The Brain That Sparked the NFL's Concussion Crisis

How a puzzling autopsy report opened a new chapter in football history

Mike Webster’s death was significant. Iron Mike. The best center in the NFL. Nine-time Pro Bowler. Hall of Famer. Four Super Bowl rings. He had played in more games—220 of them—than any other player in Steelers history.

Plenty of guys had a hard time after retiring from football—you had to adjust to a new identity and a new schedule, like coming home from war. But Webster’s reaction seemed extreme. He got lethargic. He forgot to eat. One day he peed in the oven, frightening his wife and kids. Then he wandered off, meandering through Pittsburgh. He slept under bridges, in the Amtrak station, then in his truck. Somehow, he got guns. He would walk up to strangers and rant. “Kill ’em! I’m gonna kill ’em!”

His teeth started falling out. He got Super Glue, squirted each fallen tooth, and tried to stick them back in. He wrapped his hands with duct tape and stuck a pen in the tape so he could write thousands of letters. He bought himself a taser and used it on his stomach or his thigh. He zapped himself into unconsciousness, just to get some sleep.

And now here he was in the morgue, dead at 50.

With the electric saw, the pathologist Bennet Omalu carefully cut a cap out of the skull, pulled off the cap, and gently reached inside for the brain. He was thinking about football and brain trauma. Specifically, he was thinking of dementia pugilistica—“punch-drunk syndrome,” they called it in boxers. The condition’s clinical picture was somewhat like Webster’s: “Punch-drunk syndrome” was characterized by severe dementia—delusion, paranoia, explosive behavior, loss of memory—caused by repeated blows to the head. If chronic bashing of the head could destroy a boxer’s brain, couldn’t it also destroy a football player’s brain?

Surely someone in the history of football had thought to look for dementia pugilistica. Unlike boxers, football players wear helmets, but a helmet can’t fully protect the head from damaging impact. The brain is suspended in a kind of thick jelly inside the skull, and a helmet can’t keep it from sloshing around. If you hit your head hard enough, the brain goes bashing against the walls of the skull.

Omalu had seen plenty of cases of brains destroyed within helmets. Omalu picked up Webster’s brain, carried it slowly to the cutting board, and turned it upside down and on its side and then over again. It was not at all what he expected. Regular folds of gray matter. No mush. No obvious contusions, like you find in dementia pugilistica. No shrinkage like you would see in Alzheimer’s disease. He reviewed the CT and MRI scans. All normal.

* * *

In his medical writings, Hippocrates mentioned what he called commotio cerebri—the loss of speech, hearing, and sight that could result from “commotion of the brain,” a vigorous shake or blow to the head.

The 10th-century Persian physician Abu Bakr Muhammad ibn Zakariya Razi is thought to be the first to make the distinction between the dramatic kind of brain injury— bruising and swelling and bleeding—that outright killed a person, and another, more subtle kind: an injury to the head that could make you dizzy, could even knock you unconscious, but from which you recovered. Razi was the first to use the term “cerebral concussion.”

In the early 16th century the Italian physician Jacopo Berengario da Carpi, a pioneer in the science of anatomy, came up with the idea that perhaps “brain commotion” was caused by the thrust of the soft structure of the brain against the solid case of the skull. The brain, he posited, was essentially bruised inside the skull by banging against its walls.

That would turn out to be a prescient theory. But there was little hope of advancing it, even when the microscope was invented at the end of the 16th century. Few people died from concussions, and so doctors didn’t routinely have concussed brains to autopsy. Without the underlying pathology to describe it, the word “concussion” remained a description, not a diagnosis. Most of the medical literature of the day pointed to good news: Unlike more severe forms of head injury, like crushing your skull or getting a bullet through your brain, this condition seemed temporary.

