An experimental study of pharmaceutical cannabis in fibromyalgia

I’ve had a strong interest in cannabis and pain seeing as so many of the people I’ve worked with who live with chronic pain talk about using it (it’s still illegal in New Zealand, though medical cannabis has just been legalised this year). This study is one of the growing number of studies beginning to examine the effects of cannabinoids on pain, and offers a tiny window into what might be happening. Note: the study was performed in collaboration with the cannabis producer, and one of the authors is an employee of this company. Although his role was only to comment on the protocol and final version of the paper, it’s worth noting this relationship.

The study question

In this study, the researchers were looking to understand the analgesic effect of inhaled pharmaceutical-grade cannabis as a plant rather than an extract, using four different varieties with known levels of THC and CBD. Three had active biochemicals, while one was a placebo and had neither THC nor CBD. They investigated the effects of these preparations on experimental pressure pain, electrical pain, and spontaneous pain (primary endpoints), as well as the subjective and psychotropic effects.

The participants were all women with rheumatologist-diagnosed fibromyalgia, a score on a numeric rating scale of more than 5 (where 10 = most pain imaginable), met the diagnostic criteria of the 2010 American College of Rheumatology, and therefore had a widespread pain index of greater than or equal to 7 (from 0 – 19); symptom severity score of greater than 5 (from 0 – 12), or a widespread pain index of 3 – 6, and a symptom severity score greater than 9. Participants were excluded if they had any medical, neurological or psychiatric illness, used strong opioids or other pain relief except paracetamol or ibuprofen, using benzodiazepines, or had any known allergies to the cannabis used. Other exclusion criterai included pregnancy, illicit drug or alcohol use, recent use of cannabis, breast feeding, and other pain problems apart from fibromyalgia. On the day of screening and each day of testing, urine was tested for illicit drug use. Comment: note that excluding anyone with psychiatric illness doesn’t describe whether this was current illness, illness controlled by medications – and if it doesn’t include these participants, suggests the participants are not our usual sort of person with fibromyalgia, given the high comorbidity of psychiatric illness with fibromyalgia.

Study design

Participants attended the centre five times, with the first visit being the screening session where they were also given an orientation to the experimental set-up (eg how to inhale). On subsequent visits, participants were given one of four different cannabis inhalations (in random order) with at least 2 weeks between visits. The vapour was generated using the Stroz and Brickel Volcanic Medic vapouriser which heats the plant material which is then collected in a balloon (made opaque for this study so participants couldn’t see the vapour). Participants had to inhale the vapour 3 – 7 minutes after the balloon was filled, and asked to hold their breath for 5 seconds after they’d inhaled.

Blood testing involved using an arterial line, and five ml of blood was obtained a T0 (before), 5, 10, 20, 30 , 40, 50, 60, 90, 120, and 180 minutes after the person started to inhale. This blood was analysed for CBD,THC, and its active metabolite 11‐hydroxy‐THC (11-OH-THC) plasma concentrations.

In addition, participants were asked to rate their pain on an 11 point visual analogue scale (from 0 = no pain to 10 = most severe pain imaginable), and to do this before inhaling, and at 1, 2, and 3 hours after. Two experimental pain tests were used: pressure pain test using an algometer to deliver pressure on a skin area of 1 cm square, between the thumb and index finger; pressure was applied until the person said it had become painful, and repeated three times at each time point of T 5 0 (baseline), 12, 22, 32, 42, 62, 92, 122, 152, and 182 minutes after the start of inhalation.

An electrical pain test was also used delivering a current via two electrodes placed on the tibial surface of the right leg, about 10 cm above the medial malleolus. The participants were required to indicate when they first experienced pain (threshold) and when the pain became unbearable (tolerance), and this procedure was repeated at T 5 0, 10, 20, 30, 40, 60, 90, 120, 150, and 180 minutes after the start of cannabis inhalation.

Finally, two questionnaires were also completed: the Bowdle questionnaire which is used to evaluate psychoactive aspects of cannabis use (eg psychedelic effects), and the Bond and Lader questionnaire which is used to establish the mental cloudiness and mood effects.

I won’t go into the blinding and allocation processes, but randomisation was computer-generated, and adequate steps were taken to ensure neither the investigators nor the participants were aware of the contents of the inhalation.

The results

25 people were recruited, but five withdrew after the first study visits, and interestingly three did so because of dizziness and nausea (3/5) . These participants were replaced with another patient according to the protocol. Participanats were women, around 39 years old (+/- 13 years), weighing about 82kg +/- 20kg, and 169 cm (+/- 7cm). Their NRS pain score was 7.20 +/-1.24; and all had their fibromyalgia diagnosis confirmed. Widespread body pain of 13.9 =?-2.6, symptom scale of 9.2 +/-1.3, and 14.9 +/- 2.9 tender points. (note that tender points are still difficult to identify reliably, so this continues to be an area of discussion).

All three active preparations resulted in adverse effects. Yes – all three! These effects included coughing, sore throat and bad taste, feeling high, dizzy, and nauseous. Of course, two also reported feeling high after placebo, but there were no differences in the frequency of adverse effects between the active treatments, and it should be noted, no serious adverse effects.

Interestingly, none of the treatments had an effect greater than placebo on spontaneous pain scores or electrical pain responses. So it doesn’t look like cannabis is much help with the general spontaneous pain many people with fibromyalgia experience, and I hope we don’t go around electric shocking each other!!

BUT two preparations caused a significant increase in tolerance to the pressure applied to the skin over the adductor pollicis muscle for the duration of the study. The largest effect was observed for the cannabis variety that contained high doses of both THC and CBD, allowing an additional 11kgf at 20 – 90 minutes. Active treatments vs placebo showed significantly more patients (n = 18) responded to the CBD + THC preparation with a decrease in spontaneous pain by 30%, but only N = 9 achieved 50% which is not statistically significant. At both responder rates, all other treatments had response profiles not different from placebo. Spontaneous pain scores were strongly correlated with the magnitude of drug high.

