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 Table of Contents  
Year : 2021  |  Volume : 8  |  Issue : 4  |  Page : 7-14

Piriformis Syndrome and Variants – A Comprehensive Review on Diagnosis and Treatment

1 Department of Neurosurgery, Institute of Neurosciences, Apollo Proton Cancer Centre, Apollo Specialty Hospital, Chennai, Tamil Nadu, India
2 Department of Neuroradiology, Institute of Neurosciences, Apollo Proton Cancer Centre, Apollo Specialty Hospital, Chennai, Tamil Nadu, India

Date of Submission19-Oct-2021
Date of Acceptance03-Nov-2021
Date of Web Publication24-Dec-2021

Correspondence Address:
Anil Pande
Senior Consultant Neurosurgeon, Department of Neurosurgery, Institute of Neurosciences, Apollo Speciality Hospitals, Apollo Proton Cancer Center, Chennai Adjunct Professor of Neurosurgery, Apollo Hospital Education and Research Foundation, Chennai, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/joss.joss_19_21

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Piriformis syndrome (PS) is an entrapment neuropathy caused by the compression of the sciatic nerve by the piriformis muscle (PM). PS pain is described as deep, aching type with tingling and numbness, radiating from the gluteal and perineal area down to the lower limb. Rarely, this nondisc sciatica can present with associated pudendal neuralgia due to added pudendal nerve (PN) Type 1 entrapment. Women are much more likely to develop PS than men. The diagnosis is difficult in the past due to the lack of standardized diagnostic tests. Cases can present with symptoms attributable to PS. They report sciatica, paraesthesia, numbness, and episodic sharp pain in the perineal area, which is exacerbated on prolonged sitting, standing, and walking. Magnetic resonance imaging (MRI) scans of lumbosacral spine and lumbosacral plexus are usually normal. Their clinical symptoms can be misdiagnosed with urinary tract infection. The treatment with antibiotics has no effect on pain and paraesthesia. The urine cultures are negative, consultation with a neurosurgeon is requested due to associated sciatic pain. The compression of sciatic nerve and PN by PM is rare but possible. These symptoms can be misdiagnosed and mistreated. Nondisc sciatica is no longer a rarity with the easy availability of MRI for most patients with lumbago and sciatica. The awareness of possible association of Type 1 pudendal neuralgia with PS is necessary.

Keywords: Nondisc sciatica, pelvic sciatic nerve entrapment syndromes, perineal paraesthesia, piriformis syndrome, pudendal nerve, pudendal neuralgia, pyriformis pudendal syndrome, sciatic nerve

How to cite this article:
Pande A, Gopinath RA, Ali S, Adithyan R, Pandian S, Ghosh S. Piriformis Syndrome and Variants – A Comprehensive Review on Diagnosis and Treatment. J Spinal Surg 2021;8:7-14

How to cite this URL:
Pande A, Gopinath RA, Ali S, Adithyan R, Pandian S, Ghosh S. Piriformis Syndrome and Variants – A Comprehensive Review on Diagnosis and Treatment. J Spinal Surg [serial online] 2021 [cited 2022 Aug 11];8:7-14. Available from: http://www.jossworld.org/text.asp?2021/8/4/7/333615

  Introduction Top

In 1928, Yeoman reported the first case of sciatic pain related to piriformis muscle (PM).[1] Later, Mixter and Barr[2] in 1934 linked sciatic pain to the rupture of intravertebral disc with involvement of spinal roots. In 1947, Robinson first coined the term piriformis syndrome (PS)[3] for patients presenting with pain at the sacroiliac joint, greater sciatic notch and PM that is radiating in nature and causes difficulty in walking. PS, a nondisc sciatica remained till recently a controversial clinical syndrome with claims that it was over diagnosed[4] and many others emphasizing its elusive and delayed diagnosis.[5],[6],[7] Magnetic resonance neurography (MRN) currently allows for objective diagnostic criteria for this relatively rare nondisc sciatica.[8]

PS is classified under entrapment neuropathies, caused by compression of the sciatic nerve between the hypertrophied or inflamed PM and bony pelvis. Rarely, ipsilateral PM atrophy may be seen.[9] Kulcu and Naderi[10] list conditions such as lumbar radicular herpes zoster, lumbar nerve root Schwannoma, lumbar instability, facet hypertrophy, Ankylosing spondylitis, Sacroillitis, sciatic neuritis, intrapelvic mass, and Coxarthrosis that can give rise to nondisc sciatica. PS forms a significant percentage of these cases [Table 1].
Table 1: Causes of nondisc sciatica

