Pain

One way of using a biopsychosocial framework in pain management – vi


I could write about a BPS (biopsychosocial) model in every single post, but it’s time for me to explore other things happening in the pain management world, so this is my last post in this series for a while. But it’s a doozy! And thanks to Eric Bowman for sharing an incredibly relevant paper just in time for this post…

One of the problems in pain management is that there are so many assessments carried out by the professionals seeing a person – but very little discussed about pulling this information together to create an overall picture of the person we’re seeing. And it’s this aspect I want to look at today.

My view is that a BPS approach provides us with an orientation towards the multiple factors involved in why this person is presenting in this way at this time (and what is maintaining their presentation), and by integrating the factors involved, we’re able to establish a way to reduce both distress and disability. A BPS approach is like a large-scale framework, and then, based on scientific studies that postulate mechanisms thought to be involved, a clinician or team can generate some useful hypotheses through abductive reasoning, begin testing these – and then arrive at a plausible set of explanations for the person’s situation. By doing so, multiple different options for treatment can be integrated so the person can begin to find their way out of the complex mess that pain and disability can bring.

The “mechanisms” involved range from the biological (yes, all that cellular, genetic, biomechanical, muscle/nerve/brain research that some people think is omitted from a BPS approach IS included!), to the psychological (all the attention, emotion, behavioural, cognitive material that has possibly become the hallmark of a BPS approach), and eventually, to the social (interactions with family, friends, community, healthcare, people in the workplace, the way legislation is written, insurers, cultural factors and so on). That’s one mess of stuff to evaluate!

We do have a framework already for a BPS approach: the ICF (or International Classification of Functioning, Disability and Health) provides one way of viewing what’s going on, although I can empathise with those who argue that it doesn’t provide a way to integrate these domains. I think that’s OK because, in pain and disability at least, we have research into each one of these domains although the social is still the most under-developed.

Tousignant-Laflamme, Martel, Joshi & Cook (2017) provide an approach to help structure the initial domains to explore – and a way to direct where attention needs to be paid to address both pain and disability.

What I like about this model (and I urge you to read the whole paper, please!) is that it triages the level of complexity and therefore the intervention needed without dividing the problem into “physical” and “psychosocial”. This is important because any contributing factor could be The One to most strongly influence outcome – and often an integrated approach is needed, rather than thinking “oh but the biological needs to be addressed separately”.

Another feature I like about this model is the attention paid to both pain and disability.

Beginning from the centre, each of the items in the area “A” is something that is either pretty common, and/or easily modified. So, for example, someone with low back pain that’s eased by flexion, maybe has some osteoarthritis, is feeling a bit demoralised and worries the pain is going to continue, has a job that’s not readily modified (and they’re not keen on returning) might need a physiotherapist to help work through movement patterns, some good information about pain to allay their worries, an occupational therapist to help with returning to work and sleeping, and maybe some medication if it helps.

If that same person has progressed to become quite slow to move and deconditioned, they’re experiencing allodynia and hyperalgesia, they have a history of migraine and irritable bowel, their sleep is pretty rotten, and they’re avoiding movements that “might” hurt – and their employer is pretty unhappy about them returning to work – then they may need a much more assertive approach, perhaps an intensive pain management programme, a review by a psychiatrist or psychologist, and probably some occupational therapy intervention at work plus a graded exposure to activities so they gain confidence despite pain persisting. Maybe they need medications to quieten the nervous system, perhaps some help with family relationships, and definitely the whole team must be on board with the same model of healthcare.

Some aspects are, I think, missing from this model. I’d like to see more attention paid to family and friends, social and leisure activities, and the person’s own values – because we know that values can be used to help a person be more willing to engage in things that are challenging. And I think the model is entirely deficits-based meaning the strengths a person brings to his or her situation aren’t incorporated.  Of course, too, this model hasn’t been tested in practice – and there are lots of gaps in terms of the measures that can be used to assess each of these domains. But as a heuristic or a template, this model seems to be practical, relatively simple to understand – and might stop us continuing to sub-type back pain on the basis of either psychosocial risk factors or not.

Clinicians pondering this model might now be wondering how to assess each of these domains – the paper provides some useful ideas, and if the framework gains traction, I think many others will add their tuppence-worth to it. I’m curious now to see how people who experience low back pain might view an assessment and management plan based on this: would it be acceptable? Does it help explain some of the difficulties people face? Would it be useful to people living with pain so they can explore the factors that are getting in the way of recovery?

Tousignant-Laflamme, Y., Martel, M. O., Joshi, A. B., & Cook, C. E. (2017). Rehabilitation management of low back pain – it’s time to pull it all together! Journal of Pain Research, 10, 2373-2385. doi:10.2147/JPR.S146485

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One way of using a biopsychosocial framework in pain management – v


Theories are an important part of scientific development. Theories are essentially a collection of propositions or hypotheses that build a picture of what is in order to predict or control or somehow explain what’s going on. The extent to which a theory’s predictions represent what actually happens, given a set of circumstances, allows us to place more or less faith in the adequacy (or perhaps accuracy) of that theory. The problem with social theory is that there are so many complex interactions between variables that it’s very hard to generate hypotheses that represent what actually goes on in the world – so we end up with skinny theory that explains very little, and in turn this allows naysayers to argue “oh but it isn’t so”.

A biopsychosocial framework is one of those messy, complex theoretical models of “the way people are” that beg for people to argue against it. “It’s too complex”, “it’s too broad”, “it’s too reductionist”, “it’s not clinically useful” – all points against this way of viewing people. Yet, after years of using this model, I still find myself unable to find an alternative way of attempting to understand my two clinical questions: why is this person presenting in this way at this time (and what is maintaining their situation), and what can be done to reduce distress and disability?

Social theories are not something many health professionals are introduced to during their undergraduate training. We’re not trained to understand topics like structure of societies, organisations, groups and everyday lives and how they come about. We don’t typically get trained to think about power and who defines what is normal and abnormal, or who generates names for things – classifications, taxonomies, diagnoses. We rarely get to unpack the hidden discourse of who holds power in healthcare delivery, policy development – even social spending on health.

The people I typically see, living with persistent pain, are often from what posh folks call “the wrong side of the tracks”. Many people don’t have good employment histories. They may not have savings, they may live off a benefit. They are often not well-educated, having left school to do manual work. Their daily routines might be chaotic, and the idea of “keeping fit” or “eating well” doesn’t occur to them because their lives are about getting through the day, loving the family they have, and maybe looking towards a tomorrow where things might be different.

