Posted on June 10th, 2014 by Fred Wolfe

A sharp critique of the fibromyalgia idea and the research that surrounds it

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.

As an illustration, I analyzed several iconic studies in the fibromyalgia literature, finding reason to believe that the peer review system largely failed in its role to limit authors’ conclusions to those which can reasonably be substantiated by the evidence in each publication.  Part II of my lecture is devoted to a brief analysis of 8 studies.
I found it helpful to start with a recognition that the concept of fibromyalgia can be presented as a hypothesis with several components, each one of which should be subjected to scrutiny and testing.
While I personally feel that fibromyalgia is in fact a “failed hypothesis,” no doubt many readers would be dismissive of my conclusion. Nevertheless, I hope the currently prevailing belief system will not prevent you or your readers from at least sampling and judging my ideas.” Click on the link below.


    • Thanks for your inquiry. Here’s the way I see it.

      Above all, the terms “chronic” and “widespread” need to be stripped of their obscurantist quality, as follows.

      (This is derived from detailed clinical evaluation of 176 individuals previously labeled as “fibromyalgia.”)

      1. In almost all cases, the patients got to where they were via a months-to-years cumulative pattern of 2, 3, or 4 very comprehensible painful locomotor disorders based in the natural discrepancies in resiliency of myotendinous force chains. (Typical example for women would be gluteus medius tendonopathy, trapezial-cervical strain, and a suprapinatus tendonopathy.– but see my list of 40 common locomotor ailments)
      2. Each individual ailment is notorious for being more or less enduring and yet fluctuating in intensity, easily re-awakened by physical activities which though “normal” are imprudent for the individual circumstances. Further, each of the ailments appears to the patient as a rather mysterious affliction. The archetypal patient is someone who is busy, dynamic, and responsible but who is unaware of myotendinous limitations.
      3. The patient arrives at clinic with a layman’s perception of “hurting all over” and overwhelms the clinician who is not armed, trained, and prepared to deconstruct the history and examination into its component parts. (Diffusely-perceived pain is not the same as pain coming from all over or from brain dysfunction.)
      4. The patients who tend to go further and further on the “fibromyalgia” train, courtesy of the clinician, are those who are most frustrated, most burdened by care-seeking selectors in a variety of organ systems, most neurotic perhaps, most likely to enter research studies, and who then help contribute to the artifactual “fly-paper” symptom agglomeration which publications emphasize. This then feeds back into the mystification embedded in the very foundational terms of the fibromyalgia hypothesis.

      If at step 3, the patient is instead effectively addressed by a standard history and an anatomically-informed physical examination, here is what happens in most cases: (a) the patient is relieved that the clinician knows what he is doing, (b) the patient has the opportunity to confront the annoying limitations imposed by her/his specific locomotor weak links, (c) the clinician has a menu of at least partially effective interventions to offer, and (d) even the most neurotic of the patients start look a lot more rational and many are delighted to be relieved of the burden of a confabulated psychoneurologic pariah ailment, and (e) the clinician has specific findings and metrics to follow in collaboration with the patient, the same as for any other organic ailment, and has the satisfaction of concretely fulfilling his medical, ethical, and legal duty to diagnose and treat properly.

      Thus, I favor the following substitutions:

      1. “CHRONIC” = an enduring specific problem (usually variable and in most cases mendable)
      2. “WIDESPREAD” = multifocal (but in each locus anatomically-derived)
      3. “PAIN” = a normal neurocognitive signal of one or more anatomic locomotor resiliency problem.

      And lastly my “preferred” definition of the day:

      “FIBROMYALGIA” = a term of mystification allowing clinicians to falsely attribute myotendinous pain to free-floating CNS dyscontrol, while submerging the simple yet profound truths about the construction flaws which allow 5% or more of the human race to be continuously troubled by several common locomotor disorders.

      Dr. Quintner, I trust that the above addresses at least part of what you asked. And I hope you will take my remarks with a sense of humor, since I know they go to the heart of the conventional wisdom on this subject and thus can be annoying. However, my recent review of the foundational literature (back to Dr. Traut’s Chicago paper of 1968 anyway) confirmed that even in embryonic form, “fibromyalgia” is based on unfounded assertion, and that none of its authors or authorities ever devised a series of investigations to actually test or challenge the hypothesis of CNS dysregulation. Instead, they stacked up more and more layers of self-referential fables and defective research designs, which became “orthodox” text, accepted only because we as physicians are not scientifically critical and are just reaching for any life-preserver paradigm to deal with our daily onslaught of difficult clinical issues. Then, unfortunately, the FM paradigm became congruent with the needs of industry to frame it all as a pharmacological problem. This “collaboration” has spiraled the field into depths of disrepute. Just my opinion.

      I am looking forward to reading D. Schuster’s Neurasthenic Nation ( see ) to explore Dr. Wolfe’s observation that “fibromyalgia” is playing a similar role to 19th Century “neurasthenia.”

      James H. Lampman, MD

  1. Dr Lampman, thank you for providing me with much food for thought.

    I agree with you that the Fibromyalgia label has been very loosely applied in clinical rheumatological practice. In your own words: “Fibromyalgia, in fact, is what you say when you have not provided your patient with an anatomically informed assessment.”

    But when you suggest replacing the FM construct with another anatomically informed construct – “Disorders of myotendinous resiliency” – I must part company with you.

    Some of the examples you provide as evidence lack clearly defined pathophysiology. These include: trapezial-cervical strain; thoracic cage pain syndromes; iliac crest pain/lumbago; myalgic headache; Achilles strain etc.

    Are they based on pure speculation? If so, they are reminiscent of the concept of injury to the “muscle-tendon unit” put forward by Littlejohn in 2007. No evidence for such an injury was ever provided!

    Finally, when you refer to “pain processing” (how do you process an experience?) are you in fact referring to the nociceptive apparatus?

    Reference: Littlejohn G. Regional pain syndrome: clinical characteristics, mechanisms and management. Nat Clin Pract Rheumatol 2007; 3: 504-511.

  2. I don’t have a PhD or MD, but I think I am reasonable intelligent, yet can’t quite understand this. Is there a word missing in this:
    ” 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.”

    Normal way ?? is manifested? It feels quite circular the way it is written. Am I completely missing something? The slides sure have a lot of diagrams of muscles and such- is it satire or serious? I am bewildered. Maybe I just need to study it more closely to understand your thoughts/points.

  3. Nancy: I appreciate your effort to understand my ideas. I’m no English major. Does the following help a little? Testing of the effects of pain via brain imaging (e.g. fMRI), spinal fluid chemistry, pain thresholds etc has been claimed to be different, “abnormal,” and “aberrant” in patients with chronic pain labeled as fibromyalgia … but the experiments involved comparison with healthy normal people. The comparison group is wrong. If you instead used a comparison group of patients with chronic pain from (for instance) shingles, osteomyelitis, cancer, rotator cuff disease, or painful hangnails, then you may find the same patterns of pain processing in all. That would deflate any claims that “fibromyalgia” involved some kind of special dysregulation of the CNS. In other words, if all kinds of chronic pain are handled by the brain in the same way, it actually is the expected way, the “normal” way and there is no abnormality or aberrancy involved here.

    Dr. Quintner:

    1. The term “pain processing,” as you know, is popular in the FM, neurology, and psychology literature. I use the term pain processing the same way authors in the field do — as an abbreviation for the totality of physiologic/psychologic events by which the body, brain, and psyche identify and experience pain.There is a nice review by E. Garland emphasizing that pain typically starts with nociception but becomes multidimensional and ultimately psychophysiological. [ See E. Garland here: Pain Processing in the Human Nervous System: A Selective Review of Nociceptive and Biobehavioral Pathways. Prim Care 2012 September ; 39(3): 561–571. doi:10.1016/j.pop.2012.06.013.] One of the iconically bad research papers I analyzed uses the term as applied to fMRI patterns [Evidence of augmented central pain processing in idiopathic chronic low back pain. T Giesecke et al. Arthritis & Rheumatism Volume 50, Issue 2, pages 613–623, February 2004].

    2. The term “pain processing” and the ideas behind it form part of the infrastructure of current research in the FM field. Misuse of this infrastructure has formed a screen which shields the underlying FM axioms from scrutiny. Authors have said that, via fMRI, they can “see” administered jolts of acute pain being processed in various networks of regions in the brain. Indeed, such jolts are “processed” differently in chronic pain states than in healthy normals. But that’s not enough to say it’s aberrant because similar findings are seen when acute pain is administered in patients with osteoarthritis pain, rectal pain, etc. That’s just the expected result in someone with chronic pain.

    2. I am not sure if you are using the words “anatomically-informed” construct the same way I do. FM is the antithesis of an anatomy-based understanding of pain sources– in fact most would accept that by definition it excludes or minimizes anatomic/physiologic/peripheral sources of or explanations of pain. That’s why the symbol has been Wolfe’s anatomy-free Three Graces drawing — the artistic opposite of Rodin’s Three Shades, which revels in human myotendinous anatomy. Maybe I misunderstood the first part of your comment on this. As far as the examples of myotendinous pain disorders that I gave, I didn’t predict that this would be something to part company on. I don’t think I am alone in finding that all these quite common ailments are tissue-based and use-related. They are popular subjects for study in the literature of physiatry, occupational medicine, and orthopedics, perhaps more so in Europe. Some are better-imaged and better-biopsied and better-understood than others. The underlying pathophysiology of each localized disorder needs lots of further exploration, definition, microscopic pathology, and diagnostic imaging advances. Even something seemingly simple like humeral epicondylitis, painful though it is, has relatively sparse non-inflammatory fibrocyte cellular changes — yet I guess few realistically doubt that it’s a locomotor injury disorder. Having personally experienced a selection of ailments of this type, I have little personal doubt of the circumstances that generate them and heal them (rotator cuff, tennis elbow, trigger finger, triceps strain, achilles tendonopathy, subcalcaneal pain, and trapezial-subocciptal postural strain). I, and am sure you too, have pragmatically diagnosed, treated, followed hundreds of cases of similar items over the decades. If, for the past 40 years, we had had someone the caliber of Mike Benjamin working in every university on locomotor pathophysiology, we might know a lot more about the microscopic, functional, patholologic, and imaging features of these disorders. Just historically, if you carefully read William Gowers’ lecture published in Lancet of 1903, you can see he was groping tentatively toward understanding the microscopic pathology of locomotor disorders — but at no point did he doubt that “lumbago” and shoulder-girdle ailments were tissue-based nociceptive disorders. He suggested that the intramuscular interstitium could be the source of pain. Among his points was that it was seldom to find biopsies or autopsies focused on low back pain etc, in view of the many life-threatening disorders medicine was dealing with. He had to be scapegoated over the years by FM partisans in order, again, to screen the FM neuro-interpretive hypothesis from criticism. Remember that he was not Stockman. As far as Dr. Littlejohn, I shared some thoughts with him back in 2007, and admired some of his work and his systematic approach to the locomotor force unit ranging the course from one tendo-osseous junction to the other and encompassing the diverse anatomic structures which make up the unit. I thought he put too much emphasis on the neurologic features. As far as the neurologic issue so prominent in the literature, I think it relates back to medicine’s preoccupation with pain as a problem to be physically or pharmacologically excised, altered or anesthetized, while neglecting in this case to study and solve the peripheral causes of pain.

    Enough for today. Let me know more criticisms and where you see flaws in my reasoning since this helps me to reformulate and to restudy the literature.

    James H Lampman, MD

  4. Dr Lampman, please accept my apology for inadvertently suggesting that FM is an anatomically-informed construct. Of course it is quite the opposite.

    Your hypothesis of widespread peripheral nociception is interesting but does not explain the other features said to be characteristic of FM – mood changes, fatigue, impaired cognition, sleep disturbance etc. As you would be aware, there is a body of rheumatological opinion that incriminates seemingly ubiquitous trigger points in muscles as being sources of ongoing nociception – but there is no scientific evidence in support of this speculation.

    Are you intending to publish your hypothesis in the peer reviewed literature?

  5. Thanks for clarifying.

    You raise 2 points. First, though, I prefer to re-phrase your term “widespread peripheral nociception” to exclude the word “widespread” which carries a freighted meaning similar to “diffuse” and which does not clearly demarcate my intent. It plays into the premises of “CWP” which suggests pain all over or in a pattern of regions in which the actual pathophysiology of the pain is more or less irrelevant (per the 2010 ACR suggested classification etc). A better term for me is multifocal — and with specific pathology at each of the structures identified in the physical examination. This one conceptual seed of difference eventually grows into a confident and concrete style of examination which finds no necessity to be burdened with mystifications. As a rule, when a patient says I hurt all over, it is a metaphorical statement of a frustrated individual, with the same literary meaning as “I feel as if a truck ran over me.” Here is what happens: if you say, OK then let’s get your detailed description and examine you from head to toe to see where you hurt and what’s causing it — invariably you find the several structures which are responsible — and the patient usually concurs that yes indeed I do hurt at those 3 places and I don’t hurt at these 20 other places. These are not tender points or trigger zones but actual functioning myotendinous body parts. Most are very localized and specific (e.g. a costosternal junction or a trochanteric pain; but some occur in myotendinous structures which drape over several attachments (e.g. trapezius which attaches to spine, scapular, and suboccipital points). It doesn’t take more than a few notorious tendon problems to make someone voice the “all over” perception. But there is no human ailment which literally causes pain all over when you get right down to it. [I might mention that I found 2 cases of overt malingering who had unphysiologic exams in the context of legal issues -- something Gowers called "forensic depreciation."]

    Now to the purported non-locomotor corollaries of pain that you mentioned. This has been one of the axioms or premises of the FM hypothesis right from the beginning. I think it’s artifactual. It may have resided in the minds of Traut, Smythe, Yunus etc as a cultural residual of the neurasthenia/hysteria/misogyny preoccupations of previous decades of North American medicine. They said it, so it must be right, was the logic. It continued to be a preoccupation of FM researchers uselessly seeking personality-based factors in etiology of pain. Here’s what I think. Their practice patterns, predilections, and case diagnoses pre-selected individuals who were more likely to voice complaints of various types and who seemed more neurotic than average. Those patients were the vulnerable ones who didn’t scoot off to an orthopedist or manual practitioner when told nothing was wrong with the places which hurt. They impress the researcher as a type; he collects them in the clinic; and when the researcher compares them to healthy normals, he confirms that indeed these complaints are more common. See Yunus’ 1981 study in Seminars in Arthritis & Rheumatism. No comparison with patient types involving equal amounts of different pain, nor with those with multifocal myotendinous pain. It gets built into the orthodoxy and then these non-locomotor complaints and distress get embedded in the very definition of the ailment. Contrariwise, I found that patients seen by others as fibromyalgics had some very good reasons to hurt a lot, to hurt persistently, to be frustrated, sleep-disrupted, and troubled by the long-term threat to their family responsibilities, marriages, employment, and enjoyment. [One personality trait did strike me over the years: women who were more-than-average driven in daily physical tasks and postures -- their husbands frequently confirmed "She just can't sit down and relax!" ] But they had no defect in cognition except when distracted and discouraged by discomfort and when trust in the rationality of their own body is undermined by an incorrect psychosomatic diagnosis. As far as any pathophysiologic connection with bowel and bladder issues, I am impressed only with how confabulatory the concept is. I do puzzle over why most of the cases coming to clinical attention are female. Just on theoretical grounds it’s possible that for some reason their is a greater degree of tensile discrepancy between strong and weak links in key force chains. And there are anatomic differences that make females much more likely to get gluteus medius tendonopathy (greater trochanteric pain syndrome) — which is a very common pain burden for women, fluctuating for years or decades.

    On your second point re ubiquitous trigger points as sources of ongoing pain. I wonder if you are referring to some of the work of Staud, [e.g. Enhanced Central Pain Processing of Fibromyalgia Patients is Maintained by Muscle Afferent Input: A Randomized, Double-Blind, Placebo Controlled Study. Pain. 2009 September ; 145(1-2): 96–104. doi:10.1016/j.pain.2009.05.020.] If so, I find this work interesting even though it’s cloaked in the FM terminology. If you can make pain thresholds improve both locally and generally by trapezius lidocaine injections, this to me speaks not only to the source of pain in actual trapezius structures, but to the general effect that any enduring pain has on alteration of body pain thresholds. The latter thresholds and the tender point ideology I think have served as a deep-running intellectual artifice or sleight in FM history, just cleverly obscure enough that it seems plausible, yet containing a misperception which mistakes a nonspecific signal as if it were a key part of the defining pathophysiology.

    As far as publication, yes I’d like to do that but am somewhat hampered by being in an enjoyable retirement life; and by having lost access to the detailed records of my cases. Still, I could produce and opinion article. For now, I have settled to publish a letter in A & R this month (DOI 10.1002/art.38397) emphasizing a problem in selection of control group in studies of fibromyalgia. I can send you that as an individual if you’d like to see it, but I guess I am not supposed to post it publically.

    I’ll be interested in how Dr. Wolfe configures his eventual “swan song” revision of FM thinking and I am studying some recent documents of his.

