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Libby and Tom Bates // CBS News

A brain disease best known for impacting football players who suffered concussions is now being found in soldiers

By Sharyn Alfonsi, September 16, 2018, CBS News

Until a few years ago, NFL players who struggled with severe depression, bouts of rage and memory loss in their retirement were often told they were just having a hard time adjusting to life away from the game. Doctors have since learned these changes can be symptoms of the degenerative brain disease CTE – chronic traumatic encephalopathy, caused by blows to the head.

As we first reported in January, CTE isn’t just affecting athletes, but also showing up in our nation’s heroes. Since 9/11 over 300,000 soldiers have returned home with brain injuries. Researchers fear the impact of CTE could cripple a generation of warriors.

When Joy Kieffer buried her 34-year old son this past summer, it was the end of a long goodbye.

Kieffer’s son, Sgt. Kevin Ash, enlisted in the Army Reserves at the age of 18. Over three deployments, he was exposed to 12 combat blasts, many of them roadside bombs. He returned home in 2012 a different man.

Joy Kieffer: His whole personality had changed. I thought it was exposure to all of the things that he had seen, and he had just become harder. You know, but he was — he was not happy.

Sharyn Alfonsi: So at this point, you’re thinking this decline, this change in my child is just that he’s been in war and he’s seen too much.

Joy Kieffer: Right.

Sharyn Alfonsi: Did he tell you about blasts that he experienced during that time?

Joy Kieffer: Uh-huh.

Sharyn Alfonsi: What did he–tell you?

Joy Kieffer: That they shook him. And he was having blackouts. And — it frightened him.

Ash withdrew from family and friends. He was angry. Depressed. Doctors prescribed therapy and medication, but his health began to decline quickly. By his 34th birthday, Sgt. Kevin Ash was unable to speak, walk or eat on his own.

Sharyn Alfonsi: Looking back on it now, was there anything you feel like he could’ve done?

Joy Kieffer: Uh-uh.

Sharyn Alfonsi: Because?

Joy Kieffer: Because it was– it– it was his brain. The thing I didn’t know was that his brain was continuing to die. I mean, before he went into the service he said, “you know, I could come back with no legs, or no arms, or even blind, or I could be shot, I could die,” but nobody ever said that he could lose his mind one day at a time.

His final wish was to serve his country one last time by donating his brain to science — a gesture he thought would bring better understanding to the invisible wounds of war.

Joy reached out to the VA-Boston University-Concussion Legacy Foundation Brain Bank where neuropathologist Dr. Ann McKee is leading the charge in researching head trauma and the degenerative brain disease CTE.

McKee has spent fourteen years looking at the postmortem brains of hundreds of athletes who suffered concussions while playing their sport.

Last summer, her findings shook the football world when she discovered CTE in the brains of 110 out of 111 deceased NFL players — raising serious concerns for those in the game today.

And when Dr. McKee autopsied Patriots tight-end Aaron Hernandez who killed himself after being convicted of murder, she found the most severe case of CTE ever, in someone under 30.

Now she’s seeing similar patterns in deceased veterans who experienced a different kind of head trauma — combat blasts. Of the 125 veterans’ brains Dr. Mckee’s examined, 74 had CTE.

Sharyn Alfonsi: I can understand a football player who keeps, you know, hitting his head, and having impact and concussions. But how is it that a combat veteran, who maybe just experienced a blast, has the same type of injury?

Dr. Ann McKee: This blast injury causes a tremendous sort of– ricochet or– or– a whiplash injury to the brain inside the skull and that’s what gives rise to the same changes that we see in football players, as in military veterans.

Blast trauma was first recognized back in World War I. Known as ‘shell shock,’ poorly protected soldiers often died immediately or went on to suffer physical and psychological symptoms. Today, sophisticated armor allows more soldiers to walk away from an explosion but exposure can still damage the brain — an injury that can worsen over time.

