Assessment

Pain science is not a thing


Today’s post is occasioned by reading several discussions on various forums where the term “pain science” and various adjectives to describe this kind of practice. For those who don’t want to read the rest of my ramblings: no, it’s not a thing, science is an approach to understanding phenomena, and I would have thought all health professionals would use a science-based approach to treatment.

I went on to Google, as you do, to find out when this term began its rise in popularity. Google wasn’t particularly helpful but did show that it’s been around since 2004 at least, and seems to have been centred around the US, UK and Australia in roughly May 2004. I can’t grab data from earlier than this, sadly, but I think it’s interesting to take a look at the popularity peaks and troughs…

So, what does “pain science” mean to commentators? I haven’t delved in too deeply to the social media use of the term, but given I’m a social animal and have written my blog since 2007 (which is mainly on “pain science”) I’ve encountered it many times. It seems to be related to using a neurobiological explanation for pain as an experience (referring to the phenomenon and the underlying biological processes involved) rather than focusing purely on biomechanics or tissue damage/nociception as the key force. And it does seem to tie in with the emergence of “Explain pain” as one way of helping people reconceptualise their experience as something they can influence rather than something other people need to “fix”.

Commentators who aren’t in love with the “explain pain” thing have said things like “the pain science camp” or as one person put it “There’s your manual PTs, your pain science PTs, and your just load it PTs etc”

I went on to Twitter and the hashtag #painscience was paired with #BPSModel and #PT and #physicaltherapy (or variations), #chronicpain #exercise #lowbackpain – and so on.

So what do I think pain science means if it’s not a neurobiological approach to pain management? Well – pain science is a lot like cardio-respiratory science, and neurological science, and psychological science – it’s about applying a scientific approach to understanding pain. Science has been defined as “the intellectual and practical activity encompassing the systematic study of the structure and behaviour of the physical and natural world through observation and experiment.” In this instance, Google is your friend. So science is about systematically studying phenomena through observation and experimenting. If we apply this to pain – it’s the systematic study of structure and behaviour of the phenomenon we call ‘pain’ through observation and experiment. For what it’s worth, scientific study of pain has been going on since… oh at least Descartes, but probably much earlier given that pain is a ubiquitous and essential part of human experience.

To me, understanding pain involves multiple disciplines: yes to biology, and especially neurobiology because the experience (as we understand it now) involves neurobiological processing. But it’s also about psychology
the scientific study of the human mind and its functions, especially those affecting behaviour in a given context; sociology – the study of the development, structure, and functioning of human society; the humanities – the study of how people process and document the human experience; politics – the activities associated with the governance of a country or area, especially the debate between parties having power; and Anthropology –  the study of humans and human behavior and societies in the past and present. Social anthropology and cultural anthropology study the norms and values of societies. Linguistic anthropology studies how language affects social life.

So to describe an entire approach to understanding a phenomenon as if it’s a “movement” or “camp” or “dogma” or even “tribe” suggests serious  misunderstanding of both science and of an intervention.

What is “explain pain” then, or pain neurobiology education? – it’s an explanation of some of the biological elements of our nociceptive system as they combine to produce the experience we know as pain. For some people it’s the first time anyone took the trouble to explain why the pain of a papercut feels so bad compared with, for example, the pain of a sprained ankle; and why they still experience pain despite having no “damage” as visible on imaging. It’s an attempt to give people a frame of reference from which to understand their own journey towards recovering from a painful injury/disease/problem. In itself it’s not new: explanations for pain have been used in pain management programmes since the 1970’s (and earlier, if we consider that Fordyce used explanations in his behavioural approaches to pain management), and have routinely drawn on current pain research to help provide explanations that make sense to both the person and the clinician. The distinction between earlier explanations which drew heavily on the gate control theory, and this latest iteration is that the explanations are more complex, pain is considered to be an “output” that emerges from multiple interactions between brain and body, and that’s about it. Oh and it’s been picked up and enthusiastically used by physiotherapists (and other primarily body therapists) around the world.

What’s the evidence for this approach? Well, IMHO it’s not intended to be a stand-alone “treatment” for most people experiencing pain. I see giving an explanation as integral to usual practice, just as we do when we explain why it’s not a good idea to go running on a newly sprained ankle or why we’re suggesting a mindfulness to someone with a panic disorder. So far there have been a lot of studies examining variants of “explaining pain” alone or in combination with a number of other treatments including exercise. A recent systematic review and meta-analsyis of “pain neuroscience education” for chronic low back pain found eight papers (with 615 participants) showing that in the short-term, this kind of education reduces disability (by 2.28 points on the Roland-Morris Disability Questionnaire which is a 24 point scale) in the short-term and a slightly lesser effect in the long-term  (2.18). There were greater effects when this was combined with physiotherapy, though we often don’t know exactly what is included in “physiotherapy”.  There was some evidence that this kind of education helps reduce pain scores (by 1.32) but only in combination with other physiotherapy interventions. The authors pointed out that the strength of evidence for education on pain in the short term was low to moderate, but that it doesn’t have much of an impact on pain-related fear and avoidance, or on pain catastrophising (Wood & Hendrick, in press).

To compare this with another active treatment, exposure therapy for fear of movement/reinjury in chronic low back pain, de Jong, Vlaeyen, Onghena, Goossens, Geilen & Mulder (2005) performed a careful study of six individuals, using a single case experimental design. (If you’re not familiar with this approach to research – it’s extremely rigorous and useful in a clinical setting, this link takes you to a chapter discussing its use).  The aim was to establish which part of treatment “did the work” to change behaviour, but also measured pain intensity, and fear of pain and movement.  The treatments were information about pain and mechanisms, and the activities were those the person particularly wanted to be able to do. Their findings identified that explanations do little to pain intensity, avoidance or fear – but what actually worked was doing graded exposure. In other words, experiencing something different, DOING that something different in the real world, was more effective than talking about why someone shouldn’t be afraid. A much more recent replication of this study was conducted by Schemer, Vlaeyen, Doerr, Skoluda, Nater, Rief & Glombiewski (2018) and shows the same result: doing trumps talking about doing.

