pain management

Knee pain – not just a simple case of osteoarthritis


Knee osteoarthritis is, like so many chronic pain problems, a bit of a weird one. While most of us learned that osteoarthritis is a fairly benign disease, one that we can’t do a whole lot about but one that plagues many of us, the disability associated with a painful knee is pretty high – and we still don’t have much of a clue about how the pain we experience is actually generated.  Cartilage doesn’t have nociceptive fibres, yet deterioration of cartilage is the hallmark of osteoarthritis, though there are other structures capable of producing nociceptive input around the knee joint. Perhaps, as some authors argue, knee osteoarthritis is a “whole organ disease with a complex and multifactorial pathophysiology involving structural, psychosocial and neurophysiological factors” (Arendt-Nielsen, Skou, Nielsen et al, 2015).

Central sensitisation, or the process in which spinal cord and the brain become “wound up” or more responsive to input than normal, and seems to be a factor in the pain some people experience when they have osteoarthritic knees (Fingleton, Smart, Moloney et al, 2015; Finan, Buenaver, Bounds, Hussain, Park, Haque et al, 2013), particularly in women (Bartley, King, Sibille, et al, 2016). The problem is, few people are routinely screened for central sensitisation before they receive surgical treatment (a good question is whether pain-related research is a factor in orthopaedic assessment). Why should we think about screening? Well, outcomes for joint replacements in knee OA are not as good as they are for hip OA, and a good proportion of people have more than one surgery to attempt to revise the joint but ultimately don’t obtain a satisfactory resolution of their pain.

The authors of this very useful clinically-relevant paper “Clinical descriptors for the recognition of central sensitization pain in patients with knee osteoarthritis” (Lluch, Nijs, Courtney, Rebbeck, Wylde, Baert, Wideman, Howells and Skou, 2017) openly acknowledge that although the idea of central sensitisation in humans is appealing, and seems to answer a number of important questions, the actual term “central sensitisation” can, at this time, only be measured in animal models. The use of the term in humans is not yet agreed upon, and a term I find appealing is “nociplastic”, or in other words, plasticity of the nervous system underpinning an increase in responsiveness to “actual or potential tissue damage” (to quote from the IASP definition of pain). They argue that central sensitisation may not exist in a dichotomous “yes you have it” or “no you don’t”, but instead may from a continuum from a lot to a little, and they note that pain sensitivity also exists on a continuum (a bell-shaped curve).

So what’s a good clinician to do? We can’t all go out and get involved in conditioned pain modulation or in using brain imaging, yet it seems important to establish who might respond well to joint replacement vs who might need additional input so they get a good outcome. And something that’s not going to add too much expense or complexity to an assessment process that, at least in New Zealand, is rationed because of cost. (oops, sorry not “rationed” just “waitlist management”).

The first step as described by Lluch and colleagues involves the “subjective” assessment – I loathe the word “subjective” because this is the person’s own experience, and doesn’t need to be tainted with any suggestion that it’s inaccurate or can’t be trusted. ‘Nuff said. During an interview portion of an assessment, the authors suggest using some simple measures: reports of pain above 5/10 on a numeric rating scale where 0 – no pain, 10 – extreme pain. They add increased weight to this report if there is little significant found on simple imaging of the knee, because central sensitisation is thought to be less relevant where there is severe structural changes in the knee joint.

A pain drawing can be helpful – radiating pain, pain on the contralateral leg, and pain in other body sites can be an indication of central sensitisation, while pain that is localised just to the joint itself may be an indication that a surgical approach will be more likely to help. Using the Widespread Pain Index score >7 and painDETECT score >19 (seeVisser, et al, 2016) may be a relatively simple process for clinicians to use to identify those with troublesome pain.

The behaviour of pain with/without movement may be a useful indicator: those that find movement painful, or who report increased pain after engaging in physical activity might be responding to central sensitisation, given that OA pain is usually associated with rest. Add to this a discussion about what relieves the pain and what doesn’t (where easing up on mechanical demands should reduce pain while with central sensitisation, this may not occur), and those with pain that continues after movement may need more help with central sensitisation than those who don’t.

The authors also suggest two questionnaires that may help to spot the person experiencing central sensitisation – the painDETECT or the Central Sensitisation Inventory. At this point I’m not entirely certain that the CSI measures only central sensitisation (it may simply measure somatic attention, or distress), so I’d interpret the findings carefully and make sure the clinical picture confirms or doesn’t… while the painDETECT has been used to identify those with neuropathic pain, and may be appropriate though it hasn’t been strongly confirmed for use with knee OA (it was developed for low back pain). While you’re at it, you should also assess for psychosocial factors such as the tendency to think the worse, low mood, feeling helpless, and perhaps factors such as not liking your job, having limited family support, and maybe self-medicating with alcohol and tobacco or other substances.

Finally, for today’s post (yes I’ll carry on to the clinical tests next week!), response to pharmacology may also be a useful approach to identifying those with central sensitisation. Poor response to NSAIDs (the mainstay for knee OA in NZ), weak opioids (like codeine), and perhaps not responding to things like heat or joint mobilisation, may also be useful predictors.

In summary, there are numerous indicators one can use to help establish who might not respond well to a peripheral-only treatment. While some of these measures are used routinely by enlightened clinicians, there are plenty of people who think of these responses as an indication of “poor coping” or someone who REALLY needs surgery. Unless surgeons and those who work with people with knee OA begin to examine the literature on pain in knee OA, I think we’ll continue to have patients who receive surgery when perhaps it’s not the best thing for them. More on this next week.

 

 

 

Arendt-Nielsen L, Skou ST, Nielsen TA, et al. (2015). Altered central sensitization and pain modulation in the CNS in chronic joint pain. Current Osteoporosis Reports, 13:225–234.

Bartley EJ, King CD, Sibille KT, et al. (2016) Enhanced pain sensitivity among individuals with symptomatic knee osteoarthritis: potential sex differences in central sensitization. Arthritis Care Research (Hoboken). ;68:472–480.

Finan PH, Buenaver LF, Bounds SC, Hussain S, Park RJ, Haque UJ, et al. (2013). Discordance between pain and radiographic severity in knee osteoarthritis: findings from quantitative sensory testing of central sensitization.  Arthritis & Rheumatism, 65, 363-72. doi:10.1002/art.34646

Fingleton C, Smart K, Moloney N, et al. (2015). Pain sensitization in people with knee osteoarthritis: a systematic review and meta-analysis. Osteoarthritis and Cartilage, 23:1043–1056.

Kim SH, Yoon KB, Yoon DM, Yoo JH & Ahn KR. (2015). Influence of Centrally Mediated Symptoms on Postoperative Pain in Osteoarthritis Patients Undergoing Total Knee Arthroplasty: A Prospective Observational Evaluation.  Pain Practice, 15, E46-53. doi:10.1111/papr.12311

Visser EJ, Ramachenderan J, Davies SJ, et al. (2016). Chronic widespread pain drawn on a body diagram is a screening tool for increased pain sensitization, psycho-social load, and utilization of pain management strategies. Pain Practice, 16, 31-37

Conversations about cannabis for chronic pain


The debate about cannabis and derivatives for persistent pain continues to grow in New Zealand, and elsewhere in the world. Many people I’ve treated and who are living with persistent pain say they like to use cannabis (in a variety of forms) to help with pain intensity and sleep, adding their voices to those wanting “medicinal” cannabis to be approved. In the few patients I’ve worked with who have managed to obtain a cannabis product (in NZ it has to be legally prescribed and will generally be in the form of Sativex or similar) the effect doesn’t seem as profound as the real thing (whether smoked, vaped, or in edibles).

