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This article explores and reviews the controversies
surrounding piriformis syndrome (PS) with respect to diagnosis,
investigation and treatment. While some authors have argued
that PS is analogous to other well accepted compression
neuropathies such as carpal tunnel syndrome, there is a wide
spectrum of opinions concerning the diagnosis. These range
from the belief that cases of true piriformis-induced entrapment
exist but are rare,1-5 to strongly held skepticism regarding the
piriformis muscle’s causative role.6,7 Silver and Leadbetter7
reported on a survey of 75 U.S. physiatrists and found only 72%
were confident that PS exists. Moreover, 55% felt that the
disorder was over-diagnosed, while 38% felt it was under-
diagnosed. Still other authors have argued that the syndrome is a
symptom complex and represents a myofascial pain disorder
rather than an entrapment neuropathy.2,8-10
Though many contrasting definitions exist, PS may be
defined as a neuromuscular disorder that is presumed to occur
when the sciatic nerve is compressed or involved at the level of
the piriformis muscle. It has been further subdivided into
primary and secondary forms,11,12 with primary PS comprising of
cases in which sciatic nerve entrapment occurs because of some
intrinsic abnormality within the muscle itself (for example
anomalous anatomy),13 while secondary PS is caused by direct,
often blunt trauma to the piriformis muscle.
Stewart14 has attempted to bring more consistency to the
subject by suggesting diagnostic criteria modeled upon
ABSTRACT: Piriformis Syndrome (PS) is an uncommon, controversial neuromuscular disorder that is
presumed to be a compression neuropathy of the sciatic nerve at the level of the piriformis muscle (PM).
The diagnosis is hampered by a lack of agreed upon clinical criteria and a lack of definitive
investigations such as imaging or electrodiagnostic testing. Treatment has focused on stretching,
physical therapies, local injections, including botulinum toxin, and surgical management. This article
explores the various sources of controversy surrounding piriformis syndrome including diagnosis,
investigation and management. We conclude with a proposal for diagnostic criteria which include signs
and symptoms, imaging, and response to therapeutic injections.
RÉSUMÉ: Le diagnostic et le traitement du syndrome piriforme : mythes et réalités. Le syndrome piriforme
est une maladie neuromusculaire rare et controversée dont l'étiologie présumée est une neuropathie de compression
du nerf sciatique au niveau du muscle pyramidal du bassin. Le diagnostic est entravé par le manque de consensus
concernant les critères cliniques diagnostiques et le manque d'études définitives probantes ayant recours à l'imagerie
ou à l'électrodiagnostic par exemple. Le traitement met l'accent sur les étirements, la physiothérapie, les injections
locales dont des injections de toxine botulique et la chirurgie. Cet article explore les différentes sources de
controverse entourant le syndrome du muscle pyramidal du bassin quant à son diagnostic, son évaluation et son
traitement. Nous concluons en proposant des critères diagnostiques incluant les signes et les symptômes, l'imagerie
et la réponse au traitement par injections.
Can J Neurol Sci. 2012; 39: 577-583
THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES 577
The Diagnosis and Management of
Piriformis Syndrome: Myths and Facts
T.A. Miller, K.P. White, D.C. Ross
From the Departments of Physical Medicine and Rehabilitation and Surgery, Schulich
School of Medicine and Dentistry, University of Western Ontario, London, Ontario
Canada.
RECEIVED APRIL 11, 2011. FINAL REVISIONS SUBMITTED APRIL 4, 2012.
Correspondence to: Thomas A. Miller, Schulich School of Medicine and Dentistry
University of Western Ontario, St. Joseph’s Health Care, Room 066, 21 Grosvenor
Street, London, Ontario, N6A 1Y6, Canada. Email: tmiller@uwo.ca.
REVIEW ARTICLE
Wilbourn’s15 classification of thoracic outlet syndrome.
Utilizing these criteria, he describes four distinct clinical
subtypes of PS (1) proximal sciatic neuropathies (2) neurogenic
PS (3) posttraumatic PS and (4) non specific PS. The five
components of diagnostic criteria are 1) signs and symptoms
2) electrodiagnostic findings 3) imaging 4) findings at surgery
and 5) response to surgical decompression. To date, no clinical
studies have confirmed the usefulness of this classification and
in particular, whether patients diagnosed by these criteria
respond in a predictable way to treatment.
