MORE TROUBLE IN THE LAND OF THE TRIGGER POINT

Introduction

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

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

The Delphi study

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

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

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

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

The first round

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

The second round had three elements

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

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

The third round

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

Outcomes

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

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

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

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

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

Discussion 

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

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

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

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

Conclusion

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

References

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

 

Has Your Fascia Freaked Out?

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

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

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

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

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

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

A chart has even been compiled showing the condition of the fascia at each phase, what’s happening in the body, and both the symptoms present and the respective diagnoses: https://ashleyblackguru.com/wp-content/uploads/2013/08/Fascia-Chart.pdf

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

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

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

Total Body Pain Relief

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

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

A comprehensive series of self-help tutorials is readily available on her website: https://ashleyblackguru.com/tutorials-home/

For those with fibromyalgia, a short video is used to explain the treatment: https://www.youtube.com/watch?v=JsNq9TLJWmc

So who is Ashley Black?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Frederick Wolfe MD and Brian Walitt MD MPH

References

  1. Walitt B, Nahin RL, Katz RS, Bergman MJ, Wolfe F. The Prevalence and Characteristics of Fibromyalgia in the 2012 National Health Interview Survey. PLoS One. 2015;10(9):e0138024.
  2. Walitt B, Katz RS, Bergman MJ, Wolfe F. Three-Quarters of Persons in the US Population Reporting a Clinical Diagnosis of Fibromyalgia Do Not Satisfy Fibromyalgia Criteria: The 2012 National Health Interview Survey. PLoS One. 2016;11(6):e0157235.
  3. Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33(2):160-172.
  4. Wolfe F, Clauw D, Fitzcharles MA, et al. The American College of Rheumatology Preliminary Diagnostic Criteria for Fibromyalgia and Measurement of Symptom Severity. Arthritis Care Res. 2010;62(5):600-610.
  5. Dumit J. Illnesses you have to fight to get: Facts as forces in uncertain, emergent illnesses. Soc. Sci. Med. 2006;62(3):577-590.
  6. Nettleton S. ‘I just want permission to be ill’: towards a sociology of medically unexplained symptoms. Soc. Sci. Med. 2006;62(5):1167-1178.
  7. Clauw D, Arnold L, McCarberg B. The science of fibromyalgia. Mayo Clin. Proc. 2011;86:907 – 911.
  8. Arnold L, Clauw D, McCarberg B. Improving the recognition and diagnosis of fibromyalgia. Mayo Clin. Proc. 2011;86:457 – 464.
  9. Ehrlich GE. Pain is real; fibromyalgia isn’t. J.Rheumatol. 2003;30(8):1666-1667.
  10. Wolfe F, Walitt B. Culture, science and the changing nature of fibromyalgia. Nature Reviews Rheumatology. 2013.
  11. Gowers WR. Lumbago: its lessons and analogues. Br.Med.J. 1904;1:117-121.
  12. Taylor RE. Death of neurasthenia and its psychological reincarnation A study of neurasthenia at the National Hospital for the Relief and Cure of the Paralysed and Epileptic, Queen Square, London, 1870-1932. The British Journal of Psychiatry. 2001;179(6):550-557.
  13. Wessely S. Old wine in new bottles: neurasthenia and “M.E.”. Psychol.Med. 1990;20:35-53.
  14. Beard GM. A Practical Treatise on Nervous Exhaustion (Neurasthenia), Its Symptoms, Nature, Sequences, Treatment. 5th ed. New York: E.B Treat & Company; 1905.
  15. Taylor RE. Death of neurasthenia and its psychological reincarnation: a study of neurasthenia at the National Hospital for the Relief and Cure of the Paralysed and Epileptic, Queen Square, London, 1870-1932. The British journal of psychiatry : the journal of mental science. 2001;179:550-557.
  16. Jeffery DD, Bulathsinhala L, Kroc M, Dorris J. Prevalence, health care utilization, and costs of fibromyalgia, irritable bowel, and chronic fatigue syndromes in the military health system, 2006-2010. Military medicine. 2014;179(9):1021-1029.
  17. Moynihan R, Heath I, Henry D. Selling sickness: the pharmaceutical industry and disease mongeringCommentary: Medicalisation of risk factors. BMJ. 2002;324(7342):886-891.
  18. Matheson A. The Disposable Author: How Pharmaceutical Marketing Is Embraced within Medicine’s Scholarly Literature. Hastings Cent. Rep. 2016.
  19. Fava GA. The Hidden Costs of Financial Conflicts of Interest in Medicine. Psychother. Psychosom. 2016;85(2):65-70.
  20. Barker KK. Listening to Lyrica: contested illnesses and pharmaceutical determinism. Soc. Sci. Med. 2011;73(6):833-842.
  21. Reed M, Herrmann M. The Difficulties in Developing and Implementing Fibromyalgia Guidelines. 2012.
  22. Hauser W, Urrutia G, Tort S, Uceyler N, Walitt B. Serotonin and noradrenaline reuptake inhibitors (SNRIs) for fibromyalgia syndrome. The Cochrane database of systematic reviews. 2013;1:CD010292.
  23. Uceyler N, Sommer C, Walitt B, Hauser W. Anticonvulsants for fibromyalgia. The Cochrane database of systematic reviews. 2013(10):CD010782.
  24. Wolfe F, Walitt BT, Katz RS, Lee YC, Michaud KD, Hauser W. Longitudinal patterns of analgesic and central acting drug use and associated effectiveness in fibromyalgia. European journal of pain (London, England). 2012.
  25. Clauw DJ. Fibromyalgia: a clinical review. Jama. 2014;311(15):1547-1555.
  26. Walitt B, Ceko M, Gracely JL, Gracely RH. Neuroimaging of Central Sensitivity Syndromes: Key Insights from the Scientific Literature. Curr Rheumatol Rev. 2016;12(1):55-87.
  27. Slade GD, Fillingim RB, Sanders AE, et al. Summary of findings from the OPPERA prospective cohort study of incidence of first-onset temporomandibular disorder: implications and future directions. J Pain. 2013;14(12 Suppl):T116-124.
  28. Goffaux P, de Souza JB, Potvin S, Marchand S. Pain relief through expectation supersedes descending inhibitory deficits in fibromyalgia patients. Pain. 2009;145(1-2):18-23.
  29. Potvin S, Paul-Savoie E, Morin M, Bourgault P, Marchand S. Temporal summation of pain is not amplified in a large proportion of fibromyalgia patients. Pain Res Treat. 2012;2012:938595.
  30. Ceko M, Bushnell MC, Fitzcharles MA, Schweinhardt P. Fibromyalgia interacts with age to change the brain. Neuroimage Clin. 2013;3:249-260.
  31. Morris DB. How to speak postmodern: medicine, illness, and cultural change. Hastings Cent. Rep. 2000;30(6):7-16.
  32. Chapman CR. Painful Multi-Symptom Disorders: A Systems Perspective. . In: Kruger L LA, ed. Translational Pain Research: From Mouse to Man. Boca Raton, FL: CRC Press/Taylor & Francis; Available from: http://www.ncbi.nlm.nih.gov/books/NBK57272/; 2010.
  33. Matheson A. How industry uses the ICMJE guidelines to manipulate authorship—and how they should be revised. PLoS Med. 2011;8(8):e1001072.
  34. Brown P, Morello-Frosch R, Zavestoski S. Contested Illnesses: Citizens, Science, and Health Social Movements. University of California Press; 2011.
  35. Barker KK. Electronic support groups, patient-consumers, and medicalization: the case of contested illness. J. Health Soc. Behav. 2008;49(1):20-36.
  36. Conrad P, Barker KK. The Social Construction of Illness Key Insights and Policy Implications. J. Health Soc. Behav. 2010;51(1 suppl):S67-S79.