Here’s my current position, for what it’s worth. Right now I think cannabis legislation needs an overhaul. Cannabis doesn’t seem to fit into the same class as synthetic drugs (often called “herbal highs” or synthetic “cannabis”) – for one, the plant probably contains a whole lot of substances that have yet to be fully analysed, and for another, I have yet to see a death reported from cannabis use, yet in Auckland, NZ, alone this year there have been around 9 people who have died from taking the synthetic substance, whatever it is. Cannabis seems to cause less harm than legal substances like alcohol and tobacco, and in many places in the world it’s been legalised with some interesting effects on use of opioids.

Ever since Professor David Nutt visited New Zealand a few years back, I’ve been convinced it’s time for a rethink on cannabis laws, but at the same time I’m not ready to support wholesale legalisation of “medical” marijuana. Here are a few reasons why:

  • When a doctor prescribes a drug, he or she is able to rely on the manufacturer making a consistent product, with a consistent amount of “active” ingredients, and a consistent quality. At present, with the exception of the two versions available in New Zealand, this can’t be guaranteed. Plants vary in the combination of active chemicals in them, and storage and age of the product influence the availability of those chemicals when inhaled or ingested. Just as we don’t suggest people go and grow their own opium poppies because we know that opioids are effective analgesics, I don’t think it’s time to allow people to grow their own cannabis for medicinal purposes, such as treating pain. A doctor can’t know just how much of a dose a person can get because in NZ we don’t yet have a controlled environment for cannabis production.
  • When a doctor prescribes a drug, he or she is also guided by the indications for use. So, although some medical practitioners prescribe “off-label” use for medications (a good example is nortriptyline, an antidepressant used often for pain reduction), generally there are good double-blinded, randomised controlled trials to determine whether the active drug is more effective than placebo. When we read about cannabis use for medicinal reasons we hear of its use for cancer (mainly nausea, but also pain), neuropathic pain, and in the general media we hear of its use for migraine, period pain, abdominal pain, fibromyalgia, osteoarthritis – there’s very few pain disorders that cannabis isn’t seen to be appropriate. But the truth is, we don’t really know which kind of pain (the underlying mechanism) will respond, and what pains don’t respond. It’s still a bit of a mystery – mind you, this is not any different from other medications for pain for which N=1 seems to be the mantra.

Why might I support a change to marijuana laws?

Well, an interesting study from the Northeastern United States, and published in the journal Pain, looked at the perspectives of people enrolled in legal medical marijuana clinics. It was quite a large study of 984 people, so should represent a good cross-section of those using the drug within a legal system. Participants were asked to complete an online survey, and their responses were analysed by a psychologist who was “not a cannabinoid expert”, arranging the data into themes and subthemes. (As an aside, apparently this was carried out using a “Grounded Theory perspective” based on Corbin and Strauss – BUT essentially the researchers didn’t follow grounded theory methodology throughout, and instead it should be called a thematic analysis using inductive coding. Pedant, yes!). The data was then examined to quantify the responses (another violation of GT methodology), and re-examined by another co-author for verification.

What they found was a group of people, over half women, with 2/3 indicating they’d been diagnosed with chronic pain by a medical professional. Diagnoses varied, but most (91%) had low back and neck pain, 30% with neuropathic pain, 23% with postsurgical pain, nearly 22% with abdominal pain, 20% with chronic pain after trauma/injury, 7% with cancer pain and 5% with menstrual pain.  Most people smoked cannabis either by joint, pipe or bong; some used a vaporiser, some had edibles or a tincture, and least, some sort of ointment.

The participants indicated it was on average 75% effective at reducing/treating symptoms, which is extraordinary when you realise that traditional forms of medication for neuropathic pain may reduce pain by 50% in around 1  in 4 people (Woolf, 2010). Participants spent around $3118 each year, but this was skewed because concentrates cost $3910, while topicals were $814. Joints were more expensive than vaporised product ($260 different!).

Analysing the positives of cannabis, participants reported pain relief, or at least being able to tolerate the pain more easily; while sleep benefits was the next most significant theme. Participants were encouraged that cannabis doesn’t have overdose potential, it’s natural, there are a wide range of strains with different characteristics, and limited potential for dependence.

There were numerous other positive aspects to using cannabis this way, according to the participants: things like “feeling normal”, “I am more active and able to do things I want”, being “distracted” from the pain, “able to focus”, and “able to relax”.

Negative perspectives included the cost (too expensive – in NZ Sativex is around $1000 a month – not covered by NZ pharmaceutical subsidies); some people didn’t like the smell, the effects on lungs and breathing, appetite changes (and gaining weight), and some emotional effects like anxiety or paranoia. Stigma and judgement by others also features, as did the difficulty accessing the drug, and conflict about the different laws applying to cannabis use – noting that the US has different federal and state laws.

Overall, the responses from these participants suggest a benign, mainly positive response to a drug, with negatives primarily around the social aspects – stigma from health providers, other people thinking of the participants as stoners, the legal situation and so on. For me, the limitations of this study really preclude any major judgement as to benefit or otherwise. We only know what this group of people believed, they have a vested interest in promoting benefits because negatives won’t support their belief that this is a viable treatment option, we don’t know the effect on function (particularly objective data), and we have no way of verifying the diagnoses individuals reported as the reason for prescription.

My conclusion?

It’s way past time to discuss cannabis use, health risks and health benefits. To have an open discussion about use for medicinal reasons, we need to remove the current barrier: the legal situation. While people have a vested interest in promoting the benefits over risks or adverse effects, we’re not going to have a very clear picture of what happens with ongoing use. I don’t support the use of cannabis as a medicinal product – to me there are far too many unknowns, and I think we risk wedging open a gate that has, until now, been useful for limiting the risk from pharmaceutical harms. We need to subject cannabis to the same level of rigour as any other pharmaceutical product being introduced to the market.

On the other hand, I think removing legal barriers to recreational use is about balancing the benefits and harms of this substance against other substances used for similar reasons. Alcohol and tobacco are well-known for harmful effects. Prohibition of alcohol did not work. Tobacco smoking is reducing over time courtesy of a committed campaign documenting harms, as well as raising the price via taxation. We can’t campaign around health harms for a product that isn’t legal. We can’t establish useful regulation over who produces it, who can buy it, where it can be used, the effects on work injury/vehicle injury, we can’t represent the undoubted benefits, and we look, to many people, to hold a double-standard.

And sneaking cannabis use in under the guise of “medicinal” use just isn’t on, in my humble opinion. Let’s not put medical practitioners in an unenviable situation where they’re asked to prescribe a product that is not yet examined to the level we expect for every other pharmaceutical product on the market. Let’s spend some precious research funding to establish WHO cannabis helps, WHAT it helps with, and HOW it helps – and most importantly, let’s look at whether it helps produce outcomes that surpass other approaches to persistent pain. We need to face it, currently our treatments are not very good.

 

Piper, B. J., Beals, M. L., Abess, A. T., Nichols, S. D., Martin, M. W., Cobb, C. M., & DeKeuster, R. M. (2017). Chronic pain patients’ perspectives of medical cannabis. Pain, 158(7), 1373-1379.

