Pain

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

Great expectations – and low back pain


Have you ever wondered why there are so many treatments for low back pain? Like there are actually hundreds of different ways to “treat” back pain… yet the truth is, none of them work for everyone. Actually, most of them seem to help pass the time until low back pain settles of its own accord. Until it’s back again (no pun intended!).

This post is prompted after reading a string of general news articles discussing the common non-specific low back pain – under various guises of “dead butt syndrome“, “Dr Tom: Ouch I’ve hurt my back” and the like – I think it’s time for a frank discussion about the natural history of low back pain, as found in large epidemiological studies. There’s no doubt that low back pain is a problem around the world, and I think it’s partly due to unmet expectations (along with a whole lot of other variables). The Global Burden of Disease found low back pain to be the most common reason for days lived with disability around the world – that’s more than anaemia, depression, hearing loss, migraine!

Low back pain is common in every single country in the world.

Dunn, Hestbaek & Cassidy (2013) examined the prevalence of low back pain across the life span – they found that many of us view low back pain as a simple “yes/no” question – do you have it, or don’t you. They point out that people with no back pain at the time of a survey are not all the same: some might never have had a bout ever, while some might have had several bouts but just don’t have one right now. These presentations are not the same! Those who have had a previous episode will have developed an understanding of back pain on the basis of what happened, and this will influence their expectations, and subsequent response, to treatments.

Dunn, Hestbaek & Cassidy found that children/adolescents have a point prevalence (ie at the time of the survey, they reported they had back pain) of 12%. As people get older the prevalence continues to be around 12%. The elderly, those over 60 (that doesn’t really feel old to me!), seem to have a prevalence similar to people in middle age, and activities affected by low back pain seem to increase as we age.

Given the lifetime prevalence of low back pain is around 80% (or more), following people up over time seems to paint a different picture from the point prevalence studies: it’s not the same 12% of people that has low back pain all the time. Some studies show that at least 40% of people do recover within a year of an episode (see Hestbaek, Leboeuf-Yde, & Manniche, 2003). A Danish study with 5 year follow-up found around 23% of people consistently reported no pain days during the previous year (during the study) but around 10% reported more than 30 days of back pain every time they were asked. So, while long-term low back pain isn’t common in the adult population, most people do have a couple of bouts over long periods of time.

What are the risk factors? Well one clear risk factor is having had a previous episode, although this isn’t a consistent predictor for long-term back pain. Perhaps we should take a look more closely at the natural course of acute neck and low back pain – from the Norwegian longitudinal studies. From one city in Norway, these researchers screened 9056 people between 20 – 67 years old to identify those with a brand new bout of neck or back pain in the previous month – 219 people were identified, then followed for 12 months. What these researchers found was pain decreasing rapidly in the first month, irrespective of treatment, thereafter though, back pain didn’t change for the rest of the year especially for those with pain in the neck as well as the back at the first assessment, and for those who had 4 or more pain sites in the beginning.

Now what’s really interesting about this study is that the pain reduction people experienced, particularly in low back pain, was pretty close to the pain reduction people achieved whether they had treatment, or not. Hmmmm. Next question: what if we look at all the treatments people get, and those who are in the control group, and pooled that information to find out what happens? Artus, van der Windt, Jordan & Croft examined whether just taking part in a study on low back pain might influence outcomes – so they pooled 70 RCTs and 19 cohort studies, and both sets of data showed “a rapid improvement in the first six weeks followed by a smaller further improvement until 52 weeks. there was no statistically significant different in pooled standardised mean change (a measure used to compared the pooled within-group change in pain in RCTs with cohort studies) – get this, at any time point.

But wait, there’s more!

Axen & Leboeuf-Yde (2013) looked at the trajectories of low back pain over time. They summarised four studies in primary care or the general population, finding that over the course of between 12 weeks and 12 months, participants could be divided into two to four groups: one group remained uncomfortable, perhaps staying that way over the whole 12 months (around 10 – 21%); one group also remained uncomfortable but they reported their pain as “moderate” or “mild” – around 36%; another approximately 30% experienced fluctuating or intermittent low back pain; and finally, the group we love – those who recovered and remained that way, around 30 – 58%.

