treatment

Wait and see…when do we “escalate” care for low back pain?


Prompted by reading a paper by Linton, Nicholas and Shaw (in press), today’s post is about various service delivery models for low back pain and not the content of back pain treatment.

Service delivery in New Zealand is assumed to be based on getting most bang for the buck: we have a mainly socialised healthcare system, along with a unique “no fault, 24 hour” insurance model for accidents whether at work or elsewhere, which means market forces existing in other countries are less dominant. There are, however, many other influences on what gets delivered and to whom.

Back to most bang for buck. With a limited healthcare budget, and seriously when is there ever NOT a limited budget in health, it would make sense to a thinking woman for healthcare to focus on high value treatments. Treatments that have large impact and are low cost. In low back pain, the techno-fix has limited application. Things like costly surgical approaches (synthetic disc replacements, fusions to stop vertebral movement) should be reserved for only those with clear indications for the procedure, and given on the basis of clinical need rather than in response to a distressed person. The outcomes just are not all that great (see Maher, Underwood & Buchbinder (2017) for a good review of nonspecific low back pain).

High value and low cost treatments are typically delivered by low status clinicians. Those “nonmedical” people like occupational therapists, physiotherapists, osteopaths, chiropractors and the like. Maybe it’s for this reason that these treatments are relatively poorly funded. We lack lobby power.

Back to service delivery models. Currently in Christchurch, where I live, there is a health pathway (in other words, a service delivery model) developed in collaboration with GP’s, physiotherapists, osteopaths and secondary care. The model adopted applies to ALL episodes of low back pain, and uses the STarTBack tool to triage those who may need more intensive treatment under a biopsychosocial model (mainly because of the additional risk psychosocial factors pose for these people), and to continue with treatment as usual for those with lower risk as measured by this tool.

After about six weeks, if the person hasn’t responded to treatment, clinicians are meant to refer the person to a team for review and to see whether additional treatments or another pathway might be appropriate. Unfortunately, there is no indication of the makeup of that team, and no obligation for the clinician to send the person to it. I’m not sure about clinical audit of this pathway, and again this isn’t clear.

One of the problems (amongst many) with this approach is that six weeks without responding to treatment and the time needed after this to review the file, then be referred elsewhere is a very long time to someone experiencing back pain. A very long time. By six weeks it wouldn’t be surprising if the person’s sick leave is gone. If they’re receiving ACC the processes will have kicked in, but for the person who has typical grumpy back symptoms without an “accident” initiating it, there may be nothing.

Linton, Nicholas and Shaw point out that all of the triaging approaches for low back pain hold assumptions. The three are stepped care (begin with low intensity, once that hasn’t helped progress to more intensive and so on); stratified (triage those with high risk, and treat them accordingly, while low risk get lower intensity treatment); and matched care (treatments are administered according to an algorithm based on grouping people with similar characteristics).

Stepped care

The assumptions of stepped care include that people with basic acute low back pain will recover relatively easily, while those who need more help will be fine waiting for that additional level of care. There’s an assumption that factors leading to chronic disability occur in stages – the longer a person waits the more risk factors will appear – but this isn’t actually the case. Many people present with risk factors from the very beginning (and they can be identified), while waiting only allows those problems to be cemented in place. At the same time, we know acute low back pain is quite a rare thing: most people will have their first bout of back pain in adolescence, and will have learned good and not so good habits and attitudes from that experience. Another assumption is that duration of back pain doesn’t harm, but we know delayed attention to risk factors for chronicity is harmful. Stepped care can be useful because it’s efficient, easy to implement and overtreatment is less likely – but what about the person who appears with all the risk factors evident from the beginning? These people may not get adequate or appropriate treatment from the outset.

Stratified care

In stratified care, treatment is provided according to the category of risk the person presents with, maybe circumventing some of the problems from stepped care. Stratified care assumes we’re able to identify risk factors, and that they are stable from the outset rather than changing over time. It also assumes that risk factors exert a cumulative effect with more risk factors meaning greater risk. BUT while screening can identify some risks, and those at low risk get more adequate treatment while higher intensity treatment is given to those with more risk, this approach doesn’t identify underlying mechanisms, and more comprehensive treatments addressing specific issues may not be provided. This approach may not even consider the impact of workplace factors, family dynamics, social and recreational issues. It’s also pretty challenging to implement as I think the Christchurch example demonstrates.

