Part III: The Life and Contributions of Bennet Omalu MD

Prior to being referred to as case number A02-5214, Webster was known as Iron Mike, literally one of the strongest men in the National Football league during his playing career. Even the name of the town where he was born was sounded impressive:  Tomahawk, Wisconsin.  Growing up, Webster strengthened his 6-foot one inch, 255-pound frame by working on his parent’s farm.  He played football at the University of Wisconsin and was drafted by the Pittsburgh Steelers, with a career spanning from 1974 to 1990.   In those years, Webster became the best center in the NFL and made the pro bowl 8 years in a row. 

One of Webster’s most deadly weapons was his head, and he used it both physically and intellectually.  Not only was he a smart player, but he used that head also as a battering ram against the heads and chests of his opponents.  Defensive lineman struggled to find ways to neutralize the powerful Webster.  Harry Carson, the great New York Giants linebacker, stated that his best strategy against Webster was to club him in the head, leaving him dazed and confused.  “When I would explode into Mike, it was power against power,” said Carson.  I would hit him in the face.  That’s what we were taught:  to hit a guy right in the face so hard that they’re dazed and stunned.”  (League of Denial, Mark Fainaru-Wada and Steve Fainaru, Three Rivers Press, 2013, pg 25).  Although that sounds brutal, it was a common football tactic.  Jack Lambert, Webster’s teammate, once told reporters that he “got satisfaction out of hitting a guy and seeing him lay there for a while.” (League of Denial, pg 15).  In those days, contact was constant and heavy, even in practice.  Webster wasn’t known as Iron Mike just for his considerable strength.  At one point, he participated in 5, 871 consecutive plays in the NFL until he dislocated an elbow.  He was inducted into the Pro Football Hall of Fame in 1997.  After his playing career, he frequently made office visits to doctors, trying to explain his mood swings and lack of memory, among other symptoms he was having.  When a doctor, trying to understand his condition, inquired if he had ever been in a car accident, Webster was said to have replied, “Yes, 25,000 times.” That sad, but humorful, terse answer embodies, in a nutshell, the essence of Chronic Traumatic Encephalopathy. 

What Omalu saw on the slides puzzled him.  The pathology didn’t make sense in a 50-year-old athlete.  There were plaques in the brain, called neurofibrillary tangles, made up of Tau proteins, which were heavily phosphorylated, occupying space, and strangling brain cells and axons, contributing to neuronal loss. The abnormal Tau had a predilection for the deep sulci and perivascular areas, the territory around small blood vessel, suggesting structural damage or microhemorrhages from repeated head trauma.   Tau proteins are normal and important structures in the healthy brain, often occurring in distal neuronal axon microtubules, helping to stabilize the structure of the microtubule/axon complex and help make it semi-flexible.  This Tau, though, was disorganized, random, cluttering up the axonal highways and disrupting neuronal connections.  There were also neuritic threads in the neocortex, subcortical ganglia and brainstem nuclei.  The most severe damage appeared to be in the depths or furrows of the brain, called the sulci, as opposed to the folds of the brain, or gyri.  The sulci are especially vulnerable to the mechanical stress and shearing forces sustained with repetitive head trauma. 

Dr. Omalu sat back and took another bite of his apple.  He set it on the table and rubbed his eyes, trying to process what he was observing.  He knew this was something different.  Yet, what?  His mind started to sift through facts one by one, like frames slowly moving through a movie projector.  Tauopathy was seen in Alzheimer’s disease, but there was usually an abundance of amyloid extracellularly.  It was a hallmark of the disease.  There was very little of that here.  In Alzheimer’s often started in the entorhinal cortex and hippocampus and spread to the neocortex in a predictable fashion.  Here, he was seeing the Tau proteins in the perivascular areas of the deep sulci in the absence of considerable amyloid and in a much different distribution. 

He considered Dementia Pugilistica, first diagnosed almost 100 years ago, and caused by head trauma, repetitive concussive and sub concussive blows.  He reviewed the neurohistopathological classification of Dementia Pugilistica, but it didn’t seem to fit.  This seemed different.  It caused a widen septum pellucidum, a space in the midline that separated the left and right lateral ventricles.  It was widened in boxers with Dementia Pugilistica or DP.  DP also affected the substantia nigra, the symptoms of which could mimic Parkinson’s disease with neurologic impairments such as gait disorder, tremor, cognitive defects, and bradykinesia, or slowness of movement.  The boxer Mohammed Ali was a prominent example of this condition.  Omalu was not convinced.  He doubted by Alzheimer’s and Dementia Pugilistica.  This…this was something new.  Something different, he thought.  Of that he was convinced.  After reviewing the slides with equally baffled experts in neuropathology, including one of the leading experts on Alzheimer’s Disease, Dr. Steven DeKosky, head of the department of neurology at the University of Pittsburgh, Omalu was told these findings were significant and that he needed to have a name for this disorder and he needed to publish this case report.  He was told the first step would be to name the disorder.  After researching the subject, he came up with Chronic Traumatic Encephalopathy. 

To understand where medicine is going, it is imperative to know where it has been, and understanding Dementia Pugilistica is central to that process.  We know now that DP is a variant of CTE and literature on it as a disease state dates back about 100 years.  DP falls under the umbrella of CTE, not the other way around.  To understand the story of Dr. Omalu, one must first understand the most studied form of brain trauma to date, “Punch Drunk Syndrome,” or Dementia Pugilistica.