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The prevalence of PS ranges from 6% to 17.2% of patients with back pain.[6],[11],[12] Of 750 cases referred to a pain clinic, 45 patients were diagnosed with PS using the Freiberg and pace tests.[13] PS is common in women aged 30–40 years than men with a ratio of 3-1[6] with Pace and Nagel noting that it was six times more frequent in women.[13] Women show higher susceptibility to PS than men due to the wider quadriceps femoris angle in the os coxae and due to hormone changes during pregnancy, where muscles around the pelvis, including PM, tense up to stabilize the area for birth.[6] Radiating sciatic pain is the result of neuromuscular conflict due to the close proximity of the PM and the sciatic nerve at the sciatic notch.[9] Most prevalent symptoms of PS is pain starting from the hip and lower back region, descending down the posterolateral aspect thigh radiating till the knee, ankle and heel and mostly, not reaching the toes. Patients complain about numbness, tingling and tenderness, generally on one side, which is aggravated by prolonged sitting and walking.[6],[14] Multiple dermatomes involvement with pain radiation to all toes is seen in PM, whereas pain in (L5) medial toes and (S1) lateral toes is seen in disc sciatica.[9]

Entrapment of the sciatic nerve can be seen between greater sciatic notch and ischial tuberosity. The other sites are at lower ischial tunnel, the hamstring muscle attachment, and quadratus femoris muscle. Posttraumatic PS[15] and bilateral PS caused by entrapment between the piriformis and hypertrophied hip joint capsule after arthroplasty have been reported.[16] Multipartite and accessory piriformis variants such as a split piriformis traversed by a split sciatic nerve are seen and can predispose to entrapment.

Pudendal nerve (PN) entrapment with the sacrotuberous and sacrospinous ligaments at the level of ischial spine, and at Alcock's canal (Alcock's syndrome) results in pudendal neuralgia.[9],[17] PN occurs in association with PS due to PN co-entrapment at medial inferior border of the PM at the greater sciatic notch. PN compression by PM hypertrophy results in associated pudendal neuralgia symptoms (allodynia, paraesthesia, and pain in perineal and perianal area).

The diagnosis of PS and other nondisc sciatica is difficult.[7],[18],[19] The straight leg raising test is usually negative. Resisted abduction or adduction of flexed internally rotated thigh triggers symptoms. Beatty introduced a test which caused contracture of the pyriformis rather than stretching which reproduces the pain reliably.[20] Most commonly used diagnostic tests in clinics for the diagnosis of PS are flexion adduction internal rotation and the Beatty test.[20] Solheim's, Pace and Nagel, Freiberg[21] and Laseguesigns are useful [Table 2].
Table 2: Common signs elicited in ps patients and tests conducted

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  Case Scenarios Top

A 35-year-old obese (body mass index [BMI] 25.8) female presented with a 3-year history of low back pain and left-sided sciatic pain associated with stabbing pain, paraesthesia, burning sensation. She was misdiagnosed with urinary tract infection (UTI) and referred to an urologist who suspected uric stones and associated urethral spasms. Cystoscopy was performed, a urethral stricture was identified, urethroplasty done 1 month before presentation with persistence of symptoms. The patient had no focal motor or sensory deficits. Pace and Nagel and Lasegue tests, Freiberg and Solheim'ssigns were positive. Her magnetic resonance imaging (MRI) spine was normal.

A 35-year-old diabetic woman (BMI 32) presented with a 4-year history of severe low backache, right sciatica with perineal pain and paraesthesia after 2 years of her second delivery. The persistency, intensity, and severity of perineal pain were extremely high, with a Verbal Numerical Rating Scale of 9 for pain. Four different gynaecologists misdiagnosed her as UTI repeatedly. Cystoscopy revealed normal urinary tract without any structural anomaly. She was referred to a psychiatrist for the evaluation of psychogenic pain, and the assessment results were negative. She was referred to us. Her neurological examination and MRI was normal.

A 31-year-old hypothyroid female was admitted with low back pain, bilateral sciatica pain along with perineal paraesthesia of 45 days duration. Her MRI of lumbosacral spine and plexus was essentially normal. Her neurophysiological examination revealed a L4-5 radiculopathy. She gave a history of abortion and weight gain of about 10 kg a year. She was initially suspected to have an UTI. Later, she was referred to us.

All were prescribed carbamazepine/gabapentin and advised posture correction, reduce weight, and perform stretching and strengthening exercises along with spinal flexion and extension exercises. They had relief of sciatic and pudendal neuralgia.

