Professional topics

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


While a biopsychosocial ‘model’ (or sociopsychobiological framework) has been widely adopted when attempting to understand pain, many critics argue that it just doesn’t give clinicians a clear way to integrate or prioritise clinical information and generate treatments. The ‘model’ itself has been challenged from many angles – it’s too complex, too simplistic, relies on Bertalanffy’s “general systems theory” which has itself been challenged, it’s too “fuzzy”, and of course there are many who think that psychological and sociocultural aspects of human experience are epiphenomena while will ultimately be boiled down to cellular or biological processes. Nevertheless, this framework also has considerable appeal, is widely adopted and I think can provide us with some useful heuristics for thinking about how and why a person presents in the way they do at the time they do – and helps us consider what can be done to reduce distress and disability.

Disclaimer: I work with the “fuzzy” sociopsychological aspects of pain management, and leave a great deal of the biological to those who focus on that – and believe me, the biological is usually done and done to the nth degree in most cases of persistent pain. I rarely see someone who hasn’t had their scans, Xrays, physical examinations, bloods, urine, nerve conduction, surgery, exercise or whatever looked at – but plenty of people who have never once been asked what they think is going on and what their main concern is. Oh and not had their sleep, mood, alcohol and other substance use, daily routines, relationships, work situation, community and spiritual aspects of life ever discussed. So, despite the constant banging on about “don’t forget the bio” – I really do not think this is a thing.

Where do we start with this approach?

The first place I start with my discussions is to ask “Tell me about your problems with pain.” What I’m focusing on in this discussion is when did the person first recognise that there was “something wrong” – and then what did they do about it.

Fabricio Benedetti talks about the neurobiological processes involved in a person detecting that he or she is “unwell”. He writes: “Physiology and neuroscience have a lot to say about feeling sick, for it involves sensory systems that convey different pieces of information related to peripheral organs and apparatuses, as well as brain regions that lead to conscious awareness.” (Benedetti, 2013). To me, this involves biological, psychological and social factors for when does a person recognise that “conscious awareness” means something? Benedetti goes on to say “The second step is what makes a patient “seek relief,” a kind of motivated behavior that is aimed at suppressing discomfort. This behavioral repertoire is not different from that aimed at suppressing hunger or thirst, and the brain reward mechanisms are crucial in this regard” (Benedetti, 2013). Judgements about what internal experiences mean may begin with a reflex response (automatic and based on evolutionary demands to keep safe) but what we DO about those experiences depends a great deal on what we learn from others. The people we most draw from are those around us – mother, father, siblings, people in our immediate family and extended family. And over time, the social nature of humans means we also consider the community in which we live – and wider with social media! Judgements, or appraisals (thoughts and beliefs about the meaning of these internal experiences) are, ‘fraid to say, psychological in nature. While the influences on thoughts and beliefs are – you guessed it – social.

So, how can a clinician use this information? Where’s the research? Come on – science it up woman!!

If it’s not enough to know that there are neurobiological factors underpinning our internal experience, and motivated behaviour is tied up with reward systems, then what else can we use to understand the processes of feeling ill and seeking treatment? To me, the natural first step is to look at learning mechanisms. Yep, very basic Psych 101 classical and operant conditioning mechanisms. Add in a dash of social learning theory (how we learn from watching and talking with others) and we have some rather useful experimentally-validated hypotheses to work with.

What do I mean by this?

Well, at least part of clinical reasoning is a process of recognising potential explanations for the phenomena we see. My take on clinical reasoning is that we can use case formulation to help generate a series of hypotheses to explain why a person is coming to see us in this way at this time – and what might be maintaining their current situation. In case formulation we can use “abductive reasoning” (recognising a potential “rule” or class of behaviour from a specific observation – eg we can postulate that a person’s sleep disturbance might be due to low mood, sleep apnoea, habit, operant conditioning, or a new baby, and we’ll probably collect some more information to test each of these possible explanations before deciding on the most probable reason). If we know a whole bunch of research around what humans do when they’re feeling sore and vulnerable, we are able to come up with a bunch of possible reasons for someone noticing they feel unwell, judging it in a certain way, and then deciding to do something about it.

