Clinical reasoning

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


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

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

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

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

Greenhalgh (2018), quoting Sir John Grimley Evans

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

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

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

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

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

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

Different narratives for different purposes

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

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

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

Guidelines and algorithms

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

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

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

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

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

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

 

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

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

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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 (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!

Click to the next post

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.

Assessing problems with sleep & persistent pain


Problems with sleep affect most of us from time to time. We know we might find it difficult to get off to sleep because of a busy mind, a different bedroom, changes to our schedule – but for most of us, sleep returns to our normal fairly quickly. For some of us, though, sleep problems continue for weeks, months or even years. And for people living with persistent pain, sleep can be one of the most difficult things to deal with, yet it’s also one of the most common (McCracken & Iverson, 2002). Studies of sleep problems in people with fibromyalgia show abnormal sleep continuity as well as changes in sleep architecture – this looks like increased number of times waking, a reduced amount of slow wave sleep and an abnormal alpha wave intrusion in non rapid eye movement, termed alpha-delta sleep (Dauvilliers & Touchon, 2001). People with fibromyalgia may also experience primary sleep disorder such as sleep apnoea or periodic leg movements during sleep.

The effect of rotten sleep is quite clear: pain increases the day following a disrupted night’s sleep, while high levels of pain on one day has less of an impact on subsequent sleep – but if you’ve been sleeping poorly for a while, all of this becomes something of a blur (Johnson, Weber, McCrae & Craggs, 2017; Slavish, Graham-Engeland, Martire & Smyth, 2017)! When we add in the effects of poor sleep on daily activity, and begin to unpack the relationships between sleep, pain and mood (Goerlitz, Sturgeron, Mackey & Darnell, 2017) well it’s a bit of a complicated matter, and one that I think we need to address when someone comes in for help with their pain.

Assessing unrefreshing sleep or poor sleep can be a reasonably straightforward process, but it needs to be carried out systematically. The event/s that initiate poor sleep may be very different from the events that maintain poor sleep, and while it’s interesting to know what started the sleep difficulties – in the end it’s possibly more important to work out what’s maintaining it.

The following is my attempt to outline what I look for when I’m discussing sleep with someone.

1. Is sleep really a problem? Sounds a bit odd, but some people have a strong belief that they need a certain number of hours of sleep a night, and when they’re not getting that magical number, it can be quite worrying – and actually kick off a sleep problem!

  • My key question here is do you wake feeling like you’ve had a good sleep? The number of hours of sleep is irrelevant, to a large extent, if you wake up feeling refreshed. If the person I’m talking to wakes up feeling OK I quickly swing into trying to understand why they’re worried about their sleep – and reassuring them that having a certain sleep duration is not fixed. In fact, sleep length changes over time – remember when you were a kid and slept for hours and hours? And when you were a teen and sleep in until midday if you could, but stayed up most of the night? These are pretty normal changes in pattern and nothing to worry about.

If you don’t feel refreshed, then I dig a little deeper…

2. What’s your sleep routine? This is about finding out the time someone goes to bed, how long it takes to fall asleep, what time a person wakes up, and gets up. I’ll also ask about the pre-bedtime routine: what’s the evening routine like? when do the screens go off? what’s the last drink of the evening? what’s the bedroom environment like?

  • I’m looking for a consistent bedtime at around the same time each night, a “wind down” ritual where the same things happen each night to prime the mind for sleep. I’m also looking for factors that might make it more difficult to fall asleep once in bed – screen time (devices, laptops, TV), dealing with worries, solving problems, having arguments, difficulty getting comfortable.
  • I’m also looking for a consistent wake up time, and whether the person gets out of bed then – or lies in bed and maybe falls asleep again…
  • A comfortable room temperature, a dark room, relatively little noise: all of these very basic things help keep bed for sleep (and sex) but not for much else.

The reason these basic “sleep hygiene” factors help is that our sleep pattern is malleable. It changes depending on environmental factors like light, noise and temperature. This is why we end up having jetlag – it takes a little while to adjust to the new daily light patterns (especially when you travel from Christchurch, NZ to somewhere like Norway!). Our body temperature drops during the night, our digestive processes slow down (that’s why we tend not to do “number twos” at night) and why we pee a lot less at night than during the day. Setting up a consistent routine helps us retain these habits and “teach” the mind/body to sleep at the correct time.

3. What substances do you use? I’m interested in the usual suspects: caffeine (not only coffee, but tea, energy drinks, dark chocolate), but also alcohol, the timing of medications, and that late night snack.

