Health

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 – 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 – 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.

Minding your body: Interoceptive awareness, mindfulness and living well


We all grow up with a pretty good idea of what our body feels like; what normal is. It’s one of the first “tasks” of infancy, it seems, to work out what is me and what is not. When people experience a disturbance to the way their body moves or feels, it can take some time to get used to that new way of being. In pregnancy, where the body takes on a different shape and dimension, it’s not uncommon to bump into things because the new shape hasn’t yet sunk in!

This awareness of “what my body feels like” is called interoceptive awareness (IA), and I was intrigued to read this paper by Hanley, Mehling and Garland (2017) in which IA is examined in relation to dispositional mindfulness (DM). DM is thought to be the innate tendency to notice without judging or automatically reacting to what is going on. IA may be extremely sensitive in some people – for example, people with health anxiety might notice their sweaty palms and heart palpitations and then worry that they’re about to have a heart attack, or the same symptoms in someone with social anxiety might be experienced as indications to LEAVE RIGHT NOW because EVERYONE is looking at ME.

I’m not sure of research into IA in people with persistent pain, although I am positive it’s something that has been studied (see Mehling, Daubenmier, Price, Acree, Bartmess & Stewart, 2013). As a result, in my conclusions I’m going to draw from my experience working with those living with persistent pain, and extrapolate wildly!

This study aimed to establish the relationship between various items on two questionnaires used to measure IA and DM: the MAIA (Multidimensional Assessment of Interoceptive Awareness), and the FFMQ (Five Facet Mindfulness Questionnaire). The paper itself discusses the first measure as empirically derived and confirmed by focus groups, and having associations with less trait anxiety, emotional susceptibility and depression – in other words, high scores on this measure (awareness of body sensations and judging those sensations) are associated with important factors influencing our wellbeing. The second measure is described as “one of the most commonly used self-report measures of DM”. It consists of five scales thought to measure important aspects of mindfulness (observing, not reacting and acting with awareness).

Along with these two measures, the authors examined wellbeing, which essentially was defined as a tendency to accept oneself, have a purpose, manage the environment, develop good relationships, continue to grow as a person and be independent and autonomous. We could probably argue about these dimensions in view of what may be a cultural component (autonomy may not be highly favoured in some communities).

Recruitment was via mTurk, Amazon’s crowdsourcing website. As a result participants possibly don’t represent the kinds of people I would see in clinical practice. And half of the 478 participants were excluded because people didn’t complete all the questionnaires. I could quibble about this sample, so bear that in mind when you consider the results.

Results

Turning to the results, the first finding was a good correlation between all three questionnaires, with the FFMQ more strongly correlated with psychological wellbeing than the MAIA. But these researchers wanted more! So they carried out canonical correlation analysis, which is used to correlate the latent variables present in measurement instruments. It’s complicated, but what it can tell us is how underlying aspects of two unrelated measures might fit together. In this instance, the researchers found that two of the FFMQ (non-reacting and observing) were related to six of the eight MAIA factors (attention regulation, self-regulation, trusting, emotional awareness, body listening and noticing). They also found that FFMQ ‘non-judging’ and ‘acting with awareness’ were associated with MAIA ‘not worrying’ subscale.

What does this tell us? Well, to me it’s about grouping somewhat-related items together from two instruments to work out their contribution to something else. The authors thought so too, and therefore completed a further analysis (told you it was complicated!), to look at a two-step hierarchical multiple regression where the two sets of scales were entered into equations to see how much each contributed to the psychological wellbeing score. Whew!

What they found was interesting, and why I’m fascinated by this study despite its shortcomings.

What can we do with this info?

Being mindfully observant and non-reactive seems to be associated with a person’s ability to notice and control attention to what’s going on in the body. Makes sense to me – knowing what goes on in your body but being able to flexibly decide how much to be bothered about, and what you’re going to do about those sensations will make a difference to how well you can cope with things like fatigue, hunger, the need to change body position or to sustain a position when you’re focusing on something else – like hunting!