Harrison Martland, who received his MD degree from Columbia University and was a distinguished pathologist at Newark City Hospital, was the first physician to identify “Punch Drunk Syndrome” in the medical literature.  In 1928, he was approached by a boxing promoter to review twenty-three cases the promoter suspected were “punch drunk,” and the promotor wanted medical clarification on the subject.  At the time, “punch drunk” was not a medical diagnosis known to most doctors.  There was no literature on the subject, it was not taught in medical schools, and most doctors, especially those with no connection to boxing, remained ignorant of it.  Martland examined five of the twenty-three patients himself and read elaborate charts on the remaining eighteen.  The phrase “Punch Drunk” was used in the boxing world, however, among fighters, promoters, fight fans, and sports writers, who had been using the term for decades to describe the physical and mental impairments of some boxers.  One of the cases Martland personally examined, CASE 2, was representative of what became known thereafter in the medical literature, as Punch Drunk Syndrome.  CASE 2, or N.E. (later identified as Nathan Ehrlich), was a popular Jewish fighter from Philadelphia.  CASE 2 began his professional career at age 16, in 1906, and retired in 1913. He had been knocked out only twice in his career, once for upwards of an hour, however.  He had fought against extremely good competition.  He was no slouch, he was a refined and skilled boxer.  CASE 2 had frequented many doctors, all of whom had no idea what his diagnosis was.  He had fought many times, including 27 times in 1909 alone.  Tris Dixon, in his classic book Damage, the Untold Story of Brain Damage in Boxing, further describes the scene: 

CASE 2 had suffered no previous illnesses, nor did he regularly drink alcohol.  Despite this, the subject was frequently accused of being intoxicated because of the similarity of his symptoms with drunkenness.  Case 2 retired at age twenty-three because his left hand shook involuntarily and his legs were unsteady.  Martland also indicated that there were problems with his speech because his tongue “had a tremor.”” (Damage, Tris Dixon, 2021, Hamilcar Publications, pg. 5). 

Martland found that “Punch Drunk” boxers often staggered to their corners.  There symptoms may start during their boxing careers but never progress after retirement, or turn chronic, afflicting them with horrible neuropsychiatric maladies capped by shortened lifespans.  Their speech tended to be slurred.  Their legs might drag, give out, or feel weak.  They often had tremors, slowed movements, and a tendency to fall backwards when they walked.  Long term, they also suffered violent mood swings, rage, episodes of amnesia, and mental deterioration, sometimes ending up in asylums or sanitariums.  People in the boxing industry, and fans, knew intuitively when someone was affected by “too many blows to the head”.  To them, it was the obvious what was the cause of it.  Thus, they were called “cuckoo” or “Punch Drunk.”  Physicians on the other hand, had no clue, unless they happen to follow the fight industry closely.  There was nothing in textbooks or medical school to describe the condition. 

Martland saw the constellation of symptoms as being similar to Parkinson’s disease, and he labeled this a Parkinson’s-like syndrome.  Martland did not focus on the amount of concussions or knockouts a fighter suffered, but on the amount of blows to the head he received during the duration of his career.  He postulated that the less skilled boxers, and those used for sparring practice, were more likely to develop Punch Drunk Syndrome then the more skilled boxers, who were able to avoid many blows.  This thinking was later challenged by John Corsellis in 1973, who declared the opposite; Dixon puts it succinctly in his work Damage, “Unlike the neurologists who came before him, Corsellis believed the fighters who were the most at risk were the better, more successful ones.  They had the longest careers, fought the best opponents, and took more shots to the head.”  As echoed by Claude Abrams, former Boxing News editor, “When you match the best against the best, the fight is equal.  There is no give.  The duration of these matches is usually longer and the quality and the accuracy of the punches greater.  The stakes and desire to win are higher.  Consequently, these boxers push themselves to the limit.”  (Damage, Hamilcar Publications, pg 58).

Martland published his historic paper in the Journal of the American Medical Association in 1928, and it has since become the foundational paper on traumatic brain injuries in boxers, identifying deterioration of both motor and cognitive skills. 

The early boxers, pre nineteenth century, were bare-knuckled boxers.  It has been postulated that they suffered less from Punch Drunk Syndrome because they had to become more skilled with boxing techniques, throwing an economy of punches due to the risk of breaking one’s hand on the skulls of their opponents.  When boxing gloves were invented, the punch counts escalated considerably, and, along with it, the incidence of “Punch Drunk” fighters. 

Importantly, Martland had this to say about the medical consequences of boxing.  “The condition can no longer be ignored by the medical profession or the public.  It is the duty of our profession to establish the existence or nonexistence of punch drunk by preparing accurate statistical data as to its incidence, careful neurologic examinations of fighters thought to be punch drunk, and careful histologic examination of the brains of those who have died with symptoms simulating the Parkinsonian syndrome.  The late manifestations of the punch drunk syndrome will be seen chiefly in the neurologic clinics and asylums, and such material will practically fall to the neuropathologist connected with such institutions.”  (Damage, Tris Dixon, Hamilcar Publications, 2021, pg 7).  Compare that precise and ethical statement of duty with the statements and conclusions of the physicians assembled on the Mild Traumatic Brain Injury (MTBI) Committee by the NFL, were there was no ethical call to arms, no acknowledgement of the problem or responsibility to conscientiously explore the subject and get down to the truth.  It should be noted that Martland, though a pathologist, was not presented with any autopsy specimens to examine histopathologically.  All of the 23 subjects were still living at the time, including Battling Nelson, the Michigan Wildcat, Ad Wolgast, Joe “Iron Man” Grim, Billy Papke, known as the “Illinois Thunderbolt,” and Kid McCoy, all of whom eventually committed suicide, murdered someone, or ended up in asylums with what became known as Dementia Pugilistica. 

“In writing his paper Martland had used scientific research from New York neuropsychiatrists Michael Osnato and Vincent Giliberti, published the year before and entitled “Post concussion Neurosis—Traumatic Encephalitis” as well as C. B Cassasa’s paper “Multiple Traumatic Cerebral Hemorrhages.”   Osnato and Giliberti were the first scientists to propose that exposure to traumatic brain injuries, or TBI’s, could lead to neurodegenerative changes.  Their findings were presented at an annual meeting of the American Neurological Association in 1926.  (Damage, Tris Dixon, pg 7). 

