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Don’t let go.

It’s been a little over 14 months since we got the worst call of our lives and lived a reality we wish on no one. You can relive our experience here as it will forever be etched in our lives.
The day after Andrew died we responded with the following statement:

"We are deeply heartbroken to share of the loss of Andrew Carroll, an amazing son, brother, uncle, nephew, cousin, teammate, teacher, mentor, and friend who died tragically after a fall at the Chicago O’Hare Airport. We are deeply grieving but have the assurance that he is in the loving arms of Jesus because of his decision to accept Christ. At this difficult time, what also gives us comfort is that his life meant so much to so many people and he was able to give the gift of hope by donating his organs so that others might have life. May his love for Jesus and others live through each of us. We are in the process of making arrangements for his celebration of life and hope you can join us as we honor Andrew." With love, the Carroll Family

As I wrote in the original blog post, we announced that he died as a result of a tragic fall. No one ever is prepared to share such devastating and incomprehensible news, writing words while still in complete disbelief that 20 minutes after Andrew purchased a plane ticket to fly home to St. Paul in the early morning of January 20th, he walked out the door to an overpass, climbed the railing, turned around (as the police officer described to us) and let go.

His death certificate reads jump from height resulting in death by suicide.

Through this journey of being affected by suicide, in our experience, there were no signs, to any of us that were close to him, that ever made us think he would harm himself.

“Clearly you had to of known?” asked of Chris by a woman at the visitation. No. No. No, do not ask that. If we would have known he was struggling, we would have tried to help him (as any family or friend would). But…thank you (no thank you) for asking in assumption that the answer you wanted to hear is really just trying to calm your own fears that this could happen to you. That question hurts everyone affected by suicide and is not helpful to anyone. Mental health and suicide unfortunately already carry a societal stigma and questions and assumptions like that only contribute to the trauma of this painful part of our story.

Yesterday was the final interview with the Boston University CTE Center, after the 14 month period of time that they studied Andrew’s brain. With the number of years he played hockey (collegiate + 9 years professional), the cause of death, and roles he played on his teams, we listened as the neuropathologist explained the condition of his brain at the time of his death.

The process before the final results were given included clinicians interviewing our family about his medical history. Many of the questions were basic about his mood, headaches, and eventually led to questions about trauma to the brain. In the years that he played hockey as a forward, he experienced a few concussions and a lot of trauma (as defined by the clinical definition) to the brain while engaging in hockey fights (during his professional career).

The doctor explained how the testing was conducted and the results indicated that Andrew had Chronic Traumatic Encephalopathy (CTE). According to the Boston University CTE Center, CTE is a degenerative brain disease found in athletes, military veterans, and others with a history of repetitive brain trauma. In CTE, a protein called Tau forms clumps that slowly spread throughout the brain, killing brain cells. Andrew’s frontal lobe was impacted by this protein. Currently, CTE can only be diagnosed after death through brain tissue analysis. You can read more about the diagnosis here. There are many people living with CTE and they may not even suspect they have it (as in Andrew’s case). The doctor explained that a majority, if not all, of the donations of young brains are a result of death by suicide. Research and awareness around this disease is something that is vital so that this can be prevented.

There have been many different emotions since we’ve heard this news. Many tears. On one hand it gives us more clarity, understanding that his frontal lobe of the brain was damaged and the lack of impulse control played a part in his act of desperation. But it doesn’t change the outcome, he’s gone. And that hurts so bad. Everyday.

I watched my in-laws say goodbye to their son. No parent should ever have to experience what they did. The pain each time they walk past his childhood bedroom, his stuff that had to sort through, the daily reminders he is gone. The days and holidays that come and remind you that life as you knew it will never be the same. Andrew would have never wanted them to feel this hurt.

Watching my husband, kneeling next to his only brother’s hospital bed, hearing him say his final goodbye is something I never imagined doing when we exchanged vows on our wedding day. To see him so broken, my heart aches for him as he misses his best friend. He used to wake in the middle of the night with images in the hospital that couldn’t leave his mind.

Our kids ask about Andrew all of the time. They say his name often as he was a huge part of our daily life. We open a book to read at bedtime and there is his handwriting on the inside cover, “Jacko-Happy Birthday. I can’t wait to read this to you at bedtime with Luke and Taylor.” They miss him so much.

This picture makes me smile because he came to the hospital the night Taylor was born and ate almost all the candy. Classic Andrew.
This picture makes me smile because he came to the hospital the night Taylor was born and ate almost all the candy. Classic Andrew.

While going through a stack of papers, I can remember finding the plane ticket that he purchased in the early hours of January 20th, holding it in my hand and crying out, “Just go to the gate. Come home.” Don’t let go.

One evening, Chris went over to look through Andrew’s things because he said he needed to find something. He was in Andrew’s old bedroom for awhile and came back empty handed. A few weeks later, he shared what he was looking for. The red Chicago Blackhawks shirt that Andrew wore all of the time. After searching for many minutes for it, his mom came in the room and shared that that was the shirt he was wearing that night and it was cut off of him when he was brought to the hospital. She found that shirt in his bag. Sally had to unpack that bag. Imagine that. Imagine that feeling of unpacking your son’s bag who is now gone. My heart ached. Chris left that night with another painful moment that sneaks up on the journey of grief.

As a family, we’ve all journeyed down this path of grief differently and I’ve realized that it’s never healthy to expect anyone to grieve the same way you do. People grieve in character so to expect everyone to handle a loss the same way is an unrealistic expectation. Avoiding the pain is easier than feeling it, and that has caused this road of grief to be windier and bumpier (and at times feels longer) than we wished we could say we’ve experienced.

Please remember that although a person’s smile may appear on their face, the condition of their heart may tell a different story. I’ve learned in the past year, that trauma affects the whole body and I believe we’d be much more open about the process if it was received with empathy and grace, versus someone’s judgement of the ‘appropriate’ timeline of grief. Sometimes the pieces don’t always get put back together as quickly as you’d assume they should be.

Also, please don’t expect us to move on. When you do, it’s as if we are suppose to do life not acknowledging there is a person that never existed, and a pain we are suppose to ignore. We will move forward because it’s the only choice we have. We choose to honor him and the life he lived.

Andrew was a one-of-a-kind person. He truly lived each day to the fullest. Investing in others, taking time to see and hear people whether they were 70 years old or a baby. Fully devoted to whatever he committed to. Remembering the memories we had with Andrew brings us so much joy. We’ve seen in many ways how God provides for the brokenhearted. There is peace in knowing he knew Jesus and because of that is healthy and whole again. Oh how this would be so much more difficult if he wouldn’t have accepted Christ as his Savior.

A lot of laughter comes from the memories from others and that helps heal our hearts. Please don’t hesitate to share your moment with us. One of his former teammates created a website to compile some memories of AC and you can read them here. Some of them are of his weird and crazy pre game routines and also a bet of running a sub 6 minute mile after a 5 course meal. The kid won the bet, of course. Here is a memory that means so much to us and truly exemplifies who he was.

“Selfless, encouraging, enthusiastic, courageous....these are just a few of the many traits Andrew Carroll possessed and practiced on a daily basis. I remember meeting Andrew in the locker room in Hartford, CT when we were teammates and line mates on the Connecticut Whale. One of the first things he told me when we were going to play together on the same line was "don'tworry about anything, I am always going to be the first one on the forecheck and going to try to get you the puck as fast as I can." I'm thinking to myself, "now this is my kind of winger!" Come to find out I think he just loved to forecheck and throw his body around in the form of playing physical and checking someone into the boards! But that's honestly how Andrew lived his life day in day out, selflessly putting himself out there for the benefit of others, whether on the rink or outside in his daily life. He was one of the most genuine human beings I have ever met in my life. I am not saying that just for this story or some sort of tribute to him...that is literally the truth about him. He exemplified what it meant to be a genuine, God seeking, God loving man. He lived it! Every single day! Who can say that they do that!?”

So we move forward with this new news and I kept remembering Chris’ tribute to Andrew at his funeral:

“But, regardless of how our hearts are marked by life’s events…what truly makes who we are… is our response…because that is what we can control. My response and outlook as I move forward is based on the questions I have been asking myself.

Not why or how?

But simply asking myself, what?

What can I do to honor my brother?

What can I do to carry out his legacy?

What can I do that can make me stronger, kinder, more patient?

What can I do to be mentally tough…yet also be mentally healthy?

This will not only help me grieve, but strengthen my response and mend my heart into what MAKES me.

Those simple questions, in the face of some really tough stuff will make me who I am.

I know I need to wake up each day and ask the right questions of myself. Because that’s the only thing that will carry my brother’s legacy.

And my response matters. Quite possibly, our greatest contribution in our response may not be something that I do, but rather, who may witness it. Our influence is far more powerful than any position that we hold and…this isn’t just about me.

Look at this room filled with so many people. That's a reflection of Andrew’s influence on all of us. He saw each of you. He made you feel important, and took the time to do that. May we all honor him by doing that more.

As I close, I want to share one last thing with my brother, something that I didn’t share enough….

I was out on a run early in the morning while we were in Chicago and the one thing that gave my heart peace was that I am so proud of you.

I am so proud that I am your brother, that there is only one person in this room that can call you brother. And that's me.

And I can’t even describe how proud that makes me.

THANK YOU FOR MAKING ME BETTER.”

On May 7th, it would have been his 34th birthday. There are many simple things you can do to celebrate him. Take extra time to listen to someone, and ask them questions about their life. Show up late because you were investing in someone. Wear your AC20 gear (email (carissa@jacksbasket.org), text, or call us if you need some!) and tell one person about him. Open your bible and read his life verse, Joshua 1:9, and write down what you are going to do to be strong and courageous in honor of AC and his love for Jesus.

On Sunday, May 5th, the plan is to be in the backyard on the AC20 sport court where we will be doing ‘AC Skills and Drills, so come on over with your families (stay for a little or stay as long as Andrew would have ) and help us celebrate the guy we all love and miss so much! Reach out to Chris or I, Bill or Sally, and we will give you more details! He’ll be smiling (and chirping) from Heaven.


Finally, please go tell someone how much you love them. Tell them why they matter to you. If it’s not you to verbally express it, write in a card or note. Send it. You will never regret telling someone how much they meant to you. People need to hear more often.

You make me better.

If you are hurting and need some help, please tell someone. No matter the story you are telling yourself, you are loved by God and loved by those around you. Tomorrow needs YOU. Don’t let go.

Call the suicide prevention line at 1-800-273-8255 for help.