Woolf, C: (2010). Review: Overcoming obstacles to developing new analgesics, Nature Medicine (Supplement); 16,11: 1241 – 47

Clinical reasoning in persistent pain management


I think we need to take a cold hard look at clinical reasoning in pain management and especially at how we can integrate all the various factors influencing the person sitting in front of us. There are too few papers really addressing how different professions can put their assessment findings together to generate a truly multi-faceted model of why this person is having trouble with their pain. I could find only one paper detailing interprofessional clinical reasoning for chronic pain – and it’s inside a textbook dates from 2008 (Linton & Nicholas, 2008). So it’s no wonder, when a team gets together, that we collectively find it difficult to work together.

The approach discussed by Linton and Nicholas was the way I was trained to work, so I’m biased. Nevertheless I think this is a practical and useful way of putting the jigsaw puzzle together to see how each factor influences every other factor. I’m not suggesting that every case should be formulated this way – but I do find myself using the same strategy for every person I see.

We all do a bunch of assessments when we first see a person. But then what do we do with all that material? As Linton and Nicholas say, most assessments are used to document the intensity of the problem. Case formulations try to identify the main problems experienced by the person – and then generate hypotheses about the mechanisms supporting those problems for this person sitting in front of me.

So here’s a question for y’all – if you have information on the person’s pain intensity, how much it is interfering in their life, how depressed they are, as well as understanding their fear-avoidance beliefs and catastrophising; and if you know how their family responds to them, should we simply provide our standard treatment package ( e.g. analgesic medication, home exercises, and relaxation training)?

Wouldn’t it make more sense to only target catastrophising if they seem to add to the person’s problems? And wouldn’t it be better to add home exercises only if the person seems to be avoiding activities?

Or have we got to the place where everyone gets exactly the same solutions to what, for them, is a very unique and individual problem?

A key part of case formulation is involving the individual in the process. I think it’s crucial to actively be putting their perspective into generating the hypotheses about the factors maintaining their problem – this helps them see the relevance of each piece of the treatment puzzle, and ensures we don’t over-interpret (or under-interpret) factors.

Another really good reason for case formulation is to counter our cognitive biases. We know we jump to conclusions, find patterns where there aren’t any, look for things that confirm our own beliefs, look for simple options and ignore complex and ambiguous options – and so on, and case formulation can buy us time to avoid some of these really significant problems.

So, how do they work. Linton and Nicholas use a “spaghetti diagram” – looks like a bunch of arrows connecting various factors together. It looks a bit like this:

I personally use something that looks a bit different because I like Tim Sharp’s reformulation of a CBT model.

Whatever the approach, having a structure, taking time to “fill in the gaps”, including the person living with pain, and understanding the literature that clarifies those factors important in pain and disability, will allow us to avoid some of the major cognitive bias traps. Using a common formulation across all the clinicians involved really helps all of the team know why they’re doing what they’re doing – and why the other members of the team are so important. That means we can support one another!

But the bit missing, for me, is the “what do you do when you see these patterns?” To me, it’s about identifying the person’s main concerns – what are they primarily concerned about? Often it’s not the pain intensity, but instead it’s whether they’ll be able to still work, or their sleep, or their family reactions, or loss of roles. So we need to look for factors that are influencing these aspects of their situation so we actually address the problems that the person identified (rather than our own preference!). Shock and horror ensues! That might mean the person doesn’t need to see a physio for an exercise programme – they might prefer to work on sleep management, or work.

And if the person doesn’t avoid because they’re not too bothered by their pain, why would we need to give them “pain education”? Perhaps we’d do better to treat their depression, or help with their sleep. Similarly, if someone isn’t distressed, isn’t avoiding and just needs some medication – shouldn’t they get just that? Do we seriously need them to see a psychologist, occupational therapist, physiotherapist and go to the gym four days a week? Maybe less can be more.

I guess some of my frustration lies with the fact that despite all this talk of integrating the various parts of pain management, what we often end up with is a formulaic “education, exercise and mindfulness” for everyone – irrespective of their actual needs. Is it time to talk about what we might do differently for the person who might have a tendency to catastrophise but isn’t avoiding, or for the person who is very fit but doesn’t want to sit, or the person who is having such trouble sleeping because of their pain? Let’s be a bit nuanced, folks!

Linton, S. J., & Nicholas, M. K. (2008). After assessment, then what? Integrating findings for successful case formulation and treatment tailoring. Clinical Pain Management Second Edition: Practice and Procedures, 4, 1095.

Everyday hassles of fibromyalgia


This post has been on my mind for a while now. I live with fibromyalgia (FM) and want to share some of the everyday hassles I face. This isn’t a “oh woe is me” kind of post, it’s more of a “if you’re a clinician working with someone who has fibromyalgia, these are some things to ponder”.

Diagnosis

I worked in chronic pain management for almost 20 years before I recognised that the pains I’d been experiencing most of my adult life actually added up to “…a syndrome of diffuse body pain with associations of fatigue, sleep disturbance, cognitive changes, mood disturbance, and other variable somatic symptoms”(Fitzcharles, Ste-Marie, Goldenberg et al, 2012). I’d hurt my back in my early 20’s, thankfully been seen by Dr Mike Butler and given the Melzack & Wall book “The Challenge of Chronic Pain” to read, so I wasn’t afraid of my pain and just accepted it as part of life. What I hadn’t really recognised was that not only was the pain in my lower back part of the picture, so too was the pain in my neck, shoulders, arms, hips, legs, feet, and the irritable bowel, and the gastro discomfort, and the migraines and the dysmenorrhoea. Not to mention the fatigue, rotten sleep, foggy thoughts, and low mood.

Diagnosis for people living with fibromyalgia is often delayed.  People with fibromyalgia may resist going to the GP for what seem to be short-term but painful bouts in various parts of the body. There for a couple of weeks, then shifting to another part of the body. As one person said to me “You feel a fool going to see a Dr about a pain that’s not consistent to say ‘Oh Doctor and I have pain here, and here and here and last week I had one here…especially when it might be gone next week, and that other one has already gone.'”. This experience is echoed in qualitative research where, for example in a study by Undeland and Malterud (2007) people said that although having a label was reassuring (it’s not something that will kill you!), the label itself was often difficult to obtain (doctors not being keen to label something so nebulous as FM), and even with a label health professionals and the general public “pay no attention to the name, or blatantly regard them as too cheerful or healthy looking” (Undeland & Malterud, 2007).

Treatment

One of the problems with getting the diagnosis is that very few people get relief from medication. Those that do may find their pain settles almost completely, but many others have no effective analgesia despite trying numerous combinations. I’m one of them. What this means is that “self management” is the order of the day – yet in many places this is not even considered, let alone having services to help people develop such skills.

I’ve learned that my body feels best when I maintain a consistent level of activity irrespective of the day of the week. I enjoy stretching, walking, cycling and dancing, but I also love gardening, fishing, walking the dog – and I guess I can add in doing the housework and working as part of the mix. New activities are bound to give me aches and pains that last for weeks, while stopping my usual routine also brings me aches and pains that last for weeks. So boring consistency is the name of the game. And as I’ve previously blogged that means I look for a variety of different movement options in my repertoire.

Everyday hassles

The one thing that makes my life difficult is when I develop a new pain in a part of my body that doesn’t usually feel uncomfortable. Like most people living with persistent pain, I’ve developed an awareness of “my normal” (see this study by Strong & Large, 1995, for a nice description of this aspect of living with pain, one that is not often discussed). I know the usual pattern of my pains – bellyache, low back pain, neck and upper back pain, wrists and fingers, and often, knees, headaches and facial pain. These are my normal – but when should I seek help for a new pain? After all, it could be simply a manifestation of my fibromyalgia (ie there is nothing medically to be found, and no real change in management). At the same time, these are new pains – one in my shoulder that feels like an impingement (painful arc), and one that’s possibly an adductor tendon thing that’s very localised and hasn’t moved for over 7 months.

