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John L. Quintner, Geoffrey M. Bove, Milton L. Cohen, A critical evaluation of the trigger point phenomenon, Rheumatology, Volume 54, Issue 3, March 2015, Pages 392–399, https://doi.org/10.1093/rheumatology/keu471
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Abstract
The theory of myofascial pain syndrome (MPS) caused by trigger points (TrPs) seeks to explain the phenomena of muscle pain and tenderness in the absence of evidence for local nociception. Although it lacks external validity, many practitioners have uncritically accepted the diagnosis of MPS and its system of treatment. Furthermore, rheumatologists have implicated TrPs in the pathogenesis of chronic widespread pain (FM syndrome). We have critically examined the evidence for the existence of myofascial TrPs as putative pathological entities and for the vicious cycles that are said to maintain them. We find that both are inventions that have no scientific basis, whether from experimental approaches that interrogate the suspect tissue or empirical approaches that assess the outcome of treatments predicated on presumed pathology. Therefore, the theory of MPS caused by TrPs has been refuted. This is not to deny the existence of the clinical phenomena themselves, for which scientifically sound and logically plausible explanations based on known neurophysiological phenomena can be advanced.
Introduction
The phenomena of muscle pain and tenderness in the absence of obvious disease are well recognized but poorly understood. Myofascial pain syndrome (MPS) is a popular explanatory model, which posits a local (muscle) origin of nociception called the trigger point (TrP) and advocates local treatment, primarily direct manipulation of TrPs using manual pressure or needles, the latter with and without injectate [ 1 , 2 ]. These forms of treatment are being practised worldwide by physicians, physical therapists, chiropractors and various unlicensed and unregulated practitioners [ 3 ].
But does the evidence support these concepts? Are the hypotheses generated by MPS theory scientifically sound? And are treatments based on this theoretical model beneficial?
This article will show that the theory is flawed both in reasoning and in science. In seeking a resolution, two testable hypotheses are identified that point the way to neuroscientific explanations for the observed clinical phenomena.
Evolution of MPS theory
It has long been believed that muscle pain might originate from focal lesions within connective tissues [ 4 , 5 ]. The initial description put forward by Stockman [ 6 ] was of fibrositic nodules, which were suggested to harbour low-grade inflammation that activated sensory fibres innervating muscle spindles and the interstitial tissues between muscle fibres. However, Stockman’s claim that ‘the essential lesion is a chronic inflammatory hyperplasia of white fibrous tissue in patches’ [ 7 ] has never been confirmed [ 8 ].
An infective aetiology of such nodules was proposed, but other conjectures included microtrauma, exposure to environmental extremes, nerve root irritation and psychoneurosis [ 8 , 9 ].
Kraus (cited by Simons [ 2 ]) speculated that palpable muscle hardening of unknown cause could set up a reflex increase in muscle tension, resulting in a pain–reflex–pain self-perpetuating cycle that could be disrupted by ethyl chloride sprayed onto the overlying skin or by local injections of anaesthetic. Pain theorists William Livingstone [ 10 ] and John Bonica [ 11 ] favoured this vicious circle hypothesis, as did others [ 12 , 13 ].
Speculation took a new turn when Travell and Rinzler [ 5 ] conceptualized that pain felt in voluntary muscles is myofascial in origin. Their claim, that ‘trigger areas in myofascial structures can maintain pain cycles indefinitely’ [ 5 ], was reminiscent of the vicious circle hypothesis.
Travell and Simons formalized the construct of ‘myofascial pain arising from trigger points’ [ 14 ]. Not only were TrPs described in exactly the same way as fibrositic nodules had been, but it was also asserted that they could potentially develop within every voluntary muscle and in multiple locations within a given muscle.
The theory of MPS comprised two essential components: the TrP, a localized area of tenderness or hyperirritability deep within voluntary muscle; and a predictable discrete zone of deep aching pain, which could be located in the immediate region of or remote from the TrP, and which was worsened by palpation of the TrP [ 4 , 14 ].
Travell and Simons [ 14 ] composed anatomical charts of TrPs and their characteristic pain referral patterns. However, it appears that their diagrams had ‘sometimes been chosen arbitrarily, there being no accepted standard’ [ 15 ].
Located within palpable taut bands, TrPs were said to represent shortened (contractured [ 16 ]) muscle fibres. On snapping palpation or insertion of a needle, a local twitch response could be elicited, which was accompanied by an irritable EMG response [ 14 ]. In contrast to a normal muscle, one containing a TrP was said to exhibit both antalgic inhibition when tested for its strength, and intolerance to passive stretch.
To explain the puzzling onset of pain in ostensibly lesion-free tissues, Travell and Simons [ 14 ] found it necessary to invent the latent TrP, a site of potential tenderness within a muscle unassociated with spontaneous pain but having the potential to be activated by a myriad of factors, within or outside the body. In an attempt to extend the theory to explain more widespread pain, they claimed that TrPs could self-propagate to become secondary TrPs in other muscles and even to metastasize throughout the bodily musculature.