Further research followed from Ernst Jokl in 1933 and Harry Parker in 1934, who wrote a medical paper titled “Traumatic Encephalopathy of Professional Pugilists,” while at the Mayo Clinic.  Parker stated there were two types of injuries to the brains of boxers.  Those that caused death instantly and those that caused long term deficits from repetitive blows to the head.  Jokl was one of the founding members of the pioneering American College of Sports Medicine who, ironically, honored Bennet Omalu with its man of the year award due to his pioneering research which brought awareness of CTE in the NFL.  It wasn’t until 1937 that J. A. Millspaugh suggested the name be changed from Punch Drunk Syndrome to Dementia Pugilistica, as he considered the former title demeaning to those patients afflicted.  He published this in an article in the United States Naval Bulletin. 

MacDonald Critchley was an English neurologist who published Medical Aspects of Boxing, Particularly from a Neurological Standpoint, in 1957 in the British Medical Journal.  Critchley called Dementia Pugilistica “Chronic Progressive Traumatic Encephalopathy of Boxers.”  He tried to tie in the outward signs of a life in professional boxing, cauliflower ears, the flattened noses of repeated demolition, the thick, scarred periorbital skin, to see if they correlated with the neurodegenerative disease going on inside the brain and postulated it took an average of 16 years of fighting for clinical signs to show up, based on his study of 69 boxers. 

One boxer confided in Critchley, “I can’t think properly.  And I can’t remember things; my speech has been getting bad for eighteen months…and my head goes blank at times.” (Damage, Tris Dixon, Hamilcar Publishing, pg 36).

In 1963, La Cava posed the name:  Cumulative Traumatic Encephalopathy of the boxer. 

It wasn’t until Englishman John Corsellis, a neuropathologist, published his paper “The Aftermath of Boxing,” in the journal of Psychological Medicine, that the neurohistopathology of Dementia Pugilistica took firm root.  Corsellis had established a bank of brains the had saved and fixed since 1951.  He studied the brains of 15 boxers and found they had all suffered from Dementia Pugilistica.  He established criteria such as a widened Septum Pellucidum, which in non-boxers was 1.6 mm, but 5.17 mm in fighters.  He found scarring of the inferior cerebellum from movement against the Foramen Magnum, where the brain exits the skull, from repetitive trauma from punches to the head.  He found damage to the Substantia Nigra, and neurofibrillary tangles in the medial temporal lobe in the absence of Beta Amyloid plaques.  Corsellis also postulated how different punches might transfer both accelerative force and rotational force to the brain parenchyma with ensuing tissue damage. 

Despite the known consequences of boxing, fighters continued to fight.  It was a way to become known and a way to pay their debts off and make a few extra dollars.  Afterall, it was called Prize Fighting, wasn’t it?  Some were fighting for the glory, but many for the prize.  Mohammed Ali made 3.00 dollars in his first amateur fight against Ronnie O’Keefe, another 12-year-old from Louisville, Kentucky.  This was a lot of money for a kid who had nothing and just the right type of reinforcement to continue boxing.  Many fighters chose to see the dangers of boxing through rose colored glasses.  Brain damage was always something only the other guy was going to get.  But Dementia Pugilistica turned out to be the grim reaper of boxing, felling such greats as Joe Louis, Henry Armstrong, Sugar Ray Robinson, Ali, and the less well known but superb Cocoa Kid. 

Boxing writer Springs Toledo had this to say about the Cocoa Kid.  “The Cocoa Kid eventually…wasn’t sure of his name anymore, this tattered figure wandering Times Square.  He’d shuffle over to the general delivery window at 33rd and 8th street (the post office in Manhattan) and mumble to the clerk.  His VA benefit check was his only income, but he’d often lose his service papers and had to find a way to the local veteran’s office and fill out an application for copies.  Staff had a fine time trying to sort through the misinformation he provided—he forgot where and when he was born.  “January 9, 1916, in Mexico,” he guessed on one application.  He was actually born on May 2, 1914, in Puerto Rico.”  (Damage, Tris Dixon, pg 34).  In the end, the Cocoa Kid ended up in an asylum in Chicago under a John Doe status until they matched his fingerprints and figured out that he was Herbert Lewis Hardwick, the Cocoa Kid.  He died at age 52, after a career involving a whopping 249 professional fights.  Unfortunately, a better understanding of the threat of Dementia Pugilistica did not have a significant impact on the sport of boxing, at least enough to affect large scale change to the industry.  Equally unfortunate, Omalu’s work arguably may not have significantly changed the sport of football, either. 

Boxers were not ignorant though.  Heavyweight champion of the world Sonny Liston put it in his own words:  The different parts of the brain sit in little cups like this.  When you get hit a terrible shot—pop!—the brain flops out of them cups and your knocked out.  Then the brain settles back in the cups, and you come to.  But after this happens enough times, or sometimes even once if the shots hard enough, the brain don’t settle back right in them cups, and that’s when you start needing other people to help you get around.”  (Ali, A Life, Jonathan Eig, Simon and Schuster, 2018).

Boxing is unique in the sporting world.  In other sports, such as ice hockey, football, rugby and soccer, there is always the threat of concussion.  In boxing, that’s the goal!  To give someone a concussion.  When a fighter gets knocked down by a punch to the head, whether he gets up or not, that is a concussion!  In boxing, a fighter gets all of 10 seconds to get up after a concussion.  If he does, the fight is allowed to go on, despite the fact one of the participants now has a bonafide concussion.  If he gets knocked down again, he’s had two concussions in the same fight, which is common.  It’s only after a knockout that the fight is stopped.  Fighting is the only sport (MMA included) where concussion is part of what is supposed to happen during a match.  When it’s apparent that a player is concussed in the NFL, the crowd hushes and shows concern.  In boxing, a concussion is wildly applauded. 

