The following announcement has just appeared on Myopain Seminars, one of the websites run by proponents of “dry needling”: The Federation of State Boards of Physical Therapy is working on developing a list of competencies needed for physical therapists to perform dry needling, and we would greatly appreciate your help! The Federation has developed a survey based on the Physical Therapy Practice Analysis, developed by the Federation in 2011. The survey contains a list of knowledge, skills, and activities that physical therapist have and undergo. Based on this list, the survey asks if each item is necessary to competently perform dry needling. This survey is the preliminary stage of determining the list of dry needling competencies. Although this is one of the first steps, it is critical. Please follow the link below to complete the survey. Additionally, the Federation asks that you share the survey with any colleagues or practitioners who may be performing dry needling. Please complete the survey no later than April 5, 2015. We truly appreciate your help in this endeavor! If you have any questions, please feel free to contact the Federation at any time. Link: https://survey.fsbpt.org/TakeSurvey.aspx?SurveyID=m80049l Before such a survey is undertaken, the really important question that needs to be asked and urgently addressed by the Federation is whether the currently available scientific evidence supports a continuation of the popular practice by its constituency of “dry needling” muscles and other deep tissues. Clearly, this form of treatment is irrational and therefore the answer must be an unequivocal NO!
“Name Witheld” has a website entitled http://fibromyass.com. She is not a fan of the fibromyalgia idea and has been writing asking me to post a link to her web site – something I haven’t done until now. But she has come up with a good question and I thought I’d offer a reply. “How,” she writes, “is someone with rheumatoid arthritis and fibromyalgia different than someone who just has rheumatoid arthritis?” One of the things prompting the question is a rumble that a second clinical trial of the fibromyalgia “blood test” is in the works. Something the blood test developers apparently want to do (in addition to cashing in big) is to distinguish fibromyalgia from rheumatoid arthritis (RA).
As a clinician, I know that persons with RA have swollen joints and tenderness in their affected joints. Often they have certain positive blood tests and often evidence of joint damage that is seen on X-range examination. If you ask people with RA where it hurts, they most often report problems in their affected joints. People with RA and fibromyalgia have all of the these features. But they also have pain in different, but characteristic regions–in the upper and lower back, the hips and shoulders. They are also more tender when examined in specific tender point spots. It’s not hard, and actually it is very simple and easy to identify fibromyalgia in people with RA. All you have to do is to stop and listen. As a sop to Dr. Quintner, I admit flat out that there are a lot of intellectual and logical problems with the fibromyalgia idea that he and I both acknowledge. But for now, lets suspend some disbelief. Dr. Lampman has been very correctly criticizing the nature of fibromyalgia studies. He couldn’t be more correct. People who fit the fibromyalgia diagnostic criteria have severe problems in hundreds of areas. They are always different from those without fibromyalgia. In the absence of a Gold Standard for fibromyalgia, it is hard to see how an expensive blood test could approach the current diagnostic criteria in the ability to accurately diagnose fibromyalgia, nor is it clear exactly what is being measured with the blood test.
The fibromyalgia idea is not so bad if you don’t take it too seriously.
Sometime last year I stopped posting to this blog and kind of let things go. We hadn’t been able to attract some the fibromyalgia leaders to participate, and I wondered if it was all worth the effort. I am going to try again, now. Still, we had many participants and a wide variety of comments. There are several reasons I decided to go on. First, Dr. John Quintner, who has been an inveterate source of comments, comforts and articles, suggested I should. His recent post on Trigger Points is an example of his very high quality work. It starts a discussion that has been long needed. Second, I have many comments and ideas about fibromyalgia that are very hard to express with the current system of journals and reviews. I want to publish these thoughts here. More about that to come.
The blog was designed for professionals, with the idea that professional would have a good idea of the scientific method (whatever that is) and could respond based on data and scientific analysis. Some of you might say this was a dubious belief, but at least the standard should be known to this group. Later, we opened the blog to non-professionals, including patients, provided they met certain rules. We blocked post from those who did not follow the rules; and we blocked some health professional, too. But some of the best comments we have had have come from non-professionals. See the series of important posts from “Nancy.”