This is not the picture we hear in the media. This is not what we were taught. And yes, I know there are problems with pooled data because individualised responses get ironed out. But what all this says to me is – our patients come to us expecting that low back pain should completely resolve. The reality is that for a lot of people, back pain will come and go throughout the lifetime.

What does this mean to me?

Isn’t it time to give people an idea that if they have a bout of back pain, chances are high they’ll have another. Complete resolution of low back pain may not occur for a large number of people. A new bout of low back pain may not mean a new “injury” (given we don’t know why many people develop back pain in the first place). Learning to self-manage a bout of back pain is likely to save people a load of heartache, not to mention a lot of money. And maybe it’s the latter that means it’s very hard to find clear, effective messages about just how safe a painful back is. It’s far easier to sell a message of vulnerability, of the need for treatment for that “unhappy spine” as a chiropractor in Christchurch calls it. And of course, if we continue to allow the expectation that all pain should be gone, we’re going to be in business for a very long time…

 

Artus, M., van der Windt, D., Jordan, K.P., & Croft, P.R. (2014). The clinical course of low back pain: A meta-analysis comparing outcomes in randomised clinical trials (rcts) and observational studies. BMC Musculoskeletal Disorders, 15, 68.

Axén, I., & Leboeuf-Yde, C. (2013). Trajectories of low back pain. Best Practice & Research Clinical Rheumatology, 27(5), 601-612. doi: http://dx.doi.org/10.1016/j.berh.2013.10.004

Dunn, K.M., Hestbaek, L., & Cassidy, J.D. (2013). Low back pain across the life course. Best Practice & Research in Clinical Rheumatology, 27(5), 591-600.

Hestbaek L, Leboeuf-Yde C, Engberg M, Lauritzen T, Bruun NH, Manniche C. (2003). The course of low back pain in a general population. Results from a 5-year prospective study. Journal of Manipulative & Physiological Therapeutics, 26(4):213–9.

Hestbaek L, Leboeuf-Yde C, Manniche C. (2003). Low back pain: what is the long-term course? A review of studies of general patient populations. European Spine Journal, 12(2):149–65.

Vasseljen, O., Woodhouse, A., Bjorngaard, J.H., & Leivseth, L. (2013). Natural course of acute neck and low back pain in the general population: The HUNT study. Pain, 154(8), 1237-1244.

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.

Exercise? Who me? Yoga or physiotherapy or education…


Exercise, while one of The Most Important self management approaches for persistent pain, is not an easy sell to someone who is experiencing pain. Especially not if that exercise looks like huffing and puffing, hauling on bits of metal in a gym, or wearing lycra. Not to mention the “sports drinks”…  Those things aside, exercising is a good thing. You heard it from me, and I have declared my body an exercise free zone! The thing is, what kind of exercise, for what purpose, and how to get introduced to it.

Personally I’m a fan of exercise that achieves something else other than “getting fit”. I like gardening, I love dancing, I enjoy cycling (especially to the store to get a GREAT coffee!). Walking the dog is fun. Swimming (especially snorkeling) is awesome! I like my exercise to do more than bring on the endorphins, especially as I don’t get much of that post-exertional analgesia that many people do – and believe me, they do (Ellinson, Stegner, Schwabacher, Koltyn & Cook, 2016). I like my exercise to look like the things I need or want to do, so that when I need to do ’em, I’m in fit state to get on and do ’em.

So what kind of exercise works best? One sage told me “the exercise the person does!” and there is some truth to that, so when I begin talking to someone about exercise, I’m looking for something they can do regularly, that fits into their lifestyle, that makes them feel good, and has some other benefit to them. That benefit might be the social thing – going to a box-fit class with a group of others all bent on getting their fix of play-fighting. It might be the solitary thing – long walks along the beach with the dog for company. It might be the music – in my case, it’s belly dance (and I dare anyone to do a 5 minute shimmy drill while keeping an isolated upper body, a loose shimmy and smile!).

