Pain

…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.

What to do with the results from the PCS


The Pain Catastrophising Scale is one of the more popular measures used in pain assessment. It’s popular because catastrophising (thinking the worst) has been identified as an especially important risk factor for slow recovery from pain (Abbott, Tyni-Lenne & Hedlund, 2010), for reporting high levels of pain intensity (Langley, 2011), and for ongoing disability (Elfving, Andersoon & Grooten, 2007). I could have cited hundreds more references to support these claims, BTW.

The problem is, once the PCS is administered and scored: what then? What difference does it make in how we go about helping a person think a little more positively about their pain, do more and feel more confident?

If you haven’t seen my earlier posts about the PCS, take a look at this, this, and this for more details.

Anyway, so someone has high scores on rumination, helplessness and magnifying – what does this mean? Let’s say we have two people attending the clinic, one has really high scores on all three subscales, while the other has low or average scores. Both have grumbly old low back pain, both have had exercises in the past, both are finding it tough to do normal daily activities right now.

For a good, general pain management approach to low back pain, and once red flags are excluded (yes, the “bio” comes first!) this is what I do. I establish what the person thinks is going on and ask if it’s OK to talk about pain neurobiology. Together we’ll generate a pain formulation, which is really a spaghetti diagram showing the experience as described by the person (I used guided discovery to develop it). I then ask the person what they’d be doing if their pain wasn’t such a problem for them, perhaps what they’re finding the most frustrating thing about their situation at the moment. Often it will be sleep, or driving or cooking dinner, or perhaps even getting clothes on (shoes and socks!). I’ll then begin with helping the person develop good relaxed breathing (for using with painful movements), and start by encouraging movement into the painful zone while remaining relaxed, and tie this in with one of the common activities (occupations) the person needs or wants to do. For example, I’ll encourage bending forward to put shoes and socks on while breathing in a relaxed and calm way. I’ll be watching and also encourage relaxing the shoulders and any other tense parts of the body. For someone who is just generally sore but doesn’t report high pain catastrophising, I will also encourage some daily movements doing something they enjoy – it might be walking, yoga, dancing, gardening, whatever they enjoy and will do regularly every day for whatever they can manage. Sometimes people need to start small so 5 minutes might be enough. I suggest being consistent, doing some relaxation afterwards, and building up only once the person has maintained four or five days of consistent activity. And doing the activity the person has been finding difficult.

If the person I’m seeing has high scores on the PCS I’ll begin in a similar way, but I’ll teach a couple of additional things, and I’ll expect to set a much lower target – and probably provide far more support. Catastrophising is often associated with having trouble disengaging from thinking about pain (ruminating), so I’ll teach the person some ways to deal with persistent thoughts that hang around.

A couple to try: mindfulness, although this practice requires practice! It’s not intended to help the person become relaxed! It’s intended to help them discipline their mind to attend to one thing without judgement and to notice and be gentle with the mind when it gets off track, which it will. I ask people to practice this at least four times a day, or whenever they’re waiting for something – like the jug to boil, or while cleaning teeth, or perhaps waiting for a traffic light.

Another is to use a “15 minutes of worry” practice. I ask the person to set a time in the evening to sit down and worry, usually from 7.00 – 7.15pm. Throughout the day I ask the person to notice when they’re ruminating on their situation. I ask them to remind themselves that they’re going to worry about that tonight and deliberately put that worry aside until their appointment with worry. Then, at 7.00pm they are asked to get a piece of paper and write ALL their worries down for a solid 15 minutes. No stopping until 15 minutes is over! It’s really hard. Then when they go to sleep, I ask them to remind themselves that they’ve now worried all their worries, and they can gently set those thoughts aside because they won’t forget their worry, it’s written down (I think worry is one way a mind tries hard to stop you from forgetting to DO something about the worry!). People can throw the paper away in the morning because then it begins all over again.

Usually people who score high on the PCS also find it hard to be realistic about their pain, they’ll use words that are really emotive and often fail to notice parts of the body that aren’t in pain. By noticing the worst, they find it tough to notice the best.  I like to guide people to notice the unloved parts of their body, the bits that don’t hurt – like the earlobes, or the belly button. I’ll offer guidance as to what to notice while we’re doing things, in particular, I like to guide people to notice those parts of the body that are moving smoothly, comfortably and that look relaxed. This is intended to support selective attention to good things – rather than only noticing pain.

