Research

Six old papers for pain clinicians


We’re rather flighty beasts, us clinicians. From looking at the various ads for courses on the interwebs, it seems we’re all ready to jump on to the next newest thing. This same “what’s new” attitude is present in journals as well –  “these references are very old, are there newer ones you can use?”

Here’s a question: what happens to the old stuff? Is it outdated and useless? Do really well-conducted studies have a “use-by” date? Are older therapies always less effective than the new ones? What if this urge to “refresh” means we do actually throw the baby out with the bathwater?

Some of you will know that I’m keen on reading about the history of how we manage pain. I think it helps put some of our current dilemmas into perspective – and helps us understand “legacy” beliefs: things people believe based on old ideas about how our body works. It reminds me that some of these problems are not about research evidence, but about very human issues of political clout, social inertia, and legal factors (thinking of my recent post on the ” Dynasty of the Disc“.

So, today I want to talk about reading old papers. Papers written maybe in the 1960’s or 1970’s, 1980’s and 1990’s. Even from 2000 and on!

Here are some papers I think everyone working in pain and pain management should review:

  1. Melzack, R., & Wall, P. D. (1965). Pain mechanisms: a new theory. Science, 150(3699), 971-979.

The original paper, the one that ignited new ways of thinking about pain. Not a very long paper, and yes, many of the details proposed in this paper have been revised in light of new information, but the essential groundbreaking principles, distinguishing between nociception and pain, between peripheral and central mechanisms, of the modulation that occurs at every single synapse to and from the brain, of the need for us to consider OMG the brain!  This is the bit that really grabs my attention: 2. Fordyce, W. E., Fowler, R. S., & Delateur, B. (1968). An Application of Behavior Modification Technique to a Problem of Chronic Pain. Behaviour Research and Therapy, 6(1), 105-107.

This is the original paper by Fordyce and colleagues, demonstrating that by following the principles of operant conditioning, a person with persistent and disabling pain could return to daily life. It was extraordinary in that instead of focusing on pain – it focused on behaviour. Fantastic description of behaviour therapy in action.

3. Fordyce, W. E. (1988). Pain and Suffering: A Reappraisal. American Psychologist, 43(4), 276-283.  This is another paper by Fordyce, this time discussing distinctions between pain and suffering – he clearly articulates Loeser’s “onion rings” model which has been reproduced, revised, and possibly warped out of shape in various papers since (do a Google search and see what you can find!).

4. Engel, G. L. (1977). The need for a new medical model: A challenge for biomedicine. Science, 196(4286), 129-136. doi:http://dx.doi.org/10.1126/science.847460 The classic Engel paper, written for a psychiatry audience but with a far far wider impact on healthcare since. It’s really useful to read how Engel put this model together, the context at the time, and his ideas for how it might be used. The part that really gets me is how he considers the path from being a person to being a patient – that decision-making process to seek treatment which is rarely discussed (but is, I think, a crucial indicator of the expectations the person brings to a consultation)

5. Ignelzi, R. J., Sternbach, R. A., & Timmermans, G. (1977). The pain ward follow-up analyses. Pain, 3(3), 277-280. This paper is one of the very first to show that surgical approaches to pain management don’t provide the most wonderful outcomes, at least not in comparison with those who were participants in a pain management programme. I think it’s interesting because it shows the use of long term follow-up data to demonstrate effectiveness. Who would have thought two and three year outcomes would show such differences? And I wonder what would happen today?

6. I couldn’t resist this one: Fordyce, W., McMahon, R., Rainwater, G., Jackins, S., Questad, K., Murphy, T., & De Lateur, B. (1981). Pain complaint-exercise performance relationship in chronic pain. Pain, 10(3), 311-321. Why? Because as far back as 1981 we were seeing that advice to stop doing, or to use pain as a guide, was unhelpful. Perhaps it’s time we took this one on board?

There. Old papers. Old messages – perhaps ones we have still to adopt. Can we do better? Shouldn’t we do better? Should we stop trying to create new and groovy stuff and instead implement some of these really old principles?

 

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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.

The dynasty of the disc! More history in pain management


Low back pain, despite the multitude of explanations and increasing disability associated with it, has been with humans since forever. Who knows why and I’m not about to conjecture. What’s interesting is that despite ergonomic solutions (fail), increased fitness amongst many people (also a fail), surgical solutions (fail), hands on solutions (fail, fail), and a whole bunch of “special” exercises (fail, fail, fail) we still don’t have a handle on how to reduce disability from it.