Head injuries in football can be traced back to the games inception and were very common in the early days of the sport.  In 1905, Harry Turner, playing for the Canton Professionals in the Ohio League, a precursor to the NFL, died after bolting out of the backfield with his head lowered and smashing into a pile of players, severing his cervical spinal cord and causing severe head injury.  The same year, there were eighteen deaths in college football, causing President Theodore Roosevelt to issue an ultimatum, prompting large scale reform in college football and the formation of the NCAA.  Formations such as the Flying Wedge, were banned.  In the Flying Wedge, the team with the ball assembled into a spearhead-shaped formation, with one unfortunate player at the tip of the spear, and the rest packed tightly behind, much like a pack of billiard balls waiting to be unracked.  The ball carrier was snuggly encased inside the spearhead.  The tightly formed group moved in unison, sometimes locking arms or shoulders, generating tremendous force and momentum, mowing down players on the opposing team and causing devastatingly severe injuries in its wake.  In what was called a momentum play, additional players from the back of the formation would dive over the pack, headfirst, creating even more forward force.  Players did not typically wear helmets during this era, and if they did, they were made of leather material.  There was, in essence, no real head protection.  Deaths at this time typically occurred from skull fractures, brain hemorrhages, or broken necks.  In addition to outlawing the wedge, the forward pass was legalized, thus spreading the players on the field, and further reducing mass collisions.  A neutral zone was also established, and a minimum distance between players on the same team, thus prohibiting the linking of arms.

It was not until the 1940’s that players started sporting plastic helmets, which were hard and rigid, with little internal padding.  This gave the sport a false sense of security, as players increasingly used their now “protected” heads as weapons.  In the 1960’s, improved materials and padding was introduced, and facemasks became standard.  Helmet to helmet contact remained legal and was often encouraged by coaches and players alike. The 1980’s saw polycarbonate helmets and better cushioning, with air bladders.  Concussions were observed frequently but not respected by personnel, with players often returning to the game immediately. 

In 1994, a watershed moment occurred.  Quarterbacks Vinny Testaverde, Chris Miller, and Troy Aikman, a powerhouse in the game, all suffered concussions in the same week.  In what was being termed, “the season of the concussion,” sports writers began to sound the alarm.  One writer, Bill Livingston, from Cleveland, called the situation a “disgrace,” and said the league was “making money on pain.”  As noted in the excellent book League of Denial, “The NFL…downplayed the crisis.  Greg Aiello, the leagues director of communications, repeatedly told reporters the rate of concussion since 1989 remained unchanged:  one concussion every three to four games.  Joe Maroon, a neurosurgeon who consulted for the Pittsburgh Steelers, estimated it was more like 2-4 per NFL game.  (League of Denial, Mark Fainaru-Wada and Steve Fainaru, Three Rivers Press, 2013, pg 74).  Later that year, Aikman, suffered another concussion in the NFC Championship Game against the San Francisco 49ers.  Aikman was hospitalized and according to his agent, Leigh Steinberg, he had no recollection of the game and repeatedly asked his agent why he was in the hospital.  When Steinberg told him he had suffered a concussion in the game, he asked if he had played well.  Steinberg replied affirmatively.  Aikman continued to repeat the same question, “Why am I in the hospital?” every few minutes to an increasingly worried Steinberg.

NFL commissioner Paul Tagliabue came under intense pressure from the press on the issue of concussions and football safety soon after.  As a pressure release valve, the NFL announced a scientific study of its own, and the Mild Traumatic Brain Injury Committee (MTBI) was formed.    The committee was to be headed by Dr. Elliot Pellman, the New York Jets team physician.  Pellman was not a neurologist or an internist, and, according to reports, had no knowledge of the extensive literature on concussions up until that point, despite it being a focal point of football medicine.  Despite these educational shortcomings, he treated Al Toon, a standout Jets wide receiver, for multiple concussions until the head injuries forced his early retirement.  Far from having an impressive academic educational pedigree, (Pellman attended medical school at the Universidad of Autonoma de Guadalajara, in Mexico), he was a rheumatologist by training.  Pellman and his committee set out to define the meaning of the word concussion and then instituted a battery of neuropsychological tests to monitor for concussions league wide.  The committee was dark for nine years afterwards, not publishing any findings until 2003, when they produced a series of studies ending in 2006, almost a decade after initiation of the committee.  The committee concluded there was no evidence for long term brain damage in players who suffered concussion, and that it was safe in many instances to return a player to the game on the same day of a concussion.  It also concluded that players suffered no permanent ill-effects after multiple concussions according to their studies.  To improve safety, the committee focused on ways to develop a helmet capable of limiting or preventing concussions, with the latest technology.  The committee’s work was not respected in the medical community, nor in the community of common sense, and their conclusions drew enormous criticism.  They were seen as mere lackeys to the NFL establishment.  Their take home message “Football is safe and now that we have proven what we already knew, we can all go back to enjoying the game and stop worrying.”    The committee, in response to intense criticism, was eventually disbanded in 2010, sixteen years after formation.

