive responses, such as bare fist fights to retaliate or intimidate, although Bettman says there are no "designated fighters like we used to [have] in the old game."

Bettman says roughly eight out of ten games today are played without a fight. And he characterizes the fighting that does erupt as "spontaneous emotional reaction."

"At the end of the day, it is a part of the game that is an emotional outlet," Bettman says.

The NHL's Stanley Cup playoffs continue through the end of May, with the Cup Finals slated to begin on June 3.

The interview has been lightly edited for clarity and length.

Interview highlights
On fighting during NHL games

Roughly 80% of our games do not have fights. That's probably a record low. The types of fights we have compared to years ago are spontaneous emotional reaction to what takes place on the ice. We don't have players who are designated fighters like we used to in the old game. The role of fighting in the game has evolved and really acts as the thermostat, because remember, we have a very fast, physical, emotional game where players are encouraged to have body contact. And, by the way, they happen to be carrying sticks.

On the NHL diversity and inclusion report that found 84% of league employees are white

That was a number that was not unexpected. But making the decision to have such a report and make it public is consistent with our goal of making sure that we're welcoming and inclusive and that we're going to hold ourselves accountable in a very public fashion as to how we're progressing to improve and increase our diversity. So having that report and making it public was a conscious effort to say, we're going to do better.

On some players and teams refusing to participate in NHL Pride Night events

Clubs make their own decisions. To the extent that they have Pride Nights, the elements that they put into them have always been left up to the clubs, and it's always been left to the players as to who wants to participate. And overwhelmingly, our clubs and our players support Pride Night and what it stands for. And I don't think that the notion that a couple of players on each team or on some teams we're not comfortable wearing pride jerseys is not an indictment. To the contrary, you have to be tolerant of all views and all expressions. And sometimes respect and endorsements are not the same thing.

Kaity Kline produced the audio version of this interview and Jan Johnson edited the digital.
https://www.npr.org/2023/04/19/11708023 ... in-disease

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"That's extremely young"

A Columbia University study of 6,039 former NHL players since 1967 showed enforcers (50+ career fights) died on average a decade younger than their comparable peers. Mean average age of death for fighters was 47.5. Average age of death of control group was 57.7.

The risks of fighting and repetitive head trauma are a growing concern among player safety advocates. While fighting accounts for 9% of acute concussions in NHL players, repetitive head trauma may contribute to the development of headaches, depression, personality changes, and cognitive deficits. Later effects include increased risk of neurodegenerative diseases, including chronic traumatic encephalopathy (CTE) and even suicide. A recent examination of all-cause mortality comparing National Football League (NFL) players with Major League Baseball players demonstrated that NFL players had an elevated all-cause mortality. A similar analysis of mortality rates in NHL enforcers is urgently needed to better characterize the long-term association of repetitive head trauma from fighting.

8DGUvVGI.png

Fighting and Penalty Minutes Associated With Long-term Mortality Among National Hockey League Players, 1967 to 2022
Read the entire study: https://jamanetwork.com/journals/jamane ... ultClick=1

Dr. Dave Ellemberg, a professor at Universite de Montreal and a specialist in sports medicine, said in an interview with CP he was shaken to see that athletes in the control groups died on average in their mid-50s. “That’s extremely young,” he said.
Read more: https://www.theglobeandmail.com/sports/ ... ir-fellow/

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11-Time Stanley Cup Champion, Hall of Famer Henri Richard diagnosed with stage 3 CTE | Concussion Legacy Foundation


https://concussionfoundation.org/news/p ... tage-3-cte

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"She is the first female athlete diagnosed with CTE, but she will not be the last"

A female professional athlete has been diagnosed with chronic traumatic encephalopathy, or CTE, for the first time, researchers say. The degenerative brain disease, which is believed to be caused by repeated head injuries, was diagnosed in the late Australian rules footballer Heather Anderson, who died at the age of 28 in November 2022, researchers said. It came as researchers and advocates urged new attention on how the issue might affect women in high-level sports.

