This Is Your Brain on Football
Some boys just run smoother than others, burn premium for fuel, not unleaded. Eric Pelly is a Jaguar of a kid, all throttle and forward lean, no square edges. From the age of six, he’s played two sports a season and trained with the zeal of a walk-on grinder, the peewee Clay Matthews. Crunches and pushups while he’s watching TV, hours of lifting after he’s home from school and blitzed through his class work, then out with his boys for games of flag football that turn into tackle without the pads. At one point, in middle school, he was bigger than other kids, but topped out – cruelly – at five-eight. He moped for weeks when the doctor told him that his growth plates had shut for good, then bore down harder to craft a body that would take him where he planned to go. Here’s a straight-A student at a high school so competitive that he’s barely in the top 100 in his class, but he’s still telling his mom what he’s said since grade school: I’m going to play pro football. You just watch.
That isn’t merely the Pittsburgh talking in him, though it seems like every male in this yellow-and-black town wants to be Troy Polamalu, or hit like him. Since he was old enough to walk or, more like it, run, Eric has craved contact the way fat kids crave soft serve. At 16, playing flanker for his high school team, the perennial section champs North Allegheny, he goes up for a pass, cracks helmets with a safety and bangs his head on the turf when he lands. By the time he’s 17, he’s had a couple of concussions that his parents, Joan and Mark, know about, and maybe another couple that they don’t. “I kept him out of football as long as I could – he knew I didn’t want him to play,” says Joan, an ex-flight attendant who stopped flying long ago so she could ferry her three kids to their games. “He was always so driven, but clever, too; he could talk you into anything,” she says. “In the end, he finally wore down my resistance.”
In the fall of his junior year, Eric stumbles home after taking a shot to the jaw in a backyard football game. His friends help him in, then he slides down the wall, saying, “Mom, I got another, but don’t worry.” This concussion’s different, though: The headaches last for weeks, as does the fatigue that keeps him home on school mornings. He fights through it and goes in late, but has trouble finishing exams: His eyes seem to wobble in their sockets. “He had headaches and stuff, though he didn’t talk about it much; he was hard-nosed, always going a hundred-and-ten,” says Bill Landefeld, a friend and confidante with a concussion history himself, having wrestled in high school and college. “There are certain kids that don’t know another speed and need someone to step in and slow them down. That’s what he was missing: a coach to say stop. He’d be in the gym, lifting, while he was still concussed.”
At length, Eric recovers but gives up playing football, in part to reclaim his summers from the grind of practice. Still, he can’t shake it, that need for speed; it’s wired into the dura of his brain. So when a close friend, Jon Casile, joins a high school rugby club, Eric tags along to check it out. He falls hard for the game, finding it just the right mix of skill, force and smarts – and no cheap head shots. He likes it so well, in fact, that he makes a huge leap the summer he turns 18, earning a spot on the Pittsburgh Harlequins, a semi-pro team. “We were going against men, guys who’d played college and World Cup, but Eric was so good he fit right in,” says Casile. Fast and fearless, Eric scores in bunches and becomes a starter at outside center. At an away game, however, he gets dinged carrying the ball and subs out before the half and doesn’t return. Once home, he tells no one about the blow to his head, afraid that Joan will blow her stack and squash his playing career once and for all. Just two weeks later, he’s back on the pitch, wrestling men a hundred pounds bigger. Joan watches from the stands when he makes his trademark tackle, a low, hard takedown of a bruising forward. The forward pops up again but Eric doesn’t; he’s too woozy to stand, so his teammates carry Eric to the bench. The next thing Joan knows, her son is balled up on the ground, moaning and holding his head in vice-grip pain. An ambulance is called as she races across; Eric is barely conscious when she gets there. Still, he keeps muttering “I’m OK, Mom,” as they wait for the medics to show. “It was so ingrained in him to tell me that,” she says. “Even out of it, laying across his coach’s shoulder.”
