I am overwhelmed with things to read. W.H. Auden once said that the reason to read the classics when young was that there would be little time to read them later in life for most people. I find that the pull to read something at length is a pull away from my general work, alas. But a recent trip by air gave me free time to read. At the suggestion of Dr. Brian Walitt–who is largely responsible for pushing me into new ideas, I read Oliver Sacks new book, “Hallucinations” on a Kindle. I recommend this book. Part of its relevance is that hallucinations occur in normal people. And they represent reality: things seen, heard or felt. Sacks writes:

Many cultures regard hallucination, like dreams, as a special, privileged state of consciousness— one that is actively sought through spiritual practices, meditation, drugs, or solitude. But in modern Western culture, hallucinations are more often considered to portend madness or something dire happening to the brain— even though the vast majority of hallucinations have no such dark implications. There is great stigma here, and patients are often reluctant to admit to hallucinating, afraid that their friends and even their doctors will think they are losing their minds. I have been very fortunate that, in my own practice and in correspondence with readers (which I think of, in some ways, as an extension of my practice), I have encountered so many people willing to share their experiences. Many of them have expressed the hope that telling their stories will help defuse the often cruel misunderstandings which surround the whole subject. I think of this book, then, as a sort of natural history or anthology of hallucinations, describing the experiences and impact of hallucinations on those who have them, for the power of hallucinations is only to be understood from first person accounts.

Here, then, is a sampling which I hope will give a sense of the great range, the varieties, of hallucinatory experience, an essential part of the human condition.

His favorite definition comes from William James. “An hallucination is a strictly sensational form of consciousness, as good and true a sensation as if there were a real object there. The object happens to be not there, that is all.

Could hallucinations and the Jamesian “as good and true a sensation” play a role in the mystery of fibromyalgia? Or at least suggest a model?

In a comment to a post on somatization, Dr. Marcelo Derbli Schafranski writes:

Wouldn’t it be risky to try to integrate old somatization concepts into the concept of fibromyalgia, especially those unexplained by the sensitization theories? I guess if we try harder, we possibly can do it. But my fear is to sink the somatizer (or any other definition among countless already applied for this condition, Briquet´s Syndrome, just for an example) more and more in a Procrustean Bed named fibromyalgia. As a rheumatologist, cognitive dissonance haunts me everyday.
 And Congratulations for the blog!

Dr. Schafranski’s truth– that somatization as an explanation for fibromyalgia is a bad idea–is one that most have now accepted. But there is an interesting letter to the editor of Rheumatolgy (Kinder, A., Jorsh, M., Johnston, K. & Dawes, P. Somatization disorder–a defensive waste of NHS resources. Rheumatology.(Oxford) 43, 672-674 (2004)) that deserves reading. I have excerpted a paragraph.

This lady initially presented at the age of fourteen to ear, nose and throat surgeons with recurrent sore throats and underwent a tonsillectomy. Five years later during pregnancy she developed recurrent abdominal pain and despite extensive investigations no cause was found. She had a normal delivery of a healthy child. Since this time she has been referred to 16 different hospital specialities and undergone investigations for chest pain, breast pain, facial pain, ear pain, nasal stuffiness, irritable bowel disease, menorrhagia, urinary problems and dyspareunia. She has been referred to the rheumatology department on three occasions with back pain or multiple joint pains. Her symptoms have not improved despite surgery. A retrospective 30-yr review of her hospital case notes revealed she has had 29 operations requiring general anaesthetic, 10 MRI scans, three CT scans and 25 ultrasound examinations. She attended out-patients on 204 occasions with 52 in-patient stays totalling 411 days (Table 1). She is now 44 yr old and under the care of neurologists, physicians and urologists.

I think that when psychiatrists (and the DSM) speak of somatization they mean something along the lines of this patient. When we think of the unallowed word (somatization) in fibromyalgia we mean something different: increased somatic symptom reporting and experiencing. It was such a characteristic feature that increased somatic symptoms was added as a criterion to the 2010 ACR fibromyalgia criteria. One could suggest that increased symptom report is analogous to increased pain reporting.

In our population studies the extent of body pain correlates with number of symptoms reported, as well with anxiety and depression. Such correlations occur in the general population whether or not fibromyalgia is present. Perhaps it is part of the human condition. There is a lot of literature on this subject, but no clear answers. In agreement with Dr. Schafranski, I wouldn’t try to explain fibromyalgia by “somatization,” but I would consider that increased symptom reporting is part of polysymptomatic distress which, when severe, is fibromyalgia.

Sorry to have left the blog empty for a while. A brief illness followed by a trip away from my computer was the culprit.

I hope the Journal of Rheumatology lawyers will allow me to quote this article of mine. It represented one of the several memorials to Hugh Smythe. I have left out the references, but otherwise this is the same as the J Rheum article.  Smythe had no use for what what fibromyalgia had become, and he makes that clear at the end of the article.

Hugh Smythe and the Birth of Contemporary Fibromyalgia

I had no interest in fibrositis…at the start. —  Hugh Smythe

Hugh Smythe and Harvey Moldofsky were the inventors of fibromyalgia (FM). Before them, fibrositis, as FM was then called, was a vague mishmash of descriptions and symptoms. Everybody knew what it was even if they couldn’t define it or believe in it. In 1962, the 35-year-old Smythe was on his way to being “a real rheumatologist,” as he put it, when Wallace Graham died. According to Smythe, “Graham had been given the job of writing the chapter on fibrositis for Pemberton’s and then Hollander’s textbook. Wallace died suddenly in 1962, and shortly afterwards a letter came. And at that point, Wallace had been writing a chapter on the shoulder and on ankylosing spondylitis and on fibrositis. So a letter was received by me and by Metro Ogryzlo asking us to take over those chapters. Now, I had had no interest in fibrositis as a topic, but Metro was the senior man, so I was the junior man, and got the unwanted, unloved topic of fibrositis.” And with it he became the author of the Hollander and later, the Kelley textbooks for several decades. Until publications about the new fibrositis began to come out in the early 1980s, Smythe was the primary voice of fibrositis in the English-speaking world.

