In the early sixteenth century the Italian physician Jacopo Berengario da Carpi, a pioneer in the science of anatomy, was dissecting hundreds of human cadavers and sketching his findings. He took apart skulls and examined brains and he 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 the skull 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 sixteenth 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. It was a description of the state of unconsciousness and other functional problems that resulted from impact to the head, and most of the medical literature of the day pointed out the good news: unlike more severe forms of head injury, like crushing your skull or getting a bullet through your brain, this condition was temporary.
Or was it? Did the brain really always recover from concussions? Could there be a cumulative effect from multiple such injuries to the head? That question wouldn’t get serious consideration until the twentieth century. 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 about one hundred such patients. “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 it got people like Harrison Martland, a forensic pathologist in Newark, New Jersey, thinking. He was interested in studying boxers, popular 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.”
Martland’s paper read as a plea on behalf of punch-drunk boxers everywhere who ended up going crazy and were sent to asylums where they would eventually turn into full-blown lunatics and curl up and die. It was not an unknown path; boxing was so popular it seemed everybody knew somebody who was slug nutty. Boxing was the most popular spectator sport in the United States and England, and anyone could put up their dukes and do it. The boxing booths would come to town for fairs and shows and the boxers would invite anyone to take them on and people would place bets and drink and holler. The punch-drunk boxers were the showstoppers.
“As far as I know this condition has practically not been described in medical literature,” Martland wrote. “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.”
But he didn’t have any proof. He hadn’t autopsied any boxers’ brains.
“I realize that this theory, while alluring, is quite insusceptible of proof at the present time,” he wrote. “But I am so convinced from my former studies on post-traumatic encephalitis that this is the logical deduction that I feel it my duty to report this condition.” Martland 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.
—
Prema had taken to visiting Bennet and watching his TV because she didn’t have one. Then, as long as she was visiting, she figured she may as well cook, and so the two of them began sharing meals regularly. No candlelight dinners; none of that. This was just eat, get back to work. Prema’s own studies kept her up late and she enjoyed the companionship. On the days she had hospital rotations outside the city where the buses didn’t reach, Bennet would drive her, and if she had an early morning rotation she would stay at his apartment the night before. It was convenient, they both agreed. Nothing more to it.
“I know I don’t live here and I have no right to complain, but must you store brains next to my soup?” she said one time.
He was bringing brains home, slicing them on the patio or out in the hallway. She thought it was such a curious hobby. She took photos of him doing it and they laughed. “Perhaps you might get a separate refrigerator?” she asked. She had no idea what he was studying or why he would be studying it. She was busy with her own work. She had never heard of Mike Webster and had no idea what football was.
One night, Bennet was looking in the microscope and she heard him say, “What is this? What in the world—?” He was looking at a slide from a section of Mike Webster’s frontal lobe, and he saw strange, dark splotches.
“What’s going on?” Prema said, calling from the kitchen.
“I have no idea,” he said, flipping quickly now through one slide, then another. “It doesn’t make any sense.”
“What the mind doesn’t know,” she said in a singsong voice. It was a shorthand version of the phrase Bennet had taken to repeating.
“—the eye cannot see,” he finished. “Yes, yes, exactly, Prema!” A professor had once taught him the saying and he never forgot it. You can’t know what you’re looking at unless you understand it.
He flipped to another slide, saw the same dark splotches. He sat back in his chair. “What the—?” He consulted a medical textbook, then another one, then dug into a binder of journal articles he had collected. He went back to the slides, the books, the slides. He kept finding the splotches—in Mike Webster’s brain and in the books. He became increasingly engrossed in the story unfolding on the slides, and in the books, the history of concussion and brain trauma, what people knew and when they knew it, the rhythm of the evolution of science, fits and starts and wrong turns and denial and more fits and starts.
—
Scientific proof of Martland’s 1928 theory about punch-drunk boxers wouldn’t come for another four decades. In 1973 the British neuropathologist J.A.N. Corsellis studied fifteen former boxers who had died of natural causes. He cracked open their skulls, took their brains out, and studied them. He called his brain bank the Corsellis Collection and he documented his findings, including the clinical information he was able to gather, postmortem, from family members.
Case 1 (R.H. 54/71.) This boxer’s ex-wife, a sister, and a brother were interviewed. He was a bright, healthy boy who did well at elementary school and excelled at sport. His boxing career began at a charity show when he was 11 years old and he went on to fight as a professional for the next 14 years. The number of his fights [is] estimated at 400; he lost a handful and one contest was stopped. He fought in the United States and became a British and a World Champion. As a young man he was quiet, generous, and abstemious. He married in his early 20s when he had already become a social as well as a boxing success. Soon his life became more hectic and “he changed completely.” He wenched and drank and gambled heavily. His memory began to fail him. He had three car accidents….His marriage broke up and he drifted away from his family, only returning for the occasional embarrassing visit.
He had violent outbursts, he was “knocked out” by only a small amount of alcohol, his behavior was “disgusting.” His brother remarked that “his brain was not functioning—he made mistakes in reckoning.” He could not settle in a job and he became a vagrant….At the age of 62 he was found lying neglected and louse-ridden in the boiler house of a hotel.
Case 7 (R.H. 124/71.) In this case the wife was interviewed. Her husband came from a family of boxers. He was not good at school—“he could read and write but never did.” He started boxing as a professional at the age of 16 years and during the next 20 years or so he fought an estimated 400 contests. He was a popular, successful man and he traveled on many boxing tours around the world. He retired from the ring after a particularly damaging fight, and started to teach physical training and boxing in boarding schools. He gave this up after a few years at a time when he was drinking heavily and beginning to become moody and violent. A few years later he lost a job in a printing works for hiding away to sleep and he seems not to have worked again….He had spells of “going within himself” followed by aggressive attacks on his wife and his home. He complained of violent headaches; his sexual demands gave his wife little rest. He wandered, out, half-dressed, at night and would importune for money. He had “glassy-looking eyes”; he was doubly incontinent at times….He could not be left alone. When 59 he was admitted to a psychiatric hospital and found to be grossly demented.
