Sports-Related Concussion: What Happens in the Brain?

Published by Nick Schmeed on

A concussion is a silent injury. Although an injury occurs to brain tissue, it is difficult for the outside world to recognize the problem. People can see an ankle injury as a swollen, red, and inflamed joint. But inflammation cannot be visualized in the brain. The only way to see a concussion is by looking for the appropriate signs. So, what happens in the brain during a sports-related concussion?

A concussion is an injury to the brain that results in temporary loss in normal brain function. The primary injury causes the initial signs and symptoms. Then, the secondary injury along with other external factors leads to an evolution of these signs and symptoms over time. At each stage, physical, biochemical, and molecular changes occur that may not only affect symptoms but also dictate recovery.

This article should not place fear into the minds of people. Rather, it is meant to explain a complex topic so that concussions are better understood. Understanding the pathophysiology of sports-related concussions will give greater appreciation for the methods used to prevent and treat concussions. Concussion education is one of these methods.

Basic Concussion Definition

Sports-Related Concussion Definition

A Force Causes a Sports-Related Concussion

Primary Injury in a Sports-Related Concussion

Secondary Effects of Sports-Related Concussion

Waste Accumulates After Sports-Related Concussion

Blood Flow Diminishes Following Sports-Related Concussion

Inflammation and Microglia Activation Occur in Sports-Related Concussion

Blood Brain Barrier is Damaged with Sports-Related Concussion

Inflammation Resolution in Sports-Related Concussion

Basic Concussion Definition

According to the American Association of Neurological Surgeons (AANS), a concussion is a “clinical syndrome characterized by immediate and transient alteration in brain function, including alteration of mental status or level of consciousness, that results from mechanical force or trauma.”1

This definition has a few key points. First, a concussion has temporary effects in the acute stage. Yes, a concussion can have chronic or long-lasting effects, but strictly speaking, a concussion can produce short-lived, sometimes terrifying, symptoms due to altered brain function.

Second, a concussion can but does not need to produce a loss of consciousness. Hence, a concussion is not a simple diagnosis that the public can easily see.

Lastly, a concussion results from a mechanical force or trauma. This definition fails to emphasize that the force could be to the head, neck, or body. Also, the force does not need to involve physical contact with another object like in a blast-injury.

Whether a concussion occurs in sports, on a battlefield, or in a car accident, the mechanisms are similar. However, the research prefers to distinguish between a concussion or mild traumatic brain injury that occurs in sports compared with those in other settings.

Sport-Related Concussion Definition

The preferred definition that includes more details of a sports-related concussion (SRC) comes from the 2022 Concussion in Sport Group (CISG) from the 6th international conference held in Amsterdam2:

Sport-related concussion is a traumatic brain injury caused by a direct blow to the head, neck or body resulting in an impulsive force being transmitted to the brain that occurs in sports and exercise-related activities. This initiates a neurotransmitter and metabolic cascade, with possible axonal injury, blood flow change and inflammation affecting the brain. Symptoms and signs may present immediately, or evolve over minutes or hours, and commonly resolve within days, but may be prolonged.

No abnormality is seen on standard structural neuroimaging studies (computed tomography or magnetic resonance imaging T1- and T2-weighted images), but in the research setting, abnormalities may be present on functional, blood flow or metabolic imaging studies. Sport-related concussion results in a range of clinical symptoms and signs that may or may not involve loss of consciousness. The clinical symptoms and signs of concussion cannot be explained solely by (but may occur concomitantly with) drug, alcohol, or medication use, other injuries (such as cervical injuries, peripheral vestibular dysfunction) or other comorbidities (such as psychological factors or coexisting medical conditions).

Patricios JS, Schneider KJ, Dvorak J, et al. Consensus statement on concussion in sport: the 6th International Conference on Concussion in Sport-Amsterdam, October 2022. Br J Sports Med. 2023;57(11):695-711.

The first paragraph of this definition describes how an external force leads to a primary injury in the brain followed by secondary effects. These effects cause the signs and symptoms that evolve and often resolve spontaneously within seven days.

The next paragraph displays that an SRC cannot be seen on structural imaging studies like a CT or MRI because it is a functional disturbance of brain tissue. Research settings can visualize functional issues, but functional tests are not standard care.

Lastly, the signs and symptoms, whether acute or chronic, cannot be explained solely by other conditions, injuries, or substances. While neck injury and dehydration symptoms may be present, these cannot explain all the athlete’s symptoms if an SRC truly occurred.

Let’s break it down further.

