Fig. 30.1 In piriformis syndrome, the sciatic nerve is either sandwiched between the piriformis muscle and the ischiofemoral ligament or, less commonly, adherent to the ventral surface of the piriformis muscle or the dorsal aspect of the obturator internus.
Approximately 3–4% of cases include variations involving the posterior tibial and peroneal components uniting below the piriformis muscle with or without a communicating nerve. Also included in this grouping is a variation in which the two divisions are united within the pelvis, separate at the piriformis level and reunite; effectively surrounding the muscle (Sunderland, 1868; Beaton and Anson, 1937; Sridhara and Izzo, 1985; Fishman and Zybert, 1992; Sharma et al., 2010) (Fig. 30.2). In rare cases in which the muscle is divided, a small fibrous band penetrates the nerve. This can easily result in sciatic pathology at the level of the piriformis muscle.
Fig. 30.2 In 10–30% of unselected cadavers, fibers of the posterior tibial and peroneal nerves never unite to form the sciatic nerve. In approximately half of these cases, one or both nerves pass through or above the piriformis muscle. (Reproduced with permission from Travell, JG and Simons, DG. Myofascial Pain and Dysfunction: The Trigger Point Manual, Volume 2, 2nd edn. Philadelphia, PA: Williams & Wilkins; 1998, p. 186.)
A common opinion about the pathogenesis of piriformis syndrome is that any and all of these anomalies are responsible for it (Sharma et al., 2010). However, the facts do not support this. Cadaveric studies show that anomalous passage of the sciatic nerve and the piriformis, when it occurs, is overwhelmingly bilateral (Sunderland, 1868; Beaton and Anson, 1937; Sridhara and Izzo, 1985; Fishman and Zybert, 1992; Sharma et al., 2010). Yet in our experience of 17 000 patients, the syndrome is unilateral 90% of the time it is encountered. Further, surgical reports confirm an anomalous sciatic–piriformis relationship approximately 15% of the time, the same proportion found in cadaveric studies of the general population (Fishman and Ardman, 1997). Understanding these anatomical variations is important in treating the disorder, but they do not inevitably cause it. Far from it. Tension or pressure of the muscle on the nerve causes the syndrome, but it does not appear that these anomalous nerve/muscle variations are consistently responsible for that pressure.
Anatomy books frequently picture the gemellus superior, the obturator internus and the gemellus inferior distal to the most caudal side of the piriformis muscle and adjacent to the exiting sciatic nerve (Lockhart et al., 1959); in fact, there is also a sharp-edged ligament that lurks just below the muscle, the ischiofemoral ligament (Fig. 30.1). Where we do find this compressive pressure, and resulting piriformis syndrome, is where the sciatic nerve is held against the ischiofemoral ligament under pressure by a misbehaving piriformis muscle. Its erosive influence on the sciatic nerve, developed under pressure from the tight, shortened or scarred piriformis muscle roofing the sciatic nerve at that junction, appears to be the most common cause of piriformis syndrome. Denudation of the vaso nervorum, noted in more than 100 postsurgical reports, confirms this.
There are also cases of piriformis syndrome in which adhesions attach the nerve to the piriformis muscle or, less frequently, to the obturator internus muscle. In these cases, muscular contraction raises the risk of neuropraxia through stretching. Surgical reports and specialized scans describe both the compressive and adhesive phenomena with regularity, favoring the former considerably. For our purposes, both are important, since a botulinum neurotoxin (BoNT) injection that reduces muscle motility will be effective in either case, provided the injection is well placed.
Diagnosis of piriformis syndrome
The most common causes of piriformis syndrome are:
- sedentary occupation: financial sector, vehicle driver, secretary, clinical psychology
- athletic: track and field, rowing, hockey, football, soccer
- recreational: health club, pilates, trainer
- traumatic: rear-ended in vehicle, backward fall.
Piriformis syndrome was long considered a diagnosis of exclusion, a diagnosis to consider only when other diagnoses had been ruled out. Unfortunately, this means that piriformis syndrome is not considered if other diagnoses are actually present, when in fact, clinicians may often find patients with two diagnoses.
There are two methods of specifically diagnosing piriformis syndrome: electrodiagnostic testing and the MRI neural scan.
