EPIDEMIOLOGY OF CONCUSSIONS

Centers for Disease Control, in the U.S.A. record roughly about 300K concussions per year. These are just from sport, not to mention the concussions sustained during other types of accidents, nor does this number reflect those concussions that are considered “Sub-concussive Brain Trauma” (SCBT) or Chronic Traumatic Encephalopathy (CTE).

It appears that high-school football players sustain far more concussions and more often than those athletes at the collegiate and professional level. Concussions in female athletes are on the rise as well.

In a single 80-yard drive, a NFL lineman, can sustain up to 18 SCBT’s. Over a 10 year career, they would have sustained roughly 15,000 SCBT’s! This is according to Dr. Robert Cantu, a prominent neurosurgeon from Boston MA.

SCBT is a cumulative ticking time bomb, waiting to explode. Becoming more apparent as the athlete ages, resulting in symptoms like dementia known as chronic traumatic encephalopathy (CTE), a progressive, degenerative brain disease, just to name few. This is similar to what boxer’s experience. It is known as “dementia pugilistica.” SCBT injuries are especially traumatic; due to the fact the athlete may not show any overt symptoms of a concussion, despite having received multiple blow the cranium. It is only till later in life that the athlete may show signs of Traumatic Brain Injury (TBI).

SCBT can be represented as bruising to the brain, or micro-trauma, which cannot be seen, much like if one where to sustain such an insult to the thigh, for example. These micro impacts can easily diminish the threshold of partial and/or permanent brain trauma.

TBI’s involve a sudden yet violent anterior-posterior, acceleration and de-acceleration of the brain, that may or may not be accompanied with a large amplitude rotational forces as well. It is this sudden acceleration and de-acceleration that force the brain to violently move inside the skull, only to have to come to a dead stop, and re-coil back the opposite way it came from. This action can distort the cranial membranes (i.e. falx cereberi and the tentorium cerebelli). It is this disruption, amongst other structures, that is usually compromised. The alteration of these two membranes can alter fluid dynamics of cerebral spinal fluid, as it flows throughout the cranial cavity. The disruption of these membranes can also affect brain function.

At the cellular level, according to Dr. Allen Hovda, Director of the Brain Injury Research Center at UCLA, the nerve cells become stretched or twisted, releasing potassium into the extracellular matrix, which in turn, depolarizes the cell allowing calcium to reduce cellular function. The resulting consequence is an increase in amnesia, confusion and a loss of consciousness, via the inhibition of cellular function of the impacted cells and the subsequent surrounding tissue. The inhibition of cellular function causes the brain to increase its uptake of blood glucose, which can result in a overproduction of lactic acid. The lactic acid, itself, begins to inhibit brain function. Blood flow diminishes by roughly 50%, to prevent swelling. It will take roughly 10 days before normal blood flow to the brain is restored, depending upon the extent of the damage to the surround tissue. It is during this time period, which if the athlete sustains another SCBT, which in turn, will not only delay the healing process, but also will never allow the brain tissue to completely heal itself.