After Omalu published his ground-breaking case report in Neurosurgery in 2005, the MTBI committee immediately went on the offensive.  They wrote their own flawed rebuttal to Omalu’s paper that was also published in Neurosurgery, but in May of 2006, writing “We disagree with the assertion that Omalu et al.’s recent article actually reports a case of CTE in an NFL player.”  This is based on a “serious misinterpretation of the neuropathological findings in relation to the tetrad characteristics of CTE and a failure to take an adequate history.”  The editorial was penned by Ira Casson, Elliot Pellman, and David Viano.  The basis for their rebuttal is the comparison of Omalu’s description of what he reported in the brain of Mike Webster, neurofibrillary tangles in the deep sulci, and the findings commonly found by Corsellis et al, whose seminal work classified the basic criteria for Dementia Pugilistica, specifically:   Widening of the septum pellucidum, cerebellar scarring, degeneration of the substantia nigra with no Lewy bodies, and widespread neurofibrillary tangles in the cerebral cortex and brainstem, most prominently in the medial temporal lobe gray matter.  They believe these findings were representative of what would generally be found in a case of Chronic Traumatic Encephalopathy.  Through their collective ignorance, and what they failed to note, was that Omalu was saying “You are correct, this is NOT Dementia Pugilistica.  This is something different.  A different disorder.  We now know, through hindsight, that Dementia Pugilistica is a subtype of CTE.  It falls under the CTE umbrella, with CTE findings specific to boxers.  Corsellis had even described the same histopathological findings of DP in a chronically battered woman, who suffered years of physical abuse, on autopsy.  Football players, ice hockey players, and military veterans, who suffered shockwave damage from repeated exposure to firing military grade weapons, which Omalu was also the first physician to pathological describe, have become, neuropathologically, the classic examples of CTE.  What the MTBI committee mistakenly concluded was if the Omalu findings differed from what is classically seen in Dementia Pugilistic, the only form of CTE then known and fully classified, then Omalu must be wrong, this could not be CTE.  And if it was not CTE related, then Omalu must offer another explanation for the findings in Mike Webster, other than football.  The criticism that Omalu didn’t elaborate enough on the medical history in his first paper seems petty and nonsensical, since it was generally known that Webster was a retired football player with 17 years’ experience in the NFL playing in a known collision sport and with well reported tendencies to favor an aggressive style of play, leading with his head.  His mental and physical problems were also well publicized since his death.  Furthermore, they state they knew from their own research, that since Webster was an offensive lineman, they had a “Lower incidence of mild traumatic brain injury compared with other players.”   They also note Webster had no documented history of concussion or leaving the field of play after a blow to the head.  Without knowing it, the committee was digging its own grave. They went on to note Webster may have sustained brain damage in high school or college even, there was no way to know, which could theoretically clear the NFL.  Their reasoning was not only flawed but childlike.  Finally, in their piece de resistance, they urged Omalu et al to retract the paper, a serious request in the world of science with enormous consequences.  When he refused, what followed was a full-scale assault on Omalu, his character, his findings, and his credibility, as we will later see.

While important, helmets have more to do with preventing skull fractures than concussions.  A concussion occurs with a severe blow to the head, causing the brain to be impacted and then ricochet in the opposite direction and even rattle around the enclosed brain casing.  If two opposing players were both traveling at 15 miles per hour and collided, their helmets would protect their scalp and skull, but both brains would continue trying to move forward at 15 MPH despite the bodies that carried them grinding to a sudden stop.  In another fantastical example provided for emphasis, we know the Earth rotates on its axis at approximately 1000 miles per hour.  If the Earth’s rotation were to suddenly come to an immediate halt, all life on Earth would cease to exist in a fraction of a second, because our bodies would continue to move at 1000 MPH above the now still ground.  This is the reason why using the helmet solution to prevent or lessen concussions is a foundational fallacy.  Skull injury can be lessened or prevented, but not brain injury because the moving brain is still at risk for trauma when the body comes to a sudden stop in a routine tackle, head trauma or not.  The Pellman was correct when he said that concussions were an occupational hazard of the game.  Unfortunately, what he did not or would not acknowledge was that repeated high velocity head trauma, concussive, sub concussive, or asymptomatic, could do lasting, harmful damage to the player.  CTE is a cumulative phenomenon; repeated trauma to the brain, without the need to have documented instances of concussion, as in Mike Websters case.  Webster frequented multiple doctors after his playing career, desperately trying to explain his mood swings and lack of memory, his impulsive behavior and his chronic depression and severe insomnia.  When a doctor inquired if he had ever been in a car accident and Webster replied “Yes, 25,000 times,” that sad but humorful terse, answer embodies the essence of Chronic Traumatic Encephalopathy in a nutshell. 

What Omalu saw on the slides puzzled him.  The pathology didn’t make sense in a 50-year-old athlete.  There were plaques in the brain, called neurofibrillary tangles, made up of Tau proteins, which were heavily phosphorylated, occupying space, and strangling brain cells and axons, contributing to neuronal loss. The abnormal Tau had a predilection for the deep sulci and perivascular areas, the territory around small blood vessel, suggesting structural damage or microhemorrhages from repeated head trauma.   Tau proteins are normal and important structures in the healthy brain, often occurring in distal neuronal axon microtubules, helping to stabilize the structure of the microtubule/axon complex and help make it semi-flexible.  This Tau, though, was disorganized, random, cluttering up the axonal highways and disrupting neuronal connections.  There were also neuritic threads in the neocortex, subcortical ganglia and brainstem nuclei.  The most severe damage appeared to be in the depths or furrows of the brain, called the sulci, as opposed to the folds of the brain, or gyri.  The sulci are especially vulnerable to the mechanical stress and shearing forces sustained with repetitive head trauma. 

Dr. Omalu sat back and took another bite of his apple.  He set it on the table and rubbed his eyes, trying to process what he was observing.  He knew this was something different.  Yet, what?  His mind started to sift through facts one by one, like frames slowly moving through a movie projector.  Tauopathy was seen in Alzheimer’s disease, but there was usually an abundance of amyloid extracellularly.  It was a hallmark of the disease.  There was very little of that here.  In Alzheimer’s often started in the entorhinal cortex and hippocampus and spread to the neocortex in a predictable fashion.  Here, he was seeing the Tau proteins in the perivascular areas of the deep sulci in the absence of considerable amyloid and in a much different distribution. 