As we navigate down this path, we will continue to talk about how we will honor him. We have set up an Andrew Carroll Memorial Fund so that his life continues to impact others as he did when he was living. Organizations that were close to Andrew’s heart were Hockey Ministries International (HMI) and Jack’s Basket, and a gift will be given to a foundation that supports suicide prevention and those impacted by CTE (TBD). If you would like to contribute to the memorial fund click here or send a donation directly to those organizations. We are hopeful that those living with CTE will not find themselves at a point Andrew was when he let go.

Tags Andrew Carroll, Andrew Carroll Dies at 32, CTE, Hockey

https://www.jacksbasket.org/strengthfortheclimb

Study published about former NFL and NHL players in Sept/Oct 2018 Journal of Head Trauma Rehabilitation

Conclusion: None of the retired contact sport athletes qualified as having early-onset dementia consistent with chronic traumatic encephalopathy. There were no remarkable differences in imaging, cognition, behavior, or executive function from noncontact sport athletes. The results underscore an apparent disconnect between public perceptions and evidence-based conclusions about the inevitability of chronic traumatic encephalopathy and the potential neurodegenerative effect on former athletes from contact sports.

https://journals.lww.com/headtraumareha ... _of.9.aspx

Scientists Find New Evidence of What Makes Chronic Traumatic Encephalopathy Unique
The telltale tau proteins present in the disease known as CTE display distinctive features.

SPORTS
Thursday, March 21, 2019 - 10:30

Chris Gorski, Editor


(Inside Science) -- In a study of the brains of three people diagnosed with chronic traumatic encephalopathy, or CTE, researchers have found new details about the disease that could eventually lead to ways to diagnose it earlier and treat it. The researchers say these insights show that the tau proteins found in CTE differ from those found in other neurodegenerative diseases that are also linked to abnormal collections of the same protein.

The disease now known as CTE was first described as "punch drunk syndrome" in the 1920s to capture the mental decline exhibited by some boxers. CTE is associated with repeated exposure to head impacts, such as those experienced by athletes, members of the military and others, and can lead to symptoms such as cognitive impairment, impulsive behavior and suicidal thoughts. In the new study, the researchers analyzed the brains of two boxers and one American football player diagnosed with CTE and found fundamental similarities in the disease across all three cases.

CTE can be diagnosed only after death by examining the brain for a specific pattern of tau proteins. Tau proteins are present in human brains under normal conditions, but they gather in abnormal clumps and tangles in the brains of people who have neurodegenerative diseases such as Alzheimer's and CTE.

The new research, published yesterday in the journal Nature, uses a powerful technique called cryo-electron microscopy to discern minute details, including how the tau proteins found in CTE fold and then twist into narrow structures called filaments -- features smaller than one-ten-millionth of a meter, or just a tiny fraction of the width of a human hair.

"The fact that the structures of these filaments from CTE are different from the Alzheimer's ones is important, I think, because so far that wasn't clear," said Michel Goedert, who has studied tau proteins and neurodegenerative diseases for more than 30 years at the MRC Laboratory of Molecular Biology, in Cambridge, U.K.

The new finding makes the case that Alzheimer's disease and CTE are really fundamentally different diseases, said Lee Goldstein, a researcher at Boston University's CTE Center who was not involved with the new study. "Both result in dementia eventually, but they do so likely by different molecular mechanisms."

Additionally, Goedert and his colleagues found never-before-seen pockets, called inclusions, containing some presently unknown molecules within the tau filaments of brains affected by CTE.

"So far this is the only structure of tau filament from the human brain where you see these inclusions," Goedert said. "We obviously have to figure out what it is."

That knowledge might unlock much more information about the origin of the disease. Goedert said that in CTE, the tau proteins often gather in cells located near blood vessels. It could be, he speculated, that the mystery molecules within the tau filament pocket enter the brain through the blood and induce tau to gather near the blood vessels. Or, he said, an inflammation reaction could cause tau to collect.

The researchers have thus far studied tau proteins from the brains of three people diagnosed with CTE. Goedert said that he would like to investigate proteins from more cases of CTE, but that it is difficult to produce large numbers of images. In recent years it became possible to magnify the tau protein filaments enough to notice the kinds of details revealed in the new study, and the group has published separate studies based on the brains of 19 people with Alzheimer's and nine with Pick's disease, a different affliction that also has abnormal tau proteins.

"One would always like to see more brains. But I'm pretty confident that what they're looking at is representative of the vast majority of CTE cases," said Byron Caughey, a senior investigator at the National Institute of Allergy and Infectious Diseases in Hamilton, Montana, who studies tau-associated diseases and was not involved in the new research. "But, it's a heroic effort just to get to this point."

"In all three cases [of CTE] you see this very unusual molecular pathology, and it's the same in all three. It's pretty damn convincing to me," said Goldstein.

The new research may help neuroscientists build a better understanding of how CTE develops and progresses, which in turn will help them design better ways to test for the disease, and eventually treat it, Goldstein said.

"You can say that it starts taking things out of their infancy," said Goedert.


Author Bio & Story Archive
Chris Gorski

Chris Gorski
Chris Gorski is an Editor for Inside Science and runs the Sports beat. Follow him on twitter at @c_gorski.

Recent study done on high-level rugby players.

Conclusions Despite a high number of concussions in RIRP, differences in mental health, social or work functioning were not found late after injury. Subtle group differences were detected on two cognitive tests, the cause of which is uncertain. Prospective group comparison studies on representative cohorts are required.


https://jnnp.bmj.com/content/88/6/505.long

2019 review from Nature, as high quality of a scientific journal as there is.

Abstract: The term chronic traumatic encephalopathy (CTE) has recently entered public consciousness via media reports and even a Hollywood movie. However, in contrast to general impressions, the incidence of CTE is unknown, the clinical diagnostic criteria have not been agreed upon and the current neuropathological characterization of CTE is acknowledged as preliminary. Additionally, few studies have compared the pathologies of CTE with those of other neurodegenerative disorders or of age-matched controls. Consequently, disagreement continues about the neuropathological aspects that make CTE unique. Furthermore, CTE is widely considered to be a consequence of exposure to repeated head blows, but evidence suggests that a single moderate or severe traumatic brain injury can also induce progressive neuropathological changes. These unresolved aspects of CTE underlie disparate claims about its clinical and pathological features, leading to confusion among the public and health-care professionals alike.

Our View: Results offer sobering reminder
By News Tribune Editorial Board Today at 8:00 p.m.

The sad news that broke Monday, that former Minnesota Duluth men's hockey player Andrew Carroll had Stage One CTE, was a sobering reminder: Hockey can be a rough game, a dangerously rough game — with hard checks into the boards; blows from sticks, pucks, and other players; and falls that aren't always the most graceful onto unforgiving concrete-hard iced surfaces.

Carroll, a captain for parts of all four of his seasons with the Bulldogs, from 2005 to 2009, took his own life in 2018. No one can say for certain CTE is to blame, but chronic traumatic encephalopathy is a neurodegenerative brain disease known to be caused by repeated blows to the head. And it can result in personality changes and behavioral changes. It can't be diagnosed until after death, but its signs include aggression, depression, paranoia, and suicidal thoughts.

Despite high-tech helmets and other protective equipment, former pro football players with early dementia or other ailments continue to grab most of the headlines about CTE and concussions. But CTE also has been found in the brains of former NHL players like Jeff Parker and Derek Boogaard, as well as other athletes.

Carroll's family sent his brain to Boston University for study following his death. They received word last week that Stage One CTE was detected, as KSTP-TV in the Twin Cities reported Monday.

The family hopes his death can help raise awareness and promote research and possible prevention of the disease. We all can join them in that wish, as well as in their grief, whether we're hockey fans or not.

"I think it would be honoring to my brother for sure," Andrew's brother Chris Carroll, a high school hockey coach, said in an interview with KSTP. "Knowing it will certainly impact how you see the game moving forward. In your mind and my heart right now, it will certainly change things."

Hockey can join football and other contact sports in considering and in working always to prevent the damage that can be done by the violence of their games. No more reminders of that are necessary.

https://www.duluthnewstribune.com/opini ... g-reminder

Traumatic Brain Injury


Traumatic brain injury (TBI) results from an impact to the head that disrupts normal brain function. Traumatic brain injury may affect a person’s cognitive abilities, including learning and thinking skills.

About
Diagnosis
Prevalence
Outcomes
Causes and risk factors
Treatment
Symptoms


About traumatic brain injury
The leading causes of TBI that resulted in emergency department visits were falls, being struck by an object and motor vehicle crashes. Indirect forces that jolt the brain violently within the skull, such as shock waves from battlefield explosions, can also cause traumatic brain injury. In addition, traumatic brain injury can result from bullet wounds or other injuries that penetrate the skull and brain.

Doctors classify traumatic brain injury as mild, moderate or severe, depending on whether the injury causes unconsciousness, how long unconsciousness lasts and the severity of symptoms. Although most traumatic brain injuries are classified as mild because they're not life-threatening, even a mild traumatic brain injury can have serious and long-lasting effects.

Resulting from an impact to the head that disrupts normal brain function, traumatic brain injury is a threat to cognitive health in two ways:

A traumatic brain injury's direct effects — which may be long-lasting or even permanent — can include unconsciousness, inability to recall the traumatic event, confusion, difficulty learning and remembering new information, trouble speaking coherently, unsteadiness, lack of coordination, and problems with vision or hearing.
Certain types of traumatic brain injury may increase the risk of developing Alzheimer's or another type of dementia years after the injury takes place.
​
If a head injury occurs
Traumatic brain injury injures your brain even if you don’t lose consciousness and your symptoms clear up quickly. Anyone who experiences an impact to the head and develops any symptoms of traumatic brain injury should seek medical attention, even if symptoms seem mild. Call emergency services for anyone who’s unconscious for more than a minute or two, or who experiences seizures, repeated vomiting or symptoms that seem to worsen as time passes. Seek emergency care for anyone whose head was injured during ejection from a vehicle, who was struck by a vehicle while on foot or who fell from a height of more than three feet.


Prevalence
According to the Centers for Disease Control and Prevention (CDC), approximately 2.8 million TBI-related emergency department visits, hospitalizations and deaths occurred in 2013, the latest year for which information is available.


Causes and risk factors

Preventing traumatic brain injury
Falls are the most common cause of traumatic brain injury, and falling poses an especially serious risk for older adults. According to a CDC special report analyzing data from several federal agencies, each year 56,000 seniors are hospitalized as a result of head injuries sustained in falls and 8,000 die as a result. When a senior sustains a serious traumatic brain injury in a fall, direct effects of the injury may result in long-term cognitive changes, reduced ability to function and changes in emotional health.