Apparently, being able to attend to body sensations is also part of regulating your emotional state, and if you can do this, you’ll generally experience your body as a safe and “trustworthy” place. And if you can do this when your body doesn’t feel so good yet still remain calm and accepting, this is a good thing. In the final analysis, these authors called the first cluster of statements “Regulatory awareness” – being aware of your body and regulating how you respond to it. The second cluster related more with non-judging and acting with awareness, so the authors called this “Acceptance in action”.

For people living with persistent pain, where the body often does not feel trustworthy and there’s an increased need to “ignore” or “let go” or “not judge” painful areas, it seems that one of the most important skills to learn is how to self regulate responses to IA. To take the time to notice all the body (not ignore the sore bits, nor obsess about the sore bits). This doesn’t come easily because I think for most of us, we’ve learned we need to notice pain – after all, ordinarily it’s helpful! The second part is to accept in action – in other words discriminating between unpleasant body sensations are should be worried about, and those not needing our attention is an adaptive skill. Perhaps mindfulness gives us better capabilities to discriminate between what needs to be taken into account, and what does not.

Interestingly, the least strongly associated response items were related to using words to describe what goes on in the body. For me this suggests experiential practices might be more useful to help people develop these two skills than simply talking about it. And suggests that maybe we could use meditative movement practices as a good way to develop these skills.

R.A. Baer, G.T. Smith, J. Hopkins, J. Krietemeyer, L. Toney, (2006) Using self-report assessment methods to explore facets of mindfulness, Assessment 13 27–45.

Hanley, A. W., Mehling, W. E., & Garland, E. L. (2017). Holding the body in mind: Interoceptive awareness, dispositional mindfulness and psychological well-being. Journal of Psychosomatic Research, 99, 13-20. doi:https://doi.org/10.1016/j.jpsychores.2017.05.014

W.E. Mehling, J. Daubenmier, C.J. Price, M. Acree, E. Bartmess, A.L. Stewart, (2013). Self-reported interoceptive awareness in primary care patients with past or current low back pain, Journal of Pain Research. 6

W.E. Mehling, C. Price, J.J. Daubenmier, M. Acree, E. Bartmess, A. Stewart, (2012) The multidimensional assessment of interoceptive awareness (MAIA), PLoS One 7  e48230.

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 – 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.

Conversations about cannabis for chronic pain


The debate about cannabis and derivatives for persistent pain continues to grow in New Zealand, and elsewhere in the world. Many people I’ve treated and who are living with persistent pain say they like to use cannabis (in a variety of forms) to help with pain intensity and sleep, adding their voices to those wanting “medicinal” cannabis to be approved. In the few patients I’ve worked with who have managed to obtain a cannabis product (in NZ it has to be legally prescribed and will generally be in the form of Sativex or similar) the effect doesn’t seem as profound as the real thing (whether smoked, vaped, or in edibles).

Here’s my current position, for what it’s worth. Right now I think cannabis legislation needs an overhaul. Cannabis doesn’t seem to fit into the same class as synthetic drugs (often called “herbal highs” or synthetic “cannabis”) – for one, the plant probably contains a whole lot of substances that have yet to be fully analysed, and for another, I have yet to see a death reported from cannabis use, yet in Auckland, NZ, alone this year there have been around 9 people who have died from taking the synthetic substance, whatever it is. Cannabis seems to cause less harm than legal substances like alcohol and tobacco, and in many places in the world it’s been legalised with some interesting effects on use of opioids.

