Print Page   |   Contact Us   |   Sign In   |   Join the ICS
Article Search
Information Articles: Clinical

Diagnosing and Treating Piriformis Syndrome​

Wednesday, March 13, 2019   (0 Comments)
Posted by: By Dr. Timothy Bertelsman, DC, DACO
Share |

Diagnosing and Treating Piriformis Syndrome

Piriformis syndrome, first described in 1928, arises when a hypertonic or irritated piriformis muscle compresses the proximal sciatic nerve.  (1) This pressure causes neurologic ischemia, congestion, local inflammation and radicular complaints.  (2) Researchers estimate that piriformis syndrome contributes to up to one third of all back pain. (3,4)

The piriformis muscle originates on the anterolateral surface of the mid-portion of the sacrum and inserts on the superior medial aspect of the greater trochanter.  When the hip is extended, the piriformis functions primarily as an external rotator of the thigh, with secondary contributions toward flexion. The muscle assists in abduction when the hip is flexed to 90 degrees.  (3) The sciatic nerve has a variable relationship to the piriformis muscle.  In the majority of the population, the sciatic nerve travels deep to the muscle.  Approximately one fourth of the population is anatomically predisposed to piriformis syndrome because their sciatic nerve passes through the muscle, splits the muscle or both.  (5,6) The innervation to the piriformis is somewhat variable, but typically consists of 2-3 branches, most commonly the superior gluteal nerve (70%) and the ventral rami of S1 (85%) and S2 (70%). (32)

Like many other lower extremity biomechanical problems, the presence of a Morton foot (longer second digit) is thought to be a predisposing factor.  (7) The condition is most prevalent in 40-60year-olds and affects women more frequently, possibly due to variations in Q-angle.  (4) 

Symptoms of piriformis syndrome may begin abruptly as the result of a traumatic event or may develop slowly in response to repeated irritation. Piriformis muscle irritation and hypertonicity can result from a strain, a fall onto the buttocks or catching oneself from a “near fall.” In other instances, the process may begin following repetitive microtrauma, like long distance walking, stair climbing or from chronic compression, e.g, sitting on the edge of a hard surface or a wallet. (8,9) 

Presenting complaints for piriformis syndrome include pain, paresthesia or numbness beginning in the gluteal region and radiating along the course of the sciatic nerve.  Additional symptoms may develop from local trigger point referral into the proximal thigh, sacroiliac and hip regions. (9) Symptoms are often provoked by holding any one position for longer than 15-20 minutes, particularly prolonged sitting or standing. Positional changes may provide transient relief.  Patients may report increasing discomfort when walking, running, stair climbing, riding in a car or arising from a seated position. Activities that involve hip internal rotation, like sitting cross-legged, may exacerbate symptoms. Patients with piriformis syndrome sometimes exhibit an antalgic gait.  (10)

Palpable hypertonicity and tenderness over the piriformis muscle are hallmarks of clinical evaluation.  (11,12) Tenderness from compensatory somatic dysfunction in the sacroiliac joint and associated hip musculature is likely. The obturator internus, located deep to both the piriformis muscle and sciatic nerve, is a synergistic hip external rotator and may be a co-contributor to piriformis syndrome.  (13) Clinicians should also assess the tensor fascia lata, obturator externus, adductor and gluteal muscles, particularly in chronic cases. Motion palpation and orthopedic testing may reveal sacroiliac joint dysfunction and compensatory restrictions in the spine and lower extremity.  (11)  Clinicians should evaluate the arch of the foot and assess for the possibility of a leg length inequality.  

The patient may display a slightly externally rotated hip while at rest (Piriformis sign) (15,16) Orthopedic evaluation may demonstrate painfully limited passive hip internal rotation (Freiberg sign). (11,16) FADIR test (flexion, adduction, and internal rotation) has relatively good sensitivity and specificity for piriformis syndrome and, when positive, is sometimes called the “Pace sign.”  (17,18) The Beatty test may assist in the diagnosis of piriformis syndrome.  The test is performed with the patient lying on the unaffected side and slightly abducting the affected leg a few inches off of the table.  Reproduction of the chief complaint is suggestive of piriformis syndrome.  (19)  

Patients may exhibit a positive straight leg raise.  Longstanding piriformis hypertonicity may lead to sciatic perineural adhesions with additional nerve tension signs. Neurologic evaluation of piriformis syndrome may reveal changes in sensation, reflex and motor strength.  Sciatica of piriformis origin may present with weakness or atrophy in the distal (leg) musculature, but unlike lumbar radiculopathy, piriformis syndrome is generally not accompanied by proximal (thigh) weakness.  (20)  

The diagnosis of piriformis syndrome is based on an accurate history and physical exam.  Radiographic imaging of a suspected soft tissue disorder is of limited benefit.  (21)  Advanced imaging may be an appropriate modality to rule out other sources of radicular complaints.  (17)  Diagnostic ultrasonography may show enlargement of the piriformis muscle belly producing compression on the sciatic nerve or anatomic variations in sciatic nerve location. Electrodiagnostic testing can help differentiate piriformis syndrome from lumbar radiculopathy.  (20)

Piriformis syndrome shares several common characteristics and may even co-exist with other lumbopelvic problems.  The differential diagnosis for piriformis syndrome includes: hip pathology; fracture; lumbar compression fracture; discitis; trochanteric bursitis; sacroiliitis; sacroiliac joint dysfunction; lumbar radiculopathy; spinal stenosis and viscerosomatic referred pain.  (20,25,26)

