That is not fibromyalgia which alters when it alteration finds—or is it?

In work that is slowly ambling through the review and publication practice, we show that fibromyalgia is over-diagnosed in women and under diagnosed in men, at least based on post ACR 2010 criteria; and psychosocial symptoms influence physicians more than pain. Selection and confirmation bias permeate the process. And most people diagnosed with fibromyalgia don’t satisfy criteria. In a study in a university rheumatology clinic (manuscript submitted) the agreement between staff rheumatologists (Surely, experts, right?) and published criteria was fair, at best.

While it is easy to mock definitions and diagnostic criteria, perhaps the real meaning of such data is to indicate that fibromyalgia as it occurs in the community is strongly influenced by the needs of physicians, researchers, patients and pharmaceutical companies, and that such influence is part of the de facto definition of fibromyalgia.  Oliver Sacks wrote in another setting, but appropriate to fibromyalgia, “I had not properly realized, until this time, the power of wish to distort and deny – and its prevalence in this complex situation, where the enthusiasm of doctors, and the distress of patients, might lie in unconscious collusion, equally concerned to wish away an unpalatable truth.”

Fibromyalgia? O, no! it is an not ever-fixed mark.  If this be error, and upon me prov’d, I never writ, nor no man ever lov’d.

Fibromyalgianess, polysymptomatic distress or what?

A recent FM Perplex commentator wrote, “Fibromyalgianess sounds ridiculous.” As the inventor or father of the term, I couldn’t agree more. But here’s how it all came about. The 2010 “American College of Rheumatology Preliminary Diagnostic Criteria for Fibromyalgia and Measurement of Symptom Severity” [1] proposed two variables for the diagnosis of fibromyalgia. One counted the number of painful regions a patient had (0-19) and was called the widespread pain index (WPI). The other was a score that came from combining individual scores for fatigue, unrefreshed sleep, cognitive problems and the degree of symptom reporting. That sub-scale was called the somatic symptom scale (SSS). When the WPI and SSS scales were simply summed, the result was a single (0-31) scale. The scale, which we will call the polysymptomatic distress PSD scale for now, had some astounding properties. It predicted all (bad) fibromyalgia outcomes. The greater the PSD score the more abnormal … anything you want … work disability, obesity, income, global severity, pain, quality of life, post-operative pain, and so on [2].

One interesting thing about the scale, it didn’t observe the boundaries of fibromyalgia diagnosis. In practice, we observed that the scale ranged from no symptoms to a very high score. And the scale was comprised of the key fibromyalgia symptoms. This scale, by the way, when plotted against outcomes, provided evidence that there was no simple fibromyalgia: yes or no. Instead, one should and could think of fibromyalgia simply as an artificial point on a fibromyalgia symptom scale.

In our first attempt, we called the scale the “Fibromyalgia Symptom” (FS) scale [3]. That didn’t seem to carry the full impact of the scale because the scale wasn’t just about symptoms, it was about those symptoms that were most characteristic of fibromyalgia and fibromyalgia diagnosis. It was a measure of the essence of fibromyalgia. But because the scale was an effective measure of fibromyalgia qualities in those who did, didn’t or didn’t quite meet fibromyalgia criteria, using the term “Fibromyalgia Scale” destroyed its usefulness as a general measure. So what should we call it. My first attempt was to use the term fibromyalgianess [4], which perhaps characterizes the scale pretty accurately while at the same time being a “ridiculous term,” and one that would hardly be accepted outside the pain/fibromyalgia community. I suggested a replacement term, the polysymptomatic distress (PSD) scale. And thereupon came about an ongoing and contentious argument between Dan Clauw and me. The term, polysymptomatic distress, came from the writings of the Oxford psychiatrist, Simon Wessely [5]. For whatever fibromyalgia is, it is many symptoms in many different areas.

Clauw hated the term PSD. He told me that distress meant mental symptoms, and that fibromyalgia was a pain disorder not a psychosocial disorder (back to the central pain hypothesis)—a narrow view, I thought, and I had a different view of fibromyalgia. So, when we write, Clauw uses “fibromyalgianess” or fibromyalgia symptom scale. I use the term, PSD, and I can’t think of a better term. Even those who don’t believe in fibromyalgia can use and understand PSD. Still, I have some affection for my wayward child, fibromyalgianess.


  1. Wolfe F, Clauw D, Fitzcharles MA, Goldenberg D, Katz RS, Mease P, et al. The American College of Rheumatology Preliminary Diagnostic Criteria for Fibromyalgia and Measurement of Symptom Severity. Arthritis Care Res. 2010;62(5):600-10.
  2. Wolfe F, Michaud K. Outcome and predictor relationships in fibromyalgia and rheumatoid arthritis: evidence concerning the continuum versus discrete disorder hypothesis. J Rheumatol. 2009;36(4):831-6.
  3. Wolfe F, Clauw D, Fitzcharles MA, Goldenberg D, Häuser W, Katz RS, et al. Fibromyalgia Criteria and Severity Scales for Clinical and Epidemiological Studies: A Modification of the ACR Preliminary Diagnostic Criteria for Fibromyalgia. J Rheumatol. 2011;38:1113-22.
  4. Wolfe F. Fibromyalgianess. Arthritis Rheum. 2009;61(6):715-6. Epub 2009/05/30. doi: 10.1002/art.24553. PubMed PMID: 19479689.
  5. Wessely S, Hotopf M. Is fibromyalgia a distinct clinical entity? Historical and epidemiological evidence. Baillieres BestPractResClinRheumatol. 1999;13(3):427-36. PubMed PMID: 39980.



In his seminal book Propaganda (1928) Edward Bernays [1891-1995] observed:

“The conscious intelligent manipulation of the organized opinions and habits of the masses is an important element in a democratic society. Those who manipulate this unseen mechanism of society constitute an invisible government which is the ruling power in our society.”

As this article will show, his words still ring true in the field of Rheumatology. That which commenced as conjecture on fibromyalgia has been repeatedly embellished to a stage where it has assumed the status of established knowledge or truth.

“Central sensitivity syndromes”

In 2007, Dr Muhammad Yunus from Illinois noted that a number of diverse medically controversial conditions, such as fibromyalgia, irritable bowel syndrome, tension-type headaches and chronic fatigue syndrome, had several clinical features in common. He attributed these features to “hyperexcitement of the central neurons”, which in turn led him to propose the “concept of central sensitivity syndromes (CSS)” [Yunus 2007].

A closer examination of this proposition reveals two assertions: firstly, central sensitisation (CS) of nociception was taken as the model from which a generalisation to “central sensitisation” was made; secondly it was stated that the biology of CSS is “based on neuroendocrine aberrations (including CS) that interact with psychosocial factors to cause a number of symptoms”. How these undefined biochemical aberrations within the body “interact” with such extra-corporeal “factors” was never clarified.

This concept of “central sensitivity syndromes” should be seen as a bold proposition that there may be a common pathogenesis for the symptom clusters (technically not syndromes) under consideration. Although at that time “evidence for CS is not present in all patients of the CSS family”, the proposition was plausible and indeed the author stated explicitly, “The concept of CSS seems viable”. This can be seen as an example of a conjecture being raised to the status of a truth simply because if it were true so much that is currently not understood may become so [Lipton, 2005]. But is it true?