When we sit down and take a cold hard look at what we do in pain management we can see that the field has to draw on a huge range of disciplines and fields of study to understand the problems people experiencing pain have. This is, in fact, why Bonica and colleagues first established the International Association for the Study of Pain, and why multidisciplinary (and now interprofessional) pain management teams and approaches were established. None of us can possibly hold all the knowledge needed to work effectively in the area. At the same time, as health professionals working with people, we do need to have some foundation knowledge about biology, disease, illness, psychology, sociology and anthropology. These areas of study inform us as we work hard to help people get their heads around their pain. Do we need to be experts in all of these fields? Yes – if you work completely in isolation. No – if you work within an extended team (whether co-located or otherwise). Pain research will continue to push our understanding ahead – and to be responsible health professionals, we must incorporate new understandings into our practice or we risk being unprofessional and irrelevant. I would go as far as to say we’re irresponsible and harming patients if we fail to incorporate what is known about pain as a multidimensional experience. It’s time to back away from temporary guruism and move towards a far more nuanced, and perhaps less flighty approach to understanding pain.

Pain science. No, it’s not a thing. Pain being examined through multiple scientific lenses: definitely a thing.

NB for the avoidance of doubt: pain is never a “thing” but examining pain through multiple scientific lenses involves many “things”. (Merriam-Webster – click)


de Jong, J. R. M., Vlaeyen, J. W. S. P., Onghena, P. P., Goossens, M. E. J. B. P., Geilen, M. P. T., & Mulder, H. O. T. (2005). Fear of Movement/(Re)injury in Chronic Low Back Pain: Education or Exposure In Vivo as Mediator to Fear Reduction? [Article]. Clinical Journal of Pain Special Topic Series: Cognitive Behavioral Treatment for Chronic Pain January/February, 21(1), 9-17.

Schemer, L., Vlaeyen, J. W., Doerr, J. M., Skoluda, N., Nater, U. M., Rief, W., & Glombiewski, J. A. (2018). Treatment processes during exposure and cognitive-behavioral therapy for chronic back pain: A single-case experimental design with multiple baselines. Behaviour Research and Therapy, 108, 58-67.

Wood, L., & Hendrick, P. A. A systematic review and meta-analysis of pain neuroscience education for chronic low back pain: Short-and long-term outcomes of pain and disability. European Journal of Pain, 0(0). doi:doi:10.1002/ejp.1314


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From the particular to the general – Clinical reasoning in the real world


From the particular to the general –
Clinical reasoning in the real world

I make no secret of my adherence to evidence-based healthcare. I think using research-based treatments, choosing from those known to be effective in a particular group of people in a specific context helps provide better healthcare. But I also recognise problems with this approach: people in clinical practice do not look like the “average” patient. That means using a cookie cutter, or algorithm as a way to reduce uncertainty in practice doesn’t, in my humble opinion, do much for the unique person in front of me.

I’ve been reading Trisha Greenhalgh’s recent paper “Of lamp posts, keys, and fabled drunkards: A perspectival tale of 4 guidelines”, where she describes her experience of receiving treatment based on the original description given for her “fall”. The “fall” was a high-impact cycle accident with subsequent limb fractures, and at age 55 years, she was offered a “falls prevention” treatment because she’d been considered “an older person with a fall”. Great guidelines practice – wrong application!

Greenhalgh goes on to say “we should avoid using evidence-based guidelines in the manner of the fabled drunkard who searched under the lamp post for his keys because that was where the light was – even though he knew he’d lost his key somewhere else”

Greenhalgh (2018), quoting Sir John Grimley Evans

When someone comes to see us in the clinic, our first step is to ask “what can I do for you?” or words to that effect. What we’re looking for is the person’s “presenting symptoms”, with some indication of the problem we’re dealing with. Depending on our clinical model, we may be looking for a diagnostic label “rheumatoid arthritis” or a problem “not sleeping until three hours after I go to bed”.

What we do next is crucial: We begin by asking more questions… but when we do, what questions do we ask?

Do we follow a linear pattern recognition path, where we hypothesise that “rheumatoid arthritis” is the problem and work to confirm our hypothesis?

Our questions might therefore be: “tell me about your hands, where do they hurt?” and we’ll be looking for bilateral swelling and perhaps fatigue and family history and any previous episodes.

Or do we expand the range of questions, and try to understand the path this person took to seek help: How did you decide to come and see me now? Why me? Why now?

Our questions might then be: “what do you think is going on? what’s bothering you so much?”

Different narratives for different purposes

Greenhalgh reminds us of Lonergan (a Canadian philosopher), as described by Engebretsen and colleagues (2015), where clinical enquiry is described as a complicated process (sure is!) of 4 overlapping, intertwined phases: (a) data collection – of self reported sensations, observations, otherwise known as “something is wrong and needs explaining”; (b) data interpreting “what might this mean?” by synthesising the data and working to recognise possible answers, or understanding; (c) weighing up alternative interpretations by judging; and (d) deciding what to do next, “what is the right thing to do”, or deliberation.

Engebretsen and colleagues emphasise the need to work from information from the individual to general models or diagnoses (I’d call this abductive reasoning), and argue that this process in the clinic should be “reflexive” and “informed by scientific evidence” but warn that scientific evidence can’t be replaced simply by reflexive approaches.

The reason for conceptualising clinical reasoning in this way is that a narrative primarily based on confirming a suspicion will likely reduce the number of options, narrow the range of options considered, and if it’s focused on diagnosis, may well over-ride the person’s main concern. A person may seek help, not because he or she wants a name or even treatment, but because of worries about work, the impact on family, or fears it could be something awful. And without directly addressing those main concerns, all the evidence-based treatments in the world will not help.

Guidelines and algorithms

Guidelines, as many people know, are an amalgamation of RCT’s and usually assembled by an esteemed group of experts in an attempt to reduce unintended consequences of following poorly reasoned treatment. They’re supposed to be used to guide treatment,  supporting clinical reasoning with options that, within a particular population, should optimise outcomes.

