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Authors: James A. Holstein,Richard S. Jones,Jr. George E. Koonce

Is There Life After Football? (17 page)

BOOK: Is There Life After Football?
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While the NFL admitted no legal liability, the settlement is a tacit admission that the NFL has actively prevented players from knowing the full extent to which they were inviting chronic brain disease by playing in the NFL—information vital to making informed decisions about their long-term physical and mental health.
15
The NFL's shameful complicity in suppressing information about the consequences of concussions and its attempts to thwart scientific research into concussions and their aftermath were further unmasked by media exposés such as the 2013 book
League of Denial
and an accompanying PBS
Frontline
documentary of the same title.
16
There's little question that brain injury is a much more serious problem than the NFL has wanted to admit.

Momentarily setting aside the controversy over concussion research at the heart of the lawsuit, what's most remarkable in this scenario is the sheer number of former players claiming significant brain damage from playing in the NFL. More than 4,500
living
players maintain that they have symptoms of football-related brain damage. That's nearly a quarter
of all living NFL alumni. A 2013
Washington Post
survey found that around 90 percent of former players indicate that they suffered at least one concussion while they were playing. Of those who did, two thirds say they still experience symptoms.
17
The NFL Player Care study—commissioned by the NFL itself—asked alumni respondents if they had ever been “diagnosed with dementia, Alzheimer's disease, or other memory-related disease.” While relatively few reported such diagnoses, comparisons with age peers in the general male population are shocking. Older retirees (50 and older) are five times more likely to report such diagnoses (6.1% to 1.2%), while younger alums (30–49) are 19 times more likely (1.9% to 0.1%).
18
Moreover, neurodegenerative mortality among a 1959 through 1988 cohort of NFL players was three times higher than that of the general population, and the mortality rate for this cohort due to Alzheimer's disease or ALS was four times higher.
19
While these data don't say that football wreaks havoc on
all
players, they clearly suggest that former NFL players are dramatically more likely than the average man on the street to suffer from long-term brain damage.

Every NFL player has his “bell rung.” These shots to the head are likely to cause concussions. They leave players momentarily stunned, disoriented, “seeing stars,” feeling woozy. The most pronounced symptoms may pass in a few minutes, but headaches, impaired vision, memory loss, or cognitive “fuzziness” may persist. Nevertheless, most players simply “play through” the symptoms, getting back into action as soon as they can.

The medical definition of a concussion is a bit more ominous. It's a brain injury caused by a force transmitted to the head that results in a collision between the brain and the skull that surrounds it. When someone takes a jolt to the head, the brain bangs around inside the skull case. The collision sets off organic, neurological, and chemical reactions that alter the brain and disrupt its functions. There's a wide range of possible symptoms: loss of consciousness, memory loss, slowed reaction times, cognitive impairment, drowsiness, headaches, irritability, and emotional fluctuations. Some people even go temporarily blind. Most of these symptoms, however, resolve spontaneously.
20

No two concussions are alike. Some are more serious than others, and some may persist for days, if not weeks. NFL players have “shook off” the effects of concussions since the game began. There are countless stories of players having their bells rung, but playing on, not knowing what they were doing, and remembering nothing afterwards. In one memorable instance, Cowboys quarterback Troy Aikman was “dinged”—kneed in the head—during the January 24, 1994, NFC championship game. Aikman had played well and the Cowboys beat the 49ers, but Aikman ended up in the hospital with a concussion. He couldn't remember
anything
about the game.
21
Steve Young, a contemporary of Aikman's and a fellow Hall of Famer, was once asked about how many concussions he suffered. His reply: “You mean official ones? . . . An official one is when you're knocked out and carted off the field. But I get dinged all the time and just continue to play. We might dumb down the playbook a little bit, but I couldn't count those.”
22
Jim Otto, Hall of Fame center from the AFL and NFL, probably took as many hits to the head as anyone.