The recent conjecture that peripheral pain generators can reside within muscles (i.e. myofascial tissues), and be responsible not only for spontaneous pain but also for the initiation and maintenance of profound changes within the CNS (known as central sensitization) rests upon these dubious premises [ 17 , 18 ]. Similarly, prominent rheumatologists are among those who maintain that TrPs are responsible for the initiation and maintenance of the syndrome of chronic widespread pain (FM) [ 17–23 ].
Beliefs in TrP theory and the associated concept of MPS continue to be strongly held [ 24 ], despite the fact that such beliefs exemplify circular reasoning: TrPs cause myofascial pain because painful muscles contain them [ 25 ].
Review of the evidence
Clinical diagnosis
An extensive review identified at least 19 different sets of diagnostic criteria used for the MPS/TrP syndrome, and concluded there was a lack of consistency and consensus on case definition [ 26 ]. The authors suggested that until reliable diagnostic criteria had been established, ‘there is a need for greater transparency in research papers on how a case of MTrP [ sic ] pain syndrome is defined, and claims for effective interventions in treating the condition should be viewed with caution’ [ 26 ]. A similar study found that the diagnosis of MPS from putative TrPs was based on a clinical test of unknown reliability and validity with no accepted reference standard [ 27 ].
In studies of inter-examiner reliability, examiners were given the muscle to palpate with or without an accompanying diagnosis [ 28–31 ]. In one study, extensive training coupled with the use of an algometer resulted in examiner agreement that the phenomenon could be localized [ 29 ]. Another study reported that the assessments of an individual examiner were consistent from one test to another [ 31 ], and that more experience in assessment leads to better inter-examiner agreement [ 30 ]. These studies suggest that when shown where a problem may exist, examiners may agree. However, when blinded as to diagnosis, those who claimed expertise in the field were unable to detect putative TrPs in the majority of subjects with a MPS diagnosis [32 ]. In this study, there was virtually no inter-examiner reliability for either putative TrPs or taut bands. This finding questions the reliability of the diagnostic criteria used by these experts. More recent studies [ 33 , 34 ] have also reported poor inter-examiner diagnostic reliability and poor methodological quality [ 35 ].
In summary, physical examination cannot be relied upon to diagnose a condition that is supposed to be defined by that physical examination. That is, the pathognomonic criterion for making the diagnosis of MPS is unreliable.
Pathology
The first histological analysis of fibrositic nodules reported diffuse inflammatory changes [ 9 ]. These findings were not confirmed, although tender muscles contained increased extracellular fluid [ 36 ]. The authors suggested that the resulting turgor might explain the observed finding of mechanical tenderness.
The term myogelosis describes a change in muscle structure analogous to TrPs [ 37 ]. Samples taken from unfixed cadavers following detection of such areas showed altered histology [ 37 ], but the clinical relevance to the findings on palpation is unknown.
Tissue biochemistry
Shah et al. [ 38 , 39 ] employed microdialysis to sample tissue fluid within and near to a palpated trigger zone in trapezius muscles in patients with a diagnosis of TrPs and also in normal pain-free subjects. Samples were taken from the following regions: normal (no pain, no TrP), active (pain and TrP detected) and latent (no pain, TrP detected). Samples were also taken from asymptomatic gastrocnemius muscles. Elevated levels of calcitonin gene-related peptide (CGRP), substance P (SP), norepinephrine, TNF-α, IL-1, IL-6 and low pH were reported in fluid from all sampled regions of symptomatic patients. However, elevated levels were also found in uninvolved, control muscle areas.
These reported alterations in biochemical milieu are consistent with inflammation due either to tissue damage or to altered peripheral nerve function, in contrast to pathology necessarily being in the tissue sampled [ 40 , 41 ].
EMG studies
In one study, EMG examination of TrPs failed to provide evidence of ongoing denervation or focal muscle spasm [ 42 ]. But another study did report spontaneous electrical activity (i.e. endplate noise and spikes) in regions considered to be TrPs in patients with chronic tension headache and pericranial muscle tenderness [ 43 ].
Simons et al. [ 44 ] addressed the question of whether endplate noise and spikes arise from normal endplates by performing EMG on 25 patients who met the ACR 1990 criteria for FM and 8 pain-free subjects in whom latent TrPs had been identified by manual palpation of taut bands and characteristic referral of pain [ sic ] [ 45 , 46 ]. Unfortunately, the researchers conflated the TrPs of MPS and the tender points of FM, another issue yet to be resolved [ 47 ]. They concluded that endplate noise is characteristic of but not restricted to TrPs, and that the finding could not be considered a reliable diagnostic criterion [ 45 , 46 ].
An alternative interpretation of these EMG findings is that insertional and spontaneous activity (i.e. endplate noise) from single muscle fibres generated by the activation of i.m. nerve termini irritated by the needle was being recorded [ 48 ]. Nonetheless, it is still asserted that spontaneous electrical activity is one of the characteristics of myofascial TrPs [ 49 ].
