rehabilitation

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.

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.

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.

What to do with the results from the PCS


The Pain Catastrophising Scale is one of the more popular measures used in pain assessment. It’s popular because catastrophising (thinking the worst) has been identified as an especially important risk factor for slow recovery from pain (Abbott, Tyni-Lenne & Hedlund, 2010), for reporting high levels of pain intensity (Langley, 2011), and for ongoing disability (Elfving, Andersoon & Grooten, 2007). I could have cited hundreds more references to support these claims, BTW.

The problem is, once the PCS is administered and scored: what then? What difference does it make in how we go about helping a person think a little more positively about their pain, do more and feel more confident?

If you haven’t seen my earlier posts about the PCS, take a look at this, this, and this for more details.

Anyway, so someone has high scores on rumination, helplessness and magnifying – what does this mean? Let’s say we have two people attending the clinic, one has really high scores on all three subscales, while the other has low or average scores. Both have grumbly old low back pain, both have had exercises in the past, both are finding it tough to do normal daily activities right now.

For a good, general pain management approach to low back pain, and once red flags are excluded (yes, the “bio” comes first!) this is what I do. I establish what the person thinks is going on and ask if it’s OK to talk about pain neurobiology. Together we’ll generate a pain formulation, which is really a spaghetti diagram showing the experience as described by the person (I used guided discovery to develop it). I then ask the person what they’d be doing if their pain wasn’t such a problem for them, perhaps what they’re finding the most frustrating thing about their situation at the moment. Often it will be sleep, or driving or cooking dinner, or perhaps even getting clothes on (shoes and socks!). I’ll then begin with helping the person develop good relaxed breathing (for using with painful movements), and start by encouraging movement into the painful zone while remaining relaxed, and tie this in with one of the common activities (occupations) the person needs or wants to do. For example, I’ll encourage bending forward to put shoes and socks on while breathing in a relaxed and calm way. I’ll be watching and also encourage relaxing the shoulders and any other tense parts of the body. For someone who is just generally sore but doesn’t report high pain catastrophising, I will also encourage some daily movements doing something they enjoy – it might be walking, yoga, dancing, gardening, whatever they enjoy and will do regularly every day for whatever they can manage. Sometimes people need to start small so 5 minutes might be enough. I suggest being consistent, doing some relaxation afterwards, and building up only once the person has maintained four or five days of consistent activity. And doing the activity the person has been finding difficult.

If the person I’m seeing has high scores on the PCS I’ll begin in a similar way, but I’ll teach a couple of additional things, and I’ll expect to set a much lower target – and probably provide far more support. Catastrophising is often associated with having trouble disengaging from thinking about pain (ruminating), so I’ll teach the person some ways to deal with persistent thoughts that hang around.

A couple to try: mindfulness, although this practice requires practice! It’s not intended to help the person become relaxed! It’s intended to help them discipline their mind to attend to one thing without judgement and to notice and be gentle with the mind when it gets off track, which it will. I ask people to practice this at least four times a day, or whenever they’re waiting for something – like the jug to boil, or while cleaning teeth, or perhaps waiting for a traffic light.

Another is to use a “15 minutes of worry” practice. I ask the person to set a time in the evening to sit down and worry, usually from 7.00 – 7.15pm. Throughout the day I ask the person to notice when they’re ruminating on their situation. I ask them to remind themselves that they’re going to worry about that tonight and deliberately put that worry aside until their appointment with worry. Then, at 7.00pm they are asked to get a piece of paper and write ALL their worries down for a solid 15 minutes. No stopping until 15 minutes is over! It’s really hard. Then when they go to sleep, I ask them to remind themselves that they’ve now worried all their worries, and they can gently set those thoughts aside because they won’t forget their worry, it’s written down (I think worry is one way a mind tries hard to stop you from forgetting to DO something about the worry!). People can throw the paper away in the morning because then it begins all over again.

Usually people who score high on the PCS also find it hard to be realistic about their pain, they’ll use words that are really emotive and often fail to notice parts of the body that aren’t in pain. By noticing the worst, they find it tough to notice the best.  I like to guide people to notice the unloved parts of their body, the bits that don’t hurt – like the earlobes, or the belly button. I’ll offer guidance as to what to notice while we’re doing things, in particular, I like to guide people to notice those parts of the body that are moving smoothly, comfortably and that look relaxed. This is intended to support selective attention to good things – rather than only noticing pain.

