At 46, "Terrible" Terry Norris has the lean, muscled frame of a former pro boxer. He’s just a little taller than average, with a thick, black Van Dyke framing a bright smile. Gray creeps in at the edges of his beard, but his shaved head seems the only concession to age, a paring away of the intricately razored box cut of his heyday, now some 20 years gone. These days, he teaches cardio boxing in a converted garage north of Hollywood; upstairs, he shares a loft with his wife, Tanya, who also teaches and runs his gym. During classes he looks fit and powerful, his fists still preternaturally fast. Only when he speaks, in a low, raspy murmur bordering on unintelligible, do you wonder at the damage he’s suffered.
He started boxing when he was nine years old, a black kid growing up in Lubbock, Texas, a conservative, predominantly white industrial city best known as the birthplace of Buddy Holly. His mother wanted to keep her mischievous son, "Terrible," off the streets; his father was a former fighter. At 19 he turned pro. World Boxing Council light-middleweight champion at 22. Three more titles followed; he finished his career at 47-9, with 31 knockouts, and joined the International Boxing Hall of Fame.
In more than 20 years of boxing, he suffered four knockouts and innumerable blows to the head. After losing three consecutive fights he attempted a comeback, applying for a Nevada fight license in 2000. But Dr. Margaret Goodman, a ringside doctor he’d known casually for years, greeted him at a fight and was shocked by his slurred speech. He hadn’t admitted it, but he had problems with his coordination and balance, too. Looking back, Norris says he knew there was something wrong, but told himself with time he’d recover.
On Goodman’s advice, the Nevada State Athletic Commission held a hearing on Norris’ fitness to fight. Sympathetic doctors provided him a clean bill of health, but going into the hearing, he says today, "I was hoping for a miracle. I really didn’t have a life outside of boxing." Reviewing his case, the commission saw potentially irreparable damage. "You put him in that ring and let him take more blows, he is a time bomb," said one doctor. His license to fight unanimously denied, Terry Norris, at 32, was effectively out of professional boxing.
When the NSAC refused Norris’ fight license, it hoped to prevent him from following the path of Muhammad Ali, Jerry Quarry, Floyd Patterson, and Sugar Ray Robinson — all legends of the sport struck by post-career brain illnesses, and whose decline played out with varying degrees of publicity. Aging boxers have long suffered increased risk of mental health issues, from Alzheimer’s to Parkinson’s syndrome to dementia pugilistica; these afflictions have been largely accepted, if quietly and perhaps without reflection, by fans and fighters as potential consequences inherent to the sport. Yet today, as professional football begins to face its own reckoning over brain-damaged players, boxing is receiving new scrutiny from researchers hoping to understand just what happens inside a boxer's brain during a career. And that means understanding men like Terry Norris.
Medical science has recognized the dangers of repetitive brain trauma in boxing for nearly a century. "For some time fight fans and promoters have recognized a peculiar condition occurring among prize fighters which, in ring parlance, they speak of as ‘punch drunk,’" wrote Dr. Harrison S. Martland in the Journal of American Medicine, among the first doctors to draw attention to the issue — in 1928. Two years later, most states had legalized boxing.
"Punch drunk" became a common synonym for dementia pugilistica, a medical condition that for decades applied almost exclusively to boxers. Today, dementia pugilistica is recognized as a variant of chronic traumatic encephalopathy, or CTE, a neurodegenerative disease found in the brains of some people with a history of repetitive brain trauma. It affects more than boxers, and has recently entered the public understanding largely through another sport: football.
How does a series of static injuries become a progressive, degenerative disease?
In 2002, Mike Webster became the first former National Football League player diagnosed with CTE. Just 50 when he died, after retiring Webster suffered chronic pain so bad he’d Taser himself unconscious just to be able to rest. He wrote long, meandering journal entries, then during episodes of lucidity wept at what he’d written. Unable to cope with his increasing detachment from reality, friends and family became estranged. When he died, he was living out of a black Chevy S-10 pickup truck parked on the streets of Pittsburgh, Pennsylvania.
A heart attack appeared the direct cause of death, but a young pathologist, Bennet Omalu, had a deeper question: why had Mike Webster gone so crazy? His brain appeared normal, but Omalu, obsessed with unlocking its secrets, eventually removed a thin slice and stained it. Then he put it under a microscope.
