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


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.

Preconceived bias?

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!

Sonographic evidence

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.

Tissue biochemistry

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”.

Twitch response

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.


Arendt-Nielsen L, Svensson P. Referred muscle pain: basic and clinical findings. Clin J Pain 2001; 17: 11-19.

Audette JF, Wang F, Smith H. Bilateral activation of motor unit potentials with unilateral needle stimulation of active myofascial trigger points. Am J Phys Med Rehabil 2004; 83: 368-374.

Ballyns JJ, Turo D, Otto P, Shah JP, Hammond J, Gebreab T, Gerber LH, Sikdar, S. Office-based elastographic technique for quantifying mechanical properties of skeletal muscle. J Ultrasound Med 2012; 31: 1209-1219.

Botwin K, Sharma K, Saliba R, Patel BC. Ultrasound-guided trigger point injections in the cervicothoracic musculature: a new and unreported technique. Pain Physician 2008; 11: 885-889.

Bubnov RV. The use of trigger point “dry” needling under ultrasound guidance for the treatment of myofascial pain (technological innovation and literature review). Lik Sprava 2010: 56-64.

Gerwin, RD, Dommerholt, J & Shah, JP. An expansion of Simons’ integrated hypothesis of trigger point formation. Curr Pain Headache Rep 2004; 8: 468-475.

Hall TM, Quintner JL. Responses to mechanical stimulation of the upper limb in painful cervical radiculopathy.  Aust J Physio 1996; 42: 277-285.

Hoyle JA, Marras WS, Sheedy JE, Hart DE.  Effects of postural and visual stressors on myofascial trigger point development and motor unit rotation during computer work. J Electromyogr Kinesiol 2011; 21: 41-48

Jafri MS. Mechanisms of myofascial pain. International Scholarly Research Notices Volume 2014 (2014): Article ID 523924, 16 pages.

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  1. In the section titled “Biased review of the literature,” the following sentence should read:

    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.

  2. Before the TrP empire strikes back, let me explain clearly why the outcome of this debate is relevant to the current practice of rheumatology. Certain of our key opinion leaders have suggested that nociceptive input from TrPs may be responsible for both the initiation and maintenance of Chronic Widespread Pain (aka Fibromyalgia Syndrome). Although we dealt with this issue in our recent paper published in the journal Rheumatology, their misguided opinion could be seen to give official license for “dry needlers” to assault the muscles of the many patients labeled with this condition. In the famous words of Marcus Tullius Cicero, we need to ask “Cui bono?”

  3. I appreciate your efforts on bringing the debate into the open with the hope of additional discussion. I also appreciate scientific research and its unbiased results. With that said, I do hope that this brings about tangible evidence from supporting studies very soon.
    As a layman specializing in supporting those with centralized pain/fibromyalgia syndrome and myofascial pain syndrome, I am confronted with a combination of scientific evidence supporting/not supporting Trps as a contributing factor in afferent pain, mounds of personal experience and hundreds of members giving their personal accounts on this subject matter.
    We are seeing an influx of PT’s suddenly certified in dry needling and an equal amount of patients flocking to their clinics for relief. This is not a fad, nor is this a gimmick for business. Therapists are scrambling to genuinely find ways to help us in light of the lack of alternative options for chronic myofascial pain.
    It is obvious your research is heading in the right direction and it is our deepest hope that this is an advance in the study of fibromyalgia symptoms.

  4. Dr. Wolfe,

    While I appreciate your invitation to “offer space to Dommerholt and Gerwin,” frankly, I do not see any need to continue discussing the two papers. The two papers highlighted where we differ in opinion and where we agree.

    In summary, we believe that there is growing evidence that trigger points are sources of peripheral nociceptive input than can lead to, maintain and accentuate central sensitization. We have addressed many aspects of this issue in our article FERNANDEZ-DE-LAS-PENAS, C. & DOMMERHOLT, J. 2014. Myofascial trigger points: peripheral or central phenomenon? Curr Rheumatol Rep, 16, 395. Quintner and colleagues disagree.

    We believe that research on myofascial pain is still in its infancy and we see no reason to stop exploring this clinical phenomenon. Serious research did not really start until maybe 20 years ago. Quintner feels that 50 years of investigation should be enough to refute the construct. In other words, we disagree.

    Quintner questions the ongoing research efforts conducted at the US National Institutes of Health and George Mason University and speculates that the researchers possibly failed to properly select their subjects. We do not see any reason to discredit the research by Ballyns, Sikdar, Gerber, and others. In other words, we disagree.

    Quintner feels that we assume that trigger points are anatomical lesions, which we have never expressed. He also maintains that we believe that all muscle pain is pain from trigger points, which we also do not believe. Again, we disagree.

    Quintner questions the Cinderella Hypothesis and goes back to presumed damage of fibers. We disagree.

    Lastly, Quintner believes that the trigger point theory has been well and truly refuted, and that the scientific credibility of those who offer courses in “dry needling” to physical therapists can legitimately be called into question. We disagree.

    I do not plan to continue this online exchange as I am not convinced that anything new will develop that has not already been discussed in the two papers.

    • Jan, in fact we have done much more than just disagree with you and your colleagues.

      By not heeding the warning we gave in our 1994 paper, you and your colleagues have presided over a disastrous era in musculoskeletal medicine during which time you have been passing off conjecture as factual knowledge. This is a very serious accusation which you cannot shrug off by repeatedly saying that you disagree.