Algorithms are also assembled by experts and aim to provide a clinical decision-making process where, by following the decision tree, clinicians end up providing appropriate and effective treatment.

I suppose as a rather idiosyncratic and noncomformist individual, I’ve bitterly complained that algorithms fail to acknowledge the individual; they simplify the clinical reasoning process to the point where the clinician may not have to think critically about why they’re suggesting what they’re suggesting. At the same time I’ve been an advocate of guidelines – can I be this contrary?!

Here’s the thing: if we put guidelines in their rightful place, as a support or guide to help clinicians choose useful treatment options, they’re helpful. They’re not intended to be applied without first carefully assessing the person – listening to their story, following the four-step process of data collection, data interpretation, judging alternatives, and deciding on what to do.

Algorithms are also intended to support clinical decision-making, but not replace it! I think, however, that algorithms are more readily followed… it’s temptingly easy to go “yes” “no” and make a choice by following the algorithm rather than going back to the complex and messy business of obtaining, synthesising, judging and deciding.

Perhaps it’s time to replace the term “subjective” in our assessment process. Subjective has notions of “biased”, “emotional”, “irrational”; while objective implies “impartial”, “neutral”, “dispassionate”, “rational”. Perhaps if we replaced these terms with the more neutral terms “data collection” or “interview and clinical testing” we might treat what the person says as the specific – and only then move to the general to see if the general fits the specific, not the other way around.

 

Engebretsen, E., Vøllestad, N. K., Wahl, A. K., Robinson, H. S., & Heggen, K. (2015). Unpacking the process of interpretation in evidence‐based decision making. Journal of Evaluation in Clinical Practice, 21(3), 529-531.

Greenhalgh, T. (2018). Of lamp posts, keys, and fabled drunkards: A perspectival tale of 4 guidelines. Journal of Evaluation in Clinical Practice, 24(5), 1132-1138. doi:doi:10.1111/jep.12925

Myths about exposure therapy


Exposure therapy is an effective approach for pain-related anxiety, fear and avoidance, but exposure therapy is used less often than other evidence-based treatments, there is a great deal of confusion about graded exposure, and when it is used, it is not always well-conducted. It’s not a treatment to be used by every therapist – some of us need to challenge our own beliefs about pain, and whether it’s OK to go “into” the pain a little, or even slightly increase pain temporarily!

Below are some common misconceptions and suggestions for how to overcome them:

Misconception: Exposure therapy causes clients undue distress and has adverse consequences.

Suggestions: Although exposure therapy can lead to temporary increases in anxiety and pain, it is important to remember that these symptoms are not dangerous, and that exposure is generally carried out in a very gradual and predictable way. Exposure very rarely causes clients harm, but it is important to know your clients’ medical histories. For example, a client with a respiratory condition would not be asked to complete an exposure designed to elicit hyperventilation.

I usually begin with a really clear explanation for using this approach, basing my explanation on what the person has already said to me. By using Socratic or guided discovery, I try to understand the logic behind the person’s fear: what is it the person is most worried about? Often it’s not hurt or harm, it’s worrying that they won’t sleep, or they’ll have a flare-up that will last a looooong time – and they won’t be able to handle it. These are fundamental fears about having pain and vital to work through if the person is going to need to live with persistent pain for any length of time.

Once I’ve understood the person’s reasons for being bothered by the movements and pain, then I work on developing some coping strategies. These must be carefully carried out because it’s so easy to inadvertently coach people into using “safety behaviours” or “cues” that work to limit their contact with the full experience. Things like breath control, positive self-statements, any special ways of moving, or even ways of recovering after completing the task may serve to control or reduce contact with both anxiety and pain. I typically draw on mindfulness because it helps people focus on what IS happening, not what may have happened in the past – or may happen in the future. By really noticing what comes up before, during and after a graded exposure task, and being willing to experience them as they are, people can recognise that anticipating what might happen is often far worse than what does happen.

Finally, I’ll work through the scenario’s – either pictures of movements and activities, or descriptions of the same things. I prefer photographs (based on the Photographs of Daily Activity), because these elicit all the contextual details such as the other people, weather, flooring or surface and so on that are often factors increasing a person’s concerns. We begin with the activity that least bothers the person and consistently work up from there, with practice in the real world between sessions. I’ll go out to the places the person is most concerned about, we’ll do it together at first, then the person can carry on by themselves afterwards.

Misconception: Exposure therapy undermines the therapeutic relationship and leads to high dropout.

Suggestions: If you give your person a clear reason for using this approach and deliver it well,  the person is more likely to achieve success – and this in turn strengthens your relationship. Additionally, there is evidence that dropout rates for exposure are comparable to other treatments.

There is something about achieving a difficult thing that bonds us humans, and if you approach graded exposure with compassion, curiosity, and celebration, you may find your relationship is far more rewarding and deeper than if you simply prescribe the same old same old.

Misconception: Exposure therapy can lead to lawsuits against therapists.

Suggestions: Survey data suggest that lawsuits against therapists using exposure are extremely rare. As with any kind of therapy, you can take several steps to protect yourself from a legal standpoint. Don’t forget to obtain informed consent, ensure your treatment is delivered with competency, professionalism, and ethical consideration.

The best book/resource by far for graded exposure is Pain-Related Fear: Exposure-Based Treatment for Chronic Pain, (click) by Johan W.S. Vlaeyen, Stephen J. Morley, Steven J. Linton, Katja Boersma, and Jeroen de Jong.

Before you begin carrying out this kind of treatment, check you have these skills (from the book I’ve referenced):

Vlaeyen, Johan, Morley, Stephen, Linton, Steven, Boersma, Katja, & de Jong, Jeroen. (2012a). Pain-related Fear. Seattle: IASP Press.

Assessing problems with sleep and pain – ii


Last week I wrote about my approach to assessing sleep problems in those with persistent pain. As an ex-insomniac I’ve spent a while learning about sleep so I can understand what’s going on, and why sleep can be such a problem. In this week’s post I want to dig a little deeper into what’s going on with poor sleep, as well as some of the unique features of sleep in people experiencing persistent pain.