I've had over 20 concussions myself. . . . There were so many times that I would walk off the field and my eyes would be crossed. Did you ever have that happen to you? Get hit in the head so hard your eyes were crossed? You sit there. It's strange; it's really strange. Or what about if you had amnesia for two days? When you looked at your wife and you didn't know who she was, like, who's this chick? And you couldn't remember. You got hit in the head, and you had amnesia.
23

Eventually, Aikman, Young, Otto, and hundreds of others whose bells have been rung snap out of it—more or less. For generations, that meant that they were good to go. But part of the recent concussion controversy has centered on exactly what happens over the long run when the brain is jarred enough to produce concussion symptoms.

By his own count, Mike Webster, Hall of Fame center for the Pittsburgh Steelers and Kansas City Chiefs from 1974 to 1990, played in 300 games, going back to high school, without missing a single game. He
reckoned he'd shown up for 890 of a possible 900 practices in the NFL. He'd knocked heads literally tens of thousands of times in the “pit” of the offensive line. Within a few short years of his retirement, Webster's everyday aches and pains became severe. He battled hand and foot afflictions. His teeth began to fall out. In addition to physical deterioration, many friends and associates noted that there was something wrong inside his head. He couldn't sleep. He became paranoid and behaved erratically. His speech was scattered and disjointed. His memory failed repeatedly. He lost his balance. He took on a vacant look—no emotion, no affect. His cognitive functioning slipped. He was “beat up” and “discombobulated,” according to his doctor. Ultimately, Webster became socially dysfunctional. He couldn't hold a job or live normally in the company of others. His family couldn't cope with his erratic behavior and his wife divorced him. He simply wasn't the man they had loved and grown up with. He came to rely upon Ritalin to maintain momentary focus, but eventually abused the drug and began forging dozens of prescriptions. His life became the horror story of an unbalanced, erratic transient.

Finally, Webster, with the assistance of a team of friends, doctors, and attorneys, filed for NFL disability benefits, presenting testimony from four physicians to establish that Webster had disabling brain damage due to his play in the league. The NFL, however, dragged its feet. The Retirement Plan Disability Board insisted on a fifth handpicked “independent” neurologist. When he agreed with Webster's doctors, the NFL finally granted Webster “total and permanent” disability benefits. The league's explanation for the decision included an extraordinary admission: “[Webster's] disability is the result of head injuries suffered as a football player with the Pittsburgh Steelers and the Kansas City Chiefs.” This concession would become even more significant when subsequent concussion litigation arose.
24

Webster's story, however, doesn't end with the disability board. Three years later, his maladies caught up with him, and he died, ultimately from heart problems, at age 52. During a routine autopsy, however, the forensic pathologist, Bennet Omalu, noted that the death certificate indicated
that Webster had suffered from “depression secondary to postconcussion syndrome.” Not a football fan himself, Omalu recalled media stories of football great Mike Webster's erratic behavior and tragic demise, and realized that this was the very same Webster on his examination table. The body was ravaged beyond belief, but when Omalu examined Webster's brain, it looked completely normal, a startling anomaly. Curious, Omalu got permission to study Webster's brain. His findings set off a torrent of questions, followed by a flood of research that eventually morphed into a major controversy.
25

Beneath the surface, Mike Webster's brain was anything but normal. He had a serious pathology that's come to be known as CTE. The condition is a progressive degenerative disease found in athletes (and others) with a history of repetitive brain trauma. This might include symptomatic concussions as well as asymptomatic subconcussive blows to the head. The head trauma triggers progressive degeneration of the brain tissue—the scientific literature often refers to this as a pathologic “cascade.” The pathology includes the build-up of an abnormal substance called “tau,” a protein that enables the brain to function, but that can also strangle it if the tau congeals into clumps called “neurofibrillary tangles.” These tangles can choke neurons inside the brain, causing a wide variety of problems. The changes in brain chemistry associated with CTE may begin months, years, or even decades after the last brain trauma.
26