      My deliberate choice of the title for this article – The Decline and Fall of the Trigger Point Empire – should leave you in no doubt as to what is at stake.

      Clearly there is nothing left for us to debate.

      Will you and your colleagues continue to teach “myofascial pain” theory and practice in the vain hope that no one will notice their lack of scientific credibility?

  5. Sabrina, if the treatment is based on a theory that has been refuted, I find it hard not to believe that it is either a passing fad or is being done for monetary reward. There is no rationale underlying “dry needling,” no evidence for its effectiveness, and the practice raises significant ethical considerations. Our research points in a completely different direction from intervening in peripheral tissues.

  6. I work as a physiotherapist in a pain management centre. I am not here to argue about the use of hands-on/hands-off/passive treatments like acupuncture etc., however, we need to be responsible clinicians and acknowledge the developing evidence and research. Yes, a number of patients report benefits from the passive TrP release treatments but it is the “pseudoscientific” explanations that patients have been given, that I object to. Patients deserve a proper explanation of the pain neurobiology, and what the treatments are aimed at ( “the therapist released the knot in my muscle” is NOT a helpful, or in anyway, a scientific explanation ). Our clinical practice requires that we provide patients with informed choice. A patient who primarily complains of pain needs an explanation of the pain science and we need to have the courage to say that we use treatments for which we do not have good evidence or indeed a good physiological understanding. That will help the patient to understand the complexity of persistent pain conditions ( felt in the soft tissues or elsewhere ) and why the pain felt in the muscle, can be treated and managed dealing with sensitisation of the nervous system and the impact of psychological processes in neurophysiology. It would certainly make my life a lot easier, when patients attend my clinic after years of oversimplified explanations for their pain including a number of entirely non-evidence based diagnosis. So thanks to Quinter et al. for highlighting that we cannot keep using this outdated model.

  7. john the problem with a refuted theorey is that there was a refuted theory before and one before ….
    If dry needling is a waste of time present an alternative supported treatment approach and you shall have your wish..

    • Andrew, you are quite correct about discredited theories, which is why we no longer bleed or purge our patients.

      We have critically examined the theory of pain arising from “trigger points” in muscles and found that it has no scientific evidential basis. Fred was spot on when he referred to it as “cargo cult” science.

      The practice of “dry needling” of “trigger points” in muscles now falls into the same category as many other once popular but long abandoned forms of treatment. It was never our brief to present an alternative “supported treatment approach”.

    • This is poor logic and assumes that doing something is always and inherently better than doing nothing. But better for who, the practitioner or the patient?

      And besides, why hunt fasciculations by blindly sticking in needles and introducing no small risk when you can achieve the same fasciculations (and relaxation) with simple manual techniques? It’s really not all that difficult.

  8. I did not mention another paper that Dommerholt believes is important in the debate. He and Fernadez-de-las-Penas (2014) assert: “Development or activation of TrP can result from a variety of factors, including repetitive muscle overuse, acute muscle overload, repetitive minor muscle trauma, psychological stress, and visceral disorders.” As evidence for this extraordinary claim, they cite Gerwin, Dommerholt and Shah (2004). They are here passing off what is conjecture as factual knowledge.

    The rest of the article demonstrates the fallacy known as reification, where the nebulous TrP is assigned the property of being a concrete entity or “thing” when in reality it is merely a faulty interpretation of observed clinical phenomena. To cap it off, one of the authors declares no conflict of interest!


    Fernandez-de-las-Penas C, Dommerholt J. Myofascial trigger points: peripheral or central phenomena? Curr Rheumatol Rep 2014; 16: 395.

    Gerwin RD, Dommerholt J, Shah JP. An expansion of Simons’ integrated hypothesis of trigger point formation. Curr Pain Headache Rep 2004; 8: 468-475.

  9. Sabrina, if you are interested, we have just responded to three e-letters submitted to the journal Rheumatology. The main letter is authored by some of the High Priests of Myofascial Pain theory. The second letter was authored by an academic who objected to our interpretation of the scientific method, and the third author defended the concept of myofascial “trigger points” in canines.

    The debate is now well and truly over. One cannot escape the conclusion, as was once expressed by Thomas Huxley, that “a beautiful theory has been destroyed by an ugly fact”.

