Piriformis syndrome remains an oft misdiagnosed cause of buttock and leg pain. Because of its proximity to the sciatic nerve, variant anatomic relations between the piriformis muscle and sciatic nerve have been implicated as potential etiology. However, clinical significance of anatomic variants has been disputed as no difference was identified in prevalence of variant anatomy in a surgical case series of symptomatic patients vs. random cadaveric dissections (16.2% vs. 16.9%).
Clinically the syndrome includes elements of both somatic and neuropathic pain and may be considered a myofascial pain syndrome. Piriformis syndrome remains a diagnosis of clinical exclusion, and physical exam maneuvers continue to yield poor specificity and sensitivity. Diagnostic testing of potential value may include electromyography (EMG) and magnetic resonance neurography (MRN).
Conservative treatment with physical therapy, antiinflammatory drugs, and targeted injections are effective in 75% to 80% of individuals. Most commonly employed injection techniques include fluoroscopic-guided injection with aid of a neurostimulator, and more recently ultrasound guided directly into the muscle. Advocates of an ultrasound-guided approach cite greater precision, with 19/20 cadaveric injections correctly placed into the piriformis muscle vs. 6/20 fluoroscopic injections. Should patients attain transient benefit from local anesthetic, botulinum toxin injection may be entertained. In refractory cases surgical release remains a potential curative option.
Keywordsdeep gluteal syndromes, fluoroscopic-guided injection, pathophysiology, piriformis syndrome, treatment, ultrasound-guided injection
Although piriformis syndrome (PS) was first described in 1947, leg pain originating at the ischium was thought to derive from sciatic nerve irritation as early as the 15th century and was termed “sciatica.” PS is an uncommon and often misdiagnosed cause of buttock and leg pain, with reported prevalence rates typically ranging between 5% and 8%, but it sometimes is cited as high as 36% among patients with low back pain. In this section, the following topics are discussed: (1) the anatomy of the piriformis muscle and anatomic abnormalities that cause PS, (2) etiologies of the syndrome, (3) signs and symptoms associated with the syndrome, and (4) treatments of the syndrome.
Anatomy of the Piriformis Muscle and the Sciatic Nerve
The piriformis muscle is pyramidal in shape and originates from the anterior surface of the S2–S4 sacral vertebrae, the capsule of the sacroiliac joint, and the gluteal surface of the ilium near the posterior surface of the iliac spine. It runs laterally through the greater sciatic foramen, becomes tendinous, and inserts into the piriformis fossa at the medial aspect of the greater trochanter of the femur ( Fig. 67.1 ). Ventral rami of the S1 and S2 spinal nerve course into the deep surface of the piriformis muscle to innervate it. The main function of the piriformis muscle is abduction and external rotation of the femur. The sciatic nerve, posterior femoral cutaneous nerve, gluteal nerves, and the gluteal vessels pass below the piriformis muscle.
With a typical diameter of 2 cm, the sciatic nerve is formed by the ventral rami (L4–S3) of the lumbosacral plexus and exits the pelvis through the greater sciatic foramen. As it is a mixed nerve, it contains both motor fibers, which supply the posterior thigh, hip and knee, and sensory fibers that supply the entire surface of the leg distal to the knee with the exception of the anteromedial calf and medial aspect of the foot. The sciatic nerve typically passes inferior to the piriformis muscle and then divides into the tibial nerve and the peroneal nerve, which ordinarily occurs at the superior angle of the popliteal fossa.
Anatomical variants between the sciatic nerve and piriformis muscle have been described in the literature with prevalence rates anywhere from 6.4% to 16.9%. There is a correlation between anatomical variations of the sciatic nerve and increased variability of other morphometric measurements of the lower limbs. The clinical significance of variant anatomy remains disputed, as there was no difference in rates of aberrant anatomy in a surgical case series of patients with PS versus cadaveric dissections (16.2% vs. 16.9%), questioning its importance in the pathogenesis of PS.
Six possible anatomic variants have been described between the sciatic nerve and the piriformis muscle and have been classified by the Beason and Anson Classification system ( Table 67.1 ). Anomalies of the piriformis muscle and the sciatic nerve can cause true sciatica. The compression usually occurs between the tendinous portion of the muscle and the bony pelvis. An abnormal course of the sciatic nerve or the smaller divisions, which are not as durable as the large caliber and well-sheathed sciatic nerve, are more susceptible to compression from muscle hypertrophy. A study of 250 cadavers revealed an anatomical variation in the relationship of the nerve and muscle in 11.7% of the population. The proportion of individuals with aberrant anatomy has previously been described as ranging anywhere between 8% and 21%, further demonstrating that a significant minority of the population exhibits this anatomic risk factor, which is a possible etiology of PS. However, as noted above, the clinical significance of variant anatomy remains disputed.
|Beason and Anson Classification|
|Normal anatomy||Type 1||Undivided sciatic n. passes inferior to undivided m.|
|Proximal division||Type 2||One division passes through and one inferior to m.|
|Aberrant route||Type 3||One division passes inferior and one superior to m.|
|Type 4||One division passes inferior and one superior to the m.|
|Normal division||Type 5||Sciatic n. passes through the m.|
|Aberrant route||Type 6||Sciatic n. passes superior to the m.|
Pathophysiology, Signs and Symptoms, and Treatment
The clinical presentation of PS may be due to both somatic and neuropathic pain. Myofascial pain of the piriformis muscle itself is the primary etiology of the somatic component of pain. Etiologies and predisposing factors of the syndrome include trauma to the pelvis or buttock, hypertrophy or spasm of the piriformis and/or adjacent gemelli muscles, female gender, pregnancy, anatomic abnormalities of the piriformis muscle or the sciatic nerve, true or apparent leg-length discrepancies (a minimum of half an inch difference in leg lengths), obesity, cerebral palsy secondary to hypertonicity, lumbar hyperlordosis, infection, and rarely a mass effect from space occupying lesions.