Ever since Professor David Nutt visited New Zealand a few years back, I’ve been convinced it’s time for a rethink on cannabis laws, but at the same time I’m not ready to support wholesale legalisation of “medical” marijuana. Here are a few reasons why:

  • When a doctor prescribes a drug, he or she is able to rely on the manufacturer making a consistent product, with a consistent amount of “active” ingredients, and a consistent quality. At present, with the exception of the two versions available in New Zealand, this can’t be guaranteed. Plants vary in the combination of active chemicals in them, and storage and age of the product influence the availability of those chemicals when inhaled or ingested. Just as we don’t suggest people go and grow their own opium poppies because we know that opioids are effective analgesics, I don’t think it’s time to allow people to grow their own cannabis for medicinal purposes, such as treating pain. A doctor can’t know just how much of a dose a person can get because in NZ we don’t yet have a controlled environment for cannabis production.
  • When a doctor prescribes a drug, he or she is also guided by the indications for use. So, although some medical practitioners prescribe “off-label” use for medications (a good example is nortriptyline, an antidepressant used often for pain reduction), generally there are good double-blinded, randomised controlled trials to determine whether the active drug is more effective than placebo. When we read about cannabis use for medicinal reasons we hear of its use for cancer (mainly nausea, but also pain), neuropathic pain, and in the general media we hear of its use for migraine, period pain, abdominal pain, fibromyalgia, osteoarthritis – there’s very few pain disorders that cannabis isn’t seen to be appropriate. But the truth is, we don’t really know which kind of pain (the underlying mechanism) will respond, and what pains don’t respond. It’s still a bit of a mystery – mind you, this is not any different from other medications for pain for which N=1 seems to be the mantra.

Why might I support a change to marijuana laws?

Well, an interesting study from the Northeastern United States, and published in the journal Pain, looked at the perspectives of people enrolled in legal medical marijuana clinics. It was quite a large study of 984 people, so should represent a good cross-section of those using the drug within a legal system. Participants were asked to complete an online survey, and their responses were analysed by a psychologist who was “not a cannabinoid expert”, arranging the data into themes and subthemes. (As an aside, apparently this was carried out using a “Grounded Theory perspective” based on Corbin and Strauss – BUT essentially the researchers didn’t follow grounded theory methodology throughout, and instead it should be called a thematic analysis using inductive coding. Pedant, yes!). The data was then examined to quantify the responses (another violation of GT methodology), and re-examined by another co-author for verification.

What they found was a group of people, over half women, with 2/3 indicating they’d been diagnosed with chronic pain by a medical professional. Diagnoses varied, but most (91%) had low back and neck pain, 30% with neuropathic pain, 23% with postsurgical pain, nearly 22% with abdominal pain, 20% with chronic pain after trauma/injury, 7% with cancer pain and 5% with menstrual pain.  Most people smoked cannabis either by joint, pipe or bong; some used a vaporiser, some had edibles or a tincture, and least, some sort of ointment.

The participants indicated it was on average 75% effective at reducing/treating symptoms, which is extraordinary when you realise that traditional forms of medication for neuropathic pain may reduce pain by 50% in around 1  in 4 people (Woolf, 2010). Participants spent around $3118 each year, but this was skewed because concentrates cost $3910, while topicals were $814. Joints were more expensive than vaporised product ($260 different!).

Analysing the positives of cannabis, participants reported pain relief, or at least being able to tolerate the pain more easily; while sleep benefits was the next most significant theme. Participants were encouraged that cannabis doesn’t have overdose potential, it’s natural, there are a wide range of strains with different characteristics, and limited potential for dependence.

There were numerous other positive aspects to using cannabis this way, according to the participants: things like “feeling normal”, “I am more active and able to do things I want”, being “distracted” from the pain, “able to focus”, and “able to relax”.

Negative perspectives included the cost (too expensive – in NZ Sativex is around $1000 a month – not covered by NZ pharmaceutical subsidies); some people didn’t like the smell, the effects on lungs and breathing, appetite changes (and gaining weight), and some emotional effects like anxiety or paranoia. Stigma and judgement by others also features, as did the difficulty accessing the drug, and conflict about the different laws applying to cannabis use – noting that the US has different federal and state laws.

