Diagnosis and Management of Piriformis Syndrome
SOURCE: J Am Osteopath Assoc. 2008 (Nov); 108 (11): 657-664 ~ FULL TEXT
Lori A. Boyajian-O’Neill, DO, Rance L. McClain, DO,
Michele K. Coleman, DO, Pamela P. Thomas, PhD
Department of Family Medicine, Kansas City University of Medicine,
Biosciences College of Osteopathic Medicine,
1750 Independence Ave, SEP 358,
Kansas City, MO 64106-145, USA.
Piriformis syndrome is a neuromuscular condition characterized by hip and buttock pain. This syndrome is often overlooked in clinical settings because its presentation may be similar to that of lumbar radiculopathy, primary sacral dysfunction, or innominate dysfunction. The ability to recognize piriformis syndrome requires an understanding of the structure and function of the piriformis muscle and its relationship to the sciatic nerve. The authors review the anatomic and clinical features of this condition, summarizing the osteopathic medical approach to diagnosis and management. A holistic approach to diagnosis requires a thorough neurologic history and physical assessment of the patient based on the pathologic characteristics of piriformis syndrome. The authors note that several nonpharmacologic therapies, including osteopathic manipulative treatment, can be used alone or in conjunction with pharmacotherapeutic options in the management of piriformis syndrome.
From the Full-Text Article:
Piriformis syndrome occurs most frequently during the fourth and fifth decades of life and affects individuals of all occupations and activity levels. [7-12] Reported incidence rates for piriformis syndrome among patients with low back pain vary widely, from 5% to 36%. [3, 4, 11] Piriformis syndrome is more common in women than men, possibly because of biomechanics associated with the wider quadriceps femoris muscle angle (ie, “Q angle”) in the os coxae (pelvis) of women. 
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Difficulties arise in accurately determining the true prevalence of piriformis syndrome because it is frequently confused with other conditions.
The piriformis muscle acts as an external rotator, weak abductor, and weak flexor of the hip, providing postural stability during ambulation and standing. [4, 9, 13] The piriformis muscle originates at the anterior surface of the sacrum, usually at the levels of vertebrae S2 through S4, at or near the sacroiliac joint capsule. The muscle attaches to the superior medial aspect of the greater trochanter via a round tendon that, in many individuals, is merged with the tendons of the obturator internus and gemelli muscles (Figure 1). [1, 13, 14] The piriformis muscle is innervated by spinal nerves S1 and S2 — and occasionally also by L5.
The proper understanding of piriformis syndrome requires knowledge of variations in the relationships between the sciatic nerve and the piriformis muscle (Figure 2). In as much as 96% of the population, the sciatic nerve exits the greater sciatic foramen deep along the inferior surface of the piriformis muscle. [15-17] In as much as 22% of the population, the sciatic nerve pierces the piriformis muscle, splits the piriformis muscle, or both, predisposing these individuals to piriformis syndrome. The sciatic nerve may pass completely through the muscle belly, or the nerve may split — with one branch (usually the fibular portion) piercing the muscle and the other branch (usually the tibial portion) running inferiorly or superiorly along the muscle. [7, 13-16, 18, 19] Rarely, the sciatic nerve exits the greater sciatic foramen along the superior surface of the piriformis muscle. [15-17]
Some symptoms of piriformis syndrome occur as a result of local inflammation and congestion caused by the muscular compression of small nerves and vessels — including the pudendal nerve and blood vessels, which exit at the medial inferior border of the piriformis muscle. 
There are two types of piriformis syndrome — primary and secondary. Primary piriformis syndrome has an anatomic cause, such as a split piriformis muscle, split sciatic nerve, or an anomalous sciatic nerve path. [8, 9, 20] Secondary piriformis syndrome occurs as a result of a precipitating cause, including macrotrauma, microtrauma, ischemic mass effect, and local ischemia. [1, 6, 11, 21, 22] Among patients with piriformis syndrome, fewer than 15% of cases have primary causes. [4, 11]
Figure 1. Anatomic features of the hip, including the most common orientation of the sciatic nerve, running inferior to the piriformis muscle.
