Pro-Bowler Dave Duerson's Suicide Renews Head Trauma Debate

Former Chicago Bears player Dave Duerson's suicide sparks a safety debate.

ByABC News
February 25, 2011, 5:55 PM

Feb. 26, 2011— -- When Dave Duerson, former member of the Chicago Bears who was a four-time Pro-Bowl safety, died of a self-inflicted gunshot wound at age 50 on Feb. 17, he made sure his brain was intact -- or as intact as it could be after a head-banging career in professional football.

He shot himself in the abdomen, after requesting that his brain be studied for evidence of chronic traumatic encephalopathy, a condition that has become an increasing source of concern among professional athletes. Around 20 football players who died relatively young have been found to have the brain changes associated with this condition, and some critics are now calling for a ban on the game for youth younger than 18.

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Neuropathologist Bennet Omalu, MD, who was the first to identify the condition, told MedPage Today, "There is no reason, no medical justification, for any child younger than 18 to play football, period."

It has been known since the 1920s that the repetitive brain trauma experienced by boxers sometimes led to neurologic and cognitive deterioration -- a condition that initially was termed "dementia pugilistica."

But in 2002, after the death of Pittsburgh Steelers former star center Mike Webster, known as "Iron Mike," Omalu, who then worked in the medical examiner's office in Pittsburgh, performed an autopsy on the player, whose life ended with a heart attack after years of homelessness and destitution -- he had even sold his Super Bowl rings -- as well as depression and multiple suicide attempts.

On first examining Webster's brain, Omalu was startled to find that it appeared perfectly normal. He had been expecting visible evidence of repeated damage that could cause the player's deterioration.

But he persevered, and in special analyses of brain tissue samples, he found large deposits of tau, a protein which is part of the microskeleton of brain cells. With repeated axonal injury, tau loses its self-repairing ability, becomes hyperphosphorylated, and begins to accumulate, forming neurofibrillary tangles and neuritic threads in areas of the neocortex.