REVIEW
Piriformis syndrome: implications of anatomical variations,diagnostic techniques, and treatment options
Lindsey Cassidy • Andrew Walters •
Kathleen Bubb • Mohammadali M. Shoja •
R. Shane Tubbs • Marios Loukas
Received: 17 August 2011 / Accepted: 29 January 2012 / Published online: 12 February 2012
� Springer-Verlag 2012
Abstract Details of piriformis syndrome, including the
proper diagnosis and most effective form of treatment,
continue to be controversial. While the cause, diagnosis,
and treatment of piriformis syndrome remain elusive, many
studies have been conducted to investigate newly devel-
oped diagnostic techniques as well as various treatment
options for piriformis-induced sciatica. Despite the quan-
tity of literature, few studies have demonstrated statisti-
cally significant results that support one form of treatment
over another. Thus, despite the evidence supporting the
newer treatment methodologies for piriformis syndrome,
research should continue. It is important not only to eval-
uate treatment outcomes based on associated pain relief,
but also to investigate the functional and anatomical return
that patients experience from these studied treatments in
order to fully explore the most effective form of therapy for
piriformis syndrome.
Keywords Buttock � Piriformis � Sciatic nerve �Botulinum toxin � Back pain � Sciatica
Introduction
According to Fishman et al. [7], the term ‘‘sciatica’’ was
first introduced in the fifteenth century in Florence to
describe leg pain that was thought to originate at the
ischium. Long before sciatica could be explained by her-
niation of an intervertebral disk, Yeoman [27] attributed
sciatica to inflammation of the sacroiliac joint and nearby
piriformis muscle, both of which are anatomically related
to the sciatic nerve as it exits through the greater sciatic
notch [16, 26]. The term ‘‘piriformis syndrome’’ was first
used by Robinson in 1947 when he described the syndrome
as having six key characteristics: (1) a history of trauma or
direct fall to the buttock, (2) gluteal or sacroiliac pain
radiating down the leg that often limits ambulation, (3)
gluteal atrophy, (4) a palpable sausage-shaped mass, (5)
positive Lasegue sign, and (6) exacerbation with bending
or lifting [23]. Approximately a decade after Robinson, a
surgeon by the name of Freiberg developed a more succinct
set of criteria for defining piriformis-induced sciatica.
Freiberg’s three indications for piriformis-induced sciatica
included: (1) tenderness at the sciatic notch, (2) positive
Lasegue (straight leg raise) sign, and (3) improvement with
nonsurgical treatment [7]. Despite their attempts to accu-
rately identify the characteristics that exclusively define
piriformis syndrome, there are apparent problems with both
Robinson’s and Freiberg’s definitions. While Freiberg’s
criteria encompasses problems other than piriformis syn-
drome such as sacroiliac joint derangement and gluteal
injections, Robinson’s exacting list of characteristics
selects out a fraction of piriformis syndrome cases that are
identified clinically [7]. In reviewing the literature on pir-
iformis syndrome, sciatica and other conditions associated
with low back pain, it is apparent that there are still issues
of uncertainty and controversy relating to the proper
L. Cassidy � A. Walters � K. Bubb � M. Loukas (&)
Department of Anatomical Sciences, St. George’s University
School of Medicine, St. George’s, Grenada, West Indies
e-mail: [email protected]
M. M. Shoja
Division of Neurosurgery, University of Alabama,
Birmingham, AL, USA
R. Shane Tubbs
Pediatric Neurosurgery, Children’s Hospital,
Birmingham, AL, USA
M. Loukas
Department of Anatomy, Medical School Varmia and Mazuria,
Olsztyn, Poland
123
Surg Radiol Anat (2012) 34:479–486
DOI 10.1007/s00276-012-0940-0
diagnosis and most effective form of treatment for piri-
formis syndrome.
Anatomy
The piriformis muscle is conventionally described as
originating from the anterior surface of the S2–S4 sacral
vertebrae, the gluteal surface of the ilium near the posterior
surface of the iliac spine, and the capsule of the sacroiliac
joint [5, 10, 13]. The muscle runs laterally through the
greater sciatic foramen and inserts to the piriformis fossa at
the medial aspect of the greater trochanter of the femur.
