pain management

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.

 

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?

 

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

Getting persistent pain and disability confused


As I read blogs and tweets and posts on social media, and even peer reviewed papers in journals, I often read that what we’re trying to do in sub-acute pain management is to prevent chronic pain from developing (note, when I talk about pain that goes on beyond healing, more than three months, or has no useful function, I may use the term “chronic” or I may use the more recent term “persistent” – they mean the same thing, except persistent has perhaps less baggage…).

I want to take aim at that focus – to prevent pain from persisting – and think carefully about it. Let’s take a 56 year old woman with a painful knee, a knee that’s been diagnosed as having osteoarthritis (OA). Now, although we have surgical management for OA (a knee replacement – uni-compartment or even a total knee replacement), in most cases surgeons are not enthusiastic about doing a knee replacement on a younger person, particularly someone who is active (plays netball, golf, runs, gardens). So if a knee replacement is not a thing – yet – what do we do? Most of us will know about the value of remaining active and fit, losing weight and maintaining good range of movement (see here for the NICE guidelines, 2017). We know that these things will maintain function – but they won’t stop cartilage deterioration (much, if at all), and they won’t stop the pain. No matter what we do – even medications are not always especially helpful – pain is likely to persist. Does that mean we’ve failed? Reading some of these blogs, it certainly seems it does.

Let’s take back pain – most of us will know back pain occurs periodically throughout life, from the time we’re teens, through to old age. In some people a single bout of back pain happens and then they’re fully recovered and never bothered again, but for many of us, we’ll be troubled with repeated bouts throughout our lives. And still others will have one bout than just never ends (Axen & Leboeuf-Yde, 2013; Vasseljen, Woodhouse, Bjorngaard, & Leivseth, 2013).  This is despite our best efforts to prevent the onset of low back pain, and to treat it effectively – pretty much all our treatments provide a small amount of help but only exercise has been shown to prevent a new bout after the first one (Choi, Verbeek, Wai-San Tam & Jiang, 2010) – and even then the evidence was “moderate” and only at one year.

So… when we begin to examine claims that by treating musculoskeletal problems early we can prevent pain from becoming chronic or ongoing, I think we need to stop and pause before letting the blood rush to our head.

If we can’t prevent pain from hanging around, what can we do? What is the aim of all this treatment?

Well, let’s take a quick look at the Global Burden of Disease (Hoy, March, Brooks, Blyth, Woolf, Bain et al, 2014). In this piece of work, “Out of all 291 conditions studied in the Global Burden of Disease 2010 Study, LBP ranked highest in terms of disability (YLDs), and sixth in terms of overall burden (DALYs). The global point prevalence of LBP was 9.4% (95% CI 9.0 to 9.8). DALYs increased from 58.2 million (M) (95% CI 39.9M to 78.1M) in 1990 to 83.0M (95% CI 56.6M to 111.9M) in 2010. Prevalence and burden increased with age.” [emphasis mine].

What this means is that although low back pain is not a fatal disease, that may well be the problem – people don’t die from low back pain, they live with disability all the days of their life. And worse, the burden of low back pain is increasing. And this is despite all the work we (you, me, the entire health system) is putting in.

If we can’t “get rid of” low back pain (and it looks like we don’t yet have the tools to do so), what are we trying to do?

Given our poor outcomes for completely curing low back pain, we need to aim to reduce the impact of pain on people’s lives.

And not just low back pain, but things like tennis elbow, frozen shoulder, neck pain, abdominal pain, pelvic pain, headache, migraine, osteoarthritis…

For a moment, let’s think about the effect on a person going through treatment, being promised that “pain education” will reduce their pain, that exercises will get rid of their pain, that gadget A or B will get rid of their pain, that treatment Y or Z will get rid of their pain. What do you think it feels like to be completely adherent about everything you’re being asked to do, but still feeling a failure because that pain does not go? Think of the language used by some of our colleagues – “failed back syndrome”? Who failed, exactly?