Study author’s discussion

The authors point out that none of the treatment had an effect greater than placebo on spontaneous pain, but that compared with placebo, more people responded to the combined THC + CBD preparation than the other forms – and these others had response rates no different from placebo. The pain reduction scores for spontaneous pain correlated with how high participants felt. For pressure pain threshold, an increase in pressure was tolerated by people with two preparations with THC content, while the form with CBD did not have any analgesic effect.

What do I think?

As someone living with fibromyalgia, I’m always curious about treatments that may help reduce the burden of this disorder. Unfortunately, I don’t think cannabis, at least in these forms, is going to cut the mustard. While pressure pain threshold reduced, it didn’t reach the 50% reduction in pain that we really want, and I’m not sure pressure pain is the one I’m most concerned about. I’d love for my spontaneous pain to reduce and unfortunately this study suggested that I’d have to get high to do so. Might be great for pain, but not so great for being able to DO anything! The authors point out that “the pressure pain test seems especially suited for exploring treatment effects in FM pain, as it elicits mechanical muscle stimulation through A delta- and C fibre activation and better reflects the symptoms of patients with FM, but I’m not entirely convinced myself.

The numbers needed to treat for cannabis preparations are greater than 20 – what this means is that more than 20 people need to try cannabis for ONE person to obtain a benefit. Not only that, but from this study, 5 of the original 20 people withdrew because of adverse effects, with adverse effects being very common. You’d have to be prepared to cope with coughing, dizziness, nausea, and feeling high if you wanted to use cannabis in this way.

So, at this point I’m not an advocate of cannabis for the purpose of relieving the pain that people with fibromyalgia experience. While it’s appealing, the numbers needed to treat are very high, adverse effects common, and the fact that the analgesic effects were only experienced alongside feeling high makes me very cautious. More studies are needed!

van de Donk, T., Niesters, M., Kowal, M. A., Olofsen, E., Dahan, A., & van Velzen, M. (2019). An experimental randomized study on the analgesic effects of pharmaceutical-grade cannabis in chronic pain patients with fibromyalgia. Pain, 160(4), 860-869.

Everyday hassles of fibromyalgia

This post has been on my mind for a while now. I live with fibromyalgia (FM) and want to share some of the everyday hassles I face. This isn’t a “oh woe is me” kind of post, it’s more of a “if you’re a clinician working with someone who has fibromyalgia, these are some things to ponder”.


I worked in chronic pain management for almost 20 years before I recognised that the pains I’d been experiencing most of my adult life actually added up to “…a syndrome of diffuse body pain with associations of fatigue, sleep disturbance, cognitive changes, mood disturbance, and other variable somatic symptoms”(Fitzcharles, Ste-Marie, Goldenberg et al, 2012). I’d hurt my back in my early 20’s, thankfully been seen by Dr Mike Butler and given the Melzack & Wall book “The Challenge of Chronic Pain” to read, so I wasn’t afraid of my pain and just accepted it as part of life. What I hadn’t really recognised was that not only was the pain in my lower back part of the picture, so too was the pain in my neck, shoulders, arms, hips, legs, feet, and the irritable bowel, and the gastro discomfort, and the migraines and the dysmenorrhoea. Not to mention the fatigue, rotten sleep, foggy thoughts, and low mood.

Diagnosis for people living with fibromyalgia is often delayed.  People with fibromyalgia may resist going to the GP for what seem to be short-term but painful bouts in various parts of the body. There for a couple of weeks, then shifting to another part of the body. As one person said to me “You feel a fool going to see a Dr about a pain that’s not consistent to say ‘Oh Doctor and I have pain here, and here and here and last week I had one here…especially when it might be gone next week, and that other one has already gone.'”. This experience is echoed in qualitative research where, for example in a study by Undeland and Malterud (2007) people said that although having a label was reassuring (it’s not something that will kill you!), the label itself was often difficult to obtain (doctors not being keen to label something so nebulous as FM), and even with a label health professionals and the general public “pay no attention to the name, or blatantly regard them as too cheerful or healthy looking” (Undeland & Malterud, 2007).


One of the problems with getting the diagnosis is that very few people get relief from medication. Those that do may find their pain settles almost completely, but many others have no effective analgesia despite trying numerous combinations. I’m one of them. What this means is that “self management” is the order of the day – yet in many places this is not even considered, let alone having services to help people develop such skills.

I’ve learned that my body feels best when I maintain a consistent level of activity irrespective of the day of the week. I enjoy stretching, walking, cycling and dancing, but I also love gardening, fishing, walking the dog – and I guess I can add in doing the housework and working as part of the mix. New activities are bound to give me aches and pains that last for weeks, while stopping my usual routine also brings me aches and pains that last for weeks. So boring consistency is the name of the game. And as I’ve previously blogged that means I look for a variety of different movement options in my repertoire.

Everyday hassles

The one thing that makes my life difficult is when I develop a new pain in a part of my body that doesn’t usually feel uncomfortable. Like most people living with persistent pain, I’ve developed an awareness of “my normal” (see this study by Strong & Large, 1995, for a nice description of this aspect of living with pain, one that is not often discussed). I know the usual pattern of my pains – bellyache, low back pain, neck and upper back pain, wrists and fingers, and often, knees, headaches and facial pain. These are my normal – but when should I seek help for a new pain? After all, it could be simply a manifestation of my fibromyalgia (ie there is nothing medically to be found, and no real change in management). At the same time, these are new pains – one in my shoulder that feels like an impingement (painful arc), and one that’s possibly an adductor tendon thing that’s very localised and hasn’t moved for over 7 months.

The question that keeps coming back to me is whether I’m overlooking something that can be treated, or whether it’ll just settle down like most of my pains do. Essentially I’ve just kept doing what I do and ignoring it.

The difference between my situation and those of people who are not painiacs, who don’t know that their pain is largely unrelated to the state of the tissues, is that I’m immersed in pain research all day, every day. I’m not overly bothered by these new pains. I’m continuing to exercise as normal and these pains aren’t interfering with what I need and want to do in daily life (well, perhaps a little…).