 

Too Easy To Diagnose Fibromyalgia

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

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

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

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

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

 

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

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

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

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

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

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

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

 

If Cannabis Should Meet Fibromyalgia

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

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

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

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

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

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

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

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

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

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

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

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

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

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

John Quintner

 

References:

Austin JH. Zen-Brain Reflections. Cambridge, Massachusetts: MIT Press, 2006:301-302.

Dyer O. The growth of medical marijuana. Brit Med J 2013; 347:f4755.

Farrell M, et al. Should doctors prescribe cannabinoids? BMJ 2014; 348: 348:g2737. doi: 10.1136/bmj.g2737.

Grotenhermen F, Müller-Vahl K. The therapeutic potential of cannabis and cannabinoids. Dtsch Artztebl Int 2012; 109: 495-501.

Iversen L. Cannabis and the brain. Brain 2003; 126: 1252-1270.

Lynch ME, Campbell F. Cannabinoids fro treatment of chronic non-cancer pain. A systematic review of randomized trials. Brit J Clin Pharmacol 2011; 72: 735-744.

Martin-Sanchez E, et al. Systematic review and meta-analysis of cannabis treatment for chronic pain. Pain Med 2009; 10: 1353-1368.

Vincent A, et al. Prevalence of fibromyalgia: a population-based study in Olmsted County, Minnesota, utilizing the Rochester-Minnesota project. Arthritis Care Res (Hoboken) 2013; 65(5): 786-792.

Ware MA, Desroches J Medical cannabis and pain. PAIN Clinical Updates, 2014, XXII (3).

Wolfe F, et al. The use of polysymptomatic distress categories in the evaluation of fibromyalgia (FM) and fibromyalgia severity. J Rheumatol 2015; 42(8): 1494-1501.

