Science in practice

Managing sleep problems – a medication-free approach (ii)


Last week I described the “conventional” CBT for insomnia approach (CBTi), but this week I want to introduce an Acceptance and Commitment Therapy (ACT) approach which is superficially similar to CBTi but holds to some of the fundamental principles of ACT: mindfulness, and letting go of control. As is typical for ACT, there are no hard and fast absolutes and instead there is a focus on workability – what works, in context.

Most of the content of today’s post is drawn from my personal experience and The Sleep Book by Dr Guy Meadows. There are five basic steps and according to the book it should take five weeks to get sleep sorted. I’m not as convinced about timeframes, so I’ll describe it as five steps.

  1. Discover: this step is about discovering what triggers and maintains insomnia, and focuses on why struggling to start sleeping is counter-productive. That’s right – stop struggling!
  2. Accept: well, with a name like ACT you’d expect some acceptance, right? This is not about resigning yourself to nights of poor sleep, but rather a willingness to let go of the struggle, to be fully present in the now – rather than reminiscing about the past, or predicting the future.
  3. Welcome: everything that shows up in your mind and body (after all, they’re there whether you want them or not!).
  4. Build: a new sleeping pattern by identifying how much sleep you need and when you need it.
  5. Live: during the day and sleep during the night!

Like absolutely any behaviour change, this process is not always easy! It takes persistence, courage and doing things that may not feel like sensible things to do! Let’s begin.

Discover: we do a whole heap of things to try to get to sleep – normal sleepers don’t. Normal sleepers just put their heads on the pillow, maybe let their minds wander over the day, and then gently fall asleep. When people with insomnia try to sleep, we try all manner of things to get to that state – and many of those things either prolong the sleeplessness, or actually wind it up!

Meadows describes four factors associated with the start of insomnia:

  • risks which may be getting older, being female, being a worrier or depressed, having a family history of rotten sleep, maybe being generally full-on;
  • triggers may include life stress, some medical conditions like irritable bowel or a fracture and yes, pain, and medications or alcohol, time zone changes and so on;
  • arrivals are memories, thoughts, sensations, emotions and urges that come to visit when we’re trying to get off to sleep but can’t – and these are partly the fight, flight or freeze response which happens when we begin worrying, or are part of the triggers (and we often think it’s those things that need to be got rid of); and finally
  • amplifiers, or things that are meant to be helping reduce insomnia but can actually make it worse: things like spending longer in bed, sleeping in, going to be earlier, having naps – and oddly enough, some of the things we’re traditionally advised to do to help us sleep. Things like reading in low light, having a warm bath or warm milk drink, watching TV, listening to the radio, playing with devices like the phone…. Even some of the things we do because we’re not sleeping – like getting out of bed and doing things like checking emails, doing some exercise, going to the loo – all of these things are done to try avoid the chitter-chatter of our mind, or eat least to control or distract from it, yet can paradoxically train your brain to be awake right when you really want to sleep… even things like keeping the room dark, wearing earplugs, doing relaxation, sleeping in a different bed from your partner, trying a new mattress or pillow can be a step too far and train your brain to think controlling these thoughts about sleep is the Thing To Do.

I’ll bet that, like me, most people have done all these things – and some of them are part of CBTi. There is a place for them in moderation – but it’s even better to develop the skill of not being caught up in trying to control our thoughts, worries, feelings, body sensations when we’re heading to sleep.

Now I’m sure this is where people are going “yeah but…” and giving a whole list of why your situation is different. Would you be willing to keep reading and look at some alternatives?

The risk of trying to control these arrivals and amplifiers is that while they don’t work, it’s too scary NOT to do them. Your brain learns, as a result, that sleep is a problem. And what does the brain like best? Oh that’s right – solving problems. Except that if you’ve ever tried to “make yourself” stop thinking, or feeling – have you noticed that you just can’t? Try it now: try and make yourself feel happy. Yeah… you either have to recall something enjoyable from the past, or anticipate something in the future. And while you’re doing that, your brain is cranking up. It’s worse if you try to stop yourself from thinking or worrying because that old fight, flight or freeze response kicks in and up goes your heart rate and perspiration and breathing…

So the first step of this programme is to discover all the things you’re doing to control the uncontrollable. We can’t stop feelings, thoughts, memories and so on from arriving. They just do. So fighting with them and trying hard to get rid of them just does not work – they’re there AND you’re feeling stressed because you can’t get rid of them!

