What is the pathophysiology of piriformis syndrome?

Updated: Dec 21, 2018
  • Author: Shishir Shah, DO; Chief Editor: Sherwin SW Ho, MD  more...
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Gait mechanics help in demonstrating the physiologic features of piriformis hypertrophy. When a person takes a step forward, the extremity moves from external rotation to internal rotation, and the piriformis muscle lengthens. This stretching is followed by reflex contraction. A second contraction in the initially stretched piriformis muscle occurs when the opposite foot swings forward. This gait pattern leads to hypertrophy, and the dual contraction is further exacerbated by the stretching of the piriformis muscle on the side of a shortened leg.

More commonly, piriformis syndrome is secondary to inflammation due to gluteal trauma or spasm. The effect of this inflammatory process on the sciatic nerve is chemical rather than mechanical. Several theories suggest that the following are key factors in the muscle hyperfunction or spasm that leads to an interstitial myofibrositis: extravasation of blood; release of serotonin from platelets; and prostaglandin E, serotonin, bradykinin, and histamine release.

Although no general consensus about the etiology and pathophysiology of piriformis syndrome exists, many physicians and physical therapists attribute this syndrome to a specific mechanism involving the sciatic nerve. For example, Benson and Schutzer attributed the syndrome to blunt trauma to the buttocks that results in hematoma formation and subsequent scarring between the sciatic nerve and the short external rotators. [2] Entrapment of the sciatic nerve at the sciatic trunk (where it leaves the pelvis and crosses the greater sciatic notch) is an infrequent cause. This entrapment can also occur as a result of an enlarged hypertrophic piriformis, an inflamed piriformis muscle, tumors, cysts, and pseudoaneurysms.

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