Smythe’s central contribution to the syndrome he and Moldofsky made famous was to call attention to tenderness and referred pain. Although previous authors had sporadically identified muscle tenderness, it was not mandatory to have tenderness. Smythe made it mandatory. Smythe’s interest in referred pain and tenderness came from the work of Kellgren in the UK. From Kellgren he learned that with referred pain came referred tenderness. Similarly, it was Moldofsky’s interest in sleep and fatigue, his observations of patients with fibrositis, and his attempts to induce fibrositic symptoms by interrupting sleep that led to the incorporation of these ideas into the fibrositis definition. The key paper that catapulted fibrositis into general knowledge was their “Two contributions to understanding of the ‘fibrositis’ syndrome”, which was published in 1977. Strangely, despite their common interest and fame, they published only 4 papers together, only 1 of which followed “Two contributions.”

Hugh Smythe was an extraordinary physical anatomist. In the 1989 training sessions for the 1990 American College of Rheumatology FM criteria study he taught us all how to do the tender point examinations. We were nonplussed, as he described in site after site exactly where the tenderness began and ended, and how to elicit it properly. Here was a large group of “experts” who were about to start a study where tenderness was key, and none of us could hold a candle to Hugh Smythe. But he was a good teacher, and some of the investigators learned how to do the examination.

It was the cervical spine that was of most interest to Smythe. He thought it was the source of most of the symptoms and physical findings of FM, and he wrote about it in a paper on the C6-C7 syndrome. Anyone who visited him at home was shown a pile of stones and asked to say what they were, while he smiled loudly. What they were was stone “pillows” that he acquired in Africa, and other places in the world, that people used to protect the cervical spine and make sleep comfortable.

Hugh Smythe was a kind, thoughtful scholar and teacher, who went out of his way to help people. Many of his fellows went on to be interested in FM and teach it across the world. He was kind to me when I wrote to him in 1980 about my first paper that had been rejected by Arthritis & Rheumatism and asked him why. He gave a beginner good advice, and I never made the same mistake again.

Several months before he died I spoke to him on the telephone. I wanted to get his ideas about his career and the future of FM. I asked him if there was still an interest in FM in Toronto, now (June 2012). No, he said, “I get all kinds of inquiries, and I tell them that there’s nobody in our hospital that I could refer them to that would give them the message I was giving them. Nobody in Toronto, nobody in Ontario, and nobody in Canada. And I could probably go on and say nobody in North America.”

“What do you think is going to happen with fibromyalgia now? What’s the future?” I asked. His response: “I suppose it’s going to have to be rediscovered. It’s dead now.” “And it’s going to have to be rediscovered in terms of the tenderness that you see?” I asked. “Yes. The idea that the pain is psychogenic in origin or neurogenic in origin is just ignoring all the experimental work of Kellgren and Lewis and all the stuff that we did, up to 1990 or beyond that.”

Whether Smythe was right or wrong in some of his pronouncements, he opened up a new world of observation. Perhaps when the swirling debates about FM are resolved, we will arrive “where we started and know the place for the first time.”

Although there is generally agreement that fibromyalgia treatment is unsatisfactory, most articles that discuss treatment list a whole series of ‘effective’ treatments. Often the treatments are extolled because they address specific pathways hypothesized to be important or for which drugs have been developed. As we have noted previously, many authors of treatment recommendations have received Pharma payments. Even the best authors drift toward new mechanisms, often in the face of little evidence for useful efficacy of previously hyped treatments.

One of the reasons authors get away with this behavior is that statistically effective treatments can have very weak effects, but these effects can be extolled as “effective.” Maybe one way to solve this problem would be to impose a moral requirement to describe the degree of effectiveness up front. Instead of ‘Drug A is an effective treatment for fibromyalgia’ authors should be required to state ‘Drug A is a weakly effective treatment.’

Still, in fibromyalgia you often have to take what you can get. Cognitive Behavioral Therapy (CBT) can be quite effective in some conditions. For example, effective sizes >2 have been seen in some studies of PTSD (that’s almost a cure!).^{1, 2} But metaanalyses in fibromyalgia from the ever-reliable Häuser group in Germany yield these results:³

Results. A total of 14 out of 27 RCT with 910 subjects with a median treatment time of 27 hours (range 6–75) over a median of 9 weeks (range 5–15) were included. CBT reduced depressed mood (SMD –0.24, 95% CI –0.40, –0.08; p = 0.004) at posttreatment. Sensitivity analyses showed that the positive effect on depressed mood could not be distinguished from some risks of bias. There was no significant effect on pain, fatigue, sleep, and HRQOL at posttreatment and at follow-up. There was a significant effect on self-efficacy pain posttreatment (SMD 0.85, 95% CI 0.25, 1.46; p = 0.006) and at follow-up (SMD 0.90, 95% CI 0.14, 1.66; p = 0.02). Operant behavioral therapy significantly reduced the number of physician visits at follow-up (SMD –1.57, 95% CI –2.00, –1.14; p < 0.001).

