Science in practice

…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!


Empathy and catastrophising influence pain inhibition

When I went to occupational therapy school I was introduced to nociception and the biological underpinnings of pain. I wasn’t, at that time, taught anything about the brain, attention, emotions or any social responses to pain behaviour. Like most health professionals educated in the early 1980’s, pain was a biological and physical phenomenon. I suppose that’s why it can be so hard for some of my colleagues to unlearn the things they learned way back then, and begin to integrate what we know about psychological and social aspects of our pain experience. Because pain is a truly biopsychosocial experience. Those pesky psychosocial factors aren’t just present in people who have difficulty recovering from pain, they’re actually integral to the entire experience.

Anyway, ’nuff said.

Today I stumbled across a cool study exploring two of the psychosocial phenomena that we’ve learned are involved in pain. The first is catastrophising. And if you haven’t got your head around catastrophising it’s probably time to do so. It’s one of the strongest predictors of disability (Edwards, Dworkin, Sullivan, Turk & Wasan, 2016). Catastrophising is the tendency to “think the worst” and consists of ruminating (brooding on), magnifying (over-estimating the negative impact) and helplessness (feeling as if there’s nothing you can do).  The second is empathy, or the ability to sense other people’s emotions, coupled with the ability to imagine what someone else might be thinking or feeling. Empathy is not the same as sympathy which seems to be about the emotions a person experiences while observing another’s emotional state. In fact, separate parts of the brain are involved in the two experiences (Cuff, Brown, Taylor & Howat, 2014).

Back to the study. This study examined conditioned pain modulation in partners observing their partner undergoing a painful experience. It was carried out by Gougeon, Gaumond, Goffaux, Potvin and Marchand (2016) in an attempt to understand what happens to the pain experience of people watching their loved ones in pain. The experimental protocol was (1) baseline; (2) assessing pain VAS 50; (3) pre-CPT heat pain testing (thermode preimmersion at a fixed temperature); (4) CPT (either at 201Cor71C); and (5) post-CPT heat testing (thermode postimmersion at the same fixed temperature). What they did was ask the participants to submerge their right hand in a freezing cold waterbath while video recording them. They then asked their partners to place their right hand in lukewarm water while watching the video recording. Participants were asked to rate their pain intensity.

What they found was the higher the catastrophizing score was, stronger was their descending pain inhibition when they were watching either themselves or their spouse in pain. In women, the more empathic the women were, the better was their descending pain inhibition when they observed their spouse in pain.

This is extraordinary. Firstly, the finding that there was a correlation between catastrophising score and descending inhibition contradicts other research studies – Gougeon, Gaumond, Goffaux, Potvin and Marchand suggest that although cognitive and emotional processes underlying catastrophising increase pain perception and decrease inhibition, their experimental design may have increased pain perception during the conditioned stimulus which may have triggered more conditioned pain modulation. They also suggest that the catastrophising level of participants increases their perceived pain, explaining why it correlates with conditioned pain modulation efficiency.

Secondly, women were more distraught than men by observing pain in others. Adopting the perspective of a loved-one elicited stronger activation in regions involved in the “pain” matrix than adopting the stranger’s perspective (Cheng et al), and the authors suggest that empathy is a powerful factor involved in pain modulation while observing someone in pain. This shows that descending inhibition is influenced by physical stimulus characteristics (such as intensity or location), as well as personal cognitive dimensions. A far cry from the notion that psychosocial factors play little part in modulating our pain experience.

What does this actually mean for us?

Well, to me it suggests that we need to be aware of our own empathic response to observing someone else who is experiencing pain. Let’s put it this way: if I’m an especially empathic person (and especially if I tend to catastrophise) and I see people who are experiencing pain in my clinical practice, my own emotional and cognitive response to seeing people may influence my behaviour and practice. For example, I might be less willing to tell people that I don’t have a way to reduce their pain. I might pursue more “heroic” healthcare – send people off for more treatments, try for longer with unsuccessful treatments “just in case”, I might even send people away from my care because I find it hard to tolerate being around someone who “doesn’t respond”.

