Posted on July 14th, 2015 by John Quintner

Could Fibrositis be Making a Comeback?

Introduction

As I perused the abstracts for the upcoming 4th International Fascial Research Congress (September 2015), I came upon one that made me stop and think. It related to a half-day post-conference workshop by Kirstie Segarra – Managing Fascial Health for Individuals in Fibromyalgia:

To demonstrate clearly that managing widespread pain must include treatment of the fascia as we are structured determined systems, and to decrease pain is to invite change in the structure through the fascial matrix in order to have a correlating change in the central nervous system. In this way we restore homeostasis in the client.

Could pathology within fascia have been overlooked in the search for a peripheral source of nociception in this condition? Well, it appears that this is no longer the case.

Pathophysiological considerations

Liptan [1] hypothesized that fibromyalgia could be seen as a “bodywide fasciitis,” comparable to situations characterised by more focal fasciitis (e.g. plantar fasciitis).

The culprit appears to be chronic tension within the fascia responsible for causing micro-injuries (i.e. tears) in those with a “dysfunctional” healing response. Such a response is said to result from insufficient growth hormone release consequent upon inadequate deep sleep.

In summary, Liptan argued that: “Fascial dysfunction and inflammation may lead to widespread pain and central sensitization seen in fibromyalgia.”

He explained the tender points as possibly reflecting “areas that suffer the greatest microtrauma and mechanical stress from daily activities, and thus have higher levels of fascial inflammation.”

The main evidence put forward in support of his hypothesis derived from “recent biopsy studies [which] have found increased levels of collagen and inflammatory mediators in the fascia of fibromyalgia patients.”

But is this a novel hypothesis? In the Background section of his paper, Liptan harks back to the early 1900s when the aetiology of “muscular rheumatism” was indeed a hot topic.

Muscular rheumatism

In speculating upon the pathophysiology of low back pain, the great British neurologist, William Gowers [1904] coined the term “fibrositis” and thus championed the central role of the fascia in this condition:

In all parts it seems it seems the most susceptible to the influence we call “rheumatism” … The relation of lumbago to rheumatism would alone, make us expect to find it an affection of the fibrous tissue of the muscles, the tissue in which the spindles are situated, rather than of these alone … important proof that the malady is an affection of fibrous tissue; it may spread, and it spreads by continuity of this tissue.

Gowers postulated both focal and generalised forms of “fibrositis”:

We are thus compelled to regard lumbago in particular, and muscular rheumatism in general, as a form of inflammation of the fibrous tissue of the muscles.

The pathological findings

Ralph Stockman [1913], a Scottish pathologist, soon announced:

The essential lesion is a chronic inflammatory hyperplasia of white fibrous tissue in patches and as fibrous tissue is spread throughout the body the lesions may also be widely spread or may affect only a single limited area.

But after other researchers had repeatedly failed to find biopsy evidence of fibrous tissue inflammation, the “fibrositis” construct was eventually superseded by that of “fibromyalgia” [Hench, 1976] and classified in the nebulous category of non-articular rheumatism [Atkinson, 1981].

Treatment

As did Gowers, Liptan [2010] ascribed a limited role to anti-inflammatory drugs (NSAIDs and corticosteroids), which should be used only during the initial phase of injury repair.

According to Liptan [2010] “only slow and sustained pressure will effect changes in the fascial tissue” and he recommended manual therapy techniques that “don’t cause further injury and inflammation, but rather gently break apart existing fascial restrictions and adhesions to promote tissue healing.”

He wondered whether techniques said to target the fascia, which included “Rolfing” (a technique of deep tissue manipulation) and “myofascial release,” could “help define the role of fascia in producing fibromyalgia pain.”

Based upon Liptan’s hypothesis, a pilot trial was undertaken comparing Swedish massage with myofascial release therapy (MFR), each administered over 90 minutes a week for 4 consecutive weeks [Liptan et al. 2013]. The former technique utilized moderate pressure stroking of the neck, back, arms and legs, whereas MFR consisted of “prolonged assisted stretching of painful areas of soft tissue” in the same regions.

The rationale given for MFR maneuvers is that they are designed to “break up fascial adhesions” presumed to be the consequence of tissue injuries occurring in the fascia of patients with fibromyalgia [Liptan et al. 2013]. That for Swedish massage is to increase circulation and promote general relaxation.

Although numbers were small, both forms of treatment were found to be “safe, tolerable and acceptable” with MFR producing better symptom reduction.

By contrast, the mainstay of treatment recommended by Gowers was complete rest:

Not even passive movement should be employed until it causes no pain, and then it should be most gentle. The avoidance of pain should be made the standard for all local measures.

Gowers observed that counter-irritation (cautery being the most effective form) sometimes lessens the pain, as does deep hypodermic injection of cocaine, repeated daily for 2-3 weeks.

Other treatment strategies worth trying included a Turkish bath, mild aperients and, in the most acute cases, medicinal agents such as salicylates, nitrous ether, colchicum and perchloride of mercury.

Looking ahead

Gowers conceded: “we are without any direct evidence of the real nature of these affections” but he did hope that opportunities for pathological research would be seized upon:

We cannot wonder at our ignorance, still less complain of it, for it is only quite recently that the minute structure of the sensory elements of muscle and tendon has been clearly perceived, and much of the normal structure remains obscure.

But over a century later, direct histological evidence to support the related concepts of “fibrositis” and “fascial adhesions” is still lacking.

Nonetheless, Liptan [2010] calls for the use of existing methods of in vivo microdialysis to investigate the chemical composition of fascial interstitial fluid for evidence of inflammation, as well as for evidence of activation of fibroblasts removed from fascial tissues. He did not canvass the possibility that any such inflammation might in fact be “neurogenic” [Julius & Basbaum, 2001].

As for the role of manual therapy, Liptan et al. [2013] hope that various measurement tools being developed “may provide insight into which symptom of function domains are most malleable to various types of massage intervention.”

Conclusion

To date, the search for underlying peripheral musculoskeletal pathology in fibromyalgia has not been fruitful.  Yet, a recently published book – Fascial Dysfunction: Manual Therapy Approaches (2014) – is being advertised to manual therapists with this rather astounding claim appearing in the blurb:

Fascial dysfunction is now recognized as one of the main underlying causes of musculoskeletal pain leading to impaired and reduced mobility.  [Link: http://www.amazon.com/Fascial-Dysfunction-Manual-Therapy-Approaches/dp/1909141100]

Could Gowers have been right after all? Should we now discard the term fibromyalgia and revert to his “fibrositis” model? It seems a most unlikely possibility but a critical review is urgently needed to once and for all resolve this important question.

References:

Atkinson MH. Nonarticular rheumatism. Can Fam Physician 1981; 27: 254-258.

Gowers WR. A lecture on lumbago: its lessons and analogues. Brit Med J 1904; i: 117-121.

Hench PK. Nonarticular rheumatism, 22nd rheumatism review: review of the American and English literature for the years 1973 and 1974. Arthritis Rheum 1976; 19(suppl): 1081–1089.

Julius D, Basbaum AI. Molecular mechanisms of nociception. Nature 2001; 413: 203–210.

Liptan GL. Fascia: a missing link in our understanding of the pathology of fibromyalgia. J Bodywork Mov Ther 2010; 14: 3-12.

Liptan G, Mist S, Wright C, Arzt A, Jones KD. A pilot study of myofascial release therapy compared to Swedish massage in Fibromyalgia. J Bodywork Mov Ther 2013; 17: 365-370.

Stockman R.  Discussion on fibrositis. Proc R Soc med 1913; 6: 36-39.

 

5 Comments

  1. Thank you for that lucid and interesting summary. You have accessed literature which is not as familiar to rheumatologists. Who among us, at least in the US, even knows of these journals and some of the notable efforts published there … e.g. from Guelph, Ontario: PP Purslow, Muscle fascia and force transmission, Journal of Bodywork and Movement Therapies 2010; 14: 411-417 .

    I am pleased by your lookback to the 1904 Gowers lecture on “Lumbago: Its Lessons and Analogues.” Gowers is the bete noire of CNS-focused fibromyalgia proponents because he unflinchingly sought biomechanical pathology for lumbosacral pain disorders, brachial pain (likely rotator cuff disease), thoracic cage pain, neck pain, etc. Many cases, he felt, were due to trauma, including awkward posture, in vulnerable individuals. He speculated on causation in the microscopic muscle spindles and their nerves, and also put emphasis on the tendinous attachments to bone via tissues we’d regard as fascia. Every time I read his lecture I enjoy those curious things which illuminate the medical perceptions of his time .. for instance, as you say, he critiques a variety of treatment modalities, including “free perspiration,” non-painful exercise, rest, avoidance by women of raising arms behind the head to groom hair, Turkish baths, “frequent hot fomentations,” massage, gentle electrical current, various liniments and wraps, saline laxatives, counter-irritation with cautery or with deep injections of cocaine, each method tuned to the early or late stage of the pain disorder. Gowers was skeptical of “medicinal agents” but in accepted a trial of salicylates, and of nitrous ether, citrate of lithia, and colchicum, with an option to add a small dose of perchloride of mercury in severe cases. Odd stuff, but not as odd as Lyrica and the suppositions underlying its use.

