I recently reviewed a surface EMG scan of a patient who was assessed by her Chiropractor. If you haven’t seen how these scans are performed it is definitely worth looking at the report of findings, which provide a wonderful graphic representation of muscle activity along the spine. The data is collected using a two-pronged probe, which is positioned on either side of the spinous processes and moved along the length of the spine with readings taken at each segmental level. This then gives a bar chart of muscle activity on either side of the spinal column. This is then equated to segmental levels and considered as part of a diagnosis of segmental dysfunction.
I have looked at several of these surface EMG measurement systems over the years because I have been struck by how impressed patients are by the graphics and detail reported.
My issue(s) in terms of diagnostic utility are all those related to the usefulness and accuracy of surface EMG, which seem to present such confounding challenges as to be almost clinically useless – at least in my hands. I spent too many hours trying to explain / justify variances in VMO/VL EMG ratios to patients that did not correlate with the clinical picture it became embarrassing – so I abandoned the technology.
Secondly comparing manual therapy examination to surface EMG readings I would have much more confidence in palpatory findings. Of course this doesn’t have the graphical representation or technological appearance but ultimately changing an EMG score without palpable change in muscle texture or sensitivity is of little practical value.
I also think that given the complexity of compensatory reactions we see in our patients, finding scattered areas of muscle tension distributed throughout the spine is hardly an unusual or an expected finding in clinical practice. The challenge really is in defining what is primary and what is secondary, what is clinically relevant and what is not.
There is an increasing trend within the Chiropractic and Health Promotion industry to use this type of screening as part of a wellness approach. These “physiological measures” are coupled with other measurements i.e. skin temperature, skin conductance and heart rate as supposed indicators of the state of health. I am very much in favour of the pursuit of wellness but I do wonder if this is a case of pseudo science used to substantiate a worthy cause?
Nonetheless it is undeniable that graphical reports of findings and numerical scales are certainly attractive to patients and may well enhance the compliance. Unfortunately these systems are relatively expensive and I would therefore find it hard to justify purely on the basis of increasing patient “buy-in”.
Do any of you have positive experiences with surface EMG?
Please share your thoughts.
Do you think we, as Physiotherapists, are effective in relaying our examination results and defining care pathways?
I think the Chiropractic profession handle this issue of report of findings in a very effective way. Can physiotherapy rise to the challenge?
Enjoy the clinical challenge.
Understanding the biomechanics of the thoracolumbar fascia is a necessity for clinicians using therapeutic exercise in the management of lumbo-pelvic pain. When this concept was first proposed in the 1990’s it was hypothesised to contribute almost 50% to the support of the spinal column. These approximations have been revised down to 20% in recent years.
Hope you enjoyed but more importantly found this useful. What do you think of this type of format?
Please feel free to share your thoughts in the comment’s area.
Enjoy the clinical challenge.
DavidGHTime Code(s): nc
The sacroiliac joint has now been well established to actually move yet clinicians of my generation and older would certainly be aware of the argument that the sacroiliac joint did not normally move except in pregnancy. Suffice to say that we have now moved beyond this argument for the normal population and the clinical challenge is diagnosing not only the existence of sacroiliac dysfunction but the mechanism behind the dysfunction.
Radiological imaging does not particularly add to the diagnostic work-up so we are left to rely on clinical assessment. In the last decade Vleeming and Schneider’s have advanced the concept of both “form and force closure” as the primary mechanisms maintaining sacroiliac stability.
Form & Force Closure
In brief, form closure refers to the configuration of the joint surfaces, the alignment of these surfaces relative to gravity and bodyweight, and the tension in the restraining ligaments associated with normal alignment of the segments.
Force closure refers to the interaction of multiple muscle groups, which act across the joint to enhance compression on the joint surface to assist in joint stability. This is the so-called oblique sling system, which has been conceptualised to involve the ipsilateral Glueteus Maximus and Tensor Fascia Lata in conjunction with the contra lateral latissimus dorsii. This is enhanced anteriorly by the oblique abdominal system and the contra-lateral hip adductors.
These two oblique systems effectively form an X (cross shape) on the anterior and posterior aspects of the pelvis and constitute the dynamic mechanism by which joint integrity is maintained. These concepts appear to hold some clinical validity and have provided an enhanced framework for us to approach our treatment of the sacroiliac joint.
Lee has integrated this approach with some of the traditional osteopathic models to provide a clinical algorithm for determining sacroiliac dysfunctions. This involves evaluation of:
1) Lumbar spine
2) Pelvic landmarks,
3) Sacral landmarks.
This provides a practical framework where we as clinicians can try to differentiate primary or secondary pelvic dysfunction and therefore target our treatment in the most appropriate way. Because of the functional interaction of body segments a lumbar scoliosis, for example, can have secondary effects on the sacroiliac joint alignment and conversely sacroiliac mal-alignment may produce secondary scoliosis in the lumbar spine. This is the classic “chicken and egg” scenario.
So using the above categorisations we can quantify spinal alignment using:
Palpating bony landmarks
Correlating with movement pattern in the lumbar spine.
Looking specifically at the pelvis we can define the position of the bony landmarks on the pelvis using:
as reasonably reliable landmarks to assess the positional orientation of these bones.
The spectrum of pelvic dysfunctions which have been described include:
Anterior innominate rotation
Posterior innominate rotation
Much debate exists regarding the reliability and mechanism of these syndromes so it is largely a clinical diagnosis.
