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

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Post tags: chronic myofascial pain, Myofascial pain, myofascial pain dysfunction, myofascial pain myofascial pain, myofascial pain symptoms

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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 | 2 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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TMJ and facial pain is another one of those challenging conditions where the pathology is not easy to define and several specialities can be involved in co-ordinating patient management.  These may include dentists, pain management specialists, ENT, neurology, physiotherapy and the whole myriad of allied health professionals.  It is often difficult to quantify whether the facial symptoms are primary or secondary in nature even when a specific mechanical history is reported.  One of the reasons for this is that often a traumatic mechanism involving the head and neck can simultaneously irritate multiple structures and therefore doesn’t narrow down the examination process.  Similarly mechanisms such as whiplash which do not directly involve the jaw as a point of impact also appear to be capable of inducing secondary irritation either by way of reflex changes or as a consequence of the inertia from violent head and upper thorax motion.

Specific symptom reports such as clicking, locking, opening restriction, pain on bite, fatigue on talking and slowness of speech are all frequent symptom reports from patients with primary TMJ problems.  There may well be some localised tenderness along the joint line also.

When patients describe overt locking and clicking there are a number of possibilities to be considered.

1)      Intra-articular disc pathology – This is usually a clinical diagnosis which requires arthroscopic confirmation and management.

2)      Intra-articular impingement secondary to capsular restriction – Patients in this grouping display restricted motion of the TMJ sometimes in a global pattern and sometimes direction specific.  The primary treatment strategy in this patient group is to improve joint mobility by re-evaluating the intra-articular pain pattern post-intervention.

3)      TMJ instability – This is a most challenging group where the structural constraints have become either torn or chronically elongated thus compromising stability in the region.  Patients in this category are often the poor responders to treatment or those who require on going maintenance as part of their management strategy.

Secondary TMJ Pain – Myofascial pain radiating to the face, head and jaw is extremely common.  In the presence of a post whiplash history there will often be co-existing cervicogenic signs, headaches and even neuropathic symptoms in the head and face as part of the general symptom pattern.  In clear-cut cervicogenic myofascial referral the symptoms can be reproduced by palpation of trigger points in;

Trapizus

Sternocleidomastoid

Scalene

Scapular musculature.

Specific evaluation of the face and jaw with palpatory techniques does usually not yield sufficient information but diagnostic probing using dry needling is certainly worthwhile. Combinations of manual therapy specifically to the joint condyles together with hold- relax procedures in the direction of motion restriction are all part of the tools normally used to manage this type of condition.  The therapist should be aware that intra-oral techniques are usually required so appropriate gloving and preparatory procedures are necessary.

A common clinical challenge we face is patients who have regular sleep disturbance following a traumatic neck injury.  This cycle of sleep disturbance if sustained for any period induces fatigue with subsequent diffuse increases in muscle tension.  When this cycle involves into a pattern of habitual teeth grinding, known as ‘Bruxism’ this seriously compounds the clinical management.  It is particularly important to identify in persistent head and facial pain and the clinician is looking for a pattern of temporary response to localised modalities but recurrence of symptoms on an on going basis.  Typically these patients don’t show gross range of motion restrictions but do exhibit diffuse sensitivity on palpatory testing.

The strategies used to control Bruxism may involve relaxation, dental splinting, and evaluation of bite mechanics as well as looking at other muscular skeletal and postural drivers to potential persistence of muscle hyperactivity.  Undoubtedly an interesting and challenging caseload and one that often involves collarabation of health care professionals – true multi-disciplinary pain management.

Enjoy the clinical challenge.

David.

© David for PhysioDigest - an educational resource for the musculoskeletal rehabilitation community, 2009. | Permalink | No comment | Add to del.icio.us
Post tags: cervicogenic, ENT, Facial Pain, fatigue on talking, Myofascial pain, neurology, opening restriction, pain on bite, physiotherapy, rapizus Sternocleidomastoid, Scalene, Scapular musculature.bruxism, slowness of speech, TMJ, TMJ clicking

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