League of Denial Page 19

  What Omalu was seeing under the microscope was the buildup of tau, a protein that enables the brain’s ability to function but can also strangle it. Without tau, neurons would collapse, cutting off the flow of nutrients and molecules to the cells. But sometimes, especially later in life, tau congeals into clumps called neurofibrillary tangles. These tangles slowly strangle the neurons from the inside. In neuropathology, they are one of the two defining markers in Alzheimer’s disease. The other marker is the buildup of beta-amyloid plaques: hardened proteins that surround the cells and poison them.

  The staining of the slides is what brings the tau to life; otherwise, you can’t see it. Under a microscope, tau appears as tiny brown splotches interspersed among a pattern of normal cells represented as dots, as if someone had dripped dark brown paint on a flecked marble tile. As Omalu examined the slides of Webster’s brain, he saw lots of brown splotches. He also saw signs of amyloid plaque, but the pattern didn’t look like Alzheimer’s as he had been trained to identify it. There was very little beta-amyloid, and it had taken on a slightly different form. Even stranger, the tangles of tau seemed to be distributed haphazardly throughout different parts of the brain, almost without rhyme or reason. In Alzheimer’s disease, numerous tangles are present in the hippocampus (an area of the brain involved with memory) before they are seen in the cortex (the outer part of the brain that is critical to cognition). But in Webster’s brain it was the opposite: Omalu saw many tangles in the cortex but none in the hippocampus. And besides, Webster was 50: He wouldn’t be expected to have Alzheimer’s disease.

  Omalu knew from his training that head trauma could cause tau to form tangles. The presence of a neurodegenerative disease had been chronicled in boxers since 1928, when Harrison Martland, the chief medical examiner for Essex County, New Jersey, published a landmark paper in which he used the expression “punch-drunk” as a medical term. The phrase, he noted, was already part of the vernacular of fight aficionados, who also referred to the condition as “slug-nutty” and “cutting paper dolls.” The condition was most pronounced among “poor boxers who take considerable head punishment, seeking only to land a knockout blow,” Martland wrote. In severe cases, Punch-Drunk Syndrome was characterized by “marked mental deterioration” that sometimes forced ex-fighters to be sent off to the asylum. Martland estimated that nearly half of all veteran fighters had some form of the syndrome.

  Martland has since been lionized for what is now seen as the seminal first study on head trauma and sport. But the reality was that his conclusions were not universally well received, especially by fight fans, who saw them as an unproven denunciation of the sport. It wasn’t until 1973 that dementia pugilistica, as it came to be known, was accepted as irrefutable science. A British neuropathologist, J. A. N. “Nick” Corsellis, cut open the skulls of 15 former boxers who had died of natural causes. The autopsies showed cerebral atrophy in 14 of the 15 cases. Corsellis, who put together his own brain bank, the “Corsellis Collection,” had shown for the first time that the repetitive head trauma associated with boxing led to the “destruction of cerebral tissue.”

  However, in Webster’s brain, Omalu didn’t see one of the hallmarks of dementia pugilistica: an opening in the septum pellucidum, the wall that separates the lateral ventricles in the brain. Plus, from what he had read, Webster didn’t seem to have any of the symptoms of Parkinson’s disease—slow gait, tremors, and slurred speech—that defined so many old boxers. Omalu’s working theory was that Webster may have been suffering from something similar to Punch-Drunk Syndrome, the reason behind his irritability and erratic behavior. Even that would be groundbreaking as there had never been a diagnosed case of brain damage associated with football.

  Omalu pressed on, still too reticent to come forward with his findings. He ordered additional stains of Webster’s brain tissue, paying for them out of his own pocket. He stacked up every piece of literature he could find on concussions, dementia pugilistica, head trauma, and football on his dining room table and went through it paper by paper. He read Martland, Corsellis, and numerous others on boxing as well as the recent work related to football by researchers such as Jeff Barth, Kevin Guskiewicz, and Micky Collins. He came across papers published by something called the NFL’s Mild Traumatic Brain Injury Committee, which was documenting the scientific effects of concussions in pro football.