Finally, I give more support to those who tend to be more worried about their pain than others. So I might set the goals a little lower – walking for five times a week, two days off for good behaviour rather than every day. Walking for five minutes rather than ten. And I’ll check in with them more often – by text, email or setting appointments closer together. It’s important for people who fear the worst to experience some success, so setting small goals that are achieved can build self efficacy – especially when I try hard to offer encouragement in terms of what the person has done despite the odds. So, if the person says they’ve had a real flare-up, I’ll try to boost confidence by acknowledging that they’ve come in to see me even though it’s a bad pain day, that they’ve tried to do something instead of nothing, that talking to me about the challenge shows guts and determination.

People who see the glass as half empty rather than half full are just people. Like you and I, they’re people who have a cognitive bias. With support, we can help people view their pain differently – and that process applies to all of us, not just those with high scores on the PCS.

 

Abbott, A. D., Tyni-Lenne, R., & Hedlund, R. (2010). The influence of psychological factors on pre-operative levels of pain intensity, disability and health-related quality of life in lumbar spinal fusion surgery patients. Physiotherapy, 96(3), 213-221. doi:10.1016/j.physio.2009.11.013

Elfving, B., Andersson, T., & Grooten, W. J. (2007). Low levels of physical activity in back pain patients are associated with high levels of fear-avoidance beliefs and pain catastrophizing. Physiotherapy Research International, 12(1), 14-24.

Langley, P. C. (2011). The prevalence, correlates and treatment of pain in the european union. Curr Med Res Opin, 27(2), 463-480. doi:10.1185/03007995.2010.542136

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:http://dx.doi.org/10.1080/08870440108405493

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)

What difference does it make to know about psychosocial risk factors?


The “psychosocial yellow flags” or risk factors for developing ongoing disability after a bout of acute low back pain have been promulgated in New Zealand since 1997. Introduced as part of the Acute Low Back Pain Guidelines, the yellow flags were lauded both locally and internationally and subsequently there have been many international guidelines which have adopted this kind of integration. But what exactly do we do with that information? How does it help if we find out that someone is really afraid their pain means something awful, or if they fear their life will never be the same again, or if they truly worry about doing movements that provoke their pain?

Truth to tell, although there have been a lot of studies examining the relevance of psychosocial risk factors, the uptake among clinicians has been fairly abysmal. This is particularly so among clinicians who work either mainly with acute musculoskeletal pain, or amongst those who are mainly involved in treated the body. One physio I know said she got the impression during her training that psychosocial factors “are the things we can blame when our treatments don’t work”.

I think part of the problem is the focus on assessment “technology”. There is a proliferation of questionnaires that can be used to help spot the person who’s likely to have difficulty recovering. We have STartBack, Orebro Musculoskeletal Questionnaire, Pain Catastrophising Scale, Tampa Scale of Kinesiophobia, Depression Anxiety Stress Scale, Pain Self Efficacy Scale – most of which are known by their abbreviations, so it’s like an alphabet soup! But despite knowing about these questionnaires, and perhaps even administering them to people we think might need assessment, once the results come in it’s pretty difficult to know what to do next.

So what if a person reports really high levels of catastrophising? Or that they’re very high on the Fear of Injury/Reinjury on the TSK? Or that they have the lowest ever score on the PSEQ? What on earth do you do to make an impact?

Some people are very actively engaged in “Pain Education”. It’s given to absolutely everyone because “the evidence says” it “works”. Pain reduces. People get engaged in their exercise. Life returns to normal.

Some people refer immediately on to a psychologist. Let them deal with the “difficult” patients.

Others just carry on as normal but in the back of their mind have the “out” that “Oh but they have yellow flags” – and drop their expectations accordingly.

To me that’s just not good enough, and it suggests to me that we need to learn more about what these measures mean – and what to do differently as a result.