So if you want to post, we welcome your comments. But pay attention to the rules. I repeat them here. From the “About” section:
This blog is designed to facilitate open, vigorous discussion about fibromyalgia and fibromyalgia-related issues. Say here what you think. We want to open up frank discussions of the full spectrum of fibromyalgia-related ideas and consequences. But do keep in mind Niels Bohr’s admonition, ‘It is not enough to be wrong, one must also be polite.’
Rules about posting and articles:
About comments. We want this blog to be about research and discussions concerning fibromyalgia. To post to this blog you should be a published author, have other academic credentials, or would be welcomed as a discussant in an academic journal. We make these somewhat arbitrary rules to try to exclude the general, non-scientific public. We welcome comments by all scientists and social scientists, not just those who are physicians. This blog is moderated, meaning that the editors decide what will appear. In general, we will not censor on-topic scientific posts provided authors meet the above guidelines. If you don’t fit our guidelines and think you have something to contribute, send the editors an email at email@example.com. [As a modification, we will accept post from non-profesionals provided they meet certain criteria.]
About articles. We welcome submissions of articles. By articles we mean new subject posts of varying length. They can be long. In fact, we might even publish short academic articles. If you want to submit a new-subject post, write and discuss this with the editors first at firstname.lastname@example.org.
From some previous posts: “We will not publish insulting or crude comments. They just won’t appear. If you have something to say, try to think about it in a scientific way. Provide evidence. Think about why you might be wrong. We’ll give it a try.
I (we) can’t and won’t answer personal problems. We won’t give medical advice. People with fibromyalgia know a lot. You can help us with thoughtful comments.”
Non-Professional authors who are uncertain if we will publish their comments are welcome to write to me with questions.
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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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.
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Dr. James Lampman has sent along a set of slides about fibromyalgia and his view about limitations of the fibromyalgia idea and research. It is well worth looking at, He writes
“While I developed my findings as early as 2006, this year I did a more in-depth review of the claims of the FM research community. I concluded that the published experimental studies had serious flaws and that actually none had addressed a principal research question: to determine if the pain-processing and neurochemistry of patients labeled as fibromyalgics is anything other than the normal way manifested in all patients with common kinds of enduring pain.
The human understanding when it has once adopted an opinion draws all things else to support and agree with it. And though there be a greater number and weight of instances to be found on the other side, yet these it either neglects or despises, or else – by some distinction sets aside and rejects, in order that by this great and pernicious determination the authority of its former conclusion may remain inviolate. [Francis Bacon (1620) from Novum Organum, Book 1, Aphorism XLVI.]
Introduction.The latest fads from the shadowy world of pseudo-science have always been quick to take off. For those who are keen on approaching pain sufferers with their sharp needles, the invention of Neural Prolotherapy by Dr John Lyftogt, of Christchurch in New Zealand, must have come as a godsend. A quick search on the Internet reveals that this invention is being taken seriously by a number of health practitioners who one might have expected to have known better than to accept it so uncritically.
The claims for Neural Prolotherapy “Prolo-” is short for proliferation and derives from the Latin “to regenerate or rebuild”. Prolotherapy with injectable substances that are being acclaimed as growth factors is now the subject of intensive research. But Dr Lyftogt favours hypertonic sugar injections.
Here are some remarkable extracts from his website (http://www.doctorliftoff.co.nz/):
“After the success of Neural Prolotherapy with Achilles tendonitis other persistent painful conditions of the neck, back, shoulders, elbows, wrists, knees, ankles and feet have been effectively treated by targeting the local inflamed superficial nerves with micro-injections of low dose Glucose.”
Comment: there have been no properly conducted clinical trials of Neural Prolotherapy.
“More recently Dr Lyftogt has developed effective neural prolotherapy treatment protocols for Migraine. ‘Fibromyalgia,’ CRPS, compartment syndrome and other difficult to treat persistent painful conditions.”
Comment: Again, no clinical trials have been conducted. The evidence is purely anecdotal and subject to all forms of bias.
“Neural prolotherapy is an effective novel and evolving treatment for non-malignant persistent pain, based on sound neuroscientific principles.”