An estimated 775,000 older adults are living with traumatic brain injury-related disability. Measures to reduce the risk of falls include:

Home safety and dementia

Use our online tool, Alzheimer's Navigator®, and get a personalized action list on how to prevent falls and make your home safe for someone with dementia.

Using a walker or other assistive device to compensate for mobility problems, muscle weakness or poor balance.
Having your vision checked regularly and using glasses or contact lenses that correct for changes.
Working with your doctor to watch for medication side effects or interactions among drugs you’re taking.
Avoiding household hazards, such as clutter, loose rugs or poor lighting.

Motor vehicle crashes are another common cause of traumatic brain injury. You can reduce your risk by keeping your vehicle in good repair, following the rules of the road and buckling your seat belt. You can also protect your head by wearing a helmet and other protective equipment when biking, inline skating or playing contact sports.


Dementia and traumatic brain injury
Over the past 30 years, research has linked moderate and severe traumatic brain injury to a greater risk of developing Alzheimer's disease or another dementia years after the original head injury.

One of the key studies showing an increased risk found that older adults with a history of moderate traumatic brain injury had a 2.3 times greater risk of developing Alzheimer's than seniors with no history of head injury, and those with a history of severe traumatic brain injury had a 4.5 times greater risk. Other studies — but not all — have found a link between moderate and severe traumatic brain injury and elevated risk.
There’s no evidence that a single mild traumatic brain injury increases dementia risk. However, emerging evidence does suggest that repeated mild traumatic brain injuries, such as those that can occur in sports like American football, boxing, hockey and soccer, may be linked to a greater risk of chronic traumatic encephalopathy (CTE), a form of dementia.
Previous research has shown that boxers have an increased risk of CTE, which was originally called dementia pugilistica or “punch-drunk syndrome.” The risk of CTE in boxers seems most closely tied to the number of rounds boxed, not to the number of times a boxer was knocked out, suggesting that even repeated mild traumatic brain injuries that don’t cause unconsciousness may increase dementia risk. Researchers don’t yet know whether CTE is most likely to occur following a small number of severe traumatic brain injuries, a large number of mild or very mild traumatic brain injuries, or some other pattern of head trauma. The symptoms of CTE may include memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, anxiety, suicidality, parkinsonism (movement symptoms similar to Parkinson's disease), and, eventually, progressive dementia. These symptoms may begin years or even decades after the last traumatic brain injury.
A study published in the March 23, 2016, online edition of the Journal of Neurology found that a history of traumatic brain injury may accelerate the age of onset of cognitive impairment by two or more years. These results were consistent with other studies that indicate traumatic brain injury is a significant risk factor for cognitive decline in older adults and associated with an earlier age of onset in people with mild cognitive impairment and Alzheimer’s disease.
Another study conducted by researchers at Umeå University in Sweden confirmed traumatic brain injury as a risk factor for dementia and revealed that the risk of a dementia diagnosis was highest during the first year after the injury. During this time, people who had a traumatic brain injury were four to six times as likely to get a dementia diagnosis as those without a traumatic brain injury. The study, published in PLOS Medical Journal on January 30, 2018, also concluded that a concussion or other traumatic brain injury can increase the risk of developing dementia even 30 years later.
More research is needed to fully understand the relationship between traumatic brain injury and dementia and to understand why moderate, severe and repeated mild traumatic brain injuries are at an increased risk. Current research on how traumatic brain injury changes brain chemistry indicates a relationship between traumatic brain injury and hallmark protein abnormalities linked to Alzheimer’s. Within hours after injury, severe traumatic brain injury has been shown to increase levels of beta-amyloid, one hallmark Alzheimer’s protein. And CTE, the dementia linked to repeated mild traumatic brain injury, appears to be most strongly characterized by deposits of tau protein, another Alzheimer’s hallmark. Beta-amyloid deposits are also found in some individuals with CTE.
Some research suggests that traumatic brain injury may be more likely to cause dementia in individuals who have a variation of the gene for apolipoprotein E (APOE) called APOE-e4. More research is needed to understand the strength of the link between APOE-e4 and dementia risk in those who’ve had a traumatic brain injury.
Does every hit to the head lead to dementia?
Not everyone who experiences a head injury develops dementia. There’s no evidence that a single mild traumatic brain injury increases dementia risk. Although there’s no known strategy to reduce the possible long-term risk of dementia once you’ve experienced a moderate or severe traumatic brain injury, or repeated mild traumatic brain injuries, it’s important to understand that not everyone who experiences a head injury in one of these categories develops dementia. More research is needed to confirm the possible link between brain injury and dementia and to understand why moderate, severe and repeated mild traumatic brain injuries may increase risk.


Symptoms
The severity of symptoms depends on whether the injury is mild, moderate or severe.

Mild traumatic brain injury, also known as a concussion, either doesn’t cause unconsciousness or unconsciousness lasts for 30 minutes or less. Mild traumatic brain injury symptoms may include:

Inability to remember the cause of the injury or events that occurred immediately before or up to 24 hours after it happened.
Confusion and disorientation.
Difficulty remembering new information.
Headache.
Dizziness.
Blurry vision.
Nausea and vomiting.
Ringing in the ears.
Trouble speaking coherently.
Changes in emotions or sleep patterns.
These symptoms often appear at the time of the injury or soon after, but sometimes may not develop for days or weeks. Mild traumatic brain injury symptoms are usually temporary and clear up within hours, days or weeks; however, on occasion, they can last months or longer.

Moderate traumatic brain injury causes unconsciousness lasting more than 30 minutes but less than 24 hours, and severe traumatic brain injury causes unconsciousness for more than 24 hours. Symptoms of moderate and severe traumatic brain injury are similar to those of mild traumatic brain injury, but more serious and longer-lasting.

In all forms of traumatic brain injury, cognitive changes are among the most common, disabling and long-lasting symptoms that can result directly from the injury. The ability to learn and remember new information is often affected. Other commonly affected cognitive skills include the capacity to pay attention, organize thoughts, plan effective strategies for completing tasks and activities, and make sound judgments. More severe changes in thinking skills — a hallmark characteristic of dementia — may develop years after the injury took place and the person appears to have recovered from its immediate effects.


Diagnosis
Evaluations by health care professionals typically include:

Questions about the circumstances of the injury.
Assessment of the person's level of consciousness and confusion.
Neurological examination to assess memory and thinking, vision, hearing, touch, balance, reflexes, and other indicators of brain function.
Let your physician know if you are taking medications (prescription, over-the-counter or “natural remedies”), especially blood thinners such as Coumadin and aspirin, because they can increase the chance of complications. Also inform your health care professional if you drink alcohol or take illicit drugs.

Depending on the cause of the traumatic brain injury and the severity of symptoms, brain imaging with computed tomography (CT) may be needed to determine if there’s bleeding or swelling in the brain. If you experience a traumatic brain injury, it should be noted in your permanent medical record and mentioned whenever familiarizing a new doctor with your medical history.

Outcomes
Alzheimer’s disease and other dementias that may occur as a long-term result of traumatic brain injury are progressive disorders that worsen over time. As with all dementias, they affect quality of life, shorten life span and complicate the effort to manage other health conditions effectively.


Treatment
The most serious traumatic brain injuries require specialized hospital care and can require months of inpatient rehabilitation. Most traumatic brain injuries are mild and can be managed with either a short hospital stay for observation or at-home monitoring followed by outpatient rehab, if needed.

Treatment of dementia in a person with a history of traumatic brain injuries varies depending on the type of dementia diagnosed. Strategies for treating Alzheimer's or another specific type of dementia are the same for individuals with and without a history of traumatic brain injury.

Alzheimer's disease and other dementias that may occur as a long-term result of traumatic brain injury are progressive disorders that worsen over time. As with all dementias, they affect quality of life, shorten lifespan and complicate the effort to manage other health conditions effectively. However, because CTE is a relatively new area of exploration for researchers and physicians, formal clinical guidelines for diagnosing and managing this condition do not yet exist. Several major research initiatives are under way to gain further insight into the patterns of injury and brain changes that may be implicated in CTE, and to develop new strategies for prevention, diagnosis and treatment.

Learn more: Treatment for Dementia, Treatment for Alzheimer's

Dementia help and support are available
The Alzheimer's Association can help you learn more about Alzheimer's and other dementias, and help you find local support services. Call our 24/7 Helpline at 800.272.3900.

Brain Injury Association of America (BIA) is an education, advocacy and research organization that offers support to people with brain injuries and their families. Call their information center at 800.444.6443.

Centers for Disease Control (CDC) has a traumatic brain injury section that offers information about research studies and prevention and education programs.

The Concussion Legacy Foundation provides chronic traumatic encephalopathy (CTE) information and resources.

Supporting traumatic brain injury research, the National Institute of Neurological Disorders and Stroke (NINDS) has a traumatic brain injury section that offers information about treatment, clinical trials and resources.



https://www.alz.org/alzheimers-dementia ... ain-injury

To see pictures use link at the end of article

Frequently Asked Questions about CTE

What is CTE?

Chronic Traumatic Encephalopathy (CTE) is a progressive degenerative disease of the brain found in people with a history of repetitive brain trauma (often athletes), including symptomatic concussions as well as asymptomatic subconcussive hits to the head that do not cause symptoms. CTE has been known to affect boxers since the 1920’s (when it was initially termed punch drunk syndrome or dementia pugilistica).
In recent years, reports have been published of neuropathologically confirmed CTE found in other athletes, including football and hockey players (playing and retired), as well as in military veterans who have a history of repetitive brain trauma. CTE is not limited to current professional athletes; it has also been found in athletes who did not play sports after high school or college.
The repeated brain trauma triggers progressive degeneration of the brain tissue, including the build-up of an abnormal protein called tau. These changes in the brain can begin months, years, or even decades after the last brain trauma or end of active athletic involvement. The brain degeneration is associated with common symptoms of CTE including memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, suicidality, parkinsonism, and eventually progressive dementia.
In both sets of photographs below, the brain tissue has been immunostained for tau protein, which appears as a dark brown color. Tau immunostained sections of medial temporal lobe from 3 individuals:

How do you get CTE? Can I get CTE from one concussion/hit to the head?
We believe CTE is caused by repetitive brain trauma. This trauma includes both concussions that cause symptoms and subconcussive hits to the head that cause no symptoms. At this time the number or type of hits to the head needed to trigger degenerative changes of the brain is unknown. In addition, it is likely that other factors, such as genetics, may play a role in the development of CTE, as not everyone with a history of repeated brain trauma develops this disease. However, these other factors are not yet understood.

What is a concussion?

