Piriformis syndrome is a syndrome of low back and leg pain thought to be due to chronic contracture of the piriformis muscle that causes irritation of the sciatic nerve. The syndrome involves gluteal pain often accompanied by pain radiating down the affected leg in the distribution of the sciatic. It is commonly called “hip pocket neuropathy” or “wallet neuritis”.

Two most common theories are 1) compression of the nerve between the inflamed muscle and the bony pelvis 2) compression of the nerve between the two inflamed fascicles of the piriformis muscle. Robinson observed that any inflammation or spasm of the piriformis muscle will compress the sciatic nerve whenever the leg is raised, producing the sciatica.

Pace proposed that focal hyper-irritability of the piriformis muscle resulted in a trigger-point syndrome. Sciatic neuritis is believed to result from irritation of the sciatic nerve sheath, which is caused by biochemical agents released from an inflamed piriformis muscle where the two structures meet at the greater sciatic foramen. In a series of biopsies of myofascial trigger points, Awad documented the pathologic findings of metachromatic ground substance (mucopolysaccharide), extravasated platelets, degranulating mast cells, and giant myofilaments. Based on these findings, he hypothesized the probable mechanism of “interstitial myofibrositis” to be as follows: trauma to the muscle results in extravasation of blood, release of serotonin from extravasated platelets, and degranulation of mast cells releasing histamine and heparin. Serotonin and histamine are vasoactive amines that produce vasodilation and increased vascular permeability.

Anatomy

 

The piriformis muscle is a flat, pyramidal-shaped muscle that originates from the anterior surface of the sacrum from S2 to S4 and sacrotuberous ligament, passes through the upper part of the greater sciatic notch, and inserts on the superior surface of the greater trochanter.

 

The piriformis is innervated by the nerve of L5, S1, and S2 segmental origin. The sciatic nerve emerges from the greater sciatic notch, very close to the inferior border of the piriformis muscle. The function of the piriformis muscle is to externally rotate the leg and abduct the thigh when the hip is flexed.

The sciatic nerve originates from the L4, L5, S1, and S2 nerve roots. It arises from the lumbosacral plexus and leaves the pelvis through the greater sciatic notch. It is composed of two trunks, the peroneal division and the tibial division. The sciatic nerve divides into the common peroneal and tibieal nerves at the midthigh to distal thigh region. All the hamstring muscles except the short head of the biceps femoris are innervated by the tibial division. All the muscles below the knee are innervated by the sciatic nerve. All sensory nerves except the saphenous nerve are derived from the sciatic nerve.

The location of the sciatic nerve in relationship to the muscle makes it vulnerable to irritation and entrapment secondarily to pathology involving the piriformis muscle.

In about 20%, the piriformis muscle is split and one or both parts of the sciatic nerve pass through the muscle belly, and in 10% of the population, the tibial and peroneal portions of the sciatic nerve are not enclosed in a common sheath and one portion may pierce the muscle.
Six possible anatomic variations of the relationship between the sciatic nerve and piriformis muscle have been described. The first four have been confirmed, the last two are hypothetical.
1) the sciatic nerve passing below the piriformis muscle
2) a divided nerve passing through and below the piriformis
3) a divided nerve above and below the muscle
4) an undivided nerve passing through the piriformis
5) a divided nerve passing through and above the muscle
6) an undivided nerve passing above the muscle

 

Diagnosis

 

Piriformis syndrome was mostly a diagnosis of exclusion with the symptoms of sciatica and pain in the buttock. There have been studies of diagnostic tests which may aid in identifying piriformis syndrome. The common findings on history and physical will be reviewed.

History of trauma to the buttock is commonly reported. In Durrani and Winnie's study, 92% of their patients reported either direct or indirect trauma. Direct trauma may be to the low back or buttocks. Indirect truama may be due to unusual stretching of the lumbosacral and/or hip muscles through athletic or other strenuous activities.

Women often complain of pain with sexual intercourse, dyspareunia, men may complain of rectal pain. There is pain with walking, limping, and squatting. Pain with stooping or lifting, intolerance to sitting, taking long automobile rides, and complaint of pain in the buttock.
The treatment for the sciatic pain may not yield results. History of failed laminectomy, discetomy, and chemonucleolysis, or a series of epidural steroid injections with no change in sciatica may indicate piriformis syndrome.

Robinson described six classic findings for piriformis syndrome:
1) a history of trauma to the sacroiliac and gluteal regions
2) pain in the region of the sacroiliac joint, greater sciatic notch, and piriformis muscle that usually extends down the limb and causes difficulty with walking
3) acute exacerbation of pain caused by stooping or lifting
4) a palpable sausage-shaped mass, tender to palpation, over the piriformis muscle
5) a positive Lasegue sign
6) gluteal atrophy

Durrani and Winnie used the following physical examination tests to diagnose piriformis syndrome:
1) digital palpation of the piriformis muscle for reproducing sciatica
2) rectal or pelvic examination to rule out lateral pelvic wall tenderness and reproduce sciatica
3) Freiberg’s and Pace’s signs
4) Tonic external rotation of the affected lower extremity
 

They found that 26/26 people had moderate to severe tenderness of the lateral pelvic wall along with reproduction of their sciatica during pelvic or rectal examination, 24/26 had reproduction of pain with deep digital palpation of the piriformis muscle.