Dr. Ann McKee: It’s not a new injury. But what’s been really stumping us, I think, as– as physicians is it’s not easily detectable, right? It’s– you’ve got a lot of psychiatric symptoms– and you can’t see it very well on images of the brain and so it didn’t occur to us. And I think that’s been the gap, really, that this has been what everyone calls an invisible injury.

Dr. Ann McKee: This is the world’s largest CTE brain bank.

The only foolproof way to diagnose CTE is by testing a post-mortem brain.

Sharyn Alfonsi: So these are full of hundreds of brains…

Dr. Ann McKee: Hundreds of brains, thousands really…

Researchers carefully dissect sections of the brain where they look for changes in the folds of the frontal lobes – an area responsible for memory, judgement, emotions, impulse control and personality.

Dr. Ann McKee: Do you see there’s a tiny little hole there? That is an abnormality. And it’s a clear abnormality.

Sharyn Alfonsi: And what would that affect?

Dr. Ann McKee: Well, it’s part of the memory circuit. You can see that clear hole there that shouldn’t be there. It’s connecting the important memory regions of the brain with other regions. So that is a sign of CTE.

Thin slivers of the affected areas are then stained and viewed microscopically. It’s in these final stages where a diagnosis becomes clear as in the case of Sgt. Kevin Ash.

Sharyn Alfonsi: So this is Sergeant Ash’s brain?

Dr. Ann McKee: Right. This is– four sections of his brain. And what you can see is– these lesions. The, and those lesions are CTE And they’re in very characteristic parts of the brain. They’re at the bottom of the crevice. That’s a unique feature of CTE.

Sharyn Alfonsi: And in a healthy brain, you wouldn’t see any of those kind of brown spots?

Dr. Ann McKee: No, no, it would be completely clear. And then when you look microscopically, you can see that the tau, which is staining brown and is inside nerve cells is surrounding these little vessels.

Sharyn Alfonsi: And explain, what is the tau?

Dr. Ann McKee: So tau is a protein that’s normally in the nerve cell. It helps with structure and after trauma, it starts clumping up as a toxin inside the nerve cell. And over time, and even years, gradually that nerve cell dies.

Dr. Lee Goldstein has been building on Dr. McKee’s work with testing on mice.

Inside his Boston University lab, Dr. Goldstein built a 27-foot blast tube where a mouse – and in this demonstration, a model – is exposed to an explosion equivalent to the IEDs used in Iraq and Afghanistan.

Dr. Lee Goldstein: When it reaches about 25 this thing is going to go.

Dr. Goldstein’s model shows what’s going on inside the brain during a blast. The brightly colored waves illustrate stress on the soft tissues of the brain as it ricochets back and forth within the skull.

Dr. Lee Goldstein: What we see after these blast exposures, the animals actually look fine. Which is shocking to us. So they come out of what is a near lethal blast exposure, just like our military service men and women do. And they appear to be fine. But what we know is that that brain is not the same after that exposure as it was microseconds before. And if there is a subsequent exposure, that change will be accelerated. And ultimately, this triggers a neurodegenerative disease. And, in fact, we can see that really after even one of these exposures.

Sharyn Alfonsi: The Department of Defense estimates hundreds of thousands of soldiers have experienced a blast like this. What does that tell you?

Dr. Lee Goldstein: This is a disease and a problem that we’re going to be dealing with for decades. And it’s a huge public health problem. It’s a huge problem for the Veterans Administration. It’s a huge moral responsibility for all of us.

A responsibility owed to soldiers like 34-year-old Sgt. Tom Bates.

Sgt. Tom Bates: We were struck with a large IED. It was a total devastation strike.

Bates miraculously walked away from a mangled humvee — one of four IED blasts he survived during deployments in Iraq and Afghanistan.

Sharyn Alfonsi: Do you remember feeling the impact in your body?

Sgt. Tom Bates: Yes. Yeah.

Sharyn Alfonsi: What does that feel like?

Sgt. Tom Bates: Just basically like getting hit by a train.

Sharyn Alfonsi: And you were put back on the frontlines.