Ten days later – after leaving the hospital and making a shockingly swift return to class – Eric goes back to his stopless life, though he clearly is not the same kid. “We ate lunch together and he wasn’t all there, said his head was really hurting bad,” says Landefeld, 23, now the front-desk manager of a Marriott hotel in the suburbs of Pittsburgh. “I met him in the hall and saw the same thing: He couldn’t focus or really follow the conversation,” says Adam Neugebauer, another close friend who’s now a graduate assistant at Tiffin University in Ohio. “He said he wanted to go to sleep but couldn’t that day. He had to work at his father’s shop after school.” That evening, eating dinner and discussing the frog pond in the yard, Eric suddenly seizes up, midsentence. His eyes roll back and his fists clench tight; he’s dead from a massive brain swell either before he hits the floor or within a couple of seconds of having done so. His mother screams at his sister Jenna to call 911, as Mark tries to revive him, but the cranial edema has crushed his brainstem and shorted out his heart and lungs. This boy, who was so fully and sleekly alive that he never stopped moving or multitasking from the moment he rolled out of bed, is killed at 18 by a pair of concussions that no one who saw them happen thought life-threatening. And then, two years later, comes a second shock of horror to a family blown sideways by grief. At a lab outside Boston, neuropathologists examining Eric’s brain have found clumps of poisoned cells, the brown-tinted markers of CTE, or chronic traumatic encephalopathy. It is the disease that’s dimmed the minds of retired football icons, wrought early dementia in hockey fighters and turned the brains of punched-out boxers into mush. As it can’t yet be detected in living subjects (the clumps are too small to show on current scanners), it’s been confirmed only in deceased ex-athletes whose brains were donated for study. Those players include Mike Webster, Pittsburgh’s Hall of Fame center; Terry Long, who played beside him on that Steelers line, and Justin Strzelczyk, Long’s mountainous linemate soon after Webster retired. To date, 75 subjects have tested positive at that lab, the Center for the Study of Traumatic Encephalopathy in Bedford, Massachusetts – men who won Super Bowls and hockey brawls and paid an awful price for it by their forties. To their number, add Eric Pelly, a boy who once burned to be a Steeler and, if nothing else, died like one. He very surely will not be the last.
Iron Mike Webster took his beatings better than any man who ever hiked a ball. Every day in practice, he got smacked in the mouth by Mean Joe Greene and Ernie Holmes, met the battering-ram launches of Jack Lambert and Jack Ham as he led Franco Harris through the hole – and didn’t miss a snap for six seasons. You couldn’t move him or scare him or wear him out, which is how he lasted 17 brutal years as a too-light, late-round pick from Nowhere, Wisconsin. A Super Bowl champion four times over, a no-doubt Hall of Famer and the center on the league’s all-time team, he was the face of the modern game’s dogs-of-war ethos: We Visigoths do battle for your pleasure.
But as with other titans you couldn’t knock out – Joe Louis, Johnny Unitas and Muhammad Ali, to name but three – his marble jaw was Iron Mike’s unmaking. While still in his thirties, he began to shrink, recede behind that fortress of a brow. He soon forgot everything that mattered – his kids’ birthday parties, the names of the men he’d blocked for in Pittsburgh – and slept nights in his pickup or the Amtrak station because he couldn’t remember where he happened to live. He scrawled desperate notes to himself in journals, trying to catch the cattails of his thoughts, squandered his life savings, and shot himself repeatedly with a Taser gun to get an hour’s oblivion from despair. This was worse than going mad – this was going dark, the lights in his head extinguishing as he watched. By the time he died, at 50, of a coronary, there was nothing left of Webster but the brain he gave to science, a grotesquely tangled slurry of dead connections. Fittingly, that brain has been moving mountains since. It’s a large part the reason we’re paying attention to concussions and finally thinking in earnest about their toll.