He considered Dementia Pugilistica, first diagnosed almost 100 years ago, and caused by head trauma, repetitive concussive and sub concussive blows.  He reviewed the neurohistopathological classification of Dementia Pugilistica, but it didn’t seem to fit.  This seemed different.  It caused a widen septum pellucidum, a space in the midline that separated the left and right lateral ventricles.  It was widened in boxers with Dementia Pugilistica or DP.  DP also affected the substantia nigra, the symptoms of which could mimic Parkinson’s disease with neurologic impairments such as gait disorder, tremor, cognitive defects, and bradykinesia, or slowness of movement.  The boxer Mohammed Ali was a prominent example of this condition.  Omalu was not convinced.  He doubted by Alzheimer’s and Dementia Pugilistica.  This…this was something new.  Something different, he thought.  Of that he was convinced.  After reviewing the slides with equally baffled experts in neuropathology, including one of the leading experts on Alzheimer’s Disease, Dr. Steven DeKosky, head of the department of neurology at the University of Pittsburgh, Omalu was told these findings were significant and that he needed to have a name for this disorder and he needed to publish this case report.  He was told the first step would be to name the disorder.  After researching the subject, he came up with Chronic Traumatic Encephalopathy. 

To understand where medicine is going, it is imperative to know where it has been, and understanding Dementia Pugilistica is central to that process.  We know now that DP is a variant of CTE and literature on it as a disease state dates back about 100 years.  DP falls under the umbrella of CTE, not the other way around.  To understand the story of Dr. Omalu, one must first understand the most studied form of brain trauma to date, “Punch Drunk Syndrome,” or Dementia Pugilistica.

Harrison Martland, who received his MD degree from Columbia University and was a distinguished pathologist at Newark City Hospital, was the first physician to identify “Punch Drunk Syndrome” in the medical literature.  In 1928, he was approached by a boxing promoter to review twenty-three cases the promoter suspected were “punch drunk,” and the promotor wanted medical clarification on the subject.  At the time, “punch drunk” was not a medical diagnosis known to most doctors.  There was no literature on the subject, it was not taught in medical schools, and most doctors, especially those with no connection to boxing, remained ignorant of it.  Martland examined five of the twenty-three patients himself and read elaborate charts on the remaining eighteen.  The phrase “Punch Drunk” was used in the boxing world, however, among fighters, promoters, fight fans, and sports writers, who had been using the term for decades to describe the physical and mental impairments of some boxers.  One of the cases Martland personally examined, CASE 2, was representative of what became known thereafter in the medical literature, as Punch Drunk Syndrome.  CASE 2, or N.E. (later identified as Nathan Ehrlich), was a popular Jewish fighter from Philadelphia.  CASE 2 began his professional career at age 16, in 1906, and retired in 1913. He had been knocked out only twice in his career, once for upwards of an hour, however.  He had fought against extremely good competition.  He was no slouch, he was a refined and skilled boxer.  CASE 2 had frequented many doctors, all of whom had no idea what his diagnosis was.  He had fought many times, including 27 times in 1909 alone.  Tris Dixon, in his classic book Damage, the Untold Story of Brain Damage in Boxing, further describes the scene: 

CASE 2 had suffered no previous illnesses, nor did he regularly drink alcohol.  Despite this, the subject was frequently accused of being intoxicated because of the similarity of his symptoms with drunkenness.  Case 2 retired at age twenty-three because his left hand shook involuntarily and his legs were unsteady.  Martland also indicated that there were problems with his speech because his tongue “had a tremor.”” (Damage, Tris Dixon, 2021, Hamilcar Publications, pg. 5). 

Martland found that “Punch Drunk” boxers often staggered to their corners.  There symptoms may start during their boxing careers but never progress after retirement, or turn chronic, afflicting them with horrible neuropsychiatric maladies capped by shortened lifespans.  Their speech tended to be slurred.  Their legs might drag, give out, or feel weak.  They often had tremors, slowed movements, and a tendency to fall backwards when they walked.  Long term, they also suffered violent mood swings, rage, episodes of amnesia, and mental deterioration, sometimes ending up in asylums or sanitariums.  People in the boxing industry, and fans, knew intuitively when someone was affected by “too many blows to the head”.  To them, it was the obvious what was the cause of it.  Thus, they were called “cuckoo” or “Punch Drunk.”  Physicians on the other hand, had no clue, unless they happen to follow the fight industry closely.  There was nothing in textbooks or medical school to describe the condition. 

Martland saw the constellation of symptoms as being similar to Parkinson’s disease, and he labeled this a Parkinson’s-like syndrome.  Martland did not focus on the amount of concussions or knockouts a fighter suffered, but on the amount of blows to the head he received during the duration of his career.  He postulated that the less skilled boxers, and those used for sparring practice, were more likely to develop Punch Drunk Syndrome then the more skilled boxers, who were able to avoid many blows.  This thinking was later challenged by John Corsellis in 1973, who declared the opposite; Dixon puts it succinctly in his work Damage, “Unlike the neurologists who came before him, Corsellis believed the fighters who were the most at risk were the better, more successful ones.  They had the longest careers, fought the best opponents, and took more shots to the head.”  As echoed by Claude Abrams, former Boxing News editor, “When you match the best against the best, the fight is equal.  There is no give.  The duration of these matches is usually longer and the quality and the accuracy of the punches greater.  The stakes and desire to win are higher.  Consequently, these boxers push themselves to the limit.”  (Damage, Hamilcar Publications, pg 58).