The question that keeps coming back to me is whether I’m overlooking something that can be treated, or whether it’ll just settle down like most of my pains do. Essentially I’ve just kept doing what I do and ignoring it.

The difference between my situation and those of people who are not painiacs, who don’t know that their pain is largely unrelated to the state of the tissues, is that I’m immersed in pain research all day, every day. I’m not overly bothered by these new pains. I’m continuing to exercise as normal and these pains aren’t interfering with what I need and want to do in daily life (well, perhaps a little…).

I can understand why someone might ask for help for a new pain. There are no rules saying that just because you have a persistent pain disorder you’re immune from acute musculoskeletal disorders. And sometimes by treating a new pain as an acute pain, it will vanish. Though, it must be said that outcomes for people with more than 3 or 4 persistent areas of pain with low back pain are not as good as those who only have one or two (Nordstoga, Nilsen, Vasseljen et al, 2017), nor of recovery and benefit from total hip and knee replacement (Wylde, Sayers, Odutola, Gooberman-Hill et al, 2017).

Points to ponder

So how do we as clinicians help people who must live with persistent pain?

  • Do we consider the meaning of the labels we give? And do we read around the experiences of those who have been given the diagnosis? Or do we, instead, rely on our own beliefs and biases when thinking about the way we handle diagnosis?
  • Do we give people an explanation for their pain that they can understand, or do we rely on currently favoured language and models without really considering what this means to the person? And do we ever check out how they’ve interpreted our explanations?
  • Do we ever discuss how to self-manage pain? Do we think about the practical implications of needing to learn to modify every aspect of life in the face of pain that will not just go away? When I compare the tasks of living well with persistent pain against those needed to cope with other disorders, pain can interfere with everything – do we talk about the impact on sex? on relaxation? on having a holiday?
  • Do we talk about what to do when a new pain turns up? Do we think about how someone can decide whether their pain is worth seeing someone about, or one they can handle? And do we even talk about the effect of having a persistent pain problem and then going on to have surgery? Do we teach people to recognise their “normal” pain, or are we afraid to teach people this because it might focus their attention on their pain?

I don’t have researched answers to these questions. I have my experience. And I’ve been working in this field a long time – yet somehow the voices of people living successfully with this pain are rarely heard.

 

Fitzcharles, M.-A., Ste-Marie, P. A., Goldenberg, D. L., Pereira, J. X., Abbey, S., Choinière, M., . . . Proulx, J. 2012 canadian guidelines for the diagnosis and management of fibromyalgia syndrome. http://fmguidelines.ca/

Nordstoga, A. L., Nilsen, T. I. L., Vasseljen, O., Unsgaard-Tøndel, M., & Mork, P. J. (2017). The influence of multisite pain and psychological comorbidity on prognosis of chronic low back pain: Longitudinal data from the norwegian hunt study. BMJ open, 7(5). doi:10.1136/bmjopen-2016-015312

Strong, J., & Large, R. (1995). Coping with chronic low back pain: An idiographic exploration through focus groups. The International Journal of Psychiatry in Medicine, 25(4), 371-387. doi:10.2190/H4P9-U5NB-2KJU-4TBN

Undeland, M., & Malterud, K. (2007). The fibromyalgia diagnosis – hardly helpful for the patients? Scandinavian Journal of Primary Health Care, 25(4), 250-255. doi:10.1080/02813430701706568

Wylde, V., Sayers, A., Odutola, A., Gooberman‐Hill, R., Dieppe, P., & Blom, A. (2017). Central sensitization as a determinant of patients’ benefit from total hip and knee replacement. European Journal of Pain, 21(2), 357-365.

Pacing, pacing, pacing – good, bad, or…?


There’s nothing that pain peeps seem to like more than a good dispute over whether something is good, or not so good for treatment. Pacing is a perennial topic for this kind of vexed discussion. Advocates say “But look at what it does for me! I can do more without getting my pain out of control!” Those not quite as convinced say “But look at how little you’re doing, and you keep letting pain get in the way of what you really want to do!”

Defining and measuring pacing is just as vexed as deciding whether it’s a good thing or not. Pacing isn’t well-defined and there are several definitions to hand. The paper I’m discussing today identifies five themes of pacing, and based this on Delphi technique followed by a psychometric study to ensure the items make sense. The three aspects of pacing are: activity adjustment, activity consistency, activity progression, activity planning and activity acceptance.

Activity adjustment is about adjusting how we go about doing things – approaches like breaking a task down, using rest breaks, and alternating activities.

Activity consistency is about undertaking a consistent amount of activity each day – the “do no more on good days, do no less on bad” approach.

Activity progression refers to gradually increasing activities that have been avoided in the past, as well as gradually increasing the time spent on each task.

Activity planning involves setting activity levels, setting time limits to avoid “over-doing”, and setting meaningful goals.

Finally, activity acceptance is about accepting what can be done, and what can’t, setting realistic goals, adapting targets, and being able to say no to some activities.

In terms of covering the scope of “activity pacing”, I think these five factors look pretty good – capturing both the lay sense of pacing, as well as some of the ideas about consistency and progression.

On to the study itself, conducted by Deborah Antcliffe, Malcolm Campbell, Steve Woby and Philip Keeley from Manchester and Huddersfield.  Participants in this study were attending physiotherapy through the NHS (yay for socialised healthcare! – Let’s keep that way, shall we?!), and had diagnoses of chronic low back pain, chronic widespread pain, fibromyalgia and chronic fatigue syndrome.  They completed the questionnaire either while on a waiting list, or after completing treatment, as a way to generalise findings – so this isn’t a measure of change (at least, not at this point).

Along with the APQ (the Activity Pacing Questionnaire – original name huh?!), participants completed a numeric rating scale, the Chalder Fatigue Questionnaire, Hospital Anxiety and Depression Scale, Pain Anxiety Symptoms Scale, and the Short-Form 12.  Some lovely number crunching was used – hierarchicial (sequential) multiple regression models with five separate multiple regression models of the symptoms of current pain, physical fatigue, depression, avoidance and physical functioning.

One of the confusing problems with  measuring pacing is that people may vary their use of different forms of pacing, depending on their symptoms at the time. So in this analysis, factors like pain and fatigue could be a dependent variable (ie I use pacing techniques and feel less fatigued and I’m in less pain), or they could be a confounding variable (ie I feel sore and tired, so I use these techniques).  Needless to say, the statistical analysis is complex and I don’t have a hope of explaining it!

The results, however, are very intriguing. 257 people completed the questionnaires in full, from an overall number of 311 participants. About half had completed their physiotherapy, while the other half had yet to start (ie waiting list). As usual, more people with low back pain than other conditions, and 2/3 were female. On first pass through the data, to establish correlations for inclusion in the regression  models (did your eyes just glaze over?!), the findings showed activity adjustment was associated with higher levels of current pain, depression, and avoidance, and lower levels of physical function. Activity consistency was associated with lower levels of physical fatigue, depression, and avoidance. and higher levels of physical function. Activity progression was associated with higher levels of current pain. Activity planning was significantly associated with lower levels of physical fatigue, and activity acceptance was associated with higher levels of current pain and avoidance.

