…and now what we’ve all been waiting for: What do to about central sensitisation in the clinic

For the last couple of weeks I’ve posted about central sensitisation; what it is, and how to assess for it. Today I’m going to turn to the “so what” question, and talk about what this might mean when we’re in the clinic.  Remember that most of this material comes from Jo Nijs’ recent talks at the New Zealand Pain Society.
Firstly, remember that pain is an experience that people have, underpinned by neurobiology, but also, depending on the level of analysis, on interactions with others, on systems and how they work, on culture, on individual experiences, and of course, on interacting within a body within an environment or context. Everything I say from here on is based on these assumptions.

The first point Jo Nijs makes is that when we know a bit more about the neurobiology of persistent pain associated with central sensitisation, we can use this knowledge wisely when we help someone make sense of their pain. This doesn’t mean wholesale and broadcast “I-will-tell-you-all-I-know-about-pain-neurobiology-because-I-know-you-need-to-know-it-because-I-know-it-and-think-it’s-important” which is, truth to tell, a lot more about the know-it-all than the person in front of them! We need to earn the right to give information – that means establishing that we’ve heard the other person’s story and the current meanings they’ve made from their experience. It also means asking permission to share new information. It means thinking about WHY we want to share new information.

So what if the person doesn’t use the same groovy language we use to describe his or her understanding?! So what if they’ve got some of the newer ideas slightly skewed. In the end, what’s important is that the person understands these things:

  • Pain isn’t a direct reflection of what’s happening in the tissues.
  • Pain can be influenced by many things, some of which are physical forces (heat, pressure and so forth), some of which are ideas, and some are emotions. And there are a bunch of other variables that can influence the experience, including what else is going on around the person.
  • The brain is intimately involved with our experience of pain, and it’s a two-way street from body to brain and brain to body.
  • Persistent pain is more about neurobiology than tissue damage per se (but not exclusively about neurobiology).

Our job is to make sure the person understands these things, rather than our job being about “educating” people. The end result matters, rather than any particular process.

If we look at the evidence for helping people reconceptualise their pain, there’s plenty to show that this approach is useful – it’s been a key tenet of a self-management cognitive behavioural approach to pain management since at least the late 1970’s. The later research (from Butler, Moseley and Louw et al) is simply looking at this approach within a slightly different cohort and in a different context. Rather than being integrated with an interdisciplinary pain management programme, research from these guys shows that physiotherapists (in particular) can deliver this kind of information very effectively – and that it helps reduce the fear and subsequent efforts to avoid pain (such as not moving, seeking healthcare, and being worried about pain). Yay!

It’s true that there are many different ways to influence the descending modulatory system, and release endorphins. One of them is to help people understand their pain and be more confident about moving. Another is to place hands on the person – hence massage therapy, manual therapies, manipulations and so on. Nijs believes hands on therapy has best effect after you’ve gone through some of the reconceptualisation that’s often needed (Bishop, Torres-Cueco, Gay, Lluch-Girbes, Beneciuk, & Bialosky, 2015).

Similar arguments can be made for considering sleep management and stress management as an integral part of pain management. (To be perfectly honest, I always thought this was part of what we did…). So here’s the argument: we know most people with persistent pain experience rotten sleep. We also know that people are stressed by their experience of pain. Because poor sleep is associated with increased activation of glia in the prefrontal cortex, amygdala and hippocampus, and therefore are pro-inflammatory, pain is often increased after a poor night’s sleep. Sleep medications interfere with the sleep architecture, so it’s useful to consider nonpharmacological approaches to sleep management.

Three strategies to consider:

  • CBT for insomnia – here’s one resource to use
  • ACT or acceptance and commitment therapy – I’ve written a great deal about ACT, just use the search function on this blog for more
  • Exercise – OMG yes, exercise is effective! (just not right before bedtime, kthx)

Stress management is tougher. We can’t avoid experiencing stress – and neither can we live in a bubble where we don’t ever get exposed to stress. Instead, we probably all could do with learning multiple ways of managing stress. Things like realistic evaluations of the situation, increasing our capabilities for regulating our response to stress via biofeedback if need be, and using mindfulness as a strategy for being with stress instead of fighting against it, or folding beneath it.

I haven’t cited many references in this post – not because there aren’t many, but because there are SO many! And I’ll post more next week when I start looking at the rather sexy neurobiological examinations of processes used in pain management for years (yes, we’ve been doing it for a long time, we now have great explanations for how these things might work – though effect sizes are still small.)


Bishop, M. D., Torres-Cueco, R., Gay, C. W., Lluch-Girbés, E., Beneciuk, J. M., & Bialosky, J. E. (2015). What effect can manual therapy have on a patient’s pain experience?. Pain, 5(6), 455-464.


Does central sensitisation matter?

In my last post I discussed some of the mechanisms thought to be involved in central sensitisation, and while many of the details remain pretty unknown, I think the general conclusion is that yes, it really is a thing. What do I mean by central sensitisation? Well, it’s curious, it can refer to the processes at spinal and brain levels that seem to reduce the usual descending inhibitory mechanisms, expand the areas in which neural activity takes place, and allows increased information flow to eventually reach conscious awareness. At the same time it can refer to the experience in which a person feels greater pain than anticipated, given the degree of input; pain that is distributed more widely than anticipated, given the degree of input; and/or pain that lasts longer than we’d expect, given the degree of input (Woolf, 2011). BTW most of this post is derived from talks given by Pro Jo Nijs at the recent New Zealand Pain Society Conference.

The question now is whether this really matters. After all, nociceptor inputs can trigger a prolonged but reversible increase in central nociceptive pathways – if they’re reversible, just eliminate the original nociceptive input, and voila! The sensitisation is gone. What we know, however, is that in many cases the tendency towards having long-term increased sensitivity remains, or was perhaps always present.

Well, unfortunately if someone does tend to have greater activity in the central nervous system, then it has the potential to add enormously to poor outcomes if he or she decides to have surgery. For example, individuals with this tendency experience poorer outcomes after total knee replacement; and after shoulder surgery; but not after hip-joint replacement surgery. Testing in these cases was conducted using conditioned pain modulation which involves people undergoing painful testing – when they’re already in pain! Brave souls. You can see why it’s not a popular testing procedure in mainstream surgical situations.

Adding to the view that central sensitisation matters clinically, Ferrandiz and colleagues (2016) found that central sensitisation mediates the treatment effects in people with low back pain; Jull and colleagues (2007) found the same for neck pain after whiplash; Coombes and colleagues (2015) found the same for people with chronic tennis elbow.  It seems that central sensitisation is associated with greater pain catastrophising, slower movements, higher pain reporting, poorer functioning, increased perception of pain, and fear of moving.

The question now is how best to assess for the presence of this phenomenon. Given that most people won’t want to undergo conditioned pain modulation (not to mention the need for testing equipment and skilled technicians to administer the test!), what’s needed is a reasonably simple way to identify those who have the characteristics of central sensitisation so we can plan for, and manage it, more effectively.

