Piriformis Syndrome

Jonathan S. Kirschner, MD, Patrick M. Foye, MD, Jeffrey L. Cole, MD

No one involved in the planning of this CME activity has anyy relevant financial relationships to discllose. Authors/faculty have nothing to disclose.

CME is available 6/11/2009 - 6/10/2012

Copyright: 20009

American Association of Neuromuscular and Electrodiagnostic Medicine

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CME Information Product: JR21 ‐ Piriformis Syndrome

Course Description Piriformis syndrome (PS) is an uncommon cause of that involves buttock pain referred to the leg. Diagnosis is often difficult, and it is one of exclusion due to few validated and standardized diagnostic tests. Treatment for PS has historically focused on and modalities, with refractory patients also receiving anesthetic and injections into the origin, belly, muscle sheath, or sheath. Recently, thhe use of (BTX) to treat PS has gained popularity. Its use is aimed at relieving sciatic nerve compression and inherent muscle pain from a tight piriformis. BTX is being used increasingly for myofascial pain syndromes, and some studies have demonstrated superior efficacy to corticosteroid injection. The success of BTX in treating PS supports the prevailing pathoanatomic etiology of the condition and suggests a promising future for BTX in the treatment of other myofascial pain syndromes. Intended Audience This course is intended for Neurologists, Physiatrists, and others who practice neuromuscular, musculoskeletal, and electrodiagnostic medicine with the intent to improve the quality of medical care to patients with muscle and nerve disorders.

Learning Objectives Upon conclusion of this program, participants should be able to: 1. identify the physical examination approaches to piriformis syndrome. 2. describe the diagnostic and treatment options for piriformis syndrome. 3. recognize diagnostic and interventional options using botulinum toxin.

Release Date: 6/11/2009 Expiration Date: 6/10/2012. Your request to receive AMA PRA Category 1 Credits™ must be submitteed on or before the credit expiration date. Duration/Completion Time: 2 hours

Accreditation and Designation Statements The American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM) is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AANEM designates both sections of this enduring material for a combined maximum of 2 AMA PRA Category 1 creditsTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

How to Obtain CME Once you have reviewed the materials, you can obtain CME credit by clicking on the link in the e‐mail received when you purchased this product. Answer the questions and click submit. Once your answers have been submitted, you will be able to view a transcript of your CME by logging into www.aanem.org and clicking View Profile and then My CME. INVITED REVIEW ABSTRACT: Piriformis syndrome (PS) is an uncommon cause of sciatica that involves buttock pain referred to the leg. Diagnosis is often difficult, and it is one of exclusion due to few validated and standardized diagnostic tests. Treatment for PS has historically focused on stretching and physical therapy modalities, with refractory patients also receiving anesthetic and corticosteroid injections into the piriformis muscle origin, belly, muscle sheath, or sciatic nerve sheath. Recently, the use of botulinum toxin (BTX) to treat PS has gained popularity. Its use is aimed at relieving sciatic nerve compression and inherent muscle pain from a tight piriformis. BTX is being used increasingly for myofascial pain syndromes, and some studies have demonstrated superior efficacy to cortico- steroid injection. The success of BTX in treating PS supports the prevailing pathoanatomic etiology of the condition and suggests a promising future for BTX in the treatment of other myofascial pain syndromes. Muscle Nerve 40: 10–18, 2009

PIRIFORMIS SYNDROME, DIAGNOSIS AND TREATMENT

JONATHAN S. KIRSCHNER, MD,1 PATRICK M. FOYE, MD,1 and JEFFREY L. COLE, MD2

1 Department of Physical Medicine and Rehabilitation, University of Medicine and Dentistry of New Jersey– New Jersey Medical School, Administrative Complex Building 1, 30 Bergen Street, Newark, New Jersey 07101-1709, USA 2 Kessler Institute for Rehabilitation, West Orange, New Jersey, USA