I like the idea of having variety – who says we need to do the same kind of exercise every day? So it’s a wet day and I don’t fancy taking my bike out in the rain, I can turn to my dance practice, or do the dusting, or vacuum the floors. It’s a frosty day and I can go for a brisk walk and take photographs of gorgeous sparkly frosty droplets while Sheba-the-wonderdog huffs steam and sniffs at the local scents. If it’s a warm day, why not head to the pool for a lap or two? If it’s a busy day and I don’t have time, what about some “exercise snacks”? Five minutes of exercise every 25 minutes adds some pretty quickly, so it’s lunges and chair dips and wall presses and shimmy practice in between writing.

Over time we’re seeing more research looking particularly at yoga for persistent pain of all kinds. Yoga comes in many different forms, and in this case I’m guessing the more extreme forms of hot yoga and contortion is not being studied. Some of the studies are appearing in rather eminent journals, like this one from the Annals of Internal Medicine and authored by a very large team including Saper, Lemaster, Delitto and colleagues (2017).

This study is a “non-inferiority” study, looking to establish whether yoga or physiotherapy, or indeed education, can help people living with chronic low back pain. Now I’m not going to do a blow-by-blow analysis of the study, that’s for you to do. What I am going to do is look at what the yoga consisted of – and see why, perhaps, yoga is getting so much research interest. BTW, yoga was found to be non-inferior to physiotherapy, and both yoga and PT were more likely than education to have a clinically meaningful response, although neither yoga nor PT were superior to education.

This is the basic format of the yoga class: Each class began with relaxation and meditation exercises, yoga breathing, and yoga philosophy. It continued with yoga poses and
concluded with relaxation. Pose variations and aids (such as chair, strap, and blocks) accommodated various abilities. Thirty minutes of daily home practice, facilitated by a DVD, a manual, and take-home yoga supplies, was strongly encouraged.

Yoga appeals to many because it seems to begin where people are at – it’s not huffy-puffy, things don’t jiggle, and generally the classes begin and end with the ritual of breathing and meditation. I like the idea of yoga (and yes, I’ve done a class or two!), because it doesn’t involve a lot of gadgets, you can do it alone or in a group, and it feels good. What I don’t like about yoga is the need to get effective and consistent feedback about how well you’re performing the poses, especially in the beginning, which means it can be difficult to do on your own without a teacher.

For people who find exercising both difficult and painful, yoga is a good place to start. I think attending classes is crucial (or at least having an instructor and a mirror!). Learning to use the meditation and breathing is integral to the exercise – and it’s this that I think makes yoga an effective addition to the exercise toolkit. What I’m less sure of is whether it’s better than any other form of exercise – or, in my case, the many different types of movements that I use in my weekly routine. And there’s the rub. As an occupational therapist, exercise is something people choose to do as a form of occupation (valued and meaningful activity). I also enjoy a bunch of other movement-based occupations, and to me these are as valid as yoga or the PT exercises included in this study. What my approach lacks, however, is a researched basis for it.

But here’s the thing: to date the research supporting exercise for people with persistent pain shows modest effects. And those effects are completely lost if the person doesn’t do the exercise. So why not have a wide range of whole-body movement practices to draw on, allowing the person to pick and choose and get out and do something every day, even if it doesn’t fit with our modern notions of what exercise should be?

 

 

Ellingson, L. D., Stegner, A. J., Schwabacher, I. J., Koltyn, K. F., & Cook, D. B. (2016). Exercise Strengthens Central Nervous System Modulation of Pain in Fibromyalgia. Brain Sciences, 6(1), 8. http://doi.org/10.3390/brainsci6010008

Saper, R. B., Lemaster, C., Delitto, A., & et al. (2017). Yoga, physical therapy, or education for chronic low back pain: A randomized noninferiority trial. Annals of Internal Medicine. doi:10.7326/M16-2579

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

Targeting the people who need it most


A couple of things came to mind today as I thought about this post: the first was an article in the local newspaper about a man complaining that the government is “promoting disability” because he couldn’t get surgery for a disc prolapse – and the pain was affecting his ability to work. The second was how to direct the right treatment at the right person at the right time – and how we can be derailed by either wholesale over-servicing “everyone needs treatment X”, or by overburdening people with assessment just to give a fairly basic treatment.