“Centralized pain”

Rheumatologist Dr Dan Clauw and his colleagues at the University of Michigan not only championed the cause of CSS around the world, but also have gone much further than Yunus by introducing the concept of “centralized” pain. In their paper with a tantalizing title – “maybe it (pain) is all in their head” – Phillips and Clauw [2011] likened “augmented pain transmission” and “sensory amplification” to the volume control on a radio dial. They suggested that individuals might have different “volume control settings” on “their pain and central processing”. This is an attractive metaphor, perhaps, but one that suggests lack of understanding of contemporary concepts of nociception and pain.

They followed up this paper by defining their concept of “centralized” pain [Phillips & Clauw, 2013]:

For clarity, we will use terms such as central augmentation or amplification to refer more broadly to central mechanisms that enhance perception or modulation of pain differentially between individuals. We will use the term “centralization” of pain to refer to a common process that seems to occur to a vulnerable subset of individuals with any chronic pain state, wherein pain primarily due to peripheral nociceptive input is subsequently amplified by central factors, such that both peripheral and central factors are then contributing to the perception of pain by an individual.

In this assertion, note the language: “centralization of pain … seems to occur … with any chronic pain state…” and “… pain primarily due to peripheral nociceptive input is … amplified by central factors, such that both peripheral and central factors … [contribute] to … pain”? Did they not notice the tautology inherent in these statements? Is not the experience of pain itself the “perception”, not a thing that is “perceived”? And is not “perception” an emergent function of the brain? “Modulation” of nociception may be analogous to a volume control; “amplification” of the experience of pain is not quite so linear.

The paragraph quoted above could be restated simply as, “Any chronic pain state is a function of the brain and may be influenced by many factors”.

But just how is pain to be “centralized” – and who or what does the “centralizing”? Apparently “centralized” pain can be identified “when multifocal pain occurs in conjunction with other centrally mediated symptoms, such as fatigue, insomnia, memory difficulties, and mood disturbances.” Such individuals are then said to “have centralized their pain” [Phillips and Clauw, 2013].

This implies that polysymptomatic distress in association with (multifocal) pain defines that pain as “centralized”. This diagnostic methodology could be termed “guilt by association”, which is a recognised logical fallacy.

Clauw [2014] then proclaimed: 

“Fibromyalgia can be thought of as a centralized pain state. Centralized pain is a lifelong disorder beginning in adolescence or young adulthood manifested by pain experienced in different body regions at different times. “Centralized” refers to central nervous system origins of or amplification of pain. This term does not imply that peripheral nociceptive input (i.e. damage or inflammation of body regions) is not contributing to these individuals’ pain but rather that they feel more pain than would normally be expected based on the degree of nociceptive input.”

How is it known that this is a “lifelong disorder”? How can it be determined that any one feels “more pain than normally would be expected …”? How would an observer be able to determine this [Cronje & Williamson 2006]?

A “white paper” [Arnold et al. 2016] then appeared in which fibromyalgia was said to exemplify “centralized” pain and to result from “persistent neuronal dysfunction” (See their Fig 1). Here is their argument:

“Aberrant neurochemical processing of sensory signals in the CNS may lower the threshold of pain, amplify normal sensory signals, and alter gene expression, thereby leading to hypersensitivity and central sensitization that result in chronic pain” [Arnold et al. 2016].

In this context, what is the “threshold of pain”? And how might “alter[ed] gene expression” lead to “hypersensitivity”. Of what and to what do “hypersensitivity and central sensitization” refer?

Returning to his dial-on-the-radio metaphor, Clauw [2015] asserted, “the pathophysiological hallmark is a sensitized or hyperactive central nervous system that leads to an increased volume control or gain on pain and sensory processing.”

Translated, that statement can be written as, “Increased CNS activity leads to increased pain and sensory processing”, which is a circular and tautological conjecture.

FM as a brain disorder/disease

According to Sluka and Clauw [2016], the overlapping conditions drawn together as CSS by Yunus [2007] are in fact manifestations of an underlying brain disorder with “similar underlying pathology with alterations in central nervous system function leading to augmented nociceptive processing and the development of central nervous system (CNS)-mediated somatic symptoms of fatigue, sleep, memory and mood difficulties.”

Translated, that statement can be written as, “Central sensitisation syndromes are characterised by the development of CNS-mediated symptoms attributable to altered brain function”. Or, to put it another way, a cluster of “CNS-mediated symptoms” allows the inference of a brain disorder called “central sensitisation”. This is yet another circular and self-fulfilling argument.

Further research

In 2017 the National Institute of Health awarded Michigan Medical School researchers, Drs Chad Brummett and Dan Clauw, funding of US $7.5 million to expand their work on the metaphor of the radio dial.

As Dr Clauw explained:

“For those with fibromyalgia, it’s like the brain turns up the volume control on pain processing. The high volume is often the underlying problem, more than damage or inflammation in the region of the body that hurts.”

In terms of contemporary neuroscientific knowledge of brain function, this comment makes no sense. Our brains are much more complex than are radio transmitters or receivers.


There may be validity in the proposition that the phenomenon of central sensitisation of nociception could be relevant to the pain experienced by patients who have been labeled with “fibromyalgia”. That is a theory from which testable hypotheses might be generated. Such an approach stands in marked contrast to statements such as “the brain turns up the volume of pain processing”, as if pain is a “thing” that can be “processed” including being “centralized”, or that “neuroendocrine aberrations interact with psychosocial factors” without outlining the biochemical basis of psychosocial factors, or that “chronic pain [is] caused by alterations in sensory processing in the CNS” which is equivalent to saying that the central nervous system is integral to the experience of chronic pain.

These and other statements should be seen for what they are: conjectures that appear plausible until it is recognised that their content is not amenable to hypothesis testing and thus are incapable of leading to the truth.

‘But the facts don’t exactly matter: people repeat them so often that you believe them. Welcome to the “illusory truth effect,” which is a glitch in the human psyche that equates repetition with truth [Dreyfuss 2017]’.

Such an effect is all too evident in this discourse where the main agenda is to promote fibromyalgia as a brain disease.

John Quintner & Milton Cohen


Arnold LM, Choy E, Clauw DJ, et al. Fibromyalgia and chronic pain syndromes: a white paper detailing current challenges in the field. Clin J Pain 2016; 32(9): 737-746.

Clauw DJ. Fibromyalgia: a clinical review. JAMA 2014; 311(15): 1547-1555. Clauw DJ. Fibromyalgia and related disorders. Mayo Clin Proc 2015; 90(5): 680-692.

Cronje RJ, Williamson OD. Is pain ever “normal”? Clin J Pain 2006; 22: 692–699

Dreyfuss E. “Want to make a lie seem true? Say it again. And again. And again.” WIRED 11 February 2017. Link:

Lipton P. The Medawar Lecture 2004: The truth about science. Philos Trans R Soc Lond B Biol Sci 2005; 360: 1259–69.