    James H. Lampman

    • Dr Lampman, in the words of Karl Popper, the late philosopher of science, “that which explains everything explains nothing.” Your hypothesis does not seem to be falsifiable. Whenever you cannot demonstrate local pathology at the site or sites where a person complains of pain, you are forced to postulate the existence of a nebulous “myotendinous” lesion.

      Nonetheless, from my own experience I can assure you that an enjoyable retirement is not compromised by publishing an opinion article or two.

      • Hmm. Dr. Quintner, again, I wouldn’t have guessed that one would describe the aforementioned rather specific locomotor lesions as nebulous, either conceptually or in terms of actual pathology. Nor that the rather concrete resiliency hypothesis is anything but eminently and easily testable and Popper-worthy.

        The more well-known items such as rotator cuff lesions, bicipital tendonopathy, achilles lesions, gluteus medius strain, hamstring injuries, patellar tendonopathy, etc have a gradient of use-related pathology all the way up to shredding and discontinuity. These lesions are imageable, biopsiable, operable if needed (even the gluteus medius when tearing occurs). I selected some MRI images of these for one of my slides just to emphasize that we are not dealing with imaginary, cerebral, or “nonpathologic” pain issues. The trochanteric pain syndrome, by the way, is a well-defined gluteus medius-minimis lesion which can easily show up on MRI; any bursal involvement is strictly secondary. The use of ultrasound imaging may disclose density changes at key locomotor lesions and could be clinically useful if it gets a little more sophisticated.

        I envision a not-distant future involving an advanced metabolic body scanning technology which can detect and quantify all of a patients myotendinous lesions, whether they partake of nebulosity or not.

        In any case, with or without imaging, it’s only too easy to demonstrate that the pathology is local just by injecting lidocaine, as did Staud in the article I cited. Not that injection therapy with steroid etc is always desirable, since it works temporarily very well and can delude the patient into continued imprudent use of the locomotor structure and permit further biomechanical deterioration and healing delay (e.g. lateral epicondylitis, achilles strain, supraspinatus).

        As far as falsifiability, again I didn’t suppose that to be an issue. Both the FM central augmentation theory and my myotendinous resiliency theory are easily enough falsifiable both practically and theoretically. The problem with FM research is that its advocates never bothered to falsify it, which generally would be their responsibility … although as I pointed out in my lecture, Clauw’s group inadvertently did so by using a lumbago positive control group in their 2004 study cited earlier. To falsify FM’s principal claim (that there is something unique, prototypical, or transcendent about its “generalized pain”), just run a comparison study looking at fMRI, spinal fluid chemistry etc on a contemporaneous group of agreed-upon nociceptive pain patients. Why in 40 years has no one done that to please Popper? To falsify my proposal, just find me some patients said to have no local myotendinous pathology exactly correlative to and proportionate to the pain complaints: one would examine them with standard everyday history and physical using agreed-upon techniques, and perform any and all suitable imaging & other testing, and then buttress the certainty of specific diagnoses by intervening specifically to treat the individual lesions. From 2006 to 2011 I combed through hundreds of patients and couldn’t find any who fit that description — namely generalized pain for no recognizable tissue-based reason. In fact I ran this same method of numerous patients referred to me with a claimed diagnosis of fibromyalgia.

        As far as explaining everything and nothing, such a label would be more suitable to the FM hypothesis, which self-admittedly contains a fly-paper clause — any odd symptom attaches itself arbitrarily to it (e.g. bladder irritability).

        Respectfully and with a sense of humor –

        James H. Lampman, MD

        • Dr Lampman, as you well know, the FM proponents never published an hypothesis. Their inability to put forward an explanatory model for the clinical phenomena that they gathered under the umbrella of FM has led to much confusion. I think we agree on this.

          But as far as I know, Staud’s study (2009) has never been replicated. Nevertheless, his views may well be in accord with yours, as expressed above:

          “Although it is unclear whether TrPs (trigger points) are the cause or effect of muscle injury, they represent abnormally contracted muscle fibers.” [Staud, 2006]

          And how about this argument extracted from one of his more recent publications? “Similar to CWP, FM pain appears to depend on impulse input from deep tissues, particularly muscles. In genetically susceptible individuals, such tonic impulse input results in peripheral sensitisation as well as neuroplastic changes of the central nervous system (CNS), termed ‘central sensitisation’.” [Staud, 2011]

          Staud’s understanding of these conditions appears to be grounded in as yet undiscovered pathological changes existing within deep structures, e.g. muscle, whereby supposed tonic impulse input therefrom is responsible both for local tissue changes (i.e. peripheral sensitisation) and for changes in central nervous system function (i.e. central sensitisation).

          Clearly Staud’s views are highly speculative yet they are being passed off as factual. Am I missing something here?

          Staud R. Are tender point injections beneficial: the role of tonic nociception in fibromyalgia. Current Pharmaceutical Design 2006; 12: 23-27.

          Staud R. Peripheral pain mechanisms in chronic widespread pain. Best Pract Res Clin Rheumatol 2011; 25: 155-164.

        • What needs to be falsified is the claim that central sensitization (whatever that is) causes symptoms symptoms and pain. The assertion that it does seems not falsifiable to me. Clauw writes in his manifesto-like 2014 JAMA article, “Sensitivity to bright lights, loud noises, and odors and even many visceral symptoms may be in part due to a global sensory hyperresponsiveness seen in conditions such as fibromyalgia often leads to a “pan-positive review of symptoms” that has often mischaracterized these individuals as “somatizers” as the biology of somatization is increasingly recognized as that of sensory hyperresponsiveness.

          I take your model to be “for every pain there is a lesion.” But there seem to be many people walking around without pain who have lesions.

  6. Dr. Lampman, one has to be brave or unwise to take on John and Nancy. While you have been writing I have been finishing an abstract for the ACR meeting entitled, “Symptom Increase in Fibromyalgia Is Not Consistent with the Central Sensitization or Central Hyperresponsiveness Hypothesis.” Although I agree with much that you say, I have to come down on Nancy and John’s side. I could write a lot about my personal struggles trying to understand myotendinous problems—what they were, when and how to diagnose them, and when and whether they existed. I was referred numerous patients with trochanteric bursitis (whatever that was) and various named eponymic and non-eponymic musculoskeletal disorders. I studied briefly with a trigger point guru. … did all of the musculoskeletal things. In the end, I came to the conclusion that John did: these diagnoses were many times in the eye of the beholder. There was nothing easier then labeling trochanteric pain “bursitis” and sending the patient and his bank account for a long rendezvous with the physical therapist; or to the long needles of the orthopedic surgeon. Fibromyalgia as a diagnosis is much more difficult to the conscientious physician who takes on the problems of the world with such a diagnosis.

    If you don’t believe in fibromyalgia, move a little to right and you are in the midst of Chronic Fatigue. There you have fibromyalgia without all of the musculoskeletal contradictions that make you unhappy. I found a recent interesting comment from an Institute of Medicine report on the Gulf War Syndrome. They wrote, “Chronic multisymptom illness (CMI) is a serious condition that imposes an enormous burden of suffering on our nation’s veterans. Veterans who have CMI often have physical symptoms (such as fatigue, joint and muscle pain, and gastrointestinal symptoms) and cognitive symptoms (such as memory difficulties) and may have comorbid syndromes with shared symptoms (such as chronic fatigue syndrome [CFS], fibromyalgia, and irritable bowel syndrome [IBS]) and other clinical entities (such as depression and anxiety). For the purposes of this report, the committee defined CMI as the presence of a spectrum of chronic symptoms experienced for 6 months or longer in at least two of six categories—fatigue, mood and cognition, musculoskeletal, gastrointestinal, respiratory, and neurologic—that may overlap with but are not fully captured by known syndromes (such as CFS, fibromyalgia, and IBS) or other diagnoses.”

    I am happy to call CMI fibromyalgia.

    They continue, “Despite considerable efforts by researchers in the United States and elsewhere, there is no consensus among physicians, researchers, and others as to the cause of CMI. There is a growing belief that no specific causal factor or agent will be identified.”

    I don’t quite see FM as a misdiagnosed musculoskeletal disorder, as you do. But I certainly saw real musculoskeletal problems in a proportion of patients who fit the fibromyalgia diagnosis. But this is not the place for a long essay. What I deplore as much as you do is the false causal models of fibromyalgia and central sensitization. The ACR 2010/2011 fibromyalgia criteria and polysymptomatic distress scale — particularly the PSD scale show that the symptoms that make up fibromyalgia exist on a continuum and are part of ordinary living. Maybe that is what you meant when you spoke of normal pain mechanisms. What is deplorable about fibromyalgia in the academic community is soft, bad thinking, self-serving academic stars, KOLs, and continual commercial disease promotion. In an in press article about to be published, I wrote, “Despite weak to nonexistent evidence regarding the causal association of trauma and fibromyalgia, the literature and court testimony continue to point out the association as if it were a strong and true association. Such assertions influence legal evaluations and beliefs of expert and non-expert physicians, and further the social construction of fibromyalgia. In 2007, Smith described Pseudoevidence-based medicine (PEM) “as the practice of medicine based on falsehoods that are disseminated as true evidence, then adopted by unwitting and well-intentioned practitioners of evidence-based medicine.” (52) Fibromyalgia recommendations are subtler. They have taken weak truths and added them together to give the impression of an overall association of fibromyalgia and trauma, while rarely addressing study quality, bias and strength of effect.”

  7. @ Fred. It is good to hear from you again. May I ask you to explain what is meant by “ordinary living”? It makes me recall the profound insights of Eriksen et al. who see these very same conditions as likely to be the “Total human organism’s response to overload or existential crises”. Of course, I am biased in favour of our 2011 hypothesis, which as you know is built on a large body of research from the field of evolutionary biology.

    Eriksen TE, Kirkengen AL, Vetlesen AJ. The medically unexplained revisited. Med Health Care & Philos. 2012. DOI: 10.1007/s1109-012-9436-2.

  8. Yes, I think that is a good phrase. But I mean something slightly different. In my (our) 2013 paper, “Fibromyalgia Prevalence, Somatic Symptom Reporting, and the Dimensionality of Polysymptomatic Distress: Results From a Survey of the General Population” in Arthritis Care and Research, Figure 3 demonstrates that in a general population there is a continuum of symptoms associated with x variables, in this case with polysymptomatic distress. You can have a whole series of x variables. That is, the symptoms of fibromyalgia exist on a continuum of severity. Humans [here it gets toward interpretation, not data] tend to “respond” to illness [or stress] in an almost stereotyped way. They report more symptoms of all kind, including pain, fatigue, sleep and memory problems. Symptoms are “normal.” When I have symptoms I try not to worry about them. I don’t bother about the paresthesia, muscle aches, – what Yeats called “the slow decrepitude of the flesh.”

    Even so, it is inexplicable why people differ in their response to ordinary ands non-ordinary events.

    • Dear Fred, I think we are getting closer together in our views. I still have a problem with “normal”. Would you accept that the symptoms of polysymptomatic distress are ubiquitous? If so, we might only have shifted the goal posts a little to one side but the BIG question remains unanswered – what are the likely biological explanations for symptom production? Another question then arises – why do the symptoms persist?

      • Yes, I accept that the symptoms of polysymptomatic distress are ubiquitous. I think that the presence of one pain or one body abnormality makes us more aware of others. Maybe the intensity of threat plays some role.

        A while ago, in one of our questionnaires we asked people not just whether they had symptoms, but how severe they were. Among the choices were: Yes, but it doesn’t bother me and the scaled for degrees of bother. I did this for my own interest and never published it (Hmm, maybe I should write it up for the next abstract round). What we found out was that when people endorsed a symptom (yes or no) they were endorsing more than ” Yes, but it doesn’t bother me.” This degree of concern may be one of things that moves the fibromyalgia curve to the right – some would have said this is related to the old “somatization” definition.

  9. Dr. Quintner: On the matter of presentation of the FM hypothesis by its proponents: don’t they more or less constantly present it in the first paragraph of every article and review? Often it is accompanied by a claim that there is “vast and extensive evidence” favoring central augmentation as its principal mechanism. In my slide 26 I did my best to summarize in neutral terms the chief features of the hypothesis as follows:

    *A unique or prototypical generalized intrinsic pain state.
    *Commonly pictured as tender points in anatomy-free “3 Graces” or as a diagram of sensory information ascending, descending, traversing interconnected CNS regions.
    *Independent of specific anatomic basis in the body, though it is perceived as musculoskeletal pain.
    *It is signaled abstractly by (or even defined by) bodily tender points of which the patient is said often to be unaware; and/or by widely distributed enduring pain loci which need not have local pathology
    *Its special “chronicity” sets it apart from the mundane pain we know day by day
    *The amorphous widely perceived pain, the chronicity, tender points, and reduced sensory thresholds are said to be expressions of some form of dysregulation of pain processing residing in the central nervous system.
    *The pain state of fibromyalgia is said to be part of a larger rubric of ill-defined somatic and cognitive dysfunctions

    Each feature, I felt, contained premises which are ridden with mystification and misdirection. For me personalIy, none of it is worth the time to falsify since it is on the face of it confabulatory. However, those who claim support for their central pain theory via the fMRI’s and substance P etc would self-falsify or self-destruct upon using the right “positive control” in the next study. They are deluding themselves by claiming aberrancy and abnormal sensitization when in fact they are looking at the non-aberrant and normal reflections of pain.

    I feel that we as rheumatologists ought to be the premiere diagnosticians for the spectrum of musculoskeletal pain. As such our prime responsibility is to discover the precise cause and meaning of each pain and to do it with traditional methods of analysis and deconstruction. I have found that generally rheumatologists are not “armed and prepared” with confident examination skills involving common muscle/tendon (locomotor) disorders. In fact, the bulk of our literature, texts, and fellowship training will tend to suppress interest in this matter. I know I had to pretty much self-educate on this 10 and 20 years out of training. Virtually nowhere is there a coherent presentation of the locomotor system and its spectrum of very understandable and biomechanically stereotypic disorders. Even when items are discussed they are disconnected from the actual motor use which causes them (e..g DeQuervain wrist, trigger finger, gluteus medius, rhomboid). This makes it all uninteresting and obscure/unworthy to the rheumatologist. It’s a deficiency of our training and has made rheumatology vulnerable to the mystifying influenza of the FM program. Willy-nilly the modern FM program has been transformed into a neuropharmacological agenda alien to the actual biomechanics of the body. No wonder many rheumatologists try to exclude such patients from their practices. From the other side, the cases are certainly not wanted by the neurologists either.

    Dr. Wolfe: you aptly noted that I feel that for every pain there is a lesion –and you point out but not vice versa. Very true in some respects — for instance some people with rotator cuff tearing on MRI may not have pain at a given phase, a damaged biceps tendon may not hurt much after a while, and many with degenerative lumbar disease are pain-free. An “accommodation” has been made in many cases — and likewise there are a few people who seem to easily tolerate and even behaviorally ignore destructive rheumatoid disease, OA, or AS. But by and large the pain-perceiving pathways are pretty reliable in telling humans that something new has gone wrong. That’s where we come in.

    The species is biologically and psychologically quite variable; and naturally there are a lot of people just off the rails. Yet in the office evaluation of “hurt all over and fatigued,” I found that even the most cringe-worthy pan-symptomatic individuals become understandable and become your allies in treatment once you stick to what we know and point out specifically the locomotor lesions causing the pain. That’s our first responsibility. Not doing that is equivalent to telling someone they have “chronic Lyme disease” when in fact they have multiple sclerosis or RA.

    Patients don’t usually come to a rheumatologist for contemporaneous psychological issues, irritable colon, etc — those trains are running on different platforms and we don’t have the facilities or training to capture those anyway. Taking on the existential troubles of the world is maybe too much for our modest rheumatology discipline.

    “Ordinary life” as I see it is laden with daily challenges to the flawed human locomotor system — which almost naturally we operate carelessly until brought up short by damage to one or more weak links. Our muscles are strong enough to unwittingly and commonly do real damage to concatenated structures such as tendons and tendo-osseous junctions. Our sports-medicine and orthopedic friends are more clear on this than the average rheumatologist.

    Dr. Wolfe: the IOM report you refer to provides what sounds most like an administrative list of disorders and complaints set up to decide who gets benefits. All the listed ailments are worthy and troubling. Yet they may be pathophysiologically unrelated to each other and to musculoskeletal pain. Calling all this “co-morbidity” and classifying it CMI may not really be doing the veterans a favor; what they could use is an individual analysis of each ailment and treatment of the treatable parts the same way anyone deserves.

    Dr. Quintner: Staud has been an interesting outlier and appears to be contradicting some of the accepted delusions of FM orthodoxy by studying the “periphery” and seeing that it should not be forgotten. I haven’t yet read the 2 items you cited. But I am concerned that he is looking in muscle as an isolated tissue rather than as a biomechanically active component of an entire locomotor chain — and thus is going to miss where the problems are (just as did Yunus in the electron microscopy study of 1989).

    James H. Lampman, MD

    • Dr Lampman, may I take it that you are advocating a rheumatological project that aims to define the precise cause and meaning of each pain? The project’s fundamental assumption is that the human locomotor system is biomechanically flawed and we are thereby predisposed to sustain musculotendinous injuries in the course of our daily lives. If I am reading you correctly, this constitutes a post hoc ergo propter hoc argument.