Finally, I give more support to those who tend to be more worried about their pain than others. So I might set the goals a little lower – walking for five times a week, two days off for good behaviour rather than every day. Walking for five minutes rather than ten. And I’ll check in with them more often – by text, email or setting appointments closer together. It’s important for people who fear the worst to experience some success, so setting small goals that are achieved can build self efficacy – especially when I try hard to offer encouragement in terms of what the person has done despite the odds. So, if the person says they’ve had a real flare-up, I’ll try to boost confidence by acknowledging that they’ve come in to see me even though it’s a bad pain day, that they’ve tried to do something instead of nothing, that talking to me about the challenge shows guts and determination.

People who see the glass as half empty rather than half full are just people. Like you and I, they’re people who have a cognitive bias. With support, we can help people view their pain differently – and that process applies to all of us, not just those with high scores on the PCS.

 

Abbott, A. D., Tyni-Lenne, R., & Hedlund, R. (2010). The influence of psychological factors on pre-operative levels of pain intensity, disability and health-related quality of life in lumbar spinal fusion surgery patients. Physiotherapy, 96(3), 213-221. doi:10.1016/j.physio.2009.11.013

Elfving, B., Andersson, T., & Grooten, W. J. (2007). Low levels of physical activity in back pain patients are associated with high levels of fear-avoidance beliefs and pain catastrophizing. Physiotherapy Research International, 12(1), 14-24.

Langley, P. C. (2011). The prevalence, correlates and treatment of pain in the european union. Curr Med Res Opin, 27(2), 463-480. doi:10.1185/03007995.2010.542136

What should we do about acute low back pain?


There’s no doubt that low back pain presents a major healthcare problem in all parts of the world. It’s probably the most common form of musculoskeletal pain around, it can be highly disabling – and its management is one of the most contentious imaginable. As someone once said “if there was an effective treatment for low back pain, there wouldn’t be such a range of treatments available!”

I want to take a step back and consider people living with nonspecific low back pain only, it’s by far the most prevalent, and while no-one would say there is a single diagnosis that can be applied to all forms of back pain, there seem to be some similarities in how this kind of pain responds.

What we’ve learned over the past year is that acetaminophen hardly touches the pain of nonspecific low back pain Machado, Maher, Ferreira, Pinheiro et al, 2015). This means anti-inflammatory medications (NSAIDs) are the most likely group of medications to be prescribed, or perhaps codeine. Exercise was the recommended treatment for osteoarthritis of the hip and knee, suggesting that this approach might also be recommended for low back pain.

Turning to exercise, it seems that there is no clear indication that any particular type of exercise is any better than any other exercise for low back pain (not even motor control exercise)(Saragiotto, Maher, Yamato Tie, Costa et al, 2016), and all exercise improves pain and disability – and even recurrences (Machado, Bostick & Maher, 2013). What seems important is that people get moving again, and do so quickly after the onset of their back pain.

Graded exposure has also been in the news, latest being a study using graded exposure for elderly people living with chronic low back pain, where it was found to not only improve function (reduce disability) but also found to reduce pain (Leonhardt, Kuss, Becker, Basler et al, in press). OK, pain reduction wasn’t reduced a great deal, but neither have many treatments – and at least this one has few adverse effects and improves disability.

Where am I going with this?

Well, recently I made some apparently radical suggestions: I said that

  1. sub-typing low back pain doesn’t yet seem to be consistent;
  2. that no particular exercise type seems better than anything else;
  3. that ongoing disability is predicted more by psychosocial factors than by physical findings – even when injection treatments are used (van Wijk, Geurts, Lousberg,Wynne, Hammink, et al, 2008).
  4. that people with low back pain seem to get better for a while, and often find their back pain returns or grumbles along without any particular provocation;
  5. and that perhaps treatment should focus LESS on reducing pain (which doesn’t seem to be very effective) and LESS on trying to identify particular types of exercise that will suit particular people and MORE simply on graded return to normal activity.
  6. Along with really good information about what we know about low back pain (which isn’t much in terms of mechanics or anatomy, but quite a lot about what’s harmful and what doesn’t help at all), maybe all we need to do is help people get back to their usual activities.

For my sins I was asked not to remain involved in the group planning health system pathways (I also suggested maybe osteopaths, chiropractors, massage therapists and both occupational therapists and psychologists might also be good to be involved – maybe that was the radical part because I can’t see an awful lot radical about my other suggestions!).

Here’s my suggestion – when one of the most difficult aspects of low back pain management is helping people return to normal activities within their own environment (work, home, leisure), why not call in the experts in this area? I’m talking about YOU, occupational therapists! So far I haven’t been able to find a randomised controlled trial of occupational therapy graded exposure for low back pain. I’m sorry about this – it’s possibly a reflection of the difficulty there is in even suggesting that DOING NOTHING (ie not attempting to change the tissues, just helping people return to normal activity) might be an active form of treatment, and one that could work.