Then things changed. As these researchers began adjusting for other independent variables, the patterns changed – Activity adjustment was significantly associated with higher levels of depression and avoidance and lower levels of physical function as before, but after adjustment, the association with pain was no longer significant; instead, it was significantly related to higher levels of physical fatigue. Activity consistency remained significantly associated with lower levels of physical fatigue, depression, and avoidance, and higher levels of physical function, but became significantly associated with lower levels of current pain. There were now no significant partial correlations between activity progression and any of the symptoms, whereas activity planning retained its significant association with lower levels of physical fatigue. Activity acceptance lost its significant association with current pain but retained its significant association with higher levels of avoidance.

Ok, Ok, what does that all mean? Firstly – engrave this on your forehead “Correlation does not mean causation”! What seems to be the case is that different themes or forms of pacing are associated with different symptoms. The items associated with adjusting or limiting activities were generally associated with more symptoms. So the more pain and fatigue a person experiences, it seems the more likely it is for them to choose to limit or adjust how much they do. Pacing themes involving consistency and planning were associated with improved symptoms. Using path analysis, the authors identify that activity adjustment and activity consistency play the most important parts in the relationship  between pacing and symptoms.

The take-home messages from this study are these:

  • We can’t define pacing as a unidimensional process – it seems clear to me that different people describe pacing in different ways, and that this messy definitional complexity makes current studies into the use of pacing rather challenging.
  • It seems that avoiding activities, reducing activities in response to pain or fatigue – the idea of an “envelope” of time/energy that needs to be managed to get through the day – is associated with more severe symptoms. Whether people choose this approach only when their symptoms are severe, and revert to activity adjustment and consistency when in less discomfort is not clear (correlation does not equal causation!)
  • Planning activities seems to be associated with some improved symptoms and the authors suggest that planning activities in advance might help people avoid a “boom and bust” scenario. giving a better shape to the day, a greater sense of control and achievement. Then again, it could be that when people feel better, they’re more able to plan their day, and again this study doesn’t help us much.
  • Activity progression, where the overall amount of activity gradually increases over time, wasn’t associated with either more or less pain and fatigue. I think it’s time we had a good look at whether progression helps people – or doesn’t. Rehabilitation philosophy suggests that it “should” – but do we know?
  • And finally, activity consistency was the aspect of pacing that was associated with improved symptoms – and this is certainly something I’ve found true in my own pain management.

The authors maintain that describing pacing as a multi-faceted construct is the only way forward – clearly we’re not going to agree that “pacing is X” when five different forms of pacing were derived from the Delphi study on which the APQ is based. It seems to me that we could benefit from applying this kind of nuanced definition in more areas than just pacing in pain management!

Antcliff, D., Campbell, M., Woby, S., & Keeley, P. (2017). Activity pacing is associated with better and worse symptoms for patients with long-term conditions. The Clinical Journal of Pain, 33(3), 205-214. doi:10.1097/ajp.0000000000000401

Returning to work, good or bad?- a very complex question


One of the main reasons returning to work is a priority in many healthcare systems is simply that compensation and off-work benefits is the most costly portion of the bill for people with ill health. This naturally leads to a strong emphasis in most rehabilitation, especially musculoskeletal rehabilitation in New Zealand, to help people return to work as soon as practicable. At times the process can be brutal. In my own case, after 18 months of working part-time due to post-concussion symptoms after a “mild” traumatic brain injury, I had the hard word put on me to get back to my job or I’d be sent to work back on the wards (after having spent most of my clinical career working in pain management). Not quite the supportive approach I needed when I was having to sleep for at least an hour every afternoon!

I can well remember the pressure of trying to maintain my work output to the satisfaction of my manager, keep my home responsibilities going (I had teenaged children at the time), manage all the paperwork required just to be part of a rehabilitation system, maintain my relationship which was strained just because I had no energy to play or have fun the way I used to. Oh and I had weekly rehabilitation appointments to top it all off! Not easy to keep your cool when everything seems balanced on a knife-edge.

Yet, despite the challenges of going back to work, most accounts of recovery from musculoskeletal pain find that returning to work forms a crucial element in maintaining long-term gains. The study that sparked this post is a good example: Michael Sullivan and colleagues, set in Montreal, Canada, found that returning to work helps to maintain treatment gains in people with whiplash injury. Of the 110 people enrolled in this study, 73 participants returned to work by the end of one year, while the remaining 37 remained off work. Using regression analysis, the researchers found that the relationship  between return to work and maintaining treatment goals remained significant even when confounds such as pain severity, reduced range of movement, depression and thinking the worst (catastrophising) were controlled. What this means is that something about those who returned to work seemed to help them achieve this, and it wasn’t the usual suspects of low mood or that the injury was more severe. What is even more striking is that those who didn’t return to work actually reported worsening symptoms.

There are plenty of arguments against this finding: could it be that those who didn’t return to work just didn’t respond as well to the treatment in the first place? Well – the authors argue no, because they controlled for the things that should have responded to treatment (eg range of movement, mood). Participants in the study returned to work 2 months on average after completing their treatment, and final measurement was on average 10 months later suggesting that it was something to do with being at work that made a difference.

In their discussion, the authors suggest that perhaps those who didn’t return to work were overall less physically active than those who did, compromising their recovery potential. They also note that being out of work is known to be associated with poorer mental health, so perhaps that explains the difference at the end of the trial period. In addition, they point out that perhaps ongoing stress related to having to handle disability claims processes, perhaps even the financial stress of being unable to work might have been influential.

It’s this last point that I think is interesting. There is no doubt that people who encounter the disability systems that fund their treatment and replace their income feel like their autonomy and independence has gone. They feel their world is being manipulated at the whim of case managers, treatment providers, assessing doctors, and even their family.  A sense of injustice can be detrimental to outcomes for people with whiplash, as Sullivan and colleagues showed some years ago (Sullivan, Thibault, Simmonds, Milioto et al 2009), and we know also that social judgements made about people who experience persistent pain are often negative and exert an influence on the experience of pain itself (Bliss, 2016; Schneider et al, 2016).

Working is really important to people – even in a job you don’t especially enjoy, there are important reasons you keep going (even if it’s only for the money! Money in the hand means food for you and yours, power for the lighting and heating, and even a little bit left over for jam on your bread!). In addition to the money, the most commonly asked question when you’re introduced to someone is “and what do you do for a job?” It’s a way of categorising a person, as much as we hate that idea. Work gives us social contact, routine, purpose and allows us a way to demonstrate competence. Without the anchor of working, many people who live with persistent pain feel the burden of social judgement “who are you?”, of ongoing bureaucracy (filling in paperwork), of repeated assessments to justify not being at work, of constantly being asked to attend appointments, of never feeling like time is their own. Balancing the demands of a system that judges you negatively because you are “unfit” against the demands of family and your own needs is an incredibly difficult process – but then again, so is the process of returning to a job where you fear you’ll fail and experience That Pain Again, and where, if you fail, you could lose that job entirely.

I don’t have an answer to how we can make this process easier. I do know that early return to work can be positive if handled well – but handled poorly, can be an extremely unpleasant and stressful process. Vocational rehabilitation providers need to understand both acute and persistent pain. They also need to carefully assess the psychosocial aspects of a job, not just the biomechanical demands. And someone needs to represent the needs of the person living with persistent pain and help them balance these demands carefully.

 

Bliss, Tim VP, et al. (2016)”Synaptic plasticity in the anterior cingulate cortex in acute and chronic pain.” Nature Reviews Neuroscience .

De Ruddere, Lies, et al. (2016)”Patients are socially excluded when their pain has no medical explanation.” The Journal of Pain 17.9 : 1028-1035.

