Sports Concussions - Part 2

Pathophysiology: How does a Concussion occur and what happens in the Brain?

In Part 1, we discussed what a concussion is and how do you get one. What is often not discussed in concussion educational materials for parents or even in university degrees for that matter (at least to any degree of depth that is worthwhile), is the pathophysiology of a concussion. A pathology is simply an abnormal or undesirable condition, which in our case is a concussion. Therefore, pathophysiology explains the functional changes happening in the brain during this abnormal state. If we can understand the breadth of chemical alterations that happen from a concussion (termed neurometabolic), then we will be less inclined to brush off our child’s suspected concussion as “not that bad”. I very much believe that when people hear the word concussion, they don’t truly grasp what is happening in the brain. Often it is perceived as some vague and cloudy concept that you’ve heard is bad but don’t really know why.

Biomechanics of a Concussion: What causes a concussion?

A concussion is caused by an abrupt linear and/or a rotational acceleration or deceleration of the brain within the skull. Linear accelerations (e.g., a blow to the front of the head) are measured in g-forces (g=gravity), and it has been found concussions generally occur above 95g (Marshall, 2012), but this threshold can be higher or lower for different individuals. Keep in mind fighter pilots typically handle 8-9g! Rotational forces, like from a side-on impact, increase the shear forces going through the brain. Brain tissue, which is a highly organized structure, is particularly susceptible to shear forces which can further increase damage. It has also been found that if you are unaware of the impact, you have less time to pre-emptively tense your neck muscles to dampen the forces going through the head. This is why athletes delivering a hit get hurt far less than those getting blindsided.

This mechanical energy is then transferred to the brain. The brain, which is an incredibly soft tissue composed largely of water, deforms very easily when high impact or shear forces are applied. Once the forces applied are above the threshold for sustaining a concussion, an immediate series of metabolic and physiological changes occur termed the “Neurometabolic Cascade of Concussion” (Figure 1). The following is a very high-level overview of the changes happening in the brain which cause concussive symptoms (summarized from Marshall, 2012 and Giza & Hovda, 2015)

When an impact or trauma occurs above 95g of force, the acceleration of that motion stretches and shears the neurons of the brain. This aggressive deformation opens up ion channels and depolarizes the neuron, or in other words, forces it to fire. This causes the release of the amino acid Glutamate, which binds to methyl-D-aspartate receptors. This causes large amounts of Potassium to be released out of brain cells, and consequently, large amounts of Calcium ions flow into these same cells. In conjunction with these ion changes, a decrease in Cerebral blood flow occurs, meaning less fresh blood, and therefore oxygen and nutrients, are coming to the brain. It should be noted that this instantaneous firing of large amounts of neurons is what causes many of the initial symptoms like confusion, vision issues, and balance problems...your brain is firing uncontrollably.

It is this influx of Calcium ions into the brain cells which is the real problem. Firstly, Calcium overloads the mitochondria of brain cells. Your mitochondria are the “powerhouses of the cell” and are responsible for producing ATP (or energy) for your cells to function properly via the Aerobic energy system. This overload of mitochondrial Calcium causes a dysfunction in ATP production. This means when someone suffers a concussion their brain produces less energy to function properly. There is also an increase in the production of potentially damaging free radicals. You need properly functioning mitochondria to detoxify free radicals or else they can build up and cause cell damage. 

Due to the Aerobic energy system struggling to produce energy, the Anaerobic energy system kicks in to pick up the slack. However, this energy system is not meant for long term energy production and is much more inefficient than the Aerobic (for example, it produces 9x less ATP from a single molecule of glucose compared to the Aerobic system). So the brain is burning up all remaining glucose but not producing much ATP. Finally, this influx of Calcium can damage tiny structures in the brain cells called microtubules and neurofilaments, which can disrupt neural connectivity (i.e., how brain cells communicate with each other). It is these widespread neural complications which cause symptoms like cognitive deficits, altered emotional state, and fatigue.

In essence, after a hit to the head, there is an ion imbalance in the brain causing symptoms which need to be reversed. To correct this imbalance, our brains use something called a Sodium/Potassium pump to remove Calcium from the cell and put Potassium back in. However, these pumps require a large and steady supply of ATP (energy), and in an uninjured brain this would be no problem. However, as we just discussed, the influx of Calcium causes our mitochondria to produce less ATP, therefore, we are unable to produce enough ATP to get rid of the Calcium. These pumps, combined with the fact our Anaerobic system can’t keep up with ATP demand, quickly deplete the energy reserves in the brain resulting in a hyperglycemic state, or in other words, the brain is craving a huge amount of glucose to create the energy needed to heal itself. Combined with a reduced cerebral blood flow, which is needed to help bring glucose to the brain after a concussion occurs, we have what is called an Energy Mismatch. The brain needs energy to heal but there is not enough available.

