Physical Medicine and Rehabilitation for Piriformis Syndrome

The piriformis muscle is flat, pyramid-shaped, and oblique.[7] This muscle originates to the anterior of the S2-S4 vertebrae, the sacrotuberous ligament, and the upper margin of the greater sciatic foramen. Passing through the greater sciatic notch, the muscle inserts on the superior surface of the greater trochanter of the femur. With the hip extended, the piriformis muscle is the primary external rotator; however, with the hip flexed, the muscle becomes a hip abductor. Branches from the L5, S1, and S2 nerve roots innervate the piriformis muscle, as demonstrated in the image below. Due to this innervation, a lower lumbar radiculopathy may cause secondary irritation of the piriformis muscle, which may complicate diagnosis and hinder patient progress.

A cadaver study by Iwanaga et al indicated that the superior gluteal nerve is another important source of piriformis muscle innervation. Of 20 sides from 10 cadavers studied, the investigators found that in 80%, the piriformis muscle was innervated by 2-3 nerves. Nerves originated from the superior gluteal nerve on 14 sides (70%); from the inferior gluteal nerve on one side (5%); from the L5 ventral ramus on one side (5%); from the S1 ventral ramus on 17 sides (85%); and from the S2 ventral ramus on 14 sides (70%).[8]

Many developmental variations of the relationship between the sciatic nerve in the pelvis and piriformis muscle have been observed.[9, 10, 11] In approximately 20% of the population, the muscle belly is split, with 1 or more parts of the sciatic nerve dividing the muscle belly itself. In 10% of the population, the tibial/peroneal divisions are not enclosed in a common sheath. Usually, the peroneal portion splits the piriformis muscle belly, although in rare cases, the tibial division does so.

In a study of 200 pairs of sacral roots (100 patients, none of whom had piriformis syndrome) by Russell et al, T1-weighted magnetic resonance imaging (MRI) scans revealed that 199 of the S1 nerve roots (99.5%) were positioned above the piriformis muscle, while 150 of the S2 nerve roots (75%) traversed the muscle and 50 of them (25%) were located above it. The images also showed that 194 S3 nerve roots (97%) traversed the muscle and that 190 S4 nerve roots (95%) were below it. The piriformis muscles had an average size of 1.9 cm; in 19% of the study's patients, the muscle was asymmetrical by more than 3 mm.[12]

Involvement of the superior gluteal nerve usually is not seen in cases of piriformis syndrome. This nerve leaves the sciatic nerve trunk and passes through the canal above the piriformis muscle.

Blunt injury may cause hematoma formation and subsequent scarring between the sciatic nerve and short external rotators. Nerve injury can occur with prolonged pressure on the nerve or vasa nervorum.

The etiology of piriformis syndrome can be divided into the following categories:

• Hyperlordosis

• Muscle anomalies with hypertrophy

• Fibrosis (due to trauma)

• Partial or total nerve anatomical abnormalities

Other causes can include the following:

• Pseudoaneurysms of the inferior gluteal artery adjacent to the piriformis syndrome

• Bilateral piriformis syndrome due to prolonged sitting during an extended neurosurgical procedure

• Cerebral palsy

• Total hip arthroplasty

• Fibrodysplasia ossificans progressiva (myositis ossificans)

• Vigorous physical activity

• Leg length discrepancy[13]

Piriformis syndrome remains controversial because, in most cases, the diagnosis is clinical, and no confirmatory tests exist to support the clinical findings.

Papadopoulos and colleagues proposed the following classifications for piriformis syndrome[14] :

• Primary piriformis syndrome - This designation would apply to piriformis syndrome resulting from intrinsic pathology of the piriformis muscle itself, such as myofascial pain, anatomic variations, and myositis ossificans.

• Secondary piriformis syndrome (pelvic outlet syndrome) - This classification would encompass all other etiologies of piriformis syndrome, with the exclusion of lumbar spinal pathology.

In an imaging study of 74 patients who demonstrated pathologies associated with piriformis syndrome, Vassalou et al found a greater incidence of secondary causes than primary etiologies, with the condition most often caused by space-occupying lesions in the piriformis area. The study, which employed magnetic resonance imaging (MRI) and/or computed tomography (CT) scanning, reported the most frequent imaging finding to be piriformis muscle enlargement.[15]

Frequency

United States

Given the lack of agreement on exactly how to diagnose piriformis syndrome, estimates of the frequency of sciatica caused by piriformis syndrome vary from rare to approximately 6% of sciatica cases seen in a general family practice.[3] More than 80% of adults have had at least 1 episode of disabling low back pain (LBP) in their lifetime.[16]

Mortality/Morbidity

Piriformis syndrome is not life-threatening, but it can have significant associated morbidity. The total cost of low back pain and sciatica is significant, exceeding $16 billion annually in direct and indirect costs.