Phillips K, Clauw DJ. Central pain mechanisms in chronic pain states – maybe it is all in their head. Best Pract Res Clin Rheumatol 2011; 25(2): 141-154.

Phillips K, Clauw DJ. Central pain mechanisms in rheumatic diseases: future directions. Arthritis Rheum 2013; 65(2): 291-302.

Sluka KA, Clauw DJ. Neurobiology of fibromyalgia and chronic widespread pain. Neuroscience 2016; 338: 114-129.

Yunus M. Fibromyalgia and overlapping disorders: the unifying concept of central sensitivity syndromes. Semin Arthritis Rheum 2007; 36(6):339-356.


Samuel Hahnemann was the originator of homeopathy, a system of medical treatment devised under the principle summed up by the phrase, “like is cured by like” [Hahnemann 1796]. Drugs which when given to healthy persons cause certain specific symptoms are to be given to patients when they present to their doctors with the very same symptoms.

Hahnemann argued that only infinitesimally small doses were needed because the disease produced an abnormal sensitiveness to the given drug, provided that the correct remedy had been chosen. Another principle was that a second dose should not be given until the first had ceased to act.

When homeopathy was introduced it became popular in the 19th century and probably served a useful purpose in checking the dangerously excessive drugging, bloodletting, purging, and induced vomiting that were then prevalent [Guthrie 1945; Ackerknecht, 1968].

The dogmatism of Hahnemann’s system separated it from the mainstream of scientific development [Ackerknecht, 1968] but its survival as a cult with a relatively small following suggests that it may still, at least partially, fulfill this role [Relton et al. 2017].

The technique of “dry needling” so-called myofascial trigger points (MTrPs) [Simons et al. 1999] became popular with physical therapists during the 1990s and has remained so to this day [Dunning et al. 2014].

Remarkably, the practice is based upon the same principle as that devised by Hahnemann – “like is cured by like”.

In this case the “disease” being treated is “myofascial pain” localised to a trigger point (TrP) within voluntary muscle or other soft tissues. Those who believe that this is true postulate the existence of a lesion caused by “direct trauma or overuse” [Martín-Pintado-Zugasti et al. 2018].

The recommended therapy for such pain is to insert a needle directly into the muscle where the TrP is thought to reside. However, post-injection pain is not uncommon and is caused by “tissue injury produced by the needle and the following inflammatory reaction” [Martín-Pintado-Zugasti et al. 2018]. Animal experimental studies have been confirmatory of such an injury [Domingo et al. 2013].

Some experts consider that benefit from the technique of needling can be attributed to the destruction of the allegedly dysfunctional motor endplates producing the MTrPs as well as the related sarcomere shortening of myocytes [Dommerholt et al. 2006].

Martín-Pintado-Zugasti et al. [2018] claim that post-injection pain is “fundamentally different from the pathophysiology of the MTrP itself”. They base this opinion solely on the way in which some patients describe that pain as being different to their original pain. They did not consider the possibility that the original pain might have been wrongly attributed to the MTrP and that the tissue being needled did not in fact harbour a source of nociception [Quintner et al. 2015].

The number of needle insertions and the pain perceived during needling is positively correlated with the intensity of post-needling soreness in healthy subjects [Martín-Pintado-Zugasti et al. 2015]. This observation suggests that there is a direct relationship between the amount of tissue damage caused by the needle and the intensity of post-needling soreness.

Lewitt [1979] mentioned that a “reactivation of pain may occur several hours later or on the following day” and that this usually lasts for 1-2 days. Simons et al. [1999] recommended waiting until the soreness had resolved before repeating the procedure.

There has even been a suggestion that soreness following dry needling might be seen as a “positive sign rather than a negative experience that requires special care” [Dommerholt et al. 2015]

The conclusion seems inescapable that an actual lesion is being created in muscle through dry needling in a futile attempt to heal a muscular lesion that has never been shown to exist.

In other words, Hahnemann’s homeopathic principle lives on, but in another guise as a cultish practice that today lies well outside the mainstream theory and practice of scientific medicine.


Ackerknecht EH. A Short History of Medicine. New York: The Ronald Press Company, 1968: 145.

Domingo A, Mayoral O, Monterde S, Santafé MM. Neuromuscular damage and repair after dry needling in mice. Evidence-Based Complementary and Alternative Medicine Volume 2013, Article ID 260806, 10 pages

Dommerholt J, Mayoral del Moral O, Gröbli C. Trigger point dry needling. The Journal of Manual & Manipulative Therapy. 2006; 14(4): 70–87.

Dommerholt J, Hook T, Grieve R, Layton M. A critical overview of the current myofascial pain literature – July 2015 Journal of Bodywork & Movement Therapies 2015; 19: 482-493.

Dunning J, Butts R, Mourad F, et al. Dry needling: a literature review with implications for clinical practice. Phys Ther Rev 2014; 19(4): 252-265.

Guthrie D. A History of Medicine. London: Thomas Nelson and Sons Ltd., 1945: 219-220.

Hahnemann S. Versuch über ein neues Prinzip zur Auffindung der Heilkräfte der Arzneissubstanzer nebst einigen Blicken auf die bisherigen. Journ pract Arzneykinde 1796; 2(3): 433.

Lewitt K. The needle effect in the relief of myofascial pain. Pain 1979; 6: 83-90.

Martín-Pintado-Zugasti A, Pecos-Martín D, Rodríguez-Fernández AL, et al. Ischemic compression after dry needling of a latent myofascial trigger point reduces post-needling soreness intensity and duration. PM R. 2015; 7: 1026-1034.

Martín-Pintado-Zugasti A, Mayoral del Moral O, Gerwin RD, Fernández-Carnero J. Postneedling soreness after myofascial trigger point dry needling: current status and future research. Journal of Bodywork & Movement Therapies 2018, doi: 10.1016/j.jbmt.2018.01.003.

Quintner J, Bove G, Cohen M. A critical evaluation of the “trigger point” phenomenon. Rheumatology 2015; 54: 392-399.

Relton C, Cooper K, Viksveen P, et al. Prevalence of homeopathy use by the general population worldwide: a systematic review. Homeopathy 2017;106(2):69-78. doi: 10.1016/j.homp.2017.03.002. Epub 2017 Apr 7.

Simons DG, Travell JG, Simons LS. Myofascial Pain and Dysfunction. The Trigger Point Manual, Vol 1. 2nd ed. Baltimore: Williams & Wilkins; 1999.





Behold the Mighty Trigger Point

Some clinicians are still endeavoring to prove that myofascial pain is a distinct localised clinical entity attributable to “trigger points” (TrPs) within muscles if not also other soft tissues.

There are others who continue to propose that the pain of FMS (fibromyalgia syndrome) “is largely composed of pain arising, at least partially, from TrPs” [Fernández-de-Las-Penãs & Arendt-Nielsen 2016].

It might seem therefore that MPS and FMS are two sides of the TrP coin, the label used depending on which side the coin lands. If only those TrPs could be treated!