Nijs and the Pain in Motion Research Group published the first set of criteria in 2014, from an epidemiological perspective. This classification approach involves first excluding neuropathic pain – and the group propose using IASP diagnostic criteria for neuropathic pain (see Haanpaa & Treede, 2010). If the problem is neuropathic pain (where there is a clear lesion of the nerve), then it’s managed accordingly (although we really don’t have great treatments for this kind of pain, either!).

Then they propose an algorithm which helps to clarify whether the problem is central sensitisation or “something else”.

The first question is whether the person identifies they have “disproportionate pain experience” – now this I have a problem with, because what is a “proportionate” pain experience? Given how fluid our experience of pain can be, and how poorly the experience correlates with what’s going on in the tissues, I find this a bit tough to use as a clear-cut indicator. Nevertheless, it’s the first question asked in this algorithm…

The next question relates to the person experiencing diffuse pain distribution (or, perhaps, wider spread than expected). If this is the case, eg someone has a grazed knee, but pain is experienced all over the entire leg, then it’s identified as central sensitisation. If the result is more like pain just above the knee to just below, then it’s somewhat equivocal, so the authors suggest the person completes the Central Sensitisation Inventory. This is a questionnaire I’ve discussed in the past. I’m no nearer to establishing whether it really is a useful measure than when I wrote that blog, but the measure continues to be used, and research is ongoing. Certainly, Jo Nijs and group seem to think the measure holds promise and might help to classify those at greater risk of developing problems with pain if they proceed to surgery.

So, to summarise, while the mechanisms involved in central sensitisation are still being discovered, and it’s challenging to know where normal processes end and abnormal ones begin, it definitely seems to be a clinical phenomenon affecting not only those without peripheral nociception (eg migraine), but also those with clearcut peripheral problems like osteoarthritis. Central sensitisation processes seem to underpin some of the most problematic pain problems we know of, and can get in the way of recovery even when peripheral nociceptive input has been removed – 18% of total knee-joint replacements are revised because of ongoing pain, and this pain doesn’t seem to improve after subsequent surgery (NZ National Joint Registry). There’s confusion about language – does the term refer to the mechanisms thought to be involved, or does it refer to the experience described by people? And assessing it is challenging – either go through complex and painful testing, or complete a questionnaire that may confound distress about health (and subsequent hypervigilance about body symptoms) with pain and other responses that might represent the presence of central sensitisation processes being invoked.

More challenging still is what do we do once central sensitisation is identified? Are our treatments any good? That, folks, will be explored in the next enthralling episode on Healthskills!


Baert, I., Lluch, E., Mulder, T., Nijs, J., Noten, S., & Meeus, M. (2016). Does pre-surgical central modulation of pain influence outcome after total knee replacement? A systematic review. Osteoarthritis and Cartilage, 24(2), 213-223.

Haanpää M, Treede RD. Diagnosis and classification of neuropathic pain. Pain Clinical Updates 2010; XVII.

Nijs, J., Torres-Cueco, R., van Wilgen, P., Lluch Girbés, E., Struyf, F., Roussel, N., . . . Vanderweeën, L. (2014). Applying modern pain neuroscience in clinical practice: Criteria for the classification of central sensitization pain. Pain Physician, 17(5), 447-457.

Valencia, C., Fillingim, R. B., Bishop, M., Wu, S. S., Wright, T. W., Moser, M., . . . George, S. Z. (2014). Investigation of central pain processing in post-operative shoulder pain and disability. The Clinical Journal of Pain, 30(9), 775.

Woolf, C. J. (2011). Central sensitization: Implications for the diagnosis and treatment of pain. Pain, 152(3 Suppl), S2-15.

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.

Is central sensitisation really a thing?

It seems odd to me that there’s much argument about central sensitisation in pain circles. I thought the idea of central sensitisation was well-established based on research from some years ago – but apparently there are still arguments about its relevance, and lots of debate about how to identify it clinically. This post is based mainly on a presentation by Jo Nijs from Pain in Motion, at the recent NZ Pain Society meeting in Nelson. In this post I want to briefly review the material presented by Jo suggesting that central sensitisation is a thing. I’ll write more about assessment in a future blog, or this post will be the longest ever!

Firstly, what is it and why should it matter? Researchers have long been aware that when a nerve is repeatedly stimulated, in future stimulation it will respond for longer and with more intensity – this is called long-term potentiation. Recently, the contribution of glial cells to this situation has been identified (remember glia? Those little cells whose purpose no-one really knew? Turns out they release gliotransmitters that circulate throughout the spinal cord and allow information to be transmitted widely, far from the original source of stimulation – see Kronschlager, Drdla-Schutting, Gassner, Honsek et al, (2016). Glial cells occur widely throughout the central nervous system, and while LTP is a process we’ve known about in the CNS for some time – we’ve known because this is how “memories” are formed (remember “nerves that fire together wire together”? Pathways that frequently activate develop the tendency to continue to activate together) – we’ve perhaps not been aware that this occurs in the spinal cord as well. So, LTP occurs in both the spinal cord and the brain, and there is more than one way this process is facilitated. Glial cells are one. Central sensitisation involves this process of long-term potentiation across and amongst pathways within our nervous system – it means information from peripheral regions like your big toe are more likely to be transmitted to areas in the brain responsible for attending and responding to threatening information.

Why does this matter? Well, if we think of ourselves as a finely tuned homeostatic machine, one that wants to remain in a stable state, we can think of two systems balanced with one another. One system works to facilitate information transmission (nociceptive facilitation), while the other works to reduce or modulate this transmission (endogenous hypoalgesia). If we continue with the machine analogy, we want to know about “trouble” as soon as possible – so our nociceptive facilitatory system is like an accelerator, working promptly to make sure we know about the state of play very quickly. If you’ve ever driven a race car, you’ll know how twitchy the accelerators are! The brakes on this system is our endogenous opioid system which reduces the influence of the nociceptive system so we can keep moving forward. If the brakes fail, for whatever reason, in a race car we’ll burst forward! Similarly, if the endogenous modulatory system fails, for whatever reason, far more information ascends to relevant regions in the brain for interpretation – and ouch.

What sorts of things enhance connectivity between areas of the brain that deal with nociceptive information? Well, this is where things get all woolly and psychosocial for a while (sorry guys!). From many fMRI studies, it’s possible to establish that “pain catastrophising” or the tendency to brood on pain, feel helpless about it, and regard the pain as seriously intense activates brain areas like the dorsolateral prefrontal cortex, the anterior cingulate cortex, and the insula, which in term reduces the efficiency of the opioid analgesic system (that endogenous opioid system), makes it harder to distract attention from the pain, and increases facilitation (ie the transmission of nociceptive information from lower CNS to higher). In other words, this very psychological construct has a biological component to it.

