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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 Ó 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 Á Piriformis Á Sciatic nerve Á Botulinum toxin Á Back pain Á 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 Á A. Walters Á K. Bubb Á 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
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Page 1: Piriformis syndrome: implications of anatomical variations, diagnostic techniques, and treatment options

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

Page 2: Piriformis syndrome: implications of anatomical variations, diagnostic techniques, and treatment options

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

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Page 3: Piriformis syndrome: implications of anatomical variations, diagnostic techniques, and treatment options

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

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Page 4: Piriformis syndrome: implications of anatomical variations, diagnostic techniques, and treatment options

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

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Page 5: Piriformis syndrome: implications of anatomical variations, diagnostic techniques, and treatment options

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

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Page 6: Piriformis syndrome: implications of anatomical variations, diagnostic techniques, and treatment options

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

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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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