What he saw shocked him. At the microscopic level, Webster’s brain had become a riot of black and brown skeins: deposits of a modified protein called tau. Tau normally lines the inside of the nerve cell, providing stability, but here had built up in what’s called neurofibrillary tangles. When Omalu later published his findings, those tangles became the calling card of CTE.
The human brain floats in a cushion of cerebrospinal fluid within the skull. When a shock causes rapid, jarring movement, bones, tendons, and muscles help re-stabilize the head. Floating in fluid, however, the brain has its own inertia. When the head stops moving, the brain keeps going, striking the inside of the skull.
Colloquially we call this a concussion, though doctors prefer "mild traumatic brain injury." The formal name underscores that fact that there’s no empirical test to prove a concussion. There are only recognizable symptoms, including headache, brain fog, and memory impairment.
Scientists don’t yet know how a series of mild traumatic brain injuries becomes CTE, largely because it’s nearly impossible to see accumulated tau proteins until after death. So diagnosis depends on clinical judgement and a careful reading of patient histories. Early on, CTE can usually be distinguished from other types of dementia, but later stages are more difficult to identify. The three categories of symptoms — cognitive, mood, and behavior — each carry frustratingly difficult questions. For example, when does forgetfulness cross into diagnostically relevant changes in cognition, like memory impairment and problems with planning, organizing, multitasking, and judgement? When do depression, apathy, and irritability indicate early CTE and when are they signs of other mental illnesses? What about problems with impulse control, substance abuse, aggression, and violence?
"I thought it would pass," Terry Norris says today of his slurred speech and shaky balance, "because I’ve always had this speech like that." He’s from Texas, after all, and he’s always spoken fast. Sometimes his words roll together. "So I didn’t really notice that much and didn’t want to notice that much, really," he says. But the boxing doctors were right about the underlying damage. Today he has parkinsonism, a mild form of Parkinson’s disease, and has been diagnosed with dementia pugilistica. He has memory problems and difficulty controlling his emotions. Balance and coordination often fail him. Tanya sometimes reminds him to eat, or, when his throat gets clogged with mucus, clears her own to show him how. His muscles are rigid, always contracted. He tires easily and works with a service dog, a scrappy pit bull terrier with a sweet face and a cold, pink nose. He often experiences separation anxiety, Tanya says, and the dog calms him.
When the head stops moving, the brain keeps going, striking the inside of the skull
“He has to take a medication to sleep occasionally because he does fight in his sleep," Tanya says, "I don’t go near him in his sleep.” One night, she says, "I heard him saying, ‘I’m ready, I’m ready,’" like a boxer entering the ring. Before she could move, Terry hit her. "That’s when I told the doctor, ‘Um, he’s fighting in his sleep? He’s like, jumping up and lunging at me, so I need to fix this real fast.”
Every few months, he travels to the Cleveland Clinic Lou Ruvo Center for Brain Health in Las Vegas, Nevada, where researchers are studying more than 400 active and retired fighters. It’s the first longitudinal study to examine fighters’ brains, trying to understand when changes occur, what they mean, and why only some fighters develop long-term impairments. Such knowledge could, for example, help future fighters decide when to retire and warn those at higher risk for permanent damage.
Dr. Charles Bernick, a neurologist and associate medical director at the center, leads the study. He’s disarmingly candid about how little certainty science has regarding CTE. How does a series of static injuries become a progressive, degenerative disease? Why can some people fight an entire career and emerge relatively unscathed, while others develop mild to severe chronic brain damage? Repeated brain trauma obviously plays a role, but what about other risk factors — genetics, lifestyle, diet? To these questions Bernick offers some variation of his good-natured "Well, we don’t know."
Much current CTE research focuses on football players, but Bernick says looking at fighters offers an opportunity for comparison. Tau proteins appear consistently in CTE patients, whether in fighters or football players or a circus clown repeatedly fired from a cannon. Tau tends to clump in similar patterns around blood vessels and deep in the brain’s folds. Tau accumulation correlates with the symptoms and severity of the disease, but tau may simply indicate other, less visible damage. Because it increases as the disease progresses, it’s likely the culprit. "But we don’t know that," Bernick says, "and I don’t think we can be confident that’s really the underlying problem."