A concussion has occurred any time you have had a blow to the head that caused you to have symptoms for any amount of time. You do NOT need to have lost consciousness to have a concussion. These symptoms include blurred or double vision, seeing stars, sensitivity to light or noise, headache, dizziness or balance problems, nausea, vomiting, trouble sleeping, fatigue, confusion, difficulty remembering, difficulty concentrating, or loss of consciousness. A concussion has also occurred when a person gets a “ding” or gets their “bell rung.”

What are the symptoms of CTE?

The symptoms of CTE include memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, anxiety, suicidality, parkinsonism, and, eventually, progressive dementia. These symptoms often begin years or even decades after the last brain trauma or end of active athletic involvement.

I recently had a concussion, and I am suffering from a number of the symptoms
listed above. Do I have CTE?

The symptoms of CTE generally do not present until years or decades after the brain trauma occurred or after one stops actively playing contact sports. While most concussion symptoms resolve within a few weeks, the symptoms can last for months or, in severe cases, even years. When this occurs, it is called post-concussion syndrome. Post-concussion syndrome is different than CTE, and the symptoms of post-concussive syndrome usually resolve years or decades before the onset of CTE symptoms. If you believe you are suffering from either an acute concussion or post-concussion syndrome, contact your physician. For more information on concussions, visit the Concussion Legacy Foundation’s Concussion Resources. For more information on physicians in your area who work with those suffering from brain trauma, please use the Concussion Clinics search tool.
If I have the symptoms of CTE, do I have the disease itself?
Just because you have some or many of the symptoms of CTE does not necessarily mean that you have the disease itself. There are many possible causes of these types of symptoms. If you are having difficulties, you should speak with your primary care or specialist physician.

How is CTE diagnosed?

At this time CTE can only be diagnosed after death by postmortem neuropathological analysis. Right now there is no known way to use MRI, CT, or other brain imaging methods to diagnose CTE. The CTE Center is actively conducting research aimed at learning how to diagnose CTE during life. Find out more about our research here.

Can I be evaluated at the BU CTE Center?

The BU CTE Center is a research group. At this point in time we do not offer clinical services. The best first step, if you are seeking clinical evaluation, is to speak to your primary care physician. For more information on physicians in your area who work with those suffering from brain trauma, please use the Concussion Clinics search tool.

Can you refer me to a doctor?

Unfortunately, as a small research group, the CTE Center is unable to keep a comprehensive list of doctors across the country who are familiar with brain injury and related issues. For more information on physicians in your area who work with those suffering from brain trauma, please use the Concussion Clinics search tool.

Can CTE be cured? What can I do if I think I have CTE?

Unfortunately, at this time there is no cure for CTE. However, the CTE Center is currently conducting ongoing clinical research aimed at discovering how CTE develops and progresses, risk factors for the development of the disease, and how to diagnose the disease during life. The symptoms of CTE, such as depression and anxiety, can be treated individually. If you believe you or a loved one may have CTE, please read through the Living with CTE page and talk with your physician. For more information on physicians in your area who work with those suffering from brain trauma, please use the Concussion Clinics search tool.
What’s the difference between CTE and Alzheimer’s Disease (AD)?
Although there are some similarities between CTE and Alzheimer’s Disease (AD), significant differences exist. The symptoms of CTE generally present earlier (in one’s 40s) than those of AD (in one’s 60s). The initial and most central symptoms in AD involve memory problems, while the first symptoms of CTE generally involve problems with judgment, reasoning, problem solving, impulse control, and aggression. In addition, these diseases are found to be different in postmortem neuropathological findings.

What can I do to help/how can I become involved in research?

For more information on the CTE Center’s current clinical research, check out our LEGEND study. The CTE Center also has a brain bank that studies postmortem brain and spinal cord tissue to better understand the effects of repeated brain trauma. Current and former athletes and military personnel of all ages and levels may be eligible to pledge to donate their brain (added link to pledge) and spinal cord to the BU CTE Center after death. Being a brain donor is similar to being an organ donor, and the procedure is done in such a way that the donor may have an open casket if desired. BU CTE Center personnel understand that this is a difficult time for the family of the donor, and they work hard to make the donation process as easy as possible for the family. For more information visit our Brain Donation Registry.
Do I have to be a high level amateur or professional athlete to participate in your research?
No. The CTE Center welcomes athletes of all sports and levels to participate in our research. Although some studies are restricted to specific sports and levels, other studies are open to anyone with a history of participation in organized sports or military service.
Can I participate in the Brain Donation Registry?
If you have a history of participation in organized sports and/or a history of participation in the military, you may be eligible to participate in the brain donation registry. For more information, please contact the Brain Donation Registry coordinator Madeline Uretsky by phone at 617-358-6027 or by email at muretsky@bu.edu.
For questions regarding your Brain Donation Registry Card, please contact Kelly Dean of the Concussion Legacy Foundation at 857-244-0810 or KDEAN@CONCUSSIONFOUNDATION.ORG
Can I participate in the LEGEND study?
If you have a history of participation in organized sports, you may be eligible to participate in the LEGEND study. For more information, please contact the LEGEND study coordinator by email, LEGEND@bu.edu.

http://www.bu.edu/cte/about/frequently-asked-questions/

Tau Positron-Emission Tomography in Former National Football League Players


Robert A. Stern, Ph.D., Charles H. Adler, M.D., Ph.D., Kewei Chen, Ph.D., Michael Navitsky, M.S., Ji Luo, M.S., David W. Dodick, M.D., Michael L. Alosco, Ph.D., Yorghos Tripodis, Ph.D., Dhruman D. Goradia, Ph.D., Brett Martin, M.S., Diego Mastroeni, Ph.D., Nathan G. Fritts, B.A., et al.
Abstract
BACKGROUND
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that has been associated with a history of repetitive head impacts. The neuropathological diagnosis is based on a specific pattern of tau deposition with minimal amyloid-beta deposition that differs from other disorders, including Alzheimer’s disease. The feasibility of detecting tau and amyloid deposition in the brains of living persons at risk for CTE has not been well studied.

METHODS
We used flortaucipir positron-emission tomography (PET) and florbetapir PET to measure deposition of tau and amyloid-beta, respectively, in the brains of former National Football League (NFL) players with cognitive and neuropsychiatric symptoms and in asymptomatic men with no history of traumatic brain injury. Automated image-analysis algorithms were used to compare the regional tau standardized uptake value ratio (SUVR, the ratio of radioactivity in a cerebral region to that in the cerebellum as a reference) between the two groups and to explore the associations of SUVR with symptom severity and with years of football play in the former-player group.

RESULTS
A total of 26 former players and 31 controls were included in the analysis. The mean flortaucipir SUVR was higher among former players than among controls in three regions of the brain: bilateral superior frontal (1.09 vs. 0.98; adjusted mean difference, 0.13; 95% confidence interval [CI], 0.06 to 0.20; P<0.001), bilateral medial temporal (1.23 vs. 1.12; adjusted mean difference, 0.13; 95% CI, 0.05 to 0.21; P<0.001), and left parietal (1.12 vs. 1.01; adjusted mean difference, 0.12; 95% CI, 0.05 to 0.20; P=0.002). In exploratory analyses, the correlation coefficients in these three regions between the SUVRs and years of play were 0.58 (95% CI, 0.25 to 0.79), 0.45 (95% CI, 0.07 to 0.71), and 0.50 (95% CI, 0.14 to 0.74), respectively. There was no association between tau deposition and scores on cognitive and neuropsychiatric tests. Only one former player had levels of amyloid-beta deposition similar to those in persons with Alzheimer’s disease.

CONCLUSIONS
A group of living former NFL players with cognitive and neuropsychiatric symptoms had higher tau levels measured by PET than controls in brain regions that are affected by CTE and did not have elevated amyloid-beta levels. Further studies are needed to determine whether elevated CTE-associated tau can be detected in individual persons. (Funded by Avid Radiopharmaceuticals and others.)

Supported by an investigator-initiated grant from Avid Radiopharmaceuticals (a wholly owned subsidiary of Eli Lilly) to Boston University and by grants from the National Institutes of Health (R01NS078337, U19AG024904, 1UL1TR001430, U01NS093334, P30AG19610, and P30AG13846), the State of Arizona, and the Department of Defense (W81XWH-13-2-0063, W81XWH-13-2-0064, and W81XWH-14-1-0462). All flortaucipir and florbetapir PET radiotracers were provided by Avid Radiopharmaceuticals.

Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.

This article was published on April 10, 2019, at NEJM.org.

A data sharing statement provided by the authors is available with the full text of this article at NEJM.org.

We thank the participants and investigators who participated in this study; Robert Bauer, Yinghua Chen, and Vivek Devadas for their assistance in the analysis of PET data; Amy Duffy for participant recruitment and assessments at Mayo Clinic Arizona; Alicia Chua for assistance with data analysis and the production of the figures; and Gustavo Mercier for acquisition of PET data at the Boston University Medical Campus.

Author Affiliations
From the Boston University School of Medicine (R.A.S., M.L.A., N.G.F., J.J.), Boston University School of Public Health (Y.T., B.M.), Brigham and Women’s Hospital (M.E.S.), Harvard Medical School (M.E.S.), and the Veterans Affairs Boston Healthcare System (M.E.S.) — all in Boston; Mayo Clinic Arizona, Scottsdale (C.H.A., D.W.D.), Banner Alzheimer’s Institute, Phoenix (K.C., J.L., D.D.G., E.M.R.), and Arizona State University, Tempe (D.M.) — all in Arizona; and Avid Radiopharmaceuticals, Philadelphia (M.N., M.D.D., M.A.M., M.J.P.).

Address reprint requests to Dr. Stern at Boston University Alzheimer’s Disease Center, Boston University School of Medicine, 72 E. Concord St., B-7800, Boston, MA 02118, or at bobstern@bu.edu.


April 10, 2019
DOI: 10.1056/NEJMoa1900757



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https://www.youtube.com/watch?v=O61V_x7hy-k

"Zarley Zalapski's story shows CTE isn't black and white."
https://www.theglobeandmail.com/sports/ ... and-white/

-September 9th, 2018

Something didn’t add up for Kyla Zalapski. Her older brother Zarley, a former NHL defenceman who played for Canada at the 1988 Winter Olympics, was no longer a picture of health. There were dark circles under his eyes and he had uncharacteristically put on weight. Never the most talkative guy, he had become even more withdrawn. He was lethargic and spoke of feeling “foggy.”

On the day before he died last December, Zalapski underwent a check-up in Calgary at Foothills Medical Centre’s cardiac function clinic for viral myocarditis, an inflammation of the heart muscle that had hospitalized him for almost three weeks last October. A clinic nurse told Kyla her brother was in good spirits. He had slowly been working his way back and had become an active member of the Calgary Flames’ alumni.

