Widespread pain, aka fibromyalgia – does it really belong in rheumatology?

I’ve asked it before, and I’ll probably ask it again, but does widespread pain really belong with the rheumatologists? I think the answer is rapidly becoming “No”.
The “so what” question begs: does it really matter who looks after people with widespread pain? I think the answer is “yes”, only because it’s becoming clear that helping unravel the problem of fibromyalgia (widespread pain) is going to take a different tack from looking at peripheral mechanisms alone. In fact, it could be that peripheral mechanisms are by and large irrelevant to this enigmatic disorder.

What is fibromyalgia?

Good question: there are clear diagnostic criteria for the disorder, but developed mainly for research purposes. In clinical terms, fibromyalgia is a little more tricky. Essentially, if a person says “I hurt all over”, and they also report unrefreshing sleep, foggy thinking, fatigue and sensitivity to multiple sensory modalities, chances are the person has fibromyalgia, especially if the usual diagnostic tests fail to show anything else out of order. The American College of Rheumatology released revised criteria in 2010 (Wolfe, Clauw, Fitzcharles, et al., 2010) and now doesn’t require the presence of tender points.

And this is why I don’t think it’s necessary for people to be diagnosed by a rheumatologist: there are too many people who experience this range of symptoms for diagnosis to remain the province of a single specialty. At the same time, it seems quite evident that hunting for mysterious explanations for the problem by undertaking multiple investigations is also not the answer – instead, a GP using good clinical techniques can make a diagnosis and then focus on helping the person to manage his or her symptoms quickly and without fuss.

A recent paper by Fitzcharles, Ste-Marie & Pereira (2013) argues this point, saying that “the diagnosis is made on the basis of a composite of symptoms, centred on chronic widespread pain and absence of physical findings that would indicate another condition”, and “a physical examination is required for all patients, and findings may be completely within normal limits”, and “only limited laboratory testing should be conducted for most patients” (p. E646).

What about the neurobiology?

Here’s where the situation gets a little murky, and it’s going to take a while before we really begin to understand the problem.

Neurophysiologic studies show abnormal pain processing at various levels of the nervous system, and no single unique change associated with fibromyalgia. I use the term “pain” advisedly here, because while nociception may be involved, it is not obligatory, so what we are left with is the experience of pain and some really weird abnormalities that are associated with the experience. Remember, people have pain, it’s an experience, it’s formed by the interaction of biological, psychological and social elements, and we only know about it because people do something about it – look for help.

Studies show peripheral sensitisation of the primary somatosensory neuron, central sensitisation at the dorsal horn, changes at the thalamus and gray matter of the brain, impairment or reduced functioning of the descending noxious inhibitory control mechanisms, not to mention alteration of endogenous opioid uptake. Treatments are, therefore, focused primarily on reducing the ascending information and increasing the descending inhibitory mechanisms, or working to alter the way this information is managed or prioritised by the cortex.

This means that for most people with this kind of pain, some sort of neuromodulatory drug is part of the mix – something to reduce the “reactivity” of the neural circuitry involved in processing this kind of information.  Anticonvulsants such as gabapentin or pregabalin seem to do something useful, while tricyclic antidepressants or SNRI’s are also helpful, together or separately from the anticonvulsants. BUT medications really don’t alter the pain terribly much for many people with FM. I’m one of those who fail to respond to medications. What I, and many others with fibromyalgia are left with, is learning to use the most powerful of mechanisms in the world – our fabulous cortex.

A teeny bit more neurobiology

In a paper that is in preprint right now, a group of Spanish researchers have been l0oking not just at one part of the brain, but more at the connectivity and subtle interplay between various parts of the brain while a person with fibromyalgia experiences pain. The usual culprits involved in processing nociception such as the periaqueductal gray, anterior insula, pariental operculum/secondary somatosensory cortex (SII), and the primary somatosensory cortext.