In a paper published on June 30 outlining their findings, researchers said Anderson’s family had donated her brain to the Australian Sports Brain Bank, where the analysis took place.

The family had hoped to learn "whether a lifetime of exposure to repetitive head trauma contributed to (Anderson's) death," a report co-authored by one of the researchers behind the study and published by The Conversation, said.

"She is the first female athlete diagnosed with CTE, but she will not be the last," it said. IN their June 30 report outlining their findings, researchers said "contact sports in which head injuries occur commonly" are "historically male dominated," which "likely underlies the strong male bias in CTE prevalence to date.”

"However, the last two decades have seen a rise in popularity and participation in women’s contact sports, particularly among younger women aged 15–34 years," they said.

Researchers also noted that available evidence suggested females were more susceptible to sports-related concussions than males, even when participation is controlled for. Dr. Robert Cantu, co-founder and medical director of the Concussion Legacy Foundation, a nonprofit organization based in the U.S., said research on CTE in women needed to be “urgently” accelerated to help understand the situation better.

“Research shows women have an equal or greater susceptibility to concussion in contact sports, but we don’t yet know what that means for their risk of developing CTE,” Cantu said in a statement. “We urgently need to accelerate research on CTE in women so we can prevent future cases, better understand how CTE impacts their behavior and cognition, and treat those who develop symptoms,” he said. “The first case of CTE in a female athlete should be a wakeup call for women’s sports,” Dr. Chris Nowinski, Concussion Legacy Foundation co-founder and CEO, said.

“We can prevent CTE by preventing repeated impacts to the head, and we must begin a dialogue with leaders in women’s sports today so we can save future generations of female athletes from suffering.”

CTE is a disorder that is still "not yet well understood," the Mayo Clinic says on its website. Its development is associated with repeated head injuries "often occurring in contact sports or military combat," it says.

In their report, researchers said Anderson was an avid player from 5 years of age, with a total contact sport career of 18 years.

"She had suffered one diagnosed concussion, with four other possible concussions not formally diagnosed but suspected by family," the report says.

Anderson had also served in the military for nine years and participated in amateur martial arts for three years, though no concussions were reported from those activities, the report said.

While the Mayo Clinic says "there are no specific symptoms that have been clearly linked to CTE," a number of symptoms have been recorded in those confirmed to have CTE at autopsy.

Among the symptoms associated with the disease are motor symptoms, including issues with walking and balance; cognitive impairment issues including trouble thinking, memory loss, problems with planning; behavioral changes, including impulsive behavior and aggression and mood disorders, including depression, apathy, substance misuse and suicidal thoughts or behavior.

An investigation into Anderson’s death is still underway, but the June 30 paper outlining researchers’ findings notes that “due to the circumstances surrounding the death, it is suspected the woman died by way of suicide.”

“While there are insufficient data to draw conclusions on any association between CTE and manner of death, suicide deaths are not uncommon in the cohorts where CTE is sought at autopsy,” researchers said in their report.

British newspaper The Guardian reported that Anderson's father had written in a Facebook post following her death that it was suspected she had died by suicide. “The response to the news of Heather taking her own life has shown us that she had friends, teammates, and fellow soldiers all across the country,” he wrote.

If you or someone you know is at risk of suicide, please call the National Suicide Prevention Lifeline at 800-273-8255, text TALK to 741741 or visit SpeakingOfSuicide.com/resources for additional resources.

CTE diagnosed in a female professional athlete for the first time
The disease was diagnosed in the late Australian rules footballer Heather Anderson, who died at the age of 28 in November 2022, a paper outlining the post-mortem analysis said.
Read more: https://www.nbcnews.com/news/world/cte- ... -rcna92500

Australian researchers confirm world’s first case of dementia linked to repetitive brain trauma in a female athlete
Read more: https://theconversation.com/australian- ... ete-208929

Late Australian footballer Heather Anderson first diagnosed case of CTE brain trauma in a female athlete
Read more: https://www.theguardian.com/australia-n ... esearchers

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CTE identified in brain donations from young amateur athletes
Study examined athletes who played contact sports, showed CTE symptoms, and died before age 30.