For example, we know from research studies that people who have had adverse experiences in early childhood have a greater risk of developing post-traumatic stress disorder and chronic pain (eg Afari, Ahumada, Wright, Lostoufi, Golnari, Reis & Cuneo, 2014; Jones, Power & Macfarlane, 2009). We also know that those people may develop weaker attachments to others and so feel vulnerable in relationships where high levels of trust are needed – also linked to the presence of persistent pain – and adversely affecting outcomes from multidisciplinary pain management programmes (Anno, Shibata, Ninomiya, Iwaki, Kawata, Sawamoto et al., 2015; Kowal, McWilliams, Peloquin, Wilson, Henderson & Fergusson, 2015).

These factors might mean that when we ask someone about their theory for why they have persistent pain, or what they think is going on, we might keep an ear open to listen for threats to relationships around the time of the onset of the problem dealing with pain (especially if the pain has been present for a while but the person hasn’t been looking for treatment until just now). We might also be thinking hard about the neurobiological effects of relationship breakups and how this might impinge on either coping (eg accessing strategies to manage effectively during painful experiences) or on stress responses (eg heightened vigilance to threat).

Two things: (1) This doesn’t mean persistent pain is “psychological” – it’s not, but these experiences might set the scene for neurobiological changes, both in “set-point” for threat and in resilience for dealing with threat. (2) This also doesn’t mean that we need to deal with the response to relationship stress ourselves – it might mean we listen respectfully, and bear this vulnerability in mind during our interactions, being careful not to threaten trust, and work hard to retain a sense of warmth/empathy as well as competence for this person.

Next time: More on learning theory and how these might influence the way we look at why someone seeks treatment with us, and why at this time, and what may be maintaining the behaviours we see.

 

Afari N, Ahumada SM, Wright LJ, Mostoufi S, Golnari G, Reis V, Cuneo JG., (2014). Psychological trauma and functional somatic syndromes: A systematic review and meta-analysis. Psychosomatic Medicine, 76, 2-11.

Anno, K., Shibata, M., Ninomiya, T., Iwaki, R., Kawata, H., Sawamoto, R., . . . Hosoi, M. (2015). Paternal and maternal bonding styles in childhood are associated with the prevalence of chronic pain in a general adult population: The hisayama study. BMC Psychiatry, 15(1), 181. doi:10.1186/s12888-015-0574-y

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

Jones GT, Power C, Macfarlane GJ, (2009). Adverse events in childhood and chronic widespread pain in adult life: Results from the 1958 British Birth Cohort Study. Pain 143:92-96.

Kowal, J., McWilliams, L. A., Péloquin, K., Wilson, K. G., Henderson, P. R., & Fergusson, D. A. (2015). Attachment insecurity predicts responses to an interdisciplinary chronic pain rehabilitation program. Journal of Behavioral Medicine, 38(3), 518-526. doi:10.1007/s10865-015-9623-8

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What should healthcare professionals learn?


I was lucky enough to spend two days attending the Placebo Symposium in Sydney in November this year – what an experience! A lineup of the cream of researchers exploring placebo and contextual responses (meaning responses) – all were excellent speakers and the focus was on both research and what this means to clinicians. If you’re keen to watch all you can for free over the next two weeks – click here: www.placebo.armchairmedical.tv.

At the end of the symposium, the speakers were asked a question by artist Eugenie Lee what subjects they would want taught if they had all the facilities and students with top class skills attending. This is what they said (it’s the Lennox Thompson translation, any mis-translations are entirely my responsibility):