Sgt. Tom Bates: Yes.

Sharyn Alfonsi: And that was it?

Sgt. Tom Bates: Uh-huh

When Bates returned home in 2009, his wife Libby immediately saw a dramatic change.

Libby Bates: I thought, “Something is not absolutely right here. Something’s going on. For him to just lay there and to sob and be so sad. You know, what do you do for that? How do I– how do I help him? He would look at me and say, “If it wasn’t for you, I would end it all right now.” You know, I mean, like, what do you– what do you do– and what do you say to somebody who says that? You know I love this man so much. And —

Sharyn Alfonsi: You’re going to the VA, you’re getting help, but did you feel like you weren’t getting answers?

Sgt. Tom Bates: Yes.

Sharyn Alfonsi: And so you took it into your own hands and started researching?

Sgt. Tom Bates: I knew the way everything had gone and how quick a lot of my neurological issues had progressed that something was wrong. And I just– I wanted answers for it.

That led him to New York’s Mount Sinai Hospital where neurologist Dr. Sam Gandy is trying to move beyond diagnosing CTE only in the dead by using scans that test for the disease in the living.

Dr. Sam Gandy: By having this during life, this now gives us for the first time the possibility of estimating the true prevalence of the disease. It’s important to estimate prevalence so that people can have some sense of what the risk is.

In the past year, 50 veterans and athletes have been tested for the disease here. Tom Bates asked to be a part of it.

That radioactive tracer – known as t807 – clings to those dead clusters of protein known as tau, which are typical markers of the disease.

Through the course of a 20 minute PET scan, high resolution images are taken of the brain and then combined with MRI results to get a 360 degree picture of whether there are potential signs of CTE.

Scan results confirmed what Tom and Libby had long suspected.

On the right, we see a normal brain scan with no signs of CTE next to Tom’s brain where tau deposits, possible markers of CTE, are bright orange.

Dr. Sam Gandy: Here these could be responsible for some of the anxiety and depression he’s suffered and we’re concerned it will progress.

Sgt. Tom Bates: My hope is that this study becomes more prominent, and gets to more veterans, and stuff like that so we can actually get, like, a reflection of what population might actually have this.

There is no cure for CTE.

Dr. Gandy hopes his trial will lead to drug therapies so he can offer some relief to patients like Tom.

Dr. Ann McKee believes some people may be at higher risk of getting the disease than others.

While examining NFL star Aaron Hernandez’s brain she identified a genetic bio-marker she believes may have predisposed him to CTE.

A discovery that could have far-reaching implications on the football field and battlefield.

Sharyn Alfonsi: Do you think you will ever be your old self again?

Sgt. Tom Bates: I don’t ever see me being my old self again. I think it’s just too far gone.

Sharyn Alfonsi: So what’s your hope then?

Sgt. Tom Bates: Just to not become worse than I am now.

Since our story first aired, over 100 veterans have contacted Dr. Gandy to enroll in ongoing trials to identify whether they are living with CTE. And more than 300 have reached out to Dr. Mckee about donating their brains to research.

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Junior Seau, shown at his beloved Pacific Ocean in the ESPN Films “30 for 30” documentary “Seau,” which premieres Thursday. (ESPN Films)

ESPN hits the mark with documentary ‘Seau’

By Tom Krasovic, September 20, 2018, San Diego Union Tribune

An aerial view of the Oceanside coast, in full sparkle and splendor below, grandly eases viewers into “Seau,” an ESPN Films documentary in the “30 for 30” series that debuts Thursday on the streaming service ESPN+.

It’s a sunny scene, the Pacific Ocean’s turquoise waves illuminated as they roll toward the white beach. The late Junior Seau told friends he found peace paddling on these waters, deep into his life alongside the town where he’d grown up.

Up at dawn with a yellow long-board and oar in hand, Seau had only a short walk from his beachfront home to the water.

