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 

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 

MYOFASCIAL PAIN SYNDROME

The prevalence of myofascial pain syndrome and the clinical observation of trigger points is a phenomena which most clinicians are familiar with.  Since Travell &  Simons in the 1950’s documented pain referral patterns unique to muscle there has been contentious debate regarding the legitimacy of these pain referral patterns, the true nature of trigger points, their aetiology and effective treatment strategies.  The original term for these palpable nodules was fibrositis implying an inflammatory reaction within the muscle and this led to many biopsy studies attempting to quantify local pathology in muscle.

These studies did not elicit a structural lesion implicated from the clinical observations of trigger points. Subsequent, recent work in using biochemical analysis of specific trigger points has indeed confirmed that there are local inflammatory mediators located within these tender zones.  Furthermore diagnostic ultrasound scanning can visualise these hyperactive zones within the muscle and doppler blood flow scanning suggests that there may also be some characteristic blood flow changes around trigger points (an impairment of blood flow).  The postulated mechanism for this is an alteration in capillary resistance secondary to mechanical tension within the muscle fibers.

Criteria defining trigger points

Essential Criteria:

1. Taut band palpable (when muscle is accessible).
2. Exquisite spot tenderness of a nodule in the taut band.
3. Patient’s recognition of current pain complaint by pressure on the tender nodule (this identifies an active trigger point).
4. Painful limit to full stretch range of motion.

Confirmatory observations:

1. Visual or tactile identification of local twitch response.
2. Pain or unpleasant sensation in the distribution from a trigger point in that muscle.
3. Electromyographic demonstration of spontaneous electrical activity characteristic of active loci in the tender nodule of the taut band.

Because of this frequent clinical observation of palpable nodules that aren’t tender or don’t produce a twitch response Travell and Simons postulated a differentiation between active and latent trigger points.

Active and latent trigger points

The active trigger points fulfil the criteria outlined above and the latent trigger points being palpable but not producing pain.  There is also a further sub-classification to categorise groups of trigger points into primary and secondary (satellite) groups.  The primary being the most potent source of symptoms and the secondary / satellite points being associated with synergic muscle activity involved in the same mechanism postulated mechanism of overload.  This perhaps is where the biggest clinical debate remains regarding the legitimacy of targeting palpable nodules in muscle.  According to the strict criteria they should only be painful nodules, which reproduce a twitch response and the patient’s pain.  This then raises the issue as to whether each of these clinically similar types of nodules are parts of the same phenomenon or separate distinct clinical entities.  Much of this debate has been fuelled by the Internationally accepted classification of fibromyalgia syndrome in which the diagnosis is confirmed by patients displaying 11 out of 18 predetermined paired diagnostic points as being sensitive to palpation.

Myofascial practitioners suggest that the locations of tender points associated with the fibromyalgia diagnosis are not in fact trigger points as defined by Travell and Simons and outlined in the criteria above.

Causes of trigger points

Looking further at the aetiology of trigger points (disregarding whether they are distinct entities or parts of a continuum) the issue of how they occur is obviously of interest.

Postulated factors include:

Postural asymmetry

Asymmetrical muscle loading

Excessive muscle activity

Altered patterns of recruitment,

Repetitive activation

Acute traumatic overload

Gradual traumatic strain

Non-specific non-localised factors.

While each of these categories appear  plausible in their own right they should be considered in the light of well observed and documented clinical phenomena of alternating sites of myofascial pain varying from affected to non-affected areas  and spreading diffusely away from traumatised regions. Such behaviour is not compatible with the local pathology hypotheses.  This is further challenged by the fact that depravation of sleep can induce tender points in muscles implying these phenomena can be induced from central nervous system process independent of local muscle pathology.

In clinical practice we probably see a spectrum of presentations from initial acute muscle overload, which then evolves into some central sensitised states producing a progressive expansion of sensitivity over a broader area of non-traumatised muscle.  In pain physiology terms this is described as secondary hyperalgesia – a phenomena dependent on the CNS mediation.

Another significant clinical issue is that the pain referral patterns defined by Travell and Simons, which essentially have become the clinical maps for diagnosing the presence of myofascial trigger points.  Clinical observation indicates that a significant proportion of patients who report local sensitivity on trigger point palpation and indicate re-production  of familiar symptom, do not demonstrate the precise patterning of symptoms outlined in the pain maps.  We are thus left with a scenario where we may observe a tender trigger point in an area where patients complain of symptoms but provocation of this trigger point does not elicit the full spectrum of clinical features.  We must therefore make a decision as to whether it is a legitimate target to treat in the absence of fulfilling all of the criteria previously outlined.