Sex

Some reports suggest a 6:1 female-to-male ratio for piriformis syndrome.

Piriformis syndrome often is not recognized as a cause of low back pain (LBP) and associated sciatica. This clinical syndrome is due to a compression of the sciatic nerve by the piriformis muscle; it is similar in clinical presentation to LBP with associated L5, S1 radiculopathy due to diskogenic and/or lower lumbar facet arthropathy with foraminal narrowing. (The image below demonstrates the origins of both conditions.) Not uncommonly, patients demonstrate both of these clinical entities simultaneously. This diagnostic dilemma highlights the need for patients with LBP and associated radicular pain to undergo a complete history and physical examination.

Many cases of refractory trochanteric bursitis are observed to have an underlying occult piriformis syndrome due to the insertion of the piriformis muscle on the greater trochanter of the hip. If a patient's trochanteric bursitis and piriformis syndrome are treated inadequately, both conditions remain resistant to medical management.

Examination findings may include the following:

• Piriformis muscle spasm often is detected by careful, deep palpation.

• The reproduction of sciatica-type pain with weakness results from resisted abduction/external rotation (Pace test).[3]

• The Freiberg test is another diagnostic sign that elicits pain, upon forced internal rotation of the extended thigh.[4]

• The Beatty maneuver reproduces buttock pain by selectively contracting the piriformis muscle.[5] The patient lies on the uninvolved side and abducts the involved thigh upward; this activates the ipsilateral piriformis muscle, which is a hip external rotator and, when the hip is flexed, an abductor.

• Some specialists may include a digital rectal examination, which may reveal a tenderness on the lateral pelvic wall that reproduces piriformis symptoms; this procedure is less commonly performed, as it is uncomfortable and leads to a nonspecific finding.

• A painful point may be present at the lateral margin of the sacrum.

• Shortening of the involved lower extremity may be seen.

• The patient may have difficulty sitting due to an intolerance of weight bearing on the buttock.

• The patient may have the tendency to demonstrate a splayed foot on the involved side when in the supine position.

• Piriformis syndrome alone is rarely the cause of a focal neuromuscular impairment; either a sciatic mononeuropathy or an L5-S1 radiculopathy can mimic both of these conditions, obscuring diagnosis of piriformis syndrome.

• A Morton foot may predispose the patient to developing piriformis syndrome. The prominent second metatarsal head destabilizes the foot during the push-off phase of the gait cycle, causing foot pronation and internal rotation of the lower limb. As a compensatory mechanism, the piriformis muscle (external hip rotator) reactively contracts repetitively during each push-off phase of the gait cycle , leading to piriformis syndrome.

Approximately 50% of patients with piriformis syndrome have a history of trauma, with either a direct buttock contusion or a hip/lower back torsional injury. The remaining 50% of cases are of spontaneous onset, so the treating physician must have a high index of suspicion for the problem, lest it be overlooked.

Laboratory studies generally are not indicated in the diagnosis of piriformis syndrome.

Diagnostic imaging of the lumbar spine may be helpful in excluding associated diskogenic and/or osteoarthritic contributing pathology should conservative treatment of clinically diagnosed piriformis syndrome fail to provide therapeutic benefit.

Reports in the literature on the piriformis muscle describe imaging by nuclear diagnostic studies and MRI of the pelvis,[17] but these tests are neither practical nor reliable approaches to the diagnosis of piriformis syndrome. The history and clinical diagnostic examination provide the greatest and most specific diagnostic yield for the disorder.

Magnetic resonance neurography

Magnetic resonance neurography is a newer, sensitive imaging technique that increases nerve conspicuity by suppressing the signal from adjacent soft tissue, including fat, bone, and muscle.[18] The nerve itself contains minimal fat, and its signal is unsuppressed. According to Filler and colleagues, MR neurography demonstrated piriformis muscle asymmetry and sciatic nerve hyperintensity at the sciatic notch with 93% specificity.[19] The investigators also found that the technique had a sensitivity of 64% with regard to distinguishing patients with piriformis syndrome from persons who, despite having similar symptoms, did not have the condition (p< 0.01).