I don’t want to denigrate the wonderful work many clinicians do in the field of low back pain, but I suspect much of what seems to work is “meaning response” – well-meaning clinicians who believe in their treatments, patients who believe in their therapists, treatments that appear plausible within the general zeitgeist of “why we have low back pain”, all leading to a ritual in which people feel helped and begin to do things again.

Many of us have read Ben Darlow’s paper on The Enduring Impact of What Clinicians Say to People with Low Back Pain (Darlow, Dowell, Baxter, Mathieson, Perry & Dean, 2013). We have yet to count the cost of well-meaning clinicians feeding misinformed and unhelpful beliefs (and behaviours) to people with acute low back pain. I think the cost will be extremely high.

I just wonder if we might not be able to cut out much of the palaver about low back pain if we went directly to the “feeling helped and begin to do things again” without the misinformation and cost of the rituals involved. While other clinicians can contribute – the process of doing in the context of daily life is where occupational therapy research, experience and models have focused for the discipline’s history. That’s the professional magic of occupational therapy.

 

Darlow, B., Dowell, A., Baxter, G. D., Mathieson, F., Perry, M., & Dean, S. (2013). The enduring impact of what clinicians say to people with low back pain. Annals of Family Medicine, 11(6), 527-534. doi:10.1370/afm.1518

Leonhardt C, Kuss K, Becker A, Basler HD, de Jong J, Flatau B, Laekeman M, Mattenklodt P, Schuler M, Vlaeyen J, Quint S.(in press). Graded Exposure for Chronic Low Back Pain in Older Adults: A Pilot Study. Journal of Geriatric Physical Therapy.

Macedo, L. G., Bostick, G. P., & Maher, C. G. (2013). Exercise for prevention of recurrences of nonspecific low back pain. Physical Therapy, 93(12), 1587-1591.

Machado, G. C., Maher, C. G., Ferreira, P. H., Pinheiro, M. B., Lin, C.-W. C., Day, R. O., . . . Ferreira, M. L. (2015). Efficacy and safety of paracetamol for spinal pain and osteoarthritis: Systematic review and meta-analysis of randomised placebo controlled trials (Vol. 350).

Saragiotto Bruno, T., Maher Christopher, G., Yamato Tiê, P., Costa Leonardo, O. P., Menezes Costa Luciola, C., Ostelo Raymond, W. J. G., & Macedo Luciana, G. (2016). Motor control exercise for chronic non-specific low-back pain. Cochrane Database of Systematic Reviews, (1). http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD012004/abstract doi:10.1002/14651858.CD012004

van Wijk, R. M. A. W., Geurts, J. W. M., Lousberg, R., Wynne, H. J., Hammink, E., Knape, J. T. A., & Groen, G. J. (2008). Psychological predictors of substantial pain reduction after minimally invasive radiofrequency and injection treatments for chronic low back pain. Pain Medicine, 9(2), 212-221.

Neuroplasticity: Transforming the brain


Neuroplasticity is a concept that’s taken the world by storm over the past years – take a look at this Google graph of the growth in searches for the term!Capture

 

The idea behind using the brain’s ongoing neuroplasticity is that we can influence the connections between neurones by doing and thinking differently. Great idea, and definitely one we can use. There have been many discussions about how much we can influence plasticity – or not (this post refers to education and neuroplasticity, this to an old discussion about Norman Doidge’s book – and some of the points that have been omitted). Whatever the real situation, there’s no doubt that our brains do continue developing, forming and reforming connections between synapses and generally responding to our world and the interactions we have with our world via our bodies.

Pain researchers have been particularly enraptured by the idea that the brain can develop new connections, driven it seems by a greater understanding that our experience of pain is an integration of information from the body, modulated at every step of the way by both ascending and descending influences, right until that information is processed by various parts of our brain and, in combination with past experience, expectations, beliefs, predictions for the future, current goals and priorities and in our sociocultural context, produces what we know as pain. Long, long sentence – but you know what I mean!

So, the reasoning seems to go, if pain is an output of our nociceptive system and produced via all these interactions, then neuroplasticity should mean painful experiences can be reversed using the same principles. And yes! Lo and behold! In some cases this happens – vis all the research produced by Moseley and crew in Adelaide, and promoted by the NOI group, and others.

While Lorimer’s group has produced probably the most consistent body of work in relation to therapy based on neuroplasticity, with NOI promoting many of these approaches, it’s not the only group to do so.  Today I’m taking a look at Michael Moskowitz and Marla Golden’ book Neuroplastic Transformation: Your brain on pain, and the accompanying website.