In pain management, we’ve not really spent much time examining the kinds of social relationships or social structures in which the people who really struggle with managing pain come from.  I’m not sure I’ve read very much research exploring, for example, whether people who have two jobs and live on a minimum wage experience greater difficulty developing skills in pacing their activities. I’ve not heard much from the people who live in this way expressing their understanding of what contributes to their distress and disability. I don’t see much about how uncertainty of employment pushes people into unsuitable work – while work is good for most people, what about those minimum wage jobs with unsavoury work environments, precarious employment tenure, cold, wet, smelly and physically demanding jobs with little prospect for the future? I don’t see very much about the effect of someone living on the bare bones of their threadbare trews going to see a medical specialist dressed immaculately in a bespoke suit and silk tie, with the handmade shoes and a language of healthcare that is incomprehensible to anyone other than another similarly clad specialist.

For a sociopsychobiological model of pain (yes, that’s a word, and no I haven’t got it backwards – see this) to gain traction, I think it’s timely to ponder the way our communities view persistent pain. Communities include our own healthcare communities – the manual therapy, physical therapy, occupational therapy, nursing, medical enclaves that use special language and dress in certain ways to demonstrate that we know our stuff. And we need to take a minute to understand the communities the people we hope to help come from.

At the stroke of a keyboard, the labels we give to someone – fibromyalgia, “degenerative changes”, “pre-existing condition”, “depression” – alter the treatment that person receives within healthcare. No question about it – if a person is receiving accident compensation (in NZ it’s ACC) and someone gives that kind of label to them, they’re going to the bottom of the health queue. The vagaries of our system mean that person doesn’t receive work-related rehab, they’re disentitled from ACC, no more weekly compensation, and oh yes they now go through the dehumanising process of attending the “Ministry for Social Development”.

I’m not arguing against the way our ACC legislation is written. And I’m not certain that receiving compensation is always a good thing. What I am pointing out is that when health professionals view the person in front of them as “other” – beneficiary, ACC claimant, pain patient – we are issuing a social declaration. And that means we’re exerting a degree of power over them and their lives. The labels we give have power. And this has a significant impact on the way that person views their pain, and the treatment they may receive.

I think until we begin to include, extend, and invite people living with pain to co-investigate their experience and to contribute to our health professional education (including scientific meetings), we’ll carry on thinking of ourselves as somehow superior to, and certainly more powerful than, the people we hope to treat. Hats off to Rajam Roose for developing the San Diego Pain Summit where this year she’s included a patient panel to give an insight into what it means to hear “your pain is just an output of your brain”. Can we have more please.

What can we do to reduce distress and disability? One thing we can do is begin a conversation about persistent pain being something that anyone can experience. It’s just that people without resources end up dealing with not only pain but also lack of power to change the way it’s treated.

One way of using a biopsychosocial framework in pain management – iv


And yes! There’s more to this series of posts on how I use a biopsychosocial model in practice!

Today’s post is about moving from a conceptual model to a practical model, or how we can use research in our clinical reasoning.

A biopsychosocial model (BPSM) as envisaged by Engel was a framework for clinicians to think about why this person is presenting in this way at this time (and what may be maintaining their situation), as well as what could be done to reduce distress and disability. Engel wanted clinicians to go beyond disease processes, isolated from the people experiencing them, and to explore aspects of how the person coped with everyday challenges (including health), the factors that influenced their decision that their health problem was indeed a problem, and the context of seeking healthcare.  He wanted clinicians to be scientific about how they generated hypotheses which could then be tested in clinical practice, and ultimately confirm or disconfirm the contribution of that factor.

The “bio” aspect of pain (which is a contentious word – I’ll comment in a bit) involves disease processes, trauma, all the biological aspects prior to conscious awareness of the “ouch” we know as pain. Theoretical developments in this area include all the work being conducted in terms of understanding anatomy and physiology of the human body, from molecular study (information transmission from one neurone to another); detailed understanding of spinal cord mechanisms; of the role of glia; of inflammatory processes; of genetic and epigenetic changes; of relationships between blood flow to and from various parts of the brain; of biomechanics; of normal healing processes – and so on. There’s no lack of information being generated by researchers undertaking basic science about the biological mechanisms involved in our experience of pain. Because I typically see people with persistent pain that has been present for maybe 12 months or more (usually much longer than that), I rely on the work of my colleagues to make a good diagnosis. Most people have had more investigation than is probably helpful for them, and I think we can use Clifford Woolf’s broad mechanisms as a reasonable stance when considering an underlying mechanism involved in a person’s pain. Essentially he identifies four main mechanisms: nociceptive, inflammatory, neuropathic and what is now known as “nociplastic” (where the nociceptive system appears to have a problem with processing information).

Yes, we can argue that our current state of understanding is incomplete and there is more to learn, but by working from these basic mechanisms I think we can begin to work on the “bio” part of a biopsychosocial model with a degree of confidence. For my work, anyway, these mechanisms seem to provide a reasonable framework from which the “bio” part of management can begin.

But this is where many clinicians start – and stop. Directly treating, for example, inflammation, certainly provides a reduction in pain – for example, my partner who takes Humera for his ankylosing spondylitis. He no longer experiences inflammatory pain and as his CRP levels reduced, so too did his pain. We can see similar effects when someone has a grotty old hip joint replaced, which removes nociceptive input, ultimately leaving them with a shiny new and painfree hip (in most cases). But as my partner found out, having no pain doesn’t immediately change old habits.

His situation is a nice illustration of the interaction between a disease process which responded really well to a drug that eliminates inflammation, and his beliefs and behaviour which wasn’t changed. Let me explain – once his drug kicked in and he had no pain, he found it odd not to have to think about his pain when climbing hills. It took him about a month or two to fully return to hill climbing in the way he’d done before his anky spond started. That’s right – no pain for a month or two, but that long before he felt confident to go about his activities. And he’s not a man who worries much about his pain!

To add some theory to this, his beliefs (that if he climbed hills a full speed he would inevitably end up with a very sore back) led to him having learned not to go a full pace (through both classical and operant conditioning). We could call this “pain-related fear and avoidance” – or “fear avoidance”. This is one theory that has been extensively researched, and we can integrate the hypotheses generated from this theory into our understanding of why my partner initially had some hesitation about climbing hills. Flowing on from this, we can consider treatments that have been found useful to address his hesitation.

The first treatment could be “explaining pain” to him. Now that wasn’t useful in this case because – oh yeah – his pain had gone! And although he knew his inflammatory pain wasn’t going to harm him (otherwise he’d never have been a high country fire fighter for 20 years despite his anky spond!), he didn’t like the after-effects of aggravating his pain. What helped was addressing his anxiety about the potential for a big flare-up – and this was primarily about beginning at a level that was just beyond his “normal” hill climb, and gradually progressing.