Before I get harangued for breathing the word that, ooops, our treatments don’t work very well, let me address the issue of “pain education” and pain intensity. Don’t forget that the only way we can know how much it hurts someone is by asking them. And our usual tool is that 0 – 10 scale, where 0 = no pain and 10 = most extreme pain imagined. Have you ever tried doing that on yourself? Seriously – how do you rate your own pain? Some of that pain rating is about how much we’re prepared to (capable of) putting up with. Some of that rating is about how bothered (fed up, distressed, frustrated) we are about our pain. Some of it is about “OMG I don’t know what this is and how long it’s going to go on for”.

What this means is that when someone gives an explanation it can –

  • make the experience less frightening,
  • less distressing,
  • more understandable,
  • less bothersome

and as a result, when we’re then asked for our pain intensity rating on that darned scale, we reduce the score we give our pain. It does not necessarily mean the pain has reduced in intensity – a pain scale is a means of communicating something about our experience, thus it’s a pain-associated behaviour with the purpose of communicating something. So if a person isn’t ‘convinced’ by our pain education, you know they’ll keep their score pretty high.

So, there are some people for whom we cannot reduce or get rid of their pain. It’s likely to persist. And it’s these people who can be viewed as “heartsink” patients, who hang around not getting better. Well, unless we begin looking at their experience and examine what they’re looking for (and believe me, it’s not pain reduction – it’s what pain reduction means they can do) we’re going to be stuck. And so will they. Let’s get it into our heads that pain reduction is not achievable for all, but reducing the impact of pain on life is something we can all help with. Let’s stop demonising the person who has to live with pain that doesn’t respond to all our ministrations and begin looking deeply at ourselves and why we avoid recognising that we can’t win ’em all. And let’s get on with the business of helping people do what’s important in their lives, irrespective of pain.

 

 

Axén, I., & Leboeuf-Yde, C. (2013). Trajectories of low back pain. Best Practice & Research Clinical Rheumatology, 27(5), 601-612. doi: http://dx.doi.org/10.1016/j.berh.2013.10.004

Choi, B. K. L., Verbeek, J. H., Wai-San Tam, W., & Jiang, J. Y. (2010). Exercises for prevention of recurrences of low-back pain. Occupational and Environmental Medicine, 67(11), 795-796. doi:10.1136/oem.2010.059873

Hoy, D., March, L., Brooks, P., Blyth, F., Woolf, A., Bain, C., . . . Buchbinder, R. (2014). The global burden of low back pain: Estimates from the global burden of disease 2010 study. Annals of the Rheumatic Diseases, 73(6), 968-974. doi:10.1136/annrheumdis-2013-204428

Vasseljen, O., Woodhouse, A., Bjorngaard, J.H., & Leivseth, L. (2013). Natural course of acute neck and low back pain in the general population: The HUNT study. Pain, 154(8), 1237-1244.

Back to basics about psychosocial factors and pain – v


I’ve been writing about psychosocial factors and pain but I realise that I haven’t actually defined what I mean by psychosocial factors. The strange thing about this term is that it’s often conflated with “psychological” or “psychopathological” when it’s actually not. So… where to begin?

The Collins English Dictionary defines psychosocial as: “of or relating to processes or factors that are both social and psychological in origin”, while the Oxford English Dictionary defines it as “Of or relating to the interrelation of social factors and individual thought and behaviour.” According to the Oxford, it first appeared in the American Journal of Psychology in 1890 when it was used to describe the factors associated with the increase of alcoholism. An 1899 journal used it to describe “… psycho-social phenomena, such as language, customs, rights, religion etc., arising from the action of social elements with or upon the individual mind.”

So, the term is fairly recent but seems to have always been associated with broader influences on thoughts and behaviour – that is, a reciprocal response between what individuals think and do, and what helps to shape (and also responds to) what happens in the community.

When we think about pain, the most common “psychosocial” factors seem to be psychological – things like attention (vigilance), catastrophising (thinking the worst), negative affect (low mood), treatment seeking (behaviours associated with looking for help), avoidance (not doing, not approaching). What is lacking in clinical practice, in my humble opinion, is the relationship between how these factors develop and are maintained, and how those around an individual (both family and the wider community) respond to these factors. It’s not that there is no research into these relationships – it’s that research is complex, it’s tough to conduct experiments in this field, and effecting change once relationships are identified is pretty hard. More than that, health professionals typically see individuals, not people-in-context.