“Mike was the first to say, ‘Pro football hurt my brain,’ and prove it, both in court and from the grave,” says Bob Fitzsimmons, a West Virginia attorney who fought a seven-year battle with the NFL’s pension board over Webster’s post-concussion damage. That struggle, decided in Webster’s favor four years after he died in 2002, opened the dam to thousands of new lawsuits and put the public on notice that America’s pastime was hazardous to the minds of the men who’ve played it. The point was hammered home by Dr. Bennet Omalu, a neuropathologist and then-coroner in Pittsburgh who approached Webster’s family shortly after his death for permission to examine Webster’s brain. His findings, published in Neurosurgery in 2005 to scathing denunciations from the league, established Webster as Patient Zero, the first ex-player to test positive for CTE.
Omalu, a Nigerian who knew nothing of the sport, also tested the brains of Long and Strzelczyk and reported that they, too, had “footballer’s dementia,” which contributed to their early, gruesome deaths.
In the seven or so years since his paper appeared, the focus of clinicians and league commissioners has been to try to make their violent sports safer and saner for the adults and college athletes who play them. That’s fine, as far as it goes, though it doesn’t go far enough. One Sunday this past fall, for instance, three NFL quarterbacks suffered brutal blows to the head during games but were allowed to continue playing for several series. Must someone drop dead of a subdural hematoma before the league puts neurologists on its sidelines? And what’s to be said about the players themselves, the Jay Cutlers, Alex Smiths and Michael Vicks? After thousands of scare stories about dementia in vets, won’t they bear some blame for their unhinging if, at 50, they can’t spell their own names? Or is that, like everything else now, to be settled in court, where at last count 4,000 former players were pressing claims for permanent brain damage?
Still, these are grown-ups making informed decisions about the risks they will or won’t take on. Missing in the discussion are the millions of others who can’t give legal consent: They aren’t old enough to sign the release forms. Each year, according to one study, up to 3.8 million Americans suffer a concussion on playgrounds or in contact sports, and the majority of them are children. That’s a staggering number, both in human suffering and the costs exacted on their families. It is also very surely an undercount. “The large majority of concussions don’t render kids unconscious, so neither they nor their coaches know they’ve happened,” says Dr. Robert Cantu, chair of neurosurgery at Emerson Hospital, the co-director of the Center for the Study of Traumatic Encephalopathy (CSTE) and the nation’s leading authority on concussions. “Boys in particular don’t tell us when something’s the matter. The real number is way north of 4 million.”
Cantu, the author of the recently published Concussions and Our Kids, made headline news when, on a book tour last fall, he urged parents to pull their kids from tackle football until they turn 14. Columbia- and Harvard-trained, he isn’t given to rash pronouncements or attempts to blow up football’s talent pipeline. He’s simply speaking from deep experience treating children who suffer concussions, many of whom don’t make meaningful progress in the weeks and months that follow. “About 90 percent of kids with concussions heal fine with proper rest and precautions,” he notes. For reasons not understood, though, the remaining 10 percent contract the malaise called post-concussion syndrome, or PCS. Every day in his office at this suburban hospital a half-hour west of Boston, he sees boys and girls with some of the 26 symptoms on the PCS checklist. Fatigue, dizziness, memory failure; lightheadedness, nausea, lack of focus: these can linger indefinitely in shifting clusters, costing patients a year of school or even more. The bigger blow, however, is to their mental development. “There’s an epidemic of kids whose normal trajectory is permanently stunted by head injury,” says Cantu. Over time, some “pass grades again and are thought of as fine, but might have been superior instead of average.”
