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 

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