EXPERT COMMENTARY: CHRONIC TRAUMATIC ENCEPHALOPATHY AND NFL PLAYERS
Robert Cantu, M.D., FACSM, is a clinical professor and co-director of the Center for the Study of Traumatic Encephalopathy at Boston University Medical Center. He is a 31-year member of ACSM and is an internationally recognized expert on concussions and head injuries. The comments below do not necessarily reflect the views or positions of ACSM.
Chronic Traumatic Encephalopathy (CTE) was first described more than 80 years ago by a New Jersey coroner/pathologist, Dr. Harrison Martland, in a hallmark 1928 article in the Journal of the American Medical Association (91:1103-1107;1928). The CTE clinical triad includes recent memory failure progressive to dementia, depression, and lack of impulse control. The pathology was first shown by Roberts in 1969 and involves the deposition of a toxic hyperphosphalated form of tau protein call neurofibrilary tangles. This tau, although deposited throughout the cortex, basal ganglia, brainstem and spinal cord is concentrated in the medial temporal lobe structures, amygdala, hippocampus, and entorhinal cortex.
Although Alzheimer’s disease shares tau deposition with CTE it also involves beta amyloid deposition and senile plaques which are not a feature of CTE. Thus a neuropathologist can easily distinguish between these two entities.
Although most cases of CTE have been described in boxers, in the last several years, 20 or so cases have been identified in former NFL players.
It has also been seen in players who did not play beyond college and has even been seen in one high school athlete. In addition, it has been found in battered women, a soccer player, a rugby player, and even a circus clown with repetitive head trauma. The common dominator is repetitive head trauma at both the concussive and subconcussive level. A number with this disease have had few recognized concussions but have a long history of many subconcussive blows (i.e., football linemen). Often, symptoms begin a decade or more after an athlete terminates his or her career. Once symptoms begin, they are progressive, usually over several more decades.
Soon, I will be testifying before Congress regarding the recent flap over the Michigan phone survey study of retired NFL players that found an incidence of dementia/memory related disease 19 times higher in players ages 30-49 and six times higher in retired NFL players over 50, as compared to expected prevalence in the population. While this study has serious design flaws as dementia cannot be diagnosed over the phone and “memory-related disease” is a very ambiguous term, the findings are not surprising to those of us studying CTE.
I personally believe the real message is repetitive head injury of concussive and even subconcussive levels is not a good thing and is not to be encouraged. Football, for instance, is being played in a far different manner than 50 years ago, with the helmeted head being used as a battering ram when blocking and tackling. I believe rules must not only be put in place but also enforced in order to change this behavior. The same can be said for hits to the head in hockey and other sports. If such change is not effected, I fear these sports are at risked of being dropped by many schools, something I believe that, with proper change, is not necessary.