What is the role of compression in the pathophysiology of cauda equina syndrome (CES)?

Updated: Jun 14, 2018
  • Author: Segun Toyin Dawodu, JD, MD, MS, MBA, LLM, FAAPMR, FAANEM; Chief Editor: Nicholas Lorenzo, MD, CPE, MHCM, FAAPL  more...
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Several studies in different animal models have assessed the pathophysiology of cauda equina syndrome. [3, 4] Olmarker et al, using a graded balloon pressure method in a porcine model, reported that the venules in the CE region begin to compress at a pressure as low as 5 mm Hg and the arterioles begin to occlude as the balloon pressure surpasses the mean arterial pressure. [5, 6, 7, 3, 8] Despite this, even a pressure as high as 200 mm Hg failed to completely shut off nutritional supply to the CE.

These studies showed that not only the magnitude but also the length and the speed of obstruction were also important in damaging the CE region. [9] Similar results were reported in other studies. Takahashi et al reported a reduction in blood flow to the intermediate nerve segment when 2 pressure points were applied along the path of the nerve in the CE. [10]

Others have studied compound action potentials in afferent and efferent segments of nerves in the CE region after application of balloon compression. [11, 12, 13] These researchers reported that 0-50 mm Hg of pressure did not affect the action potentials (the threshold for disturbances in action potentials was 50-75 mm Hg), and significant deficits were observed when pressure rose to 100-200 mm Hg.

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