There’s a couple of problems though:

  1. How do we choose who to give a questionnaire to? – do we rely on “intuition” or do we give them out to everyone?
  2. Which questionnaires do we use? There’s no “gold standard” – just a mix of various measures that tap into part of the picture…
  3. How much do we rely on strong RCT’s examining whole treatment packages, versus how much do we rely on principles of behaviour change and knowledge of the underlying theories relevant to pain and disability?
  4. What if our clinical reasoning models are completely silent on the work involved in supporting people who present with these risk factors – what if our clinical reasoning models suggest that this work is not all that important compared with the “real” work of tissues and muscles and movement?

Here are my thoughts on what we can do.

I think we should give screening questionnaires to everyone who comes in with an acute bout of musculoskeletal pain, and I think there are a couple that really work well – Orebro is clearly one of them, PCS or PASS are both useful, and I think it’s helpful to screen for mood problems. Why do I think everyone needs these? Well, it’s easier to give them to everyone than to rely on our terribly inaccurate intuition. The risk of failing to identify someone who needs more support is high (and the consequences of omitting this is serious). By routinely administering screening measures we can de-stigmatise the process (though there shouldn’t be any stigma associated with understanding that pain involves the whole person!). We can make the administration easy by integrating it within routine clinic entry process – and by using electronic forms of each questionnaire we can make entering and scoring them easy.

We then need to learn what the questionnaires actually measure – not just the total score, but the subscales as well. Then we need to use those subscale scores to understand what we need to ask the person when we see them face-to-face. This helps us begin to understand the person and how they came to develop these beliefs and attitudes, and in doing so we can develop greater empathy for their experience – and alter our treatments to reflect their needs.

For management, I think we have to, at this stage, step beyond the RCT for evidence. There’s a few reasons for this: one is that RCTs naturally omit individual responses to the treatment meaning we lost the detail as to who responds to which aspect of the treatment. Another is that RCTs often group patients together to ensure power is reached – but in doing this, omit important individual differences. And finally, each person we see is a unique individual with a unique interaction between the various factors influencing their presentation – and there are simply insufficient RCTs to account for these differences. Does this mean we stop using evidence? Oh no!! It just means we need to look at the principles behind many treatments – what are the guiding principles and why might they apply to this person at this time? Finally we need to monitor outcomes so we can establish whether our approach actually helped.

Finally, I think our clinical reasoning models need to include important aspects of treatment that we vary, often without being aware that we do.

For example, if we see someone who scores very high on the PCS and tends to ruminate or brood on the negative, we can’t go ahead and give that person the same set of exercises or activities we’d give someone who is quite confident. We’ll need to lower the physical demands, give really good explanations, take the time to explain and de-threaten various sensations the person may experience, we’ll probably need to move slowly through the progressions, and we’ll definitely need to take time to debrief and track progress.

These “invisible” aspects of treatment are, I think, often the most important parts – but they’re often not mentioned in clinical protocols, and perhaps our skill in titrating the challenges we give our patients is not well developed. These factors incorporate psychological techniques of behaviour change – things like reinforcement, motivational interviewing, problem solving, Socratic questioning, how to fade support, how to bolster confidence, how to vary the environment, and how to avoid pliance and tracking (or going along with things rather than truly integrating the learning). If we want to work with people and help them change their lives, we need to learn how people change behaviour. That means, I’m afraid, learning some psychology…!

A new year


So 2016 is over, and 2017 is here. As usual, I find the new year to be a time for reflecting on what is important in life, and what I’d like to see more of this year. Usually I’ll want more balance. More space between frantic activity. Maybe even less frantic activity! And I pretty much always want to learn something new. But this year I want to be a bit different. Yes I’ve been thinking about what’s important, and yes I want more balance, but this year I want to work on a new project as part of this blog.

