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Pathophysiology of Concussion

Pathophysiology of Acute Concussions

 

Fundamentally, an acute concussion can be viewed as a neurometabolic problem.

 

A blow to the head or body causes movement of the brain with axonal shearing and lateral fluid percussion. Focal contusions related to coup-contrecoup injury can mimic moderate to severe injury but secondary metabolic effects are also produced at sites distal to the injury.

 

A concussion induces massive neuronal firing with release of excitatory neurotransmitters such as glutamate. These neurotransmitters cause the neurons to continue firing while at the same time causing a massive influx of calcium into the cell. Calcium influx disrupts the ability of the mitochondria to make the ATP necessary for returning the cell to homeostasis. Secondary injuries to surrounding cerebrovasculature cause further injury due to ischemia and cytotoxic cascades. Giza and Hovda referred to this as the neurometabolic cascade of concussion.

 

We still don’t know the exact course of neurometabolic recovery of concussions in humans but evidence points towards 30 days as a timeframe for full recovery for most individuals. The consensus is that young brains may take even longer to recover due to brain maturational processes that appear to extend well towards 25 years of age. Unfortunately the time frame for concussion symptom recovery is usually between 3-15 days. When post-concussed individuals with baselines were tested after symptomatic recovery, 38% of them continued to exhibit at least one neurocognitive decrease.

 

The worry therefore is when to make the return to play decision. If a second injury is sustained during the period of metabolic recovery then a new metabolic cascade will ensue and will push cellular energy production even lower, possibly below the threshold of cell survival. These injuries can be catastrophic, will very likely be more severe and will take significantly longer to recover.

 

Signoretti S1, Lazzarino G, Tavazzi B, Vagnozzi R. The pathophysiology of concussion. PM R. 2011 Oct;3(10 Suppl 2):S359-68.

 

Broglio SP1, Macciocchi SN, Ferrara MS. Neurocognitive performance of concussed athletes when symptom free. J Athl Train. 2007 Oct-Dec;42(4):504-8.

 

Christopher C. Giza and David A. Hovda.The Neurometabolic Cascade of Concussion. J Athl Train. 2001 Jul-Sep; 36(3): 228–235.

 

Vagnozzi R1, Signoretti S, Cristofori L, Alessandrini F, Floris R, Isgrò E, Ria A, Marziali S, Zoccatelli G, Tavazzi B, Del Bolgia F, Sorge R, Broglio SP, McIntosh TK, Lazzarino G. Assessment of metabolic brain damage and recovery following mild traumatic brain injury: a multicentre, proton magnetic resonance spectroscopic study in concussed patients. Brain. 2010 Nov;133(11):3232-42.

 

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