      For the record, I have never been part of the FM orthodoxy. Since 1993 Milton Cohen and I have published a number of articles that have been severely critical of the FM construct. Elsewhere on this blog I have commented on the reluctance of the FM orthodoxy to engage in serious debate. Hopefully you will stir them from their slumber.

  10. “Patients don’t usually come to a rheumatologist for contemporaneous psychological issues, irritable colon, etc — those trains are running on different platforms and we don’t have the facilities or training to capture those anyway. Taking on the existential troubles of the world is maybe too much for our modest rheumatology discipline.”

    I once published an article on psychological issues, I pointed out that psychologists see patients when they are bad, but rheumatologists see them over a life-time over good and bad times, particularly with RA. I said we know more about the psychological lives of our patients than psychologists. In my practice beginning around 1974 I started to collect PE and self-report data in a computer (I wrote the software). So for every patient visit I has pain, global HAQ, fatigue and in the beginning anxiety and depression data. I thought what patients wanted from me was support and an interface to the world as they, as often was the case in those day, progressed to disability and dissolution of plans and often lives. I think we should use psychological skills and do have a part in the existential troubles of the world.

    I do admit that sometimes I missed the anatomic problems in some FM patients. Slapping my hand to my head, how could I have missed something that obvious I sometimes said. It occurred when I prejudged patients and didn’t look hard enough.

    FM occurs in RA frequently. Treating the RA better often made the FM better. But both RA and FM were there. If you don’t believe in FM, then just say exaggerated or increased pain and general distress. One thing about FM, if you are looking for it you find people who meet criteria that you might not have thought had FM because the symptoms were not flagrant. My self-report scale for fatigue was most helpful.

    If one uses self-report you see all sorts of things you never would have suspected.

    So, I would say, if you have anatomic lesion that you can fix that makes “FM” go away, then thats what we should do. But I would guess that it turns out to be a small fraction. I don’t care if people believe in FM or not – as long as they pay attention to patient symptoms.

    One last comment. I collected RA data from many physicians. Often they were very certain. “My patients always ….” Some MDs swore by one biologic while others by another. Steroids were good and bad. I learned early on in my data collection that many of my successes were not successes. They just went to other doctors and “got disability.” On justifiably famous Boston Rheumatologist to me that patients went first to another justifiably famous rheumatologist who treated them with state of the art treatments – then they came to me. All of this should make us humble and uncertain in our judgements. Montaigne knew that.

  11. Dr. Wolfe: agreed on first principles: the importance of support, guidance, and empathic interaction which is a large part of our professional persona and is helpful to each patient and helps maintain a valuable relationship which sometimes is the only half-rational thing in the patient’s life.

    However, apart from basic internal medicine skills, it can be a misstep to try to handle certain problems alone (e.g. neurologic problems, or bowel and bladder symptoms which can easily portend inflammatory or malignant lesions we don’t claim expertise in) or to lead patients to expect actual psychological counseling and the availability which goes with it (which can be time-consuming, hazardous to both parties, and is seen to be outside our scope of practice when things go wrong). Sometimes the most supportive and sound thing is to make the right referral and it’s something which only strengthens the physician-patient relationship (“He cared enough to find the right doctor for my problem.”) I’m saying this not to suggest you disagree with it but just to clarify.

    Further, the numerous tribulations, slings, arrows, errors, and mischances in the daily practice of medicine are humbling for most of us. They are bearable only because they are usually outnumbered by the successes in diagnosis, prognosis, and treatment. I am not sure what specific thought of Montaigne you refer to. But I did touch his burnished shoe recently, on the seated statue in front of the Sorbonne. And I stayed at a Holiday Inn. This reminds me that Paris Descartes University is down the block from there and set off a memory that Descartes once dissected brains and felt that nerve impulses were carried to the brain much as pulling a bell rope would ring a bell — I liked the wonderfully mechanical analogy — which presaged how the 30 different somatosensory receptors would eventually be understood to ring those cerebral bells at a distance. I digress; please allow my peccadilloes.

    As far as RA and FM, all I can say in response is that myotendinous disorders occur contemporaneously with any disease that happens to be there. Once a famous lupus investigator admitted that the lupus features were much easier to manage than “fibromyalgia” features in those patients. Made me wonder what examination techniques were being used. By the way, we differ in the recognition of “exaggeration” and “increased distress” — I gradually understood that the amount of pain and angst voiced by my patients was about right for the objective problems I found .. (These were the patients for whom I un-diagnosed FM in favor of the 3 or so myotendinous pain sources.) If you couldn’t rest or focus or perform because of bilateral trochanteric pain, humeral epicondylitis, and recurring myalgic headaches, you’d be very justified in complaining pretty loud.

    You desire to diagnose an intrinsic generalized disorder of pain and/or distress — but to properly do that you’d want first to exclude the simple biomechanical issues I emphasize. After you do that, fine. But you might not be surprised at this point that I believe there is actually nothing left to diagnose, pain-wise, after finding the mechanical problems. I evidently am not persuading you — but we should at least agree where we differ. You say you found that my kind of myotendinous problems were in the eye of the beholder and you place little reliance on searching for them since you decided they were kind of imaginary.. naturally you need to replace that with a non-biomechanical paradigm. I find the myotendinous problems very real, biologically based in simple Renaissance anatomy, imageable in many cases even, but why waste the resources, very stereotypical, very orthopedic in a medical kind of way, and usually easy to identify since they are so common, and virtually never being countered by later clinical developments for each patient. I think the mechanical thing is a big fraction. In fact, all. Therefore I don’t need FM or anything attached to it. And I am very critical of its underlying premises, research status, and future. My guess is that in 20-30 years medical historians will look back and wonder how it went so wrong — just as they did with the acid-stress theory of peptic ulcer. The entire research output of FM will disappear since it was wrong right out of the gate. But then each of us and the medical world itself are on a rocky journey with a lot of byways so it’s nothing new. Again, sorry if I am being annoying and provocative. I concur that the patient is the thing and everything we do should be to serve him/her. My intent is not to be too ad hominem.

    Dr. Quintner: please, I apologize if I inadvertently suggested that there is anything orthodox about you. This is clearly not the case. However, you do appear to be a logician, and one versed in Latin, which I admire. You state my “project for rheumatology” (I appreciate the phrase) is to determine the precise cause and meaning of each pain. I am proud to associate myself with that project since it echoes that of my personal intellectual hero, Giov. Battisti Morgagni, whose very anatomy theater I have visited in Padua. More than any other, he helped banish the illusory and all-explanatory humoral theory of disease and replace it with organ-derived pathology, with careful autopsy dissections and correlations of some 700 of his patients. I take it as a QED that the anatomic substrate of human and animal locomotor systems not only DOES give rise to stereotypic types of injury as it is used, but in fact is PREDESTINED by virtue of its structure to do so, and very few humans escape some feature of it. The clinical project would involve accurately identifying the process for each individual patient. The logic underlying this is similar to recognizing that because of certain vulnerabilities in innate & acquired immunity we are prone to an array of microbial infections and that’s the project of the infectious disease specialist. There’s no propter there, just pragmatic physiology and medicine, sensu stricto.

    James H. Lampman, MD

  12. @ Dr Lampman. The main weakness I see in your argument is the assumption that pain felt in musculoskeletal tissues must always originate within those tissues. Is this fair comment?

  13. Not really. The only assumption is that the clinician will make his best effort to accurately diagnose each problem individually. If an osteoporotic fracture, malignant lesion, infection, discogenic lesion, or autoimmune disorder presents with pain near or within a locomotor structure (perhaps mimicking one of the common tendonopathies), or is referred into that structure from an adjacent site, then the clinician has to capture that. Index of suspicion, accurate diagnostic technique, and selective testing are required. PMR, Parkinson’s, peripheral neuropathy, and paraneoplastic disorders such as hypertrophic osteoarthropathy all could, for a time, mimic benign myotendinous pain. I’ve encountered each of these. That’s what being a clinician involves. But that being said, the common lesions of concern in my discussion are hundreds of times more common than the rarities and are just not that hard to pin down pretty confidently.

    Gentlemen: I’ll have to go on hiatus since I’ll be away from my office and my wife is rescinding my computer privileges anyway since I’ve been overdoing it. See you again soon …….. James H. Lampman MD

    • Dr Lampman, I suggest that you are merely replacing one tautological construct (Fibromyalgia) with another (myotendinous disorder). I am using ‘tautology’ in its logically defined meaning – a statement that will turn out to be true in every circumstance or, as some say, in every possible world. This is not to say that your argument is invalid. However, I wish you well with the project.

  14. OK one last rejoinder while my wife is cooking breakfast.

    Neither paradigm can be dismissed with a logician’s syllogism.

    The problem with FM is not tautology — it’s that it’s just plain wrong. There is no cerebral dyscontrol going on. In fact the CNS is doing its job trying to receive, report, and integrate somatosensory messages from (in this case) biomechanical sources in the body. And sufferers can describe it any way they choose. Whether to the listener it seems amplified or seems understated, and whether it is accompanied by high or low levels of distress, our job is still the same: find and address the actual biologic issues.

    The problem with Myotendinous Resiliency is that it evidently does not partake of the mystic liturgy of the priests of pain processing — it is simple, relies only on elementary anatomic knowledge, it is matched point-to-point only with injured locomotor sites, it is not monolithic or grandiose, does not claim comprehensive correlation with every misery of human existence, and does not involve a futile search for pharmacologic balm.

    There is no tautology in calling for the primacy of simple biomechanical examination. For some, this appears to involve some very arcane knowledge. In any case, If, upon taking the 5 minutes to do this favor for a patient, the examiner finds nothing he can precisely correlate to the patient’s complaints, he is free to devolve the diagnostic process into whatever mystic explanation is desired. I have yet to find circumstances where this is required.

    That’s my last word — until the next one.

    • Dr Lampman, I concede that your hypothesis of Myotendinous Resiliency is simple but therein lies its fundamental problem. Beware! You may be treading the same rocky path as did the pioneers of Myofascial Pain/Trigger Point theory. As it turns out, they were “not even wrong” but their High Priests promoted this theory far and wide to the detriment of countless innocent muscles who were repeatedly subjected to dry and wet needling etc.

  15. Dr. Quintner: Thanks for that insight and others you have provided.

    The truly scientific literature on actual treatment of some of the common myotendinous disorders is remarkable slim and lightweight. Witness the few good publications on humeral epicondylitis and greater trochanteric pain syndrome. Note that as far as treatment, I limit myself to pointing out that there is a menu of options available and that any quick “success” with medication or injection can be illusory and deceptive. One of the few sources available to me 30+ years ago was the first edition of R Sheon’s “Soft Tissue Rheumatism” which at least collected some of the common knowledge about it — though jumbled in with segments on FM, trigger points etc. There were 2 Czech authors back in the 60′s-70′s who listed and advocated the exploration of the numerous common enthesopathies (a new word back then)– The road forked then — I sigh to think how far medicine would be with this if it had followed that trail instead of being confounded by FM.

    • Dr Lampman, I agree with your last remark – “I sigh to think how far medicine would be with this if it had followed that trail instead of being confounded by FM.” But to be fair to North American rheumatology of the 1980s, the trails that were available for them to follow were not well sign posted. For the record, I know that the enthesopathy trail has been followed by my Australian compatriot, Dr A. Breck McKay.

  16. I am reminded of a Mitch Hedberg joke: ‘If you find yourself lost in the woods, f@&$ it, build a house. “Well, I was lost, but now I live here. I have severely improved my predicament.”‘

    Harsh? Perhaps. I don’t mean to be flip- just point out that there may not be an answer to the experience we call fibromyalgia that makes logical sense. Sometimes a conclusion is the place where you got tired of thinking.

    Most patients live in an uncomfortable space between competing paradigms. Doctoring styles range from identifying and treating the source of the pain to accepting and acknowledging the mystery of pain. We do our best to know who to trust to give us the best care.

    In the meantime patients mostly just feel like crap and have to live around that, regardless of the philosophizing going on regarding the validity of the definition of the experience.

  17. Nancy for your sake, and for that of others in your situation, I hope we are all still thinking. Paradigm shifts can only be identified in retrospect. Let us hope that we are moving into a new paradigm where the validity of the experience of patients (sufferers) is not being questioned.

    • John and Nancy,

      And a few small drops of rain …

      Your comments, as always, have been useful to me. So here are some thoughts. Maybe this is the article I want to write.

      We need again to think that what is being called fibromyalgia is a syndrome, by which I mean a sometimes unclear set of symptoms that may have many causes or pathways. The enemy of understanding and dealing with this syndrome is certainty and pomposity. I see academia and industry with its goals of self-agrandisement and money as an evil, one that creates and sustains parts of the syndrome. I also see that illnesses are sustained by society. I think there is room for Dr. Lampman’s views, too, at least to some extent.

      John, yours and similar work suggests reasonable observed mechanism. Factors that we know exist based on research are stress, psychological factors, societal factors. We have measured to some degree stress and change in pain sensitivity (to avoid the word central sensitization for a moment). We know that pain is real (whatever that means).

      Now, I want to be very careful in how the following is interpreted, and remember that I have spoken of different pathways. Society does not always sympathize with suffering if it judges the suffering is self-induced – or it doesn’t sympathize much. Perceived deviant behaviors, beliefs or lifestyle are suspect. If society perceives that fibromyalgia is the result of such things, then there is disapprobation and suspicion. In the U.S. the institution of social insurance (Medicare disability) was opposed by many who were afraid of self-reported disability and social causes. Such arguments continue. My point is not to take sides, but to suggest that these issues will always be important.

      So when we speak of fibromyalgia as if it were one thing, with one group of patients, one set of mechanisms, we do harm. So if there is to be a paradigm shift it should be to a multi-pathway – multi-person syndrome.

      • Fred, I do not see how people can avoid taking sides in this controversial area of medicine. Dr Lampman’s views illustrate what I see as the urgent need to develop a logical, scientifically-based, unambiguous and non-stigmatizing taxonomy for chronically painful conditions.

        Of course this huge challenge would aim to fill a yawning credibility gap, despite the best efforts of those responsible for developing ICD-10, DSM-V and the IASP Taxonomy.

        I do not envisage Fibromyalgia Syndrome as having a place in such a classification, nor will Myofascial Pain Syndrome or Disorders of Myotendinous Resiliency. Attempts to formulate a mechanism-based classification have not progressed beyond the key descriptors of Nociceptive and Neuropathic, but at least there are operational criteria for each of them. The clinical phenomena of the vast majority of those with the Fibromyalgia label are not encompassed by this terminology. I agree with you and Dr Lampman that “central sensitization” is unsatisfactory as an organizing principle, mainly on the ground that its operational criteria are delightfully vague. But there is no other generally accepted organizing principle available. Milton Cohen and I do have a suggestion that might prove to be acceptable but our work in this area is still “under construction”.

        Do you agree that this sort of challenging project might drive the much needed paradigm shift?

    • I see the article in A & R for July with another report on reduced small-fiber skin nerve density in patients labeled fibromyalgia. I would be curious as to the interpretation given this information by Drs. Wolfe and Quintner.

      Personally, I find it very interesting, along with certain similarly-designed prior reports (e.g. Oaklander, Argoff). However, it may be of note that again the control group is healthy normal individuals. Thus it is not addressed whether changes in small fibers are perhaps just a consequence of any type of chronic pain — (including those with multiple common myotendinous pain disorders whom I feel are identical to the FM patients in these studies).

      Certainly the findings are so preliminary and biologically odd that I feel it’s unwarranted to run a study of the therapeutic use of IVIG, which is what Oaklander has been doing at Mass. General.

      • Note the detailed report of 6 patients with acute calcific tendinitis of the gluteus medius, authored by N. Paik of Korea, in the June number of Semin. Arth Rheum. Four of the six were women. I’ve seen one such case; but much more commonly, there are cases of simple tendonopathy at that site, without visible calcification — similar no doubt to supraspinatus tendonopathy, where very seldom do we see the overt calcium deposits we used to note on films. The gluteus medius is an under-reported form of myotendinous pain and is often minimized as a “non-pathologic” tender point, etc, in the FM paradigm.

      • Dr Lampman, may I suggest that pain (a lived experience) cannot be an agent of pathological change.

        In my opinion, FM label has been a convenient label we have used for patients with a particular set of symptom clusters. It is not therefore surprising that a small percentage of them will harbour identifiable disease processes, such as “small fiber peripheral neuropathy”. By eliminating known causes (diabetes mellitus, underlying malignancy, vitamin deficiency, exposure to toxic chemicals) the investigators suggest that a peripheral immune-mediated process may be responsible for the nerve damage.

        There is an increasing awareness that immunopathology involving the nervous system “can be traced to components of the microbiome and to the genetic pathways that pathogens within the microbiome dysregulate in order to survive.”

        This could be the reason why Oaklander’s group are trialing IVIG.

        Reference: Proal AD. Inflammatory disease and the human microbiome.