    As to the modern perception of causation in patients labeled as “fibromyalgia” sufferers, I favor looking at the underlying bio-neuro-mechanical features of each localized source of pain (including those features attributable to all locomotor system components, among them fascia). We owe our patients this much — especially in view of the scientific failure of the CNS theory — a failure so disastrous that its survival depends on shared illusions — particularly based around the fallacy of the normal control group.

  2. Dr Lampman, I share with you a great admiration for WR Gowers as a pioneer in clinical neurology. His paper on neuralgia is particularly remarkable for its clear descriptions of the various clinical presentations and for its prescience on possible central mechanisms involved in nerve pain [1].

    In my article, I was tempted to include these apt observation from Elliott [2]: “We have seen that there has been a progressive reduction in the number of conditions which can be attributed to fibrositis, and that the application of rigorous clinical discipline coupled with new technical methods threatens to continue the process of dismemberment … This thesis does not seek to shut the door on fibrositis as a clinical entity, and it would be unfortunate if the hypothesis of myofascial inflammation were to be replaced, at this stage, by a facile generalization that muscle tenderness is always due to spasm of skeletal muscle.”

    References:
    1. Gowers WR. Neuralgia; its etiology, diagnosis, and treatment. Wood’s Medical and Surgical Monographs 1890; 5(1): 3-56.
    2. Elliott FA. Aspects of “fibrositis”. Ann Rheum Dis 1944; 4: 22-25.

  3. “As to the modern perception of causation in patients labeled as “fibromyalgia” sufferers, I favor looking at the underlying bio-neuro-mechanical features of each localized source of pain (including those features attributable to all locomotor system components, among them fascia).”

    Dr Lampman, you may be interested to learn that there are others who seem to share your views, although they have extended them to medical conditions that are way beyond fibromyalgia, as we rheumatologists understand it.

    Here are some excerpts taken from an article by a prominent physical therapist, John F Barnes: “What is fibromyalgia really? What do fibromyalgia, chronic fatigue syndrome, chronic pain, headaches, pelvic/menstrual pain and dysfunction, and PMS have in common? These are simply different labels of a common denominator, unrecognized myofascial restrictions. Myofascial restrictions do not show up in all the standard tests that are now performed, nor have most health professionals been taught how to recognize them.”

    Having once identified the particular myofascial restriction in each case, Barnes claims that “Myofascial release is utilized for the treatment of menstrual pain and/or dysfunction, back and pelvic pain, and other inflammatory disorders. It can treat the unpleasant and/or painful symptoms of pregnancy and childbirth, recurrent bladder pain and infection, painful intercourse, sexual dysfunction, elimination problems, coccygeal pain, painful episiotomy scars and the list goes on.” He is confident that “these problems can in many cases be substantially alleviated or eliminated by myofascial release, nontraumatically and gently.”

    Myofascial release evidently has the added benefit of relieving the emotional pain associated with past unpleasant events or traumas. According to Barnes: “The painful memories or emotions from beatings, rapes, molestations, or miscarriages seem to be stored in the body’s memory … As myofascial release frees the adhered tissue, the trapped emotions and painful memories fade away leaving the person with a sense of peace.”

    Link: http://www.myofascialrelease.com/downloads/articles/Fibromyalgia.pdf

  4. Dr. Quintner, you are at your best in employing understatement and wry humor in handling Dr. Barnes’ Freud-like claims.

    As for me, I gained a “sense of peace” and fading of “trapped emotions and painful memories” some ten years ago when I shed concerns with the mystic weight of chronic widespread pain, finding solace in knowing that each limb or axial pain originated in rationally understood anatomic issues sculptured into the human form.

  5. Dr Lampman, the only connection I could find with Sigmund Freud (1856-1939) relates to his views on neurasthenia (a 19th century label for the fibromyalgia symptom cluster) as a “masturbation neurosis”:
    “Neurasthenics merge into anxiety neurosis in consequence of masturbation as soon as they refrain from this manner of sexual gratification.” [From Ch. VI. Selected Papers on Hysteria and other Psychoneuroses, 1912.]

    Barnes derives his inspiration from contemporary cellular biology, which does indeed include “anatomic issues sculptured into the human form”.

    I will briefly enlarge upon this matter, as rheumatologists may wish to have some knowledge and understanding of the various types of physical treatment on offer to their patients with fibromyalgia, and to be in a better position to help them discern what may be useful and what may be a waste of their time and money.

    In Massage Magazine, Barnes (2014) gives more than a passing nod to science and describes his work as “restoring the body’s microenvironment,” which he rightly sees as “critical to our health”. Barnes’ focus is solely upon fascia, which he describes as “truly the architecture of life”:

    “The cells’ cytoskeletons are influenced by the extracellular matrix, i.e. the fascia, which are in a constant tug of war. Balance is important to health.” [Barnes, 2014]

    Biologists accept that a fundamental requirement of cells is their ability to transduce and interpret their mechanical environment in response to physical forces and that this ability contributes to regulation of growth, differentiation and adaptation in many cell types [Ingber, 1997; Palmisano et al. 2015]. This is not a new concept:

    “The ancient Greek philosopher Aristotle considered shape as the soul of all living entities. Cell biologists are beginning to see the profound role of shape in a more modern sense. Shape exerts a powerful influence on life: on the one hand, it affects how cells build and repair organs, and on the other hand, it can become malevolent, undermining health. As we refine our understanding of the power of shape, we may be able to bend it to help people.” [Piccolo S, 2014]

    According to Barnes, physical treatment of patients with fibromyalgia is to be targeted at fascial “restrictions,” which can only be detected by well-trained therapists (Barnes has instructed more than 100,000 therapists worldwide in his Myofascial Release Approach):

    “In the practice of Myofascial Release, we focus on finding the restrictions in the individual, generating the proper amount of pressure, and waiting a sufficient amount of time-five minutes or longer-for a number of important physiologic processes to occur. These include piezoelectricity, mechanotransduction and ultimately, resonance, which is another word for the release we hope to help our clients achieve.” [Barnes, 2014]

    So patients with fibromyalgia could well harbour a multitude of “myofascial restrictions,” and be completely unaware of them. How well do Barnes’ theories translate into clinical practice?

    Surprisingly, the important question of inter-observer reliability in detecting Barnes’ “restrictions” is yet to be addressed.

    Nevertheless, two controlled trials of “myofascial release therapy” in fibromyalgia have been published by Spanish researchers [Castro-Sánchez et al., 2011 (a); Castro-Sánchez et al., 2011 (b)].

    In the former study, those in the experimental group attended twice-weekly for treatment administered according to a strange protocol that included: “release of the falx cerebri by frontal lift, release of tentorium cerebelli by synchronization of temporals, deep fascia release in temporal region, suboccipital release, compression–decompression of temporomandibular joint, global release of cervicodorsal fascia, release of pectoral region, diaphragm release (transverse slide), transverse diaphragmatic plane, lumbosacral decompression, release of psoas fascia and release of fascia of the lumbar square.”

    The investigators did not address the question as to whether “restrictions” actually existed at any or all of these disparate anatomical sites.

    In the latter study, the experimental group underwent release of their “myofascial restrictions” for 90 minutes weekly. Treatment was specifically directed at the sites of the 18 “painful points” reported by the American College of Rheumatology. Presumably the therapist spent 5 minutes treating each of these sites in turn. Neither study documented the number of myofascial “restrictions” detected in the respective control groups.

    Both studies, which are not really comparable in design, concluded that these techniques of manual therapy administered regularly for 20 weeks produced better outcomes at one and six months than sham therapy with a disconnected “magnotherapy” device.

    The main conclusion I draw is that there does seem to be quite a large credibility gap to bridge between Barnes’ theory of “myofascial restrictions” and its translation into clinical practice, at least for patients with fibromyalgia.

    However, it appears there are still those who believe that pathological changes reside in the region of the “tender points” once said to be associated with fibromyalgia. But of that there is no evidence!

    Yes, fibrositis never really disappeared and is definitely making a strong comeback.

    References:

    Barnes JF. Therapeutic insight: The John F. Barnes’ myofascial release perspective – how mechanotransduction may affect cells. Massage Magazine, October 23, 2014. http://www.massagemag.com/therapeutic-insight-the-john-f-barnes-myofascial-release-perspective-how-mechanotransduction-may-affect-cells-27154/

    Castro-Sanchez AM, Matarán-Peñarrocha GA, Morales MA, et al. Effects of myofascial release techniques on pain, physical function, and postural stability in patients with fibromyalgia: a randomized controlled trial. Clin. Rehabil 2011 (a); 25 (9): 800-813.

    Castro-Sánchez AM, Matarán-Peñarrocha GA, Granero-Molina J, et al. Benefits of massage-myofascial release on pain, anxiety, quality of sleep, depression, and quality of life in patients with fibromyalgia. Evidence-based Complementary and Alternative Medicine 2011 (b), Article ID 561753, 9 pages. doi: 10.1155/2011/561753.

    Ingber DE. Integrins, tensegrity, and mechanotransduction. Gravitational and Space Biology Bulletin 1997; 10(2): 49-55.

    Palmisano M, Bremner SN, Hornberger TA, et al. Skeletal muscle intermediate filaments form a stress-transmitting and stress-signaling network. Journal of Cell Science 2015; 128: 219-224.
    Piccolo S. Twists of fate. Scientific American, October 2014: 75-81.