I can understand why someone might ask for help for a new pain. There are no rules saying that just because you have a persistent pain disorder you’re immune from acute musculoskeletal disorders. And sometimes by treating a new pain as an acute pain, it will vanish. Though, it must be said that outcomes for people with more than 3 or 4 persistent areas of pain with low back pain are not as good as those who only have one or two (Nordstoga, Nilsen, Vasseljen et al, 2017), nor of recovery and benefit from total hip and knee replacement (Wylde, Sayers, Odutola, Gooberman-Hill et al, 2017).

Points to ponder

So how do we as clinicians help people who must live with persistent pain?

  • Do we consider the meaning of the labels we give? And do we read around the experiences of those who have been given the diagnosis? Or do we, instead, rely on our own beliefs and biases when thinking about the way we handle diagnosis?
  • Do we give people an explanation for their pain that they can understand, or do we rely on currently favoured language and models without really considering what this means to the person? And do we ever check out how they’ve interpreted our explanations?
  • Do we ever discuss how to self-manage pain? Do we think about the practical implications of needing to learn to modify every aspect of life in the face of pain that will not just go away? When I compare the tasks of living well with persistent pain against those needed to cope with other disorders, pain can interfere with everything – do we talk about the impact on sex? on relaxation? on having a holiday?
  • Do we talk about what to do when a new pain turns up? Do we think about how someone can decide whether their pain is worth seeing someone about, or one they can handle? And do we even talk about the effect of having a persistent pain problem and then going on to have surgery? Do we teach people to recognise their “normal” pain, or are we afraid to teach people this because it might focus their attention on their pain?

I don’t have researched answers to these questions. I have my experience. And I’ve been working in this field a long time – yet somehow the voices of people living successfully with this pain are rarely heard.


Fitzcharles, M.-A., Ste-Marie, P. A., Goldenberg, D. L., Pereira, J. X., Abbey, S., Choinière, M., . . . Proulx, J. 2012 canadian guidelines for the diagnosis and management of fibromyalgia syndrome.

Nordstoga, A. L., Nilsen, T. I. L., Vasseljen, O., Unsgaard-Tøndel, M., & Mork, P. J. (2017). The influence of multisite pain and psychological comorbidity on prognosis of chronic low back pain: Longitudinal data from the norwegian hunt study. BMJ open, 7(5). doi:10.1136/bmjopen-2016-015312

Strong, J., & Large, R. (1995). Coping with chronic low back pain: An idiographic exploration through focus groups. The International Journal of Psychiatry in Medicine, 25(4), 371-387. doi:10.2190/H4P9-U5NB-2KJU-4TBN

Undeland, M., & Malterud, K. (2007). The fibromyalgia diagnosis – hardly helpful for the patients? Scandinavian Journal of Primary Health Care, 25(4), 250-255. doi:10.1080/02813430701706568

Wylde, V., Sayers, A., Odutola, A., Gooberman‐Hill, R., Dieppe, P., & Blom, A. (2017). Central sensitization as a determinant of patients’ benefit from total hip and knee replacement. European Journal of Pain, 21(2), 357-365.

Pain, by any other name, still hurts

Whether we call it “widespread pain”, fibromyalgia, or any of the myriad other names it’s been given over centuries, pain that occurs in all four quadrants of the body and is accompanied by poor sleep, low mood, and “foggy thinking” is common. I can say this because a soon-to-be published meta-analysis of widespread pain (aka fibromyalgia) has found that approximately 10 – 15% of the population (or more accurately 11.8% with 95% confidence intervals of 10.3 to 13.3) report widespread pain of this type (Mansfield, Sim, Jordan, Jordan & Jordan, in press). More women than men report it, and those over 40 years old were also more likely to report it. Curiously (or not) these researchers found differences in prevalence depending on geographic variation and some cultural differences.

Diagnostic labels, and how we determine who is ill and who isn’t, is a field of study I’m fascinated by. Not so long ago, women with “the vapours”, or fainting spells, were considered to have “hysteria” or “wandering womb”. Low back pain has been variously painted as “railway spine”, rheumatism, lumbago, evil humours, “inflammation of the white fibrous tissue of the body” – and yes, the discs, degeneration of the joints, spinal irritation, nerve roots, facet joints …. ad infinitum (Allan & Waddell, 1989). Designating a set of human experiences as a particular form of health problem, and therefore worth treating has enormous implications for the individual, the treater and society. (For a longer paper on historical approaches to back pain, go here.

An interesting study by Adlrich and Eccleston (2000) looked at a social construction of what “everyday pain” means to a wide range of people. Using Q sort, which involves generating a big number of statements about the topic, then asking people to sort those statements into various piles with similar meanings, these researchers found that people believe that pain is a sign of malfunction; pain-as-self-growth (it makes us who we are, pain is essential for survival); pain-as-spiritual-growth (pain is an essential part of being human and makes the sufferer stronger through spiritual growth); pain-as-alien-invasion (pain is something external that invades and takes over who we are); pain-as-coping-and-control (pain gives us necessary information to alert us); pain-as-abuse (a negative experience inflicted upon individuals from powerful others); pain-as-homeostatic-mechanisms (regulates and shouldn’t be fought against); and finally pain-and-power (pain should not be used to obtain power over another).

Back to fibromyalgia. FM has a complex history. I think I mentioned a couple of weeks back that the orthopaedic surgeons I work with said to me “Is that even a thing?” when I mentioned my interest in this widespread pain problem. What? 11% of the population experiences it, and they wonder if it’s a “thing”?! The problem with FM is that there’s no imaging technique, no blood test, no objective method for diagnosing it – but there are a constellation of studies that have given us some ideas about how people with FM differ from those who don’t. Things like the pressure point threshold – the pressure at which pain is reported when a small pointed thing is poked into the skin (without breaking the skin); problems with descending inhibition in quantitative sensory testing; changes in brain structure such as increased functional connectivity. But of course, these things can’t be carried out in routine examinations – or could they?

