in Hip injuries
Chris Mallac looks at the relevant anatomy and biomechanics of the tensor fascia latae. He explains, what role it plays in pain and dysfunction, and what can be done in the presence of a tight and overactive TFL muscle MORE
Chris Mallac explains the relevant anatomy and functional biomechanics of the piriformis muscle, highlights the role it plays in musculoskeletal dysfunction and looks at management options in cases of muscle dysfunction
The piriformis muscle (PM) is well-known in the fraternity of sports medicine as a significant muscle in the posterior hip. It is a muscle that has a role in controlling hip joint rotation and abduction, and it is also a muscle made famous due to its ‘inversion of action’ in rotation. Furthermore, the PM also grabs attention due to its role in the contentious ‘piriformis syndrome’, a condition implicated as a potential source of pain and dysfunction, not only in the general population but in athletes as well.
The name piriformis was first coined by Belgian Anatomist Adrian Spigelius in the early 17th century. Its name is derived from the Latin word ‘pirum’ meaning ‘pear’ and ‘forma’ meaning ‘shape’ – ie a pear shaped muscle (see Figure 1)1.
The PM originates on the anterior surface of the sacrum and is anchored to it by three fleshy attachments between the first, second, third and fourth anterior sacral foramina2. Occasionally its origin may be so broad that it joins the capsule of the sacroiliac joint above and with the sacrotuberous and/or sacrospinous ligament below3 4.
PM is a thick and bulky muscle, and as it passes out of the pelvis through the greater sciatic foramen, it divides the foramen into the suprapiriform and infra-piriform foramina5. As it courses antero-laterally through the greater sciatic foramen, it tapers out to form a tendon that is attached to the superior-medial surface of the greater trochanter, commonly blending with the common tendon of the obturator internus and gemelli muscles6.
The nerves and blood vessels in the suprapiriform foramen are the superior gluteal nerve and vessels, and in the infrapiriforma fossa are the inferior gluteal nerves and vessels and the sciatic nerve (SN)7. Due to its large volume in the greater sciatic foramen, it has the potential to compress the numerous vessels and nerves that exit the pelvis.
PM is closely associated with the other short hip rotators that lie inferior such as the superior gemellus, obturator internus, inferior gemellus and obturator externus8. The primary difference between the PM and other short rotators is the relationship to the SN. The PM passes posterior to the nerve whereas the other otators pass anterior (see figure 2).
A few anatomical variants have been found with the PM:
The other hotly debated issue is the relationship between the PM and the SN. The conclusion is that there are several anatomical variations of the PM and its SN relationship. The sub-types of this variation include15 16 17:
It is also believed that two other very uncommon variations occur (see E and F below).
Type A is the most common variation, showing the SN passing below the PM
The primary functional roles of the PM are;
As the PM is the most posterior of the hip external rotators due to its attachment on the anterior surface of the sacrum, it has the greatest leverage to exert a rotation effect on the hip joint. It is often seen clinically that the PM appears to be tight and hypertonic, while the other short hip rotators that are closer to the axis of rotation become inhibited and hypotonic.
The most contentious issue related to the function of the PM is its ‘reversal-offunction role’ or ‘inversion of action’ role. Many authors have suggested that as the hip approaches angles of 60-90 degrees and greater, the tendon of the PM shifts superiorly on the greater trochanter. As a result, its line of pull renders it ineffective as a hip external rotator; however it does contribute to internal hip rotation. Therefore it reverses its rotation role at high hip flexion angles23 24 25.
The function of the PM at varying joint angles is an important consideration for the clinician who is evaluating and treating ‘piriformis syndrome’. Often it has been advocated to stretch the hip into flexion, adduction and external rotation to stretch the PM over the glutes by utilising the ‘reversal of function’ concept.
However, more recent anatomical dissection studies have shown that the attachment of the PM onto the greater trochanter can be variable and in some instances it may insert in a position whereby it is unable to reverse its function, for example in a more posteriorly placed attachment26. Therefore, stretching the PM into external rotation when the hip is flexed beyond 90 degrees – based upon reversal of function – would be ineffective as a treatment or misleading as an examination technique27.
Many decades ago, the role that the PM played in creating sciatic-like symptoms was first suggested by Yeoman (1928) when it was considered that some cases of sciatica may originate outside the spine28. This was supported soon after when Freiberg and Vinkle (1934) successfully cured sciatica by surgically dividing the PM29. Based on cadaver dissections Beaton and Anson (1938) gave the hypothesis that the spasm of the PM could be responsible for the irritation of the SN30.
The term ‘piriformis syndrome’ was first coined by Robinson in 194731 and was applied to sciatica thought to be caused by an abnormality in the PM (usually traumatic in origin) with emphasis on ruling out more common causes of sciatica such as nerve root impingement from a disc protrusion. It soon became an accepted clinical entity – but with no consensus about the exact clinical signs and diagnostic tests to differentiate it from other sources of sciatica32 33.
Piriformis syndrome can be defined as a clinical entity whereby the interaction between the PM and SN may irritate the SN and produce posterior hip pain with distal referral down the posterior thigh, imitating ‘true sciatica’. Isolating the dysfunction to this region usually follows exclusion of the more common causes of buttock pain and sciatica.