I don’t think there will be many people who haven’t seen this:
I’ve never quite worked out why, when you search for imagines of disc bulges (or rather, prolapse of the nucleus pulposus – herniated or ruptured disc was the term preferred by Mixter and Ayer (1935) who proposed the notion of disc prolapse being the cause of “injuries to the spine” (Allan & Waddell, 1989), you end up with these nasty red glowing areas (see below). I think it’s because how else do you convey the idea that this is meant to be “the source of pain”.

Let’s dig back a little into history. Allan and Waddell (1989) describe the “modern” concept of the disc based on four papers: Goldthwaite (1911); Middleton & Teacher (1911); Dandy (1929) and Mixter and Barr (1934). Pathologists had described the presence of these prolapses when conducting postmortem examinations – but their patients couldn’t tell them whether they hurt, and neither was there any clinical awareness of any relationship between pain and disc prolapse. In 1911, two papers described patients with massive disc prolapses – one was a fatal case of paraplegia after a disc prolapse followed by Middleton and Teacher conducting lab experiments to see whether injury (force applied to the disc) could produce a prolapse (Middleton & Teacher, 1911). Goldthwaite described a case of paresis (not pain) after manipulation of the back, presuming that a “displaced sacroiliac joint” was responsible and identified that the nerve at the lumbosacral joint could be compressed – this was supported by later authors.

Cushing, a surgeon, performed a laminectomy which didn’t turn out well – but identified that “narrowing of the canal” might be responsible for the person’s pain, and from there the disc was blamed as the cause of “many cases of lumbago, sciatica and paraplegia”.  This narrative was followed up by other clinicians, and Mixter and Barr (1934) increased the attention given to these theories. Ultimately this led to a meeting of the minds where Mixter and Barr (Mixter being a neurologist, Barr an orthopaedic surgeon) carried out an investigation into enchondromas and and normal discs. What were thought to be tumours were mainly “normal cartilage”.  Mixter and Ayer (1935) went on to pursue the idea of disc prolapse being involved in not only cases where neurological changes were evident, but also low back pain.

Mixter and Ayer (1935) found that surgical responses were not very good – while leg pain was fixed patients still complained of a painful back. Their paper, however, emphasised that lesions of the disc were caused by “trauma” (even though history of even minor trauma was only found in 14 of their 23 cases). Canny men that they were, they noted that if trauma was involved it would “open up an interesting problem in industrial medicine”: who caused the trauma?

Well, like many ideas of the time, this one took root in an exciting climate of medical and surgical discovery – detailed descriptions of the techniques and procedures used were published, but even at that time outcome measures were not reported because, in their words “the question of liability, compensation and insurance loom large on the horizon and add complications compounded to an already knotty problem”. The meme of physical trauma to the back causing disc prolapse and subsequent back pain caught hold of the imagination, and although initially diagnosed using a myelogram, very quickly became replaced (in the name of avoiding complications, cost, discomfort and potentially missing ‘concealed’ discs) by clinical history and neurological examination.

Over the years 1930 – 1950, anaesthetics and surgery became safer and more routine – and accepted, after all look at how these surgeons patched up the brave soldiers! But by the 1970’s the enthusiasm began to wane as more patients reported adverse outcomes, and continued to experience pain.  So… it was decided disc prolapses should only be surgically managed in the case of sciatica rather than simply low back pain – but what about disc degeneration? Surely that could be the “cause”! And yes, we know that even though normal age-related changes were present, these were ignored, along with the somewhat tenuous relationship between disc changes and pain… Instead cadaver biomechanical studies were used to confirm that the disc could bulge with certain forces, and because the problem was now “degenerative” there was no cure – it would ‘inevitably’ progress. Thus the surgical fusion was brought in to play to reduce the “wear and tear” on the disc to “stabilise” the joint (though instability hadn’t been found, and fusion didn’t produce great results).

What was really striking was the move during this period towards rest as treatment. Previously bonesetters (predecessors of osteopathy and chiropractic and manual medicine) manipulated and then quickly mobilised people with low back pain. The hands-on treatment provided short-term relief but the real cure was to keep doing. Orthopaedics, however, based both on knowledge of fracture and tissue healing and ongoing use of surgery for low back pain, emphasised rest to allow “inflammation” to heal. Whether there was any inflammation is moot – what took root in the minds of medical and other practitioners was the need to rest until the pain was gone.