  18. Dr. Quintner: I am glad to see you are still out there. Here’s some responses to the two items you raised.

    1. The term nociceptive/nociception seems to refer to the entire neurocognitive process of perceiving something as obnoxious. It would therefore not be a type of impairment but more of a recognition of & response to a certain stimulus. No doubt the pain perceived at the greater trochanteric attachments is due to objective damage at tendon & closely related anatomic structures. But the individual’s experience of pain, stiffness, tenderness could be felt along a whole spectrum from intense to minimal or none, I suppose. I’d say the first thing is to recognize the anatomic pathology. Then the art of medical management comes in when dealing with the individual person’s issues and for some that surely involves “impairment” relative to certain daily functions. This may seem semantic but for me it goes back to de-mystifying and eliminating the cerebral dyscontrol concept embedded in the term fibromyalgia. [As you know, I find that even after 40+ years of study, there is not a shred of evidence showing that the brain handles pain differently in FM-labeled patients than in those who have chronic pain from some other source.]

    2. For the papers on small fiber neuropathy — I’d prefer that the authors (a) use the term “patients labeled as fibromyalgia” in their presentation; (b) display the results to detect a biologic gradient; and (c) provide a positive control group rather than solely “normals.” The use of only normal controls in this setting is the origin of unending nonsense. What says that an equal number of people with, e.g. chronic pancreatitis pain or chronic gluteus medius tendonopathy pain, do not have similar reduction in skin nerve fibers? And similar levels of various nonspecific cytokines? Is there a protective loop in which chronic pain affects density of fibers — thus a consequence rather than cause of pain?

    • Dr Lampman, I think you have missed my important point. Chronic pain (an experience) cannot be a causal agent of bodily pathology, e.g. having an effect on the density of nerve fibers.

      I agree with you that positive controls should be studied on the ground that people with various painful conditions may share mechanisms of disordered bodily function, as exemplified by their profiles of expression and regulation of stress-related genes.

  19. Actually I did not miss your point — and I do accept with you that the isolated emotional-cognitive experience of pain itself (the subjective “lived experience”) is not going to produce pathologic pruning of peripheral nerves.* My countervailing point would be that the objective pathology behind the subjective pain experience could generate immunologic intermediaries (chemical or cellular) which might be involved in such “pruning” — and that this might even be a normal feedback loop feature of many kinds of ailment — and would for instance act to reduce the nociceptive response (not amplify it). (And it would have nothing to do with the so-called FM.) Presumably the greater quantity of pathology would generate the most nerve pruning — thus my interest in the “gradient.” Not sure anyone has looked at this possibility — certainly not the authors of the several studies mentioned.

    *[Note, though, it's a cultural-literary theme that all kinds of harm are inflicted by the body's hormonal axes in pain & stress settings--not really well supported in literature... for instance in the exaggerated claims historically made by Hans Selye on behalf of the tobacco industry]

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Posted on January 27th, 2014 by John Quintner


 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 (

“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.” [1]

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.” [2]

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.” [3]

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



  1. I attended Dr. Liftogt’s seminar and used what he taught right away and the my patients are quite happy. I am researching the science to help me better explain it my patients, however, just because I don’t understand it doesn’t mean it does not exist.
    Example of my first patient:
    He is a 36 y/o Marine; he injured his left shoulder in 2003 carrying something heavy at work. He was eval by his PCM, sports med, ortho, neurology, and pain management as his sx’s progressed to the point that he had n/t, pain, and slight weakness to the arm. He had a complete w/u that was not revealing and had undergone extensive PT and various forms of treatment. His sx’s improved enough that he could continue his work as a Marine. However, the n/t and pain never went away. He gave up figured he would live like this for the rest of his life. I saw him earlier this year after he came back from a 6 month deployment to Jordan where he woke with worsening sx’s including noting the arm seemed rudier. I did the standard w/u with xray f/u and MRI with consult for NCV/EMG and neurology. I prepared by telling him I was concerned and that I will need to get vascular surgery involve pending what neuro says. I saw him the day after I got back from the seminar. I pulled him back to my office to review his w/u with him and his consult to neurology. THey too agree that vascular needs to weigh in. I told him about the seminar and thought this would help him, he gave it a chance as nothing had worked before. I palpated him out and inject based off of the course material. My Marine was smiling from ear to ear as his sx’s went away. It lasted for almost a week and he came back because he hurt his lower back. I treated his back pain and touched up his shoulder issue. He came limping in; full of sweat due to pain. He walked out and thanked me for my work.
    Again, I can’t explain the science. All I can tell you is that I have about 50 patients now that have responded well to this treatment including my wife, who is also a doctor. It is easy to scoff at something because it goes against what we are taught, especially yourself who is a trained pain doctor. It is not worth arguing a point with others who can’t or won’t open their. Rather, let them see it when they are hurt and need your help. This is the same experience I have when I use manual medicine and acupuncture in my Family Medicine clinic, my patients are skeptical, and walk away as believers. Here’s to hope.

  2. @ Tam, if you read the post carefully, you will see that I have deliberately refrained from commenting upon the efficacy of neural prolotherapy. Apart from anecdotal favourable reports such as yours, there is no evidence upon which to base an informed opinion. I applaud your intention to research the science behind the responses that you have obtained.

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Posted on January 8th, 2014 by Fred Wolfe

Evidence-based Medicine (EBM) and Fibromyalgia

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.



  1. In reply to Fred Wolfe’ s comment, your perspective on EBM is what one would expect in an ideal world. Unfortunately we don’t live in an ideal world and there are many “natural” treatments and cures available that are most likely just money making enterprises. There are also many physicians that treat their patient despite the lack of EBM for the patient’s illness. In decades past, patients with Chronic Fatigue Syndrome and Fibromyalgia have received little to no treatment for these illnesses, because doctors either thought “it was all in their head” or were at a loss of how to treat these patients. As a result many of these patients were mostly ignored by doctors. I attended a Grand Rounds one early morning to hear a physician speak about Fibromyalgia treatment. He spent the hour talking about how crazy these patients are and advising doctors to eliminate these patients from their office schedule, because they will exhaust and frustrate the doctor. My point is there is little evidence available regarding the treatment of these illnesses and Fibromyalgia has only recently been acknowledged as a legitimate illness. Many doctors still believe Fibromyalgia is “just depression”. These patients are desperate for effective treatment and a cure. So while these patients wait for EBM, should they continue to be ignored? Those physicians that attempt to treat patients when there is no EBM available are practicing the art of medicine. I admire those doctors that don’t abandon their patient in the midst of uncertainty. A doctor’s ongoing care provides a patient emotional support and hope, which are key components for a patient to heal. Those physicians that first “do no harm” and secondly stand by their patient have a great deal of courage.

    • @ Valda. I take your point but it should also be said that most if not all doctors do not have a coherent and plausible story to relate to those of their patients who have been awarded the diagnostic label of Fibromyalgia. This deficiency is compounded both by the lack of availability of reliable effective evidence-based treatment and the relatively short consultation time set aside for clinician/patient interaction. Many patients who have been subjected to ineffective and potentially harmful polypharmacy have voted with their feet. The current situation for these patients could be best described as grim.
      My hope is that rapid advances in the field of epigenetic research will give us tools to switch off stress-response genes that appear to be the major players in the perpetuation of widespread pain and the other clinical features of Fibromyalgia. Of course, I may be way off the mark.

      • I think you are right on the mark. I am currently dealing with the hazards of polypharmacy and undesirable drug interactions. I’m still waiting to here the verdict 3 weeks later. I am too hopeful that research catches up with the needs of fibromyalgia patients. Meanwhile, I’m going for quality of life and not quantity so I may shorten my life in the process, but at present I don’t see a better option for me. Unfortunately the advances for fibromyalgia treatment may not benefit me, but will benefit those that come after me.

    • I think your point is overstated when you write: “So while these patients wait for EBM, should they continue to be ignored? Those physicians that attempt to treat patients when there is no EBM available are practicing the art of medicine.”

      There are plenty of EBM rated treatment data. Please look at this report from Germany.

      It isn’t that there are good treatments just sitting there waiting for EBM, the problem is that (very) effective treatments are just not available. No one wants to prevent treatment or interfere with treatment discovery. The German Guidelines can tell you which treatments are not recommend based on EBM and make some recommendations as to what seems to be effective. So there is evidence. Physicians “.…practicing the art of medicine” should stay away from treatments that don’t work.

      My disagreement with the German guidelines is they do not consider the degree of effectiveness, only the presence or absence of any effectiveness. And they do not consider the duration of effectiveness. Warm water helps many symptoms, but it doesn’t help enough or last long enough.

      When physicians tell patients, “Here is something that might help,” we (all of us – we are all in this together) expect that that the treatment advised will not be harmful or impoverishing, and will be based on some reasonable evidence. And we want there to be a test: we will stop treatments that don’t work or work well enough.

  2. Quite a dilemma.

    Unfortunately quality evidence to feed into the evidence base does not come cheap, a particular issue in historically underfunded areas such as FMS and CFS. While we may bemoan the lack of effective treatments for both conditions we won’t even reach the stage of justifying the cost of an appropriately powered RCT while the current evidence base consists of small, piecemeal and unreplicated studies.

    Adequate research funding is an inescapable limitation on the quality of data on which to base clinical decisions. So, in the meantime, without clarity as to the underlying pathology of either condition and in the absence of evidence of effective treatments, what can be offered that is not based on opinion or anecdote?

    Treatment of ‘co-morbidities’ is standard practice which can much improve quality of life even if, in the context of the primary diagnosis, may be considered merely ‘palliative’. Recent research suggests that a substantial proportion of FMS patients have small fibre polyneuropathy while in CFS a similarly large proportion are shown to have autonomic dysfunction. I can’t guarantee that all of the studies are high quality in terms of sample size etc but the findings have been replicated.

    Neither condition is of course specific to either FMS or CFS but both can result in substantial morbidity and in the case of autonomic dysfunction, its presence may predict both increased morbidity and mortality. Both can be objectively diagnosed and may be amenable to treatment.

    So while we await quality evidence of etiology and effective treatments of FMS and CFS; would it not make sense to screen patients for these conditions (whether we consider them co-morbidities, perhaps intrinsic to the conditions or just plain misdiagosis) and treat then accordingly. I assume treatments of peripheral neuropathy and autonomic dysfunction are more likely to be evidence based?

    As a final point, I fear there may be a danger of conflating the use of RCTs (a methodology which is a useful tool to control for various biases as already discussed) with a ‘seal or approval’ or ‘quality guaranteed’ imprimatur for research. This may well be true when the methodology is used appropriately and analysis and reporting is of the same standard. But the use of a RCT methodology does not guarantee this nor does it guarantee that any research has any external validity.

    The use of a ‘gold standard’ methodology shouldn’t negate the need for critical appraisal.

  3. While I largely agreed with the value of EBM, I do think that it needs to be acknowlwdged that people dealing with trying to manage their symptoms are typically going to have go try, and often fail to respond, to many therapies before arriving at something that helps. These n=1 trials are necessary given the vauge diagnosis and wide varieties of presentations of what we call fibromyalgia. I read an interesting essay on the importance of failure today, that I think applies here:

    “We fail when we attempt something. This is enough to show the value of failure, as it equates with effort. To not try to do something so as to avoid failure is much worse, as it represents inertia or, worse, the paralyzing fear of failure. In the sciences and the arts, if you don’t fail you are not creating. Every poet, every painter, every scientist collects a much larger number of failures than successes. Unconvincing lines, unsatisfactory brushwork, wrong hypotheses. Without failure we can’t move forward.

    Success is failure’s progeny.”


    • @ Nancy. EBM also informs us about treatment that has been shown not to work. Yet people in pain willingly undergo such treatment! As an example, “dry needling” of muscles is extremely popular in both our countries and is carried out by keen physical therapists who believe that inflicting more pain upon their patients is not only scientifically justified but also good ethical practice. It seems almost impossible to convince these therapists otherwise! Perhaps someone should form a Society for the Prevention of Cruelty to Innocent Muscles!

      • John – I agree with you, but since the treatments that have EBM that suggest efficacy are often suggested and often fail the n=1, patients are left with a crapshoot approach of trying other things, or wallowing in a limbo of uncomfortable stasis. Neither option feels acceptable to many, so the crap shoot begins.

        • Nancy, I see no problem if people want to pay for treatment that has been shown not to work or is of dubious benefit. However, for them to expect a third party to reimburse them for payment is quite unreasonable. Why should quack treatment, even when performed by supposedly intelligent registered health professionals, be subsidized in such a manner? Those who run our systems of health care have to rely upon EBM in deciding where our health dollars are to be spent to obtain the best returns. The day of reckoning may not be that far away.

          • I agree with you when you say “However, for them to expect a third party to reimburse them for payment is quite unreasonable.” What I am trying to explain, perhaps not very well, is how difficult it is for people with the fibromyalgia diagnosis to find something that helps – to the point that they may continue to take an FDA approved drug, say Lyrica, beyond what would be a reasonable trial, only because EBM medicine is suggesting it SHOULD be working, and doctors having little else to offer them. I am not suggesting trying every fad or quack treatment until one sticks, or you go broke. I just don’t think the EBM in the case of fibromyalgia is very robust… Some degree of trial and error is the necessary result.

          • Nancy, EBM means the provision of a quality score and a measure of overall effectiveness; and it means sensible use of the data and of treatments. Lyrica has limited effectiveness. Beyond the limited effect in RCTs, two reasonably good observational studies show people stop taking the drug, and one shows no long term benefit.

            So, rather than concluding that EBM says take Lyrica, it suggests a weak effect that probably will not last as well as a low level of toleration. And it is expensive.

  4. Fred, I haven’t overstated that patients are ignored by the medical community. I am living evidence of that. I have been sick for 20 years and have only recently found doctors that would treat me. When I would tell a doctor that I was sick they would do a cardiac panel and check my cholesterol, which was fine by the way. Many fibromyalgia patients don’t know where to go to get help. I rest my case.

  5. @ Nancy. In relation to the pharmacological treatment of patients with Fibromyalgia Syndrome, there is evidence available that should inform both the prescriber and the consumer. The NNT (Number Needed to Treat) for Lyrica is 10, for Cymbalta it is 6.4 and for a combination of Tramadol and Paracetamol it is 6.2.

    This means that to achieve a pain reduction of 50% or more, compared to placebo, one would have to treat 10 patients with Lyrica before one patient would say it is a useful drug.

    The evidence for NNH – Number Needed to Harm – is also available for each of the aforementioned drugs.

    Unfortunately, there is widespread unawareness (amongst both clinicians and patients) of this readily available evidence-base. This is why we discuss these matters upfront in our various educational workshops held for people in pain.

  6. Fred and John- thank you! Points well taken. Too bad reality has not caught up. Pharma advertising is not reflecting the research – no surprise. Educating the consumer patient is a critical factor in moving forward. Glad to hear, John, about your educational efforts.

  7. Yes, but a very common tautology. I am not sure if funding is still available. There are many articles and books about the CAM initiative, including why it was undertaken and whether it was useful.

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Posted on January 5th, 2014 by Fred Wolfe

Mud baths. Again! Science marches 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]


  1. Hi! Of course mud baths relieved pain in fibromyalgia, which is related to the stiffness and associated pain from fibromyalgia. So does a hot bath, hot shower, hot tub and heating pad. It has nothing to do with mud. These are all temporary relief measures that the majority of fibromyalgia sufferers are aware of. The difficult for us all is sorting through the fog of false promised cures and the real treatments that actually provide benefit. There are many people benefitting from our misery! Thanks for a great post! Warmly, Valda

  2. This is indeed a bemusing research study! The proteonomics measurements are the cake on the icing. Huh? What was the hypothesis that connected mud baths, fibromyalgia and gene expression? Would love to interview these folks at a poster session – could be entertaining. Or very sad.

    But isn’t this evidence based medicine? They took an intervention (ahem) and measured outcomes, right? How is it any worse than Lyrica studies? Lyrica seems as ludicrous as mud baths, honestly. Calms pain signals is the claim, right? Maybe warm mud calms pain signals. (I am being facetious of course. )

    • Yes, it is EBM. And EBM suggests that it is low quality evidence. When I first went into practice many years ago I bought a “paraffin” bath to treat RA patients with, as had been recommended by authorities. It was fun to use and it smelled good. All of the staff would dip their hands into it on cold mornings. But it wasn’t any better than hot water. I never used it on real patients (couldn’t see charging them for it) and eventually gave it away to a patients who wanted a bath. But then, there are Spas, and mud baths are used in Europe. EBM suggests we that we evaluate therapies, including their costs.

      • Dear Fred. Funny about that. I also purchased a wax bath and eventually used it to lubricate my bicycle chain. Not sure if this was evidence-based but it sure worked well.

        In a more serious vein, is there any funding available to evaluate such therapies? In my brief search I noticed this extraordinary statement appearing in a fact sheet on the NIH – NCCAM (National centre for Complementary and Alternative Medicine) website: “Fibromyalgia is a disorder that causes muscle pain and fatigue.” Tautological? You bet.

        Anyway, the site does provide consumers with a wealth of up-to-date information on CAM.

      • It must have been the times. I also had a paraffin wax bath and I used to enjoy dipping my hands in the warm wax. Did it help? Well, my hands were very soft and it was fun to play with. I wonder if they are still out there? Seriously, how can it not help? Deep, penetrating warmth always makes my muscles feel better. Even though it’s a momentary fix, it brings back times where there was no pain and it’s welcomed.

