Concussion: The Basic Science

I just gave a talk this weekend at the 26th Annual Trauma and Emergency Symposium here in Wilmington about the concussion controversy.  If you ask me the only controversy about concussion at this point is how some organized sports leagues (hint: begins with and N and ends in and L and its sport is not played on ice) continue to deny the long-term impacts of concussion.  I won’t get into that though.  Yet.  I would like to devote a few posts here at Spinal (con)Fusion to concussion as I do think it is a pressing public health issue here in our sports crazed nation.  The first post in this series will discuss some of the basic science of concussion, specifically sports concussions.

First of all, let’s define what a concussion is.  There are several fancy medical definitions for concussion but it essentially involves a transfer of kinetic energy to the brain after a blow to the head followed by transient neurological symptoms.  These symptoms can be physical symptoms (like headache, nausea and light sensitivity), emotional symptoms (like irritability), or symptoms of memory or balance.  The important thing is that the symptoms are transient and should resolve within a week or so.  Symptoms that persist longer may indicate a more serious condition.

As with many traumatic injuries concussion involves primary and secondary injury.  The primary injury is the actual blow to the head during which kinetic energy is immediately transferred to the brain.  Remember:


so that the bigger and faster the two colliding players are, the more kinetic energy transferred.  In 2003 the NFL’s Mild Traumatic Brain Injury (MBTI) Committee headed by Dr. Elliot Pellman (a rheumatologist) published its first of 16 papers on concussion in the journal Neurosurgery.  In that paper they looked at NFL game video of head impacts from 1996-2001.  From 31 off those impacts they could get enough data to recreate the impacts using crash test dummies. The found that the average speed of impact was almost 21mph and the average magnitude of impact for players who sustained concussion was 98g (as in g-force).   Some of the impacts were greater than 130g!  More recently concussion researchers have used special helmets implanted with sensors to more accurately measure the location and magnitude of impacts in real time (see figure 1).  These studies have shown that even 9-12 year olds playing Pop Warner can generate hits with magnitudes over 100g.  This is concerning given how much brain development occurs at that age.


Figure 1. The Head Impact Telemetry System (HITS)

The secondary injury involves the events that happen on a cellular level shortly after the primary injury.  First, the kinetic energy of the impact causes stretching and even shearing of the axons of neurons (the critical messaging pathways between the cells in your brain.)  The force of the impact also disrupts the membranes of the neurons.  To backtrack a bit, cells in your body maintain very precise gradients of electrolytes inside and outside of the cell membrane.  These electrolyte gradients are then used to power the pumps in the membrane that in turn generate energy for the cell to use.  When the membranes of the cells are torn after a blow to the head, electrolytes that were inside the cell (potassium, or K+ , is the main one) leak out and those that were outside of the cell (Sodium, Na+, and calcium, Ca++) leak in.  This is bad for two reasons.  First, the power pumps go into overdrive to try to restore those gradients.  This causes an “energy crisis” in the cell as its stores of glucose (the main source of cellular energy in the brain) become depleted for up to 7-10 days.  Second, high levels of Ca++ inside of the cell can a) cause further damage to axons thereby causing death of the neuron, and b)trigger the release of glutamate, high level of which are toxic to neurons.  Finally, blood flow to the brain decreases after concussion and also may not normalize for 7-10 days (see figure 2).  So between the decreased glucose levels, the altered levels of electrolytes and finally the decreased blood flow to the brain, it’s no wonder why a concussed player can feel lousy for over a week after their injury.


Figure 2. Graph demonstrating depressed glucose levels and cerebral blood flow rates for 7-10 days.  Source: Giza et al, 2014.

Thanks for reading.

J. Alex Thomas, M.D.


Giza, C., & Hovda, D. (2014). The New Neurometabolic Cascade of Concussion. Neurosurgery, 75(4), 24–33. 

Pellman, E. J., Viano, D. C., Tucker, A. M., Casson, I. R., & Waeckerle, J. F. (2003). Concussion in Professional Football: Reconstruction of Game Impacts and Injuries. Neurosurgery, 53(4), 799–814. 

Dashnaw, M. L., Petraglia, A. L., & Bailes, J. E. (2012). An overview of the basic science of concussion and subconcussion: where are we and where are we going. Neurosurgical Focus, 33(6): E5.


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