Matched care

In matched care risk factors are identified and treatments are matched to the person’s needs, and like stratified care it assumes that risk factors can be identified, are stable, and that they can form a “profile” or subtype. This approach also assumes that tailoring interventions to individual risk will be more efficient than alternatives. There’s some support that screening can identify some risks, and that profiles can be constructed – but this continues to be a work under progress. Some of the limitations are the emerging nature of research into grouping people according to multiple indicators is complex, particularly at the beginning of treatment, and treatments matching profiles are therefore also under development. It’s a very complex approach to implement so I can understand why local health authorities may be reluctant to embark on this strategy. It’s also back to the problem of assuming that people’s risk profiles are stable over time.

What do we do?

One part of me thinks, well it doesn’t matter really because as a lowly nonmedical person I have very little influence over health systems, the perverse incentives that drive them, and absolutely no political clout whatsoever. BUT I know that the “wait and see” six weeks before reviewing progress is not helping. And the current considerations fail to integrate those important workplace, family, socio-economic and contextual factors that are hard to quantify.

We already know that low back pain guidelines are routinely ignored by most clinicians in favour of “what I do” and “it’s worked before” and “the guidelines are biased so I won’t follow them”. There’s also the fear that by identifying psychosocial risk factors we’re condemning people to the “back pain is really in your head” meme (it’s even something I’ve been accused of. FWIW I think low back pain is far more complex and is multifactorial. Psychosocial factors are certainly more useful at predicting disability than biomechanical or diagnostic ones, but this doesn’t mean the problem is purely psychological. <steps off soapbox>). Furthermore, it’s clear that not only do physiotherapists feel poorly-prepared to identify and work with psychosocial factors (Singla, Jones, Edwards & Kumar, 2015; Zangoni & Thomson, 2017), so also do medical practitioners although for different reasons (Coudeyre, Rannou, Tubach, Baron, Coriat, Brin et al, 2006). It’s difficult to open Pandora’s box when you only have 10 minutes with a patient.

As Linton, Nicholas and Shaw (in press) point out, training is needed before clinicians can feel both confident and efficient at screening and then managing low back pain via an integrated multidimensional model. “Role” delineation (who can contribute to the various aspects of treatment?) and the paucity of funding for allied health within primary care, especially in New Zealand makes this approach an aspiration. 

Naturally I’d like to see a range of different health professionals involved in developing health pathways. Not just professionals, but people well-versed in understanding the research literature and those with effective knowledge translation skills. I’d love to see high value and low cost treatments provided rather than techno-fix approaches, especially when the high value treatments are significantly safer and develop personal self efficacy and locus of control. Wouldn’t that be a thing to see?

  • Coudeyre, E., Rannou, F., Tubach, F., Baron, G., Coriat, F., Brin, S., … & Poiraudeau, S. (2006). General practitioners’ fear-avoidance beliefs influence their management of patients with low back pain. Pain, 124(3), 330-337.
  • Linton, S. J., Nicholas, M., & Shaw, W. Why wait to address high-risk cases of acute low back pain? A comparison of stepped, stratified, and matched care. Pain. in press
  • Maher, C., Underwood, M., & Buchbinder, R. (2017). Non-specific low back pain. The Lancet, 389(10070), 736-747.
  • Singla, M., Jones, M., Edwards, I., & Kumar, S. (2015). Physiotherapists’ assessment of patients’ psychosocial status: are we standing on thin ice? A qualitative descriptive study. Manual Therapy, 20(2), 328-334.
  • Zangoni, G., & Thomson, O. P. (2017). ‘I need to do another course’-Italian physiotherapists’ knowledge and beliefs when assessing psychosocial factors in patients presenting with chronic low back pain. Musculoskeletal Science and Practice, 27, 71-77.
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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

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.

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

Teamwork: Gaps or overlaps?


For many years now, interprofessional/multidisciplinary teams have been considered the best model for delivering pain management. This stems from studies conducted right back as far as J J Bonica in 1944 (Bonica, 1993), and originally referred to teams consisting of several medical specialties. Bonica later initiated a multidisciplinary/interdisciplinary pain programme in 1960, including 20 people from 14 medical specialties “and other health professions”. In 1977, Bonica and Butler classified pain programmes into five groups – major comprehensive multidisciplinary programmes – more than six disciplines and involved in education and research; comprehensive multidisciplinary – four to six disciplines and involved in education and research; small multidisciplinary – 2 or 3 disciplines; syndrome-oriented specialising in single diagnoses; and modality-oriented using a single treatment. There were, at the time, 327 facilities around the world – including New Zealand (The Auckland Regional Pain Service).