  Discussion Top

Nondisc sciatica is a large group of heterogeneous etiologies [Table 1] that commonly involves the sciatic nerve, many are very rare, for example, venous varix.[22] These are frequently misdiagnosed when compared with common disc sciatica. Lumbar MRI is inconclusive in an estimated 1 million cases.[23] The diagnosis of PS has been termed controversial,[5],[18] but recent literature is replete with evidence that it is probably underdiagnosed, undertreated, and underreported.[19] PS is an entrapment neuropathy caused by the compression of the sciatic nerve alone or with its branches by hypertrophy, inflammation, injury or irritation of PM and entails a number of symptoms such as low back, gluteal and perineal pain, numbness, and paraesthesia.

PS may be caused the hypertrophy, anatomical variations of PM and the sciatic nerve and intrinsic pathology of the PM itself, for example, myositis ossificans of PM[24] and intra-piriformis lipoma[25] among others.

Anatomical correlation

PM originates from the anterior surface of S2–S4 sacral vertebrae, the superior margin of the greater sciatic notch and the sacrotuberous ligament. PM exits the pelvis in the greater sciatic foramen and becomes tendinous, and then attaches to the superior portion of the greater trochanter [Figure 1]. PM acts as a lateral rotator, weak abductor, and weak flexor of the hip, providing postural stability during standing and walking.
Figure 1: Diagram showing relationship of the piriformis muscle and sciatic and pudendal nerve. a= Pyriformis, b= Sciatic Nerve, c= Posterior Femoral Cutaneous Nerve, d= Pudendal Nerve, e= Nerve to Obturator Internus

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Anomalies and variations in the anatomy of PM commonly range from 1.5% to 38.8%.[26],[27] Beason and Anson classification[27],[28] in 1937 built on the earlier work of Parson and Keith in 1896 is as follows:

  • Type A. Undivided nerve below a undivided muscle
  • Type B. Division of the nerve between and below an undivided muscle
  • Type C. Division of the nerve below and above an undivided muscle
  • Type D. Undivided nerve between heads
  • Type E. Division between and below divided heads
  • Type F. Undivided nerve above an undivided muscle.

The sciatic nerve leaves the greater sciatic foramen beneath the PM (96%). The sciatic nerve is either undivided in relationship to PM. Division into a transiting fibular branch and a tibial branch that courses above or below the PM is possible. The sciatic nerve in 22% pierces and/or splits the PM (Type D) predisposing these individuals to PS.[29] The sciatic nerve crossing over the PM is very rarely seen. Varenika et al.[30] found anatomical variations in sciatic nerve course in the relationship to the PM in 12%–20% of MRI scans evaluated. Conventional anatomical classification of PM with sciatic nerve is as follows:

  • Type 1: sciatic nerve passes below the PM (observed in 87%)
  • Type 2: one division passes through the PM and another below it (observed in 13%)
  • Type 3: sciatic nerve exits above the PM (noted rarely).

Chen[31] reported release of entrapment in a bipartite PM by the dissection of the lower head. PS can involve the superior gluteal nerve, pudendal, posterior femoral cutaneous, and inferior gluteal nerves. PS may be associated with pudendal neuralgia, as PN exits the pelvis at the inferior aspect of PM. The muscle hypertrophy can compress the PN against the posterior edge of the sacrospinous ligament. Sometimes, reduced diameter of the greater sciatic notch due to posterior orientation of ischial spine is seen.[32] Spinner et al.[33] describe a case of PS, where, variant anatomy and peroneal nerve conflict with the PM were coexistent. The PN innervates the muscles of perineum and pelvic floor, the external anal sphincter and external urethral sphincter. In PN entrapment, PM spasms and sacral dysfunction stress the sacrotuberous ligament, which in turn entrap the PNs at the exit of the greater sciatic notch causing perineal pain and paraesthesia [Table 3].
Table 3: Nantes diagnostic criteria for pudendal neuralgia by pudendal nerve entrapment

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Entrapment of PN[9] can be classified into four major types depending on its location:

  • Type I – PN gets compressed at the level of PM (noted in 3.5% of cases)
  • Type II – Entrapment of PN occurs at the level of ischial spine (observed in 9% of cases)
  • Type III – Entrapment occurs in the Alcock's canal on the medial surface of obturator internus (noted in majority of cases)
  • Type IV – Entrapment occurs at its distal branches (noted in 9% of cases).

The anatomical relation of the PN to the sacrospinous and sacrotuberous ligaments could be a risk factor for pudendal compression. PM is attached to the anterior sacrospinous ligament and to the pelvic portion of the sacrotuberous ligament. As the tension increases within the PM, subsequent stretch on these ligaments narrow down the space between them. This results in the compression of the PN, resulting in additional pudendal neuralgia.