Conclusion. CBT can be considered to improve coping with pain and to reduce depressed mood and healthcare-seeking behavior in FM.

 Shafran (2009) points out that CBT is underused and may not be provided correctly.¹ In the US my experience is that it is difficult to get CBT and to get it paid for. That’s just an impression. Perhaps someone has better data.

1.  Shafran, R. et al. Mind the gap: Improving the dissemination of CBT. Behav Res Ther 47, 902-9 (2009).

2.  Ehlers, A. et al. A randomized controlled trial of cognitive therapy, a self-help booklet, and repeated assessments as early interventions for posttraumatic stress disorder. Archives of General Psychiatry 60, 1024 (2003).

3.  Bernardy, K., Füber, N., Köllner, V. & Häuser, W. Efficacy of cognitive-behavioral therapies in fibromyalgia syndrome‚Äîa systematic review and metaanalysis of randomized controlled trials. The Journal of rheumatology 37, 1991-2005 (2010).

I came across ‘A patient survey of the impact of fibromyalgia and the journey to diagnosis’ while performing a Google Scholar search.¹ There were some interesting data in this open access paper, but also many problems—the type you might expect in a retrospective, highly selected sample. And the results were pretty much what one might expect, as these questions had been reported on over and over again for many years.

The paper made the point repeatedly that there was delay in diagnosis. They concluded ‘Patients who reported dissatisfaction with treatment also reported waiting longer to receive a work-up, diagnosis and care for their fibromyalgia. By the time the patient presents to the physician who actually diagnosed their condition, the fibromyalgia journey has already begun (on average over 2 years). The association between chronicity of symptoms and worse response to treatment suggests that earlier diagnosis and treatment may lead to improved treatment response and reduced impact of the condition.’ Why should these highly selected data on highly selected patients suggest this?

To use a six letter word: Pfizer. It seems as if three of the seven authors were Pfizer employees, and two were employed by a company hired by Pfizer. Correspondence from this UK paper ‘should be addressed to Pfizer’—in New York. The lead author received fees for consulting to Pfizer. The authors AG and EK were employed by Harris Interactive who was commissioned and funded by Pfizer Inc to develop and conduct the survey. And there is more. As for the Pfizer employees and hires: ‘TL and JK made substantial contributions to the conception and design of the survey and interpretation of data and were involved in reviewing and critiquing the manuscript for important intellectual content. AG made substantial contributions to conception and design, acquisition of data, and analysis and interpretation of data and was involved in reviewing and critiquing the manuscript for important intellectual content. EK made substantial contributions to the conception and design of the survey, interpretation of data and was involved in reviewing and critiquing the manuscript for important intellectual content.’

It gets better: ‘The survey was commissioned and funded by Pfizer Inc, New York, NY. Janet Bray MPharmS who provided medical writing (!) services which were funded by Pfizer Inc.

Journal charges were also met by Pfizer Inc. I would summarize it this way. Pfizer commissioned the study, paid for it, carried it out, wrote it and interpreted it. One of the messages of the paper is to diagnose more people with fibromyalgia and treat it better. Guess with which drug?

1.   Ernest Choy, Serge Perrot, Teresa Leon, Joan Kaplan, Danielle Petersel, Anna Ginovker and Erich Kramer: A patient survey of the impact of fibromyalgia and the journey to diagnosis. BMC health services research 10, 102 (2010).

There appears to be a modern obligation to eschew Cartesian Dualism and to and rail against it as the cause of multiple ills. According to Cohen and Quinter, ‘When seen through this Cartesian dualistic frame, pain sufferers appear to a clinician either as a disordered bodily machine or as a disturbed mind.’ In the absence of evidence of a “disordered machine,” the clinician ‘defaults to an inference of a “disturbed mind.”’¹ But the dualistic dilemma can be seen in any number of lights. Sometimes the dualism problem is phrased as a Mind-Brain problem; Kirmayer calls it the Mind-Body problem, and illuminates it as a cultural issue:²

Although Western medicine has often been characterized, and criticized, as dualistic and reductionistic, contemporary biomedical physicians are largely unconcerned with the metaphysical “world-knot” of the mind-body problem. Science seems to be slowly untangling this knot, offering a multitude of empirical correspondances between physiology and behaviour that constrain philosophical speculation. Modern biology explains mindful action as an emergent property of the hierarchical organization of the nervous system. A more sophisticated version of this materialism recognizes that mind and consciousness are not simply functions of the isolated nervous system but can be better understood as emergent properties of social systems, that is, of interactions between many individual organisms.

That is, it is being worked out.

However, biology leaves unexplored an aspect of the mind-body problem that is essentially ethical. This residual mind-body problem occurs because mind and body symbolize contrasting poles in human experience: the voluntary or intentional and the involuntary or accidental. It is because the contrast between willful action and impersonal accident is central to both the private sense of self and the public concept of the person that mind-body dualism persists in Western thinking about morally significant events like sickness and disability.