Recently Kumbhare et al. [2017] reviewed the very limited literature that in their opinion justifies the use of ultrasound-guided injection techniques in the treatment of patients in whom “trigger points” are thought to be the cause of their pain. Have they found the ultimate solution?

The significant problems that bedevil this article quickly become evident from an analysis of the opening sentences:

Myofascial pain syndrome (MPS) is a common regional musculoskeletal pain syndrome that can cause local or referred pain.   In other words, a pain syndrome is said to cause itself, which is of course a logical impossibility!

The authors then appear to accept the existence of pathophysiological entities for which there is no evidence: It [MPS] is characterized by myofascial trigger points (MTrPs), which are hard, palpable discrete localized nodules located within taut bands of skeletal muscle and can be painful on compression. However, such nodules have never been objectively demonstrated – histologically, ultrastructurally, biochemically or electrically. So how can it be known that they are the primary cause of musculoskeletal pain?

To be fair, the authors do point out that diagnosis is difficult, not least because palpation is unreliable and there are no accepted standardized clinical criteria for the diagnosis of MTrPs. Yet Khumbare et al. [2017] advise clinicians to rely on palpation to detect taut bands in muscle prior to applying the ultrasound probe to these regions. To find what? Some studies report finding hypoechoic regions, whereas others report the regions of interest to be hyperechoic. Elsewhere in the article the authors favour the former possibility but provide no reason for this choice.

So, what is the “gold standard” for the identification of a phantom? And if, as the authors concede, there are no data on inter-rater reliability when using ultrasonography and no consensus within the literature on what can be identified, how can they logically – let alone ethically – recommend injection therapy?

The only valid conclusion that can be drawn from this article is that the authors are locked into a bogus construct about which they are hopelessly confused [Quintner & Cohen 2015; Quintner et al. 2015].


John Quintner, Milton Cohen, Asaf Weisman.



Fernández-de-Las-Penãs C, Arendt-Nielsen L. Myofascial pain and fibromyalgia: two different but overlapping disorders. Pain Manag 2016; 6: 401-408.

Kumbhare D, Singh D, Rathbone A, et al. Ultrasound-guided interventional procedures: myofascial trigger points with structured literature review. Reg Anesth Pain Med 2017; 42: 407-412.

Quintner JL, Cohen ML. Myofascial pain: a bogus construct. In: Hutson M, Ward A, eds. Oxford Textbook of Musculoskeletal Medicine, 2nd ed. 2015: 132-142.

Quintner J, Bove G, Cohen M. A critical evaluation of the “trigger point” phenomenon. Rheumatology 2015; 54: 392-399.







Some clinicians have suggested that myofascial trigger points (MTrPs) might be responsible for the widespread pain that characterises fibromyalgia [2,4], thus conflating two controversial constructs, one of which has been refuted [5,6].

Because the nature of the trigger point (TrP) has been a controversial issue for many years, notwithstanding its refutation, any attempt to formulate a generally accepted definition would attract interest.

The Delphi study

A Delphi study is one method of arriving at a consensus in a systematic interactive way. The process aims to determine the extent to which experts agree about a given issue and in areas where they disagree, to achieve a consensus opinion.

Fernández-de-las-Peñas and Dommerholt [3] conducted a Delphi study amongst 60 international MPS/TrP experts who were selected on the basis of what they considered was “established knowledge,” their “familiarity with MPS and TrPs” and “their ability to influence policy related to MPS (myofascial pain syndrome).”

The authors presumed that the participants were equivalent in knowledge and experience [1]. But this important assumption was never tested.

The questions put to the Delphi panel were formulated following a comprehensive review of the MPS/TrP literature, but obviously excluding that which refuted the construct. They were introduced over three rounds.

The first round

Participants were asked to rate the relative importance (as either “essential” or “confirmatory”) of four symptoms and four palpatory findings considered to be indicative of the “trigger point” phenomenon. Responses by 70% or more participants to each question were then made available and evaluated by the panel.

The second round had three elements

From the list generated in the first round, participants were invited to select three answers that might enable them to identify “active” and “latent” TrPs.

  • They were also asked whether they believe a relationship existed between “active” TrPs and clinical pain (one would have thought that this would be axiomatic).
  • Members were invited to briefly summarize their beliefs on the differences between “active” and “latent” TrPs.
  • Lastly, they addressed the question as to whether they believed TrPs were located in particular anatomical regions, as had been originally proclaimed by Travell and Simons in their Trigger Point Manual [7].

The third round

The sole topic for discussion in the final round was whether referred pain can be considered an essential criterion for the diagnosis of “active” or “latent “TrPs.


Consensus was reached on a cluster of three criteria necessary for identification of a TrP: (i) a taut band in a muscle; (ii) a hypersensitive spot, and (iii) referred pain.

TrP diagnosis required that at least 2 of 3 of these criteria were present. Remarkably, a finding of local tenderness was not considered necessary for the diagnosis of a TrP.

A taut band in muscle was required for the diagnosis of both the “latent” and “active” TrP. Whereas the “latent” TrP exhibited a hypersensitive spot, there was no agreement that this was a necessary requirement for an “active” TrP. However, it was also remarkable that the majority of the experts agreed that palpating “the spot” reproduced the patient’s symptoms.

Pain was considered by most experts to be “referred” whenever it spread to a distant area or was described as a dull ache.

There was no agreement that the anatomical locations of TrPs coincided with the specific locations mapped (and marked with an X) as set out in the Trigger Point Manual [7]. Furthermore, the majority of experts did not support the idea of a distinct referred pain pattern from TrPs present in any given muscle.


Clearly, their lack of agreement on the important questions suggests either that the members of the Delphi panel did not all possess the same level of knowledge and experience, or that the questions put to them highlighted a state of conceptual confusion amongst those who were “inside the tent”.

In the Introduction to their paper, Fernández-de-las-Peñas and Dommerholt [3] confidently asserted that MPS is characterized by the presence of MTrPs.

However, in the light of the Delphi study, they conceded that “The conceptual association between MPS and TrPs has been questioned” and “We do not currently know if MPS is due only to TrPs, or if MPS is an independent pain condition.”

Given that the detection of TrPs had to date been a sine qua non for MPS, should an examiner not be able to detect their presence, how can that examiner be expected to make a diagnosis of MPS? The authors have (again) demonstrated that their construct is a mirage.


This study can only be seen as a desperate attempt by its devotees to stave off the inevitable conclusion that the MPS/TrP conjectures made so long ago by the late Drs Travell and Simons [7] can now once and for all be consigned to the dustbin of medical history.