Overall, the responses from these participants suggest a benign, mainly positive response to a drug, with negatives primarily around the social aspects – stigma from health providers, other people thinking of the participants as stoners, the legal situation and so on. For me, the limitations of this study really preclude any major judgement as to benefit or otherwise. We only know what this group of people believed, they have a vested interest in promoting benefits because negatives won’t support their belief that this is a viable treatment option, we don’t know the effect on function (particularly objective data), and we have no way of verifying the diagnoses individuals reported as the reason for prescription.

My conclusion?

It’s way past time to discuss cannabis use, health risks and health benefits. To have an open discussion about use for medicinal reasons, we need to remove the current barrier: the legal situation. While people have a vested interest in promoting the benefits over risks or adverse effects, we’re not going to have a very clear picture of what happens with ongoing use. I don’t support the use of cannabis as a medicinal product – to me there are far too many unknowns, and I think we risk wedging open a gate that has, until now, been useful for limiting the risk from pharmaceutical harms. We need to subject cannabis to the same level of rigour as any other pharmaceutical product being introduced to the market.

On the other hand, I think removing legal barriers to recreational use is about balancing the benefits and harms of this substance against other substances used for similar reasons. Alcohol and tobacco are well-known for harmful effects. Prohibition of alcohol did not work. Tobacco smoking is reducing over time courtesy of a committed campaign documenting harms, as well as raising the price via taxation. We can’t campaign around health harms for a product that isn’t legal. We can’t establish useful regulation over who produces it, who can buy it, where it can be used, the effects on work injury/vehicle injury, we can’t represent the undoubted benefits, and we look, to many people, to hold a double-standard.

And sneaking cannabis use in under the guise of “medicinal” use just isn’t on, in my humble opinion. Let’s not put medical practitioners in an unenviable situation where they’re asked to prescribe a product that is not yet examined to the level we expect for every other pharmaceutical product on the market. Let’s spend some precious research funding to establish WHO cannabis helps, WHAT it helps with, and HOW it helps – and most importantly, let’s look at whether it helps produce outcomes that surpass other approaches to persistent pain. We need to face it, currently our treatments are not very good.

 

Piper, B. J., Beals, M. L., Abess, A. T., Nichols, S. D., Martin, M. W., Cobb, C. M., & DeKeuster, R. M. (2017). Chronic pain patients’ perspectives of medical cannabis. Pain, 158(7), 1373-1379.

Woolf, C: (2010). Review: Overcoming obstacles to developing new analgesics, Nature Medicine (Supplement); 16,11: 1241 – 47

Great expectations – and low back pain


Have you ever wondered why there are so many treatments for low back pain? Like there are actually hundreds of different ways to “treat” back pain… yet the truth is, none of them work for everyone. Actually, most of them seem to help pass the time until low back pain settles of its own accord. Until it’s back again (no pun intended!).

This post is prompted after reading a string of general news articles discussing the common non-specific low back pain – under various guises of “dead butt syndrome“, “Dr Tom: Ouch I’ve hurt my back” and the like – I think it’s time for a frank discussion about the natural history of low back pain, as found in large epidemiological studies. There’s no doubt that low back pain is a problem around the world, and I think it’s partly due to unmet expectations (along with a whole lot of other variables). The Global Burden of Disease found low back pain to be the most common reason for days lived with disability around the world – that’s more than anaemia, depression, hearing loss, migraine!

Low back pain is common in every single country in the world.

Dunn, Hestbaek & Cassidy (2013) examined the prevalence of low back pain across the life span – they found that many of us view low back pain as a simple “yes/no” question – do you have it, or don’t you. They point out that people with no back pain at the time of a survey are not all the same: some might never have had a bout ever, while some might have had several bouts but just don’t have one right now. These presentations are not the same! Those who have had a previous episode will have developed an understanding of back pain on the basis of what happened, and this will influence their expectations, and subsequent response, to treatments.

Dunn, Hestbaek & Cassidy found that children/adolescents have a point prevalence (ie at the time of the survey, they reported they had back pain) of 12%. As people get older the prevalence continues to be around 12%. The elderly, those over 60 (that doesn’t really feel old to me!), seem to have a prevalence similar to people in middle age, and activities affected by low back pain seem to increase as we age.

