I read with dismay the latest news that chronic traumatic encephalopathy (CTE) has been identified in a young man who played mostly amateur soccer. Patrick Grange played soccer throughout his childhood and in college and even in semi-pro leagues. He developed amyotrophic lateral sclerosis (ALS) in his mid-20s and died at age 29. His brain was studied and the pathology reported is a grade 2 case (out of a 4-point scale) of CTE.

Here I want to make two points. First, this news further deepens parents’ and young people’s dilemmas regarding sports. The most commonly played organized sport among youth in the world, even in the latecomer U.S., is soccer (or football in the parlance of the world outside of the U.S.). Much was made of Patrick Grange’s penchant for head-butting the ball. However, it is not clear at all that Mr Grange’s CTE was a result of his head-butting proclivities. His parents report that he suffered from at least 3 serious concussions. Regardless of which injuries were in the straw-pile that broke the camel’s back, I think that most parents recognize that soccer can be a dangerous sport. Weighing the positive physical and social benefits of team sports against the potential for future disability is a personal judgment call. The influence of future harm upon the final decision is greatly impacted by discounting as discussed in a previous post.

The second point to be made here is the connection between ALS and CTE. ALS is often called Lou Gehrig’s disease because the great New York Yankee died of ALS just before his 38th birthday. The key symptoms associated with ALS are distinctive. Both motoneurons (the neurons that innervate skeletal muscles) and corticospinal neurons (the neurons that excite motoneurons to produce volitional movement) die in ALS. In other diseases such as polio or stroke, only the motoneurons or only the corticospinal neurons, respectively, are affected. So the combination of symptoms resulting from motoneuron and corticospinal neuronal death is what marks ALS. It appears that several athletes with CTE have also shown the clinical signs of ALS. The question is whether they have ALS or whether the CTE has produced ALS-symptoms through a different mechanism. This question was addressed in 2010. Personally I think that the small sample size of that study – 12 patients were studied, 3 of whom had ALS – is just too small to answer this question. You may wonder if Lou Gehrig might have had CTE and the answer is that that is a distinct possibility as he suffered at least one notable concussion. We will never know because he was cremated after his death.

What difference does it make whether an individual’s ALS-symptoms are caused by ALS or by a distinct mechanism associated with CTE? The answer is that diseases that look alike but result from different mechanisms have to be treated differently. For example, an ischemic stroke (produces its damage by blocking blood flow and thereby oxygen delivery) and a hemorrhagic stroke (produces its damage by bursting a vessel) in the same spot will present indistinguishable symptoms. However, the former should be treated by blood-thinners; not so much for the latter. Unfortunately, no treatment (beyond palliative care) exists for either ALS or CTE. So for now, this debate is interesting but not of practical consequence.