Lower limb strains: What a modified slump test can reveal

Mark Alexander proposes a novel approach to the diagnosis and treatment of lower limb strains

Most sports therapists have at some time come across patients suffering from lower limb injuries that appear to be chronic calf or hamstring muscle strains, yet there is no evidence of tears or strains on MRI or ultrasound scans(1,2,3). These conditions are commonly explained or diagnosed as lumbar (central nervous system) and/or neural (peripheral nervous system) in origin.

But frustratingly these muscle injuries are chronically recurrent, especially in the older athlete, despite our best efforts. So is there something we are missing in our assessment and treatment of these recurrent muscle conditions to ensure optimal injury prevention and management?

Here we explore a new neural interface concept involving the smaller nerves perforating through the fascia that surrounds muscle tissue, creating a potential neural entrapment. The focus will be on the calf/ lower leg, although this phenomenon may not be exclusive to this area, with the hamstring potentially being involved as well. These chronic muscle injuries have been explained as being either intraneural, which involves the nerve conducting or nerve connective tissue; or extraneural, which is external to the nerve tissue. Extraneural issues generally occur at interfaces defined as the surrounding tissue or material adjacent to or in contact with the nerve tissue(4).

We commonly think of neural interfaces as the sites where nerves pass through, over or around structures such as bone, muscle, ligaments and tendons. These are considered vulnerable points where stresses can be applied to the nerves. Pathomechanical and pathophysiological changes can occur to the nerve resulting in inflammation, adhesions and fibrosis(4).

One interface that hasn’t previously been described in the sports injury literature, however, is where specific nerves perforate or pass through fascia supplying muscles and skin with innervation(5). For example the medial sural nerve, a cutaneous branch of the tibial nerve, descends between the two gastrocnemius heads and at the mid-calf level moves outwards towards the skin, perforating the deep fascia. There, it joins with the peroneal communicating branch of the common peroneal nerve to form the sural nerve which supplies the skin to the lateral foot(6,7). This has been confirmed during superficial and deep dissection of the lower leg of a cadaver.

The region where the medial sural branch of the tibial nerve perforates the deep fascia anatomically correlates with a common site of tightness and apparent strain in the calf muscle. This is one example of an ignored interface that may lead to nerve entrapment, which I believe to be a common source of symptoms with chronic calf strains and tightness.

This neural interface is a likely point of irritation based on the amount of translational movement of lower limb nerves during movement. In one study the tibial nerve glided 10mm with hip motion and 2 mm with knee motion; the sciatic nerve glided 24mm with hip motion and 7 mm with knee motion(8). This joint movement occurs during running and so may produce some gliding of the cutaneous branch of the tibial nerve (medial sural nerve) through the deep fascia. Over time, if there is neural or fascial tightness, this may lead to neural irritation at the interface, and hence inflammation, adhesions and potentially fibrotic neural entrapment in the long term. There is MRI evidence of this occurring to the tibial nerve in the popliteal fossa (back of the knee joint) but not the medial sural nerve, where it perforates the deep fascia of the leg(9). Although there is no empirical evidence to support this concept, clinically adhesions can be felt in the calf muscle in the same anatomical region.

With regard to fascial movement, there have been studies that show movement of fascia in the lumbar region of cadavers from artificial muscular force of transversus abdominis and latissimus dorsi(10). Studies have measured the movement of the calf aponeurosis but not the fascia(11). But if the concept of fascial movement is extrapolated to the calf, when the muscles contract during walking and running, there may be some gliding of deep fascia in relation to the medial sural nerve. This may also lead to irritation and neural entrapment where the nerve perforates the deep fascia.

How to test

Neural and fascial length and palpation are the only ways to assess this condition in the clinic. I believe that a novel modified slump test performed in a lumbar lordotic position, as described by Purdam(12), could specifically sensitise and test the length of fascial tissue more than neural tissue (see Figure 1, above). The normal slump test is a measure of nerve length and some could argue that the test also involves the fascial system, but when performed in a lumbar lordosis there is a release of the proximal nerve structures which may specifically measure the length of the fascial structures.

Palpation is the most accurate form of assessment for this condition and can be done with the patient lying supine, knees bent and feet flat, so the muscle, nerve and fascia are off-stretch. This enables more accurate palpation of the nerves and adhesions within the muscle, and of any increased muscle tone. In symptomatic people, there are obvious adhesions in the mid-calf, deep between the two gastrocnemius heads, where the nerve perforates the fascia. Palpation usually reproduces both their site and type of pain.