TL;DR - a blow to the head leads to a neural ion imbalance, which causes cellular dysfunction (symptoms) and a reduced ability to produce ATP. There is an increased demand for energy to return the brain back to normal, but a lack of available energy to fulfill these demands. This impaired metabolic state can last up to 7-10 days (or longer) as the body works overtime to return ion concentrations back to normal. This is why symptoms persist for many days after the initial incident. 

During this period of time where energy need is high but energy availability is low is why appropriate management is so crucial. The brain is vulnerable to suffering a second, and often worse, concussion. Being in an already compromised state, and then suffering another blow, can cause an even worse cascade of events. This will plunge the brain further into energy debt with even less ability to produce ATP, taking much longer to return to normal (read: months) and can result in much worse symptoms. This is why avoiding putting an athlete back into sport, prior to being properly cleared, is very important. A concussion is not a bruise, it is not something someone can “walk off”, it is not having your “bell rung”...it is a highly complex change in brain chemistry that if not understood could result in misdiagnosis and premature return to play, which can have dire long-term consequences.

Figure 1. The Neurometabolic Cascade of Concussion (from Marshall, 2012)

Returning too Soon: What are the Risks?

The importance of proper recognition, evaluation, and management of a concussion is to ensure brain chemistry and function return to normal. If an athlete is still experiencing symptoms, no matter how mild, they can still suffer serious problems if they return to sports too soon. The following section will explore the risks of sending an athlete back into sports prematurely.

Probably the most alarming reason for going back too soon is the possibility of second impact syndrome (SIS). This occurs when an athlete sustains a second impact to the head before the initial injury has completely healed. The pathophysiology of SIS is theoretically thought to be due to the ionic imbalance and energy deficit of the initial concussion creating an environment that cannot manage a second impact to the head (Marshall, 2012). This creates further calcium influx, mitochondrial dysfunction, and the inability to regulate cerebral blood flow which causes cerebral swelling, increased brain pressure, brain herniation, and ultimately coma and/or death. Fortunately, SIS is exceedingly rare with less than 20 reported cases in the literature as of 2012 (McCrory, 2012), and its rarity might be more due to underlying genetic factors rather than impact alone. Even though SIS is rare, what is known is that there is a period of brain vulnerability post-concussion. With decreased ATP availability signifying incomplete recovery, a second concussion can lead to even greater energy deficits (i.e., worse symptoms) and longer recovery times.

Just because SIS is unlikely, doesn’t mean there aren’t significant risks with returning too early. A concussion decreases cognitive ability and reaction time, therefore increasing the athlete’s risk of suffering another concussion or injury to another body part. Studies have found athletes are 2-3.4 times more likely to suffer a lower-body injury post-concussion (Lynall, 2015; Herman, 2017), suggesting that the brain struggles to coordinate movement after it is injured. It can also prolong symptoms and recovery times due to the prior energy deficit, and because of the brain's vulnerable state it can take a much smaller impact to cause a secondary injury. A decrease in reaction time and cognitive ability can also affect sport skills and performance, particularly if those skills require refined motor control. 

What is particularly concerning for parents, is the long term impacts of sports-related concussion. Chronic Traumatic Encephalopathy, or CTE, is a neurodegenerative disease associated with repetitive brain trauma that overtime can result in executive dysfunction (i.e., planning, problem-solving, time management), memory impairment, depression, and poor impulse control (Harmon, 2013). Unfortunately little is known about CTE, but it should be stressed that a single concussion has not been linked with developing CTE. Another long term concern is Chronic Neurocognitive Impairment (CNI), resulting in cognitive impairments or depression later in life. The prudent thing to do, as more research is needed in both of these areas, is to ensure proper education, evaluation, and management of concussions to ensure proper recovery and avoid putting a vulnerable brain back into sports too soon.

We hope this review of what actually happens in the brain during a concussion proves useful in understanding the severity of concussions.

Part 3 will look at managing concussions and how to return athletes to school and sport.

~Coach Gies