  Finally, in the spring of 2003, Omalu was ready to seek a second opinion. He turned to his mentor, Ronald Hamilton, the neuropathologist who had helped train him during his two-year fellowship at UPMC. Hamilton was renowned as the first neuropathologist to show that Lewy bodies—abnormal masses of protein that develop in nerve cells and are commonly associated with Parkinson’s disease—were twice as common in Alzheimer’s patients than previously had been known. He had a close and somewhat paternalistic relationship with Omalu. Hamilton viewed his protégé as bright and ambitious but also a bit flamboyant and given to hyperbole. In forensic pathology—particularly Cyril Wecht’s brand of forensic pathology—certainty and authority under the bright lights are valued. Not so in neuropathology, in which scientific debates are more measured and deliberate than the fierce advocacy required in the courtroom. Omalu spoke in pronouncements, an attitude that earned him a warning from the head of the neuropathology program that he might not make it in academia if he kept it up. “That’s everybody’s experience with him. Bennet has a powerful personality, and at first it’s just like, What?” said Hamilton. “And then you start listening to him more and more—if you have the patience. And you start to realize that he’s really right on the mark. It’s just that his personality really drives some people nuts.”

  For his part, Omalu viewed Hamilton not only as a great scientist but as his introduction into a broader world. With characteristic bluntness, he announced one day: “Hamilton is gay. And Hamilton was the one who changed my attitudes toward gay people. I was very homophobic. I thought that gay people are bad people. Hamilton was the first gay person I had met. He was such a good guy; he was so good to me. For the first time in my life I realized that I had been fed lies by the church, by my family and society, that this guy is a good guy with a heart, who cared for me.”

  One afternoon, Omalu dropped by Hamilton’s office at Presbyterian University Hospital and asked if he would look at a special case he had been assigned at the coroner’s office.

  “What’s the case?” Hamilton asked.

  “I’m not going to tell you; just look at it,” said Omalu.

  This was a favorite game among pathologists. You wanted the second opinion to come with a clean slate, not even a suggestion of bias. Omalu’s biggest fear was that Hamilton would look at the slides and tell him that what he was seeing was “no big deal,” perhaps a variant of Alzheimer’s that Hamilton had seen many times before.

  Hamilton put a slide under the microscope. Then another. Then another.

  This wasn’t Alzheimer’s disease, not even early Alzheimer’s. The game was getting intriguing. Hamilton looked at more slides, keeping his thoughts to himself. This was something he had taught Omalu: Don’t muse. Wait until you’re ready to make a diagnosis.

  “Is this patient a boxer?” he asked finally.

  That made the most sense. He figured it would not be unheard of for the body of a boxer to show up at the coroner’s office. Maybe he had died in the ring and this was a case of dementia pugilistica.

  “No, this guy is not a boxer,” Omalu said, a smile coming over his face. “He’s an NFL football player. A Pittsburgh Steeler. This is Mike Webster.”

  Hamilton’s jaw dropped, literally.

  He knew immediately it was a new discovery, one with profound implications. In some ways Hamilton thought it was obvious; why hadn’t it been discovered before? But he had no doubts. The pathology—the haphazardly formed tangles, the scarcity of beta-amyloid—proved it.

  “I mean, if I had really felt any kind of hesitation about the diagnosis whatsoever, I would have said no,” said Hamilton.
“But it was so obvious, so logically beautiful. These are boxers with helmets on that are hitting each other all the time. And Bennet was feeling the same way. So we both came to the same conclusions without being unduly influenced. He didn’t say, ‘I want you to look at this case. It’s a brand new case of something that’s gonna be really big.’ He just said, ‘I want you to take a look at this case and tell me what you think.’ ”

  Hamilton, half in jest, said they should call it “dementia footballistica.”

  It was a once-in-a-lifetime discovery.

  “I knew this was a billion-dollar kind of finding when I saw it,” he said.

  Hamilton knew he needed more firepower. Omalu would be seen as a nobody—young, eccentric, and Nigerian. He wasn’t even officially a neuropathologist. Hamilton didn’t want to see him or the findings dismissed out of hand. Hamilton was known and respected, but he knew he needed to go higher.