No major studies are under way to try to count those kids or to determine why their symptoms don’t improve. “We have barely enough funding to study adults, and the neural setup is different in kids,” says Dr. Ann McKee, the neuropathologist who runs the brain bank for CSTE. At her warren of labs at the VA Hospital in nearby Bedford, Massachusetts, McKee, a handsome blonde working 60-hour weeks to whittle down a backlog of cases, hands across slides of the brains she’s examined – 10-micron-thin sections sealed in wax. The first one she shows me belonged to a boy who collapsed during a game in 2010. Nathan Stiles was as special as Eric Pelly – National Honor Society student, senior homecoming king and a running back for the football team – who had life by the throat at his Kansas high school when he returned, unhealed, from a prior concussion. Doctors had done a scan of his brain and found no swelling after the first concussion, despite his complaints to coaches and his parents about recurring headaches. But PCS is a crisis of molecular scale, a firestorm of ions leaking in and out of neurons to wreak havoc on their tiny connections. You can’t catch that on an MRI and won’t be able to in the near future. The only way to detect it is through a thorough examination by a concussion-savvy doctor or neurologist. Nathan went to his family physician, who after further testing and confirming he was headache-free cleared him to play less than a month after the concussion.
In his final game, he was playing well on both sides of the ball when he suddenly stumbled off, holding his head. There’d been no big collision, no helmet-to-helmet takedown, but with post-concussive kids, even a trivial blow can touch off fatal swelling in the brain. On the sideline, Nathan swooned and was deeply unconscious before the trainer reached him. Hours later, he was brain-dead in an ICU, where his devastated parents were saying goodbye and signing forms to donate his bone and tissue.
“It’s called second-impact syndrome and only affects kids, or people under the age of 25,” says McKee. “We think it’s the immaturity of their nervous system – it can’t handle the flux of salts and ions that an older, more developed brain can. But we’re not really sure of that yet. It’s an area of intense debate.”
Nathan had another thing in common with Eric Pelly. When McKee stained sections of his brain with a chemical marker, she found small but significant clumps of poisoned tau, the primary culprit in CTE. Tau is a structural protein in axons, those long-armed fibers that link nerve cells together, carrying messages and nutrients up the line. In concussions, where the brain is violently shaken, bouncing against the hard walls of the skull, the primary damage isn’t bruises and bleeds but rotational and linear stretching and tearing. Anchored like a disc drum around the brainstem, the brain swivels hard in one direction, then snaps back hard in the other, stressing the membranes of its axons. Tiny holes appear in them, leaking potassium out and letting calcium in. This sends the system into a four-bells freakout: The axons shut down, trying to pump the calcium out, the nerve cells they’re tied to flood with stimulants and tau proteins fall off their skeletal ladder, piling like sticks on the axon floor. No drug exists now that can fix this mess or halt the neural meltdown once it has begun. Happily, the brain can rewire itself if given proper time and rest. Axons seal up again after swabbing themselves clean, switched-off neurons power back online and the rungs of tau reattach themselves to carry the chemical mail to other cells.
But in an age when pro players still hide their concussions as a red badge of courage and commitment, it’s essential to define what “proper rest” means – and what the lack of it portends for injured brains. “Physical rest is crucial, but so is cognitive rest, avoiding all kinds of mental exertion,” says Cantu. He orders his patients to switch the television, laptop and Xbox off till their cluster of symptoms has cleared. He concedes that it’s hard to do nothing for days, particularly for teens who spend half their lives communing with screechy boxes. But failure to let the nervous system mend sets up patients, first, for PCS and, second, for future concussions. And it’s those repeat insults to an unhealed brain that phosphorylate, or poison, the tau proteins. Once toxified, tau rots out the cells that house them, then slowly spreads to neighboring cells, killing them from the inside out.
Now, a high school safety will feel none of this happening, nor will a 30-year-old lineman. Stage one of the disease is either asymptomatic or marked by mild attention lapses. But in stage two (typical onset: the forties), the brain’s roll gate comes down with a thud. Short-term recall begins to fail, as do judgment, planning and coordination. Depression creeps in, along with fits of rage and/or psychotic breaks, and the frontal cortex of the brain, which coordinates things like focus and motor movement, begins to break down. Stage three sufferers, often men in their fifties, see their brains shrink as the major centers – the amygdala (keeper of emotion) and the hippocampus (memory) – continue to erode. By the final stage, dementia is total and often joined by other evils: Parkinson’s, ALS or seizure disorder. As distinct from Alzheimer’s, which kills patients, on average, seven to 12 years after diagnosis, CTE sufferers can live for decades in pitch-black confusion and distress. It’s a fate you would wish on no one you know, least of all your strapping teenage son.