  1. Altschuld JW, Thomas PM Considerations in the application of a modified scree test for Delphi survey data. Evaluation Review 1991; 15 (2): 179-188.
  1. Fernández-de-Las-Peñas C, Arendt-Nielsen L. Myofascial pain and fibromyalgia: two different but overlapping disorders.Pain Manag 2016; 6(4): 401-408. doi: 10.2217/pmt-2016-0013
  1. Fernández-de-las-Peñas C, and Dommerholt J. International Consensus on Diagnostic Criteria and Clinical Considerations of Myofascial Trigger Points: A Delphi Study. Pain Medicine 2017 (in press). doi: 10.1093/pm/pnx207
  1. Liptan GL. Fascia: a missing link in our understanding of the pathology of fibromyalgia. J Bodywork Mov Ther 2010; 14: 3-12.
  1. Quintner JL, Cohen ML. Referred pain of peripheral neural origin: an alternative to the “Myofascial Pain” construct. Clin J Pain 1994; 10: 243-251.
  1. Quintner JL, Bove GM, and Cohen ML. A critical evaluation of the trigger point phenomenon. Rheumatology (Oxford) 2015; 54: 392-399.
  1. Travell JG, Simons DG. Myofascial Pain and Dysfunction: the Trigger Point Manual. Williams and Wilkins: Baltimore, 1983.


Has Your Fascia Freaked Out?

The belief that painful lesions exist within the muscle and/or fascia of those with fibromyalgia remains a popular one, despite the absence of any supporting pathophysiological evidence. But, to be entirely fair, the very name of the condition suggests that such an association might indeed exist.

However, the upshot of this incorrect belief is that people with fibromyalgia are being confronted by a bewildering array of therapies, products and appliances targeted at their muscles and/or fascia.

One of the most remarkable therapeutic devices currently being advertised and marketed to them is a white plastic clawed implement known as the FasciaBlaster.

The sales pitch correctly points out that fibromyalgia is “the second most common symptom ailment that affects the muscular (sic) skeletal system next to osteoarthritis” and that people with the condition often either have to change their job or leave the workforce.

Then follows an astounding revelation: “fibromyalgia is NOT a biological abnormality in the nervous system or a physicological (sic) disorder– it’s something that is caused throughout life that triggers a TOTAL FASCIA FREAK OUT!”

But evidently there are 7 phases of this “fascia freak out” and those who are in phases 3 to 7 have real cause for concern and require treatment, which fortunately can be self-administered should they choose to purchase the said implement.

A chart has even been compiled showing the condition of the fascia at each phase, what’s happening in the body, and both the symptoms present and the respective diagnoses:

So how can fascia “freak out” and cause mischief to its owner?

According to Ashley Black, inventor of the FasciaBlaster, “Nerves flow through the fascia, and tight fascia can cause pinched nerves, tingling sensations and numbness. In addition, the nerve is what fires the muscle, so if the nerve supply is limited, muscle output is lessened.” Evidently tight fascia can also restrict joints and “choke out muscles, causing a host of orthopedic problems.” And fascia can even trap fat, causing cellulite! Such entrapment suggests a potential cosmetic role for the FasciaBlaster.

It turns out that Ashley Black believes that many illnesses of unknown origin “such as Fibromyalgia, Migraines,“itis” (sic), Chronic Fatigue Syndrome, IBS, Restless Leg Syndrome, nerve pain, tender points, and many more are rooted in the fascia system”:

Total Body Pain Relief

She even suggests her own test: “A good way to check if fascia could be part of your total body pain is to pinch your forearm or the top of your leg and pull up and away from the bone. If the skin does not pull up easily, then fascia is at least part of the problem.”

Ashley Black’s implement is claimed to be the only self-treatment tool “designed to break up fascial adhesions and restore healthy fascia.” Moreover, “with consistent use, users can expect relief from pain, tightness, and restriction as well as improved muscle performance, mobility, circulation, nerve activity, and total body function.”

A comprehensive series of self-help tutorials is readily available on her website:

For those with fibromyalgia, a short video is used to explain the treatment:

So who is Ashley Black?

On her website Ashley describes herself as an “inventor, best-selling AUTHOR, fasciology expert and the owner of an exploding multi-million dollar business”:

Apart from having attained “guru” status, Ashley Black does not claim to have any health professional qualifications or to have performed any research to support either her idiosyncratic views on fascia (quaintly termed “fasciology”) or her claims for therapeutic success that can be achieved by those with fibromyalgia who use her implement on a regular basis.

From the above on-line information, one can only conclude that that the aphorism of Johann Wolfgang von Goethe [1749-1832] still rings true: “Nothing is more terrible than to see ignorance in action.”

From: Maxims and Reflexions, I (translated by John Stuart Blackie in The Wisdom of Goethe).

75% of Persons in the General Population Diagnosed with Fibromyalgia Don’t Have It, But It Is Worse Than That…

In September 2016, Brian Walitt and I fell prey to what I have to call a hoax. We received an email from a journal inviting us to submit a commentary. Most of such invitations come from journals that are poorly rated or are frankly fraudulent in that their main purpose is to get authors to pay for publications rather than function as a legitimate scientific conduit. When I read the invitation, I saw Journal of Headache and Pain. Not a journal I usually follow, I looked it up on their web page and found it had a good impact factor: “The Journal of Headache and Pain is specifically dedicated to researchers … Impact Factor 3.497.” So this would be a good place to send an invited commentary. But I didn’t look close enough. It didn’t actually say Journal of Headache and Pain; it said  Journal of Headache and Pain Management. By the time we figured it all out JHPM “accepted” our article and sent us a bill for $1298. We withdrew the article and told them not to publish it, and that we would not pay the bill. They said it was too late. They published it anyway – not peer reviewed and poorly proof-read, with many glaring errors put in during the “publishers” editing.

It is an important article about fibromyalgia. You can get a PDF at And we print it in its entirety below from our clean copy.

In studies of fibromyalgia in 2015 and 2016, we applied fibromyalgia criteria to the 2012 National Health Interview Survey (NHIS), the principle source of information on the health of the civilian US population, and observed that 75% of persons in the US population reporting a physician diagnosis of fibromyalgia did not satisfy fibromyalgia criteria. 1,2 Persons with a fibromyalgia diagnosis who did not report symptoms specific and severe enough to satisfy diagnostic criteria constitute 1.3% of the US population. We will call this group criteria-negative fibromyalgia (C- FM). These persons were nearly exclusively white women (82.2% white, 92.7% women).

Criteria positive fibromyalgia (C+ FM), persons reporting symptoms severe and specific enough to satisfy fibromyalgia criteria positive fibromyalgia was prevalent in 1.7% of the US population. The C+ FM group was much less exclusive, with no ethnic predisposition and a more modest gender disparity of 2.3:1. However, only 27% of the C+ FM group also had a physician diagnosis of fibromyalgia [0.5% of US population]. We will refer to this less common instance when criteria positivity and physician diagnosis occur together as FM++.

Although the prevalence percentages seem small, the absolute numbers of people affected by our findings are not. By our calculations almost 3 million people who do not meet fibromyalgia criteria have been given a fibromyalgia diagnosis. At the other end of the spectrum, there are almost 3 million persons who satisfy fibromyalgia criteria, but have not been diagnosed with the disorder by a physician. It appears likely that many of their physicians when presented with the opportunity to diagnose fibromyalgia decline to make such a diagnosis. Data such as these call into question the usual 2-4% population estimates of fibromyalgia, and the validity of previous epidemiological studies of fibromyalgia that were not designed to identify physician diagnosis. We expect that the majority of the subjects considered to have fibromyalgia in these studies had not been diagnosed as having fibromyalgia.