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Posted on May 23rd, 2015 by John Quintner

THE TRANSMUTATION OF FIBROMYALGIA

Fibromyalgia was officially recognised in 1990 when a Multicenter Criteria Committee of the American College of Rheumatology recommended the term be used as a means of classifying patients presenting with chronic widespread pain and tenderness [1].

Pain was considered to be “widespread” when it was experienced in all four quadrants of the body (i.e. on both the left and right sides and above and below the waist).

Tenderness was assessed over 18 specifically chosen tender points. When patients with widespread pain were judged by their clinician to be hypersensitive at 11 or more of these points, the diagnosis of Fibromyalgia could be applied.

Some 20 years later, the criteria for diagnosis were broadened by the introduction of a symptom severity scale score to replace the tender point count. Widespread pain remained a diagnostic criterion [2].

The clinical problem of “RSI” (repetitive strain injury)

In Australia the term “RSI” (repetitive strain injury) came to be broadly applied to all conditions characterised by neck and/or upper limb pain presenting in an occupational context.

“RSI” embraced localised conditions, such as carpal tunnel syndrome, dorsal wrist tenosynovitis, lateral epicondylitis and rotator cuff “tendonitis”, along with poorly understood conditions characterised by diffuse pain felt in the neck, pectoral girdle and arms, often accompanied by positive sensory symptoms, cramp, loss of muscle strength, and vasomotor abnormalities [3,4].

A vigorous medical debate had taken place during the 1980s over the categorization of the sub-group of patients with diffuse pain. On the one side were those who espoused the theory of muscle overuse injury, whilst on the other side were those who argued that those with these conditions were reflecting psychological distress that was manifest as somatic symptoms [5].

However, the homogeneity of presentation of these patients implied not only a common pathophysiology but also one that could be attributed to dysfunction of the nociceptive system itself, consistent with what was then the current definition of “neuropathic” pain. This explanatory model was proposed on the basis of careful clinical observation integrated with current knowledge of mechanisms of nociception [3,6].

Fibromyalgia becomes a regional condition

The 1980s brought the dreaded “RSI” (repetition strain injury) with interaction between Fibromyalgia Syndrome and the medico-legal system [7].

One of the key proponents in Australia of fibromyalgia, Geoffrey Littlejohn, was keen to extend the construct to subsume these syndromes of less diffuse pain, which were then being called “RSI”. He and his colleagues argued that these conditions were in fact a “subset” of fibromyalgia. 

They conjectured: Mechanisms similar to those in generalised fibromyalgia are likely to operate, although to a lesser extent, in patients with primary chronic localised pain or localized fibromyalgia [8].

This reconceptualisation of “primary chronic localised pain” as “regional fibromyalgia” presumed the validity of a parent syndrome.

However this exercise was an example of the logical fallacy known as “begging the question,” and was particularly problematic when the diagnostic credibility of both conditions was being hotly contested.

In the absence of knowledge or theory regarding the pathogenesis of fibromyalgia, these authors nonetheless took a bold step to explain the pathogenesis of local pain that became regional.

To accomplish this, Littlejohn invented the concept of “simple injury to the muscle-tendon unit” but neglected to provide any pathological evidence to support the existence of such an entity:

The majority of patients with the “RSI problem” have a chronic pain syndrome, which, although it may be triggered by a simple injury to the muscle-tendon unit, is not due to persisting tissue damage of injury. Extensive investigations seeking out tissue damage will only show age-related changes which do not explain the diffuse symptoms” [9].

Thus, in summary, “RSI” is seen as a complex pathophysiological pain problem where clinical features may be approached using the paradigm of localised fibromyalgia syndrome” [9].

This step needs to be dissected in order to understand the transmutation of fibromyalgia.  A diffuse pain syndrome of unknown pathogenesis was invoked to explain “regional” or “local” apparently similar conditions of allegedly known pathogenesis.  There was never a “paradigm” of “localized fibromyalgia syndrome”; it was never proposed that (diffuse) fibromyalgia syndrome could be “triggered by a simple injury to the muscle-tendon unit”.

These assertions were and are entirely conjectural.

Medico-legal implications

Littlejohn’s next contribution was to downplay the nexus between “localised fibromyalgia syndrome” and work-related factors. This strategy was to have important implications for those with the condition who might be seeking workers’ compensation payments, particularly so in New Zealand [10].

Fibromyalgia can also occur as a syndrome of localised or regionalized pain and a low pain threshold. This situation is common after otherwise short-lived “soft tissue” injuries involving spinal areas, particularly in the context of compensation” [11].

Littlejohn defined “low pain threshold” in terms of sensitivity at the arbitrarily chosen “tender points” in fibromyalgia, which he claimed to be “characteristic regions used clinically to define pain threshold” – a circular argument – and that “sensitivity at these points is increased in pain-free subjects, but to an even greater extent in patients with fibromyalgia syndrome.”

But defining “sensitivity” in terms of the stimulus being applied is highly subjective and influenced by contextual effects and, as Littlejohn noted, this diagnostic criterion (along with widespread pain) has not been validated for medicolegal or disability purposes.

Furthermore, he did not produce evidence to support his claim that “low pain thresholds were common” after short-lived “soft tissue injuries” involving spinal areas. Yet again, conjecture was being passed off as established knowledge.

Littlejohn [12] then raised the spectre of psychogenesis:

The regional features seem to relate to local biomechanical factors around the spine, either postural or secondary to simple strains. When central sensitisation occurs it is likely that central neurophysiological factors, including psychological influences, allow for the amplification of otherwise subclinical spinal reflexes. These in turn cause regional pain, tenderness, muscle tightness and dermatographia.

The concept of “otherwise subclinical spinal reflexes” is yet another of Littlejohn’s conjectures. Furthermore, he failed to explain the mechanism(s) by which “central neurophysiological factors” could be responsible not only for their amplification but also for the various clinical phenomena.

Finally, Littlejohn [13] announced “operational” criteria for a diagnosis of localised fibromyalgia. But in fact they were Littlejohn’s own non-validated criteria [12]:

Regional pain syndromes are also referred to as localised fibromyalgia. Although no validated classification or diagnostic criteria exist for these condition, operational or clinically useful criteria have been proposed: regional pain and regional lowering of pain threshold, and the presence of sleep disturbance, fatigue, muscular stiffness and emotional distress in the absence of a primary nociceptive cause for pain.

“Using this model, regional pain syndrome appears to be on a spectrum between the simple self-limited aches and pains of everyday life and persistent musculoskeletal syndromes such as fibromyalgia.”

Littlejohn’s pronouncements are tautological: if regional pain syndrome is in fact localized fibromyalgia syndrome, then it follows that fibromyalgia is generalised regional pain syndrome.

What was achieved?

Where has this transmutation of fibromyalgia taken us? Has any light been shed on diffuse or regional pain syndromes?

Littlejohn attempted to fill gaps in our understanding of  “RSI” by interpolating his personal views on Fibromyalgia into the debate.  However all he achieved was to introduce circular arguments based on conjecture.   How did the guardians of the literature allow that to happen?

John Quintner (Physician in pain medicine and rheumatology)

Milton Cohen (Specialist pain medicine physician and rheumatologist)

References:

1. Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombadier C, Goldenberg DL, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Arth Rheum 1990; 33: 160-172.

2. Wolfe F, Clauw DJ, Fitzcharles MA, Goldenberg DL, Katz RS, Mease P, et al. The American College of Rheumatology preliminary diagnostic criteria fibromyalgia and measurement of symptom severity. Arthritis Care Res 2010; 62-600-610.

3. Cohen ML, Arroyo JF, Champion CD, Browne CD. In search of the pathogenesis of refractory cervicobrachial pain syndrome. Med J Aust 1992 ; 156: 432-436.

4. Cohen ML, Arroyo JF, Champion GD. The relevance of concepts of hyperalgesia to “RSI”. In: Bammer G, ed. Working Paper No. 31. Canberra: Australian National University, 1992.

5. Quintner JL. The Australian RSI debate: stereotyping and medicine. Disabil Rehab 1995; 17(5): 256-262.

6. Quintner JL, Elvey RL. The neurogenic hypothesis of RSI. In: Bammer G, ed. Working Paper No. 24. Canberra: Australian National University, 1991.

7. Reilly P, Littlejohn GO. Fibrositis/fibromyalgia syndrome: the key to the puzzle of chronic pain. Med J Aust 1990; 226-228.

8. Granges G, Littlejohn GO. Pressure pain thresholds in pain free subjects, in patients with chronic regional pain syndrome, and in fibromyalgia syndrome. Arthritis Rheum 1993; 36: 642-646.