Then, that night, Zalapski went to sleep and never woke up. The cause of death was eventually diagnosed as a hemorrhagic stroke, the result of a blood clot from his faulty heart. He was 49.

Kyla wanted to know if Zarley had any other health issues lurking in his brain. She was aware he had suffered at least two concussions in his 12-year NHL career, but unsure if he had ever missed a game because of one. To check all possibilities, she had his brain sent to Toronto to be examined. When the results came back from neuropathologist Dr. Lili-Naz Hazrati, it was more than Kyla expected.

An occasional fighter, but hardly one of the game’s physical players, Zarley Zalapski had Chronic Traumatic Encephalopathy (CTE). Not only that, he had more tau (abnormal brain protein) than what was found in another former NHL defenceman, Steve Montador, who died three years ago at age 35.

That might have closed matters for some people, but not Kyla, who says the science on CTE is not always cut and dried. And her doubts are echoed by many in the scientific-research community.

“Concussions and the neurological damage from concussions are real and we need to find better ways to prevent and treat them,” says Kyla, who flew to Toronto and spent six hours with Hazrati going over Zarley’s results and learning everything she could about them. “We also know CTE is a collection of tau. But that’s as far as science takes us … so much more research is needed before we can jump to conclusions.”

Researchers and experts have continuously examined CTE after Dr. Bennet Omalu found it for the first time in a former NFL player 16 years ago. The possibility that concussions or the newly labelled “sub-concussive hits” lead to CTE was given added clout when Boston University’s CTE Center announced last year that it had located CTE in all but one of 111 brains belonging to former NFLers. The findings sent shock waves around the continent and had some calling for a ban on youth football.

And yet dozens of papers published yearly in North American medical journals offer differing observations or call for more data before stoking fears that what has happened in the NFL can be extrapolated into the general population. Loyola University neuropsychologist Christopher Randolph, a CTE skeptic, wrote it was important to specify that BU’s 111 brains were “a sample of convenience, consisting of brains donated by family members who were concerned about pre-mortem behavioral and/or cognitive changes. Little attention has been paid to the fact that the majority of these brains contain evidence of known neurodegenerative disorders.” Randolph’s article was published in July under the title “CTE is not a real disease.” He has been roundly criticized for suggesting that.

The significance of the Zalapski discovery is that it underscores how large the divide remains between what we know about CTE and what we don’t. There are brain specialists who say there is no scientific correlation between concussions and tau and no scientific way to connect the CTE pattern of tau to clinical symptoms such as depression and suicide. It’s also uncertain how, or if, CTE is influenced by genetics, pre-existing conditions, environmental factors, drug and alcohol usage and mere aging.

Hazrati, who has performed autopsies on hundreds of brains in her career, has added to the debate with some curious discoveries. She found CTE in the brain of a man who never suffered a head injury and did not play contact sports, said to be the first known case of its kind. Conversely, she did not find CTE in the brain of John Forzani, the former Calgary Stampeders’ offensive lineman who played seven seasons in the CFL and suffered more than one concussion.

Hazrati has tried to allay worries that anyone who experiences a concussion is at risk of having CTE. In a paper she co-authored with Nicole Schwab, Hazrati noted that the “commonly cited case series studying CTE are limited by methodological biases, pathological inconsistencies, insufficient clinical data, and a reliance on inherently biased postmortem data.”

“This is not a black-and-white issue,” Hazrati says from her office at the Hospital for Sick Children in Toronto. “The tool – CTE – that I’m supposed to use to make a diagnosis of a disease is still not very evolved. We have much more work to do.”

Zarley Zalapski, born in Edmonton, was selected by the Pittsburgh Penguins with the No. 4 pick in the 1986 NHL draft. He built a reputation as a minute-muncher. At 6 foot 1 and 215 pounds, his fitness level and calm under pressure allowed him to eat up a lot of ice time most every night. He was a strong skater with a flair for jumping into the offensive play. As for fighting, he tried to avoid it for a simple reason – “you can’t score from the penalty box,” he told his family.

Zalapski scored 99 goals and recorded 285 assists in the NHL. He also played overseas for several seasons before retiring in 2010.

The defenceman’s problems became noticeable to his family during his playing years with the Flames, from 1993-94 to 1997-98. A non-drinker, non-smoker and non-drug user, Zalapski saw a number of holistic doctors in an effort to snap out of his doldrums. He had the amalgam fillings replaced in his teeth. He opened a health-food store and underwent vitamin therapy. He was diagnosed with chronic fatigue and had a number of food allergies.

“It was an evolution of things,” says Kyla, herself a former competitive athlete who owns and operates a Calgary fitness club. ”He wasn’t somebody you could ask, ‘Are you okay?’ It was very difficult to have that conversation with him.”

Well before Zarley’s death, Kyla was looking for information on athletes adjusting to retirement and how it plays on their mental health. One of the people she contacted was Merril Hoge, the former NFL running back and ESPN analyst who had retired from pro football because of too many head injuries. His last, in a 1994 game with the Chicago Bears, almost killed him. He was revived after his heart stopped beating for 10 seconds. Five years prior, Hoge was a Pittsburgh Steeler when Zalapski was a Pittsburgh Penguin. The two were part of a civic helmet-safety campaign and posed for photos.

“Kyla reached out to me because Zarley was struggling with his transition from hockey life to life’s work,” Hoge says. “In the interim, he passes. Well, because of this hysteria about CTE, right away people are going to think CTE killed him. CTE has never killed a soul. The paranoia of it, you can argue has.”

Dread and self-diagnosis have proved to be a dangerous combination. Several athletes, from the NFL to the NHL, have killed themselves suspecting they not only had CTE but were doomed because of it. Their deaths left families and friends asking heartfelt questions – why and how did it happen? Montador’s family is still planning to move ahead with a lawsuit against the NHL, claiming the league concealed information concerning concussions and their long-term effects.

In searching for answers to her brother’s death, Kyla Zalapski was told by Hoge she should talk with Dr. Peter Cummings. A neuropathologist and BU associate professor who earned his Master’s degree in pathology at Dalhousie University, Cummings is a strong advocate of saving kids from concussions and the possibility of head trauma. He went about protecting his 12-year-old son by not even allowing football to be shown on television for fear he’d want to play it.

His son was ultimately introduced to football via a video game and was determined to play for real. Cummings decided to do his homework. He was encouraged to see how rule changes – such as having as few as six players on the field per side instead of 11, limiting player contact and removing punts and kickoffs – had improved safety. He then read the science behind CTE and was perturbed at how incomplete the picture was.

“Nobody really knows much about it,” Cummings says. “To think we have CTE solved in a nice, wrapped little box in the space of four, five years doesn’t make any sense.”

Cummings, who now coaches youth football, is at odds with the way CTE is treated in the mainstream and social media. Given the speed at which today’s news travels, and the limitations of our attention span, “nobody has the time to go and read the actual [research] paper,” he points out. “This is where the information age, especially Twitter, can be a dangerous place. There is such a huge discrepancy between what the science is saying and what the headlines are saying that it terrifies me as a parent, doctor and coach.

“The worst part,” Cummings adds, “is anyone who dares speak out against this is labelled a ‘denier, a flat-worlder’ or worse. This is science, and science should always be questioned freely and openly. That’s not happening here.”

Kyla Zalapski insists she is neither pro- nor anti-CTE, nor is she in this pursuit for any financial gain. Her intent is to better separate fiction from fact so that the exact information can assist others.

“I feel I owe it to my brother and all the other people struggling to find answers to ask the right questions and to stand up even when my voice may be unpopular with some,” she says. “Zarley was a principled player and a principled man. He didn’t follow the crowd, he stood up for what he believed was right and he always sought the truth. I plan to take his lead and do the same.”

Currently CTE can only being diagnosed by cadaver brains.

Unfortunately that makes the science somewhat limiting. CTE in Iraq and Afghanistan veterans is, again unfortunately, the group easiest to study. Hopefully we can, like in the aftermath of every war, further the science of medicine.

Merril Hoge, co-author of new book are way off target in discussing football, CTE
Christine Brennan, USA TODAYPublished 6:28 p.m. ET Oct. 24, 2018 | Updated 6:29 p.m. ET Oct. 24, 2018

SportsPulse: USA TODAY Sports' Nancy Armour says that Tyler Hilinski's autopsy makes one thing clear: CTE, and therefore football, is what led to the promising young Washington State quarterback's suicide. USA TODAY Sports

The national conversation about sports, head trauma, concussions and CTE took a curious turn this week. An op-ed written by the co-authors of a new book with the provocative title “Brainwashed: The Bad Science Behind CTE and the Plot to Destroy Football” debunks the ground-breaking work of Dr. Ann McKee at Boston University and chastises the news media for picking on football as a cause of CTE.
Ask the authors who’s behind this plot to destroy our most popular game, as I did in a phone interview Wednesday, and there’s no clear answer. It took several tries before co-author Merril Hoge, a former NFL player and ESPN analyst, mentioned “the headlines…the New York Times…Concussion Legacy (Foundation)…Boston University.”
So far this season, the NFL appears to be having a resurgence in interest and TV ratings, so as plots go, this one doesn’t seem to be working very well. When presented with that information, Hoge said it’s more about youth football, trying to destroy that.
One might look at it another way, as seeing concerned parents reassessing their children’s sports preferences, with more emphasis on avoiding head injuries and other serious problems not only in football, but in all kinds of youth sports, including soccer, ice hockey and basketball.

The plot twists can come quickly in this saga. Hoge is an interesting pitchman for the “let’s not come down too hard on football” crowd, considering he was forced to retire from the game after two concussions.

More: Researchers close in on CTE diagnosis in living, one brain at a time
More: NFL had 'intervention' with seven teams on concussion rates

NEWSLETTERS
And he and co-author Peter Cummings, an assistant professor of anatomy and neurobiology with the Boston University School of Medicine who has also written a book titled “The Neuropathology of Zombies,” employ an unorthodox way of making their case.
Well into our nearly one-hour-long conversation about their Yahoo Sports op-ed and other theories in defense of football, I asked them both if football causes head injuries.
“Sure, definitely,” Cummings said, quickly and willingly. “I don’t think anyone would deny that it causes head injury.”
Just as swiftly, he said, “Again, here we are, what do you mean by head injury?”
Hoge interrupted. “I think you need to define what you mean by head injury. I could say slipping in the shower causes a head injury because that’s how my son got his first concussion.”
So I followed up: Does football cause CTE?
“There’s no scientific evidence of that,” Hoge said.
“I don’t think we know the answer to that yet,” Cummings said.
If this is a battle between these co-authors and the nation’s renowned experts, it’s time to invoke the mercy rule.