Central sensitisation has been identified in many different pain problems, ranging from osteoarthritis in the knee (Akinci, Al Shaker, Chang, et al, 2016), post-cancer pain (Lam, 2016), shoulder pain (Sanchis, lluch, Nijs, Struyf & Kangasperko, 2015), and yes, those messy complicated ones like whiplash (Coppieters, Ickmans, Cagnie, Nijs, et al, 2015), low back pain (Sanzarello, Merlini, Rosa, Perrone et al, 2016) and fibromyalgia (Walitt, Ceko, Gracely & Gracely, 2016). Rates of central sensitisation vary from 10% in shoulder pain to 100% in fibromyalgia. For some good reading on central sensitisation in these disorders, take a look at the references I’ve cited.

So yes, central sensitisation is a thing, and it results in increased pain experiences that last longer and spread. Why do some people experience while others don’t? Now we’re venturing into rather more speculative areas, but some findings seem clinically useful. People who have, in their early years, experienced physical and/or psychological trauma, those who tend to catastrophise or have unhelpful beliefs (often inaccurate beliefs) about their pain,  those who have poor sleep, and those who have an elevated stress response seem more likely to have pain that fits with what we’d expect with central sensitisation (See Nijs & Ickmans, 2014).

Why does this occur? Well, stress increases release of glutamate and this in turn increases CNS excitability (makes sense – let’s react faster to everything, at least for a short time). At the same time, stress reduces GABA and serotonin, and as a result inhibition is reduced (the brakes come off). If we add microglial activity to the mix (remember that’s going to increase the connectivity between neurones), and if we add ongoing release of adrenaline in because the stress has been continuing for a while, we’re going to end up with activated glial activity in the prefrontal cortex, amygdala and hippocampus, all important areas for detecting salience and making decisions to act. These glial cells release chemicals known to increase neuroinflammation, reducing hippocampal activity (ultimately reducing volume of neurones in this area), increasing the size of the amygdala (which means it’s more capable of responding to threat), and reducing the prefrontal cortex size, reducing the capacity to make considered decisions (Kregel, Meeus, Malfliet et al, 2015). Ew… nasty! In longterm stressful situations, it seems our brains adapt – and not in a helpful way when it comes to experiencing pain. Whatever you do DON’T say to your patients  “Oh and by the way, your back pain means your brain is inflamed and parts of your brain are shrinking” – this is NOT helpful!

Next post I’ll discuss assessing for central sensitisation – but before I do, remember that central sensitisation is not the only factor at play in ongoing pain. In fact, some people don’t seem to develop central sensitisation even with ongoing nociception from either disease processes, or inflammation. We don’t really know why. What we do know is that simply treating peripheral nociceptive input when central sensitisation is present may fail to help the person – so keeping an eye out for it is important.


Akinci, A., Al Shaker, M., Chang, M. H., Cheung, C. W., Danilov, A., Jose Duenas, H., . . . Wang, Y. (2016). Predictive factors and clinical biomarkers for treatment in patients with chronic pain caused by osteoarthritis with a central sensitisation component. International Journal of Clinical Practice, 70(1), 31-44.

Coppieters, I., Ickmans, K., Cagnie, B., Nijs, J., De Pauw, R., Noten, S., & Meeus, M. (2015). Cognitive performance is related to central sensitization and health-related quality of life in patients with chronic whiplash-associated disorders and fibromyalgia. Pain Physician, 18(3), E389-401.

Kregel, J., Meeus, M., Malfliet, A., Dolphens, M., Danneels, L., Nijs, J., & Cagnie, B. (2015). Structural and functional brain abnormalities in chronic low back pain: A systematic review☆. Paper presented at the Seminars in arthritis and rheumatism.

Kronschläger, M. T., Drdla-Schutting, R., Gassner, M., Honsek, S. D., Teuchmann, H. L., & Sandkühler, J. (2016). Gliogenic ltp spreads widely in nociceptive pathways. Science, 354(6316), 1144-1148. doi:10.1126/science.aah5715

Lam, D. K. (2016). Emerging factors in the progression of cancer-related pain. Pain Management, 6(5), 487-496.

Nijs, J., & Ickmans, K. (2014). Chronic whiplash-associated disorders: To exercise or not? The Lancet, 384(9938), 109-111.

Sanchis, M. N., Lluch, E., Nijs, J., Struyf, F., & Kangasperko, M. (2015). The role of central sensitization in shoulder pain: A systematic literature review. Seminars in Arthritis & Rheumatism, 44(6), 710-716.

Sanzarello, I., Merlini, L., Rosa, M. A., Perrone, M., Frugiuele, J., Borghi, R., & Faldini, C. (2016). Central sensitization in chronic low back pain: A narrative review. Journal of Back & Musculoskeletal Rehabilitation, 29(4), 625-633.
Walitt, B., Ceko, M., Gracely, J. L., & Gracely, R. H. (2016). Neuroimaging of central sensitivity syndromes: Key insights from the scientific literature. Current Rheumatology Reviews, 12(1), 55-87.

A surfeit of learning

It’s been a busy few weeks as I’ve been at the San Diego Pain Summit and then the New Zealand Pain Society meeting where wonderful speakers presented on topics like exercise for pain, cognitive functional therapy, central sensitisation, opioid use in New Zealand, sensory profiles and other such topics. The chance to meet and spend time with clinicians who are passionate to not only learn about pain, but apply what they’ve learned in clinical practice is something I can’t miss.

What’s difficult, though, is deciding what to apply on Monday morning after having been to meetings or events where there’s so much new material to absorb. And that’s one of the problems, I think, in our clinical practice today. The years when it was relatively easy to do the same old, same old, have (thankfully!) gone – but in its place is the challenge of sifting through that new information and deciding what and how to do it.

So today I thought I’d go through some of the practices I’ve used – maybe it will help someone else?

Firstly, I try to take just one thing away from a meeting. If I absorb more than this, it’s fine, but one new thing is usually quite enough for me! Someone made the point that changing habits is hard – and, just for a moment, think about what we expect the people we treat to do, and then think about that last conference and what you intended to do, but just didn’t… Without  intention, planning and support to change what you do, you’ll carry on doing what’s easy, what’s worked before, and what feels “comfortable”. So be kind to yourself and pick just one thing. For me, that one thing is to feel OK about teaching people to ask “and what does that mean to you?” when someone is telling me their story about their pain.

Next, I let the rest of the information I heard just sit and percolate a while. This means I might casually read something related, or I might review the speaker’s slides or recordings, but I don’t do this in a way that I’m madly trying to cram in action points. This is because I’ve chosen one thing to do, and that’s enough. The rest of the information won’t just disappear because I’m letting it rest, it’s just going to connect with other concepts and pop out later when I stumble on it while reading something else.

To apply what I’ve learned, I plan. Yep, you heard it, I plan! Just like our clients, we need to make specific action plans if we’re going to do things differently. I think there are two factors to apply: the first is how important I think the concept/action is to me, the second is how confident I am to make a change.