In the study by Mansfield and colleagues, the justification for conducting a meta-analysis was that to plan interventions and develop a rationale for prioritising the condition requires data. Clinicians need to know the underlying prevalence so they can factor this problem in when they’re trying to diagnose a disorder. If a problem is fairly widespread in the population, and particularly amongst certain groups of people (women, middle-aged, and from certain geographical areas) then it’s worth knowing about, particularly if there are implications for problems, say after surgery.

The question occurring to me is, if this problem is as widespread as indicated by Mansfield, Sim, Jordan & Jordan (in press), why are there so many health professionals who don’t know about it?

Is it because it occurs more in women than men? There’s some research suggesting that when women attend for care, their treatment is different from men (Bernardes, & Lima, 2011, Richardson & Holdcroft, 2009; Stenberg, Fjellman-Wiklund & Ahlgren, 2012; Werner & Malterud, 2003)), and women’s pain from heart attack differs from mens (more diffuse, not always that left-sided, crushing pain), while women may be prescribed more medications for mood management when men are given analgesia. While women are over-represented in chronic pain statistics, they are not studied in experimental studies nearly as often as men. But men find it far more difficult to deal with the “masculinity” scripts within society and their experience of being disabled with chronic pain – it’s very hard to be “manly” and strong when you hurt all over (Ahlsen, Mengshoel, Sobrakke, 2012).

Is it because there are no “objective” diagnostic tests? Fibromyalgia can be a “diagnosis of exclusion”, the diagnosis a person gets given once all the diagnostic tests come back with no abnormality detected. But to me this doesn’t make a lot of sense – there’s no argument about the common headache, yet there’s no diagnostic test for that. I wonder if the old lumbago problem would be in a similar category had the anatomy of the spine not had quite such a lot of impact.

Is it because it’s been a diagnostic hot potato for a long time? What I mean by this is it’s had so many names and proposed mechanisms that no-one believes it’s “real” any more. Well, maybe, but are back pain, CRPS or whiplash any different?

I’m not sure why fibromyalgia has such deniability amongst a group of health professionals, and I’m sure cynics reading this will suggest something about not being able to use a scalpel on it, but I’m not convinced it’s simply that, either. The thing is, fibromyalgia by any name is common and has profound consequences for people who live with it. It’s hard to make sense of. It defies a simply Cartesian “body/mind” split. It exhausts and fogs and constrains life for many people. It complicates recovery from surgery, influenza, even concussion. It’s hard to explain – drawing on the term “central sensitisation” can bring on arguments about tautology (how can pain be explained by the presence of pain?). There are few treatments, and these have a very limited effect.

At the same time as wanting fibromyalgia to be recognised by my colleagues, I don’t want to suggest a hard-out diagnosis awareness campaign. The risks of people being mislabelled, or diagnosed correctly but then unhelpfully managed or even given a label that invites derision, is at this point in history far too great. Mostly I’d just like people living with fibromyalgia to realise that although it’s “real” it doesn’t need to define who we are.



Ahlsen, Birgitte, Mengshoel, Anne M., & Solbrække, Kari N. (2012). Troubled bodies – troubled men: a narrative analysis of men’s stories of chronic muscle pain. Disability & Rehabilitation, 34(21), 1765-1773. doi: 10.3109/09638288.2012.660601

Aldrich, Sarah, & Eccleston, Chris. (2000). Making sense of everyday pain. Social Science & Medicine, 50(11), 1631-1641. doi:

Allan, David B, & Waddell, Gordon. (1989). An historical perspective on low back pain and disability. Acta Orthopaedica, 60(s234), 1-23. doi: doi:10.3109/17453678909153916

Bernardes, Sonia F., & Lima, Maria Luisa. (2011). On the contextual nature of sex-related biases in pain judgments: The effects of pain duration, patient’s distress and judge’s sex. European Journal of Pain, 15(9), 950-957.

Bernardes, Sonia F., & Lima, Maria Luisa. (2011). A contextual approach on sex-related biases in pain judgements: The moderator effects of evidence of pathology and patients’ distress cues on nurses’ judgements of chronic low-back pain. Psychology & Health, 26(12), 1642-1658.

Mansfield, Kathryn E., Sim, Julius, Jordan, Joanne L., & Jordan, Kelvin P. A systematic review and meta-analysis of the prevalence of chronic widespread pain in the general population. Pain.

Richardson, Jen, & Holdcroft, Anita. (2009). Gender differences and pain medication. Women’s health, 5(1), 79-90.

Stenberg, G., Fjellman-Wiklund, A., & Ahlgren, C. (2012). “Getting confirmation”: gender in expectations and experiences of healthcare for neck or back patients. J Rehabil Med, 44(2), 163-171. doi: 10.2340/16501977-0912

Werner, Anne, & Malterud, Kirsti. (2003). It is hard work behaving as a credible patient: encounters between women with chronic pain and their doctors. Social Science & Medicine, 57(8), 1409-1419.

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.

Exercise and chronic pain
One of the most consistent recommendations in cognitive behavioural therapy approaches for chronic pain is for people to exercise. Exercise is thought to help reduce pain, improve physical fitness and support participating in social, professional and domestic activities. By being fit people can manage their daily activities at a lower percentage of their maximum aerobic capacity and, hopefully, minimise the risk of flare-up.

While the overall premise of exercise is clear, the details of how often, what kind and the best approach for recovery after exercising are rather less. The problem for people with chronic pain is that moving HURTS.  Some people have even argued that chronic pain is, in essence, an activity intolerance disorder.

Daenen, Varkey, Kellmann & Nijs (2014) have attempted to clarify the state of play in exercise for chronic pain, and propose some interesting guidelines for clinicians. You see, one type of chronic pain is not the same as another – and neither is one form of exercise exactly like another.

How does exercise “work”?