Images of human brain cross sections. use link at bottom to see images

Researchers found brain abnormalities associated with CTE, such as thalamic notch (top left) and degradation of the fornix (top right), in a brain bank sample from young athletes who played contact sports and died before age 30. The bottom images are of a control brain. McKee lab, Boston University CTE Center.
What
In a study of 152 deceased athletes less than 30 years old who were exposed to repeated head injury through contact sports, brain examination demonstrated that 63 (41%) had chronic traumatic encephalopathy (CTE), a degenerative brain disorder associated with exposure to head trauma. Neuropsychological symptoms were severe in both those with and without evidence of CTE. Suicide was the most common cause of death in both groups, followed by unintentional overdose.

Among the brain donors found to have CTE, 71% had played contact sports at a non-professional level (youth, high school, or college competition). Common sports included American football, ice hockey, soccer, rugby, and wrestling. The study, published in JAMA Neurology, confirms that CTE can occur even in young athletes exposed to repetitive head impacts. The research was supported in part by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health.

Because CTE cannot be definitively diagnosed in individuals while living, it is unknown how commonly CTE occurs in such athletes. As in all brain bank studies, donors differ from the general population and no estimates of prevalence can be concluded from this research. Most of the study donors were white, male football players with cognitive, behavioral, and/or mood symptoms. Their families desired neuropathologic examination after their loved one’s early death and donated to the Understanding Neurologic Injury and Traumatic Encephalopathy (UNITE) Brain Bank. There were no differences in cause of death or clinical symptoms between those with CTE and those without.

Nearly all the athletes with CTE were found to have a mild form (stages I or II, on a four-stage scale) in the study led by Ann C. McKee, M.D., chief of neuropathology at VA Boston Healthcare System and director of the Boston University CTE Center. Those with CTE were more likely to be older (average age at death 25.3 years vs. 21.4). Among athletes who played football, those with CTE had a significantly longer playing career (2.8 years longer, on average) compared to those without CTE. Notably, the study includes what the authors believe to be the first report of CTE in an amateur female soccer player.

All athletes in this study had shown clinical symptoms, regardless of CTE status, as reported by those who knew them. Clinical symptoms of depression, apathy, difficulty controlling behaviors, and problems with decision-making were common, even among donors without CTE.

Taken together, the findings demonstrate that evidence of CTE can be found in young, symptomatic athletes who play contact sports; however, more studies are needed to understand the relationship between repeated head injury, white matter damage, CTE, and clinical symptoms. Given that 58% of the brain donors who died at a young age did not have evidence of CTE, the causes of severe symptoms in this group are likely due to multiple factors.

This study was funded in part by NINDS (U01NS086659, U01NS093334, U54NS115266, R01NS078337, R56NS078337, K23NS102399), the National Institute on Aging (NIA) (RF1AG057902, 5R01AG062348, R01AG061028, K23AG046377, P30AG13846), and the National Center for Advancing Translational Medicine (NCATS) (UL1TR001430).

Additional support came from the Andlinger Foundation, National Football League, MacParkman Foundation, National Operating Committee on Standards for Athletic Equipment, Nick and Lynn Buoniconti Foundation, the Alzheimer’s Association, the Concussion Legacy Foundation, World Wrestling Entertainment, the US Department of Defense, and the US Department of Veterans Affairs.

Who
Nsini Umoh, Ph.D., TBI program director, NINDS Division of Neuroscience

To arrange an interview, please contact NINDSPressTeam@ninds.nih.gov(link sends e-mail).

Article
McKee AC, et al. “Neuropathological and Clinical Findings in Young Contact Sport Athletes Exposed to Repetitive Head Impacts.” August 28, 2023. JAMA Neurology. DOI: 10.1001/jamaneurol.2023.2907(link is external).