9. Littlejohn GO. Key issues in repetitive strain injury. J Musculoskel Pain 1995; 3(2): 25-33.

10. Rankin DB. Viewpoint: the fibromyalgia syndrome: a consensus report. NZ Med J 1999; 112: 18-19.

11. Littlejohn GO. Med J Aust 1996; 165: 387-391.

12. Littlejohn GO. Clinical update on other pain syndromes. J Musculoskeletal Pain 1996: 163-179.

13. Littlejohn GO. Fibromyalgia syndrome and disability: the neurogenic model. Med J Aust 1998; 168(8): 398-401.

 

 

4 Comments

  1. In their post on “The Transmutation of Fibromyalgia” Quintner and Cohen rail against a renaming and reinterpreting of fibromyalgia. In the US, one often sees the famous quotation from US Supreme Court Justice Potter Stewart who wrote of pornography that he couldn’t define, but “I know when I see it.” It can be that way with fibromyalgia, too. The idea that fibromyalgia could be “local” or regional can be found in the initial description of “fibrositis” in the first decades of the 20th century, and it is repeated in many articles and description before the “official” definition of fibromyalgia of the 1990 American College of Rheumatology criteria. Yunus, in 1981, in his defining on article on fibromyalgia, “Primary Fibromyalgia (Fibrositis): Clinical Study of 50 Patients With Matched Normal Controls,” writes of localized fibromyalgia: “Localized forms of fibrositis, e.g., cervical fibrositis of taxi drivers, gluteal and back fibrositis of bus drivers and localized fibrositis due to trauma (obvious or due to repetitive use) may be recognized by history, involvement of limited (one or two) anatomic sites’ and by the usual absence of non-musculoskeletal symptoms …” In the more recent literature one finds phrases such as “incomplete fibromyalgia;” one author writes of “pre-fibromyalgia” to identify patients who have some but not all of the criteria requisite findings. More recently, the description of the polysymptomatic distress scale and the suggestion that fibromyalgia may be part of a continuum of distress further weakens the classic definition and understanding of the syndrome. In such setting, “I know it when I see” has more than a little utility.

    Some see fibromyalgia as a “central pain disorder,” some as a somatoform condition, some as an invented illegitimate disorder. How one sees it often depends on the beliefs of the observer. I am comfortable in seeing it as part of continuum of polysymptomatic distress in which fibromyalgia is a shorthand for the end of that continuum. When the collection of symptoms and beliefs that we call fibromyalgia becomes reified and then is further split into compartments (local or regional fibromyalgia) we enter a world of religious like beliefs. Quintner and Cohen ask about “the guardians of the literature” (tongue in cheek, I hope). Last week I reread a book that I hadn’t read since childhood, “The Emperor’s New Clothes.” John, Milton, the guardians are in that story.

  2. Fred, would you agree that the fundamental error made by Yunus et al. [1981] was that they mistook their “symptom cluster” for a “syndrome”?

    A “symptom cluster” is a stable group of two or more concurrent symptoms that appear at face value to be related to one another and to be independent of other groupings of symptoms. [Kim et al. 2005]

    One way of understanding the concept of a “symptom cluster” is by way of its analogy with recognizable but imaginary patterns seen within constellations of stars in the night sky. They might appear to be close to one another but in fact they have no real connection and can be light years apart.

    Based on this misconception Yunus et al. [1981], and those who followed them, constructed Fibromyalgia, a process that can be likened to building an edifice of bricks but without using any mortar to bind them together.

    As you know, I am not comfortable with seeing fibromyalgia as “part of a continuum of polysymptomatic distress”. The application of such a descriptor tells us absolutely nothing about the underlying pathogenesis and pathophysiology of the distress.

    References:

    Kim H, McGuire DB, Tulman L, Barsevick AM. Symptom clusters; concept analysis and clinical implications for cancer nursing. Cancer Nursing 2005; 28: 270-282.

    Yunus M, et al. Primary fibromyalgia (fibrositis): clinical study of 50 patients with matched normal controls. Semin Arthritis Rheum 1981; 11: 151-171.

  3. “Fred, would you agree that the fundamental error made by Yunus et al. [1981] was that they mistook their “symptom cluster” for a “syndrome”?” That’s a little to vague and uncertain. I think there were many different errors made.

    “As you know, I am not comfortable with seeing fibromyalgia as “part of a continuum of polysymptomatic distress”. The application of such a descriptor tells us absolutely nothing about the underlying pathogenesis and pathophysiology of the distress.” I think it is an accurate description: the symptoms – all of them- increase together with increasing severity. They begin at minimal levels ands continue to the most severe. I take this for many reasons to suggest that the process is a “normal” one in that it is probably present in the population generally. We concentrate on it when the symptoms are disturbing to us or to the patients. The PDS scale allows us to model this “distress” in a way that we can show that it is associated with severe medical illness, social disadvantage, psychological issues. It helps us to measure some of the issues in “underlying pathogenesis and pathophysiology of the distress,” but doesn’t get to the bottom of it all. In some work I was examining recently, I found the PSD scale was 3 units greater in those below the median income and 2 units greater in smokers than non-smokers. This this type of the thing suggests psychosocial factors play some role in the fibromyalgia and PSD severity. The nice thing about PSD thinking is that you don’t have to believe in a whole series of hypotheses to see it function. But I think that here “less is more.” Unless you believe that FM is a distinct entity or disease ….

  4. Fred, in other words, the term FM functions as an idiom of distress.

    In the words of Eriksen and Risor: “The fundamental symptom experience is embedded in a cultural context, affects families and relationships, and will be subject to communication and interpretation.”

    They go on to argue that “unexplained conditions still largely resist medical approaches focusing on explanation, diagnosis and treatment … they concern life-world related phenomena which largely fall outside the medical gaze … trying to deal with this challenge from an interdisciplinary standpoint, an adequate response could be to receive and interpret such thinking by applying philosophical/existential and sociocultural theories and models.”

    I think we have arrived at the same destination.

    Reference: Eriksen TE, Risor MB. What is called symptom? Med Health Care and Philos DOI 10.1007/s11019-013-9501-5

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Posted on April 2nd, 2015 by John Quintner

ARE THEY ASKING THE RIGHT QUESTION?

The following announcement has just appeared on Myopain Seminars, one of the websites run by proponents of “dry needling”: The Federation of State Boards of Physical Therapy is working on developing a list of competencies needed for physical therapists to perform dry needling, and we would greatly appreciate your help! The Federation has developed a survey based on the Physical Therapy Practice Analysis, developed by the Federation in 2011. The survey contains a list of knowledge, skills, and activities that physical therapist have and undergo. Based on this list, the survey asks if each item is necessary to competently perform dry needling. This survey is the preliminary stage of determining the list of dry needling competencies. Although this is one of the first steps, it is critical. Please follow the link below to complete the survey. Additionally, the Federation asks that you share the survey with any colleagues or practitioners who may be performing dry needling. Please complete the survey no later than April 5, 2015. We truly appreciate your help in this endeavor! If you have any questions, please feel free to contact the Federation at any time. Link: https://survey.fsbpt.org/TakeSurvey.aspx?SurveyID=m80049l Before such a survey is undertaken, the really important question that needs to be asked and urgently addressed by the Federation is whether the currently available scientific evidence supports a continuation of the popular practice by its constituency of “dry needling” muscles and other deep tissues. Clearly, this form of treatment is irrational and therefore the answer must be an unequivocal NO!

2 Comments

  1. As I see it, the more important task to be carried out by the Federation of State Boards of Physical Therapy is that of ensuring its constituency of physical therapists adheres to its Code of Ethics.

    Principle 6 C of the current Code of Ethics mandates that Physical Therapists shall evaluate the strength of evidence and applicability of content presented during professional development activities before integrating the content or techniques into practice.

    There is now sufficient evidence* available
    to suggest that dry needling “myofascial trigger points,” as is currently being performed by physical therapists, lacks a sound scientific evidence base. The fact that many physical therapists currently offer this form of treatment is not relevant.

    The Federation of State Boards is in a unique position to help physical therapists to critically evaluate the various commercially sponsored professional development opportunities being offered under the banner of “dry needling”. Much more than a survey of members will be necessary to determine whether ethical practice is being maintained.

    *Shah JP, Thaker N, Heimur J, Aredo JV, Sidkar S, Gerber L. Myofascial trigger points then and now: a historical and scientific perspective. PM R 2015 Feb 24. pii: S1934-1482(15)00079-9. doi: 10.1016/.pmrj.2015.01.024. {Epub ahead of print] Review.

  2. To everyone “out there”:

    I know it may appear that I am talking to myself, and even that I may harbour an as yet undiagnosed psychiatric condition. But I do suspect that many health professionals read the material which is posted on Fibromyalgia Perplex, courtesy of Professor Wolfe. The ongoing discussions that I have seen taking place on other social media bear witness to this.

    There can not be many physical therapists from English-speaking countries who are unaware of the important debate that has been taking place over MTrP theory and practice. So far it has been a one-sided debate, as the other side is hoping that sooner or later some scientific evidence will turn up to support their strongly held position – a hypothesis that “trigger points” in muscles exist and are a primary source of nociceptive input to the central nervous system. Samuel Beckett’s play – “Waiting for Godot” – springs to mind.

    I do accept that if no one is actually listening, I have indeed wasted my time. But it is mine to waste! Rest assured that I will not waste it by seeking psychiatric opinions.

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Posted on March 27th, 2015 by admin

A couple of points on fibromyalgia

“Name Witheld” has a website entitled http://fibromyass.com. She is not a fan of the fibromyalgia idea and has been writing asking  me to post a link to her web site – something I haven’t done until now. But she has come up with a good question and I thought I’d offer a reply. “How,” she writes, “is someone with rheumatoid arthritis and fibromyalgia different than someone who just has rheumatoid arthritis?” One of the things prompting the question is a rumble that a second clinical trial of the fibromyalgia “blood test” is in the works. Something the blood test developers apparently want to do (in addition to cashing in big) is to distinguish fibromyalgia from rheumatoid arthritis (RA).