  • When sleep onset is a bit fragile it’s probably best not to have coffee and allied substances after mid-afternoon, and for some people (like me!) it’s best not to have them after lunch.
  • Medications for persistent pain are often sedating, so people need to know how to use this side effect for the best – and that often means taking medications earlier than first thought.
  • It also means for us, recognising that some medications alter sleep architecture (particularly meds given for, paradoxically, insomnia!). Alcohol might help people get to sleep but it changes the sleep architecture, preventing you from falling into that deepest sleep phase – and waking you up to pee halfway through the night, if you don’t do that already!
  • I also check whether people are smokers, and if they are, whether they wake in the morning absolutely gasping for a smoke, or whether they smoke during the night. Nicotine withdrawal can keep someone awake during those brief periods before and after dreaming sleep, so may need to be managed with patches.
  • Food is also something I check – snacks at midnight are the stuff of school stories, but can become a learned behaviour that we associate with being awake at that time, and maintain disrupted sleep. Maybe a mid-evening protein-based snack is a better option.

4. What’s going through your mind (or what’s your mind telling you) about your sleep? Having hopefully dealt with the basics of sleep hygiene (though I haven’t included exercise yet – that’s coming!), I’m keen to understand the person’s mind chatter about their sleep.

  • Worries, rumination and attempts at problem-solving (yes I’ve solved the problem of world peace!) can all keep us from falling asleep. What we do about those thoughts depends on the sleep management approach we’re using.
  • Often, the worries are actually worries about not sleeping – that paradoxically keep us from falling asleep! Feeling bothered about “how am I going to cope tomorrow if I don’t sleep”, or “I’m going to be so tired tomorrow, I know I won’t manage” are really common.
  • Along with worries about not sleeping, every other unsolved problem seems to pop up courtesy of your mind – this can happen because the person is too busy during the day to stop and ponder (and it’s quiet at night… fewer distractions!) so it’s worth finding out what is going through the person’s mind and dealing with those issues.

5. What’s your pattern of sleeping through the night? This is about the pattern of arousals – when, how long for, what the person does during these times.

  • Some understanding of normal sleep architecture is useful here so you can help the person understand why waking just before/just after dreams occurs.
  • Reviewing the habits at these times helps to understand the factors that maintains being awake at the wrong times! Waking briefly but without being aware of it is normal, but when internal or external factors intrude during lighter periods of sleep, we become more aware of being awake and can begin to do things that keep us awake, like watching TV, turning the radio on, having a snack, worrying.

To be continued…

These are some of the very fundamentals of assessing sleep problems. Next week I’ll review some more – and the week after look at strategies that can help!

 

Dauvilliers, Y., & Touchon, J. (2001). Le sommeil du fibromyalgique : Revue des données cliniques et polygraphiques (sleep in fibromyalgia patients: Clinical and polysomnography pattern.). Neurophysiologie Clinique/Clinical Neurophysiology, 31(1), 18-33. doi:https://doi.org/10.1016/S0987-7053(00)00240-9

Goerlitz, D., Sturgeron, J., Mackey, S., & Darnall, B. (2017). (395) sleep quality and positive affect as mediators of daily relationship between pain intensity and physical activity. The Journal of Pain, 18(4), S73.

Johnson, M., Weber, J., McCrae, C., & Craggs, J. (2017). (397) the catch 22 of insomnia and chronic pain: Exploring how insomnia and sleep impact the neural correlates of chronic pain. The Journal of Pain, 18(4), S73-S74.

McCracken, L. M., & Iverson, G. L. (2002). Disrupted sleep patterns and daily functioning in patients with chronic pain. Pain Research & Management, 7(2), 75-79.

Slavish, D., Graham-Engeland, J., Martire, L., & Smyth, J. (2017). (394) bidirectional associations between daily pain, affect, and sleep quality in young adults with and without chronic back pain. The Journal of Pain, 18(4), S73.

Pain – or disability?


One of the fundamental distinctions we need to make when working with people who experience pain is to understand the difference between experiencing pain – and the behaviour or actions or responses we make to this experience. This is crucial because we can never know “what it is like” to experience pain – and all we have to rely on as external observers is what we see the person doing. Differentiating between the various dimensions associated with our experience of pain makes it far easier to address each part in the distinct ways needed.

Let me explain. We know the current definition of pain – an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in such terms (IASP, 1979). One of the key points of this definition was to remove the need for nociception as a requirement for pain to be present. So when we unpack what we understand about pain, the first step is to recognise that it’s an experience. Something we can never share with another person – just like we can’t share joy, the taste of a great craft beer, or what a lover’s touch is like.

We therefore have an inexact relationship between two concepts: nociception, or the biological mechanisms at play until the point at which we are conscious of pain; and pain, or the experience of what it is like to have an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in such terms.

But wait, there’s more. Given that this experience is a subjective, internal and personal experience – how do we know when someone is experiencing pain?