  10. I am not sure about the intricacies of the debate about the existence and treatment of “trigger points.” My feeling is that the trigger point discussion does steer us away from verifiable and rational understanding of the locomotor system. However, at the least we must credit that the advocates are proposing pathology elsewhere than in the recesses of the central nervous system. Recall that Gower accepted that one should look within the intramuscular fibrous tissue for sources of pathology and pain.
    I continue to marvel that many modern authorities give credence to evidence that the CNS is the source of the symptoms felt by patients labeled as fibromyalgia. I find the evidence base is seriously flawed right out of the gate – often by what I term the “fallacy of the normal control.”
    Below, I’ll give four examples from recently published literature to illustrate. The key flaw in each experimental design is comparing cases labeled “fibromyalgia” to healthy normals instead of to controls who have other forms of pain, fatigue, etc. This flaw prevents one from seeing anything distinctively different about the so-called FM cases – in fact it allows the authors to mistakenly claim that any difference whatsoever from the normal controls means something specific about the FM cases. A classic historical example is the work of I. Jon Russell, who felt it was worthy to perform CSF studies in 62 people to demonstrate that substance P was different in “FM” cases than in than normals – not bothering to check that CSF substance P might well be similarly altered in any form of pain (e.g. pancreatitis, osteoarthritis, burns). [Arthritis & Rheumatism 37; 1593–1601, November 1994]
    Anyway, sampling the recent literature suggests that the “fallacy of the normal control” still dominates the thinking of prominent investigators. Not a one has ever actually set out to determine if there is anything unexpected and different in the brain mechanisms of patients said to exemplify a disorder called fibromyalgia. That’s their critical defining hypothesis, so why not test it? Stop comparing it to exclusively normal controls! Do they really think it unnecessary to show that their findings are truly different than in lupus arthritis/fatigue, or in ankylosing spondylitis, or in chronic rotator cuff attrition? Are they that obtuse – or perhaps just wouldn’t know what to do if each of the “abnormalities” in brain chemistry & function are found to be the same in pretty much any kind of enduring pain ailment? And thus not even relevant to the discussion of what these FM cases actually have?

    Here are the examples:

    1. Altered White Matter Integrity in the Corpus Callosum in Fibromyalgia Patients Identified by Tract-Based Spatial Statistical Analysis. Dajung J. Kim et al. Arthritis & Rheumatology Volume 66, Issue 11, pages 3190–3199, November 2014. COMMENT: 19 FM vs 21 healthy controls.

    2. Reduced insular γ-aminobutyric acid in fibromyalgia. Bradley R. Foerster et al. Arthritis & Rheumatism. Volume 64, Issue 2, pages 579–583, February 2012. COMMENT: 16 FM vs 17 healthy controls.

    3. Are Fibromyalgia Patients Cognitively Impaired? Objective and Subjective Neuropsychological Evidence. Valentina Tesio et al. Arthritis Care & Research. Volume 67, Issue 1, pages 143–150, January 2015. COMMENT: 30 FM vs 30 healthy controls.

    4. Neuromuscular fatigue and exercise capacity in fibromyalgia syndrome. Damien Bachasson et al. Arthritis Care & Research Volume 65, Issue 3, pages 432–440, March 2013. COMMENT: 11 FM vs 11 healthy controls.

  11. Dr Lampman, I agree with your impression that the “trigger point” discussion has steered us “away from a verifiable and rational understanding of the locomotor system”. But what I find even more remarkable is the blind faith in their infallibility shown by the high priests of the discredited theory of pain arising from myofascial “trigger points”.

    • Yes there is a certain catechismal belief system that gets in there. But we all have some of that, I suppose.

      In my personal practice of medicine, I went through a phase in the mid-80s in which I was impressed by the focality and intensity of trapezial & rhomboid myotendinous pain in quite a few patients, and turned to offering local xylocaine injections for a while –finding initially that I could offer occasional improvement; but in fact most cases got better seemingly on their own, from self-healing. Later, I took on many patients with a complaint of “pain all over” ( many previously diagnosed as FM) — and found by concrete anatomic examination that each had diverse distinct sources of pain. For example, rotator cuff, epicondylitis, trochanteric/gluteus medius pain, trapezial strain, and strain at iliac crest insertions. There were no cases for which specific locomotor or other ailments could NOT be found. And plenty of patients who agreed, following examination, that they didn’t have “pain all over” even though it kind of felt like it to them, as a subjective descriptor. I gave up on using terms such as myofascial and trigger points, fibromyalgia, central pain etc., since those terms submerge the concrete findings under a kind of mystery veil. Eventually I came to the belief that the peripheral nociceptive and central interpretive systems were doing exactly what they should do for anyone with pain sources. There was no need to propose unique CNS dysfunction and, for those who believed it, no credible experimental proof. This lack of proof is what I discussed in my previous note.

    • I did not address neuroplasticity, either to favor or not favor it. And of course the last thing we want is to carry a burden of “untenability.” It just wouldn’t do.

      I do address the objective biomechanical ailments to which the mammalian physique is vulnerable by virtue of its locomotor structure. I don’t value “trigger points”/myofascial points if they are disconnected from the biomechanics or if they are seen as mysterious potentiators of centrally-maintained pain. Nor do I accept “tender points” as abstract signals of CNS hypersensitivity, nor do I find a need for the term fibromyalgia (whose fundamental axioms are flawed).

  12. Dr Lampman, by not addressing neuroplasticity you are taking pain neuroscience back to the mid-20th century. Be that as it may, how can you distinguish between primary and secondary hyperalgesia in deep bodily structures, such as muscles? This is the very rock upon which myofascial pain theory has foundered.

  13. Not at all. My remarks subsume your concerns about neuroplasticity. For instance, the reference #1 (Kim, A & R, 2014) suggests that the corpus callosum of study patients is modified compared to healthy controls. I can accept that — but my point is that he has not shown that the modification is any different than for controls with various kinds of enduring pain. It’s not shown to be a unique kind of plasticity, nor does it even bear on the issues inherent in the FM hypothesis. He and other investigators who want to work with the “central pain” hypothesis essential to FM have the responsibility to critically examine and buttress their assumptions. They are not doing it. This goes back to the late ’60’s then, when the bankrupt psychosomatic tendencies of previous decades crept unchallenged into musculoskeletal medicine, gripped the psyche of a subset of rheumatologists, and overwhelmed any sense of scientific skepticism. The FM hypothesis became orthodoxy and currently, in my opinion, is incommensurate with science. This incommensurability becomes intense when you ask the lead authors to show that the “FM” patient has an abnormal nervous system compared, for instance, with a patient with persistent painful rotator cuff tendinitis, chronic pancreatitis, or burn pain. Such authors, so deeply submerged in illogic, typically can’t even register it as a valid question.