Having reviewed the five main areas that are fundamental (and can/should be assessed by anyone working with people who experience persistent pain), the next area I want to look at with people is mood. There are two primary psychopathological contributors to poor sleep: the first we’ve dealt with last week (Question 4 – what’s going through your mind…) which is by far and away the most common initiator and maintainer of insomnia, and it doesn’t even need to be a diagnosable anxiety disorder! The second, you’ll probably have guessed, is depression.

Depression is common in people with both rotten sleep and ongoing pain (Boakye, Olechowski, Rashiq, Verrier, Kerr, Witmans et al, 2016), and there are some suggestions that pain and depression may be related and similar neurobiological processes may be involved for both (increased limbic activity being one of them). In depression, there is increased activity in the HPA Axis, reduced BDNF (brain-derived neurotrophic factor), and reduced 5HT with increased pro-inflammatory cytokines . In persistent pain, there may be activity in the HPA Axis, there is certainly reduced BDNF except in the spinal cord, and reduced 5HT, along with increased pro-inflammatory cytokines. And in sleep disturbances there is also increased activity in the HPA Axis, redced BDNF, reduced 5HT and guess what… increased pro-inflammatory cytokines. And all three interact with one another so that if you happen to be depressed, you’re more likely to experience pain that goes on, and your sleep will also reduce your mood and increase your pain. And the reverse. All very messy indeed!.

What this means is that assessing for low mood and the impact on sleep is important – if someone’s describing waking well before they usually do, in the wee small hours (anywhere from 3 – 5am if they usually wake at 7.00am) I’m ready to screen for low mood. To be honest I always assess for that anyway! Depression is also associated with low motivation and loss of “get up and go” so this is likely to interact with poor sleep, creating a very tired person.

There are three other very important aspects of sleep I like to assess for: sleep apnoea, where someone stops breathing for seconds to minutes at a time, often snorting awake, and this may be associated with snoring and daytime sleepiness. Often the person won’t be aware of their sleep apnoea, so it can be helpful for a bed-partner to let you know whether this is a feature of your patient’s sleep.

The next are a group of movement disorders of sleep, many of which are associated with the third area I assess, which are medications.

Movement disorders of sleep include restless leg syndrome – that feeling of absolutely having to move the legs, usually at night, and relieved by getting up to walk around, but in doing so, making it difficult to sleep. Another is periodic limb movement disorder of sleep, which can be every 5 – 30 seconds of leg twitching all night long, and in some cases, whole body twitching though this is less frequent and less rhythmic. This latter problem may not be noticed by the person – but their bed-mate will know about it! – and this problem may be associated with both sleep apnoea and restless leg, AND some doses of antidepressants. Another common contributor to these problems is low iron levels – worth checking both iron and medications!

Finally with medications, I like to understand not only what the person is taking, but also when they’re taking them. Several points are important here: some medications are usually sedating such as tricyclic antidepressants but in some people nortriptyline can paradoxically increase alertness! If that’s the case, timing the dose is really important and should be discussed with either the prescribing doctor, or a clinical pharmacist. Opioids depress respiration (ie slow breathing down) so can be problematic if the person has sleep apnoea AND is taking opioids, the drive to inhale may be less, causing more frequent and deeper periods without breathing normally. For restless legs and periodic limb movement disorder, some antidepressants (venlafaxine is one of them) in high doses can cause the twitching and once the dose is reduced, this fades away, at least a bit.  There is a very small amount of research suggesting that NSAIDs can influence sleep quality in some people also.

The effects of poor sleep are many: anything from micro-sleeps during the day (problematic while driving or operating machinery!), to more irritability, sluggish responses, less concentration and more difficulty solving problems. Pain is associated with more frequent micro-wakenings during the night (Bjurstrom & Irwin, 2016) but findings with respect to whether deep sleep, REM sleep or light sleep were consistently more affected weren’t clear.

Having completed my assessment, more or less, I can also use a few pen and paper measures: Wolff’s Morning Questions (Wolff, 1974), Kryger’s Subjective Measurements (1991), Pittsburgh Sleep Quality Index (Bysse, Reynolds, Monk et al, 1989) and the Sleep Disturbance Questionnaire (Domino, Blair,& Bridges, 1984) are all useful. Speaking to the partner is an excellent idea because I don’t know about you but I never snore but my partner swears I do! Who do you believe?!

People experiencing insomnia are not very reliable when describing their own sleep habits – we’re terrible at noticing when we’re actually asleep or awake in those early stages of sleep, so we typically think we’ve slept less than we actually have. We also do a whole lot of things to avoid not sleeping – and these can actually prolong and extend our sleeplessness!

We’ll discuss what to do about the factors you may have identified in your sleep assessment in next week’s instalment, but you can rest assured it’s not crucial for you to do anything yourself about some things. For example, if someone has sleep apnoea, referring for a sleep study is important, but not something YOU need to do! But please make sure a referral is suggested to someone who can make it happen. Similarly with medications and sleep movement disorders, it’s not something you should tackle on your own – please discuss managing these with a specialist sleep consultant, psychiatrist, or the person’s own GP. Mood problems – treat as you would any time you find someone with a mood problem.

Next week – off to the Land of Nod: A roadmap?!

 

Boakye, P. A., Olechowski, C., Rashiq, S., Verrier, M. J., Kerr, B., Witmans, M., . . . Dick, B. D. (2016). A critical review of neurobiological factors involved in the interactions between chronic pain, depression, and sleep disruption. The Clinical Journal of Pain, 32(4), 327-336.

Buysse DJ, Reynolds CF 3rd, Monk TH, et al. The Pittsburgh Sleep Quality Index: a new instrument for psychiatric practice and research. Psychiatry Res 1989; 28(2):193–213.

Domino G, Blair G, Bridges A. Subjective assessment of sleep by Sleep Questionnaire. Percept Mot Skills 1984;59(1):163–70.

Kryger MH, Steljes D, Pouliot Z, et al. Subjective versus objective evaluation of hypnotic efficacy: experience with zolpidem. Sleep 1991;14(5):399–407.

