High-impact activities like football are known to cause creeping brain damage that can't easily be detected until after death. But promising research may give rise to new methods of diagnosing chronic traumatic encephalopathy.
In 1996, the brain of an alcoholic dwarf circus clown perplexed scientists with a disease normally limited to boxers. Over 15 years of being shot from a cannon at a circus, the clown developed dementia pugilistica, or as its 1928 discoverer Harrison Martland called it, "punch drunk." Less than ten years after the publication of a study on that cannon-rattled brain, an autopsy diagnosed deceased NFL Hall of Famer Mike Webster with the same condition, but now called chronic traumatic encephalopathy (CTE). An upswell in public interest and research following this death brought to light the danger that brain injuries present for athletes in all contact sports. A string of suicides and bizarre deaths by professional athletes, primarily football and hockey players, catalyzed a movement of more than 100 athletes to donate their brains for scientific study.
Junior Seau is the most recent athlete to donate his brain. The day after Junior Seau's suicide last week, the co-directors of the Boston University Center for the Study of Traumatic Encephalopathy published a paper, titled "Chronic traumatic encephalopathy: neurodegeneration following repetitive concussive and subconcussive brain trauma," in the medical journal Brain Imaging and Behavior. Even though Corsellis first identified the signs of CTE in the brains of boxers in 1973, significant gaps remain in our knowledge of this disease.
MORE ON SPORTS INJURY
Repeated blows to the head -- from football tackles, blasts from a circus cannon or some other trauma -- put the brain at risk for CTE. Although typically associated with concussions or serious head injuries, brains of football players with CTE but without any concussive history demonstrate that repeated, less severe "subconcussive" injuries provide sufficient trigger for this disease. While individual trauma may produce short-term symptoms, the effects of CTE manifest years after the injuries as the disease progresses and the brain breaks down. Yet many athletes with recurrent head injuries evade CTE; it appears repeated head trauma are necessary, but not sufficient, to trigger CTE. Researchers believe that the nature of the head trauma -- and the severity, frequency, and age of the recipient -- may play a role in whether or not CTE develops. But, for now, why the disease overtakes some and spares others remains a mystery.