“Subcutaneous prolotherapy with a series of percutaneous near nerve injections has been shown to be an effective treatment for a variety of recalcitrant painful conditions caused by prolonged neurogenic inflammation.”
Comment: This is the logical fallacy called circular argument: the conclusion is assumed before the evidence is presented. Dr Lyftogt offers no evidence that these conditions are associated with “prolonged neurogenic inflammation”.
The “sound neuroscientific principles”
Dr Lyftogt targets the “guilty” superficial nerves by injecting 5% Mannitol or 5% dextrose and thereby claims to modulate the neurogenic inflammation that he believes is responsible for “neuropathic pain”. He refers to the work of a highly regarded authority:
“Quintessential to the working hypothesis that subcutaneous prolotherapy treats prolonged pathological neurogenic inflammation is the work by Douglas W Zochodne from the Neuroscientific Research Unit at Calgary University.” 
When contacted by the author, Professor Zochodne replied: “I can indicate that I have no interest in it, have not endorsed it or plan to endorse it and am disappointed our work would be quoted for something without evidence.”
But there is more!
“The author hypothesizes that subcutaneous prolotherapy injections of hypertonic glucose and 0.1% lignocaine induce apoptosis of proliferating peptidergic noceffectors (i.e. SP and CGRP) and neovessels by reducing VEGF (vascular endothelial growth factor) levels and restoring “effective repair processes” with reduction of pain.” 
Comment: In this author’s opinion, this is pure speculation.
On his website and in a recent email to Associate-Professor Geoff Bove, a world leader in experimental studies of nervi nervorum (“the nerves of the nerves”), Dr Lyftogt claims that his injections target specific receptors (TRPV1) present on the nervi nervorum.
“The very small nerve fibers, innervating the nerve trunk, identified as unmyelinated C-fibers or ‘Nervi Nervorum’ are responsible for pain and swelling of the protective sheath of the nerve trunk. This was already demonstrated 125 years ago by Professor John Marshall from London and called neuralgia. It is now called ‘neurogenic inflammation’.”
Comment: Dr Marshall was in fact advocating “nerve stretching” in his Bradshaw Lecture given in London. Fortunately, this form of treatment has long been abandoned as being both ineffective and potentially dangerous.
Dr Bove made the following personal response to Dr Lyftogt in relation to his facile incrimination of the nervi nervorum:
“Dextrose does not do anything to TRPV1 receptors, and it is certainly not selective for abnormal ones (and there is no knowledge that those exist). You are not targeting nervi nervorum other than in your mind; they are few and far between on the small peripheral nerves, and maybe nonexistent. Regardless, you have nothing to offer regarding the injected dextrose reducing their function and thus reducing neurogenic inflammation, or reducing neurogenic inflammation at all.
The bottom line
According to Dr Lyftogt: “The growing scientific evidence supporting the view that neuropathic pain syndromes are caused by unremitting peripheral neurogenic inflammation involving the autonomic and sensory nerves may lead to renewed interest in prolotherapy and neural therapy as these treatments are effective and seem to target the PNS.” 
However, Dr Lyftogt has yet to demonstrate the presence of the unremitting (enhanced) neurogenic inflammation that he claims to have identified and treated with his sugar injectates.
The question as to the efficacy of Neural Prolotherapy, as practiced and taught around the world by Dr Lyftogt, is outside the scope of this article. There are no published trials upon which to base any firm conclusions.
Anecdotally, there may be face validity for this treatment but to date there has been no discussion of placebo effect, observer bias, expectation bias, reversion to the mean of the conditions being treated etc.
But what is abundantly clear is that published animal experimental research by leading neurobiologists Professor Douglas Zochodne and Associate-Professor Geoffrey Bove does NOT in any way support Dr Lyftogt’s hypothesis. This should be the end of the story but I suspect that the aphorism by Francis Bacon is as true today as it was over 400 years ago. All we can do is hope that good science will triumph over its rival.
Author: Dr John Quintner, Physician in Rheumatology and Pain Medicine
Dr Quintner accepts full responsibility for the content and opinions expressed in this article.
1. Lyftogt J. Subcutaneous prolotherapy treatment of refractory knee, shoulder and lateral elbow pain. Australasian Musculoskeletal Medicine November, 2007: 83-85.