Our observations in the NHIS of large numbers of apparently over and under diagnosed subjects, including that C- FM is far better predicted by demographic factors than symptom reporting, offer essential insights into the nature of historical and contemporary fibromyalgia. Whether fibromyalgia is determined by the tender point examination of the 1990 fibromyalgia criteria or by the symptom assessment tools of the 2010/2011 criteria, 3,4 fibromyalgia assessments are always subjective; they are influenced by biologic, psychosocial and environmental factors and, in clinical settings, by the beliefs and biases of physicians and patients. A C- FM diagnosis of fibromyalgia can legitimize vague and difficult or distressing symptoms, allowing entrée into official diagnosis and government approved treatments, or providing a way toward official disability status. All doctors and patients have to do is agree on the diagnosis. There is no reliable way to dispute such a diagnosis, and such a C- FM diagnosis can be “helpful” to the patient and to the physician who struggle to handle a difficult problem and sometimes a difficult patient.

The utility of a C- FM or a FM++ diagnosis depends on a general societal acceptance of fibromyalgia as a “real” disease. Fibromyalgia is one of a series of contested illnesses whose “nature and existence are contested as to whether they are primarily mental, psychiatric, or biological. They are causally undetermined: their etiology is likewise contested as to social, genetic, toxic and personal possibilities.” “They have fuzzy boundaries and are each cross-linked to other emergent illnesses as subsets, mistaken diagnosis, and comorbid conditions. They are legally explosive: each condition is caught up in court battles, administrative categorization and legislative maneuvering.” 5 For patients, there is a battle to establish and sustain the legitimacy of fibromyalgia, as “society does not readily grant permission to be ill in the absence of disease.” 6

The current dominant paradigm holds that fibromyalgia is a central pain disorder in which there is only a small role for psychosocial and environmental determinants. 7,8 Such a viewpoint is not consistent with the NHIS results nor the long history of expansions and contractions of similar somatic illnesses. It is wise to remember George Ehrlich’s admonition: “When one has tuberculosis, one has tuberculosis, whether or not it is diagnosed. The same is true for cancer, rheumatoid arthritis, hookworm infestation — really, of the gamut of diseases. But not for fibromyalgia (FM). No one has FM until it is diagnosed.” 9 One of the implications of Ehrlich’s statement is that the diagnosis of fibromyalgia is discretionary, and that patient level psychosocial factors and external societal factors influence that discretion.

A C- FM diagnosis requires that the physician buy into the fibromyalgia concept. With C+ FM this buy-in does not occur or is only partial. Many persons (C+ FM) who satisfied NHIS criteria for fibromyalgia reported receiving alternative diagnoses, such as rheumatoid arthritis (15.3%), gout (3.3%), lupus (1.4%), low back pain (21.7%), and non-specific “arthritis” (47.5%). 1,2 The constellation of severe symptoms can be clinically interpreted and diagnosed in many different ways, perhaps influenced by clinician and patient beliefs and their resultant interactions. Published diagnostic criteria appear to be ignored in C+ FM and used only as a vague guide in determining what fibromyalgia is in clinical practice (C- FM, FM++).

What these data mean, practically, is that psychosocial and environmental forces and physician and patient belief strongly affect fibromyalgia diagnosis and status. The distinguished medical historian Edward Shorter characterized fibromyalgia as a “psychic epidemic, an illness attribution that spreads epidemically, then is forgotten.” We have previously noted that the growth of fibromyalgia and its precursor, fibrositis, began in the 1980s, 10 after years of virtual neglect following the 1904 description of fibrositis 11 and the veritable shutdown of the fibromyalgia lookalike, neurasthenia, which was complete by 1930. 12,13 The neurasthenia shut down followed loss of societal support with the recognition that neurasthenia was not a condition of over-sensitive reflexes and was better considered within a psychological framework.14,15

Somatic symptoms and syndromes have always existed, but what drives the modern diagnosis of fibromyalgia? Three essential stakeholders: 1) the pharmaceutical industry (Pharma); 2) physicians with intellectual conflicts of interest (COI) and ties to Pharma; and 3) patient support organizations. In trying to understand why fibromyalgia over diagnosis (C- FM) exists, we noted that a recent five-year study of health care utilization in the US military observed an increase in fibromyalgia prevalence from 0.307% to 0.522%. 16 The authors stated “…we strongly suspect that the rise in FMS prevalence between 2006 and 2008 is due to drug marketing activities between September 2005 and October 2008, the period when Pfizer “illegally promoted the sale and use of Lyrica [pregabalin] for a variety of off-label conditions (including chronic pain. . .) . . . [and] offered and paid illegal remuneration to health care professionals to induce them to promote and prescribe Lyrica … .” “By 2008, manufacturers of these drugs began direct consumer marketing and increased grant monies for FMS provider education and research, and for FMS advocacy groups… . In 2008, Pfizer provided about $4 million in grants to U.S. physicians, nurses, and other health professionals to educate them about FMS. Coinciding with these marketing costs are FMS clinical guidelines developed by consensus and literature reviews. The 2009 guidelines, based on a meeting funded by “an independent educational grant from Pfizer,” were developed by U.S. experts with documented conflicts of interest with manufacturers of FMS-approved drugs.”

Pfizer-sponsored publications state that “Although awareness and understanding of FM have improved, it is thought that FM remains undiagnosed in as many as 3 of 4 people with the disorder (Data on file. Decision Resources report 2009. Pfizer, New York, NY) 7,8. Such articles then point out the presumed medical hazards of delayed diagnosis and go on to advocate active treatment: “Better health outcomes and quality of life can be achieved by patients with FM with effective treatments developed as a result of an enhanced understanding of the disorder. Clinicians, both individually and in collaboration with other health care professionals and their patients, can improve patient care with vigilant recognition and diagnosis of FM.” — The conclusion of the Pfizer organized and financed “Fibrocollaborative” with “editorial support” also funded by the pharmaceutical company.8 While these paragraphs on the extensive role of Pharma are incomplete, a large literature exists that the reader may consult. 17-21

The evidence that current medical practice has led to better health outcomes is non-existent; the general ineffectiveness of pharmacological therapies outside of the clinical trial setting has been well characterized by meta-analysis22,23 and longitudinal population 24 and insurance database studies. Our data show that there a millions of potential customers provided more physicians can be taught to diagnose fibromyalgia, a job that has been done very well so far by Pharma.