Accepted 18 January 2009

Originally described by Robinson in 1947, pirifor- (CT), magnetic resonance imaging (MRI), ultrasound, mis syndrome (PS) is a constellation of symptoms and peripheral nerve stimulator guidance have been that include low back or buttock pain referred to the described.3,4,7 A novel approach to treating PS involves leg (described in Papaddapoulos and Khan).24 It is the use of botulinum toxin (BTX) in an attempt to often underdiagnosed and mistaken for more com- alleviate both sciatic nerve compression from a normal mon conditions such as facet arthropathy, sacroili- or hypertrophic piriformis and relieving inherent piri- 13 itis, lumbar disk disease, and . There formis muscle pain by relaxing it. BTX is being used is some disagreement as to whether PS is a distinct increasingly for pain syndromes of myofascial origin,17 clinical entity and whether it involves neuropathic and some studies have shown superior efficacy to cor- pain from compression of the sciatic nerve as it ticosteroid injection.8,23 courses through the piriformis muscle or myofascial In this review we look at the history, physical pain from a tight, hypertrophic, and tender pirifor- examination approaches, and diagnostic and treat- 22,27,28 mis without nerve entrapment. ment options for PS. We include a comprehensive Treatment for PS has traditionally included physi- literature review regarding the use of BTX, with a cal therapy focused on muscle and connective tissue discussion of the various diagnostic and interven- stretching, and a combination of local anesthetic and tional techniques. corticosteroid injections into the piriformis muscle belly, muscle sheath, or sciatic nerve sheath. Injection METHODS techniques that involve a combination of electromyo- graphy (EMG), fluoroscopy, computed tomography A review of the literature was performed using PubMed and the search terms “piriformis syndrome” and “botulinum toxin.” A total of 11 articles were Abbreviations: ACh, acetylcholine; BTX, botulinum toxin; CMAP, com- identified, 6 of which were of an experimental de- pound motor action potential; CT, computed tomography; EMG, electromyo- graphy; FAIR, flexion, adduction, internal rotation; FTP, FAIR test positive; sign. The rest were descriptions of technique, case HNP, herniated nucleus propulsis; MNCV, motor nerve conduction velocity; reports, and reviews. Additional background infor- MRI, magnetic resonance imaging; MUAP, motor unit action potential; NCS, nerve conduction study; PS, piriformis syndrome; SNAP, sensory nerve ac- mation was taken from the aforementioned 11 arti- tion potential; VAS, Visual Analog Scale cles and their reference lists. Key words: botulinum toxin; myofascial pain; nerve compression syn- dromes; piriformis syndrome; sciatica Correspondence to: J. S. Kirschner; e-mail: [email protected] HISTORY © 2009 Wiley Periodicals, Inc. Published online 22 May 2009 in Wiley InterScience (www.interscience.wiley. The idea that the piriformis muscle could be a com). DOI 10.1002/mus.21318 source of pain arose out of a search for an etiological

10 PS Diagnosis and Treatment MUSCLE & NERVE July 2009 The piriformis is intimately related to the sciatic nerve, and numerous anatomic variations have been described. The ventral rami of L4 through S3 nor- mally converge at the inferior border of the pirifor- mis to form the sciatic nerve, which then emerges through the greater sciatic foramen inferior to the piriformis.18 In approximately 12% of cases the com- mon fibular and tibial divisions of the nerve separate proximal to or at the level of the piriformis. The passes anterior or ventral to the pirifor- mis, and the common fibular nerve passes superfi- cially dorsal or through it. It is unclear whether these anatomic variations are responsible for or contribute to pathology, as some asymptomatic patients have these variations and some symptomatic patients do not.

HISTORY AND PHYSICAL EXAMINATION Epidemiologic data on PS is inconsistent, but it is FIGURE 1. The anatomy of the piriformis and surrounding struc- estimated to be responsible for 6–8% of the yearly tures. The piriformis is a pear-shaped muscle that originates from cases of low and sciatica in the USA.8 The the anterior border of the second through fourth sacral segments. diagnosis is largely clinical and is one of exclusion. It extends inferolaterally through the greater sciatic foramen and attaches to the superior margin of the greater trochanter. Herniated nucleus propulsus (HNP), facet arthrop- athy, , and lumbar muscle strain must be ruled out, although due to compensatory biome- explanation for sciatica long before the role of the chanical factors it is possible for the piriformis syn- herniated intervertebral disk was known. In 1928, drome to develop concurrently or as a sequelum of Yeoman attributed sciatica to inflammation of the these other conditions. and nearby piriformis muscle, both of The history usually involves pain in the buttock which are anatomically related to the sciatic nerve as with or without ipsilateral radiation down the poste- it exits through the greater sciatic notch (described rior thigh. The pain is exacerbated with activity, in Parziale, et al).30 Robinson was the first to use the prolonged sitting, or walking. The patient may walk term “piriformis syndrome” (PS) in 1947.24 He de- with a limp and hold the leg in a shortened and scribed six key features: a history of trauma or direct externally rotated position while supine.25 Condi- fall to the buttock; gluteal or sacroiliac pain radiat- tions or activities that promote internal rotation of ing down the leg that often limits ambulation; glu- the hip, such as a Morton’s foot, leg-length discrep- teal atrophy; a palpable sausage-shaped mass; posi- ancy, or cross country skiing may exacerbate pirifor- tive Lase`gue sign; and exacerbation with bending or mis pain, as the muscle is activated to promote ex- lifting (described in Pappadapoulos and Khan). ternal hip rotation.21 Physical examination may demonstrate tender- ANATOMY ness to palpation at the greater sciatic notch or over The piriformis is a flat, pear-shaped muscle that the piriformis muscle belly. It is made worse with originates from the anterior border of the second deep laterally directed palpation on pelvic or rectal through fourth sacral segments, the superior margin examination.20 There may be a trigger point over of the greater sciatic notch, and the sacrotuberous the piriformis muscle with radiation down the sciatic ligament.18 It extends inferolaterally through the distribution, or a palpable sausage-shaped mass, glu- greater sciatic foramen to attach to the superior teal atrophy, and positive Lase`gue sign, as described margin of the greater trochanter (Fig. 1). The piri- by Robinson.24 A thorough neuromuscular examina- formis is innervated by the ventral rami of S1 and S2, tion should be performed. If weakness or sensory which join to form the nerve to the piriformis. With loss is elicited, the diagnosis of PS becomes less the leg extended, the piriformis is mainly a hip likely, except in the more chronic presentations external rotator. With the leg flexed, it is a hip where secondary disuse atrophy may be present. Pro- abductor.25 vocative physical examination maneuvers have been