  3. I find some interesting research as well. This, I can assure you, will be discussed as well as the latest scientific method in my writings. Did you know that there was also a study where drinking helped relieve symptoms of Fibromyalgia? Maybe I’m not so far away from the scientific process…..they’ll try anything to cure Fibromyalgia. @Nancy….don’t you love those Lyrica commercials? I especially like the side effects. This is sad…..we’ve come back to mud.

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Posted on January 5th, 2014 by Fred Wolfe

Ethical Treatment

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.









  1. I completely agree with you about interventions for chronic pain being, in the main, experiments.
    It’s the premise upon which good cognitive behavioural therapy is based – “let’s explore and test whether these hypotheses hold for you, in the context of your life”.
    This makes the clinical relationship collaborative rather than hierarchical, and allows the individual with pain to use outcomes he or she truly values. An excellent clinical tool in this endeavour is to use single subject case design where the individual becomes his or her own control (,,

    EBH also includes patient values, because ultimately it’s the person receiving the treatment who needs to make the decision about whether an intervention should be implemented or not. Sometimes this is forgotten by clinicians who are unaware of treatment options thus fail to let the patient know about them, or who have a single approach that is trotted out like a recipe for every person.

    My question is: why is it so difficult for doctors, in particular, to let people with chronic pain know that the likelihood is that their pain will persist? Why not give people the real situation so they can come to terms with it? The situation in chronic pain management is very similar to that in cancer so many years ago – let’s not tell the patient because it might be too much for them to hear. What if, by failing to let people know how poorly our treatments work on pain, we were actually prolonging disability and distress? How ethical is that?

  2. Hi! I am a retired RN and also believe strongly in EBM. I have found that the experience of fibromyalgia patients frequently leads to anecdotal observations that may then lead to well-designed research and therefore EBM. The multi-factoral fibromyalgia symptoms may be all related or components of the whole, but I do believe there is a place for these anecdotal observations. We can all hopefully learn from each other, but meanwhile the false promises of a cure will continue. Wherever there is money there is greed and manipulation. I also embarked on a journey through Integrative Medicine and other “holistic” treatments in an effort to prove I’m really sick. Fibromyalgia patients aren’t taken seriously unless they have tried everything and demonstrated that they have a real illness and it isn’t “just depression”. It’s a tough journey that isn’t for the faint of heart. Warmly, Valda

  3. Thank you, Dr. Wolfe, for writing about my experience and observation. In some respects the health care system has become depersonalized. I get pushed through pain management; the average time seen is 3 minutes (and yes, I timed it). I’m not trying to push doctors under the bus; they are pushed and have time limits and have to comply with corporate policy. Another problem is Fibromyalgia is big money and certain kinds of clinics will “ride the wave.” It’s a shame but until cause is discovered things like this will happen. What all of us try to do, whether it be from physicians and researchers or those of us who are bloggers/advocates, is educate and bring awareness. I hope you won’t limit comments again. No one would expect you to allow your blog to become frivolous but sometimes opinion can bring knowledge and sometimes opinion can expose those who would treat patients in their own best interest. Thank you once again for allowing all comments. It really does help.

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Posted on December 27th, 2013 by Fred Wolfe

“We are here to help each other to get through this thing, whatever it is.” –Mark Vonnegut (from abetternhs)

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: 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.


  1. @ Fred. The Scientific Paradigm has for far too long overshadowed The Interpretive Paradigm, much to the detriment of contemporary clinical practice in Rheumatology and Pain Medicine. The 10-minute consultation is ample evidence of this imbalance. By choosing to work exclusively in the former (Scientific) paradigm, we have indeed failed many of our patients. Can we heed the words of Vonnegut? What an extraordinary challenge lies before us!

  2. @ The Shambler. Surely you would agree that the placebo effect is not a foreign concept to the practitioner? In fact it pervades every regimen of treatment offered in the context of chronic pain.

    But in relation to The Guaifenesin Protocol that has been recommended for courageous patients with Fibromyalgia Syndrome, the words of the anonymous author of “A Dose for Quacks” (Punch, 1845) seem to be quite apt today: “Great outcry has been raised of late in the Lancet and other journals, against Quacks and Quackery. Let them not flatter themselves that it is possible to put either down. The Quack is a personage too essential to the comfort of a large class of society, to be deprived of his vocation. He is, in fact, the Physician of the Fools, – a body whose numbers and respectability are by far too great to admit of anything of the kind. We propose that every Quack should not only be suffered to call himself what he is not, but should be compelled to call himself what he is.”

    • I tried to set out some rules for posting and comments, and Shambler’s comments broke those rules. I apologize for the not knowing enough about blogs to have prevented all of such posts. But I think I may have got it right now.

      To repeat, “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.

      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.

      In addition, there is a basic level of science that we require. Posts that don’t meet that level will not be accepted or will be removed.

      • The sincerity of the post took my breath away and I keep reading it over and over again. Sometimes patients forget that frustration works both ways. Chronic pain has been turned over to pain management specialists who practice in much the same way. How do you treat the whole person in ten minutes? As much as Fibromyalgia patients tend not to be believed or believe that catastrophizing is involved how can the cycle be broken?

  3. @ Rosemary Lee. From what I have read in the “social media,” I think the cycle has been well and truly broken. Due to so many historical factors way beyond our control, it appears to me that the interface between physician and patient, the central arena for the development of trust, meaning and healing, is no longer at the forefront of clinical practice.

    Pain sufferers are demanding a “better deal” from their various health care system(s). Thankfully, Australia is slowly moving forward in this direction. Perhaps the USA could learn something us!

    Here are a few selected references that might be helpful in this respect:

    Quintner JL, Buchanan D, Cohen ML. Katz J, Williamson O. Pain medicine and its models: helping or hindering? Pain Medicine 2008; 9: 824-834.

    Davies SD, Quintner JL, Parsons RW et al. Pre-clinic group education sessions reduce waiting times and costs at public pain medicine units. Pain Medicine 2011; 12: 59-71.

    Davies SD, Hayes C, Quintner JL. System plasticity and integrated care: informed consumers guide clinical reorientation and system reorganization. Pain Medicine 2011; 12: 4-8.

    Lyon P, Cohen ML, Quintner JL. An evolutionary stress-response hypothesis for chronic widespread pain (Fibromyalgia Syndrome). Pain Medicine 2011; 12: 1167-1178.

    Cohen ML, Quintner JL, Buchanan D, Nielsen M, Guy L. Stigmatization of patients with chronic pain: the extinction of empathy. Pain Medicine 2011; 12: 1637-1643.

    Slater H, Briggs AM, Bunzli S, Davies SJ, Smith AJ, Quintner JL. Engaging consumers living in remote areas of Western Australia in the self-management of back pain: a prospective cohort study. BMC Musculoskeletal Disorders 2012, 13: 69.

    Slater H, Davies SJ, Parsons R, Quintner JL, Schug SA. A policy-into-practice intervention to increase the uptake of evidence-based management of low back pain in primary care: a prospective cohort study. PLoS ONE 2012; 7(5):e38037.doi.pone.0038037.

    Briggs AM, Slater H, Bunzli S, Jordan JE, Davies SJ, Quintner JL. Consumers’ experiences of back pain in rural Western Australia: access to information and services, and self-management behaviours. BMC Health Services Research 2012, 12:357 doi:10.1186/1472-6963-12-357.

    Slater H, Briggs AM, Smith AJ, Bunzli S, Davies SJ, Quintner JL. Implementing evidence-informed policy into practice for healthcare professionals managing people with low back pain in Australian rural settings: a preliminary prospective single cohort study. Pain Med 2014; (in press).

    • John, Let me be a little cynical. No, let me put it another way. Besides questionnaires about process, shouldn’t you measure outcome in terms of symptoms, work ability, system and personal costs. treatment and adverse effects? Why not in a controlled study?

      In the past, each decade has brought new insights and methods, but perhaps little change.

      Realistically, what sort of effect size should we expect from your programs [compared with controls]?

      • Fred, I agree with you. However, I have little doubt that our inter-disciplinary patient-centred approach has the potential to produce much better outcomes (however measured) for people in pain than has the purely biomedical reductionist approach that we previously relied upon. I may be wrong but, as I see it, our constituency has for quite valid reasons deserted us.

        PS as we speak, outcomes are being studied in a number of centres.

  4. From Tomlinson’s article on Empathy

    “One reason empathy can serve power is by standing in the way of understanding. This can have important implications for doctors and patients. Brene Brown, one of the most widely quoted researchers in the field of empathy, says that ‘staying out of judgement’ is one of the four qualities of empathy. Patients often complain about being judged by doctors, and teaching empathy to doctors seeks, in part to overcome this. But a lack of judgement is at odds with critical, analytical, skeptical or otherwise thoughtful ways of responding to what our patients tell us about their illnesses. The practice of medicine is especially demanding because we are expected to be empathetic and skeptical at the same time.”

    “It is also important to note that patients do not always want or need empathy so much as thorough professionalism.”

    “Empathy is not about judgement or sympathy – it is about non-judgmental acknowledgement that things may suck, and it is hard and complicated and not easily quantified or systematically approached. This is the crux of what, I think, patients with fibromyalgia struggle with among their family, friends and physicians. But it is a complex problem, as patients also want answers, to be able to systematically address their symptoms to make meaning our of what appears to have no meaning at times. Feelings, emotions, and yes, pain, seem to cry out (ahem) for meaning and purpose for their existence. Yes, often, acknowledgement of the lack of obvious meaning is perhaps a way past the confusion, a way forward. ”

    “People who live with chronic sorrow need accompaniment,” said Kaethe Weingarten. By this, she means that clients with chronic sorrow need someone to be with them as they discover how they will interact with the limitations of their minds and bodies. It means showing them the way to peace, teaching them how to tolerate the inconsistency of their lives with support, education, and even humor. It also means requires self-care so that the therapist can be aware of the client’s own boundaries while they take this journey with their client. Weingarten does not believe chronic sorrow can be fixed or healed. But she believes it can be lived with and she suggests compassionate witnessing and companionship as ways to do that.”

    Is There a Solution for Chronic Sorrow?

    I refer to the article on “chronic sorrow”, because I feel that patients with the label of fibromyalgia are perhaps dealing with similar concerns. Having an ambiguous diagnosis, filled with societal prejudice, and that can lead to an existential crisis from dealing with all the unknowns (and unknowable), and feeling like crap “for no reason” leads many to a kind of chronic sorrow. I can assure you – feeling like crap is not a “choice” and can’t be willed away. Accepted to a certain degree – perhaps. But I don’t believe that anyone chooses to have experiences we call fibromyalgia, despite physician inferences to the contrary.
    - Nancy

  5. I agree Nancy, no-one would choose to experience the fatigue and pain of fibromyalgia. Accepting that it is present, being aware of it but not defined by it, and having a reason for living has made it a part of me that I can acknowledge and work with. I’ve not experienced prejudice from health professionals, but I rarely seek help from anyone for FM. I have experienced societal pressure from time to time as I set limits on what I will and won’t do in my life. How different is that from what anyone else has to do, though? Parents have to set limits on what they can and cannot do because children absorb time and energy. Similarly with paid employment as it takes time away from other pursuits (watch those poor junior doctors try to work 60 hour weeks!).

    I’ve worked in a chronic pain management centre for many years. I no longer do so as I pursue my academic and research career – hoping to offer some guidance to those clinicians who will encounter people who have chronic pain, whether they “want” them, or not! People with FM and other chronic pain problems are throughout the health system – we also get tonsillitis, COPD, diabetes, cancer – but we’re at greater risk of poor pain management because people are less aware of our particular requirements.

    I do not believe that every person with chronic pain requires a clinical psychologist. Neither do I believe any particular form of therapist or clinician is more – or less – important in managing chronic pain. I hope that every clinician has the skills and attitude towards people with chronic pain that will enable an empathic approach.

    The current health system around the world fails to value face-to-face interactions as the critical element in a clinical endeavour. The only way this situation will change is if people with chronic pain, researchers, clinicians, teachers and the broader community make it clear that treating individuals as cogs or gidgets on a production line is ineffective. To me, this means researchers must begin to address the “active ingredients” involved in interpersonal relationships, to learn how to maximise its effects, help clinicians to refine and improve their skills, and explore how best these so-called “placebo” effects (meaning responses) can be used.

    PS, I truly, truly loathe the term “pain sufferer”. I have pain, but I don’t suffer. I experience pain, but it doesn’t represent a threat to my identity. Suffering is about loss of identity and personhood – let’s not label the experience of pain as necessarily equivalent to losing who a person really is.

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Posted on December 21st, 2013 by Fred Wolfe

From the Neuroskeptic blog


Neuroskeptic is an important blog. A recent post addresses the publication process in science. You can read it also to understand how bad research gets published. We reviewers (and writers) don’t really know what to do with bad studies. Almost every bad study can get published somewhere.

Fixing Science’s Chinese Wall

By Neuroskeptic | December 21, 2013 5:59 am

In science we very often want certain things to be true.

Sometimes, this desire comes from noble reasons: we want a vaccine to work, because that would save many lives. Other times our motivations are less altruistic: we want our vaccine to work because then we will get lots of citations, a promotion, and a raise.



Scientists wanting things to be true is a fact, and a problem. Which is why science has evolved methods to prevent our desires from distorting the findings. For example, we use double blind trials to ensure that the researcher’s preferences and expectations can’t influence the outcome measurements. We use statistical inference with an agreed standard (p = 0.05) to determine the significance of findings, rather than leaving it up to individuals to pick what they want to consider signal and what noise.

These systems are designed to protect observations from the whims of the observers. As Feynman famously said“Science is a way of trying not to fool yourself… and you are the easiest person to fool.” It is rather like how in business, banks and other firms are required to have a ‘Chinese Wall‘ – a cordon around certain information to ensure that it can’t reach certain people. This is intended to prevent conflicts of interest influencing those branches of the company whose job is to provide impartial advice to the public or other departments.

However, there is a gap in science’s Wall between data and desire – the publication process. Whether the results of a particular experiment get published in a peer-reviewed journal depends upon at least three people:

  • the researcher(s) themselves, who decides which results to submit, in what form
  • the journal editor(s), who decides whether submissions are ‘interesting’
  • the peer reviewer(s), who advises the editor on whether submissions are ‘good’

All of these people are scientists, with their own agenda and desires. They get to decide the fate of scientific results – knowing what those results are. So the desires of researchers get to influence what’s published, and the result is publication bias. This influence would be considered unscientific if it were allowed to happen within the conduct of a given experiment – but once the results are in, we allow it.

There is an alternative. Journals ought to peer review and accept articlesbefore the work has been begun (preregistration with pre-peer review.) This ensures that science is published or not on the basis of the strength and originality of the methods, independent of what the results happen to be.

This would do for the later stages of the scientific process what double-blinding and randomization have done for the earlier, experimental stages. The Chinese Wall would be complete.

One Comment

  1. It appears to me that journal editors also have a responsibility to ensure that the Editorials they solicit are written by authors who are honest and as free from bias as is possible. An uncritically written editorial published in a prestigious scientific journal can be quite damaging to the reputation of the researcher(s) and to the cause of scientific progress. Another chink in The Chinese Wall?

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Posted on December 16th, 2013 by Fred Wolfe

Some reading

Nancy Ryan pointed me to a couple of good articles that I’d like to recommend. The first is about medical evidence. It’s kind of complicated, but really detailed and good. I strongly recommend it if you have the stomach for some hard work. Find it at .

Another superb piece is a video on aspects of neuroscience by a leader in the field. It’s easier to understand and may to your insight about the issue. Try the first article and video here: .


  1. I have to plead guilty to not understanding your comment. I just don’t know what “The crude Odds Ratio for reporting p&f in the best quintile for amitriptyline, celecoxib and fluoxetine were 1.18, 1.28 and 1.21 respectively. Whereas those for FDA approved meds SNRIs/anti-convulsant avg 1.04″ means. Tell me where I can look up the information and I will do so.

    Given the small values, I suspect you are telling me that conventional treatment is of little use. If that is the case, I agree, and have written the same many times.

  2. Trigger is a difficult word. People sometimes use it when they want to “mean” cause but don’t want to say cause. For example, if trauma really causes FM, then trigger and cause are the same thing. But if trauma makes available the legal and disability system, then it isn’t a true cause. Don’t get me wrong, I am not saying that either of these interpretations is correct; I am merely trying to differentiate causes from events on the pathway to FM diagnosis. I prefer not to use the word trigger.

    I am writing a paper on trauma and FM right now. Because it is almost impossible to prove that trauma causes FM in an individual person, we usually rely on studies of many person for guidance. Most FM trauma studies are of poor quality. The best studies come from the UK. They show that automobile trauma but not other trauma has a slight association with the subsequent development of “widespread pain.” But if the analysis adjusts for psychological factors present before trauma, the effect of trauma disappears. That is, the weak effect of of trauma can not be demonstrated when the level of psychological factors are the same in those experiencing trauma and not experiencing trauma.

