First up, these next two Clinical Kits are an aggregation of ideas that have been brewing for several years and brought about from clinical observation and trying to make sense of the available research in regards to trigger points and myofascial pain syndrome. Many of you will appreciate there is plenty of discussion going on about the nature and relevance of trigger points. For this reason don't take these ideas as gospel. We can’t deny the existence of trigger points, but the how and why is very much under discussion.
I happily confess to have mostly looked at this from a clinical standpoint, and then gone looking for information that might explain what I see - so there is a degree of bias in this premise. I would love to hear the thoughts and comments from other colleagues on this subject.
This first of two Clinical Kits looks at the history and possible mechanism of trigger points and the second Clinical Kit looks at clinical findings and an alternative viewpoint on classifying trigger points.
A Brief of History of Trigger Points
In the early work of Travell & Simons (22, 24), the ‘trigger point’ was thought to primarily be the centre of the myofascial pain problem. Trigger point dysfunction was attributed to muscle dysfunction and due to the ongoing nature of ‘spasm'. In the absence of EMG findings, it was hypothesised that trauma caused a release of calcium ions from the damaged sarcoplasmic reticulum. This local release activated the actin/myosin complex using local supplies of ATP to exhaustion. Associated circulation dysfunction (trauma, ischaemic contraction) prevented the normal calcium pump from removing accumulated calcium and hence the contraction was maintained (22). This was modified and presented as the 'Integrated Trigger Point Hypothesis' in their second text edition (23). A review of this integrated hypothesis was undertaken in 2004 to take into account new muscle pathophysiology research (10).
Two common clinical factors were identified in the updated Integrated Trigger Point Hypothesis. One was a motor dysfunction, the taut, palpable band and the other being a sensory dysfunction, pain. The mechanism(s) causing the taut band is unknown, but altered endplate/neuromuscular junction (NMJ) activity, leads researchers to believe this is the initiation site. Researchers have found increased concentrations of Ach in synaptic cleft, and changes in Ach receptors, that are considered consistent with increased NMJ electrical activity. Furthermore botulinum neurototoxin type A (BoNT-A) (which blocks Ach release) reduces end plate noise in rabbits’ myofascial trigger points and is injected to induce flaccid paralysis in humans. It has been found that BoNT-A when applied in the periphery, is transported via axoplasmic flow to the central nervous system and that for certain types of pain this transport is necessary to gain relief (19). It has been noted when palpating a taut band and localising the spot of maximal pain, there is a marked increase in low frequency electrical activity, localised to the NMJ of the taut band. In studies that have blocked or inhibited sarcomere contraction, this occurred at the NMJ.
In regards to the presence of pain, Gerwin et al states ”myofascial pain occurs because of the release of substances from damaged muscle, such as adenosine triphosphate (ATP), bradykinin (BK), 5-hydroxytryptamin (5-HT, serotonin), prostaglandins, and potassium (K+), and from the extracellular fluid around the TrP, such as protons (H+), from the acidic milieu” (10). They build an argument on pain provocation via chemical release (SP and CGRP) secondary to muscle overuse (exercise) and damage, causing an energy crisis, vascular constriction and a subsequent hypoxic state. An active trigger point (one that is symptomatic) has a demonstrable chemical milieu with elevated levels of substance P (SP), calcitonin gene related peptide (CGRP), BK, (5-HT), and assorted cytokines. Conversely the pH is lower, about pH 5, consistent with hypoxia and ischemia. This is in comparison to both latent trigger points and normal tissue.
For me a problem with this line of thinking is the obvious clinical consideration that lots of people damage & overload muscles doing eccentric exercises, and get delayed onset muscle soreness, but not trigger points. For me the reverse is truer. Quite often clients haven’t done anything unusual and have no idea what initiated their trigger points. If they haven’t experiencd a physical overload how does the muscle enter a hypoxic state, or is the hypoxic state a secondary consequence rather than an initiating factor?
So What Maybe Going On?
Initially the focus has been on the muscle side of the NMJ, with emphasis on the muscle being the source of the trigger point. What about the neural side?
To state the obvious, the NMJ is junction between neural system and muscular system. The commonly discussed mechanism is that an action potential is propagated down the motor nerve, reaching its terminal. Voltage gated channels release calcium into the neuron that binds with proteins, triggering the release of Ach into the NMJ. The Ach diffuses across the NMJ binding onto the membrane of the muscle fibre. With sufficient bindings a muscle contraction can occur.
Aside from electrical propagation, there is another characteristic of the nerve that seems to have been overlooked; axoplasmic flow. The ‘what flow’ you ask!
Axoplasmic flow (axonal transport)serves the function of overcoming the distance between cell body, in the dorsal root ganglion and the target tissue e.g. muscle, skin experienced by nerve cells when compared with other cell types, (21). Axoplasmic flow transport travels in both directions; antegrade, away from cell body and retrograde, toward cell body and at different speeds.
Anterograde Transport. Proteins are transported in the anterograde direction at different speeds. The rapid transport component moves at a rate of 410mm/day (1.7cm/hr) in the sciatic nerve. The speed of rapid transport may be slower in other nerves, but it is never less than 100mm/day. Rapid transport carries mainly membrane bound materials such as plasma membrane proteins and synaptic vesicles. In contrast, slow transport in the anterograde direction moves at a rate of only 1-3mm/day. Slow transport carries soluble enzymes and structural proteins such as the microtubule protein, tubulin.