Moul DE, Hall M, Pilkonis PA, et al. Self-report measures of insomnia in adults: rationales, choices, and needs. Sleep Medicine Reviews, 2004;8(3):177–98.

Wolff BB. Evaluation of hypnotics in outpatients with insomnia using a questionnaire and a self-rating technique. Clin Pharmacol Ther 1974;15(2):130–40.

Clinical reasoning – and cognitions


Possibly one of the most hotly discussed aspects of clinical reasoning and pain relates to thoughts and beliefs held by both people experiencing pain and the clinicians who work with them. It’s difficult to avoid reading papers about “pain education”, “catastrophising”, “maladaptive thinking”, but quite another to find a deeper analysis of when and why it might be useful to help people think differently about their pain, or to deal with their thoughts about their experience in a different way.

Cognition is defined by the APA Dictionary of Psychology as

1. all forms of knowing and awareness, such as perceiving, conceiving, remembering, reasoning, judging, imagining, and problem solving. Along with affect and conation, it is one of the three traditionally identified components of mind.

2. an individual percept, idea, memory, or the like. —cognitional adj. —cognitive adj.

Cognitions are arguable The Thing most accessible to ourselves and most distinctive about humans – indeed, we call ourselves “homo sapiens” or “wise man” possibly because we can recognise we have thoughts! Although, as you can see from the definition above, many aspects of cognition are not as readily available to consciousness as we might imagine.

From the early days of pain management, explanations about the biology of pain have been included. Indeed, since 1965 when Melzack and Wall introduced the Gate Control Theory, in which modulation and descending control were identified, clinicians working in pain management centres have actively included these aspects of pain biology as part of an attempt to help people with pain understand the distinction between hurting – and being harmed (see Bonica, 1993).

The purpose behind the original approaches to “explaining pain” were to provide a coherent explanation to people in pain as to the “benign” nature of their experience: in other words, by changing the understanding people held about their pain, people were more likely to willingly engage in rehabilitation – and this rehabilitation largely involved gradually increasing “up time” and reducing unhelpful positions or activity levels. Sound familiar? (see Moseley & Butler, 2015).

Of course, in the early days of pain management, specific relationships between thoughts and both automatic and volitional behaviour were unclear. What we know now is that if I wire someone up to a biofeedback machine, measuring say heart rate variability, respiration and skin conductance, and then I mention something related to the person’s appraisals of their pain – maybe “Oh this really hurts”, or “I don’t think I’ll sleep tonight with this pain” those parameters I’m measuring will fluctuate wildly. Typically, people will experience an increase of physiological arousal in response to thinking those kinds of thoughts. In turn, that elevated arousal can lead to an increased perception of pain – and increased attention to pain with difficulty taking attention off pain (see Lanzetta, Cartwright-Smith & Eleck, 1976; Crombez, Viane, Eccleston, Devuler & Goubert, 2013).

So, the relationship between what we think and both attention to pain and physiological response to those thoughts is reasonably well-established, such that if someone reports high levels of catastrophising, we can expect to find high levels of disability, and reports of higher levels of pain. So far, so good. BUT how do we integrate these findings into our clinical reasoning, especially if we’re not primarily psychologically-oriented in our treatments?

The answer has been to dish out “pain education” to everyone – giving an explanation of some of the biological underpinnings of our experience. But for some of our patients this isn’t useful, especially if they have already heard the “pain talk” – but it has only hit the head and not the heart.

As Wilbert Fordyce was known to say “Information is to behaviour change as spaghetti is to a brick”. In other words – it might hit the brick and cover it, but it doesn’t change the brick, and neither does it move the brick!

You see, cognitions are not just “thoughts”, nor thoughts we are consciously aware of. Cognitions include implicit understanding, attention, the “feeling of what it is like to” and so on. And as occupational therapists and educators have found over the years, experiential learning (learning by doing) is one of the most powerful forms of behaviour change available (Kolb, 2014). People learn by experiencing something different. This is why cognitive behavioural approaches such as Acceptance and Commitment Therapy (ACT) so strongly endorse experiential elements.

Rather than attempting to change someone’s head knowledge of pain=harm, it might be more useful to help them experience doing something different and help them explore and generate their own conclusions from the experience.

I think both occupational therapists and clinicians who provide opportunities for movements and experiences (such as massage therapists, physiotherapists, osteopaths, chiropractors, myotherapists etc) are in an ideal position to guide people through new experiences – and then help them explore those new experiences. Rather than telling people what to think or believe (especially amongst those folks who are unconvinced by “book learning”!) we’re in a good position to help them work out what’s going through their minds – and what it feels like to do something differently. Instead of convincing, we can help people ponder for themselves. This is the essence of graded exposure: going from “OMG I can’t do that!” to “Oh yeah, I can master this”. It’s the difference between reading about how to ride a bicycle – and actually getting on a bike to learn to ride.

I agree that cognitive processes are really important in understanding a person’s experience of pain. I think, though, we’ve focused on overt thoughts to the detriment of trying to understand other aspects of cognition. We need to spend some more time exploring attention and distraction from pain; memories and how these influence pain; and to examine some of the implicit features of our understanding – and instead of approaching changes to thinking/understanding via the hammer of information dumping, maybe we can ponder the opportunities that arise from helping people experience something different and new.

 

 

Bonica, J. J. (1993). Evolution and current status of pain programs. Journal of Pharmaceutical Care in Pain & Symptom Control, 1(2), 31-44. doi:10.1300/J088v01n02_03

Crombez, G., Viane, I., Eccleston, C., Devulder, J., & Goubert, L. (2013). Attention to pain and fear of pain in patients with chronic pain. Journal of Behavioral Medicine, 36(4), 371-378.
Kolb, D. A. (2014). Experiential learning: Experience as the source of learning and development (2nd Ed), Pearson Education: New Jersey.
Lanzetta, J. T., Cartwright-Smith, J., & Eleck, R. E. (1976). Effects of nonverbal dissimulation on emotional experience and autonomic arousal. Journal of Personality and Social Psychology, 33(3), 354.