A Force Causes a Sports-Related Concussion

An SRC can occur from any force directly or indirectly to the head. However, not every impact to the head will cause a concussion. The force must be transmitted to the brain at the appropriate magnitude and direction to move the brain within the skull. The movement of the brain is what causes the SRC.

When watching a football game, there may be multiple head impacts that seem hard enough to cause an SRC; however, one should not look for the force of impact. Rather, the acceleration and direction of an athlete’s head after the impact are the determining factors on how much force the brain receives.

More specifically, a force must cause one’s head to rotate quickly in one or multiple planes of movement. It is the rotational acceleration of the head, and therefore the brain, which causes a sports-related concussion.3

When a force causes the head to aggressively move back and forth, the brain also rotates back and forth and side to side around different axes. Because the brain is sitting in cerebrospinal fluid, it can move freely; therefore, the cerebrum (‘big brain’) not only bangs against the inside of the skull but also rotates on top of the brainstem below.

The main type of brain cell that sends electrical signals is a neuron. A neuron has a cell body where the DNA is located and extensions that send or receive signals. The small tree-branch extensions are dendrites that receive signals, whereas the long axon sends signals. Some axons are very short while others travel longer than the length of your leg.

The direct force with the skull causes blunt trauma to neurons and their cell bodies. At the same time, the rotation causes shearing force to the axons—the connections—between brain regions. Most axons are insulated by fatty sheaths made of myelin, so damage occurs mostly to the insulation of axons, yet the axon itself can be disturbed.

Primary Injury in a Sports-Related Concussion

The initial focal areas of damage are the primary injury. The outside of the brain receives more of the blunt trauma, whereas midline structures deep in the brain succumb to shearing forces.

As the cerebrum rotates on top of the brainstem, the inner most axons and neuron cell bodies experience the most shearing force. Think about if you were to ring out a wet towel. The inner fibers of that towel will have the most stress and release the most water. A similar process happens to innermost or midline parts of the brain, except these damaged cell membranes release more than just water.

When the neuron cell membranes are disrupted, it causes electrolyte imbalances. Sodium and calcium flow into the cell and potassium flows out, which dysregulates the resting state of an electrical cell.4 This causes unwanted activation and over firing of neurons.

When neurons fire, they release neurotransmitters, which are cell signaling molecules to tell another neuron to fire. Unwanted activation leads to the release of excitatory neurotransmitters like glutamate. The more glutamate released, the more neurons are activated leading to excitotoxicity.

Excitotoxicity occurs because there is no control or regulation of electrolytes, especially calcium, moving into the neurons. Calcium is important to properly activate neurons for learning; however, too much calcium in the cell signals damage causing the cell to undergo controlled cell death, also known as apoptosis.

This primary injury and release of electrolytes basically stuns neurons. This results in the initial signs and symptoms, and potential loss of consciousness, of a sports-related concussion.

Secondary Effects of Sports-Related Concussion

After the primary injury to the brain, there are many other subsequent events that promote more damage to surrounding brain regions. These secondary effects lead to the secondary injury. These effects are functional, versus structural, because there is not enough damage to be visible on standard imaging like an MRI or CT scan.

They can be small and short-lived or expansive and progress for days or weeks. The variability depends on both the force of initial brain injury and the environment that contains the brain, which highly depends on each athlete.

Waste Accumulates After Sports-Related Concussion

Besides the electrolytes leaking into and out of the cell, large protein molecules in the cell are released. Glial fibrillary acidic protein (GFAP), tau protein, and amyloid beta peptide are proteins in cells that help maintain proper structure and are essential for growth and repair.

These proteins leak from the damaged cells and can clump together, which leads to disruption of axons and blockage of neural connections. They can be used as blood biomarkers for concussion and TBI5; however, it is not yet a common clinical practice to test for them.

The body has systems in place to remove waste from the brain like veins going back to the heart and the glymphatic system that drains toxins through the lymph. The glymphatic flow to remove waste is most active at night during deep sleep. If sleep was not prioritized, there may already be waste accumulation.

Additionally, previous head injuries and poor spinal movement can disrupt glymphatic flow. If this is the case, there may already be toxin build up, protein clumping, and disruption of neurotransmission.

Blood Flow Diminishes Following Sports-Related Concussion

When a concussion occurs, there is decreased blood flow to the brain to prevent excessive swelling and pressure.6 At the same time, the processes that convert blood sugar or glucose into energy are greatly diminished. In fact, the neurons shut down the channels that allow glucose into the cell. This leads to an energy crisis.

The cell needs energy to repair its membrane, reestablish the resting potential by moving calcium and sodium out and potassium in, and hence, decrease further damage. In order to make energy, the cell needs glucose (or another fuel source) and oxygen, but the lack of blood flow along with decreased glucose uptake and processing prevents energy production.