I’ve been asked to take a look at this by a follower, and it’s been an interesting and fun project to work on.

The book is a spiral bound, colour printed A4 sized book with large print (yay!) and gorgeous illustrations of brain sections and neurones and other beautiful diagrams relevant to understanding the brain. The principles underpinning the book are that if we can understand a bit more about the brain, we can harness the functions so we can train our brain to be a little more settled and out of pain. The three neuroplastic rules are: What is fired is wired; What you don’t use you lose; When you make them you break them; when you break them you make them.  The premise is that it’s possible to reverse the changes that occur when a person is experiencing persistent pain – “treathment that uses the basic principles of neuroplasticity to change the brain pathways back to normal function and anatomy”. The authors discuss using thoughts, images, sensations, memories, soothing emotions, movements and beliefs to modify the experience.

The process of treatment involves four phases: Rescue, Adjustment, Functionality and Transformation, or RAFT. Rescue involves generating hope that pain can be changed by providing information about neuroplasticity, and developing a partnership between clinician and person living with pain. Adjustment involves “stabilising” the pain disorder – using a multi-modal approach including medications, injections, and psychosocial treatments to increase activities while reducing pain – emphasising that adjusting to the pain disorder is not the end goal. Functionality involves the person, every time he or she experiences pain, challenging the experience with non-painful stimuli. In other words, every time the person becomes aware of his or her pain, they need to use thoughts, beliefs, images, sensations, movements and emotions to “reverse the neuroplastic processes that cause persistent pain”. Finally, Transformation involves using the experience of overcoming pain to establish new ways to give pleasure.

What I like about this approach is that it is explained and illustrated very well, using up-to-date information and illustrations. It strongly supports self-management or the person being as much part of the treatment as any clinician. That’s good – because, as any of us who have ever tried to change a habit know very well, change is hard! And that’s probably one of the three main concerns I have about employing this approach as a core pain treatment.

My concerns:

  1. Reversing or altering cortical pathways is truly difficult – and it’s perhaps not possible to completely reverse, especially if the problem has been present for a long time. Here’s why: can anyone remember learning to ride a bike? Remember all that falling off, the wobbling, the stopping and starting, the weaving all over the place? How many hours did it take to learn to do that successfully, smoothly and to the point where you were safe to ride in traffic? Now, for some of you, it will have been YEARS since you jumped on a bike. Do you forget how to ride? No. You might wobble a bit, but you don’t actually forget. Similarly, in phobic states, pathways associated with avoiding the feared stimulus remain “wired together” even when new pathways associated with approaching the stimulus are developed. What this means is that it’s possible for a spider phobic to remain somewhat jumpy around a spider even after treatment has reduced the screaming heebie-jeebies. When we think about pain and the myriad associations between the experience, context, interoception (internal body feeling-sense), memories, emotions, language, treatment visits, investigations – there are so many connections that become wired together as a result of experiencing persistent pain that to completely reverse it is an almighty monumental challenge requiring hours or dedicated practice.
  2. While the principles of a neuroplastic approach are well-known, there are some differences in the approach depicted in this book that I’m not aware of being tested formally in pain research. For example, while it’s nice to have a pleasant smell or memory brought to mind, I’m not aware of studies showing that doing this changes memory for pain (or pain intensity). I may well be wrong about this and I’d love someone even more geeky than me to bring some studies to my attention.
  3. My third reservation relates to the well-established research showing that persistent pain is not easily changed, and meanwhile, in the pursuit of pain reduction, many people lose out on good things in life. While people are sitting in waiting rooms, spending time with therapists, monitoring and checking on pain intensity, it becomes very difficult to carry on with valued actions. There are many ways to make space to have your pain and live as well. This doesn’t mean you need to give up hope of pain reduction, but it does mean the focus moves from this as a life focus and on to the things that make life of any kind worthwhile. Maybe the two approaches can go hand in hand, but to my mind the very intensive nature of the approach within this book means that attention must be shifted away from valued actions and towards doing the things that this book argues will reverse pain.

Overall I like the approach within this book – I like that it’s person-centred, positive, uses underlying principles and encourages the person to be actively involved in his or her treatment. There’s no way you can be a passive recipient with this approach! I would love to see some more in-depth study of the effects of this treatment, even in a series of single-subject experiments. I think it could be very helpful, but I’m a little concerned at the focus on pain reduction as the primary goal, and the time and energy this approach demands.

Pain exposure therapy – what is it?


Thanks to an enquiry on my About page, I’ve been prompted to read a little about pain exposure therapy. This is a little-known approach to helping people with CRPS type I (the type that is NOT associated with a peripheral nerve injury. Type II is the same phenomenon but IS associated with an injury to the nerve.)