Bonica didn’t comment on the team structure of these facilities, nor on the mix of “other health professions” involved. There has been a significant reduction in the numbers of comprehensive pain management centres, particularly in North America since the 1990’s. Fragmented, unidimensional treatment seems to be far more common than integrated multidimensional approaches.

Why might teamwork and structure of teams be important in pain management?

I like this discussion of why interprofessional/interdisciplinary teams might be more effective in pain management than multidisciplinary: “Multidisciplinary teams are unable to develop a cohesive care plan as each team member uses his or her own expertise to develop individual care goals. In contrast, each team member in an interdisciplinary team build on each other’s expertise to achieve common, shared goals. Therefore, it is crucial to indicate that multidisciplinary teams work in a team; whereas, interdisciplinary teams engage in teamwork.”

The argument for interprofessional teams in pain management is that by drawing on a common model of pain, each profession can align their treatments to meet the person’s goals, using a common framework, language and broad principles. But, and it’s a big but, this model depends on mutual trust, respect and time spent together developing a common understanding of each team member’s contributions. This is not something in which many health professionals have much training. For a good discussion of ways to foster good dynamics, Youngwerth and Twaddle’s 2011 paper is a nice place to start.

Why write about this now?

I was prompted to write about this because of a set of questions I was posed by a group of clinicians from another profession. We ostensibly work in a team, under the ACC Pain Contracts which specify a “multidisciplinary” approach. The questions, however, reflected both a lack of knowledge about pain management group programmes, and a lack of respect for the clinical skills provided by the people who deliver the programme I’ve developed. And it’s not the first instance of such behaviour.

I rarely criticise New Zealand healthcare policy, at least not on the pages of this blog. In this instance, though, I think it’s time to point out some of the issues that are present in the way pain contracts are being delivered since late 2016.

For those who’re not aware, ACC is NZ’s only personal injury insurer, owned by the country, with no-fault, 24 hour cover. That means anyone who has an accidental injury in NZ firstly can’t sue, and secondly has their treatment and rehabilitation paid for. Like most personal injury insurance companies, ACC’s main problem is the burden of long-term claims where often the main issue preventing return to work and case closure is persistent pain. As a result, pain services have been provided under ACC rehabilitation policy under a “provider-funder split” model since 2000.

ACC contracts providers to deliver pain management services. These services were to involve a number of designated professions, and these professionals were to be at least two years post-graduation, and to have completed postgraduate education in pain and pain management. And no, I don’t think a weekend course counts as “postgraduate education”. Unfortunately, the remuneration under these contracts is incredibly low. Remuneration rates are pre-determined by ACC, so that occupational therapy and physiotherapy are given one hourly rate, psychologists have a higher rate, and medical practitioners have the highest rate of all. There’s no variation in rates to fund experienced clinicians, so everyone gets the same amount irrespective of skill level. There is little to no allowance for team meetings, and there’s no allowance for screening or reporting included in the funding for the group programme I’ve developed.

Aside from the low funding, there are other concerns for me. There has been no auditing of the providers delivering these services. As a result, large businesses naturally try to maximise profit, employing entry-level clinicians for the contracts. Incredibly challenging for new graduates who have had limited exposure to persistent pain and pain management, and often apply acute pain management principles to chronic conditions. And that risks prolonging disability and exacerbating distress of people needing help.

Secondly, because these are new contracts, with quite different requirements from earlier iterations, groups have had to recruit a great many clinicians. Some of those clinicians presumed, I think, that their professional qualification is sufficient to work with people who have persistent pain. Even if their training had no pain content. ACC considers professional registration to be quite sufficient to practice in this area. While some of these clinicians are very experienced – pain management is not simple, and it is specialised. I have heard of practitioners continuing to use gate control theory as their primary “pain education”. While it’s an advance on being told you have “somatic disorder”, it doesn’t exactly reflect modern pain concepts. Again, using outdated information risks prolonging disability and exacerbating distress in a group of vulnerable people.