Physician support for fibromyalgia has been a very important force, as it has driven acceptance of the idea of central pain and a neurobiological basis of fibromyalgia.25 However, there is no evidence that central neurological alteration is the cause of the pain of fibromyalgia; all findings to date have been derived from cross-sectional studies unable to determine whether the observed difference reported represents a risk factor, an epiphenomenon, an endophenotype, or is causal.26 Despite the frequent claims that the rapid pace of neurobiological discovery means that definitive proof is right around the corner, the prospective studies needed to investigate fibromyalgia causality still await conception. The single attempt to prospectively understand the neurobiological mechanisms of “central pain” disorders was the OPPERA study of temporomanibular disorder (TMD), which concluded that ‘TMD is a complex disorder with multiple causes consistent with a biopsychosocial model of illness’.27 Failure to demonstrate a reducible neurobiological causality, along with a host of anomalous observations that are not consistent with central sensitization26,28-30, has been willfully ignored or fought against. It remains hard to find “academic” articles that move beyond the idea of “central pain” or that consider a strong biocultural 31 or complex systems component to the disorder, although important publications exist that do this. 32

The role physicians in publishing data on fibromyalgia must be mentioned. Index Medicus now (September 2016) lists 9,366 article addressing fibromyalgia, and the tangible and intangible benefits physicians receive from publishing are substantial. 19,33 Why do independent investigators do fibromyalgia studies? Because it is easy to find patients and there are always abnormalities. If you look hard enough almost any question can seem publishable and justified as an incremental increase in scientific understanding.

Finally, there has been an enormous and often quite successful effort by patient support groups to legitimize fibromyalgia and support fibromyalgia physicians. These efforts have been documented elsewhere. 20,34-36 For patients and their advocates, the suffering of fibromyalgia is a self-evident demonstration of legitimacy, even if the scientific reasons used to establish its medical legitimacy may not be.

We acknowledge some limitations to the NHIS study. Our data refer predominantly to the United States. The NHIS data used surrogate fibromyalgia criteria that we developed and validated. It is likely actual criteria, had they been available, would led to modestly different results. In addition, in writing about C- FM, some cases might include previous FM++ subjects who improved to the extent that they now longer satisfied criteria. Studies in the clinical literature suggest this may be a much as 25% of criteria negative subjects. However, in the NHIS setting that percentage is likely to be lower and certainly not higher.

In summary, the majority of clinical fibromyalgia cases in the US do not reach levels of severity considered to be diagnostic. Rather, fibromyalgia is disproportionally dependent on socially-constructed factors rather than the symptoms themselves. Diagnostic criteria appear to be used only as a vague guide by clinicians and patients, allowing for substantial diagnostic expansion of fibromyalgia.

Frederick Wolfe MD and Brian Walitt MD MPH


  1. Walitt B, Nahin RL, Katz RS, Bergman MJ, Wolfe F. The Prevalence and Characteristics of Fibromyalgia in the 2012 National Health Interview Survey. PLoS One. 2015;10(9):e0138024.
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  3. Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33(2):160-172.
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  5. Dumit J. Illnesses you have to fight to get: Facts as forces in uncertain, emergent illnesses. Soc. Sci. Med. 2006;62(3):577-590.
  6. Nettleton S. ‘I just want permission to be ill’: towards a sociology of medically unexplained symptoms. Soc. Sci. Med. 2006;62(5):1167-1178.
  7. Clauw D, Arnold L, McCarberg B. The science of fibromyalgia. Mayo Clin. Proc. 2011;86:907 – 911.
  8. Arnold L, Clauw D, McCarberg B. Improving the recognition and diagnosis of fibromyalgia. Mayo Clin. Proc. 2011;86:457 – 464.
  9. Ehrlich GE. Pain is real; fibromyalgia isn’t. J.Rheumatol. 2003;30(8):1666-1667.
  10. Wolfe F, Walitt B. Culture, science and the changing nature of fibromyalgia. Nature Reviews Rheumatology. 2013.
  11. Gowers WR. Lumbago: its lessons and analogues. Br.Med.J. 1904;1:117-121.
  12. Taylor RE. Death of neurasthenia and its psychological reincarnation A study of neurasthenia at the National Hospital for the Relief and Cure of the Paralysed and Epileptic, Queen Square, London, 1870-1932. The British Journal of Psychiatry. 2001;179(6):550-557.
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  16. Jeffery DD, Bulathsinhala L, Kroc M, Dorris J. Prevalence, health care utilization, and costs of fibromyalgia, irritable bowel, and chronic fatigue syndromes in the military health system, 2006-2010. Military medicine. 2014;179(9):1021-1029.
  17. Moynihan R, Heath I, Henry D. Selling sickness: the pharmaceutical industry and disease mongeringCommentary: Medicalisation of risk factors. BMJ. 2002;324(7342):886-891.
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  20. Barker KK. Listening to Lyrica: contested illnesses and pharmaceutical determinism. Soc. Sci. Med. 2011;73(6):833-842.
  21. Reed M, Herrmann M. The Difficulties in Developing and Implementing Fibromyalgia Guidelines. 2012.
  22. Hauser W, Urrutia G, Tort S, Uceyler N, Walitt B. Serotonin and noradrenaline reuptake inhibitors (SNRIs) for fibromyalgia syndrome. The Cochrane database of systematic reviews. 2013;1:CD010292.
  23. Uceyler N, Sommer C, Walitt B, Hauser W. Anticonvulsants for fibromyalgia. The Cochrane database of systematic reviews. 2013(10):CD010782.
  24. Wolfe F, Walitt BT, Katz RS, Lee YC, Michaud KD, Hauser W. Longitudinal patterns of analgesic and central acting drug use and associated effectiveness in fibromyalgia. European journal of pain (London, England). 2012.
  25. Clauw DJ. Fibromyalgia: a clinical review. Jama. 2014;311(15):1547-1555.
  26. Walitt B, Ceko M, Gracely JL, Gracely RH. Neuroimaging of Central Sensitivity Syndromes: Key Insights from the Scientific Literature. Curr Rheumatol Rev. 2016;12(1):55-87.
  27. Slade GD, Fillingim RB, Sanders AE, et al. Summary of findings from the OPPERA prospective cohort study of incidence of first-onset temporomandibular disorder: implications and future directions. J Pain. 2013;14(12 Suppl):T116-124.
  28. Goffaux P, de Souza JB, Potvin S, Marchand S. Pain relief through expectation supersedes descending inhibitory deficits in fibromyalgia patients. Pain. 2009;145(1-2):18-23.
  29. Potvin S, Paul-Savoie E, Morin M, Bourgault P, Marchand S. Temporal summation of pain is not amplified in a large proportion of fibromyalgia patients. Pain Res Treat. 2012;2012:938595.
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Too Easy To Diagnose Fibromyalgia

In his post on Cannabis, John Quintner refers to “Too Easy To Diagnose Fibromyalgia.” One might think I would be offended by this offhand categorization, as I have spent much of my professional life working on fibromyalgia diagnosis. (Wolfe, Smythe et al. 1990, Wolfe, Clauw et al. 2010, Wolfe, Clauw et al. 2011, Wolfe, Clauw et al. 2016) Look what he says. A “constellation of symptoms …exists in varying degrees of severity within all communities. These symptoms are non-specific and include widespread pain and tenderness, fatigability, sleep disturbance, cognitive impairment, mood changes etc. When present together in various combinations they are currently understood as reflecting “polysymptomatic distress” (Wolfe, Walitt et al. 2015). Self-diagnosis is not at all uncommon, through the agency of electronic media and support groups.” Worse than that, “…there is no objective marker or test for fibromyalgia, and it has been said that the condition can co-exist with any other painful condition, theoretically the label may be applied to many of the one in five members of the general population who report persistent pain and associated distress.”