After his sixth concussion, Chris Nowinski was home in bed, climbing the walls in the middle of the night. Not out of boredom or captive angst; he was actually asleep but standing bolt-upright, trying to scale the wall above his pillow. “I dreamt that someone was falling, and I needed to reach them,” he says. Nowinski, six-five and 260 at the time, a Harvard lineman-turned-wrestler on the brink of big stardom on the World Wrestling Entertainment tour, proved a hard man to reason with that night. “My girlfriend tried to wake me up but couldn’t do it,” he says. “I jumped head-first off the bed over a nightstand. And even after I landed, I was still asleep. That was what it took to scare me straight.”
Nowinski was 24 and a cash-cow prospect, the first Ivy grad to grace the mat of a Vince McMahon production. Just two years out of wrestling school, he’d vaulted the ranks of maulers to become a pay-per-view sensation named Chris Harvard. There were millions to be made before he turned 30, then the inevitable pivot to action movies or some other self-branding pot of gold. But Nowinski up and quit then, in 2003, afraid for his life and in constant pain. He’d had headaches before from prior concussions – two of them suffered as an All-Ivy tackle, four in his short time wrestling – but nothing like the ones that set in now and lasted five years without letup. “Excruciating migraines in the back of my head that would work their way forward,” he says. “Some days I could handle them, some days not. That was when the beer handled them.”
Medications proved useless or made things worse, wreaking havoc on his sleep cycle. “I’d act out dreams that I was choking to death, or put my girlfriend in a headlock and wake up to her screaming.” He saw a half-dozen doctors over the next couple of years before he found his way to Cantu’s office. “Till then, I’d thought this was my first concussion because none of the others knocked me out,” says Nowinski, mortified by his then-naiveté. “He said, ‘Yeah, but you’ve been hit and seen stars or heard ringing?’ and I said, ‘Of course, man, that’s all the time.’ He goes, ‘Well, those are concussions,’ and that was the ‘aha’ moment. Every guy I ever played with had those.”
Though slowed by his migraines and sleepwalking follies (chasing rabbits in his bedsheets, accosting imaginary intruders at his front door), Nowinski resolved to warn other athletes of the catastrophic risks they were courting. He read every study he could get his hands on, interviewed clinicians and ex-players by the dozens, then sat down to write a book, with Cantu’s support, that he hoped would change the state of play in sports. Published to wide acclaim in 2006, Head Games: Football’s Concussion Crisis made him the leading – and for a while, at least, the only – activist on an issue he was about to break wide. Over the next year, he talked the family of Andre Waters into donating for study the brain of the ex-Eagles safety after he shot himself to death at 44; talked the mother of Justin Strzelczyk into doing likewise after her son died in a wrong-way, high-speed chase at the age of 36; talked Teddy Johnson, the Patriots linebacker, into going public about his post-concussion syndrome; and persuaded the family of Chris Benoit to donate the brain of the superstar wrestler after he killed his wife, young son and himself. Each of the dead athletes tested positive for CTE, the most floridly afflicted being Benoit; all of 40 at his death, he presented the brain of an 80-year-old, punch-drunk boxer.
Having emphatically made his point, in a series of page-one bombshells, about the price being paid in collision sports, Nowinski could have honorably quit the scene for a lucrative job in biotech. (He was working part-time as a management consultant.) Instead, he went all in on head trauma, co-founding, with his friend and mentor Cantu, the Boston-based Sports Legacy Institute (SLI), a high-profile firm committed to ending the concussion epidemic and finding a cure for the related illnesses. Beginning in 2007, he single-handedly built a brain bank, cold-calling the families of hundreds of dead athletes and persuading many of them to donate tissue. Cantu, for his part, recruited McKee to perform the neuropathological studies, forging an alliance with Boston University to create the Center for the Study of Traumatic Encephalopathy, which received a $1 million gift from the NFL in 2010. That gift, among others, grew the scope of their inquiry: What the researchers have learned from their investigations these last couple of years has stunned everyone, including themselves.
