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.

© David for PhysioDigest - an educational resource for the musculoskeletal rehabilitation community, 2009. | Permalink | 4 comments | Add to del.icio.us
Post tags: fibromyalgia, myofascial muscle pain, myofascial neck pain, Myofascial pain, myofascial pain dysfunction, myofascial pain symptoms, trigger point injections

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