    Human events and human illness is rarely cause and effect. Instead there are usually multiple factors involved. In complex societies, the number of contributing factors is large. One is rarely able to to identify and measure all of the factors.

  3. Dear Manuel,

    Thanks for sending a copy or your letter. These observations are interesting, and I look forward to seeing where this all goes. What makes me dubious that this will turn out to be important is that is seems inconsistent with pre-diagnosis symptoms, with non neuropathic symptoms, and with the observation that FM is part of a continuum – in which case we should see evidence of this abnormality in non-criteria positive patients as well. I am also worried about sample selection and representative patients and controls. Replication and confirmation in different sample is required. But the authors (and you and your work) are of high quality. So I look forward to future developments.


  4. I have personally been the receipient of the genetically-susceptible defense. I was struck by a car going 35 mph. (I was at a complete stop and the driver failed to notice). It was a few years later that I was diagnosed with Fibromyalgia. This brings me to a couple of questions. First, there are theories out there that state trauma can be a trigger for Fibromyalgia. I have an opinion on this one but what is your feeling on this? It isn’t a blanket statement because quite a few people are involved in accidents that have worse injuries than I and don’t develop Fibromyalgia. I guess I ask the 64 thousand dollar question…..what is the trigger?

    I, too, believe that research has run amok. There are articles that point to just about everything causing Fibromyalgia, however, there seems to be too many changes in the central nervous system for researchers not to find evidence and conclude this is truly not in our heads. I believe that stress can cause a great deal but I think doctors take that a little too lightly and then give us the sage advice “to just calm down.” What is my doctor telling his patients right now? Basically, it’s all in management. His feeling is that it is more of a neurological problem and there are clinical subgroups. He told me to read the overview of the Canadian Consensus. (I don’t know that he tells all his patients to read that!)

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Posted on December 16th, 2013 by Fred Wolfe

Comments from people with fibromyalgia

I had hoped when starting this blog that it might have been possible to engage other physicians and researchers into an ongoing discussion of fibromyalgia. It is, after all, a controversial subject. But with one or two exceptions, we have been unable to get physicians and researchers to participate. Too bad.

More recently we have been receiving comments from people with fibromyalgia – those that doctors tend to call patients. In the original documentation for the blog we wrote that the blog would be only for researchers and those with academic credential. They idea was to have discussions among researchers. Since the blog started we have had thousands of spam posts; they are filtered out pretty well by a spam filer.  But we have often also had comments that came in from people with fibromyalgia, and from others. Although it was in the original plan, I have decided that we might try patients’ comments. Up to now they have been mostly blocked. But let me make a few rules based on the unpublished comments I have seen already.

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.


  1. First, I want to thank you for opening up to Fibromyalgia patients. I believe there is much we can learn from each other. Next, I understand your frustration. There should have been interest, promise and an opportunity to put your heads together to find a cause for this elusive syndrome. Unfortunately, Fibromyalgia patients encounter this attitude all the time. Quite a few doctors just don’t care. The ones that do and try to help are treasures.

    There is an article that is pointing once again to antivirals being used. This would lend itself to the belief that this syndrome is inflamation based. The test being developed would document high levels of pro-inflammatory cytokines. The article poses an interesting theory? Is pain inflammation gone haywire?

    • There is no research support for the idea that fibromyalgia is inflammation based. Cytokines are normal cell products that participate in inflammation and non-inflamation based settings. Preinflammatory is really a meaningless term in the context of fibromyalgia.

      An article “pointing to anti-virals being used” or a “test being developed” is not a scientific approach to fibromyalgia. If we want to talk about science we we must use the language and methods of science. For treatments we require randomized control trials; for proposed scientific idea we ask for rigorously documented peer-reviewed studies. Progress in fibromyalgia requires no less.

      It is not too difficult to teach oneself enough about science. But it does take some study. There is no conspiracy against new idea. Bu they need to be proposed and support using the methods of science.

      Fred Wolfe

      Fred Wolfe

  2. Fred, I have previously expressed my disappointment that too few of our colleagues have been prepared to contribute their views (and thoughtful comments) on the important issues that have been raised so far in Fibromyalgia Perplex. However, could it be that the “caravan” of rheumatology has not heeded the barking dogs and has moved on regardless? Is this a fair description of the “state of play” in North American rheumatology with regard to fibromyalgia?

    • John, I am very cynical about fibromyalgia research. Every day I get abstracts emailed to me from PubMed (Nation Library of Medicine). I am astounded how much that is published is repetitive non-information. I attribute much of this to the “Publish or Perish” mentality and the growing number of medical journals where almost anything can get accepted. For some doctors who have made a career of fibromyalgia its just publish and publish and publish again. There are so many problems that fibromyalgia patients have that one could almost publish forever, and without really saying much.

      I think that many FM experts don’t want to debate or be challenged.

      • Hello guys!! Sorry for the absence.

        Can we discuss the only consistent therapy that we have of FM, RSD/CRPS, and actually all chronic stubborn pain syndromes is actually a half century old and that is Myofascial Release therapy with hands-on and with dry/wet needling + Vitamins, minerals (magnesium) and trace elements + Mindfulness + Stress Management + Sleep Hygiene + Forgiveness + Self care home exercise program!! Works best when used in a set regular daily, weekly and monthly program.

  3. Thank you Dr. Wolfe for allowing comments. I understand your frustration. It’s disheartening to look around and find disinterest when so much good could be accomplished. I’ve been looking at recent research which is pointing toward using an antiviral…i.e. gamma globulin which would be appropriate if the diagnosis is actually small fiber neuropathy. I’m going to include the link and would be interested in your opinion. They also discuss proinflammatory cytokines. They think this could be the cause of Fibromyalgia. It seems to me that this is both ends of the spectrum…antivirals yet a CNS problem because of the high levels of proinflammatory cytokines.


    • John, I am very cynical about fibromyalgia research. Every day I get abstracts emailed to me from PubMed (Nation Library of Medicine). I am astounded how much that is published is repetitive non-information. I attribute much of this to the “Publish or Perish” mentality and the growing number of medical journals where almost anything can get accepted. For some doctors who have made a career of fibromyalgia its just publish and publish and publish again. There are so many problems that fibromyalgia patients have that one could almost publish forever, and without really saying much.

      I think that many FM experts don’t want to debate or be challenged.

    • See my comments above. The group that published the small fiber neuropathy article is well respected. But there are a number of objections to their theory, and more work is required to better understand it and fit it in to the total picture of fibromyalgia. Go to the follow-up letters to neuropathy article for additional comments. In my view, it would be malpractice to use an expensive, unproven therapy for a preliminary and confirmed hypothesis.

      • Dear Fred: There is no one, but two well respected groups of investigators that have recently shown that the majority of fibromyalgia patients have small fiber neuropathy. Here is a copy of my letter to the editor commenting the first publication. There is no doubt: fibromyalgia’s sensory neuropathy is a real as in other neuropathic pain syndromes. With my best wishes!!

        Small fibre neuropathy, fibromyalgia and dorsal root ganglia sodium channels.

        To the Editor:
        In their elegant study, Üçeyler et al, provide objective evidence of small fibre neuropathy (SFN) in patients with fibromyalgia (FM). They conclude that FM may be a neuropathic pain syndrome (Üçeyler et al 2013). SFN is a disorder of the peripheral nerves resulting in sensory changes and sympathetic dysfunction.

        For years, we have proposed that FM is a neuropathic pain syndrome based on the following 3 arguments: (1) FM is a stimulus-independent pain state. There is no structural damage that could explain the pain intensity. (2) The presence of allodynia as an essential feature of FM. (3) The presence of paresthesias as a distinctive feature of FM (Martinez-Lavin et al 2003). It seems difficult to ascribe an etiology other than neuropathic pain to a syndrome with such characteristics.
        Among neuropathic pain syndromes, we proposed that FM pain is sympathetically maintained based on the following three issues. (1) The high frequency of physical or psychological trauma as a triggering event. (2) Diverse heart rate variability studies showing the FM patients have changes consistent with ongoing sympathetic hyperactivity (Lerma et al 2011). (3) A double-blind study showing that norepinephrine injections rekindle FM pain (Martinez-Lavin et al 2002)

        Based on animal models of sympathetic pain, we focused our attention on dorsal root ganglia (DRG) as potential sympathetic-nociceptive short-circuit sites in cases of FM. DRG contain the sensory fibres cell bodies. Trauma and/or infection trigger sympathetic sprouting within DRG via nerve growth factor over-expression. Such aberrant neuroplasticity enables catecholamines and sympathetic traffic to induce sensory neuron firing. Sodium channels play a pivotal role in this hyperexcitability. A sodium channel isoform (NaV1.7) encoded in gene SCN9A of chromosome 2q24.3 is predominantly expressed in the DRG pain-sensing neurons and sympathetic ganglia neurons and their fine-diameter axons.
        In a pilot study, we described a particular SCN9A sodium channel gene variant (rs6754031 GG genotype) associated to severe FM (Vargas-Alarcon et al 2012). On the other hand, Faber et al reported that a gain of function mutations in sodium channel NaV1.7, which render dorsal root ganglion neurons hyperexcitable, are present in a substantial proportion (28.6%; 8 of 28) of patients meeting strict criteria for SFN (Faber et al. 2012). This preliminary information raises the possibility that some cases of FM and SFN may have underlying DRG sodium channelopathy.
        Üçeyler et al study reinforces our proposal of FM as sympathetically maintained neuropathic pain syndrome. Sympathetic dysfunction provides a coherent explanation for the multiple non-pain related FM symptoms (Martinez-Lavin 2012).
        Manuel Martinez-Lavin MD
        Chief, Rheumatology Department
        National Institute of Cardiology. Mexico.

        Faber CG, Hoeijmakers JG, Ahn HS, Cheng X, Han C, Choi JS, Estacion M, Lauria G, Vanhoutte EK, Gerrits MM, Dib-Hajj S, Drenth JP, Waxman SG, Merkies IS Gain of function Naν1.7 mutations in idiopathic small fiber neuropathy. Ann Neurol. 2012 ;71:26-39.
        Lerma C, Martinez A, Ruiz N, Vargas A, Infante O, Martinez-Lavin M Nocturnal heart rate variability parameters as potential fibromyalgia biomarker: correlation with symptoms severity. Arthritis Res Ther. 2011;13:R185
        Martinez-Lavin M, Vidal M, Barbosa RE, Pineda C, Casanova JM, Nava A Norepinephrine-evoked pain in fibromyalgia. A randomized pilot study [ISRCTN70707830]. BMC Musculoskelet Disord. 2002;3:2
        Martínez-Lavin M, López S, Medina M, Nava A.Use of the Leeds assessment of neuropathic symptoms and signs questionnaire in patients with fibromyalgia. Semin Arthritis Rheum. 2003 Jun;32(6):407-11.
        Martinez-Lavin M Fibromyalgia: When distress becomes (un)sympathetic pain. Pain Res Treat. 2012;2012: 981565
        Uçeyler N, Zeller D, Kahn AK, Kewenig S, Kittel-Schneider S, Schmid A, Casanova-Molla J, Reiners K, Sommer C. Small fibre pathology in patients with fibromyalgia syndrome. Brain. 2013 Mar 9. [Epub ahead of print]
        Vargas-Alarcon G, Alvarez-Leon E, Fragoso JM, Vargas A, Martinez A, Vallejo M, Martinez-Lavin M. A SCN9A gene-encoded dorsal root ganglia sodium channel polymorphism associated with severe fibromyalgia. BMC Musculoskelet Disord. 2012;13:23.

        • @ Dr Martinez-Lavin. Thank you for my drawing attention again to your intriguing hypothesis.

          Do you have any idea how the dorsal root ganglia might come to “know” when the organism (person) has been exposed to physical (including infection) and/or psychological trauma? In other words, what do you think is happening “upstream”?

          • Dear John: In the animal model, physical trauma induces sympathetic sprouting within the dorsal root ganglia via excessive nerve growth factor production. This sympathetic sprouting establishes shot-circuits between the sympathetic nervous system and the pain pathways. In such circumstances, sympathetic activity and/or norepinephrine induce pain. We propose that similar mechanisms operate in fibromyalgia. Lets remember that the cerebrospinal fluid of fibromyalgia patients contains high nerve growth factor levels.
            Additionally, dorsal root ganglia are infective agent sanctuaries. Herpes virus, borrelia and other agents may home in such immune-privilege places. Dorsal root ganglia clearly participate in post-herpetic neuralgia.
            To Fred: Many chronic conditions are a continuum. You don’t expect to have well established neuropathy in pre-diabetes.
            Kind regards.

          • Dear Manuel,

            To link neuropathy to FM, studies need to investigate 1) multiple unselected patients with fibromyalgia; 2) study other pain patients; 3) investigate neuropathy along the continuum of polysymptomatic distress (PSD) because every other manifestation of FM exists along that continuum. Unlike diabetes which is not symptomatic at the start, FM is defined by symptoms – symptoms that exist in a continuum. Should we expect sensory neuropathy in FM criteria negative widespread pain?. How about in those with 9 or 10 tender points? I believe a great deal of additional studies must be done to understand neuropathy and fibromyalgia. If,as many have shown, prediagnosis increase in somatic symptoms is present in those who later are diagnosed as FM, how can this fit in with the idea of neuropathy as a cause of FM? Could neuropathy be an effect of treatment, etc. Since one can see FM in 20-25% of those with rheumatoid arthritis, should we expect to find neuropathy there? I keep an open mind about FM, but I need a large number of well done studies to done to make what is going clearer.

        • @Dr Martinez-Lavin

          This recent abstract appears to bring the total to three as well as correlating reduced fibre density with reduced habituation of evoked potentials. Without access to the full paper I can’t tell if the findings of reduced fibre density fully met the clinical criteria for small fibre neuropathy :

          Update on laser-evoked potential findings in fibromyalgia patients in light of clinical and skin biopsy features.
          de Tommaso M, Nolano M, Iannone F, Vecchio E, Ricci K, Lorenzo M, Delussi M, Girolamo F, Lavolpe V, Provitera V, Stancanelli A, Lapadula G, Livrea P.
          J Neurol. 2013 Dec 24. [Epub ahead of print]

          Could I also ask if you’re aware of the work of Kathleen and Alan Light at the University of Utah, USA, examining the signalling of pain and fatigue (via the DRG) in FMS and CFS patients and in particular the importance of exercise challenge?

          This is a useful review that refers back to their previous findings :

          Review Article
          Genetics and Gene Expression Involving Stress and Distress Pathways in Fibromyalgia with and without Comorbid Chronic Fatigue Syndrome
          Kathleen C. Light, Andrea T. White, Scott Tadler, Eli Iacob, and Alan R. Light

          Pain Research and Treatment
          Volume 2012 (2012), Article ID 427869

  4. I’m a researcher, educator and a person with fibromyalgia – have had my head down writing my thesis this last year so haven’t had the head space to keep up with your blog. I think dialogue between all individuals with an interest in FM would be the very best thing we can get.
    I’m very comfortable with debating – but for me currently I think the main problem is poor understanding of chronic pain per se.
    FM is yet another of the elusive, complicated entities that we haven’t got our head around. Reading the literature I think it’s likely to be a disorder that has more than one subtype, more than one contributing factor, and more than one solution. Small fibre neuropathy may contribute to some forms of FM, but I doubt it’s the be-all and end-all for this enigmatic disorder.
    I’ve found that developing effective balance in life, maintaining good humour and having something I want to do has kept me going. No medications cut it for me, so I mainly put it to one side and don’t let it rule my life.
    Rest assured, as I finish my PhD, I’ll be entering the publish or perish cycle too – but hopefully because I have a greater emphasis on teaching, I’ll also be able to keep it real.

    • There are different “triggers” that flip the switch so why would the medications work for all? The approved medications never worked for me and I found the side effects worse than the pain…so why bother? I do think it’s interesting that Dr. Rice’s theory about the AV shunts, and the note that women tend to have more of the small fibers than men which is why more women get Fibromyalgia, an interesting path to follow. I still don’t think it is the cause. I think it is another trigger…just a lay persons opinion. Bonnie, I’ve always thought there were subtypes. It isn’t proven but it just makes sense. I agree Nancy….we are in this neverending loop. There seems to be a new hypothesis every day…Fibro is the new darling (or money maker) and it seems to be a free for all. I do think that Dr. Rice is making some advances though. I’ve been in contact and he genuinely wants to help and prove that Fibromyalgia is not a somatic disorder and is evidence based.

    • @ Bronnie. You are indeed in a privileged position to contribute to this blog! Do we know what story or stories rheumatologists and other clinicians are telling their patients these days? It would also be interesting to know what the academic rheumatologists are teaching their students about fibromyalgia. What is happening in your part of the world?

      • Let me get the ball rolling. There is a body of expert opinion suggesting that yet to be described pathology within muscle can both initiate and maintain central sensitisation (said to be one of the characteristics of FM). This conjecture is being passed off as fact. Here are some examples:

        “Myofascial pain syndrome can accompany other MTU injuries and is commonly seen in patients with regional pain syndrome, complex regional pain syndrome and FMS.” [Littlejohn, 2007]

        The author has invented his own pathology, “the injured muscle-tendon unit”:

        “… it is thought that trauma or injury to a component of the muscle-tendon unit (MTU) precedes regional pain syndrome in most cases.”

