Chris Mallacoffers a radical view of the diagnosis and causes of hamstring pain
A 25-year-old professional rugby union tight head prop forward presented with hamstring pain in his right leg that had come on during a game three days earlier, after a collapsed scrum. The player had played on with the injury but was aware of the hamstring whenever in a forward lean position such as scrums, breakdowns and when tackling. He had a history of low back tightness and symptoms over the years, with magnetic resonance imaging scans showing mild L1/2 and L5/S1 disc degeneration. His low back symptoms had never caused him to miss a game.
On examination the patient’s standing posture showed increased thoracic kyphosis (mid-spine curvature) with overdeveloped thoracic erector spinae muscles (particularly on the right), increased lumbar lordosis (arching of the low back) and anterior pelvic tilt. Stretch tests showed the hip flexors to be tight, and both hamstrings, with right side straight-leg raise (SLR) restricted to 70 degrees and left to 85 degrees. Knee extension with hip flexed to 90 degrees while lying supine was about 45 degrees (from vertical) on the right and 30 degrees on the left. Both stretch tests reproduced posterior thigh symptoms in the right hamstring.
While the rugby player’s hamstring strength proved normal, the tests reproduced his awareness of symptoms in the hamstring. He had increased muscle tone in the gluteals, hamstrings, and in particular erector spinae on the right and latissimus dorsi on the left. A standing latissimus dorsi length test (see box above) showed the left latissimus to be tighter than the right. Slump testing (see below) was positive for hamstring symptoms on the right.
The combination of the collapsed scrum and tightness exhibited in the left latissimus and right erectors made me think initially of the myofascial system in the trunk and arms as being a contributing factor in this player’s posterior thigh symptoms. It is known among ‘rugby therapists’ that tight head props tend to exhibit paraspinal muscle spasm on the right because of the asymmetrical forces acting across the spine during scrums, and latissimus and shoulder tightness on the left because of the left arm being the ‘binding’ arm in scrums.
While I had not ruled out the possibility of a hamstring injury, as a quick and experimental ‘fix’, I used this player as the proverbial guinea pig to assess the response of his slump test after I’d done some deep soft tissue massage and releases of the right paraspinal and left latissimus dorsi muscles. I deliberately avoided the lumbar areas, gluteals and the hamstrings.
Upon retesting, his straight-leg raise showed an improvement from 70 degrees to 80 degrees on the right, with some awareness of symptoms in the hamstring; his left knee extension went from 45 degrees to 30 degrees (same as right side), and he felt mild sensation on his hamstring strength tests. The slump test had markedly improved, with symptom awareness through the left gluteal but not the hamstring.
I continued treating the hamstring, gluteals and hip flexor trigger points. After three days of treatment, the player was back in full training, symptom free.
What makes this case interesting is that treatment directed to a non-neural tissue resulted in an improvement in a ‘neural’ test such as the slump test. Is it possible that the interconnecting myofascial system of the trunk and limbs is a factor in producing false-positive slump tests?
The slump test
Physiotherapists use this test widely to help assess and treat lumbar spine and posterior thigh symptoms. When Maitland introduced the test in 1978(1), it was a means of assessing the mobility of structures within the vertebral canal that can lead to pain.
These include the spinal cord and its associated outer layer, the nerve roots, posterior ligaments and posterior discs. It is also suggested that the test can assess the mobility of peripheral nerves. As a straight leg raise and cervical flexion both increase tension in the spinal cord, combining both movements should increase the tension in the spinal cord more than either technique performed in isolation.
Perform the slump test with the patient supported sitting on a bed/plinth, with the backs of both knees flush up against the edge of the bed and the shins and feet hanging suspended. The patient places their hands behind their back and bends at the hips and trunk to ‘slump’ their chest towards the knees. They then fully flex their cervical spine (chin on to chest), a position maintained by the examiner.
The knee of the limb to be assessed is manually extended. If it reaches full extension, the ankle is dorsiflexed. If this reproduces the patient’s symptoms, they are asked to extend their cervical spine. If the nervous system is implicated in producing the symptoms, these will reduce. Alternatively, the patient may be instructed to plantarflex and dorsiflex the ankle. Again, symptoms associated with spinal cord and sciatic/tibial nerve should lessen in plantarflexion. Issues with the common and deep peroneal nerve may be reproduced with plantarflexion and inversion.
The slump test assesses adverse mechanical tension in the nervous system. It is thought that it may assess the development of tension or pressure within the nervous system, as well as movement of the nervous system relative to its interfaces(2). In order for the test to be considered positive, a number of criteria must be satisfied(2):
*The test reproduces all or part of the patient’s symptoms
*The symptoms reproduced are different to those reproduced in the other limb (unilateral symptoms); or if symptoms are bilateral, they should be different compared with what is known to be normal
*Sensitising and desensitising movements either provoke or relieve the pain. For example, ankle dorsiflexion/plantarflexion should increase/decrease hamstring symptoms.
However, a positive slump test does not necessarily imply a mechanical disorder of the nervous system. Symptoms may be neural in origin or caused by the interface between neural tissue and an adjacent structure. These include:
* the intervertebral discs and associated ligaments in the spinal canal
*the intervertebral foramen (exit points for nerves)
Slump and hamstring symptoms
There is little evidence on the role of the slump test in posterior thigh symptoms. The two studies worthy of note have looked at Australian Rules (AFL) players and rugby players.