This superficially looks like “exercise” – but it’s exercise with a twist. My partner is as fit as a buck rat. His cardiovascular fitness was fine. Gradually increasing his hill walking wasn’t about increasing fitness – it was about helping him approach an activity that he was a tad concerned might flare his pain up, leading to a rotten night’s sleep (as it had in the past). In fact, this “treatment” was almost all about reducing avoidance by exposing him to things that increased his anxiety just a bit – enough for him to establish that the rotten sleep consequence didn’t happen.

So a biopsychosocial approach to his recovery involved the biological which quickly resolved his pain but left him with some concerns (reasonable ones I think) about pushing himself too hard. Addressing those concerns by taking a theory developed originally from phobia research, applying it to his situation and developing a treatment based on this theory, has led to his return to full participation. Using research-based information to address another part of “why is this person presenting in this way at this time, and what might be maintaining this situation” involves thinking beyond the disease process, and into understanding the problems the person identifies. It means thinking beyond a single discipline. It means reading widely and thinking creatively. That was a good part of Engel’s original proposition.

 

One way of using a biopsychosocial framework in pain management – iii


Before Christmas and the New Year break I was writing about how I use a biopsychosocial model in pain management – and I haven’t finished!

To review: The first post was about the context or the ideas behind Engel’s original model, and my two key clinical questions – why is this person presenting in this way at this time, and what can be done to reduce distress and disability?

The second post was about classical and operant conditioning and why these models are useful when we’re thinking about what a person does when they’re sore – and how their actions communicate to people around them. I also pointed out that many of these actions are not conscious, but have been learned and shaped from childhood, leading to a myriad of ways people express themselves when they’re in pain.

One of the criticisms of this approach to pain management is that “the model” isn’t scientific (therefore doesn’t lend itself to generating hypotheses that can be tested), and a second is that it’s “too fuzzy” and doesn’t specify what should be “in” and what should be “out” in clinical reasoning. I don’t agree with either of these statements and today I hope to present why.

Is a BPSM truly a “model”? What’s a model anyway? – one definition I’ve found is “In science, a model is a representation of an idea, an object or even a process or a system that is used to describe and explain phenomena that cannot be experienced directly.” In other words, they’re like a metaphor, bridging between something known and something abstract or unfamiliar. Models may be extremely detailed and mathematical, but may also be conceptual and broad. BPSM is probably the latter – a conceptual model from which we’ve developed some useful and testable hypotheses.

Engel himself described this as a scientific model, saying that it “enables the physician to extend application of the scientific method to aspects of everyday practice and patient care heretofore not deemed accessible to a scientific approach” (Engel, 1980, p.  535). He goes on to say that the doctor’s tasks are to find out what and how the patient is feeling, then to explanations (hypotheses) for the patient’s feelings and experiences, and then to test those hypotheses via clinical and laboratory studies (p. 536). Engel had some ideas about how a physician might generate hypotheses – based on his knowledge of general systems theory (von Bertalanffy, 1968). Engel appealed to von Bertalanffy’s idea that systems are a hierarchically arranged series of units, with the level of analysis dependent upon the complexity and unit of measure. In other words, molecular analysis is appropriate when cells and physiology are the unit of analysis, while the quality and influence of social connections are appropriate when looking at the influence of community and legislation on an individual’s behaviour.

The notion that a BPSM approach is “too fuzzy” and doesn’t provide structure is quite true: there’s not a lot of explanation as to how the various levels within a hierarchical system might interact. Interestingly, I think this problem is still relevant today!  While we know a lot about the brain, and a little about the mind – we don’t know how brain produces “mind”, although some philosophers and neuroscientists have taken a stab at it (thinking Andy Clark amongst others here). Similarly, although we know a lot about thoughts, beliefs and even relationships, we don’t know nearly as much about how thoughts and beliefs are adopted by a community, although Daniel Dennett has some thoughts about this.

So, it’s hardly surprising that when it comes to pain, we struggle to understand how biological processes, psychological processes and social ones interact to produce the experience of one person presenting for treatment at this time in this way – but this does not mean we should ignore what we DO know, which is that within each domain there is much to explore!

My preference is to draw on Brian Haig‘s idea of an Abductive Theory of Scientific Method, and in particular this paper on clinical reasoning, scientific method and abductive reasoning. The basic idea is that we recognise the existence of a phenomenon because either we’ve seen it before, or we’ve read about it. We distinguish between random events and a phenomenon because these appear to be consistent and repeated. Then we begin to generate some hypotheses to explain the presence of this phenomenon. Abduction is the process of studying what we see/observe/know (“facts”) and developing a theory to explain them (or generating a hypothesis). We then go about testing that hypothesis – and while we never truly confirm it, we can reject an alternative hypothesis tested against the first. As a result we arrive at what we can call a plausible explanation – something that “makes sense”, given what we’ve observed, and what we know about the world and how it works.

More about this geeky stuff next week. Meanwhile I think it’s worth pondering this: in “usual science” we somehow arrive at a hypothesis, and then set about testing it. No-one, it seems, knows where the original hypothesis comes from – and it’s rarely truly acknowledged. Researchers typically look for “gaps in the literature”, something that hasn’t been asked or answered yet, but what if you happen to be a clinician? I think clinicians routinely observe “interesting things” that, if we took some time to measure them, might be a phenomenon. Something that hasn’t yet been explained. I also think we have opportunities to be scientific about how we investigate what we see and do, if we’re prepared to be systematic and think about how we might control for confounds/bias. And I think those edges between levels within a hierarchy or between domains might be fruitful areas for clinicians to be exploring – bringing us to a practical application of Engel’s BPSM.

ENGEL, G. L. 1980. The clinical application of the biopsychosocial model. The American Journal of Psychiatry, 137, 535-544.

HAIG, B. D. 2008. Scientific method, abduction, and clinical reasoning. Journal of Clinical Psychology, 64, 1013-1018.

The new year begins


For some of you, the New Year has already started, but I’ve been in a lovely position where I’ve been on leave and haven’t yet started “work” – though the work of living is always present!

It’s traditional at this time to year to review the past year and plan for the coming months, so today’s post is a few musings on both.

Last year I noticed I’d been working on this blog for nearly 10 years! Astonishing really, because it was intended to be a learning experience for me during my recovery from a mTBI. It kinda grew like Topsy, and here I am 10 years down the road still blogging, albeit not so often as in the first couple of years. Over that time I’ve commented on a whole bunch of articles, made a few blunders, and put my thinking out in the public arena in a way that Academic journals just don’t really allow.