Obese individuals have excessive accumulation of lipids in adipose tissues, as well as in nonadipose tissues such as skeletal muscles. Increase in the bulk of PM, results in narrowing of the greater sciatic foramen size, which in turn leads to the compression neuropathy of the sciatic and PNs. Lumbar lordosis increases significantly with increasing BMI and trunk weight. With the hyper-lordosis, the sacrum tilts downward and forward. This may be associated with “rotational malalignment,” which refers to excessive anterior or posterior rotation in the sagittal plane in relation to the fixation of innominate bones. In a person with rotational malalignment, a posterior innominate rotation, with relative superior and anterior rotation of sacrum and posterior coccyx movement, separates the piriformis origin and insertion. When combined with medial rotation of the innominate, the tension within the PM causes further reduction of the available space beneath the muscle, through which the sciatic nerve and PN transverses through the greater sciatic foramen. Over a period of time, chronic increase in the piriformis tension along with the narrowing of outlet size results in PN compression. Other factors that can predispose are weight gain and ligament laxity.

Clinical features

The most common clinical presentation of PS include pain, paraesthesia and numbness radiating from lower back and gluteal area down to the thigh and leg and tenderness with palpation over the PM.[34] Pain is caused mainly due to the compression of sciatic nerve by PM. For some patients, palpable “sausage-shaped” mass is present in the gluteal area.

The symptoms include perineal and genital paraesthesia, constant burning, sensory loss, numbness, the areas as well as urinary and fecal incontinence.[32] Dyspareunia and male impotency have also attributed to piriformis compression of the PN and blood vessels. Similar clinical presentation of perineal pain in a male patient who was referred to family practitioners, urologists, neurologists, and psychiatrists over a long period of time, before eventually been diagnosed.[35] There has been limited literature on pudendal neuralgia associated with PS.


The diagnosis and even definition of PS have been reported to be difficult in the past[32],[36] due to the lack of standardized objective tests and definite pathophysiology to support the existence of this syndrome. A combination of medical history and physical assessment of the patient along with neurologic and radiologic testing are essential to make an accurate diagnosis. Using advanced radiography and neurophysiological tests, other pathologic conditions such as lumbosacral radiculopathies, intervertebral disc pathology, compression fractures, spinal stenosis, facet syndrome, primary sacral dysfunction, sacroiliitis, and trochanteric bursitis have to be ruled out and thus, narrow the differential diagnosis toward PS. A few pathologies may concurrently present with PS.[37] Banerjee[38] in an early report on sciatic nerve entrapment emphasised the importance of electrophysiology in diagnosis. Fishman and Zybert[39] used a delay in the H-reflex by internally rotating an adducted, flexed the affected leg to confirm the diagnosis electrophysiologically.

Ultrasound is being used to diagnose the PS, and both enlarged PM and sciatic nerves are seen compared with normal side. The sciatic nerve has decreased echo intensity and unclear perineurium[40] which in turn may be used to guide therapeutic injections.

Computed tomography (CT) and MRI scans evaluation was done to pick up the enlargement of PM and one of the early reports[41] was of a 27-year-old female where the PM enlargement was documented by CT and MRI reports with pudendal neuralgia, MRI of the spine and magnetic resonance neurography (MRN) with both 1.5 and 3 tesla machines are frequently used to confirm the diagnosis.[42] High-resolution 3 Tesla MRI and three-dimensional image acquisition along with novel fat suppression methods and improved coil designs allowing for state of the art MRN.

[Figure 2] shows diagnostic and therapeutic evaluation of PS.[8] In MRN studies, abnormal sciatic nerves are characterized by higher nerve to vessel SI ratios and abnormal and enlarged fascicular shape with increased T2 hyperintense signals. PM shows fatty infiltration, edema, and atrophy.[42] Sciatic nerve variants are classified usually according to the Beason and Anson classification and one large radiological study[43] found 19.2% variant anatomy. Lewis et al.[44] state that MRN, the best diagnostic procedure of choice, is proving that PS was being underdiagnosed in the past. MRN techniques using short-tau inversion recovery (STIR) sequences have made diagnosis both reliable and sensitive. Multiple qualitative and quantitative criteria of the sciatic nerve and the regional skeletal muscles (high nerve to vessel ratio SI ratios (cut-off value of 0.89), increased T2 hyperintensity and abnormal fascicular shape of nerve and increased fatty infiltration, edema, and atrophy of muscles) compared to the normal side are used to diagnose sciatic neuropathy.[45] Filler et al.[23] reported a 93% specificity and 64% sensitivity using MRI features such as PM asymmetry and sciatic nerve hyperintensity in distinguishing patients with PS. In another MRI study,[14] pyriformis asymmetry was common with up to 8 mm difference. The S1 root was seen above the PM in 99%, S2 was seen traversing in 75%, and S3 roots traverses the muscle in 97%.There was earlier no precise pathognomonic imaging, laboratory and electrophysiology criterion to detect the PN involvement. The diagnosis of PN entrapment in PS remains primarily clinical,[46] which results in frequent misdiagnosis and sometimes in unnecessary surgery.
Figure 2: Magnetic resonance imaging images (a- T2 axial, b- Coronal STIR, c- MR neurography) showing the anatomy of the structures around the piriformis muscle. Piriformis muscle (long arrow) is seen coursing through the greater sciatic foramen (left side in this magnetic resonance imaging), with sciatic nerve (short arrow), pudendal nerve vessels , nerve to obturator internus (x), inferior gluteal nerve-vessels (+) seen passing inferior to the piriformis muscle. Superior gluteal nerves (△) is seen passing through suprapiriform foramen