Normally, there is activity between the perietal operculum/SII and the various sensory cortices such as the auditory, visual, primary somatosensory cortex and posteria insula. This is called the “default mode” and seems to provide support for Melzack’s “neuromatrix” theory where this network is assumed to monitor and maintain “normal representation” of the body. In people with fibromyalgia, there is reduced functional connectivity between these regions.  Interestingly, there were increased functional connections between the parietal operculum/SII and the posterior cingulate cortext, precuneus, ventral putamen and ventral insula. Subjective pain ratings were positively correlated with measures of functional connectivity between the parietal operculum and PCC, ACC, left angular gyrus (also parts of the default mode network), and the left prefrontal cortex.

The authors conclude that “Overall the data suggest a strong association of clinical pain with a general weakening of sensory integration in fibromyalgia.” They point out that the amgydala and the insula are two major parts of the descending limbic input to the PAG – suggesting down-regulation of the cerebral influence on the PAG. Normally the PAG provides a “brake” on ascending sensory information – if, in people with FM, this is not working properly, it provides some explanation for the poor sensory filtering in people with fibromyalgia.

What the authors argue is that because non-nociceptive information is downregulated, it provides an opportunity for more nociceptive information to reach various parts of the brain – and this occurs not just in pain, but also in other sensory modalities such as scent, sound and vision. A bit like migraineurs perhaps? Anyway, these researchers argue that “spontaneous pain may be a consequence of partial damage in the nociceptive system with a subsequent nociceptive system hyperexcitability and a secondary inhibition of the transmission of tactile signals.”

What does this mean for treatment?

Some treatments are based on providing competing information between nociceptive and non-nociceptive input – things like peripheral nerve stimulation, whole-body vibration therapy, heated water body stimulation – and probably far closer to my heart, whole body movement, body awareness and cognitive behavioural therapy. These provide opportunities for people with FM to develop (refine, enhance) discrimination between various body states and sensory inputs. By learning to be more aware of what is really happening in the body, paying mindful attention to what is, rather than what has happened or might happen, and by carefully structuring these experiences to grade the complexity and psychosocial variables associated with them including the emotions associated with them, people with FM may begin to “retune” the out of sync central mechanisms involved in sensory processing.

To me this means we need to go beyond a biomedical approach to managing fibromyalgia, or widespread pain. We need to incorporate occupational therapists, who have specific training in analysing occupations (activities) and can grade the complexity of these occupations to titrate the level of input to where the individual needs it. We need physiotherapists to guide movements and grade complexity of movement patterns. We need to work as a team to help people understand and reconceptualise their role in managing fibromyalgia – and overall, we need to help people with FM learn to live well despite their pain. My question is: should this be the province of a single speciality in medicine? I don’t think so, I think it belongs to us all, and especially to people living with the problem.

Fitzcharles, Mary-Ann, Ste-Marie, Peter A., Pereira, John X., & Iglar, Karl. (2013). Fibromyalgia: evolving concepts over the past 2 decades. Canadian Medical Association Journal. doi: 10.1503/cmaj.121414

Pujol, J., Macià, D., Garcia-Fontanals, A., Blanco-Hinojo, L., López-Solà, M., Garcia-Blanco, S., Poca-Dias, V., Harrison, B., Contreras-Rodríguez, O., Monfort, J., Garcia-Fructuoso, F., & Deus, J. (2014). The contribution of sensory system functional connectivity reduction to clinical pain in fibromyalgia PAIN® DOI: 10.1016/j.pain.2014.04.028

Wolfe, F., Clauw, DJ., Fitzcharles, M-A., et al. (2010). The American College of Rheumatology Preliminary Diagnostic Criteria for Fibromyalgia and Measurement of Symptom Severity. Arthritis Care Research (Hoboken), 62, 600-610.


  1. Bronnie, to answer some of your important questions, it might be a good idea to start with an hypothesis. How about the one referenced below that we published in 2011? It seems to be the only coherent scientific explanatory model currently available. It contains implications for patient management along the lines that you favour.

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

  2. Yes I agree – I haven’t incorporated it yet because I’m still working my way through it and the implications of it. I agree it’s a good hypothesis for testing and especially for explaining how FM originates. What’s also interesting is that the recommendations don’t really differ from what we’ve been suggesting for years – only perhaps a little more refined in how we might apply it.