Martland published his historic paper in the Journal of the American Medical Association in 1928, and it has since become the foundational paper on traumatic brain injuries in boxers, identifying deterioration of both motor and cognitive skills. 

The early boxers, pre nineteenth century, were bare-knuckled boxers.  It has been postulated that they suffered less from Punch Drunk Syndrome because they had to become more skilled with boxing techniques, throwing an economy of punches due to the risk of breaking one’s hand on the skulls of their opponents.  When boxing gloves were invented, the punch counts escalated considerably, and, along with it, the incidence of “Punch Drunk” fighters. 

Importantly, Martland had this to say about the medical consequences of boxing.  “The condition can no longer be ignored by the medical profession or the public.  It is the duty of our profession to establish the existence or nonexistence of punch drunk by preparing accurate statistical data as to its incidence, careful neurologic examinations of fighters thought to be punch drunk, and careful histologic examination of the brains of those who have died with symptoms simulating the Parkinsonian syndrome.  The late manifestations of the punch drunk syndrome will be seen chiefly in the neurologic clinics and asylums, and such material will practically fall to the neuropathologist connected with such institutions.”  (Damage, Tris Dixon, Hamilcar Publications, 2021, pg 7).  Compare that precise and ethical statement of duty with the statements and conclusions of the physicians assembled on the Mild Traumatic Brain Injury (MTBI) Committee by the NFL, were there was no ethical call to arms, no acknowledgement of the problem or responsibility to conscientiously explore the subject and get down to the truth.  It should be noted that Martland, though a pathologist, was not presented with any autopsy specimens to examine histopathologically.  All of the 23 subjects were still living at the time, including Battling Nelson, the Michigan Wildcat, Ad Wolgast, Joe “Iron Man” Grim, Billy Papke, known as the “Illinois Thunderbolt,” and Kid McCoy, all of whom eventually committed suicide, murdered someone, or ended up in asylums with what became known as Dementia Pugilistica. 

“In writing his paper Martland had used scientific research from New York neuropsychiatrists Michael Osnato and Vincent Giliberti, published the year before and entitled “Post concussion Neurosis—Traumatic Encephalitis” as well as C. B Cassasa’s paper “Multiple Traumatic Cerebral Hemorrhages.”   Osnato and Giliberti were the first scientists to propose that exposure to traumatic brain injuries, or TBI’s, could lead to neurodegenerative changes.  Their findings were presented at an annual meeting of the American Neurological Association in 1926.  (Damage, Tris Dixon, pg 7). 

Further research followed from Ernst Jokl in 1933 and Harry Parker in 1934, who wrote a medical paper titled “Traumatic Encephalopathy of Professional Pugilists,” while at the Mayo Clinic.  Parker stated there were two types of injuries to the brains of boxers.  Those that caused death instantly and those that caused long term deficits from repetitive blows to the head.  Jokl was one of the founding members of the pioneering American College of Sports Medicine who, ironically, honored Bennet Omalu with its man of the year award due to his pioneering research which brought awareness of CTE in the NFL.  It wasn’t until 1937 that J. A. Millspaugh suggested the name be changed from Punch Drunk Syndrome to Dementia Pugilistica, as he considered the former title demeaning to those patients afflicted.  He published this in an article in the United States Naval Bulletin. 

MacDonald Critchley was an English neurologist who published Medical Aspects of Boxing, Particularly from a Neurological Standpoint, in 1957 in the British Medical Journal.  Critchley called Dementia Pugilistica “Chronic Progressive Traumatic Encephalopathy of Boxers.”  He tried to tie in the outward signs of a life in professional boxing, cauliflower ears, the flattened noses of repeated demolition, the thick, scarred periorbital skin, to see if they correlated with the neurodegenerative disease going on inside the brain and postulated it took an average of 16 years of fighting for clinical signs to show up, based on his study of 69 boxers. 

One boxer confided in Critchley, “I can’t think properly.  And I can’t remember things; my speech has been getting bad for eighteen months…and my head goes blank at times.” (Damage, Tris Dixon, Hamilcar Publishing, pg 36).

In 1963, La Cava posed the name:  Cumulative Traumatic Encephalopathy of the boxer. 

It wasn’t until Englishman John Corsellis, a neuropathologist, published his paper “The Aftermath of Boxing,” in the journal of Psychological Medicine, that the neurohistopathology of Dementia Pugilistica took firm root.  Corsellis had established a bank of brains the had saved and fixed since 1951.  He studied the brains of 15 boxers and found they had all suffered from Dementia Pugilistica.  He established criteria such as a widened Septum Pellucidum, which in non-boxers was 1.6 mm, but 5.17 mm in fighters.  He found scarring of the inferior cerebellum from movement against the Foramen Magnum, where the brain exits the skull, from repetitive trauma from punches to the head.  He found damage to the Substantia Nigra, and neurofibrillary tangles in the medial temporal lobe in the absence of Beta Amyloid plaques.  Corsellis also postulated how different punches might transfer both accelerative force and rotational force to the brain parenchyma with ensuing tissue damage. 

Despite the known consequences of boxing, fighters continued to fight.  It was a way to become known and a way to pay their debts off and make a few extra dollars.  Afterall, it was called Prize Fighting, wasn’t it?  Some were fighting for the glory, but many for the prize.  Mohammed Ali made 3.00 dollars in his first amateur fight against Ronnie O’Keefe, another 12-year-old from Louisville, Kentucky.  This was a lot of money for a kid who had nothing and just the right type of reinforcement to continue boxing.  Many fighters chose to see the dangers of boxing through rose colored glasses.  Brain damage was always something only the other guy was going to get.  But Dementia Pugilistica turned out to be the grim reaper of boxing, felling such greats as Joe Louis, Henry Armstrong, Sugar Ray Robinson, Ali, and the less well known but superb Cocoa Kid. 