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Tiel did a critical review of the clinical features and treatment strategies of PS, in which he recommends be termed as nonlocalizing sciatica.[7]

Conservative treatment

The mainstay of treatment continues to be conservative.[11],[47] Initial conservative therapies include osteopathic manipulative treatment and physical therapy alone or in combination with pharmacotherapeutic options (anti-inflammatory drugs, analgesics, and muscle relaxants). Lessons learnt from pharmacological treatment of other neural conflict syndromes, especially trigeminal neuralgia allow for a significant relief with carbamazepine, baclofen, gabapentin, and pregabalin. These may be required for extended periods with other concurrent disease-modifying efforts.

Ultrasound, computed tomography, and magnetic resonance imaging scans-guided injections

For patients with persistent pain, more aggressive therapy such as local injection of anaesthetic and corticosteroid preparations were recommended, which in turn confirms the diagnosis through therapeutic success. Intervention by ultrasound,[48] CT and MRI-guided injections[49],[50],[51],[52] can confirm the diagnosis and be therapeutic too. Both steroid[37],[53] and botulinum toxin[12]-guided injections have been used. Recurrence of the pain may warrant repeat injections of bupivacaine hydrochloride or Botulinum toxin.


For rare cases of unrelenting severe pain, surgical decompression of the PM is an optional treatment.[54],[55] Freiberg[54] in 1937 pioneered surgical access to relieve symptoms. Minimal access surgery using electromyography and newly reported techniques to determine the compressive neuropathy has been proven successful in large-scale outcome studies.[9] Surgical management through decompression of the PN inferior to the PM may be indicated following failed conservative and pharmacological treatment.[35] Laparoscopic surgery involving decompression of the sacral plexus or resection of the PM has been shown to be effective partially. Minimal access surgery for pelvic entrapment of the sciatic nerve using an incision 3 cm superior medial edge of greater trochanter of femur with trajectory toward the piriformis tendon. Gluteal tendon incision placement of a minimally invasive self-retaining retractor separating gluteal muscle fibers to reach the prepiriformis fascia and underlying piriformis fat pad. Depending on the morphological variations of the femoral neck and trochanter height the piriformis can vary from a vertical to horizontal relationship to the sciatic nerve.

All three patients discussed here had higher BMI, contributing to increased bulk of PM. These patients were presented to the neurosurgical clinic mainly due to the sciatica pain, but were investigated by other specialities for perineal paraesthesia. The delay of diagnosis in our patients was due to the complexity of the urogenital symptomatology. These patients were repeatedly referred to gynecologists, urologists, nephrologists, and psychiatrists. They were repeatedly misdiagnosed and treated for UTI. After the consultation with a neurosurgeon for sciatic pain evaluation, these patients were diagnosed with PS along with sciatica. The perineal pain and paraesthesia were specifically due to the associated compression of PN.[46] These three case reports discuss the unusual clinical added symptomatology of pudendal neuralgia in patients with PS, suggesting that this could be a variant of PS. All three patients reported pain reduction and improvement in mobility with medical therapy and physical intervention.

  Conclusion Top

Nondisc sciatica is caused by many pathologies involving the sciatic nerve. PS is not so rare, also could be a causative factor of nondisc sciatica. Additional entrapment of PN can lead to perineal pain and paraesthesia. The sciatica and type 1 peudendal nerve compression can be undiagnosed or misdiagnosed as nonneural symptoms, as illustrated by these three cases. The clinical presentation of pudendal neuralgia symptoms in patients is an uncommon clinical variant of PS and may be termed the piriformis pudendal syndrome.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

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  [Figure 1], [Figure 2]

  [Table 1], [Table 2], [Table 3]


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