About the National Institute on Aging (NIA): NIA leads the U.S. federal government effort to conduct and support research on aging and the health and well-being of older people. Learn more about age-related cognitive change and neurodegenerative diseases via NIA’s Alzheimer's and related Dementias Education and Referral (ADEAR) Center website. Visit the main NIA website for information about a range of aging topics, in English and Spanish, and stay connected.

NINDS is the nation’s leading funder of research on the brain and nervous system. The mission of NINDS is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

NIH…Turning Discovery Into Health®

https://www.nih.gov/news-events/news-re ... r-athletes

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A Former Hockey Enforcer Searches for Answers on C.T.E. Before It’s Too Late
Chris Nilan fought more than 300 times during a pro hockey career, then had years of addiction and anger problems. A high-risk candidate for chronic traumatic encephalopathy, Nilan is being studied by Boston University.


By David Waldstein
Reporting from Terrasse Vaudreuil, Quebec, and Boston
• Sept. 22, 2023
Page 68 of Boston University’s Hope Study questionnaire asks, “Have you ever injured your head or neck in a fight or been hit by someone?”
For Chris Nilan, a simple yes could never convey the whole story.
Listen to This Article
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Listen to this story in the New York Times Audio app on iOS.

The answer stretches out over 300 bare-knuckle fights as a professional hockey player, and countless other brawls on the street corners of Boston beginning in his childhood. Most times, Nilan was the one dispensing the punishment. But hockey fights almost always involve mutual, bone-crushing blows, fists jackhammering from powerful shoulders, sometimes fracturing bones, tearing tissue and rattling brains.
The Hope Study, run by B.U.’s Chronic Traumatic Encephalopathy Center, has been measuring the brain health of living subjects with Alzheimer’s disease and related dementias since 1996. Nilan, curious about the condition of his brain after years of furious on-ice battles and eager to help with the research, turned to B.U., where participants return each year to repeat extensive testing, and eventually donate their brains. C.T.E. can only be diagnosed posthumously, but the Hope Study’s testing can provide valuable clues while patients are alive.
One of the key elements of the research is the background questionnaire, where subjects detail any history of brain impacts.
Nilan had played only a few N.H.L. games when, one night in 1980 as a rugged rookie for Montreal, he dropped his gloves and fought Boston’s Stan Jonathan and Terry O’Reilly, two of the most feared pugilists in league history. The bouts came in consecutive periods — hockey’s equivalent of boxing Muhammad Ali and Mike Tyson within an hour of one another.
Nilan, who was labeled Knuckles before he even turned pro, survived that night, plus 12 more seasons of fighting and scoring goals (118, including the playoffs). He won a Stanley Cup in 1986 with Montreal and was named an All-Star in 1991. Over his 13 years in the league, he fought an astonishing 316 times, the third most in N.H.L. history, according to the N.H.L. Fight Card database.
All of it was followed, coincidentally or not, by years of agonizing drug addiction, alcohol abuse and anger issues before Nilan settled into a quiet life in a Montreal suburb. An engaging, humorous sort with a Boston accent thicker than Chahles Rivah sludge, Nilan now hosts the “Raw Knuckles” podcast, fishes, cooks, reads every day — mainly books on military history — runs addiction recovery groups and spends quiet time with his fiancée, Jaime Holtz.
But if there was ever a high-risk candidate for C.T.E., the degenerative neurological disease associated with repeated impacts to the head or a body blows harsh enough to rattle the skull, Nilan would seem to fit the category.
Researchers have long suggested that the more hits to the head someone receives, including subconcussive ones, the more likely they are to develop cognitive and neurological problems later in life. A study earlier this year of football players’ brains suggested that the cumulative impact of multiple hits can also play a role.
Thirty years after retiring from an uncompromising, violent and successful career, and with the encouragement of the widow of a fellow enforcer who had the disease, Nilan signed up for the Hope Study.
“I don’t worry about having C.T.E.,” Nilan said. “But sometimes you wonder.”
Ten years ago, there might have been more concern. Nilan’s past substance abuse and outbursts of rage mirror some of the behavior exhibited by other hockey enforcers following retirement, players like Bob Probert, Derek Boogaard, Wade Belak, Todd Ewen and Steve Montador. All of them were diagnosed with C.T.E., which can only be detected after death.
More than a dozen hockey players have been diagnosed with C.T.E., and not all of them fighters. The most recent was Henri Richard, a small, skillful center for the Canadiens who died in 2020, the kind of player Nilan was paid to protect.