Ultrasonography

Diagnostic ultrasonographic imaging of the piriformis muscle for the assessment of muscle morphology has demonstrated a significant correlation of piriformis muscle morphology abnormality, especially in patients with lumbosacral/buttock pain and pain ascending stairs, referred pain to the posterior thigh on the symptomatic side, and reproduction of pain with needling of the piriformis muscle.

The results of electrodiagnostic testing for piriformis syndrome usually are normal. Reports of positional H-reflex abnormalities can be found in the literature;[20, 21] however, such findings have not been widely accepted or reproduced.

There are several treatment approaches to piriformis syndrome, ranging from nonoperative treatment with physical therapy, costicosteroid injections, and self-stretching to operative management by piriformis muscle surgical release.

Physical Therapy

Because there is no definitive method to accurately diagnose piriformis syndrome, treatment regimens are controversial and have not been subjected to randomized, blind clinical trials. Despite this fact, numerous treatment strategies exist for patients with this condition.

Functional biomechanical deficits associated with piriformis syndrome may include the following:

• Tight piriformis muscle

• Tight hip external rotators and adductors

• Hip abductor weakness

• Lower lumbar spine dysfunction

• Sacroiliac joint hypomobility

Functional adaptations to these deficits include the following:

• Ambulation with the thigh in external rotation

• Functional limb length shortening

• Shortened stride length

Once the diagnosis has been made, these underlying, perpetuating biomechanical factors must be corrected.

Consider the use of ultrasound and other heat modalities prior to physical therapy sessions. Before piriformis stretches are performed, the hip joint capsule should be mobilized anteriorly and posteriorly to allow for more effective stretching. Soft-tissue therapies for the piriformis muscle can be helpful, including longitudinal gliding with passive internal hip rotation, as well as transverse gliding and sustained longitudinal release with the patient lying on his/her side. Addressing sacroiliac joint and low back dysfunction also is important.

A home stretching program should be provided to the patient. These stretches are an essential component of the treatment program. During the acute phase of treatment, stretching every 2-3 hours (while awake) is a key to the success of nonoperative treatment. Prolonged stretching of the piriformis muscle is accomplished in either a supine or an orthostatic position with the involved hip flexed and passively adducted/internally rotated.

Extracorporeal shock wave therapy

Radial extracorporeal shock wave therapy has emerged as a nonoperative treatment option for piriformis syndrome. A randomized, controlled trial by Ahadi et al comparing radial extracorporeal shock wave therapy with corticosteroid injection for the treatment of piriformis syndrome found that pain and quality of life significantly improved in both of the report’s cohorts. However, pain reduction was more rapid in the radial shock wave treatment group, with a decrease in pain noted at 1-week follow-up visit, sooner than in the corticosteroid injection treatment group. Otherwise, there was no significant difference between the cohorts. Radial extracorporeal shock wave therapy is a novel non-invasive treatment of piriformis syndrome, with few adverse side effects.[22]

Due to lack of objective clinical trials, no consensus exists on the overall treatment of piriformis syndrome. In most cases, conservative treatment (eg, stretching, manual techniques, injections, activity modifications, natural healing, modalities such as heat and ultrasound) is successful.

Injection therapy

Injection therapy can be incorporated if the situation is refractory to the aforementioned treatment program. For effective injection, the piriformis muscle must be localized manually by digital rectal examination. The piriformis muscle is then injected using a 3.5-inch (8.9-cm) spinal needle. Care must be taken to avoid direct injection of the sciatic nerve. Fluoroscopic or ultrasonographic imaging guidance can significantly enhance the effectiveness of the piriformis muscle injection, because this deep muscle cannot otherwise be directly visualized.[23, 24]

Failure or partial failure of piriformis syndrome treatment may be secondary to an underlying obturator internus muscle injury, since this problem can be obscured by piriformis syndrome. The obturator internus muscle is inferior to the piriformis muscle and is also an external hip rotator. It originates at the medial surface of the pubis and passes through the lesser sciatic notch to insert on the greater trochanter. Physical examination demonstrates a trigger point that is more caudal than that in piriformis syndrome. Injection therapy would require direct visualization by fluoroscopy, due to the small size and location of this muscle.