Other studies report varying incidence of PS (8% to “rare”) in
patients presenting with low back/buttock pain.2-5,16-23 Many of
these studies are hampered by a retrospective design and are
weakened by a lack of uniform inclusion criteria. Due to
insufficient data, it is difficult to re-classify patients in these
studies using Stewart’s14 criteria. It is not feasible to utilize
statistical techniques such as meta-analysis to bring clarity to
treatment outcomes.
The diagnosis of PS remains difficult and controversial.
Review of this subject is hampered by a lack of standardized and
accepted diagnostic criteria, making objective, rigorous
comparison of different syndromes impossible. It is hoped, that
upon review of this article, the reader will have an appreciation
of these controversies and an enhanced ability to assess and treat
patients presenting with symptoms suggestive of piriformis
syndrome.
Clinical Anatomy
Understanding the manifestations of piriformis-induced
entrapment requires familiarity with the anatomy of the muscle
and surrounding structures. The piriformis muscle originates at
levels S2-S4 on the ventrolateral aspect of the sacrum, and
inserts into the piriform fossa of the greater trochanter.24 It is
innervated by a nerve that originates in the S1 and S2 segments.
However, considerable variation exists, with the S2 and S3 nerve
roots said to pass through the muscle in some symptomatic
patients,13 and in a large percentage of asymptomatic live
controls25 and cadavers.26,27 The muscle’s main functions are 1)
to externally rotate the thigh and 2) to abduct the thigh when the
hip is flexed.11,22,24 It also can be a weak hip flexor.
Clinical Findings
Due to its location within the sciatic notch and relative to the
sacral nerve roots, symptoms that are said to be characteristic of
PS are buttock pain which radiates into the ipsilateral thigh and
leg.28,29 Pain may be exacerbated by prolonged sitting, walking,
walking up inclines, and certain other movements.28 In a recent
review, Hopayian et al29 found reported incidences of buttock
pain, low back pain and exacerbation of symptoms due to sitting,
to occur in 95%, 63% and 97% of the population respectively.
Estimates of dyspareunia frequency were unreliable in their
review.
To diagnose PS, studies of the usefulness and frequency of
positive signs/symptoms on physical examination are hampered
by the absence of a gold standard. Physical signs however, may
be grouped into those which are generally positive for sciatic
THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES
578
(1)
There is no convincing evidence that the piriformis is anything more than a rare to very rare cause of sciatic nerve entrapment
(2)
The evidence that exists suggesting otherwise is based upon flawed studies and/or reasoning
(3)
Studies on patients who have undergone surgery for other reasons, as well as on cadavers, have demonstrated that piriformis-
induced sciatic nerve compression is either uncommon or highly non-specific
(4)
Electrophysiologic and imaging studies suggesting pathology generally are non-specific and, consequently, potentially
misleading
(5)
Numerous other causes of the symptoms are at least as likely
(6)
The label ‘piriformis syndrome’ is therefore misleading, and should be changed to a more general term that does not implicate
any particular anatomic structure
(7)
Injections and surgical manipulations of the piriformis muscle are being performed too commonly and usually without adequate
justification.
Table 1: Arguments against Piriformis Syndrome
(1)
Piriformis syndrome is a reasonable explanation for at least a significant proportion of the vast majority of patients with
sciatic-like symptoms whose pain is not explained by other, more accepted diagnoses
(2)
The anatomic location of the piriformis muscle corresponds exactly with the area of focal tenderness observed in these
patients.
(3)
The course of the muscle relative to the sacral nerve roots explains the results of a host of provocative tests that often
are positive in these patients
(4)
A variety of imaging and neurodiagnostic tests now confirm the presence of piriformis pathology
(5)
Numerous patients have responded very well to either focal injections or surgical manipulation of the piriformis,
thereby implicating it as the cause of symptoms in those cases.
Table 2: Arguments for Piriformis Syndrome
nerve “irritation”, and those which are thought to be more
specific to PS. Of the former, the more common physical signs
include limited straight leg raising, a positive Lasègue sign,
diminished ankle and/or hamstring reflexes and motor weakness
in the L4-S1 myotomes.
