Reducing Concussions in Football?

The awareness and medical implications of concussions in professional sports have increased significantly over the last half-decade, especially in National Football League (NFL). The direct responsibilities of both the NFL and players to manage the concussion question have previously been outlined in the blog here. Unfortunately neither party, especially the players, has administered those responsibilities appropriately. While behavior still needs to be adjusted to reduce concussion probability, there may be biological strategies that can help maximize positive health outcomes for athletes with regards to concussions.

Various concussion research has involved evaluating rugby-based headgear as well as other helmet designs, custom-fitted mouth guards and face shields (in ice hockey).1-4 The general conclusions are that no particular type of headgear, including rugby-based, reduces the probability of acquiring a concussion any more effectively over most other types of helmets and there is no strong evidence that mouth guards or face shields reduce concussions.4,5 In addition significant amounts of research has focused on post-concussion symptoms and recovery. However, less research has been conducted on secondary factors to developing concussions. For example football has changed significantly in many ways since the early professional days in the 50’s and 60’s; one way that could be very relevant to concussion development is the means in which the brain processes and consumes oxygen.

There are two chief theories that attempt to explain the biological origins of a concussion. First, some believe that the first step involves a significant level of at least one type of force, linear, rotational or angular, that is directly or indirectly applied to the head leading to the disruption of cell membranes in various neurons throughout the brain. This disruption creates an influx of potassium ions to the cells resulting in depolarization and the release of neurotransmitters, usually glutamate.6 The release of glutamate creates a cascade of depolarization among various neuronal networks. Sodium-potassium pumps operate at greater than normal capacity to correct the unnatural and uncontrolled potassium influx, which leads to an energy shortage (excessive consumption of ATP and glucose) resulting in excess lactate accumulation.7-9 All of these elements work in consort to generate neurological imbalance and damage.

Some also believe there is a loss of glucose metabolizing efficiency due to excessive metabolization during the initial stages of the concussion. This loss of metabolizing efficiency is due in part to inefficient lactic acid removal after the concussion event, at least in rodents, which leads to reduced blood flow for a number of days after a concussion event.7,10 Interestingly enough this lack of blood flow could explain why an individual has a higher concussion probability rate (vs. baseline) for a number of days after the initial concussion event because there is less cerebral blood flow and greater ability to produce slosh and other forces. Whether or not calcium accumulation results in cell death through a secondary pathway is unclear.11

Second, some believe that rapid acceleration/deceleration of the brain due to forces and collisions create “slosh” (movement of liquid inside containers that are undergoing motion). Slosh occurs in tissues and fluids with differing densities (white matter, skull, spinal fluid, blood, gray matter, etc.) because they accelerate/decelerate at different rates leading to shearing forces and even hydrodynamic cavitation.12,13 Cavitation is the formation of vapor cavities in liquid born from a rapid change to a lower pressure (below saturated vapor pressure of the liquid). After these cavities are formed an increase in pressure results in their implosion creating shockwaves. These shockwaves create damage throughout the brain.14

Whether or not concussions are driven by functional or structural changes is still an open question. While structural damage has been demonstrated in some brains of humans, commonly resulting in a state similar to Alzheimer’s disease, these changes appear to require numerous concussions over a relatively short period of time (decade or less). Overall it is highly likely that concussions are driven by temporary functional changes, which is why the symptoms are only temporary.

An interesting element about concussions is that both rams and woodpeckers can tolerate head impacts much larger than those that are thought to induce concussions in humans. For example typical football impacts generate 25 to 50-g of force whereas rams ramming each other during demonstrations of supremacy generate 500-g and woodpeckers generate 1200-g numerous times a day.15 This ability to experience head trauma without detrimental outcome is thought to be managed by manipulating intracranial volume and pressure. Both animals have different methodologies behind this ability; rams utilize a carbon dioxide-mediated response to altitude and woodpeckers utilize altered jugular outflow.12,15 These methods create efficient brain compacting, which reduces motion and shearing forces. Clearly altering jugular outflow is not reasonable for humans, but it may be possible to incorporate information from an altitude response to reduce the probability of concussions.

Some of the central features that drive a concussion occur within the skull, which is why no helmet can ever clinically claim to reduce concussions because they cannot directly influence forces inside the cranium. However, playing at an increased altitude (venues at or exceeding 644 ft.) appears to decrease the probability of developing a concussion. A recent study of concussion occurrence in the NFL calculated a 30% reduction at higher altitudes.15 Recall from above that one of the elements that is thought to causes concussions is the brain “sloshing” around creating various forces and cavitation. Clearly one of the methods to reduce the probability of concussions is to increase intracranial volume that would allow the brain to reduce “slosh”.15,16

Some have argued that inadequate adjustment to altitude reduces the ability of players to exert maximum effort thus reducing the amount of force applied when running, blocking and tackling thereby reducing the probability of concussions. However, studies in the past have demonstrated that there is no significant enhancement of fatigue at the 644 ft. threshold; therefore, this “reduced force” reasoning should not be applicable. If concussion probability reduction occurred only at higher altitudes like 2000 ft. then it would be more plausible, but that is not the case.