Elsewhere³ he puts somatic symptoms (the essence of fibromyalgia –FW) in a table of  ‘Interpretive Frameworks and Potential Meanings of Somatic Symptoms’ where they can represent an:

1. Index of disease or disorder

2. Symbolic expression of intrapsychic conflict.

3. Indication of specific psychopathology

4. Idiomatic expression of distress

5. Metaphor for experience

6. Act of positioning with a local world

7. Form of social commentary or protest

Movement disorders (sometime called conversion symptoms) are a problem for neurologists who are uncertain what to make of patients with such disorders:⁴

The key clinical feature that separates patients with functional movement disorders from those with organic movement disorders is that the movements have features that one would usually associate with voluntary movement (distractibility, resolution with placebo, and presence of pre-movement potentials), but patients report them as being involuntary and not under their control. There seem to be just two logical explanations for this feature: either movements are deliberately feigned or there must be a brain mechanism that allows voluntary movement to occur but to be experienced subjectively as involuntary. Understanding this mechanism would seem to be key to understanding the development of symptoms and their treatment.

And a survey of British neurologists concerning conversion disorders reported,⁵

The neurologists endorsed psychological models but did not understand their patients in such terms. Rather, they distinguished conversion from other unexplained conditions clinically by its severity and inconsistency. While many did not see this as clearly distinct from feigning, they did not feel that this was their problem to resolve. They saw themselves as ‘agnostic’ regarding non-neuropathological explanations … One reason for the model’s persistence may be that it is employed as a diagnostic device, used to differentiate between those unexplained symptoms that could, in principle, have a medical explanation and those that could not.

 Hill notes:⁶

 … conditions that do not readily fit the clinician’s model of care and practice can place patients in moral jeopardy. Carl May and colleagues found that physicians quickly make evaluative judgments of patients’ motives, the legitimacy of their symptoms, and the congruence between the physician’s and the patient’s conceptual model of illness.

 Banks⁷ noted of patients with chronic fatigue (fibromyalgia’s first cousin) that

In the realms of symptoms, aetiology and treatment evaluation, lay people in the CFS clinic have quite distinct ideas about what their problems are and how they might be analysed and managed—ideas that are often in conflict with those of medical professionals. Thus, lay sufferers, for example, operate within a different conceptual terrain from that of many professional experts. They are more likely to refer to a disease (myalgic encephalomyelitis or ME), rather than a syndrome. They call upon different kinds of hypotheses to explain their symptoms. They hold to conflicting ideas about the order of causal sequences, and they give emphasis to different kinds of phenomena in their accounts of illness. As a consequence, clinical consultations can often take on the form of a political contest between physician and patient to define the true and real nature of the patient’s disorder—a micro political struggle in which neurological symptoms can be re-framed as psychiatric symptoms, and psychiatric symptoms as neurological. In short, a contest in which the demarcation lines between mind and body are continually assessed and re-defined, and the tenets of ‘biomedicine’ are constantly challenged

In an email, Nancy Ryan calls attention to an article by Siri Hustvedt entitled, ‘Philosophy matters in brain matters.’⁸ Hustvedt is a highly regarded writer who happens to suffer from migraine and ‘medically unexplained seizures,’ and wrote about it in a book called ‘The Shaking Woman or A History of My Nerves’ that was published in 2009. Another name for her problem is psychogenic non-epileptic seizures (PNES), which the Wikipedia describes as ‘events superficially resembling an epileptic seizure, but without the characteristic electrical discharges associated with epilepsy. Thus, PNES are regarded psychological in origin, and may be thought of as similar to conversion disorder.’

It’s not possible to summarize Hustvedt’s important article—read the whole article, but the abstract gives the flavor:

Purpose: Although most neuroscientists and physicians would argue against Cartesian dualism, Descartes’s version of the psyche/soma divide, which has been controversial since he proposed it in the seventeenth century, continues to haunt contemporary neurological diagnoses through terms such as functional, organic, and psychogenic. Drawing on my own experiences as a person with medically unexplained seizures, I ask what this language actually means if all human experience has an organic basis.

Methods: Close reading of a textbook chapter on psychogenic seizures.

Results: I expose the author’s unreflective embrace of psyche and soma as distinct entities, his inherent bias against illnesses labeled psychogenic, and the implicit sexism of his position. I further argue that even when a patient’s symptoms are not alleviated, heightened self-consciousness and narrative framing can strengthen his or her sense of agency and have therapeutic benefits.

Conclusion: The ethical treatment of patients requires a respect for their stories.

She concludes,  ‘Although some empathy in one’s doctor is certainly desirable, an ethical position requires respect, above all, the simple recognition that the patient in front of you has an inner life as full and complex as your own.’

If it is not entirely clear what these illnesses mean or what dualism means, we can value as being complete and correct Hustvedt’s call: ‘The simple recognition that the patient in front of you has an inner life as full and complex as your own.’

For now, one path, quoted by Scheurich⁹ and in line with Kirmayer’s ideas,  is that that we should understand clinical problem simultaneously as diseases, dimensions, behaviors, and life stories. Things are true or false or unclear depending on who we are and where we are. But the patient in front of us has an inner life as full and complex as our own.

1.            Cohen, M., Quintner, J., Buchanan, D., Nielsen, M. & Guy, L. Stigmatization of patients with chronic pain: the extinction of empathy. Pain Medicine (2011).

2.            Kirmayer, L.J. in Biomedicine examined 57-93 (Springer, 1988).

3.            Kirmayer, L.J. & Young, A. Culture and somatization: clinical, epidemiological, and ethnographic perspectives. Psychosomatic Medicine 60, 420-430 (1998).

4.            Edwards, M.J. & Bhatia, K.P. Functional (psychogenic) movement disorders: merging mind and brain. The Lancet Neurology 11, 250-260 (2012).

5.            Kanaan, R., Armstrong, D., Barnes, P. & Wessely, S. In the psychiatrist’s chair: how neurologists understand conversion disorder. Brain 132, 2889-2896 (2009).