You see, being empathic and catastrophising tends to elevate feelings of distress in the presence of pain. If we don’t have effective ways to manage our own distress when we are in the presence of someone who is indicating they’re sore, we’re at greater risk of developing burnout and of feeling frustrated (Gleichgerrcht & Decety, 2014).

For this reason I’m a fan of using mindfulness because it does help people to step back from the emotional judgements of experience, and in particular the negative impact such judgements have on both interactions and emotions (Dobkin, Bernardi & Bagnis, 2016).


Cheng Y, Chen C, Lin CP, et al. Love hurts: an fMRI study. Neuroimage. 2010;51:923–929.

Cuff, B. M. P., Brown, S. J., Taylor, L., & Howat, D. J. (2014). Empathy: A review of the concept. Emotion Review, 8(2), 144-153. doi:10.1177/1754073914558466

Decety, J., Yang, C.-Y., & Cheng, Y. (2010). Physicians down-regulate their pain empathy response: An event-related brain potential study. Neuroimage, 50(4), 1676-1682.

Dobkin, P. L., Bernardi, N. F., & Bagnis, C. I. (2016). Enhancing clinicians’ well-being and patient-centered care through mindfulness. Journal of Continuing Education in the Health Professions, 36(1), 11-16.

Edwards, R. R., Dworkin, R. H., Sullivan, M. D., Turk, D. C., & Wasan, A. D. (2016). The role of psychosocial processes in the development and maintenance of chronic pain. The Journal of Pain, 17(9, Suppl), T70-T92.

Gleichgerrcht, E., & Decety, J. (2014). The relationship between different facets of empathy, pain perception and compassion fatigue among physicians. Frontiers in behavioral neuroscience, 8, 243.

Gougeon, V. M., Gaumond, I. P., Goffaux, P. P., Potvin, S. P., & Marchand, S. P. (2016). Triggering descending pain inhibition by observing ourselves or a loved-one in pain. Clinical Journal of Pain, 32(3), 238-245.

End-of-year musings

It’s my last post for the year. It has been an extraordinary year, lots of surprises, shocks and enough excitement for anyone! I’m not even going to start on the political changes, here in NZ we’ve had yet another major earthquake, excitement as ACC (our national accident insurer) sets up new pain service contracts (with a LOT of people who haven’t been involved in pain management before… there’s an experiment in the making!), and continuing road cone carnage on the streets of Christchurch.

On the pain news front, I can’t think of any incredibly ground-breaking news – although one medic advised that “Virtually all cases of low back pain can now be diagnosed definitively by criterion standard methods as to source and cause.” That same medic also argued that a paper by Maher, Underwood & Buchbinder (2016) on non-specific low back pain, published in The Lancet, represented “the views of non-evidence-based troglodytes who (a) have apparently not read any scientific papers since 1966, and (b) have vested interests in “managing” non-diagnosed patients so their practices remain busy and they reinforce each other’s views that the burden of low back pain cannot be eased.” I’ll leave the critiquing of that view to those with more time and energy than I have!

It’s also been a year in which various commentators have critiqued the “biopsychosocial model” as it’s applied in musculoskeletal pain.  Some have pointed out that this is an unscientific model, it’s not a theory that can be tested and therefore can’t point to “truth” or whatever approximation we can currently identify. Others have argued that by adopting this framework, practitioners must either be versed in “life, the universe and everything” – or perhaps become exactly what advocates of this approach decry: reductionists. I’m not sure I follow this argument, but those that raise it are intelligent, articulate and far more thoughtful than those who believe that Maher, Underwood & Buchbinder are “troglodytes” or have “vested interests”.

I continue to hold that a biopsychosocial perspective explains more, and is of practical use when we consider the various factors that might influence why this person is presenting in this way at this time, and what might be done to reduce their distress and disability. Here’s my take.