As a clinician, I know that persons with RA have swollen joints and tenderness in their affected joints. Often they have certain positive blood tests and often evidence of joint damage that is seen on X-range examination. If you ask people with RA where it hurts, they most often report problems in their affected joints. People with RA and fibromyalgia have all of the these features. But they also have pain in different, but characteristic regions–in the upper and lower back, the hips and shoulders. They are also more tender when examined in specific tender point spots. It’s not hard, and actually it is very simple and easy to identify fibromyalgia in people with RA. All you have to do is to stop and listen. As a sop to Dr. Quintner, I admit flat out that there are a lot of intellectual and logical problems with the fibromyalgia idea that he and I both acknowledge. But for now, lets suspend some disbelief. Dr. Lampman has been very correctly criticizing the nature of fibromyalgia studies. He couldn’t be more correct. People who fit the fibromyalgia diagnostic criteria have severe problems in hundreds of areas. They are always different from those without fibromyalgia. In the absence of a Gold Standard for fibromyalgia, it is hard to see how an expensive blood test could approach the current diagnostic criteria in the ability to accurately diagnose fibromyalgia, nor is it clear exactly what is being measured with the blood test.

The fibromyalgia idea is not so bad if you don’t take it too seriously.

 

2 Comments

  1. My response to Katrine belongs elsewhere on this blog (The Decline and Fall of the Trigger Point Empire).

    I have viewed the various opinions of “Name Witheld” that are highly critical of Fibromyalgia-as-a-diagnosis and, colorful language aside, they are not without substance. I cannot agree with my colleague Professor Wolfe that “the fibromyalgia idea is not so bad if you don’t take it seriously.” Milton Cohen and I have always taken the clinical phenomena associated with the condition very seriously but, from the outset, we have railed against the tautological issue raised by the name given to it. In the spirit of advancing the discussion, I have suggested to “Name Witheld” that a close reading of our 2011 paper might lead to a better understand of the condition. I have also posted on his/her Facebook page an excellent summary of the paper’s content prepared by Dr Pamela Lyon. To the best of my knowledge our paper contains a sound theoretical basis for the condition, and advances a testable (and refutable) hypothesis based upon this theory.

  2. Katrine, I neglected to thank you for your comment. I hope that increasing numbers of your colleagues will share your disapproval of the pseudo-scientific explanations currently being given to so many people in pain. The scientific evidence informs us that passive treatment modalities have little or no place in contemporary pain management. The emphasis is now being placed on facilitating a “third space” engagement between clinician and patient. It is in this space that pain education can be effectively delivered. Delivering it at the point of a needle is a very poor substitute!

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Posted on March 6th, 2015 by admin

We are back

Sometime last year I stopped posting to this blog and kind of let things go. We hadn’t been able to attract some the fibromyalgia leaders to participate, and I wondered if it was all worth the effort. I am going to try again, now. Still, we had many participants and a wide variety of comments. There are several reasons I decided to go on. First, Dr. John Quintner, who has been an inveterate source of comments, comforts and articles, suggested I should. His recent post on Trigger Points is an example of his very high quality work. It starts a discussion that has been long needed. Second, I have many comments and ideas about fibromyalgia that are very hard to express with the current system of journals and reviews. I want to publish these thoughts here. More about that to come.

The blog was designed for professionals, with the idea that professional would have a good idea of the scientific method (whatever that is) and could respond based on data and scientific analysis. Some of you might say this was a dubious belief, but at least the standard should be known to this group. Later, we opened the blog to non-professionals, including patients, provided they met certain rules. We blocked post from those who did not follow the rules; and we blocked some health professional, too. But some of the best comments we have had have come from non-professionals. See the series of important posts from “Nancy.”

So if you want to post, we welcome your comments. But pay attention to the rules. I repeat them here. From the “About” section:

This blog is designed to facilitate open, vigorous discussion about fibromyalgia and fibromyalgia-related issues. Say here what you think. We want to open up frank discussions of the full spectrum of fibromyalgia-related ideas and consequences. But do keep in mind Niels Bohr’s admonition, ‘It is not enough to be wrong, one must also be polite.’

Rules about posting and articles:

About comments. We want this blog to be about research and discussions concerning fibromyalgia. To post to this blog you should be a published author, have other academic credentials, or would be welcomed as a discussant in an academic journal. We make these somewhat arbitrary rules to try to exclude the general, non-scientific public. We welcome comments by all scientists and social scientists, not just those who are physicians. This blog is moderated, meaning that the editors decide what will appear. In general, we will not censor on-topic scientific posts provided authors meet the above guidelines. If you don’t fit our guidelines and think you have something to contribute, send the editors an email at fmperplex@gmail.com. [As a modification, we will accept post from non-profesionals provided they meet certain criteria.]

About articles. We welcome submissions of articles. By articles we mean new subject posts of varying length. They can be long. In fact, we might even publish short academic articles. If you want to submit a new-subject post, write and discuss this with the editors first at fmperplex@gmail.com.

From some previous posts: “We will not publish insulting or crude comments. They just won’t appear. If you have something to say, try to think about it in a scientific way. Provide evidence. Think about why you might be wrong. We’ll give it a try.

I (we) can’t and won’t answer personal problems. We won’t give medical advice. People with fibromyalgia know a lot. You can help us with thoughtful comments.”

Non-Professional authors who are uncertain if we will publish their comments are welcome to write to me with questions.

 

 

 

3 Comments

  1. In restarting the blog, I noticed a number of comments had been sent in but had not been posted. There is supposed to be system to notify me when post come in, but it didn’t seem to have been working. In any event, I have seen to it that the comments are posted. Replies should be coming soon. In the parlance of the day, “my bad.”

    • Dr Wolfe, I am very concerned by your new assertion that fibro is not a diagnosis of exclusion. It should be. I was diagnosed with fibromyalgia repeatedly for 2 years, told I was in denial about my fibromyalgia when I insisted I do not believe in it and I must have something else. It turns out I have kidney failure which was not diagnosed until I literally collapsed. My nephrologist does not believe in fibromyalgia, I hurt all over because my immune system was attacking my kidneys. I got better as soon as I started dialysis and learned to not eat so much fruit. How irresponsible is it to say that overworked GPs should just diagnose fibro based solely on someone meeting the 2010 criteria you helped write? How many other conditions cause someone to hurt all over for 3 months, and have other random symptoms like nausea? Have you seen the recent studies with fibro patients where they thought they found nerve differences, but it turned out these people had nerve differences caused by neuropathy, caused by diabetes and hepatitis? Or the others who declared they had found a thyroid difference in fibro patients, but later found out the people they were looking at actually had a thyroid problem?

      • What we mean by “fibromyalgia is not a diagnosis of exclusion” is that it is possible to have fibromyalgia and other diseases at the same time. For example, rheumatoid arthritis and fibromyalgia, cancer and fibromyalgia, and renal failure and fibromyalgia. To call something fibromyalgia and not identify renal failure is a terrible medical error. Almost all medical problems can coexist with fibromyalgia. It is the job of the physician to identify all important medical conditions. Even so, fibromyalgia is not a common problem in renal failure. See Bardin T. Musculoskeletal manifestations of chronic renal failure. Curr Opin Rheumatol 2003;15:48-54.

        You really should cite references for the statements, “Have you seen the recent studies with fibro patients where they thought they found nerve differences, but it turned out these people had nerve differences caused by neuropathy, caused by diabetes and hepatitis? Or the others who declared they had found a thyroid difference in fibro patients, but later found out the people they were looking at actually had a thyroid problem?” And it is important to be clear about the quality of evidence and the ability to understand causation in small,non-randomized studies and case reports.

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Posted on March 5th, 2015 by Fred Wolfe

THE DECLINE AND FALL OF THE TRIGGER POINT EMPIRE

Below we publish Quintner, Bove and Cohen’s Response to Dommerholt and Gerwin: Did we miss the point? The  Dommerholt and Gerwin article is a reply to Quintner, Bove and Cohen’s important refutation of the trigger point concept. If you haven’t seen it, you should read it. It is a landmark in the trigger point debate. We publish this additional commentary here in the spirit of encouraging discussion, as it is hard to bring debate and discussion to convention medical journals. Similarly, we offer space to Dommerholt and Gerwin. – Fred Wolfe, MD

THE DECLINE AND FALL OF THE TRIGGER POINT EMPIRE

It should by now be obvious to those who have read our paper (Quintner et al. 2015) that we do not share the same beliefs as do Dommerholt and Gerwin (2015), who mounted a spirited defense of their preferred theory of myofascial pain arising from trigger points (MTrP).

This is a most important academic debate. Both Robert Gerwin and Jan Dommerholt claim to have studied and worked with the founders of MTrP theory, Drs Janet Travell and David Simons. They lecture and teach around the world under the banner of Myopain Seminars. “Dry needling” of MTrPs is their favoured treatment modality for pain that is deeply felt within muscles.

The position taken by Dommerholt and Gerwin

In summary, Dommerholt and Gerwin (2015) have made their position quite clear:

Based on our understanding of the literature, Quintner et al. have not presented any convincing evidence to believe that the Integrated TrP hypothesis should be laid to rest” and that “insufficient evidence is to be taken that further studies are needed …” and that “Quintner et al have not succeeded in providing sufficient evidence that the current TrP hypotheses should be rejected.”

Dommerholt and Gerwin have raised a number of important issues and made accusations that impugn our scientific credibility. They have very publicly thrown down the gauntlet.