Imaging studies
Seven patients with a 3-year history of myofascial pain associated with the presence of a taut band in the upper trapezius muscle were examined using magnetic resonance elastography [ 50 ]. A signature chevron-like pattern was reported, with its leading edge coincident with the physician-identified taut band. The authors did not offer diagnostic criteria nor make any comment on the relationship of a taut band to a TrP. A subsequent study of eight subjects, four of whom were said to have MPS and four of whom did not, is open to the same criticism [ 51 ].
Attempts were made to visualize TrPs using diagnostic US of the anterior abdominal wall of 10 patients [ 52 ]. The points in question appeared as a mixed echoic area in the rectus abdominis muscle that became prominent on injection of local anaesthetic solution [ 52 ]. They conceded that the findings could have been coincidental. Also, the image presented is consistent with the normal sonographic appearance of abdominal muscles [ 53 ].
In another study, 44 patients with acute cervical pain and at least one putative TrP identified by palpation in the upper trapezius were evaluated using sonoelastography and Doppler imaging [ 54 ]. The authors claimed to have measured TrP size and to have distinguished normal muscle from active and latent TrPs. Although the data on which these assertions were made were not presented, the authors found no correlation between claimed TrP area and pain pressure threshold. The absence of pain-free control subjects is yet another flaw. These methodological concerns do not lend credibility to the findings.
Animal models
Animal models are often informative about pathophysiology in ways that are impossible to demonstrate in humans. To be considered relevant, models must have symptomatic and/or pathological similarities to the condition being studied. For TrP research, no such model exists.
Simons and Stolov [ 55 ] biopsied ostensibly normal canine muscles, seeking to correlate palpated taut bands with morphological and histological changes. The findings were negative, given that there was no indication of pain or a pathological condition present prior to these studies. The researchers observed ‘rubbing palpation produced a transient contraction which could be primarily responsible for the sensation of a hardness palpated in the dog muscles’ [ 55 ]. This is the myotatic reflex, which correlates with the twitch response also evocable on palpation of normal human muscle [ 56 ].
Based upon the conjecture that ‘… latent TrPs can be identified in almost all skeletal muscles of normal adults’ [ 14 ], a rabbit model of TrPs was proposed [ 57 , 58 ]. Rabbit leg muscles were palpated until they exhibited a myotatic reflex. Such muscles were considered to contain taut bands and, by assumption, TrPs. A number of papers have since been published using this model [ 58–65 ], but have not offered evidence of clinical relevance.
Delayed onset muscle soreness
Studies of delayed onset muscle soreness (DOMS) have been undertaken using eccentric exercise to cause symptoms, in both humans and animals. Although DOMS has been related to TrPs in only one study [ 66 ], this model was proposed for MPS [ 67 ]. The relevant experiment was performed in humans and used eccentric exercise of the extensor digitorum of the middle finger [ 66 ]. Following the development of DOMS, the muscle was palpated, revealing a tender band judged to be taut. However, since the muscle itself is a band, relating the description to TrPs seems meaningless. It should be noted that DOMS is self-limiting, whereas whatever phenomenon is occurring with chronic muscle-related pain is not. The relevance of DOMS to TrPs remains unclear.
Integrated hypothesis
Dommerholt et al. [ 68 , 69 ] postulated that low-level isometric muscle contraction or eccentric or submaximal concentric contractions could result in muscle dysfunction or damage, and that the formation of TrPs would follow. According to Gerwin et al. [ 70 ], excessive release of acetylcholine from dysfunctional neuromuscular endplates might be responsible for the taut band phenomenon (i.e. focal muscle contraction modulated by muscle spindle afferents) and that these bands could in turn produce muscle ischaemia, apparently by compressing adjacent capillaries supplying the muscle. This physiological process could precipitate an energy crisis in the relevant working muscle, which would respond by releasing proinflammatory molecules, thereby activating nociceptive neurons. Although there is no experimental evidence in support of this hypothesis, others [ 71 , 72 ] have accepted the motor endplate and the energy crisis theories of tonic muscle hyperactivity and TrP formation.
Recent studies of induced muscle pain in humans has not provided evidence for a reflex increase in fusimotor drive and spindle discharge [ 73 , 74 ]. In fact, persistent musculoskeletal pain is associated with decreased agonist muscle tone [ 75 ]; in other words, digital pressure or other stimuli that evoke pain will decrease the tone of the muscle stimulated. The validity of the paradigm that correlates endplate activity or noise with pain arising from the TrP became further suspect when it was reported that injection of botulinum toxin A in the region of a TrP had no effect on pain intensity or mechanical pain thresholds, but did significantly reduce motor endplate activity and the EMG interference pattern [ 76 ]. Finally, the vicious circle hypothesis has now been laid to rest by microneurographic recordings in humans performed during sustained muscle pain [ 73 , 74 ]. The integrated hypothesis remains conjecture in the face of conflicting data.