Bernick and his team hope to change the fundamental problem of CTE diagnosis — that it’s visible only in sectioned brains — with PET (positron emission tomography) imaging. PET scanning typically uses glucose molecules tagged with a radioactive tracer and injected into the body. The tracer reveals how the glucose gets metabolized: how different areas of the brain use it for energy, or how metabolization by cancerous cells differs from that of healthy ones.
Using PET scanning and a radioactive tracer molecule that binds to tau proteins, researchers have found physical signs of CTE in living patients, albeit in a very small study. Making tau visible in living brains would be a major advance. Still, even with a hypothetical, excellent tracer, researchers don’t yet understand basic questions such as how much tau is acceptable, if the tau itself is harmful, and how to turn an image into sound medical advice. Nevertheless, imaging a lot of brains is a first step.
Since 2002, when Mike Webster’s brain revealed its roil of malformed proteins, football’s CTE crisis has only become more public. Bennet Omalu published his findings on tau protein in 2005, in the journal Neurosurgery. The NFL, which had long downplayed the risk of concussions among players, dismissed the research, even calling for a retraction. But Omalu found CTE in the brain of Terry Long, a former player who’d killed himself at 45 by drinking antifreeze. Soon dozens of former players were diagnosed with CTE. Terry Bradshaw, Brett Favre, and Troy Aikman have worried publicly about their post-NFL mental health. Former NFL players Andre Waters and Junior Seau committed suicide; both had shown signs of CTE. In 2010, a 17-year-old football player in Spring Hill, Kansas died hours after a homecoming game; his brain showed CTE, the youngest reported case to date.
The legal consequences have begun. In 2011, former Atlanta Falcons safety Ray Easterling filed suit against the NFL, charging a "concerted effort of deception and denial" about the risks of long-term brain trauma to anyone who played football. Thousands of former players joined the suit; by late 2013, they’d reached a $765 million settlement to cover as many as 20,000 injured players, providing money for compensation, testing, research, and education. In January, the presiding judge rejected the settlement, concerned whether payouts would be adequate and fair. (Easterling committed suicide in 2012 at age 62. He was later diagnosed with CTE.) Many other players and families have filed suits against the NFL. And in 2013, a group of retired National Hockey League players sued the organization over its handling of head injuries.
"They need a federal commission. It’s the only way it's going to get fixed."
Yet among boxers — where the dangers of brain injury, whether labeled dementia pugilistica or CTE, have been long recognized if woefully under-acknowledged, and where no fighters are protected by unions or a cohesive regulatory system — little has changed. The protections provided professional football and hockey players don’t exist in boxing or mixed martial arts, and even reaching the highest levels of those sports doesn't guarantee benefits such as insurance, disability, severance pay, or pensions. Combat sports are regulated at the state level: there’s no national body defining medical standards or deciding who gets to fight.
When it comes to medical fitness, some states have fairly extensive requirements, while others aren’t so rigorous. In California, for example, professional fighters must have HIV antibody, Hep B surface antigen, and Hep C antibody testing; they also need a physical, an eye exam, an EKG, an MRI of the brain, and a neurological exam. But for amateurs? Just an annual physical. If New York rejects you because you’ve had a subdural hematoma — bleeding in the brain — you can always try Nevada, where that won’t stop you from receiving a fight license. Fighters admit it’s easy enough to get passable medical documentation, no matter your actual health.
"They need a federal commission. It’s the only way it's going to get fixed," says Dr. Margaret Goodman, a neurologist who formerly chaired the Nevada State Athletic Commission medical advisory board and served as a ringside physician. She shrugs in disgust, seated cross-legged on the living room floor of her Nevada home, a golden retriever sitting calmly by her side. She’s been saying this for a long time.
A fight license is like a driver’s license, she says: you have to earn it. She knows Norris’ pain at being denied a license in 2000. "It must have been horrible for him," she says. "It was horrible for us." But she took her role seriously. She sees herself as protecting fighters in the face of greed and callousness, but also, sometimes, their own will to fight. "It’s so hard for them to make these decisions for themselves," she says. Often it’s not just a paycheck they’re giving up, but their very sense of self. But today Norris recognizes just how lucky he was. "It’s good that Margaret was there," he says. "Thank God she saved me. She saved my life."