[090662-IMAGE10]

Treatment

The treatment is performed in the same assessment position using transverse frictions across the line of the nerve where it perforates the deep fascia. Treatment time should only be 2 to 3 minutes as the technique is quite painful.

It is wise to teach patients to friction themselves at home for 2 to 3 minutes daily, to maintain treatment effectiveness.

I would reassess their modified lordotic slump test and then reassess a functional task such as running or hopping to determine if any improvement has occurred. Anecdotally results occur quite rapidly within two to three treatments.

Mr J’s calf strain

Mr J is a 43-year-old keen runner who had completed five marathons and had a long history of calf strains and tightness deep in the mid-belly of his right calf. He felt vulnerable to calf strains during most runs espe- cially after 10km. Massage and stretching had never alleviated the symptoms. He also had numerous treatments on his back with spinal mobilisations and also neural mobilisations in the slump and straight-leg raise positions with little benefit as the problem continued to recur.

On assessment his slump and straight-leg raise tests were symmetrical and only slightly restricted. The modified slump test in lumbar lordosis was symmetrical in range but he had a sensation of tightness and shearing at end of range in the area of his calf tightness. His lumbar spine assessment revealed nothing significant. His ankle range of motion and biomechanics were symmetrical and similarly not remarkable. During hopping and calf raises, after 5-6 reps he had a vague feeling of burning and tightness on the right side.

On palpation the right calf had noticeably more tone, and deep in the calf between the two gastroc heads there was a palpable adhesion about the size of a pea. When this adhesion was frictioned it reproduced the exact site of his symptoms and was extremely painful. The patient described it as like a knife being poked into his leg. On palpation there was nothing similar felt on the left side.

Treatment involved four sessions over two weeks of deep frictions and daily self-treatment at home, with one day off every three to four days to reduce the local bruising from treatment. The patient continued to run but reduced his mileage to 4-5km for two weeks. Ice was applied after runs. He also performed three stretches that were aimed at the neural and fascial system, such as the low back rotational stretch, the hamstring straight-leg raise stretch and the calf stretch.

On assessment after two weeks, the patient could run for 10km symptom-free, which he hadn’t been able to achieve for 12 months. The muscle tone was symmetrical. While there was still a small detectable adhesion on the right-hand side, it wasn’t excruciatingly tender as it had been. The patient continued his self-treatment and stretches and he was able to complete his sixth marathon three months later.

References

1.Connell DA et al (2004) ‘Longitudinal study comparing sonographic and MRI assessments of acute and healing hamstring injuries’ Am J Roentgenol2004 Oct; 183(4):975-84

2.Gibbs N et al (2004) ‘The accuracy of MRI in predicting recovery and recurrence of acute grade one hamstring muscle strains within the same season in Australian Rules football players’ J Sci Med Sport2004 Jun; 7(2):248-58

3.Verrall GM et al (2001) ‘Clinical features and MRI characteristics predictive for recurrent hamstring muscle strain injuries’ www.ausport.gov.au/ fulltext/2001/acsms/papers/VERR1.pdf

4. Butler DS (1991) Mobilisation of the Nervous System, Churchill Livingstone, Edinburgh

5. Gray’s Anatomy (2000) Anatomy of the Human Body, Lea & Febiger, Philadelphia. 20th Ed

6. Mestdagh H et al (2001) ‘Origin and make-up of the human sural nerve’ Surg Radiol Anat2001 Sep; 23(5):307-12

7. Ortiguela M et al (1987) ‘Anatomy of the sural nerve complex’ J Hand Surg [Am]1987 Nov; 12(6):1119-23

8. Babri AS et al (2003) ‘Longitudinal excursion of peripheral nerves of the human lower limb’ International Society of Biomechanics XIXth Congress, p24

9. Kim S et al (2006) ‘Role of magnetic resonance imaging in entrapment and compressive neuropathy – what, where, and how to see the peripheral nerves on the musculoskeletal magnetic resonance image: part 1. Overview and lower extremity’ Eur Radiol2006 Mar

10. Barker PJ et al (2004) ‘Tensile transmission across the lumbar fasciae in unembalmed cadavers: effects of tension to various muscular attachments’ Spine15; 29(2):129-138 11. Muramatsu T et al (2001) ‘Mechanical properties of tendon and aponeurosis of human gastrocnemius muscle in vivo’ J Appl Physiol90: 1671-1678

12. Purdam C (2000) Australian Institute of Sport. personal communication