  1. Importance: While simply selecting the single thing I take away from a meeting implies that I think it’s important, it’s worth considering why I decided it’s so important. So I list a few reasons I valued that concept. For me, it was the idea that we can uncover more of the real concerns of a person if we ask what it means to them, we can be more able to hear what the person really wants. I also took the idea that anyone: PT, OT, MT, Osteo, Chiro, Doc, Nurse ANYONE can ask this question. This is important to me because if that question isn’t asked, the person may go on fearing the worst even if they appear to be “doing well”. And we cannot rely on “someone else” asking this question. Even if we’re not psychologists, and so think that beliefs and attitudes are out of scope, we ARE experts in how the human body works. We know structure and function. This means we have a responsibility to help people understand what’s going on their body rather than living in ignorance or confusion.
  2. Confidence: It’s not enough to think that something is important. We need to make it easy to make a change. This means identifying what might get in the way of change and planning around that. It also means identifying what might make it easy to change and structuring life so it’s not hard. It could mean writing some “cheat sheets” giving brief phrases to use (Alison Sim and I used this approach in our recent workshop), or it might mean a poster in a prominent place to act as a reminder. It might mean removing something from the environment so you don’t use it as easily. It could mean simplifying for a couple of times. For me it will mean working through possible arguments people make against asking those questions about meaning, using open-ended questions. Often the questions relate to time available in clinic, scope of practice questions, “opening Pandora’s box” questions, “what do I say next” questions, or the “it’s not my focus” questions. I’ll work on responses to these in advance so I can explore what these mean to the clinician before asking if it’s OK to explain my perspective.

I ask myself “what would it look like if I applied this new strategy?”, or “how would I know I was using this strategy?”. I also take time to review how I’ve gone using that new strategy – recording myself, asking someone to sit in on a session, even just reviewing against the “cheat sheet” to see what I used, and what I could have used.

If you take a moment to review my process, hopefully you’ll see the elements of a motivational approach to behaviour change. I’ve written quite a bit about motivation – hope this helps you too!


What is pain for?

We’re told we need pain – without the experience, we risk harming our bodies and living short lives. With pain, and for most people, we learn to not go there, don’t do that, don’t do that AGAIN, and look at that person – don’t do what they’re doing! Thirst, hunger, fear, delicious tastes and smells, the feelings of belonging, of safety and security, of calm and comfort: all of these are experiences we learn about as we develop greater control over our bodies.

Pain is an experience we learn to associate with actual or possible threat to “self”. Let’s take a moment to think about what “self-hood” means.

If I ask you “who are you?” you’ll tell me your name, probably your occupation, maybe where you live and who you live with. Baumeister (1997) suggests our sense of self is about “the direct feeling each person has of privileged access to his or her own thoughts and feelings and sensations.” He goes on to say “it begins with the awareness of one’s own body and is augmented by the sense of being able to make choices and initiate action.” We learn about who we are through interacting with the environment, but also as we interact with other people and begin to sort through our roles, contributions and relationships.

Of course, our sense of self changes over time and is reciprocally influenced by choices we make as well as opportunities (and threats) around us, both environmental and social.

We work really hard to avoid threats to our sense of self. For example, I’ll bet we’ve all seen that person who steadfastly refuses to stop colouring his hair, wearing the same clothing styles as he did in his 20’s, holding on to the same habits as he did at the same age even when he’s now in his 50’s, has a paunch, and still looks for partners 20 years younger than he is…  He still believes he’s that young stud despite the evidence in the mirror. And of course the same applies to women perhaps more so!

So what happens when our mind/body is threatened? How do we know it? And what do we do about it?

In this instance I’m not talking about social threats, though there’s interesting research suggesting that being socially excluded has similar neurobiological effects as being physically threatened (or experiencing pain – though this may reflect the distress we experience when we’re hurt and when we’re socially excluded – see Iannetti, Salomons, Moayedi, Mouraux & Davis, 2013; Eisenberger, 2015). I’m instead talking about threats to our physical body. Those threats may be violence from another person, physical trauma to the body, or the threat of physical harm to the body. When we experience these kinds of threats, and once an aspect of mind/body has disentangled the threat evaluation from whatever other goals we’re currently engaged in, we experience pain. Tabor, Keogh and Eccelston (Pain, in press) define pain in terms of action: an experience which, as part of a protective strategy, attempts to defend one’s self in the presence of inferred threat.

So pain is there to help us maintain an intact sense of self in the presence of threat – threat that we’ve inferred from our context (or drawn a conclusion from incomplete data). It’s part of a system that works to maintain “us” in the face of multiple threats that we encounter.

Tabor, Keogh and Eccleston also argue that pain is an experience designed to intrude on awareness to show that “boundaries have been reached and action must be taken”. Pain is one way our mind/body can give us an indication of boundary – just how much, or how little, we can do. For example, I experience pain when I bend my thumb down to reach my wrist – it’s one way I can learn how far I can bend without disrupting something! The purpose of that pain is to help “me” defend against doing really dumb things, like stretching my thumb out of joint!

Interestingly, when we feel overwhelmed by our pain, when we can’t defend against it (because it feels too intense, has meanings that threaten our deepest sense of self) we tend to withdraw from responding to everything else – our conversations stop, we don’t notice other people or events, we pull into ourselves and ultimately, we can lose consciousness (think of the accounts of early surgery without anaesthesia – the surgeons were kinda grateful when the patient lapsed into unconsciousness because at last they weren’t writhing to get away – see Joanna Bourke’s book “The Story of Pain” for some harrowing stories!).

When we lose consciousness, our sense of self disappears. We lose contact with the “what it is to be me”.

Our sense of self also disappears when we experience pain we can’t escape and we can’t make sense of. Throughout the time while people are trying to label their pain, establish the meaning of their symptoms, and while people are searching for a solution to their pain, people’s experience of both time and “who I am” is threatened (Hellstrom, 2001).

To me, this is one of the primary problems associated with pain – and one we’ve almost completely ignored in our healthcare treatments. All our treatments are aimed at helping “get rid of the pain” – but what isn’t so often incorporated in these efforts is a way of engaging and rebuilding a resilient sense of self. So while the pain may ebb away, the “self” remains feeling vulnerable and threatened, especially if there’s any hint of pain returning.

What can we do better? Perhaps talk about what vision a person has of themselves as a “self”. Help them work towards becoming the “self” they believe they are – or at least helping them express the underlying values that their “self” has previously been expressing. That way perhaps people can find flexible ways to express that “self” – which will make them more capable of living well under any circumstances.


Baumeister, R. F. (1997). Identity, self-concept, and self-esteem: The self lost and found. Hogan, Robert [Ed], 681-710.

Bourke, J. (2014). The story of pain: From prayer to painkillers: Oxford University Press.

Eisenberger, N. I. (2015). Social pain and the brain: Controversies, questions, and where to go from here. Annual review of psychology, 66, 601-629.