Yet the former Chargers linebacker, role model and local philanthropist was then also writing in a journal of bouts with depression, memory loss and perceived guilt. There were headaches, too, and nights plagued by insomnia. “Buddy,” he’d told a friend and professional soccer player who’d suffered a brain injury from heading a ball, “I’ve had a concussion since I was 15.”

Diary entries also revealed feelings of humiliation and embarrassment over not living up to expectations of others and himself, and of feeling used by others.

“The world has nothing for me,” Seau pens in one entry, the cursive words all too legible.

One of Seau’s surviving adult children, after reading the grim line aloud, wonders why his father didn’t regard his family as something in this apparent world of nothing.

Why couldn’t they have been a lifeline for him to reach out and grasp?

“Seau,” produced and directed by Kirby Bradley, lets viewers draw their own conclusions about a complicated life that ended one May morning six years ago, at age 43, with a self-inflicted gunshot wound to the chest, but not before we hear from an array of family members, friends and experts in football and brain science.

At the end of the 90-minute film, themes of redemption and hope are raised.

“Let’s all walk from here being better for having known Junior Seau and the impact he had on our lives,” NFL quarterback Drew Brees, a former Chargers teammate of the Hall of Fame linebacker, concludes near the film’s end.

Former Chargers lineman Aaron Taylor notes that in death, Seau drew extraordinary attention to the link between head trauma and a degenerative brain disease, CTE, revealed in a tissue sample sent to a brain scientists at the family’s request.

Exciting beginnings and success are a thread to the film, followed often by bitter detours or hurtful endings.

Seau took to sports at Oceanside High with a passion that rivaled his stunning blend of size, speed and agility. If he was slamming into football ball-carriers or catching passes, scoring baskets or throwing the discus and shot, he was a “force of nature” for the green-and-white-clad Pirates, observers said.

A flood of football scholarship offers came to the small home where Seau and his brothers slept in a tiny garage.

Jubilation ensued when Seau chose USC, keeping him close to his parents and siblings and the tight-knit Samoan-American community in Oceanside. A similar celebration arose in 1990 when the Chargers drafted him fifth overall. “I’m a real momma’s boy,” Seau said, pulling on a blue team cap.

Playing for his beloved “Diego,” he led the long-struggling Chargers to the playoffs in just his third season, and their first Super Bowl two years later. “Now the world is gonna know the San Diego Chargers,” he told some 70,000 celebrants in Mission Valley after the team returned from claiming the 1994 AFC title in Pittsburgh.

The flip side?

If Oceanside lost a game in which he played, Junior lost his lunch money. It was the price his father exacted.

The thrill of signing with USC gave way to humiliation when a failed admittance test made him ineligible as a freshman. His father refused to talk to him in response, deeming the failure an embarrassment to the family. After a dominant junior year with USC, there would be no senior year. Making money was the next step, in no small part because he wanted to support his parents and other family members.

The Chargers couldn’t build upon their Super Bowl season, and the team’s constant losing wore on Seau.

When the Chargers traded him in the spring of 2003, after 13 seasons with the club, Seau was hurt that the team — Stay Unclassy, San Diego? — called not him but his agent to tell him the news. “I know that was hard on him,” said the agent, Steve Feldman.

Gina Seau was working for the Chargers in marketing when she first met Seau early in his NFL career.

She recalled “very kind eyes” and a “very soft voice” that almost “didn’t match the size and stature.”

The two would marry, but erratic behavior that Gina Seau linked to numerous football-related head injuries — “My head is on fire,” he told her — led to a divorce in 2002. The two remained friends. Believing that driving off a steep coastal cliff in October 2010 wasn’t an accident, Gina pleaded with her former husband to get help.

Here’s hoping that if there’s a “Seau II,” events yet to transpire bring more developments of redemption. Say, a cure for CTE.

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Ann C. McKee, chief of neuropathology at the VA Boston Healthcare System, which houses the world’s largest brain bank devoted to CTE research, examines a brain earlier this month.(Photo: Robert Deutsch, USA TODAY)

Researchers close in on CTE diagnosis in living, one brain at a time

By Nancy Armour, August 24, 2018, USA TODAY

BOSTON – Submerged in chemicals in the stainless-steel bowl is the key to life and, researchers hope, death.