Given the lifetime prevalence of low back pain is around 80% (or more), following people up over time seems to paint a different picture from the point prevalence studies: it’s not the same 12% of people that has low back pain all the time. Some studies show that at least 40% of people do recover within a year of an episode (see Hestbaek, Leboeuf-Yde, & Manniche, 2003). A Danish study with 5 year follow-up found around 23% of people consistently reported no pain days during the previous year (during the study) but around 10% reported more than 30 days of back pain every time they were asked. So, while long-term low back pain isn’t common in the adult population, most people do have a couple of bouts over long periods of time.

What are the risk factors? Well one clear risk factor is having had a previous episode, although this isn’t a consistent predictor for long-term back pain. Perhaps we should take a look more closely at the natural course of acute neck and low back pain – from the Norwegian longitudinal studies. From one city in Norway, these researchers screened 9056 people between 20 – 67 years old to identify those with a brand new bout of neck or back pain in the previous month – 219 people were identified, then followed for 12 months. What these researchers found was pain decreasing rapidly in the first month, irrespective of treatment, thereafter though, back pain didn’t change for the rest of the year especially for those with pain in the neck as well as the back at the first assessment, and for those who had 4 or more pain sites in the beginning.

Now what’s really interesting about this study is that the pain reduction people experienced, particularly in low back pain, was pretty close to the pain reduction people achieved whether they had treatment, or not. Hmmmm. Next question: what if we look at all the treatments people get, and those who are in the control group, and pooled that information to find out what happens? Artus, van der Windt, Jordan & Croft examined whether just taking part in a study on low back pain might influence outcomes – so they pooled 70 RCTs and 19 cohort studies, and both sets of data showed “a rapid improvement in the first six weeks followed by a smaller further improvement until 52 weeks. there was no statistically significant different in pooled standardised mean change (a measure used to compared the pooled within-group change in pain in RCTs with cohort studies) – get this, at any time point.

But wait, there’s more!

Axen & Leboeuf-Yde (2013) looked at the trajectories of low back pain over time. They summarised four studies in primary care or the general population, finding that over the course of between 12 weeks and 12 months, participants could be divided into two to four groups: one group remained uncomfortable, perhaps staying that way over the whole 12 months (around 10 – 21%); one group also remained uncomfortable but they reported their pain as “moderate” or “mild” – around 36%; another approximately 30% experienced fluctuating or intermittent low back pain; and finally, the group we love – those who recovered and remained that way, around 30 – 58%.

This is not the picture we hear in the media. This is not what we were taught. And yes, I know there are problems with pooled data because individualised responses get ironed out. But what all this says to me is – our patients come to us expecting that low back pain should completely resolve. The reality is that for a lot of people, back pain will come and go throughout the lifetime.

What does this mean to me?

Isn’t it time to give people an idea that if they have a bout of back pain, chances are high they’ll have another. Complete resolution of low back pain may not occur for a large number of people. A new bout of low back pain may not mean a new “injury” (given we don’t know why many people develop back pain in the first place). Learning to self-manage a bout of back pain is likely to save people a load of heartache, not to mention a lot of money. And maybe it’s the latter that means it’s very hard to find clear, effective messages about just how safe a painful back is. It’s far easier to sell a message of vulnerability, of the need for treatment for that “unhappy spine” as a chiropractor in Christchurch calls it. And of course, if we continue to allow the expectation that all pain should be gone, we’re going to be in business for a very long time…

 

Artus, M., van der Windt, D., Jordan, K.P., & Croft, P.R. (2014). The clinical course of low back pain: A meta-analysis comparing outcomes in randomised clinical trials (rcts) and observational studies. BMC Musculoskeletal Disorders, 15, 68.

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

Dunn, K.M., Hestbaek, L., & Cassidy, J.D. (2013). Low back pain across the life course. Best Practice & Research in Clinical Rheumatology, 27(5), 591-600.