The protective effect of higher altitudes may directly involve the rate of oxygen flow to the brain. The chief change relative to oxygen at higher altitudes is a drop in oxygen partial pressure throughout the body, especially the brain. For example alveolar oxygen partial pressure drops from 103 to 98 when moving from 0 to 1000 ft.17,18 This reduced partial pressure lowers the available oxygen in the blood for consumption by various organs including the brain. With a greater demand for oxygen cerebral blood flow increases, which increases intracranical volume and decreases the probability of concussion. This relationship between oxygen and altitude could also explain why there is not an empirical linear relationship in the above study between altitude and oxygen for after a certain point players become fatigued by the lack of ambient oxygen and resort to supplementing oxygen consumption with outside sources. This supplementation could explain why Denver, the highest altitude playing field in the NFL, did not have the lowest rate of concussion.15

The relationship between oxygen-related blood flow and concussions also can influence the rate of inertial cavitation. The skull can be considered a rigid vessel with a reduced compliance (due to increased intracranial volume) the probability of inertial cavitation decreases because there is less sudden directional changes in near-by fluids reducing the formation of vapor cavities.13,14,19,20 Therefore, increased cerebral blood flow reduces both the force and the cavitation elements associated with potential concussion progression.

So how is cerebral blood flow controlled naturally? The brain has a much higher metabolic requirement for oxygen than other organs and uses approximately 20% of existing oxygen to maintain normal function. Under normal biological operation blood flow to the brain is constant due to vascular resistance provided by large arteries and parenchymal arterioles and tight gap junctions.21,22 Flow is increased through the dilation of upstream vessels avoiding downstream microvascular pressure.23 Overall blood flow rates are controlled by vasodilation of distal to proximal arterial and myogenic mechanism24 maintaining a cerebral blood flow at approximately 50 mL per 100 g per minute as long as cerebral perfusion pressure (CPP) is between 50-60 and 160 mmHg.25

If CPP falls below 50-60 mmHg cerebral ischemia occurs and the body attempts to compensate by increasing oxygen extraction from blood and increasing blood flow to the brain.26,27 Part of the reason blood flow needs to increase is because the partial pressure of oxygen drops hemoglobin saturation from 100% to 50%.28 There is a rather linear relationship between blood flow and CPP below 50-60 mmHg, but there is little change in metabolism regardless of oxygen partial pressure.28 Under these hypoxic conditions cerebral arteries and arterioles reduce vascular resistance increasing vasodilation and smooth muscle hyperpolarization.

An increase in CO2 concentration has a similar effect to reducing oxygen concentration because of a decrease in oxygen partial pressure. In response cerebral blood flow is increased through similar methods as above (cerebral arteries and arterioles dilation).29 The biological effect of CO2 inhalation is rather significant where a solution of 5% CO2 increases cerebral blood flow by 50% and a 7% CO2 solution increases blood flow by 100%.30 The chief mechanism behind hypercapnic vasodilation is the direct influence of extracellular hydrogen on vascular smooth muscle as changes in CO2 partial pressure along does not change cerebral artery diameter.31,32

With the above information it appears that increasing the ratio of CO2/oxygen in the blood will increase the rate of blood flow to the brain, which will decrease the probability that an individual suffers from a concussion. Outside of playing at altitude what are the methods to increase cerebral blood flow? One long term solution could be breathing conditioning where continuous periods of holding one’s breath would increase CO2 concentration in the blood stream over a very short period of time which could lead to the expansion of carotid arteries increasing blood flow to the brain.

However, breathing conditioning is a long-term solution that many individuals may not have the time or the inclination to undertake, so is there a short-term solution that can temporarily increases cerebral blood flow? One possibility that springs to mind is the consumption of a specific carbonic acid beverage (basically a stronger version of soda/pop). Whether or not this method would be viable is unclear as there is almost no empirical information regarding how the consumption of such a beverage would influence cerebral blood flow or other systems and organs.

Another question is whether or not the use of mouth-to-mask ventilation increases concussion risk by temporarily reducing cerebral blood flow. While there appears to be no direct evidence regarding this question, anecdotal evidence involving the drop-off of concussion reduction at very high altitudes (Mile High Stadium in Denver for example) appears to support this idea.
Basically the technical aspect of this question is how does the brain respond with respects to blood flow to a brief (15-30 seconds) inhalation of 50-100% oxygen and what is the residence time of this response? The answer to this question could change the use of mouth-to-mask ventilation to only emergency situations rather than an augmented pick-me-up after a 26-yard run in order to avoid increasing the chance of a concussion in the next play.

There are numerous behavioral methods to reduce the probability of concussions in football including ensuring that defensive players tackle properly (no leading with the head) and proper neurological evaluation after significant head contact. However, another avenue of concussion prevention has remained generally unexplored. Based on some preliminary evidence it appears that devising a strategy to increase cerebral blood flow to act as a “biological helmet” could go a long way to decreasing the probability of concussion development. The one significant caveat to the development of such a method would be determining any long-term detrimental effects associated with multiple temporary increases to cerebral blood flow. Overall it is important to investigate biological methods as well as material methods and behavioral solutions to prevent concussions in sports.

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