  • Inform students about the contextual effects of every single clinical encounter and treatment
  • Help them focus on supporting patients to develop helpful expectations about treatments
  • Read Stanislovski (A good doctor [healthcare professional] is about being a good actor)
  • Always remember: we’re treating people not tissues
  • Use words wisely (they can heal – and harm)
  • Listen to your patients (and show them you’re listening)
  • Interprofessionalism is a thing
  • Talk with your patients not at them
  • Train together with your allied health colleagues
  • Ignore “placebo” or contextual effects at your peril
  • “Placebo” will eventually die – but the effect of context lives on in every treatment
  • Communication skills training needs more than a taste – to learn these skills takes time and intensity
  • Emphasise not just empathy – but also competence – these two factors contribute enormously to the “meet the therapist moment” (generating a sense of trustworthiness)
  • Introduce neurobiology from the beginning of the course
  • Learn [much much much more] about pain throughout the programme – not just the neurobiological systems but the psychological and social
  • Develop greater understanding of research methodologies for studying treatments and their effects

What were my take-away points from this whole conference?

As a longtime convert to Dan Moerman’s re-labeling to meaning response of what we often call “placebo effect”, the key points I took away were these (and you’ll see them pop up again and again in my blogs I’m sure):

  • Every healthcare encounter involves four things: a person seeking help, a person hoping to deliver help, a treatment ritual, and a social context. These can’t be divided if we hope to understand the outcome of treatment.
    • We need to understand the person seeking help – how they identify their illness, how they frame recovery, what their main concern is, and the context in which they are experiencing their illness.
    • We need to understand the person hoping to deliver help – how they view their contribution, how they view the person seeking help, the way they frame their treatment, the context in which they’re given the authority to help, and how they frame recovery.
    • We need to explore the treatment ritual – from the packaging, the meaning (to both parties) of the artifacts, the procedures, the words and actions – all of these have meaning, as marketing companies undoubtedly know (and exploit).
    • We need to examine the social context – the communities in which we live, the way illness and wellbeing are defined, the way healing is understood, how treatments are recognised, the impact of language and interpretation of that language and the way language evolves over time, how communities view treatment seekers and treatment givers, historical understanding and how this influences who, what, why and how therapeutic interactions are enacted.
  • The psychological is underpinned [as much as we can detect for now] by neurobiology, at one level of analysis. Neurobiological processes are incredibly complex and we don’t understand them very well. As we do, many of the influences decried as “woolly” or “fluffy” by some of my colleagues are, I think, going to be uncovered and found to be extraordinarily complex interactions between neurobiological systems. And yes, they will be complex – beyond most mortal’s understanding. This doesn’t mean they’re woo, or that they can be disregarded.
  • A other levels of analysis, sociopsychological processes are incredibly important contributors to the way treatments are sought – and treatments have effects. This means we’re unlikely to understand them in any simplistic sense. So to deride these processes as irrelevant or “unscientific” simply because they don’t fit in with an existing model of cause and effect (particularly if they don’t fit with a simple 1+2+3=6 model) probably means there’s a lot of learning needed. Simply because an empirical basic science or RCT doesn’t show “what’s going on” does not mean the concept under study is “not science” – it just means a scientific methodology that accommodates these complexities is needed. Not everything can be reduced to an experimental design – qualitative research is valid for some very important questions.
  • Communication – what and how we express meaning to another, and how this is interpreted and responded to by that other – occurs everywhere and all the time. Whether we attend to it or not. Meaning-making is something humans just do. So maybe as health professionals we should invest rather more than we do in training ourselves to be skilled at communicating. This means recording our interactions, reviewing them, getting to know the effect of what we communicate and training ourselves to be just as careful with our communication as we are with prescribing anything else. Because it could be that our communication is the most potent ingredient in our treatment.

“A good listener is not only popular everywhere, but after a while he knows something.” —Wilson Mizner

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.

Manage pain – or aim to cure? Why I’m committed to pain management


Prominent researchers, clinicians and commentators seem to suggest that aiming to help people live with their pain is aiming too low. That pain cure or at least reduction is The Thing To Do. It’s certainly got a bit of a ring to it – “I can help get rid of your pain” has a sex appeal that “I can help you live with your pain” doesn’t have. And I can recognise the appeal. Persistent pain can be a scourge for those who live with it; it can eat away at every part of life. Imagine waking up one day to find NO PAIN! Excited much?