Boxing writer Springs Toledo had this to say about the Cocoa Kid.  “The Cocoa Kid eventually…wasn’t sure of his name anymore, this tattered figure wandering Times Square.  He’d shuffle over to the general delivery window at 33rd and 8th street (the post office in Manhattan) and mumble to the clerk.  His VA benefit check was his only income, but he’d often lose his service papers and had to find a way to the local veteran’s office and fill out an application for copies.  Staff had a fine time trying to sort through the misinformation he provided—he forgot where and when he was born.  “January 9, 1916, in Mexico,” he guessed on one application.  He was actually born on May 2, 1914, in Puerto Rico.”  (Damage, Tris Dixon, pg 34).  In the end, the Cocoa Kid ended up in an asylum in Chicago under a John Doe status until they matched his fingerprints and figured out that he was Herbert Lewis Hardwick, the Cocoa Kid.  He died at age 52, after a career involving a whopping 249 professional fights.  Unfortunately, a better understanding of the threat of Dementia Pugilistica did not have a significant impact on the sport of boxing, at least enough to affect large scale change to the industry.  Equally unfortunate, Omalu’s work arguably may not have significantly changed the sport of football, either. 

Boxers were not ignorant though.  Heavyweight champion of the world Sonny Liston put it in his own words:  The different parts of the brain sit in little cups like this.  When you get hit a terrible shot—pop!—the brain flops out of them cups and your knocked out.  Then the brain settles back in the cups, and you come to.  But after this happens enough times, or sometimes even once if the shots hard enough, the brain don’t settle back right in them cups, and that’s when you start needing other people to help you get around.”  (Ali, A Life, Jonathan Eig, Simon and Schuster, 2018).

Boxing is unique in the sporting world.  In other sports, such as ice hockey, football, rugby and soccer, there is always the threat of concussion.  In boxing, that’s the goal!  To give someone a concussion.  When a fighter gets knocked down by a punch to the head, whether he gets up or not, that is a concussion!  In boxing, a fighter gets all of 10 seconds to get up after a concussion.  If he does, the fight is allowed to go on, despite the fact one of the participants now has a bonafide concussion.  If he gets knocked down again, he’s had two concussions in the same fight, which is common.  It’s only after a knockout that the fight is stopped.  Fighting is the only sport (MMA included) where concussion is part of what is supposed to happen during a match.  When it’s apparent that a player is concussed in the NFL, the crowd hushes and shows concern.  In boxing, a concussion is wildly applauded. 

Head injuries in football can be traced back to the games inception and were very common in the early days of the sport.  In 1905, Harry Turner, playing for the Canton Professionals in the Ohio League, a precursor to the NFL, died after bolting out of the backfield with his head lowered and smashing into a pile of players, severing his cervical spinal cord and causing severe head injury.  The same year, there were eighteen deaths in college football, causing President Theodore Roosevelt to issue an ultimatum, prompting large scale reform in college football and the formation of the NCAA.  Formations such as the Flying Wedge, were banned.  In the Flying Wedge, the team with the ball assembled into a spearhead-shaped formation, with one unfortunate player at the tip of the spear, and the rest packed tightly behind, much like a pack of billiard balls waiting to be unracked.  The ball carrier was snuggly encased inside the spearhead.  The tightly formed group moved in unison, sometimes locking arms or shoulders, generating tremendous force and momentum, mowing down players on the opposing team and causing devastatingly severe injuries in its wake.  In what was called a momentum play, additional players from the back of the formation would dive over the pack, headfirst, creating even more forward force.  Players did not typically wear helmets during this era, and if they did, they were made of leather material.  There was, in essence, no real head protection.  Deaths at this time typically occurred from skull fractures, brain hemorrhages, or broken necks.  In addition to outlawing the wedge, the forward pass was legalized, thus spreading the players on the field, and further reducing mass collisions.  A neutral zone was also established, and a minimum distance between players on the same team, thus prohibiting the linking of arms.

It was not until the 1940’s that players started sporting plastic helmets, which were hard and rigid, with little internal padding.  This gave the sport a false sense of security, as players increasingly used their now “protected” heads as weapons.  In the 1960’s, improved materials and padding was introduced, and facemasks became standard.  Helmet to helmet contact remained legal and was often encouraged by coaches and players alike. The 1980’s saw polycarbonate helmets and better cushioning, with air bladders.  Concussions were observed frequently but not respected by personnel, with players often returning to the game immediately. 

In 1994, a watershed moment occurred.  Quarterbacks Vinny Testaverde, Chris Miller, and Troy Aikman, a powerhouse in the game, all suffered concussions in the same week.  In what was being termed, “the season of the concussion,” sports writers began to sound the alarm.  One writer, Bill Livingston, from Cleveland, called the situation a “disgrace,” and said the league was “making money on pain.”  As noted in the excellent book League of Denial, “The NFL…downplayed the crisis.  Greg Aiello, the leagues director of communications, repeatedly told reporters the rate of concussion since 1989 remained unchanged:  one concussion every three to four games.  Joe Maroon, a neurosurgeon who consulted for the Pittsburgh Steelers, estimated it was more like 2-4 per NFL game.  (League of Denial, Mark Fainaru-Wada and Steve Fainaru, Three Rivers Press, 2013, pg 74).  Later that year, Aikman, suffered another concussion in the NFC Championship Game against the San Francisco 49ers.  Aikman was hospitalized and according to his agent, Leigh Steinberg, he had no recollection of the game and repeatedly asked his agent why he was in the hospital.  When Steinberg told him he had suffered a concussion in the game, he asked if he had played well.  Steinberg replied affirmatively.  Aikman continued to repeat the same question, “Why am I in the hospital?” every few minutes to an increasingly worried Steinberg.