The principle assumption of quantifying bony pelvic orientation is that the pelvic position will determine the position of the sacrum and therefore mal-alignments of the pelvis should be prioritised over sacral mal-alignments when they are observed to co-exist.
In general the principles of correction are either to use manipulative thrust procedures, joint mobilisation or muscle energy / myofascial techniques to help to realign the pelvic structures using the leverage of the torso or lower limbs. This then leaves us in a situation of assessing the sacral position within the corrected pelvic rim and then ascertaining the sacral orientation. A number of sacral dysfunctions have been categorised.
1) Nutated sacrum
2) Counter- nutated sacrum
3) Oblique axis twist indicating a spinning mechanism where one side of the sacrum lies deep and the other lies more superficial.
Assessing sacral position within the pelvis is challenging clinically, produces more inter-tester variability and is harder to be confident with. However it is well worthwhile using this clinical algorithm to define joint mal-alignments clinically and plan treatment strategies.
Crossing the first hurdle of defining the dysfunction the challenge is then to determine why mal-alignments have occurred and whether we can assess breakdowns in functional control (force closure mechanisms) which may be associated with overload- but that’s another day’s work and a discussion for another time
Enjoy the clinical challenge.
Lumbar pain on flexion is one of the commonest symptom reports clinicians hear when treating patients low back pain. There are a number of clinical reasoning processes, which need to be considered.
Much of the literature focuses on the changes in intra-discal pressure associated with spinal flexion implying that spinal flexion pain is associated with increased disc strain reproducing symptoms. In order to strengthen the hypothesis of disc related flexion pain the clinician needs to establish other components of discogenic characteristics to support the hypothesis.
These can range from the overtly obvious…..
gross global movement restriction
positive neuro-provocation tests
to the other end of the spectrum where symptoms are only produced on flexion and only localised in the lumbar spine. Of course acknowledging that any of the spinal elements may reproduce pain on flexion and this produces a list of potential targets to include:
posterior longitudinal ligament
local segmental musculature
Symptom Location – clues to aetiology
The ability to localise symptoms can give the clinician some clues as to the possible structures involved, but in cases of centralised pain this does not particularly enhance diagnostic accuracy other than to reduce the likelihood of facet joint involvement.
Interestingly typical treatment approaches for flexion related pain is to use extension/McKenzie’s extension protocols, passive accessory intervertebral motion to facilitate extension (Maitland). Undoubtedly this strategy is helpful for patients when improvements in tolerance for extension related treatments show simultaneous improvement in flexion capacity. And for those that don’t?…….
What do we do for patients whose flexion does not improve with extension regimes?
The caseload of interest here are the patients who might be categorised as non-specific low back pain who have persistent problems with spinal flexion. Here is a list of tips for things to evaluate when accessing this function:
- Spinal segment flexion range.
- Hamstring flexibility.
- NeuroDynamic sensitivity.
- Proximal trunk control.
- Pelvic rotation on femoral heads.
- Sacroiliac nutation.
- Hip extensor muscle function on flexion (eccentric control).
- Hip extensor muscle function on return to upright (concentric control)
- Paraspinal / abdominal co-activation on return to upright.
- Lumbal-pelvic rhythm on flexion.
11. Lumbal-pelvic rhythm on return to upright.
Evaluating each of these components allows the clinician to determine mechanisms of breakdown and plan treatment strategies to facilitate recovery. Exploring these mechanisms is relevant for non-responders to extension regimes.
Enjoy the clinical challenge.
The basic mechanics of gait and propulsion dictate that the extensor chain mechanism must operate in an integrated way to convert ground reaction force into forward momentum. From a clinical perspective we are interested in the integrated activity of ankle plantar flexion, hip and knee extension and controlled but stable trunk alignment on the propelling limb. There are a number of potential mechanisms of breakdown in this region, which can be broadly categorised as:
motion impairment deficiencies
muscle power deficiencies.
Impairment of ankle dorsi flexion range inhibits the ability of the foot to act like a pivot and allow body weight to transfer in front of the axis of the ankle joint in order to facilitate propulsion.
Impairment of knee extension effectively shortens the length of the standing leg and reduces the efficiency of forced transmission through the lower limb. Typically in association with impaired knee extension is an increased co-activation of the hamstrings and quadriceps with the net result of a stiffening of the limb and reduction in “fluidity” of knee motion.
The next component of the extensor chain is the ability to extend the hip. In cases where postural alignment tends to be flexed the centre of gravity remains anterior to the axis of the hip joint producing a perpetual flexion moment. This is perpetuated by sustained hip/flexor muscle activity in conjunction with the anterior abdominal wall. In order for the hip to function freely there needs to be passive range of hip extension and sufficient power within the prime hip extensors (gluteus maximus) to generate the propulsion.
In clinical practice impairment of this fundamental component of gait is exceedingly common and often results in a combination of compensatory strategies. One compensatory strategy for impairment of hip extension is to induce excessive sacroiliac torsion producing increased anterior rotation of the innominate bone. This may subsequently produce secondary strain through the lumbosacral junction or induce a motion pattern of lumbar hyperextension in order to bring the leg behind the body. Not only is this movement pattern inefficient but produces a high risk of tissue overload in the zones of compensation.
- How can we detect breakdowns in the extensor chain function?
- What are the implications of a hyperlordotic strategy for hip extension in relation to trunk stability?
- What are the implications of anterior innominate rotation as part of the facilitatory mechanism of leg extension?
Share your thoughts and …..
Rise to the clinical challenge.