The tendinous part of the muscle, passing through the
greater sciatic foramen, often blends with the tendons of
the obturator internus and the gemelli [11]. The piriformis
muscle functions as an external rotator of the hip joint
when the thigh is extended and as an abductor of the hip
joint when the thigh is flexed [11]. Typically, the gluteal
nerves, gluteal vessels, sciatic nerve, and the posterior
femoral cutaneous nerve pass below the piriformis muscle
[13]. The piriformis muscle is innervated by branches of
the L5, S1, and S2 spinal nerves [4]. More specifically, the
ventral rami of S1 and S2 join together to form the nerve to
the piriformis [11, 16]. The gluteus medius, gluteus mini-
mus, and tensor fasciae latae are all innervated by the
superior gluteal nerve, which arises proximal to the piri-
formis muscle, and is thus often spared in cases of piri-
formis syndrome [11]. There are six commonly described
anatomical relationships between the sciatic nerve and
piriformis muscle that were originally described by Beaton
and Anson [2]: (A) the sciatic nerve passing below the
piriformis muscle, (B) a divided sciatic nerve passing
through and below the piriformis muscle, (C) a divided
nerve passing above and below the muscle, (D) an undi-
vided sciatic nerve passing through the piriformis muscle,
(E) a divided nerve passing through and above the muscle,
or (F) an undivided sciatic nerve passing above the piri-
formis muscle [2, 18, 19]. In his review of multiple
cadaveric studies from the late 1800s until 2009, Smoll
[24] presented the overall reported incidence of these six
variations in over 6,000 dissected limbs. The first rela-
tionship A was found in 83.1% of limbs, whereas rela-
tionships B, C, D, E, and F occurred in 13.7, 1.3, 0.5, 0.08,
and 0.08%, respectively [24]. In approximately 12% of
cases, the common fibular and tibial divisions of the sciatic
nerve separate proximal to or at the level of the piriformis
muscle. The tibial nerve passes anterior or ventral to the
piriformis, and the common fibular nerve passes superfi-
cially dorsal to or through the muscle. It is not clear
whether these anatomic variations are responsible for or
contribute to the pathology of piriformis syndrome, as
some asymptomatic patients present with these variations
and some symptomatic patients do not [16]. To the best of
our knowledge, we were able to identify the six variations
as previously described as well as an additional one, a
subset of B (Figs. 1, 2, 3, 4, 5, and 6). In this variation, the
sciatic nerve appeared to pass below the piriformis muscle,
but a smaller accessory piriformis, with its own separate
tendon, passed between the common fibular and tibial
portions of the sciatic nerve, creating the impression that
the sciatic nerve was passing both through and below the
piriformis muscle (Fig. 2b).
In attempts to explain possible causes of piriformis
syndrome, cadaver studies have been conducted to explore
anatomic abnormalities involving both the piriformis
muscle and the sciatic nerve. In a study conducted by
Benzon et al. [4], 36 cadavers were examined for the
anatomic relationship between the sciatic nerve, piriformis
muscle, and sacroiliac joint. The authors specifically
focused on the anatomic abnormalities of the piriformis
muscle and the sciatic nerve, the distance from the lower
border of the sacroiliac joint to the sciatic nerve, and the
width of the sciatic nerve at its widest point [4]. Benzon
et al. [4] found both components of the sciatic nerve
passing below the piriformis muscle in 65 of 66 (98.5%)
dissections of specimens. The remaining dissection showed
the piriformis muscle to be split, with the tibial component
of the sciatic nerve passing below the piriformis muscle
and the common peroneal (or common fibular) nerve
passing through the muscle [4]. In a study conducted by
Beaton and Anson in 1938 involving 240 cadaver speci-
mens, 90% of cases demonstrated the sciatic nerve exiting
posterior to and beneath the piriformis muscle [3]. The
Fig. 1 Type A: Gross anatomy image depicting an undivided sciatic
nerve passing below the piriformis muscle. Anatomical position is
defined
480 Surg Radiol Anat (2012) 34:479–486
123
remaining 10% of cases in this particular study demon-
strated anatomic variations that Beaton and Anson further
classified into their six different types [3, 11]. Jawish et al.