While positive findings on physical examination of an
individual patient are indicative, the true sensitivity and
specificity of any one or combination of these signs remains
undetermined.9,14,28,30-32
Physical findings thought to be more specific for PS include
external tenderness over the sciatic notch, or tenderness of the
piriformis muscle on either rectal or vaginal examinations.
Three eponymous tests are also suggestive of PS when positive:
1) the Freiberg test (forceful internal rotation of the hip with the
patient supine), 2) the Pace test (reproduction of buttock pain
with resisted hip abduction), and 3) the Beatty test (reproduction
of buttock pain with abduction of the thigh against gravity with
patient in lateral decubitus position). Exacerbation of pain in the
“FAIR” position (affected hip flexed, adducted and internally
rotated) is also a suggestive sign.
Diagnostic Imaging
Diagnostic imaging is invaluable in ruling out other causes of
sciatic nerve irritation such as lumbar disk disease and
radiculopathy, however, controversy exists as to the value of
imaging modalities to document/confirm the presence of
piriformis-related nerve root entrapment.
Although computed tomography may be useful for excluding
pathologies such as hematoma and pelvic tumours, it is not
generally useful in diagnosing PS.9Magnetic resonance imaging
(MRI) and MR neurography (MRN) have been utilized in a
number of studies to diagnose PS,33-36 yet these studies are
limited to case reports in which specific atypical anatomy was
confirmed at time of surgery. In contrast to this, Sayson37 and
Barton28 found pre-operative MRI failed to diagnose atypical
anatomy that was found intra-operatively. Further undermining
the significance of positive findings on MRI reports, is the study
by Russell et al25 who examined the piriformis muscle and
sciatic nerves in 100 patients who did not have symptoms of PS.
Findings showed that almost one in five subjects had greater
than 3mm of asymmetry in the size of their piriformis muscles,
with a maximum of 8mm, and the percent of nerve roots that
traversed the muscle was < 1% at S1, but 95% and 97% at S2
and S3, respectively. The S4 root was located below the muscle
in 95% of cases.
Magnetic resonance neurography is a relatively new
technique that was developed specifically to enhance the
imaging of nerves.38-40 Filler et al38 defined MRN as “tissue-
selective imaging directed at identifying and evaluating
characteristics of nerve morphology: internal fascicular pattern,
longitudinal variations in signal intensity and calibre, and
connections and relations to other nerves or plexuses.” Its ability
to identify peripheral nerve pathology has been documented
from numerous body sites, including the neck, back, pelvis and
extremities.38
In a widely known study, Filler et al40 utilized MRN to
prospectively investigate 239 patients with sciatica-like pain, in
whom either standard testing had failed to yield a diagnosis or
who had a failed lumbar disk surgery. Results showed that 67%
of this group were diagnosed with PS. Using a validated
outcomes scale (for lumbar disc surgery), 76% experienced a
good or excellent outcome after piriformis surgery. Due to the
specific findings, this study has been cited as validating PS as a
true clinical entity. Tiel5however, disagrees with Filler’s40
conclusions citing methodological and technical problems.
As Tiel5and Stewart14 have both pointed out, there is,
however, the inherent dilemma of tautology, using treatment
response as the standard for diagnosis given the absence of any
way to reliably confirm the diagnosis of PS. In essence, it creates
a self-fulfilling and highly-convenient prophesy where patients
who recover had the condition we thought they had. Moreover,
as Filler41 argues, the dramatic and prolonged response seen in
the majority of patients who had failed all prior attempts at
treatment and were treated by guided injection, strongly
implicate the piriformis as being somehow involved in the pain
mechanism. A critical analysis of the 239 patients with radiating
leg pain revealed that roughly half of the cohort (46%) had been
diagnosed with failed back surgery syndrome, i.e. what is often
referred to as the poorly understood condition of post
discectomy sciatica.40 Similarly, it is difficult to reconcile that
15% (24 patients) of the 162 patients who had the ultimate
diagnosis of PS, had complete relief after a single diagnostic
injection. This is difficult to appreciate given the underlying
potential pathophysiology.