Teams to deliver pain contracts were often assembled in haste. Processes of induction, continuing education, developing a common clinical model, knowledge of other professionals’ contributions have all suffered as a result. Multidisciplinary practice is the norm – as one person I know used to put it, it’s “serial monotherapy”. Decision-making processes haven’t been developed, and integrating a clinical model common to all – and therefore abolishing a hierarchical structure – has just not happened. Instead a hierarchical, patch-protecting, and disjointed model where professionals are pitted against one another to gain some kind of dominance is emerging. A far cry from a mutually-respectful, integrated, non-hierarchical interprofessional team environment that research suggests is best for delivering pain management (Gatchel, McGeary, McGeary & Lippe, 2014).

When high value, low cost treatments for persistent pain are under-funded, and when costly yet ineffective treatments such as surgery continue being delivered, it’s the people who most need help who are harmed. I suppose what’s even more concerning is that despite 1 in 5 NZers living with pain lasting more than three months, and ACC claimants representing a small proportion of those living with pain, there is no New Zealand strategy for chronic pain management. People on ACC are, in most ways, rather lucky despite the failings of this contracting system.

The pain contracts could have represented an opportunity for innovation and an expansion of understanding between professions, what has happened instead is a tendency to deliver formulaic, ritualised programmes with gaps and overlaps, as a result of underfunding, poor quality control and both ignorance and power play in some instances.

We used to be world leaders in pain management. We have failed to capitalise on our headstart.  We should do better. We must do better for people living with pain.

 

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

Gatchel, R. J., McGeary, D. D., McGeary, C. A., & Lippe, B. (2014). Interdisciplinary chronic pain management: past, present, and future. American Psychologist, 69(2), 119.

Youngwerth, J., & Twaddle, M. (2011). Cultures of interdisciplinary teams: How to foster good dynamics. Journal of Palliative Medicine, 14(5), 650-654.

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

 

 

 

One way of using a biopsychosocial framework in pain management – i


While a biopsychosocial ‘model’ (or sociopsychobiological framework) has been widely adopted when attempting to understand pain, many critics argue that it just doesn’t give clinicians a clear way to integrate or prioritise clinical information and generate treatments. The ‘model’ itself has been challenged from many angles – it’s too complex, too simplistic, relies on Bertalanffy’s “general systems theory” which has itself been challenged, it’s too “fuzzy”, and of course there are many who think that psychological and sociocultural aspects of human experience are epiphenomena while will ultimately be boiled down to cellular or biological processes. Nevertheless, this framework also has considerable appeal, is widely adopted and I think can provide us with some useful heuristics for thinking about how and why a person presents in the way they do at the time they do – and helps us consider what can be done to reduce distress and disability.

Disclaimer: I work with the “fuzzy” sociopsychological aspects of pain management, and leave a great deal of the biological to those who focus on that – and believe me, the biological is usually done and done to the nth degree in most cases of persistent pain. I rarely see someone who hasn’t had their scans, Xrays, physical examinations, bloods, urine, nerve conduction, surgery, exercise or whatever looked at – but plenty of people who have never once been asked what they think is going on and what their main concern is. Oh and not had their sleep, mood, alcohol and other substance use, daily routines, relationships, work situation, community and spiritual aspects of life ever discussed. So, despite the constant banging on about “don’t forget the bio” – I really do not think this is a thing.

Where do we start with this approach?

The first place I start with my discussions is to ask “Tell me about your problems with pain.” What I’m focusing on in this discussion is when did the person first recognise that there was “something wrong” – and then what did they do about it.

Fabricio Benedetti talks about the neurobiological processes involved in a person detecting that he or she is “unwell”. He writes: “Physiology and neuroscience have a lot to say about feeling sick, for it involves sensory systems that convey different pieces of information related to peripheral organs and apparatuses, as well as brain regions that lead to conscious awareness.” (Benedetti, 2013). To me, this involves biological, psychological and social factors for when does a person recognise that “conscious awareness” means something? Benedetti goes on to say “The second step is what makes a patient “seek relief,” a kind of motivated behavior that is aimed at suppressing discomfort. This behavioral repertoire is not different from that aimed at suppressing hunger or thirst, and the brain reward mechanisms are crucial in this regard” (Benedetti, 2013). Judgements about what internal experiences mean may begin with a reflex response (automatic and based on evolutionary demands to keep safe) but what we DO about those experiences depends a great deal on what we learn from others. The people we most draw from are those around us – mother, father, siblings, people in our immediate family and extended family. And over time, the social nature of humans means we also consider the community in which we live – and wider with social media! Judgements, or appraisals (thoughts and beliefs about the meaning of these internal experiences) are, ‘fraid to say, psychological in nature. While the influences on thoughts and beliefs are – you guessed it – social.