6.            Hill, T.E. How clinicians make (or avoid) moral judgments of patients: implications of the evidence for relationships and research. Phil Ethics Hum Medicine 5 (2010).

7.            Banks, J. & Prior, L. Doing things with illness. The micro politics of the CFS clinic. Social science & medicine (1982) 52, 11 (2001).

8.            Hustvedt, S. Philosophy matters in brain matters. Seizure (2013).

9.            Scheurich, N. Moral attitudes & mental disorders. Hastings Center Report 32, 14-21 (2002).

Previously, I raised the questions, ‘What is fibromyalgia?’ ‘When does fibromyalgia begin? Based on data that suggests strongly that fibromyalgia represents the end of a continuum of polysymptomatic distress, I stated that people who didn’t quite reach the end of the continuum could be considered to be on the pathway to criteria positive fibromyalgia. I also thought that fibromyalgia could be considered to be a trait disorder rather that a state disorder. I wrote about this in the blog on February 20, 2013: ‘Fibromyalgia as a Trait (and a Continuum) Disorder.’ I want to reprint a little of that post below:

Because fibromyalgia is a symptom based disorder, rather than a disease, it ‘officially’ begins when a person satisfies fibromyalgia criteria and is diagnosed by a physician. Prior to the 2010 criteria, that meant satisfying the 1990 ACR fibromyalgia criteria and its requirement of the tender point examination. The 2010 criteria require only self-reported symptoms that are convincing to the physician. Because the evaluations required by the criteria are almost never performed in primary care practice except when fibromyalgia is expected, and then only rarely, there is no way to know whether a patient had fibromyalgia prior to formal diagnosis. In fact, some people could have had fibromyalgia for decades—without ever knowing it: as Ehrlich acidly pointed out, ‘No one has FM until it is diagnosed.’

Applied to fibromyalgia, trait means the tendency of those with fibromyalgia to respond to physical or mental stress in a stereotyped way—by increasing pain, fatigue and the other symptoms of fibromyalgia. Katz and Wolfe put it this way:

‘…a diagnosis of fibromyalgia is most often permanent in the sense that it tends to represent a trait rather than a state. As such, a person may have “a little” or even no fibromyalgia for a while and much fibromyalgia during other periods. For example, fibromyalgia characteristics may become more prominent during periods of physical and/or mental stress and may relent or decrease during periods of better health or tranquility…. Patients considered to have fibromyalgia may not meet formal ACR criteria on some or all occasions.’

Examination of the life history of fibromyalgia patients shows that many have extensive somatic symptoms, functional illnesses, complaints of fatigue and pain before a formal diagnosis of fibromyalgia can be made. Dan Wallace, the fibromyalgia author and a strong proponent of the idea that trauma can cause fibromyalgia writes, ‘In our experience, a review of the medical record would show that 90% of the time, myofascial or FM‑associated complaints were present prior to the injury.’ In many court cases, a detailed review of patients records prior to diagnosis will also show repeated medical visits for fibromyalgia related symptoms. The 2010 American College of Rheumatology criteria identify excess somatic symptom reporting as a characteristic of fibromyalgia, and excess somatic symptom reporting is often found prior to diagnosis.

Wolfe et al. reported the results of six-center longitudinal study of fibromyalgia. They found that patients with ‘fibromyalgia were more likely to have lifetime surgical interventions, including back or neck surgery, appendectomy, carpal tunnel surgery, gynecologic surgery, abdominal surgery, and tonsillectomy, and were more likely than other rheumatic disease patients to report comorbid or associated conditions;’ and they emphasized that tonsillectomy is an intervention that occurs in childhood.  Most of the observed events occurred before fibromyalgia was formally diagnosed.

These results are key to understanding the limitations of the ideas and clinical concepts of fibromyalgia. Here are just a few of the issues they raise.

How does trauma cause fibromyalgia if fibromyalgia existed (in an attenuated form?) before the trauma? Does it make sense to call 11 tender points fibromyalgia (1990 criteria) and to call 9 tender points not fibromyalgia? If fibromyalgia exists in a continuum, how can we say that fibromyalgia is associated with (or caused by) central sensitization (CS)? For certain we know that the 8, 9 or 10 tender point patient will also be found the have CS.

Although the idea of a dichotomous fibromyalgia may be useful clinically, it is an untruth in fibromyalgia research and in the understanding of pain and symptoms.

The March number of ‘SPINE’ contains a remarkable article entitled, ‘Health, Social, and Economic Consequences of Neck Injuries.’ Fortunately, it is free to all readers at http://journals.lww.com/spinejournal/Fulltext/2013/03010/Health,_Social,_and_Economic_Consequences_of_Neck.14.aspx? Neck injuries as “whiplash” is a disputed condition; and additionally, many people labeled as whiplash will satisfy fibromyalgia criteria. Whiplash and fibromyalgia often are discussed together in the context of traumatic causation. I bring this up at this time because the pain, suffering, costs and psychosocial issues are similar in these two overlapping syndromes. Below, I excerpt some of the text to make some points, but you need to read the full article to get the unedited version.

The authors used records from the Danish National Patient Registry 1998–2009. All patients with a diagnosis of neck injury and their spouses were identified and compared with randomly chosen controls matched for age, sex, geographical area, and civil status.

The register contributed 94,224 patients, and 372,341 matched controls were identified. Patients with neck injury had significantly higher rates of health- related contacts, medication use, and higher socioeconomic costs than controls. To a lesser extent, they also had lower employment rates, and those employed generally had lower incomes.