    My personal preferences in thinking about this, as you know, relate to my proposal that the neurologic system’s structure, metabolism, and function are actually normal (within the usual broad biologic variability) in the patients we encounter in the office. While the usual neurotic behavioral nonsense is layered on pretty thick in some, when you get right down to examining these cases anatomically, there isn’t such a great a mystery that we need to accept a far-out theory (central pain) in the absence of evidence. Just take a look at the fleshy mechanical anatomy and be impressed with the multiple opportunities for pain. As far as all the flutter over brain imaging in FM pain, it has veered into a realm called “neurotrash” since it fails to compare positive pain controls, which I believe would simply demonstrate the normal modes, pathways, and connections that the brain has in dealing with any chronic pain issue.

    Re: Travell etc in the 1950’s — a valiant effort to address a spectrum of symptoms.. I recall reading the big red book in the 1980’s and using it to try to understand certain cases of rhomboid, trapezial, intercostalis, and peripelvic pain cases — but ultimately I found it unsatisfactory since at the time it didn’t go concretely enough into commonsense locomotor causes and mechanisms. When current authors propose that normal daily forms of use-trauma can set up pain foci in mechanical locomotor structures, I would concur that’s a valuable avenue to pursue. But I’d prefer they not see “myofascial” points as isolated structures — instead of connected components of the kinetic chains and fabrics which power the body’s locomotion.

    • Dr Lampman, we have had this discussion before. Suffice it to say that I still do not find either the peripheralist or the centralist explanations of the clinical phenomena embraced by the FM construct to be scientifically satisfactory.

      It is disappointing that Jan Dommerholt has signed off because I would be interested to learn how he and others who offer expensive courses to demonstrate “dry needling” of innocent muscles will respond now that the theoretical underpinnings of their teachings have been critically examined and found to be pseudo-scientific.

      My best guess is that they will shrug off this challenge and carry on regardless, thereby perpetuating what I can only see as a monumental hoax being carried out by physical therapists (and some medical practitioners who by virtue of their training should know better) upon people in pain.

  14. Whilst this debate has been taking place, the practice of “dry needling” of “trigger points” by physical therapists has aroused the interest of the US National Center for Acupuncture Safety and Integrity, which alleges that this form of therapy was first described over two thousand years ago in the Yellow Emperor’s Inner Classic.

    If this is the case, physical therapists are using a technique indistinguishable from traditional Chineseacupuncture.

    Recently, in the State of Washington, the practice of “dry needling” was found to be outside the scope of practice of physical therapists. The Washington East Asian Medicine Association supports bill HB1042 which has been introduced in the Senate in an effort to clarify this matter.

    It is ironical that this furore seems to be all about safeguarding the public from needles being wielded by enthusiastic physical therapists who have not undergone the extensive training required of intending acupuncturists. That “dry needling” of myofascial “trigger points” is based on pseudo-scientific theory and is lacking in evidence of efficacy seems to have escaped the attention of the legislators.

  15. Very interesting.

    The history of medicine evidently is that of an uneasy rough-and-tumble mix-up between science and various alternatives, with the legal structure not giving unique dominance in the marketplace to any one of multiple trends and schools of therapeutics. As best I can tell, medical treatment was never about efficacy as such. Look at homeopathy and acupuncture. And scientific criteria have always been easily overcome by culturally-driven notions and frank silliness. Our profession, which sanctioned bone-marrow transplants for breast cancer, has less than perfect credibility. Rheumatology has wrongly accepted CNS-altering medications for muscular pain, hyaluronate injections and glucosamine/chondroitin for osteoarthritis, oral gold for RA, etc. with evidence for relevant clinical impact which is borderline, mangled, or just nonsense. And cardiology is being ridiculed for misinterpretation of the data on the diet/heart issue.

    I recently read Erika Janik’s “Marketplace of the Marvelous: The Strange Origins of Modern Medicine,” with subtitle “An entertaining introduction to the quacks, snake-oil salesmen, and charlatans, who often had a point.” [There is a nice summary at It’s especially good on mesmerism, Christian Science, and various diet & water therapies of the 19th Century.

    In dealing with benign but annoying physical ailments, practitioners probably do little harm and fill a need. However, you’d think that the legal structure would hold such practitioners to the same medico-legal liability we have — and not dismiss them so lightly when the aches are part of a threatening medical condition, diagnosis of which is delayed because of incomplete training. Dr. Quintner is troubled by the underpinnings of trigger-point theory. I applaud his efforts, but those efforts might be wasted. This may not go away quickly — and even then only when replaced by the next phase of alternatives — and then later, similar alternatives will likely continue even after scientific medicine gets it right. It’s tiresome.

    So how, then, do WE get it right?

    • Thank you Dr Lampman for your most relevant observations. How do we get it right? That is the quest of medical science when it is applied to problem solving. However, it needs to be accompanied by a ready willingness to admit that we may have been wrong when the evidence points in this direction.