Treatment
Non-invasive interventions that have been advocated include compression of the TrP, spray and stretch, transcutaneous electrical stimulation and, more recently, high-intensity focused US [ 77 ]. Invasive treatments have included injection of local anaesthetic agents, injection of CSs, injection of botulinum toxin, needle acupuncture and dry needling [ 78 ].
In their systematic review, Cummings and White [ 79 ] were unable to find evidence that needling therapies have any specific effect. Their later review of 1517 studies found only seven that were of high enough quality for meaningful analysis [ 80 ]. Rickards [ 81 ] also found limited strength of evidence for any treatment of TrPs.
Another review remarked upon the heterogeneity of the populations being treated, and the lack of widely accepted standard diagnostic criteria for MPS [ 82 ]. This review also concluded that there was insufficient evidence to support the use of most interventions.
A systematic review of botulinum toxin A for TrP treatment located 21 randomized controlled trials, with 12 eligible for consideration but only five suitable for inclusion, and concluded that the current evidence does not support any therapeutic value [ 83 ]. Again, these authors reported that the data were limited and that the patient populations were heterogeneous.
These studies provide little evidence that dry needling of TrPs is associated with a treatment effect compared with standard care [ 3 ]. They are based on small sample sizes, uncertainty as to whether TrPs were the sole cause of pain, as well as neglect of technical issues such as the variability in the location of TrPs and the depth of needle insertion.
With these results in mind, why do many clinicians insist that their treatments work? One explanation is that the treatments are rarely performed in an isolated fashion; that is, treatment is accompanied by manual therapy, home exercises and stretching.
Contextual effects could explain the plethora of anecdotal responses to treatment [ 84 , 85 ]. This is not unexpected when a medical treatment with high face validity is based solely on practical experience rather than reflecting a rational approach based on pathogenesis. Apparent effectiveness of any treatment may be attributed to the natural history of the particular problem being treated, regression to the mean, and the expectation of something being done to the area in question. This can lead to the fallacy known as post hoc ergo propter hoc (after this, therefore because of this), when the treatment offered in fact had nothing to do with the pathogenesis of the condition towards which it was directed. A recent study comparing dry needling with manual compression, in which there was no control group, exemplifies this critical methodological issue [ 86 ].
One common factor shared by most therapies is that they elicit pain at the site of their application; that is, they are noxious stimuli. If they do work, this similarity suggests a common mechanism of action. One possible mechanism is counterirritation, or application of a competing noxious stimulus [ 87 , 88 ]. It is not surprising that a noxious stimulus applied in the region where pain is experienced, whether or not there is local pathology present at that site, would elicit a transient reduction in pain intensity by recruiting those higher order brain regions responsible for anti-nociception [ 89 , 90 ]. In conclusion, the vast majority of studies and meta-analyses do not support the prediction from MPS theory that focal treatment of TrPs is effective.
An impasse
In 1976, Simons hoped that: ‘It would now appear possible to resolve much of the conflicting data of the past by carefully distinguishing trigger from reference zones, and acute from chronic lesions using modern electrodiagnostic, biochemical, histochemical, and ultramicroscopic techniques’ [ 1 ]. Some three decades later, he conceded that acceptance of the concept of TrPs had been hampered by two outstanding considerations: the lack of a diagnostic gold standard and the lack of generally recognized pathogenesis [ 91 ].
We propose that sufficient research has been performed to allow TrP theories to be discarded. The scientific literature shows not only that diagnosis of the pathognomonic feature of MPS (the TrP) is unreliable, but also that treatment directed to the putative TrP elicits a response that is indistinguishable from the placebo effect. As these conclusions refute MPS, formulating a plausible scientific explanation for pain perceived by patients as coming from their muscles remains a challenge.
Towards explaining the clinical phenomena
In our opinion, current neuroscientific hypotheses can form the basis for collaborative scientific investigation to explain the clinical phenomena. We offer two for consideration, neither of which relies on local pathophysiology.
Neuritis model
Nerve inflammation as a source of pain was discussed in the 19th century [ 92–97 ], but focused research on nerve inflammation as a primary disease aetiology has been limited.
Quintner and Cohen [ 25 ] hypothesized that the TrP was an area of what was then called secondary hyperalgesia occurring in muscles that are structurally and physiologically unimpaired. Noting the remarkable proximity of TrPs to known peripheral nerves, these authors argued that sensitization of the axons within the nerves, possibly by inflammation, may inform the underlying mechanism. Subsequent research has emerged in support of this hypothesis.
Focal inflammation of peripheral nerves leads to ectopic axonal mechanical sensitivity and spontaneous discharge of some but not all of the nociceptors within the inflamed nerve [ 98–101 ]. These changes can be expected to lead to focal areas of neurogenic inflammation and possibly to sensitization in the muscle innervated. If confirmed, they can inform further investigation that might be highly relevant to explaining the phenomenon of chronic muscle pain.