Hellstrom, C. (2001). Temporal dimensions of the self-concept: Entrapped and possible selves in chronic pain. Psychology & Health, 16(1), 111-124. doi:

Iannetti, G. D., Salomons, T. V., Moayedi, M., Mouraux, A., & Davis, K. D. (2013). Beyond metaphor: Contrasting mechanisms of social and physical pain. Trends in Cognitive Sciences, 17(8), 371-378.

Tabor, A., Keogh, E. and Eccleston, C. (2016) Embodied pain— negotiating the boundaries of possible action. Pain. ISSN 0304- 3959 (In Press)

“I know my pain doesn’t mean I’m damaging myself – but I still have pain”

In the excitement of helping people understand more about pain neuroscience, which I truly do support, I think it’s useful to reflect a little on the history of this approach, and how it can influence the experience people have of their pain.

If we go right back to the origins of pain self management, in the groovy 1960’s and 1970’s – the first truly significant work in chronic pain self management came from Wilbert Fordyce (Fordyce, Fowler & Delateur, 1968). Bill Fordyce was a clinical psychologist working in the Department of Physical Medicine and Rehabilitation, University of Washington, Seattle, Washington. He noticed that when people were given positive reinforcement (attention, and social interaction) for “well” behaviour, and ignored or given neutral responses to reports of pain, their “up-time” or activity levels increased. Interestingly for occupational therapists, in the paper I’ve cited, occupation was used as an integral part of the programme and occupational therapy was a part of the programme (somewhat different from most clinics nowadays!)  Thus the operant conditioning model of pain behaviour and disability was first developed.

As practice progressed, clinicians began discussing the gate control theory of pain to help people understand how incredibly powerful descending pain modulation could be. Included in those discussions was the distinction between “hurt” and “harm” – that simply because something hurt, did not mean it was a sign of harm in the tissues.

As the 1980’s wore on, interdisciplinary pain management programmes became popular, with much of the work involving helping people reappraise their pain as “noise in the system”, and encouraging participants to develop strategies to increase activity levels and at the same time employ approaches to “close the gate” and thus reduce pain intensity.  I started working in pain management in the mid-1980’s when not only did I develop a patter to explain gate control, chronic pain, the relationship between the brain and what was going on in the tissues, I also started using the case formulation approach I still use today.

The key effects of this approach were pretty profound: people said to me they had never realised their pain wasn’t a fixed thing. The commonplace examples I used to explain why the relationship between their pain and what was going on in the tissues was complicated and uncertain made sense – everyone had heard of phantom pain, everyone knew of people who played rugby and didn’t feel the pain until after the game, everyone had heard of hypnosis for pain, and people also recognised that when they felt bad, so their pain felt worse but when they were busy and happy doing things, their pain was less of a problem.

I’ve attached one of the original examples of “explaining pain” to this post.simple-explanation-of-biopsychosocial-model-of-chronic-pain

Now the interesting thing is that during the 1970’s, 80’s, and 90’s, there was still a lot of talk about ways to abolish chronic pain. Loads of nerve cutting and burning, lots of surgical fusing and metalwork, heaps of pharmacological strategies were all the rage. People felt sure there was a way to stop all this chronic pain from appearing – and the answer was to begin early, before pain behaviour was established, before people got the wrong idea that their pain was intractable.  As a result the “yellow flags” or psychosocial risk factors for chronicity were developed by Kendall, Linton & Main (at least in NZ). This created a great flurry of ideas about how to “get people moving”, and “assess and manage yellow flags” which have subsequently flourished and become a veritable rainbow of flags.

Sadly, I haven’t seen any significant reduction in the rates of chronic pain, or rates of disability associated with chronic pain – although there do seem to be fewer people having five or six or more surgeries for their lower back pain. Instead, there’s a far greater emphasis on “explaining pain” from the beginning – a good thing, you’d think! But hold on… a recent conversation on Facebook suggests that the purpose of explaining pain may have been misconstrued, perhaps even over-interpreted…

When we begin to untangle some of the elements involved in our experience of pain, we can see that at least part of the “yuk factor” of pain lies in our appraisal or judgement of what the pain signifies. Let me give you an example – say you were walking down a dark alley and someone approached you with a loaded syringe. They stab you with the needle! What do you do? Well – probably you’d run for the nearest Emergency Department, and my bet is that you’d be well aware of the sting of the needle as it went in. Now think about the last time you got your flu jab – same stimulus, but your response is likely to be quite different. You’ll notice the sting of the needle, but it will quickly fade, and you’ll generally be calm and matter-of-fact about it. Your appraisal of the sting is quite different from what I guess you’d be thinking if you’d been stuck by a needle in a dark alleyway.

When people are asked to rate their pain intensity, at least some of the “score” given on a visual analogue scale can be attributed to the “distress” portion of the pain experience. The part that we can attribute to “what this experience signifies to me”. And this is the part that an explanation about pain can influence – and thus pain intensity ratings can and do drop once a helpful explanation is given. BUT it does not change the biological elements, nor the “attention grabbing” aspects of pain (well, maybe the latter can be a little bit changed because if we don’t think of the experience as representing a threat, we can more readily put it aside and focus on other more important things).

Why is this important? Well, in the enthusiasm to explain pain to everyone, I think sometimes the application can be a bit blunt. Sometimes it becomes an info-dump, without really taking the time to listen to what the person is most concerned about. It may not be that they think their pain represents harm – instead it may be that they’re not sleeping well, or that they’re finding it hard to concentrate at work, that they’re worried about the effect of pain on their ability to drive safely. Because quite apart from the “yuckiness” of pain, pain intensity also has an effect on cortical processing space. And an explanation of the mechanics doesn’t take away the poor sleep, the worries about work, or make it easy to drive home. And there are times when the person remains unconvinced by an explanation – or has “head knowledge” but it makes no difference to what they’re doing. From our own experience in life, we know there’s a big difference between reading about something – and actually doing it. Experiential learning trumps “head knowledge”

Do I think it’s important to explain pain neurobiology? Most of the time, yes. But we need to do this with care, compassion and sensitivity.  We need to think about why we’re doing it. And we need to recognise that for some people, explanation doesn’t change their pain intensity, it just changes their judgement about the meaning of their pain – and if their concerns are about the effect of pain on their life, then an explanation may not be the most useful thing. And most of all, we need to remember that reducing pain intensity is not really the most important outcome: doing more is probably more important.


Fordyce, Wilbert E., Fowler, Roy S., & Delateur, Barbara. (1968). An Application of Behavior Modification Technique to a Problem of Chronic Pain. Behaviour Research and Therapy, 6(1), 105-107. doi:

Okifuji, Akiko, & Turk, Dennis C. (2015). Behavioral and Cognitive–Behavioral Approaches to Treating Patients with Chronic Pain: Thinking Outside the Pill Box. Journal of Rational-Emotive & Cognitive-Behavior Therapy, 33(3), 218-238. doi: 10.1007/s10942-015-0215-x

Flexibility: not just movement variability

For many therapists, learning the Right Way to treat a person experiencing pain means following rules. Observe this, identify that, follow the yellow brick road and end up with the right result. The problem is that people don’t always respond in the way the rules suggest meaning both clinician and patient can be confused about what to do next. While it’s normal to generate clinical heuristics, or rules of thumb, these can limit the way we approach helping someone.