[14] further elaborated on the remaining 10% of cases
reviewed by Beaton and Anson, indicating that in 7% of
cases the piriformis and sciatic were divided, with one
branch of the sciatic nerve passing through the split and the
other branch passing distal to the piriformis muscle. In 2%
of these cases, only the sciatic nerve was found divided and
in the remaining 1% of cases the piriformis muscle was
divided by the sciatic nerve. Pokorny et al. [20] also looked
at topographic variations of the piriformis muscle and
sciatic nerve to try and justify anatomical reasons for
neurological deficits after total hip arthroplasty. After a
cadaveric study, their numbers came out similar to those
reported by Beaton and Anson nearly 70 years earlier.
Their conclusion, however, was that after total hip arthro-
plasty, the disruption of certain muscular origins can result
in stretching of the sciatic nerve, and some variants pre-
dispose the nerve to stretching more than others [20].
Fig. 2 a Type B: Gross anatomy image depicting a divided sciatic
nerve passing through and below the piriformis muscle. b Type B:
Gross anatomy image depicting a divided sciatic nerve passing
‘‘through and below’’ the piriformis muscle, with an accessory
piriformis splitting the sciatic nerve. The accessory piriformis had an
independent tendon and defined muscle belly separate from that of the
larger piriformis muscle
Fig. 3 Type C: Gross anatomy image depicting a divided sciatic
nerve passing above and below the piriformis muscleFig. 4 Type D: Gross anatomy image depicting an undivided sciatic
nerve passing through the piriformis muscle
Surg Radiol Anat (2012) 34:479–486 481
123
As mentioned in the article by Halpin et al. [11], it has
been reported that the tibial division of the sciatic nerve is
less frequently involved in piriformis syndrome than the
peroneal (or fibular) division because the tibial division is
located more medially in the sciatic notch. Babinski et al.
[1] described another anatomical variation in which the
tibial nerve passed inferior, and the common fibular nerve
superior to the superior gemellus muscle, and concluded
that such variations may contribute to the prevalence of
piriformis syndrome [1].
Windisch et al. [26] also considered anatomic variation
as a cause for piriformis syndrome, and looked at the shape
of the muscle, nature of the musculotendinous junction,
diameter, insertion, and fusion of the piriformis tendon
with other tendons in 112 cadaveric specimens. The
extensive variability they found with each of these
parameters led them to conclude that a purely anatomical
cause for piriformis syndrome is rare, and that other
diagnoses should be considered in a patient workup [26].
Pathophysiology
According to Filler et al. [6], piriformis syndrome is the
most common cause of persistent sciatica in patients for
whom a proper diagnosis was not established and for whom
the routine spine-centered approach for treatment failed.
Ratnatunga et al. [21] more specifically noted that in those
sciatica patients who failed to improve with standard
treatment, up to 68% had piriformis syndrome. Although
piriformis syndrome is considered to be uncommon, it is
often an undiagnosed cause of buttock and leg pain [4]. In
approximately 50% of cases of piriformis syndrome, there
is a history of trauma that is usually not dramatic and may
occur several months before the initial presentation of
symptoms [4]. Inflammation of the piriformis muscle will
result in the release of prostaglandin, histamine, bradyki-
nin, and serotonin. These inflammatory mediators may
contribute to the irritation of the sciatic nerve, thereby
resulting in a pain–spasm–inflammation–irritation cycle.
The inflamed, spastic, or stretched muscle may compress
the sciatic nerve between the tendinous portion of the
piriformis muscle and the bony pelvis [4]. A patient with
sciatic nerve entrapment may experience neurological
deficits and show abnormal electrodiagnostic findings.
However, in a typical patient with piriformis syndrome,
neurological deficits are not the chief complaint [4]. Most
often, a patient presenting with piriformis syndrome will
complain of buttock pain with or without radiation to the
ipsilateral leg; this pain usually extends from the sacrum to
the greater trochanter of the femur, though it may radiate to
the posterior thigh and down to the knee if there is
involvement of the posterior cutaneous nerve of the thigh
[4]. Patients who experience pain related to piriformis
syndrome will complain of aggravated pain after prolonged
periods of sitting or upon rising from a seated position.
Pain may also occur with bowel movements due to the
proximity of the piriformis muscle to the lateral pelvic
wall. In addition, pain may worsen after sitting on hard
surfaces with a wallet in the back pocket [4]. Other factors
reported to contribute to the etiology of piriformis
Fig. 6 Type F: Gross anatomy image depicting an undivided sciatic
nerve passing above the piriformis muscle
Fig. 5 Type E: Gross anatomy image depicting a divided sciatic
nerve passing through and above the piriformis muscle
482 Surg Radiol Anat (2012) 34:479–486
123
syndrome include gluteal traumas, piriformis muscle
hypertrophy and spasticity in athletes, piriformis muscle
fibromyositis, early branches of the sciatic nerve in the
pelvis, passing of the tibial and fibular nerves in different
tunnels, complications of total hip arthroplasty, and
complications of cesarean section under spinal anesthesia
[9].