Some people would argue that my analysis is lightweight because I don’t leap into the depths of statistical analysis and research design in my commentaries. Others think I spend far too much time pondering the psychosocial and – how could I – omitting the biological. Some don’t like my reference to a biopsychosocial “model”, while others wonder what an occupational therapist is doing writing about pain psychology.

Blogging is a personal pursuit without written rules.  I muse about things as part of my own processing, plus to hopefully put some useful content out online for those who don’t have the pleasure of ready access to articles. I’m interested in some of the research questions even poorly conducted research articles can pose. I’m intrigued by the relevance (or not) of findings to my own setting here in NZ. I’m fascinated by connections drawn by authors as they ponder the implications of their research question, findings and works by other people.

I write about topics that mean something to me. It’s a completely personal selection, reflecting papers I’ve recently read, topics discussed in social media, patients I’ve seen, and conversations I’ve had.

What’s the impact of blogging on anything or anyone? Well, that depends on the kind of “impacts” you’re talking about. Through blogging I’ve made contacts with clinicians and researchers (and social media people) from around the world. I’ve been able to contribute to some pretty special meetings. I’ve been asked to speak, to write, and have been in touch with so many people who have got in touch with me because of this platform.

My aim apart from satisfying my own curiousity, is to share information and help to translate from academic journals to the real world. Information locked up in journals isn’t likely to help a clinician who can’t access them! And reading, reflecting on, and integrating research into daily clinical practice is difficult. I hope some of what I write about helps to bridge that gap.

Why would an occupational therapist from New Zealand do this? Well the first question I’ll answer is why an occupational therapist – why not? And because occupational therapists are possibly the ultimate scavengers in terms of taking something that’s been explored by another discipline and applying it to their client’s own real-world setting. Occupational therapists apply clinical reasoning to help people DO in the real world, so in a sense we’re really translational scientists, applying what’s known from research into the unique context of our clients and what they need and want to do. As an occupational therapist I think I bring some unique skills to the process of translating research to clinical practice, and besides, I’ve been in this field for a few years now, so I want to temper some of the enthusiasm for whizzbang new things with some of the wisdom from older research. You know, the 1980’s and 1990’s produced some really foundational research in pain and pain management.

Why from New Zealand? What does NZ have in common with the “rest of the world”? We’re a relatively well-developed country, with a partly socialised healthcare system that struggles with many of the same problems as other developed countries with or without a socialised healthcare system. NZ struggles with a biomedically-dominated model of disease holding sway, limiting the availability of allied health professionals who focus on a more wholistic (no, it’s not a dirty word) view of health and wellbeing. Allied health professionals everywhere in the world have difficulty being heard over the clamour of medicine with it’s one-shot, high-tech and super-simple view of disease. Our work is not sexy. Our work involves being with people, and our currency is the time we spend communicating with people. We don’t rely on a brief consultation and a quick flick of a prescription, a jab of a needle or a slice of the knife. Our work is about messy human life, behaviour change, taking the time to listen to what’s important to our clients/patients and step-by-patient-step supporting them to achieve their goals.

Over the 10 years I’ve been writing, I’ve constantly heard bickering between various factions in allied health care. Mainly <puts on teacher face & granny glasses> amongst physically-oriented therapists. Mainly about trivia as to whether treatment X is “better than” treatment Y. Niggling time and again over ridiculously inflated claims, “trademarking” approaches that have been in practice for oh at least 30 years, heated arguments about whether nociception is important (well of course it is, duh), whether biomechanics is important (well yeah, just not all the time wrt pain), whether tape/laterality/neural stretches/posture/”correct technique” and on ad nauseum is crucial. Meh. The differences between us all are far less than the commonalities – and it’s only with the commonalities that we’ll actually make a change to the way pain management is done here in NZ, or the rest of the world.

So this year I intend to focus even more on allied health pulling together, looking for what we have in common, drawing comparisons with a reductionist model (whether that’s biomedical or biomechanical), and encouraging us to get involved in system change. Are you with  me?

 

One way of using a biopsychosocial framework in pain management – ii


Last week I discussed case formulation as one way of using a biopsychosocial framework in pain management, and I reviewed Benedetti’s description of the process of becoming aware that something’s wrong, seeking relief from that discomfort, then the “meet the therapist moment”, and finally the “receiving the therapy” steps along the way. Benedetti considers this within a neurobiological model (Benedetti, 2013), while Engel (1977) used general systems theory to frame his critique of the original biomedical model.

This week I want to look at a behavioural model. I do this partly because I think it’s been a long time since this model was brought into our discussions about pain and pain behaviour, and I do it because I think we can understand a great deal about why different people respond differently to their pain when we look at behaviour alone – before we even begin to look at beliefs or attitudes about pain.

Let’s do a little revision (Psych 101). In a behavioural model, we’re looking at two main forms of conditioning: Pavlovian or classical conditioning, and operant or instrumental conditioning. In the case of pain, we also need to revisit the distinction made between the experience (pain), and our behavioural response to that experience (pain behaviours). Pain behaviours are typically filtered or influenced by what we think is going on (judgements about the meaning of pain – eg super-scary crumbling back, or I just did too much gardening), what we’ve learned to do, and the context in which we’re experiencing pain. That context can be current (eg I’m in Church and it’s very quiet so I’d better not swear as I hit my toe against the pew!), or past (eg last time I kicked my toe against the pew and swore, everyone looked at me – how embarrassing!), or even future (eg if I swear when I kick my toe against the pew, I’ll never be able to show my face here again!). It’s the learned part I want to discuss today.

Pain behaviours range from reflex withdrawal responses (lifting the foot up while straightening the other leg to support me when I stand on a tack), to quite complex behaviours we’ve learned are relevant in our environment (filling out a claim form for compensation and treatment).

We probably developed pain behaviours as part of our evolutionary development: the reflex withdrawal behaviours don’t require conscious thought, so they begin in infancy (actually, before), and rely on spinal mechanisms (eg Rohrbach, Zeiter, Andersen, Wieling & Spadavecchia, 2014), with various parts of the brain becoming involved as part of strategies to avoid threat (see Damasio and Damasio (2016) for some insights into evolutionary aspects of withdrawal reflex). But because we have a developed cortex, we’ve learned ways of suppressing our responses, depending on social context – and on responses from others around us.