I’ve been pondering this as I’m reading Villatte, Viullatte and Hayes Mastering the clinical conversation: Language as intervention. I posted last time I wrote about the problems that language can pose for us as we attend to the concepts and relationships those word generate for us rather than noticing what is actually happening right here and now. I was originally thinking of the people we work with and treat, but now I want to turn my attention to us – because we too can be imprisoned within rules that function well in one context – but hamper flexible responses in other contexts.

The rules we follow

Some of the rules we learn during our initial clinical training can be very helpful – for example, we learn that we need to attend to what people say and do; we learn to suppress our judgements about the person as “likeable” or “unlikable” (hopefully); we learn the importance of using correct terminology with one another. Other rules are far less helpful: in my case, learning that people “should” use a raised toilet seat after hip replacement (almost irrespective of the bathroom they have, the alternatives they’d already organised, or whether it actually reduced the risk of hip dislocation) meant that I tried to give the things out to people who didn’t actually need them. I quickly stopped doing that after I found too many of those toilet seats dumped on the roadside inorganic rubbish collection! And I became more sensitive to who, what, when and where. And I changed my thoughts once I read the research suggesting those “hip precautions” perhaps don’t hold up to scrutiny (for example: Schmidt-Braekling, Waldstein, Akalin, et al, 2015; Ververeli, Lebby, Tyler & Fouad, 2009).

We follow many other clinical rules – for example, we attend to certain features of a person’s presentation because we’ve been told it’s important. Depending on the model or theory we hold about the problem, we’ll attend to some things and not others.

Similarly in terms of our treatments – we’ve been told that some treatments are “good” and others not so. Some of us follow these rules very strictly – so patients are told to move in certain ways, to avoid certain movements, to do six repetitions of an exercise, to stop for a break every hour – and some of us have even been quite frustrated because the patients we’ve been advising tell us these rules aren’t working. We think “but they should”!

Explaining pain

A good example of this is the push to ensure every person experiencing pain gets an explanation for their pain. We’ve seen the evidence showing it’s a good thing, and we’ve even learned a set of phrases that we’ve been told “work”.

BUT is this a rule we should always follow?


In some instances giving pain education is unhelpful. Times I can think of are when a person is presenting with high pain intensity and in an acute situation – or when they’re stuck with an explanation they prefer and aren’t ready to consider another, or when they have other more important concerns.

Based on what I’ve been reading, perhaps we need to consider some alternative ways of looking at this “rule”.

Here’s the thing: for some people, at the right time, and when the person is being helped to discover for themselves, learning about pain neurobiology is a really good thing. But if we apply this as a rule, we risk becoming insensitive to other things the person might need AND to whether the education has had the intended effect. For some people, it’s not the right thing – the outcome for THAT person might be seen in increased resistance to your therapeutic approach, or arguing back, or them simply not returning because we “didn’t listen” or “told me it’s all in my head”. For others, this information might be useful but not as important as identifying that they’re really worried about their financial situation, or their family relationships, or their mood is getting them down, or they’re not sleeping…

Am I suggesting not to do pain education? Not at all. I’m suggesting that instead of developing a rule that “everyone must have pain education because it’s good” (or, for that matter, any other “must”), clinicians could try considering the context. Ask “is this important to the client right now?”, “what effect am I hoping for and am I measuring it?”, “how can I guide the person to draw their own conclusions instead of telling them?”

In other words, attending to those contextual cues might just help us think of a bunch of alternative ways to help this person achieve their goals. And if we then ask the person to collaborate on HOW to reach those goals, suggesting the plans are experiments that both of you can evaluate. This helps reduce our human tendency to latch onto an idea, and then create a rule that isn’t always helpful.


Schmidt-Braekling, T., Waldstein, W., Akalin, E. et al. Arch Orthop Trauma Surg (2015) 135: 271. doi:10.1007/s00402-014-2146-x

Ververeli P, Lebby E, Tyler C, Fouad C. Evaluation of Reducing Postoperative Hip Precautions in Total Hip Replacement: A Randomized Prospective Study. ORTHOPEDICS. 1; 32: doi: 10.3928/01477447-20091020-09 [link]

Villatte, M., Viullatte, J., & Hayes, S. (2016). Mastering the clinical conversation: Language as intervention. The Guilford Press: New York. ISBN: 9781462523061

Words are never enough – but does that stop us?

Pain may be said to follow pleasure as its shadow; but the misfortune is that in this particular case, the substance belongs to the shadow, the emptiness to its cause. CHARLES CALEB COLTON, Lacon

I can bear any pain as long as it has meaning. HARUKI MURAKAMI, 1Q84

But pain … seems to me an insufficient reason not to embrace life. Being dead is quite painless. Pain, like time, is going to come on regardless. Question is, what glorious moments can you win from life in addition to the pain?  LOIS MCMASTER BUJOLD, Barrayer

Language is not just words, but what those words symbolise. We use movements of lips, tongue and throat to produce symbols we relate to other things. We then use the relationships we learn through symbols to frame or structure our experiences – language is a “form of cooperation that builds on the social nature of humans groups and enhances a culture of eusociality in which humans thrive” (Villatte, Villatte & Hayes, 2016. p. 28). What this means is that humans learn to connect concepts together through language which represents concepts only because of a shared social understanding – and in sharing this understanding we feel connected.

Why am I talking about language? Well, relational frame theory is a theory of human behaviour that helps us understand how language can exert an influence on us through the way we understand symbolic relations.We learn symbolic relationships by interacting with our world – children learn concepts of  “I – you” (that you and I are different, but that I can take your perspective by imagining I was in your place); “here-there” (that here is where I am, but there is another place – and I can move to that place); “now – then” (what is happening now will become then soon) by handling objects, ultimately understanding that the concepts only make sense within the context of “here”, or “I”, or “now”.   To be empathic, we need to learn to take the perspective of another, see and feel things from another person’s point of view, and be willing to experience those feelings (Villatte, Villattee & Hayes, p.32).

To be empathic to another’s pain, we need to take the perspective of another, to be willing to experience “what it might feel like” from the other person’s shoes.

Why are symbolic relations important?

In Christchurch, as many people know, over the past five years we have been through over 10,000 earthquakes of more than 3 on the Richter Scale. The thought of having an earthquake, to someone raised in NZ, is a distinct possibility. We have small ones all the time. Then in September 2010 we had the first big earthquake. It happened in the middle of the night (early morning), when all was dark, and it was violent! Later that day we had many aftershocks, and I can remember my heart pounding and feeling anxious in the aftermath. What has happened since, though, is that I’ve learned to associate the word “earthquake” with a whole lot of concepts – a rumbling noise from a truck driving past, the deep rumble of earthworks, EQC (our national insurer), road cones, detours, heritage buildings being knocked down, having no water or power. I keep a look out for exits, I brace at the rumble of a truck, one of the topics of conversation is “how is your house” and I remember the fatigue of constant aftershocks in the middle of the night.

