Concussion series, Part 1: Pathophysiology

Over the past few years concussions have become quite the “buzz word” in sports. Many years ago, no one really cared about concussions, and then all of a sudden, we’ve gone to the other extreme – everyone who gets hit has a concussion.

Concussions are a very serious topic. It is a mild traumatic brain injury (mTBI). Back in the day, the scale of brain injury would be: concussion, mild TBI, moderate TBI, severe TBI. Now concussions and mTBI should be, and are, interchangeable. That is because concussions ARE a form of brain injury. Many people believe that in order to sustain a concussion you need to have Loss of Consciousness or be hit in the head. In the above video, the hit was clean shoulder to shoulder, and Toews was conscious. But Toews sustained a concussion in that play. Loss of consciousness is also not a predictor of how severe the concussion is, nor will it dictate the length of recovery for the athlete.

It is not just a physical syndrome (headaches, nausea, vomiting, dizziness etc…) but is it a metabolic syndrome as well – it is an energy mismatch in the brain, leading to a large ATP deficit. The old theory/hypothesis of why concussions happened is the “coupe/contrecoupe” theorem shown below.

concussion1.png In this hypothesis, it states that the brain impacts the front of the skull and then impacts the back of the skull, creating two sites of injury. However, it has actually been shown that concussions are more widespread throughout the brain that just that. The new hypothesis is that concussions are “acceleration/deceleration” injuries that create shearing of the neuronal axons.


In the above image, shearing causes damage to the axons and also results in the energy mismatch that the literature has shown. When an athlete (really, any one in general too) experiences a concussion, action potentials are firing constantly at first (excitatory phase) and then when all of the ATP is used up, they become fatigued and lethargic (spreading depression phase).

If we all think back to physiology 101 (It been a long time since I’ve taken that class, and it was a memory I’d like to forget, haha), the concentration gradient inside a resting cell is as follows: K+ high inside, Na+ and Ca+2 high outside the cell. When there is shearing of the neuronal axons, there is also an resultant deformation of the cell membrane, leading to opening of ion channels and the ions flow down their respective gradients. This creates action potentials and causes the release and increase of Excitatory Amino Acids (EAAs): most notably, Glutamate. In order to restore the ion concentration balance to its resting state, we need activation of the Na+/K+ pumps – requires a lot of ATP. The release of glutamate triggers the activation of N-methyl-D-aspartate (NMDA) leading to an influx of calcium into the cell. Ca+2, however, has an affinity for the mitochrondria and when there is a large influx of it into the cell, it creates dysfunction within the electron transport chain – reduces the cell’s ability to create ATP, furthering the energy crisis.screen-shot-2016-09-27-at-9-12-58-am

In the above image, you can see the influx of calcium as well as NMDA in the middle of the cell body. An interesting point that has been made in the literature is that Mg+2 fits into one of the NMDA receptors like a plug. It’s been hypothesized that if you are sufficient in your body’s Mg+2 levels, then it can control how much calcium influxes into the cell and may decrease your recovery time. Many of the physical signs and symptoms can be derived from the underlying pathophysiology described above (headaches, fatigue, dizziness, inability to focus etc..).

That was a lot of physiology in one post. Take some time to wrap your head around the information. One of the big points I will be making in this series is that you have to recover physically AND metabolically to be considered 100% recovered from a concussion. However, many will not show signs and symptoms around day 8-10, but research has shown they are still not metabolically recovered – you will still be at risk for second impact syndrome and return to play at this point may further delay your recovery.


Giza, C., Hoda, D. The neurometabolic cascade of concussion. J of Athletic Training. 2001;36(3):228–235

Giza, C., Hoda, D. The new neurometabolic cascade of concussion. Congress of Neurological Surgeons. 2014;75(4):524-533

Signoretti, S. et al The Pathophysiology of concussion. American Academy of Physical Medicine and Rehabilitation. 2011;3: S359-S368

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