Piriformis Syndrome

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:

• Positive Lasegue sign
• Tenderness at the sciatic notch
• Relief of symptoms with traction

In 1947, Robinson coined the term piriformis syndrome and proposed 6 cardinal features:

• History of trauma to the sacroiliac and gluteal region
• Pain in the sacroiliac joint, greater sciatic notch and the piriformis muscle, extending down the leg and causing difficulty walking
• Acute exacerbations brought on by stooping or lifting and relieved by traction on the affected leg
• Presence of a tender, palpable, sausage-shaped mass over the piriformis muscle
• Positive Lasegue sign
• Gluteal atrophy

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:

• Undivided sciatic nerve passing below the piriformis muscle (commonest)
• Divided sciatic nerve passing through and below the piriformis muscle
• Divided sciatic nerve passing above and below the piriformis muscle
• Undivided sciatic nerve passing through the piriformis muscle
• Divided sciatic nerve passing through and above the piriformis muscle
• Undivided sciatic nerve passing above the piriformis muscle

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.

• Numerous examination maneuvers have been described to assess for piriformis syndrome. No single finding is reliable in all cases, but a careful systematic examination should provide a reasonable clinical picture.
• Posterior pain is nonspecific. The overlying gluteus maximus and other closely related soft-tissue structures can be painful to palpation. Palpation for the piriformis should be localized directly posterior to the hip joint, close to the sciatic notch. Focal palpation may also recreate some of the patient’s radicular symptoms.
• A positive straight leg raising test is more likely to be indicative of lumbar nerve root irritation. Typically, straight-leg raise may produce localized posteriorhip discomfort, but this is often nonspecific for a variety of conditions.
• Freiberg sign: With the hip extended, passive internal rotation and resisted external rotation of the leg are both maneuvers that may reproduce pain around the area of the piriformis
• Pace sign: In flexion, the piriformis becomes an abductor, so resisted abduction of the flexed hip is another provocative test
• Piriformis stretch: At 90° of flexion passive adduction and internal rotation can produce symptoms.

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).

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.

• Establishing a diagnosis
• Imaging if needed to confirm the diagnosis
• Patient education
• Management of pain (non-pharmacological, medications, interventional treatments