A Cry for Help – Will the NFL listen?

[TW for suicide, gun violence, bodily damage from long-term football play]

From the LA Times:

[Dave Duerson] is the former Chicago Bears safety, most notably with the 1985 Super Bowl champs, and a businessman who grew a food company into a multimillion-dollar success. He had 11 years in the NFL and was selected to four Pro Bowls. […]

Thursday, Duerson shot himself to death in his home in Florida. He was 50.

It took a day or so for the official word that it was suicide. It took another day or so for the real shocker to be revealed.

He shot himself in the heart, not the head. He did so, it became obvious, because he had left a request with relatives that he wanted his brain tissues examined. Word now is that that will be done at the Boston University Center for the Study of Traumatic Encephalopathy.

Chronic traumatic encephalopathy, or CTE as it is now known, first acquired public recognition when it was identified in the brain tissue of former Philadelphia Eagles player Andre Waters after his suicide in 2006. There have been other cases of CTE found in the brain tissue of former football players who committed suicide. It has been a murky concept for years, its connection to football injuries denied by most involved with the game, including medical personnel. Determining the presence of CTE can be done only on a deceased brain.

So Duerson gave his to medical science in the only way he could right now.

From NFL Fanhouse:

In a suicide note he sent to friends, Duerson asked that his brain be donated to the Center for the Study of Traumatic Encephalopathy at Boston University School of Medicine. The Center has been leading the way in research into how brain damage — including injuries suffered in collisions on the football field — can lead to health problems later in life. One theory is that people who have a history of repetitive brain trauma are more likely to experience depression, and studying Duerson’s brain may help researchers determine whether brain damage suffered on the football field led to the depression that ultimately caused him to take his life.

From The Chicago Tribune:

Chris Nowinski, co-director of the Center for the Study of Traumatic Encephalopathy at Boston University School of Medicine, said Duerson’s family contacted him to examine Duerson’s brain for abnormalities related to chronic traumatic encephalopathy (CTE), a degenerative brain disease found in those who have a history of repetitive brain trauma, including concussions. […]

“NFL players are at higher risk for CTE than normal people and probably other athletes as well,” Nowinski said. “Of the 14 former NFL players we’ve completed studies on, 13 of them had the disease.”

From The New Yorker (from Jan 31, 2011):

What we now know, from reading Schwarz, is that retired N.F.L. players are five to nineteen times as likely as the general population to have received a dementia-related diagnosis; that the helmet-manufacturing industry is overseen by a volunteer consortium funded largely by helmet manufacturers; and that Lou Gehrig may not actually have had the disease that bears his name but suffered from concussion-related trauma instead. (Since 1960, fourteen N.F.L. players have had a diagnosis of amyotrophic lateral sclerosis, which is about twelve more than you would expect from a random population sample.) […]

“The reality is you’re going to need about twenty fixes that reduce risk by a couple of percentage points each,” Chris Nowinski said. “There’s still going to be four downs. Still going to be a football. Still going to be eleven guys on the field—and touchdowns. Other than that, everything’s in play.” […]

From Fink’s research, for instance, I know that the rate of reported concussions in the N.F.L. did not decline after the stern warnings in October; it increased. Some of this may be attributable to greater conscientiousness on the part of players and medical staffs, which is a good thing, but the “disturbing” hits, as the league’s Ray Anderson called them, were just as prevalent, if not more so, as the season wore on. When I called Fink, he told me about a friend of his who plays in the N.F.L., a longtime taxi-squad member who had finally caught on as a starter. Earlier this season, the friend showed up in the concussion database that Fink compiles from news reports and other sources. “I texted him and asked how it happened,” he said. “He texted back, ‘I’m always concussed, they just caught me this week.’ ” […]

Some of the most effective proposed reforms seem to involve limiting contact during practice, and forbidding children to tackle until adolescence or beyond. (Developing brains are vulnerable to “second-impact” syndrome.) “Seventy-five per cent of the hits are in practice,” Nowinski said. “You could drop the exposure by fifty per cent without changing the game at all.” You could, perhaps, but it does also make you wonder about a game whose preservation is couched largely in terms of reducing the frequency with which people really play it.

From The New Yorker (from Oct 19, 2009):

She has now examined the brains of sixteen ex-athletes, most of them ex-football players. Some had long careers and some played only in college. Some died of dementia. Some died of unrelated causes. Some were old. Some were young. Most were linemen or linebackers, although there was one wide receiver. In one case, a man who had been a linebacker for sixteen years, you could see, without the aid of magnification, that there was trouble: there was a shiny tan layer of scar tissue, right on the surface of the frontal lobe, where the brain had repeatedly slammed into the skull. It was the kind of scar you’d get only if you used your head as a battering ram. […]

What seems to have caused his concussion, in other words, was his cumulative exposure. And why was the second concussion—in the game at Utah—so much more serious than the first? It’s not because that hit to the side of the head was especially dramatic; it was that it came after the 76-g blow in warmup, which, in turn, followed the concussion in August, which was itself the consequence of the thirty prior hits that day, and the hits the day before that, and the day before that, and on and on, perhaps back to his high-school playing days.

This is a crucial point. Much of the attention in the football world, in the past few years, has been on concussions—on diagnosing, managing, and preventing them—and on figuring out how many concussions a player can have before he should call it quits. But a football player’s real issue isn’t simply with repetitive concussive trauma. It is, as the concussion specialist Robert Cantu argues, with repetitive subconcussive trauma. It’s not just the handful of big hits that matter. It’s lots of little hits, too. […]

The HITS data suggest that, in an average football season, a lineman could get struck in the head a thousand times, which means that a ten-year N.F.L. veteran, when you bring in his college and high-school playing days, could well have been hit in the head eighteen thousand times: that’s thousands of jarring blows that shake the brain from front to back and side to side, stretching and weakening and tearing the connections among nerve cells, and making the brain increasingly vulnerable to long-term damage. […]

In one column, the HITS software listed the top hits of the practice up to that point, and every few moments the screen would refresh, reflecting the plays that had just been run on the field. Forty-five minutes into practice, the top eight head blows on the field measured 82 gs, 79 gs, 75 gs, 79 gs, 67 gs, 60 gs, 57 gs, and 53 gs. One player, a running back, had received both the 79 gs and the 60 gs, as well as another hit, measuring 27.9 gs. This wasn’t a full-contact practice. It was “shells.” The players wore only helmets and shoulder pads, and still there were mini car crashes happening all over the field.


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