Nilan is 65 and sober now, still with a sharp wit and a vivid memory of a tumultuous and violent life that intersected closely with some of Boston’s most infamous figures, including James Bulger, the murderous crime boss, known as Whitey, who was Nilan’s father-in-law.
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A Family History of Dementia
On April 17, Nilan entered the Hope Study. He and Holtz answered background questions from their home over a video conference call with researchers, who asked about Nilan’s family and behavioral history, his moods, his memory, his mother’s dementia and his career on the ice.
A few weeks later, he went to Boston for the cognitive and medical testing, and a month after that he received results that can give participants a snapshot of their brain health at that moment.
Nilan went into the study feeling healthy and robust, perhaps even a bit lucky. He empathizes with players who suffered from the same dangerous work that he did, but points no fingers.
In 2013, a group of former players sued the N.H.L. for not doing enough to address head injuries. Nilan was asked to join but declined, believing the sport did not cause his past substance abuse issues, and he does not regularly suffer from depression.
But because of his nearly unmatched history of fighting in hockey, Nilan has emerged as an important subject for researchers studying the effects of repetitive brain impacts and ways to detect it before death.
Even if he does not have C.T.E. or show signs of cognitive impairment, researchers will want to know why not, and what can be learned from it.
“That’s huge,” said Dr. Michael Alosco, the co-director of clinical research at Boston University’s C.T.E. Center. “Why do some people get it, and some don’t? What is different about them? It could be very informative for treatment and prevention.”
‘A Window Into the Brain’
A year ago, Dani Probert was a guest on Nilan’s podcast. They discussed her husband’s career and the time he tangled with Nilan on the ice. They recalled how Nilan and Bob Probert had become good friends after hockey, Probert’s addictions and his death in 2010 from a heart attack, at 45 years old.
Dani Probert explained that when she donated her husband’s brain to B.U.’s C.T.E. research center, she had difficulty answering an accompanying questionnaire about her husband’s life and career. She knew Probert was considered hockey’s heavyweight champion. But she did not know the details of every brutal punch, every check into the boards or fall to the ice.
She urged Nilan to answer those questions now, while he still could. A year later, Nilan joined the Hope Study and pledged to donate his brain.
“It’s vital to get athletes like Chris to participate,” said Chris Nowinski, the co-founder of B.U.’s C.T.E. Center and of the Concussion Legacy Foundation.
Over a day and a half in Boston, Nilan underwent a battery of medical, cognitive and neurological exams designed to help researchers learn the causes and effects of repetitive head impacts that can lead to C.T.E., and perhaps one day design a test that will detect it in living patients.