Biopsychosocial model

When we look into the original biopsychosocial model, we need to understand the context in which Engel first developed it. He was a psychiatrist, and at the time psychiatry was under threat from psychologists in particular, who were strongly advocating that many mental illnesses were actually “problems of living”. Things like alcohol abuse, forms of mood disorder, relationship issues and the like were seen as disorders influenced by learning and environment rather than biology. Psychiatrists were perhaps on the way to being sidelined from the very area in which they claim expertise. Engel, influenced by general systems theory and cybernetics, proposed a way for psychiatrists to remain relevant: look at the person as part of a wider system in which each element in the system could influence and be influenced by the next. Engel used this approach as a way to frame conversations with the patients he saw – attempting to understand how and why they were seeking help, and especially, attempting to understand the person and his or her priorities. I think that’s admirable.

How the model has evolved since then is an interesting tale. I first encountered the model during my occupational therapy training, where it was a foundation to viewing people-in-context. It was presented as a bit old hat (I started training in 1979), and was replaced in my profession by Gary Kielhofner’s Model of Human Occupation. This model similarly draws on general systems theory, and argues for the relevance of volition and habits as well as capacity from a biological/performance stance to undertake occupation and of course, contexts such as environment which includes the social environment. MOHO incorporates much of what we consider to be biopsychosocial – in fact, occupational therapy as a profession is based on the idea that people actively engage in purposeful and meaningful activities (occupations) that are formed out of the affordances available to them by virtue of biology, psychology and social elements within an environmental context.

So what?

For a model, or theory, to have value it needs to offer something that existing models or theories don’t. It needs to be more parsimonious (make fewer assumptions), explain more (be more consilient), hold together with existing knowledge (cohere), and predict more (Thagard, 1978).

For a clinician, a theory must also be useful in terms of explaining why this person is presenting in this way at this time, and directing what can be done to reduce distress and disability. Why these questions? Because people actively make decisions to seek treatment. They evaluate their experience in light of their past experiences, prevailing community beliefs about the trajectory of their problem, family influences, and yes, legislative influences. These are possibly more important than the biology of their problem – because we’re not going to treat someone who doesn’t believe they have a problem!

As clinicians I think we need to ponder exactly what we consider to be “treatment”.

When my fracture is reduced and immobilised, that is “treatment” – but it’s not actually ‘healing’ my bones, it’s actually up to my body to do the work. What immobilisation does is create an environment in which my body can heal itself. But the problem of a broken bone is not “treated” just by immobilisation. Treatment has to include the rest of my recovery – and involve prevention strategies too. My recovery will need to include restoring function. And some of that restoration will be by guiding me through various movements that increase tissue tolerance as well as my confidence that my limb will support me. My recovery also has to include me understanding and learning from my experience – will I jump off that cliff again? Will I leave the toys all over the floor again? Will I walk on a slippery path again?

I think clinicians simply create an environment in which people can recover. And we need to go beyond measuring range of movement or strength to establish that recovery has occurred. Recovery isn’t just about returning to “normal” whatever that is. It’s about moving beyond this interruption and into new possibilities and new challenges. It’s really about being able to be who we really are. While that’s primarily the person’s own responsibility, our job as clinicians is to create an environment where it’s possible. While a biopsychosocial model/theory/framework makes life complex, using this approach allows us to be aware of more of the factors relevant to recovery and growth than simply looking at people as if they’re bits of meat, bone, and juice.

In the new year

I’ve been blogging since 2007. In that time I’ve written over a thousand posts all on the topic of pain. Almost all of my posts are on the theme of how we can remember that we are working with people. Other human beings who have their own thoughts, beliefs and priorities. Humans who make sense of their situation as best they can. People who, like us, hold cognitive biases, and feel emotions, and get stuck, and hold values. My real focus is on how we can integrate these things into clinical reasoning – because until we do, we’re ignoring what matters most to the people we seek to serve.


Engel, G. L. (1977). The need for a new medical model: A challenge for biomedicine. Science, 196(4286), 129-136. doi:10.1126/science.847460

Maher, C., Underwood, M., & Buchbinder, R. (2016). Non-specific low back pain.  The Lancet. doi:10.1016/S0140-6736(16)30970-9

Thagard, P. R. (1978). The best explanation: Criteria for theory choice. The Journal of Philosophy, 75(2), 76-92.