Referred pain and tenderness (allodynia)
Kellgren [ 102–104 ] reported the critical observation that, in addition to referred pain, referred tenderness could be induced by targeted injections of hypertonic saline into tissues such as interspinous ligaments, periosteum, cancellous bone, or voluntary muscle. His studies and those of others [ 105 , 106 ] showed that nociception in deep tissues can induce the phenomena of remote localized pain and tenderness. This relegates the TrP to being a site of secondary allodynia reflecting altered central nociceptive mechanisms [ 107 ].
Conclusion
The construct of MPS caused by TrPs remains conjecture. All working hypotheses derived from this conjecture have been refuted and therefore the theory can be discarded. In contrast, evolving insights into the neurobiology of nociception and pain suggest plausible hypotheses that form a basis for advancing knowledge and therapeutics in this challenging area.
Disclosure statement : The authors have declared no conflicts of interest.
The theory of myofascial pain based on trigger points is conjecture that has been put forward as established knowledge.
The key phenomenon of muscle tenderness demands a robust plausible explanation based on neurobiology.
Clinicians cannot ignore the important role of contextual factors when evaluating outcomes of their treatment for myofascial pain syndrome.
Comments
Sir,
We thank Lluch et al. for their comments on our recent article [1].
The primary premise of their discussion is that there exists a pathological lesion in muscle (the trigger point) that is responsible for local and radiating pain. Despite substantial research efforts, there is no evidence supporting the existence of trigger points. The nebulous concept of the trigger point has been put forward as if it were true. Our paper asserts that the truth lies elsewhere. Studies based on a faulty premise can only perpetuate the fundamental logical error.
Lluch and colleagues write, "The new hypotheses they propose have never been tested and at this point in time are perhaps interesting, but otherwise more or less irrelevant." Are they asserting that hypotheses that test an alternative to their beliefs are irrelevant, even before they are tested?
References
1. Quintner JL, Bove GM, Cohen ML. A critical evaluation of the trigger point phenomenon. Rheumatology 2015; 54:392-99.
Conflict of Interest:
None declared
Sir,
We thank John Sharkey for his comments on our recent article [1]. We would like to respond to his points.
Firstly, he mentions not presenting "evidence to support their claims". Our claim is that the evidence does not support the existence of the trigger point as a pathological entity: in this exercise we are not required to present evidence that tests an alternative hypothesis.
Secondly, Sharkey's defence of the concept of the latent trigger point merely reasserts the conjecture of his mentor.
He writes, "[t]here are still many questions concerning the nature of MPS and the aetiology and pathophysiology of the myofascial trigger point is (sic) still somewhat elusive. " It is clear that he accepts that trigger points exist. In doing so, he - as do many others - is accepting a proposed explanation as a fact, because, according to Lipton, "the activity of explanation itself supposes truth." [2].
The scientific principle that we have followed is that of Sir Karl Popper: repeated refutations of hypotheses generated by a theory should lead to rejection of that theory [3].
References
1. Quintner JL, Bove GM, Cohen ML. A critical evaluation of the trigger point phenomenon. Rheumatology 2015; 54:392-99. 2. Lipton P. The Medawar Lecture 2004: The truth about science. Philos Trans R Soc Lond B Biol Sci 2005;360:1259-69. 3. Popper KR. Objective knowledge: an evolutionary approach. Oxford: OUP, 1979.
Conflict of Interest:
None declared
Sir,
We thank Elizabeth Frank for her response to our recent article [1]. In reply, we would like to bring to the attention of readers the three errors of reasoning contained in that response.
Firstly, although she apparently agrees with us that refutation of the myofascial trigger point (MTrP) construct would imply that its translation into the context of chronic pain in other species is invalid, Frank nonetheless argues the contrary, that "the human is a naturally occurring model of myofascial pain in the dog."
Secondly, defining a pathological entity by its putative response to therapy - this problem has apparently responded to myofascial trigger point therapy, therefore what was being treated is a myofascial trigger point - is a classical circular argument.
Thirdly, Frank's suggestion that "MTrPs are not only a feature of mammalian myofascial pain but also one that has been evolutionarily conserved in skeletal muscle" again begs the very question about MTrPs that we raised and addressed in some considerable detail in our article. We have shown that MTrPs arise solely out of the conjectures of Travell and Simons [2].
Frank also mentions the rabbit model of MTrPs; however, as we described in our article there is no such valid model, since the work was performed on normal rabbits [3].
One cannot deny the validity of Frank's own observations that a non- or minimally-noxious physical stimulus applied to sensitive soft tissues of a sentient being may be associated with clinical benefit. However that does not imply that a definite pathological entity has been specifically treated, especially if the existence of that entity was presumed based on findings in an invalid model that was inappropriately taken across species.
Frank's dismissal of the "all too commonly used placebo excuse", in the face of increasing scientific understanding of placebo phenomena, in fact detracts from her own observations.
