The cause of Dave Duerson's death in February was the bullet that he fired into his chest. But the public has been given reason to believe that the seeds for Duerson's suicide were sown decades before, during his career as a hard-hitting NFL safety. And that may be wrong. All those hits, the story goes, damaged Duerson's brain, leading him to develop neurological and psychological problems—particularly depression—with the expectation of an even darker future. Duerson may have believed that football left him with an irreversible brain condition called Chronic Traumatic Encephalopathy (CTE), which was the root of all that plagued him. Like many struggling, aging former athletes, Duerson, at age 50, had reason to think of CTE as a time bomb in his head. He shot himself in his chest, so that his brain could be studied.
Last week Boston University's Center for the Study of Traumatic Encephalopathy announced that it had discovered CTE in Duerson's brain. (CTE can only be detected and measured after death.) The finding was not unexpected. "I would not be surprised if we eventually learn that this type of pathology is present in the vast majority of participants in contact sports," says Jonathan Katz, a San Francisco neurologist. What concerns Katz and many of his colleagues is the prevailing perception that CTE, and therefore participation in sports that might produce it, is a cause of a range of neurological conditions, including depression, dementia and a disease that mimics ALS. The public's belief in this link has been shaped by the BU researchers and disseminated by, among others, The New York Times, which has printed 35 articles since 2005 on CTE. That belief may provide some comfort for surviving family members, like relatives of the 21-year-old Penn linebacker Owen Thomas, who hanged himself in April 2010 and whose brain was found to have CTE. Yet, says Katz, "Sadly, there is absolutely no proof that CTE plays a role in causing any of the myriad clinical conditions from which these athletes have suffered."
As Duerson went through middle age he went bankrupt, his home went into foreclosure, his marriage dissolved. Robert Cantu, a neurosurgeon and codirector of the BU clinic, concludes that those developments stemmed from the CTE found in a part of Duerson's brain that governs memory, emotion and impulse control. "We believe, more probably than not, because that is the area of the brain that was damaged, that this is what caused his problems," says Cantu. Such a conclusion, however, might amount to "drawing a bull's-eye after seeing where the arrow hit." That was an analogy used by the authors of one of two letters published in the Journal of Neuropathology and Experimental Neurology, which last year ran an article by the BU team suggesting that CTE can cause an ALS-like disease—letters signed by a total of 19 prominent neurologists who strongly criticized the finding.
Several widely accepted beliefs concern experts. One is that CTE is definitely a causative, and not a parallel, condition in those with neurological symptoms. A consequence of this thinking is that those with symptoms may assume that they are suffering from the untreatable brain damage of CTE instead of other independent causes—depression or other disorders—which might be treatable. Cantu allows that the sample of brains examined by his clinic is self-selected. "We have not gotten a lot of brains of asymptomatic people who died naturally and had no issues," he says. "[They come from] a very skewed population of people who have accidentally died or have taken their own lives." There is likely an enormous population of former participants in contact sports whose brains exhibit CTE, and yet who experience no noticeable neurological symptoms.
Another criticism is that it has not been satisfactorily proved that CTE, which is usually painted in the media as both "degenerative" and "progressive," is either. Cantu and his colleagues have made these conclusions because the symptoms they have associated with CTE are "relentlessly progressive" and because they found more of it in older former players like Wally Hilgenberg, a linebacker who died of ALS in 2008 at the age of 66, than they did in younger former players like Duerson. The sample size, however, is small. BU has examined 15 brains of former NFL players and found CTE in 14 of them. It is impossible to know if Duerson's brain showed more signs of CTE when he died at age 50 than when he stopped playing at 33.
Causality brings comfort, though, and Duerson's family now feels certain of the cause of the downward spiral that led to his final act. "We have been given the gift of closure," said one of Duerson's sons, Tregg, last week.
"Trying to tie everything into these sports injuries can be a distraction from the real problems," cautions Richard Barohn, chairman of the neurology department at the University of Kansas. "In [Duerson's] case it might have been more than a distraction. It might have been totally damaging." Cantu shares that worry. "I'm concerned that some people, whether they are football players or not, may come to some decisions that could be very, very wrong, and do things that are very destructive," he says.
Former participants in contact sports who experience neurological symptoms should not assume that CTE has left them with incommutable death sentences, and they should seek professional help. There remains a disturbingly strong possibility that the treatment for what afflicted Dave Duerson might have included regular psychological therapy, and not a bullet to the chest.
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