Exercise is “planned, structured and repetitive bodily movements that are performed to improve or maintain one or more components of physical fitness” (Howley, 2001).  Aerobic exercise at approximately 70% or more of maximum aerobic capacity sparks production of endorphins and descending inhibitory mechanisms (serotonergic, opioidergic, adenosinergic systems); it also reduces weight, strengthens muscles and increases bone density. People without chronic pain experience pain inhibition for up to 30 minutes after aerobic exercise, but this period is much shorter for those involved in resistance training (just a couple of minutes). Researchers think that endogenous opioids and growth factors are released, supraspinal nociceptive inhibition occurs, releasing beta-endorphins from the pituatary and hypothalamus and these enable analgesia by activating mu-opioid receptors in both the periphery and central nervous systems.

…And if you have fibromyalgia?

People with sensitised nervous systems, and in particular those people with dysfunctional descending inhibitory mechanisms, such as those with fibromyalgia, do not experience this endogenous analgesia. Instead, they can have increased pain possibly through a reduced pain threshold after exercise – myofibre (muscle fibre) damage is a normal part of exercise, but is associated with lactates and oxidative stress, and these can be potent contributions to nociception. In an individual with poor descending inhibition, this nociceptive input can trigger a flare-up of symptoms.

Stress responses

Daenen, Varkey, Kellman & Nijs (2014) also point out that people with chronic pain can have abnormal stress responses, with increased activity of the sympathetic nervous system, and problems associated with the HPA axis. What this means is that people with some forms of chronic pain are chronically “stressed”, that is, they’re exposed to stressors simply from having chronic pain, and this changes the homeostatic response of the HPA axis and sympathetic nervous system. This can lead to excessive fatigue and difficulty recovering from exercise, because exercise is also a stressor in which growth hormone, testosterone, cortisol, epinephrine, and norepinephrine are released. Normally this enables the body to gradually adjust to a stressor and maintain homestasis – by exercising in small but regular amounts, and allowing enough time to recover in between, the body becomes more able to respond to stressors.

In people who are chronically stress, failing to provide adequate recovery periods can lead to ongoing sensitisation of nociceptors and increased experience of pain. Daenen, Varkey, Kellman & Nijs (2014) consider that dysfunctional reactivity of the HPA axis contributes to exercise intolerance in people with fibromyalgia.

What does this mean for exercise for people with chronic pain?

I think this means we need to be careful about how we go about prescribing exercise. The purpose of exercising is generally to ensure people can manage their everyday activities with a little room to spare in terms of activity tolerance. My study suggests that people who cope well with pain use exercise more for their mental health than to improve fitness or muscle strength. And this group of people used low-level cardiovascular exercise such as walking, cycling, dancing and tai chi as their preferred form. Some people used their daily activities as their form of exercise – things like gardening, vacuuming the floor, washing windows, hanging out washing, cleaning the car.

I think we need to ensure we are very clear as to the goals of exercise. Why this particular set of exercises?

We also need to be clear that one size does not fit all. If a person doesn’t enjoy going to a gym, this shouldn’t be the ONLY form of exercise they’re exposed to. If the person doesn’t have an activity intolerance, maybe they need to develop recovery strategies rather than changing their exercise form.

We need to be aware that increases in pain intensity are likely for some people who have pain such as fibromyalgia. People with this type of pain problem may benefit from developing both an exercise form they enjoy and therefore can do consistently (I like to bellydance and garden!), AND to develop effective recovery strategies. Perhaps helping people use strategies such as mindfulness and diaphragmatic breathing as part of a cool-down could be a good option.

Finally, I think it’s important to avoid implying that people who have dysfunctional endogenous analgesic systems are simply “noncompliant”, need “psychological” input, or just need more encouragement. Maybe it’s time to reconsider the kind of exercise and recovery we’re prescribing, and titrate it according to the individual’s response to exercise.


Daenen, L., Varkey, E., Kellmann, M., & Nijs, J. (2014). Exercise, not to Exercise or how to Exercise in Patients with Chronic Pain? Applying Science to Practice The Clinical Journal of Pain DOI: 10.1097/AJP.0000000000000099

Howley ET. Type of activity: resistance, aerobic and leisure versus occupational physical activity. Med Sci Sports Exerc 2001;33:S364-9; discussion S419-20.

Non-drug approaches for people with fibromyalgia
No-one wants to be told their pain is “in your head”. But given our increasingly sophisticated understanding of pain neurobiology, there’s plenty of reason to agree that thinking, feeling and doing things differently makes life far more rewarding and rich than feeling helpless, fatigued and sore. Some proponents of purely biomedical interventions argue that if only the “source of the nociception” was found, the nerve “zapped” or anaesthetised, then all this psychosocial claptrap could be safely ignored because people “return to normal”. I think this belief shows ignorance and perhaps even arrogance because people process and attribute meaning to everything that happens to them.

I originally entitled this post as “psychological” approaches for people with fibromyalgia, but I’ve changed it after reflecting that we actually do not know which of the various parts of non-drug therapy are most useful for people. There are some core components in self-management approaches, these include explanations (or reconceptualising pain), graded return to life’s activities or occupations, exercise (again, graded), and often some work around thoughts/beliefs/emotions that might get in the way of returning to activities, and some practical problem-solving and goal-setting to help people work out how they’re going to “get on with it”.

While the assumptions are cognitive behavioural in origin – that is, people can take control of what is happening around them, and respond differently even if the pain doesn’t change – most of what happens involves doing things differently in order to bring more of what the person values back into their life, rather than having life dominated by pain.

I’ve written before about ACT, Acceptance and Commitment Therapy, and I find it quite appealing. The ACT approach involves developing skills to be fully present, work towards living a life aligned with your personal values, being mindful of what is (rather than worry about what was, or what might be), being committed to taking action even if the process isn’t always happy-happy, joy-joy. I like it, and in my research it seems to fit quite nicely with what people naturally do. In ACT the coping strategies used don’t fall into “good” or “bad” dichotomies, instead they’re evaluated according to how well they’re working in light of each individual’s values. I like the respectful attitude towards people’s personal values and beliefs, and the flexibility of using “what works” and experiential therapy rather than sitting in a clinic room talking.