Learning the associations (symbolic relations) between the experience at the time of an earthquake and all these other things such as words, movements, actions and emotions means that as a person living in Christchurch, the word “earthquake” and the sight of road cones and the rumble of a truck have all gained additional meaning or salience to me.

Simply by remembering a particular day (for us it was September 22, 2011), or by looking at a road cone, or diggers operating in a trench in a road, I have emotional, cognitive, motivational and perceptual responses. This is the power of a symbol, once learned.

And once learned, that association will never be unlearned – I will always remember that trucks rumbling by sound a lot like the start of an earthquake, and I will probably always have a quick little bracing response that I may not even notice (but hitch me up to biofeedback and I’ll be skin conductance will be increased).

What does this have to do with pain?

In the same way that I learned about earthquakes being associated with a whole bunch of things that hadn’t been connected before September 2010, from the time we are born we develop associations between our experiences of pain and other things including language.

For the most part we learn that pain is associated with something not so good happening to our body. We learn that it’s something we don’t really want to experience, and so we try to avoid it (mainly). We learn words that are associated with that experience – “ouch!”, “hurt”, “painful”, “ache”. We also develop emotional, cognitive, motivational and perceptual responses to this experience. We learn that certain movements bring pain on, while others alleviate it; we learn that some people respond with sympathy to our words or movements while others don’t respond.

The thing about symbolic relations is that “the simplest act of remembering by using names and symbols … means that anytime, anywhere, we can remember past painful or difficult events based on a few cues…the past can become present through symbolic relations” (Villatte, Villatte & Hayes, 2016, p. 33). While nonhuman animals can become fearful in situations that are similar to those they’ve felt threatened in, humans can experience the same emotions and responses even when a word is spoken – like earthquake for me brings on a heightened awareness of how vulnerable I am when the ground shakes.

What this learned association means is that for all humans, there are many cues that will elicit the same response as the actual event. And given the ubiquity of pain and the words we use to describe pain – and the associations we develop since we’ve been children – it’s no wonder that changing some of the more unhelpful associations and responses we have to the experience is a challenge.

Over the next few weeks I’ll be posting about relational frame theory and how this theory can help us understand why words can be used to help – and harm – and how to implement useful verbal strategies in sessions to help our clients see their pain from a different frame.

Villatte, M., Viullatte, J., & Hayes, S. (2016). Mastering the clinical conversation: Language as intervention. The Guilford Press: New York. ISBN: 9781462523061

Ambiguity and uncertainty

Humans vary in how comfortable we are with uncertainty or ambiguity: Tolerance of ambiguity is a construct discussed in cognitive and experimental research literature, and refers to the willingness to prefer black and white situations, where “there is an aversive reaction to ambiguous situations because the lack of information makes it difficult to assess risk and correctly make a decision. These situations are perceived as a threat and source of discomfort. Reactions to the perceived threat are stress, avoidance, delay, suppression, or denial” (Furnham & Marks, 2013, p. 718).  Tolerance to uncertainty is often discussed in relation to response to stress and emotions associated with being in an ambiguous situation, or it may refer to a future-oriented trait where an individual is responding to an ambiguous situation in the present. Suffice to say, for some individuals the need to be certain and clear means they find it very difficult to be in situations where multiple outcomes are possible and where information is messy. As a result, they find ways to counter the unease, ranging from avoiding making a decision to authoritatively dictating what “should” be done (or not done).

How does this affect us in a clinical setting? Well, both parties in this setting can have varying degrees of comfort with ambiguity.

Our clients may find it difficult to deal with not knowing their diagnosis, the cause of their painful experience, the time-frame of its resolution, and managing the myriad uncertainties that occur when routines are disrupted by the unexpected. For example, workers from the UK were interviewed about their unemployment as a result of low back pain. Uncertainty (both physical and financial) was given as one of the major themes from interviews of their experience of unemployment (Patel, Greasley, Watson, 2007).  Annika Lillrank, in a study from 2003, found that resolving diagnostic uncertainty was a critical point in the trajectory of those living with low back pain (Lillrank, 2003).

But it’s not just clients who find it hard to deal with uncertainty – clinicians do too. Slade, Molloy and Keating (2011) found that physiotherapists believe patients want a clear diagnosis but feel challenged when they’re faced with diagnostic uncertainty. What then happens is a temptation to be critical of the patients if they fail to improve, to seek support from other more senior colleagues, and end up feeling unprepared by their training to deal with this common situation. The response to uncertainty, at least in this study, was for clinicians to “educate” care-seekers about their injury/diagnosis despite diagnostic uncertainty (my italics), and a strong desire to see rapid improvements, and tend to attribute lack of progress to the client when either the client doesn’t want “education” or fails to improve (Slade, Molloy & Keating, 2003).

Physiotherapists are not alone in this tendency: There is a large body of literature discussing so-called “medically unexplained diseases” which, naturally, include chronic pain disorders. For example Bekkelund and Salvesen (2006) found that more referrals were made to neurologists when the clinician felt uncertain about a diagnosis of migraine. GP’s, in a study by Rosser (1996) were more likely to refer to specialists in part because they were uncertain – while specialists, dealing as they do with a narrower range of symptoms and body systems, deal with less diagnostic uncertainty. Surprisingly, despite the difference in degree of uncertainty, GP’s order fewer tests and procedures yet often produce identical outcomes!

How do we manage uncertainty and ambiguity?

Some of us will want to apply subtypes, groupings, algorithms – means of controlling the degree of uncertainty and ambiguity in our clinical practice. Some of the findings from various tests (eg palpation or tender point examination) are used as reasons for following a certain clinical rule of thumb. In physiotherapy, medicine and to a certain extent my own field of occupational therapy, there is a tendency to “see nails because all I have is a hammer” in an attempt to fit a client into a certain clinical rule or process. We see endless publications identifying “subtypes” and various ways to cut down the uncertainty within our field, particularly with respect to low back pain where we really are dealing with uncertainty.

Some of these subgroupings may appear effective – I remember the enthusiasm for leg length discrepancies, muscle “imbalance”, and more recently neutral spine and core stability – because for some people these approaches were helpful! Over time, the enthusiasm has waned.

Others of us apply what we could call an eclectic approach – a bit of this, a bit of that, something I like to do, something that I just learned – and yes, even some of these approaches seem to work.

My concern is twofold. (1) What is the clinical reasoning behind adopting either a rule-governed algorithm or subtyping approach or an eclectic approach? Why use X instead of Y? And are we reasoning after the fact to justify our approach? (2) What do we do if it doesn’t work? Where does that leave us? As Slade, Molloy & Keating (2003), do we begin blaming the patient when our hammer fails to find a nail?