2. Lyftogt J. Prolotherapy for recalcitrant lumbago. Australasian Musculoskeletal Medicine May 2008: 18-20.
3. Lyftogt J. Pain conundrums: which hypothesis? Australasian Musculoskeletal Medicine November 2008: 72-7
Montori and Guyatt in their recent article “Corruption of the Evidence as Threat and Opportunity for Evidence-Based Medicine” discuss some of the current concerns with EBM. They define EBM as “…conscientious, judicious, and explicit use of the best available evidence from clinical care research in making health care decisions …” They link EBM to two principles: “The first principle is that the higher the quality of the evidence the more confident the decision-maker.” “The second principle of evidence-based medicine is that the evidence alone never tells one what to do. Making sound decisions requires the clinician to expertly assess the patient’s personal, social, and clinical context and integrate this information with the values and preferences of the informed patient and the best available evidence.”
People with FM and their doctors sometimes make use of very low quality evidence. What does that mean? The results of low quality evidence are likely to be wrong—different from what we expected. High quality evidence means that we can be very confident in the results of the study. Knowing the quality of evidence is very important when people with FM consider treatment options.
Some comments to the blog speak of the value of “opinion.” Opinion is not evidence. If, after speaking to many people with FM, I believe that guaifenesin [is or is not] an effective treatment, that is opinion not evidence. If a doctor treats many patients with guaifenesin and observes its effect, that is (before and after) evidence, but it is very low quality evidence because of the multiple biases that will always be present in that type “study.” Sometimes that sort of evidence is called a “case series.” If a randomized controlled trial (RCT) was performed and yielded high quality evidence we could be assured of the value of guaifenesin. In fact, positive case series and a negative RCT have been performed. They lead to the conclusion that guaifenesin is not effective. Doctors and patients should be happy with results like this because it means we now know not to use guaifenesin. In a sense, this is the model that EBM brings to us: to evaluate the quality of evidence and to make use of the information.
If a pharmaceutical company or a doctor distorts or withholds evidence and still calls the process EBM, then EBM is corrupted. Some pharmaceutical companies have published positive studies and withheld negative ones, leading to EBM distortion. We need to demand the best quality evidence.
Even so, just because there are RCTs that are high quality, it does not mean that the evidence is correct or useful at the clinical level. For example, if a study shows benefit over three months that does not mean that treatment will continue to be effective. If people stop taking the medication because of insufficient effect, side effects or costs, an “effective” medicine can turn out to be useless. Long term studies, such as we do in the National Data Bank for Rheumatic Diseases can give some idea of long-term effectiveness. Such studies are difficult to do, are open to bias, are never as good as RCTs, and are almost never supported by pharmaceutical companies, as they have nothing to gain.
So when I go to the doctor and receive a suggestion for treatment, I want to know what is the quality of the evidence that led to the recommendation, how effective is the treatment, how long will it last, what are the side effects, how much does it cost? That’s what you should want to know, too. We want kind and empathetic physicians, but we need scientific answers not opinions, not low quality evidence. Doctors who use unorthodox treatments have an ethical responsibility to perform and publish the results of their treatments in peer-reviewed journals. Otherwise patients who receive such treatment are little more than experimental subjects who do not even know they are being experimented on.
If you are interested in new research about fibromyalgia, register at Pubmed on the web and you will soon receive daily abstracts of breaking advances. This abstract came today and caught my eye. Mud baths? Really! Does anyone really think that mud baths are a truly useful therapy for FM? What also caught my eye was all of the “sophisticated” and expensive tests that were done and what it all costs. Are the laboratory results meaningful? Who paid for this study and why? You should note the conclusion, “Our results showed that the thermal treatment might have a beneficial effect on the specific symptoms of the disease.” And “the mud-bath treatment gives longer lasting results.”
If you can do a study like this, why not one comparing red wine with white wine (appropriately blinded, of course). I, for one, would like to see a trial of Chianti versus Riesling.