      The “dry needling” brigade has been preparing for this eventuality by directing its gaze from the “myo-” to the “fascial”. Fascination with the fascial components of the musculoskeletal system is now in fashion. There are entire conferences being devoted to diagnosing and treating imaginary fascial dysfunctions! Yes, it is tiresome but we should not forget that Henry VIII enacted legislation to protect the quacks from the wrath of the physicians of the day. They have since continued to flourish

  16. I do need to say that there is a large body of respectable scientific research that has been directed at the anatomy, physiology and biomechanics of fascial tissues and in particular their interface with other musculoskeletal tissues. How this research will translate into clinical practice is not at all clear. There are a number of important issues facing physical therapists, not the least being how to reliably diagnose the presence of “fascial dysfunctions”. I hope that we do not see a repeat of the “trigger point” debacle. Another important issue is that of assessing whether therapeutic massage (in all its variations) applied to such dysfunctions serves any useful purpose. These therapies go under the name “myofascial release” but no one seems to know what exactly is being “released”.

  17. The diversity of fascial structures interests me — especially the type linked in as part of the locomotor system, as stabilizers, force transmitters, attachment, and sensors. The sheer bulk of fascia visible on dissection is impressive. Those big multiple aponeurotic attachments at the iliac crest and all the multi-directional trapezial attachments are remarkable. Not enough is known about the underlying physiology– but I like the title of an essay written long ago by an orthopedist named Richard Brand –“What do tissues and cells know of mechanics?”

    You’d think that with a combination of MR and sonographic study we’d be able to astutely visualize and localize very specific abnormalities. And more than just rotator cuff, achilles, trochanteric/gluteus minimis areas. Examples: latissimus dorsi (1) and tensor fascia lata (2).

    I personally feel that each and every person labeled “fibromyalgia” is set up to be biomechanically very vulnerable to inadvertent and recurrent auto-traumatic myo-tendinopathy. (Some of it is as simply provoked as by habitual stress shoulder elevation via the trapezius.) And that future advances in imaging will allow this to be demonstrated by the proper experimental design. The reason I think this is that by hands-on examination I was unable to find ANY labeled “FM” cases who lacked good concrete biomechanical explanations for each pain complaint (the most common areas voiced being trapezius/neck, rotator cuff, elbow, iliac crest, and lateral trochanter). Here’s the experiment: take 20 wide-ranging pain cases “authoritatively” labeled elsewhere as fibromyalgic — perform a standard detailed individual history and anatomic musculoskeletal/neurologic exam on each one, followed by a panel of MRI/sonographic imaging of each currently prominent pain area — and compare the findings to either normals or people selected for distinct agreed-upon rheumatologic and neurologic disorders. In addition, you’d compare the findings from patients with just one region of pain (e.g. isolated trochanteric/gluteus medius pain). You could even do fMRI brain imaging on them all to top it off, if you desire. My prediction is that you’d find that there is nothing wrong with the CNS or pain thresholds etc in any of the patients in any group, but a lot wrong with specific locomotor components “peripherally.”

    1. Sonography and MRI of latissimus dorsi strain injury in four elite athletes. Pedret C et al. Skeletal Radiology. May 2011, Volume 40, Issue 5, pp 603-608.

    2. Sonographic findings of tensor fascia lata tendinopathy: another cause of anterior groin pain. C Bass et al. Skeletal Radiology March 2002, Volume 31, Issue 3, pp 143-148

  18. The website you flagged is very interesting and well done and I’ll place it on my list of places to visit from time to time.

    As far as acupuncture and needling, I convinced myself by 1970 that acupuncture can be dismissed; and by 1975 that the concept of “needling” has no value except in a quite different sense– a very limited pragmatic way using local corticosteroid for symptom relief at mechanical sites such as rotator cuff, deQuervain, and greater trochanteric — and even then only if the patient significantly modifies the behavior pattern which produced the problem. Transiently dampening irritative pain at a locomotor source has to be followed by physiologic healing. No doubt that’s why, for instance, injection therapy for humeral epicondylitis so often fails when the patient resumes imprudent strains.

    Naturally I would not want to be seen supporting any theory that even resembles much less “resonates” with something you disdain!

    With the diverse locomotor myotendinous and aponeurotic tissue sites in mind, and with knowledge of the daily trauma of mammalian life, and with knowledge of the imaging and surgical findings across an array of musculoskeletal structures …… can you actually find any patients where the BEST explanation of their pain findings is that NOTHING proportionately physical is wrong with them and that their problem is primarily a neurologic interpretive dysfunction? And if so, would you, at least in thought, be willing to submit those patients to independent evaluators from the fields of orthopedics, physical medicine, neurology, and rheumatology — as part of my “experiment” described above?

    I regret being retired now and thus unavailable to participate!

    • Dr Lampman, I doubt whether such an experiment will ever be undertaken, as there would be major problems interpreting the data.

      We know that people can experience pain in the absence of discernible tissue damage and that discernible tissue damage can be present in the absence of pain. Furthermore, the examining clinicians would need to be able to distinguish between primary and secondary (referred) hyperalgesia (allodynia).

  19. Dear Fred, without labouring the point, findings from a recently published and important study in the journal PAIN put yet another nail in the coffin of the practice of “dry needling” so-called “myofascial trigger points”.