PS Diagnosis and Treatment MUSCLE & NERVE July 2009 11 DIAGNOSTIC TESTS Diagnostic modalities such as CT, MRI, ultrasound, and EMG are mostly useful in excluding other con- ditions rather than clinching a diagnosis of PS. MRI may be useful in identifying anatomic anomalies that may lead to sciatic or lumbosacral nerve root com- pression, such as accessory piriformis muscle fi- bers,15 and can anatomically assess the piriformis muscle itself, including its associated tendons, bur- sae, and surrounding structures (Fig. 5). Although many studies failed to show consistent radiographic abnormalities, there have been case reports of pa- tients with clinical evidence to support PS and a markedly enlarged piriformis with enlargement and compression of the sciatic nerve on MRI.26 CT and ultrasound lack the sensitivity and resolution of MRI in assessing the piriformis muscle itself. They are useful in identifying mass lesions like hematomas, pelvic tumors, aneurysms, endometriosis, and ab- scesses that may similarly cause buttock pain and sciatic nerve compression.28 EMG examination is often normal; however, with long-standing compression, abnormal spontaneous activity may be seen in muscles innervated by the sciatic nerve (particularly common fibular divi- 16 FIGURE 2. The Freiberg maneuver. The examiner passively sion). Normal lumbosacral paraspinal muscles can internally rotates the extended thigh. help differentiate sciatic compression from lumbo- sacral radiculopathy. Nerve conduction studies (NCS) are also usually normal, but in some cases conduction slowing or sensory nerve action potential described, although clear sensitivity and specificity (SNAP) or compound motor action potential values have not been determined. Freiberg’s maneuver involves forcefully internally rotating the affected leg while the patient is supine in an attempt to stretch the irritated piriformis and provoke sciatic nerve compression (Fig. 2).2 Using 130 cadaveric limbs Pec´ina showed that passive in- ternal rotation of the hip compressed the piriformis against the common fibular nerve in the 20.77% of cases where it passed through the muscle, whereas external rotation relieved it.22 Others have used elec- trophysiologic studies to suggest that maximal sciatic compression is obtained with the affected hip in the flexion, adduction, internal rotation (FAIR) posi- tion.11 The Pace maneuver (Fig. 3) elicits pain by ab- ducting the hip while in the seated position. This activates the piriformis rather than stretching it.19 Another active test, proposed by Beatty, involves hav- ing the patient lie on the affected side with the knee and hip flexed (Fig. 4). Abducting the thigh to raise the knee off the table elicited deep buttock pain in those with PS, but back and leg pain in those with FIGURE 3. The Pace maneuver. Pain in the buttock is repro- lumbar disk disease.2 duced with resisted hip abduction in the seated position.

12 PS Diagnosis and Treatment MUSCLE & NERVE July 2009 FIGURE 4. The Beatty maneuver. Pain in the buttock, but not the lumbar spine, is reproduced with the patient actively abducting the thigh in the lateral decubitus position.