Hestbaek L, Leboeuf-Yde C, Engberg M, Lauritzen T, Bruun NH, Manniche C. (2003). The course of low back pain in a general population. Results from a 5-year prospective study. Journal of Manipulative & Physiological Therapeutics, 26(4):213–9.

Hestbaek L, Leboeuf-Yde C, Manniche C. (2003). Low back pain: what is the long-term course? A review of studies of general patient populations. European Spine Journal, 12(2):149–65.

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.

Primary pain disorders


In a move likely to create some havoc in compensation systems around the world (well, at least in my corner of the world!), the International Association for the Study of Pain has worked with the World Health Organisation to develop a way to classify and thus record persistent pain conditions in the new (draft) ICD-11. While primary headache disorder has been in the classification for some years, other forms of persistent pain have not. Recording the presence of a pain disorder is incredibly important step forward for recognising and (fingers crossed) funding research and treatment into the problem of persistent pain. As the IASP website states:

Chronic pain affects an estimated 20 percent of people worldwide and accounts for nearly one-fifth of physician visits. One way to ensure that chronic pain receives greater attention as a global health priority is to improve the International Classification of Diseases (ICD) diagnostic classification.

The classifications are reasonably straightforward, with an overall classification of “chronic pain”, and seven subcategories into which each type of pain can be placed.

Now there will be those who are uncomfortable with labelling a symptom (an experience, aporia, quale) as a separate diagnosis. I can understand this because pain is an experience – but at the same time, just as depression, which is an experience with clinical and subclinical features, so too is pain. There is short-term and useful pain, serving as an alert and warning, and typically an indication of the potential or actual threat to bodily integrity. Just as in depression which has short-term and usually useful episodes of sadness, withdrawal and tearfulness (as in grief). At the same time, there are periods when sadness becomes intractable and unhelpful – and we call this depression. Underlying both of these situations are biological processes, as well as psychological and social contributors. Until now, however, persistent pain has remained invisible.

The definition of chronic pain, at this time, is the IASP one from the 1980’s:

“Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. Often, pain serves as a symptom warning of a medical condition or injury. In these cases, treatment of the underlying medical condition is crucial and may resolve the pain. However, pain may persist despite successful management of the condition that initially caused it, or because the underlying medical condition cannot be treated successfully.

Chronic pain is pain that persists or recurs for longer than three months. Such pain often becomes the sole or predominant clinical problem in some patients. As such it may warrant specific diagnostic evaluation, therapy and rehabilitation. Chronic pain is a frequent condition, affecting an estimated 20% of people worldwide. This code should be used if a pain condition persists or recurs for longer than 3 months.”

Chronic Primary Pain is defined as “…chronic pain in one or more anatomical regions that is characterized by significant emotional distress (anxiety, anger/frustration or depressed mood) and functional disability (interference in daily life activities and reduced participation in social roles). Chronic primary pain is multifactorial: biological psychological and social factors contribute to the pain syndrome. The diagnosis is appropriate independently of identified biological or psychological contributors unless another diagnosis would better account for the presenting symptoms. Other chronic pain diagnoses to be considered are chronic cancer pain, chronic postsurgical or posttraumatic pain, chronic neuropathic pain, chronic headache or orofacial pain, chronic visceral pain and chronic musculoskeletal pain. Patients with chronic primary pain often report increased depressed and anxious mood, as well as anger and frustration. In addition, the pain significantly interferes with daily life activities and participation in social roles. Chronic primary pain is a frequent condition, and treatment should be geared towards the reduction of pain-related distress and disability.” (definition are found here)

The definition doesn’t require identified biological or psychological contributors – so people with primary pain would be those who have fibromyalgia, persistent low back pain, perhaps even “frozen” shoulder. The main requirement is that the person is distressed by it, and that it interferes with life. Now here’s a bit of a problem for those of us who have learned to live well with our persistent pain – I experience widespread pain, but generally I’m not distressed by it, and seeing as I’ve lived with it since my early 20’s, I find it hard to work out whether I’m limited by it, or whether I’ve just adjusted my life around it, so it doesn’t really get in the way of what I want to do. Technically, using the draft definition, I might not be given the label. Does this mean I don’t have chronic primary pain?