 

Most Fibromyalgia Research is Worthless

Most Fibromyalgia Research is Worthless

I make it a point to try to be aware of all fibromyalgia research that is published by using PubMed’s free subscription service (http://www.ncbi.nlm.nih.gov/pubmed/). I get to read all of the abstracts this way and if I find articles that are of special interest to me I try to download them. PubMed reports 659 publications in the last 12 months relating to fibromyalgia. For those who are interested, there are 9,366 articles listed in the all the years that data are available. For 1990, the year the American College of Rheumatology 1990 fibromyalgia criteria were published, PubMed cites 95 articles. If you think that after all these years of research you and your patients are much better off, think again. A kind, conscientious physician treating a fibromyalgia patient in 1980 or 1990 will have done as well as the 2016 health workers with access to all of these new publications and expensive if not very efficacious medications.

Of all the 9,366 articles on fibromyalgia indexed in PubMed 1,268 have an attached tag of “clinical trial.” You can get a flavor for the research by looking at the two most recent articles. The first is titled, “The Effects of a Gluten-free Diet Versus a Hypocaloric Diet Among Patients With Fibromyalgia Experiencing Gluten Sensitivity-like Symptoms: A Pilot, Open-Label Randomized Clinical Trial.” That led me to ask myself. “Why would anyone want this information or want to do such a study?” The authors sav, “Patients with fibromyalgia frequently present with symptoms similar to those experienced by patients with gluten-related disorders, raising the possibility that a subgroup of these patients could be experiencing underlying gluten sensitivity. This study aimed to evaluate the effects of a gluten-free diet (GFD) compared with a hypocaloric diet (HCD) among patients with fibromyalgia? Well, the reason they did it was [they say] “…the possibility that a subgroup of these [fibromyalgia] patients could be experiencing underlying gluten sensitivity.” One reason for publications like this one is not quite the old “publish or perish.” Instead, think that the authors like a little of the glory that comes from being “scientists” and publishing “research.”

The second article is “Safety and efficacy of pregabalin in adolescents with fibromyalgia: a randomized, double-blind, placebo-controlled trial and a 6-month open-label extension study.” This is a special class of article,” one sponsored, funded, written and analyzed by Pfizer and led by physicians with a very long conflict of interest list. Pfizer has a long history of government fines, corrupt practices and ghost (or semi-ghost) written articles. The article concludes, “while this trial did not meet its primary efficacy outcome, improvements in secondary outcomes of pain and impression of change, together with a safety profile that was consistent with the known profile in adults with FM, suggest that patients might benefit from pharmacological treatments.” This isn’t the first time in Pfizer clinical trials that the authors point out the effectiveness of drugs that failed to meet their primary outcome goals. Few know that “Pfizer” is an old Klingon word that means beware.

Bad study design is a big problem

1) Normal controls. Most non-treatment studies of fibromyalgia make use of “normal” controls. This turns out to be a fatal flaw because persons with fibromyalgia virtually always have more severe abnormalities than healthy persons. They will suffer more, have greater costs, social disruption, pain, comorbidity, psychological distress. It doesn’t matter what you study if it is perceived to have some internal meaning. Studies against normals will tell you just what you always knew, fibromyalgia patients have more problems than those without fibromyalgia. Additional studies showing that patients with fibromyalgia have more of A, B and C are valueless. More than valueless, they tend to make clear that the authors don’t really understand the nature of fibromyalgia. Pfizer sponsors many studies that show how bad it is to have fibromyalgia.

If one wants to understand how those with fibromyalgia differ from those with pain who do not satisfy fibromyalgia, then controls have to come from pain groups. Because persons with fibromyalgia also usually have other comorbid illnesses and differences in psychosocial status, good studies of fibromyalgia need to seek similar (not normal) controls and have sufficient appropriate covariates. Many MRI studies, for example, that use normal controls may find differences that are not so much due to fibromyalgia as to other common comorbid symptoms. An example of this problem is that published studies began to report peripheral nerve abnormalities in fibromyalgia compared with normal controls. However, non-fibromyalgia pain controls also had such abnormalities. A number of early studies touted fibromyalgia vs. control data as examples of underlying abnormalities in fibromyalgia.

2) Biased studies and blinding. Convenience sample of volunteers with fibromyalgia as well as normal controls are usually biased, often in ways that are difficult to fully understand. Such biases are very common and truly invalidate studies, and statements by authors that there may be “limitations” never solve the problems. Fibromyalgia studies often have diagnosis and outcomes evaluated by persons who have an interest in the outcome. Studies that do this often get the results that the authors want.

3) Fibromyalgia studies are often underpowered, poorly analyzed and described. Only a small fraction follow guidelines for proportion publications.

4) Fibromyalgia studies often ask participants to remember events from many years in the past, something that always leads to unreliable data.

5 P-Hacking or taking multiple looks at the data before picking the analyses is common.

Why do “investigators do fibromyalgia studies? Because it is easy to find patients and there are always abnormalities. If you look hard enough almost any question can seem publishable.  As I sit here with a cat at my side and sun streaming in the window, I wonder if cats or weather have something to do with fibromyalgia? Not a bad guess; more than 2,000 hits on pets and fibromyalgia in Google scholar. Weather and fibromyalgia? More than 5,000 hits. Chinese food? Not so good. Only 103 hits.