Diagnosis
While often described as ‘‘difficult to substantiate,’’ the
incidence of piriformis syndrome has been estimated to be
the true diagnosis in 6–8% of patients experiencing
symptoms of low back pain and sciatica. These percentages
indicate an incidence of 4.8–6.4 million cases annually
[10]. Piriformis syndrome has been an elusive diagnosis,
often one of exclusion, designated by clinicians only when
adequate inquiry suggests no spinal cause of significant
sciatic pain. Piriformis syndrome is also sometimes refer-
red to as a one of the ‘‘non-discogenic causes of sciatica’’,
resulting from the compression of the sciatic nerve by the
piriformis muscle in the neutral and piriformis stretch test
position [9]. Ever since Mixter and Barr’s 1934 publica-
tion, diagnostic attention related to piriformis syndrome
has focused on intramedullary and foraminal causes of
sciatica [7]. Although piriformis syndrome was once
thought to be an exclusively clinical diagnosis, recent
reports demonstrate the diagnostic value of electromyog-
raphy. Although electromyography examination is often
normal in patients with piriformis syndrome, long-standing
compression may result in abnormal spontaneous activity
of the muscles innervated by the sciatic nerve (particularly
the common fibular division) [17]. Electromyography is
able to detect myopathic and neuropathic changes includ-
ing a delay in the H-reflex with the affected leg in a flexed,
adducted, and internally rotated position as compared with
the same H-reflex in the normal anatomic position. A
prolongation of the H-reflex test by three standard devia-
tions has recently been recommended as the physiologic
criterion for piriformis syndrome. This particular finding
suggests entrapment of the sciatic nerve by the hip
abductor and external rotator, or the piriformis muscle, as
the nerve passes underneath [4]. According to Kirschner
et al. [16], the FAIR maneuver (flexion, adduction, and
internal rotation) had a sensitivity of 85% in identifying
piriformis syndrome and 82% in identifying normal legs
when using a cutoff of two standard deviations above the
normal H-reflex. Other neurography findings in patients
with piriformis syndrome have demonstrated ipsilateral
piriformis muscle atrophy, despite previous reports of pir-
iformis muscle hypertrophy as an image finding in piri-
formis syndrome [6].
Prior to the use of magnetic resonance imaging (MRI),
piriformis syndrome, otherwise referred to as entrapment
neuropathy of the sciatic nerve, was often misdiagnosed as
lumbar radiculopathy [21]. The use of computed tomog-
raphy (CT) for viewing soft tissues of the pelvis in cases of
piriformis syndrome may show an abnormal uptake by or
enlargement of the piriformis muscle, whereas MRI may
confirm an enlarged piriformis muscle, but with normal
intensity [4]. Although there has been emphasis on the
diagnostic value of various imaging techniques, recent
studies confirm that imaged abnormalities may not be the
cause of pain. On the contrary, nearly every clinician has
found significant, even unbearable pain related to sciatica
in individuals with normal CT, MRI, myelogram, and
conventional electromyography [7].
Differential diagnoses of piriformis syndrome encom-
pass all other causes of low back pain and sciatica such as
spinal stenosis, facet syndrome, sacroiliac joint dysfunc-
tion, trochanter bursitis, pelvic tumor, endometriosis and
various conditions that involve irritation of the sciatic
nerve. As previously mentioned, the diagnosis of piriformis
syndrome is most often made on the basis of exclusion of
the aforementioned possibilities [15]. The use of a newly
introduced neuroradiological technique (Magnetic Reso-
nance Neurography) along with the established imaging
methods (MRI) used for evaluating unexplained chronic
sciatica have led to the identification of variable changes
relating to the piriformis muscle and the sciatic nerve
which could further be demonstrated with surgical explo-
ration. According to Kanakis et al. [15], ‘‘these new
imaging methods further contributed to the acceptance of
piriformis syndrome as a distinct nosological entity in the
medical world.’’