What do we do with those questionnaires?

Courtesy of many influences in pain management practice, you’d have to have been hiding under a rock or maybe be some sort of dinosaur not to have noticed the increasing emphasis on using questionnaires to measure factors such as pain catastrophising, depression or avoidance. The problem is I’m not sure we’ve all been certain about what to do with the results. It’s not uncommon for me to hear people saying “Oh but once I see psychosocial factors there, I just refer on”, or “they’re useful when the person’s not responding to my treatment, but otherwise…”, “we use them for outcome measures, but they’re not much use for my treatment planning”.

I think many clinicians think psychosocial questionnaires are all very well – but “intuition”  will do “…and what difference would it make to my treatment anyway?”

Today I thought I’d deconstruct the Pain Catastrophising Scale and show what it really means in clinical practice.

The Pain Catastrophising Scale is a well-known and very useful measure of an individual’s tendency to “think the worst” when they’re considering their pain. Catastrophising is defined as “an exaggerated negative mental set brought to bear during actual or anticipated painful experience” (Sullivan et al., 2001). The questionnaire was first developed by Sullivan, Bishop and Pivik in 1995, and the full copy including an extensive manual is available here. Keep returning to that page because updates are made frequently, providing more information about the utility of the measure.

The questionnaire itself is a 13-item measure using a 0 – 4 Likert-type scale from 0 = “not at all” to 4 = “all the time”. Respondents are instructed to “indicate the degree to which you have these thoughts and feelings when you are experiencing pain”.

There are three subscales measuring three major dimensions of catastrophising: rumination “I can’t stop thinking about how much it hurts”; magnification “I worry that something serious may happen”; and helplessness “It’s awful and I feel that it overwhelms me”.

To score the instrument, simply sum all the responses to all 13 items, but to get a better idea of how to help a person, the subscale calculations involve the following:

Rumination: sum items 8,9,10, and 11

Magnification: sum items 6,7, and 13

Helplessness: sum items 1,2,3,4,5, and 12

There’s not a lot of point in having numbers without knowing what they mean, so the manual provides means and standard deviations relating to a population individuals with injury leading to lost time from work in Nova Scotia, Canada.

thingClinicians are typically interested in whether the person sitting in front of them is likely to have trouble managing their pain, so the manual also provides “cut off”scores for what could be described as “clinically relevant” levels of catastrophising. A total score of 30 or more is thought to represent the 75th percentile of scores obtained by individuals with chronic pain.

The “so what” question

Cutting to the chase, the question is “so what”? What difference will getting this information from someone make to my clinical reasoning?

Leaving aside the enormous body of literature showing a relationship between high levels of catastrophising and generally poor responses to traditional treatments that address pain alone (including surgery for major joint replacement, recovery from multiple orthopaedic trauma, low back pain, shoulder pain etc), I think it’s helpful to dig down into what the three subscales tell us about the person we’re working with. It’s once we understand these tendencies that we can begin to work out how our approach with someone who has high levels of rumination might differ from what we’ll do when working with someone who has high levels of helplessness.

As an aside and being upfront, I think it’s important to remember that a questionnaire score will only tell you what a person wants you to know. Questionnaires are NOT X-rays of the mind! They’re just convenient ways to ask the same questions more than once, to collect the answers and compare what this person says with the responses from a whole lot of other people, and they allow us to organise information in a way that we might not think to do otherwise.  I also think it’s really important NOT to label a person as “a catastrophiser” as if this is a choice the person has made. People will have all sorts of reasons for tending to think the way they do, and judging someone is unprofessional and unethical.


Rumination is that thing we do when a thought just won’t get out of our mind. You know the one – the ear worm, the endless round and round, especially at night, when we can’t get our mind off the things we’re worrying about. If a person has trouble with being able to drag his or her attention away, there are some useful things we can suggest. One theory about rumination is that it’s there as a sort of problem solving strategy, but one that has gone haywire.