The question is whether ACT is any better or worse than any other psychological treatment – such as “traditional” cognitive behavioural therapy.

The jury is out. Frankly I am not sure it’s as much about the particular model or type of therapy used as it is about the way in which it’s introduced to the person. There are CBT clinicians who seem to be able to come alongside a person, help them work out for themselves whether their thinking is helpful or not, and help them shift their perspective nicely. Then there are CBT clinicians who leave people feeling as if they have “stinking thinking” or “maladaptive thoughts”, who “have” to change their way of life, who “must” do therapy “homework” – and blame the patient for failing to do “homework” or being “noncompliant”.  I can, of course, say the same about ACT clinicians and indeed any other form of clinician!

Where does this leave us?

Well, I’m not sure that much has changed in the 20 or so years I’ve been working in this field. What has happened is stronger evidence to show that thoughts, beliefs, emotions and behaviour are linked, and directly influence our experience of pain. People still need to understand, or make sense, of what’s happening to them, get more active and have more of what they want in their lives rather than feeling controlled by pain.

How we achieve this probably depends as much on the person who has pain as the clinician.

We also know that fruitlessly seeking pain reduction leads to demoralisation, frustration and increasing disability.

While I’ve put “fibromyalgia” as the type of chronic pain two of the papers I’ve cited refer to, really I’m not convinced that the problems people experience from their pain differs terribly much depending on the diagnosis. The effect of pain that goes on is the same – a diminishing sense of self identity, increased sense of helplessness and overall difficulty doing and being well. Addressing these effects is far more worthwhile in people’s lives than trying to control, avoid or abolish pain – because some pains just don’t go away.

Luciano, J., Guallar, J., Aguado, J., López-del-Hoyo, Y., Olivan, B., Magallón, R., Alda, M., Serrano-Blanco, A., Gili, M., & Garcia-Campayo, J. (2014). Effectiveness of group acceptance and commitment therapy for fibromyalgia: A 6-month randomized controlled trial (EFFIGACT study) PAIN®, 155 (4), 693-702 DOI: 10.1016/j.pain.2013.12.029
BERNARDY, K., FUBER, N., KOLLNER, V., & HAUSER, W. (2010). Efficacy of Cognitive-Behavioral Therapies in Fibromyalgia Syndrome — A Systematic Review and Metaanalysis of Randomized Controlled Trials The Journal of Rheumatology, 37 (10), 1991-2005 DOI: 10.3899/jrheum.100104
Williams ACDC,, Eccleston C,, & Morley S (2012). Psychological therapies for the management of chronic pain (excluding headache)in adults. Cochrane Database of Systematic Reviews (11) DOI: 10.1002/14651858.CD007407.pub3


NB: I have amended the first paragraph because it may have been viewed as unnecessarily pejorative towards a single type of clinician. The truth is, I point the finger at any clinician from any background or discipline if I think what is being done is harmful, illogical or maintains distress and disability, including my original profession of occupational therapy.  I was being simplistic to suggest a single profession is at fault. It’s not the profession per se, it’s the attitude that I strongly object to.  To those who were upset by my original wording, here’s an invitation: if you’re able to demonstrate HOW you integrate biopsychosocial approaches in your practice, I’ll publish it. That’s the beauty of dialogue, and particularly social media.

‘Psychological therapy’ works for fibromyalgia!
An ‘enigmatic’ disorder – this is what Perry Nicassio calls fibromyalgia. I hadn’t thought of it that way, because so many chronic pain problems seem to be equally ‘enigmatic’! It’s a common disorder, affects many more women than men, has a multiplicity of effects on people ranging from fatigue, poor sleep, widespread aching, other pain sensations such as stabbing or needle-like pains that can appear anywhere in the body, often with low mood and loss of function.  There are few medications that seem to help, and many people never seek treatment for their pain.  If people do look for treatment, they can be faced with skepticism from some health providers, despair from others, and offered a multiplicity of treatments that don’t seem to do an awful lot to change the situation.

Have I painted a bad enough picture? It’s only so the good news looks really good!  And the good news is that in a recent meta-analysis of psychological therapies, there was a consistent finding that both short-term and longer term outcomes improved with this kind of input.  OK, the effect sizes were small – but they were maintained, and the good thing about cognitive behavioural therapy (which was found to be the most effective ‘brand’ of therapy) is that once learned, no-one can take it away again, unlike medications!

The mainstay treatments for fibromyalgia include regular exercise – it seems that hydrotherapy is popular, but so is tai chi, pilates, walking, and really, anything that keeps the whole body moving.  People with fibromyalgia also respond to learning more about their disorder – information is power! And to cognitive therapy – identifying unhelpful thinking and working with these to check out their helpfulness and accuracy, and then identifying new ways of viewing the situation.  Other therapies commonly used, and studied in this meta-analysis, include biofeedback and relaxation training; sleep restriction and other forms of sleep management (eg sleep hygiene, cognitive therapy); activity management such as scheduling, pacing, planning, and graded increases in activity; behavioural strategies such as positive reinforcement for well behaviour and contingency management for illness behaviour; problem solving and communication strategies.

These don’t sound particularly different from the kind of therapy that most people with chronic pain receive within a cognitive behavioural approach.  In other words, a full package of pain management strategies within a cognitive behavioural approach seems to have the best short-term and long-term effect on things like sleep, pain intensity, mood, activity level – and even catastrophising!

There are always questions raised in studies like this.

Why were only 23 studies from the original 1530 identified? Methodological limitations hampered inclusion of many of these studies – too few details provided in the research paper, no control groups, limited descriptions of how people were selected for the treatment and what happened to people who dropped out, or other treatments such as pharmacology were continued so that good conclusions couldn’t be drawn from the results.