References
1. Quintner JL, Bove GM, Cohen ML. A critical evaluation of the trigger point phenomenon. Rheumatology 2015; 54:392-99.
2. Travell JG, Simons DG. Myofascial pain and dysfunction. The trigger point manual. Baltimore: Williams and Wilkins, 1983.
3. Hong CZ, Torigoe Y. Electrophysiological characteristics of localized twitch responses in responsive taut bands of rabbit skeletal muscle fibers. J Musculoskel Pain 1994; 2: 17-43.
Conflict of Interest:
None declared
Dear Sir, Quintner et al.'s recent paper in Rheumatology (1) claimed that, while they did not deny the existence of the clinical phenomena, the explanation for myofascial pain syndrome (muscle pain and tenderness in the absence of evidence for local nociception) caused by trigger points lacks external validity. The paper reflected an obvious emotive frustration with claims that therapists who offer treatment of myofascial trigger points had uncritically accepted the diagnosis of myofascial pain syndrome (MPS) and its system of treatment. The authors claimed to have critically examined the evidence and stated that MPS and myofascial trigger points are inventions that have no scientific basis (experimental or empirical). Their paper boldly claims to have refuted the theory of MPS caused by trigger points. I am the programme leader for a Masters degree in Neuromuscular Therapy, a clinical anatomist and exercise physiologist working for the department of clinical sciences University of Chester/National Training centre, Ireland. As such I have an appetite for and warmly welcome critical evaluations regarding any topic generally and specifically that of MPS and the role of myofascial trigger points. Unfortunately Quintner et al. is positively anorexic when it comes to providing evidence to support their claims. Much of what Quintner et al. criticize deserves criticism. The very nature of scientific investigation leads to new questions and often falls short of conclusive answers. This is the reason many papers finish with more research is required. Yes, there are still many questions concerning the nature of MPS and the aetiology and pathophysiology of the myofascial trigger point is still somewhat elusive. However significant ground has been made and we are moving forward in our understanding of the mechanisms involved but, as with the majority of syndromes, these issues remain in the realm of theories. That is the nature of science. Science is both stable and malleable; it is not the final word. Science continues to test and challenge previous assumptions and challenges but it must do so on scientific principles. Quintner et al. fall short on this point on several grounds.
First, the references provided by Quintner et al. are not current as the majority of the research they site is post 2011. The paper contains biased opinions and false unsupported claims more akin to finger pointing than scientific scrutiny. Quintner et al.'s claim that "Travell and Simons found it necessary to invent the latent TrP" was offensive. This is a misleading claim and not at all an accurate reflection of the scientific process. Noting that patients reported pain that they did not recognise as fitting the active trigger point phenomenon such that irritation of the trigger point did not refer in the pattern typically observed but only locally. Travel and Simons gave this palpable hard nodule the name latent trigger point to add to their findings. In this regard they developed a concept for further scientific investigation. To use emotive terms such as they "found it necessary to invent" seems a rather pernicious comment to make. Overall the Quintner et al.'s paper is weak and fails to provide much more than opinions peppered with bias. The author's use the popular technique of quote mining, where misquoting or selective phrasing (i.e. leaving out an important part of a passage or quoting a line out of the context in which it was originally written) is obvious to those familiar with the research quoted. Where is the research to support the hypotheses of Quintner et al.?
The language used by these experienced authors is surprisingly emotive and not befitting a scientific review paper. I openly declare my own bias as David G. Simons was my mentor and wrote the forward to my first book on the topic of Myofascial trigger points (MtPs) 92). That said, I am fully prepared to change my views and opinions regarding the topic of MPS and the involvement of the MtPs based on investigations that have verified the quality and validity of the research. Quintner et al.'s hypothesis of an inflammatory neuritis to explain myofascial pain is a welcomed hypothesis but has yet to bring forward supportive research regarding the underlying mechanisms of myofascial pain and myofascial trigger points. In the time honoured fashion, I say, "Further research is required."
Reference
1. Quintner JL, Bove GM and Cohen ML. A critical evaluation of the trigger point phenomenon. Rheumatology 2015; 54: 392-99.
Conflict of Interest:
None declared
Sir, we read with great interest the article by Quintner et al. in which the authors claim to refute the concept of myofascial trigger point (MTrP) pain [1]. Unfortunately, we feel that the authors have expressed many biased opinions, based mostly on highly selective references in support of their assumptions.
We had high expectations of the review as the authors promised to provide a better explanation of the phenomenon of MTrPs. To our surprise, the two current neuroscientific hypotheses proposed by the authors are no different from what they had proposed 20 years ago without any compelling evidence of their alternative to the myofascial pain construct or any up-to-date references in support of their argument [2].