Electrodiagnostic Testing
Electrodiagnostic testing is frequently normal in patients with
a clinical diagnosis of PS. It is very useful in ruling out other
causes with similar symptoms such as radiculopathy, focal
LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES
Volume 39, No. 5 – September 2012 579
Figure: The Anatomy of the Sciatic nerve, piriformis muscle, and
surrounding structures.
entrapment neuropathy, and/or a sciatic nerve palsy. Perhaps the
first report using electromyelogram (EMG) to diagnose PS was
from Kipervas42 in 1976. In the English language literature,
Synek43 in 1987 was the first to write about using
electrophysiologic studies for this purpose, reporting the
detection of short latency somatosensory evoked potentials in
four patients. One of the patients had PS while the other three
had spondylopathic cervical radiculopathy, meralgia
paraesthetica, and allodynia secondary to a femoral nerve injury.
The patient with PS occurred after a fall on a concrete surface,
and she demonstrated a sciatic nerve injury with clinical findings
of weakness and sensory loss that correlated with the
electrophysiology, and axonal loss and denervation on needle
EMG, as well as abnormal motor, sensory and H reflex studies.43
This, in our opinion, is a traumatic sciatic nerve injury at the
level of the piriformis muscle, and not Piriformis syndrome per
se. Benson and Schutzer44 reported abnormal EMG findings in
the distribution of the inferior gluteal nerve and the tibial and
peroneal divisions of the sciatic nerve in six of eight patients
who were later shown to have adhesions between the piriformis
muscle, sciatic nerve and the roof of the greater sciatic notch.
They suggested that these findings confirmed extra pelvic
compression of the sciatic nerve. No specific needle EMG or
further information regarding their EMG findings was provided.
In 1990, Chang and Lien45 reported on the comparison of
EMG versus spinal nerve stimulation in patients with L5 or S1
radiculopathies. They found that in 17 patients with objective
clinical evidence of radiculopathy including a neurological
deficit, the EMG was abnormal in 10 (59%), whereas amplitude
and area differences in spinal nerve stimulation were noted in 16
(94%) and 12 patients (71%), respectively. More recently, Chang
et al46 measured motor nerve conduction velocity using magnetic
stimulation in the sciatic nerve in patients who met all three
criteria for diagnosis proposed by Fishman et al47 (sciatica or
gluteal pain in the FAIR position, focal tenderness in the sciatic
notch and a positive Lasègue sign). They detected significant
slowing of motor nerve conduction velocity in the gluteal
component of the L5 root (L5 root to gluteal fold) versus healthy
controls, whereas there was no difference in CMAP amplitude
recording from the tibialas anterior (TA) or gastrocnemius.
Looking specifically at the use of electrodiagnostic testing in
patients with piriformis syndrome while using an epidural
electrode positioned at S3-4, Nakamura et al48 recorded action
potentials from the cauda equina in two patients with piriformis
syndrome symptoms. Recording was completed with the hip and
knee fully extended, the hip flexed and then the hip both flexed
and internally rotated in order to stretch the piriformis muscle
and increase its compressive effect upon the sciatic nerve. They
detected a 30% decrease in amplitude in the piriformis-stretch
position on the symptomatic side, versus just a 10% decrease in
the other two hip positions on the contralateral side. Similarly,
Fishman et al47 documented significant prolongation of both the
posterior tibial and peroneal H-reflexes in symptomatic patients
whose hips are in the FAIR position (flexed, adducted and
internally rotated), and noted that when clinical criteria and
response to treatment were used to define it, a more than three
standard deviation increase (specific for the condition) was
found 83% of the time. Interestingly, the results of these last two
studies47,48 coincide with the results of a study on ten cadavers,26
in which the FAIR or piriformis “stretch” position resulted in
narrowing of the infra-piriformis foramen, the sciatic nerve
being closer to the ischial spine of the hip, and an increase in the
angle between the sciatic nerve and the transverse plane. The
Fishman studies are the only ones in the current literature to
demonstrate abnormalities and prolongation in the FAIR
position of the H-reflex.32,47 This conclusion must be treated
with caution, as a critical review of the data in this non-standard
diagnostic test suggests that the data does not make intuitive
sense. As such, replication in another setting is required but most
importantly must be done in a standardized fashion in patients