And that, dear ones, is how the epidemic of disability (the effect on function, limitations on what people can do, on participation) was born. It’s called iatrogenesis, or what health professionals can do to increase harm, inadvertently or not. And it’s still happening today.

We should not lay the blame for ongoing harm at the feet of orthopaedic surgeons and neurologists of the day. It was a perfect storm of media attention, community fascination with technology and miracles performed as a result of the war, the heroic soldiers and their equally heroic surgeons, the courts (in the case of industry as responsible for trauma to civilians), and of course the insurers – all over the period between 1880 – and until even today.  While outcomes are being more widely reported in orthopaedic surgery (and other treatments), changing clinical behaviour, community attitudes and the legacy of our history is slow. Cognitive dissonance is a thing… and even though 1965 saw gate control theory revolutionise our thinking about the way pain is produced, the implications are not yet fully accepted.

 

Allan, D. B., & Waddell, G. (1989). An historical perspective on low back pain and disability. Acta Orthopaedica Scandinavica, 60(sup234), 1-23.

Each time we face our fear, we gain strength, courage, and confidence in the doing – Theodore Roosevelt


I’m not certain Theodore Roosevelt actually said that – but who cares?! It’s a great statement. For the person living with persistent pain, though, it can be the last thing you want to hear. After all, it’s tough enough getting up and just doing the normal things let alone challenge yourself! So… how can a health professional help?

Let’s briefly recap. Self efficacy is the confidence I can do something successfully if I wanted to. It’s a robust predictor of many health behaviours including exercise, stopping smoking, eating healthily and coping well with persistent pain (Jackson, Wang, Wang & Fan, 2014; Williams & Rhodes, 2016). It was first introduced as a concept by Bandura as part of his theoretical model of behaviour change, and further discussed in an experimental study in a paper investigating systematic desensitisation processes, arguing that this approach to treatment created and strengthened expectations of personal efficacy (Bandura & Adams, 1977). Bandura argued that people develop a sense (expectation) of self efficacy from their own performance, watching others succeed, being persuaded by someone that yes indeed you have the skills to achieve, and also awareness of physiological arousal from which people can judge their own level of anxiety.

Self efficacy is more than a simple “general confidence” construct, however. It’s far more selective than this. For example, although I believe I can successfully dance in my lounge with no-one there and the curtains closed, this does not translate to me dancing on a stage on my own in the spotlights with an audience watching! Self efficacy refers to confidence to succeed and produce the outcome I desire in a given context – and that’s extremely important for pain management, and in particular, exercise for people experiencing pain.

How does self efficacy improve outcomes? There are at least two ways: (1) through the actions taken to manage or control pain (for example, gradually increasing activity levels but not doing too much) and (2) managing the situations associated with pain (for example, people with low self efficacy may avoid activities that increase pain, or cope by using more medication (Jackson, Wang, Wang & Fan, 2014).

To examine how self efficacy affects outcomes, Jackson and colleagues (2014) conducted a meta-analysis of papers examining this variable along with other important outcomes. Overall effect sizes for relationships between self efficacy and all chronic pain outcomes were medium and highly significant. This is really important stuff – we don’t find all that many studies where a single variable has this much predictive power!

As a moderator, the adjusted overall effect size (r=.50) of self efficacy and impairment was larger than the average effect sizes of meta-analyses on relations between disability and fear-avoidance beliefs, and pain as a threat for future damage and challenge for future opportunities. Self efficacy has stronger links with impairment than cognitive factors such as fear-avoidance beliefs and primary appraisals of pain (Jackson, Wang, Wang & Fan, 2014).  Age and duration of pain were the strongest moderators of these associations and suggest that reduced self-efficacy can become entrenched over time. In other words – as time passes, people experience fewer opportunities for success and begin to expect they won’t ever manage their pain well.

An important point is made by these authors: how we measure self efficacy matters. They found that self efficacy measures tapping “confidence in the capacity to function despite pain” had
stronger associations with impairment than did those assessing confidence in controlling pain or managing other symptoms.

Bolstering self efficacy – not just about telling people they can do it!

Given that self efficacy is domain-specific, or a construct that refers to confidence to do actions that lead to success in specified situations, here are a few of my questions:

  • Why are most people attending pain management programmes provided with gym-based programmes that don’t look at lot like the kinds of things people have to do in daily life? It’s like there’s an expectation that “doing exercise” – any exercise – is enough to improve a person’s capabilities.

    BUT while this might increase my confidence to (a) do exercise and (b) do it in a gym – but does it mean I’ll be more confident to return to work? Or do my housework?

