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.
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