Chris Borland, a star rookie linebacker for the 49ers, announced in March of 2015 that he would retire early from football. He had 2 concussions and walked away from a multimillion-dollar contract and possible superstardom. He said, “I don’t think it’s worth the risk.” The NFL estimates that 30% of former players will develop dementia.

The term chronic traumatic encephalopathy is new, but the disorder was recognized as far back as 1928 when a Dr Harrison Martland described a condition in boxers who were recognized to be “punch-drunk” that was similar to Parkinson’s. The condition seemed irreversible and worsened steadily, even after retirement from boxing. Severity correlated with the number of professional bouts. Muhammad Ali was the poster child. A similar syndrome has been reported in non-athletes who had repetitive brain injuries, such as abuse victims, veterans, autistic patients with head-banging behavior, and in fact a circus clown. The sports most likely to cause chronic traumatic encephalopathy (CTE) are professional football, hockey, rugby, professional wrestling, and soccer. There is evidence that repetitive “subconcussive” head trauma, meaning that the trauma affects the brain but does not cause symptoms, may contribute to CTE. Thus, athletes who were never recognized to have a concussion may still be at increased risk.

There are many unanswered questions. Is there a threshold number of concussive or subconcussive injuries that will increase risk? The National Institutes of Health recently funded 2 large research projects, utilizing funds contributed by the NFL.

The symptoms of CTE are usually mood disorders, headaches, cognitive difficulties, suicidal ideation, difficulties with speech, and aggressive behavior. These athletes tend to have poor impulse control and are short-tempered.

Understanding why some athletes develop CTE and others do not is a major public health challenge.

See Neurology, October 27, 2015, page 1442 and 1504.

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