Why “Centralized” Is Unacceptable As A Descriptor For The Pain Of Fibromyalgia

Why “Centralized” Is Unacceptable As A Descriptor For The Pain Of Fibromyalgia

The search is on for a third pain descriptor for chronic pain that is more appropriate for the large group of people whose pain is not associated with tissue damage (i.e. “nociceptive pain”) or with demonstrable nerve damage (i.e. “neuropathic pain”).

A recent article in the prestigious journal PAIN outlines the need for such a third descriptor and suggests the following candidates: “nociplastic”, “algopathic” and “nocipathic” [Kosek et al. 2016].

It is important to recognise that these descriptors are not diagnoses, just as “pain” itself is not a diagnosis. However they are intended to imply underlying neurophysiological mechanisms.

But another candidate has recently appeared upon the scene – “centralized pain” [Clauw 2014]. In this context, centralized refers to “central nervous system origins or amplification of pain”. Given that pain as an experience always originates from within the nervous system, and that pain is not a “thing” that can amplify itself, this proposition does not make sense.

The term “centralized” can refer only to an anatomical location within the central nervous system. Not only does the word itself not imply a mechanism but also it creates potential for confusion with conditions such as “central post-stroke pain” (which is technically “neuropathic”) and quite different from the phenomena that underlie Fibromyalgia.

Therefore “centralized” has no legitimate place as a descriptor for pain.

 

John Quintner & Milton Cohen

 

References:

Clauw DJ. Fibromyalgia: a clinical review. JAMA 2014; 311(15): 1547-1555,

Kosek E, Cohen M, Baron R, et al. Do we need a third mechanistic descriptor for chronic pain states? Pain 2016; 157(7): 132-186.

FIBROMYALGIA AND THE SARNO CONNECTION

Have you struggled with chronic pain or another medically unexplained symptom for a long time? Have you tried everything to alleviate your pain, but nothing worked? Have you had doctors tell you they “just can’t find anything wrong?”

Then you may have Tension Myositis Syndrome (TMS). TMS is a condition that causes real physical symptoms that are not due to pathological or structural abnormalities and are not explained by diagnostic tests. In TMS, symptoms are caused by psychological stress.

http://www.tmswiki.org/ppd/An_Introduction_to_Tension_Myositis_Syndrome_(TMS)

Introduction

People with fibromyalgia who are desperate for pain relief might well be tempted to read on to find out more about Tension Myositis Syndrome (TMS). At face value it does appear to be a genuine medical condition. But when they delve into its origins, there may be some unwelcome surprises.

Tension Myositis Syndrome, also known as Tension Myoneural Syndrome and Mind Body Syndrome, was originally described in 1981 by Dr John Sarno, a retired professor of Clinical Rehabilitation Medicine at New York University School of Medicine, and attending physician at the Howard A. Rusk Institute of Rehabilitation Medicine at New York University Medical Center.

This article will trace the development of Dr Sarno’s ideas over the past four decades and will show how he and his followers have tackled the vexed problem of the relationship between mind and body by inventing a psychologically based condition (TMS) together with an imagined musculoskeletal lesion. As an aside, their strategy bears more than a passing resemblance to that of those who pioneered the now discredited concept of the “myofascial trigger point”.

What is TMS?

According to Sarno (1998) TMS is “a benign (though painful) physiologic aberration of soft tissue (not the spine) and it is caused by an emotional process.” He suggests that this process is the result of “specific, common emotional situations”. The various soft tissues that can be affected in this peculiar disorder include muscles, nerves, tendons and ligaments (Sarno, 1998).

As Coen and Sarno (1989) explained:

“Of approximately 4000 patients with neck, shoulder and back pain seen by physiatrist author (JES) over 15 years, over 95% were diagnosed as having TMS. What stands out most from our clinical material are the contributions of tension and chronic character defences to musculoskeletal symptoms, and then the uses made of pain (for dependency, defence of narcissistic preoccupation with the pain, for punishment, and to express anger against caretakers (internal and external).

We emphasise the relative ease of helping patients out of their back pain syndrome … Empathic explanation of the role of anxiety and defensive states in causing back pain, together with reassurance that this is a reversible self-limited process, usually leads to recovery.

The capacity to tolerate one’s affective life seems, in effect, to preclude the back pain syndrome. We believe that the more able patients are to tolerate what they feel, including their anxiety, vigilance, mistrust, anger and depressive feelings, the less troubled they will be by back pain.”

To further confuse the issue of nomenclature, Sarno proposed that TMS syndrome be relabelled “the mind body syndrome,” which includes the musculoskeletal disorder now referred to as “musculoskeletal mind-body syndrome (MMS), as well as a large variety of other psychophysiologic conditions involving other systems (Rashbaum & Sarno, 2003).