Case 13 (R.H. 125/71.) The patient’s daughter was interviewed….He joined the Royal Navy at 14 years and rose to Petty Officer rank. During this time he boxed as an amateur and won a Royal Naval Championship in his weight. He won “several cups and many canteens of cutlery”; he took part in exhibition bouts; he was knocked out several times. He had cauliflower ears and a deformed nose. His wife had described him as good-tempered and popular at that time with a keen sense of responsibility and strict personal standards….He became “more vague” and “spoke more slowly.” He began to neglect his appearance and he complained that he could not grip things or get on a bus. His sight and his memory seemed a little faulty….He became violent after two pints of beer, sometimes “fighting with his wife.”…He wandered away bemused and had to be taken to a mental hospital. He was then 53. On admission he was mildly confused and complained of blackouts. His wife, from whom he was separated, but who was still concerned for him, said that his personality had been changing for the worse….He could not recall his address or the date…completely disoriented and needed help with dressing….The deterioration continued. He became incontinent, paranoid, and aggressive. He ate off the table with his fingers; a cigarette packet he called a flower; he undid buttons when asked to put his tongue out. He continued to have blackouts and a few days after a convulsion he died from bronchopneumonia, aged 57 years.
“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. Bruised and bashed, swollen and atrophied, 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.”
“A single punch,” Corsellis wrote, “or even many punches, to the head need not visibly alter the structure of the brain but there is still the danger that, at an unpredictable moment and for an unknown reason, one or more blows will leave their mark. The destruction of the cerebral tissue will have then begun and, although this will usually be slight enough in the early stages to be undetectable, it may build up, if the boxing continues, until it becomes clinically evident. At this point, however, it could be already too late, for destroyed cerebral tissue can never be replaced, while the further danger exists that the process of degeneration could smoulder on even after the boxing had stopped.”
In his dining room, Bennet looked at the photos of the Corsellis Collection; he had this article in his collection of journal articles in his binder. He looked at the photos he had taken of Mike Webster’s brain before he sliced into it. He put these images side by side. The Corsellis brains were bruised and bashed, swollen and atrophied. Webster’s was not.
Bennet had imagined finding evidence of dementia pugilistica when he looked at Mike Webster’s brain. He imagined irregular folds in irregular patterns as in the Corsellis Collection.
But now he was looking at Mike Webster’s brain under the microscope.
And now he was reading what Corsellis saw in the boxer 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.
Corsellis could have been dictating Bennet’s findings. These were precisely the changes he was finding in Mike Webster’s brain under the microscope.
“Everywhere,” Bennet said to Prema that night while he looked. “It’s all over the place! What are these clumps doing here?” he said, in his highest-pitched voice, the squeak that came out when he was angry or excited or both.
The clumps he found in Mike Webster’s brain were buildups of a protein called tau. Tau belongs in a healthy human brain. It acts as a kind of lubricant. But in concentrated masses, it forms clumps called neurofibrillary tangles. With the proper staining, these tangles announce themselves under a microscope and show up as dark splotches, random stars spitting rays.
“Everywhere,” Bennet said, flipping through a series of slides of Webster’s brain. Tau tangles were kind of like sludge, clogging up the works, killing healthy brain cells—in this case cells in regions of the brain responsible for mood, emotions, and executive functioning. This was why boxers went crazy. This was why Mike Webster went crazy, too.
“Just everywhere,” Bennet said again and again into the night. He was finding tau tangles in the same regions as the Corsellis brains—and in other regions, too. Maybe this wasn’t dementia pugilistica, but it was similar.
What do you do with something you notice that no one else has ever noticed before? Do you believe your eyes? Why had no one reported seeing something like this before?
Because no one had ever gone looking for a disease like that in a football player’s brain before.
Was a professional football career similar to a boxer’s when it came to head injury? To the untrained eye—which Bennet definitely was when it came to both American football and boxing—it seemed similar.
What the mind doesn’t know, the eye can’t see. But what the mind knows too well, the eye can miss altogether.
—
It was a warm day in May 2003 when Bennet 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.
“Bennet?” Hamilton said. He took off his glasses and extended his hand.
“You like the suit?” Bennet said, standing in the doorway with his arms outstretched, like, ta da! He had taken to wearing his best suits even to run errands.
“I see ol’ Cyril is treating you well,” Hamilton said.
“He taught me that a black man must dress impeccably to get respect,” Bennet said.
Hamilton smiled. He had forgotten about this; Bennet had a way of blatantly referring to matters others considered indelicate.
“The gay life is good?” Bennet asked.
Hamilton shook his head. How do you even answer something like that? Bennet had never met a gay man before Hamilton, and he found the concept fascinating and culturally enriching.
“It’s really great seeing you again, Bennet,” Hamilton said.
“Your shirt is thin and lifeless,” Bennet said. “Have you considered starch?”
“Please, Bennet, please come in.”
“I have something for you
to look at,” Bennet said, and he handed him the tray of slides. “Take your time with it.”
“Now?”
“Can you?”
Hamilton rolled over an office chair for Bennet and told him to sit and he turned to his microscope and began looking at the slides.
“You’re not going to tell me what I’m looking at?” Hamilton said.
“No. Like the old days. See what you come up with.”
This was sport for neuropathologists. A guessing game. Can you look at the pathology and guess what the patient was suffering from?
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,” Bennet said. And so Hamilton took his time. One slide after the other, while Bennet twirled in the chair like a kid on a playground. 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.
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