Inflammation and Microglia Activation Occur in Sports-Related Concussion

Aside from the energy crisis, a local inflammatory process begins. Like an ankle injury, tissue damage causes molecules to release from cells known as damage-associated molecular patterns (DAMPs). These DAMPs activate the local immune cells to initiate inflammation.7

In the brain, the immune cells—microglia—recognize the DAMPs leading to their activation and signaling for help to fight the damage. This initial microglial activation promotes inflammation and increases free radicals or oxidants that help kill any possible infections but also cause further damage to cells.

The local inflammation and microglial activation can spread if not well-controlled. Further exacerbation occurs by the excessive glutamate neurotransmitter, described above, causing excitotoxicity across brain networks.

Blood Brain Barrier is Damaged with Sports-Related Concussion

On top of the brain cell disruption, a concussion often compromises the blood brain barrier (BBB).8 A type of supporting cell called astrocytes form the BBB by wrapping its arm-like extensions around the blood vessels in the brain. This forms a barrier that only allows small molecules like electrolytes, oxygen, and glucose to pass through. Other larger molecules need specific channels to enter the brain.

When the BBB is damaged, it causes an unregulated influx of large molecules. Some may be beneficial, but some are toxins and inflammatory signals that promote neuroinflammation. Inflammation is a natural part of healing and is beneficial; however, when uncontrolled inflammation lasts, the wider spread of damage can disrupt more brain regions and networks.

Inflammation Resolution in Sports-Related Concussion

This inflammatory response takes approximately 4-6 hours to develop but can extend up to a couple of days. Hence, the progressing secondary effects lead to the evolution of concussion symptoms.

If uncontrolled, inflammation leads to expanded damage of the myelin sheaths that insulate axonal connections. This is diffuse axonal injury and can result in inefficient connections among brain networks.

It is important to limit the damage during this time and to begin inflammation resolution. Practically, this begins with concussion prevention strategies followed by timely initiation of concussion management. Additional posts regarding nutrition, supplementation, exercise, and sleep will discuss these topics.

Conclusion

In summary, a sports-related concussion is an injury to the brain that results in temporary loss of neurologic function. An SRC requires a force to the head or body that produces rotational acceleration of the head. This is necessary for brain movement and rotation within the skull causing the primary injury.

The primary injury is due to blunt trauma to neurons and shearing forces to axons. Damaged cell membranes lead to electrolyte dysregulation, excitotoxicity, and inflammation. Other secondary effects that promote widespread disruption include waste accumulation, lack of blood flow and nutrients, blood brain barrier damage, and microglial activation.

While every sports-related concussion affects different brain areas and produces different symptoms, prevention and management strategies can be employed to limit the damage caused by the primary injury and secondary effects.

References

  1. Agarwal N, Thakkar R, Than K. American Association of Neurological Surgeons. Updated 2021. Accessed March 6, 2022. https://www.aans.org/en/Patients/Neurosurgical-Conditions-and-Treatments/Concussion
  2. Patricios JS, Schneider KJ, Dvorak J, et al. Consensus statement on concussion in sport: the 6th International Conference on Concussion in Sport-Amsterdam, October 2022. Br J Sports Med. 2023;57(11):695-711.
  3. Meehan, WP, III. Kids, sports, and concussion: a guide for coaches and parents. 2nd ed. Praeger, an imprint of ABC-CLIO, LLC; 2018.
  4. Capizzi A, Woo J, Verduzco-Gutierrez M. Traumatic Brain Injury: An Overview of Epidemiology, Pathophysiology, and Medical Management. Med Clin North Am. 2020;104(2):213-238.
  5. Bogoslovsky T, Wilson D, Chen Y, et al. Increases of Plasma Levels of Glial Fibrillary Acidic Protein, Tau, and Amyloid β up to 90 Days after Traumatic Brain Injury. J Neurotrauma. 2017;34(1):66-73.
  6. Giza CC, Hovda DA. The new neurometabolic cascade of concussion. Neurosurgery. 2014;75 Suppl 4(0 4): S24-S33.
  7. Simon DW, McGeachy MJ, Bayır H, Clark RS, Loane DJ, Kochanek PM. The far-reaching scope of neuroinflammation after traumatic brain injury [published correction appears in Nat Rev Neurol. 2017 Aug 04; Nat Rev Neurol. 2017;13(3):171-191.
  8. Sahyouni R, Gutierrez P, Gold E, Robertson RT, Cummings BJ. Effects of concussion on the blood-brain barrier in humans and rodents. J Concussion. 2017;1:10.1177/2059700216684518.