Fighters need protection, she says, the same way NFL players have protection: for contracts, medical testing, insurance, and licensing. She knows that fighters (and their trainers) seek out lax rules; it’s impossible to imagine brain-damaged NFL players staying in the game just by playing in a different state. Only standardized rules will provide serious oversight. "Until something like that happens," she says, "it’s kind of a free-for-all."
The first time I got knocked down was Julian Jackson," Norris says, "That was like the scariest moment of my life." He sits on a black leather love seat in his loft, dressed in sleek athletic gear and a light jacket. He says interviews make him nervous, but he appears wholly calm. His wife is making tea nearby; she sets a plastic squeeze-bottle of agave nectar on the table. His service dog lies at the top of the stairs looking down at him.
In 1989, Julian Jackson was the WBA junior middleweight champion. Norris was an up-and-comer, barely 22. After leaving Lubbock, he’d gone to San Diego, California to train with his brother. He didn’t dream of becoming a boxer, but he had talent and he needed something to do. Sparring with world champions, he realized he might earn his place among them. So he made himself a promise: he’d get the belt. He’d give his father, the man who trained him, the man who raised him, a championship.
And he did — four times over. The first was the best: in 1990, he handily dispatched the WBC light-middleweight champion, John Mugabi. "I was the king of the world, I was so happy," he says. "I couldn’t stop laughing, couldn’t stop smiling." The memory moves through him, as he pantomimes his hooks and jabs. His hands became busier, the delicate fingers clenched, the smooth calluses of his knuckles like crested smudges of oil paint.
His dad was there: the master, the mentor, the trainer. "He told me he wanted to be champion, and I was champion, and it was the greatest feeling ever," he says. His voice breaks. His eyes are wet. He looks up at Tanya as his words slow down. "It was a dream come true: for me, my family. My dad."
Before that, though, there was Julian Jackson and his world title. Jackson caught Norris with a right in the second round and sent him to the canvas. He’d never been hit that hard before, he says, "so I just took it as a major learning experience." He came to his senses in time to see Julian Jackson raise his gloves in victory.
"That’s one fight that I haven’t watched," he says, "Never. I’ve never watched that fight."
Terry Norris still gets offers to fight. Fourteen years after being denied a fight license due to a suspected brain injury, after filing for California disability benefits due to a brain injury, he still gets asked to step back into the ring. In the name of competition, entertainment, a paycheck. "If he ever boxed again, I’d leave him," Tanya Norris declares.
She speaks of the heartache and frustration of watching other, older fighters stay in the ring. It’s what provoked them to create the Final Fight Foundation. She watched it happen with her husband. By the last three fights, she says, "The look in his face … I couldn’t sleep that night when I saw that. The look in his face was like, he just wanted to stop. But he couldn’t."
After Terry learned he could no longer fight in Nevada, his manager drove him to the airport. On the way, Terry confronted him about whether he’d had Terry’s best interests at heart. Then Terry got on a plane to San Diego and the two never spoke again. "And then," he says, "life starts. Life as a normal person starts. I had to try to pull things together and make a normal life."
With Final Fight they want to make it easier for fighters to make a normal life. They want to address the problems that have plagued fighting sports for decades: lack of health insurance, trustworthy financial services, and non-biased counseling. They want a fighters’ union. And to help prepare families to talk about difficult things like retirement plans or neurological symptoms.
Terry climbs the stairs from the gym and leans into the kitchen counter, watching with a slight smile as Tanya rails against the current state of boxing and the trouble with old fighters. He chimes in about Manny Pacquiao’s potentially dire financial situation; Tanya exclaims, "How do you know all the gossip?" Pacquiao has reportedly squandered $200 million.
"It’s because his eye is already crossed!" she says. "They don’t understand, when the eye crosses, the career’s over. That’s all you have to do, is look for it." She points at Terry, who is chuckling quietly. "He has it, he has a crossover eye. It’s over when that happens. You can’t fight anymore."
Terry knows he can’t fight anymore, and he knows the damage wrought on fighters left to fend for themselves, who, at their careers’ end find themselves adrift physically, financially, and emotionally. "I hope we can change it," he says, in that voice ravaged by years in the ring. "I hope that I can change it. This sport really needs some help, and it’s a great sport, but it needs some help protecting the guys that made it."