This requires us to make a clinical judgement on the relative degree of

“comparability” of the physical signs elicited from trigger point palpation.

If they do not fulfil the above described criteria are they still legitimate targets for therapy?

How do we prioritise targets for treatment in the presence of diffuse localised point tenderness within a group of synergic muscles?

We then of course need to consider what our treatment options for myofascial pain syndrome but that’s a discussion for another day.

Enjoy the clinical challenge.

David.

Psychosocial Social Concepts in Primary Care – 10 Tips for practical application.

As clinicians we have been bombarded with research outlining the important role of psychosocial issues in clinical outcomes.  I have often wondered why these models have been applied to low back pain and whiplash but don’t seem to feature on the radar of many other chronic conditions we  see routinely.  Maybe it’s a case of chronic conditions such as osteoarthritis, ankylosing spondylitis, degenerative joint disease etc having more defined pathology and are therefore being a more acceptable diagnosis to patients thereby deflecting them from further questioning or seeking more treatment.

Regardless there is a vast array of measurement tools available for quantifying

psychosocial components. These include:

McGill Pain Questionnaire

SF36 Health status Questionnaire

Oswestry LBP Disability Questionnaire

Fear / Avoidance Index

Pain Catastrophization Index

Visual Analog Sacale

to name a few.

Taken in conjunction with the now widely accepted concept of Flags;

Red

Yellow

Black

Blue

Orange

we have a huge battery of questionnaires and a framework which can be used to elucidate individual characteristics and tendencies.  I have spent several years enquiring about the merits of these scales in primary care and arguing that specific questions interspersed within a subjective examination yield more direct information than a “profile questionnaire” yielding information about individual tendencies. For example “when are you planning on returning to work?” will yield some specific answers ranging from “never” to “when you get me better” to “when they say their sorry” etc…. Such responses present the clinician with an opportunity to challenge beliefs, identify obstacles or alter a management plan. Several authors of these tools acknowledge the basis of this argument but cite the lack of “research validity” for the approach I’ve outlined. I’ll let you be the judge of that!!!

One of the big challenges in an acute presentation is whether to initiate these type of investigating tools as part of a routine assessment protocol or whether to try to identify high risk patients relatively early in the intervention and alter management strategies accordingly.  On the face of it this might seem like an obvious management plan but there are some very real practical limitations to implementing it.

Firstly – if every acute patient is going to be screened using psychosocial profiling from day one then there are large numbers of patients who are going to be asked a lot of questions which they may perceive as being highly irrelevant to their primary (musculoskeletal) problem and the reason they consulted Physiotherapy.

I think this is particularly significant in the Private Care Sector where we deal with patients who are unlikely tolerate some of the enquiring questions contained in the questionnaires and the  perception of the type of treatment to be administered .  Remember again we are talking about an acute setting here not a chronic pain management setting where the patient mindset is in a different place.

Secondly, the challenge if we wait for recognition signs of slow response to treatment or unpredictable features which emerge as part of one-to-one contacts, three or four sessions into care, is how do we change our management strategy and sell it to a patient in a credible way?  By “selling to the patient” I mean providing a credible explanation for their symptoms, which may be contradictory to what was initially stated, based on the physical findings alone on initial assessment.  This is a major major issue, which is never discussed in formal literature but as clinicians, one which we must find practical strategies to address if we are to be in a position to deliver care.

So the issue of therapist credibility surfaces in two respects: Firstly,in that the explanatory mechanism of a patient’s symptoms may need to change as the therapist gets more information from increased patient contact time and behavioural observation.

Secondly, how do we start to change our rating scale factors to shift the hypothesised mechanism of symptoms from being nociceptive to more predominantly psychosocial?  Of course as in all things in life this is never a clear cut classification as there will be degrees of pain mechanisms in all presentations which may alter and vary as time goes by – ie they are dynamic.

We have discussed pain mechanisms in previous posts. So how do we rise to this challenge of changing our clinical hypothesis to facilitate a different management strategy and delivering that message effectively to our patients in order to achieve compliance?  This again is another un-talked about subject.  The therapist can feel assured in the knowledge that they are following International best practise guidelines to deliver a message which appears entirely credible to the therapist but does not appear so to the patient.  This is a classic situation of “blame the patient” for not listening to the message.  The challenge for the clinician therefore is to recognise early signs, which require a change in the hypothesis of symptom mechanisms. It also means careful consideration of the type of clinical discussions which occur in the early phases of a patient /therapist interaction. (and I don’t mean being “wishey washy/vague” when reporting clinical findings – just systematic and analytical).

