"Head Injuries III"
"Head Injuries III"
HEAD INJURIES, PART III
By Dr. Ken
Once the brain is accelerated and forced to move, it then will come to rest. If it moves slowly enough within the skull, the fluid that it floats in will prevent it from striking the inner part of the skull. If it does hit the inside part of the skull, some cells will be damaged. If damage occurs through actual cell breakdown/destruction, current theory holds that the series of chemical responses that follow will produce the symptoms that we know as “concussion.” As serious and as damaging is the response of the brain cells, especially the axons we spoke of last month, to rapid movement, especially rapid rotational movement. Even if cells aren’t actually “broken”, the stretching that takes place leads to the same, or similar response chemically. Recall from our previous installments of Helmet News, that rotational acceleration can cause very serious injury to the cervical spine or neck. If our readers also recall that the brain, when an analogy is made to a clump of mayonnaise, is susceptible to having its cells stretched as compared to compressed. If a glancing blow occurs that sends the head “spinning” or glancing off of the point of contact, acceleration and subsequent deceleration is such that cells may be stretched significantly. Getting thrown hard and fast to the turf will also set the brain in motion to the extent that damaging tissue stretch may occur. Once this happens past a certain, definite threshold the chemical cascade or response begins.
The damaged cells begin to leak potassium. They then uptake calcium to a point where “calcium sinks” are formed in the area of damage. There is a reduction in the amount of magnesium that is usually in the brain or axonal cells. This takes place when glucose metabolism (and glucose is the primary fuel of the brain cells) increases markedly following injury. The increase is influenced by the changes that are taking place chemically. Unfortunately, with the higher demand for glucose or sugar, there is a decrease in the brain’s blood flow. The blood is what carries nutrients (glucose) and oxygen to the cells. Thus in light of this increased need for oxygen and fuel, there is a decreased delivery. This forces the brain to use a type of metabolism that requires an absence of oxygen (anaerobic Glycolysis to those who recall chemistry or physiology class). This in turn results in an accumulation of waste products called lactate. This makes the area more acidic which is followed by damage to the cell membranes or borders. This leads to further cell function alteration and the start of edema (build up of fluid in the brain). This is called a “cascade” by researchers because once the event begins, one aspect of it follows another in turn, until what appeared to be a minor blow, causes an awful lot of damage to the tissues and changes in behavior. “Gee, it didn’t seem as if he was hit that hard” is a commonly heard remark. The contact did not have to be “that hard”, it merely had to cause stretch of the axons and the beginnings of the chemical responses and the entire sequence followed. It is the chemical response, the step-by-step dysfunction that leads to, and determines the overall damage, immediate effect, and long-range effect of the concussion. This metabolic disruption will also determine how vulnerable the athlete will be to another concussion as the more widespread the chemical response is and the longer it lasts, the more danger the athlete will be in once he returns to the field. Even if the changes in behavior don’t seem “so bad” he may have had the type of chemical response that actually has him in a lot of potential difficulty. Changes in chemical behavior and blood flow can last for days, making the athlete at risk, for days or weeks following the incident.
If the damage is severe enough or the chemical reaction is widespread or long lasting enough, what may have begun or appeared to be a “concussion”, can become a more severe traumatic brain injury (TBI). In summary, it’s not the hit, or even the cell damage from the hit that can cause devastating problems; it’s the tissue and chemical responses that are the ultimate determinant of the athlete’s injury. Does the response of the helmet make a difference? See more Helmet News in the following months.