Patients with neck injury had already presented negative social and health-related status up to 11 years before the first diagnosis, which became more pronounced for those with the highest costs. The health effects on costs were present regardless of age group and sex, and it was also seen for the patients’ spouses. The increased expenses during subsequent years cannot be explained by the injury alone, because these patients already had elevated expenses prior to the injury. This indicates some selection of increased vulnerability for both patients and their spouses.

Of particular note is that both patients and their spouses exhibited a pre-existing social, economic, and morbidity impact several years before the accident.

That higher health care costs seen for both patients and spouses prior to the injury speak for a trend that low-threshold sickness behavior leads to both choosing spouses with similar behavior and, in case of an injury, contact the health care system with a lower threshold.

The economic impact of neck injuries is often considerable. As can be seen in Figures 3 and 4, even at the time of diagnosis, patients generally had incurred significant health- related expenses earlier in life. Such prediagnostic burdens have been described for various chronic and progressive disorders, such as multiple sclerosis, Parkinsonism, and sleep-disordered breathing, but these are associated with long-lasting and prediagnostic courses. The previously mentioned proportion of patients with chronic neck pain— starting acute without an evident trauma—is often classified as having a neck “injury.” A proportion of them are probably characterized as having comorbidity and miscellaneous psychosocial aspects influencing their ability to cope with back and neck pain.

Even in chronicity after whiplash injuries, such aspects frequently are present as well. Also, for other distinct trauma, those patients with neck injury who develop chronic courses tend to be associated with lower social classes.

Consequently, we conclude that sequelae of neck injuries, including injury reports sent to NPR, tend to occur more often among more vulnerable people and that development of chronicity is more likely among high-risk groups. In this case, risk indicators could typically be: age, female sex, neck pain, mood, low physical activity, psychological factors, and low social class. It is interesting to note that similar effects also occur for the spouses, although it is well known that people choose spouses with characteristics comparable with their own.

In studies from the UK about chronic widespread pain (CWP), pre-existing psychosocial characteristics explained the development of CWP following trauma.¹ And, as I have noted previously, fibromyalgia patients had increased medical and surgical costs and events prior to the diagnosis of fibromyalgia.²

1.  Jones, G.T. et al. Role of road traffic accidents and other traumatic events in the onset of chronic widespread pain: Results from a population‚Äêbased prospective study. Arthritis Care & Research 63, 696-701 (2011).

2.   Wolfe, F. et al. A prospective, longitudinal, multicenter study of service utilization and costs in fibromyalgia. Arthritis Rheum 40, 1560-70 (1997).

Below, I have posted an article by Milton Cohen & John Quintner. It is a much shortened version of their 2011 publication [Cohen, M., Quintner, J., Buchanan, D., Nielsen, M. & Guy, L. Stigmatization of patients with chronic pain: the extinction of empathy. Pain Medicine (2011)]. The original article is, I believe, rather better, conveying more of their thinking and logic. Although copyright law prevents us from reprinting that version, you can, if you hurry, download a PDF version of their work by searching for the title in scholar.google.com.

There is much in their article with which I disagree, and I will follow-up with a longer post on some of the issues I see. But for now, read below or, better, get the original article from the web.

Chronic Pain and the Negation of Empathy by Milton Cohen & John Quintner

 Health professionals usually regard empathy as a positive attribute to be conveyed by them to their patients.¹ Empathy denotes the capacity of the clinician to sense the emotions and feelings of the patient.²

Derived from the Greek empatheia for “in suffering or passion,” empathy implies a shared phenomenology wherein a person is able to both accept and understand the expression of another person’s experience because it reflects the formers own experience.³

Empathy functions as a foundation for other acts (e.g. compassion, prosocial behaviour) that allow one to enter the experience of the “other” in an intuitive manner without the necessity of having to share that same experience, especially at an emotional level, as is the case for sympathy.⁴  In medical practice, the patient’s lived experience of pain is a common substrate for empathy.

However, empatheia includes the sharing of strong negative emotions, such as those that may accompany a sense of personal danger or hostility or prejudice,⁵ which could be directed at a clinician, especially when the legitimacy of that patient’s distress is in doubt and their presentation challenges the clinician’s expectation of a linear relationship between the severity of pain and the extent of tissue damage.⁶ Often there may be no discernible evidence of the latter.

The simulation theory of empathy proposes an analogical mapping process from one person’s situation to another.⁷  Such mapping occurs automatically at an unconscious level, but it can also depend on rule-based reasoning, making it more deliberate and theoretical.⁸ It is used both to produce the experience and to decode it when the “other” is experiencing it.

Neuroscientific research supports the existence of this reciprocal process, suggesting that the act of observing others who are experiencing pain triggers activation of neural networks that have been implicated in the direct lived experience of pain.⁹

Importantly, these networks also include those that have been found to accompany the observation of strong negative emotional expressions such as disgust, fear, anger and sadness.⁹

Empathy may then mutate into a projection of negative emotion and judgment towards the other person and even a conscious avoidance of compassion.6 When empathy is extinguished, and compassion disappears, we have coined the term “negative-empathy”.

“Negative-empathy” allows community-based stereotypes of chronic pain sufferers to pervade the clinical encounter.¹⁰ As stereotypes may contain negative emotional valence (e.g. “putting it on,” “all in the mind”),  “negative-empathy” on the part of their health professionals can become a significant component of the complex process of stigmatisation of chronic pain sufferers.