(CMAP) amplitude loss may be seen, particularly in thigh in the FAIR position (Figs. 6 and 7); and (4) the common fibular nerve.5 electrodiagnostic studies that excluded myopathy or In an attempt to create objective electrophysi- neuropathy (Table 1). ologic criteria to aid in diagnosis, Fishman and Zy- There was a mean H-reflex prolongation of 1.87 bert compared H-reflexes in the affected leg in sub- ms in limbs with PS when tested in the FAIR position jects with clinical evidence of PS in their normal (Fig. 8). The FAIR maneuver had a sensitivity of 85% contralateral legs. They theorized that, because the in identifying PS and 82% in identifying normal legs H-reflex involves both afferent and efferent circuits, when using a cutoff of 2 standard deviations (SDs) it would be twice as sensitive at picking up slowing.11 above the normal H-reflex (1.36 ms). The FAIR test Subjects were included if they had: (1) positive La- has subsequently been used as an inclusion criterion se`gue sign at 45°; (2) tenderness at the sciatic notch; in therapeutic trials for the treatment of PS,8 al- (3) increased pain in the sciatic distribution with the though repeat studies have failed to reproduce its diagnostic accuracy.

FIGURE 6. The FAIR (flexion, adduction, internal rotation) ma- FIGURE 5. Normal MRI of the piriformis muscle with 3-Tesla neuver. The hip is passively flexed, adducted, and internally

T2-weighted SPAIR (fat saturation) axial MRI of the . P, rotated by the examiner, reproducing buttock pain radiating down piriformis muscle; S, sacrum; SN, sciatic nerve; TC, Tarlov cyst. the leg.

PS Diagnosis and Treatment MUSCLE & NERVE July 2009 13 FIGURE 8. The H-reflex performed in the FAIR position. Tibial H-reflex with the thigh flexed, adducted, and internally rotated. E1 ϭ active electrode; E2 ϭ reference electrode; Gnd, ground electrode. FIGURE 7. The anatomy of the piriformis and surrounding struc- tures in the FAIR position. The sciatic nerve is compressed with the hip passively flexed, adducted, and internally rotated. H-reflex latencies in patients in the neutral hip po- sition with PS compared with controls, but the FAIR test was not performed. Chang et al.5 studied magnetic NCS and conven- tional NCS and EMG in 30 controls and 30 cases of TREATMENT PS diagnosed by Fishman’s clinical criteria (Table 1).11 Patients with PS had significant slowing of the Conservative treatment of PS includes symptomatic motor nerve conduction velocity (MNCV) in the relief of muscle and nerve pain with nonsteroidal gluteal segment of the sciatic nerve with magnetic anti-inflammatory drugs, muscle relaxants, and neu- stimulation of the L5, but not S1, nerve root. There ropathic pain agents such as gabapentin, nortripty- was a strong negative correlation between sciatic line, and carbamazepine. The mainstay of treatment, MNCV and disease duration (r ϭϪ0.68, P Ͻ 0.01). however, is piriformis stretching, which aims to cor- There was no significant difference, however, in rect the underlying pathology by relaxing a tight SNAP or CMAP values obtained in PS patients and piriformis, and related muscle stretching to relieve controls using standard sural, common fibular, and nerve compression. Because the piriformis lies deep tibial NCS. Some patients had CMAP loss in the in the gluteus maximus, using moist heat or ultra- 21 tibialis anterior and gastrocnemius muscles, but the sound prior to stretching is most often suggested. diagnostic sensitivity of CMAP amplitude was Stretches can be done in both the standing and Ͻ0.167. Twenty-three percent (7 of 30) of patients supine positions, and they involve hip and knee had abnormal needle EMG findings, including 5 in flexion, hip adduction, and internal rotation of the the tibialis anterior and 2 in the gastrocnemius. thigh, as in the FAIR position. This may take some There were no significant differences in F-wave or time for patients to tolerate, as this is the same position used to provoke piriformis pain. After stretching, lumbosacral stabilization, hip strengthen- ing exercises, and myofascial release are per- Table 1. Fishman’s clinical criteria. formed.20 1. Positive Lase` gue sign at 45° For those who have failed after utilizing the afore- 2. Tenderness at the sciatic notch mentioned treatment, various therapeutic injections 3. Increased pain in the sciatic distribution with the thigh in the may be considered, including local anesthetic, cortico- FAIR position steroid, BTX, or a combination of the three. In fact, 4. Electrodiagnostic studies that exclude myopathy or neuropathy response to local anesthetic injection has been used to both diagnose and treat PS. In refractory cases, surgical