The foundations of treatment for piriformis syndrome include stretching, myofascial release and correction of underlying biomechanical dysfunction. Patients may need to temporarily limit provocative activities, including hill and stair climbing, walking on uneven surfaces, intense downhill running or twisting and throwing objects backward (i.e. firewood).  Patients should avoid sitting on one foot and take frequent breaks from prolonged standing, sitting and car rides.  Women should be cautious to limit sustained hip external rotation and abduction during gynecologic procedures or intercourse. (T&S). Stretching of the piriformis muscle is crucial and may be performed with seated, prone or quadruped maneuvers.  (26) 

Clinicians should be judicious in the application of soft tissue manipulation in order to avoid additional irritation to the sciatic nerve. Soft tissue release and stretching exercises may be appropriate for any associated myofascial concerns in the piriformis, gluteus, obturator, tensor fascia lata, hamstring, lumbar erectors and hip adductors. Sciatic nerve flossing may be helpful. Manual manipulation may be necessary to correct lumbar, sacroiliac and lower extremity joint dysfunction.  (28,29) Some studies have shown benefit from heat, ice and ultrasound, particularly when applied prior to manual treatments.  (30) NSAIDs may provide benefit in the early stages of management.

Strengthening exercises should be directed at the abductor, adductor and gluteal muscles.  Clinicians should be alert to the possibility of lower crossed syndrome and formulate appropriate rehab plans to deal with any biomechanical dysfunction.  Structural leg length inequalities may require the use of a heel lift. Patients with a loss of the longitudinal arch of the foot would benefit from arch supports or orthotics.  

Medical co-management with muscle relaxants, steroids, trigger point injections or Botox may be considered for recalcitrant cases.  (17,31)  

1. Yeoman W. The relation of arthritis of the sacroiliac joint to sciatica. Lancet. 1928;ii:1119-22.
2. Williams PL, Warwick R. Gray's Anatomy. 36th ed. Philadelphia, Pa: WB Saunders Co; 1980.
3. Papadopoulos EC, Khan SN. Piriformis syndrome and low back pain: a new classification and review of the literature. Orthop Clin North Am. 2004;35:65-71.
4. Pace JB, Nagle D. Piriformis syndrome. West J Med. 1976;124:435-439.
5. Beason LE, Anson B.J. The relation of the sciatic nerve and its subdivisions to the piriformis muscle. Anat Record. 1937;70:1-5.
6. Pecina M. Contribution to the etiological explanation of the piriformis syndrome. Acta Anat (Basel). 1979;105:181-187.
7., retrieved 10/13
8. Foster MR. Piriformis syndrome. Orthopedics. 2002;25:821-825
9.  Travell J, Simons D. Myofascial Pain and Dysfunction, Vol 2. Williams and Wilkins 1992.  pp 186-214
10. Magee DJ. Orthopedic Physical Assessment. 3rd ed. Philadelphia, Pa: WB Saunders Co; 1997.
11. Chaitow L. Soft Tissue Manipulation: A Practitioner's Guide to the Diagnosis and Treatment of Soft-Tissue Dysfunction and Reflex Activity. 3rd ed. Rochester, Vt: Healing Arts Press;1988
12. TePoorten BA. The piriformis muscle. J Am Osteopath Assoc. 1969;69:150-160
13. Meknas K, Christensen A, Johansen O. The internal obturator muscle may cause sciatic pain. Pain. 2003;104:375-380.
16. DiGiovanna EL, Schiowitz S, Dowling DJ, eds. An Osteopathic Approach to Diagnosis and Treatment. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins;2005 17. Boyajian-O'Neill, LA.; McClain, RL.; Coleman, MK.; Thomas, PP. (Nov 2008). "Diagnosis and management of piriformis syndrome: an osteopathic approach.". J Am Osteopath Assoc 108 (11): 657–64.
18. Magee DJ. Orthopedic Physical Assessment. 3rd ed. Philadelphia, Pa: WB Saunders Co; 1997.
19. Beatty RA. The piriformis muscle syndrome: a simple diagnostic maneuver. Neurosurgery. 1994;34:512-514.
20. Fishman LM, Dombi GW, Michaelsen C, Ringel S, Rozbruch J, Rosner B, et al. Piriformis syndrome: diagnosis, treatment, and outcome—a 10-year study [review]. Arch Phys Med Rehabil. 2002;83:295-301.
21. Benson ER, Schutzer SF. Posttraumatic piriformis syndrome: diagnosis and results of operative treatment. J Bone Joint Surg Am. 1999;81:941-949.
23. Fishman LM, Schaefer MP. The piriformis syndrome is underdiagnosed. Muscle Nerve. 2003;28:646-649.
25. Grant JH. Leg length inequality in piriformis syndrome. J Am Osteopath Assoc. 1987;87:456
26. Prather H. Sacroiliac joint pain: practical management. Clin J Sport Med. 2003;13:252-255. 
28. DiGiovanna EL, Schiowitz S, Dowling DJ, eds. An Osteopathic Approach to Diagnosis and Treatment. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins;2005 29. Mayranda N, Fortin J, et al. Diagnosis and Management of Posttraumatic Piriformis Syndrome: A Case Study Journal of Manipulative and Physiological Therapeutics Volume 29, Issue 6, July–August 2006, Pages 486–491
30. Steiner C, Staubs C, Ganon M, Buhlinger C. Piriformis syndrome: pathogenesis, diagnosis, and treatment. J Am Osteopath Assoc. 1987;87:318-323.
31. van Tulder MW, Scholten RJ, Koes BW, Deyo RA. Nonsteroidal anti-inflammatory drugs for low back pain: a systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine. 2000;25:2501-2513.
32. Iwanaga J. et al. The Majority of Piriformis Muscles are Innervated by the Superior Gluteal Nerve. Clin Anat. 2018 Nov 8. doi: 10.1002/ca.23311. [Epub ahead of print] 



#ICSClinical #ICSClinicalDiag

Membership Software Powered by YourMembership  ::  Legal