What is the postulated mechanism?

Physical symptoms are said to occur when the unconscious mind senses that repression of emotions may fail and an “emotional eruption” is imminent. The conflict is between “the reasonable, intelligent, moral, conscious mind and the childish, primitive archaic mind that continues to have a strong influence on the unconscious” (Rashbaum & Sarno, 2003).

Repressed unconscious emotions (e.g. rage) can trigger abnormal autonomic nervous system activity, apparently resulting in mild ischaemia (i.e. lack of blood supply) and mild oxygen deprivation that can adversely affect muscles, nerves & tendons. These changes in physiology are supposedly manifested by muscle pain, nerve pain, tendon pain, paraesthesias (“pins and needles”) and muscle weakness.

There is of course no scientific evidence whatsoever to support these wild guesses.

TMS & fibromyalgia

Sarno (1998) decided to characterize fibromyalgia as a severe form of “musculoskeletal mind-body syndrome” with multiple ischemic foci involving muscle, nerve, and tendon. Rashbaum and Sarno (2003) chided the American College of Rheumatology (ACR) because although the diagnosis required the identification of 11 of a potential 18 tender points in the trunk, arms, and legs, it did not make the connection between the emotions and clinical findings.”

Resorting to psychoanalytic theory, Sarno made the connection by proposing that fibromyalgia was caused by “the psychosomatic avoidance of psychic conflict.” He even gave the pain a purpose, which was “to distract attention from frightening, threatening emotions and to prevent their conscious expression.” Fibromyalgia therefore signified the person’s abject failure to resolve his or her own psychic conflict:

Physical symptoms occur when the mind senses that repression of emotions may fail and an emotional eruption is imminent. The conflict is between the reasonable, intelligent, moral, conscious mind and the childish, primitive archaic mind that continues to have a strong influence on the unconscious.

Current status of Sarno’s ideas

Schechter et al. (2007) published outcomes of a “mind-body” treatment offered to a convenience sample of 51 patients with persistent low back pain and a diagnosis of TMS (note that Sarno is referenced in relation to making this diagnosis). The primary goal of this program was “to raise patient awareness of how emotional issues, including repressed emotions, affect their physical pain” by counseling and educating patients on “how psychological factors can manifest as physical pain” and learn to begin “thinking psychologically,” instead of “structurally,” about their pain.

The authors conceded the many limitations of this study, with financial and logistical constraints forcing them to conduct a case series study instead of a randomized clinical trial. The authors’ lack of specific criteria for a diagnosis of TMS and their inability to precisely standardize the program for all patients makes interpretation of this paper impossible.

However, Dr Howard Schubiner and his co-workers are others who continue to advocate John Sarno’s ideas. As he informs those who visit his blog site:

Your body is producing pain because it’s manifesting unresolved stress, possibly from your childhood, or from stressful events in your adulthood, or from your present circumstances, and as a result of your personality traits (which affects how you respond to stress and how much pressure you tend to put upon yourself).

http://mind-body-blog.blogspot.com.au/2008/02/mindbody-syndrome-tension-myositis.html

In a more recent publication, Lumley et al. (2015) have restated these views:

We view the key pathological process in both unresolved trauma and internal conflict to be the avoidance or suppression of one’s primary or adaptive emotions, which then activates neural pathways that trigger, augment, or maintain pain and other symptoms.

In the meantime, Hsu et al. (2010) reported the results of a randomized controlled trial of Dr Schubiner’s program of intervention – Affective Self-Awareness (ASA) – developed at Providence Hospital.

Without going into details, the 24 of the 45 participants who attended Dr Schubiner’s three 2 hour small group sessions over three weeks and had read one of Dr Sarno’s standardized texts (Sarno, 1998) reported less pain and improved physical functioning compared to those in the 21 wait-listed control group. Members of the latter group were “free to engage in any interventions on their own, as recommended by their providers …”

It comes as no surprise that the authors reported:

Individuals with fibromyalgia in this study appeared to accept the central message of the intervention: that the experience of pain in fibromyalgia is real, that fibromyalgia pain is processed in the central nervous system, that unrelated emotional experiences can initiate and perpetuate physical symptoms, and that the mind-body link can be tapped to empower individuals with fibromyalgia to more effectively diminish pain and associated symptoms.

The authors conceded that they had no idea as to the mechanisms responsible for the benefits of the ASA intervention. But at least they did acknowledge the possible contribution of various contextual factors.

The pivotal research question posed by Schubiner et al. (2012) is to “determine if targeting unresolved stress and emotions offers an advance in the treatment of chronic non-structural pain.”

Hsu et al (2010) do intend to conduct a larger study that will “not only assess the efficacy of this type of intervention in comparison to an active control group, but will allow for assessment of mediating and moderating variables to help determine mechanisms of action and subgroups of patients that respond best to this intervention.”