Sociologist Erving Goffman¹¹ defined stigmatisation as a process by which the reactions of a community to specific personal characteristics reduce a person’s identity “from a whole and usual person to a tainted, discounted one”, causing that person to be discredited, devalued, rejected and socially excluded from having a voice.

Because clinical relationships are morally charged, chronic pain sufferers are also at risk of being placed in “moral jeopardy” by their clinicians.¹² Should they fail to validate the effectiveness claimed by their health professionals, or should they challenge their clinicians’ power to control the relationship, patients may acquire negative labels denoting that their motives are suspect and the legitimacy or reality of their symptoms doubted.

Moreover, clinicians can themselves encounter the same lack of validation should their choice of treatment happen to conflict with the views of regulatory authorities.¹³ The prescribing of opioid medications is a case in point.¹⁴

Remediation of negative empathy might commence with an examination of binary terminologies that are readily found both in medical teaching and clinical practice: objective/subjective; normal/abnormal; body (nociception)/mind (somatisation). Recognition of how these dualistic frames can work against patients’ best interests would be integral to a program that seeks not to perpetuate them. The stage would then be set for the emergence of pain theories with greater explanatory power.

Such theories would transcend the body/mind dualistic frame attributed to Descartes.¹⁵ They would incorporate the findings from neuroscience as they compel clinicians to accept empathy in all its connotations as being of fundamental importance to the understanding and management of patients presenting with complex pain states.

A new model of clinical engagement will emerge, one that is both scientifically and ethically obliged to discard conceptual frames that perpetuate negative stereotypes. There must be no hidden rules of the consultation (such as those governed by power imbalance) that might hinder a rapprochement between clinician and patient.

In proposing what might be termed a social neuroscience paradigm, we invoke the concept of the intersubjective or “third space” ^16,17 which allows for many different ways of communication. In this space, the experiences of both patient and clinician are shared and negotiated, neither being an “expert” compared with the other, thereby resisting socially or culturally determined stereotypes.

1.   Gallagher RM. Empathy: a timeless skill for the pain medicine toolbox. Pain Med 2006; 7: 213-4.2.   Preston SD, de Waal FBM. Empathy: its ultimate and proximate bases. Behavioral and Brain Sciences 2002; 25: 1-72.

3.   Wispé L. History of the concept of empathy. In: Eizenberg N, Strayer J, eds. Cambridge: Cambridge University Press, 1987: 17-37.

4.   Stein E (1917). On the problem of Empathy. Stein W, transl. Washington: ICS Publications, 1989.

5.   Craig KD, Versloot J, Goubert L, Vervoort T, Crombez G. Perceiving pain in others: automatic and controlled mechanisms. J Pain 2010; 11: 101-8.

6.   Shaw LL, Batson CD, Todd RM. Empathy avoidance: forestalling feeling for another in order to escape the motivational consequences. Journal of Personality and Social Psychology 1994; 67: 879-87.

7.   Barnes A, Thagard P. Empathy and analogy. Dialogue: Canadian Philosophical Review 1997; 36: 705-20.

8.   Gallese V, Ferrari PF, Umiltà MA. The mirror matching system: a shared manifold of intersubjectivity. Behavioral and Brain Sciences 2002; 25: 35-6.

9.   Budell L, Jackson P, Rainville P. Brain responses to facial expressions of pain: emotional or motor mirroring? Neuroimage 2010; 53: 355-63.

10.   Krendl AC, Macrae CN, Kelley W, Fugelsang JA, Heatherton TF. The good, the bad, and the ugly: an fMRI investigation of the functional anatomic correlates of stigma. Social Neuroscience 2006; 1: 5-15.

11.   Goffman E. Stigma: notes on the management of spoiled identity. New York: Prentice Hall, 1963.

12.    Hill TE. How clinicians make (or avoid) moral judgments of patients: implications of the evidence for relationships and research. Philos Ethics Human Med 2010; 5:11. Published online 2010 July 9. doi: 10.1186/1747-5341-5-11.

13.   Notcutt W, Gibbs G. Inadequate pain management: myth, stigma and professional fear. Postgrad Med J 2010; 86: 453-8.

14.   Nicolaidis C. Police officer, deal-maker, or health care provider? Moving to a patient-centered framework for chronic opioids management. Pain Medicine; 2011; 12: 890-7.

15.   Descartes R (1649). The Passions of the Soul. Steven Voss (trans.) Indianapolis: Hackett Publishing, 1989.

16.   Quintner JL, Buchanan D, Cohen ML. Katz J, Williamson O. Pain medicine and its models: helping or hindering? Pain Medicine 2008; 9: 824-34.

17.   Husserl  E. Cartesian Meditations: an Introduction to Phenomenology, transl. Dorian Cairns. The Hague: Martinus Nijhoff, 1973.