The electrophysiological method is the oldest. The diagnosis is made by measuring the delay of the H-reflex when the piriformis muscle is stretched against the sciatic nerve (Fig. 30.3). This is done by first recording an H-reflex for the posterior tibial and peroneal nerves bilaterally in the anatomical position. Then, the patient is placed in the lateral decubitus position and the affected leg is forcibly urged into flexion, adduction and internal rotation (FAIR test). The posterior tibial and peroneal H-reflexes are then re-elicited. We generally press diagonally downward on the knee in order to control hip motion while raising the ankle (Fig. 30.4). This is well tolerated by most patients. After testing 88 normal individuals in our laboratory, the mean prolongation seen in the FAIR test was 0.01 milliseconds and the standard deviation (SD) was 0.62 milliseconds (Fishman et al., 2002a). A delay of 3SD (1.86 milliseconds) of either branch of the sciatic nerve’s H-reflex in the FAIR position is taken to denote piriformis syndrome (Figs. 30.5 and 30.6).
Fig. 30.3 The H-reflex is electrophysiological initiation and measurement of the monosynaptic Achilles tendon reflex. It is named after Paul Hoffmann, who discovered it in 1910. S1 and S2, first and second stimuli; R1 and R2, recording electrodes; G, ground. Illustrated by Mayank Pathak, from author’s original.
Fig. 30.4 When a patient is in 90 degrees of hip and knee flexion, forcibly adducting and internally rotating the leg to the level of the patient’s or joint’s tolerability (FAIR test) may compress the sciatic nerve or stretch it sufficiently to delay the H-reflex significantly (1.86 ms). Illustrated by Mayank Pathak, from author’s original.
Fig. 30.5 Comparing the H-reflex in the anatomical position with one elicited in flexion, adduction and internal rotation will either confirm or refute the presence of piriformis syndrome according to whether the FAIR test generates a delay equal to or greater than 1.86 ms.
Fig. 30.6 Frequency curves for the H-reflex showing percentage with a standard deviation (SD) delay (full lines) compared with 88 normals and the percentage within each group that attained that particular prolongation of the H-reflex with FAIR positioning (dotted lines): normals (N), piriformis syndrome (PS); contralateral posterior tibial reflex (CPT), contralateral peroneal reflex (CP). Because the H-reflex crosses the piriformis muscle in both afferent and efferent limbs, the delay generated by compression is doubled, amplifying FAIR test discrepancies in patients with piriformis syndrome. Patients with piriformis syndrome can be clearly separated from normals in this FAIR test (n = 687) (Fishman et al., 2002a).
The electrodiagnostic approach may be tempered by comparing side-to-side H-reflexes in the anatomical position with each other and with normal values, as a clue to radiculopathic involvement. It is also useful to seek additional electromyography (EMG) findings cephalad to the piriformis muscle, as well as in the muscle itself, as the S1 and S2 fibers that innervate the piriformis muscle do not pass under it. Unfortunately, nature has missed an opportunity for a feedback loop here, as with pronator syndrome, for if the innervation of these muscles passed below them, spasm would reduce their stimulus for further tightening, limiting compression of the sciatic and median nerves, respectively.
Findings from EMG suggestive of piriformis syndrome may be confined to one branch of the sciatic nerve with no involvement of the hamstrings, glutei, piriformis or tensor fascia latae. Further, discrepancy in the sural sensory nerve action potentials, with reduction in the amplitude on the affected side, is consistent with the clinical diagnosis of piriformis syndrome in the context of the usual clinical criteria – sciatica, pain worsened by sitting, and tenderness in the mid-buttock. Attempts to use a 50% reduction in sural sensory nerve action potentials as a criterion for piriformis syndrome indicate that it only correlates in 30% with the FAIR test. However, placing pickups on the peroneus longus and stimulating just behind the fibular head produces a peroneal H-reflex more than 80% of the time.
The second diagnostic method is neural scanning, a technique that shims the MRI for the pelvis, does a standard MRI study and a fat-suppression study, then proceeds to digitally subtract the fat-suppression study from the standard one, leaving the myelin-rich peripheral nerves in fairly sharp relief (Filler et al., 2005) (Fig. 30.7). This imaging method can detect nerve swelling proximal to and nerve attenuation distal to the site of entrapment, it may note pudendal and medial femoral cutaneous nerve involvement and can detect ischial tunnel syndrome if these are present. It may also reveal bifurcation of the piriformis muscle and the sciatic nerve or other anomalous situations, including gluteal arterial and obturator internus complications in the course of the sciatic nerve or its components. At the time of writing there are five centers in the USA where the test is performed.
Fig. 30.7 Neural scanning. (a) Piriformis muscle showing the asymmetrically enlarged left muscle. (b,c) Axial and coronal sections. Arrows indicate sciatic nerves. (d) The curved neurographic image of hyperintense left sciatic nerve with loss of fascicular detail. Piriformis syndrome is on the reader’s right in each image. (With permission from Filler et al., 2005.)
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