So, how can a clinician use this information? Where’s the research? Come on – science it up woman!!

If it’s not enough to know that there are neurobiological factors underpinning our internal experience, and motivated behaviour is tied up with reward systems, then what else can we use to understand the processes of feeling ill and seeking treatment? To me, the natural first step is to look at learning mechanisms. Yep, very basic Psych 101 classical and operant conditioning mechanisms. Add in a dash of social learning theory (how we learn from watching and talking with others) and we have some rather useful experimentally-validated hypotheses to work with.

What do I mean by this?

Well, at least part of clinical reasoning is a process of recognising potential explanations for the phenomena we see. My take on clinical reasoning is that we can use case formulation to help generate a series of hypotheses to explain why a person is coming to see us in this way at this time – and what might be maintaining their current situation. In case formulation we can use “abductive reasoning” (recognising a potential “rule” or class of behaviour from a specific observation – eg we can postulate that a person’s sleep disturbance might be due to low mood, sleep apnoea, habit, operant conditioning, or a new baby, and we’ll probably collect some more information to test each of these possible explanations before deciding on the most probable reason). If we know a whole bunch of research around what humans do when they’re feeling sore and vulnerable, we are able to come up with a bunch of possible reasons for someone noticing they feel unwell, judging it in a certain way, and then deciding to do something about it.

For example, we know from research studies that people who have had adverse experiences in early childhood have a greater risk of developing post-traumatic stress disorder and chronic pain (eg Afari, Ahumada, Wright, Lostoufi, Golnari, Reis & Cuneo, 2014; Jones, Power & Macfarlane, 2009). We also know that those people may develop weaker attachments to others and so feel vulnerable in relationships where high levels of trust are needed – also linked to the presence of persistent pain – and adversely affecting outcomes from multidisciplinary pain management programmes (Anno, Shibata, Ninomiya, Iwaki, Kawata, Sawamoto et al., 2015; Kowal, McWilliams, Peloquin, Wilson, Henderson & Fergusson, 2015).

These factors might mean that when we ask someone about their theory for why they have persistent pain, or what they think is going on, we might keep an ear open to listen for threats to relationships around the time of the onset of the problem dealing with pain (especially if the pain has been present for a while but the person hasn’t been looking for treatment until just now). We might also be thinking hard about the neurobiological effects of relationship breakups and how this might impinge on either coping (eg accessing strategies to manage effectively during painful experiences) or on stress responses (eg heightened vigilance to threat).

Two things: (1) This doesn’t mean persistent pain is “psychological” – it’s not, but these experiences might set the scene for neurobiological changes, both in “set-point” for threat and in resilience for dealing with threat. (2) This also doesn’t mean that we need to deal with the response to relationship stress ourselves – it might mean we listen respectfully, and bear this vulnerability in mind during our interactions, being careful not to threaten trust, and work hard to retain a sense of warmth/empathy as well as competence for this person.

Next time: More on learning theory and how these might influence the way we look at why someone seeks treatment with us, and why at this time, and what may be maintaining the behaviours we see.

 

Afari N, Ahumada SM, Wright LJ, Mostoufi S, Golnari G, Reis V, Cuneo JG., (2014). Psychological trauma and functional somatic syndromes: A systematic review and meta-analysis. Psychosomatic Medicine, 76, 2-11.

Anno, K., Shibata, M., Ninomiya, T., Iwaki, R., Kawata, H., Sawamoto, R., . . . Hosoi, M. (2015). Paternal and maternal bonding styles in childhood are associated with the prevalence of chronic pain in a general adult population: The hisayama study. BMC Psychiatry, 15(1), 181. doi:10.1186/s12888-015-0574-y

Benedetti, F. (2013). Placebo and the new physiology of the doctor-patient relationship. Physiological Reviews, 93(3), 1207-1246. doi:10.1152/physrev.00043.2012

Jones GT, Power C, Macfarlane GJ, (2009). Adverse events in childhood and chronic widespread pain in adult life: Results from the 1958 British Birth Cohort Study. Pain 143:92-96.

Kowal, J., McWilliams, L. A., Péloquin, K., Wilson, K. G., Henderson, P. R., & Fergusson, D. A. (2015). Attachment insecurity predicts responses to an interdisciplinary chronic pain rehabilitation program. Journal of Behavioral Medicine, 38(3), 518-526. doi:10.1007/s10865-015-9623-8