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Managing sleep problems – a medication-free approach (i)


I’ve recently completed two posts on assessing sleep problems in people experiencing persistent pain, and today I turn my attention to strategies for managing sleep problems – without medication. Why without medication? Because to date there are no medications for insomnia that don’t require a ‘weaning off’ period, during which time people often find their original sleep problems emerge once again… I’m not completely against medications for sleep or pain – but I think they need to be used with care and full disclosure about the effects, side-effects, and the need to eventually withdraw from them.

The approach I’m advocating is a modified form of cognitive behavioural therapy for insomnia (CBTi). CBTi is a form of treatment that is now considered to be first line therapy by both the British Association for Psychopharmacology (Wilson, Nutt, Alford, Argyropoulos, Baldwin, Bateson et al, 2010), and the American College of Physicians (Qaseem, Kansagara, Forciea, Cooke, Denberg et al, 2016). It includes sleep hygiene, cognitive therapy for the thoughts and beliefs associated with sleep, and sleep restriction for those who clinically need it. The modified version I advocate is based on Dr Guy Meadows ACT-based approach and I’ll cover that next week, but I’ll describe the classical CBT approach first.

Basic principles

The basic idea behind a CBT approach to insomnia is that although the initiating event may be out of our control, it’s unlikely to be maintaining the problem – and the factors maintaining the problem are typically the habits people have, and the thoughts and beliefs about their sleep problem.

Sleep is a behaviour that is infinitely malleable, as anyone who has travelled far enough on long-haul flights will know (and parents of small babies as well!). There are cues we use to decide when we should head to bed, and how long we should stay asleep. Bodies in turn respond to these cues and modify automatic processes such as digestion, urine production, and body temperature to ensure we stay asleep for as long as needed. When those cues change – for example, we’re in a new time zone when it’s light at the “wrong” time, and we’re hungry at the “wrong” time, we have trouble staying asleep until the body adjusts. Some people say we can manage a two-hour time zone shift every 24 hours, but in some sensitive people even a one-hour daylight savings change can upset the apple-cart!

If sleep is a habitual behaviour, then we can manipulate the cues to our benefit when sleep is elusive. We learn to associate things like the routine we follow prior to going to bed, light in the room, the “winding down” process we use, and even the timing of our snacks and drinks as a way to signal to the body/mind that we’re sleepy/tired.

There are three basic steps in CBTi: stimulus control (aka sleep hygiene), cognitive therapy, and sleep restriction – with the usual relapse prevention steps an essential part as well.

Sleep hygiene (stimulus control)

The basis of sleep hygiene is to control the stimuli associated with going to sleep so that we clearly indicate to the body/mind that it’s time to get to sleep. That means some basic “rules” around what we do in the time preceding getting into bed, and what we do when in bed trying to sleep.

The golden rule is that the bed is for sleep and sex – not for worrying in, not for watching TV or using the computer or phone or tablet, not for arguing in, not for talking on the phone. If you’re awake in bed for longer than 20 minutes, it’s time to get out of bed until you’re sleepy/tired (more on this in a moment), keeping the lights down low, doing something tedious or boring, then returning to bed to actually sleep.

Simple, commonsense things like keeping the room dark and warm, blocking out the worst of the noise, NOT using a TV or radio or any other noise-making device to go to sleep, ensuring caffeine intake is limited, having a regular bedtime and wake-up time, not taking naps through the day and timing when exercise and relaxation are undertaken are all part of sleep hygiene and most of us are aware of these steps. If they’re not familiar to you, this site is a good one – click.

Cognitive therapy

The cognitive therapy part is about managing the thoughts and attitudes that can exacerbate the sleep problem – things like having a busy mind, worrying about not being able to sleep, believing that it’s crucial to have a certain number of hours of sleep or the next day will be awful, getting that sinking dread as bedtime approaches, following any number of almost (and sometimes actual) obsessive rituals to achieve sleep – and so on…

As usual, with any conventional CBT, dealing with these thoughts involves firstly reality testing – Is it true that you must have a certain number of hours of sleep or the next day will inevitably be terrible? Must the room be absolutely silent or sleep will elude you? Then challenging or disputing those thoughts – “It’s possible I’ll feel tired tomorrow, but I can still function even if I’m not at my best”, “It might take me longer to fall asleep but I’ll get to sleep even though I can hear a clock ticking”.

These simple approaches are reasonably easy to implement – and they are effective. But if sleep is still a problem, and the person isn’t getting more than 4 hours sleep a night, it’s time to bring in the big guns.

Sleep restriction

There are two parts of altering sleep habits that are particularly challenging: getting out of bed after 20 minutes of being awake (especially in the wee hours of the morning!); and using sleep restriction. Neither are easy, yet both are effective.