Kornberg and Lew(3)showed how using slump as a treatment modality in AFL players with Grade 1 hamstring strains is more beneficial in returning athletes to sport than standard physio alone (defined as massage, ultrasound, progressive flexibility and strength work).
Turl and George(4)studied male rugby union players with a history of repeated Grade 1 hamstring strains. They found that 57% of the experimental group (hamstring strain group) had a positive slump compared with none of the control group. They suggest that adverse neural tension is related to repeated Grade 1 hamstring strains, but do not ascribe a cause and effect relationship between adverse neural tension and hamstring strain.
Despite the lack of empirical evidence, physiotherapists and athletics trainers world-wide heavily incorporate slump mobilisations/stretching in the management of ‘hamstring strains’. Furthermore, it is clinically evident that a significant proportion of hamstring victims produce a positive slump test.
However, the question remains: is it possible that there is a different anatomical source for these posterior thigh symptoms reproduced with slump testing? Specifically, might it be that symptoms emanating from the myofascial system of the trunk and limbs can reproduce ‘hamstring’ sensations?
The thoraco-lumbar fascia (TLF) is a dense connective tissue structure that covers the lower thoracic and lumbar areas of the back. Some important muscles and fascia (connective tissue) blend with the TLF. In particular, Vleeming et al(5)have shown the importance of the relationship between the posterior layer of the TLF and muscles such as latissimus dorsi, transversus abdominis, internal and external obliques, gluteus maximus/ minimus, erector spinae and trapezius.
In a landmark study of the role, the TLF plays in load transfer between the spine, pelvis, legs and arms, Vleeming(5)showed how tension in various muscles can impart a tensioning effect over the TLF. This study highlighted how leg muscles can interact with spinal and arm muscles via the TLF. That is, tension in one muscle group may impart tension to another more distant muscle group via the TLF. In summary, the important findings from this study are:
* Contraction of the opposite-side latissimus dorsi and same-side gluteus maximus and erector spinae will increase tension in the superficial layer of the TLF
* Contraction of the trapezius will increase tension in the superficial layer, but to a lesser degree than above
* Contraction of the biceps femoris will increase tension in the deep layer of the TLF.
Barker and Briggs(6)support this anatomical finding by suggesting that the biceps femoris is continuous with the sacrotuberous ligament (STL), blending with the long dorsal sacroiliac joint ligament and then the posterior layer of the TLF. This in effect connects the hamstring to the back of the head via the TLF and the thoracic extensors/fascia.
From these anatomical studies, Vleeming and colleagues propose that a number of myofascial ‘slings’ exist that help the body to transfer force from upper to lower body and vice versa. There are three main slings:
* Posterior oblique sling– latissimus dorsi, TLF and opposite gluteus maximus
*Anterior oblique sling– external oblique, abdominal fascia and contralateral adductor
* Posterior longitudinal sling– erector spinae, long dorsal sacroiliac ligament, sacrotuberous ligament and biceps femoris.
So to return to our question: does the slump test assess solely neural mobility or might it also be positive for tension in the myofascial system? Might the test in fact tension the entire myofascial system from the cervical spine muscles and fascia all the way down to the lower limb muscles and fascia? And for this type of false-positive result to be possible, we would also need to discover how it was possible for tension in one part of the system to reproduce pain and sensations in a more distal component of the system.
The interesting idea highlighted in this case study, is that the myofascial system can be considered an alternative source of dysfunction in soft-tissue injury. The work being published by Vleeming et al will one day redefine how anatomists and biomechanists describe muscle attachments and the invest- ments that the fascia has with muscles. No longer will muscles be considered as running solely from bone to bone, but from bone to extensive fascial tissue, the muscle tissue itself and bone.
This, in turn, will lead those involved in the study of movement to consider how force is transferred from one part of the body to another using this complex network of fascial sleeves and slings. Similarly, therapists and those involved in sports medicine will need to reconsider the role that the fascial system has in pain syndromes as well as implications for the prescription of rehabilitation protocols after injury to the musculoskeletal system.
1.Maitland GD (1978) ‘Movement of pain sensitive structures in the vertebral canal in a group of physiotherapy students’ Proceedings of the Inaugural Congress of Manipulative Therapists, Sydney
2.Butler (1998) Adverse mechanical tension in the nervous system: a model for assessment and treatment. In ‘Adverse Neural Tension reconsidered’ Australian Journal of PhysiotherapyMonograph Number 3, 1998, pp19-31
3.Kornberg C and Lew P (1989) ‘The effect of stretching neural structures on grade one hamstring strains’ Journal of Orthopaedic and Sports Physical Therapy13:481-487
4.Turl SE and George KP (1998) ‘Adverse neural tension: A factor in repetitive hamstring strain?’ Journal of Orthopaedic and Sports Physical Therapy 27:16-21
5.Vleeming A, Pool-Goudzwaard AL, Stoeckart R, van Windergen JP and Schnijders CJ (1995) ‘The posterior layer of the thoracolumbar fascia. Its function in load transfer from spine to legs’ Spine. 20(7):753-758
6.Barker PJ and Briggs CA (1999) ‘Attachments of the posterior layer of the lumbar fascia’ Spine. 24(17):1757-1764