A multidisciplinary approach to study the effects of balneotherapy and mud-bath therapy treatments on fibromyalgia. Clin Exp Rheumatol. 2013 Nov-Dec;31(6 Suppl 79):111-20Authors: Bazzichi L, Da Valle Y, Rossi A, Giacomelli C, Sernissi F, Giannaccini G, Betti L, Ciregia F, Giusti L, Scarpellini P, Dell’osso L, Marazziti D, Bombardieri S, Lucacchini A
OBJECTIVES: To study the effects of both balneotherapy and mud-bath therapy treatments in patients affected by primary fibromyalgia (FM) using rheumatological, psychiatric, biochemical and proteomic approaches.
METHODS: Forty-one FM patients (39 females, 2 males), who fulfilled the American College of Rheumatology criteria received a 2-week thermal therapy programme consisting of therapy once daily for 6 days/week. Twenty-one patients received mud-bath treatment, while the other twenty balneotherapy. Pain, symptoms, and quality of life were assessed. Oxytocin, brain-derived neurotrophic factor (BDNF), ATP and serotonin transporter levels during therapy were assayed. Comparative whole saliva (WS) proteomic analysis was performed using a combination of two-dimensional electrophoresis (2DE) and mass spectrometry techniques.
RESULTS: We observed a reduction in pain, FIQ values and improvement of SF36 in both groups of patients treated with mud-bath or balneotherapy. The improvement of the outcome measures occurred with different timing and duration in the two spa treatments. A significant decrease in BDNF concentrations was observed either after balneotherapy or mud-bath therapy when assayed after twelve weeks, while no significant change in oxytocin levels, ATP levels and serotonin transporter were detected. Significant differences were observed for phosphoglycerate mutase1 (PGAM1) and zinc alpha-2-glycoprotein 1 (AZGP1) protein expression.
CONCLUSIONS: Our results showed that the thermal treatment might have a beneficial effect on the specific symptoms of the disease. In particular, while balneotherapy gives results that in most patients occur after the end of the treatment but which are no longer noticeable after 3 months, the mud-bath treatment gives longer lasting results.
PMID: 24373369 [PubMed - in process]
A few days ago “Rosemary Lee/Seeking Equilibrium” made the following comment which I have edited somewhat.
When I was first diagnosed I spent thousands (and we’re not talking four figures) on anything and everything that I could do to help manage my symptoms. I was a real estate broker for a national homebuilder and was used to running around building sites and homes in every stage of the building process. I wanted to get rid of this thing called “Fibromyalgia” and truly believed I could make it go away through nutritional supplements, acupuncture, massage, trigger point injections, epidurals, IV therapies and any other homeopathic cure I could fine. You name it, I’ve probably done it. I think the statement, “where profits are involved” is a revealing one. I probably helped a few doctors put their children through college. While I’m not discounting the benefit of taking care of oneself and managing symptoms I’d like to reiterate that at this point in time, there is no cure. I’ve become highly suspect of the new “science” that claims they can cure Fibromyalgia. If it was true, this discussion wouldn’t be necessary. I “think” (obviously not a scientific hypothesis) that a combination of continued stress due to a high volume-high stress career and trauma led to my experience with Fibromyalgia. … I can say that my experience with needles has not been a good one. It has not led to any release or improvement in pain and has actually increased it.
As a physician, I saw many people with similar experiences. I came to believe that treatments for which there was not good evidence for efficacy were, and should be treated as, experiments—at least by physicians. Making good use of the placebo effect notwithstanding, ethical treatment requires not fooling yourself or the patient, having a good approximation of truth about what you are recommending or not recommending, and always keeping the best interests of the patients in mind.
Among dubious therapies there was back surgery or arthroscopy, ill-directed physical therapy, hurriedly put together hospital pain clinics, epidural injections, places where patients received hundred of musculoskeletal injections, chelation therapy, megavitamin therapy, and all of the other treatments (and more) that Rosemary Lee mentions. Physicians sometimes called these surgical and medical treatments “remunerectomies” and “medical remunerectomies.” There are many reasons for such treatments. Some doctors truly believed they were helping patients. But some mixed idealism with greed, and some were sociopaths. I saw several patients die when irrational treatments were imposed and necessary therapies terminated. Physician friends in other countries are appalled when I tell them stories like this. So I have no idea of the worldwide prevalence of these behaviors.