Reflexive responses are those associated with classical conditioning – and lead us to learn relationships between previously non-threatening stimuli and both withdrawal responses and the physiological arousal that goes with them. For example, if I bend over to make the bed and OUCH! my back suddenly gets really sore. I straighten up very carefully – and I’ve learned something: next time I bend over to make the bed, I’ll be remembering and preparing for that OUCH! to happen once again. The bed and bending forward movement become associated, in my mind, with that OUCH! Of course, for most of us, once we make the bed a few more times (make that many times), we’ll learn that OUCH! doesn’t inevitably follow the bend, so we gain confidence to repeat that movement without preparing for the OUCH! Now what do you think might happen if I never had an opportunity to make the bed again? Say, if I have a really protective person in my life who stopped me every time I go to do it – will that association I have in my mind persist, or will it reduce? This is, in essence, what is thought to happen when someone develops so-called “fear avoidance”. Note: the experience of pain does not have to re-occur for me to avoid bending and begin to rev my nervous system up. What needs to happen is for the first instance to be pretty strong, and for me to not test my belief again. It’s the behaviour that persists (avoidance) because by avoiding something I believe will be OUCH! I avoid experiencing OUCH! And by avoiding that experience, I never test whether OUCH! happens every time, or just that once.

Let’s look at the other really powerful learning mechanism: operant conditioning. In this situation, the likelihood of me repeating my behaviour is increased or reduced, depending on responses in the environment. So, let’s take my bending forward and experiencing OUCH! If my partner (bless him) then decided to fuss over me, make me a cup of tea and tell me not to worry about making the bed ever again – AND if I liked that idea – my response is likely to be to avoid making the bed. I might even go as far as wincing a bit when walking, so he makes me another cup of tea and fusses over me. I might talk about my back pain because he’s so concerned about me (or I really want him to be concerned about me) and if he carries on fussing, I’m likely to carry on with these behaviours. Now picture that in a two-year-old kid – every time the kid trips and cries, some concerned parent comes picks him up, something the kid likes, it’s probable that kid will learn that this is normal, and something to do when he hurts. For more on learning theory, Johan Vlaeyen summarises the state of play in a review paper from 2015 (Vlaeyen, 2015).

We’re smart, us humans. We learn to predict and remember patterns even from imprecise data – it doesn’t take much for us to put two and two together, particularly when it’s something relevant to surviving! Whenever I’m listening to someone telling me their story about why they’re presenting in this way at this time, and what is maintaining their situation, I keep thinking about the various learning mechanisms involved. Social context and the people around us and how they respond to us exert a powerful force on what we do – and many times we’re not even aware of why we do what we do.  Knowing this stuff means that when I’m listening to someone’s story I try very hard to factor in those things that may have influenced what the person does, rather than just thinking the person is aware of doing all they are doing.

 

Benedetti, F. (2013). Placebo and the new physiology of the doctor-patient relationship. Physiological Reviews, 93(3), 1207-1246. doi:10.1152/physrev.00043.2012

Damasio, A., & Damasio, H. (2016). Pain and other feelings in humans and animals. Animal Sentience: An Interdisciplinary Journal on Animal Feeling, 1(3), 33.

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

Rohrbach, H., Zeiter, S., Andersen, O. K., Wieling, R., & Spadavecchia, C. (2014). Quantitative assessment of the nociceptive withdrawal reflex in healthy, non-medicated experimental sheep. Physiology & behavior, 129, 181-185.
Vlaeyen, J. W. (2015). Learning to predict and control harmful events: Chronic pain and conditioning. Pain, 156, S86-S93.

What’s the biggest barrier to learning more?


Reading and engaging with clinicians online and face-to-face, it’s clear to me that effectively integrating psychosocial factors into daily clinical reasoning, especially amongst physical or manual therapists, is a real challenge. There’s enough research around showing how poorly these factors are identified and then factored in to change what we do and how we do it for me to be convinced of this. What intrigues me, though, is why – given psychosocial risk factors have, in NZ, been around since 1997 – it’s still a problem.

It’s not ignorance. It’s not holding an alternative viewpoint. It’s not just that clinical reasoning models don’t seem to integrate these factors, or that our original training kinda partitioned the various “bits” of being human off – I think that it’s probably that we think we’re already doing well enough.

Image result for dunning kruger effect

This effect has a name – Dunning-Kruger effect. Now, don’t be put off by this term, because I know in some social media circles it’s used to bash people who are  maybe naive, or haven’t realised their lack of knowledge, and it can feel really awful to be told “well actually you’re ignorant”, or “you’re inflating your skill level”.  The thing is, it’s a common experience – we all probably think we’re great car drivers – but in reality we’re all pretty average.

The same thing occurs when we consider our ability to be:

  • empathetic
  • responsive
  • good listeners
  • client-centred
  • collaborative

Another important effect found in clinicians is that we believe our experience as clinicians means we’re better at aspects of clinical care, and especially at clinical reasoning. Over time we get better at recognising patterns – but this can actually be a problem for us. Humans are excellent at detecting patterns but as a result we can jump to conclusions, have trouble stopping ourselves from fixating on the first conclusion we draw, begin looking for things to confirm our hunch, overlook things that don’t fit with the pattern we’ve identified, and basically we begin to use stereotypes rather than really looking at the unique person sitting in front of us (see Croskerry, Singhal & Mamede, 2013a, b).

The effect of these biases, and especially our bias towards thinking we do better than we actually do (especially regarding communication skills and psychosocial factors) means we’re often completely unaware of HOW we communicate, and HOW poorly we pick up on psychosocial factors.

So often I’ve heard people say “Oh I use intuition, I just pick up on these psychosocial issues” – but the problem is that (a) we’re likely to over-estimate how well we pick up on them and (b) our intuition is poor. The risk for our patients is that we don’t identify something important, or alternatively, that we label something as a psychosocial risk factor when it’s actually irrelevant to this person’s problem.

Clinical reasoning is difficult. While recognising patterns becomes easier over time because we have a far broader range of patterns we’ve seen before, at the same time

  • research is expanding all the time (we can be out of date)
  • we can get stuck prematurely identifying something that isn’t relevant
  • we get hooked in on things we’ve just read about, things that happen rarely, things that remind us of something or someone else

Hypothetico-deductive reasoning is an alternative approach to clinical reasoning. It’s an approach that suggests we hold some ideas about what’s going on in our mind while collecting more information to test whether this is the case. The problem here is that we look for information to confirm what we think is happening – rather than looking for something to disconfirm, or test, the hypothesis we hold. So, for example, we might observe someone’s pain behaviour and think to ourselves “oh that person is doing that movement because of a ‘dysfunctional movement pattern’. We can assume that the reason for this movement pattern is because of underlying dysfunction of some sort – but we fail to test that assumption out to see whether it might in fact be a movement pattern developed because someone told the person “this is the way you should move”, or the person is moving that way because of their beliefs about what might happen if they move differently.