with an established set of agreed upon diagnostic criteria in order
for implementation into electrophysiological laboratories. The
H-reflex itself requires further discussion. Most electro-
physiological laboratories perform H-reflex from the soleus or
gastrocnemius and there are normative and side-to-side
comparison data available. There is no such data available for
the peroneal H-reflex recording from the tibialis anterior,
peroneus longus or extensor digitorum longus (EDL). The
original study by Fishman et al47 which describes this technique
has a number of significant flaws related to the onset latency of
the monosynaptic response. We have suggested that the H-reflex
is more sensitive as a diagnostic tool to amplitude than to a delay
in onset latency.49 The recording of H-reflexes with facilitation
is required for the tibialis anterior, peroneus longus or EDL and
is fraught with many technical difficulties. The motor control
literature would suggest that when using the H-reflex to
document motoneuron excitability, or when assessing
facilitation and inhibition, there are complex influences on the
activity dependent changes in the motor pathway.50,51 The effects
of hip joint angle on H-reflex excitability in humans suggests
that there are many important factors that may impact the
amplitude, with depressed H-reflex excitability with the hip
flexed.52 At best, this makes commenting on amplitude a
challenge and at worst, makes the H-reflex highly suspect as an
accurate diagnostic tool. Conceptually however, the idea of
obtaining a long latency response from a peroneal innervated
muscle makes sense but requires validation, in a clinical setting,
using the proposed criteria.
Electrodiagnostic testing requires proximal stimulation above
the piriformis muscle, with an attempt to demonstrate focal
slowing and or conduction block across the piriformis muscle.
This requires near nerve stimulation or root stimulation in the
prone plus FAIR positions in order to reproduce symptoms. This
technique has not been published nor is it available in most
standard electrodiagnostic laboratories. In our opinion, the
results of the Chang et al study,46 requires further study.
Proposed EDX Criteria in evaluating patients with Sciatic Nerve
Injury/ Palsy(*):
1. Standard Motor and Sensory studies in the lower limb
bilaterally with a > 50 % reduction of CMAP and/or SNAP
amplitude with side-to-side comparison
2. Greater than 1 msec difference between sides of Soleus H-
reflex latency
3. Evidence of axonal loss in muscles innervated by the sciatic
nerve on needle EMG of muscles below the piriformis
muscle, and paraspinal muscle EMG must be normal to
exclude a radiculopathy
THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES
580
*The term palsy is an old fashioned word and strictly speaking
means muscle weakness. As such, a nerve cannot suffer a palsy.
This term is often used/misused when discussing nerve damage.
As stated above further research is needed to determine the
side-to-side differences of H-reflexes from the soleus and
peroneus muscles in various postions e.g. FAIR. Furthermore,
electrophysiological studies are providing important and
objective neurophysiological information about clinical
conditions that may mimic PS, not diagnose it.
Treatment of Piriformis Syndrome
Initial non-operative treatment typically consists of
medications (non-steroidal anti-inflammatory drugs (NSAID),
muscle relaxants, other medications effective in neuropathic pain
such as pregabalin or gabapentin) and physiotherapy.
Physiotherapy concentrates on piriformis stretching, and
isometric strengthening. Therapists often use the FAIR position
described above in education and treatment. However, there have
been no reported studies in physiotherapy that compare one
technique to the other. The technique of post-isometric relaxation
is a common and helpful addition as are the stretching techniques
of reciprocal inhibition.53,54
Local injection therapy is a mainstay and may be both
diagnostic and therapeutic. Injections may include local
anaesthetic, steroid, both a local anaesthic and steroid or, more
recently, botulinum toxin (BTX). Fishman et al32 studied 353
patients with a diagnosis of PS (using standardized criteria) with
a combination of physiotherapy and a local injection of lidocaine
and triamcinolone. Results showed that 79% of patients
experienced at least a 50% reduction in pain at an average of 16
months post-treatment. Different studies report a variety of
methods to guide injections including imaging,18,20,40,55,56
fluoroscopy16,57,58 and EMG.21,32,59,60
In terms of prolonged pain relief, some of the most
encouraging results are found with the use of botulinum toxin.