  • How often are people attending gyms told to “push on”, or to “stop if it hurts”? And what effect does this have on people?

If their confidence is low, being told “just do it” is NOT likely to work. People need to experience that it’s possible to do things despite pain – and I think, to be able to handle a flare-up successfully. Now this is not going to happen if we adopt the line that getting rid of all pain is the aim, and that flare-ups should be avoided. If we want people to deal successfully with the inevitable flare-ups that occur, especially with low back pain, then we need to (a) be gentle, and grade the activities in an appropriate way (b) have some “ways of coping” we can introduce to people rather than simply telling them they can cope or reducing the demands (c) have other people around them also coping well (and that includes us health professionals)

  • Ensure we attribute change to the person, not to us.

That’s right: not to our sparkling personality, not to our special exercises, not to the machines we use, not to the techniques we have – you get the drift? Progress must be attributed to the person and his or her skills and perseverance. Because, seriously, all this arguing over which exercise regime is best doesn’t stack up when it’s actually self efficacy that predicts a good outcome.

And for case managers who may read this: just because someone has successfully completed an exercise programme, or a vocational programme with exercise as a component, this does not mean the person can manage successfully at work. Well, they may manage – but they may utterly lack confidence that they can. Context matters.

 

Bandura, A., & Adams, N. E. (1977). Analysis of self-efficacy theory of behavioral change. Cognitive Therapy and Research, 1(4), 287-310.

Estlander AM, Takala EP, Viikari-Juntura E., (1998). Do psychological factors predict changes in musculoskeletal pain? A prospective, two-year follow-up study of a working population. Journal of Occupational and Environmental Medicine 40:445-453

Jackson, T., Wang, Y., Wang, Y., & Fan, H. (2014). Self-efficacy and chronic pain outcomes: A meta-analytic review. The Journal of Pain, 15(8), 800-814.

Williams, D. M., & Rhodes, R. E. (2016). The confounded self-efficacy construct: Conceptual analysis and recommendations for future research. Health Psychology Review, 10(2), 113-128.

The confidence that you’ll succeed if you try…


Self efficacy. It’s a word bandied about a lot in pain management, and for a group of clinicians in NZ, it’s been a shock to find out that – oh no! They’re not supporting self efficacy with their patients very much! It means “confidence that if I do this under these conditions, I’ll be successful”.

Self efficacy is part of Bandura’s social learning theory (click here for the Wikipedia entry) where he proposed that much of psychological treatment is driven by a common underlying mechanism: to create and strengthen expectations of personal effectiveness. Bandura recognised that we don’t always have to personally experiment through trial and error in order to learn. Self efficacy expectations were thought to develop from personal experience (let me do, and I’ll learn how); watching other people try (show me, and I’ll see if you succeed, then I’ll copy you); verbal persuasion that aims to convince that you have the capabilities to manage successfully (encourage me, let me know I can, and I’ll try); and how physiologically aroused or alert you are (if I feel confident inside, I’ll try but if I feel anxious or stressed I’m less inclined to) (Bandura, 1977).

Bandura and colleagues established that “different treatment approaches alter expectations of personal efficacy, and the more dependable the source of efficacy information, the greater are the changes in self-efficacy.” (Bandura & Adams, 1977, p. 288). The conclusions drawn from this mean that treatments where people DO and succeed are more effective at enhancing their belief in self efficacy, while watching others, or being told how to do something are far weaker at building this effect.

Bandura began working on this theory while pondering how psychological treatments, particularly for systematic desensitisation or graded exposure, generated their effects. Systematic desensitisation aimed to reduce arousal levels and thus avoidance while being in a relaxed state – therefore the person is exposed to increasingly “aversive” stimuli (stimuli you want to avoid) while remaining calm and relaxed. Bandura thought that there were other factors involved in avoidance behaviour, developing his theory that expectations of negative consequences alone can generate fear and defensive behaviour and that this isn’t necessarily reflected in autonomic arousal and actions. Bandura hypothesised that reducing physiological arousal improved performance not by eliminating a drive to escape – but instead by increasing the confidence that the person can successfully manage the situation.

For parents, the idea that if you believe you can do what you set out to do, is embodied in the little book “The Little Engine That Could” (Piper, 1930/1989). Remember? The little engine that couldn’t because all the bigger engines said so, but then tried and tried and believed he could – and he did!

So, what does this have to do with pain management?