14 PS Diagnosis and Treatment MUSCLE & NERVE July 2009 dissection of the sciatic nerve or splitting of the pirifor- received Food and Drug Administration (FDA) ap- mis muscle may be indicated. proval for the treatment of strabismus, blepharo- spasm, and hemifacial spasm in 1989. In the USA, it and . In 2002, Fishman has since been indicated for use in cervical dystonia, and colleagues9 reported a 10-year study on the di- primary axillary hyperhidrosis, and frown lines.29 It agnosis, treatment, and outcome of patients with PS. is commonly used off-label for the treatment of cer- Patients were included if they had two of following vicogenic headache, overactive bladder, and focal three clinical features: (1) pain where the sciatic dystonias and spastic conditions due to cerebral nerve travels below the piriformis muscle in the FAIR palsy, stroke, traumatic brain , and other up- position; (2) tenderness to palpation at the same per motor neuron disorders.17 location; or (3) positive Lase`gue sign and/or a 3-SD BTX is being used increasingly for the treatment of prolongation of the H-reflex in the FAIR position. various musculoskeletal pain conditions. Exact mecha- Each of their patients received an injection of 1.5 ml nisms are not known, but BTX presumably relieves of 2% lidocaine and 0.5 ml (20 mg) of triamcinolone pain by relaxing painfully spastic muscles. BTX-A has acetonide using a 3.5-inch 23–25G spinal needle been shown to act at the level of the muscle spindle by followed by a standardized physical therapy proto- inhibiting gamma motor neurons and blocking type Ia col. Seven injections were performed with EMG afferent signals, thus affecting both motor and sensory guidance; the remainder were performed “blinded,” pathways. BTX-A may derive some of its analgesic effect using anatomical landmarks and the point of maxi- by inhibiting the release of substance P from nerve mal discomfort. Patients were followed at 6, 12, 24, terminals, as has been shown to occur in embryonic rat 26, and 48 months, either by in-person, telephone, cells in vitro.1 Although research is limited, BTX has or mail interviews. Patients with two of the three been used effectively to treat myofascial pain in various clinical features of PS (n ϭ 537) had an average conditions including chronic neck pain, lateral epi- FAIR test prolongation of Ͼ5 SD above the mean. condylitis, , stiff-man syndrome, and PS Using a 3-SD cutoff, 468 of these patients were FAIR (Table 2).17 test positive (FTP), for a sensitivity of 0.881 and a One of the earliest studies to examine the use of specificity of 0.832. Seventy-nine percent of FTP pa- BTX-A for treatment of PS included patients with tients achieved at least 50% improvement in symp- myofascial pain originating from the anterior toms; however, 75.5% of those who were FAIR test scalene, iliopsoas, or piriformis muscles.23 Forty pa- negative yet had two of the three clinical features tients participated and received 0.5% bupivicaine in also had improvement. Taken together, participants addition to BTX-A or methylprednisolone (MP). improved an average of 71.7%, suggesting the effi- The majority of the patients received injections into cacy of corticosteroid and lidocaine injection com- the piriformis (23 total muscles), whereas 10 scalene bined with physical therapy in treating PS; however, and 7 iliopsoas muscles were injected. The groups there was no control group in their study. differed significantly at baseline, with the group re- ceiving BTX-A having higher Visual Analog Scale Botulinum Toxin. BTX inhibits the presynaptic re- (VAS) pain scores (P ϭ 0.006). This effect was nul- lease of acetylcholine (ACh) at the neuromuscular lified at 30 days postinjection; the BTX-A group had junction, leading to muscle paralysis and wasting. It lower VAS scores than the MP group, but this only is the strongest neurotoxin identified to date,17 and approached statistical significance (P ϭ 0.06). At 60 has long been associated with muscle paralysis lead- days, the BTX-A group demonstrated statistically sig- ing to respiratory failure, especially in infants con- nificant pain reductions compared with the MP suming raw honey. There are seven serotypes, A–G, group (P Ͻ 0.0001). The data were not subanalyzed and all but one (type G) are produced by Clostridium by muscle injected, so it is unclear how much benefit botulinum.17 BTX type A is commercially available as was derived from piriformis muscle injection specif- Botox (Allergan, Inc., Irvine, California) and Dys- ically. The doses used for piriformis injection were port (Ipsen, Ltd., Berks, UK), and type B as Myob- 80 mg of MP, 100 units of BTX-A, and 2 ml of 0.5% loc/Neurobloc (Solstice Neurosciences, San Fran- bupivicaine. Both groups received the same total cisco, California). The different BTX subtypes all volume of injectate, with the exception of the BTX-A inhibit exocytosis of ACh vesicles from nerve termi- iliopsoas group, which for unknown reasons re- nals but do so through different intracellular actions ceived 1 more milliliter of bupivicaine than the MP and with varying degrees of potency.1 group. All patients benefited 2–3 minutes after the BTX-A was first used therapeutically to treat es- injection of bupivicaine, suggesting the patients were otropia in children in the late 1970s.17 The drug indeed suffering from PS. More patients in the MP