More specifically, complaints of buttock pain with distal referral of symptoms are not unique to the PM. Similar symptoms are prevalent with the more clinically evident lower back pain syndromes and pelvic dysfunctions. Thus, a thorough evaluation of these regions must be performed to exclude underlying pathology34. It has been suggested that piriformis syndrome’ is responsible for 5-6% of cases of sciatica35 36. In the majority of cases, it occurs in middle-aged patients (mean age 38 yr)37 and is more prevalent in women38.
PS may be caused by or relate to three primary causative factors;
Janvokic (2013) has presented a number of causative factors in PS48;
Typical symptoms reported in piriformis syndrome include:
Conventional imaging such as X-ray, CT scan and MRI tend to be ineffective in diagnosing piriformis syndrome.
However, some value may exist in electrodiagnostic testing.
It is beyond the scope of this paper to discuss in detail the process of electrodiagnostic testing; the reader is directed to references for more a more detailed description of how these tests are administered65 66 67. However the purpose of these tests is to find conduction faults in the SN. Findings such as long-latency potentials (for example the H reflex of the tibial nerve and/or peroneal nerve) may be normal at rest but become delayed in positions where the hip external rotators are tightened68 69 70.
It is accepted that the tibial division of the SN is usually spared, the inferior gluteal nerve that supplies the gluteus maximus may be affected and the muscle becomes atrophied71. However testing of the peroneal nerve may provide more conclusive results as is more likely to be the impinged portion of the SN. The H-wave may become extinct during the painful position of forced adduction-internal rotation of the affected leg72.
Stewart 2003 argues that piriformis syndrome is an often over-used term to describe any non-specific gluteal tenderness with radiating leg pain73. He argues that only in rare cases is the PM implicated in nerve compression of the SN to truly qualify as a piriformis syndrome. He cites only limited evidence and cases where the diagnosis of piriformis syndrome can be made.
McCory (2001) supports this argument by stating that it is more likely that (given the anatomical relationship of the PM to the various nerves in the deep gluteal region) the buttock pain represents entrapment of the gluteal nerves, and the hamstring pain entrapment of the posterior cutaneous nerve of the thigh, rather than the SN alone74 This would explain the clinically observed phenomenon in the absence of distal sciatic neurological signs. Whether the PM is the cause of the compression has not been clearly established. It is possible that the obturator internus/gemelli complex is an alternative cause of neural compression. He suggests using the term ‘deep gluteal syndrome’ rather than piriformis syndrome.
When it is believed that a piriformis syndrome exists and the clinician feels that a diagnosis has been made, the treatment will usually depend on the suspected cause. If the PM is tight and in spasm then initially conservative treatment will focus on stretching and massaging the tight muscle to remove the PM as being the source of the pain. If this fails, then the following have been suggested and may be attempted75 76:
Here, we will focus on therapist-directed interventions such as stretching of the PM and direct trigger point massage. It has always been advocated that PM stretches are done in positions of hip flexion greater than 90 degrees, adduction and external rotation to utilise the ‘inversion of action’ effect of the PM to isolate the stretch to this muscle independent of the other hip external rotators.
However, recent evidence from Waldner (2015) using ultrasound investigation discovered that there was no interaction between hip flexion angle and the thickness of the PM tendon in both internal and lateral hip rotation stretching – suggesting that the PM does not invert its action77. Furthermore, Pine et al (2011)78 and Fabrizio et al (2011)79 in their cadaveric studies found that the PM insertion is a lot more complex and varied than first thought. It is possible that the PM may invert its action only in some subjects but not others.
Therefore, due to the disagreements and confusions over the ‘inversion of action’ concept, it is recommended that the clinician ‘covers all bases’ and performs two variations of a PM stretch – stretches in flexion, adduction and external rotation and stretches in flexion, adduction and internal rotation. Examples of these stretches are given in figures 5-7 above.
The best approach to palpate the PM trigger points is in the position suggested by Travel and Simons80 and this is shown below. In this position, the clinician can feel for the deep PM trigger points and apply a sustained pressure to alleviate the trigger points – and also apply a flush massage to the muscle in this position. In this position the large gluteus maximus is relaxed and it is easier to feel the deeper PM
The PM is a deep posterior hip muscle that is closely related anatomically to both the sacroiliac joint and the sciatic nerve. It is a hip external rotator at hip flexion angles of neutral to 60 degrees of hip flexion, an abductor when in flexion and also contributes to hip extension.
It has been previously accepted that the PM will ‘invert its action’ or ‘reverse its function’ after 60 degrees of flexion to become a hip internal rotator. However, recent ultrasound and cadaveric studies has found conflicting evidence that this ‘inversion of action’ may in fact not exist.
PM is a muscle that is a dominant hip rotator and stabiliser, and thus has a tendency to shorten and become hypertonic. Therefore, stretching and massage techniques are best utilised to reduce the tone through the muscle. Furthermore, it has also been implicated in compression and irritation of the sciatic nerve – often referred to as piriformis syndrome’.
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