But other questions are also raised.  What are the mechanisms that psychological therapies are working on?  How do they work?  Why is that something that influences pain intensity can also influence sleep quality and mood problems?  Does this mean these problems are linked somehow?  Could this mean that if we addressed just sleep, for example, these other problems might resolve themselves?

Are all people with widespread pain actually experiencing fibromyalgia? If there is a spectrum of symptoms, ranging from full-blown low mood, poor sleep, deactivation and tender points along with the aching, and all points in between, does this mean that different parts of the central nervous system are affected? Is it all one disorder?  Would being able to identify subgroups help with treatments?

These are the same sort of arguments that plague low back pain management – and given the somewhat more straightforward conceptual models of back pain, I would hope things like sub-groups and specific treatments might be slightly clearer – but this is not the case!  So I guess that fibromyalgia may also present a more vexing problem, and the research questions will continue to flow.

I can’t summarise the state of play regarding treatment for fibromyalgia any better than the authors of this meta-analysis:

Clinicians treating fibromyalgia patients with psychological methods should keep in mind that they can successfully work with their patients on several goals, such as reducing pain, sleep problems and catastrophizing and elevating mood and daily functioning. However, both clinicians and patients should also be aware that the effects will likely be rather small and require a high number of sessions to occur. Fibromyalgia is a heterogeneous disease and there is evidence that some drugs  or exercise is moderately effective for treating the disorder. Multicomponent therapies have been shown to be effective, although only in the short-term. Thus, based on the results of this study, we suggest treating fibromyalgia patients with a combination of methods that include psychological interventions as a major component.

What does this mean for clinicians who are not psychologists? Well, I can’t find evidence to suggest that clinicians of other persuasions can’t be effective at delivering a cognitive behavioural approach to pain management.

The basics of this type of therapy are common to occupational therapists, physiotherapists, nurses, social workers and others – what might be needed now is a concerted effort by ‘non-psychologists’ to establish ways of integrating psychological strategies within the treatment paradigms of these professions.

For me, I continue to focus on goals that the person wants – usually things like sleep management, ability to return to work, being able to manage the household activities, return to leisure activities – the sort of things I discussed in yesterday’s post about what patients want.   Good pain management is really about using the most effective tools to help people achieve these goals, and to me, the goals represent what my core profession values the most – occupation.

Nicassio, P. (2010). Psychological approaches are effective for fibromyalgia: Remaining issues and challenges Pain, 151 (2), 245-246 DOI: 10.1016/j.pain.2010.08.011
Glombiewski, J., Sawyer, A., Gutermann, J., Koenig, K., Rief, W., & Hofmann, S. (2010). Psychological treatments for fibromyalgia: A meta-analysis Pain, 151 (2), 280-295 DOI: 10.1016/j.pain.2010.06.011

Pain and rheumatology: an overview of the problem
One of the most common reasons to visit a doctor is musculoskeletal pain. And one of the first symptoms of a rheumatological disorder is pain – so it’s great to find this succinct overview of pain in rheumatological disorders. I think one of the saddest findings I’ve read recently (I blogged about it a while ago) is that people who see a rheumatologist may have their disease process managed – but their pain problem may remain untouched. There is a misconception that pain is simply ‘a response to inflammation’ or ‘joint derangement’ – but it’s never really that simple!

This paper by Montecucco, Cavagna, & Caporali identifies five groups of pain disorder in rhematological diseases: acute pain, like gout, related to local tissue damage with nociceptive activation; chronic pain, which may be triggered by tissue damage or disease, but is often perpetuated by other factors such as central nervous system involvement – the three remaining groups of pain disorder are all subsumed under this chronic pain heading; inflammatory pain, such as rheumatoid and some osteoarthritis, involves increases in pain especially over night, with reduction after activity, and often with morning stiffness; mechanical pain, which is often a feature of osteoarthritis where the joint mechanics are altered – this pain is often worse during the day and relieved somewhat with rest, and although there may be some stiffness in the morning it usually lasts about 10 minutes or so; and the final type of pain is neuropathic pain, not often thought to be a feature of rheumatological problems, but involves disease or trauma to the somatosensory system – it could be peripheral, or it could be in the CNS and it may also be in response to heightened sensitisation secondary to the initial disease.

The authors briefly discuss fibromylagia – I posted about this recently also, discussing a paper that suggests perhaps FM doesn’t belong with rheumatologists at all, because it’s becoming apparent that it is a disorder of the central nervous system involved increased sensitivity to nociceptive input, probably associated with reduced functioning of the descending inhibitory pathways. Their suggestion is that it is ‘not clearly classifiable as inflammatory or mechanical’, but they’re not prepared to include it in the neuropathic group because the pain experience is slightly different.
Neuropathic pain is thought to be more commonly perceived as burning, tingling, hyperalgesia especially to hot or cold, and often involving allodynia.

The paper goes on to review the epidemiology of rheumatic pain. I don’t think there would be many who would argue that chronic pain associated with these problems is common and this paper indicates there is research to suggest it is an increasing burden even in developing countries such as Vietnam, Peru and China. Despite this increasing prevalence, the underlying disorders vary from country to country.

The burden of pain is also discussed – rheumatic diseases are probably the most prevalent cause of functional limitation that does not reduce life expectancy. While pain doesn’t kill, people live a long time with poor function, lowered quality of life, and use a wide range of support services including health care in this time.

I was struck by the estimates of the economic cost of pain in these disorders – 1 – 2.5% of GNP in USA, UK, France and Australia. OA is thought to cost the USA more than $60 billion per year.

The final quite brief section in this paper draws attention to the different ways in which people express their pain – I couldn’t agree more. Psychosocial factors are integral to the pain experience, so it makes sense to include psychosocial management along with disease management. Would that this happened where I work – sadly, though, the rheumatology clinics don’t routinely have pain management using any approach let alone a cognitive behavioural one! And this despite many studies showing the effectiveness multi and interdisciplinary pain management using a cognitive behavioural approach on the lives of people with these painful conditions.