Lang21 reported on 20 patients treated with 5000 units of BTX-
B and noted that 95% of patients reported fair to excellent
improvement in pain. Fishman60 attempted to establish dose-
response curves for BTX-B in PS and concluded that 12,500
units was safe and most efficacious. Porta10 and Childers31 both
reported positive outcomes using BTX-A in PS. Childers31
inclusion and exclusion criteria would meet the proposed criteria
outlined below.
There are no prospective, randomized trials that use surgery
to treat PS. Rather, a number of small case studies report positive
results using non-validated outcome measures.41,44,61 Benson44
reported on 14 patients with post-traumatic PS that were treated
with piriformis tenotomy and sciatic neurolysis. Eight of the 14
patients underwent pre-operative EMG testing and of the eight
patients, six showed extra-pelvic compression of the sciatic
nerve. On a non-validated outcome scale, the study reported that
there were 11 excellent and 4 good results. Filler and
colleagues40 have described the use of surgical resection for PM
in 62 patients with piriformis syndrome who had not obtained
relief by local anaesthetic injections. They found 59% had an
excellent outcome and 4% showed no benefit. Both Tiel5and
Stewart4have criticized the conclusions of this paper.
Most surgeons treating patient(s) with symptoms suggestive
of PS require a reasonable yet unsuccessful period of
conservative treatment (i.e. physiotherapy, imaging and
electrodiagnostic findings) in order to rule out other causes of
sciatic nerve involvement. A brief yet consistent response to
injection with local anaesthetic and/or BTX may also be
involved. Utilization of these treatments may increase the
frequency of symptom improvement, however there are no
guarantees.
CONCLUSIONS
The diagnosis of PS remains controversial due to a lack of
definitive diagnostic criteria. Stewart’s4,14 suggestion to base the
diagnosis on a template previously utilized for thoracic outlet
syndrome (TOS) is reasonable but must be reviewed as the use
of such criteria to diagnose TOS has not completely stopped the
controversy of that diagnosis in the upper extremity. Papers such
as that of Hopayian29 are useful attempts to bring some clarity to
the diagnostic criteria.
In conclusion, from the perspective of the electromyographer,
there is a role for EMG, nerve conduction studies, and nerve
stimulation in the diagnosis and management of PS. The
specifics and magnitude of their roles however, must be tested
further within the confines of formal comparative clinical trials.
It appears at present that the most important aspect of
electrodiagnostic testing is for ruling out more common
conditions and evaluating the differential diagnosis (e.g.,
peroneal nerve entrapment, an L5 radiculopathy, or a sciatic
nerve palsy).
We do not feel that criteria are required for the entity
described by Stewart,4,14 as neurogenic or post-traumatic PS.
These are proximal sciatic neuropathies which can be
differentiated from the controversial entity known as PS. We
suggest that the following criteria be used to describe the non-
specific piriformis syndrome:
Proposed Criteria for the classification of Piriformis Syndrome
1. Buttock and leg pain made worse with sitting, stair climbing
and/or leg crossing
2. Pain and tenderness to palpation of the sciatic notch area
(piriformis muscle) and pain with increased PM tension
3. No evidence of axonal loss to the sciatic nerve on
electrophysiological testing
4. No evidence of abnormal imaging or other entity that could
explain the presenting features of sciatica (e.g.
radiculopathy, tumor, etc.)
5. Reduction of > 60% of buttock and leg pain with diagnostic
injection into the piriformis muscle under radiographic
imaging (Fluoroscopic or Ultrasound) and or EMG guidance
Given that a true gold standard for diagnosis is difficult to
establish, it is suggested that a positive outcome from standard
PS treatments on a prospective trial would validate the criteria.
This analysis would be similar to how other syndromes are
evaluated and studied and will include the development of
diagnostic criteria. We are proposing that as in the classification
and diagnosis of rheumatic diseases, a set of criteria can be used
as guidelines for classification of disease syndromes, for the
purpose of patients taking part in clinical investigation. One
LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES
Volume 39, No. 5 – September 2012 581
must be cautious in such application because criteria can be
developed with several different purposes in mind, e.g. to
classify a group of patients, diagnose individual patients, or to
estimate disease frequency and or to determine prognosis. In
this case we are suggesting the above as diagnostic criteria, as a
way to select patients for future therapeutic trials.
ACKNOWLEDGEMENTS
The authors thank Heather Askes for assistance with the
manuscript.
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