What is the pathophysiology of postconcussive syndrome (PCS)?

Updated: Jul 25, 2019
  • Author: Roy H Lubit, MD, PhD; Chief Editor: David Bienenfeld, MD  more...
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Answer

The pathophysiology of postconcussive syndrome (PCS) results from contusions and diffuse axonal injury (DAI). Disruption of axons triggers a cascade of further insults, including calcium influx, excitotoxin release, phospholipase activation, and lipid peroxidation.

Postmortem studies of traumatic brain injury (TBI) have demonstrated pathological changes that cannot be detected by conventional neuroimaging studies. In fact, much of the pathology of TBI is under the threshold of detection in conventional MRI, which in humans is approved only to be done at 3 Tesla or less. Even when standard structural neuroimaging of the brain reveals no visible abnormality, underlying structural, biochemical, or electrophysiological abnormalities may be present. [11]  Diffusion tensor imaging frequently will show evidence of white matter damage when there are no observable problems on a standard MRI.

For example, Govindaraju et al examined volumetric proton spectroscopic imaging of the whole brain in mild TBI (mTBI) patients 1 month postinjury. [12] This method provides a mechanism for detecting biochemical perturbations of the brain brought on by injury that would not necessarily show-up in standard imaging. The authors found “widespread metabolic changes following mTBI in regions that appear normal...” on conventional MRI. This supports the notion of nonspecific damaging effects from mTBI that occur at a subtle, microscopic level of injury [13] and that one can have a significant brain injury, yet have normal conventional structural imaging. This has also been shown by Gaetz et al. [14]


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