The problem with intuition and these other cognitive biases is that they simplify our clinical reasoning, and they reduce effort, so they’re easy traps to fall into. What seems to help is slowing down. Deliberately putting a delay in between collecting information and making a decision. Holding off before deciding what to do. Concurrently, we probably need to rely less on finding “confirming” information – and FAR more on collecting information across a range of domains, some of which we may not think are relevant.

That’s the tough bit. What we think is relevant helps us narrow down our thinking – great for reducing the amount of information we need to collect, but not so great for testing whether we’ve arrived at a reasonable conclusion. My suggested alternative is to systematically collect information across all the relevant domains of knowledge (based on what’s been found in our research), wait a bit and let it settle – then and only then begin to put those bits and pieces together.

Why doesn’t it happen? Well, we over-estimate how well we do this assessment process. We do jump to conclusions and sometimes we’re right – but we wouldn’t know whether we were right or not because we don’t check out alternative explanations. We’re pushed by expectations from funders – and our clients – to “set goals” or “do something” at the very first assessment. We feel guilty if we don’t give our clients something to take away after our initial assessment. We want to look effective and efficient.

Great quote?

For every problem, there is a solution that is simple, elegant, and wrong. H.L. Mencken.

If you’d like to question your own practice, try this: Record your session – and transcribe that recording. Notice every time you jump in to give advice before you’ve really heard your client. Notice how quickly you form an impression. Examine how often you look for disconfirmation rather than confirmation. See how often you ask about, and explore, those psychosocial factors. It’s tough to do – and sobering – but oh how much you’ll learn.

Croskerry, P., Singhal, G., & Mamede, S. (2013). Cognitive debiasing 1: origins of bias and theory of debiasing. BMJ Quality & Safety, 22(Suppl 2), ii58-ii64. doi:10.1136/bmjqs-2012-001712

Croskerry, P., Singhal, G., & Mamede, S. (2013). Cognitive debiasing 2: impediments to and strategies for change. BMJ Quality & Safety, 22(Suppl 2), ii65-ii72. doi:10.1136/bmjqs-2012-001713

The gap in managing pain


If you’ve read my blog for any period of time you’ll know that I like practical research, and research that helps clinicians do what they do with humanity, compassion and evidence. One really enormous gap in the field is rarely mentioned: how do clinicians pull their assessment findings together and use them for clinical reasoning? Especially if you’re part of an interprofessional team (or work in a biopsychosocial framework). The silence in the pain literature is deafening!

There are any number of articles on what can be included in an initial assessment, most of them based on the idea that if factor X is an important predictor, it oughta be assessed. So we have a proliferation of assessments across (mainly) the biopsychological spectrum, with a teeny tiny bit of social (family relationships) thrown in, if you’re lucky. There are numerous papers proposing treatments for aspects of pain – anything from medications, to movement treatments, to cognitive treatments (yes, pain education), and behavioural treatments – but after reading them it almost feels like authors think anyone with pain that’s going on longer than we’d hope “should” have That Treatment, and then of course the person will be just fine.

Except that – there are just as many people with persistent pain today as there were 20 years ago, perhaps more (given the global burden of disease shows that low back pain is The Most Common problem associated with years lived with disability). In other words, all our treatments across all our specialties don’t seem to be having the impact that the research papers suggest they ought to. What gives?

I think it’s time to take a leaf from some of the better-conducted pharmacological studies. Yes, I said that! What I mean is that given our treatments especially for low back pain seem to have broadly the same or similar effects, maybe we need to look beyond the grouped analyses where individual differences are lost within the grouped data, and head to some of the sub-analyses proposed and used by Moore, Derry, Eccleston & Kalso (2013). In this paper, they advocate using responder analysis – who, exactly, gets a good result?

At the same time, I think we need to get much better at assembling, integrating and using the multitude of assessments people complete for us when we start treating them. Several points here: yes, we all carry out assessment but how well do we put them together to “tell the story” or generate a set of hypotheses to explain the crucial questions:

Why is this person presenting in this way at this time? And what can be done to reduce distress and disability?

I think case formulations may take us a step towards better use of our assessments, better clinical reasoning, better teamwork, and, most of all, better collaboration with the person we hope to help.

Case formulations are not new in psychology. They’re really a cornerstone of clinical psychological reasoning – assembling the information gathered during assessment into some sort of explanatory framework that will help the therapist generate possibly hypotheses about predisposing factors, what precipitated the problem, what perpetuates the problem, and any protective factors. Psychologists are no less prone to arguing about whether this approach works than anyone else – except they do some cool studies looking at whether they’re consistent when generating their formulations, and sadly, formulations are not super-consistent with each other (Ridley, Jeffrey & Robertson, 2017).

BUT here’s why I think it might be a useful approach, especially for people with complex problems associated with their pain:

  1. Case formulations slow our clinical reasoning down. “Huh?” you say, “Why would that be good?” Well because rapid clinical judgements on the basis of incomplete information tend to lead us towards some important cognitive biases – anchoring on the first possible idea, discounting information that doesn’t fit with that idea, we notice weird stuff more than the commonplace, we fill in information based on stereotypes, generalities and past histories, and we don’t shift from our first conclusion very easily. By taking time to assemble our information, we can delay drawing a conclusion until we have more information.
  2. By completing a consistent set of assessments (instead of choosing an ad hoc set based on “the subjective”) we reduce the tendency to look for confirmation of our initial hunch. I know this isn’t usual practice in some professions because that “subjective” history is used to guide assessments which are then used to determine a diagnosis – but the risk is that we’ll look for assessments that confirm our suspicions, meanwhile being blinded to possible alternative explanations (or hypotheses or diagnoses).
  3. Working together with the expert on their own situation (ie the person seeking help!) we build collaboration, a shared understanding of the person’s situation, and we can develop an effective working relationship without any hint of “one-up, one-down” that I can see appeals to “experts” who like to point out the “problems” with, for example, posture, gait, motor control and so on – all which may have little to do with the patient’s pain, and a whole lot more to do with creating a “listen to me because I Know Things” situation.
  4. Other team members can contribute their assessments, creating a common understanding of the various factors associated with the person’s situation. Common goals can be developed, common language about what might be going on, common treatment aims and enhanced understanding of what each profession contributes can happen when a formulation includes all the wonderful information collected across the team.
  5. If one of the treatments doesn’t work (ie the hypothesis doesn’t hold up to testing) there are other options to draw on – we’re not stuck within our own clinical repertoire, we can think across disciplines and across individual clinical models and become far more confident about knowing when to refer on, and how we can support our colleagues.

But, you know, I looked in the pain journals, searched far and wide – and I found few examples of case formulation for persistent pain. The best paper I’ve found so far is from a textbook – so not readily accessible. It’s Linton & Nicholas (2008) “After assessment, then what? Integrating findings for successful case formulation and treatment tailoring”. Where is the rest of the research?!!