BUT here are some of the areas currently being explored.

Clinician behaviour – there would be few readers of this blog who are unfamiliar with Ben Darlow’s work on the power of what clinicians say (Darlow, Dowell, Baxter, Mathieson, Perry & Dean, 2013), though he’s not the first research to begin to look at this – Tamar Pincus and others have also reviewed the influence of practitioners beliefs on what they do for people with persistent pain (Parsons, Harding, Breen, Foster, Pincus, Vogel & Underwood, 2007).  The broad conclusions from this body of work, of which these two are tiny tips of a very large iceberg, is that what clinicians believe about pain and chronicity and hurt/harm influences both their treatment recommendations and their attitude towards people experiencing persistent pain, and has a direct effect on chronicity in the acute stages of a pain problem.

Family responses – Herta Flor and colleagues explored the impact of persistent pain on family relationships way back in the 1980’s, while much more recently,  Burns, Post, Smith, Porter et al (in press) investigated the interaction between spouse criticism and the effect on pain intensity and behaviour in people with persistent low back pain. Chan, Connelly & Wallace (2017) established that poor peer relationships influenced both emotional functioning and persistent pain amongst adolescents, while treatment seeking amongst adolescents was found to be associated with elevated treatment seeking in their parents (Stone & Wilson, 2016). Whether the relationships are genetic (in family patterns of persistent pain and disability), or learned (social learning theory) or a mix of both – it looks like how others respond and behave in relation to pain and disability has a strong influence on persistent pain in an individual.

Work – This, naturally, has been the place of many a study trying to establish a relationship between biomechanical factors and the onset and maintenance of pain, but it has also been the location for studies examining social relationships like supervisory responses, peer relationships, employer flexibility along with the personal effects of workplace stress on the body. I’m not going to review the myriad studies, but point you to a good systematic review of prognostic factors for return to work by Steenstra, Munhall, Irvin, Oranye, Passmore et al (2016) to demonstrate just how many factors have already been identified.

I’ve barely touched the surface of the social aspects influencing our experience of pain and disability. It’s evident that these factors have been identified – but let me ask you this: How often do you identify and then provide an intervention for these social factors? And if not, why not? And if not you – who?

 

Burns, J. W., Post, K. M., Smith, D. A., Porter, L. S., Buvanendran, A., Fras, A. M., & Keefe, F. J. (2017). Spouse criticism and hostility during marital interaction: effects on pain intensity and behaviors among individuals with chronic low back pain. Pain.
Chan, S. F., Connelly, M., & Wallace, D. P. (2017). The Relationship Between Pain Characteristics, Peer Difficulties, and Emotional Functioning Among Adolescents Seeking Treatment for Chronic Pain: A Test of Mediational Models. Journal of Pediatric Psychology, jsx074.
Darlow, B., Dowell, A., Baxter, G. D., Mathieson, F., Perry, M., & Dean, S. (2013). The enduring impact of what clinicians say to people with low back pain. The Annals of Family Medicine, 11(6), 527-534.
Flor, H., Turk, D. C., & Scholz, O. B. (1987). Impact of chronic pain on the spouse: marital, emotional and physical consequences. Journal of psychosomatic research, 31(1), 63-71.
Parsons, S., Harding, G., Breen, A., Foster, N., Pincus, T., Vogel, S., & Underwood, M. (2007). The influence of patients’ and primary care practitioners’ beliefs and expectations about chronic musculoskeletal pain on the process of care: a systematic review of qualitative studies. The Clinical journal of pain, 23(1), 91-98.
Steenstra, I. A., Munhall, C., Irvin, E., Oranye, N., Passmore, S., Van Eerd, D., … & Hogg-Johnson, S. (2016). Systematic review of prognostic factors for return to work in workers with sub acute and chronic low back pain. Journal of occupational rehabilitation, 1-13.
Stone, A. L., & Wilson, A. C. (2016). Transmission of risk from parents with chronic pain to offspring: An integrative conceptual model. Pain, 157(12), 2628-2639.

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.