Clinical reasoning

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


More on sleeping the ACT way. Step one was discover – all the things you’re doing to help yourself sleep, but in your attempts to control the uncontrollable (thoughts, feelings, memories, worries, sensations, the environment and so on). And hopefully you’ve seen that these things can be counter-productive. That flash new pillow and bed is pretty useless if you travel somewhere. The pills need to be stopped at some point – and then you have to withdraw from them. And the thoughts, and sensations (including pain) just carry right on there not matter what you do.

So step two is to accept: accept what you can control, and what you can’t. Radically, this means changing some of the things you do to get to sleep – like pills (but get medical help for this process), doing relaxation, wearing your eyeshades and earplugs, getting up and doing things when you can’t sleep. It usually means a bit of mind chatter!

The common mind chatter is “I’ll fail”; “I know I won’t sleep and then I’ll be useless the next day”; “if I can’t sleep with my pills and earplugs, how will I sleep without them?”; “I’ll feel lousy the next day”; “I’ve slept this badly my entire life, it’s too late for me”; “why me? It’s a punishment”; “but I’ve got [a new job, a baby, a puppy, going on holiday]”; “I’m too tired”

It’s likely, as you begin doing this, you’ll be in bed wide awake – and it’s at this point you can choose. In that moment, you can decide to listen to your mind – or think of your mind as holding an opinion, but one you do not have to follow. In ACT language, what you’re doing here is learning to accept, or be willing to sit with (lie with), to make room for not sleeping rather than struggling to control it. You can’t control your risk factors, you can’t control that you’ve learned to be awake at this time. You can’t control your thoughts about this – but you can lie there and just notice the things your mind is dumping on your doorstep. This isn’t “giving up” – this is radical willingness to come alongside and be with your own sleeplessness.

The best way to learn to do this is – you guessed it, mindfulness.

Now mindfulness is NOT about getting you to fall asleep. You may fall asleep or feel drowsy which is cool, but if you try to use mindfulness “to fall asleep” you’re again trying to control the problem and mindfulness can then become an empty process. You ARE allowed to let your mind wander… just gently bring it back to where you want it to be. Practicing mindfulness can be done anywhere and everywhere – for a few short seconds while cleaning your teeth, sitting in the car, walking through a door – or longer, like at the end of the day, or in the morning.

Some ways to be mindful: notice your senses by bringing your mind to sounds, sights, smells, tastes, touch. Just list all the things you experience – like “a bird chirp”, “the weight of my legs on the seat”, “the smell of coffee”…and as your mind wanders off, as it will, bring it back gently to what you want to focus on.

Another one to try: close your eyes for a few seconds and notice any thoughts or images that pop into your mind. List it – thought, image, work worry, dinner planning.

This skill is one of the most important and useful skills when you’re learning to sleep again. When you lie in bed wide awake, it’s easy to get caught up in the content of what your mind is bringing to  you, rather than just noticing that you are thinking. The problem is, thoughts your mind brings often lead to that heart thump and dry mouth that keeps you wide awake! Instead, directing your focus on to your breathing, or your body contact on the bed, are simple things that help you just notice and be in the present.

If you have pain, mindfulness is one way of letting you experience the ache without that “Oh no, it’s really bad tonight” judgements of that ache. Gently letting yourself notice where you’re sore – and equally, where you’re not sore – and guiding your mind around your body, noticing every part, the painful and the non-painful – allows you to be present with your pain, without fighting against it. Practicing this skill many times during the day really helps you develop this skill. And don’t be surprised if your mind starts trying to either judge or solve the problem of pain, because that is simply the mind doing what it’s done since forever. Be kind to your mind, and bring your attention back to your breath, or your left earlobe, or your belly button, or your little toe…

At night, in bed, mindfulness is not about helping you relax and fall asleep. What it’s there for is to help you guide your mind away from being caught up in the content of your thoughts or feelings or sensations, and back onto just noticing that you are thinking, and bringing your attention onto something like your breath. It can be scary doing this at night because we often want to get out of bed or control what we’re thinking and force ourselves into sleep. And you know it doesn’t work! What mindfulness does is let your brain and mind know that being awake isn’t a threat – remember the flight, fright, freeze response? By letting your mind know you’re not buying into the horror stories, and instead you’re being OK with simply lying there noticing, you’re teaching your mind to let go of the struggle.

  • Start with feeling the sensation of the bed against your body, from the toes to the head. When your mind begins “minding”, bring your attention to your breath. If you get the urge to move or get up (actually, your mind brings the urge), notice it and choose to stay in bed, and bring your attention back to your breath or touch.

Welcome: You’ll find your mind will have a good go at dumping scary thoughts on you when you decide to be present and stay. Remember it’s your mind’s opinions – and be gentle with your thoughts, feelings and yourself. Stay with it, notice your breathing, make room to feel a bit tired (because you were going to be tired anyway, right?!), and be kind, but firm, with your mind, and bring your attention to your breath yet again. You’re resting your body while you’re lying down, and that’s a good thing.

If you find you have a frequent flyer – a thought or worry or sensation that comes visiting when you’re trying to sleep  – you can simply name it “Hi worry”, or “thinking”, or “here you are scared”, or “back again, pain”. Welcoming the thoughts or feelings may feel odd –  but once you’ve noticed it, labelled it, and then welcomed it, go back to your breathing or noticing your body. You can become quite creative with this process – if you have a vivid imagination for visual images, try projecting your thoughts onto a movie screen, or turning them into cartoon letters, or characters from a movie (my pain is a grumpy witch!), or a ball of string all tangled up, or a scrunched towel.  Some people have taken to imagining their thoughts as different voices – squeaky “I’m scared” or deep “I’ll never sleep tonight” – these strategies are ways to help you step back from the content of what your mind is telling you, and see your thoughts as simply thoughts made by your mind.

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


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

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

Basic principles

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

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

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

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

Sleep hygiene (stimulus control)

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

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

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

Cognitive therapy

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

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

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

Sleep restriction

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

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

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

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

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

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

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

 

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

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

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

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

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.

Clinical reasoning – and cognitions


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

Cognition is defined by the APA Dictionary of Psychology as

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

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

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

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

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

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

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

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

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

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

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

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

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

 

 

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

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

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

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


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

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

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

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

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

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

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

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

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

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

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

 

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

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

Clinical reasoning in pain – emotions


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

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

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

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

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

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

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

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

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

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

 

 

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

 

 

 

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

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

 

 

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

 

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

 

 

 

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


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

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

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

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

But.

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

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

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

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

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

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

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

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

 

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

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

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


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

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

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

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

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

What did they find?

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

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

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

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

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

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

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

 

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

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

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

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

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