Mindfulness can help so that people can notice their thoughts but not get hooked up into them. I like to use this both as a thought strategy, but also as a way of scanning the body and just noticing not only where the pain is experienced, but also where it is not.

“Fifteen minutes of worry” can also help – setting aside one specific time of the day (I like 7.00pm – 7.15pm) where you have to write down everything you’re worried about for a whole fifteen minutes without stopping. By also telling yourself throughout the day “I’m not worrying about this until tonight” and afterwards saying “I’ve already worried about this so I don’t need to right now”, worrying and ruminating can be contained. By being present with the thoughts during that 15 minutes, the threat value of the thought content is also reduced.


This is the tendency to think of the worst possible thing rather than the most likely outcome, and it’s common! Magnification can really increase the distress and “freeze” response to a situation. If a person is thinking of all the worst possible outcomes it’s really hard for them to focus on what is actually happening in the here and now. There’s some adaptive features to magnification – if I’ve prepared for the worst, and it doesn’t happen, then I’m in a good situation to go on, but in some people this process becomes so overwhelming that their ability to plan is stopped in its tracks.

Once again, mindfulness can be really useful here, particularly paying attention to what is actually happening in the here and now, rather than what might happen or what has happened. Mindful attention to breathing, body and thoughts can help reduce the “freeze” response, and allow some space for problem solving.

Of course, accurate information presented in nonthreatening terms and in ways the person can process is important to de-threaten the experience of pain. This is at the heart of “explain pain” approaches – and it’s useful. What’s important, however, is to directly address the main concern of the person – and it may not be the pain itself, but the beliefs about what pain will mean in terms of being a good parent, holding down a job, maintaining intimacy, being responsible and reliable. It’s crucial to find out what the person is really concerned about – and then ensure your “reassurance” is really reassuring.


Helplessness is that feeling of “there’s nothing I can do to avoid this awful outcome so I won’t do anything”. It’s a precursor to feelings of depression and certainly part of feeling overwhelmed and out of control.

When a person is feeling helpless it’s important to help them regain a sense of self efficacy, or confidence that they CAN do something to help themselves, to exert some sort of control over their situation. It might be tempting to aim for focusing on pain intensity and helping them gain control over pain intensity, but because it’s often so variable and influenced by numerous factors, it might be more useful to help the person achieve some small goals that are definitely achievable. I often begin with breathing because it’s a foundation for mindfulness, relaxation and has a direct influence over physiological arousal.

You might also begin with some exercise or daily activities that are well within the capabilities of the person you’re seeing. I like walking as a first step (no pun intended) because it doesn’t require any equipment, it’s something we all do, and it can be readily titrated to add difficulty. It’s also something that can be generalised into so many different environments. In a physiotherapy situation I’d like to see PTs consider exercises as their medium for helping a person experience a sense of achievement, of control, rather than a means to an end (ie to “fix” some sort of deficit).

To conclude
Questionnaires don’t add value until they’re USED. I think it’s unethical to administer a questionnaire without knowing what it means, without using the results, and without integrating the results into clinical reasoning. The problem is that so many questionnaires are based on psychological models and these haven’t been integrated into physiotherapy or occupational therapy clinical reasoning models. Maybe it’s time to work out how do this?

Sullivan M J L, Bishop S, Pivik J. The Pain Catastrophizing Scale: Development and validation. Psychol Assess 1995, 7: 524-532.

Main, C. J., Foster, N., & Buchbinder, R. (2010). How important are back pain beliefs and expectations for satisfactory recovery from back pain? Best Practice & Research Clinical Rheumatology, 24(2), 205-217. doi:doi:10.1016/j.berh.2009.12.012

Sturgeon, J. A., Zautra, A. J., & Arewasikporn, A. (2014). A multilevel structural equation modeling analysis of vulnerabilities and resilience resources influencing affective adaptation to chronic pain. PAIN®, 155(2), 292-298. doi:

Clinical reasoning “think aloud”

Occupational therapists are keen on helping people return to doing the things they value – meaningful activity, or participating in valued occupations (same thing, essentially). So, a person might come to see me because they have low back pain and want to work out how to get to work.