“We started out thinking concussion was just a metabolic injury,” meaning a short-term shift of neural compounds, says Cantu. But looking at distinct groups of teenage athletes who’d suffered sports concussions (kids who’d died by suicide, as well as those from second-impact syndrome), they saw structural changes in the brains of both cohorts: early, focal pockets of CTE, in some teens, and long-term swelling of the axons. That dovetailed with the data from brand-new studies on boys during football season; it showed permanent damage in seemingly healthy teens who had never had a recognized concussion. This meant that every hit mattered, from peewees on, and counted toward an unknown threshold number past which brain cells began their die-off. “I’ve seen serious cognitive injuries in a nine-year-old boy,” says Cantu of a Pop Warner player he treated. “He lost the ability to remember names, as well as math and vocabulary, for the better part of a year. I never felt comfortable letting him play collision sports again.”
Though Cantu has also tended to dozens of pro athletes, some of whom have had “over 50 concussions in the course of their careers,” the thrust of his concern is school-age kids, whose risk for harm is grave and growing more so. Part of this owes to the professionalizing of hobbies: Kids now play and practice one or more sports eight to 10 months a year, so there’s much more exposure to blunt-force trauma – and much less downtime to heal. The other factor is basic physiognomy: Kids have gotten bigger and faster in the past decade but lack mature muscle in and around their necks to brace for the hits they see coming, so the whiplash damage is more severe than in men who’ve built bull necks. “Kids’ heads are almost full size by the age of four, but their musculature obviously isn’t, so you get the bobblehead effect on the brain,” says McKee. This is especially true for girls in contact sports: They’re twice as apt as boys to sustain a concussion playing soccer, lacrosse or ice hockey. And those games pale beside the mother of head trauma: competitive cheerleading meets. In 2011, 37,000 cheerleaders were taken to ERs, many from being dropped on, or kicked in, the skull during aerial maneuvers. Only football results in more catastrophic injuries – and those boys have the benefit of helmets.
Clearly, things must change, and better equipment isn’t the answer. “The best helmets in the world don’t stop rotational forces, where the brain whips around and snaps back,” says Cantu. Nor, despite the efforts of SLI and its counterparts around the country – the Brain Injury Research Institute, headed by Omalu, Dr. Julian Bailes of Chicago and Fitzsimmons, the West Virginia lawyer; the Brain Injury Research Center at UCLA, directed by the neuroscientist Dr. Dave Hovda, whose work on setting protocols for blast-injured soldiers has saved countless troops from permanent brain woes – are scientists much closer to a drug or hormone that will mitigate the fallout from concussions. Trials are under way for anti-tau compounds that may or may not break up toxic bundles, but earlier versions have been rousing busts in the grail for a dementia drug. There’s more cause for hope on the detection front: New scanners being tested have been able to spot tau in the deep-brain folds, with the help of a radioactive compound. When and if they’re approved by the FDA, the devices could alert young athletes and their families long before the onset of CTE. “If we identify it early, we can maybe arrest it just by stopping the activity that caused it,” says Cantu.
Still, the best prognosis is to avoid it altogether, and there’s slow but steady progress along those lines. A search is well along, at SLI and elsewhere, for the bio-markers of mild brain trauma, proteins found in blood or spinal fluid that tell doctors of an unhealed concussion. “Again, given time, most brains heal themselves and don’t start the pathogenic process – even after multiple concussions,” says Cantu. But that, of course, opens a great conundrum: Why do oft-concussed quarterbacks like Steve Young and Joe Montana appear perfectly lucid in their fifties, while men with fewer recognized knockouts develop dementia at that age? “Clearly, there’s genetic variability here, just as it’s harder to knock certain men out than others,” says Cantu. “We’re trying to identify those genetic factors, so that if a kid tests positive for the markers, his parents can hold him out of contact sports.”