I’ve been writing for so many years, and one of my main reasons for doing so is to bridge the gap between what’s found in research, and what clinicians are doing in their practice. I want to inform and I want to infuse that information with a strong sense that alongside what we know from research we need to remember these things:

  1. We work with people – not doing things TO people (even if we do things to people), but we have a window of maybe an hour in a clinic in which everything we say and everything we do is pondered over by the people we see. And believe me, people will interpret what we say and do and then make their own decision about what happens next.
  2. We could all become a patient. That’s a bit humbling because we don’t expect we’ll develop a problem, but pain is indiscriminate – it will affect anyone and everyone. Trouble recovering is somewhat more discriminating – some people are at more risk than others, but here’s the thing: there are SO MANY variables that have been known to influence recovery that we can never be truly certain that we’ll be able to dodge that bullet. So, you and I can become a patient, and our recovery may also be complex, and we may need to swallow the bitter truth that rehabilitation is plain hard work.
  3. People don’t exist in isolation. Most of our treatment philosophy and techniques focus on the person with pain. Just that person. Not their family, their employer, their friends or colleagues or mates. Just that individual. But we know that people live within a community. And that community is pretty big – especially when we think of the connections made around the interwebs! And for every time we see “a person” we ALSO need to see “a person-in-context”.
  4. We get it wrong. We all do. We fail. We don’t reason clearly. We get hooked up in our own biases. We ignore things. We look for things that confirm our own beliefs. We notice things we want to notice, and conveniently ignore things we don’t want to notice. And we often don’t even know we’re doing it. That’s a constant and ongoing tendency we all need to work hard to counter.
  5. Research often omits important variables. This world is complicated. There are so many factors influencing what happens, when, where and why. Researchers can’t control everything. And because people are messy, complicated and ornery beings, the people we see (and ourselves) don’t always fit within the parameters of what’s been found in a research study. This doesn’t mean research findings aren’t important, it just means we need to temper our tendency to adopt a new and groovy thing just because a piece of research suggests it’s very cool. And we need to recognise that, especially here in NZ, studies conducted elsewhere in the world may not work as well here in our country. And that applies everywhere and to all human-oriented research. Context is critical. What people want and believe in is also critical. Qualitative research begins to bridge the gap between experimental designs and individual variability – but it’s often considered less valuable than quantitative research.
  6. People living well with chronic pain need to inform our practice. Why? Because we can learn so much from people who have been able to see life differently. Who have taken gems from wherever they’ve found them, been able to integrate those gems into their daily lives, and are now in the best position to help us learn what worked for them – and most importantly, why it’s worked.
  7. We’re biopsychosocial beings. People are biological beings, with psychological processes that influence their actions, many of which have been picked up from the social context in which they live. Those psychosocial factors are integral to living, not some add-on, after-the-fact mess that only applies if our treatments don’t work. We ALL actively process what happens to us, and interpret these things in light of what we already know and what we think might happen next. Yes I know this model is incomplete. I know some people can think of it as reductionist. Others think it’s messy and non-scientific. Still others believe it’s useless and impractical. But whether it’s an “accurate” way of thinking about people or not, I think it can be a helpful framework from which we can begin to explore situations where people are involved.

The new project

I’ve written thousands of words. Usually about 1200 once a week on this blog alone. My intention this year is to collate that writing and sort it into some semblance of order. I intend to post short summaries on topics and link to some of my older work for details. And maybe, just maybe, there could be a book at the end of it! Whatever I manage, this year I will be learning new things, and I will be posting them up here. So keep visiting! Ask questions and comment. Be part of the conversations that can change our approach to helping people with pain. Want to join me?

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.

… a little more about Pain Catastrophising subscales


I’ve been writing about the Pain Catastrophising Scale and how to use this instrument in clinical practice these last two posts here and here because the construct of catastrophising (thinking the worst) has become one of the most useful to help identify people who may have more distress and disability when dealing with pain. Today I want to continue with this discussion, but looking this time at a large new study where the subscales magnification, rumination and hopelessness have been examined separately to understand their individual impact on pain severity and disability.

Craner, Gilliam and Sperry looked at the results of 844 patients with chronic pain prior to taking part in a group programme (a heterogeous sample, rather than a single diagnosis, so this group probably look at lot like those admitted to high intensity tertiary chronic pain management services such as Burwood Pain Management Centre here in Christchurch).  Most of the participants were female, European/white and married, and had chronic pain for an average of 10.7 years. Just over half were using opioid medication to manage their pain.

Along with the PCS, participants also completed some very common measures of disability (Westhaven-Yale Multidimensional Pain Inventory – MPI) and quality of life (SF-36), and the CES-D which is a measure of depression.