This paper is a very brief summary of pain in rhematological disorders, but as an overview it does what it oughta. I like the many references, and they’re all quite recent, so if you’re wanting to get your head around pain in these problems, it is a worthwhile paper to get hold of.

Montecucco, C., Cavagna, L., & Caporali, R. (2009). Pain and rheumatology: An overview of the problem European Journal of Pain Supplements DOI: 10.1016/j.eujps.2009.07.006

Fibromyalgia: an overview

I didn’t intend to get into a theme this week, but this paper arrived in my inbox this morning, and given both the prevalence of fibromyalgia, and the often ‘fuzzy’ management that can be provided, I thought it might be worthwhile taking a look at it.  The paper itself is a pre-print, but has been revised earlier this year and is probably the final version.

The outline of the paper covers diagnostic criteria, and briefly discusses the place of neuroimaging (if only we could get that done readily here!), but notes that many other conditions overlap or mimic FM such as hypothyroidism, tendonitis, ankylosing spondylitis, as well as chronic fatigue, suggesting some sort of common pathway in either the peripheral or central nervous system, raising the possibility of some common treatment approach.  So far though, it’s not clear – and it’s important to rule out these other conditions that all have their own management approach before deciding that FM is what the problem is.

The next section of the paper reviews the current state of knowledge around pathophysiology as a basis for treatment and rehabilitation.  Both peripheral and central sensitisation seem implicated in FM, leading to amplification of sensory impulses that alter pain perception.  Increased excitation of various peripheral structures can in turn lead to neuroplastic changes in the central nervous system – winding up the whole experience for the person in the middle of it!

Imamura, Cassius & Freni, the authors of this paper, briefly review some of the factors thought to play a role in the reduced threshold for neuronal firing, including elevated levels of substance P, calcitonin gene-related peptide, bradykinin, and so on.  Included in their review are CNS factors such as the altered non-REM sleep of people with FM – and that this is associated with the severity of symptoms; the association between depression and FM; and neuroimaging studies showing a change in regional cerebral blood flow to pain-related structures in people with FM.

If these aspects of FM can be explained to people with the pain problem it could make a significant difference to their own attitude toward their pain.  For many people, it can take several years before a diagnosis of FM is made: during this time the beliefs and approaches of many practitioners can influence their understanding of their pain – and sadly, some practitioners are not empathic and can take a somewhat pejorative approach to people with the disorder.  Knowledge can lead to understanding – and understanding can lead to a sense of empowerment.

Moving through the paper, the authors indicate that treatment needs to be based on the proposed model of fibromyalgia.  That is, it needs to address central mechanisms rather than peripheral ones (so, no more NSAIDs, opioids or corticosteroids!), and the overall approach needs to be ‘rehabilitative’ – I’d suggest biopsychosocial as the model!  The shift is from curing the problem to improving health status and health -related quality of life.

There are two arms of management for fibromyalgia:

(1)  pain relief through medication and ‘physical’ strategies to reduce peripheral and central sensitisation

(2)  cognitive behavioural approaches to manage sleep, fatigue, mood, cognitive problems, headache, migraine and other problems associated with FM.

Although the authors suggest ‘education’ as a cornerstone – I’d rather suggest helping the person to reconceptualise their problem as one of pain processing.  Education can be seen as simply providing information – reconceptualising is about helping the person see themselves and their pain problem as something they can manage, something only they can do – and something they can do.

The remainder of the paper looks at pharmacological approaches and the rationale for using tricyclic antidepressants and/or serotonin/norepinephrine-reuptake inhibitors, and tramadol because of their effect on reducing afferent transmission at the dorsal horn or increasing the activity of the descending inhibitory pain systems.

It should be noted that even these drugs don’t always reduce the pain and all have their own array of side-effects – so they need to combined with self management.

Nonpharmacological approaches are then reviewed.  This is where the interdisciplinary team can take the lead because these approaches are both effective – and once learned, don’t consume health resources in quite the same way as medications can.

Exercise gets the nod – remembering that exercise can include enjoyable daily activities such as walking, gardening, dancing and playing with the dog, not just going to a gym!

Electrical stimulation – this is suggested, although as far as I know, it’s not readily available – Imamura et al. indicate transcranial direct current stimulation as an effective approach, but I haven’t heard much of this as a strategy available in New Zealand.  (If anyone has, let me know).  I’m also not entirely comfortable with this as a self management strategy – it sounds pretty invasive and requires health care input, at least initially.

Acupuncture – this is less well-documented, and results are, as these authors say, ‘controversial’.  They suggest that ‘clinical benefits seem to be of small magnitude and of short duration’ – my main concern would be that unless the person can ‘do it themselves’, it will involve more appointments, so I’d not be comfortable with it as a self management approach.  I hold a similar view of injections – Imamura et al suggest that ‘concomitant myofascial pain, along with instruction in relaxation techniques, may benefit some patients with an associated mysfascial pain component.’ 

The final area reviews, very, very briefly, cognitive behavioural therapy.  The authors indicate its use for ‘associated psychological and psychiatric comorbidity’, but I’d be inclined to challenge this.  The perception of pain involves thoughts and beliefs about the meaning of pain – and the effect of reconceptualising fibromyalgia as not being a ‘life sentence’ or a ‘constant struggle’, and understanding what some of the mechanism are, will bring about changed perception.  Distress reduction, increased sense of self efficacy and more effective approaches to activity, relaxation, cognitions, as well as effective communication skills and working on relationships – these are all integral to living a good life despite pain.

Overall – this is a nice, brief review especially of some of the pathophysiology of fibromyalgia and the rationale for the treatment approaches suggested.  There are plenty of good references, and while it’s not an ‘easy’ read, it’s quite brief and contains the essentials.


From Imamura, M., Cassius, D., & Fregni, F. (2009). Fibromyalgia: From treatment to rehabilitation European Journal of Pain Supplements DOI: 10.1016/j.eujps.2009.08.011