Moseley, G. L., & Butler, D. S. (2015). Fifteen years of explaining pain: The past, present, and future. Journal of Pain, 16(9), 807-813. doi:10.1016/j.jpain.2015.05.005

Clinical reasoning in pain – emotions


The current definition of pain includes the words “unpleasant sensory and emotional experience” so we would be surprised if we encountered a person with pain who wasn’t feeling some sort of negative emotion, am I right? Yet… when we look at common pain assessments used for low back pain, items about emotions or worries are almost always included as indicators of negative outcomes (for example, STarTBack – Worrying thoughts have been going through my mind a lot of the time, I feel that my back pain is terrible and it’s never going to get any better, In general I have not enjoyed all the things I used to enjoy). And while the screening questionnaires have been validated, particularly for predictive validity (ie higher scores obtained on these measures are associated with poorer outcomes), I wonder how much we know, or think we know, about the relationship between emotions and pain. Perhaps its time for a quick review…

Firstly, let’s define emotions (seems easy!) “Emotions are multicomponent phenomena; (2) emotions are two-step processes involving emotion elicitation mechanisms that produce emotional responses; (3) emotions have relevant objects; and (4) emotions have a brief duration.” (Sander, 2013). There are thought to be six evolutionarily shaped basic emotions such as joy, fear, anger, sadness, disgust, and surprise (Ekman, 1992); but as usual there are complications to this because emotions are also examined in terms of their valence – negative or positive – and arousal (similar to intensity, but in terms of how much our physiology gets excited).

There are two main brain areas involved in processing both pain and unpleasant stimuli in general are the amygdala and the prefrontal cortex. These areas don’t exclusively deal with pain but with stimuli that are especially salient to people (remember last week’s post?), and researchers are still arguing over whether particular areas are responsible for certain emotions, or whether “emotions emerge when people make meaning out of sensory input from the body and from the world using knowledge of prior experience” based on basic psychological operations that are not specific to emotions (Lindquist et al., 2012, p. 129) . I’m quoting from an excellent book “The neuroscience of pain, stress and emotions” by Al, M. Absi, M.A. Flaten, and M. Rogers.

Now researchers have, for years, been interested in the effects of emotions on pain – there is an enormous body of literature but luckily some good reviews – see Bushnell et al., 2013; Roy, 2015 ;  Wiech and Tracey, 2009. What this research shows, essentially, is that pain is reduced by positive emotions, and increased by negative emotions. Now we need to be somewhat cautious about over-interpreting these results because they’re mainly conducted in experimental designs with acute experimental pain – people are shown pictures that elicit certain emotions, then poked or zapped, and asked to rate their pain (and their emotions, usually). It’s thought that the way these emotions influence pain is via our descending inhibitory pathways. Now the situation with real people experiencing pain that is not experimentally administered is probably slightly different – a lot more salient, a lot more worrying, and far less controlled. Nevertheless it’s worth knowing that when you’re feeling down, you’re likely to rate your pain more highly. If the emotion-eliciting stimuli are particularly arousing (ie they’re REALLY interesting) then the effect on pain ratings is greater. Experimenters also found pain reduces responses to pleasant stimuli, but there isn’t such a strong relationship with negative stimuli.

The valence (positiveness or negativeness – if that’s a word LOL) activates motivational systems either pleasant = appetitive, or unpleasant = defensive. Arousal or alertness gives us a clue as to how much motivation we have to either move towards or away from the stimulus. The degree of arousal affects our pain experience – so the more negative and angry we are, we rate our pain more highly; while the happier and jollier we are, we rate our pain as less intense. BUT, as for most things in pain, it’s complex – so once we get more than moderately angry/alert/aroused, the less we experience pain. The diagram below shows this kind of relationship – from the same book I quoted above (it’s worth getting!).

Does this mean we should freak people out so they experience less pain? Don’t be dumb! Being that alert is really exhausting. But what this diagram can explain is why some people, when they’re first attending therapy and are asked to do something out of the ordinary and just so slightly threatening (like lifting weights, or jumping on a treadmill) might report higher pain intensity – because we’ve caught them at the moderate arousal level where pain is facilitated.

Clinically, what this information means is that if we’re hoping to improve someone’s pain via pleasant or positive emotions, we’d better make sure they’re fairly high energy/arousing – a hilarious comedy perhaps – because lower intensity pleasure doesn’t affect pain much.

We should, at all costs, avoid eliciting fear and worry, or anger in the people we treat – because this increases pain intensity. This means giving people time to get used to our setting, what we’re asking them to do, and the intensity of whatever activity we’re going to do with them. In graded exposure, we should give people skills in mindfulness well before we begin doing the exposure component – because it’s likely to evoke higher than usual pain intensity if they can’t “be with” the increased anxiety that emerges during this kind of treatment.

And finally, if someone is experiencing anger, depression, sadness or anxiety – this is a normal psychological reaction integral to our experience of pain. It’s not necessarily pathological – though it probably increases the pain intensity the person reports.

I think we could promote far more scheduling pleasurable experiences as a routine part of therapy. What makes people smile, feel joy, have a good belly laugh? When was the last time they watched a comedy or joked with their family? Therapy can be fun, just see my friend Alice Hortop’s work on comedy as therapy (https://alicehortop.com/)!

 

 

Ekman, P.  (1992). An argument for basic emotions. Cognition and Emotion, 6, 169–200.

 

 

 

Flaten, M. A. (2016). The neuroscience of pain, stress, and emotion : Psychological and clinical implications. In Al, M. Absi, M. A. Flaten, & M. Rogers (Eds.), Neuroscience of Pain, Stress, and Emotion: Amsterdam, Netherlands : Elsevier.

K.A. Lindquist, T.D. Wager, H. Kober, E. Bliss-Moreau, L.F. Barrett, (2012). The brain basis of emotion: a meta-analytic review. Behavioral and Brain Sciences, 35 (03),  121–143

 

 

Roy, M. (2015). Cerebral and spinal modulation of pain by emotions and attention. Pain, Emotion and Cognition, 35–52.