CTE is insidious. It may lead to memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, cognitive impairment, and, eventually, progressive dementia.
27
As the disease progresses, symptoms become more severe and broader in scope. Memories fail. Victims can't concentrate or focus their attention. The brain's executive functioning declines; victims' organizing capacity fails, they can't plan things out, they exhibit poor judgment, and multitasking suffers. Sometimes speaking becomes disjointed or difficult. Victims become uncharacteristically irritable, impulsive, or aggressive. Some become completely apathetic at times, in complete contrast to other outbursts of aggressive behavior. Others suffer from depression, paranoia, even
suicidal tendencies. Instrumental activities are compromised so that routines of everyday life become impossible. Ultimately, full-blown dementia may set in. While CTE may have symptoms similar to Alzheimer's disease and other neurodegenerative conditions, its organic presentation is different. Equally important, whereas Alzheimer's disease and other dementias appear later in life, CTE shows up in relatively young people.
28
Mike Webster was only 52, and the interior of his brain was laced with tangles of tau.

Given the statistical evidence of widespread aftereffects of head injuries, how likely is it that former NFL players are actually suffering the ravages of CTE? Clearly, all of them aren't symptomatic. But most have had concussions and thousands claimed some sort of brain damage in the 2013 law suit. For years, the NFL steadfastly denied that concussions were common, or that they had any lasting health consequences. Moreover, the league completely rejected the notion that head injuries sustained playing in the NFL
caused
lasting brain damage or disease. These denials were at the heart of the former players' lawsuit. The NFL, they argued, had been deceptive by denying the harmful effects of head injuries and suppressing information about the dangers of playing in the league. Without all available information, the suit argued, players could not make intelligent, informed decisions about the risks they were taking.

Late in 2013, award-winning journalists Mark Fainaru-Wada and Steve Fainaru pulled back the curtain on the NFL's deception in a relentless account of how, for decades, league officials manipulated information about the incidence, prevalence, and consequences of concussions in the NFL.
League of Denial
vividly details how the NFL misrepresented data, conducted questionable research, and attempted to suppress and discredit research others were doing on concussions and their aftermath. Along the way, the NFL compromised the professional peer review process to get its own research published in scientific journals, exerted illegitimate influence to suppress other scientists' research findings, and attacked the work and character of legitimate researchers who produced findings contrary to the NFL party line.
29

The NFL was covering up a mounting body of evidence that Mike Webster's case was far from unique. In a staggering series of tragedies, former NFL players Andre Waters, John Grimsley, Terry Long, Dave Duerson, Ray Easterling, and Junior Seau committed suicide. Tom McHale died of a drug overdose. Justin Strzelczyk was killed in a car crash after leading police on a 37-mile high-speed chase. Each man had exhibited striking behavior and mood changes leading up to his death. Autopsies showed they
all
had CTE. In the past few years, autopsy after autopsy of the brains of former players have shown signs of CTE. By the fall of 2013, Boston University researcher Dr. Ann McKee had examined the brains of 46 deceased former NFL players. Forty-five of them had CTE.
30

While there's a notable sampling bias in the collection of the cases studied—brains tend to be donated for study by families of deceased players who were suspected of having brain disease—the consistency of these findings is compelling. Moreover, not a single case of CTE has been found that wasn't preceded by some sort of brain trauma.
31
Does this mean that all NFL players have or will get CTE? No. Does it mean that every player who suffers a concussion will develop CTE? Again, the answer is probably no. It's nearly impossible to establish a certain causal link between suffering a concussion and developing CTE. Given the evidence currently available, it's also difficult to establish the likelihood that a former player, or a player who suffered a concussion, will develop CTE. The incidence and prevalence of the disease are still unknown. But some scientists—such as Ann McKee, who has probably examined more postmortem cases of CTE than anyone—are willing to speculate:

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