* * *

Mike Webster’s brain sat for two weeks in a white plastic bucket of formaldehyde at the morgue. When it was firm enough, Omalu pulled it out and put took a scalpel to the frontal lobe, cutting a section from it about the width of a stick of gum. He did the same to the parietal, occipital, and temporal lobes. He took the four slices to the lab at the University of Pittsburgh, where he had just finished his neuropathology training and knew the technicians and their particular expertise. He said nothing about whose brain he was giving them.

Omalu told the technician to shave each block of Mike Webster’s brain into microscopic slivers, then mount the slivers onto glass slides and stain them to bring any unusual patterns of cells into view.

He told the technician to submit the bill for the tissue processing to him personally, not to the coroner’s office. It would cost a few thousand dollars for just the first batch of slides, but he didn’t want any of the techs at the morgue involved in the paperwork, didn’t want anyone looking over his shoulder or making fun of him for indulging a personal curiosity.

The first time Omalu looked at the slides, nearly a month later, he didn’t see anything but clean tissue. The first slide didn’t show anything abnormal. Neither did the second or the third.

Puzzled, Omalu reviewed Webster’s death certificate and the photos he had taken of Webster’s body. The hospital report said Webster had died at Allegheny General Hospital from an acute myocardial infarction. He suffered from “depression secondary to post-concussion syndrome,” suggesting the syndrome was a contributory factor to his death, thus making it accidental.

Omalu thought about the term “post-concussion syndrome.” It was something he hated about being a doctor: People always wanting a name for something, doctors inventing them. As if naming had anything to do with healing, let alone science. You couldn’t come up with a more vague term than “post-concussion syndrome.”

* * *

For centuries, no one really considered the question of whether the brain really always recovers from concussions, or of whether there could be cumulative effects. But in the early 1900s, researchers like Michael Osnato and Vincent Giliberti, a pair of New York neuropsychiatrists, began finding patterns of mental degeneration in patients who had sustained mild head injuries. “It is no longer possible to say that concussion is an essentially transient state which does not comprise any evidence of structural cerebral injury,” the authors concluded in a 1927 Journal of the American Medical Association article. “Not only is there actual cerebral injury in cases of concussion, but in a few instances complete resolution does not occur, and there is a strong likelihood that secondary degenerative changes develop.”

That was a significant claim, and Harrison Martland, a forensic pathologist in Newark, New Jersey, took notice. Martland was interested in studying popular boxers athletes of the day, many of whom were exhibiting strange behaviors. Fans called them “cuckoo,” “goofy,” or “slug nutty” and people enjoyed screaming at them as they staggered around the ring like intoxicated fools. What was going on in their brains?

“Punch Drunk” was the title of Martland’s article in the October 13, 1928, issue of JAMA. “Punch drunk most often affects fighters of the slugging type,” he wrote, “who are usually poor boxers and who take considerable head punishment, seeking only to land a knockout blow. It is also common in second-rate fighters used for training purposes, who may be knocked down several times a day.”

“As far as I know this condition has practically not been described in medical literature,” he continued. “I am of the opinion that in punch drunk there is a very definite brain injury due to single or repeated blows on the head or jaw which cause multiple concussion hemorrhages in the deeper portions of the cerebrum.”

Martland didn’t have any proof—he hadn’t autopsied any boxers’ brains— but he posited that a boxer’s brain was bruised, and that the bruises formed scars and caused the brain to atrophy. He said he believed that nearly one half of fighters who stayed in the ring long enough would develop the condition.

“The condition can no longer be ignored by the medical profession or the public,” he wrote.

And yet it was. People loved boxing.

Scientific proof of Martland’s 1928 theory about punch-drunk boxers didn’t come until 1973, when the British neuropathologist J.A.N. Corsellis cracked open the skulls of 15 former boxes who had died of natural causes and studied their brains. He called his brain bank the Corsellis Collection and supplemented his findings with whatever clinical information he was able to gather from the family members of the deceased.

“The Aftermath of Boxing,” Corsellis titled his paper. He told the case histories and followed each with a description of what he found when he looked inside the skulls of the dead boxers: unusual and specific damage to the tissue, with irregular folds in irregular patterns. There was no question, even before examining the tissue under a microscope, that the boxers had sustained cerebral damage. Corsellis called the disease “dementia pugilistica.”