The idea behind sleep restriction is to reduce the amount of time being in bed while not actually being asleep. Simple huh? So that period from when you first hop into bed and until you actually fall asleep is called sleep latency – and the longer your sleep latency, the less sleep you actually get. You become inefficient at sleeping, and worst, your body/mind learns that it’s OK to be in bed wide awake, and as I mentioned earlier, people begin to associate even going into the bedroom as a negative thing which revs up the autonomic nervous system making it even more difficult to fall asleep.

The nuts and bolts are to work out what time you actually fall asleep, and only go to bed at that time. So if you stay awake until 2.00 or 3.00am, you only go to bed at 2.00am. And you keep your morning wake-up time the same as normal. Yes, this means you end up being only able to sleep for the time between 2.00am and 7.00am! Ouch!

The idea is to extinguish the “habit” of being awake while in bed, reducing the association between being in bed and wide awake, while getting you absolutely tired and sleepy that you fall asleep into a deep sleep quickly. Once this falling asleep part happens regularly (usually for a week or so) then it’s possible to begin a very gradual process of bringing the bedtime back to a more reasonable hour – I usually suggest 15 minute increments, returning to the previous step if falling asleep begins to be difficult.

The process is reasonably difficult – not because it’s hard to stay awake (after all, the person has been practicing it for some time!) but because of the mind chatter. It’s truly tough when your mind starts having a go at you, suggesting you can’t sleep, or you’ll be so incredibly tired you won’t cope, or you’ll be cranky and that it’s dangerous and how on earth  will you go at work without any sleep? And this is where having access to a really good clinician can be helpful, although there are apps that provide a pretty good alternative if a human isn’t available.

For a detailed examination of the literature on sleep restriction therapy, Kyle, Aquino, Miller, Henry, Crawford, Espie & Spielman (2015) provide a really good systematic analysis of how sleep restriction is employed in research trials.  For a plain language version of CBTi, this is a good description – click

As I mentioned above, I’ll be going through a slightly different version of CBTi – an Acceptance and Commitment Therapy approach to insomnia that is also gaining popularity and an evidence base. Come right on back next week for that exciting episode!

 

Kyle, S. D., Aquino, M. R. J., Miller, C. B., Henry, A. L., Crawford, M. R., Espie, C. A., & Spielman, A. J. (2015). Towards standardisation and improved understanding of sleep restriction therapy for insomnia disorder: A systematic examination of cbt-i trial content. Sleep Medicine Reviews, 23, 83-88.

Manber, R., Simpson, N. S., & Bootzin, R. R. (2015). A step towards stepped care: Delivery of cbt-i with reduced clinician time. Sleep Medicine Reviews, 19, 3-5.

Qaseem, A., Kansagara, D., Forciea, M., Cooke, M., Denberg, T. D., & for the Clinical Guidelines Committee of the American College of, P. (2016). Management of chronic insomnia disorder in adults: A clinical practice guideline from the american college of physicians. Annals of Internal Medicine, 165(2), 125-133. doi:10.7326/M15-2175

Wilson, S., Nutt, D., Alford, C., Argyropoulos, S., Baldwin, D., Bateson, A., . . . Wade, A. (2010). British association for psychopharmacology consensus statement on evidence-based treatment of insomnia, parasomnias and circadian rhythm disorders. Journal of Psychopharmacology, 24(11), 1577-1601. doi:10.1177/0269881110379307

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

When philosophy and evidence collide: is an occupation-focused approach suitable in pain management?


I have often described myself as a renegade occupational therapist: I like statistics, I think experimental research is a good way to test hypotheses, I don’t make moccasins (though I occasionally wear them!), I’m happy reading research and figuring out how I can apply findings into my clinical practice.

Occupational therapy is a profession that continues to evolve. The origins of occupational therapy lie back in the “moral” model of treatment for mental illness when advocates found that giving people things to do helped them become well (mind you, some of the reasons for admission to a “mental asylum” were things like “wandering womb”, novel reading, laziness and “female disease” read it here on Snopes). As time passed, occupational therapy was a way to “occupy” troops recovering from war wounds, and later, tuberculosis. At various points, occupational therapists have tried to enclose practice within prevailing models: anatomical, biomechanical, neurological. And then the scope broadens and the profession returns to “occupation” and all it means. Out of this latest movement, and informing occupational therapy practice today is the idea of “occupational science” – this is the “basic science” examining the factors that underpin occupational therapy practice (Yerxa, 1990).

Unlike most “basic sciences”, occupational science draws on areas of knowledge including anthropology, sociology and political science; all social sciences that bring their own philosophical biases to understanding social phenomena. Occupational science is about “what people do in daily life” – those routines, rituals, practices, customs and daily doings that support us in our roles, shape our place in the social world, and help us form an understanding of who we are in the world. Things like how we go about getting up, the way we serve a meal, the way we dress ourselves, how we go from one place to another, the hobbies and fun things we do – all fundamental building blocks of daily life. Occupational therapy, therefore, informed by occupational science, is focused on helping people participate in daily life as fully and equitably as possible, irrespective of health status, gender, ethnicity, religious belief, age and so on.