  He called up Steve DeKosky, chairman of UPMC’s Department of Neurology, director of the Alzheimer’s Disease Research Center, and an internationally renowned expert in Alzheimer’s and related neurodegenerative diseases. Hamilton knew that if Steve DeKosky concurred that this was a new syndrome and was willing to stake his name and reputation on it, that would stamp it as serious science. DeKosky didn’t have time for games, and so Hamilton called him up and told him the story: how Omalu had an interesting case involving a 50-year-old man, how there were tangles of tau throughout the cortex but not in the hippocampus and very little beta-amyloid. Hamilton said he originally thought it was a boxer, only to be told by Omalu it was a 17-year veteran of the National Football League.

  “Really?” said DeKosky.

  DeKosky immediately flashed back to a conversation a few years earlier at a meeting of the Alzheimer’s Association. A colleague had recounted speaking with a representative from the NFL Hall of Fame who was concerned about the plight of retired players. Too many were showing up at the annual induction ceremony with serious memory problems. DeKosky had been fascinated. He wondered about the connection between all those hits and the problems that were surfacing in Canton. DeKosky did a little research and found that the president of the Hall of Fame Players Association was a lawyer named Ron Mix, a Hall of Famer himself who had played 11 seasons as an offensive tackle, mostly with the Chargers. DeKosky wrote Mix, introducing himself and laying out the design for a longitudinal study that would track Hall of Famers over time. DeKosky never heard back. He hadn’t thought about it much until Hamilton’s phone call.

  Even then, DeKosky was skeptical. He knew Omalu and viewed him the way almost everyone else did: “a wickedly smart guy” but cocky and prone to exaggeration. Hamilton told Omalu to pay DeKosky a visit.

  Omalu figured he might get 5 to 10 minutes. Omalu, after all, was little more than a student; DeKosky was the department chair.

  Omalu handed over the slides. DeKosky examined them under a microscope.

  DeKosky was stunned. Hamilton had been right.

  “This will change everything,” DeKosky thought to himself. “This will change everything forever.”

  He felt that Omalu had discovered “a new syndrome. Or, actually, the rediscovery of the physics that says if you beat the hell out of a human brain, this is one of the kinds of degenerative processes that occurs. I knew it was going to change everything, but quite frankly, it was so controversial that I just thought it’s going to take a long time before this is accepted.”

  But that sealed it: If Steve DeKosky agreed, the only other step was to take it public by publishing the research in a medical journal.

  That was no small task. It would be another year before the paper was completed. Omalu needed to expand on his research into head trauma and brain injury. DeKosky had to compile a clinical history of Webster by interviewing his family and creating a portrait of how his brain had short-circuited after his retirement. There was also the question of what to call the syndrome. Omalu thought it was critical that he come up with a name already in circulation so that if anyone attacked the findings, he could point to its earlier use in the medical literature. He also wanted something with a good acronym for lay people to remember and understand. In his review of the literature, Omalu saw references to chronic insanity, chronic encephalopathy, traumatic neurosis, traumatic encephalopathy, and occasionally chronic traumatic encephalopathy. Those terms, he thought, were all used generally, not to describe a specific disorder such as dementia pugilistica. He settled on chronic traumatic encephalopathy, or CTE. He thought it was easy to remember, and the language fit: Chronic meant long-term, traumatic referred to trauma, and encephalopathy was a damaged brain.

  To a man, the researchers thought they were providing a service to the NFL. DeKosky resurrected his letter to the Hall of Fame, explaining Omalu’s findings and expressing the researchers’ interest in doing a long-term study.

  Omalu titled the paper “Chronic Traumatic Encephalopathy in a National Football League Player.” He was the lead author. Hamilton, as the senior neuropathologist, also was listed, along with two of Omalu’s colleagues who contributed a section on genetics. In scientific literature, the position of final author is traditionally bestowed as a gesture of respect for the scientist who made the research possible, the “senior author.” Omalu initially picked DeKosky, an obvious choice. He had validated the findings, and his presence gave the paper stature. But Wecht, the coroner, was irate. He was Omalu’s mentor, the man who had made him. Webster had been autopsied in his lab. In the end, “Wecht really didn’t have anything to do with” the paper, said DeKosky, but he ceded the position, in part because he worried that Omalu might “be fired if he ticked the guy off too much.”

  The paper laid out the story of Mike Webster’s brain, though it didn’t name Webster directly, instead describing the subject as a “50-year-old professional football player who died approximately 12 years after retirement from the NFL.” Any true football fan who read it—not that any would—could have deduced from the “premortem history” that it was Iron Mike. The authors described the subject as an offensive lineman who was drafted into the NFL at 22 and played 17 seasons, 245 games overall, including 177 consecutive games in a 10-year window and 19 playoff games. Telephone interviews with family members revealed a man suffering from depression, memory loss, and signs of Parkinson’s disease.