The Centers for Disease Control and Prevention says CTE “is believed to be caused in part by exposure to repetitive head impacts, including concussions as well as subconcussive trauma.” It also says “the greatest risk factor for CTE is the number of years of exposure to repeated head or brain injuries.”

The NFL itself has chimed in on this question. At a Congressional hearing in 2016, Jeff Miller, then the NFL’s executive vice president for health and safety, said there is a link between football and CTE.
"Well, certainly, Dr. McKee's research shows that a number of retired NFL players were diagnosed with CTE, so the answer to that question is certainly yes, but there's also a number of questions that come with that," Miller said.

In their op-ed, Hoge and Cummings call the evidence of football causing CTE “pseudoscience,” laying out their case by saying that McKee’s 2017 bombshell study that found signs of CTE in 110 out of 111 brains of former NFL players had no control group as a comparison — no brains, say, from people who did not play football.
The only problem with that contention is that a 2015 Mayo Clinic study co-authored by McKee tested the brains of 198 individuals who had no exposure to contact sports in their lives — and not a single one of those 198 brains showed signs of CTE.

To recap: CTE was present in the brains of 110 out of 111 ex-NFL players, and in the brains of zero out of 198 people who did not play contact sports.

“I’m happy to ask Merril Hoge who to draft No. 1 next year,” Chris Nowinski, Ph.D., CEO of the Concussion Legacy Foundation, said in a phone interview, “but we shouldn’t be asking him how to design research studies.”
Jokes aside, there’s a bigger issue at play, Nowinski said.

“Every time a football industry person belittles the issue of CTE within their sport, they are not just hurting football families, they also are hurting military families who need the science community to continue working together to find a cure for CTE.”

Now that’s a plot worthy of our attention.


https://www.usatoday.com/story/sports/c ... 750125002/

Tragic story of CTE, important new details in article and video

On January 24, 1987, Todd Ewen, a young right-winger for the St. Louis Blues, knocked the Detroit Red Wings’ notorious tough guy, Bob Probert, unconscious with one bare-knuckled punch to the head. Ewen was a new recruit, just 21 years old, and the punch immediately solidified his place in the Blues’ lineup—as well as his role in the National Hockey League as one of the many players who regularly fought members of the opposing team.

Later that same game, Ewen and Probert fought again, despite Probert having been out cold on the ice less than an hour before. This frequency of violence was typical. Ewen would go on to play 11 seasons, a soldier in the vast army of so-called “enforcers” in that era of the NHL. He would fight almost every game, mashing his fists into a pulp that doctors were forced to reconstruct with wire and screws.

Ewen and Probert’s destinies intertwined after they first met on the ice. Probert was just a year older than Ewen, and he had a similarly grueling decade-plus career. After the two men retired from hockey—in 1998 and 2002, respectively—both started to forget things. They angered quickly. Each would be dead before his 50th birthday.

Their deaths were among the earliest to fan the flames of a national debate about the lasting effects of hockey's brutality on its players' brains. But through a twist, Ewen would become a key figure in the NHL's controversial defense of the sport.

During his playing days, Ewen was a gentle renaissance man when he wasn’t on the ice. He wrote children’s books and crafted models out of hockey tape for his young fans. In 1998, Ewen retired from professional hockey and returned to the St. Louis suburbs to live with his wife, Kelli Ewen. After retiring, Kelli noticed changes in Todd. “We just saw some aggression that we hadn't previously seen,” she says. “Mood swings, irritability, and not sleeping. Just a pattern of things that was alarming to me.”

Todd’s behavior only became more erratic. During one episode, he choked Kelli and the police had to intervene. In time, depression and reclusiveness replaced Todd’s anger. He routinely became lost and disoriented in the streets around his own home.

Todd confided in Kelli that he feared he may have Chronic Traumatic Encephalopathy, or CTE—a neurodegenerative disease that most experts agree is linked to repetitive head trauma. Research on the disease has largely focused on former professional football players, but it has also been discovered in former NHL players. In 2010, Probert, the Red Wings’ bruiser, became the second NHL player to be diagnosed with CTE. His death was followed in quick succession by the deaths of four other former players’, all under the age of 40, all diagnosed with CTE.

In 2013, 10 former players launched a class-action suit against the NHL for their negligence regarding head injuries. Todd was aware of the suit but declined to participate. He ended his life in the basement of his home on the afternoon of September 19, 2015.

Damage to the brain caused by hits to the head has been observed for nearly a century. CTE was originally studied in boxers in the 1920s as dementia pugilistica. In the early 2000s, the Nigerian-American neuropathologist Bennet Omalu described the pathology of CTE following research on former pro football players. Since then, CTE has been found in the brains of hundreds of athletes across a wide range of sports. It manifests as small lesions of a protein called tau, which kill the surrounding neurons. The consequences are devastating. Anger, personality changes, and memory loss are common.

After Todd’s death, Kelli and many others were convinced he had CTE. Kelli had Todd’s brain sent to the Canadian Concussion Centre to be analyzed. Six months later, the center’s neuropathologist, Lili-Naz Hazrati, called with shocking results: Todd did not have the disease.

The NHL seized on Hazrati’s negative diagnosis in its defense of the player’s ongoing head-injury class-action suit and in public statements by the league’s commissioner. The NHL’s attorneys argued that Todd Ewen died by suicide because he believed he had CTE, therefore it would be dangerous for the league to warn players about the disease because they might kill themselves in fear. The NHL contracted 19 expert witnesses, including Hazrati, who in their testimonies injected doubt into the science of CTE. (The NHL did not respond to multiple requests for interviews.)

In April 2017, Hazrati invoiced the NHL $25,000 for her work on the trial. In her expert report and in a subsequent deposition on March 2, 2018, she claimed there was no link between CTE and head trauma and that CTE was not a disease at all. In an email response to my repeated requests for an interview, however, a representative provided a statement that appeared to conflict with this claim, saying that “Dr. Hazrati does not deny that concussions can cause damage to the brain, potentially resulting in a progressive neurodegenerative disease.” (Hazrati declined multiple interview requests.)

The science of CTE in inherently contentious. Currently the disease can only be diagnosed posthumously, and since it appears to present itself most commonly in professional athletes, researchers are forced to navigate a complicated web of relationships with athletes, sports leagues, and fellow scientists. The very existence of the disease poses an existential threat to certain sports leagues. While most researchers agree on the basic premise that CTE is a neurodegenerative disease linked to head injury, a cottage industry of CTE deniers has nevertheless sprung up. Hazrati’s research features heavily in the former pro-footballer turned commentator Merril Hoge’s 2018 book, Brainwashed: The Bad Science of CTE and The Plot to Destroy Football.

In 2014, Arland Bruce III, a retired Canadian Football League player accused The Canadian Concussion Centre, citing Hazrati’s research, of obfuscating the science of CTE in a lawsuit against the CFL and the Concussion Centre’s parent company. The case went to the Supreme Court of Canada, who declined to hear it. Kelli, too, held onto her doubts. She says she repeatedly asked Hazrati to retest Todd’s brain but Hazrati declined. Eventually Kelli had sections of Todd’s brain sent from the Canadian Centre to Boston, where a world-leading expert on CTE, Ann McKee, could retest them. In late 2018, McKee announced her own conclusions from the tests: Todd did in fact have CTE.

By 2018, over 140 former players had joined the class-action suit against the NHL. In July of that year, they were denied class-action status due to conflicts between applicable state laws. The NHL offered a settlement to players in the suit which amounted to roughly $22,000 per player with up to $75,000 in medical treatment. According to a lawyer representing players in the case, most involved are expected to take the settlement.

In November, Hazrati told the Canadian sports network TSN that she does not dispute McKee’s findings, but noted that she was “surprised to see that Todd had so very little [of the] disease for an enforcer.”

Meanwhile, McKee’s positive diagnosis relieved any doubts Kelli had about her husband’s condition. But the results were only partial vindication. The NHL so far has not acknowledged any link between head injuries sustained during the game and CTE. Hockey players still slam into each other day after day. The NHL has taken incremental steps to limit fighting and hits to the head, but as CTE is being found in growing number of hockey players, there’s arguably far more the league could do to save future players from Todd’s path.

The Tragic Post-Hockey Life of an NHL ‘Enforcer’
For 11 seasons, Todd Ewen fought in almost every game he played. He didn’t live to his 50th birthday.
Read more: https://www.theatlantic.com/health/arch ... ry/587818/

The NHL’s Deadly Denial: The Dangers of Hockey and CTE
Watch at:
https://www.youtube.com/watch?v=T_VSieTCMXI

Greybeard, thanks for posting these articles/links. GB

Tator says there is direct hockey concussions-CTE link, disagrees with Bettman
The Canadian Press
Gregory Strong
May 2, 2019
4:58 PM EDT

Last Updated
May 2, 2019
4:59 PM EDT

TORONTO — Renowned concussion specialist Dr. Charles Tator says he disagrees with Gary Bettman’s statement before a parliamentary panel where the NHL commissioner questioned any direct link between multiple hockey concussions and chronic traumatic encephalopathy (CTE), a degenerative brain condition associated with repeated blows to the head.

Tator, a University of Toronto neurosurgery professor, said Thursday that there is a conclusive link.

“In my view there is,” Tator said. “We don’t know how many players with multiple concussions will get it. That’s an important rider.”

CTE, which can only be diagnosed after death with a brain autopsy, can be profoundly debilitating with symptoms that include memory problems, personality changes, aggression and depression. Bettman weighed in on the link issue on Wednesday in Ottawa.

“I don’t believe there has been, based on everything I’ve been told — and if anybody has information to the contrary, we’d be happy to hear it — other than some anecdotal evidence, there has not been that conclusive link,” Bettman said.

Tator said that information is available on the Canadian Concussion Centre website (www.canadianconcussioncentreuhn.com), adding he’d be happy to meet with Bettman to discuss further if interested. He also dismissed the suggestion that there has not been a conclusive link.

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“It’s spelled Steve Montador,” Tator said. “Just repeat the Steve Montador case as a retort to what Bettman says. How many Steve Montadors does he need to convince him of the relationship?”

Montador, who played 571 career NHL regular-season games, was diagnosed with CTE after his death in 2015. He was 35.

“I personally counted in Steve Montador’s records that he had at least 19 concussions and his brain at autopsy showed CTE,” Tator said. “So why doesn’t Gary Bettman acknowledge that?”

A special committee of MPs has spent months holding hearings on the issue of concussions in sports and a report is expected to be tabled in the coming weeks. Several experts and athletes appeared before the cross-party panel and Bettman and his deputy Bill Daly were the final witnesses.

The committee has focused on amateur athletics but could recommend concussion protocols for pro sports.

The subject of the link between athlete concussions and CTE has also been a hot topic on the gridiron in recent years.

In November 2017, CFL commissioner Randy Ambrosie said there is not enough evidence to confirm a connection between football head injuries and CTE.

However, Jeff Miller, the NFL’s top health and safety officer, acknowledged the link during a discussion on concussions convened by the U.S. Congress in March 2016. It marked the first time a senior league official conceded football’s connection to CTE.

Bettman, meanwhile, told the parliamentary panel that hockey is safer for players and different in terms of physical contact from football, where there are repeated blows to players’ heads.

Tator noted that more football player brain samples have been examined than those from hockey players.

“So the information is, let’s say, less compelling,” he said. “But in my view, it’s sufficiently documented already to say, ‘Yes, in some players, CTE is from repetitive blows to the head.”‘

The NHL has faced criticism for its handling of head injuries despite a long list of rules, studies and league-player committees focused on safety. The league reached a settlement last year with hundreds of retired players who claimed harm from head injuries while playing, but the NHL did not admit fault or wrongdoing.

“We have said definitively that repetitive concussions in some hockey players cause CTE,” Tator said. “We have had other players who have had dozens of concussions — literally dozens — who don’t have CTE. And that’s the frustration is that not everyone gets it and we have not yet learned who’s going to get it and who isn’t.

“Some brains can tolerate more blows to the brain than other brains. There’s a great individual variation.”

Awareness of concussions and CTE has risen significantly in recent years and researchers have been delving deeper into the subject.

“We see patients who have a single concussion who have symptoms afterwards for years and years,” Tator said. “Then we see other people who’ve had dozens of them and don’t show any deterioration clinically and at autopsy their brains are clean. So that, we haven’t figured out yet — why some get it and some don’t.

“But there is no doubt in our view that some do have brain degeneration called CTE after repetitive blows and unfortunately many of them are very good athletes.”

https://nationalpost.com/pmn/sports-pmn ... th-bettman

We have found CTE in every former NHL player we have examined and we have also found it in amateur hockey players, some of whom had no significant fighting exposure

When NHL Commissioner Gary Bettman testified Wednesday before a Canadian goverment hearing, he misrepresented his meeting with Boston-based CTE researchers, they say. Neuropathologist Dr. Ann McKee has found CTE in the brain of every NHL player she tested for the disease.

Statement:
NHL Commissioner Gary Bettman’s comments at Wednesday’s Parliament Hill Subcommittee on Sports-Related Concussions in Canada included the statement: “Dr. Ann McKee…told me in my office that hockey and football are not the same. We don’t have the repetitive head contact and impact that some of the other sports do. While we understand that this is an issue that needs to be constantly followed and focused on, there have not be conclusive determinations.”

Mr. Bettman misrepresented our 2012 conversation. Our research at Boston University and the VA-BU-CLF Brain Bank clearly shows that Chronic Traumatic Encephalopathy (CTE) is associated with ice hockey play. We have found CTE in every former NHL player we have examined and we have also found it in amateur hockey players, some of whom had no significant fighting exposure. We would be delighted to have Mr. Bettman visit the Brain Bank and discuss our research on CTE and repetitive brain trauma so that any future statements will more accurately reflect the state of the science.

Ann McKee, MD
Chief of Neuropathology, VA Boston Healthcare System
Director, BU CTE Center & VA-BU-CLF Brain Bank

Chris Nowinski, PhD
Co-Founder & CEO, Concussion Legacy Foundation

https://mobile.twitter.com/rwesthead/st ... 4772621312

Dementia-related marker found in former pro athletes with concussion history
Linda Carroll

(Reuters Health) - Levels of a protein called tau in spinal fluid may help predict which former pro athletes with multiple concussions will end up with long lasting effects from their history of jolts to the brain, a new study suggests.

Elevated tau levels found in some concussed former athletes were associated with signs of damage to brain-cell connection bundles on brain scans and with poorer performance on cognitive tests, the study team reports in Neurology.

Past research suggests that elevated levels of certain versions of the tau protein are a marker of brain cell damage and degeneration, the authors note.

“We’re moving closer to being able to tell at a single-person level, what they might be in danger of developing,” said study coauthor, Dr. Carmela Tartaglia, the Marion and Gerald Soloway Chair in Brain Injury and Concussion Research at the University of Toronto.

The elevated levels of tau found in some of the athletes in the study “make us concerned that there is neurodegeneration going on,” Tartaglia said. “But we don’t know if they have CTE. That can be determined only after death.”

CTE, chronic traumatic encephalopathy, is a neurodegenerative disease that other studies have linked to repeated jolts to the brain. Currently it can only be diagnosed on autopsy.

One important finding from the new study, Tartaglia said, is that not all people who experience multiple concussions end up with long-lasting brain damage. And that falls in line with what has been observed in the past.

“Lots of people are exposed to repetitive head injury,” Tartaglia said. “But it definitely looks like not everybody gets this. We’re going to have to start looking very hard at what the difference is between the two groups.”

For the new study, Tartaglia and her colleagues recruited 22 male former pro athletes - most of them former Canadian Football League players or pro hockey players, and one snowboarder. For comparison, they also recruited five healthy volunteers and 12 volunteers who had been diagnosed with Alzheimer’s disease, both groups a mixture of men and women.

All 39 participants agreed to undergo lumbar punctures so that the researchers could examine their cerebrospinal fluid for levels of tau. They also agreed to take cognitive tests and to undergo a type of brain scan, diffusion tensor imaging, that can provide information on the integrity of the white matter that sheathes long brain-cell connections known as axons.

Tau levels were highest among the volunteers with Alzheimer’s and lowest in the healthy control group. Among the former athletes, 12 out of 22 had higher levels of tau compared to the healthy controls, but lower than the volunteers with Alzheimer’s. The other athletes had tau levels comparable to those of the healthy controls.

When the researchers analyzed just these two groups of athletes, they found that the number of concussions an individual experienced or the number of years he played were not related to his levels of tau.

They also noted that higher tau levels did correlate well with poor performance on the cognitive tests and with brain scan findings. In the brain scans of athletes with higher levels of tau, there were signs of white matter damage.

The small study does show that axonal degeneration related to brain injuries can persist for months and years, said Dr. Douglas Smith, director of the Center for Brain Injury and Repair at the Perelman School of Medicine in Philadelphia, who wasn’t involved in the research.

Smith’s group has found that “in severe traumatic brain injury there is ongoing axonal degeneration and white matter loss,” he said. “This study tends to support the idea that this may also be the case in some individuals with repeat concussion exposure.”

While the findings show that elevated tau levels appear to indicate some type of injury process is going on in the brain, they can’t tell you whether this is going to develop into CTE, said Michael Alosco, associate director of the Alzheimer’s Disease Center Clinical Core at Boston University, who wasn’t involved in the study.

Nevertheless, Alosco said, “it does suggest a pathway through which repeated head trauma leads to white matter injury and also that elevations in total tau could be used to detect that injury.”

SOURCE: bit.ly/2DX0zpc Neurology, online May 8, 2019.


https://www.reuters.com/article/us-heal ... SKCN1SE2S0

HHOF Dryden's 16 questions to ask Bettman on Wednesday

On Wednesday, NHL commissioner Gary Bettman will appear before a government of Canada parliamentary subcommittee on concussions in sports.

The committee began its hearings in November. It heard, first of all, from athletes — boys, girls, women, men — from many different sports. The athletes talked about their experiences, the brain injuries they suffered, the symptoms they felt, the diagnoses and treatments they received and the life effects they live with — about how their lives have changed and what that means for them and those around them.

It heard from medical people, from researchers who have made the brain their life’s study and doctors who have made the health and well-being of their patients their life’s work, from those who know the most and the best about what is known and isn’t known, about what they are able to do and what they aren’t and what others must do.

It heard from the leaders of other sports, whose job is also to make the decisions that affect the welfare of their players and their games. It asked them what they have done and, more importantly, what they will do to significantly reduce brain injuries in their sport in the future.

Here are some questions the subcommittee might ask Bettman:

1. Is there a connection between chronic traumatic encephalopathy (CTE) and hockey?

2. Jeff Miller, the NFL’s vice-president of health and safety, when asked in 2016 if there is a link between football and neurodegenerative diseases like CTE, replied, “The answer to that question is certainly yes.” Is Mr. Miller wrong?

3. Scientists can never know something for certain and forever. That is the nature of science. They can only know the best that anyone can know at any particular time. Do you believe it’s the job of any decision maker to make decisions based on the best information available at that moment?

4. Many present and former NHL players have talked about the symptoms they’ve experienced after their brain injuries. Do you believe there is a link between depression, memory loss, anxiety, routine problem solving, anger control and blows to the head such as those that occur in hockey?

5. You were asked in a deposition a few years ago in 2015 if you had spoken to family members of deceased players about the symptoms they had experienced and you answered, “I don’t believe so.” Have you talked to any players since who have suffered brain injuries, not only in a “How’re you doing?” way, but about their day-to-day life, how it has been affected, what they can and can’t do? Have you talked with any of their wives or partners or children?

6. In a letter to Sen. Richard Blumenthal of Connecticut, you made reference to former NHL player Todd Ewen, who after experiencing many life-changing symptoms over many years and believing he might have CTE killed himself. After a post-mortem examination showed no sign of CTE, you admonished your critics in your letter and suggested “a more measured approach consistent with the medical community consensus would be a safer, more prudent course.” Further examination of Ewen’s brain, done at the initiative of his widow Kelli, however, did show CTE. What do you think now? Have you spoken with Kelli since that time?

7. In an interview you did a year ago with WFAN radio in New York, you were asked, in relation to brain injuries and the NHL, “You’re doing everything you can?” and you responded “We do what we believe is appropriate.” What do you mean by that?

8. You have been the commissioner since 1993, over 26 years, what changes have you seen in the game?

9. Do you have children or grandchildren who play hockey? What do you see when you watch them play? What rules relating to hits to the head apply in their games? Under these rules, the kids develop their amazing skills and playing strategies and someday some of them will play in your league. Many who did grow up this way are there now. When they reach the NHL, why do they have to unlearn what they have already learned so well?

10. Do you believe you have a responsibility to kids who play hockey?

11. Paul Byron of the Canadiens was suspended for three games for a head hit on Florida’s MacKenzie Weegar. Weegar received a concussion and missed the following four games. The next time they played against each other, Weegar challenged Byron to a fight, Byron “manned up” and was helped off the ice with a concussion. He missed the next two games; Weegar wasn’t suspended. These incidents happened more than two months apart — this wasn’t spontaneous, it wasn’t about anger, nobody “just lost it.” This was, as some players and commentators said, about a “code.” An “eye for an eye.” In this case, a brain for a brain. This is 2019. What do you think about “the code?”

12. Do you think there is a difference between a blow to the head from a stick or an elbow or a shoulder or a fist? Why isn’t a hit to the head a hit to the head?

13. Do you believe the NHL has a problem with brain injuries?

14. It is a great privilege to play in your league — the experiences the players have, the money they earn, the attention and esteem they receive. It’s especially wonderful when a player is able to realize the full reward of these benefits for all of his life. For many, their post-career lives are diminished by brain injuries. Why can’t they have both?

15. We have heard about the life effects experienced by your present and former players from brain injuries, we’ve heard about the limits of what scientists, doctors and equipment makers can do. We have asked the other sports decision makers who have appeared here the same question: what steps are you going to take to make the game you lead just as exciting, challenging and wonderful to play and to watch, but less life changing for its players?

Commissioner Bettman, what is your plan?

DRYDEN: NHL needs to address these concussion issues
Read more and watch video clips at: https://torontosun.com/sports/hockey/nh ... ken-dryden

Art of Darkness: a Story of CTE - 2016 Neuro Film Festival - YouTube


https://www.youtube.com/watch?v=m8PHoWQ_s-g

Hockey’s strategy of willful denial stands out


The day after Mother’s Day was the eighth anniversary of the death of N.H.L. player Derek Boogaard. As usual, his mother, Joanne, spent a quiet day of reflection at home in Regina, Saskatchewan, and continued a tradition of writing a letter to her dead son to be published in the Regina Leader-Post.

This year’s letter lamented a missed call from him the night he died. It detailed life events involving his siblings, nephews and nieces, who mostly know “Uncle Derek” from photographs and stories told.

The end of her letter, however, was directed as much to the league as it was to Derek.

“NHL still has a lot of work to do in acknowledging and accepting responsibility for players who have passed and those who are out there with CTE and don’t even know it,” she wrote, referring to chronic traumatic encephalopathy, the degenerative brain disease caused by repeated blows to the head.

Derek Boogaard, who had C.T.E., was 28 and a prized enforcer for the Rangers when he died of an accidental overdose of painkillers and alcohol in 2011. His death and subsequent diagnosis ushered in a period of awareness of the long-term, sometimes fatal, repercussions of brain injuries in hockey. Only football seemed to be more dangerous among major team sports in the United States.

With the Stanley Cup finals underway, Joanne Boogaard and a growing group of former players worry that people have moved on to a stage of acceptance — that the N.H.L. has emerged from its concussion crisis by steadfastly denying that hockey has any responsibility for the brain damage quietly tormenting players and their families.

Other factors contribute to the lower sense of urgency around head injuries in the sport compared to the N.F.L., including hockey’s lower profile in the sports landscape, and fewer deaths making headlines.

But hockey’s strategy of willful denial stands out.

During Commissioner Gary Bettman’s annual state of the league address before Game 1 of the finals on Monday, neither Bettman nor any of his questioners uttered the words “concussion,” “brain,” “safety” or “C.T.E.”

Lawsuits that the Boogaards filed against the N.H.L. churned through the courts for years but were ultimately dismissed, mostly on technicalities over jurisdiction and timing. The N.H.L. has batted away similar lawsuits from other families and accepted no blame in the death of Boogaard or others racked by concussions or brain disease.

Last year, the N.H.L. settled a case with hundreds of retired players who had sued the league for hiding the dangers of head hits. The $19 million deal was far from the $1 billion settlement the N.F.L. made with former players five years previous.

“There’s been a lot going on in the last eight years, with a lot of hockey players that have died and a lot of others who are suffering,” Joanne Boogaard said from her home. “I don’t want people to forget him. And I don’t want people to think it’s over, that it’s all better. It’s not.”

Unlike football, in which the sheer number of C.T.E. cases (more than 100 in the N.F.L.) and the N.F.L.’s eventual public admission that there is a correlation between its game and brain disease forced concussions into the regular conversation around football, hockey has avoided such a shift.

“You have this strange cultural disconnect where, presumably, the players can read newspapers and educate themselves on these issues, and their employer, in sharp contrast, doesn’t appear to want to educate them and prevent these injuries,” said Stephen Casper, a historian of neurosciences and a professor at Clarkson University.

Two things seem certain: One, more players will die and be found to have C.T.E. “This is one of those fields where the more you know, the less good the news is,” said Ken Dryden, the author and Hall of Fame goaltender.

Two, the N.H.L. will deny playing a part. It is what the league has done since the start.

After Boogaard’s death, Bettman was asked by The New York Times about a possible link between hockey and C.T.E.

“There isn’t a lot of data, and the experts who we talked to, who consult with us, think that it’s way premature to be drawing any conclusions at this point,” he said in 2011.

On May 1, Bettman sat before a Canadian parliamentary committee investigating concussions in sports. He was asked again about hockey and C.T.E.

“I don’t believe there has been, based on everything I’ve been told — and if anybody has information to the contrary, we’d be happy to hear it — other than some anecdotal evidence, there has not been that conclusive link,” Bettman said.

Although there are uncertainties surrounding C.T.E., which only can be positively diagnosed posthumously, it has been linked to dementia-like symptoms including memory loss, depression and impulsivity. Scientists remain unsure why some seem to get it and others do not, for example.

There are at least nine publicly known cases of deceased N.H.L. players found to have had C.T.E., including Boogaard, Bob Probert, Steve Montador and Todd Ewen. Other cases are pending examination. Several other players who never reached the N.H.L. and died before age 40 had the disease, including Andrew Carroll and Kyle Raarup.

Last year’s deal between the N.H.L. and some former players gave the illusion that the concussion matter had been settled, but the effect was more like hitting a reset button. The few who declined the settlement or never joined the broader case can continue their individual claims; they are expected to receive instructions on how to proceed at a hearing in Minneapolis on June 16.

Among those moving forward is the family of Montador, who played 10 years in the N.H.L. and died in 2015 at age 35. A long-pending lawsuit filed by Montador’s estate argues, among other things, that the N.H.L. “utterly failed to provide him with crucial medical information on the permanent ramifications of brain trauma.”

Montador’s father, Paul, is eager to resume the fight with the N.H.L. in court.

“My son would be alive if it wasn’t for the way the N.H.L. handled the concussion issues, and had it recognized the impact of concussions, and eventually C.T.E., has on its players,” Paul Montador said.

Montador watched Bettman’s recent testimony in Ottawa. Like others, he was disappointed but not surprised.

“Had they handled this differently from the start, he wouldn’t have to act like a lawyer,” Montador said. “He could act like a human being.”

The day before Bettman’s testimony, Kelli Ewen, the widow of Todd Ewen, filed a lawsuit against the N.H.L. in federal court in California. The complaints include negligence, fraudulent concealment and wrongful death.

Todd Ewen played 11 seasons in the N.H.L. and killed himself in 2015 at age 49, fearing he had C.T.E.

Lili-Naz Hazrati, a neuropathologist with the Canadian Concussion Centre, examined Ewen’s brain and concluded that he did not have C.T.E. — a surprising revelation later deemed to have been incorrectly others, including scientists at Boston University’s Chronic Traumatic Encephalopathy Center.

In the nearly three years between those competing diagnoses, Hazrati served the N.H.L. as a witness in its litigation, and Bettman used the erroneous Ewen results to argue against links to C.T.E. He criticized “media hype” and “fear mongering” in a 2016 letter to Senator Richard Blumenthal of Connecticut.

Critics paint Bettman and the N.H.L. as sports’ equivalent of tobacco sellers or climate-change deniers — purposely clouding issues that few still debate in order to protect their own interests.

“It’s hard to know what’s going to push the N.H.L. to the side of right on this,” said Chris Nowinski, a co-founder of the Concussion Legacy Foundation, which is affiliated with Boston University’s C.T.E. Center. “What’s clear is that it’s not science that’s going to convince them.”

Dryden sees a simple solution: Use rules to eliminate most hits to the head. Concussions will never be fully extinguished, perhaps not in any sport, but Dryden believes any hit to the head — whether accidental or not, whether with a shoulder, stick, fist or elbow — should be penalized.

“Football faces an immense challenge — the real answers, they’re tough,” Dryden said. “In hockey, they aren’t. That’s the part that is so aggravating.”

For now, the N.H.L. has tickled the issue with its rule book, penalizing hits that appear to target the head and allowing officials to determine whether they were avoidable or not.

“The brain isn’t impressed by all these explanations and distinctions,” Dryden said.

The league still endorses a culture of bare-knuckle fighting (the video game NHL 19 includes it, boosting the energy level of the winner’s team) — though fights are in decline, something Bettman applauds while arguing, without evidence, that some level of fighting is necessary as a “thermostat” to deter more violent acts.

Early in the playoffs this year, the superstar Alex Ovechkin of the defending champion Washington Capitals was involved in a notable one.

Two weeks later, at the parliamentary hearing, Bettman said, “I don’t believe there’s much we can do” to reduce head injuries. He promoted the league’s concussion protocols, “updated regularly,” he said, since 2010.

“The deep contradiction is, if all science is anecdotal, as Mr. Bettman said during his testimony, then why bother having these protocols?” Casper said. “What are they for?”

Joanne Boogaard still waits for someone from the N.H.L. to say that, yes, they could have done more to help stem Derek’s onset of C.T.E. symptoms and, perhaps, save his life.

She and her ex-husband, Len, no longer expect that kind of forthrightness. They did not want to be part of the settlement because they did not want the N.H.L.’s money.

“It’s not a money thing,” Joanne Boogaard said. “Just be responsible. Be a leader of the sport.”

The N.F.L. Has Been Consumed by the Concussion Issue. Why Hasn’t the N.H.L.?
Read more and see the photos at: https://www.nytimes.com/2019/05/31/spor ... gaard.html

Contact sport participation and chronic traumatic encephalopathy are associated with altered severity and distribution of cerebral amyloid angiopathy
https://link.springer.com/article/10.10 ... 19-02031-x

What is your ultimate goal here?

Is it to make people more aware of CTE? I think people are aware.

Is it for better equipment? I believe equipment manufacturers are making progress with what is available.

Is it to ban hockey & football? I think most everyone knows that there is risk involved, but some believe that the risk is worth it....