With a focus on not only helping people participate in occupations, but also using occupation as therapy, it’s not surprising to find a plurality of approaches to treatment. I have seen art used to help people with persistent pain represent the impact of pain on their sense of self – and to celebrate changes that have happened as a result of pain management. I have seen gardening used to help people become stronger, more confident to move and to reconnect with a hobby they had given up because of pain. I have seen people begin new hobbies (geocaching anyone?) as part of occupational therapy. I have used excursions to the local shopping mall to help people regain confidence and reduce their fear of crowded places where they might get bumped. Graded exposure is also an approach occupational therapists use to help people generalise their emerging skills to approach feared movements instead of avoiding them.

What I hope I don’t see is a return to a compensatory model for persistent pain. You know what I mean here: using gadgets or aids to “make life easier” when a person is dealing with persistent pain. Things like a special long-handled tool so people can pick something up from the floor – fine in a short-term situation like immediately post hip arthroplasty, but not so much when the problem is longstanding fear and avoidance. A special vacuum-cleaner so the person doesn’t have to bend – it’s so much easier yes, but it doesn’t address the underlying problem which can be remedied.

Why is a compensatory model not so good for persistent pain management? Well, because in most instances, though not all, the reason a person isn’t doing a movement when they’re sore is not because they cannot – but because that movement increases or might increase pain, and no-one really wants to increase pain, yeah? By providing a gadget of some sort, or even working through a way to avoid that movement, occupational therapists who use this sort of approach are ignoring the strong evidence that this reinforces avoidance as a strategy for managing pain, doesn’t address the underlying fear, and risks prolonging and actually reinforcing ongoing disability. This approach is harmful.

Helping people do things that might hurt isn’t a very popular idea for some clinicians and a lot of people living with persistent pain. It feels at first glance, like a really nasty thing to do to someone. BUT graded exposure is an effective, occupationally-focused treatment for fear of movement and fear of pain (Lopez-de-Uralde-Villaneuva, Munos-Garcia, Gil-Martinez, Pardo-Montero, Munoz-Plata et al, 2016). Used within an acceptance and commitment therapy model, graded exposure becomes “committed action” that’s aligned to values – and engaging in valued occupations is exactly what occupational therapy is all about.

Of course, not everyone enjoys this kind of work. That’s OK – because there are others who DO enjoy doing it! And it’s all in the way that it’s done – a framework of values, commitment, mindfulness and, that’s right, “chat therapy” – which some occupational therapists believe is right outside their scope of practice.

Now unless someone works in a vacuum, via some sort of mind-to-mind process, I cannot think of any therapist who doesn’t communicate with the person they’re working with. Humans communicate effortlessly and continuously. And “chat therapy” is about communicating – communicating skillfully, carefully selecting what to respond to and how, and focusing on clinical reasoning. Of course, if that’s ALL the treatment is about, then it’s not occupational therapy, but when it’s used in the aid of helping someone participate more fully in valued occupations using CBT, ACT, DBT or indeed motivational interviewing is one of the approaches occupational therapists can employ both within an occupation as therapy and occupation as outcome model.

I firmly believe that occupational therapists should follow an evidence base for their work. While I openly acknowledge the paucity of occupational therapy-specific research in persistent pain, particularly using occupation as therapy, there is plenty of research (carried out by other professions) to support approaches occupational therapists can adopt. After all, we already use developmental models, neurological models, sociological models, anthropological ones and yes, psychological ones. And that’s without venturing into the biomechanical ones! So it’s not an unfamiliar clinical reasoning strategy.

What makes occupational therapy practice in pain management absolutely unique are two things: a complete focus on reducing disability through enabling occupation, and a commitment to bringing skills developed “in clinic” outside into the daily lives and world of the people we are privileged to work with. What we should not do is focus on short-term outcomes like reducing (avoiding) bending with some new technique, while being ignorant of other occupational approaches. We are a fortunate profession because all of what we do is biopsychosocial, let’s not forget it.