Nilan had his blood and spinal fluids drawn and was scheduled for magnetic resonance imaging of his brain. He tackled cognitive and memory tests involving word games, number sequences, short stories and mazes. One of the key tests is a lumbar puncture to draw spinal fluids that Dr. Alosco calls “a window into the brain.”
There are more than 400 participants in the program now, and about one third have been exposed to repetitive head impacts. Originally it focused on Alzheimer’s disease, but in recent years its C.T.E. research has expanded.
During the first day of testing in Boston, the city of his youth, Nilan had lunch with Dr. Alosco, who was curious about Nilan’s career and upbringing. Dr. Alosco asked if Nilan fought in college hockey and in high school. Nilan did not, but he casually mentioned some street fights. Asked how many, Nilan replied, “Oh, gosh, I couldn’t even tell you.”
More Than an Enforcer
In some ways, Nilan’s contribution to the study was an opportunity to do in retirement what he loved most as a player, defending teammates.
“If what I do now can help them figure out ways to detect C.T.E. earlier,” Nilan said, “maybe guys in the future can be forewarned and saved from further damage.”
On the ice, if an opposing player dared jam a stick blade into Guy Lafleur’s ribs or throw an elbow at Guy Carbonneau, they or their own enforcer answered to Nilan. When the other team was stocked with notorious tough guys, Nilan was the one expected to drop the gloves, absorb the crunching pain, and then weld someone’s eyes shut with his infamous knuckles.
“You’d go into Philly or Boston and you could see there were guys before the game who were scared,” Nilan said. “But I couldn’t be scared. I was the one they looked to blow the bugle, carry the flag and charge in there.”

Nilan accumulated 3,584 penalty minutes over the regular season and playoffs, the fifth-most in league history, and he played almost 300 fewer games than the top four offenders. He twice set the Canadiens record for most penalty minutes in a season: 338 in the 1983-84 regular season, and 358 the following year.
“I was a menace,” he said.
He was also one of the Canadiens’ most popular players, as much for his energetic goal celebrations as his fists. More than just a fighter, Nilan could play. In opposing arenas, he was the target of hatred and boos, even in Boston. But those who played alongside Nilan adored him.
“Chris Nilan was one of the absolute best teammates I ever had,” said Tony Granato, who played 13 years in the N.H.L., including his first two with Nilan on the Rangers, from 1988 to 1990.
A goal scorer, Granato recalled a game against the Pittsburgh Penguins in 1988 when he almost engaged in his first fight. When he returned to the bench, Nilan slid over hard and lectured him never to drop his gloves again. If there was a problem — with anyone — he should tell Nilan, who would take care of it. Nilan did the same for Brian Leetch, the star Rangers defenseman.
“There is guilt on my part for all the punishment he and those guys had to take for us,” Granato said. “But that was their job, and they took pride in it. No one did it better than Knuckles.”
Memory, Now and Five Years Ago
Chris Nilan is a quintessential Bostonian of a certain time and demographic, the kind they make movies about: A tough, working-class hockey player of Irish descent, hundreds, if not thousands, of local kids yearned to be just like him. He was born on Feb. 9, 1958, at the Faulkner Hospital in West Roxbury, Mass., the son of Henry and Leslie Nilan, a hard-working, blue collar couple who raised their four children in a strict household. Chris still found his way into scraps as a kid, and soon discovered he was a capable and fearless fighter. Often, he said, it was in defense of others. Later, he mixed it up with groups of kids and young adults on the streets and in the bars of Boston.
He met Karen Stanley at Northeastern University and they fell in love. When people asked about Bulger, Nilan would point out that he married Karen, not her stepfather. He described their 1981 wedding, with Henry Nilan’s Green Beret buddies on one side, Bulger and his cohorts on another and Nilan’s hockey pals up the middle.
“We could have invaded a small country,” Nilan said with a laugh.
Several years later, Bulger was photographed with the Stanley Cup after Nilan’s Canadiens won it in 1986. Nilan stresses he was never aware of Bulger’s criminal activities, but described tension between Bulger and his own father, an honest, taxpaying working man who disapproved of the then-reputed gangster’s “lifestyle.”
Once, when both sets of parents were visiting Montreal, Bulger bought Nilan’s mother an expensive fur coat, which upset Nilan’s father. Bulger adored Nilan’s fearless and pugnacious demeanor.
Waking In The Night, Punching or Kicking
At 6 feet, 205 pounds, Nilan was shorter and lighter than many of his opponents, like the 6-foot-5, 225-pound Dave Brown, whom he fought six times. Nilan relied on his remarkable stamina and developed a kind of rope-a-dope technique, tucking his head into one shoulder to protect his face and head and pouncing when the other fighter tired or allowed an opening. He quickly emerged as one of the most courageous and terrifying players in the league, willing to trade blows with any heavyweight.
Fighting is far less common in today’s N.H.L. than it was in the 1980s and ‘90s, as the league has ushered in rules modifications and a faster style of play, even though Gary Bettman, the league commissioner, still denies a link between fighting and C.T.E. Nilan opposes a ban on fighting, but acknowledges being sickened when a player is knocked unconscious in a fight.
It never happened to him, but in his later seasons, after he was traded to the Rangers and the Bruins, the fighting secretly wore him down.
“I fought right to the end, but it was getting harder on me,” he said. “Fight one guy and then fight another guy the next period or next shift. I’d come back to the bench and tell myself, ‘I’m losing that little edge,’ which you can never own up to. So you hide it.”
In the years after his career ended, his hands, knees and back throbbed from 13 years of pounding and too many surgeries. Nilan began ingesting Percocet, a prescription pain killer, and then became addicted to Oxycodone and alcohol, a familiar combination for many retired enforcers.