I like evidence based medicine (EBM). Nancy Ryan in a private email sent me the following:
”The drug industry’s corporate mission is to make us all sick however well we feel. As for EBM screening programmes, these are the combine harvester of wellbeing, producing bails of overdiagnosis and misery.”
EBM is being terribly misused. But the idea of EBM is eminently correct. It tells us three things about a treatment: 1) how good is the evidence; 2) Is the treatment effective? 3) How effective is the treatment? Among the rules of EBM is that opinion is not evidence.
Rosemary Lee’s observation, “While I’m not discounting the benefit of taking care of oneself and managing symptoms I’d like to reiterate that at this point in time, there is no cure” colors all patient physician interactions. Should we try something else? Maybe it will work this time? How can I disappoint this patient?
Back to experiments. Let’s define experiment again. A treatment experiment is one for which there is not good experimental evidence for effectiveness. If you want to treat a patient which such methods, I believe you have an ethical responsibility to tell the patient everything about the treatment including that there are no good studies that have yet shown the treatment to be effective. Second, doctors might consider collecting longitudinal data on patients relative to effectiveness, including those who take the treatment but never come back. To rely on a study or studies, they must be of high quality, and there are published rules about data quality. Opinion is not evidence. Poor quality studies are not evidence.
Perhaps in future postings and comments to this blog people will distinguish between opinion and EBM quality evidence when they write. Otherwise I may have to restrict postings.
In an email, Nancy Ryan pointed me to a blog posting about empathy in the abetternhs blog. Not only was she right about that topic, but it introduced me to Jonathon Tomlinson’s extraordinary blog. As I read his work in the next few hours I came upon one posting called “How Doctors Respond to Chronic Pain.” I’d like to refer you to it: http://abetternhs.wordpress.com/2013/09/07/pain/. Fibromyalgia is never mentioned, but it is clearly about fibromyalgia. I learned a lot from this extraordinary, most-human-and-decent-of-men who wrote that article. Listen to this:
Please don’t come back!
My forehead thumped down on my desk after a ten minute appointment that had stretched out to over half an hour, I felt completely exhausted and still I had another 17 patients to see and I was now running 25 minutes late. It wasn’t just that I felt exhausted, I felt useless and demoralized and more than that, I felt angry, really pissed off.
I had spent the last 30 minutes listening to Sharon describe her pains, which shifted from the somatic – how they feel, to despair – how she feels, and anger – how she feels about me. Why didn’t I know what was wrong with her? Why didn’t I refer her for more investigations? Why didn’t I send her to a [another] specialist? Why didn’t I listen? At some point I tried to introduce the idea that perhaps a pain-psychologist might help but this merely ignited the oil I’d been trying to pour on troubled waters. “You don’t even know what’s wrong with me and now you’re trying to tell me it’s all in my head, you’re not listening to me!” she all but screamed at me, tears welling up in her eyes. “No, no, no, not at all!” I actually held my hands up in front of me in self-defence, “but pain, whatever the cause, is always emotional and physical.” I believed what I was saying as I dug myself deeper into a hole I wasn’t going to dig myself out of. She was in fighting form and I was floundering. She took advantage, “You’ve done nothing for me, nothing! I want to see someone else.” I’ve been her doctor for almost 10 years and have seen her health deteriorate dramatically, her marriage take the strain and recover, her children in and out of illness and her husband through his redundancy and depression and more. I’d visited her at home and referred her to rheumatologists, physiotherapists and a pain clinic. I felt like I had nothing else left to offer. Her killer blow left me speechless. “I don’t know what to say,” I admitted, defeated, barely able to maintain eye-contact. She stood up and left.
Tomlinson then continues in a long exposition that is filled with links and commentary. It has a doctor and a patient perspective, and underlines the difficulty we all feel.
Many US doctors don’t want to see fibromyalgia patients, and some refuse to do so. They should all read Tomlinson’s blog.
He writes, “My motivation for writing this essay came out of despair. My intention was to confront and examine why I felt like that and in my conclusion I will try to articulate what I might be able to do about it.” I post the link and recommend it. I wish I had read it years ago.