There can be no doubt that this formidable (and impossible?) task will continue to tantalize future generations of researchers who have embraced Dr Sarno’s ideas.

Conclusion

It is indeed unfortunate that Dr Sarno’s outdated theories, which were always highly speculative and heavily influenced by insupportable psychoanalytic theory, continue to influence some clinicians in their approach to patients with fibromyalgia. Their laudable aim may have been to close the mind-body split but in effect they have only succeeded in widening the gap and, in so doing, have inadvertently shifted the blame for their pain onto their patients.

References:

Coen SJ, Sarno JE. Psychosomatic avoidance of conflict in back pain. J Am Acad Psychoanal 1989; 17(3): 359-376.

Hsu MC, Schubiner H, Lumley MA, et al. Sustained pain reduction through affective self-awareness in fibromyalgia: a randomized controlled trial. J Gen Intern Med 2010; 25 (10): 1064-1070.

Lumley MA, Schubiner H, Carty JN, Ziadni MS. Beyond traumatic events and chronic low back pain: assessment and treatment implications of avoided emotional experiences. Pain 2015; 156; 565–566.

Rashbaum IG, Sarno JE. Psychosomatic concepts in chronic pain. Arch Phys Med Rehabil 2003; 84 (Suppl. 1): S76-S80.

Sarno JE. The mind-body prescription: healing the body, healing the pain. New York: Warner Books, 1998.

Schechter D, Smith AP, Beck J, et al. Outcomes of a mind-body treatment program for chronic back pain with no distinct structural pathology – a case series of patients diagnosed and treated as tension myositis syndrome. Altern Ther Health Med. 2007; 13(5): 26-35.

Schubiner H, Burger A, Lumley M. P02.147. Emotions matter: sustained reductions in chronic non-structural pain after a brief, manualized emotional processing program. BMC Complement Alt Med 2012; 12 (Suppl 1): P203.

 

 

TO KILL A MYOFASCIAL TRIGGER POINT

“Remember it’s a sin to kill a mockingbird.” That was the only time I ever heard Atticus say it was a sin to do something, and I asked Miss Maudie about it. “Your father’s right,” she said. “Mockingbirds don’t do one thing but make music for us to enjoy … but sing their hearts out for us. That’s why it is a sin to kill a mockingbird.”

The late Harper Lee struck an intense moral chord in the USA with her acclaimed novel – To Kill a Mockingbird (1960).

But does the innocent mockingbird have anything in common with the “myofascial trigger point (MTrP)”? Is it a sin to kill a MTrP?

There are physical therapists who firmly believe that MTrPs can cause considerable harm to people:

Myofascial TrPs are a preventable cause of musculoskeletal pain, they cause dysfunctions, such as blurry vision, erectile dysfunction, balance disturbance and dizziness, irritable bowel, diarrhea, vomiting, voice disturbances, and loss of fine motor control. They can cause colic in babies or contribute to falls in the elderly–and in the rest of us [Starlanyl & Sharkey, 2013].

Furthermore, in their eyes the potential havoc that MTrPs can wreak extends even to fibromyalgia (aka chronic widespread pain).

In their recent book Starlanyl and Sharkey (2013) make this promise to their readers:

“You will discover how TrPs can cause or maintain fibromyalgia and why the ability to control the TrPs directly affects the control of FM symptoms … the key to controlling trigger points is identifying and controlling perpetuating factors.”

Accordingly, Starlanyl and Sharkey (2013) see fit to issue a stern warning to those individuals who are unfortunate enough to harbour MTrPs:

If the perpetuating factors are not brought under control, satellite TrPs can develop in muscles that overwork trying to compensate for the TrP-weakened ones, or in muscles in the referral zone. Once primary TrPs develop satellite TrPs in other body areas, life, and treatment, becomes more complex. The satellites themselves can develop more satellites involving more of the body. Trigger points can cause body-wide pain.

On close examination, these perpetuating factors, of which the list is exceedingly lengthy, turn out to have only been figments of the fertile imagination of the original proponents of the MTrP theory [Travell & Simons, 1983].

The belief that MTrPs can be “controlled” has spawned a worldwide industry of therapists eager to kill (“deactivate”) them by various drastic methods, which include needling, compression, and manual release.

On her website Starlanyl (2014) advises therapists to proceed cautiously, as follows:

“Use the least invasive option for therapy, with the understanding that most treatment options may activate more TrPs and cause a temporary increase in pain. Toxins and waste materials trapped in the myofascia (sic) must be processed by the body and be eliminated, and that can only proceed so fast. It takes a while for the Gordian knot to unravel, and the process is not fun for the patient.

Starlanyl (2014) describes: “… a cadre of patients with too many TrPs to count, in multiple levels in multiple muscles. They have chronic myofascial pain (CMP). The muscles may be so tight and swollen that you can’t see them move beneath the skin, and the pain levels escalate. These patients may have had multiple surgeries and procedures. There may have been multiple traumas. There may be a wide variety of perpetuating factors.”

