Let’s Talk About Concussions

Traumatic brain injuries elicit a spectrum of debility and can have massive impacts on quality of life both physically and mentally.  The purpose of this article is to examine the pathophysiology of traumatic brain injuries to understand the nature of the brain on a cellular level relative to the trauma and why some of the symptoms manifest as they do.  Several therapeutic options will be discussed which serve to address the particular dysfunctional patterns and can offer a means to a faster recovery and decrease the occurrence of post concussive syndrome.

 A concussion is a metabolic, physiologic and microstructural injury to the brain and is defined as any transient neurologic dysfunction resulting from a biomechanical force. Loss of consciousness is a clinical hallmark of concussion but is not required to make the diagnosis. Other symptoms include confusion, disorientation, unsteadiness, dizziness, headache, and visual disturbances. These postconcussive deficits occur with minimal detectable anatomic pathology and often resolve completely over time, suggesting that they are based on temporary neuronal dysfunction rather than cell death. Neuronal dysfunction can occur due to ionic shifts, altered metabolism, impaired connectivity, or changes in neurotransmission. Thus, a complete understanding of the phenomenon of concussion requires knowledge of the underlying pathophysiology of this injury

 Most commonly we think of a concussion due to a blunt force trauma such as that which typically occurs with sport and which elicits a coup and contrecoup brain injury, though brain injury can occur from other mechanisms as well.  With the mechanical insult comes a cascade of metabolic events which initiates disturbance to the delicate neuronal homeostatic balance. 

WHEN YOU HIT YOUR HEAD THERE IS A …

Release of Excitatory Neurotransmitters such as Glutamate

Glutamate is responsible for sending signals between nerve cells and is involved in learning and memory. Glutamate binds NMDA receptors on the cells. This signals for the movement of ions into and out of the cells in the brain and excessive amounts causing great disturbances in ion homeostatic balance which carries a range of negative effects outlined below.

Damaged Mitochondria
With a persistent increase in calcium entering the cells, the excess calcium gets sequestered within the mitochondria thereby impairing its function and ability to produce ATP or energy.

Increased Glucose
Metabolism in an effort to re-establish normal ion concentrations within neuronal cells, the sodium potassium pump has to work in overdrive. This pump

requires the use of ATP which is generated from qlucose metabolism. When a traumatic brain injury occurs cerebral blood flow can be decreased as much as 50%. With the hypermetabolism of glucose and the decrease in cerebral blood flow a disparity between the glucose demand and glucose supply creates an energy crisis and the cells become vulnerable. Additionally the mitochondrial damage that has occurred due to the calcium influx further exacerbates the energy crisis.

It's a vicious cycle!

Lactic Acid Accumulation

Lactate is a byproduct of glycolysis, the breakdown of glucose to produce ATP, or energy. Because of the up-regulation of glycolysis in an effort to meet the increased energy demands to re-establish normal ion concentrations within the cell. and due to the damage incurred to mitochondria leading to their inability to produce ATP, an abundance of lactate is produced. Elevated levels of lactate leads to metabolic acidosis, altered blood brain barrier permeability, membrane damage and cerebral edema. all of which leads to the dysfunction of neurons.

Inflammation and Free Radical Production
The excess intracellular calcium leads to the production of free radicals and inflammation within the affected and surrounding cells. The production of free radicals leads to DNA damage, dysfunction of brain derived neurotrophic factor and disruption of the membrane structure of cells. It is suggested that it is the production of free radicals and inflammation that is ultimately the culprit of both acute and long term post concussive symptoms.

A Reduction in Magnesium
When traumatic brain injury occurs there tends to be a decrease in magnesium which can lead to neuronal dysfunction. Low levels of magnesium creates an environment where particular receptor channels may be unblocked more easily leading to a greater influx of calcium which creates the issues outlined in the points above. Magnesium is necessary for maintaining membrane potential and initiating protein synthesis therefore these crucial processes will be impaired in the environment of low magnesium.

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The early events of the traumatic brain injury physiologic cascade are a steady and persistent increase of calcium flow into the cells, mitochondrial dysfunction with decreased energy metabolism, decreased cerebral glucose metabolism and reduced cerebral blood flow and axonal injury.  The later events of the cascade include recovery of glucose metabolism and cerebral blood flow, delayed cell death, chronic alterations in neurotransmission and axonal disconnection.  

The clinical signs and symptoms of impaired coordination, memory, attention and cognition are due to underlying neuronal dysfunction and all or some combination of the processes stated above.