 

López-de-Uralde-Villanueva, I., Muñoz-García, D., Gil-Martínez, A., Pardo-Montero, J., Muñoz-Plata, R., Angulo-Díaz-Parreño, S., . . . La Touche, R. (2016). A systematic review and meta-analysis on the effectiveness of graded activity and graded exposure for chronic nonspecific low back pain. Pain Medicine, 17(1), 172-188. doi:10.1111/pme.12882

Yerxa, E. J. (1990). An introduction to occupational science, a foundation for occupational therapy in the 21st century. Occup Ther Health Care, 6(4), 1-17. doi:10.1080/J003v06n04_04

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

When it hurts – but it’s important to keep doing


To date, despite years of research and billions of dollars, there is no satisfactory way to reduce pain in all people. In fact, our pain reduction treatments for many forms of persistent pain are pretty poor whether we look at pharmaceuticals, surgery, psychological treatments or even exercise. What this means is there are a lot of disillusioned and frustrated people in our communities – yet life carries on, and people do keep doing!

In an effort to understand what might help people who don’t “find a cure”, researchers and clinicians have been looking at mediators. Mediators are factors that explain a relationship between two variables. In the study I’m examining today, the predictor is pain intensity, and the criterion variable is participating in valued life activities (the things we want or need to do). The research question was whether self-efficacy and/or pain acceptance mediated engaging in valued life activities.

Ahlstrand, Vaz, Falkmer, Thyberg and Bjork (2017) used a cross-sectional study to explore relationships between the variables above in a group of people with rheumatoid arthritis (RA), drawn from three rheumatology registers in South East Sweden. Participants were required to have confirmed RA; be between 18 – 80 years; have had RA for four years or more; and have data included in the quality register – a total of 737 people agreed to take part (from a total of 1277 meeting entry criteria).

The researchers used the Swedish versions of Health Assessment Questionnaire (Wolfe, 1989) to establish degree of difficulty in daily activities, as well as the Valued Life Activities scale (Katz, Morris & Yellin, 2006); the Arthritis Self-Efficacy Scale (Lorig, Chastain, Ung, Shoor & Holman, 1989); and the Chronic Pain Acceptance Questionnaire (Wicksell, Olsson & Melin, 2009).
The statistical analyses included Chi-square tests of independence to identify significant differences in categorical factors due to gender, and steps were taken to establish whether there were gender differences for pain acceptance, self-efficacy and valued life activities. Pearson correlations were used to explore the relationships between acceptance, self efficacy and the valued life activities summary score, and then univariate regressions were undertaken to test each individual factor (eg pain, pain acceptance and self efficacy on valued life activities). Then, only the significant contributors in univariate analyses where entered into the hierarchical linear regression models. The tests were to establish whether self-efficacy would predict valued life activities after acceptance and pain scores were considered.

Finally, structural equation modelling was used to examine the contribution and influence of pain, activity engagement and self-efficacy on difficulties performing valued life activities. A note here: The authors used the structure of the ICF model to name the constructs in their structural equation model.

What did they find?

The people who responded to this survey tended to be less active than those who were on the registers but didn’t respond, so we need to keep this in mind when we interpret their results. They found that women reported slightly more pain than men, but there were no differences between men and women on all measures except that men scored more highly on the symptom control subscale of the self-efficacy measure. A point to note here is that, unlike the Pain Self Efficacy Questionaire, this measure includes attempts to reduce or control pain and/or disability, so it’s a slightly different construct from the PSEQ which measures confidence to engage in doing things despite the pain.

In terms of pain, pain acceptance, and arthritis self-efficacy, there were low to moderate associations between these and engaging in valued life activities. In fact, all pain acceptance and self-efficacy constructs measured in this study were associated with performing valued life activities. In other words, when people are confident, and willing to do things and engage in activities despite pain, the more valued activities they actually do. In fact, one of the more striking findings was a negative relationship between activity engagement and performing valued life activities – those with lower activity engagement scores reported great difficult engaging in what was important to them (not especially surprising given that both scales are about doing what’s important and getting on with life).

Now for the really geeky model: structural equation modeling found a rather complex relationship between all the variables – so complex I’m going to include the diagram.

What does it show? Well, there’s a relationship between pain intensity and valued activity engagement – the more pain, the less people do what’s important. BUT this is mediated by “personal factors” (remember the ICF labels). These personal factors are the pain acceptance activity engagement, self-efficacy for pain and self-efficacy for symptoms. Interestingly, pain willingness, the other subscale on the pain acceptance scale, wasn’t correlated.

Or is it surprising? To my mind there are some interesting conceptual issues with this study. Firstly, in a group that is self-selected and represents slightly more disability than those who didn’t respond, it’s not surprising that pain intensity and disability were correlated. This is something we see often pre-treatment in chronic pain settings. It’s also no surprise to me that the Arthritis self-efficacy scales were associated with valued activities, and with activity engagement – the arthritis self-efficacy scales ask “How certain are you that you can decrease your pain quite a bit?”; “How certain are you that you can that you can make a small-to moderate reduction in your arthritis pain by using methods other than taking extra medication?” amongst other questions. These suggest that pain reduction is a primary aim in arthritis management. The Chronic Pain Acceptance Questionnaire, however, is a very different beast. The Activity Engagement scale is about doing things that are valued (similar to the Valued Life Activity scale), while the  Willingness scale is about being willing to live life again despite pain – for example “I am getting on with the business of living no matter what my level of pain is.”; “It’s not necessary for me to control my pain in order to handle my life well.”.