He eventually found heroin and took it intravenously. In 2015 his mother had a stroke and Nilan went to visit her at Faulkner, the hospital where he was born. He asked a drug dealer to meet him there and he shot up in a maintenance closet. The next thing he knew, he was on a gurney with a nurse calling his name, yet another overdose victim.
Had he gone outside to find the dealer that night, instead of insisting they meet at the hospital, Nilan likely would not have survived.
He does not hide from the harrowing memory, or others, like the time decades ago when he savagely beat a young man who had hit his teenage daughter and was arrested in the assault. He grapples with the anguish he has inflicted on others, on himself, his family and Holtz.
And yes, he still wakes up, perhaps three or four times a year, throwing punches at the air in reaction to a nightmare, usually that he is being carjacked.
Problems With Anger
Nilan met Holtz in rehab and she has been his stanchion, guiding him out of relapses and back to recovery. The researchers asked Holtz about Nilan’s memory and moods and if he displayed moments of rage. She explained that several years ago, she told Nilan that if he did not get his anger under control, she would leave him.
“He would lose his temper for the smallest things,” she said. “Chris acknowledged those issues in his life and is completely different now. All of that has changed. He faced some hard truths and emotions and dealt with them. Growing up, that is how he was raised.”
Nilan adored his father, who died in 2021, and is immensely proud of him. Henry Nilan was a Green Beret in the Army reserves and a draftsman at Draper Labs in Cambridge, Mass., and he worked hard to provide for his family. He also hit Chris as punishment, sometimes in the chest, sometimes a slap to the back of the head, sometimes a punch, until Chris was about 16 and finally threatened to run away.
Growing up in that environment, he says, led to much of his anger and propensity to violence, not his career as an enforcer.
Have You Had Any Concussions?
Concussions are a concern, but not a prerequisite for C.T.E. Rather, the condition is believed to result from repeated impacts to the head.
“With C.T.E., concussions have been overemphasized,” Nowinski said.
Nilan recalls four possible concussions. One was from an opponent’s shoulder during play that left him dazed. Another time, as a fight wound down, Nilan’s opponent fell on top of his head as it struck the ice. Nilan saw stars. A third time was during a street altercation in Boston when he was struck in the head with a full bottle of beer and was, “out on my feet.” Lastly, several years ago he rolled his car into a ditch and was ejected out the back window, unconscious.
“I never felt any long-term symptoms,” he said. “I never had problems with light, or noise, or sleeping.”
‘Are you ready to hear the results?’
Nilan and Holtz sat in Nilan’s podcast studio in their home on June 8 and listened to Dr. Alosco and Hannah Bruce, a fellow researcher, present the findings. Nilan was eager to hear the results, and was also looking forward to interviewing Jim Montgomery, the Bruins’ head coach, for the podcast before heading out for a round of golf.
Holtz was nervous.
The results cannot rule out C.T.E., but they were very good for Nilan. His cognitive, memory and motor tests showed he was well within the normal range for his age, gender and education. In most he was above average. Had there been any reason for concern, Dr. Alosco would have recommended clinical care for diagnosis and treatment, which he did not consider necessary at the time.