Now here comes some statistical analysis: multiple hierarchical regression! Age, sex, duration of pain and use of opioids were entered into the equation and found to account for only 2.0% variance of the pain severity subscale of the MPI – but once the PCS was added in (subscales entered separately) an additional 14% of the variance was accounted for, but the helplessness subscale was the only one to contribute significantly to the overall variance.

When Pain Interference was  entered as the dependent variable, all the same demographic variables as above contributed a meagre 1.2% of the variance, but when the Pain Severity subscale scores were added, 25.5% of the variance was explained – while the combined PCS subscales contributed 6.5% of the variance. Again, helplessness was the only subscale to contribute to Pain Interference.

Moving to quality of life – the physical subscale of the SF-36 was used as the dependent variable, and once again the demographic variables accounted for only 1.5% variance in physical QOL, with Pain Severity accounting for 23%. PCS subscales contributed only 2.6% of the variance, with only the magnification subscale being identified as a unique contributor. When the mental health subscale was used, again demographics only accounted for 1.2% of variance, with pain severity accounting for 12.4% of the variance. This time, however, the PCS subscales contributed 19.5% of the variance with both Magnification and Helplessness contributing to the variance.

Finally, examining depression, demographics contributed a small amount of variance (3.3%), with pain severity additing 9.8% of variance. The PCS subscales were then entered and contributed a total of 21% to the prediction of depression with both Magnification and Helplessness contributing to the overall depression variance.

The so what factor

What does this actually mean in clinical practice? Well first of all this is a large group of patients, so we can draw some conclusions from the calculations – but we need to be a little cautious because these participants are a group who have managed to get into a tertiary pain management facility. They’re also a group with a large percentage using opioids, and they were pretty much all European – and from North America, not New Zealand. I’m not sure they look like the people who might commonly come into a community-based facility, or one where they’d be referred directly from a GP or primary care centre.

At the same time, while this group may not look like the people most commonly seen for pain management, they share some similar characteristics – they tend to magnify the “awfulness” of pain, and then feel helpless when their pain is bothering them. Surprisingly, I thought, ruminating or brooding on pain wasn’t a unique contributor and instead the helplessness scale contributed the most to pain severity, pain-related interference (disability associated with pain), poor mental health quality of life, and low mood, while magnification scale contributed to poorer physical health quality of life, mental health quality of life and low mood.

What this means for practice

The authors suggest that the construct measured by the helplessness subscale might be a factor underlying poor adaptation to life’s difficulties in general, leading to passivity and negative emotions. They also suggest that magnification might be a unique contributor to perceiving obstacles to doing the things we need to do every day, while hopelessness might mean people are less likely to participate in enjoyable activities and then in turn contribute to feeling low.

Importantly, the authors state: “We offer that simply collapsing the 3 dimensions of this phenomenon (ie, rumination, magnification, helplessness) may actually conceal nuanced relationships between specific dimensions of catastrophizing and outcomes that would might inform treatment approaches.” Looking at the overall scores without thinking about the subscales is going to give you less information to use for individualising your treatment.

In a clinical setting I’d be reviewing the individual subscales of the PCS alongside both disability and mood measures to see if the suggested relationships exist in the scores this person has given.

I’d be taking a look at the repertoire of coping strategies the person can identify – and more, I’d be looking at how flexibly they apply these strategies. Extending the range of strategies a person can use, and problem-solving ways to use these strategies in different activities and contexts is an important part of therapy, particularly occupational therapy and physiotherapy. Another approach you might consider is helping people return to enjoyable activities that are within their tolerance right here, right now. By building confidence that it’s possible to return to things that are fun we might counter the effects of helplessness, and help put pain back where it belongs – an experience that we can choose to respond to, or not.

I’d also be taking a look at their tendency to avoid feeling what their pain feels like, in other words I’d like to see if the person can mindfully and without judging, complete a body scan that includes the areas that are painful. This approach is intended to help people notice that alongside the painful areas are other nonpainful ones, and that they can successfully be with their pain and make room for their pain rather than attempting to block it out, or over-attend to it. The way mindfulness might work is by allowing people to experience the sensations without the judgement that the experience is bad, or indicates some terrible catastrophe. It allows people to step back from the immediate reaction “OMG that’s BAD” and to instead take time to view it as it actually is, without the emotional halo around it.