In this article I do not intend to address each and every accusation raised in their “rebuttal”, but will examine those that seem to be most relevant. Our shorter and more focused response is currently available as an article “in press” and we understand that it will be published in the July issue of the Journal of Bodywork and Movement Therapy.

Preconceived bias?

Dommerholt and Gerwin appear to have interpreted as bias our seizing upon the lack of epistemological discipline shown by the original proponents of MTrP theory (Travell & Rinzler, 1952; Travell and Simons 1983).  We first exposed the major flaws in this theory in 1994 (Quintner & Cohen, 1994). To date, these flaws have not been acknowledged, let alone addressed by proponents of the theory. It was this lack of response that prompted our second paper on the subject (Quintner et al. 2015).

Biased review of the literature?

“Quintner et al’s paper is a biased review of the literature replete with unsupported opinions and accusations.”

Limitations of space in Rheumatology meant that the many studies that have been undertaken based upon the premise that TrPs were potential sources of nociception resulting from localised muscle damage could not be included. But when arguing from a false premise (i.e. in this case an unwarranted assumption regarding the properties of TrPs), no amount of evidence can ever rectify such a fundamental fallacy of logical reasoning.

Discrediting MTrP research?

“In doing so, they specifically discredit much of the research on myofascial TrPs that has been published as unreliable, without providing any alternative studies specifically done on the pain phenomena that is attributed to TrPs.”

Dommerholt and Gerwin concede that several aspects of “myofascial pain” remain elusive and are not well understood, and that “a distinct mechanistic understanding of this disorder does not exist.” Therefore, as they appear to agree with us, there is no need to resile from the first proposition.

As for the second proposition, it was not our brief to provide “alternative studies specifically done on the pain phenomenon.”  But at the very least our paper calls for such studies to be undertaken as a matter of priority. Furthermore, in our paper we have pointed a way towards achieving this objective.

Our use of “theory” and “hypothesis”

Dommerholt and Gerwin are critical of our use of “theory” and “hypothesis” and claim that we have used them in a non-scientific manner.

“Scientific inquiry commonly starts with observations, followed by the development of hypotheses, which through experiments are confirmed, modified, or refuted. Through repeated experimental testing of the hypothesis it is continually refined until a theoretical basis can be constructed that addresses different aspects of the hypothesis.”

A theory is a generally accepted explanation for an observed set of phenomena. Hypotheses can be deduced from theory. Refutation of (the claims made by) a hypothesis should lead to modification of the theory. Repeated refutations of hypotheses generated by modified theory should lead to refutation of the theory.  In this way, even cherished theories such as MTrP can be contested.

We did mention the face validity of the generally accepted explanation for the phenomena associated with the MTrP, but in our paper we went on to argue strongly against it on the grounds that its proponents were lacking in epistemological discipline.

Diagnosis of trigger point

We acknowledge that there has not been a study to demonstrate the minimum essential features of the TrP needed to identify it for diagnosis and treatment purposes.”

Although Dommerholt and Gerwin agree with the absence of agreement about the pathognomonic feature of their explanatory model, despite 50 years of investigation, they still argue that more studies are needed. But we fail to see how such studies would avoid the twin errors of confirmation bias and circular argument.

The nature and validity of latent TrPs

“The differentiation between normal muscle tissue, active and latent TrPs reflects the degree of contraction, as confirmed objectively by vibration elastography. Their mechanical attributes are, however, not directly correlated with pain pressure threshold scores (Ballyns et al 2012), which Quintner et al interpreted as another nail in the coffin of the TrP hypothesis.

… Ballyns et al. clearly were able to distinguish and visualize contractured nodules on muscle that were only painful when stimulated (Ballyns et al. 2012).

Ballyns et al. (2012) were indeed able to provide an objective assessment of relatively superficial soft tissue, but did not make a comment as to whether the reported abnormalities in painful muscle were consistent with “contractured nodules”.

They did find regions that were “stiffer” than surrounding muscle tissue and equated them with “active” trigger points. Some of the smaller regions of stiffness were said to represent “latent” trigger points. One may well ask on what grounds were they able to make these inferences?

In the section dealing with patient selection, Ballyns et al. did not explain how they were able to exclude from the study those patients whose pain and tenderness was likely to have been referred into the muscle(s) being studied.

Sikdar et al (2009) claimed to have excluded those with “neck and shoulder conditions” including cervical radiculopathy. But did they really exclude patients whose pain may have been referred into these muscles from, for example, cervical zygapophyseal joints? We think not!

Sonographic evidence

Sonography is not only used for research and possible diagnostic purposes, but can also be applied to guide trigger point needling (Botwin et al. 2008, Bubnov 2010, Suh et al. 2014) and to objectively measure the outcome of TrP interventions such as dry needling. (Maher et al, 2013)

In a preliminary study Maher et al. (2013) found that the shear modulus of the upper trapezius muscle with MTrPs was significantly reduced after dry needling of the most painful TrP and also when the subjects assumed the prone position from supine lying. These changes were accompanied by palpable reductions in stiffness.  The authors did not address the important questions as to whether these reductions were transient and whether pain relief accompanied them.

Pathogenesis of the trigger point

Apparently, they believe that TrPs are some kind of anatomical entity, although there has never been a credible anatomic pathology associated with myofascial TrPs.”

Yet, in the studies we reviewed, and in the various other studies cited by Dommerholt and Gerwin, the authors assumed that an anatomical lesion actually existed. This logical fallacy is known as “begging the question”.

Quintner et al. refer to “fibrositic nodules” which have nothing in common with TrPs and their relevancy escapes us.”

But they go on to assert that TrPs are “palpable as hard nodules within a band of contractured fibres …”

They would appear to have contradicted themselves!

Use of animal studies

The majority of the studies of electrical activity of the TrP were carried out on animals and were based on palpation of locally contracted muscles.”

Our difficulty in accepting data derived from findings in muscles from normal animals is covered in our paper. Moreover as Dommerholt and Gerwin acknowledge “there has not been a study to demonstrate the minimum essential features needed to identify it for diagnosis and treatment purposes.” If this issue has yet to be resolved in humans, we fail to see how it has been resolved in animals.

Tissue biochemistry

Quintner et al. criticize the findings of Shah et al (2003, 2005, 2008), who have reported higher concentrations of neurotransmitters and cytokines in the extracellular fluid in the immediate vicinity of TrPs as being non-specific.”

In fact we made no such criticism but did offer two possible neuroscientific explanations for these findings, the most likely one being “neurogenic inflammation”.

Muscle pain versus myofascial pain

Perhaps Quintner et al. would consider our reasoning an example of conjecture, but the facts are that a low pH is common at active TrPs, and can cause muscle pain and hyperalgesia.”

We suggest that Dommerholt and Gerwin have fallen into the trap of conflating all pain felt in muscles with pain in muscles said to arise from supposed “myofascial TrPs”.

Twitch response

Quintner et al. … suggest that a local twitch response, which is an entirely different feature of the taut band, is nothing more than a myotatic stretch reflex.”

According to Audette et al. (2004) the literature does indeed differentiate the “localised twitch response” from a myotatic stretch reflex.

In a discussion by Simons (1976), “two features suggest a hyperirritable spinal reflex phenomenon: the increased motor unit response with increasingly vigorous palpation and the simultaneous activation of adjacent palpable bands.”

It should be noted that mechanical irritation of a hypersensitive peripheral nerve appears to generate a motor efferent response with activation of at least a subset of the motor neuron pool (Hall and Quintner, 1996).

Central sensitization induced by TrPs

 Some of the phenomena that seem to trouble Quintner et al. result from the fact that TrPs induce central sensitization and referred pain. Muscles do have nociceptors and activation of those nociceptors can initiate and perpetuate central sensitization.”

We are indeed troubled by the first proposition. It has yet to be shown that MTrPs are capable of activating nociceptors. But we have no argument with the second proposition.

It is true that Mense (2008) did accept (albeit with some reservation) the notion of MTrPs as potential peripheral generators of nociceptive activity. But following his brief summary of the hypothesis proposed by Simons (2004), he commented “this supposed mechanism leaves many questions unanswered but is currently the only comprehensive hypothesis on the origin of MTrPs.”

 We agree with Mense that there are still unanswered questions.

Low–level isometric contractions and TrP formation

 In 2006 and 2011, two complementary studies … explored whether the Cinderella Hypothesis could apply to the formation of TrPs.” Both studies provided evidence that low-level exertions can lead to the formation of TrPs (Treaster et al. 2006, Hoyle et al. 2011)

This conjecture concerns low threshold motor units, termed “Cinderella” fibers, which are being continually recruited and overloaded during low-level static exertions. It is not made clear how could one ever know this? Presumably damage to such fibers provides the basis for nociceptive input in these situations. This conjecture forms the central plank of the Integrated Hypothesis (Gerwin et al 2004).

In the second study, the authors concede that their findings were solely dependent on the expertise of a clinician not only to palpate the upper division of the trapezius muscle to locate and diagnose a taut band as a MTrP but also to rate its “sensitivity”.

Readers are then asked to accept the dubious proposition that once the examiners had located a TrP, “all detected trigger points in the trapezius and surrounding muscles were released by a combination of percussion, stretch and relaxation techniques” immediately prior to the commencement of the experimental task (approximately 60 minutes of computer typing). Following task completion, the subjects were then re-examined by the same clinicians to detect recurrence of any MTrPs, which were again duly “released”.  Surface EMG was recorded from a grid overlying the identified MTrPs.