When the preferred treatment fails to kill the MTrP(s), the blame then shifts from the therapist to the pain sufferer, who without any shadow of doubt must harbour one or more of these so-called perpetuating factors.

It may be a sin to kill a mocking-bird – but has any one ever seen a “dead” MTrP, let alone be able to identify and describe its true nature? No doubt there are some who would see it as sinful should therapists not try to “kill” as many MTrPs as possible in their attempts to alleviate human suffering. However the published research on outcomes for “treating trigger points” suggests that they are not easy to kill [Cohen & Quintner, 2008; Quintner et al., 2015].

Could this apparent resistance to destruction be explained by their very non-existence? Unless and until this is appreciated, the MTrP will continue to mock its followers.

 

John Quintner

 

References:

Cohen ML, Quintner JL. The horse is dead: let myofascial pain syndrome rest in peace [letter]. Pain Medicine 2008; 9: 464-465.

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

Starlanyl DJ, Sharkey J. Healing through trigger point therapy: a guide to fibromyalgia, myofascial pain and dysfunction. Berkeley, California: North Atlantic Books, 2013.

Starlanyl D. Fibromyalgia and trigger points for care providers, 2014. Available at: http://www.fmcmpd.org/physinfo.htm Accessed 13th May 2016.

Travell JG, Simons DG. Myofascial pain and dysfunction: the trigger point manual. Baltimore: Williams and Wilkins, 1983.

LA DOULOU (Provençal word for pain)

Many patients with fibromyalgia are desperately seeking out non-drug measures to relieve their pain and improve their quality of life. This article was inspired by the struggles of one of France’s most eminent 19th century writers against his unfortunate predicament. His eloquent words will resonate with all who suffer chronic pain. — John Quintner

LA DOULOU (Provençal word for pain)

I only know one thing, and that is to shout to my children ‘long live Life!’.

But it’s so hard to do, when I am ripped apart by pain.”

From his anecdotal journal entries (translated by Julian Barnes), we can get an idea of how the French novelist, playwright and poet Alphonse Daudet [1840-1897] addressed his extremely painful neurosyphilitic condition i.e., tabes dorsalis. Its manifestations are due to degeneration of the posterior columns and nerve roots of the spinal cord. In today’s parlance, such pain would be described as neuropathic.

Fortunately, syphilis (in all its manifestations) is curable with antibiotics and now rarely seen. But there are many other medical conditions, such as fibromyalgia and complex regional pain syndrome (CRPS), which can be associated with severe pain that is poorly controlled by the currently available medications.

I asked my colleague Melanie Galbraith, physiotherapist, to comment from the point of view of a pain sufferer upon Daudet’s methods for obtaining pain relief. Melanie experiences intractable cervical radicular (neuropathic) pain.

With the permission of Professor Abraham Olivier* the following excerpts have been transcribed directly from his book “Being in Pain” (2007):

  1. By means of imagination

Daudet: “It’s hilarious, this land of neurotics, filled with shouting, trumpet calls, sirens.”

From such passages, which refer to the people he meets at thermal stations within various health spas, it is apparent that he describes the land of pain in terms of fantasy, of theatre, of tragedy.

I argued (Chapters 4 and 5) that imagination can change a bodily state like pain into an unreal object, even while it remains a bodily state. In this way imagination can make pain vanish behind a mask. We cannot place ourselves into a space of fantasy without any pain, for we remain beings embedded in bodies. But our bodies can change our states of pain by projecting in the place of the land of pain a space of fantasy. Indeed, according to Daudet, this has the effect of a morphine injection (p. 175).

Melanie: “meets at thermal spas” – Heat – it’s a very under-utilised form of treatment for chronic pain. Sometimes when my pain is at a high level I’ll imagine being at the beach on a hot, summer’s day and scrunching the warm, white beach sand between my toes.

Daudet’s use of imagination as a strategy for pain management is supported by recent research, which has found encouraging but inconclusive evidence that guided imagery can alleviate both muscular and non-muscular pain (Posadzki & Ernst, 2011; Posadzki et al, 2012)

Of course, there is a limit to imaginative projection. Theatre is not endless and as the music fades away the pain will return. But the same goes for morphine. Why not try fantasy instead? … But again, it is one thing to use fantasy as an additional tool to physiological therapy, another to integrate it as a primordial means to treat pain. I advocate the latter. Daudet demonstrates the power of this approach: it is like a morphine injection.

Melanie: It would be great – but … when my pain is at a maximum, it’s as if your ‘beach scene’ has been overtaken by a violent storm with booming thunder, torrential rain and blinding lightning. Added to this, vicious waves are crashing against the ‘sea wall’ and threatening to ‘burst the dam’.

  1. By means of relocation

Daudet: “One ought to go to different baths each season”

On the one hand, Daudet turns the thermal station into a place of fantasy. On the other hand, he thinks a literal change of space to be as important as positing an imaginative space.