Botulinum toxin

A study by Al-Al-Shaikh et al indicated that botulinum toxin (BoNT) alleviates piriformis syndrome by causing atrophy and fatty degeneration of the piriformis muscle. In the study, which involved 20 patients with piriformis syndrome, MRI scans of the piriformis muscle from 12 patients who underwent BoNT treatment were compared with those from eight patients who did not. In the treated patients, the piriformis muscles demonstrated significantly decreased volume and thickness and increased fatty infiltration, with patients experiencing significant pain relief as well, while the untreated patients showed no significant changes in muscle size or thickness.[25]

A randomized, double-blind, controlled trial by Fishman et al suggested that piriformis syndrome can effectively be treated with incobotulinumtoxinA chemodenervation. Patients in the study were treated with physical therapy, as well as with either incobotulinumtoxinA or placebo, with the incobotulinumtoxinA group showing greater improvement in the visual analog scale score and in posterior tibial H-reflex delay on the flexion, adduction, and internal rotation (FAIR) test.[26]

Surgical management is the treatment of last resort for piriformis syndrome. Surgery for this condition involves resection of the muscle itself or of the muscle tendon near its insertion at the superior aspect of the greater trochanter of the femur (as described by Mizuguchi).[6] These procedures may be effective and may not cause associated superimposed postoperative disability. However, because surgical decompression is usually performed later in a chronic state, it may not, even if successful, bring about complete resolution of associated chronic piriformis syndrome pain.

Physiatrists or sports medicine physicians should be the primary consultants for this musculoskeletal condition. Consultation with an orthopedic surgeon for severe or refractory piriformis syndrome is indicated when surgical decompression is being considered.

Prior to physical therapy sessions, the use of ultrasound and the spray-'n-stretch myofascial treatment is helpful. Manual muscle medicine, including facilitated positional release, may also be helpful.

Injections with steroids, local anesthetics, and botulinum toxin type B (12,500 U) have been reported in the literature for the management of piriformis syndrome.[27, 28, 29, 30, 31, 32] No single technique is universally accepted. Localization techniques include manual localization of the muscle or localization with fluoroscopic, ultrasonographic, and electromyographic guidance. The piriformis muscle, after localization with a digital rectal examination, can be injected with a 3.5-inch (8.9-cm) spinal needle. Care should be taken to avoid direct injection of the sciatic nerve. Randomized comparison of ultrasound-guided imaging versus nerve stimulator with fluoroscopic imaging for piriformis muscle injections shows similar outcomes and without statistically significant differences in imaging or needling technique or total procedure time.[33]

In a prospective, double-blind, randomized, controlled trial, Misirlioglu et al found that although local anesthetic injections were effective in piriformis syndrome, the addition of corticosteroid to the local anesthetic did not increase the treatment’s efficacy.[34]

Medical acupuncture, including vigorous, direct, deep needling of the piriformis muscle, is performed to reduce piriformis muscle spasm and pain.[35]

No specific medication management of piriformis syndrome is indicated. The use of muscle relaxant medication can be beneficial, but this remains a nonspecific treatment.

See the list below:

• Piriformis syndrome usually is treated effectively with conservative measures. Please refer to the Treatment section for a discussion of treatment recommendations.

See the list below:

• Inpatient care is necessary only if surgical intervention is warranted. Surgery is the last-resort treatment for severe cases of piriformis syndrome.

See the list below:

• No method of preventing piriformis syndrome has been demonstrated. The best means of prevention is to maintain biomechanical balance through the restoration of a more physiologic weight-bearing distribution; this necessitates a level pelvis/sacral base and equal leg lengths, which can be achieved by using heel-lift therapy if necessary. This treatment approach also prevents recurrences of piriformis syndrome, especially if the underlying etiology is a leg-length discrepancy. The patient also must engage in a general stretching program that includes the bilateral piriformis muscles.

See the list below:

• The most significant complication of piriformis syndrome is a failure to recognize, diagnose, and treat this painful condition. If left untreated, a patient may undergo unsuccessful back surgery for a disk herniation; however, a coexisting occult piriformis syndrome can result in a failed back syndrome.

• Another complication is inadvertent direct injection of the sciatic nerve, which usually results in a nondisabling and temporary sciatic mononeuropathy.

See the list below:

• The prognosis of piriformis syndrome depends on early recognition and treatment. Because it is a soft-tissue syndrome, the condition has a tendency to become chronic, usually due to late diagnosis and treatment (which lead to a less favorable prognosis).

See the list below:

• For conservative measures to be effective, the patient must be taught, via an aggressive, home-based stretching program, to maintain piriformis muscle flexibility. He/she must comply with the program even beyond the point of discontinuation of formal medical treatment.