“I kind of thought,” Nilan began, then paused and shook his head. “Look, I’m a special case.”
Everyone on the call laughed, but it could be true. Dr. Alosco said Nilan is in a very high-risk group and urged him to remain vigilant with his sobriety and a healthy lifestyle. He also asked him to return for the yearly research follow-ups, and Nilan said he would.
At the end of the meeting, Dr. Alosco stressed that researchers want to know the factors that have made Nilan appear resistant so far to degenerative neurological disease, whether genetics, medical history, the types of head impacts, his lifestyle or other factors.
“That’s why your data might be so valuable to answer who is resilient to these long-term effects of repetitive head impacts,” Dr. Alosco told Nilan.
Nilan was upbeat afterward, as he prepared to head out of the house. But not because of the results.
“Either way,” he said with a clap of his hands, “I was going to play golf.”
Audio produced by Kate Winslett.
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Former Minnesota Wild player Chris Simon has died at age 52

Simon died Monday night in his hometown of Wawa, Ontario, a spokesperson for the NHL Players’ Association who has been in touch with the late forward’s agent, said Tuesday.

Simon died by suicide, his family said Wednesday.

Simon’s family blamed his death on CTE, the degenerative brain disease chronic traumatic encephalopathy, in a statement released through agent Paul Theofanous. “We will not be releasing any further details at this time and ask for privacy during this very difficult time,” the family wrote. “We appreciate everyone who shares in our tragic loss.”

There’s no way to confirm CTE while a person is alive, though doctors can identify suspected cases based on symptoms and neurological exams.

Simon played 857 regular-season and playoff games over 15 NHL seasons from 1993-2008. Over his career, he fought more than 100 times and racked up 1,824 penalty minutes to rank 67th in league history.

“For a big tough player, he was also a very kind, caring individual who was always respectful and grateful for advice,” former agent Larry Kelly said in a text message to The Associated Press.

Simon won the Stanley Cup with Colorado in 1996 and was part of runs to the final with Washington in 1998 and Calgary in 2004. He also spent time with the Quebec Nordiques before they became the Avalanche and played for Chicago, Calgary, Minnesota and the New York Rangers and Islanders, before finishing with five seasons in the KHL from 2008-13 and retiring.

“Chris was a great guy, a beloved teammate and an important part of our first championship season,” said Joe Sakic, Colorado’s president of hockey operations who was captain when the team won in 1996. “He was a really good hockey player who could score goals, was a big presence in the dressing room and was the first person to stand up and defend his teammates. Off the ice, he was an unbelievable guy and a caring father, son, brother and friend.”

Simon on the ice was a respected teammate and fan favorite, though he occasionally crossed the line and faced supplemental discipline. The NHL suspended him eight times totaling 65 games, including a 25-game ban in March 2007 while he was with the Islanders for cross-checking the Rangers’ Ryan Hollweg in the face and 30 games for stomping on the leg of Pittsburgh’s Jarkko Ruutu that December.

Philadelphia drafted Simon in the second round of the 1990 draft and sent him to the Nordiques as part of the 1992 trade that got the Flyers prized prospect Eric Lindros.

Simon, who was of Ojibwa descent, was considered a role model for First Nations hockey players across Canada.

“Chris Simon was most definitely an intimidating guy on the ice,” former teammate Mike Commodore posted on social media. “We spent a lot of time together during Flames ’04 run since we were both living in the hotel. … He couldn’t have been nicer to me. RIP Chris. You will be missed.”

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This story includes discussion of suicide. If you or someone you know needs help, please call the National Suicide Prevention Lifeline at 988.
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