What Happens During a Concussion?
The Centers for Disease Control and Prevention (CDC) defines concussion as a traumatic brain injury (TBI) caused by a bump, blow, or jolt to the head or by a hit to the body that causes the head and brain to move rapidly back and forth. This sudden movement can cause the brain to bounce around or twist in the skull, stretching and damaging brain cells and creating chemical changes in the brain. The most recent population data estimates 2.5 million traumatic brain injury–related emergency room visits, hospitalizations, and deaths occur each year in the United States(1), making it one of the most common neurological conditions.
Concussion may cause a variety of impairments that can impact an individual’s ability to return to meaningful activities such as an athlete returning to sport, a student returning to school, a civilian returning to work, or a service member returning to duty. Due to the frequency of concussions, which some reports estimate to occur every fifteen seconds in the United States, and the detrimental effects concussion can have on function, the Centers for Disease Control and Prevention (CDC) has labeled concussion a major public health issue that is accompanied by considerable personal and socioeconomic costs(2). The annual economic burden associated with concussion has been estimated to be $16.7 billion USD, with an estimated direct cost of $35,000 to $45,000 USD per patient(3,4).
At the moment of injury, the brain is exposed to a number of different vectors of stresses and strains. Classically, these have been described in terms of acceleration–deceleration or coup counter coup injuries along with rotational forces. As these stresses and strains are placed on the various tissues of the brain, the neuronal tracts are stretched, and this contributes to one of the more important pathological findings in human TBI: that of diffuse axonal injury. Similar to the action of ringing out a wet towel, the brainstem and pathways associated with the brainstem undergo torsional and sheering forces placing the neuronal tissue in very compromising positions. This results in disruption or interference of transmission of electrical impulses as well as microscopic and molecular changes to the neuronal structure.
On top of the primary mechanical damage done to the brain and neural structures after a mild traumatic brain injury there are also secondary injuries, described as the neuro-metabolic cascade. This neuro-metabolic cascade consists of an influx of sodium and calcium into the cell and forcing potassium out of the cell, that of which is opposite of the normal resting gradient. This ionic flux which leads to an energy crisis uses a considerable amount of the cell’s energy reserve in an attempt to restore the ionic gradient back to neutral by pumping calcium and water out of the cell and back to where they belong. A direct consequence of the excessive calcium influx is release of excessive glutamate, a potent excitatory molecule. Glutamate then binds to N-methyl-d-aspartate (NMDA) receptors on neighboring neurons leading to calcium influx and release of more glutamate into the extracellular space. This process, referred to as excitotoxicity, leads to a self-perpetuating cycle of hyperexcitability and cellular instability.
In an effort to restore the proper polarity within the cell the sodium potassium pump works overtime leading to a depletion of the intracellular energy reserves. This is due to the fact that in order to turn the sodium potassium pump it requires energy in the form of ATP which is dependent upon glucose. These ionic shifts in cellular energy metabolism occur in a setting where blood flow to the brain is diminished(5). which creates a mismatch between energy supply and demand(6). The problem here is not only the increased metabolic demand, but that glucose itself is not stored within the brain, and the delivery of this fuel depends on the corresponding increase in blood flow to the brain(7). Meaning the brain has a job to do but not enough resources available to complete the task at hand.
TBI is a complex dynamic process that initiates a multitude of cascades of pathological cellular pathways. Its symptomatic presentation varies with each individual, injury type, injury severity, age and gender, making it challenging to diagnose, understand and treat(8) making it even more difficult for you as the patient to find a qualified provider who is adequately trained to serve you in the highest manner possible. If you would like to learn more about Peak Brain Performance Centers and how we can help you, schedule a complimentary phone consult and lets get you back to the person you want to be.
References:
1. Cancelliere C, Coronado VG, Taylor CA, Xu L. Epidemiology of isolated versus nonisolated mild traumatic brain injury treated in emergency departments in the United States, 2006-2012: sociodemographic charac- teristics. J Head Trauma Rehabil. 2017;32(4):E37-E46.
2. Collins MW, Kontos AP, Okonkwo DO, et al. Statements of Agreement from the Targeted Evaluation and Active Management (TEAM) Approaches to Treating Concussion Meeting held in Pittsburgh, October 15-16, 2015. Neurosurgery. 2016;79(6):912-929.
3. Humphreys I, Wood RL, Phillips CJ, Macey S. The costs of traumatic brain injury: a literature review. Clinicoecon Outcomes Res. 2013;5: 281-287.
4. Marshall S, Bayley M, McCullagh S, et al. Updated clinical practice guidelines for concussion/mild traumatic brain injury and persistent symptoms. Brain Inj. 2015