The cranium is an un-yielding house for the brain. Even the smallest bit of swelling in the brain can be a problem because the bony cranium does not expand.

Recently, Will McKamey, a Navy football player, died at the age of 19. He had been in a coma since falling unconscious and unresponsive after an unremarkable practice involving no noticeable blows to his head. A couple of years ago, while still in high school, Mr McKamey suffered a severe concussion, after which he was hospitalized. This year, Mr McKamey had been examined by four “independent” neurosurgeons and had received multiple scans (both MRI and CAT). Nothing suggested to medical personnel that Mr McKamey had anything to worry about and he was cleared for resuming his football career.

I am guessing that “independent” means that the neurosurgeons don’t work for the team. But it is hard to imagine that they are doing the exams for free; and equally hard to imagine that the high school league office pays them. Maybe independent means that the four physicians are unrelated to each other. If a reader knows the answer to this, please fill us all in.

This case is just so tragic, in large part because it was so avoidable. We need to recognize that we do not know who can safely resume everyday activity and gentle exercise after a head trauma. Knowing when a person can once again safely participate in contact sports is an even more mysterious art. Furthermore, I argue here that concussion is not a useful term or concept. We should be worried about all head trauma whether or not we are able to discern any immediate symptomatic or anatomical consequences.

Blows to the head can produce dramatic and sudden consequences such as unconsciousness, confusion, and anterograde amnesia. When this happens, we call the event a concussion. When no symptoms are evident, the event is sub-concussive. Unfortunately sub-concussive head trauma is not without dire consequences that can occur either acutely or after a long delay.

Let’s look at what happens when the brain bumps violently into the skull. Neurons are excited by the mechanical impact and they release gads of neurotransmitter. The released neurotransmitter overly excites other neurons, which in turn leads to excitotoxicity (a toxic reaction to too much excitement, really), and cell death. Axons may be stretched so much that the grip between the axon and the surrounding myelin sheath is disrupted, leading to an eventual demyelination. Some cells may be so strongly affected that they break open, die, and release substances that in turn harm nearby, intact, and previously healthy cells. Blood vessels may break open, leaking blood into the brain, causing a tiny “brain bruise.” The brain is likely to swell, producing an increase in pressure within the unyielding cavity of the cranium.

Head trauma may also initiate a degenerative cascade related to that which occurs in Alzheimers (AD) or Parkinsons (PD) Disease. this biochemical cascade promotes the production and aggregation of proteins such as beta-amyloid, alpha-synuclein, and tau which can ultimately lead to plaques and tangles in the brain, cardinal pathological signs of AD and PD. People may be more or less susceptible to this consequence from head trauma just as some of us are more or less susceptible to developing AD. For example, some forms (aka alleles) of the ApoE gene increase a person’s risk of developing AD.

In sum, lots of bad stuff can happen after you hit your head. The big, big problem is that we don’t know how to predict which blows to the head will resolve and which will go on to create either a delayed dementia or a vulnerability such as that which Mr McKamey clearly possessed.

My plea is that we recognize our ignorance. After a trauma, we may not see any symptom or sign that the brain is in fact in dire straits, severely damaged, and within a whisper of going over the edge and past the point of no return. Err on the side of caution.

Treat all head trauma as the potentially lethal event that it is.