02/03/2026
Piriformis Syndrome
Piriformis syndrome is best understood as a disorder of altered load sharing and neuromuscular control at the deep posterior hip. The piriformis muscle lies in a confined anatomical corridor between the sacrum and the greater trochanter, with the sciatic nerve traveling immediately adjacent to it. Under normal conditions, the piriformis acts as a dynamic stabilizer of the hip and sacroiliac joint, modulating femoral rotation and pelvic alignment during gait. Pathomechanics arise when this stabilizing role becomes excessive, sustained, or poorly coordinated.
A primary pathomechanical driver is chronic overactivation of the piriformis due to faulty hip and pelvic mechanics. Weakness or delayed activation of the gluteus maximus and gluteus medius shifts rotational control demands onto the piriformis. As femoral internal rotation and adduction increase during stance, the piriformis contracts more forcefully to counteract these motions. Over time, this leads to increased resting tone, loss of extensibility, and elevated intramuscular pressure within the piriformis.
This increased muscle tension alters the mechanical environment of the sciatic nerve. Depending on anatomical variation, the sciatic nerve may pass beneath, through, or above the piriformis. When the muscle shortens or develops trigger points, compressive forces act directly on the nerve, while repeated hip motion produces friction and tethering. These combined compressive–shear stresses reduce neural glide, increase intraneural pressure, and sensitize the nerve, producing buttock pain and distal sciatic symptoms.
Trigger point pathomechanics play a major role in symptom presentation. Active trigger points within the piriformis generate referred pain patterns that closely mimic radicular pain, extending down the posterior thigh. This pain is not caused by direct nerve root compression but by sustained sarcomere contraction, local ischemia, and abnormal afferent signaling. The resulting motor–sensory feedback loop perpetuates muscle guarding, further increasing piriformis tone and neural irritation.
Pelvic asymmetry significantly amplifies piriformis loading. Sacroiliac joint dysfunction, leg length discrepancy, or habitual unilateral weight bearing alters sacral orientation. These changes modify the piriformis length–tension relationship, forcing one side to remain chronically shortened while functioning as a stabilizer. The obturator internus and other deep rotators may also become inhibited, increasing reliance on the piriformis and compounding neuromuscular imbalance.
Neural pathomechanics extend beyond simple compression. A hypertonic piriformis limits normal excursion of the sciatic nerve during hip flexion, extension, and rotation. Restricted nerve mobility increases tensile strain during sitting, squatting, or crossing the legs, explaining symptom provocation in prolonged seated postures. Repeated exposure to these abnormal stresses leads to peripheral nerve sensitization and lowered pain thresholds.
Piriformis syndrome is a pathomechanical cascade rather than an isolated muscle problem. Poor hip stability, altered pelvic alignment, excessive femoral rotation, trigger point development, and impaired neural mobility interact to overload the piriformis and irritate the sciatic nerve. Effective resolution requires restoring balanced load distribution across the hip complex, improving gluteal control, normalizing pelvic mechanics, and re-establishing healthy muscle–nerve interaction rather than focusing solely on stretching or local pain relief.