My first step is to understand what it is about the back pain that seems to be stopping the person from doing the tasks involved in their work. I usually begin by taking a history – what does the person understand about how their back pain came on, what’s their theory as to why it’s there, what have they done to help their recovery, how are they managing the everyday things they need to do right now. I ask about sleep, sex, personal care, daily routine, and in doing so I’m finding out about the person’s beliefs and attitudes towards their pain, their ability to regulate their arousal level, their mood, their confidence, the influence of others around them (both supportive – and those more subtle influences like their response when the person does something). I’m very careful to try to understand the contexts in which the person is having trouble – and what factors in the context might be supporting change.

In my mind I’m trying to establish a set of possible reasons for this person coming to see me at this time and in this way. I’m running through the various influences I know affect a person’s ability to engage in normal daily activities. Because I have a strong psychology background, I’ll consider functional behavioural analysis, but I’m also sensitive to personal values, cultural norms, and yes, even biological factors such as strength, range of movement, and motor control.

I can try to influence two things: the demands of the tasks in the context of work, and the capabilities of the person, but I need to keep a couple of things in mind.

  1. What is the effect of my intervention in the medium to long-term, not just the short-term?
  2. What does this person need in this context right now?

Depending on my clinical formulation, and the overall theoretical model I’m using, I can approach the decision-making in many different ways. As you’ve probably guessed, I’m a fan of Acceptance and Commitment Therapy, so my end goal is to help this person develop the ability to respond flexibly to the demands of any situation. I want to keep in mind that what I do now can have a long-term influence on what they’ll do over time. Some occupational therapists may instead focus primarily on “what will solve the problem for this person right now” without always thinking about the long-term impact.  As a result, we can see some people with low back pain being given special seating, perhaps a new bed, some adaptive equipment so they can achieve the goal of “doing” – but at the same time, being unaware of the constraints this can put on the person being able to participate in other contexts.

For example, if my client is having trouble getting to work because he thinks his car’s seat should be fixed. If my focus was purely on helping him drive his car in comfort, I could consider assessing his car and giving him some cushioning to make it more supportive. There, problem fixed! But, let’s take a look at the effect of that intervention in the medium term. While he can drive to and from work, he’s learned that he “needs” a special seat or cushioning to help stop his discomfort. He’s also learned that his back pain is something he “shouldn’t” experience.

Based on what he’s learned from my intervention, what do you think can happen if he continues to experience back pain in the work setting?

His personal model of pain will have developed a couple of interesting quirks (and ones we often see in clients) – he’s learned that posture influences his back pain, and that there is a posture that “fixes” it. He’s learned that he should have his back in a particular position to be comfortable. He’s also learned that because he can influence his sitting position in the car, he “should” be able to influence his sitting position in other contexts – like, perhaps, his office desk or the seat in his digger. He might even, if his belief that his back “should” be in a particular position is especially strong, begin to try to keep his back in this position while doing other activities like walking or carrying things, or using tools. Most insidiously, he has learned that his back pain is something he should not have. It’s a sign to him that he has to “fix” his sitting position or he’s doing something wrong. But back pain is common, many factors influence it, and it often doesn’t settle completely.

If I instead want him to be able to respond flexibly to many different settings, I’ll need to think more carefully about my intervention. My underlying reasoning has to capture the workability of any suggestions I make – and workability not just in the car while driving, but at work, while doing other tasks, at other times.

I may work together with him to find out what it is about the pain in his back that particularly bothers him. Pain itself is usually not the problem – it’s what the pain represents, the effect on doing things both here and now, and in the future. In my client’s case, perhaps his back pain is particularly frustrating for him because he values getting to work and feeling ready for anything. He doesn’t want to feel like his goals are being blocked (he doesn’t want to feel exhausted and not ready for work), he doesn’t want his back pain, and his mind is telling him he needs to be “ready for anything” even though he is in the middle of a bout of back pain. In ACT terms, he’s avoiding the negative feeling of frustration, of potential failure, of feeling exhausted and his back pain, and he’s doing what all humans do – trying to control those emotions so that he doesn’t feel them! Makes perfect sense – except that the solution (giving him a cushion for his vehicle) could pose its own problems.