When I ask students, their answer is “oh you can see grimacing, wincing, or they tell you” – and it’s true! But let’s notice something: they’re all behaviours. Things people do, either involuntarily or voluntarily, to signal that they’re sore. Behaviours or actions are not a direct indication of “what it is like” to experience pain. Like nociception and pain, there is an inexact relationship between what someone does when they’re experiencing pain – and their resultant behaviour. So we now have three somewhat overlapping concepts: nociception (biology), pain (experience), and behaviours (actions). They overlap because there is no direct 1:1 relationship between these concepts – although in some cases it may seem like there is.

What else influences our pain experience? If you’ve been paying attention to my blog these last few weeks, you’ll know that thoughts or beliefs and emotions also influence both our experience of pain and our behaviour. For example, if we know that the pain we’re experiencing is for good (such as post-surgical pain after hip replacement), we tend to be more forgiving, or at least more willing to experience it than if someone attacked us with a scalpel down some back alley! We have plenty of evidence that simply knowing the supposed cause, and something about the biology of pain, can help people to feel a little differently about it (emotions), and to move differently (behaviour) (Moseley & Butler, 2015; Tegner, Frederiksen, Esbensen & Juhl, in press), while emotions in both experimental and clinical studies have been shown to strongly affect pain intensity – and subsequent behavioural responses (Orenius, Raij, Nuortimo, Naatanen, Lipsanen, & Karlsson, 2017). Once again, the relationships are not exact – which is almost always the case when we’re studying complex systems!

Because thoughts, beliefs and emotions have both impacts on nociceptive processes and on pain experience and behaviours, I’ve depicted them as overlapping (if there was a way to show this in 3-D believe me, I would!).

But wait, there’s more!

We know context makes an enormous difference to a person’s experience of pain AND the behaviours they take in response to their pain. While contextual factors don’t directly influence nociception, these factors do influence thoughts and beliefs, emotions, and behaviour. For example, we know that in adolescents with pain, parental responses influence the amount of treatment seeking (Stone, Bruehl, Smith, Garber & Walker, 2018); and that spouses or partners of people living with pain can affect both pain intensity and behaviour because of the way they interact (Burns, Post, Smith, Porter, Buvanendran, Fras & Keefe, 2018). We also know that in different communities, responses to pain can differ: people who pursue body suspension (being pierced and suspended by hooks) are supported by those around them to “hang in there” (no pun intended!). Factors such as legislation make a difference to pursuing treatment, while treatment itself can perpetuate disability and may even increase attention to pain.

Why bother explaining all this?

The implications of understanding these associations are quite profound. Firstly, nociception is a small but important contributor to our pain experience. Most pain starts with a nociceptive stimulus, even if it ultimately ends up less influential than cortical ‘interpretive’ processes. Secondly, the experience we have of pain is something we can’t share – and thirdly the only way we can begin to infer that another person has pain is via their behaviours, or what they do. This means pain measures like the visual analogue scale, FACES scale, numeric rating scale are not direct measures but are used by people to give a message about their pain. All behaviour is influenced by both our thoughts/beliefs and emotions and contextual factors including who is nearby, past responses they’ve made to our messages, what’s normal or expected in various contexts, and the purpose we believe our behaviour will serve. And of course, many of the influences and behaviours we do are not things we’re consciously aware of because we’ve been doing them since we were born.

So when I think about what we might do to help someone with their pain, I firstly acknowledge that I can’t directly influence someone’s own experience. I’m working to influence what they do about their pain, their relationship to their pain, their beliefs and understanding, their emotions and how they communicate this to other people around them. And to me, the first step is being ready to hear what people believe about their pain. Only after I’ve successfully conveyed this to the person can I ever begin to come alongside them to help them change what they do.

 

Burns, J. W., Post, K. M., Smith, D. A., Porter, L. S., Buvanendran, A., Fras, A. M., & Keefe, F. J. (2018). Spouse criticism and hostility during marital interaction: effects on pain intensity and behaviors among individuals with chronic low back pain. Pain, 159(1), 25-32.

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

Orenius, T. I., Raij, T. T., Nuortimo, A., Näätänen, P., Lipsanen, J., & Karlsson, H. (2017). The interaction of emotion and pain in the insula and secondary somatosensory cortex. Neuroscience, 349, 185-194.

Porreca, F., & Navratilova, E. (2017). Reward, motivation, and emotion of pain and its relief. Pain, 158, S43-S49.

Stone, A. L., Bruehl, S., Smith, C. A., Garber, J., & Walker, L. S. (2018). Social learning pathways in the relation between parental chronic pain and daily pain severity and functional impairment in adolescents with functional abdominal pain. Pain, 159(2), 298-305.

Tegner, H., Frederiksen, P., Esbensen, B. A., & Juhl, C. (2018). Neurophysiological pain-education for patients with chronic low back pain-a systematic review and meta-analysis. The Clinical Journal of Pain.