One night, Omalu was looking in the microscope at Webster’s brain and saw strange, dark splotches. He flipped to another slide, saw the same dark splotches. He consulted a medical textbook, then another one, then dug into a binder of journal articles he had collected—a binder that included photos of the Corsellis Collection.

Omalu looked at the images of Corsellis’s brains, then back at the photos he had taken of Webster’s brain before he sliced into it. The Corsellis brains were bruised and bashed, swollen and atrophied. Webster’s was not.

But then he read what Corsellis saw in the boxers’ brains under a microscope.

The hippocampal neuronal population was considerably depleted. . . . Many neurofibrillary tangles in the nerve cells of the frontal and temporal cortex . . . particularly marked in the anteromedial temporal gray matter including the amygdaloid nucleus, the hippocampus and the parahippocampal gyrus.

He looked again at Webster’s brain under the microscope. Corsellis could have been dictating Omalu’s findings.

The “neurofibrillary tangles” that Corsellis had described—and that Omalu was seeing in Webster’s brain—were buildups of a protein called tau, which in a healthy human brain acts as a kind of lubricant. But in unhealthy brains, the protein can form clumps.

These concentrated masses acted like kind of like sludge, clogging up the brain and killing healthy cells—in this case, cells in regions responsible for mood, emotions, and executive functioning. This was what happened to boxers. It appeared to be what happened to Webster, too.

It was a warm day in May 2003 when Omalu drove up to the University of Pittsburgh to see his former professor, the neuropathologist Ronald Hamilton, who had been his teacher through his two-year fellowship training. “I have something for you to look at,” Omalu said, and he handed him the tray of slides. Hamilton flipped through the first two slides, then dropped his shoulders in boredom.

“You’re bringing me an Alzheimer’s case?” he said. “You do realize I spend my day with these—”

“No, keep looking,” Omalu said. He needed Hamilton’s read on this. Hamilton was the expert—he’d made a significant discovery about abnormal masses of proteins in the brains of Alzheimer’s patients during his decades-long career looking in microscopes.

“Huh,” Hamilton said, having finally figured the puzzle out. “So how did you end up with a boxer down at that morgue?”

“It’s not a boxer,” Omalu said.

Omalu explained the major difference between dementia pugilistica and his finding. The brain didn’t look battered at all on gross examination, he said. It looked perfectly normal. It wouldn’t be something a pathologist would have cause to go looking for. There would be no signs of it in a normal autopsy. You would have to know the clinical history. You would have to then go cut the brain, stain it with these particular stains, and then look at it under the microscope. You would have to go through all the steps Omalu went through, following no protocol, following the call of only his own blind curiosity.

“Dementia footballistica,” Hamilton joked. He kept going back to the slides. “This is crazy. This has never been identified before.”

Omalu and his former professor then paid a visit to the chair of the University of Pittsburgh Department of Neurology, Steve DeKosky, the director of the Alzheimer’s Disease Research Center, who was preeminent in the field of neurodegenerative diseases.

He knew brains. And he’d had his own questions about the NFL and brain trauma. Alzheimer’s researchers in his circle of colleagues had been talking about retired NFL players reportedly having memory problems. He had reached out to the NFL Hall of Fame and suggested a design for a large longitudinal study that would track Hall of Famers over time. The suggestion was never acknowledged—no one from the association had even written back to him—and the slight had made DeKosky ever more curious.

And now Hamilton was appearing in his office with a former fellow—that odd man who chose to work at the morgue instead of pursuing an academic career—with something to say about the brain of an NFL player. The three sat and repeated the guessing game, only this time DeKosky was the one looking in the microscope.

“You have my attention,” DeKosky said, and he got up to close the door. Soon, Omalu would have America’s.

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This article has been adapted from Jeanne Marie Laskas’s book, Concussion.