I can position my intervention in a couple of different ways. Honouring the value he places on being ready for anything at work, I can talk to him about how well that’s working for him right now, given he’s having a bout of back pain. Could he be willing to allow himself to be less “ready for anything” while he recovers from his back pain? I could also suggest that he could take the time to be present to his back pain, to be aware of and experience his back – and his feet, arms, shoulders and breath – while driving to work, so that he can notice the times when it’s really bothering him, and when it bothers him less, and that along with his back pain he also has areas of comfort and strength. I could provide him with a cushion – but ask him to think about what happens when he has to sit in other chairs, and ask about the workability of carrying a cushion wherever he goes.

The point is that while occupational therapists can help people do the things they want and need to do, some of our efforts can constrain people’s options over time. We don’t live the lives of our clients – but sometimes we can assume the client’s priority is to solve an immediate problem, while overlooking the other competing values the person also holds dear.

I’ve included some readings that have informed this blog post – while they’re not directly referenced in my post, they help inform my clinical reasoning.

Damsgard, E., Dewar, A., Roe, C., & Hamran, T. (2011). Staying active despite pain: Pain beliefs and experiences with activity-related pain in patients with chronic musculoskeletal pain. Scandinavian Journal of Caring Sciences, 25(1), 108-116. doi: 10.1111/j.1471-6712.2010.00798.x

DeGood, Douglas E., & Cook, Andrew J. (2011). Psychosocial assessment: Comprehensive measures and measures specific to pain beliefs and coping. Turk, Dennis C [Ed], 67-97.

McCracken, Lance M., & Vowles, Kevin E. (2014). Acceptance and Commitment Therapy and Mindfulness for Chronic Pain: Model, Process, and Progress. American Psychologist, 69(2), 178-187.

Stenberg, Gunilla, Fjellman-Wiklund, Anncristine, & Ahlgren, Christina. (2014). ‘I am afraid to make the damage worse’ – fear of engaging in physical activity among patients with neck or back pain – a gender perspective. Scandinavian Journal of Caring Sciences, 28(1), 146-154. doi: 10.1111/scs.12043

Trompetter, Hester R., ten Klooster, Peter M., Schreurs, Karlein M., Fledderus, Martine, Westerhof, Gerben J., & Bohlmeijer, Ernst T. (2013). Measuring values and committed action with the Engaged Living Scale (ELS): Psychometric evaluation in a nonclinical sample and a chronic pain sample. Psychological Assessment, 25(4), 1235-1246.

van Huet, H, & Williams, D. (2007). Self-Beliefs About Pain and Occupational Performance: A Comparison of Two Measures Used in a Pain Management Program. OTJR: Occupation, Participation and Health Vol 27(1) Win 2007, 4-12.

“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

Guide, don’t instruct: how we talk within sessions

Do you remember your favourite teacher in school? Mine was Mrs Jackson, teacher of my Form 2 class (I think I was 12 years old). She was an outstanding teacher because she expected that we’d do well. She also didn’t tell us what to do – she helped us explore. And if there was one thing I’d like to have happen in therapy sessions with clients, it would be that we learn how to guide instead of instructing.

It’s only recently that I’ve learned why guiding and facilitating is so much more helpful than telling or instructing, and yes it’s because I’ve been reading Villatte, Villatte & Hayes Mastering the Clinical Conversation.

Have you ever noticed that when we give an instruction like “Sit up straight” or “Use your core” our clients attend to how well they’re doing just that – sitting up straight, or using the core – and at the very same time, they no longer attend to other aspects of their movement (or the context, or even the purpose of the movement). It’s a human tendency to focus on a particular set of features of our environment – and it certainly helps us cognitively because it means we don’t have to attend to everything all at once. BUT at the same time, it means we become relatively insensitive to other features occurring at the same time.