Now with the first man, I don’t know his clinical situation – what I do know is that there are many people every day who must learn to live with their pain because there simply is not an effective treatment of any kind, and that amongst these people are those go on to live wonderful lives despite their pain. I wonder if this man has ever been offered comprehensive self management for while he waits for his surgery. Whether the government could spread some funding away from surgery as the primary option for such pain problems – and instead provide better funding for the wider range of approaches offered through the interdisciplinary pain management centres (approaches which include injection procedures, physiotherapy, psychology, occupational therapy and medications). When there is an effective treatment (and this is arguable in the case of disc prolapse – in fact, it’s difficult to know whether even MRI imaging can give a clear indication of who might respond best to what treatment (Steffens, Hancock, Pereira et al, 2016), we should be able to give it, provided it fits within our country’s health budget. Ahh – that’s the problem, isn’t it… expensive treatments mean fewer people can get basic treatment. And with lumbar disc prolapse, the evidence for surgery is less favourable than many people recognise (Deyo & Mirza, 2016) – they state:

“Patients with severe or progressive neurologic deficits require a referral for surgery. Elective surgery is an option for patients with congruent clinical and MRI findings and a condition that does not improve within 6 weeks. The major benefit of surgery is relief of sciatica that is faster than relief with conservative treatment, but results of early surgical and prolonged conservative treatment tend to be similar at 1 year of follow-up. Patients and physicians should share in decision making.”

So here we have a person with lots of pain, experiencing a great deal of distress, and reducing his work because of pain and disability. My question now (and not for this person in particular) is whether being distressed is equivalent to needing psychological help. How would we know?

There’s been a tendency in pain management to bring in psychologists to help people in this kind of situation. Sometimes people being referred for such help feel aggrieved: “My problem isn’t psychological!” they say, and they’re quite correct. But having a problem that isn’t psychological doesn’t mean some psychological help can’t be useful – unless by doing so, we deny people who have serious psychological health problems from being seen. And in New Zealand there are incredible shortages in mental health service delivery – in Christchurch alone we’ve had an increase in use of mental health services of more than 60% over the past six years since the massive 2010/2011 earthquakes (The Press).

People living with persistent pain often do experience depression, anxiety, poor sleep, challenges to relationships and in general, feeling demoralised and frustrated.  In a recent study of those attending a specialist pain management centre, 60% met criteria for “probable depression” while 33.8% met criteria for “severe depression” (Rayner, Hotopf, Petkova, Matcham, Simpson & McCracken, 2016). BUT that’s 40% who don’t – and it’s my belief that providing psychological services to this group is allocating resources away from people who really need it.

So, what do we do? Well one step forward might be to use effective screening tools to establish who has a serious psychological need and who may respond just as well to reactivation and return to usual activities with the support of the less expensive (but no less skilled) occupational therapy and physiotherapy teams. Vaegter, Handberg, & Kent (in press) have just published a study showing that brief psychological screening measures can be useful for ruling out those with psychological conditions. While we would never use just a questionnaire for diagnosis, when combined with clinical assessment and interview, brief forms of questionnaires can be really helpful for establishing risk and areas for further assessment. This study provides some support for using single item questions to identify those who need more in-depth assessment, and those who don’t need this level of attention. I like that! The idea that we can triage those who probably don’t need the whole toolbox hurled at them is a great idea.

Perhaps the New Zealand politicians, as they begin the downhill towards general elections at the end of the year, could be asked to thoughtfully consider rational distribution of healthcare, and a greater emphasis on targeted use of allied health and expensive surgery.

 

Deyo, R. A., & Mirza, S. K. (2016). Herniated Lumbar Intervertebral Disk. New England Journal of Medicine, 374(18), 1763-1772.

Hahne, A. J., Ford, J. J., & McMeeken, J. M. (2010). Conservative management of lumbar disc herniation with associated radiculopathy: A systematic review. Spine, 35(11), E488-504.

Koffel, E., Kroenke, K., Bair, M. J., Leverty, D., Polusny, M. A., & Krebs, E. E. (2016). The bidirectional relationship between sleep complaints and pain: Analysis of data from a randomized trial. Health Psychology, 35(1), 41-49.