As it evolved, somatization became a way to think about and classify unexplained symptoms. The word somatization fell out of favor because it always implied psychogenicity. It was an hypothesis that was often inconsistent with observed data, and was mired in different schools of psychiatric thought and argument. For better or worse, it lacked face validity to many physicians. Still, it stayed around because it described common symptoms and situations that didn’t fit in otherwise and which, at some level, made at least a little sense. In a previous post, John Quinter writes disparagingly of somatization: It ‘in fact only reflects the medical observer’s “psychologization” of the clinical problem.’ John’s comment exposes the opposition to somatization and a psychosocial basis for fibromyalgia. Dan Clauw, together with a group of truly expert co-authors, writes

In the final analysis, physical versus psychologic distinctions regarding unexplained symptoms might rest on preconception and perspective rather than a priori hypothesis testing. Historically, observers of syndromes of unexplained symptoms have often drawn differing conclusions from like presentations. Whereas some observers have preferred to see a common physiological mechanism that explains symptoms, others have postulated common psychologic traumas ranging from childhood abuse to current stressors. Still others have invoked the tendency for some individuals to seek relief from social predicaments and for some clinicians and scientists to derive novel illnesses that accommodate them.¹

Beginning at the end of the 20^th, a clearer recognition of the limitations of the somatization concept was acknowledged. Sharpe wrote in 2006 ‘The assumptions that (a) bodily pathology can always explain bodily symptoms, (b) psychopathology can always explain bodily symptoms in the absence of bodily pathology, and (c) dichotomizing bodily symptoms into biomedical and psychiatric types is clinically useful were all found to have questionable validity and utility.² He wrote further that ‘Alternative multiaxial diagnostic approaches for the classification of bodily symptoms are proposed. These are intended to (a) give greater prominence to bodily symptoms in their own right, (b) allow etiology to be conceptualized in terms of multiple factors, and (c) provide the basis for integrating medical and psychiatric approaches to patient care.

Such ideas are also found in the designation of illnesses like fibromyalgia and similar disorders as `somatic syndromes disorders,’ ‘physical symptom disorders,’ ‘functional symptoms disorders,’ ‘somatic and multisomatic symptom disorders.’ It became clear that the line between psychiatric conditions and physical ones was difficult to draw, and as Sharpe said, etiology should be to be ‘conceptualized in terms of multiple factors.’

‘Somatization’ was also confounded by the specialties that invoked it. The psychiatrists clearly had in mind a psychiatric disorder—the type of illness that I never saw in my patients with fibromyalgia. The primary care physician input, led by the careful, thoughtful and ultimately very helpful work of Kurt Kroenke and others in his group, noted that somatic symptoms were ubiquitous and mostly transitory. Rheumatologists saw a different pattern in chronic pain patients: persistent increased numbers of somatic symptoms and symptom severity.

Kroenke developed as series of Patient Health Questionnaires (PHQ) that identified those with many somatic symptoms, and he couched descriptive language in non-psychiatric terms. In 1997 he wrote, ‘For clinical or research use in primary care, the DSM-IV diagnostic criteria for somatization disorder are too restrictive, while the criteria for un- differentiated somatoform disorder are overly inclusive. In this article, we examine the validity of multisomatoform disorder, defined as 3 or more medically unexplained, currently bothersome physical symptoms plus a long (≥2 years) history of somatization.’³ In 2012, he developed an 8-item question that could be used together with the (disputed) DSM-5 Somatic Symptom Disorder. The items included GI-GU problems, back pain, joint and muscle pain, headaches, chest pain, dizziness, fatigue, trouble sleeping. It is a veritable checklist for fibromyalgia, but is neutral as to psychogenicity—as was the multisomatoform disorder.

Without intending it, the 2010 ACR fibromyalgia made clear the prominence of somatic symptoms in fibromyalgia. Given multiple painful regions, the diagnosis of fibromyalgia is dependent on somatic symptoms. Maybe, as some have suggested, fibromyalgia should be considered as a kind of somatic pain disorder. Noll-Hussong in 2011 used the term, ‘Pain-predominant multisomatoform disorder.’⁴ Not a bad phrase for fibromyalgia, to my mind.

Collecting data on the number (or the number and severity) of somatic symptoms provides insights into fibromyalgia. Symptoms increase with age; people with fibromyalgia report many more symptoms than non-fibromyalgia, regardless of criteria. Symptoms exist in a continuum and correlate with psychological variables. Symptoms cannot easily be explained by the central sensitization hypothesis, though this is often suggested. We have recently published that patients with fibromyalgia report more hearing loss and hair loss than those with rheumatoid arthritis or osteoarthritis, and hair loss is a non-sensory ‘symptom.’⁵

Quintner has written that pain constitutes an ‘aporia, a space and presence that defies us access to its secrets.’⁶ But somatic symptoms are not hidden and may provide important information about fibromyalgia that includes psychocultural dimensions. Somatization, the word that dare not speak its name, is gone. But what rough beast, its hour come round at last, Slouches towards Bethlehem to be born?

1. Clauw, D.J. et al. Unexplained symptoms after terrorism and war: an expert consensus statement. Journal of occupational and environmental medicine 45, 1040-1048 (2003).

2. Sharpe, M., Mayou, R. & Walker, J. Bodily symptoms: New approaches to classification. Journal of psychosomatic research 60, 353-356 (2006).

3. Kroenke, K. et al. Multisomatoform disorder: an alternative to undifferentiated somatoform disorder for the somatizing patient in primary care. Archives of General Psychiatry 54, 352 (1997).

4. Noll-Hussong, M. et al. Sensation of pain and empathy in patients with pain-predominant multisomatoform disorder-Results of the PISO Imaging Study. Psychother Psych Med 61, A061 (2011).

5. Wolfe, F., Rasker, J. & Häuser, W. Hearing loss in fibromyalgia? Somatic sensory and non-sensory symptoms in patients with fibromyalgia and other rheumatic disorders. Clinical and experimental rheumatology (2012).

6. Quintner, J.L., Cohen, M.L., Buchanan, D., Katz, J.D. & Williamson, O.D. Pain medicine and its models: helping or hindering? Pain Medicine 9, 824-834 (2008).