Retrograde Transport. The rate of retrograde transport is about half that of anterograde transport. The function of retrograde transport is not well understood but it is thought that it is important in regulating metabolism of the cell. For example, when an axon is cut, the signal inducing cell body chromatolysis, is probably carried by retrograde transport, taking proteins, enzymes, mitochondria, organelles (3-5) & neurotransmitters (16).
Neuropathy symptoms (motor, sensory & autonomic) have been attributed to neurotrophic denervation (axoplasmic flow reasons) rather than impulse disuse (17). Using certain alkaloids that block axoplasmic transport but still allow normal conduction and hence muscle contraction; trophic signs of degeneration will occur. McComas (20) in four case studies demonstrated that target tissue (muscle) functioned normally in the absence of impulse conduction.
Axoplasmic transport provides;
Chemicals responsible for development of axonal mechanical sensitivity (to pressure & stretch) (7)
Vital nutrition for the nerve and target tissue. Korr (18) reported that nerve axons transmit nerve cell proteins not only for itself but after several days also for the associated target muscle cell. Selective proteins cross the nerve/muscle cell junction and are synthesized by the muscle to form muscle proteins. Hence there are proteins manufactured by nerve cell bodies that are transported via axoplasmic flow, destined specifically to provide normal muscle cell function
Neurotransmitters to convey information across the synapse to target tissues
Feedback mechanism to the cell body from the neuron and target tissue (2)
Changes in axoplasmic flow rate or quality can result from;
Decreased blood supply
Tissue inflammation (acute) with the presence of histamine (1)
Presence of selected chemicals; colchicine and vinblastine without inflammation (7)
Nerve compression as low as 20mm Hg (3-5). Clinically these pressures and higher are demonstrated at sites of peripheral neuropathy (9) and result in axonal mechanical sensitivity
Lets have a closer look at the last possibility, nerve compression, in more detail.
Acute entrapment is at most, momentarily painful (15).
Ongoing entrapment however causes an alteration in fast antegrade axoplasmic transport of mechanically sensitive ion channels. Their localised deposition (responsible for impulse propagation), results in ectopic neural pacemaker sites formation (6). These are generally massed within a small region of the nerve; as in a nerve end neuroma, or they may be disseminated throughout a nerve, resulting in axonal mechanical sensitisation (AMS) and sensitisation of the nerve’s target tissue (8). No abnormal nerve findings are present with AMS.
Clinically we see chronic nerve entrapment causing sensitisation of the nerve trunk nervi nervorum, such that light palpation of the distal nerve trunk produces a painful response = mechanical allodynia (14). With one lesion the rest of the nerve trunk may become supersensitive or hyperactive (11).
An ectopic neural pacemaker site (ENPS) can display lowered threshold to depolarisation, increased rate of spontaneous discharge, after discharge properties and become hypersensitive to a broad range of physical, chemical and metabolic challenges (8).
Other clinicians have noticed similar things and written of their observations in different ways. Gunn (11) coined the phrase of ‘prespondylosis’ following research to describe the range of peripheral neuropathy symptoms that preceded a radiological diagnosis of spondylosis. Gunn et al. (12, 13) based this upon impulse denervation rather than altered axoplasmic flow.
Clinically clients that have spondylosis seem much more likely to develop associated trigger points. The Double Crush Syndrome as described first by Upton & McComas in 1973 (25) found of the 115 patients with median (carpal tunnel) or ulna (cubital tunnel) nerve lesions, 70% had clinical evidence of a neural lesion in the neck. The authors proposed that minor serial impingements created a net deficiency effect and predisposed the rest of the nerve to an entrapment neuropathy.
It only takes a small amount of pressure to reduce axoplasmic flow
Reduced axoplasmic flow can occur with and without inflammation & in both cases, AMS develops to pressure & stretch stimulation
With reduced axoplasmic flow, ENPS can form, sensitising the nerve and associated muscles to other potential stresses e.g. chemical (SP, BK, CGRP, 5HT), mechanical (compression, continuous low load) and temperature (less than 10C & greater than 42C)
It seems that we currently look at trigger points as all being homogenous. Are they? While superficially they seem the same, could part of the variability of treatment effects reflect the assumption that trigger points all have the same cause? We certainly fell into this trap with the management of non specific chronic low back pain. Now as we differentiate patterns of lumbar pain, our interventions are more appropriate and effective. Perhaps if we look at trigger points as being heterogeneous and not lump them all into the same treatment model, we will likewise start to become aware of different patterns of presentation.
I am wondering therefore, could a trigger point reflect a minor peripheral nerve compression, (impeding normal axoplasmic flow) and resulting in AMS? With this neural pathway sensitised, then there are a variety of other internal and external stresses that superimposed could ‘activate’ a trigger point, making it symptomatic. This could explain in part the variety of trigger points presentations, including 'the spread' of trigger points the variable response to treatment.
In the next blog I will be looking at clinical features and how I classify trigger points. Trigger points don’t seem to follow the three musketeers motto of ‘All for one and one for All!’
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19. Matak I. Working where it really matters: Botulinum toxin A targets pain hypersensitivity in the CNS http://www.bodyinmind.org/botulinum-toxin-a-pain-cns/. [1/8/2014.
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21. Oztas E. Neuronal Tracing. Neuroanatomy 2: 2-5, 2003.
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