McParland, J. L., & Eccleston, C. (2013). “It’s not fair”: Social justice appraisals in the context of chronic pain. Current Directions in Psychological Science, 22(6), 484-489.

Schneider, Peggy, et al. “Adolescent social rejection alters pain processing in a CB1 receptor dependent manner.” European Neuropsychopharmacology 26.7 (2016): 1201-1212.

Sullivan, M. J., Thibault, P., Simmonds, M. J., Milioto, M., Cantin, A. P., Velly, A. M., . . . Velly, A. M. (2009). Pain, perceived injustice and the persistence of post-traumatic stress symptoms during the course of rehabilitation for whiplash injuries. Pain, 145(3), 325-331.

Sullivan, M., Adams, H., Thibault, P., Moore, E., Carriere, J. S., & Larivière, C. (2017). Return to work helps maintain treatment gains in the rehabilitation of whiplash injury. Pain, 158(5), 980-987. doi:10.1097/j.pain.0000000000000871

The “Subjective” – and really hearing


I’m not a physiotherapist. This means I don’t follow the SOAP format because it doesn’t suit me. The first letter is intended to represent “subjective” – and when I look up the dictionary meaning of subjective and compare it with the way “subjective” notes are thought about, I think we have a problem, Houston.

Subjective is meant to mean “based on personal feelings” or more generally “what the person says”. In the case of our experience of pain, we only have our personal feelings to go on. That is, we can’t use an image or X-ray or fMRI or blood test to decide whether someone is or isn’t experiencing pain.

Now the reason I don’t like the term “subjective” when it’s part of a clinical examination is that so often we contrast this section with so-called “objective” findings.  Objective is meant to mean “not influenced by personal feelings”, and is intended to represent “facts” or “the truth”. Problem is… how we determine truth.

Let’s think about how the information we obtain fits with these two ideals, and how we use it.

Subjective information is all the things we ask a person about – their thoughts, beliefs, feelings, understanding and their own experience. Subjective information might even include the person’s report of what they can and can’t do, how they feel about this and what their goals are.

Objective information, on the other hand, is all the things we as clinicians observe and measure. Now here’s my problem. By calling this information “objective” we’re indicating that we as clinicians hold a less-than-subjective view of what we see. Now is that true? Let’s think about the tests we use (reliability, validity anyone?). Think about the choices we make when selecting those tests (personal bias, training variability, clinical model…). Think about the performance variables on the day we do the testing (time of day, equipment and instruction variability, observational awareness, distractions, recording – oh and interpretation).

Now think about how that information is used. What value is placed on the objective information? It’s like a record of what actually was at the time. If you don’t believe me, take a look at what’s reported in medico-legal reporting – and what gets taken notice of. The subjective information is often either overlooked – or used to justify that the client is wrong, and what they can actually do is contained in the “objective”.

Given the predictive validity of a person’s expectations, beliefs and understanding on their pain and disability over time, I think the label “subjective” needs an overhaul. I think it’s far more accurate to call this “Personal experience”, or to remove the two labels completely and call it “assessment”. Let’s not value our own world view over that of the people we are listening to.

How do we really hear what someone’s saying? Well, that’s a hard one but I think it begins with an attitude. That attitude is one of curiosity. You see, I don’t believe that people deliberately make dumb decisions. I think people make the best decisions they can, given the information they have at the time. The choices a person makes are usually based on anticipating the results and believing that this option will work out, at least once. So, for example, if someone finds that bending forwards hurts – doesn’t it make sense not to bend over if you’re worried that (a) it’s going to hurt and (b) something dire is happening to make it hurt? In the short term, at least, it does make sense – but over time, the results are less useful.

Our job, as clinicians, is to find out the basis for this behaviour, and to help the person consider some alternatives. I think one of the best ways to do this is to use guided discovery, or Socratic questioning to help both me and the client work out why they’ve ended up doing something that isn’t working out so well now, in the long term. I recorded a video for the Facebook group Trust Me, I’m a Physiotherapist (go here for the video) where I talk about Socratic questioning and Motivational Interviewing – the idea is to really respect the person’s own experience, and to guide him or her to discover something about that experience that perhaps they hadn’t noticed before. To shed a little light on an assumption, or to check out the experience in light of new knowledge.

Learning Socratic questioning can be tricky at first (Waltman, Hall, McFarr, Beck & Creed, 2017). We’re not usually trained to ask questions unless we already know the answer and where we’re going with it. We’re also used to telling people things rather than guiding them to discover for themselves. Video recording can be a useful approach (see Gonsalvez, Brockman & Hill, 2016) for more information on two techniques. It’s one of the most powerful ways to learn about what you’re actually doing in-session (and it’s a bit ewwww at first too!).

We also really need to watch that we’re not guiding the person to discover what we THINK is going on, rather than being prepared to be led by the client as, together, we make sense of their experience. It does take a little time, and it does mean we go at the pace of the person – and we have to work hard at reflecting back what it is we hear.

So, “subjective” information needs, I think, to be valued far more highly than it is. It needs to be integrated into our clinical reasoning – what the person says and what we discover together should influence how we work in therapy. And we might need to place a little less reliance on “objective” information, because it’s filtered through our own perspective (and other people may take it more seriously than they should).

 

Gonsalvez, C. J., Brockman, R., & Hill, H. R. (2016). Video feedback in CBT supervision: review and illustration of two specific techniques. Cognitive Behaviour Therapist, 9.
Kazantzis, N., Fairburn, C. G., Padesky, C. A., Reinecke, M., & Teesson, M. (2014). Unresolved issues regarding the research and practice of cognitive behavior therapy: The case of guided discovery using Socratic questioning. Behaviour Change, 31(01), 1-17.
Waltman, S., Hall, B. C., McFarr, L. M., Beck, A. T., & Creed, T. A. (2017). In-Session Stuck Points and Pitfalls of Community Clinicians Learning CBT: Qualitative Investigation. Cognitive and Behavioral Practice, 24(2), 256-267.

Mulling over the pain management vs pain reduction divide


I’ve worked in persistent pain management for most of my career. This means I am biased towards pain management. At times this creates tension when I begin talking to clinicians who work in acute or subacute musculoskeletal pain, because they wonder whether what I talk about is relevant to them. After all, why would someone need to know about ongoing management when hopefully their pain will completely go?

I have sympathy for this position – for many people, a bout of tendonosis, or a strained muscle or even radicular pain can ebb away, leaving the person feeling as good as new. While it might take a few months for these pain problems to settle, in many instances there’s not too much need for long-term changes in how the person lives their life.

On the other hand, there are many, many people who either don’t have simple musculoskeletal problems (ie they’re complicated by other health conditions, or they have concurrent issues that make dealing with pain a bit of a challenge), or they have conditions that simply do not resolve. Good examples of these include osteoarthritis (hip, knee, shoulder, thumbs, fingers) and grumbly old lower back pain, or peripheral neuropathy (diabetic or otherwise). In these cases the potential for pain to carry on is very present, and I sometimes wonder how well we are set up to help them.

Let’s take the case of osteoarthritis. Because our overall population is aging, and because of, perhaps, obesity and inactivity, osteoarthritis of the knee is becoming a problem. People can develop OA knee early in their life after sustaining trauma to the knee (those rugby tackles, falling off motorcycles, falling off horses, running injuries), or later in life as they age – so OA knee is a problem of middle to later age. People living with knee OA describe being concerned about pain, especially pain that goes on after they’ve stopped activities; they’re worried about walking, bending and maintaining independence – and are kinda pessimistic about the future thinking that  “in 10 years their health would be worse and their arthritis would be a major problem” (Burks, 2002).