Graded exposure is an approach commonly adopted to help those people who are afraid of, or phobic about, a “thing”. Most of us will know about spider phobia treatment where people are progressively encouraged to stay with feelings of anxiety and distress while being shown and eventually handling a spider. Graded exposure has also been used to help people who are fearful of experiencing painful flare-ups and therefore avoid doing things – it’s been a successful approach especially for people who report high levels of pain catastrophising (or, as I like to put it, “freaking out” at fluctuations in pain). I’ve reported on graded exposure several times in my blog over the years, and use the approach myself with great success. BUT this approach requires some foundation skills for both the clinician AND the person living with pain.

Before I delve into the skills I think clinicians and people living with pain need, let me outline the treatment and it’s rationale.

The basis for this treatment is the idea that if pain is going to be present, and it no longer represents an indication of the state of the tissues, then avoiding movements is no longer necessary for tissue healing. At the same time, people generally don’t want to do things that flare pain up, and so they tend to avoid those movements. The issue is then much more about how to gradually get used to the fluctuations in pain (ie freak out less) while at the same time beginning to do things with the painful limb. Supporting this approach is some basic science that suggests the less we use an area of our body, the more distorted our brain’s representation of that area becomes.

So, after discussing basic information about pain and tissues, in pain exposure therapy, clinicians work together with the person living with pain to:

  • begin doing movements that are usually avoided
  • avoid responding to any behaviour that is usually associated with experiencing pain – things like grimacing, groaning, saying ouch, and rubbing the area
  • provide progressively more demanding input to the painful area despite changes in reported pain
  • encourage increased normal use of the area within daily life – eg holding onto bottles, cups, utensils, putting shoes and sox on, walking normally

In addition, clinicians use this type of therapy also prescribe many exercises to be carried out frequently through the day despite painful flareups. Sometimes clinicians will restrain the other unaffected limb so that the painful limb HAS to be used just to get things done.

Some of you reading this blog will be reminded of the work by Doidge in which a very similar approach is used during rehabilitation from stroke or traumatic brain injury – by using the limbs in a normal way, new neuronal pathways are developed, allowing the limb to eventually return to pretty much normal function.

Others of you will probably be saying “how cruel!” and “but Moseley and Butler say don’t do things that increase pain because – neurotags!”

Here’s my take on it.

Currently there exist very few, if any, randomised controlled trials of this approach for CRPS I. Actually, there are few RCTs for ANY form of CRPS and ANY treatment for CRPS.

This means we don’t have a great deal of evidence to go on when trying to decide the best approach for managing the functional problems experienced by people living with CRPS. We know that for some people mirror therapy is helpful, while there is less support for graded motor imagery (Bowering, O’Connel, Tabor, Catley et al, 2013).  We know there are very few pharmaceuticals that provide any pain reduction for people living with CRPS. There is “low quality evidence that bisphosphonates, calcitonin or a daily course of intravenous ketamine may be effective for pain when compared with placebo” (O’Connell, Benedict, McAuley, Marston et al, 2013), but otherwise very little else has been shown to have any effect at all either on pain intensity or function.

We do know that physiotherapy and occupational therapy focusing on function rather than pain reduction may have some longterm positive effects (O’Connell, Benedict, McAuley, Marston et al, 2013), and we also know that graded exposure treatments for other types of pain problem, especially low back pain, have been effective (studied since 2001).

BUT here’s the thing. Unless the person living with chronic pain is comfortable with the idea that this approach directly confronts their fear of painful flare-ups, it’s just not going to float. Both the clinician and the person living with pain need to understand the underlying principles of this approach – and have some skills to deal with the very likely distress that will emerge when pain inevitably flares up.

What we should also know is that this approach does not try to reduce pain – although for many people, according to one study (Barnhoorn, Oostendorp, van Dongen et al, 2012) pain does reduce. Yet for others, pain increases – but people can do more.

Where do I stand on this?

I think it’s worth a try but only if the person conducting the therapy is VERY comfortable with the underlying principles of graded exposure as it’s used for phobia. AND has skills to manage their own discomfort at seeing someone else experiencing high levels of distress. To me this means having had some additional training in graded exposure for phobia, and lots of practice at using mindfulness and other forms of maintaining empathy despite seeing another person being distressed. It’s not easy to be empathic without either losing your own cool – or “giving in” to the distress of the person – and that just undoes the therapy.

It also means the person participating in the therapy, ie the patient, must be completely on board with it, and not just the person but also his/her healthcare team AND family. AND have some skills to deal with distress that comes with exacerbations of pain. This approach is not for the faint-hearted, or for anyone who feels coerced into participating in the treatment without feeling very confident that they can maintain their involvement.