And even worse than that, Brian Walitt and I applied surrogate criteria to the US National Health Interview Survey and found that fibromyalgia is often not diagnosed when the symptoms fit, but that most people who are diagnosed with fibromyalgia don’t satisfy criteria for fibromyalgia. (Walitt, Katz et al. 2016)

Last week, I read a new publication from Dan Clauw’s group, the inveterate and ubiquitous promulgators, that stated, “Fibromyalgia (FM) is the current term for chronic widespread musculoskeletal pain for which no alternative cause can be identified.” (Sluka and Clauw 2016) With that characterization Clauw threw out all of the criteria: fibromyalgia is simply “chronic widespread pain.”

And fibromyalgia as chronic widespread pain isn’t something you have to have now. It can come and go. Once fibromyalgia, always fibromyalgia. Using such definitions the prevalence of fibromyalgia can be seen to exceed 20%. I am reminded of Derek Summerfield’s comment, “… If on average 1 in 4 or 6 of the people going about their ordinary business on the street outside my house as I write are diagnosable as ‘cases’ of mental illness, we need to re-examine our models before we examine the people.” (Sluka and Clauw 2016)

So what good are criteria? They keep people a little more honest. When applied, they should prevent people with trivial problems being diagnosed with fibromyalgia. They set obvious limits of validity and reliability that all of us and institutions and courts should be aware of. And they should make us think a diagnosis of fibromyalgia is not always the best or only way of approaching symptoms and distress.


Sluka, K. A. and D. J. Clauw (2016). “Neurobiology of fibromyalgia and chronic widespread pain.” Neuroscience.

Walitt, B., R. S. Katz, M. J. Bergman and F. Wolfe (2016). “Three-Quarters of Persons in the US Population Reporting a Clinical Diagnosis of Fibromyalgia Do Not Satisfy Fibromyalgia Criteria: The 2012 National Health Interview Survey.” PloS one 11(6): e0157235.

Wolfe, F., D. Clauw, M. A. Fitzcharles, D. Goldenberg, W. Häuser, R. S. Katz, P. Mease, A. S. Russell, I. J. Russell and J. B. Winfield (2011). “Fibromyalgia Criteria and Severity Scales for Clinical and Epidemiological Studies: A Modification of the ACR Preliminary Diagnostic Criteria for Fibromyalgia.” J Rheumatol. 38: 1113-1122.

Wolfe, F., D. Clauw, M. A. Fitzcharles, D. Goldenberg, R. S. Katz, P. Mease, A. S. Russell, I. J. Russel, J. Winfield and M. B. Yunus (2010). “The American College of Rheumatology Preliminary Diagnostic Criteria for Fibromyalgia and Measurement of Symptom Severity.” Arthritis Care Res 62(5): 600-610.

Wolfe, F., D. J. Clauw, M.-A. Fitzcharles, D. L. Goldenberg, W. Häuser, R. L. Katz, P. J. Mease, A. S. Russell, I. J. Russell and B. Walitt (2016). “2016 Revisions to the 2010/2011 Fibromyalgia Diagnostic Criteria.” Seminars in Arthritis and Rheumatism.

Wolfe, F., H. A. Smythe, M. B. Yunus, R. M. Bennett, C. Bombardier, D. L. Goldenberg, P. Tugwell, S. M. Campbell, M. Abeles, P. Clark and et al. (1990). “The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee.” Arthritis Rheum 33(2): 160-172.

Wolfe, F., B. T. Walitt, J. J. Rasker, R. S. Katz and W. Häuser (2015). “The Use of Polysymptomatic Distress Categories in the Evaluation of Fibromyalgia (FM) and FM Severity.” The Journal of rheumatology 42(8): 1494-1501.


If Cannabis Should Meet Fibromyalgia

Down through the ages Indian hemp (cannabis) spread from land to land. In China it was during the Wei dynasty that the famous physician Hoa Tho was able to prepare from it the sedative “Mario” which could very quickly throw the patient into so profound a sleep it was “as if he had drunk himself to death.” [from: “Triumph Over Pain” by René Fülöp-Miller, 1938: 23]

Various cannabis preparations are still widely used throughout the world, mainly for recreational purposes. But, as James Austin (2006) points out: Marijuana is often the first “herb” to lure innocents through the gate and down the garden path toward major “theobotanicals.”

Almost half of all 18-year-olds in the United States and in most European countries admit to having tried marijuana one of more times. Some have suggested that perhaps up to 10% of that teenage group can become regular users (Iverson, 2003).

In recent years concerted political efforts have been made in many countries to legalize the growing and prescribing of cannabinoids for specific medical conditions. Fibromyalgia has been included as one of a number of chronically painful conditions in which cannabis might be indicated:

The particular constellation of symptoms to which the name fibromyalgia has been attached exists in varying degrees of severity within all communities. These symptoms are non-specific and include widespread pain and tenderness, fatiguability, sleep disturbance, cognitive impairment, mood changes etc. When present together in various combinations they are currently understood as reflecting “polysymptomatic distress” (Wolfe et al. 2015). Self-diagnosis is not at all uncommon, through the agency of electronic media and support groups.

Indeed, this symptom cluster has been found in 2% (or more) of the general population (Vincent et al. 2013). According to the American College of Rheumatology, the “diagnosis” is most frequently made between the ages of 20 to 50. By the age of 80, approximately 8% of adults will meet the ACR criteria for fibromyalgia.

However, given that there is no objective marker or test for fibromyalgia, and it has been said that the condition can co-exist with any other painful condition, theoretically the label may be applied to many of the one in five members of the general population who report persistent pain and associated distress.

In the United States chronic pain is the most common reason given by patients reporting “medical use” of cannabis (Dyer, 2013). It follows that if fibromyalgia is listed as a “specific indication” for cannabinoids, considerable diagnostic “leakage” is bound to occur. Those who wish to continue to use “medicinal” cannabis for recreational purposes would not find it difficult to fulfill the “diagnostic criteria” for fibromyalgia.

What an enormous commercial market for cannabinoid preparations would be created!

In the words of Ware & Desroches (2014): The medical use of cannabis is not an end in itself; the patient demanding cannabis and refusing to consider other options may have motivations other than amelioration of pain and improvement in quality of life.

But is there any evidence that would justify the prescribing of cannabinoid preparations for those presenting with chronic pain and specifically for those diagnosed with fibromyalgia?

Three reviews of variable quality have been published (Martin-Sanchez et al. 2009; Lynch et al. 2011; Grotenhermen & Müller-Vahl 2012). Farrell et al. (2014) provided an overview of the first two reviews and also conducted their own literature review.

According to Farrell et al (2014): “… the effectiveness of cannabinoids in treating other chronic pain (e.g. fibromyalgia) is unclear and any benefit is likely to be modest. Mild to moderate adverse effects are often reported and long-term safety has not been established.”

So if unproven cannabinoids were to be legitimised as “treatment” for “too-easy-to-diagnose “fibromyalgia”, it is not too difficult to foresee an iatrogenic disaster that could sideline the hard-earned reputation of scientific medicine.

John Quintner



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