To someone living with osteoarthritis, especially knee osteoarthritis, it can seem that there is only one solution: get a knee replacement. People are told that knee replacements are a good thing, but also warned that knee replacements shouldn’t be done “too soon”, leaving them feeling a bit stranded (Demierre, Castelao & Piot-Ziegler, 2011). Conversations about osteoarthritis are not prioritised in healthcare consultations – in part because people with knee osteoarthritis believe that knee pain is “just part of normal aging”, that there’s little to be done about it, and medications are thought to be unpleasant and not especially helpful (Jinks, Ong & Richardson, 2007).

I wonder how many healthcare professionals feel the same as the participants in the studies I’ve cited above. Do we think that knee OA is just something to “live with” because the problem is just part of old age, there’s an eventual solution, and meanwhile there’s not a lot we can do about it?

When I think about our approach to managing the pain of osteoarthritis, I also wonder about our approach to other pains that don’t settle the way we think they should. Is part of our reluctance to talk about pain that persists because we don’t feel we know enough to help? Or that we feel we’ve failed? Or that it’s just part of life and people should just get on with it? Is it about our feelings of powerlessness?

In the flush of enthusiasm for explaining the mechanisms of pain neurobiology, have we become somewhat insensitive to what it feels like to be on the receiving end when the “education” doesn’t reduce pain? And what do we do when our efforts to reduce pain fail to produce the kind of results we hope for? And the critical point, when do we begin talking about adapting to living well alongside pain?

What does a conversation about learning to adapt to pain look like – or do we just quietly let the person stop coming to see us once we establish their pain isn’t subsiding? I rather fancy it might be the latter.

Here’s a couple of thoughts about how we might broach the subject of learning to live with persistent pain rather than focusing exclusively on reducing pain:

  • “What would you be doing if pain was less of a problem?” My old standby because in talking about this I can begin to see underlying values and valued activities that I can help the person look at starting, albeit maybe doing them differently.
  • “What do you think are the chances of this pain completely going away?” Some might say this is about expectancy and I’m setting up a “nocebic” effect, but I argue that understanding the person’s own perspective is helpful. And sometimes, when a person has persistent pain and a diagnosis like osteoarthritis, their appraisal is less about catastrophising and more about holding a realistic view about their own body. It’s not about the appraisal – it’s about what we do about this. And we can use this perspective to built confidence and increase the importance of learning coping strategies.
  • “If I could show you some ways to deal with pain fluctuations, would you be interested in learning more?” All episodes of pain that persists will have times when pain is more intense than others – flare-ups are a normal part of recovering from, and living with persistent pain. Everyone needs to know some ways of going with, being flexible about or coping with flare-ups. I teach people not to focus exclusively on reducing pain during these flare-up periods. This is because even during rehabilitation we don’t want to use pain as a guide (it can be a cruel task-master). We know that rehabilitation can increase (temporarily) pain while the body habituates to new movement patterns, the brain gets used to new input, and the homunculus gets redefined. It’s great to be able to teach strategies that increase the sense of safety, security and down-regulation that can be lost in the initial onslaught of pain.

To summarise, not all pain problems settle. We can help everyone to be more resilient if we begin talking about ways of coping with flare-ups even during subacute pain, particularly if we avoid an excessive focus on trying to avoid them. Instead, we can begin to help people feel confident that flare-ups always settle down, and that they can manage them effectively by using effective self management.

 

Burks, K. (2002). Health concerns of men with osteoarthritis of the knee. Orthopaedic Nursing, 21(4), 28-34.

Cohen, E., & Lee, Y. C. (2015). A mechanism-based approach to the management of osteoarthritis pain. Current Osteoporosis Reports, 13(6), 399-406.

Demierre, M., Castelao, E., & Piot-Ziegler, C. (2011). The long and painful path towards arthroplasty: A qualitative study. J Health Psychol, 16(4), 549-560. doi:10.1177/1359105310385365

Jinks, C., Ong, B. N., & Richardson, J. (2007). A mixed methods study to investigate needs assessment for knee pain and disability: Population and individual perspectives. BMC Musculoskeletal Disorders, 8, 59.

…and now what we’ve all been waiting for: What do to about central sensitisation in the clinic


For the last couple of weeks I’ve posted about central sensitisation; what it is, and how to assess for it. Today I’m going to turn to the “so what” question, and talk about what this might mean when we’re in the clinic.  Remember that most of this material comes from Jo Nijs’ recent talks at the New Zealand Pain Society.
Firstly, remember that pain is an experience that people have, underpinned by neurobiology, but also, depending on the level of analysis, on interactions with others, on systems and how they work, on culture, on individual experiences, and of course, on interacting within a body within an environment or context. Everything I say from here on is based on these assumptions.

The first point Jo Nijs makes is that when we know a bit more about the neurobiology of persistent pain associated with central sensitisation, we can use this knowledge wisely when we help someone make sense of their pain. This doesn’t mean wholesale and broadcast “I-will-tell-you-all-I-know-about-pain-neurobiology-because-I-know-you-need-to-know-it-because-I-know-it-and-think-it’s-important” which is, truth to tell, a lot more about the know-it-all than the person in front of them! We need to earn the right to give information – that means establishing that we’ve heard the other person’s story and the current meanings they’ve made from their experience. It also means asking permission to share new information. It means thinking about WHY we want to share new information.

So what if the person doesn’t use the same groovy language we use to describe his or her understanding?! So what if they’ve got some of the newer ideas slightly skewed. In the end, what’s important is that the person understands these things:

  • Pain isn’t a direct reflection of what’s happening in the tissues.
  • Pain can be influenced by many things, some of which are physical forces (heat, pressure and so forth), some of which are ideas, and some are emotions. And there are a bunch of other variables that can influence the experience, including what else is going on around the person.
  • The brain is intimately involved with our experience of pain, and it’s a two-way street from body to brain and brain to body.
  • Persistent pain is more about neurobiology than tissue damage per se (but not exclusively about neurobiology).

Our job is to make sure the person understands these things, rather than our job being about “educating” people. The end result matters, rather than any particular process.

If we look at the evidence for helping people reconceptualise their pain, there’s plenty to show that this approach is useful – it’s been a key tenet of a self-management cognitive behavioural approach to pain management since at least the late 1970’s. The later research (from Butler, Moseley and Louw et al) is simply looking at this approach within a slightly different cohort and in a different context. Rather than being integrated with an interdisciplinary pain management programme, research from these guys shows that physiotherapists (in particular) can deliver this kind of information very effectively – and that it helps reduce the fear and subsequent efforts to avoid pain (such as not moving, seeking healthcare, and being worried about pain). Yay!

It’s true that there are many different ways to influence the descending modulatory system, and release endorphins. One of them is to help people understand their pain and be more confident about moving. Another is to place hands on the person – hence massage therapy, manual therapies, manipulations and so on. Nijs believes hands on therapy has best effect after you’ve gone through some of the reconceptualisation that’s often needed (Bishop, Torres-Cueco, Gay, Lluch-Girbes, Beneciuk, & Bialosky, 2015).

Similar arguments can be made for considering sleep management and stress management as an integral part of pain management. (To be perfectly honest, I always thought this was part of what we did…). So here’s the argument: we know most people with persistent pain experience rotten sleep. We also know that people are stressed by their experience of pain. Because poor sleep is associated with increased activation of glia in the prefrontal cortex, amygdala and hippocampus, and therefore are pro-inflammatory, pain is often increased after a poor night’s sleep. Sleep medications interfere with the sleep architecture, so it’s useful to consider nonpharmacological approaches to sleep management.