  The first sentence got right to the point: “We present the results of the autopsy of a retired professional football player that revealed neuropathological changes consistent with long-term repetitive concussive brain injury.” Translation: This football player got brain damage from the daily pounding of his sport.

  The authors described it as a “sentinel case that draws attention to a possibly more prevalent yet unrecognized disease.” They recommended additional study to explore this “emergent professional sport hazard.”

  Omalu first submitted the paper to the prestigious Journal of the American Medical Association (JAMA). Three days later the paper was rejected. Omalu sent out a disappointed e-mail to his collaborators and suggested that they try submitting the paper to a journal called Neurosurgery. Reviewing the literature, Omalu had come to believe that Neurosurgery was “the official journal of the NFL committee on MTBI,” as he wrote to Hamilton and DeKosky.

  Submitting the paper to Neurosurgery made sense, because Omalu, Hamilton, and DeKosky all believed the NFL would welcome their discovery. Linking football and brain damage wasn’t great news, of course, but the league, they thought, would have to confront the implications that football causes brain damage and react accordingly, if only to protect the product.

  They were scientists. In the years to come, they would all look back and reflect ruefully on how naive they had been.

  “I thought they were gonna call me and embrace me and say, ‘Motherfucker, you’re such a hero,’ ” Omalu said. “I thought they were just gonna come and embrace me and give me a kiss on my cheek.”

  9

  THE DISSENTERS

  The NF
L rolled out Paper Number 5 in Neurosurgery in November 2004. By then, the league’s Mild Traumatic Brain Injury Committee had moved well beyond concussion videos and crash-test dummies. With each new study, the NFL was mounting a scientific argument. In essence, that argument amounted to this: Don’t worry, be happy. Concussion rates in the NFL are extraordinarily low. The number of concussions is a meaningless predictor of future injuries; theoretically, one can have an infinite number of concussions and still be fine. There is no link between football and brain damage because football players don’t get brain damage. To those on the other side of the argument, there was a kind of ham-fisted logic about this science of denial. NFL Commissioner Paul Tagliabue had created a research arm that exactly mirrored his skepticism about the so-called concussion crisis.

  NFL Paper Number 5 dealt with the modest 8 percent of players who had missed at least one game because of a concussion, described by Pellman and his colleagues as “the most severely injured of the NFL concussion cases.” Who were these players, and what happened to them? To start with, they were mostly quarterbacks, defensive backs, wide receivers, and kick returners “injured in high-speed, high-acceleration collisions.” Although this observation ignored the violence taking place in the Pit, it made some sense. The players on the perimeter were being hit with extraordinary force. It stood to reason that the most spectacular collisions were likely to result in the most severe injuries. Quarterbacks, who were often exposed and used their brains more than any other players, were perhaps most sensitive to the effects of concussions, as seen in the cases of Aikman, Young, and many others. Not surprisingly, these players had more acute symptoms: lingering memory loss, disorientation, sensitivity to light, lethargy, and so on.

  From there, Pellman and his colleagues went on to draw a number of conclusions that left some of the nation’s leading concussion researchers shaking their heads in wonderment. One finding was that even these severely injured players recovered very quickly and, when they returned, were not at greater risk for further injury. This conclusion ran counter to nearly all previous research, which held that one concussion left you predisposed to another. But the NFL’s logic was the same as in the previous studies: The fact that players went back on the field was an indication that they were fine; otherwise team medical personnel wouldn’t have cleared them. It is perhaps germane to note again that nearly half of the NFL’s concussion committee was made up of team doctors. Pellman, who was one, commended them for their superb diagnostic skills. He noted that only a small percentage of these players had been allowed back on the field the same day they suffered their injuries, an indication that “NFL team physicians and athletic trainers are extremely effective in screening out the most severely injured players on the sidelines within a short period of time after injury.” NFL doctors might actually be “overly conservative and cautious,” Pellman and his colleagues posited, in light of how quickly the players recovered and the risk of long-term brain damage—a risk that Pellman and his colleagues calculated was exactly zero: