MYOFASCIAL PAIN SYNDROMES – Unanswered Questions?

Developments in the field of Myofascial pain syndromes over the  last decade has seen  significant evolution from the initial classification of trigger points as taut bands with research seeking to identify physical lesions and define location. Most of this development has been in the field of:

Biochemistry

Radiographic imaging

Elastography

Microdialysis techniques

Integration with our current understanding of pain mechanisms

Debate has now moved beyond whether Myofascial taut bands as entities actually exist into a more refined analysis of:

Identifying patient subgroups

Alternative etiological mechanisms

Identifying optimal management strategies.

The first point to recognise is that the cause of trigger points is still a matter of speculation. Travelle and Simons originally described both active and latent trigger points – latent to describe the concept of the clinical recognition of a palpable nodule, which was not reproducing symptoms.  The working assumption is that latent trigger points can exist without pain but then become activated for some reason.  As Robert Gerwin has alluded to trigger point tenderness does not occur except in regions of muscle hardness.  But regions of muscle hardness occur without local or referred pain.

It is currently “assumed” that the muscle hardness or taut band that occurs in the absence of pain is the first abnormality and that active trigger point is a more developed or second stage of the trigger point.  However this still remains hypotheses at this point.

Jay Shah amongst others has contributed largely to our knowledge on the biochemistry of the trigger points using microdialysis techniques.  This has indicated that there is a local mechanism of nerve sensitisation involving release of local neurotransmitters, hydrogen ions, potassium and cytokines, which are all classically associated with a peripheral inflammatory response (peripheral sensitisation).  The activation of these pathways also feeds into a central sensitivity state, which can become self-sustaining and independent of the peripheral components or essentially be a mirror of the state of peripheral sensitivity.

If the mechanical hypotheses of inducing trigger points is extrapolated there is a potential cascade of events involving neurotransmitters as alluded to above and also the release of acetylcholine at the motor end plate which amplifies motor end plate discharge and is thought to be associated with the development of localised muscle contractions – however this is only one of a number of theories.

Studies many years ago by Professor Patrick Wall indicated that taut bands can be produced in muscles simply by persistent depravation of sleep over a forty-eight hour period.  Clearly this mechanism is not associated with a mechanical event.  This raises the tantalising question of the chronic persistent myofascial pain syndrome in which:

Fatigue

Sleep disturbance

Muscle pain

are part of an integrated triad which is often challenging to resolve clinically.  What does appear evident from clinical observation is that mechanical muscle overload can occur at different ends of the spectrum from an acute severe overload that doesn’t induce fibre disruption but initiates sustained physical overload of  muscle fiber with the presumption of initiating the biochemical responses alluded to earlier.

At the other end of the spectrum is a low load, sustained activity associated with postural, ergonomic or occupational factors which by its nature is a less severe mechanical effect but cumulative over a longer period of time.

Other factors associated with the development of trigger points are:

Weakness

Hypoxia

Ischaemia

Central sensitisation

Referred pain

Gender

Hypermobility

The Diagnostic challenge

According to Jay Shah regarding this particular issue “validation of clinical diagnosis by palpation with these and other objective tests e.g. magnetic resonance & elastography would help establish the reliability of the clinical examination not as interrater reliability but in terms of the reliability of the physical examination to identify those patients whose myofascial trigger points is verifiable by other mean.

Current laboratory studies that show abnormalities would have to be validated themselves by showing that they independently identify trigger points that can be treated resulting in pain relief and improved function”.

Robert Gerwin adds “ there remains a need to develop a consensus on the clinical features required to diagnose myofascial trigger points.  There is also a need to develop objective laboratory criteria that can be used to standardise a diagnosis for the purposes of research.  They may have clinical value if they can be used to confirm an examination made by physical examination.  Elastography needs to be studied in a variety of trigger point pain syndromes”.

Treatment

The current treatment spectrum encompasses:

Stretch & spray

Local soft tissue mobilisation

Direct trigger point pressure

Dry needling

Injection therapy

Comparison of these modalities is still in its infancy other than anecdotal clinical evidence.

So in summary still much to do in this area of myofascial pain syndromes.

Enjoy the clinical challenge.

David

GHTime Code(s): 3acb9 00a7c nc nc nc 

The Patient’s Perspective

Knowing what patients are thinking and saying about your Practice is an important aspect of patient management, which is rarely discussed amongst professionals.  On our first patient encounter we have no idea of their historical beliefs about Physiotherapy, their expectations, their fears, their level of compliance, their commitment to finding a definitive solution, their financial circumstances or their social environment.

On initial reflection our initial impression maybe that we cannot influence many of these variables because they are either outside our remit, outside our scope of practise or simply beyond our control.  Previous posts on this blog have referred  to psychosocial flags and extrapolated beyond the well known Red and Yellow flags to the more recently updated concept of Orange, Black and Blue flags.  If you are rusty on what those definitions refer too you can review them here and here.

It raises the very contentious issue of defining what variables are modifiable and which are not. This is contentious because Health Economists tell us repeatedly that education, socio-economic standing, geographical location and social structure are predictive factors of the utilisation of Health Services.  These factors are also strongly associated with poor outcomes, which then raises the obvious question – why bother?  In my own working environment, which is a Private Clinic, patients either self-fund or are reimbursed by a third party payer.  I naively thought many years ago that patients who were paying for treatment would be more motivated to achieve a rapid resolution of their situation and demonstrate enhanced compliance with recommended regimes.  Twenty-two years of experience, with twenty in the private sector, has convinced me that this is not the case.

However, I have concluded that patient expectations of a solution are certainly high in this environment – but that does not always translate into shifting the locus of control from the clinician to the patient in terms of compliance.  Perhaps it is a case of patients paying and therefore expecting the solution to be passively provided?  Whilst it is undoubtedly a pressure which clinicians in this environment will be aware of, it is frequently an untalked about subject and not particularly conducive to developing a good therapist/patient relationship when the initial discussion approaches ability to pay.

My dentist colleagues suggests that not discussing money at the outset of treatment is indicative of a lack of confidence of the therapist and a self-depreciating view of the value of the service provided.  Whilst this maybe one explanation I would contend that the Public’s perception of good dental hygiene – having the “Hollywood” smile is probably far more pervasive and well established than having optimal musculoskeletal health.  Dentists have shifted their paradigm from being “tooth extractors” to being preservers delivering prophylactic care and self enhancement services. I am still of the view that most patients consult physiotherapists when something has failed rather than to enquire about musculoskeletal health. We have a road to travel in this department.

On this basis the value that is attached by a patient to Physiotherapy relative to Dentistry I suspect is somewhat different unless they have had positive previous experiences.  Ultimately it comes down to individual choices and I have never come across a patient who has terminated their satellite TV subscription service, stopped smoking or reduced their frequency of pub visits in order to fund Physiotherapy.  Of course this may have happened without formal discussion but I suspect it would be a rare circumstance?

How frequently in clinical practice do you ask if patients are satisfied with the service  they are getting and whether it is meeting patient expectations?

Do patients get the message that you are satisfied with the rate of progress?

If patients have plateaued or are failing to respond are you comfortable approaching this subject in the knowledge that it is the pathology hindering resolution rather than therapist inadequacy?

Or is it a skill deficit?

This leads us then into a terrain which we have previously discussed regarding defining the patient’s prognosis and either confronting the issue of a poor outcome or making rational decisions for onward referral to other health professions who can be of practical assistance.  It is far to frequent an occurrence for Physiotherapists to send the patient back to the G.P. or for surgical consult when these strategies do not influence the practical management but simply abdicate the therapist from having a frank (and potentially unpleasant) conversation with the patient.  If we want to be respected as a profession we need to bear this responsibility as part of our duty of care.  We will return to this issue in subsequent posts no doubt.

Enjoy the clinical challenge

David

GHTime Code(s): fba08 b7bcf nc 

Core Stability – current concepts

Todays posting is a slide presentation by Prof Eyal Lederman on core stability.  This is a subject we have discussed previously when considering core stability and functional movement and I thought another perspective would be useful at this point. I first became aware of Eyal’s work from a book he published in 1998 called “Fundamentals of Manual Therapy” by Churchill Livingstone. I’ve drawn from this text frequently for information on the basic sciences relating to manual Therapy such as :

Tissue repair
Fluid mechanics
Motor Control
Muscle Tone
Pain Mechanisms
Modes of therapeutic effect

The presentation servers as an excellent literature review as well as a thought provoking perspective on a common clinical issue.

Follow the link below to access

www.physiodigest.com/?attachment_id=5278

We also looked at core stability and gait mechanics in a previous post dealing with practical applications in a clinical setting.

Enjoy the clinical challenge.

David

GHTime Code(s): af2d3 445f6 nc 52974 9dffe 4f947 

Sacroiliac joint – Kinetic Tests

Much has been written about the sacroiliac joint Kinetic tests and their value in differential diagnosis of lumbar pelvic dysfunction. My good friend and colleague Howard Turner has written extensively on this subject many of you will know his work in teaching “A combined approach to the sacroiliac joint”. Howard has developed an assessment protocol incorporating variations of kinetic tests to evaluate the mechanical competence of the lumbar pelvic area and to assist with diagnosis of mechanisms of dysfunction and therefore selection of appropriate treatment techniques.

Like many aspects of diagnostic testing and most in musculoskeletal physiotherapy very few tests are definitive taken in isolation and the current trend is to use clinical prediction rules which group a number of tests in order to confirm or refute positivity. This allows the examiner to conclude with greater confidence when a group of tests are positive even in the presence of some non-positive tests.

Assessment of sacroiliac dysfunction – Foundations.

1. Active straight leg raise test.

2. Pain provocation test.

3. Kinetic tests.

4. Positional assessment.

5. Leg-length tests.

6. Passive movement assessment.

In previous posts I have discussed the role of positional assessment and Leg length testing in relation to mechanical assessment of the pelvic girdle. Today we will focus our discussion on the kinetic tests as they have been formally described. Several renowned authors have written on this topic over the years the most notable being Philip Greenman (an osteopath), Diane Lee (Canadian physiotherapist), Richard DonTingy (US physiotherapist) and Howard Turner (Australian Physiotherapist)  referred to above who has been conducting courses in the British Isles and internationally for the last 15 years on this topic.

Kinetic Tests

Forward Flexion in standing / sitting.

Hip Extension in standing.

Hip Flexion in standing (Stork / Fowler / Guillet Test).

Lateral Flexion in standin.

Rotation in standing / sitting.

When interpreting Kinetic tests it is important to recognize that the evidence of dysfunction does not infer a mechanism of pathology.

The pathology may lie in the articular system, the myofascial system.

The pathology may be local to the pelvic girdle and sacroiliac joint.

The pathology may be secondary to lumbar spine or general postural alignment characteristics

The interpretation of “positivity” is based on the extent of variance from expected norms and the number of positive tests.

The selection of legitimate targets for intervention is based on the degree of deviation on the kinetic tests rather than the side of dominant pain.

Those of you who treat the sacroiliac joint dysfunction frequently are well aware of the propensity of this joint to demonstrate alternating sides of symptoms which can sometimes leave a therapist “chasing pain” rather than identifying primary underlying mechanisms.

1. Forward Flexion in standing

Therapist : palpates inferior aspect of PSIS inferiorly

Patient : flexes forward to end of range.

Normal : PS IS move symmetrically bilaterally

Dysfunction: asymmetrical movement of PS I S. which may be early or late in the movement pattern or the PS I S. moves more Cephalad on flexion

2. Hip extension in standing

Therapist: palpates the idiom and sacrum on one sacroiliac joint.

Patient : extends the hip.