Linton, S. J., & Nicholas, M. K. (2008). After assessment, then what? Integrating findings for successful case formulation and treatment tailoring. Clinical Pain Management Second Edition: Practice and Procedures, 4, 1095.

Moore, A., Derry, S., Eccleston, C., & Kalso, E. (2013). Expect analgesic failure; pursue analgesic success. BMJ: British Medical Journal (Online), 346.

Ridley, C. R., Jeffrey, C. E. and Roberson, R. B. (2017), Case Mis-Conceptualization in Psychological Treatment: An Enduring Clinical Problem. J. Clin. Psychol., 73: 359–375. doi:10.1002/jclp.22354

Back to basics about psychosocial factors and pain – iv


Part of the definition of pain is that it is “a sensory and emotional experience” – in other words, emotions of the negative kind are integral to the experience of pain. Is it any wonder that poets and authors have written so eloquently about the anguish of unrelieved pain? As I write this, I’ve been pondering the way “psychosocial” has been used when discussing pain, as if those factors aren’t experienced by “normal” people, as if the way we feel about pain and the way people who struggle with their pain feel are two entirely different things.

Chris Eccleston, someone I admire very much, writes about a “normal psychology of chronic pain” and makes some incredibly useful points: that pain is a normal feature of human life. Pain is an everyday occurrence (watch kids playing in a playground – every 20 minutes kids communicate about pain, Fearon et al, 1996). In New Zealand one in five people report experiencing pain lasting six months or longer. Pain really is all around us – and it’s normal and indeed part of the experience itself, to feel negative emotions such as fear, anger, sadness, anxiety, and such when we’re sore.

So why have emotions been lumped in with “other factors” as part of the negative way psychosocial factors are interpreted today? I personally think it’s partly a hangover, in NZ at least, from the way our stoic forebears viewed “weakness”. There wouldn’t be many families in New Zealand who haven’t heard something like “man up”, or “big boys don’t cry”, or “pull yourself together” with great All Blacks who played on despite broken ribs or arms – who didn’t give in when they were injured being held up as examples we should emulate. At the same time pain isn’t given much space in our health professional training programmes – and when it is, it’s primarily viewed in a neuroanatomical way, as we’re taught about spino-thalamic tracts, and nociceptors, and not much else. In fact, I think the gate control theory is still being taught as the main theory in some programmes (despite it being revised and replaced with more sophisticated models).

So what is normal? I really like Acceptance and Commitment Therapy, as you’ve possibly noticed. Amongst one of the many reasons I like it so much is its view of suffering. Within ACT, being psychologically inflexible is the problem – that is, working hard to avoid or control experiences we don’t want, getting caught up in thoughts as if they’re Truth instead of our mind’s opinion of things, being attached to someone’s idea of who and what we are, living in the past or predicting the future, and failing as a result to take actions that line up with what our personal values are. When we get stuck thinking there’s only one way to deal with a situation, and when we forget about what’s important in our lives because we’re working so hard to avoid certain experiences – these aren’t seen as pathological, but instead are just part of the way our mind/language and experience tangle us up. The beauty is that there are ways out of being stuck but they’re counter-intuitive.

What do I mean? Well if we all have negative emotions about pain, why do only some of us struggle with that experience and get stuck? For some people it’s because they’re trying so hard not to feel pain that they spend time and energy doing things to control it and in the process stop doing things that matter. Think of the many appointments and the ups and downs of hope that it will all go away with this magic thing – then despair as it doesn’t work. Just the amount of time people spend waiting for and attending appointments can take time away from being with family, working, living…Now to me, this is not psychopathology. This is what normal minds do – try to fix a problem using strategies that have always worked in the past.

At the same time, given pain is a negative experience, doesn’t it make sense to monitor what went on last time you tried to lift that box, go to work, drive the car… AND doesn’t it make sense to anticipate what might go wrong if you try it again? This isn’t about being depressed, anxious or any other kind of pathology – this is just what we’ve learned to do, and our minds are trying incredibly hard to make it work again.

When I mentioned that a solution might be counter-intuitive, what I mean is recognising that trying to control or avoid an experience that comes with us wherever we go because it’s part of us, can trip us up. Instead, we might do better if we soften our attempts to control or avoid our experience of pain. Maybe spending time exploring pain and doing things alongside pain is possible – especially if the things we want to do are important to us. Don’t believe me? Think about marathon runners – they feel the pain (hit the wall) and still keep running! Why? Because it’s important to them to get to the end.

Now I’m not suggesting that ALL people will find this approach helpful, and I’m NOT denying that many people with persistent pain experience depression, anxiety, rotten sleep and generally feel demoralised. What I AM saying is that if we approach everyone with the misguided idea that psychosocial factors exist only in “those people”, we’re wrong. Any one of us will experience negative emotions if pain is present – and even more if pain persists. This is a normal response to a challenging and inherently aversive experience. Of course, if we’ve experienced depression, adverse life events, turmoil in our home and work life, and the stigma of not being believed, the potential to then become angry, depressed, and fed up is only greater. Let’s not make a negative experience worse by stigmatising people with the notion that “psychosocial factors” makes them any different from anyone else.

 

Eccleston, C. (2011). A normal psychology of chronic pain. Psychologist, 24(6), 422-425.

Fearon, I., McGrath, P.J., Achat, H. (1996). ‘Booboos’: The study of everyday pain among young children. Pain, 68, 55-62.

Vowles, K. E., Witkiewitz, K., Levell, J., Sowden, G., & Ashworth, J. (2017). Are reductions in pain intensity and pain-related distress necessary? An analysis of within-treatment change trajectories in relation to improved functioning following interdisciplinary acceptance and commitment therapy for adults with chronic pain. Journal of consulting and clinical psychology, 85(2), 87.

Back to basics about psychosocial factors and pain – iii


Last week I discussed some of the areas in the brain, and basic principles, that are currently thought to influence our pain experience. This week I thought I’d introduce one of my favourite ways of considering pain mechanisms, mainly because it helps me think through the four main kinds of mechanisms, and can influence our treatment approach. At this stage I want to raise my hand to acknowledge the following:

  • My gratitude to Dr John Alchin, longtime friend and colleague, who first pointed this paper out to me and has shared it with hundreds of people who go to see him at the local tertiary pain management centre.
  • We know this is a simplified, under-developed approach to mechanisms underpinning pain, but it’s helpful nevertheless.
  • Most of our patients will have a combination of mechanisms involved in their experience, not just one.
  • This approach to mechanisms doesn’t include the psychological or social – just the primary biological processes.
  • Throughout this blog, when I use the word “pain” I mean the experience we have once whatever mechanisms involved filter up through to our awareness. So while I talk about peripheral mechanisms, they’re only experienced as pain once we become aware of them – and that process involves a whole lot of what I discussed in my last post .