Pain catastrophising is a useful construct – but I think we need to become more nuanced in how we use the scores from the questionnaire.

Craner, J. R., Gilliam, W. P., & Sperry, J. A. (2016). Rumination, magnification, and helplessness: How do different aspects of pain catastrophizing relate to pain severity and functioning? Clinical Journal of Pain, 32(12), 1028-1035.

When do we need to say we’ve done enough?


This post is food for thought for both clinicians and people living with pain. It has come about because of a conversation on Facebook where some clinicians felt that people with pain are only being offered the option to “learn to live with pain” when their pain intensity could either be reduced or go completely.  And this conversation is one repeated countless times around the world when those living with persistent pain seek help for their disability and distress.

I’m going to declare my hand right now: I think a the problem in chronic pain management isn’t that people get offered “pain management” or “learning to live with pain” or “accepting pain” too often – I think it’s not happening often enough, nor soon enough. But let me unpack this a little more…

We know that in New Zealand at least one person in every six lives with chronic pain that has gone on for more than six months (Dominick, Blyth & Nicholas, 2011). We also know the seven day prevalence of low back pain in New Zealand is 35% (men) and 48% (women) (Petrie, Faasse, Crichton & Grey, 2014).

Treatments for painful conditions abound. From the simple over-the-counter approach (medication, anti-inflammatory creams, hot packs, cold packs) to hands-on therapies (massage, osteopathy, chiropractic, physiotherapy), to exercise therapies (Pilates, core strengthening, gym programmes, spin classes, walking, exercise in water), and finally to the multitude of invasive therapies (injections, neurotomies, decompression surgery, fusion). There is no shortage of treatments that aim to get rid of pain, fix the problem and get life back to normal. And for the most part these treatments provide modest improvement in both pain intensity and functional gains. For low back pain it seems there is no single wonderful treatment that works for everyone – hence the proliferation of treatments! (cos if there was a single treatment that worked, we’d all be offering it – like we do with a broken bone or appendicitis).

Here’s a question: if pain “management” (ie helping people learn to live with their pain) was the main offering to people living with pain, wouldn’t there be a heap of places to get this kind of treatment? At least in New Zealand there are relatively few pain management centres although there are many, many places to go for pain reduction.

I’ve tried to find studies looking at how people are told they have persistent pain that won’t be cured. Strangely, I have had incredible difficulty finding such studies. They may be there in the research literature – but they’re fairly uncommon and hard to find. And given how poorly low back pain guidelines are followed despite being promulgated since at least 1997, even if there were studies examining the best way to convey this news, I’d be surprised if anything was routinely incorporated into clinical practice.

So, in my opinion there are many more clinicians offering to help reduce pain than there are those offering to help people “learn how to live with pain”.

I was asked recently “when you do decide to stop pursuing pain reduction?” I think I said “it’s ultimately the decision of the person living with pain” – but it’s complicated by the way we as a culture perceive this option. I think most people would be horrified to think “I’m going to have a lifetime of living like this” when our beliefs about pain are influenced by and attitude that “pain = suffering”, “pain is unnatural”, “pain is a sign of something badly wrong”, “pain is something to get rid of”. I know when I was told “I’m sorry but there’s nothing more we can do for your pain” I was terribly upset thinking I had a lifetime of feeling awful to look forward to! I was 22 and had low back pain that would not go away after 18 months. I’m now 52 and I still have pain – but I can tell you that I have done almost everything I’ve wanted to including SCUBA diving, tramping, fishing, dancing, working full time (overtime), and parenting.

When do we begin to think about living with pain rather than curing it? I think we need to take a hard look at what this sentence means.

Firstly it means living. Life continues whether we’re feeling like we’re moving forward, or we’re putting things on hold to pursue a particular goal. Life doesn’t actually stop – but the things we want to experience, the things we want to do change over time. Our focus at the age of 22 is quite different from our focus at age 52 – and I hope it will change again at age 82! We don’t get to hit the replay button and live life all over again. We get one shot at it. This could feel quite awful if we’re contemplating a life where looking for pain relief is our primary goal – especially when that process involves an endless round of hope then despair as treatments are tried – and then don’t quite work out. Even the process of looking for treatments is slow, fraught with anxiety, and it eats up time in a week. For me, taking time out from living to pursue a treatment that may work means a process of weighing up the costs against the benefits. The costs include time, energy, emotional investment in the result, and the discomfort of the treatment itself. The benefits? Well, that depends.