 

Barnhoorn, K. J., van de Meent, H., van Dongen, R. T. M., Klomp, F. P., Groenewoud, H., Samwel, H., . . . Staal, J. B. (2015). Pain exposure physical therapy (pept) compared to conventional treatment in complex regional pain syndrome type 1: A randomised controlled trial. BMJ Open, 5(12), e008283. doi:10.1136/bmjopen-2015-008283

Barnhoorn, K. J., Oostendorp, R. A., van Dongen, R. T., Klomp, F. P., Samwel, H., van der Wilt, G. J., . . . Frolke, J. P. (2012). The effectiveness and cost evaluation of pain exposure physical therapy and conventional therapy in patients with complex regional pain syndrome type 1. Rationale and design of a randomized controlled trial. BMC Musculoskeletal Disorders, 13, 58.

Barnhoorn, K. J., Staal, J. B., van Dongen, R. T., Frolke, J. P., Klomp, F. P., van de Meent, H., . . . Nijhuis-van der Sanden, M. W. (2014). Are pain-related fears mediators for reducing disability and pain in patients with complex regional pain syndrome type 1? An explorative analysis on pain exposure physical therapy. PLoS ONE [Electronic Resource], 10(4), e0123008

Bowering, K. J., O’Connell, N. E., Tabor, A., Catley, M. J., Leake, H. B., Moseley, G. L., & Stanton, T. R. (2013). The effects of graded motor imagery and its components on chronic pain: A systematic review and meta-analysis. Journal of Pain, 14(1), 3-13

Ek, J. W., van Gijn, J. C., Samwel, H., van Egmond, J., Klomp, F. P., & van Dongen, R. T. (2009). Pain exposure physical therapy may be a safe and effective treatment for longstanding complex regional pain syndrome type 1: A case series. Clinical Rehabilitation, 23(12), 1059-1066.

O’Connell Neil, E., Wand Benedict, M., McAuley, J., Marston, L., & Moseley, G. L. (2013). Interventions for treating pain and disability in adults with complex regional pain syndrome- an overview of systematic reviews. Cochrane Database of Systematic Reviews, (4).

van de Meent, H., Oerlemans, M., Bruggeman, A., Klomp, F., van Dongen, R., Oostendorp, R., & Frolke, J. P. (2011). Safety of “pain exposure” physical therapy in patients with complex regional pain syndrome type 1. Pain, 152(6), 1431-1438.

Stigma and chronic pain


Stigma is about devaluing and discrediting behaviours made by people towards those who have or are “different” from the average Joe or Josie Bloggs. For people experiencing and living with chronic pain, stigma may occur because the “average” experience of pain is associated with actual or potential tissue damage (or described in these terms) and for most chronic pain the “issues in the tissues” are less than expected by people holding a biomedical viewpoint.  Add to this that most people in the world know about acute pain which settles as expected whereas chronic pain persists, seems “disproportionately” bad in comparison with what’s expected.

De Ruddere and Craig (in press) have reviewed the literature to understand what is known about stigma and chronic pain, and what can be done about it. I thought it an apt paper to include in this blog because almost every person with chronic pain has, at some point, said they don’t feel their pain is either being taken seriously, or is accepted as real, or feel like they’re not being believed. Of course, pain is not the only condition where self-report is the only thing that we can use to determine the experience – depression, anxiety, post-concussion syndrome, fatigue are among the common experiences that are not given the kind of acknowledgement that we give to fractures or appendicitis or asthma.

People living with chronic pain say their partners, family and friends don’t seem to believe them, and that health professionals think their pain is exaggerated, imagined. They feel they’re being told it’s their fault, to “pull yourself together”, just “harden up” and often feel they’re being told to go away because they don’t have a real problem. Whether this is in fact the case undoubtedly depends on the persons involved – but it’s a common story and one I’ve heard in my clinical experience over and over and over again.

I guess some of the worst things I hear about stigma is that experienced by people seeking help for their pain from health professionals. If things don’t seem to add up, in the eyes of the observer, then people experiencing chronic pain can get less sympathy, are disliked, thought of as less meriting help, and often suspected of simply wanting attention.