Rayner L, Hotopf M, Petkova H, Matcham F, Simpson A, McCracken LM. Depression in patients with chronic pain attending a specialised pain treatment centre: prevalence and impact on health care costs. Pain. 2016;157(7):1472-1479. doi:10.1097/j.pain.0000000000000542

Steffens, D., Hancock, M.J., Pereira, L.S. et al.(2016) Do MRI findings identify patients with low back pain or sciatica who respond better to particular interventions? A systematic review. European Spine Journal 25: 1170. doi:10.1007/s00586-015-4195-4

Vaegter, H. B. P., Handberg, G. M. D., & Kent, P. P. Brief psychological screening questions can be useful for ruling out psychological conditions in patients with chronic pain. Clinical Journal of Pain.

…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.

What is pain for?


We’re told we need pain – without the experience, we risk harming our bodies and living short lives. With pain, and for most people, we learn to not go there, don’t do that, don’t do that AGAIN, and look at that person – don’t do what they’re doing! Thirst, hunger, fear, delicious tastes and smells, the feelings of belonging, of safety and security, of calm and comfort: all of these are experiences we learn about as we develop greater control over our bodies.

Pain is an experience we learn to associate with actual or possible threat to “self”. Let’s take a moment to think about what “self-hood” means.

If I ask you “who are you?” you’ll tell me your name, probably your occupation, maybe where you live and who you live with. Baumeister (1997) suggests our sense of self is about “the direct feeling each person has of privileged access to his or her own thoughts and feelings and sensations.” He goes on to say “it begins with the awareness of one’s own body and is augmented by the sense of being able to make choices and initiate action.” We learn about who we are through interacting with the environment, but also as we interact with other people and begin to sort through our roles, contributions and relationships.

Of course, our sense of self changes over time and is reciprocally influenced by choices we make as well as opportunities (and threats) around us, both environmental and social.

We work really hard to avoid threats to our sense of self. For example, I’ll bet we’ve all seen that person who steadfastly refuses to stop colouring his hair, wearing the same clothing styles as he did in his 20’s, holding on to the same habits as he did at the same age even when he’s now in his 50’s, has a paunch, and still looks for partners 20 years younger than he is…  He still believes he’s that young stud despite the evidence in the mirror. And of course the same applies to women perhaps more so!

So what happens when our mind/body is threatened? How do we know it? And what do we do about it?

In this instance I’m not talking about social threats, though there’s interesting research suggesting that being socially excluded has similar neurobiological effects as being physically threatened (or experiencing pain – though this may reflect the distress we experience when we’re hurt and when we’re socially excluded – see Iannetti, Salomons, Moayedi, Mouraux & Davis, 2013; Eisenberger, 2015). I’m instead talking about threats to our physical body. Those threats may be violence from another person, physical trauma to the body, or the threat of physical harm to the body. When we experience these kinds of threats, and once an aspect of mind/body has disentangled the threat evaluation from whatever other goals we’re currently engaged in, we experience pain. Tabor, Keogh and Eccelston (Pain, in press) define pain in terms of action: an experience which, as part of a protective strategy, attempts to defend one’s self in the presence of inferred threat.

So pain is there to help us maintain an intact sense of self in the presence of threat – threat that we’ve inferred from our context (or drawn a conclusion from incomplete data). It’s part of a system that works to maintain “us” in the face of multiple threats that we encounter.

Tabor, Keogh and Eccleston also argue that pain is an experience designed to intrude on awareness to show that “boundaries have been reached and action must be taken”. Pain is one way our mind/body can give us an indication of boundary – just how much, or how little, we can do. For example, I experience pain when I bend my thumb down to reach my wrist – it’s one way I can learn how far I can bend without disrupting something! The purpose of that pain is to help “me” defend against doing really dumb things, like stretching my thumb out of joint!

Interestingly, when we feel overwhelmed by our pain, when we can’t defend against it (because it feels too intense, has meanings that threaten our deepest sense of self) we tend to withdraw from responding to everything else – our conversations stop, we don’t notice other people or events, we pull into ourselves and ultimately, we can lose consciousness (think of the accounts of early surgery without anaesthesia – the surgeons were kinda grateful when the patient lapsed into unconsciousness because at last they weren’t writhing to get away – see Joanna Bourke’s book “The Story of Pain” for some harrowing stories!).