        In the absence of evidence to support the existence of “muscle-tendon unit trauma or injury”, these beliefs are highly conjectural. Nevertheless the author asserts, as if true, that nociceptive input therefrom is involved in the genesis of (regional) pain. Of course there is no evidence of this.

        Here is another quote from the same paper:

        “Myofascial pain syndrome results from pain generated by local areas of muscle and is identified clinically by the presence of exquisitely sensitive palpable thickening in a muscle belly, which causes both local and referred pain sequelae (sic) on stimulation.” [Littlejohn, 2007]

        Translated, this asserts that a “pain syndrome” is caused by local pain that can be identified by local sensibility that causes pain elsewhere. Circular argument?

        Another author [Staud, 2011] is guilty of the the same logical error of passing speculation off as fact:

        “… FM pain appears to depend on impulse input from deep tissues, particularly muscles. In genetically susceptible individuals, such tonic impulse input results in peripheral sensitisation as well as neuroplastic changes of the central nervous system (CNS), termed ‘central sensitisation’.”

        This claim, again couched in indicative rather than subjunctive language, is based on imagined pathological changes occurring within deep structures, such as muscle, which are held responsible both for local changes in nerve function (peripheral sensitisation) and changes in the central nervous system (central sensitisation).

        Finally, how about these statements as further examples of conjecture?

        “These associations suggest that FM can be mechanistically related to one or more focal pain conditions … a predominant localisation of FM pain (sic) in cervical or lumbar dermatomes reinforces this possibility …”. [Vierck, 2006]


        “Once the generalized sensitization of FM has developed from focal pain at any location, relatively minor trauma at another location is likely to generate a new focus of chronic pain.” [Vierck, 2006]

        My main reason in pointing out these logical errors of argument is the hope that intelligent readers will be much more critical of expert opinion that is being presented as established knowledge but which in fact is highly conjectural. By the way, I do not expect the various authors to thank me!


        Littlejohn G. Regional pain syndrome: clinical characteristics, mechanisms and management. Nat Clin Pract Rheumatol 2007; 3: 504-511.

        Staud R. Peripheral pain mechanisms in chronic widespread pain. Best Pract Res Clin Rheumatol 2011; 25: 155-164.

        Vierck CJ Jr. Mechanisms underlying development of spatially distributed chronic pain (fibromyalgia). Pain 2006; 124: 242–262.

        • John, Passing speculation off as fact underlies much of the writing about FM. My reading is that FM ideas contain a minority of truth and majority of speculation. I wonder if you have noted the idea of “genetically susceptible individuals.” It is particularly prominent in the in the trauma-causes-fibromyalgia literature where it provides defense against error. If trauma doesn’t cause fibromyalgia it is only because the person wasn’t “genetically susceptible.” It is an unfalsafiable idea.

          • Fred, it sounds to me like yet another logically flawed argument – post hoc ergo propter hoc.
            You would also have noticed that circular arguments abound in the FM literature.
            Here are a few examples:
            “…chronic FM results from a gradual progression to a chronic condition …” (p. 244). [Vierck, 2006]
            The author is arguing here that a specific condition (i.e. “chronic FM”) results from a progression to itself.
            “Due to the fact that pain is not only worsened by chronic stress but is also an important stressor in its own right, reductions in stress will likely have a positive effect on chronic pain and FM/CWP.” [Staud, 2011]
            Both pain and stress are reified by the author, who then argues in a circle – stress worsens pain which worsens stress etc.
            “MTPs cause pain and spasms in the muscle or muscle fibres.” [Staud, 2011]
            In this example, “myofascial trigger points” are reified as being causative agents (of themselves).
            “Fibromyalgia (FM) is the most common cause of chronic, widespread pain in the United States.” [Dadabhoy & Clauw [2008]
            Here fibromyalgia is synonymous with chronic widespread pain and is claimed to cause itself – this of course is a logical impossibility.

            It is little wonder that most of the FM experts have been loath to contribute to this forum.

            Additional reference:
            Dadabhoy D, Clauw DW. Musculoskeletal signs and symptoms. E. The Fibromyalgia Syndrome. In: Klippel JH, Crofford LJ, White PH, eds. Primer on the Rheumatic Diseases. New York: Springer, 2008: 87-93.

        • First congratulations to Dr Wolfe for establishing this site. Professionals networking within and outside their own field is key to rapid progress I believe.

          Thanks also for opening the site to patients. I hope I can qualify in this respect. I have a diagnosis of CFS (so I do fit in with the notion of ‘polysymptomatic distress’ as Simon Wessely would have it) but my ‘diagnosis’ was along the lines of DR “I think you have fibromyalgia” – ME “I don’t have the classic tender points” (sic – this was the 1990′s), DR “OK then – chronic fatigue syndrome it is”.

          Anyway – John expresses some concerns over the lack of mechanisms which might explain how a discrete peripheral ‘trauma’ might result in a complex multi-symptom syndrome and central sensitization.

          I’ve been doing a little informal research myself (of the review and hypothesis generation type naturally – I’m now medically retired) and have proposed a ‘neuroinflammatory model’ of CFS and ‘overlap syndromes’.

          My last ‘blog’ discussed the concept of spreading neuroinflammation in complex regional pain syndrome as a possible analogue model for CFS and FMS :

          Very interested in hearing what your thoughts!

          • @ Mark. Thanks for directing my attention to your hypothesis. I hope you will proceed to publish it in an appropriate journal so that it can be critically evaluated.

            In the meantime, could you please explain to me the difference between the concept of “neuroinflammation” and that of “neurogenic inflammation”? The latter has been well defined experimentally and seems to me to be the relevant pathophysiology in the condition known as complex regional pain syndrome.

          • Detailed and complex work. But I was always taught the key error in the flesh was in the muscles, Trigger Points fed by mineral deficiencies that lead to myofascial pain and dysfunction and all the rest of the cellular and sub-cellular immune and metabolic derangement.

            Further evidence is the fact that Myofascial Release Therapy with hands-on and with needles is highly effective at releaving pain and misery.

          • Science is in the mind of the beholder especially when profits are involved.

            The validity of a face to face encounter depends on the outcomes based on the results and relief the patients feel after therapy. The beauty of C. Gunn’s IMS therapy is that the patients walk out of the office with 10-30% improvement in pain and range of motion.

            The science I use in the office is try and see, sort of a heuristic like approach that mankind has used since we climbed out of trees. Vital method especially when traditional medicine has completely failed a lot of patients.

            What is your definition of science as it relates to day-to-day office based medicine?

          • @John Quintner

            Thanks John. If you’re referring to that particular blog then I can’t claim any credit. I was just summarising other published research that appeared to me to provide a viable model to bridge the gap between peripheral ‘stressors’ (of various types as have been associated with the onset of syndromes such as CFS and FMS) and the resulting complex multi-system symptoms that appear to be centrally mediated (mood, fatigue, chronic widespread and ‘disproportionate’ pain, cognitive and autonomic dysfunction etc). My own ‘original’ musings are contained in a series of previous blogs that I do hope to write up in a format that I could submit for publication. That’s a work in progress.

            Regarding the difference between neuroinflammation and neurogenic inflammation (as I understand it from limited reading on the subject) I’ll give it a go. Starting first with ‘neuroinflammation’ – the term now appears to be firmly established as describing a stereotypical process that occurs following trauma, infection etc most often in the context of the central nervous system. Chronic neuroinflammation has been proposed as an underlying pathology in a wide range of mood, neuropsychiatric and neurodegenerative conditions. There’s little sense in me trying to summarise the complex chain of events following glial priming and/or activation when others can do it better :

            Cytokines and Chemokines at the Crossroads of Neuroinflammation, Neurodegeneration, and Neuropathic Pain


            Perhaps its a difference in terminology only. From my perspective I would conceptualise the term neurogenic inflammation as relating primarily to the inflammatory processes following an initiating focal nerve injury resulting in the peripheral symptoms of CRPS while the dependant chronic CNS neuroinflammation resulting directly or indirectly from focal or systemic inflammation may explain the persistent of pain plus the numerous multi-systemic ‘co-morbidities’.

            You could speculate that there’s little reason to suspect that peripheral glial cells would respond differently to those in the brain and the two terms may be synonymous but I’m very happy to be told otherwise.

  5. If the hypothesis (or gut feeling) is that fibromyalgia is a functional disorder (pain without a cause) no amount of research like the one on small fiber neuropathy is ever going to convince them this could be the cause of fibromyalgia symptoms. Finding a cause negates the definition and it no longer is fibromyalgia. We are stuck in a loop where the hypothesis rules the definition.

    • @ Nancy. From the research literature we have a pretty good idea of possible “causes” but almost a total lack understanding of mechanisms. I would not equate the 19th-century term “functional disorder” with “pain without a cause.”

      Where the FM experts have hit a metaphorical brick wall is that they have not been able to transcend body/mind (substance) dualistic thinking. Tragically for those who have been awarded the FM label, such thinking remains rampant in our Western society.

      I know that I have said all this before but it does bear repeating, FM is going the way of neurasthenia which started life in the mid-19th century as a fashionable and acceptable functional disorder of the nervous system but it virtually disappeared in the first half of the 20th century as pseudo-psychological explanations for the symptomatology (i.e. pain, fatigue, cognitive disturbances, mood changes etc.) grew in popularity.

      • I have to disagree. The name given to a symptom set is just a name to help in the language of communication. That name has absolute nothing to do with the cause, treatment or the nuance of the disease itself.

        The errors in this conversation are what is science and what is medicine, they both involve a bit of human nature and insights. So any attempts at separating out the data as just data is erroneous. Both science and medicine are about knowledge, experimentation, experience, observation and our innate imagination.

  6. Unfortunately @John “pain without a cause” is used to imply the old “functional disorder” meme. It isn’t helpful. I agree we have hit a brick wall. The questions remains – how do we move forward to get out of the quagmire? What will best help people “awarded the diagnosis” as you like to say? Telling them there is nothing there and to just “get over it” is demoralizing and unhelpful. Clearly people are not feeling right. Like Bronnie says – meds are not the answer but putting it “to the side” is often quite difficult. Learning to adapt is crucial, yes, but people want to know the why – that is not unreasonable.

    • Dear Nancy. I agree with you, which is why we have offered our evolutionary stress-response hypothesis for chronic widespread pain (FM). Manuel has also provided us with a very detailed hypothesis. Both hypotheses are well grounded in biological science and, importantly, both are testable.

      We have emphasised the role of substance P, whereas Manuel’s group has zeroed in on nerve growth factor. In fact the former neurotrophin regulated the production of the latter, so we may not be far apart in our thinking.

      In my view, which is shared by others, that with which our patients are faced and we are trying to explain goes to the very heart of our humanness – our state of being as living organisms.

      I leave you with a quote from a very important paper: “Wherever the medical ways of thinking come up against a boundary, we must by way of uninhibitedness of thinking constantly address this, in a phenomenological sense, urgent matter.”

      Eriksen T et al. The medically unexplained revisited. Med Health Care and Philos DOI 10.1007/s11019-012-9436-2.

    • These guys are attempting to make us see a ghost, that they don’t even clearly see.

      Nancy the issue IMO is the denial of Travell et al trigger points in muscles. Because TPs are easy to deny because on one is trying to prove they entity exist. Something is the cause of all this pain and dysfunction.

      The truth is that if the TPs and the perpetuation factor surrounding this issue are addressed then healing is much more complete. Simple to my puny brain and common sense trumps data and statistics.

  7. Dear Fred
    I do not see that Manuel has invoked neuropathy as being a cause of FMS. He has provided an elegant explanation of this clinical and recently observed pathological phenomenon.
    As we know, there is no clear line of demarcation along the continuum of symptoms that you have defined as being those of “polysymptomatic distress”.
    Therefore making a diagnosis of FMS is an arbitrary decision of the clinician and even more so since we dispensed with the requirement of performing a tender point count. The tender point count for FMS (i.e. 11 or more of 18 possible tender points) never made any sense to me.
    In my opinion, the stress-response hypothesis does have considerable explanatory power and we are now gaining a better understanding of how these responses are regulated. Both neurotrophins (e.g. nerve growth factor) and substance P could well be important biomarkers of stress response system activation.

  8. 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, accupuncture, 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. @ Stephen, 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. While I have found tools that work for me on the fair days, on the “bad” days there isn’t much that I’ve found that brings relief. While I appreciate the doctors work to bring relief to those with Fibromyalgia, I don’t believe it can be a blanket “cure” for all those who are suffering with the pain and fatigue. Neuroinflammation? Sounds very interesting @Mark and thank you for the link to the article.

  9. My question to Stephen Rodrigues is: how much of life is a person giving up in order to find a life without pain? The constant pursuit of pain abolition can so easily interfere with the good things happening in life in the meanwhile.

    In my study of people who cope well with chronic pain (mixed diagnoses), people who recognised that pain will be present in the future, and began to accept this, also began to engage in life again and their mood/disability/distress reduced. This didn’t mean they stopped investigating pain reduction approaches from time to time and as new therapies emerged, but it did mean they invested less energy in the outcome – and importantly, although pain didn’t change, they felt they were “living well”.

    The key ingredients in learning to live well, taken from the data provided by participants in my study, were: knowing hurt doesn’t equal harm; having a label that allows conversations around the same set of symptoms to occur; hearing and accepting that pain is likely to continue; having important things to get on and do in life; and using a flexible set of coping strategies to persist with the important things in life.

    Irrespective of whether a cure for FM emerges or not, people who have FM (or have had it), will need these same ingredients. Most particularly, they need the motivation that propels them to use coping strategies to get on with life.

    In my experience, personally, clinically, and through research, using time and energy to find a cure is outweighed by the gains experienced by living life.

    • I agree that once patients realize that they are not going to die of a dreaded miserable painful death they begin to heal. One of my initial points I make to patients is for them to stop the pursuit of the answer and used that energy on themselves. By the time they get to me they would have spent a decade looking for the cause, hope and disappointment over and over until no hope at all.

      CBT, mindfulness, meditation, Kabat-Zinn, forgiveness, exercise etc all are a part of the protocol. I strongly suggest that they modify life work social family fun balance.

      For a lot just the mental is just a part of the illness and they need a lot of tissue work and the opposite is true. Without the needles and tissue work we are subjecting these poor souls to a life of pain.

      I’m here to expose all of my authors as they are the pioneers, safe and effective, labor intensive and time consuming. Some folks may need to be seen weekly for 4-5 months, some for a year and some I have been seeing for half a decade. So the key is to attack pain in the early stages and not pawn patients off on pills.

      • Stephen, it seems that with the assistance of stainless steel needles, you are pioneering what might be called “hole-istic” therapy. Have you ever considered adding Bach Flower remedies, colonic irrigation, reflexology, and moxibustion to your regimen? Evidence of their efficacy is at least as impressive as that in support of your “dry needling and tissue work” inflicted upon innocent muscles.

        • @Quintner, I am not the pioneer, I’m the curious student who discovered an alternate path in search of techniques to help my patients. Most who had failed traditional medicine based in the scientific methods devoid of grace for the sake of profits or fame. Only by serendipity did I stumble upon the textbooks, which in my opinion, were intentionally hidden from view under blankets of deceptions and disdain.

          It has taken a lot of time to deconstruct all of my thought patterns set in by 15 years of traditional medicine. I wanted to find what was making my patients feel better. The farther away I got from all my logical scientific paradigms, there it was under my nose.

          It’s about the metallic needle and the muscle performing microsurgery! Simple pure and true, the beauty of which will be true forever. Some open minded young curious scientist will pin down the details. Oh my friend the devil is in the muscles, whether it is a microbe, a DNA error, combo metabolic/cellular disagreement or cellular defect, it’s there with 100% certainty.

          My job now it to promote this key which will unlock a lot of soul suffering under the present regime of ideology and dogma.

          The hole’listic is a good one! Thanks I’ve been collecting them for a longtime. “Try Acupuncture, it won’t hurt a bit”

          For corrections, aromatherapy, reflexology, CBT, yoga, sauna and heat therapy, music therapy, jogging, brushing are all part of a recipe of therapies. Moxi is a way of adding heat energy into the microsurgery, I don’t used anymore due to time constraints and hassles. Colonic flushing, I have not experienced and do not recommend as of today. The treatment package will removing the crap that has accumulated from this crazy world and allow the body to heal. This package is a gift from our creator. So if you have a beef with it, talk to Him.

    • @bronnie,

      You make good points, however when the pain becomes extremely disabling and forcing a person to be nonfunctional, the quest relieve the pain becomes Paramont. In my opinion, Sorting out the amount of function decrease and the amount of functional disabling that the pain has caused would be a useful factor in choosing subjects for chronic pain studies. So much of the published and recommended information on chronic pain is totally useless to somebody in extreme pain. In that case, There is no way to “get on with your life”.

  10. @Stephen Rodrigues: Given the wealth of evidence supporting lifestyle modification, mindfulness, CBT etc I wonder if they might be the active ingredients in your wholistic therapies, as opposed to any needling or other hands-on therapies?
    If, as you suggest, “the devil is in the muscles”, how do you account for central processing changes?
    And if your approaches are effective, why not subject them to scientific study? Abandoning scientific reasoning reduces your thoughts to anecdote – and the plural of anecdote is not evidence.