While the authors argue that this study shows the value of self efficacy, stating “Active management promotes a sense of confidence, or self-efficacy, for dealing with pain that is associated with improved participation in daily activities and wellbeing.” I think the Arthritis Self-Efficacy Scale’s focus on controlling pain and other symptoms is incompatible with the constructs implied in the CPAQ. The ACT (Acceptance and Commitment Therapy) approach to pain is, as I’ve mentioned many times, a focus on engaging in valued activities irrespective of pain intensity – a more achievable goal for many than becoming confident to reduce pain as the ASES measures.

To their credit, the authors also indicate that men and women who continue to experience pain despite optimal medical treatment might benefit from strategies to increase their confidence to manage their own symptoms – but that a focus on pain control instead of participation despite pain is probably unhelpful. They go on to say that “by focusing on pain aceptance and activity engagement despite pain, self-management strategies may change the focus from pain control to a more flexible engagement in valued activities.” I couldn’t agree more – and I wish they’d used the Pain Self Efficacy Questionnaire instead of the ASES in this study. Maybe we need more discussion about appropriate measures in rheumatology research.

 

Ahlstrand, I., Vaz, S., Falkmer, T., Thyberg, I., & Björk, M. (2017). Self-efficacy and pain acceptance as mediators of the relationship between pain and performance of valued life activities in women and men with rheumatoid arthritis. Clinical Rehabilitation, 31(6), 824-834. doi:10.1177/0269215516646166

Katz PP, Morris A and Yelin EH. (2006). Prevalence and predictors of disability in valued life activities among individuals with rheumatoid arthritis. Annals of Rheumatology Diseases. 65: 763–769.

Lorig K, Chastain RL, Ung E, Shoor S and Holman HR. (1989). Development and evaluation of a scale to measure perceived self-efficacy in people with arthritis. Arthritis & Rheumatism, 32(1): 37–44.

Wicksell RK, Olsson GL and Melin L. (2009). The Chronic Pain Acceptance Questionnaire (CPAQ)-further validation including a confirmatory factor analysis and a comparison with the Tampa Scale of Kinesiophobia. European Journal of Pain, 13: 760–768.

Wolfe F. (1989). A brief clinical health assessment instrument: CLINHAQ. Arthritis & Rheumatism,  32 (suppl): S9

Thinking the worst – and willingness to do things despite pain


Catastrophising, perhaps more than any other psychological construct, has received pretty negative press from people living with pain. It’s a construct that represents a tendency to “think the worst” when experiencing pain, and I can understand why people who are in the middle of a strong pain bout might reject any idea that their minds might be playing tricks on them. It’s hard to stand back from the immediacy of “OMG that really HURTS” especially when, habitually, many people who have pain try so hard to pretend that “yes everything is really all right”. At the same time, the evidence base for the contribution that habitually “thinking the worst” has on actually increasing the report of pain intensity, increasing difficulty coping, making it harder to access effective ways around the pain, and on the impact pain has on doing important things in life is strong (Quartana, Campbell & Edwards, 2009).

What then, could counter this tendency to feel like a possum in the headlights in the face of strong pain? In the study I’m discussing today, willingness to experience pain without trying to avoid or control that experience, aka “acceptance”, is examined, along with catastrophising and measures of disability. Craner, Sperry, Koball, Morrison and Gilliam (2017) recruited 249 adults who were seeking treatment at an interdisciplinary pain rehabilitation programme (at tertiary level), and examined a range of important variables pre and post treatment.  Participants in the programme were on average 50 years old, mainly married, and white (not a term we’d ever use in New Zealand!). They’d had pain for an average of 10.5 years, and slightly less than half were using opioids at the time of entry to the programme.

Occupational therapists administered the Canadian Occupational Performance Measure, an occupational therapist-administered, semi-structured interview designed to assess a person’s performance and satisfaction with their daily activities (Law, Baptiste, McColl, Opzoomer, Polatajko & Pollock, 1990). The performance scale was used in this study, along with the Chronic Pain Acceptance Questionnaire (one of my favourites – McCracken, Vowles & Eccelston, 2004); the Pain Catastrophising Scale (Sullivan, Bishop & Pivik, 1995), The Patient Health Questionnaire-9 (Kroenke, Spitzer & Williams, 2001); and The Westhaven-Yale Multidimensional Pain Inventory (Kerns, Turk & Rudy, 1985).