Clinical presentation
Common symptoms of piriformis syndrome include hip
pain, buttock pain, dyspareunia in females, sciatica, and
intolerance to sitting. Other reported signs include a dis-
crepancy in leg length, tenderness over the sciatic notch,
isolated atrophy of the gluteus maximus muscle, dyses-
thesia of the posterior aspect of the thigh, and tenderness
over the rectal wall with or without a sausage-shaped mass
that may be laterally localized during rectal examination
[11].
Treatment
Treatment options for lower back pain and sciatica related
to piriformis syndrome include the more conservative
option of physical therapy, the use of anti-inflammatory
Surg Radiol Anat (2012) 34:479–486 483
123
agents, injections of local anesthetics and corticosteroids,
and the more recently studied option of botulinum neuro-
toxin injections. A mainstay of treatment according to
Kirschner et al. [16] involves piriformis stretching, which
ultimately aims to correct the underlying pathology by
relaxing the tight piriformis muscle, thereby relieving sci-
atic nerve compression. Stretching can typically be per-
formed in a standing or supine position and involves hip
and knee flexion, hip adduction, and internal rotation of the
thigh (FAIR). Considering that this is the same position
often used to provoke piriformis pain for diagnostic pur-
poses, it will often take some time for patients to tolerate
the stretching exercises involved in the conservative
treatment methods [16]. These stretching exercises are
often followed by lumbosacral stabilization, hip strength-
ening exercises, and myofascial release [16]. Reus et al.
[22] noted that in cases of piriformis syndrome where
conservative treatments (stretching exercises, massages,
heat, ultrasound, non-steroidal anti-inflammatory drugs,
and myorelaxant medications) are ineffective, the pirifor-
mis muscle can be injected with local anesthesia and ste-
roids, or with botulinum toxin. In cases where hypertrophy
and inflammation of the piriformis muscle leading to sci-
atic nerve compression, irritation, and swelling were
thought to cause the radiating leg pain associated with
piriformis syndrome, perisciatic injection of steroid and
local anesthetic at the site of nerve compression were
shown to successfully reduce nerve swelling, reduce ecto-
pic discharge, and facilitate the recovery of nerve con-
duction after injury [22]. As cited by Reus et al. [22], a
study conducted by Hanania and Kitain recommended
using lower concentrations of local anesthetics to prevent
motor block in the sciatic nerve that is often associated
with higher concentrations of the local anesthetic [12].
Fishman et al. [7] conducted a study investigating the use
of lidocaine and corticosteroid injections for treating piri-
formis syndrome. Included in the study were patients who
were found to have two out of the three following clinical
features: (1) pain where the sciatic nerve travels below the
piriformis muscle in the FAIR position, (2) tenderness to
palpation at the same location, (3) positive Lasegue sign
and or 3-SD prolongation of the H-reflex in the FAIR
position. Of the 537 patients who presented with two of the
three clinical features of piriformis syndrome, 468 were
included in the FAIR test positive (FTP) group based on a
3-SD prolongation cutoff. Of the FTP patients, after an
average of 10.2 months follow up, 79% achieved at least
50% improvement in symptoms after injection with lido-
caine and corticosteroids. Of the 109 patients meeting less
than two clinical piriformis criteria, 82 (75.2%) improved
50% or more (average improvement was 57.9%). Only 30
of 45 (67.6%) of patients meeting fewer than two criteria
and having negative FAIR tests improved 50% or more
(with an average improvement of 52.5%) [7]. From their
results, Fishman et al. [7] found that participants improved
an average of 71.7%, suggesting a substantial efficacy for
corticosteroid and lidocaine injection combined with
physical therapy in treating piriformis syndrome. Accord-
ing to the authors of the study, the FAIR test, along with
injection and physical therapy and/or surgery, appears to be
an effective means for diagnosing and treating piriformis
syndrome [7]. However, this study contained an inherent
weakness with its lack of a control group [16].
Although adequate relief from low back pain is not
always possible, emerging evidence suggests that botu-
linum neurotoxin injections may play a role in effectively
treating pain disorders related to piriformis syndrome [25].
The mechanism behind the use of botulinum neurotoxin
injections involves the blockage of nerve impulses, effec-
tively rendering muscles unable to contract and leaving
them in a state of relaxation, paralysis or both [25].