Why did I suggest compensation systems might be interested in this new classification? Well, in New Zealand, if a person has a pre-existing condition, for example they have osteoarthritic changes in their spine even if it’s not symptomatic (ie it doesn’t hurt), and then lodges a claim for a personal injury caused by accident, they may well find their claim for cover is declined.  What will happen if someone who has fibromyalgia, has an accident (say a shoulder impingement from lifting something heavy overhead), and the problem fails to settle? I think it’s possible they’ll have their claim declined. Low back pain is probably the most common primary pain disorder. Thousands of people in New Zealand develop low back pain each year. Few will have relevant findings on imaging – and even if imaging shows something, the potential for it to be directly related to the onset of low back pain is open to debate. Especially if we consider low back pain to be a condition that doesn’t just appear once, but re-occurs thereafter (1-7). What will this mean for insurers?

I don’t know where this classification will lead insurers, but from my perspective, I can only hope that by incorporating chronic pain into the ICD-11 we will at least begin to show just how pervasive this problem is, and how many people need help because of it. And maybe, just maybe, governments like the New Zealand government, will begin to take persistent pain seriously and make it a national health priority.

  1. Dunn, K.M., Hestbaek, L., & Cassidy, J.D. (2013). Low back pain across the life course. Best Practice & Research in Clinical Rheumatology, 27(5), 591-600.
  2. Artus, M., van der Windt, D., Jordan, K.P., & Croft, P.R. (2014). The clinical course of low back pain: A meta-analysis comparing outcomes in randomised clinical trials (rcts) and observational studies. BMC Musculoskeletal Disorders, 15, 68.
  3. 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.
  4. 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.
  5. Campbell, P., Foster, N.E., Thomas, E., & Dunn, K.M. (2013). Prognostic indicators of low back pain in primary care: Five-year prospective study. Journal of Pain, 14(8), 873-883.
  6. 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
  7. Hoy, D. G., Smith, E., Cross, M., Sanchez-Riera, L., Buchbinder, R., Blyth, F. M., . . . March, L. M. (2014). The global burden of musculoskeletal conditions for 2010: an overview of methods. Annals of the Rheumatic Diseases, 73(6), 982-989. doi:10.1136/annrheumdis-2013-204344

Exercise? Who me? Yoga or physiotherapy or education…


Exercise, while one of The Most Important self management approaches for persistent pain, is not an easy sell to someone who is experiencing pain. Especially not if that exercise looks like huffing and puffing, hauling on bits of metal in a gym, or wearing lycra. Not to mention the “sports drinks”…  Those things aside, exercising is a good thing. You heard it from me, and I have declared my body an exercise free zone! The thing is, what kind of exercise, for what purpose, and how to get introduced to it.

Personally I’m a fan of exercise that achieves something else other than “getting fit”. I like gardening, I love dancing, I enjoy cycling (especially to the store to get a GREAT coffee!). Walking the dog is fun. Swimming (especially snorkeling) is awesome! I like my exercise to do more than bring on the endorphins, especially as I don’t get much of that post-exertional analgesia that many people do – and believe me, they do (Ellinson, Stegner, Schwabacher, Koltyn & Cook, 2016). I like my exercise to look like the things I need or want to do, so that when I need to do ’em, I’m in fit state to get on and do ’em.

So what kind of exercise works best? One sage told me “the exercise the person does!” and there is some truth to that, so when I begin talking to someone about exercise, I’m looking for something they can do regularly, that fits into their lifestyle, that makes them feel good, and has some other benefit to them. That benefit might be the social thing – going to a box-fit class with a group of others all bent on getting their fix of play-fighting. It might be the solitary thing – long walks along the beach with the dog for company. It might be the music – in my case, it’s belly dance (and I dare anyone to do a 5 minute shimmy drill while keeping an isolated upper body, a loose shimmy and smile!).