    In the words of the authors, “[T]his is the first study to investigate the effect of adding dry needling to a standard exercise intervention for the treatment of chronic WAD (whiplash-associated disorder).”

    Their overall conclusion was that “dry needling combined with exercise provides some statistically significant effects over sham dry-needling and exercise in people with chronic WAD, However, these effects are not clinically worthwhile.”

    It will be interesting to see whether the proponents of MPS/TrP theory and practice (dry needling) will respond to the findings of this study, which did not make any comment as to the rationality of this form of treatment except to say that is “commonly used by various practitioners including physicians and physical therapists in the treatment of musculoskeletal pain conditions with such techniques growing in popularity.”

    I hope that alarm bells are now ringing loud and clear in the ears of these practitioners and of those who are marketing expensive courses in “dry needling”.

    Reference: Sterling M, Vincenzino B, Souvlis T, Connelly LB. Dry-needling and exercise for chronic whiplash-associated disorders: a randomized single-blind placebo-controlled trial. Pain 2015; 156: 635-643.

  20. Those who have been following the debate would no doubt be interested to read three e-letters published on the website of the journal Rheumatology in response to our paper – A critical evaluation of the trigger point phenomenon.

    Our replies to each of these e-letters can also be viewed at this website address:

    Here is my brief summary of the debate (with apologies to Baroness Orczy):

    “They seek them here, they seek them there,
    Those Therapists seek them everywhere.
    Are they in muscle or are they in nerve?
    Those demned elusive TPs will drain all of their reserve!”

    Now that the theory of pain arising from myofascial “trigger points” has been soundly refuted, these could be the last words ever written about myofascial “trigger points”.

    But this is only wishful thinking.

    The reality is that regardless of this most inconvenient truth, therapists who worship at the Temple of the Trigger Point will continue on their merry way, poking, prodding and needling innocent muscles and other tissues. They seem oblivious all criticism.

    For those who are perplexed, here is some excellent advice from Moses ben Maimon (Maimonides) [1135-1204]:

    If anyone declares to you that he has actual proof, from his own experience , of something which he requires for the confirmation of his theory, – even though he be considered a man of great authority, truthfulness, earnest words and morality, yet, just because he is anxious for you to believe his theory, you should hesitate.

    from: Aphorisms According to Galen (Quoted in Bulletin of the Institute of the History of Medicine 1935; 3: 555.)

    • Yes, “But this is only wishful thinking. The reality is that regardless of this most inconvenient truth, therapists who worship at the Temple of the Trigger Point will continue on their merry way, poking, prodding and needling innocent muscles and other tissues. They seem oblivious all criticism.”

      Baroness Orczy was not a part of my youth, but Lewis Carroll’s “The Hunting of the Snark” was. This line remains with me as the triggerists sail forth:

      This was charming, no doubt; but they shortly found out
      That the Captain they trusted so well
      Had only one notion for crossing the ocean,
      And that was to tingle his bell.

      John Quintner’s article is likely to have important long-term effects. On cannot simply assume the revealed truth is correct and then believe in and practice what has taken on qualities of religious certainty.. Rather, there must be scientifically valid studies before one picks up the needle or spray or -whatever. The science of medicine requires true blinding and unbiased selection, estimates of reliability, probability of success and failure, and long-term follow-up. Many years ago, when I began practice followed a few year later by collection of data on patients who never returned to the clinic, I learned that my then cherished beliefs about the correctness and effectiveness of what I was doing and what my teachers had imparted was false. Belief is not enough. Studies designed for political purposes or to demonstrate a point of view are not enough.

      Over the years I have had correspondence with physicians who have had special techniques and therapies. “Why not due a proper trial,” I would say. But they never had enough time or money, they just kept doing what they believed in, right of wrong (mostly wrong, I think). Pain and muscle pain are difficult problems. The physician in the examining room wondering what he or she could possibly do is easily drawn to the mysterious trigger point idea, known to specialists and wise men, but associated fortunately with substantial remuneration.

      John Quintner’s articles are important because they expose nonsense and bad science. Although I mostly write about fibromyalgia these days, the same skepticism needs to be placed there, perhaps even more importantly, as political and economic engines create a different mass reality.

      Fred Wolfe

      Fred Wolfe

  21. Dear Fred, a recent review by Shah et al. (2015) supports my impression that physical therapists who place “dry needles” into the tender muscles of their patients, and otherwise poke around there, have been “flying by the seat of their pants”.

    Shah et al. (2015) concede: “To date, the pathogenesis and pathophysiology of MTrPs and their role in MPS remain unknown” and that “It remains unknown whether the nodule is an associated finding, whether it is a causal or pathogenic element in MPS, and whether or not its disappearance is essential for effective treatment.”

    They also pose a number of rather embarrassing questions for researchers to answer:

    1. What is the etiology and pathophysiology of MPS?
    2. What is the role of the MTrP in the pathogenesis of MPS?
    3. Is the resolution of the MTrP required for clinical response?
    4. What is the mechanism by which the pain state begins, evolves and persists?
    5. Although the presence of inflammatory and noxious biochemicals has been established, what are the levels of anti-inflammatory substances, analgesic substances, and muscle metabolites in the local biochemical milieu of muscle with and without MTrPs?
    6. How does a tender nodule progress to a myofascial pain syndrome?
    7. Which musculoskeletal tissues are involved, what are their properties, and how do these change with treatment?