However, all this is probably years, and many millions of dollars, away, and meanwhile, the carnage goes on. When eight-year-olds are hitting each other – in tackle practice – with roughly the same G-forces as college players, what’s badly needed is a paradigm shift, a universal up-draft in thinking. Happily, there are signs. Forty states have passed legislation modeled on the Zachary Lystedt Law, so named for a 13-year-old boy in Washington state who nearly died from second-impact syndrome. It requires that everyone connected with school athletics (parents, coaches and the players themselves) be educated in the symptoms and perils of concussions; that any child suspected of having a concussion be pulled from the game or practice field, and that he or she be barred from returning to play until cleared by a physician. The NFL has thrown its weight behind the law; Commissioner Roger Goodell has urged the governors of holdout states to enact Lystedt or similar legislation. And heavy grassroots work by Nowinski and others has helped spread the gospel about concussions; they go town by town and school by school. Finally, SLI developed a hit-count program for kids, aimed at reducing the number of full-pad practices at every level of youth football. “We’ve put in pitch-count limits to protect kids’ elbows,” says Nowinski. “Why wouldn’t we do likewise to protect their brains? Isn’t that the obvious place to start?”
Well, obvious to kids and a growing number of coaches, who’ve been open to the idea of limited hitting. The door slams shut, though, when talking to parents, many of whom insist on toughening their sons for NFL careers they’ll never have. “Whether it’s starting kids later or doing fewer drills, we hear the same thing over and over,” says Cantu. “It’s ‘I’m not signing him up for flag football. My kid needs to learn how to tackle.'”
For the first two years after Eric died, Joan sat on her couch in a nimbus of grief, surrounded by pictures of her son. There were many months of counseling in a group for bereaved families, and a deep bench of friends dropping by with food to fill the empty hours. It took all her strength, though, to get Jenna off to school and drive her to her dance lessons; everywhere else, people asked how she was doing, attempts at consolation that pricked her heart. A private woman and a devout churchgoer with no taste for media attention, Joan declined to go public about his CTE, though as the then-youngest person to contract the disease, Eric’s case was important medical news. (Nathan Stiles, 17, has since supplanted him.) Meanwhile, his tissue sat in fixative at the CSTE brain lab. On the SLI website, he was identified only as John Doe, High School Football Player.
When her sadness began, at length, to lift enough to return to some version of her life, Joan decided to tour Bedford and come to terms with Eric’s remains. But as she browsed the SLI website, she was pained by the thought that he was anonymous. She saw less and less sense in keeping silent about CTE; there was a duty to other mothers to speak out. Last spring, she phoned Cantu and asked to change the case heading: “I needed Eric’s name on the record.” Around the same time, she got a call. Katie Couric wanted to fly her to New York and tell the story of her son.
In the greenroom during the taping, Joan and Cantu met the family of a 16-year-old girl with PCS. A New Jersey hockey player who’d suffered three concussions, the girl, like her mother, was deeply concerned about playing the game again. Not so her gung-ho father, who insisted she return when doctors cleared her. “He was being a real jerk about toughing it out and getting a scholarship to college,” says Joan. “I could feel my blood boil as we waited there. Luckily, Dr. Cantu did the talking.”
After she and the doctor filmed their segment, they went back to the greenroom. Watching on the monitor, the girl and her mother had been deeply impacted by Eric’s story. They asked Cantu for advice; he answered with a question: What were the girl’s dreams in life? “She said, ‘I want to be a doctor.'” Cantu looked at the girl’s father and said, “She’ll need every healthy brain cell that she has.” The man glared back and said, “You haven’t convinced me. I’ll need more evidence than that.”
Joan, a mild woman stirring cream into her coffee, turned purple recalling the exchange. “I wanted to say to him, ‘What more evidence do you need? Isn’t my son’s death enough?'”
This story is from the January 31st issue of Rolling Stone.
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