Microtrauma to the piriformis muscle may occur from overuse injuries as observed in athletes or individuals performing heavy manual labor. A history of trauma is usually elicited in approximately 50% of the cases. The trauma is usually not dramatic and may occur several months before the initial symptoms. Trauma to the gluteal musculature leads to inflammation and spasm of the muscle. Inflammatory mediators such as prostaglandins, histamine, bradykinin, and serotonin are released from the inflamed muscle and may irritate the sciatic nerve resulting in a pain–spasm–inflammation–irritation–pain cycle. The stretched, spastic, and inflamed piriformis muscle may compress the sciatic nerve between the muscle and the bony pelvis.
Other investigators consider PS to be a form of myofascial pain syndrome. Isolated involvement of the piriformis muscle is uncommon and usually occurs as a part of soft tissue injuries resulting from rotation and/or flexion movements of the hip and torso. For this reason, some authors now favor the term “deep gluteal syndrome” instead of PS to describe gluteal sciatic nerve entrapment. In addition to the piriformis muscle, pathology involving the superior and inferior gemelli muscles and the obturator internis can lead to buttock pain with or without lower extremity radiation.
The differential diagnosis of PS includes the myriad causes of low back pain and radiculopathy. Facet syndrome, sacroiliac joint dysfunction, trochanteric and ischial bursitis, myofascial pain syndrome, pelvic tumor, endometriosis, and conditions irritating the sciatic nerve should be considered in the differential diagnosis of PS. These conditions can be ruled out by a complete medical history and physical examination. Diagnosis of PS is usually arrived at only after exclusion of these possibilities. In a review of 55 studies, the most common features of PS identified were :
External tenderness over the greater sciatic notch
Aggravation of the pain on prolonged sitting
Augmentation of the pain with maneuvers that increase piriformis muscle tension
Patients with PS usually complain of buttock pain with or without radiation to the ipsilateral leg. The buttock pain usually extends from the sacrum to the greater trochanter because of the muscle’s insertion on the medial aspect of the greater trochanter. Gluteal pain radiating to the ipsilateral leg is usually present if the piriformis muscle irritates the sciatic nerve. The pain is aggravated by prolonged sitting, as in driving or biking, or when getting up from a seated position. Pain can occur with bowel movements due to the proximity of the piriformis muscle to the lateral pelvic wall, and is worse after sitting on hard surfaces.
Physical examination of the patient may reveal a pelvic tilt or tenderness in the buttock. On palpation the contracted piriformis may feel like a spindle/sausage-shaped mass in the buttock, and there may be piriformis tenderness on rectal and pelvic examinations. The pain is aggravated by hip flexion, adduction, and internal rotation. However, when hip flexion exceeds 90 degrees, the piriformis muscle is elongated with external rotation and this heel-contralateral knee maneuver (HCLK) may reproduce pain. Neurologic signs are usually absent, although there may be numbness in the lower leg or foot from compression of the sciatic nerve by the piriformis muscle. The straight leg raise test may be normal or limited with numbness occurring when the sciatic nerve is irritated. The physical examination signs found in Table 67.2 may be helpful in confirming the presence of PS.
|Diagnostic Test||Performance of Test||Positive in PS|
|Pace sign||Pain/weakness with seated abduction of hip against resistance||30%–74%|
|FAIR test||Flexion, abduction, internal rotation causing pain||—|
|Lasègue sign||Pain with voluntary flexion, adduction, and internal rotation of the flexed hip||NR|
|Freiberg sign||Pain with forced internal rotation of the extended hip||32%–63%|
|Palpation of piriformis line||Trigger point tenderness to palpation with extended thumb on the lateral third of the piriformis line with patient in Sims’ position||59%–92%|
|Beatty maneuver||Reproduction of buttock pain when painful leg is flexed and knee is elevated several inches off the table||NR|
|Hughes test||Pain caused by maximal internal rotation of the painful limb followed by maximal external isometric rotation||NR|
|Atrophic changes||Gluteal atrophy, shortening of the limb on affected side||NR|
|Internal palpation||Pain with palpation of medial end of PM by rectal or vaginal exam. Examiner may also palpate a mass along lateral pelvic wall.||100%|
|External palpation||Tenderness to palpation over the piriformis muscle||38.5%|
|HCLK (heel contralateral knee)||Hip flexion > 90 degrees with lateral rotation may reproduce buttock and sciatica symptoms after several seconds||NR|