Below we publish Quintner, Bove and Cohen’s Response to Dommerholt and Gerwin: Did we miss the point? The Dommerholt and Gerwin article is a reply to Quintner, Bove and Cohen’s important refutation of the trigger point concept. If you haven’t seen it, you should read it. It is a landmark in the trigger point debate. We publish this additional commentary here in the spirit of encouraging discussion, as it is hard to bring debate and discussion to convention medical journals. Similarly, we offer space to Dommerholt and Gerwin. – Fred Wolfe, MD
THE DECLINE AND FALL OF THE TRIGGER POINT EMPIRE
It should by now be obvious to those who have read our paper (Quintner et al. 2015) that we do not share the same beliefs as do Dommerholt and Gerwin (2015), who mounted a spirited defense of their preferred theory of myofascial pain arising from trigger points (MTrP).
This is a most important academic debate. Both Robert Gerwin and Jan Dommerholt claim to have studied and worked with the founders of MTrP theory, Drs Janet Travell and David Simons. They lecture and teach around the world under the banner of Myopain Seminars. “Dry needling” of MTrPs is their favoured treatment modality for pain that is deeply felt within muscles.
The position taken by Dommerholt and Gerwin
In summary, Dommerholt and Gerwin (2015) have made their position quite clear:
“Based on our understanding of the literature, Quintner et al. have not presented any convincing evidence to believe that the Integrated TrP hypothesis should be laid to rest” and that “insufficient evidence is to be taken that further studies are needed …” and that “Quintner et al have not succeeded in providing sufficient evidence that the current TrP hypotheses should be rejected.”
Dommerholt and Gerwin have raised a number of important issues and made accusations that impugn our scientific credibility. They have very publicly thrown down the gauntlet.
In this article I do not intend to address each and every accusation raised in their “rebuttal”, but will examine those that seem to be most relevant. Our shorter and more focused response is currently available as an article “in press” and we understand that it will be published in the July issue of the Journal of Bodywork and Movement Therapy.
Dommerholt and Gerwin appear to have interpreted as bias our seizing upon the lack of epistemological discipline shown by the original proponents of MTrP theory (Travell & Rinzler, 1952; Travell and Simons 1983). We first exposed the major flaws in this theory in 1994 (Quintner & Cohen, 1994). To date, these flaws have not been acknowledged, let alone addressed by proponents of the theory. It was this lack of response that prompted our second paper on the subject (Quintner et al. 2015).
Biased review of the literature?
“Quintner et al’s paper is a biased review of the literature replete with unsupported opinions and accusations.”
Limitations of space in Rheumatology meant that the many studies that have been undertaken based upon the premise that TrPs were potential sources of nociception resulting from localised muscle damage could not be included. But when arguing from a false premise (i.e. in this case an unwarranted assumption regarding the properties of TrPs), no amount of evidence can ever rectify such a fundamental fallacy of logical reasoning.
Discrediting MTrP research?
“In doing so, they specifically discredit much of the research on myofascial TrPs that has been published as unreliable, without providing any alternative studies specifically done on the pain phenomena that is attributed to TrPs.”
Dommerholt and Gerwin concede that several aspects of “myofascial pain” remain elusive and are not well understood, and that “a distinct mechanistic understanding of this disorder does not exist.” Therefore, as they appear to agree with us, there is no need to resile from the first proposition.
As for the second proposition, it was not our brief to provide “alternative studies specifically done on the pain phenomenon.” But at the very least our paper calls for such studies to be undertaken as a matter of priority. Furthermore, in our paper we have pointed a way towards achieving this objective.
Our use of “theory” and “hypothesis”
Dommerholt and Gerwin are critical of our use of “theory” and “hypothesis” and claim that we have used them in a non-scientific manner.
“Scientific inquiry commonly starts with observations, followed by the development of hypotheses, which through experiments are confirmed, modified, or refuted. Through repeated experimental testing of the hypothesis it is continually refined until a theoretical basis can be constructed that addresses different aspects of the hypothesis.”
A theory is a generally accepted explanation for an observed set of phenomena. Hypotheses can be deduced from theory. Refutation of (the claims made by) a hypothesis should lead to modification of the theory. Repeated refutations of hypotheses generated by modified theory should lead to refutation of the theory. In this way, even cherished theories such as MTrP can be contested.
We did mention the face validity of the generally accepted explanation for the phenomena associated with the MTrP, but in our paper we went on to argue strongly against it on the grounds that its proponents were lacking in epistemological discipline.
Diagnosis of trigger point
“We acknowledge that there has not been a study to demonstrate the minimum essential features of the TrP needed to identify it for diagnosis and treatment purposes.”
Although Dommerholt and Gerwin agree with the absence of agreement about the pathognomonic feature of their explanatory model, despite 50 years of investigation, they still argue that more studies are needed. But we fail to see how such studies would avoid the twin errors of confirmation bias and circular argument.