The second part of that sentence is “with”. Living with pain. To me this means establishing my willingness to experience something I don’t enjoy – and believe me, I’m not a fan of pain! If all I have to look forward to is pain, pain, pain I’m not keen on doing it. BUT I am keen on living and bringing pain along with me (because frankly, my pain is coming along for the ride anyway). Living with pain to me means making room to experience pain fluctuations while doing things that bring value and meaning to my life. It means I ache – but I have a beautiful garden. I have sore legs – but I’ve been dancing. I have an aching back and neck and arms – but my house is clean. Here’s the thing: even if I didn’t work in my garden, dance or clean my house I’d STILL be sore! And I’d be bored, feel like I hadn’t achieved anything, and would have had to ask other people to help because many of those things still need doing.

The thing is, pain ≠ suffering.

When do we make a decision to stop pursuing pain reduction? Well, if I’m honest I’m still on the lookout for something that will help reduce my pain. And I think anyone who does live with persistent pain would agree that we don’t really want to have this experience, just like people who have cancer don’t want it, or diabetes or stroke or any of the myriad other chronic conditions humans are prone to getting, especially as we age. When asked, I’m sure most people with chronic pain would say “Yes” to pain reduction as a goal. BUT, and this is important, living life as fully and richly as we can is just as important.  I would bet that anyone with any of those chronic conditions would also just love to have them cured too.

But pain is a funny thing, there are myths and unhelpful beliefs coming from clinicians and our cultural norms about pain being a bad thing that must go. Compared with the beliefs and attitudes about other chronic conditions, this is unhelpful. We don’t find health professionals constantly pursuing treatments to “get rid of” diabetes, the focus is on management. And we accept that people who have cancer may choose to no longer accept treatment – and we support them by providing good hospice care. How often do people with chronic pain get (a) support to make a decision to live with their pain and (b) support to learn to do this well without feeling like second class citizens who have failed. We even have a group of clinicians calling people who haven’t responded to their treatments “failed back syndrome” as if the person’s back has failed rather than the treatment failing.

What makes me decide to pursue a new treatment that promises to reduce my pain? Well, it has to fit into my life. It can’t interfere with what’s important to me in terms of time, energy or discomfort. The odds need to be pretty good for me to even look at it – I want to see more than a single research paper showing its effectiveness. I would have to trust the clinician, and they’d have to respect me and my lifestyle and priorities. I’d want to make sure that clinician was going to stick with me and help me decide whether it’s worth doing. I’d want to see that the treatment would help me achieve my goals and priorities – otherwise I’m not really interested.

Is this because I’m weird (say yes!)? Or that I have less intense pain than other people? (nope, because you can’t compare my pain with anyone else’s, and because pain intensity ratings are strongly influenced by distress, mood, anxiety, how much pain interferes with life, attention, culture yada yada yada (Linton & Shaw, 2011). I think it’s because right now I’m too busy living, I get more joy and satisfaction from doing things that make me feel like myself. But remember I’ve been doing this since I was 22. And it’s a process. And I’m weird. I am a pain geek.

The thing is, unless clinicians promote living well with pain as an equally valid option to trying to get rid of it, people will continue to think that it’s impossible to have a really good life unless their pain is gone. And that, to me, is a tragedy, because we only have one life to live.

 

Dominick, C., Blyth, F., & Nicholas, M. (2011). Patterns of chronic pain in the New Zealand population. New Zealand Medical Journal, 124(1337), 63-76.

Linton, S. J., & Shaw, W. S. (2011). Impact of psychological factors in the experience of pain. Physical Therapy, 91(5), 700-711. doi:10.2522/ptj.20100330

Petrie KJ, Faasse K, Crichton F, Grey A. How Common Are Symptoms? Evidence from a New Zealand National Telephone Survey. BMJ Open. 2014;4(6). doi: 10.1136/bmjopen-2014-005374.