The effect of this kind of behaviour from those charged with the duty to care is on distress and disability. People who feel misunderstood or maligned by treatment providers may receive less care and as a result, are able to do less, and feel rejected – social rejection and chronic pain share some similar neurobiological pathways (Eisenberger, 2012). Additionally, because the people experiencing the pain probably also hold similar beliefs to those who reject them (because the most common beliefs about pain are that there’s something going on in the tissues, and pain should fit with that tissue damage), they begin to doubt themselves, question their own responses, wonder if they really are as badly off as they feel. I know I felt this during my recovery from mild traumatic brain injury, when I wondered if I was actually just wanting a break from having to do things – yet at the same time I couldn’t doubt the performance deficits I experienced every day, and the need to sleep for several hours a day because otherwise I just could not function.

De Ruddere and Craig posit some reasons for other people stigmatising those living with chronic pain. One is that with acute pain, behavioural responses are often involuntary, automatic responses such as reflex withdrawal, vocalisations (groaning), or facial expressions. These elicit a primitive caring response in most people. Yet with chronic pain, many of the responses are less reflexive, and more voluntary – such as withdrawing from doing things or describing pain. These are usually thought to indicate that we’ve thought about them, and we’re doing them on purpose or deliberately.  When these behaviours take place alongside the general belief that pain “should” be acute and related to tissue damage, not showing automatic pain behaviours begins to look kinda fishy.

In evolutionary biology, altruistic behaviour towards others is based on an underlying assumption that if we do to others, they will do to us in turn. A sort of reciprocity. When people don’t look like they’re genuinely in pain (ie their behaviours aren’t the same as those carried out with acute pain), suspicions rise – “Are you really hurt, or are you wanting to get something for nothing?”

De Ruddere and Craig suggest some other theoretical explanations for the high level of suspicion applied to people with chronic pain, but I think this evolutionary one is an especially challenging one to deal with. Most treatment approaches attempt to upskill people living with pain to be able to communicate their problems effectively, and to reduce the frequency and interference of pain behaviour. This is only half the answer. We need to continue giving healthcare providers a deep understanding of a biopsychosocial approach: that pain is ALWAYS involves biological processes, psychological processes and is set within a social context, so that healthcare delivery goes well beyond assuming that “if the pain is gone the person is back to normal”.

Get this paper once it comes out in print. I think it’s time the social aspects of our pain management treatments were given more airtime, and this paper provides some exciting direction for future research and clinical practice.

 

 

 

De Ruddere L & Craig KD. (2012). Understanding stigma and chronic pain: a state of the art review. Pain.

Eisenberger NI. The pain of social disconnection: examining the shared neural underpinnings of physical and social pain. Nature Reviews Neuroscience 2012;13(6):421-434.DOI: 10.1038/nrn3231

Waitangi Day – or how to live together in unity


Today is New Zealand’s Waitangi Day ‘Mondayisation’ – the actual day was Saturday 6th Feb. It’s an important day in New Zealand because it’s the day when two completely different nations signed a treaty allowing certain rights between them – and allowed my ancestors to travel from Ireland and England to settle in the country I call my home. Unlike many country’s celebrations of nationhood, Waitangi Day is almost always a time of turbulence, dissension and debate. This is not a bad thing because over the years I think the way in which Maori (Tangata Whenua, or original settlers) and non-Maori settlers (Tangata Tiriti) relate in our country is a fantastic example of living together well. Not perfectly – but certainly in a more integrated way than many other countries where two completely different cultures blend.

Thinking of Waitangi Day, I’m reminded of the way in which the multidimensional model of pain attempts to integrate biological, psychological and social factors to help explain this experience and how such a primitive response to threat can ultimately lead to adaptation and learning – in most cases – or the most profound misery and disability in others.

Like the treaty relationship in New Zealand, there’s much room for discussion and debate as to the relative weight to place on various components of the model.  And like the treaty relationship, there are times when each part is accused of dominating and not giving the other/s due credit. Truth, at least to me, is, we need all of us (and all the factors) to integrate – not to become some bland nothing, but to express the components fully.

Just last week I was astonished to find that a clinician thought that I believed low back pain is “psychological”. Absolutely astonished because this has never been my position! While this blog and much of my teaching and reading is around psychological and more recently social factors influencing pain and disability, my position has never been to elevate the influence of these factors over the biological. I suppose I shouldn’t be surprised – it’s hard to deal with the state of play in our understanding of low back pain which finds that many of the assumed causal mechanisms (like disc prolapses, poor “core” muscles, the biomechanics of lifting and so on) just don’t apply. It’s also really difficult to know that so far there are no particular exercise treatments that work more effectively than any other. Cognitive dissonance anyone? Just because these factors are less relevant than presumed does not mean that (a) I think low back pain is psychological and (b) that all biological factors are irrelevant. What it does mean is that we don’t know. I’ll say that again. We. Don’t. Know. Most back pain falls into this “nonspecific” group – and by calling it “nonspecific” we are actually admitting that We. Don’t. Know.