It’s a human brain. That of a man who played college football in the 1950s, to be exact. His family donated his brain to get answers for themselves, but what’s found could lead to more answers about chronic traumatic encephalopathy, the devastating neurodegenerative disease linked to concussions and repetitive head trauma from football and other contact sports.

“Our main objective, our overarching goal, is to help the people who are living. To be able to diagnose this disease during life,” says Ann McKee, chief of neuropathology at the VA Boston Healthcare System, which houses the world’s largest brain bank devoted to CTE research.

“If we can diagnose it, we can monitor it and test therapies to see if they’re effective in treating this disease,” says McKee, director of the CTE Center at Boston University’s School of Medicine. “It would really dramatically increase our ability to point out genetic susceptibilities for this. We’d be able to look at how much is too much in certain individuals or certain positions in certain sports.”

As another football season begins, it inevitably leads to questions and fears about head trauma and its long-term damage. How many hits are too many? What can parents do to protect their children or players do to protect themselves? Are athletes in certain sports more susceptible?

Most important, which athletes will develop CTE – or Parkinson’s or ALS (amyotrophic lateral sclerosis) – and why?

The answers will come from brains such as the one McKee dissected this month, when USA TODAY Sports toured the brain bank.

The brain bank has more than 500 brains, most of them donated by former athletes or their families who suspected CTE because of mood swings, behavioral changes, depression or dementia. Of those brains, more than 360 had CTE, McKee says.

SEARCHING FOR CLUES

The arrival of a brain sets two teams in motion. One set of clinicians talks to the family to find out more about the donors. Did they play any sports? If so, what and for how long? When did they start? Did they experience any other kind of head trauma, say from an automobile accident, domestic violence or military service? Did they have drug or alcohol problems? How did their mental health change, and when did that occur?

Separately, and usually without any information about the person whose brain it was, McKee and her researchers study the brain. It is cut in half, and one half is stored in a minus-80-degree freezer, so it will be available for molecular, genetic and biochemical studies.

The other half is then photographed and sectioned. After removing the brain stem, McKee uses what looks like a bread knife to cut slices of the brain about a quarter-inch thick.


Ann C. McKee slices the brain into segments about a quarter-inch thick as part of in-depth, time consuming research on the organ. McKee hopes the work will unlock answers to CTE. (Photo: Robert Deutsch, USA TODAY)
 
Simply by looking at the brain, McKee can tell a few things. The brain of this man, who was in his 80s when he died, has shrunk, noticeably smaller than it should be for a man who once played football. The folds of the brain, normally pressed tightly against one another, are loose and have gaps between them, some large enough that the tip of a finger could be inserted.

She points to the ventricles, chambers in the middle of his brain that are filled with fluid during life. They should be small, but these are “just gigantic.”

“As the brain shrinks, they expand. What this indicates is there’s been enormous shrinkage of the brain,” McKee says. “Those are huge.”

The hippocampus, a section in the middle of the brain that controls memory, is small but not abnormally so for a man in his 80s. If it was, that could be an indication of Alzheimer’s. But a membrane that runs from one side of the brain to the other, normally thick like a rubber band, has shrunk. In some spots, it’s almost invisible.

“This is looking more like frontal predominant atrophy, and that could mean CTE because Alzheimer’s almost always affects the hippocampus,” McKee says. “At this point, I always want to know, ‘What is it? Let’s look under the microscope.’ But you have to wait.”

CTE can’t be seen by the naked eye, and it takes at least three weeks to prepare slides of the brain tissue.


 
CTE is caused by tau, a protein in the brain released as a result of head trauma. When tau clumps together, it damages brain cells and can change the brain’s function. Though tau causes Alzheimer’s, McKee says, the tau that causes CTE looks distinctly different.

Under a microscope, it can be seen in telltale brown spots.