Let’s paint a scenario. Allan comes to see a hands-on therapist because he has a sore back. He believes that hands-on therapy is the thing, because others have said it’s really good. He goes, gets his treatment and wow! Things improve! The next time he has a sore back (because, you know, it almost always comes back) what does he do? Well, on the basis of his past experience, he heads to his hands-on therapist, because he’s confident this will help his pain. The problem is, his therapist has moved town. He’s a bit stuck now because in his town there are not many therapists doing this particular kind of treatment – what does he do? He doesn’t believe that anyone else can help, and he has no belief that he can manage by himself. He has little self efficacy for managing his own back pain.

Self efficacy is not about whether a person can do certain movements, it’s about believing that the person can organise skills to achieve goals within a changing context – not just what I will do, under duress, but what I can do, what I’m capable of doing, and what I say I’ll probably do.

Self efficacy is not a belief that a specific behaviour will lead to a certain outcome in a certain situation, it’s the belief that I can perform that behaviour to produce the outcome.

So, self efficacy isn’t a generalised attitude – it’s a specific belief about certain actions, certain outcomes in certain situations. It’s not a personality trait like hardiness, or resilience, or general confidence or self-esteem, it’s about being confident that I can generate a solution to a problem in a particular part of my life.

The times when we’re least confident are often when we’re facing a new experience, or we’ve had a bad experience previously. Particularly if we’ve seen other people fail at the same thing, or succeed but do so with much fear and loathing. In the case of pain, there are ample opportunities to have a bad experience in the past, and to learn from other people around us that – oooh back pain is something to be afraid of, and you can’t manage it alone – you need to get help from someone else. Consequently, many people have very low self efficacy for successfully dealing with a bout of low back pain.

And health professionals: we can foster this.

How? By implying that success is due to what we do, rather than being a natural process of recovery. By suggesting it’s something about our “magic hands” or pills, or injections or surgery or special exercises, or “using the core correctly”. In doing so, we’re generating a belief that the person cannot manage alone. That it’s not what the person does, but the magic hands, pills, injections, surgery, special exercises or using the core…

Damush, Kroenke, Bair, Wu, Tu, Krebs and Poleshuck (2016) found that self management approaches to pain increase self efficacy, self management actions, and reduced pain intensity and depression in a group of community patients with chronic musculoskeletal pain and depression. A typically tough group to work with because confidence to succeed at anything is pretty low in depression. Self management aims to ensure the credit for recovery lies with the person doing things that help – creating and supporting a belief that the person has the capability to successfully manage their situation. The techniques? Simple strengthening and stretching exercises, progressive muscle relaxation, and visualisation, in a group setting. Strategies that typically don’t need technology, but do provide support. Information about the natural history of recovery was included – so people were given realistic and optimistic information about their recovery, whether it meant pain reduction, or not. The usual goal setting, problem-solving, and positive self talk were encouraged, and people set goals each week to achieve – maybe based on something from the session, or something the person wanted to do for themselves.

This is not a high-tech approach. This is simple, straightforward pain management as it has been done for years (right back as far as the mid-1970’s and Sternberg!). And through it, these people become increasingly confident that they could successfully manage their own mood and pain independently. As a business model it’s probably not the best for repeat business – but oh how good for those participants who could go away and live their lives without having to think of themselves as patients.

More on self efficacy in the next couple of weeks – we can help people to become confident that they can succeed at managing their pain if it should happen again.

 

Bandura, A. (1977). Self-efficacy: Toward a unifying theory of behavioral change. Psychological Review,  84, 191-215.

Bandura, A., & Adams, N. E. (1977). Analysis of self-efficacy theory of behavioral change. Cognitive Therapy and Research, 1(4), 287-310.

Damush, T., Kroenke, K., Bair, M., Wu, J., Tu, W., Krebs, E., & Poleshuck, E. (2016). Pain self‐management training increases self‐efficacy, self‐management behaviours and pain and depression outcomes. European Journal of Pain, 20(7), 1070-1078.

Maddux, J. E. (2016). Self-efficacy Interpersonal and intrapersonal expectancies (pp. 55-60): Routledge.

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

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.

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

Occupational therapists’ knowledge of pain


I am mightily bothered by health professionals’ lack of knowledge about pain. Perhaps it’s my “teacher” orientation, but it seems to me that if we work in an area, we should grab as much information about that area as possible – and pain and pain management is such an important part of practice for every health professional that I wonder why it’s so often neglected. So, to begin exploring this, I completed a search looking at occupational therapists’ knowledge of pain – and struck gold,  kinda.