I’ve long advocated working to generate multiple hypotheses to explain how and why a person is presenting in this way at this time. It’s a case formulation approach where, collaborating with the person and informed by broad assessment across multiple domains that are known to be associated with pain, a set of possible explanations (hypotheses) are generated. Then we systematically test these either through further clinical assessment, or by virtue of providing an intervention and carefully monitoring the outcome. This approach doesn’t resolve uncertainty – but it does allow for some time to de-bias our clinical reasoning, it involves the client in sorting out what might be going on, it means we have more than one way to approach the problem (the one the client identifies, not just our own!), and it means we have some way of holding all this ambiguous and uncertain information in place so we can see what’s going on. I know case formulations are imperfect, and they don’t solve anything in themselves (see Delle-Vergini & Day (2016) for a recent review of case formulation in forensic practice – not too different from ordinary clinical practice in musculoskeletal management IMHO) . What they do is provide a systematic process to follow that can incorporate uncertainty without needing a clinician to jump to conclusions.

I’d love your thoughts on managing uncertainty as a clinician in your daily practice. How do you deal with it? Is there room for uncertainty and ambiguity? What would happen if we could sit with this uncertainty without jumping in to treat for just a little longer? Could mindfulness be useful? What if you’re someone who experiences a great deal of empathy for people who distressed – can you sit with not knowing while in the presence of someone who is hurting?


Bekkelund, S., & Salvesen, R. (2006). Is uncertain diagnosis a more frequent reason for referring migraine patients to neurologist than other headache syndromes? European Journal of Neurology, 13(12), 1370-1373. doi:
Delle-Vergini, V., & Day, A. (2016). Case formulation in forensic practice: Challenges and opportunities. The Journal of Forensic Practice, 18(3), null. doi:doi:10.1108/JFP-01-2016-0005
Furnham, A., & Marks, J. (2013). Tolerance of ambiguity: A review of the recent literature. Psychology, Vol.04No.09, 12. doi:10.4236/psych.2013.49102
Lillrank, A. (2003). Back pain and the resolution of diagnostic uncertainty in illness narratives. Social Science & Medicine, 57(6), 1045-1054. doi:
Patel, S., Greasley, K., Watson, P. J. (2007). Barriers to rehabilitation and return to work for unemployed chronic pain patients: A qualitative study. European Journal of Pain: Ejp, 11(8), 831-840.
Rosser, W. W. (1996). Approach to diagnosis by primary care clinicians and specialists: Is there a difference? Journal of Family Practice, 42(2), 139-144.
Slade, S. C., Molloy, E., & Keating, J. L. (2012). The dilemma of diagnostic uncertainty when treating people with chronic low back pain: A qualitative study. Clinical Rehabilitation, 26(6), 558-569. doi:10.1177/0269215511420179

Did it help? Questions and debate in pain measurement

Pain intensity, quality and location are three important domains to consider in pain measurement. And in our kete*of assessment tools we have many to choose from! A current debate (ongoing debate?) in the august pages of Pain (International Association for the Study of Pain) journal shows that the issue of how best to collate the various facets of our experience of pain is far from decided – or even understood.

The McGill Pain Questionnaire (MPQ) is one of the most venerable old measurement instruments in the pain world.  It is designed to evaluate the qualities of pain – the “what does it feel like” of sensory-discriminative components, evaluative components, and cognitive-affective components. There are 20 categories in the tool, and these examine (or attempt to measure) mechanical qualities, thermal qualities, location and time.  Gracely (2016), in an editorial piece, compares the McGill to a set of paint colour samples – if pain intensity equals shades of grey, then the other qualities are other coloures – blue, green, red – in shades or tints, so we can mix and match to arrive at a unique understanding of what this pain is “like” for another person.

To begin to understand the MPQ, it’s important to understand how it was developed. Melzack recognised that pain intensity measurement, using a dolimeter (yes, there is such a thing – this is not an endorsement, just to prove it’s there), doesn’t equate with the qualities of pain experienced, nor of the impact of previous experiences. At the time, Melzack and Wall were working on their gate control theory of pain, so it’s useful to remember that this had not yet been published, and specificity theory was holding sway – specificity theory arguing that pain is a “specific modality of cutaneous sensation”, while pattern theory held that the experience reflects the nervous systems ability to “select and abstract” relevant information (Main, 2016).  So Melzack adopted a previous list of 44 words, carried out a literature review, and recorded the words used by his patients. Guided by his own three dimensional model of pain, he generate three groups of descriptors to begin to establish a sort of “quality intensity scale”. These were then whittled down to 78 words that have been used since, and by used I mean probably the most used instrument ever! Except for the VAS.

There are arguments against the MPQ – I’m one who doesn’t find it helpful, and this undoubtedly reflects that I work in a New Zealand context, with people who may not have the language repertoire of those that Melzack drew on. The people I work with don’t understand many of the words (‘Lancinating‘ anyone?), and like many pain measures, the importance or relevance of terms used in this measure are based on expert opinion rather than the views of those who are experiencing pain themselves. This means the measure may not actually tap into aspects of the experience of pain that means a lot to people living with it. Main (2016) also points out that interpreting the MPQ is problematic, and perhaps there are alternative measures that might be more useful in clinical practice. Some of the criticisms include the difficulty we have in separating the “perceptual” aspects of pain from the way pain functions in our lives, and the way we communicate it, and the MPQ doesn’t have any way to factor in the social context, or the motivational aspects of both pain and its communication.

In a letter to the editor of Pain, Okkels, Kyle and Bech (2016) propose that there should be three factors in the measurement – symptom burden (they suggest pain intensity), side effects (or medication – but what if there’s no medication available?), and improved quality of life (WHO-5). But as Sullivan and Ballantyne (2016) point out in their reply – surely the point of treatment is to improve patient’s lives – “we want to know if it is possible for the patient’s life to move forward again. However it is also important that we do not usurp patients’ authority to judge whether their life has improved” (p. 1574). What weighting we give to, for example, pain reduction vs improved quality of life? I concur. Even the MPQ with all its history doesn’t quite reflect the “what it means to me to experience this pain”.

Did it help? Answering this critical question is not easy. Pain measurement is needed for furthering our understanding of pain, to ensure clinical management is effective, and to allow us to compare treatment with treatment. But at this point, I don’t know whether our measures reflect relevant aspects of this common human experience.  Is it time to revisit some of these older measures of pain and disability, and critically appraise them in terms of how well they work from the perspectives of the people living with pain? Does this mean taking some time away from high tech measurement and back to conversations with people?


(*pronounced “keh-teh” – Maori word for kitbag, and often used to represent knowledge)

Gracely, R. H. (2016). Pain language and evaluation. Pain, 157(7), 1369-1372.

Main, C. J. (2016). Pain assessment in context: A state of the science review of the mcgill pain questionnaire 40 years on. Pain, 157(7), 1387-1399.

Okkels, N., Kyle, P. R., & Bech, P. (2016). Measuring chronic pain. Pain, 157(7), 1574.

Sullivan, M. D., & Ballantyne, J. (2016). Reply. Pain, 157(7), 1574-1575.