 

Sander, D. (2013). Models of emotion: the affective neuroscience approach. in J.L. Armony, P. Vuilleumier (Eds.), The Cambridge handbook of human affective neuroscience, Cambridge University Press, Cambridge, pp. 5–56

 

 

 

Clinical reasoning and why models of low back pain need to be integrated


Clinical reasoning has been defined as “the process by which a therapist interacts with a patient, collecting information, generating and testing hypotheses, and determining optimal diagnosis and treatment based on the information obtained.” (thanks to https://www.physio-pedia.com/Clinical_Reasoning#cite_note-Higgs-1). The model or lens through which we do these processes naturally has a major influence on our relationship with the person, the information we think is relevant, the hypotheses we develop, and ultimately the problems we identify and how we treat them. No arguments so far, yes?

So when we come to thinking about pain, particularly where a “diagnosis” can’t be readily established – or where the treatment doesn’t directly address a proposed causal factor – clinical reasoning should be led by some sort of model, but how explicit is our model, really? And, what’s more, how well does the research support our model, and the relationships between variables?

I’m thinking about my approach as an occupational therapist where my interest in assessment is to identify why this person is presenting in this way at this time, and what might be maintaining their current predicament; and my aim is to identify what can be done to reduce distress and disability, while promoting participation in daily occupations (activities, things that need to be done or the person wants to do). For many years now I’ve used a cognitive behavioural model first developed by Dr Tim Sharp who has now moved into Positive Psychology. His reformulation of the cognitive behavioural model works from the “experience” of pain through to responses to that experience, but incorporates some of the cyclical interactions between constructs. The model doesn’t include inputs to the “experience” component from the nociceptive system – but it could.

Many other models exist. Some of them are quite recent – the STarT Back Tool, for example, provides a very simplified screening approach to low back pain that some people have identified as a clinical reasoning model. Another is by Tousignant-Laflamme, Martel, Joshi & Cook (2017), and is a model aimed at pulling all the various approaches together – and does so with a beautifully-coloured diagram.

But.

You knew there would be one! What I think these two models omit is to generate some relationships between the constructs, particularly the psychological ones. You see, while it’s a cyclical interaction, there are some relationships that we can identify.  And over the next few weeks I’ll be writing about some of the known associations, just to begin to build a picture of the relationships we can assess before we begin generating hypotheses.

For example, we know that the nervous system, and in particular our mind/brain, is never inactive and is therefore never a completely blank slate just waiting for information to come into it, but we also know there are relationships between the intensity/salience/novelty of a stimulus that attract attention, and that this competes with whatever cognitive set we have operating at the time (Legrain, Van Damme, Eccleston, Davis, Seminowicz & Crombez, 2009). So one relationship we need to assess is current contexts (and there are always many), and the times when a person is more or less aware of their pain.

Now, what increases the salience of a stimulus? For humans it’s all about meaning. We attribute meaning to even random patterns (ever seen dragons and horses in the clouds?!), so it’s unsurprising that as we experience something (or watch someone else experiencing something) we make meaning of it. And we generate meanings by relating concepts to other concepts – for a really good introduction to a very geeky subject, head here to read about relational frame theory. Relational frame theory is used to explain how we generate language and meanings by relating events with one another (The Bronnie translation! – for an easier version go here). Wicksell and Vowles (2015) describe this, and I’m going to quote it in full:

As described by relational frame theory, the theoretical framework underlying ACT, stimulus functions are continuously acquired via direct experiences, but also through their relations with other stimuli [5]. This implies that a behavioral response is not due to just one stimuli but rather the relational network of stimuli. Pain as an interoceptive stimulus is associated with a large number of other stimuli, and the actions taken depend on the psychological function(s) of that relational network of stimuli. A seemingly trivial situation may therefore elicit very strong reactions due to the associations being made: a relatively modest pain sensation from the neck trigger thoughts like “pain in the neck is bad,” which in turn are related to ideas such as “it may be a fragile disk,” and “something is terribly wrong,” that eventually lead to fatalistic conclusions like “I will end up in a wheelchair.” Thus, even if the initial stimulus is modest, it may activate a relational network of stimuli with very aversive psychological functions.

In other words, we develop these networks of meaning from the time we’re little until we die, and these mean any experience (situation, context, stimulus, event, action) holds meaning unique and particular to the individual. And these networks of meaning are constructed effortlessly and usually without any overt awareness. Each event/experience (yeah and the rest) then has further influence on how we experience any subsequent event/experience. So if you’ve learned that back pain is a Very Bad Thing, and you’ve done so since you were a kid because your Mother had back pain and took herself to the doctor and then stopped playing with you, you may have a very strong network of relationships built between low back pain, resting, healthcare, abandonment, sadness, anger, loneliness, fear, mother, father, pills, treatment – and the this goes on.

So when we’re beginning to construct a clinical reasoning model for something like low back pain we cannot exclude the “what does it mean” relationship. Every time someone experiences “ouch!” they’re processing a network of associations and relationships and behaviours that go on to influence their response to that experience – and affect attention to it and subsequent response to it.

Over 1000 words and I’ve not even started on emotions and pain!

Take home message: Even if we think we’re not addressing “psychological” stuff – we ARE. Omitting the “what does it mean to you?” and failing to factor that in to our clinical reasoning and subsequent treatment means we’re walking uphill on a scree slope. Oh, and telling someone they’re safe does not change those associations, especially if they’re longstanding. There’s more needed.

 

Legrain V, Damme SV, Eccleston C, Davis KD, Seminowicz DA, & Crombez G (2009). A neurocognitive model of attention to pain: behavioral and neuroimaging evidence. Pain, 144 (3), 230-2 PMID: 19376654

Sharp, T. J. (2001). Chronic pain: A reformulation of the cognitive-behavioural model. Behaviour Research and Therapy, 39(7), 787-800. doi:http://dx.doi.org/10.1016/S0005-7967(00)00061-9

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

Wicksell, R. K., & Vowles, K. E. (2015). The role and function of acceptance and commitment therapy and behavioral flexibility in pain management. Pain Management, 5(5), 319-322. doi:10.2217/pmt.15.32

Using more than exercise for pain management


In the excitement and enthusiasm for exercise as a treatment for persistent pain, I wonder sometimes whether we’ve forgotten that “doing exercise” is a reasonably modern phenomenon. In fact, it’s something we’ve really only adopted since our lifestyle has moved from a fairly physically demanding one, to one more sedentary (Park, 1994). I also wonder if we’ve forgotten that exercise is intended to promote health – so we can do the things we really want or need to do. Remembering, of course, that some people find exercise actually exacerbates their pain (Lima, Abner & Sluka, 2017), and that many folks experience pain as an integral part of their exercise (think boxing, marathon running, even going to a gym – think of the pain of seeing That Much Lycra & Sweat).