The nature and validity of latent TrPs
“The differentiation between normal muscle tissue, active and latent TrPs reflects the degree of contraction, as confirmed objectively by vibration elastography. Their mechanical attributes are, however, not directly correlated with pain pressure threshold scores (Ballyns et al 2012), which Quintner et al interpreted as another nail in the coffin of the TrP hypothesis.”
“… Ballyns et al. clearly were able to distinguish and visualize contractured nodules on muscle that were only painful when stimulated (Ballyns et al. 2012).
Ballyns et al. (2012) were indeed able to provide an objective assessment of relatively superficial soft tissue, but did not make a comment as to whether the reported abnormalities in painful muscle were consistent with “contractured nodules”.
They did find regions that were “stiffer” than surrounding muscle tissue and equated them with “active” trigger points. Some of the smaller regions of stiffness were said to represent “latent” trigger points. One may well ask on what grounds were they able to make these inferences?
In the section dealing with patient selection, Ballyns et al. did not explain how they were able to exclude from the study those patients whose pain and tenderness was likely to have been referred into the muscle(s) being studied.
Sikdar et al (2009) claimed to have excluded those with “neck and shoulder conditions” including cervical radiculopathy. But did they really exclude patients whose pain may have been referred into these muscles from, for example, cervical zygapophyseal joints? We think not!
“Sonography is not only used for research and possible diagnostic purposes, but can also be applied to guide trigger point needling (Botwin et al. 2008, Bubnov 2010, Suh et al. 2014) and to objectively measure the outcome of TrP interventions such as dry needling. (Maher et al, 2013)
In a preliminary study Maher et al. (2013) found that the shear modulus of the upper trapezius muscle with MTrPs was significantly reduced after dry needling of the most painful TrP and also when the subjects assumed the prone position from supine lying. These changes were accompanied by palpable reductions in stiffness. The authors did not address the important questions as to whether these reductions were transient and whether pain relief accompanied them.
Pathogenesis of the trigger point
“Apparently, they believe that TrPs are some kind of anatomical entity, although there has never been a credible anatomic pathology associated with myofascial TrPs.”
Yet, in the studies we reviewed, and in the various other studies cited by Dommerholt and Gerwin, the authors assumed that an anatomical lesion actually existed. This logical fallacy is known as “begging the question”.
“Quintner et al. refer to “fibrositic nodules” which have nothing in common with TrPs and their relevancy escapes us.”
But they go on to assert that TrPs are “palpable as hard nodules within a band of contractured fibres …”
They would appear to have contradicted themselves!
Use of animal studies
“The majority of the studies of electrical activity of the TrP were carried out on animals and were based on palpation of locally contracted muscles.”
Our difficulty in accepting data derived from findings in muscles from normal animals is covered in our paper. Moreover as Dommerholt and Gerwin acknowledge “there has not been a study to demonstrate the minimum essential features needed to identify it for diagnosis and treatment purposes.” If this issue has yet to be resolved in humans, we fail to see how it has been resolved in animals.
“Quintner et al. criticize the findings of Shah et al (2003, 2005, 2008), who have reported higher concentrations of neurotransmitters and cytokines in the extracellular fluid in the immediate vicinity of TrPs as being non-specific.”
In fact we made no such criticism but did offer two possible neuroscientific explanations for these findings, the most likely one being “neurogenic inflammation”.
Muscle pain versus myofascial pain
“Perhaps Quintner et al. would consider our reasoning an example of conjecture, but the facts are that a low pH is common at active TrPs, and can cause muscle pain and hyperalgesia.”
We suggest that Dommerholt and Gerwin have fallen into the trap of conflating all pain felt in muscles with pain in muscles said to arise from supposed “myofascial TrPs”.
“Quintner et al. … suggest that a local twitch response, which is an entirely different feature of the taut band, is nothing more than a myotatic stretch reflex.”
According to Audette et al. (2004) the literature does indeed differentiate the “localised twitch response” from a myotatic stretch reflex.
In a discussion by Simons (1976), “two features suggest a hyperirritable spinal reflex phenomenon: the increased motor unit response with increasingly vigorous palpation and the simultaneous activation of adjacent palpable bands.”
It should be noted that mechanical irritation of a hypersensitive peripheral nerve appears to generate a motor efferent response with activation of at least a subset of the motor neuron pool (Hall and Quintner, 1996).
Central sensitization induced by TrPs
“Some of the phenomena that seem to trouble Quintner et al. result from the fact that TrPs induce central sensitization and referred pain. Muscles do have nociceptors and activation of those nociceptors can initiate and perpetuate central sensitization.”
We are indeed troubled by the first proposition. It has yet to be shown that MTrPs are capable of activating nociceptors. But we have no argument with the second proposition.
It is true that Mense (2008) did accept (albeit with some reservation) the notion of MTrPs as potential peripheral generators of nociceptive activity. But following his brief summary of the hypothesis proposed by Simons (2004), he commented “this supposed mechanism leaves many questions unanswered but is currently the only comprehensive hypothesis on the origin of MTrPs.”
We agree with Mense that there are still unanswered questions.