Figure 2. Variations in the relationship of the sciatic nerve to the piriformis muscle: (A) the sciatic nerve exiting the greater sciatic foramen along the inferior surface of the piriformis muscle; the sciatic nerve splitting as it passes through the piriformis muscle with the tibial branch passing (B) inferiorly or (C) superiorly; (D) the entire sciatic nerve passing through the muscle belly; (E) the sciatic nerve exiting the greater sciatic foramen along the superior surface of the piriformis muscle.
Piriformis syndrome is most often caused by macrotrauma to the buttocks, leading to inflammation of soft tissue, muscle spasm, or both, with resulting nerve compression. [1, 8, 9, 11, 21] Microtrauma may result from overuse of the piriformis muscle, such as in long-distance walking or running or by direct compression. An example of this kind of direct compression is “wallet neuritis” (ie, repetitive trauma from sitting on hard surfaces).
Symptoms of piriformis syndrome are shown below in Figure 3. The most common presenting symptom of patients with piriformis syndrome is increasing pain after sitting for longer than 15 to 20 minutes. Many patients complain of pain over the piriformis muscle (ie, in the buttocks), especially over the muscle’s attachments at the sacrum and medial greater trochanter. Symptoms, which may be of sudden or gradual onset, are usually associated with spasm of the piriformis muscle or compression of the sciatic nerve. Patients may complain of difficulty walking and of pain with internal rotation of the ipsilateral leg, such as occurs during cross-legged sitting or ambulation. [1, 6, 8, 9, 11, 21, 23]
Figure 3. Clinical symptoms of piriformis syndrome.
Figure 4. Clinical signs of piriformis syndrome.
Spasm of the piriformis muscle and sacral dysfunction (eg, torsion) cause stress on the sacrotuberous ligament. This stress may lead to compression of the pudendal nerves or increased mechanical stress on the innominate bones, potentially causing groin and pelvic pain. [6, 9, 22] Compression of the fibular branch of the sciatic nerve often causes pain or paresthesia in the posterior thigh. [1, 6, 8, 9, 11, 21, 23]
Through compensatory or facilitative mechanisms, piriformis syndrome may contribute to cervical, thoracic, and lumbosacral pain, as well as to gastrointestinal disorders and headache. [9, 22]
Clinical signs of piriformis syndrome are shown below in Figure 4. These clinical signs relate, either directly or indirectly, to muscle spasm, resulting nerve compression, or both. Tenderness with palpation over the piriformis muscle, especially over the muscle’s attachment at the greater trochanter, is common. Patients may also experience tenderness with palpation in the region of the sacroiliac joint, greater sciatic notch, and piriformis muscle — including pain that may radiate to the knee. [1, 6, 8, 9, 11, 21, 23]
Some patients have a palpable “sausage-shaped” mass in the buttock caused by contraction of the piriformis muscle. [6, 9, 24] A contracted piriformis muscle also causes ipsilateral external hip rotation. When a patient with piriformis syndrome is relaxed in the supine position, the ipsilateral foot is externally rotated (Figure 5) — a feature referred to as a positive piriformis sign. [6, 9, 11, 21] Active efforts to bring the foot to midline result in pain. [1, 9, 24] Many patients with piriformis syndrome also have positive Lasègue, Freiberg, or Pace signs (observed in tests described in the next section of the present article), and these patients may exhibit an antalgic gait. 
Figure 5. Ipsilateral external rotation of the lower extremity in a patient who is relaxed in the supine position, a positive piriformis sign. (Photograph by Michael D. Roach.)
Sacral plexus nerves that innervate the tensor fascia lata, gluteus minimus, gluteus maximus, adductor magnus, quadratus femoris, and obturator externus muscles are also subject to irritation by the piriformis muscle. Ipsilateral muscle weakness may occur if piriformis syndrome is caused by an anatomic anomaly or if it is chronic in duration. [1, 4, 6, 8, 9, 11, 13, 17, 21, 22] Range-of-motion evaluation may reveal decreased internal rotation of the ipsilateral hip in such cases. 
