Dave Duerson, a four-time National Football League (NFL) Pro Bowl defensive back with two Super Bowl rings, sent a farewell text-message this past winter to family members, then committed suicide by shooting himself in the chest. Duerson, only 50 years old, had been experiencing emotional as well as memory problems. He was convinced that he suffered from chronic traumatic encephalopathy (CTE), a brain-degeneration condition found in other former football players. In his text message, Duerson asked that his brain be autopsied. Days later, a group of CTE-specialists at Boston University reported that his brain did show signs of the condition.
These researchers portray CTE as a progressive brain disorder that can originate from head trauma, including impacts that are too minor to cause concussions. As such, CTE could affect anyone who participates in high-impact sports, is exposed to bomb-blast shock-waves—on the battlefield, for example—or otherwise experiences significant or routine head knocks. CTE specialists have reported finding signs of the disease in a college football player who had committed suicide at age 21, as well as in former pro hockey players, pro wrestlers, and a former boxer. These researchers also recently reported finding the brain pathology and muscle-weakness signs of amyotrophic lateral sclerosis (ALS) in CTE patients—suggesting that some ALS cases may originate, as CTE, from head injuries.
“We’ve now examined over 55 CTE cases in individuals who have suffered repetitive brain trauma—any brain trauma, even from epilepsy that’s very poorly controlled, or combat injuries,” says Ann McKee, a Boston University pathologist who has co-authored several CTE studies.
But the dramatic claims being made for CTE have been met with skepticism by some researchers. “One of the biggest problems is that we don’t know how many players don’t have it,” says William Barr, an expert on sports neuropsychology at New York University. “If it truly is common, wouldn’t we be seeing many more so-called demented football players, for example?”
Origins of the CTE controversy
CTE originated as an alternative term for dementia pugilistica, a neurodegenerative syndrome seen in boxers. It was first applied to football players by a county pathologist in Pennsylvania, Bennet Omalu, who in 2002 performed an autopsy on the body of Mike Webster, a former NFL star. Webster had died of a heart attack at 50, after years of worsening psychiatric and cognitive problems. Although Omalu found that Webster had indeed died of heart disease, he also found something unusual in Webster’s brain: a distinctive pattern of deposits of abnormally clumped tau proteins. Tau deposits occur in Alzheimer’s, fronto-temporal dementia (FTD), and other “tauopathies,” but the pattern of deposits in Webster’s cortex seemed new, and they were unaccompanied by deposits of Alzheimer’s-associated amyloid beta protein. Omalu, and subsequently several other researchers—mostly from the CTE research group where McKee works at Boston University—found similar pathological signs in the brains of other former football players, sparking widespread media reports and alarm about CTE.
As Barr points out, studies to determine the prevalence of the condition among former athletes or others with recurrent head trauma haven’t yet been done. “They have to start taking cohorts to study together,” he says. “For example, take the class of 1960 at a big football-powerhouse university, and compare the men who were on the football team to those who were on the debate team.”
Researchers also don’t yet know how the abnormal protein deposits in the brains of CTE cases could lead to cognitive and behavioral problems such as suicide. “Suicide is a very complex thing; we know of no gene or neuronal abnormality that causes it,” Barr says. “I guess that you could compare suicide rates in those who have this tauopathy, with those who have Alzheimer’s disease and with those that don’t have this tauopathy; but that would be a hard study to design, because suicide is not that common.”
One line of research on former football players may even conflict with the CTE hypothesis. About six years ago, a group led by a sports medicine researcher at the University of North Carolina, Kevin Guskiewicz, surveyed roughly 2,500 former NFL players. They found evidence of an unusually high incidence of memory problems, and the memory problems were correlated with the number of recalled concussions. Subsequently, in a study led by neuropsychologist Christopher Randolph at Loyola University School of Medicine in Chicago, they compared a sample of these former players to a sample of mostly elderly patients with mild cognitive impairment (MCI), which often presages Alzheimer’s dementia. The former players showed a pattern on tests like the pattern of the older MCI patients, as if the hard knocks to their brains had allowed the MCI process to begin early. But these former NFL players with cognitive problems appeared to be on a path to getting MCI and Alzheimer’s. They did not appear to have the more complex neuropsychological signs of CTE.
“Certainly there is reason to believe that there is a cumulative effect of both concussive and subconcussive insults,” Guskiewicz says. “But the CTE studies have found this [brain pathology] in younger deceased football players—an 18-year old, I think a 21-year old—and so it begs the question, is it really years of head insults that causes this, or is it something else?”
The cognitive and behavioral declines seen in some former athletes with CTE findings at autopsy also resemble the symptoms of FTD, which has been linked to head trauma. According to the Mayo Clinic’s description: “Frontotemporal lobe dementia is an umbrella term for a diverse group of uncommon disorders that primarily affect the frontal and temporal lobes of the brain—the areas generally associated with personality, behavior and language… Some people with frontotemporal dementia undergo dramatic changes in their personality and become socially inappropriate, impulsive, or emotionally indifferent, while others lose the ability to use and understand language.” According to Guskiewicz, “there are a number of [researchers] who claim that CTE is probably just a subclassification of FTD.”
McKee insists that CTE is a distinct disorder: “It’s not FTD, and it’s not Alzheimer’s.” She and her colleagues also are continuing their CTE research, including a project to detail the pattern of spread of the pathology in CTE-affected brains; studies of battlefield blast-injury cases—“we’re seeing in blast injury [brains] the same changes that we see in athletes in early stages of their disease”—and even a mouse model of blast-injury CTE. The latter, she says, “could give us the mechanism of the disease, and that would allow us to come up with real therapeutic strategies as well as prophylaxis and ways to prevent this disorder.”
Guskiewicz and his colleagues are pursuing their own further studies, including brain-imaging of former NFL players with MCI-like memory problems. But as he notes, the research has far to go: “There are still a lot of unknowns.”