The authors speculated that MTrPs may be one causal pathway for pain during low-level static exertions and both postural and visual demands may play a role in muscle activation patterns, perhaps contributing to MTrP development and related discomfort.

Based on our assessment of these rather unusually designed studies, we cannot agree with Dommerholt and Gerwin that they “provided evidence that low-level exertions can lead to the formation of TrPs.”

 New evidence provided by Dommerholt and Gerwin

“Rather than ignoring the worldwide developments in this field, we prefer the approach by Jafri, who critically reviewed the current thinking and contributed to a more in-depth understanding of possible underlying mechanisms (Jafri 2014)”.

Our problem with the approach of Jafri (2014) is that in his introductory remarks he begged the question that is at the heart of this debate:

While myofascial pain syndrome is complex in its presentation, the onset and persistence of myofascial pain syndrome are known to be caused by myofascial trigger points.”

Jafri accepts without reservation the opinion of David Simons (2004), one of the main proponents of MTrP theory. Unfortunately the remainder of his paper fails to rise above the level of conjecture.

Moseley confirmed that especially myofascial TrPs and joints are widely held to be common contributors to somatic referred pain.”

We acknowledge, as does Moseley (2012), that such an opinion is widely held amongst physical therapists. However, Moseley then asserts: “trigger points are present in all patients with musculoskeletal pain …” Drawing an analogy here with the universal generalization that “all swans are white” seems inescapable. The observation of one black swan (or of one patient without a trigger point) falsifies the argument.

When discussing somatic referred pain Moseley suggested that “disrupted transmission” happens within the central nervous system and he viewed “somatic referred pain from TrPs and joints as the brain’s efforts to localize the pain in response to ambiguous input.”

We are not aware of evidence for such “disrupted transmission” or for “ambiguous input” associated with referred pain phenomena.

But we can agree with Moseley’s concluding remarks: “This is a field where clinical practice may change as new evidence emerges, or new evidence may underscore the validity of current clinical practice.

 Hypotheses of Quintner et al.

Dommerholt and Gerwin dealt mainly with one of the two explanatory models we advanced in our paper – that based upon the “neuritis” model. They accepted the model of “referred pain and tenderness” but asserted that its maintenance “is dependent on ongoing nociceptive input from the site of primary muscle pain.”

Some of their concerns about the “neuritis” model can easily be resolved when one accepts the readily available evidence that pain of peripheral nerve origin may not necessarily be accompanied by changes in cutaneous sensation, by objective signs of motor deficit or by changes detected on conventional electrodiagnostic examination (Quintner and Cohen, 1994).

Dommerholt and Gerwin prefer to rely upon evidence from the experimental studies of Arendt-Nielsen and Svensson (2001) and Rubin et al. (2009) to support the importance of “ongoing nociceptive input from the site of primary muscle pain in maintaining the phenomenon of referred pain.” But no such experiment has been shown to mimic the clinical situation.

We do not doubt that nociceptor fibres innervate muscles and that they can be activated by a variety of noxious stimuli. We agree that central mechanisms are important in explaining the phenomena of referred pain. However, it has yet to be demonstrated that a hypothetical “painful lesion” residing in “myofascial” tissues can be responsible for initiating and maintaining a state of central hypersensitivity.

Conclusion

As we have shown, Dommerholt and Gerwin (and others) have been arguing from the false premise of an unwarranted assumption – that MTrPs are primary sources of nociception. No amount of evidence they can adduce will rectify this logical error. 

But if, as we believe, MTrP theory has been well and truly refuted, the scientific credibility of those who offer courses in “dry needling” to physical therapists can legitimately be called into question.

Prepared by John Quintner, Physician in Rheumatology and Pain Medicine, first author of “A critical evaluation of the trigger point phenomenon (2015).” He writes here on behalf of his co-authors.

References:

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

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

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

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

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

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

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

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

Jafri MS. Mechanisms of myofascial pain. International Scholarly Research Notices Volume 2014 (2014): Article ID 523924, 16 pages. http://dx.doi.org/10.1155/2014/523924

Maher RM, Hayes DM, Shinohara M. Quantification of dry needling and posture effects on myofascial trigger points using ultrasound shear-wave elastography. Arch Phys Med Rehabil 2013; 94; 2146-2150.

Mense S. Muscle pain mechanisms and clinical significance. Dtsch Arztebl Int 2008; 105: 214-219.

Moseley GL. 2012. Pain: why and how does it hurt? In: Brukner P, Khan K, eds. Clinical Sports Medicine, 4th ed. Sydney: McGraw-Hill Aust Pty Ltd. 2012: 41-53.

Quintner JL, Cohen ML. Referred pain of peripheral neural origin: an alternative to the “Myofascial Pain” construct. Clin J Pain 1994; 10: 243-251.

Quintner JL, Bove GM, Cohen ML. A critical evaluation of the “trigger point” phenomenon. Rheumatology 2015; 54: 392-399

Rubin TK, Henderson LA, Macefield VG. Changes in the spatiotemporal expression of local and referred pain following repeated intramuscular injections of hypertonic saline: a longitudinal study. J Pain 2010; 11: 737-745.

Sikdar S, Shah JP, Gebreab T, Yen RH, et al. Novel applications of ultrasound technology to visualize and characterize myofascial trigger points and surrounding soft tissue. Arch Phys Med Rehabil 2009; 90: 1829-1838.

Simons DG. Electrogenic nature of palpable bands and “jump sign” associated with myofascial trigger points. In: Bonica JJ, Albe-Fessard D, eds. Adv Pain Res Ther (vol.1). New York: Raven Press, 1976: 913-926.

Suh MR, Chang WH, Choi HS, Lee, SC. Ultrasound-guided myofascial trigger point injection into brachialis muscle for rotator cuff disease patients with upper arm pain: a pilot study. Ann Rehabil Med 2014; 38: 673-681.

Simons DG. Review of enigmatic MTrPs as a common cause of enigmatic musculoskeletal pain and dysfunction.  J Electromyogr Kinesiol 2004; 14: 95–107.

Travell J, Rinzler SH.  The myofascial genesis of pain. Postgrad Med 1952: 11: 425-434.

Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. Baltimore: Williams and Wilkins, 1983.

Treaster D, Marras WS, Burr D, Sheedy JE, Hart D.Myofascial trigger point development from visual and postural stressors during computer work. J Electromyogr Kinesiol 2006; 16: 115-124.

 

35 Comments

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

    Limitations of space in Rheumatology meant that the many studies that have been undertaken based upon the premise that TrPs were potential sources of nociception resulting from localised muscle damage could not be included.

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

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

  4. Dr. Wolfe,

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

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

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

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

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

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

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

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

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

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

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

      Clearly there is nothing left for us to debate.

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

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

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

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

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

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

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

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

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

    References:

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

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

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

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

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

    Here are the examples:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

  15. Very interesting.

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

    I recently read Erika Janik’s “Marketplace of the Marvelous: The Strange Origins of Modern Medicine,” with subtitle “An entertaining introduction to the quacks, snake-oil salesmen, and charlatans, who often had a point.” [There is a nice summary at http://www.goodreads.com/book/show/17797396-marketplace-of-the-marvelous. It’s especially good on mesmerism, Christian Science, and various diet & water therapies of the 19th Century.

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

    So how, then, do WE get it right?

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

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

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

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

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

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

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

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

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

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

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

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

    I regret being retired now and thus unavailable to participate!

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

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

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

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

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

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

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

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

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

    Our replies to each of these e-letters can also be viewed at this website address: http://rheumatology.oxfordjournals.org/letters/

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

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

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

    But this is only wishful thinking.

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

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

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

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

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

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

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

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

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

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

      Fred Wolfe

      Fred Wolfe

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

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

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

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

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

    Reference: Shah JP, Thaker N, Heimur J, et al. Myofascial trigger points then and now: a historical and scientific perspective. PM R 2015; available at http://dx.doi.org/10.1016/j.pmrj.2015.01.024

  22. Pingback: Mechanosensitivity: “The doctor poked, and prodded, and scratched his chin. He could find nothing wrong”

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

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

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

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

    Here it is, reproduced in full:

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

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

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

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

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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.

45 Comments

    • 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 http://muse.jhu.edu/books/9780813552224 ) 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.

    • Yes. You are missing something. This is more likely because you do not have a PhD or MD and do not deal clinically with patients. Dr. Lampman’s points are perfectly normal English and are not circular whatsoever.

  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?

          References:
          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. http://www.discoverymedicine.com/Amy-D-Proal/2014/05/22/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]

  20. Hello. I found your slides quite interesting. I found my way to them after reading a New York Times article on Fibromyalgia. I have been fascinated/angered by Fibromyalgia since finding out about it in the early 2000’s. I guess angered mostly by the fact that it is within the same class of diseases as SLE or Lupus, which I have. I also have unexplained aches and memory problems as well as suffering from a disease which can at times flare while I appear outwardly healthy. Yet at the same time, I’ve also suffered from seizures, hair loss, kidney disease, which can not be seen as just self-diagnosed or self-reported. I guess the idea that my self-reported pain, fatigue, and cognitive problems are in itself diagnosed as a separate illness just… doesn’t sit well with me. I guess I’m curious how a knowledgeable health professional may be able to differentiate Lupus from Fibromyalgia with only those symptoms. I think most times I don’t even go to an urgent care facility or see a doctor for symptoms that are termed “Fibromyalgic” because I actually don’t know what normal tiredness or pain is because I’ve had Lupus since I was 11. To imagine that people flood emergency rooms for feeling tired or “hurting all over” just seems to diminish and minimize diseases with measurable and independently assessable symptoms like Lupus. Sorry if I offend anyone… but my question stands: how may a doctor, with all his knowledge and instruments, tell the difference between Lupus tired and pain and Fibromyalgia tired and pain?

