Assessment

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.

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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

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

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

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

What’s the biggest barrier to learning more?


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

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

Image result for dunning kruger effect

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

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

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

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

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

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

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

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

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

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

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

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

Great quote?

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

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

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

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

The gap in managing pain


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

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

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

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

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

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

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

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

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

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

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

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

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

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