PS Diagnosis and Treatment MUSCLE & NERVE July 2009 15 Table 2. Studies on the use of botulinum toxin in treating BTX-A for the treatment of PS. They randomized 10 piriformis syndrome. patients to receive either 100 units of intramuscular Study (year) Intervention Results BTX-A or saline in a 20-week crossover design, based on a presumed 10-week effect of BTX-A. Subjects ϩ Porta (2000) 0.5% BC 100 U Change in VAS scores at 30 were required to have: experienced pain for Ն3 Botox or 80 mg days: P ϭ 0.06; at 60 MP days: P Ͻ 0.001 months; VAS scores of at least 5/10 on 3 consecutive Fanucci (2001) 200 U Botox 77% of those who had MRI days; two of the following symptoms—pain with pal- follow-up showed a pation between the greater trochanter and the sa- decreased signal intensity crum, pain with ipsilateral digital rectal examina- Childers (2002) 100 U Botox or Significant improvement (P tion, or pain with the Beatty maneuver. Patients were saline Ͻ 0.05) in pain intensity, spasm, distress, and excluded if they had evidence of HNP on imaging or interference with activities spontaneous activity in the paraspinal muscles on in the Botox group EMG. Injections were performed midway between compared with placebo the greater trochanter and the sciatic notch using Fishman 1.5 ml 2% LC 20 50% improvement at last both EMG and fluoroscopic guidance. Correct place- (2002) mg TL vs. two visits following 20 mg placebo vs. 200 TL vs. placebo injection: P ment was indicated by the generation of large motor U Botox ϭ 0.001; Botox vs. TL: P unit action potentials (MUAPs) with active hip ex- ϭ 0.044; Botox vs. ternal rotation and with medial to lateral spread of placebo: P ϭ 0.001 contrast along the piriformis distribution. Patients Fishman Myobloc dose Combined with PT, 88.9% underwent H-reflex testing and motion analysis test- (2004) of patients finding study injected with 12,500 U ing at baseline and throughout the study. had 50% increase on the VAS scores decreased for pain intensity, distress, VAS spasm, and interference with activities in the BTX-A Lang (2004) 5000 U Myobloc Significant reduction in hip group. This effect diminished but persisted for all per affected and buttock pain at 4, 12, but one measure (spasm) at the end of 10 weeks, side and 16 weeks Yoon (2007) 150 U Dysport vs. Pain in Dysport group at 4, although BTX-A has been reported to only have a 5mgDXϩ 1% 8, and 12 weeks vs. 10-week effect. There were no differences in hip LC baseline P Ͻ 0.0001 motion or H-reflex latency in both groups at base-

BC, bupivicaine; MP, methylprednisolone; PT, physical therapy; VAS, Visual line or after either injection. The investigators attrib- Analog Scale; DX, dexamethasone; TL, triamcinolone; LC, lidocaine. uted this to the lack of sciatic nerve compression as an etiologic explanation of PS. Later in 2002, Fishman and colleagues reported a group were noncompliant with the stretching proto- double-blind, placebo-controlled study on the use of col, which the investigators suggest was due to their BTX-A in 72 cases of PS diagnosed by the FAIR test.8 higher pain levels. Subjects were included if the H-reflex of their af- In 2001, Fanucci and colleagues used CT guid- fected limb was 1.86 ms (3 SDs) greater in the FAIR ance to inject 200 units of BTX-A into 30 patients position than in the anatomic position. Patients re- with clinical and electrophysiologic criteria sugges- ceived 2.0-ml injections under EMG guidance, either tive of PS.7 All patients underwent a confirmatory 200 units of BTX-A mixed with saline, 1.5 ml of 2% diagnostic injection with 3 ml of 2% lidocaine. The lidocaine and 20 mg (0.5 ml) of triamcinolone, or 2 test was considered positive if patients had preinjec- ml of saline. Patients were then placed on the same tion pain with the Lase`gue maneuver at 60° or force- therapy program used in the study that described the ful internal rotation of the flexed leg while supine validity of the FAIR test in diagnosing PS, twice that resolved postinjection. All 30 patients had pos- weekly for 12 weeks,11 and were followed every other itive diagnostic tests and immediately received a sec- week for 12 weeks. Clinical improvement was de- ond injection with 200 units of BTX-A. Twenty-six fined as at least 50% improvement on the VAS on patients had symptom relief within 5–7 days. The each of the last two visits postinjection. Sixty-five other 4 patients did not report benefit and received percent of BTX-A patients, 32% of triamcinolone ϩ the BTX-A injection 4 weeks later. They subse- lidocaine patients (P Ͻ 0.05), and 6% of patients quently became pain-free. The method of assessing given a placebo (P ϭ 0.001) satisfied this endpoint. pain and acceptable cut-off level were not specified The average improvement level or the time required in the study. to achieve pain relief was not specified. Unlike pre- Childers et al.6 were the first to report a random- vious studies, there was no statistically significant ized, double-blind, controlled trial on the use of benefit of triamcinolone and lidocaine over placebo