  21. (Sorry, my previous comment was made before reading through the comments, and I believe my question has been more or less answered, in my mind, at least)

    A few comments, and please I hope you take these as a bit more serious than a layperson – I am doing my PhD in Psychology, although the more difficult medical terms escape me.

    Any diagnosis based solely on self-reported data is perplexing. In psychology, it’s been shown time and time again that self-reported data is unreliable. A person given a questionnaire to measure said persons personality as part of his application for a job is always going to report himself in a more favorable light. A person who takes himself to a doctor is looking to walk out with a diagnosis and a prescription. He is going to report symptoms that can only be self reported since anything else might prove he doesn’t need to be there. Pain, fatigue, cognitive problems all fall in that range. I once read in a book about falsifiability that an example of an unfalsifiable hypothesis is that of saying there are little green men that live in the brain – except they hide if you try to observe or measure them in any way. As a Lupus patient, Dr. Lampman’s assessment is correct -my subjective pain and fatigue has usually been mirrored in an objective abnormality in my lab results. Thus my self-reported pain can be verified objectively which makes it more than little green men residing in my brain – can the same be said of Fibromyalgia pain, which avoids all measurement except self-report?

    I don’t think I’m completely against the idea of Fibromyalgia – if more objective proof surfaces I have no problems “changing sides”. As it were, though, it seems research is focused on scrambling to legitimize a disease that may or may not be deserving of a diagnosis. Again, this comment is not made to offend what may in time, be proven as an objectively assessable disease, but the current inadequacies in which diagnosis is made.

    By the way, I very much enjoyed your whole site Dr. Wolfe. Thank you!

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Posted on January 27th, 2014 by John Quintner

SUGAR-COATED NERVES: THE PSEUDO-SCIENCE OF NEURAL PROLOTHERAPY

 The human understanding when it has once adopted an opinion draws all things else to support and agree with it. And though there be a greater number and weight of instances to be found on the other side, yet these it either neglects or despises, or else – by some distinction sets aside and rejects, in order that by this great and pernicious determination the authority of its former conclusion may remain inviolate. [Francis Bacon (1620) from Novum Organum, Book 1, Aphorism XLVI.]

Introduction.The latest fads from the shadowy world of pseudo-science have always been quick to take off. For those who are keen on approaching pain sufferers with their sharp needles, the invention of Neural Prolotherapy by Dr John Lyftogt, of Christchurch in New Zealand, must have come as a godsend. A quick search on the Internet reveals that this invention is being taken seriously by a number of health practitioners who one might have expected to have known better than to accept it so uncritically.

The claims for Neural Prolotherapy “Prolo-” is short for proliferation and derives from the Latin “to regenerate or rebuild”. Prolotherapy with injectable substances that are being acclaimed as growth factors is now the subject of intensive research. But Dr Lyftogt favours hypertonic sugar injections.

Here are some remarkable extracts from his website (http://www.doctorliftoff.co.nz/):

“After the success of Neural Prolotherapy with Achilles tendonitis other persistent painful conditions of the neck, back, shoulders, elbows, wrists, knees, ankles and feet have been effectively treated by targeting the local inflamed superficial nerves with micro-injections of low dose Glucose.”

Comment: there have been no properly conducted clinical trials of Neural Prolotherapy.

“More recently Dr Lyftogt has developed effective neural prolotherapy treatment protocols for Migraine. ‘Fibromyalgia,’ CRPS, compartment syndrome and other difficult to treat persistent painful conditions.”

Comment: Again, no clinical trials have been conducted. The evidence is purely anecdotal and subject to all forms of bias.

“Neural prolotherapy is an effective novel and evolving treatment for non-malignant persistent pain, based on sound neuroscientific principles.”

“Subcutaneous prolotherapy with a series of percutaneous near nerve injections has been shown to be an effective treatment for a variety of recalcitrant painful conditions caused by prolonged neurogenic inflammation.”

Comment: This is the logical fallacy called circular argument: the conclusion is assumed before the evidence is presented. Dr Lyftogt offers no evidence that these conditions are associated with “prolonged neurogenic inflammation”.

The “sound neuroscientific principles”

Dr Lyftogt targets the “guilty” superficial nerves by injecting 5% Mannitol or 5% dextrose and thereby claims to modulate the neurogenic inflammation that he believes is responsible for “neuropathic pain”. He refers to the work of a highly regarded authority:

“Quintessential to the working hypothesis that subcutaneous prolotherapy treats prolonged pathological neurogenic inflammation is the work by Douglas W Zochodne from the Neuroscientific Research Unit at Calgary University.” [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.

Conclusion

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.

References

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

 

7 Comments

  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.

  3. Let me first state but I am not a physician and my position is purely anecdotal. I have suffered chronic pain for over two years and after multiple MRIs x-rays and meetings with multiple physicians including orthopedic surgeons who all concluded the only relief from the pain was a total hip replacement due to chronic arthritis and the degenerative condition of my hip joint. I recently heard from my primary physician about this procedure being performed by a pain management physician who had attended and trained under Dr. Lyfogt. While I do not necessarily understand the science of these injections I can only say I experienced immediate and significant pain relief from this treatment. As others may have noted while the science of exactly how this works may not be fully understood that does not mean it does not work. 100 years ago doctors were experimenting with practices that produced significant advances in medical care yet they fully did not understand them. I suspect the future will bear out the same as to this treatment protocol. I would recommend this treatment highly particularly for those skeptical of this protocol or who may experience chronic pain and be in need of relief.

  4. As a rheumatlogogist with 25 years of experience (NSAIDs, DMARDs, biologicals, steroids you name it) simple subcutaneus Dextrose 5% is certainly working fasciapain (check the book of Carla Stecco Functional Atlas of the Human Fascial Systeem) and I use it for frozen shoulders, crista iliac pain, tractus iliotibialis pain etc. It is much more effective than local steroids combined with local anesthetics. The reason for little evidence is because it is cheap and pharmaceutical companies are not interested. I agree there are no placebo controlled trials but this is also the case with treatment of frozen shoulders or pain around the trochanter major etc. I would be glad to participate in trials regarding this treatment.

  5. Dear Dr van den Brink. As there is no scientific evidence to support them, in my opinion your claims of specific therapeutic efficacy of dextrose injections must be taken with a pinch of salt. Any benefit therefrom is more likely to be attributable to the influence of contextual factors (i.e. placebo responses). I would not waste effort, time and money on conducting RCTs based upon this conjecture.

  6. Dear Dr Quintner,

    As a gynaecologist specialized in pain, I treat pudendal neuropathy since 20 years. I have learned neural prolotherapy with Dr John Lyftogt and it has changed completely my practice and the life of my patients.
    In my experience, NPT is very effective on perineal pain but also on Maigne syndrome (pain in lower abdomen), Tennis Elbow, back pain, frozen shoulder, cervicalgia., knee and feet pain. I have tried this method with lots of my patients who didn’t find a solution with more classical approaches (physiotherapy, corticoids injection, ultrasounds…). I can say that it is more effective than classical methods and therefore than placebo.
    Please try it ! Make a RCT if you want and begin to think out of the box to better help your patients.

    “Toute vérité franchit 3 étapes. D’abord elle est ridiculisée. Ensuite, elle subit une forte opposition. Puis elle est considérée comme ayant toujours été une évidence” Arthur Schopenhauer

    Jacques Beco md
    Université de Liège
    Belgium

  7. Dear Dr Beco,

    On my reading, Schopenhauer’s quotation concerns truth rather than conjecture. The theory upon which this treatment is based is scientifically unsound. Your evidence is anecdotal and subject to many forms of bias, not the least being confirmation bias.

    It is the responsibility of proponents of neural prolotherapy to conduct the RCT. In the meantime, neural prolotherapy must remain in the category of unproven remedies.

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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.

 

16 Comments

  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.

      http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2703259/

      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.”

    From http://www.npr.org/blogs/13.7/2014/01/08/260752365/a-tribute-to-failure?sc=tw&cc=share

    • @ 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. I hadn’t heard of the needling, causing pain to sufferers of FM. Indeed as a massage practitioner I was taught that over vigorous massage could leave the patient/client exhausted if not following the treatment then the following day.

    I am one of those who treat without having a good evidence base for everything I do. (There are areas of my practice where there is a good evidence base for the essential oils I choose.) I keep careful records and those I have seen with FM tell me the treatment has helped. However I have no controls and the numbers (five over the past two years) are not significant.

    While I don’t have the time to organise it, I would be more than happy to put my information into some larger database and to ask my clients whether they would be willing to be interviewed as part of a study. However I don’t have the time to organise such a study, contacting the number of therapists that would be needed, and agreeing a treatment protocol in order to produce statistical validity. What I can do is post something with my professional body to see if they are able to do this.

  8. 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

Abstract

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]

6 Comments

  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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