Rules or instructions have their place, or they wouldn’t still be being used in therapy – but their utility depends on how rigidly they’re applied. It makes sense for a super athlete to really focus on certain aspects of their performance, especially when they’re training, and especially when there’s one particular set of movements that will maximise their performance. For people living with pain, however, life is not about a set of performance goals. Instead, it’s about being able to respond adeptly to the constantly changing demands of their lives. And one thing people living with pain often have trouble with is being able to notice what’s happening in their own bodies.

Let’s unpack this. People living with chronic pain live with ongoing pain in certain parts of the body – and human tendencies being what they are, we try to avoid experiencing those sore bits, so our attention either skips over the painful area or it focuses almost exclusively on the sore bits and not on other parts (technically this could be called experiential avoidance). By working hard to avoid experiencing the sore bits, or alternatively focusing entirely on those sore bits, people living with pain often fail to notice what actually happens during movement.

As therapists, we can complicate this. We can instruct people (give them rules) about the movements they “should” be doing. We try to ‘correct’ posture. We advise people to use specific lifting techniques. We say “use your core”.

The effect of these instructions is to further lead our patients away from experiencing what is happening in their body. Instead of becoming aware of the way their bodies move, they attend to how well they’re following our instructions. Which is fine – until the person experiences a flare-up, or moves into a new environment with different demands, or perhaps we complete our sessions and discharge them into the wild blue yonder.

So, people with chronic pain can progressively become less aware of how their body actually feels as they do movements, and at the same time, try to apply rules we’ve given them that may not be all that helpful in different contexts.

We end up with the plumber trying hard to crawl under a house, carrying all her tools, while at the same time being worried that she’s not “using her core”. Or the piano teacher trying to “sit up properly” while working with a student on a duet. And the nurse, working one day in a busy ward with heavy patients, and another day in a paediatric ward, trying to “lift properly” using the same technique.

If we want to help people respond effectively to the widely differing contexts they’ll experience in everyday life, perhaps we need to take some time to help people learn to trust their own body, to experience both painful areas – and those that aren’t painful. We might need to help people work out fundamental principles of movement to enable them to have movement variability and flexibility – and to adjust and adapt when the contexts change.

To do this, we need to think about the way we help people learn new ways of moving. There are two fundamentals, I think.

  1. Guiding people to attend to, or notice, what is – including being OK about noticing painful parts of the body. The purpose behind this is to help people become aware of the various movement options they have, and the effect of those options on how they feel. We might need to guide people to consider not only pain, but also feelings of strength, stability, responsiveness, reach, movement refinement, subtlety, delicacy and power. To achieve this, we might need to spend time developing mindfulness skills so people can experience rather than attempting to change what they experience. The art of being willing to make room for whatever experience is present – learning to feel pain AND feel strength; feel pain AND relaxation; feel comfort AND power.
  2. Guiding people to use their own experience as their guide to “good movement”. In part, this is more of the same. I use words like “experiment” as in “let’s try this as an experiment, what does it feel like to you?”, or “let’s give it a go and see what you think”, or “I wonder what would happen if….” For example, if a person tries to move a box on a ledge that’s just out of reach, how many of you have told the person “stand a bit closer?” While that’s one way of helping someone work out that they might be stronger if they’re close to a load, what happens if the ground underfoot is unstable? The box still needs to be moved but the “rule” of standing close to a box doesn’t work – what do you think might happen if the person was guided to “Let’s try working out how you can move the box. What’s happening in your body when you reach for it?” then “What do you think you might change to make you feel more confident?” (or strong, or stable, or able to change position?).

When we try guiding rather than instructing, we honour the person’s own choices and contexts while we’re also allowing them to develop a superior skill: that of learning to experience their own body and to trust their own judgement. This ultimately gives them more awareness of how their body functions, and the gift of being flexible in how they approach any movement task.

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