Angelica Reyes and Cary Brown conducted a survey of Canadian occupational therapists, to explore how well occupational therapists knew their stuff.

Members of the Canadian Association of Occupational Therapists were asked to participate and a total of 354 therapists (mainly from Ontario, Alberta and Nova Scotia) took part. Curious that few were from British Columbia where I know of quite a few occupational therapists working in the area, but there you have it.  Over half of the respondents had 10 years or less experience – so they were fairly recent graduates and should reflect a “current” educational bias. Only 5% of the total number of members of CAOT responded, so this is a fraction of the occupational therapists working in Canada – but you’d think the motivated (ie knowledgeable) would be more likely to respond than those who don’t work in the area….

What they found was consistent with previous studies (prior to 2000) showing that these respondents, who were surveyed using the City of Boston’s Rehabilitation Professionals’ Knowledge and Attitude Survey (Rochman & Herbert, 2015), had disturbing “potential knowledge gaps” in the following areas:

  • children’s ability to feel pain;
  • use of analgesics in orthopedic pain
  • use of nondrug treatments
  • thermal modalities
  • prevalence of malingering
  • impact of therapists’ values on assessment of veracity
  • mind/body dualism in chronic pain
  • measurement of pain intensity
  • effect of under-treatment on chronicity
  • prevalence of patients who over-report pain
  • prevalence ofpatients who are likely to become addicted if treated with opioids.

Of particular concerns was 45.7% of participants believed that malingering is common; 38% believed that pain intensity can be objectively measured, 39.7% believed people with pain over-report their pain, and 59.8% believed that opioid addiction is likely to occur in more than 5% of the patient population.

OUCH!

So, it seems that these occupational therapists had some very outdated ideas about pain, and in particular, seem to have missed the point that because pain is a biopsychosocial experience, we have no way to determine whether someone is “faking” – or malingering.

Now, I will lay good money on a bet that if we were to carry out this very same survey amongst any other health profession, we’d still arrive at these rather unsavoury findings. Folks, I live in a pain nerd bubble and I still hear these kinds of discussions amongst knowledgeable health professionals, so it’s unsurprising that so many people hold these beliefs. Beliefs that will hamper developing good relationships with the people we want to help, and beliefs that fly in the face of what we know about pain.

I am SO not pointing the finger at Canadian occupational therapists, neither am I pointing the finger at my profession alone. I think this lack of understanding reflects many things:

  1. Pain is a complex experience, and the legacies of ancient models lingers everywhere (dualism, medical model, reductionism, etc);
  2. We devote very little time in our professional training to learning about pain – and often, it’s limited to “here is the nociceptive system”;
  3. The research around pain has exploded over the last 15 years – it’s hard to keep up, which is why I blog;
  4. The problem of persistent pain is under-estimated, so if a person works in paediatrics, older person’s health, neurology, brain injury, spinal cord injury – it’s quite probable that pain is almost completely ignored, because “it’s not relevant”. After all, pain is something for specialist pain services, yes? NO
  5. Prevailing attitudes within the healthcare community are that pain is a difficult area to understand – and “should” be treated with medication or surgery otherwise….

You can see that this year’s IASP Global Year for Excellence in Pain Education has much to do.

Did you know that IASP have produced NINE comprehensive curricula – including occupational therapy  (thank you to Emeritus Professor Jenny Strong, Professor Cary Brown and Dr Derek Jones for developing this wonderful resource). This means there is no reason for us not to begin integrating this import area of practice into our undergraduate training.

Research examining occupational therapy’s contribution within pain management is in its infancy – but oh how my occupational therapy heart went pit-a-pat when, at the Australian and New Zealand Pain Society Scientific Meeting I presented alongside two other occupational therapists with PhD’s (or nearly there!) to a room full of clinicians, not just occupational therapists. While we have little specifically occupational therapy research, occupational therapists have been and are continuing to be part of research efforts around the world. And what clinicians do is apply what is learned into the daily lives of the people we work with. That, friends, is what occupational therapy is about – helping people live full, rich lives doing what’s important to them.

Reyes, A. N., & Brown, C. A. (2016). Occupational therapists’ pain knowledge: A national survey. Disability and Rehabilitation: An International, Multidisciplinary Journal, 38(13), 1309-1317.

Rochman D, Herbert P. Rehabilitation professionals knowledge and attitudes regarding pain (COBS). Accessed 18 March 2015. Available from: http://prc.coh.org/html/rehab_professionals.htm.