Low–level isometric contractions and TrP formation
“In 2006 and 2011, two complementary studies … explored whether the Cinderella Hypothesis could apply to the formation of TrPs.” Both studies provided evidence that low-level exertions can lead to the formation of TrPs (Treaster et al. 2006, Hoyle et al. 2011)
This conjecture concerns low threshold motor units, termed “Cinderella” fibers, which are being continually recruited and overloaded during low-level static exertions. It is not made clear how could one ever know this? Presumably damage to such fibers provides the basis for nociceptive input in these situations. This conjecture forms the central plank of the Integrated Hypothesis (Gerwin et al 2004).
In the second study, the authors concede that their findings were solely dependent on the expertise of a clinician not only to palpate the upper division of the trapezius muscle to locate and diagnose a taut band as a MTrP but also to rate its “sensitivity”.
Readers are then asked to accept the dubious proposition that once the examiners had located a TrP, “all detected trigger points in the trapezius and surrounding muscles were released by a combination of percussion, stretch and relaxation techniques” immediately prior to the commencement of the experimental task (approximately 60 minutes of computer typing). Following task completion, the subjects were then re-examined by the same clinicians to detect recurrence of any MTrPs, which were again duly “released”. Surface EMG was recorded from a grid overlying the identified MTrPs.
The authors speculated that MTrPs may be one causal pathway for pain during low-level static exertions and both postural and visual demands may play a role in muscle activation patterns, perhaps contributing to MTrP development and related discomfort.
Based on our assessment of these rather unusually designed studies, we cannot agree with Dommerholt and Gerwin that they “provided evidence that low-level exertions can lead to the formation of TrPs.”
New evidence provided by Dommerholt and Gerwin
“Rather than ignoring the worldwide developments in this field, we prefer the approach by Jafri, who critically reviewed the current thinking and contributed to a more in-depth understanding of possible underlying mechanisms (Jafri 2014)”.
Our problem with the approach of Jafri (2014) is that in his introductory remarks he begged the question that is at the heart of this debate:
“While myofascial pain syndrome is complex in its presentation, the onset and persistence of myofascial pain syndrome are known to be caused by myofascial trigger points.”
Jafri accepts without reservation the opinion of David Simons (2004), one of the main proponents of MTrP theory. Unfortunately the remainder of his paper fails to rise above the level of conjecture.
“Moseley confirmed that especially myofascial TrPs and joints are widely held to be common contributors to somatic referred pain.”
We acknowledge, as does Moseley (2012), that such an opinion is widely held amongst physical therapists. However, Moseley then asserts: “trigger points are present in all patients with musculoskeletal pain …” Drawing an analogy here with the universal generalization that “all swans are white” seems inescapable. The observation of one black swan (or of one patient without a trigger point) falsifies the argument.
When discussing somatic referred pain Moseley suggested that “disrupted transmission” happens within the central nervous system and he viewed “somatic referred pain from TrPs and joints as the brain’s efforts to localize the pain in response to ambiguous input.”
We are not aware of evidence for such “disrupted transmission” or for “ambiguous input” associated with referred pain phenomena.
But we can agree with Moseley’s concluding remarks: “This is a field where clinical practice may change as new evidence emerges, or new evidence may underscore the validity of current clinical practice.
Hypotheses of Quintner et al.
Dommerholt and Gerwin dealt mainly with one of the two explanatory models we advanced in our paper – that based upon the “neuritis” model. They accepted the model of “referred pain and tenderness” but asserted that its maintenance “is dependent on ongoing nociceptive input from the site of primary muscle pain.”
Some of their concerns about the “neuritis” model can easily be resolved when one accepts the readily available evidence that pain of peripheral nerve origin may not necessarily be accompanied by changes in cutaneous sensation, by objective signs of motor deficit or by changes detected on conventional electrodiagnostic examination (Quintner and Cohen, 1994).
Dommerholt and Gerwin prefer to rely upon evidence from the experimental studies of Arendt-Nielsen and Svensson (2001) and Rubin et al. (2009) to support the importance of “ongoing nociceptive input from the site of primary muscle pain in maintaining the phenomenon of referred pain.” But no such experiment has been shown to mimic the clinical situation.
We do not doubt that nociceptor fibres innervate muscles and that they can be activated by a variety of noxious stimuli. We agree that central mechanisms are important in explaining the phenomena of referred pain. However, it has yet to be demonstrated that a hypothetical “painful lesion” residing in “myofascial” tissues can be responsible for initiating and maintaining a state of central hypersensitivity.
As we have shown, Dommerholt and Gerwin (and others) have been arguing from the false premise of an unwarranted assumption – that MTrPs are primary sources of nociception. No amount of evidence they can adduce will rectify this logical error.
But if, as we believe, MTrP theory has been well and truly refuted, the scientific credibility of those who offer courses in “dry needling” to physical therapists can legitimately be called into question.
Prepared by John Quintner, Physician in Rheumatology and Pain Medicine, first author of “A critical evaluation of the trigger point phenomenon (2015).” He writes here on behalf of his co-authors.
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