In most cases of piriformis syndrome, the sacrum is anteriorly rotated toward the ipsilateral side on a contralateral oblique axis, resulting in compensatory rotation of the lower lumbar vertebrae in the opposite direction (Figure 6). [6, 21] For example, piriformis syndrome on the right side would cause a left-on-left forward sacral torsion with L5 rotated right. Sacral rotation often creates ipsilateral physiologic short leg. [6, 9, 21, 26] Facilitation and compensatory somatic dysfunctions may lead to cervical, thoracic, and low back pain. [6, 9, 21, 26] TePoorten  reported decreased range of motion at vertebrae T10 and T11, tissue texture changes at T3 and T4, pain and decreased range of motion of the contralateral C2, and ipsilateral occiput-atlas lesion in patients with piriformis syndrome.
Osteopathic Manipulative Treatment
The goals of osteopathic manipulative treatment (OMT) for patients who have piriformis syndrome are to restore normal range of motion and decrease pain. These goals can be achieved by decreasing piriformis spasm. Indirect osteopathic manipulative techniques have been used to treat patients with piriformis syndrome. The two indirect OMT techniques most commonly reported for the management of piriformis syndrome are counterstrain and facilitated positional release. [1, 26] Both techniques involve the principle of removing as much tension from the piriformis muscle as possible.
Three tender point locations can be addressed with counterstrain — at the midpole sacrum, piriformis muscle, and posteromedial trochanter.  To position a patient for counterstrain treatment, the patient is generally asked to lie in a prone position with the affected side of the body at the edge of the examination table. In performing the counterstrain technique, the osteopathic physician brings the patient’s affected leg over the side of the table, placing it into flexion at the hip and knee, with abduction and external rotation at the hip (Figure 8).
Facilitated positional release can also be achieved from the position shown in Figure 8, with compression through the long axis of the femur from the knee toward the sciatic notch. This additional compressive force can reduce patient treatment time from 90 seconds when performing counterstrain to 3 to 5 seconds when performing facilitated positional release. 
Direct OMT techniques can be performed using either active or passive methods. The direct OMT techniques that are the most useful in treating patients with piriformis syndrome include muscle energy, articulatory, Still, and high velocity/low amplitude.  The muscle energy technique can be applied in the management of piriformis spasm, as well as for associated dysfunctions of the sacrum and pelvis. No absolute contraindications are defined for the muscle energy technique. The patient must understand the required amount of muscular force and the correct direction of this force for the technique to be effective. 
Articulatory OMT techniques are applied by advancing and retreating from a restrictive barrier in a repetitive manner to advance that barrier and increase the range of motion. The presence of osteoarthritis can limit the applicability of this technique secondary to articulatory pain.  The Still technique, a specialized form of articulatory treatment, is begun by placing a joint in a relaxed position away from restrictive barriers. Then, with an arching motion, compression is applied to the level of dysfunction and moved toward the restrictive barrier while the patient is passive and relaxed. No absolute contraindications are defined for the Still technique. 
High velocity/low amplitude technique is most often used in cases of piriformis syndrome to correct associated sacral and pelvic somatic dysfunctions. Extreme caution should be exercised when using this manual technique with individuals who have osteoporosis. 
There are many gaps in knowledge regarding piriformis syndrome. An increase in the breadth and depth of our understanding of this condition is necessary for optimal patient care. Additional research is needed for patients with piriformis syndrome, primarily concerning epidemiologic factors, risk factors, and optimal treatment. The length of time from symptom onset to initial presentation is not known and needs to be studied further. The proportion of patients presenting with low back pain who demonstrate symptoms and signs consistent with piriformis syndrome is also unknown and merits further consideration.
Piriformis syndrome is a complex condition that is often not considered in the differential diagnosis of chronic hip and low back pain. To aid diagnosis, several tests have been developed to recreate the pain by actively contracting or passively stretching the piriformis muscle and compressing the sciatic nerve. Radiographic studies and neuroelectric tests are primarily used to narrow the differential diagnosis toward piriformis syndrome by ruling out other pathologic conditions.
A holistic approach to diagnosis involves a thorough neurologic history and physical assessment of the patient, inclusive of the osteopathic structural examination, based on the pathologic characteristics of piriformis syndrome. Osteopathic manipulative treatment can be used as one of several possible nonpharmacologic therapies for these patients. Nonpharmacologic therapies can be used alone or in conjunction with pharmacologic treatments in the management of piriformis syndrome in an attempt to avoid surgical intervention.