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Leaping Too Far Too Soon

Gilbert and Johnson use the timely and controversial issue of a purported association between American tackle football and chronic traumatic encephalopathy (CTE) as a vehicle for proposing substantial changes in the way football is played and coached in order to reduce the risk of long-term neurologic damage in players. They provide insightful analysis of the substantial benefits associated with youth football and the ethical conundra faced by coaches, parents, and young athletes when confronted with the risks associated with participation. However, the authors’ argument is based upon the assumption that a causal link between participation in contact sports and CTE has been established scientifically, thus implying that every athlete who participates in contact sports is at significant risk for the development of a debilitating neurological condition from degenerative pathology affecting the brain. The scientific reality as of 2011 is that we do not have irrefutable scientific evidence, or even a preponderance of evidence, that concussion or any form of head injury is causally related to late neurological impairment. Therefore, the authors’ call for sweeping changes in football in the name of preventing CTE is premature at best. The initial case report on a possible link between football and CTE was by Omalu and colleagues in 2005 and described the case of a 50-year-old retired National Football League (NFL) player who died from myocardial infarction and underwent autopsy with complete neuropathological examination. Premorbid medical history included depression, cognitive deficits, and parkinsonian symptoms. Examination of the brain revealed many amyloid plaques as well as some neurofibrillary tangles and tau-positive neuritic threads throughout the neocortex. In 2006, Omalu and colleagues reported the case of a 45-year-old retired NFL player who committed suicide by ingesting ethylene glycol. His premorbid history included a diagnosis of major depressive disorder with multiple suicide attempts. Pathological evaluation of his brain indicated the absence of amyloid plaques but sparse to frequent tau-positive neurofibrillary tangles and threads in all regions of the brain. The authors were careful to note confounding fac-