Piriformis syndrome is a useful term that characterizes the symptoms caused by compression/irritation of the sciatic nerve by the piriformis muscle as it exits the sciatic notch. The etiology is variable, and the pathogenesis is incompletely understood. Other processes may mimic this condition, and piriformis syndrome can coexist with other disorders including disease of the lumbar spine or hip joint.
The first mention of the piriformis muscle as a cause of sciatica is attributed to Yeoman in 1928. He postulated that, because of its anatomic proximity to both the sciatic nerve and sacroiliac joints, fibrosis of the piriformis associated with sacroiliac periarthritis could cause sciatica. This was before Mixter and Barr’s landmark article in 1934 that first recognized rupture of the intervertebral disc as a leading cause in many cases of radicular pain. After this report, other causes of sciatica generally fell out of favour.
In 1937, Freiberg proposed the following characteristic features of sciatic pain caused by compression from the piriformis:
In 1947, Robinson coined the term piriformis syndrome and proposed 6 cardinal features:
The piriformis muscle originates from the anterior surface of the second through fourth sacral vertebrae, the sacrotuberous ligament, and the superior margin of the sciatic notch. It exits the pelvis through the sciatic notch and inserts on the superior aspect of the greater trochanter at its posteromedial corner. The function of the piriformis changes depending on the position of the hip. In extension, the piriformis externally rotates the hip, whereas in flexion, it becomes an abductor. The sciatic nerve arises from the lumbosacral plexus and includes fibers from the L4-S1 nerve roots. Distally, it divides to form the tibial and perineal nerves. As the sciatic nerve exits the sciatic notch, it lies below piriformis muscle.
Numerous variations of the anatomy in this region have been described:
The symptoms associated with piriformis syndrome occur from compression of the sciatic nerve by the piriformis muscle. The cause of this compression and subsequent nerve irritation is variable. Piriformis syndrome can result from overuse or repetitive trauma.
The piriformis muscle is under strain during the entire gait cycle and it is postulated that it may be more prone to hypertrophy than other muscles in the region. Gait abnormalities may accentuate this, especially if they result in increased internal rotation or adduction such as with a leg length discrepancy. Overtraining may be implicated as well as repetitive trauma, whether from exercise or sitting on hard surfaces (‘wallet neuritis’).
Acute trauma has been described in numerous cases of piriformis syndrome. A blunt blow to the buttock is believed to result in hematoma formation and subsequent scarring between the sciatic nerve and the short external rotators.
Anomalous anatomic relationships of the sciatic nerve with the piriformis muscle have also been implicated in the development of piriformis syndrome. It is postulated that the nerve is more susceptible to compression by the muscle because of the variant anatomy.
Sitting for prolonged periods of time is typically uncomfortable and becomes increasingly intolerable. Patient characteristically describe posterior hip and buttock pain and a variable pattern of radicular symptoms. These distal symptoms may be ill defined but follow the pattern of the sciatic distribution. These sensations may range from numbness and paresthesias to just a cramping sensation.
Gait, posture, and alignment should be carefully checked. Pelvic obliquity or leg length discrepancy may be a contributing factor, potentially correctable with therapy or inserts. Thorough assessment for lumbar spine disease is mandatory because this is the most likely origin for the sciatica-type symptoms. Careful examination of the hip, pelvis, and sacroiliac joint is also important. These could prove to be the primary pain generator, or piriformis syndrome may coexist with pathology from these other sites. Anatomically, the piriformis is intimately associated with the sacroiliac joint. Motor, sensory and deep tendon reflex examinations are routinely performed but objective deficits are uncommon in association with piriformis syndrome.
There are no specific radiographic features associated with piriformis syndrome, but imigaging may help to rule out other radiographically identifiable processes. For recalcitrant cases MRI of the pelvis is prudent to rule out a mass effect within the sciatic notch or intrapelvic lesions. MRI of the lumbar spine is important to rule out lumbar nerve root pathology.
EMG studies may help to rule out other causes of pain. It is rare that piriformis syndrome will result in measurable electromyogram or conduction deficits. If abnormalities are noted, there should be selective preservation of the superior gluteal nerve, which exits the notch above the piriformis muscle. A prolonged H:-reflex latency may be indicative of piriformis syndrome and this finding is accentuated if the hip is placed in a position of flexion, abduction, and internal rotation (Fishman et al).
Patients should be is counseled on lifestyle modifications to avoid offending activities. Simple oral analgesics and anti-inflammatory medications may be useful as well. Supervised physical therapy, including specific stretching exercises of the piriformis is an important component of management of piriformis syndrome.
This should be reserved for cases that do not respond to conservative treatments. Because of its deep location and relation to adjacent neurovascular structures, the piriformis injection is best performed under imaging guidance, ideally ultrasound.
Piriformis injection is also an important diagnostic tool. If relief is obtained even on a temporary basis, it helps to substantiate the diagnosis of piriformis syndrome.
Injection of local anaesthetic and steroid in to the piriformis muscle can be therapeutic and help resolve the pain on a long-term basis.
There are limited studies for botulinum toxin A injections for piriformis syndrome; however, Childers and colleagues showed analgesic benefit from botulinum toxin A injections into the piriformis under guidance.
Botulinum toxin A has been shown to act at the level of the muscle spindle by inhibiting gamma motor neurons and blocking type Ia afferent signals, thus affecting both motor and sensory pathways. Botulinum toxin A may derive some of its analgesic effect by inhibiting the release of substance P from nerve terminals.