Quintner and colleagues opted for a narrative and non-systematic review format to express their opinions. At times they seem to deliberately cite one particular sentence of an article, which appears to be out of context, and at the same time ignore other relevant aspects from the same article. For example, when the authors cited Lewit's observation about Travell's diagrams of referred pain as "sometimes been chosen arbitrarily, there being no accepted standard", careful reading of the source reveals that Lewit did not address referred pain [3]. Granted, the patterns were empirically derived and to date, most have not been subjected to scientific study. In the same paper, Lewit reported that "dry needling is highly effective in the therapy of chronic myofascial pain. Immediate analgesia without hyperesthesia (the needle effect) can be produced by needling precisely the most painful spot"[3]. Quinter et al. suggested that "treatment directed to the putative TrPs elicits a response that is indistinguishable from the placebo effect", despite recent evidence that the treatment of MTrPs is superior to placebo, something the authors overlooked or conveniently did not include in their analysis [4].
The authors suggested that contextual factors or counter-irritation would mainly be responsible for the responses achieved with MTrPs treatments. Therapeutic interventions are always mediated by different physiological mechanisms and other contextual factors, as was succintly summarized by Cagnie et al for dry needling [5]. In fact, the placebo- effect and activation of descending control pathways secondary to application of noxious stimuli (i.e., counterirritation) were discussed as potential physiological mechanisms underlying effects of MTrPs interventions [5], however, they are not exclusive to MTrP therapies, and they do not minimize other established physiologic effects of MTrP treatments.
We agree with Quintner and colleagues that the vicious cycle hypothesis explaining muscle pain from MTrPs should rest in peace. Quinter and colleagues' reference to the pain adaptation model as an alternative (i.e., "persistent musculoskeletal pain is associated with decreased agonist muscle tone") is, however, not appropriate either. Recent models suggest that motor adaptation to pain is more complex that the simple inhibition of agonists in response to pain. The new motor adaptation theory proposed by Hodges and Tucker contends that muscle activity in the presence of pain is redistributed between and within muscles, in such a way that inhibition and facilitation can occur in agonist and antagonist muscles aiming to protect tissues at least initially of more injury and pain [6]. The role of MTrPs in this proposed motor control dysfunction is currently unknown [7].
The authors mention that the physical examination of MTrPs is unreliable, citing an older study with methodological issues [7], and ignoring more recent studies demonstrating good inter- and intrarater reliability. Nevertheless, we agree that more research is needed to validate the set of clinical indicators.
Quintner et al. conclude that "the vast majority of studies and meta-analyses do not support the prediction from MPS theory that focal treatment of TrPs is effective." Unfortunately, Quintner et al ignored pertinent aspects of the current hypotheses. There is much evidence that MTrPs are hypoxic and therefore feature a significantly lowered pH. Local treatments improve the oxygen supply, normalize the pH, remove peripheral nociception from MTrPs, and reduce pain.
In summary, the paper by Quintner et al. does not achieve its stated objective. There is little evidence based on the paper that the current thinking about myofascial pain and MTrPs should be discarded. The new hypotheses they propose have never been tested and at this point in time are perhaps interesting, but otherwise more or less irrelevant.
Authors: Lluch E(1), Mayoral O(2), Cagnie B(3), Dommerholt J(4), Gerwin RD(5)
Affiliations: (1) PT, Department of Physical Therapy, University of Valencia, Valencia, Spain. Departments of Human Physiology and Rehabilitation Sciences, Faculty of Physical Education & Physiotherapy, Vrije Universiteit Brussel, Belgium. Pain in Motion Research Group, http://www.paininmotion.be
(2) Hospital Provincial de Toledo, Spain
(3) Department of Rehabilitation Sciences and Physiotherapy, Ghent University, Ghent, Belgium
(4) Pain & Rehabilitation Medicine, Bethesda, MD, USA. Johns Hopkins University, Baltimore, MD, USA
(5) Bethesda Physiocare, Bethesda, MD, USA. PhysioFitness, Rockville, MD, USA. Myopain Seminars, Bethesda, MD, USA
References
1. Quintner JL, Bove GM, Cohen ML. A critical evaluation of the trigger point phenomenon. Rheumatology 2015; 54: 392-99.
2. Quintner JL, Cohen ML. Referred pain of peripheral nerve origin: an alternative to the "myofascial pain" construct. Clin J Pain. 1994; 10:243-51.
3. Lewit K . The needle effect in the relief of myofascial pain. Pain 1979; 6: 83-90.
4. Mayoral O, Salvat I, Martin MT, Martin S, Santiago J, Cotarelo J, Rodriguez C.Efficacy of myofascial trigger point dry needling in the prevention of pain after total knee arthroplasty: a randomized, double- blinded, placebo-controlled trial. Evid Based Complement Alternat Med 2013; 694941. doi: 10.1155/2013/694941.Epub 2013 Mar 27.
5. Cagnie B, Dewitte V, Barbe T, Timmermans F, Delrue N, Meeus M. Physiologic effects of dry needling. Curr Pain Headache Rep. 2013; 17:348.
6. Hodges PW, Tucker K. Moving differently in pain: a new theory to explain the adaptation to pain. Pain 2011; 152(3 Suppl): S90-98.