When we lose consciousness, our sense of self disappears. We lose contact with the “what it is to be me”.

Our sense of self also disappears when we experience pain we can’t escape and we can’t make sense of. Throughout the time while people are trying to label their pain, establish the meaning of their symptoms, and while people are searching for a solution to their pain, people’s experience of both time and “who I am” is threatened (Hellstrom, 2001).

To me, this is one of the primary problems associated with pain – and one we’ve almost completely ignored in our healthcare treatments. All our treatments are aimed at helping “get rid of the pain” – but what isn’t so often incorporated in these efforts is a way of engaging and rebuilding a resilient sense of self. So while the pain may ebb away, the “self” remains feeling vulnerable and threatened, especially if there’s any hint of pain returning.

What can we do better? Perhaps talk about what vision a person has of themselves as a “self”. Help them work towards becoming the “self” they believe they are – or at least helping them express the underlying values that their “self” has previously been expressing. That way perhaps people can find flexible ways to express that “self” – which will make them more capable of living well under any circumstances.

 

Baumeister, R. F. (1997). Identity, self-concept, and self-esteem: The self lost and found. Hogan, Robert [Ed], 681-710.

Bourke, J. (2014). The story of pain: From prayer to painkillers: Oxford University Press.

Eisenberger, N. I. (2015). Social pain and the brain: Controversies, questions, and where to go from here. Annual review of psychology, 66, 601-629.

Hellstrom, C. (2001). Temporal dimensions of the self-concept: Entrapped and possible selves in chronic pain. Psychology & Health, 16(1), 111-124. doi:http://dx.doi.org/10.1080/08870440108405493

Iannetti, G. D., Salomons, T. V., Moayedi, M., Mouraux, A., & Davis, K. D. (2013). Beyond metaphor: Contrasting mechanisms of social and physical pain. Trends in Cognitive Sciences, 17(8), 371-378.

Tabor, A., Keogh, E. and Eccleston, C. (2016) Embodied pain— negotiating the boundaries of possible action. Pain. ISSN 0304- 3959 (In Press)

Empathy and catastrophising influence pain inhibition


When I went to occupational therapy school I was introduced to nociception and the biological underpinnings of pain. I wasn’t, at that time, taught anything about the brain, attention, emotions or any social responses to pain behaviour. Like most health professionals educated in the early 1980’s, pain was a biological and physical phenomenon. I suppose that’s why it can be so hard for some of my colleagues to unlearn the things they learned way back then, and begin to integrate what we know about psychological and social aspects of our pain experience. Because pain is a truly biopsychosocial experience. Those pesky psychosocial factors aren’t just present in people who have difficulty recovering from pain, they’re actually integral to the entire experience.

Anyway, ’nuff said.

Today I stumbled across a cool study exploring two of the psychosocial phenomena that we’ve learned are involved in pain. The first is catastrophising. And if you haven’t got your head around catastrophising it’s probably time to do so. It’s one of the strongest predictors of disability (Edwards, Dworkin, Sullivan, Turk & Wasan, 2016). Catastrophising is the tendency to “think the worst” and consists of ruminating (brooding on), magnifying (over-estimating the negative impact) and helplessness (feeling as if there’s nothing you can do).  The second is empathy, or the ability to sense other people’s emotions, coupled with the ability to imagine what someone else might be thinking or feeling. Empathy is not the same as sympathy which seems to be about the emotions a person experiences while observing another’s emotional state. In fact, separate parts of the brain are involved in the two experiences (Cuff, Brown, Taylor & Howat, 2014).

Back to the study. This study examined conditioned pain modulation in partners observing their partner undergoing a painful experience. It was carried out by Gougeon, Gaumond, Goffaux, Potvin and Marchand (2016) in an attempt to understand what happens to the pain experience of people watching their loved ones in pain. The experimental protocol was (1) baseline; (2) assessing pain VAS 50; (3) pre-CPT heat pain testing (thermode preimmersion at a fixed temperature); (4) CPT (either at 201Cor71C); and (5) post-CPT heat testing (thermode postimmersion at the same fixed temperature). What they did was ask the participants to submerge their right hand in a freezing cold waterbath while video recording them. They then asked their partners to place their right hand in lukewarm water while watching the video recording. Participants were asked to rate their pain intensity.