    • I don’t think scientific study is what everyone thinks it is!
      via wiki: The scientific method seeks to explain the events of nature in a reproducible way.[54]

      So the basic premise of the method is try and see, you throw a ball up in comes down.
      You cut yourself with a knife and it heals.
      You massage a tense tight muscle and it feels better.
      You insert a fine wire into a tense tight muscle and it relaxes.
      You insert a fine wire into a muscle and you create a hole or wound in the muscle and this wound seals off to quickly heal leaving no visible scar.

      If you repeatedly insert a wire into muscles and the patient states, that feels better than before and that is better than taking a pill or feels better than even the back surgery did, that is evidence. Collect all these cases and you have a positive pattern. Use this pattern in the community and you have a procedure that is safe and effective to promote or the well-being of all.

      All the data, research and evidence has been collected and validated. The proper questions are “why do we ignore all this information?” or “why are we so obsessed with finding out the exact molecular-chemical evidence when people need help now with a therapy that is safe and effective.”

      IMO, there can only be a few reasons why we are in this quagmire;
      The discovery team is looking for fame.
      Our present system is trying to save face, because if this data gets out the populace will be furious and start to sue.
      The economy is dependent on these miserable souls to use as cash cows, to perform unnecessary surgeries, use is drug experiments, justify further research and development etc. and to support a burgeoning market of supplements and probiotics and fake cures.

  11. I wouldn’t suggest using wikipedia as an authoritative reference!
    This one might be more helpful: a method of procedure that has characterized natural science since the 17th century, consisting in systematic observation, measurement, and experiment, and the formulation, testing, and modification of hypotheses: criticism is the backbone of the scientific method (
    Interestingly, it’s the systematic part that seems to provoke so much angst – systematic alludes to the need for removing or controlling for extraneous variables.
    “If you repeatedly insert a wire into muscles and the patient states, that feels better than before and that is better than taking a pill or feels better than even the back surgery did, that is evidence. Collect all these cases and you have a positive pattern. Use this pattern in the community and you have a procedure that is safe and effective to promote or the well-being of all.” – how do you control for these variables in your description of method? Could it be that “operator variables”, or interpersonal skill and the expectation a person holds for a treatment to be effective that makes the difference between feeling better or not feeling better? Could this be carried out with less interference with everyday life and greater sense of self-efficacy for the individual experiencing pain without needing a needle, or any other hands-on intervention?
    I argue, naturally, that this is the case, and put to you that self-management approaches offer this – but only once the person with pain has been unequivocally advised that pain is most likely to persist no matter what interventions are offered. One of the most tragic things I see in clinical practice are people who hold onto the notion that their pain CAN be cured completely if only they find “the right treatment” (or combination of treatments) – meanwhile their lives fall apart, relationships are soured, they lose opportunities for work, their self esteem reduces and they put incredible amounts of money into ongoing treatments that offer hope, but actually deliver prolonged suffering. Suffering being defined as “threat to loss of self-identity”.
    To my mind, holding onto hope that “life can return to normal” for years because some clinician has suggested that repeat passive modalities will ultimately abolish pain, is about the worst kind of situation for any person to be in. Life doesn’t return to “normal” after many years – it becomes something else. And in the interim, the individual has missed out on being the father he wants to be, the kind of partner she wants to be, enjoying sport and recreation and all the rich things (including grief about losses than ultimately enables letting go and filling life with other good things) that life is. That’s tragic, and I have seen it far too often.

    I don’t think the practitioners are always deliberately at fault – they genuinely believe that what they’re doing is a good thing. Unfortunately, like blood-letting and trepanation, belief doesn’t mean it’s actually effective.

  12. I think I asked this question, and wonder if you could answer it: “how do you control for these variables in your description of method? Could it be that “operator variables”, or interpersonal skill and the expectation a person holds for a treatment to be effective that makes the difference between feeling better or not feeling better? Could this be carried out with less interference with everyday life and greater sense of self-efficacy for the individual experiencing pain without needing a needle, or any other hands-on intervention?”

    Unless you clone yourself, if the active agents involved in treatment are not examined using scientific method, no-one else can do what you do because the component parts are not understood. This means an awful lot of patients for you to see.

    The distinction between bloodletting and trepanation of old and what is carried out today is in appropriate patient selection – I think the same should apply to treatments for people who have pain.

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Posted on September 30th, 2013 by Fred Wolfe


I practiced medicine long enough to have been wrong many times—wrong about diagnosis, wrong about treatment, and wrong about prognosis. But it is not just me alone, being wrong and not knowing goes along with being a doctor. Patients, on the other hand, want certainty. Why does it hurt here? What’s the cause? Could it be a, b or c? How long will it last? Should I have surgery? What will happen? My local newspaper publishes ads from different kinds of practitioners, local hospital and doctors, about new medicines and treatments. How come they all know what often seems not clear to me?

I have grown old enough to have to go to doctors these days. They are all kind and polite to me, but I know that they often don’t know the answers to my questions. Young resident physicians who get to talk and examine me as part of their medical training offer advice. If I do this I say (tongue-in cheek), will I live longer? How much longer? How do you know? How do you know? What’s the evidence?

Recently someone sent a comment to FM Perplex complaining that many doctors didn’t know the correct diagnosis, and the doctors gave the wrong treatments. Doctors, she said, didn’t try to find out the right treatments. They weren’t interested.

Sometimes is just is not clear what the cause of the (let’s say) musculoskeletal pain is. People will get different answers depending upon what kind of practitioner he sees: orthopedist, osteopath, family doctor, chiropractor, physical therapist, nutritionalist, rheumatologist, physiatrist, and on and on. The success of most of these specialists who have such divergent ideas is related to the fact that most people get better regardless of what we do (or what we call it). Back pain almost always goes away. But in the minds of many, the last treatment was the one that worked. The treatment that you received when your pain went away was the one that worked.

I collect and study data for my research, and I also ask about physician and patients beliefs. Some of my doctors believe drug A is really good and almost always works. For some, though, it is drug B—drug A just never works. You get the idea—people have false beliefs. Sometimes false beliefs come to doctors because patients who don’t get better change doctors while those who improve stay with them. If you only see your successes … well you see the problem.

With respect to treatment, the most important scientific advance has been the randomized placebo controlled trial (RCT). Such trials can tell us what testimonials can never tell us: whether a drug or other treatment works and how well it works. If studies are done correctly, we can be pretty sure about treatments. Practitioners who use treatments that are not supported by strong evidence are not practicing scientific medicine, and remember I said strong evidence. Some practitioners have posted comments here about non-mainstream treatments. They’ve seen it work. How can we doubt them? But remember, problems get better on their own, even some problems that have been around for a long time. Be wary of diagnoses. One mans impingement syndrome is another’s cervical syndrome (or … whatever). The science of medicine has ways of determining which diagnosis is reliable [the extent to which doctors agree].

How much one believes in a diagnosis or treatment has nothing to do with the effectiveness of the treatment. Those of us who spend time trying to tell people about effectiveness do not do so to impugn treatments, but to spread knowledge. Most doctors want to use the right treatment, but often it isn’t clear what the right treatment is or whether there is a right treatment. Better by far a physician who understand his or her limitations, and often doesn’t know, than a quack or charlatan or con man who supports, with religious certainty, treatments for which there is little to no scientific evidence.


  1. @ Fred. In a recent paper, Rosenmann and Nasti (2012) warn us that “… diagnoses neither predict the phenomena and outcomes seen in clinical practice nor relate well to contradictory research findings. In particular, diagnoses rarely seem to explain the patient’s problem … the diagnosis can be understood only as it is used within the context of activities that give it meaning. The term is understood by looking at the activities of the profession that uses it, NOT by reference to an object or specific mental process.”

    Their wise words seem particularly relevant to our discourse on Fibromyalgia.

    Rosenmann S, J. Psychiatric diagnoses are not mental processes: Wittgenstein on conceptual confusion. Aust NZ J Psychiatry 2012; 46: 1046-1052.

    • John, I agree. The type of diagnosis problems in psychiatric illnesses and fibromyalgia are similar. In my post I was addressing a comment sent to us from a patient who said several doctors told her she had a cervical syndrome, but the doctor who told her she had a shoulder impingement syndrome was able to help her. He, she said, had the diagnosis right. People, of course, get better sometimes regardless if the diagnosis is correct.

  2. I understand that this comment will never be published but it will be moderated. You wondered why patients want certainty. You also stated that you had grown old enough to visit doctors. The two are not mutually exclusive. There is a reason that patients with Fibromyalgia want certainty. After being shuffled off from physician to physician who are not interested in discourse, I finally found one who was interested enough to get to the bottom of the symptoms and spent time actually speaking to me and had a belief that “it may not be perfect but we will try to get you feeling better.” That, Dr. Wolfe, is all most people want. They want communication and a person who is sincerely interested in them. It’s kind of like this blog. I understand that you don’t want the general public blocking up the comment channel so you don’t allow them to comment. If they aren’t published, you won’t allow the comment. There it is. All people want is intelligent communication and not general disinterest.

  3. Rosemary Lee ( sent in a comment about the above post. One of the things she said was this: “There is a reason that patients with Fibromyalgia want certainty. After being shuffled off from physician to physician who are not interested in discourse, I finally found one who was interested enough to get to the bottom of the symptoms and spent time actually speaking to me and had a belief that “it may not be perfect but we will try to get you feeling better.” That, Dr. Wolfe, is all most people want. They want communication and a person who is sincerely interested in them.”

    I agree with that completely. That kind of interest and care is what everyone should get. It’s given best I think in the atmosphere of some uncertainty “ …. we call it fibromyalgia … there is a lot we don’t know about it, but here is how we can help.” The enemy is certainty, saying that it is a, b or c, and that it should be treated with x, y and z.” Pandering is the enemy of interest, understanding, empathy and decency.

  4. @ Fred. Unfortunately those who administer systems of personal injury compensation and income support demand certainty in medical diagnosis. Herein lies a dilemma for the honest and caring physician.

  5. I would argue that the symptoms themselves are evidence enough that something has gone awry. That should suffice. Judgment that implies lack of the probable cause is just that – a judgement. And this kind of judgment is demeaning and not helpful. Back to the mental vs physical dichotomy that doesn’t have useful utility when it comes to pain syndromes. “Pain has an element of blank…”

  6. Great post, thank you. “In the minds of many, the last treatment was the one that worked. The treatment that you received when your pain went away was the one that worked.” Yes! And how seductive for clinicians, to be given credit for a cure! And for patients to believe that “it couldn’t have been a coincidence.”

    This is The Timing Problem: it’s not just that the pain went away, but that it finally went away right after a novel treatment. To the patient, this cannot possibly be a coincidence, and most will fiercely reject that explanation. But it’s the mental equivalent of a paper finger trap: you’ll never get out of it if you keep pulling in the same direction. People will spend their whole lives stuck scoffing at coincidence as an explanation for their recovery, never looking deeper, because they are not wrong. The timing was probably not a coincidence … but not because the treatment worked. It is usually due to the non-specific alchemy of the therapeutic encounter — just the right story or stimulus gives a nice helpful boost to an inevitable recovery, creating the powerful illusion: “Well, that finally did the trick!” But this is not as easy to understand or as comfortable to believe in. And as every magician knows, the most effective illusion is not the one that is the most difficult to see through — it’s the one that nobody even tries to see through in the first place.

    • Nancy, no doubt Paul will respond. Why would such people feel the need to look for other explanations? There is a large literature on the subject of placebo effect, expectation bias, confirmation bias, the fallacy of post hoc ergo propter hoc, and regression to the mean.

      As Rosemary Lee noted, people with the label Fibromyalgia crave certainty – both in diagnosis and treatment. I cannot blame them for this.

      But there are many health care practitioners who are prepared to give their customers whatever they want. Hence the proliferation of today’s equivalent of the “snake oil salesman”. They tote their wares under such fancy names as Trigger Point therapy, Neural Prolotherapy and Cranio-Sacral Therapy, plying their trade to gullible and desperate pain sufferers who flock to their doors or tents, as the case may be.

      There is usually at least a modicum of science being used to bolster their claims but it is far outweighed by their speculative and outlandish sales pitch. This is not a new problem for Medicine as evidenced by what was known as the Herbalists or Quack’s Charter (1542) in the days of England’s King Henry VIII. The King found it necessary to protect “unauthorized practitioners” from the wrath of the dominant physicians. Over the centuries, such a demarcation has become somewhat blurred. But that is another story.

  7. Thank you Fred. But then I think what Paul means is they shouldn’t be “looking deeper”, but rather they should “stop looking.” And that I agree with. And perhaps that is what he meant. Problems often resolve with time, not intervention. I have had my share of encounters of the kind which this post and your comment is referring to. One in particular is frustrating, as I enjoyed the initial “treatment” of basic palliative massage therapy but had to drop the massage when they insisted on me trying a wacky supplement and I got tired of repeatedly saying no thanks – not interested! I honesty think they believed the snake oil “works”, which makes it all the more disappointing and frustrating. And sad for other patients naive and vulnerable to the sales pitches and claims. They want to believe that someone cares and wants to assist in proactively precipitating a change. Sad state of affairs. But even good doctors are complicit. Seasoned veterans like myself and others I know are wising up to the state of fibromyalgia treatment I am happy to report. But trying to educate the newbies is a delicate and tricky business. There is a fine line between hope for better days and acceptance that things may be as “good as it gets” and to leave “well enough” alone.

  8. When I was young, I had some strange, vague health problems. Eventually I seemed to be cured by a treatment — that is, my symptoms finally went away in the aftermath of a specific intervention. I settled for the obvious theory that the treatment had worked. For many years I gave alternative medicine credit for my cure and rejected the idea that the timing of my recovery was any kind of a coincidence. It was not a coincidence, but there was no specific treatment effect either. What originally impressed me as powerful kind of medicine — energy medicine — eventually looked much more like a fascinating social and psychosomatic phenomenon, a particularly robust placebo effect. For many years I resented and resisted that kind of explanation because my recovery “couldn’t have been a coincidence,“ but eventually I came to find it much more satisfying and complete understanding. Meanwhile, the idea that I had gotten a chi repair started to seem rather shallow and quaint!

        • Paul, what a coincidence! We are just about ready to submit a comprehensive critical review paper on this very topic. It will be titled – “The nerve of those trigger points”. The paper is a follow up to our 1994 paper, which I see you have referenced. Nothing has changed since then. You will not therefore be surprised by our conclusion (which is still in draft form):

          ‘The theory of “myofascial pain caused by trigger points” has been exposed as conjecture on both logical and scientific grounds. The proclamation on which the theory is based constitutes the fallacy of a circular argument, in which the conclusion is assumed before the evidence is put. Both “trigger points” and the “vicious cycles” that maintain them are inventions with high face validity but little scientific basis, whether from experimental (interrogating the suspect tissue itself) or empirical (assessing the outcome of treatments predicated on presumed pathology) approaches.’

  9. That’s great, John. I look forward to reading it (and citing it). Thanks for the sneak preview.

    I arrived quite late to the skeptical party about trigger points. I remember how fascinating it was for me to discover that you had been so rigorously critical of the energy crisis hypothesis … at least three years before I had even heard of a trigger point. I probably didn’t experience my first flickers of intellectual uncertainty on the topic until about a decade ago, and even then my doubts simmered for years more before amounting to much. But things are moving along now. And this blog has been a valuable part of the process. I haven’t commented much, but I’ve been reading!

  10. This is months late, but I would like to pose a clinical question to John, Fred, Paul, and others. As a PT, this is a scenario that arises somewhat frequently. When a patient talks about “knots” and needing them “worked out”, how do you provide science-based education to help them?

    It’s a challenge for me clinically to be clear and concise in lay-terms and would love to hear your opinions.

  11. John, thank you for the reply. I’d like to ask for further clarification. Is that your opinion because the patient’s belief is that hands-on treatment is needed to diminish his pain? Or is it your opinion that manual therapy is of benefit regardless of belief?

  12. Thanks John. This is something that has been coming up a lot in PT circles as of late. The latest fashion is to “leverage patient expectations”, as performing the treatment for someone who expects it to make them feel better often times feels better (via contextual effects). I for one am not a big fan of that treatment when it reinforces erroneous beliefs (my spine’s out of place and causing my pain and needs adjustment, i have knots in my upper back that cause my pain and need to be worked out, etc.). Even though it’s low hanging fruit for a clinician, rarely do i treat that way. I don’t see a way around it but to educate and promote exercise, self-efficacy, neuroscience education, etc. Sometimes I feel as though I am fighting a losing battle, however.

  13. Wyatt, I am aware of the gradual erosion by quality research studies of many of the cherished belief systems that have for so long underpinned our therapeutic endeavours in the area of musculoskeletal medicine. Yes, it can be a losing battle because if you do not give your patients what they want, your colleague down the road will be happy to do so. There are also those pseudo-scientific fringe dwellers (who now come under the rubric of CAM) who will be quite happy to ply their wares to gullible patients. Maintaining your professional integrity is the most important tactic to employ in this unequal battle.

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