Injections of botulinum neurotoxin may take up to
2–4 days to take effect and the effects can last from 3 to
6 months before these injections can be repeated [25]. A
review conducted by Waseem et al. [25] to determine the
effects of botulinum toxin injections on pain, function,
disability (including return-to-work) and patient satisfac-
tion in adults with lower back pain included three ran-
domized trials consisting of a total of 123 patients. The first
study demonstrated that botulinum neurotoxin injections
were more effective in reducing pain at 3 and 8 weeks and
improving function at 8 weeks as compared to saline
injections [25]. The second trial revealed that botulinum
neurotoxin injections were a more effective treatment
option for patients with sciatica attributed to piriformis
syndrome as compared to injections of corticosteroid plus
lidocaine or placebo [25]. The final study concluded that
botulinum neurotoxin injections were better at treating pain
and improving function than acupuncture in patients
diagnosed with third lumbar transverse process syndrome
[25]. All three studies involved the use of botulinum toxin
serotype-A at varying doses of 100, 200 and 300 units [25].
In another randomized study cited by Reus et al. [22],
Graboski et al. [8] compared botulinum toxin injections
with injections of local anesthetics in the treatment of
myofascial pain syndrome and found no statistically sig-
nificant differences between either types of treatment.
Thus, based on the results of their study and the high cost
of botulinum toxin, the authors advised against using it as a
first line of treatment for piriformis syndrome.
Surgery is another treatment option for piriformis syn-
drome, and is described in 2005 study by Filler et al. [6].
The surgical approach involves the disconnection and
resection of the piriformis muscle using a minimal access
technique, which may explain the complete absence of gait
dysfunction in the group of patients at all stages during
484 Surg Radiol Anat (2012) 34:479–486
123
follow up [6]. The resection process removes the muscle
when chronic spasm has not been relieved by injections, or
when hypertrophy leads to crowding of the greater sciatic
foramen, and when atrophy leads to a tight band of short-
ened muscle. The neural element involved in surgical
treatment includes neuroplasty of the distal lumbosacral
plexus, sciatic nerve, posterior femoral cutaneous nerve,
and superior and inferior gluteal nerves. This further
ensures an optimal outcome because interoperative find-
ings often reveal the presence of adhesions of these nerves
[6]. In their study on the surgical outcomes for piriformis
syndrome patients, Filler et al. [6] reported 82 patients with
initial and 76 with long-term good or excellent outcomes.
In three of these patients (5%), recurrence was observed in
the first 2 years. Two of these three underwent reoperation
and went on to experience lasting relief, while the third
patient experienced recurrence of pain. The follow-up
period for patients in the study who underwent surgical
treatment for piriformis syndrome ranged from 6 months to
6.5 years (mean of 2 years). There was a smaller subset of
patients (23 cases) who attended follow-up sessions for
over 2 years and maintained good or excellent outcomes at
greater than 70% [6]. According to the findings of the
study, none of the surgical patients reported any gait
abnormality or other surgery-related disabilities. Compli-
cations included only one wound hematoma in a patient on
coumadin therapy, and three superficial wound infections
that responded to oral antibiotic therapy. More importantly,
92% of the patients who underwent surgical treatment for
piriformis syndrome reported returning to work or to pre-
surgical activity level within 2 weeks of the operation [6].
Conclusions
In reviewing the literature regarding piriformis syndrome,
it is apparent that there continues to be uncertainty sur-
rounding the cause, diagnosis, and treatment of this elusive
syndrome. Several variations of the relationship between
the piriformis muscle and sciatic nerve exist, and these may
be the cause of chronic low back pain in cases where other
diagnoses have already been excluded. Despite recent
studies focused on newly developed imaging techniques
used for diagnosis, patients continue to present with
symptoms of piriformis syndrome without any abnormal
imaging findings. It is also important to note that a patient
may have abnormal imaging findings without ever expe-
riencing symptoms related to piriformis syndrome. When it
comes to treatment options available for piriformis syn-
drome, many options have been studied. Although more
recently explored options, such as injections of the piri-
formis muscle with botulinum neurotoxin, may be effective
in relieving painful symptoms to a degree, the evidence is
still somewhat inconclusive. To further assess the value of
treatment options available for piriformis syndrome, it is
necessary to take a closer look not only at the effective pain
relief achieved by the various treatments, but also at the
long-term functional outcome associated with the various
treatments related to piriformis syndrome.
Conflict of interest The authors declare that they have no conflict
of interest.
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