“CTE is very focal. In fact, in its early stages, it’s in the crevices. It just piles up. And that’s around blood vessels,” McKee says. “That’s very different. Alzheimer’s never does that.”

As CTE progresses, those clusters or clumps of tau will spread, and the disease will become more severe. That’s why, in the early stages of disease, stages 1 and 2, the symptoms usually relate to behavioral changes or mood swings. In stages 3 and 4, the disease is exhibited in memory loss.

“We think there may be more pathology in the young players than we’re appreciating just with the tau protein,” McKee says. “We think there’s maybe white matter structural changes or maybe inflammatory changes that are responsible for that loss of control, which is so difficult for the individuals.”

‘EVERY CASE IS A MYSTERY’

Once the slides have been examined, the pathologists and clinicians will come together for a conference. At this point, neither knows what the other does. The clinicians detail what they’ve learned about the brain donor’s history and suggest a diagnosis. The pathologists will then say whether the brain tissue confirms it.

“Every case is a mystery,” McKee says. “It’s not the same way you usually solve a mystery. I solve the pathology first, and then you go back and find out (the history). And then you try and put the two together.”

Some former players and their families once were reluctant to donate their brains, but that stigma largely has disappeared. So much so that McKee said brains arrive at the Boston bank almost every day.

Though that lengthens the time it takes to reach a definitive diagnosis, it will shorten the time before a living diagnosis can be found. In addition to the work done in her lab, McKee shares tissue samples with researchers around the world.

“What we want to do is establish the risk, educate people, educate parents, educate players,” McKee says. “So if they’re unwilling to risk that future self, if they’re unwilling to take that risk because it’s too high for them personally, we want to give them enough data so they can make a very sound and wise decision.”

When that day comes, it will change sports forever.

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CARSON, CA – AUGUST 03: Bronze medal winner Dave Mirra speaks in a press conference after the Rally Car race during the summer X Games 14 at Home Depot Center on August 3, 2008 in Carson, California. (Photo by Christian Petersen/Getty Images)

Months after committing suicide, Dave Mirra has become the first action sports athlete to be diagnosed with CTE

by Robert Silverman, vocativ.com (May 24, 2016)
 
After BMX biking legend Dave Mirra committed suicide on February 4 of this year, his wife had his brain tested for chronic traumatic encephalopathy. Sadly, the result came back positive, rife with tau proteins dotting both his temporal and frontal lobes after years of enduring an unknown amount of concussive and sub-concussive trauma. This makes Mirra the first action sports athlete to be diagnosed with CTE.

The neuropathologist went so far as to equate the condition of his brain to that of NFL players and other contact sport athletes that have been posthumously diagnosed with the disease. “I couldn’t tell the difference,” Dr. Lili-Naz Hazrati said.

In an exclusive interview with ESPN: The Magazine, Mirra’s wife Lauren describes the agonizing final weeks of his life, the transformation of his formerly vibrant personality into something different and darker, prone to wild mood swings and unprovoked crying jags or bouts of exhaustion, his mind clouded and wracked with depression.

“I remember seeing him sitting on our bed one day, in the last month of his life,” she said. “I had just gotten out of the shower and saw him hunched over with the blankest lost look. I sat down next to him and held his hand. I said, ‘What is wrong? Are you OK?’ And he just shrugged his shoulders. He couldn’t even speak. He didn’t know. He couldn’t put it into words. He was lost. He was helpless. It was completely different from who he was.”

“He was gone. I could see straight through him,” she continued. “It was the hardest thing to see, looking at someone you love, and you can’t have a conversation with them, and you can see straight through their eyes.”

Lauren Mirra doesn’t know what her exact plans might be for the future, but her overarching hope is that she’ll be able to find a forum in which to speak out, to encourage best practices and prevention measures, without coming across as an ideologue out to ban action sports altogether.

“Through him we have an opportunity to help and change,” she said. “Beauty from ashes. That’s how I will always choose to see it.”

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