Now here’s where the fun begins, because there is some serious statistical analysis going on! Hierarchical multiple regression analyses is not for the faint-hearted – read the info about this approach by clicking the link. Essentially, it is a way to show if variables of your interest explain a statistically significant amount of variance in your Dependent Variable (DV) after accounting for all other variables. Or, in this study, what is the relationship between pain catastrophising, acceptance and pain severity – while controlling for age, gender, opioids use, and pain duration. The final step was to enter a calculation of the interaction between catastrophising and acceptance, and to enter this into the equation as the final step. A significant interaction suggests one of these two moderates the other – and this is ultimately captured by testing the slopes of the graphs. Complex? Yes – but a good way to analyse these complex relationships.

Results

Unsurprisingly, pain catastrophising and acceptance do correlate – negatively. What this means is that the more a person thinks the worst about their pain, the less willing they are to do things that will increase their pain, or to do things while their pain is elevated. Makes sense, on the surface, but wait there’s more!

Pain catastrophizing was significantly (ps < .01) and positively correlated with greater perceived pain intensity, pain interference, distress due to pain, and depression – and negatively correlated with occupational therapist-rated functioning. Further analysis found that only pain catastrophising (not acceptance) was associated with pain severity, while both catastrophising and acceptance predicted negative effect (mood) using the WHYMPI, but when the analysis used the PHQ-9, both pain catastrophising and pain acceptance uniquely predicted depressive symptoms.  When pain interference was used as the dependent variable, pain acceptance uniquely predicted the amount of interference participants experienced, rather than catastrophising. The final analysis was using the performance subscale of the COPM, finding that pain acceptance was a predictor, while catastrophising was not.

What does all this actually mean?

Firstly, I found it interesting that values weren’t used as part of this investigation, because when people do daily activities, they do those they place value on, for some reason. For example, if we value other people’s opinions, we’re likely to dress up a bit, do the housework and maybe bake something if we have people come to visit. This study didn’t incorporate contexts of activity – the why question. I think that’s a limitation, however, examining values is not super easy, however it’s worth keeping this limitation in mind when thinking about the results.

The results suggest that when someone is willing to do something even if it increases pain, or while pain is elevated, this has an effect on their performance, disability, the interference they experience from pain, and their mood.

The results also suggest that catastrophising, while an important predictor of pain-related outcomes, is moderated by acceptance.

My question now is – what helps someone to be willing to do things even when their pain is high? if we analyse the CPAQ items, we find things like “I am getting on with the business of living no matter what my level of pain is.”;  “It’s not necessary for me to control my pain in order to handle my life well.”; and “My life is going well, even though I have chronic pain.”. These are important areas for clinicians to address during treatment. They’re about life – rather than pain. They’re about what makes life worth living. They’re about who are you, what does your life stand for, what makes you YOU, and what can you do despite pain. And these are important aspects of pain treatment: given none of us can claim a 100% success rate for pain reduction. Life is more than the absence of pain.

 

 

Craner, J. R., Sperry, J. A., Koball, A. M., Morrison, E. J., & Gilliam, W. P. (2017). Unique contributions of acceptance and catastrophizing on chronic pain adaptation. International Journal of Behavioral Medicine, 24(4), 542-551.

Kerns IVRD,TurkDC, Rudy TE. (1985) West Haven-Yale Multidimensional Pain Inventory (WHYMPI). Pain. 23:345–56.

Kroenke K, Spitzer RL, Williams JB. The PHQ-9: validity of a brief depression severity measure. Journal of General Internal Medicine. 16(9), 606-13.

Law M, Baptiste S, McColl M, Opzoomer A, Polatajko H, Pollock N. (1990). The Canadian Occupational Performance Measure: an outcome measure for occupational therapy. Canadian Journal of Occupational Therapy. 57(2), pp82–7.

McCracken LM, Vowles KE, Eccleston C. (2004). Acceptance of chronic pain: component analysis and a revised assessment method. Pain. 107(1–2), pp159–66.

Quartana PJ, Campbell CM, Edwards RR. (2009) Pain catastrophizing: a critical review. Expert Reviews in Neurotherapy, 9, pp 745–58.

SullivanMLJ, Bishop SR, Pivik J. (1995). The Pain Catastrophizing Scale: development and validation. Psychological Assessment. 7:524–32.

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 – iii


Before Christmas and the New Year break I was writing about how I use a biopsychosocial model in pain management – and I haven’t finished!