16 PS Diagnosis and Treatment MUSCLE & NERVE July 2009 (P ϭ 0.10). This may be because milder cases of PS that may have been amenable to steroid and lido- caine were FAIR test negative and were excluded from the study. In 2007, Yoon and colleagues used CT guidance to inject 150 units of Dysport, equivalent to 50 units of Botox, into 20 patients.31 Nine controls received 5 mg of dexamethasone and 1% lidocaine. The Ko- rean version of the Short Form-36 (SF-36) health survey was assessed at baseline and at 4, 6, and 12 weeks postinjection. Pain intensity scores were signif- icantly lower in the BTX-A group at all follow-up time-points; in fact, the control group was withdrawn at 4 weeks for ethical reasons due to lack of improve- ment. The SF-36 subscales for physical functioning, bodily pain, general health, vitality, and social func- tioning were all significantly improved as well. Ad- verse effects were mild and short-lived, including flu-like syndrome for 2 days, ecchymosis for 2 days, FIGURE 9. Fluoroscopic myogram of the piriformis. Note contrast worsening pain for 2–3 days, and transient numbness flow along the distribution of the piriformis muscle. for Ͻ72 hours. In 2004, Fishman and colleagues performed the first reported dose finding study on BTX-B, using the FAIR test as both inclusion criteria and outcome mea- five percent of patients reported good to excellent sure.10 Patients again were considered FTP if they had subjective pain relief, and side effects were minimal a 1.86-ms prolongation of the H-reflex latency with the and transient. This study was not blinded, physical affected limb in the FAIR position compared with the therapy was not included, and electrodiagnostic in- anatomic position. Imaging studies and physical signs clusion criteria were not utilized. and symptoms were not used for inclusion. Cohorts of 8 consecutive patients received injec- Injection Techniques. Techniques utilizing needle 8 3 tions with 5000, 7500, 10,000, or 12,500 units of BTX-B. EMG, peripheral nerve stimulation, fluoroscopy, ul- 27 7 VAS scores, adverse effect profiles, and FAIR tests were trasound, CT, and multimodality guidance have 4,12 assessed at 0, 2, 4, 8, and 12 weeks. All injections were been described. Earlier reports involved blinded performed using EMG guidance with the hip and knee injection using the greater trochanter and sacroiliac flexed at 90°. Each patient then received physical ther- joint as anatomic landmarks. Advantages to using guid- apy twice a week for 12 weeks according to the previ- ance obviously include more accurate placement of ously described standardized protocol. injectate and avoidance of anomalous neurovascular Patients who received 12,500 units of BTX-B structures. Disadvantages include added cost, in- showed the greatest clinical improvement 3 weeks creased procedure time, contrast reactions, and radia- postinjection but then regressed over the next 5 tion exposure. One validated method of piriformis weeks. The investigators postulated that the patients injection involves injecting one fourth to one third of who felt the most relief overused their muscles, lead- the way along an imaginary line drawn from the ace- ing to their pain recurrence. tabulum to the sacroiliac joint. The needle is inserted In 2004, Lang reported a 20-patient case series to the level of the ischium and retracted until maximal on the use of BTX-B in PS. Patients were included if MUAP activity is appreciated on EMG while the leg is they had: (1) 5/10 pain on a VAS for at least 3 externally rotated.12 If MUAPs are generated when the months; (2) physical examination signs suggestive of leg is extended, then the needle is likely in the gluteus PS; and (3) a good response to a diagnostic anes- maximus and is advanced further. Other investigators thetic injection.14 EMG guidance was used to inject have described injection halfway along a line connect- 5000 units of BTX-B into each affected piriformis (4 ing the sciatic notch and the greater trochanter.6 Ra- patients received bilateral injections). At the end of dio-opaque contrast dye is then injected and successful the 16-week study, all patients had significant im- placement confirmed with medial to lateral spread of provement in their VAS scores for buttock, hip, low contrast along the piriformis distribution (Fig. 9). If back, and overall pain, but not thigh pain. Seventy- the needle is superiorly or inferiorly misplaced, it may