Clifford Woolf wrote this paper in 2010, and although the research into mechanisms has continued unabated, I think it provides clinicians with a reasonable guide to considering how best to tackle treatment. He begins by dividing the mechanisms into “useful” and “useless” pain – ie pain that is useful for adaptation, survival, warning, alerts. Just as it’s possible to have dysfunction or disease of our cardiac, pulmonary, gastro-intestinal, and skeletal systems, I think it’s just as plausible that we can have something go wrong with our nociceptive system. In fact, because of its complexity, it seems probable to me at least that there are many different ways this system can fail to work properly. But more about that shortly! Let’s begin with the useful pain.

Nociceptive pain – is considered to be pain that is, as Woolf puts it, our “early-warning physiological protective system”. When we touch something super cold, super hot, or a chemical that can harm us (think chilli pepper!), or meet a mechanical force that activates mechano receptors, our high threshold nociceptors are activated – well in advance of tissue damage, I quickly add. This process activates withdrawal – even in simple single-celled animals – and saves us from harm. When combined with behavioural responses including vocalisation, grimaces and other pain behaviours, we signal to everyone around us that we’re in danger, and others shouldn’t do what we’ve just done (Melzack, Dennis, Kosterlitz & Terenius, 1980).  For me, the cool thing about nociceptive pain is that once you’ve removed that stimulus (got rid of the chilli on your lips, let go of the ice-cube or the hot mug of coffee, or shifted in your seat to relieve your butt) the pain simply goes away. Just like that. How cool?!

Inflammatory pain – is also a useful pain to have. Unlike nociceptive pain, inflammation involves disruption to the tissues, triggering a release of a whole bunch of neurochemicals and cells that quickly lower the point at which nociceptors will fire (making you much more sensitive to mechanical, chemical and temperature input), and increasing the blood supply to allow foreign material, dead cells and spent neurochemicals to be whisked away. Inflammation is reasonably easy to see in the periphery (though not so easy in the internal organs because the innervation is more diffuse) and you’ll all have had it – think sunburn (I know you’re not meant to, but everyone gets sunburned at least once, especially in our NZ sun). With sunburn you’re red, hot and often swollen, and you really know it when you step into the shower! That experience of ouch! to your usual shower temperature (and the ouch! when you towel down) is allodynia, or the experience of pain when a usually comfortable stimulus is applied. You’ll experience hyperalgesia if your mate comes along and slaps you on your sunburned shoulders!

Now both of these mechanisms are useful because they alert us to threat, they make it more difficult to move around, and we often respond to them with changes in our behaviour that act as a signal to others around us. Let’s turn the attention to two mechanisms where there is something gone awry with the nervous system – in other words, useless pain.

Neuropathic pain – is defined by IASP as “pain caused by a lesion or disease of the somatosensory nervous system.” What this means is that there must be an identifiable lesion in the nervous system somewhere – something that can be imaged or tested to demonstrate damage. This could be in the periphery – think of radial nerve entrapment with its characteristic tingling, deep aching and burning over the distribution of the nerve. It could be in the spinal cord itself – think of a complete spinal cord injury where the person is unable to move from the lesion down, and who also gets the same tingling, aching, burning and electric shock pain over the same area. A simple example would be radicular pain where the nerve root is compressed – and this can be seen on imaging, and where the pain is experienced over the same nerve distribution. The final group in this nasty set of neuropathies is when someone has a stroke, where part of the brain is damaged leading to intractable, deep, aching pain with electric shock-like pain just to make it nastier. For a great paper reviewing neuropathic pain, Finnerup and colleagues wrote one published in 2016 (see below), describing a grading system to indicate possible, probable and confirmed neuropathic pain. The hallmark of this pain is that it doesn’t represent tissue damage except in the area of the nervous system where the lesion is located. In other words, that pain down the leg is not where the problem lies in radicular pain – it’s near the spinal cord. So this pain doesn’t have a function for survival – it’s just a horrid nuisance.

The final mechanism is poorly understood – even less well understood than neuropathic pain. This is where ostensibly the nervous system appears intact. The pain experience might be in multiple parts of the body, it could be just in the head (migraine, for example), or it could be just in the shoulder (frozen shoulder maybe?), or it might be everywhere (fibromyalgia). The name isn’t even completely determined – it’s called “dysfunctional” by Woolf, and he collapsed this and neuropathic pain into one mechanism, but I prefer to keep it separate because it’s more helpful for management especially when a neuropathy might be amenable to surgery. Another term, and one I like, is nociplastic – referring to the idea that it’s the unhelpful neuroplasticity of our nervous system that has over-responded to potential threat (Kosek, Cohen, Baron et al, 2016). Some would argue that this mechanism is partly a general tendency to a lower nociceptive threshold, maybe genetic, maybe behavioural (ie we’ve learned to monitor and respond to threat perhaps because of early life experiences), perhaps a diathesis-stress where the predisposition exists but it’s not brought into expression until a stressor, perhaps a virus or an injury, exerts an influence on homeostasis.

Ultimately, pain is an experience that we’ve all had, and one that has individual meaning for each of us based on our previous experiences, predictions for the future, current goals, culture and biology. What a mechanisms-based approach to pain management might mean is better and more accurate management for each one. So we’d be looking to remove that bunion so people can walk more easily; reduce the inflammation in an auto-immune disease; decompress a squished nerve in neuropathic pain and look to altering plasticity in nociplastic pain. But pain is weird and as I said at the very beginning, it’s entirely possible to have more than one mechanism involved – and because pain is not just biology, we’d be foolhardy to think that just by down-tuning the intensity, everyone so treated will go “back to normal”. More on that next week!

 

 

Finnerup NB, Haroutounian S, Kamerman P, et al. Neuropathic pain: an updated grading system for research and clinical practice. Pain. 2016;157(8):1599-1606. doi:10.1097/j.pain.0000000000000492.
Kosek, E., Cohen, M., Baron, R., Gebhart, G. F., Mico, J. A., Rice, A. S., … & Sluka, A. K. (2016). Do we need a third mechanistic descriptor for chronic pain states?. Pain, 157(7), 1382-1386.

Melzack, R., Dennis, S. G., Kosterlitz, H. W., & Terenius, L. Y. (1980). Phylogenetic evolution of pain-expression in animals. Pain and Society, 13-26.

Woolf CJ. What is this thing called pain? The Journal of Clinical Investigation. 2010;120(11):3742-3744. doi:10.1172/JCI45178.