Below is a checklist of strategies which maybe helpful in the clinic.

1 Be familiar with the content of international guidelines on management of acute LBP.

2. Develop an opinion o these guidlines (ie agree, disagree or select elements)

3 Evaluate the type of patient you are dealing with (ie tense, easygoing, enquiring, intimidated, hopeless, unrealistic, naive, diligent, self directed, victim etc…)

4 On the basis of your evaluation above be selective about the type of words used to describe symptoms.(ie  pain v’s symptoms, problems v’s disabilities etc).

5. Avoid the pitfall of” information overload” in patients who won’t / can’t process this.

6. Avoid , at all costs, the pitfall of” information overload” in patients who will mal-process / distort the information presented.

7 Be guarded about contradicting professional opinions which are contrary to your own (even if you think they are off-the-wall”). Careful dissection of inappropriate advice needs supportive analysis, not dismissal, and is the difference between alienating a patient and keeping them on board to deliver care.

8.Identify predictable /familiar elements of pain patterns which responses can be mapped.

9. Identify clinical /subjective response characteristics which are improving from treatment – even if the overall patient perception is of “no change”.

10 Eliminate / reduce “Nociceptive” pain mechanisms ie clinical signs of pain, stiffness, muscle spasm, loss of movement before concluding an alternative symptom mechanism (psychosocial). Blaming all symptoms on stress, tension, strained relationships, smoking, excessive weight is a sure-fire way to lose credibility.

I think there are a few more points to add to this list but that should suffice for some mental marination.

Enjoy the clinical challenge.

David

NERVE SENSITIVITY – ALTERED NEURODYNAMICS

Detection of abnormal nerve sensitivity is a fundamental part of the clinical examination in musculoskeletal medicine.

Symptoms originating from frank neurological compression (defined as entrapment neuropathies) generally do not pose a diagnostic dilemma and the clinical features of “hard” neurological signs i.e.

Sensory

Motor

Reflex loss

are relatively easy to detect.

However subtle neural sensitivity often manifests itself in the absence of hard neurological signs as measured by the classic tests of muscle power, tendon reflex’s and sensory testing.  The landmark work of David Butler & Bob Elvey has been central to the integration of neural sensitivity assessment for musculoskeletal clinicians and has give physiotherapists potent weapons in their armoury.  Technically speaking, this classification of pain is considered as peripheral neuropathic pain as defined by the International Association for the Study of Pain and is distinct from pain originating from other peripheral tissues because of the nature of the symptoms produced and its response characteristics.

The principals of neural sensitivity testing is with a battery of mechanical provocation tests where the clinician’s objective is to detect mechanical hyperalgesia (an abnormally painful response to a normally non-painful stimulus) by virtue of a positive response to pain provocation testing.  These tests are devised along anatomical lines with attempts to either elongate or produce motion i.e. targeting nerve trunk or individual peripheral nerves.

The response is considered abnormal if it either….

reproduces the patient’s pain

reproduces atypical responses associated with nerve sensitivity

or elicits protective responses by virtue of reflex muscle spasm preventing full exploration of the test.

The spectrum of symptoms which may indicate a peripheral neuropathic pain mechanism involve descriptions of symptoms such as….

Lines of pain

Clusters of symptoms along a limb

Sharp shooting stabbing pains

Throbbing

Pulsing

Feelings of compression

Circular “band’s” around particular parts of a limb

Difficult to describe vague sensations (dysaesthesia).

The clinician must be aware of identifying these symptom characteristics and also to identify if they are reproduced or enhanced by neural sensitivity provocation testing neurodynamic testing.

If they are not it may well indicate that the mechanism of pain is still neural but not residing in the peripheral nerve tissue but rather be a central pain state.  This again according to the International Association for the Study of Pain is a neuropathic pain mechanism but does not reside in the peripheral tissues and therefore should not be treated as a mechanical phenomenon.

Failure of clinicians to identify non-mechanical mechanisms of symptom generation is a major reason for poor treatment outcomes, poor patient compliance and a low perception of the physiotherapy profession. We must ensure our clinical skills are up to the job.

Enjoy the clinical challenge
David