So why do I keep hammering on about this not very glamorous, certainly very challenging and at times unrewarding area of practice?

Here’s the thing. Persistent pain is extremely common. Not only is low back pain responsible for the most years lived with disability globally (Hoy, Bain, Williams, March, Brooks, Blyth, Woolf, Vos & Buchbinder, 2012), painful disorders like osteoarthritis increase with an aging population, and post-surgical pain is a problem for ~ 12% of people undergoing hip replacement, between 20 – 50% women undergoing mastectomy, and we all recognise the pain after limb amputation (between 50 – 80%) (Reddi & Curran, 2014). In New Zealand one person in five experiences persistent pain that goes beyond three months…

And our treatments, whether they be pharmaceuticals, procedures, surgeries or even groovy new things like mirror therapy or graded motor imagery don’t guarantee complete pain relief for 100% of patients. In fact, each new wave of therapy provides some pain relief for some people some of the time. And we shouldn’t be completely surprised about this because our nociceptive system is extraordinarily complex – and needs to be active because without pain we’re not likely to live long…or prosper. In fact, I’ll go out on a limb here and suggest that our nociceptive system with associated thoughts, emotions and behavioural responses has built-in redundancy simply because it’s there to protect us against potential harm. And every body system has at least one disorder/disease/dysfunction, so why would we think our “pain” system is immune?

So why do I spend time learning about management when I could be focused on reducing pain?

Well one reason is my clinical orientation. I’m an occupational therapist at heart (true, warped by contact with psychologists and physiotherapists), but essentially I’m about helping people do the things they need and want to do in daily life. My tools of trade are first of all focused on helping people work out the occupations (activities) that make them feel like themselves and then helping them do those things – and secondarily, and as a result of this focus, on helping people deal with their pain experience. Sometimes the latter involves helping people develop awareness of exactly how much or how little of their body and life is taken up with pain, helping them develop “wiggle room” so they can feel they have a little more space to be who they are, helping them find new ways to do those occupations that make them feel like themselves so the pain doesn’t take up quite so much room in their sense of self. Sometimes I do focus on obvious ways that people respond to their experience that may actually be making that experience much more unpleasant than it needs to be.

Another reason for me is that with a primary focus on pain reduction, we can forget the reason people want pain reduced – which is to go on and live life. And when we’re unsuccessful at reducing pain – where do those people go for help? What does it feel like to seem to “fail” a treatment again? and again? Who helps those people have good quality of life when they feel demoralised, the treatment options are exhausted and the clinicians who so desperately want to help them have no more ideas?

And as I mentioned above – there are no absolute cures for most forms of persistent pain. Nothing in my reading of the research around the world suggests that researchers have hit upon a jackpot and found a way to eliminate persistent pain 100%. What that means is there are likely to be people who will never experience complete relief from their pain. And others for whom the treatment is unavailable because of cost, side effects, intrusion on life, or because the treatment violates their values.

And because there are people who need to live with persistent pain until we have a “universal cure”, researchers and clinicians still need to refine and innovate the pain management strategies that will need to be used.

I’m not the person to make the decision about whether pain reduction or pain management is the best option. That’s not my job as a clinician or a researcher – I’m there to help people weigh up the costs and the benefits of treatments, and examine how best we can help those who can’t get rid of their pain. The thing is: if clinicians don’t know that there are viable ways of living well with pain (or they reject these as inferior or second class in comparison with pain reduction or elimination) how will they support their patients to make their own decisions? Or will they neglect to offer the approaches they don’t know about? And what kind of a choice is that?

 

 

 

Hoy, D., C. Bain, G. Williams, L. March, P. Brooks, F. Blyth, A. Woolf, T. Vos and R. Buchbinder (2012). A systematic review of the global prevalence of low back pain. Arthritis & Rheumatology 64(6): 2028-2037.

Reddi, D., & Curran, N. (2014). Chronic pain after surgery: pathophysiology, risk factors and prevention. Postgraduate medical journal, 90(1062), 222-227.

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.