PS Diagnosis and Treatment MUSCLE & NERVE July 2009 17 be located in the gemelli or obturator internus, respec- 7. Fanucci E, Masala S, Sodani G, Varruciu V, Romagnoli A, Squillaci E, et al. CT-guided injection of botulinic toxin for tively. percutaneous therapy of piriformis muscle syndrome with In conclusion, PS is a controversial diagnosis, but preliminary MRI results about denervative process. Eur Ra- it is likely an underdiagnosed cause of refractory diol 2001;11:2543–2548. sciatica. There are now validated objective measures 8. Fishman LM, Anderson C, Rosner B. BoTox and physical therapy in the treatment of piriformis syndrome. Am J Phys to aid in diagnosis, such as the FAIR test and re- Med Rehabil 2002;81:936–942. sponse to local anesthetic injection. Traditional 9. Fishman LM, Dombi GW, Michaelson C, Ringel S, Rozbruch treatment focusing on physical therapy and cortico- J, Rosner B, et al. Piriformis syndrome: diagnosis, treatment and outcome—a 10-year study. Arch Phys Med Rehabil 2002; steroid plus local anesthetic injection has been 83:295–301. shown to be effective in some studies, but not oth- 10. Fishman LM, Konnoth C, Rozner B. Botulinum neurotoxin ers.31 Several randomized, controlled trials demon- type B and physical therapy in the treatment of piriformis syndrome: a dose-finding study. Am J Phys Med Rehabil 2004; strated better efficacy with BTX-A over both placebo 83:42–50. and corticosteroid plus lidocaine. BTX-B has also 11. Fishman LM, Zybert PA. Electrophysiologic evidence of piri- been used effectively to treat PS, but it has not been formis syndrome. Arch Phys Med Rehabil 1992;73:359–364. assessed in a comparative trial vs. BTX-A or cortico- 12. Fishman SM, Caneris OA, Bandman TB, Audette JF, Borsook D. Injection of the piriformis muscle by fluoroscopic and steroid and lidocaine. BTX seems to be a logical electromyographic guidance. Reg Anesth Pain Med 1998;23: treatment choice, because it reverses the presumed 554–559. underlying pathophysiology of PS by leading to muscle 13. Kirkaldy-Willis WH, Hill RJ. A more precise diagnosis for low-back pain. Spine 1979;4:102–109. weakness, atrophy, and relief of sciatic nerve compres- 14. Lang AM. Botulinum toxin type B in piriformis syndrome. sion. Corticosteroid and lidocaine injection may pro- Am J Phys Med Rehabil 2004;83:198–202. vide enough temporary analgesia to allow patients to 15. Lee EY, Margherita AJ, Gierada DS, Narra VR. MRI of piri- participate in physical therapy, but it does not correct formis syndrome. Am J Rehabil 2004;183:63–64. 16. McCrory P, Bell S. Nerve entrapment syndromes as a cause of the underlying pathophysiology of PS and often pain in the hip, groin and buttock. Sports Med 1999;27:261–274. needs to be repeated. The effects of BTX-A have 17. Monnier G, Tatu L, Michel F. New indications for botulinum been shown to persist for up to 3 months, thus toxin in rheumatology. Joint Bone Spine 2006;73:667–671. 18. Moore KL, Dalley AF. Clinically oriented anatomy. 1999, p decreasing the need for repeat injection. As physi- 334, 334t, 554–555. cians better understand the mechanisms of myofas- 19. Pace JB, Nagle D. Piriformis syndrome. West J Med 1976;124: cial pain, the uses of BTX will likely increase over 435–439. time with proper application. Future studies need to 20. Papadapoulos EC, Khan SN. Piriformis syndrome and low back pain: a new classification and review of the literature. examine the role of other BTX subtypes, including Orthop Clin N Am 2004;35:65–71. duration of effect and safety profile and the use of 21. Parziale JR, Hudgins TH, Fishman LM. The piriformis syn- BTX for other compression neuropathies. drome. Am J Orthop 1996;25:819–823. 22. Pec´ina M. 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