 

Lasegue’s sign is pain in the vicinity of the greater sciatic notch with extension of the knee with the hip flexed to 90 degrees and tenderness to palpation of the greater sciatic notch also involving pain on voluntary adduction, flexion, and internal rotation. Freiberg’s sign is pain with passive internal rotation of the hip. Pace’s sign is pain and weakness in association with resisted abduction and external rotation of the affected thigh, different source says internal rotation of hip. The piriformis sign is pain with tonic external rotation of the affected lower extremity.

 

A diagnostic maneuver for piriformis syndrome was described by Robert A. Beatty. It is performed with the patient lying with the painful side up, the painful leg flexed, and the knee resting on the table. Buttock pain is produced when the patient lifts and holds the knee several inches off the table. It relies on contraction of the muscle, rather than stretching which reproduces one of the proposed mechanisms for piriformis syndrome. A modification to this maneuver was proposed by Robert M. Titelman. Hold the patient’s affected thigh and leg slightly above the other so it is slightly medially rotated. The patient relaxes the lower membrane, while being held in the same position. Have the patient laterally rotate against your resistance, but while still holding the leg to keep the abductors relaxed and the thigh from abducting. This would eliminate the abduction and extension involved in Beatty's diagnostic maneuver.

Diagnostic Studies

Imaging studies for piriformis syndrome may demonstrate inflammation or hypertrophy of the piriformis muscle. Bone scan may demonstrate abnormal uptake in the soft tissues of the pelvis in the distribution of the piriformis muscle. In a case report, computed tomography and magnetic resonance imaging showed an enlarged piriformis with normal and homogenous muscle signal intensity (demonstration of atrophy or fibrous tissue replacement of the piriformis muscle). Imaging may demonstrate other causes of sciatica such as herniated nucleus pulposa or extrinsic compression of the sciatic nerve by tumor or abscess.

Myelography can show the enlargement of the piriformis muscle and also demonstrate the correct placement of the needle within the muscle. However, Durrani and Winnie had 6 piriformis syndrome patients with myelograms, all of which were negative.

Electromyography has been used to aid in the diagnosis of piriformis syndrome. Fishman and Zybert have studied the use of the H-reflex in electrodiagnostic studies. The H-reflex is an electrically stimulated version of the Achilles reflex. Subjects were tested in the anatomically prone position and then placed in a lateral decubitus position. H-reflex was reexamined with the hip flexed, maximally adducted, the knee flexed, and passive rotation of the thigh internally. They concluded that there was significant delay in the H-reflex in the affected limb. Durrani and Winnie had 8/18 patients which had electromyographic evidence of radiculopathies.

Relief of pain produced by infiltration of the piriformis muscle with local anesthetic is considered to be a diagnostic sign.

 

Treatment

 

Treatment of piriformis syndrome should include correction of any abnormal biomechanics caused by posture, pelvic obliquity, leg-length inequality, or ankle/foot problems.

 

Nonsteroidal anti-inflammatory drugs, analgesics, and muscle relaxants may be prescribed to reduce local prostaglandin-mediated inflammation, pain and spasm. Piriformis stretching exercises with heat therapy may be sufficient to relieve the pain. Other relatively conservative treatments include ultrasound treatment, transrectal massage, rectal diathermy, and transcutaneous electrical stimulation.

 

Trigger point injections could be considered diagnostic and therapeutic. Local anesthetics and osteopathic manipulation work by reducing muscle spasm, restoring joint motion, and keeping the patient ambulatory. The local anesthetic apparently reverses the hyperirritability of the piriformis muscle and produces relief that outlasts the duration of the medication. Sarapin, an aqueous distillate of Sarracenia purpurea, blocks C-fiber pain transmission without affecting motor or sensory function and may be useful when used as part of the injectate. Injection of Botulinum toxin type A into the piriformis muscle could provide longer lasting relief than local anesthetics. Botulinum toxin type A is a protein produced by the Clostridium botulinum bacteria. It inhibits the release of the neurotransmitter acetylcholine thus causing muscle relaxation.

 

Caudal epidural steroid injection has been used since it is a well established treatment for low back pain. Solutions deposited in the caudal epidural space would be expected to diffuse along the nerve root sleeves and hence along the proximal part of the sciatic nerve. This was subsequently demonstrated with computerized tomographic evidence. The sacral innervation of the piriformis muscle may also have some bearing on its success. The caudal epidural injection consisted of 60-80 mg of triamcinolone with 15 ml of 0.25% bupivicaine. This is believed to relieve sciatic nerve irritation and piriformis muscle spasm.

 

Perisciatic injection of steroid have been successful in recalcitrant cases of piriformis syndrome. Perineural injection of steroid has been shown to reduce nerve swelling, reduce ectopic discharge, and facilitate recovery of nerve conduction following nerve injury. The perisciatic injection of steroid is thought to reduce swelling and irritation of the sciatic nerve while piriformis muscle injections relax the muscle and reduce nerve compression.