Normal: the PS I S raises cephalad relative to the sacrum

Dysfunction: PS I S. and sacrum move together

3. Hip Flexion in standing (Stork / Gillet / Fowler tests)

Therapist: palpates Ilium and sacrum of one SI joint

Patient: flexes they hit to 90° flexion.

Normal: PS I S. drops caudad relative to sacrum

Dysfunction: increased or decreased movement of Ilium relative to sacrum

4. Rotation in standing

Therapist: palpates Ilium and adjacent sacral segment.

Patient: rotates their torso.

Normal: sacrum lifts relative to PS I S.

Dysfunction: increased or decreased movement of sacrum relative to ilium

PS : the trunk  should rotate to the side of the tested S.i. joint.

5. Lateral flexion in standing

Therapist: palpates Ilium and sacrum of one SI joint.

Patient: performs lateral flexion.

Normal: PSIS drops and sacrum lifts on the side to which lateral flexion occurs

Dysfunction: increased or decreased movement of Ilium relative to sacrum

Clinical Thoughts?

1. Why does the Ilium move cephalad in standing flexion?
2. Why does the ilium move inferiorly relative to the sacrum in Gillet test?
3. How does the coupling of motion occur between Lumbar spine, Sacrum and Ilium in trunk rotation?
4. How do the pelvic biomechanics in lateral flexion occur ie how is the coupled motion achieved?

Enjoy the clinical challenge.

David

GHTime Code(s): nc 8daa9 

Neurodynamic Testing – Coming of Age?

Neurodynamic or adverse neural tension assessment as a concept of examination and treatment became popular in the 1980’s.  I had recently cause to reflect on how far things have come when I received a letter from my local Consultant Rheumatologist indicating that a patient he had assessed demonstrated a mild positive “Slump test”.  What was most satisfying from my perspective was that the slump test  (pioneered by a Physiotherapist) and utilised in routine musculoskeletal clinical practice has now transcended inter-disciplinary boundaries.

You may recall that Jeff Maitland was the first to describe the concept of a slump when he observed that patients reported an increase in their low back pain when flexing their head to get into a car seat.  This coincided with a body of anatomical work from a Swedish Orthopaedic Surgeon Alf  Nachemson, who performed much of the basic science research looking at neural tissue movement, its relationship to the interface and the mechanisms of pathophysiology.

Other pioneer’s in the field of peripheral neuropathic physiology were Sir Sidney Sunderland and Goran Lunborg.  Both of these researchers contributed vastly to the understanding of peripheral nerve physiology and most importantly the nerve pressure gradient, which is the mechanism for understanding normal homeostasis across a peripheral nerve.  In the early 1980’s two Australian Physiotherapists Bob Elvey and David Butler simultaneously described nerve sensitivity tests for the upper limb, which became known as the Brachial Plexus Tension Tests and have more recently been defined as the Upper Limb Neurodynamic Tests.  These have become so widespread in Undergraduate Physiotherapy Curriculum’s that testing for neural sensitivity either in the axial skeleton or the peripheries is now considered a mandatory component of any physical examination performed by competent Manual Therapist’s.

My colleagues in Occupational Medicine tell me that it is becoming more prevalent to see Occupational Physicians describing normal or positive upper limb tension test responses in patients they examine.  Over the years I have spent some considerable time training, studying and teaching with some of the above-mentioned experts and trying to impart some of this knowledge on the G.P. training schemes for which I have input.  I must sadly acknowledge that I have never received a letter from a G.P. describing altered neurodynamics and do wonder whether these concepts have reached the broader aspects of application in musculoskeletal primary care.

Do any of you have evidence of neurodynamic evaluation by your referring physicians?

Perhaps this is a secret which should be kept amongst Physiotherapists and used as a silver bullet to resolve challenging pain problems where altered neurodynamics form part of the symptom pathology?

Let us know your thoughts.

PS The positive Slump test reported was actually localised dorsal sacroiliac ligament pain with pseudo sciatica from Piriformis syndrome but that’s a discussion for another day!!

Enjoy the clinical challenge.

David

GHTime Code(s): nc nc nc 087bf nc 

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