What they found was the higher the catastrophizing score was, stronger was their descending pain inhibition when they were watching either themselves or their spouse in pain. In women, the more empathic the women were, the better was their descending pain inhibition when they observed their spouse in pain.

This is extraordinary. Firstly, the finding that there was a correlation between catastrophising score and descending inhibition contradicts other research studies – Gougeon, Gaumond, Goffaux, Potvin and Marchand suggest that although cognitive and emotional processes underlying catastrophising increase pain perception and decrease inhibition, their experimental design may have increased pain perception during the conditioned stimulus which may have triggered more conditioned pain modulation. They also suggest that the catastrophising level of participants increases their perceived pain, explaining why it correlates with conditioned pain modulation efficiency.

Secondly, women were more distraught than men by observing pain in others. Adopting the perspective of a loved-one elicited stronger activation in regions involved in the “pain” matrix than adopting the stranger’s perspective (Cheng et al), and the authors suggest that empathy is a powerful factor involved in pain modulation while observing someone in pain. This shows that descending inhibition is influenced by physical stimulus characteristics (such as intensity or location), as well as personal cognitive dimensions. A far cry from the notion that psychosocial factors play little part in modulating our pain experience.

What does this actually mean for us?

Well, to me it suggests that we need to be aware of our own empathic response to observing someone else who is experiencing pain. Let’s put it this way: if I’m an especially empathic person (and especially if I tend to catastrophise) and I see people who are experiencing pain in my clinical practice, my own emotional and cognitive response to seeing people may influence my behaviour and practice. For example, I might be less willing to tell people that I don’t have a way to reduce their pain. I might pursue more “heroic” healthcare – send people off for more treatments, try for longer with unsuccessful treatments “just in case”, I might even send people away from my care because I find it hard to tolerate being around someone who “doesn’t respond”.

You see, being empathic and catastrophising tends to elevate feelings of distress in the presence of pain. If we don’t have effective ways to manage our own distress when we are in the presence of someone who is indicating they’re sore, we’re at greater risk of developing burnout and of feeling frustrated (Gleichgerrcht & Decety, 2014).

For this reason I’m a fan of using mindfulness because it does help people to step back from the emotional judgements of experience, and in particular the negative impact such judgements have on both interactions and emotions (Dobkin, Bernardi & Bagnis, 2016).

 

Cheng Y, Chen C, Lin CP, et al. Love hurts: an fMRI study. Neuroimage. 2010;51:923–929.

Cuff, B. M. P., Brown, S. J., Taylor, L., & Howat, D. J. (2014). Empathy: A review of the concept. Emotion Review, 8(2), 144-153. doi:10.1177/1754073914558466

Decety, J., Yang, C.-Y., & Cheng, Y. (2010). Physicians down-regulate their pain empathy response: An event-related brain potential study. Neuroimage, 50(4), 1676-1682.

Dobkin, P. L., Bernardi, N. F., & Bagnis, C. I. (2016). Enhancing clinicians’ well-being and patient-centered care through mindfulness. Journal of Continuing Education in the Health Professions, 36(1), 11-16.

Edwards, R. R., Dworkin, R. H., Sullivan, M. D., Turk, D. C., & Wasan, A. D. (2016). The role of psychosocial processes in the development and maintenance of chronic pain. The Journal of Pain, 17(9, Suppl), T70-T92.

Gleichgerrcht, E., & Decety, J. (2014). The relationship between different facets of empathy, pain perception and compassion fatigue among physicians. Frontiers in behavioral neuroscience, 8, 243.

Gougeon, V. M., Gaumond, I. P., Goffaux, P. P., Potvin, S. P., & Marchand, S. P. (2016). Triggering descending pain inhibition by observing ourselves or a loved-one in pain. Clinical Journal of Pain, 32(3), 238-245.