While it’s become “exercise as medicine” in modern parlance (Pedersen & Saltin, 2015; Sallis, 2009; Sperling, Sadnesara, Kim & White, 2017), I wonder what would happen if we unpacked “exercise” and investigated what it is about exercise that makes it effective by comparison with, say, activities/occupations that incorporate whole body movement?

One of the factors that’s often omitted when investigating coping strategies or treatments, especially lifestyle/self management ones, is the context and meaning people give to the activity. Context is about the when, where and how, while meaning is the why. Whether the positives (meaning, and values people place on it) outweigh the negatives (let’s face it, the lycra and sweat and huffing and puffing does not inherently appeal) are factors that enhance (or not) adherence to exercise and activity. One positive is a sense of flow, or “an optimal subjective psychological state in which people are so involved in the activity that nothing else seems to matter; the experience itself is so enjoyable that people will do it even at great cost, for the sheer sake of doing it”(Csikzentmihalyi, 1990, p. 4). I can think of a few things I lose myself in – reading a good book; fishing; paddling across a lake; photography; silversmithing; gardening…

Robinson, Kennedy & Harmon (2012) examined the experiences of flow and the relationship between flow and pain intensity in a group of people living with persistent pain. Their aim was to establish whether flow was an “optimal” experience of people with chronic pain. Now the methodology they used was particularly interesting (because I am a nerd and because this is one technique for understanding daily lived experiences and the relationships between variables over time). They used electronic momentary assessment (also known as ecological momentary assessment) where participants were randomly signaled seven times a day for one week to respond to a question about flow. Computationally challenging (because 1447 measurement moments were taken – that’s a lot of data!), although not using linear hierarchical modeling (sigh), they analysed one-way between group analyses of variance (ANOVA) to explore differences in pain, concentration, self-esteem, motivation, positive affect and potency across four named states “flow, apathy, relaxation and anxiety”. We could argue about both the pre-determined states, and the analysis, but let’s begin by looking at their findings.

What did they find?

People in this study were 30 individuals with persistent pain attending a chronic pain clinic. Their ages ranged from 21 – 77 years, but mean age was 51, and there were 20 women and 10 men (remember that proportion). People had a range of pain problems, and their pain had been present for on average 68 months.

The contexts (environments) in which people were monitored were at home, or “elsewhere”, and, unsurprisingly, 71% were at home when they were asked to respond. Activities were divided into self-care, work and leisure (slightly less time in work than in leisure or self care respectively).  The purpose of the activities were necessity (35%), desire (40%), or “nothing else to do” (18%). And most people were doing these things with either alone or with family, with very small percentages with friends, colleagues or the general public.

Now we’d expect that people doing things they feel so wrapped up in that nothing else matters should experience lower pain – but no, although this was hypothesised, pain intensity scores during flow trended lower – but didn’t actually reach significance. When we add the findings that concentration, self-esteem, motivation, and potency mean scores were highest in the flow state and mean scores were lowest in the apathy and anxiety states, we can begin to wonder whether engaging in absorbing activities has a major effect on pain intensity – or whether the value placed on doing the activities is actually the most important feature for people with pain. Interestingly, people felt their flow experiences while outside the home: this happened rather less often than being in the home, where apathy was most present. So… doing something absorbing is more likely to occur away from home, while remaining at home is associated with more apathy and perhaps boredom. Finally, flow occurred in work settings more than elsewhere, suggesting yet again that work is a really important feature in the lives of all people, including people living with pain. Of course that depends on the kind of work people are doing…and the authors of this paper indicate that people with persistent pain in this study have few places in which they can do highly engaging activities, even including work.

What does this mean for exercise prescription?

Engaging people in something that holds little meaning, has little challenge and may not be in the slightest bit enjoyable is probably the best way to lose friends and have clients who are “noncompliant”. I think this study suggests that activities that provide challenge, stimulation, movement possibilities, the opportunity to demonstrate and develop skill – and that people find intrinsically lead to flow – might be another way to embrace the “movement is medicine” mantra. I wonder what would happen if we abolished “exercises” and thought about “movement opportunities”, and especially movement opportunities in which people living with pain might experience flow? I, for one, would love to see occupational therapists begin to examine flow experiences for people living with pain and embraced the creativity these experiences offer for the profession.

 

 

Csikszentmihalyi, M. (1990). Flow: The psychology of optimal experience. New York: Harper Collins.

Lima, L. V., Abner, T. S., & Sluka, K. A. (2017). Does exercise increase or decrease pain? Central mechanisms underlying these two phenomena. The Journal of physiology, 595(13), 4141-4150.

Park, R. (1994). A Decade of the Body: Researching and Writing About The History of Health, Fitness, Exercise and Sport, 1983-1993. Journal of Sport History, 21(1), 59-82. Retrieved from http://www.jstor.org/stable/43610596

Pedersen, B. K., & Saltin, B. (2015). Exercise as medicine–evidence for prescribing exercise as therapy in 26 different chronic diseases. Scandinavian journal of medicine & science in sports, 25(S3), 1-72.

Robinson, K., Kennedy, N., & Harmon, D. (2012). The flow experiences of people with chronic pain. OTJR: Occupation, Participation and Health, 32(3), 104-112.

Sallis, R. E. (2009). Exercise is medicine and physicians need to prescribe it!. British journal of sports medicine, 43(1), 3-4.

Sperling, L. S., Sandesara, P. B., Kim, J. H., & White, P. D. (2017). Exercise Is Medicine. JACC: Cardiovascular Imaging, 10(12).

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

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

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