    Will ethical therapists now take your advice and down needles, at least until these questions are properly answered? Will those who run courses in “dry needling” now admit that their teaching has been based upon flawed theory and many conjectures?

    Reference: Shah JP, Thaker N, Heimur J, et al. Myofascial trigger points then and now: a historical and scientific perspective. PM R 2015; available at

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  23. Walt, thanks for your contribution. Slowly but surely the Trigger Point Empire is crumbling, its proponents being unable to withstand the critical gaze that has now been cast upon its firmly held tenets. I can almost sense their feelings of disappointment as increasing numbers of physical therapists no longer believe implicitly in their teachings!

    The words of Percivall Pott [1714-1788] still ring true:

    “The desire of health and ease, like that of money, seems to put all understandings, and all men, upon a level; the avaricious are duped by every bubble; the lame and the unhealthy by every quack. Each party resigns his understanding; swallows greedily, and for a time believes implicitly, the most groundless, ill-founded, and delusory promises; and nothing but loss and disappointment ever produce conviction.” From Chirurgical Works, Vol I, “General Remarks on Fractures and Dislocations”

  24. I am indebted to Myopain Seminars for alerting me to an abstract which was presented this week at the TRI International Conference on Tinnitus in Ann Arbor Michigan.

    Here it is, reproduced in full:

    Wijtmans E, Teachey W, Levine R
    The Therapy Network, Virginia Beach, VA, USA
    AIM/OBJECTIVES: Increase understanding of the importance of identifying and treatment of myofascial trigger points (MTrPs) in the treatment of tinnitus of musculoskeletal origin.
    METHODS: Research, 1 literature review, 2 and 10 years clinical practice experience.
    RESULTS/DISCUSSION: It is well established that muscles can give referred pain and symptoms to areas outside the muscle itself. In addition, on physical examination the following can be demonstrated: MTrPs, muscle shortening, muscle stiffness, taut bands, and occasionally associated regional autonomic changes. Referred symptoms into the head and neck can include facial pain, sinus pain, ear pain, headaches, dizziness, throat discomfort, hoarseness, lacrimation, perceived hearing loss, ear fullness, itching in the ears, and tinnitus.
    The phenomena and existence of MTrPs is well recognized. They are believed to be responsible for these referred symptoms. In the case of tinnitus, the primary responsible muscles are the sternocleidomastoid and masseter muscles, and to a lesser extent the lateral pterygoid muscle. However, all the muscles of mastication, the upper trapezius, the levator scapulae, and all the cervical musculature are directly and indirectly involved.
    Traditional diagnostics, like radiographs, CT, MRI, and bloodwork do not identify or exclude the existence of MTrPs. Recent studies demonstrate that they can be identified by 2D and 3D sonography. However, in the clinical setting examination of the presence of MTrPs in the taut band relies on skilled hands and experience. Treatment of the referred symptom, such as tinnitus, involves deactivation of these MTrPs. This can be accomplished through (sustained) digital pressure, but will be more effectively achieved by injection or dry needling of the MTrP. In addition, the treatment will be much more effective if a so-called “local twitch response” (LTR) is obtained. Shah et al at NIH, demonstrated the vast changes that occur after the LTR in the biochemical milieu of MTrPs, in normalizing levels of the pH, and of neurotransmitters like bradykinins, substance P, TNF-α, norepinephrine, CGRP, IL-1β, and others. Overuse and abuse of muscles leads to the development of MTrPs. Common scenarios are a forward head posture, an uneven loading of the muscles during exercise or work related activities, trauma, and persistent muscular contractions from a physical cause (repetitive motions), or an emotional cause (stress response). There may also be exacerbating or perpetuating biochemical factors, like micronutrient deficiencies, which should be excluded. Unfortunately, despite emerging research and decades of treatments, examination and treatment of MTrPs to combat tinnitus is not yet well studied or recognized. As part of this oral presentation, I will demonstrate specific examination techniques and show a brief video of the treatment of MTrPs using dry needling.
    CONCLUSION: Thorough physical examination for potential MTrPs and their subsequent treatment should be an essential component of the evaluation and management of patients with tinnitus.
    1 Teachey WS, Wijtmans EH, Cardarelli F, Levine RA. Tinnitus of myofascial origin. Int Tinnitus J. 2012;17(1):70-73
    2 Teachey WS. Otolaryngic Myofascial Pain Syndromes Curr Pain Headache Rep. 2004 Dec;8(6):457-62.

    Myofascial trigger points, which have never been shown to exist, can apparently be a cause of tinnitus, lacrimation, hoarseness, deafness etc. Of course, this is sheer nonsense!

    But I find it astonishing that such pseudo-scientific claptrap was accepted for a podium presentation at a scientific meeting and, moreover, that it was allegedly well-received. What willcome next?