Three strategies to consider:

  • CBT for insomnia – here’s one resource to use
  • ACT or acceptance and commitment therapy – I’ve written a great deal about ACT, just use the search function on this blog for more
  • Exercise – OMG yes, exercise is effective! (just not right before bedtime, kthx)

Stress management is tougher. We can’t avoid experiencing stress – and neither can we live in a bubble where we don’t ever get exposed to stress. Instead, we probably all could do with learning multiple ways of managing stress. Things like realistic evaluations of the situation, increasing our capabilities for regulating our response to stress via biofeedback if need be, and using mindfulness as a strategy for being with stress instead of fighting against it, or folding beneath it.

I haven’t cited many references in this post – not because there aren’t many, but because there are SO many! And I’ll post more next week when I start looking at the rather sexy neurobiological examinations of processes used in pain management for years (yes, we’ve been doing it for a long time, we now have great explanations for how these things might work – though effect sizes are still small.)

 

Bishop, M. D., Torres-Cueco, R., Gay, C. W., Lluch-Girbés, E., Beneciuk, J. M., & Bialosky, J. E. (2015). What effect can manual therapy have on a patient’s pain experience?. Pain, 5(6), 455-464.

 

Does central sensitisation matter?


In my last post I discussed some of the mechanisms thought to be involved in central sensitisation, and while many of the details remain pretty unknown, I think the general conclusion is that yes, it really is a thing. What do I mean by central sensitisation? Well, it’s curious, it can refer to the processes at spinal and brain levels that seem to reduce the usual descending inhibitory mechanisms, expand the areas in which neural activity takes place, and allows increased information flow to eventually reach conscious awareness. At the same time it can refer to the experience in which a person feels greater pain than anticipated, given the degree of input; pain that is distributed more widely than anticipated, given the degree of input; and/or pain that lasts longer than we’d expect, given the degree of input (Woolf, 2011). BTW most of this post is derived from talks given by Pro Jo Nijs at the recent New Zealand Pain Society Conference.

The question now is whether this really matters. After all, nociceptor inputs can trigger a prolonged but reversible increase in central nociceptive pathways – if they’re reversible, just eliminate the original nociceptive input, and voila! The sensitisation is gone. What we know, however, is that in many cases the tendency towards having long-term increased sensitivity remains, or was perhaps always present.

Well, unfortunately if someone does tend to have greater activity in the central nervous system, then it has the potential to add enormously to poor outcomes if he or she decides to have surgery. For example, individuals with this tendency experience poorer outcomes after total knee replacement; and after shoulder surgery; but not after hip-joint replacement surgery. Testing in these cases was conducted using conditioned pain modulation which involves people undergoing painful testing – when they’re already in pain! Brave souls. You can see why it’s not a popular testing procedure in mainstream surgical situations.

Adding to the view that central sensitisation matters clinically, Ferrandiz and colleagues (2016) found that central sensitisation mediates the treatment effects in people with low back pain; Jull and colleagues (2007) found the same for neck pain after whiplash; Coombes and colleagues (2015) found the same for people with chronic tennis elbow.  It seems that central sensitisation is associated with greater pain catastrophising, slower movements, higher pain reporting, poorer functioning, increased perception of pain, and fear of moving.

The question now is how best to assess for the presence of this phenomenon. Given that most people won’t want to undergo conditioned pain modulation (not to mention the need for testing equipment and skilled technicians to administer the test!), what’s needed is a reasonably simple way to identify those who have the characteristics of central sensitisation so we can plan for, and manage it, more effectively.

Nijs and the Pain in Motion Research Group published the first set of criteria in 2014, from an epidemiological perspective. This classification approach involves first excluding neuropathic pain – and the group propose using IASP diagnostic criteria for neuropathic pain (see Haanpaa & Treede, 2010). If the problem is neuropathic pain (where there is a clear lesion of the nerve), then it’s managed accordingly (although we really don’t have great treatments for this kind of pain, either!).

Then they propose an algorithm which helps to clarify whether the problem is central sensitisation or “something else”.

The first question is whether the person identifies they have “disproportionate pain experience” – now this I have a problem with, because what is a “proportionate” pain experience? Given how fluid our experience of pain can be, and how poorly the experience correlates with what’s going on in the tissues, I find this a bit tough to use as a clear-cut indicator. Nevertheless, it’s the first question asked in this algorithm…

The next question relates to the person experiencing diffuse pain distribution (or, perhaps, wider spread than expected). If this is the case, eg someone has a grazed knee, but pain is experienced all over the entire leg, then it’s identified as central sensitisation. If the result is more like pain just above the knee to just below, then it’s somewhat equivocal, so the authors suggest the person completes the Central Sensitisation Inventory. This is a questionnaire I’ve discussed in the past. I’m no nearer to establishing whether it really is a useful measure than when I wrote that blog, but the measure continues to be used, and research is ongoing. Certainly, Jo Nijs and group seem to think the measure holds promise and might help to classify those at greater risk of developing problems with pain if they proceed to surgery.

So, to summarise, while the mechanisms involved in central sensitisation are still being discovered, and it’s challenging to know where normal processes end and abnormal ones begin, it definitely seems to be a clinical phenomenon affecting not only those without peripheral nociception (eg migraine), but also those with clearcut peripheral problems like osteoarthritis. Central sensitisation processes seem to underpin some of the most problematic pain problems we know of, and can get in the way of recovery even when peripheral nociceptive input has been removed – 18% of total knee-joint replacements are revised because of ongoing pain, and this pain doesn’t seem to improve after subsequent surgery (NZ National Joint Registry). There’s confusion about language – does the term refer to the mechanisms thought to be involved, or does it refer to the experience described by people? And assessing it is challenging – either go through complex and painful testing, or complete a questionnaire that may confound distress about health (and subsequent hypervigilance about body symptoms) with pain and other responses that might represent the presence of central sensitisation processes being invoked.

More challenging still is what do we do once central sensitisation is identified? Are our treatments any good? That, folks, will be explored in the next enthralling episode on Healthskills!

 

Baert, I., Lluch, E., Mulder, T., Nijs, J., Noten, S., & Meeus, M. (2016). Does pre-surgical central modulation of pain influence outcome after total knee replacement? A systematic review. Osteoarthritis and Cartilage, 24(2), 213-223.

Haanpää M, Treede RD. Diagnosis and classification of neuropathic pain. Pain Clinical Updates 2010; XVII.

Nijs, J., Torres-Cueco, R., van Wilgen, P., Lluch Girbés, E., Struyf, F., Roussel, N., . . . Vanderweeën, L. (2014). Applying modern pain neuroscience in clinical practice: Criteria for the classification of central sensitization pain. Pain Physician, 17(5), 447-457.

Valencia, C., Fillingim, R. B., Bishop, M., Wu, S. S., Wright, T. W., Moser, M., . . . George, S. Z. (2014). Investigation of central pain processing in post-operative shoulder pain and disability. The Clinical Journal of Pain, 30(9), 775.

Woolf, C. J. (2011). Central sensitization: Implications for the diagnosis and treatment of pain. Pain, 152(3 Suppl), S2-15.

Wylde, V., Sayers, A., Odutola, A., Gooberman‐Hill, R., Dieppe, P., & Blom, A. (2017). Central sensitization as a determinant of patients’ benefit from total hip and knee replacement. European Journal of Pain, 21(2), 357-365.