To review: The first post was about the context or the ideas behind Engel’s original model, and my two key clinical questions – why is this person presenting in this way at this time, and what can be done to reduce distress and disability?

The second post was about classical and operant conditioning and why these models are useful when we’re thinking about what a person does when they’re sore – and how their actions communicate to people around them. I also pointed out that many of these actions are not conscious, but have been learned and shaped from childhood, leading to a myriad of ways people express themselves when they’re in pain.

One of the criticisms of this approach to pain management is that “the model” isn’t scientific (therefore doesn’t lend itself to generating hypotheses that can be tested), and a second is that it’s “too fuzzy” and doesn’t specify what should be “in” and what should be “out” in clinical reasoning. I don’t agree with either of these statements and today I hope to present why.

Is a BPSM truly a “model”? What’s a model anyway? – one definition I’ve found is “In science, a model is a representation of an idea, an object or even a process or a system that is used to describe and explain phenomena that cannot be experienced directly.” In other words, they’re like a metaphor, bridging between something known and something abstract or unfamiliar. Models may be extremely detailed and mathematical, but may also be conceptual and broad. BPSM is probably the latter – a conceptual model from which we’ve developed some useful and testable hypotheses.

Engel himself described this as a scientific model, saying that it “enables the physician to extend application of the scientific method to aspects of everyday practice and patient care heretofore not deemed accessible to a scientific approach” (Engel, 1980, p.  535). He goes on to say that the doctor’s tasks are to find out what and how the patient is feeling, then to explanations (hypotheses) for the patient’s feelings and experiences, and then to test those hypotheses via clinical and laboratory studies (p. 536). Engel had some ideas about how a physician might generate hypotheses – based on his knowledge of general systems theory (von Bertalanffy, 1968). Engel appealed to von Bertalanffy’s idea that systems are a hierarchically arranged series of units, with the level of analysis dependent upon the complexity and unit of measure. In other words, molecular analysis is appropriate when cells and physiology are the unit of analysis, while the quality and influence of social connections are appropriate when looking at the influence of community and legislation on an individual’s behaviour.

The notion that a BPSM approach is “too fuzzy” and doesn’t provide structure is quite true: there’s not a lot of explanation as to how the various levels within a hierarchical system might interact. Interestingly, I think this problem is still relevant today!  While we know a lot about the brain, and a little about the mind – we don’t know how brain produces “mind”, although some philosophers and neuroscientists have taken a stab at it (thinking Andy Clark amongst others here). Similarly, although we know a lot about thoughts, beliefs and even relationships, we don’t know nearly as much about how thoughts and beliefs are adopted by a community, although Daniel Dennett has some thoughts about this.

So, it’s hardly surprising that when it comes to pain, we struggle to understand how biological processes, psychological processes and social ones interact to produce the experience of one person presenting for treatment at this time in this way – but this does not mean we should ignore what we DO know, which is that within each domain there is much to explore!

My preference is to draw on Brian Haig‘s idea of an Abductive Theory of Scientific Method, and in particular this paper on clinical reasoning, scientific method and abductive reasoning. The basic idea is that we recognise the existence of a phenomenon because either we’ve seen it before, or we’ve read about it. We distinguish between random events and a phenomenon because these appear to be consistent and repeated. Then we begin to generate some hypotheses to explain the presence of this phenomenon. Abduction is the process of studying what we see/observe/know (“facts”) and developing a theory to explain them (or generating a hypothesis). We then go about testing that hypothesis – and while we never truly confirm it, we can reject an alternative hypothesis tested against the first. As a result we arrive at what we can call a plausible explanation – something that “makes sense”, given what we’ve observed, and what we know about the world and how it works.

More about this geeky stuff next week. Meanwhile I think it’s worth pondering this: in “usual science” we somehow arrive at a hypothesis, and then set about testing it. No-one, it seems, knows where the original hypothesis comes from – and it’s rarely truly acknowledged. Researchers typically look for “gaps in the literature”, something that hasn’t been asked or answered yet, but what if you happen to be a clinician? I think clinicians routinely observe “interesting things” that, if we took some time to measure them, might be a phenomenon. Something that hasn’t yet been explained. I also think we have opportunities to be scientific about how we investigate what we see and do, if we’re prepared to be systematic and think about how we might control for confounds/bias. And I think those edges between levels within a hierarchy or between domains might be fruitful areas for clinicians to be exploring – bringing us to a practical application of Engel’s BPSM.

ENGEL, G. L. 1980. The clinical application of the biopsychosocial model. The American Journal of Psychiatry, 137, 535-544.

HAIG, B. D. 2008. Scientific method, abduction, and clinical reasoning. Journal of Clinical Psychology, 64, 1013-1018.

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.

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