  25. What will come next? How about dry needling canine and feline ‘trigger points”? Given that the theory of “myofascial pain arising from trigger points” has been refuted, and therapeutic outcomes of treatment based upon this theory have been found wanting in humans, why inflict such treatment upon dumb animals? But despite there being no evidence that “trigger points” actually exist in humans, felines or canines, “trigger point therapy” appears to be flourishing in certain veterinary circles. Is it ethical for veterinarians to treat their animal patients using outdated theory and practice derived from flawed studies of human beings? There are those who believe that the answer is in the affirmative. Here is the link:

  26. The controversy over “dry needling” of “trigger points” continues to excite passions amongst physical therapists. The traditional acupuncturists are vigorously defending their turf against the politically inspired incursions by the “dry needlers”. Courses in “dry needling” are still being marketed, despite the fact that their scientific credibility has been severely dented. But at long last, academic physical therapists in North America have been much more visible in their opposition to “dry needling,” which they see as having no place in rational therapy for musculoskeletal pain. Here is a link to the latest on-line discussion:

  27. I was very interested to see that some of the leading Myofascial Pain/Trigger Point theorists have shifted their position. Realising that the scientific evidence supporting “dry needling” of myofascial trigger points is sorely deficient and that the theory underlying it has been refuted, they have drawn heavily upon scientific evidence which is said to support the practice of traditional Chinese acupuncture.

    In a recently published paper, Butts et al. [2016] make some remarkably heretical admissions:

    1. “… as Hong suggests, spinal manipulation and and needling techniques may work additively to treat trigger point related dysfunction.”

    2. “It is therefore unlikely that clinicians are able to accurately target trigger points in a reliable fashion with monofilament needles between 0.025 mm and 0.35 mm wide.”

    3. “The fact that never entered the muscle tissue suggests that the LTR (localised twitch response] may not be a crucial component of the treatment.”

    4. “These findings support the commonly held belief that needle insertion is not enough to relieve pain.”

    5. “It also provides direct evidence that trigger points should not be the only target of DN (dry needling) treatment.”

    But what is also of great concern is their (unreferenced) conclusion: “Dry needling has gained increased popularity in Western-based medicine over the past 20-30 years. Physicians, osteopaths, chiropractors and physical therapists presently use needling modalities to treat muscles, ligaments, tendons, subcutaneous fascia, scar tissue and peripheral nerves for the management of a number of neuromusculoskeletal conditions.” These conditions include fibromyalgia, arthritis & headaches!

    This Ancient Mariner might say: “Needles, needles everywhere, but when will they stop to think?” [Apologies to Samuel Taylor Coleridge]

    Reference: Butts R, Dunning J, Perreault T, et al (2016) Peripheral and spinal mechanisms of pain and dry needling mediated analgesia: a clinical resource guide for health care professionals. Int J Phys Med Rehabil 4:327. doi:10.4172/2329-9096.1000327

  28. The Sunrise Review conducted this year by the Washington State Department of Health has determined that “dry needling” does not come within the scope of practice of Physical Therapists.

    This finding is a defeat for the American Physical Therapy Association, which has vigorously maintained that the practice of “dry needing” is entirely different from that of needle acupuncture, as practiced within Chinese Traditional Medicine.

    The full report is quite lengthy (over 700 pages) but it is comprehensive.

    Of particular interest, the Review concluded that the effectiveness of “dry needling” is in doubt and that further studies would be necessary to reverse this impression.

    It is fair to conclude that “dry needling” (as promoted by the APTA) is not acceptable as a modality of treatment on the grounds that its underlying theory has been refuted and that physical therapists who practice it are really offering a form of acupuncture for which most of them have not been properly trained.

    Of even more interest, the Sunrise Review did not comment on dry needling’s lack of rationale and science; but in any case, it appears to have arrived at the correct decision.…/Docum…/2000/DryNeedlingFinal2016.pdf

  29. Further to the above comment on the findings of the Sunrise Review, the Washington State Health Department made some recommendations should physical therapists still wish to include “dry needling” within their scope of practice:

    (a) With adequate training that includes a clinical component, dry needling may fit within the physical
    therapist’s scope of practice in treating neuromusculoskeletal pain and movement impairments.

    (b) Evidence provided in this review demonstrates a low rate of serious adverse events from physical
    therapists performing dry needling in other states, the United States military, and Canada.

    (c) Furthermore, the legislature may wish to consider adding dry needling to the physical therapist
    scope of practice through proposed legislation that includes additional safety requirements such as:
    – Requirements for dry needling-specific education;
    – Requirement for a supervised clinical practice experience to be defined in rule;
    – Requirement for physical therapists to obtain written informed consent from the patient on a form
    that clearly identifies the risks and benefits of dry needling and information on the physical
    therapist’s dry needling training. Recommend looking to Colorado for potential language;

    (d) Clear authorization for physical therapists to use acupuncture needles in the practice of dry
    needling subject to the limitations in statute;

    (e) Clear limitation that the use of acupuncture needles is only authorized within the physical
    therapist’s management of neuromusculoskeletal pain and movement impairments, and require
    referral to an authorized practitioner of acupuncture for use of acupuncture needles for any other
    purpose; and

    (f) Amend the definition of dry needling to remove the statement “Dry needling does not include the
    stimulation or treatment of acupuncture points and meridians.”

    Of more importance, Washington State Senator Randi Becker, Chair of the Senate Health Care Committee, who initially requested the review, asked the State Health Department to “review the evidence on the efficacy of dry needling.”

    As mentioned above, such evidence of efficacy was not presented, for the obvious reason that it does not exist.

  30. Dry Needling in the State of Virginia?

    The issue of competency of Physical Therapists to perform “dry needling” is again under vigorous discussion:

    Comments are now being invited and it is interesting to read some of them.

    Naturally, Professor Geoff Bove and I have presented a strong case against the practice of “dry needling”.

    We are outnumbered but at least we have no conflicts of interest to declare!

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