This illustrates once more that space is not, as traditionally thought, some place (a container or extension) belonging to the external environment, but the perspective we adopt toward our environment.

This may be taken as a useful therapeutic insight – we may even label it as space therapy: moving away as a means of removing pain, that is, changing our perspective as a means to change the quality of pain.

But if it would help, then anyone can find a means to travel. If not by plane or car or boat, then our feet, or at the end our fantasy may carry us to places that harbour new perspectives (p. 176)

Melanie: If only Medicare would fund a ‘week away’! Whilst working in the UK I saw many, many patients whose pain improved or disappeared altogether when they were away somewhere that was warm and ‘stress-free’! I’m convinced we could save a mountain of health dollars if doctors could ‘prescribe a holiday’! It’s much cheaper (and likely MUCH more effective!) than a range of ‘interventions’ such as spinal injections, drugs and surgery.

  1. By means of compassion

Returning from a sojourn at a thermal station could cast patients into desolation. This could mean extreme loneliness even to someone in a caring family.

Daudet conjures up a dialogue between two ataxic patients to demonstrate this desolation, but also to suggest compassion as a means to counter it. One patient is a bachelor, the other a family father. They discuss whether it is better to be alone while suffering or not.

The family father argues that it is better to be alone: firstly, because it is a terrible weight on a household to have someone around whose pain drags on for years. Furthermore, it adds to your own suffering to see how the pain, which always appears new to you, becomes familiar and wearisome to others. Moreover, the responsibility of taking care of your family while in pain increases your burden. Finally, family life has taught him to keep his pain to himself rather than to show it, but not showing it is a big constraint.

The bachelor counters quite sharply and forcefully: the lack of someone who cares adds to the loneliness the pain brings about, yet it is important to care for others, for your family, instead. Eventually caring for them helps you to get away from yourself, which in turn supports them in caring for you. Compassionately taking another or another’s perspective could thus be an effective means to step out of one’s misery. In this sense compassion entails a liberating perspective (p. 177).

Melanie: This is the classic situation of “the grass is always greener on the other side of the fence.” As I was alone (not in a relationship) when my chronic pain started, I often thought: “how nice it would be to have someone to care for me”. At other times, especially when pain is high, I think: “thank goodness I can shut myself away”. It’s a relief to not feel like a burden on someone else, but I didn’t choose this life situation for myself so surely I have as much “right” as the next person to have a fulfilling relationship with a significant other?

  1. By means of consultation

This does not so much refer to meetings with doctors as to discussions with fellow-patients. Such talks often consisted in the exchange of advice.

To be clear, Daudet knew how to be self-critical about such advice: “Patients giving one another advice: ‘This is what you have to do.’ ‘But does it work?’ ‘No.’ ‘Are you any better?’ ‘No.” ‘So why are you giving me advice?’ Lunacy.”

But Daudet did give advice … to those who are weak; Daudet recommended that they treat pain as an unwanted guest to whom no special attention should be accorded. Daily life should be continued as normally as possible … this advice has a strong underpinning once we see pain as bodily perception … as a change of perspective changes the quality of pain, it is certainly possible to adopt a perspective to drive out the unwanted guest … Daudet’s advice for those who do not scare too easily is that they should dare to examine their pain carefully … the question is: how can the body remove its pain by means of thinking? Once we rephrase the question, we are much closer to the possibility of realizing the power of the bodily axis our perception pivots on (p. 177).

Melanie: If I disclose my own pain problem, my patients appear to appreciate the fact that a health professional “understands what they are going through”. Despite pain being a “unique experience” – personal to the individual, I’ve found patients seem to let go their defenses when they know I’m “one of them”. Sometimes, I’ve found it’s the ONLY thing that will ‘get them on board’ and try some new strategies for managing their pain.

*Abraham Olivier is Professor and Head of the Department of Philosophy at the University of Fort Hare. In addition to this he is Co-Founder and Co-Chair of the Centre for Phenomenology in South Africa (http://saphenomenology.wordpress.com/). He was Editor of the South African Journal of Philosophy and secretary of the Southern African Philosophical Society (PSSA). Olivier obtained his PhD from the University of Tübingen and has held lecturing and research posts at the Universities of Tübingen, Stellenbosch, Hamburg and Padua. He is the author of Being in Pain as well as numerous international peer-reviewed articles.

References:

Daudet A. In the Land of Pain. Transl. Barnes J. New York: Alfred A Knopf, 2003.

Olivier A. Being in Pain. Frankfurt am Main: Peter Lang, 2007: 161-200.

Posadzski P, Ernst E. Guided imagery for musculoskeletal pain: a systematic review of randomized clinical trials. Clin J Pain 2011; 27: 648-653.

Posadzki P, Lewandowski W, Terry R, et al. Guided imagery for non-musculoskeletal pain. J Pain Symptom Manage 2012; 44: 95-104.