7. Dommerholt J. Dry needling: peripheral and central considerations. J Manual Manipul Ther 2011; 19: 223-37.
Conflict of Interest:
None declared
Sir, Quintner et al. [1] believe that the myofascial trigger point (MTrP) construct as lacking in external validity. However, lack of external validity would imply an inability to translate the MTrP model to chronic pain in other species.
Frank [2], based solely on the descriptions of Travell and Simons [3,4], used the human MTrP model to develop a diagnostic and therapeutic approach to pain syndromes unresponsive to conventional medical or surgical therapy in the dog. Features used included symptoms; initiating and perpetuating factors; palpation findings; active and latent MTrPs, response to treatment; and a range of treatment modalities including dry needling. The conclusion at the time, based on over 600 cases, that the human was a very good model for canine myofascial pain syndromes is contrary to the review by Quintner et al. who suggest no model is relevant to the condition being studied exists. Further, based on additional features of human chronic pain and the treatment to date of several thousand animals, I would conclude that the human model is a naturally occurring model of myofascial pain in the dog.
Individual dogs treated for myofascial pain have failed to respond to multiple conventional medical (up to 11 medications) and surgical interventions (at times repeated procedures on the same joint) and often a range of one or more complementary therapies; frequently over years (duration 1 day to 11 years); after consulting multiple practitioners (up to 7 veterinarians in 3 states) and referrals coming from veterinarians at the primary to specialist/tertiary level. Clinically, these cases may have pain of unknown origin; a range of neuro-musculo-skeletal anatomical and/or functional abnormalities present; or chronic pain after major or minor injury or surgery. Therapeutically, these animals have steadfastly resisted both conventional dogma and the all too commonly used placebo excuse by typically experiencing increasing frequency and severity of symptoms.
Wall [5] stated that "disturbed behavior that responds to anti-pain therapies" is an alternative definition of pain, with response to analgesic therapy being a very useful objective measure of pain. MTrP therapy is a human anti-pain therapy. "Response to appropriate treatment is the gold standard to measure the presence and degree of pain" in veterinary medicine [6]. Dog owners consistently report a pattern of response to MTrP therapy in the treatment of myofascial pain. Presenting abnormalities include pain related alteration of gait, uncharacteristic behaviour, loss of function, inability to perform activities of daily living, decreased activity levels and exercise intolerance, All consistent with chronic pain behaviour in dogs [6]. Response to therapy leads to a spontaneous return to what owner's describe as normal behaviour and function for that individual with improved quality of life. All of which are ultimate goals for veterinary chronic pain management.
Contrary to Quintner et al., the rabbit model of MTrPs has clinical relevance to treating myofascial pain in rabbits. I have successfully treated not only chronic pain due to MTrPs in dogs but also rabbits, cats, goats, ferrets and horses as well as palpating MTrPs in a clinically affected Australian saltwater crocodile. Anecdotally, MTrP therapy has also been used to treat clinically affected aquarium sharks [7].
Pain perception is likely to be under considerable evolutionary pressure and extraordinary conservation of mechanisms of nociception across different species is recognized [8]. Rather than refuting the myofascial construct, the wide range of clinically affected and treated animal species may instead suggest that MTrPs are not only a feature of mammalian myofascial pain but also one that has been evolutionarily conserved in skeletal muscle.
1. Quinter JL, Bove GM, Cohen ML. A Critical Evaluation of the trigger point phenomenon. Rheumatology 2015; 54: 392-99.
2. Frank EM. Myofascial trigger point diagnostic criteria in the dog. J Musculoskel Pain 1999; 7: 231-37. 3. Travell JG, Simons DG. Myofascial pain and dysfunction. The trigger point manual Vol 1. Baltimore: Williams and Wilkins, 1983.
4. Travell JG, Simons DG. Myofascial pain and dysfunction. The trigger point manual Vol 2. Baltimore: Williams and Wilkins, 1992.
5. Wall PD. Defining "Pain in Animals." In Short CE, Van Poznak A, eds. Animal Pain. New York: Churchill Livingstone, 1992: 63-79.
6. Mathews K, Kronen PW, Lascelles D, Nolan A, Robertson S, Steagall PVM, et al. Guidelines for recognition, assessment and treatment of pain. J Sm Anim Prac 2014; 55:E10-68.
7. Reddy M. How to massage a shark? Carefully. The Age. 2006 May 20. Available from: http://www.theage.com.au/news/national/how-to -massage-a-shark-carefully/2006/05/20/1147545568020.html. Date last accessed 17 January 2015.
8. Neely GG, Rao S, Costigan M, Mair N, Racz I, Milinkeviciute G, et al. Construction of a global pain systems network highlights phospholipid signaling as a regulator of heat nociception. PLoS Genet. 2012; 8:e1003071. Available from: www.plosgenetics.org. Date last accessed 17 January 2015.
Conflict of Interest:
None declared