I like the idea of having variety – who says we need to do the same kind of exercise every day? So it’s a wet day and I don’t fancy taking my bike out in the rain, I can turn to my dance practice, or do the dusting, or vacuum the floors. It’s a frosty day and I can go for a brisk walk and take photographs of gorgeous sparkly frosty droplets while Sheba-the-wonderdog huffs steam and sniffs at the local scents. If it’s a warm day, why not head to the pool for a lap or two? If it’s a busy day and I don’t have time, what about some “exercise snacks”? Five minutes of exercise every 25 minutes adds some pretty quickly, so it’s lunges and chair dips and wall presses and shimmy practice in between writing.

Over time we’re seeing more research looking particularly at yoga for persistent pain of all kinds. Yoga comes in many different forms, and in this case I’m guessing the more extreme forms of hot yoga and contortion is not being studied. Some of the studies are appearing in rather eminent journals, like this one from the Annals of Internal Medicine and authored by a very large team including Saper, Lemaster, Delitto and colleagues (2017).

This study is a “non-inferiority” study, looking to establish whether yoga or physiotherapy, or indeed education, can help people living with chronic low back pain. Now I’m not going to do a blow-by-blow analysis of the study, that’s for you to do. What I am going to do is look at what the yoga consisted of – and see why, perhaps, yoga is getting so much research interest. BTW, yoga was found to be non-inferior to physiotherapy, and both yoga and PT were more likely than education to have a clinically meaningful response, although neither yoga nor PT were superior to education.

This is the basic format of the yoga class: Each class began with relaxation and meditation exercises, yoga breathing, and yoga philosophy. It continued with yoga poses and
concluded with relaxation. Pose variations and aids (such as chair, strap, and blocks) accommodated various abilities. Thirty minutes of daily home practice, facilitated by a DVD, a manual, and take-home yoga supplies, was strongly encouraged.

Yoga appeals to many because it seems to begin where people are at – it’s not huffy-puffy, things don’t jiggle, and generally the classes begin and end with the ritual of breathing and meditation. I like the idea of yoga (and yes, I’ve done a class or two!), because it doesn’t involve a lot of gadgets, you can do it alone or in a group, and it feels good. What I don’t like about yoga is the need to get effective and consistent feedback about how well you’re performing the poses, especially in the beginning, which means it can be difficult to do on your own without a teacher.

For people who find exercising both difficult and painful, yoga is a good place to start. I think attending classes is crucial (or at least having an instructor and a mirror!). Learning to use the meditation and breathing is integral to the exercise – and it’s this that I think makes yoga an effective addition to the exercise toolkit. What I’m less sure of is whether it’s better than any other form of exercise – or, in my case, the many different types of movements that I use in my weekly routine. And there’s the rub. As an occupational therapist, exercise is something people choose to do as a form of occupation (valued and meaningful activity). I also enjoy a bunch of other movement-based occupations, and to me these are as valid as yoga or the PT exercises included in this study. What my approach lacks, however, is a researched basis for it.

But here’s the thing: to date the research supporting exercise for people with persistent pain shows modest effects. And those effects are completely lost if the person doesn’t do the exercise. So why not have a wide range of whole-body movement practices to draw on, allowing the person to pick and choose and get out and do something every day, even if it doesn’t fit with our modern notions of what exercise should be?

 

 

Ellingson, L. D., Stegner, A. J., Schwabacher, I. J., Koltyn, K. F., & Cook, D. B. (2016). Exercise Strengthens Central Nervous System Modulation of Pain in Fibromyalgia. Brain Sciences, 6(1), 8. http://doi.org/10.3390/brainsci6010008

Saper, R. B., Lemaster, C., Delitto, A., & et al. (2017). Yoga, physical therapy, or education for chronic low back pain: A randomized noninferiority trial. Annals of Internal Medicine. doi:10.7326/M16-2579