  3. Thanks for yet another thoughtful post. I strongly agree to your conclusion, however, I feel inclined to think that your aspects on the role of brain imagery and pain is somewhat reductionistic. Maybe I’m just being sensitive on this particular topic (brain imagery) because I don’t think the correlations between findings and symptoms (brain activity and pain) are as obvious as many authors seem to conclude. First of all the functional imagery techniques (BOLD and ASL) cannot yet give us any clear data regarding the structure they are predicting to be active – i.e. it’s somewhat of a guess to predict that a particular set of neurons are more active. Secondly work by more critical (and insightful?) researchers suggest that brain (cortical) activity may not at all correlate with activity but – if anything – rather with salience (e.g. Iannetti & Mouraux 2010).
    Once again thanks for a great blog. Keep the posts coming!

    1. I probably don’t know enough to comment on how these findings directly correlate but in this study I thought the design used was able to control many of the variables – control group, correlations with well known & regarded measures, & the linear relationship between fMRI, pain severity & the psychometric measures helps convince me that there are some grounds for their claims of dysfunctional connectivity between these regions. It’s very early in the process of using fMRI so I think there’s a lot of progress to be made in understanding & developing the technology, but it has given us some insights into ways our brains work that we couldn’t get any other way. I’ve read Iannetti & Mouraux but I’m not yet at the point where I can thoughtfully comment on the points they raise. I’m a novice in neurobiology!

      1. But clearly not in understanding neither pain nor patients! All I’m saying is that you are more likely to be correct than any current imaging technique…

    1. Ian, it is an interesting review but does not answer the fundamental questions raised by Bronnie. I have engaged extensively with the authors on the weblog Fibromyalgia Perplex, that was commenced a year or two ago by Professor Wolfe. We are still a fair way apart in our world views.

      1. For what it’s worth, I think he has some merit in the notion of a psychocultural disorder, but I think this applies to ALL names for diseases. The words we use, and the way we categorise signs and symptoms are shaped by, and shape, our community understanding of what a problem is, and what we should do about it. In NZ this is particularly relevant: we call pains in the head “headache”, but a pain in the back is called “back injury”. Where’s the injury? Are there signs of injury, or does the person express their experience of pain, receive a name that “fits” within our sociocultural belief system, and then act accordingly? The relevance of calling something “injury” in NZ is that if it meets the criteria for “injury” as identified in the Accident Compensation Corporation legislation, treatment is essentially free. If it’s NOT an injury, treatment is either nonexistant, or self-funded.
        Getting a name for the experience is part of the process of “making sense of pain”. It provides verification of the experience, says to the individual (and the community) that this problem is “real” and therefore the person is entitled to be “ill”, seek “treatment”, and get “well”. Without a label, the experience can remain mysterious, difficult to understand, unacknowledged and the person can remain stuck, without a way to express his or her experience in a form that others can recognise. Undoubtedly this is part of the reason that some health professionals would prefer to categorise weird pain problems like FM as psychiatric.
        I think we need to be much more aware of the social aspects both of diagnosing and of illness and treatment. And yes, I think there is a continuum in FM, from quite severe and intense pain/fatigue/fogginess through to rather less intense problems. But as for every pain, intensity is not inevitably correlated with degree of disability or illness.

      2. @ Bronnie. We are in the process of devising a new Taxonomy for Pain Medicine. The issues you raise are all highly relevant to this exercise. Can I run a draft by you for comment?

  4. Hi, directed to your blog by a link in a massage forum. I currently have four people with this diagnosis on my books as an aromatherapist and am constantly reminded of the concept of the patient/client being the expert in their own illness. All four are very different in how much pressure on different parts of their body is right for them, which oils help and which don’t etc. (There are some common factors with the oils but also clear differences.)

    I will probably write some more on this subject when I feel I have learned enough to do so!

    1. Thanks for stopping by! I hope you find information you’re after – and let me know if there are any topics you’d like me to write about. cheers Bronnie

    2. These are very important observations! People are unique in so many different ways. Touch is a very important potential therapeutic tool, but your four patients are likely to be hypersensitive to mechanical forces. This is due to complex changes that have taken place in their central nervous system, changing the way they process sensory stimuli. They are also likely to be hypervigilant.

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