How do people assume that because I point out that we don’t know the causal mechanisms of low back pain but we DO know the critical importance of psychosocial factors on disability associated with low back pain – and the treatments that can mitigate these factors – that I believe back pain is psychological? I think it’s a simple fallacy – some people believe that because a person responds to psychosocial interventions this therefore means their problem is psychological. This is not true – and here are some examples. Exercise (a physical modality) is shown to be an effective treatment for depression. Does this mean depression is a purely biological disorder? Biofeedback provides visual or auditory information related to physical aspects of the body like blood pressure, heart rate, and muscle tension – does this mean that blood pressure is “psychological”? Diabetes management often includes learning to resist the urge, or “urge surf” the impulse to eat foods that increase blood sugar levels – does this mean diabetes is psychological?

Here’s my real position on nonspecific low back pain, which is let me remind you, the most common form of low back pain.

Causes – not known (Golob & Wipf, 2014), risk factors for onset are mainly equivocal but one study found the major predictor of an onset was – prior history of low back pain, with “limited evidence that the combination of postural risk factors and job strain is associated with the onset of LBP” (Janwantanakul, Sitthipornvorakul,  & Paksaichol, 2012), exercise may prevent recurrence but mechanisms of LBP remain unclear (Macedo, Bostick and Maher, 2013), while subgroup analysis carried out by therapists were “underpowered, are only able to provide exploratory or insufficient findings, and have rather poor quality of reporting” (Mistry, Patel, Wan Hee, Stallard & Underwood, 2014).

My take from this brief review? The mechanisms presumed to be involved in nonspecific low back pain are unknown.

Treatments – mainly ineffective but self-management provides small effects on pain and disability (moderate quality) (Oliveira, Ferreira, Maher, Pinto, Refshauge & Ferreira, 2012), “the evidence on acupuncture for acute LBP is sparse despite our comprehensive literature search” (Lee, Choi, Lee, Lee, Shin & Lee, 2013), no definitive evidence supports the use of orthoses for spine pain (Zarghooni, Beyer, Siewe & Eysel, 2013), acetaminophen is not effective for pain relief (Machado, Maher, Ferreira, Pinheiro, Lin, Day et al, 2015), and no specific exercises are better than any other for either pain relief or recovery – not even motor control exercises (Saragiotto, Maher, Yamato, Costa et al, 2016).

My take from this set of references is that movement is good – any movement, but no particular form of exercise is better than any other. In fact, the main limitation to exercise is adherence (or actually continuing exercising after the pain has settled).

The factors known to predict poor recovery are pretty clear – catastrophising, or thinking the worst (Kim, Cho, Kang, Chang, Lee, & Yeom, 2015), avoidance (usually arising from unhelpful beliefs about the problem – see commentary by Schofferman, 2015), low mood – which has also been found to predict reporting or treatment seeking of low back pain (see this post from Body in Mind, and this one).

What can I take from all of this? Well, my view is that because psychosocial factors exert their influence at multiple levels including our nervous system (see Borkum, 2010), but also our community understanding of what is and isn’t “illness” (Jutel, 2011) and who to see and what to do about it, the problem of nonspecific low back pain is one of the purest forms of an integrated biopsychosocial and multifactorial health concern in human life. I therefore rest my case: nonspecific low back pain is not psychological, but neither is it biomechanical or biological only. It is a biopsychosocial multifactorial experience to which humans are prone.

The best we can do with our current knowledge base is (1) limit and avoid the use of nocebic language and attempts to explain low back pain via biomechanical or muscle control mechanisms, (2) be honest about the likelihood of low back pain recurring and our treatments essentially doing very little, and (3) encourage return to normal activity by doing normal activity including exercise. Being honest about the state of play in our knowledge is a good starting point for better understanding – sounds a lot like race relations, doesn’t it?

 

Borkum, J. M. (2010). Maladaptive cognitions and chronic pain: Epidemiology, neurobiology, and treatment. Journal of Rational-Emotive & Cognitive Behavior Therapy, 28(1), 4-24. doi:http://dx.doi.org/10.1007/s10942-010-0109-x

Golob, A. L., & Wipf, J. E. (2014). Low back pain. Medical Clinics of North America, 98(3), 405-428.

Janwantanakul, P., Sitthipornvorakul, E., & Paksaichol, A. (2012). Risk factors for the onset of nonspecific low back pain in office workers: A systematic review of prospective cohort studies. Journal of Manipulative & Physiological Therapeutics, 35(7), 568-577.

Jutel, A. (2011). Classification, disease, and diagnosis. Perspectives in Biology & Medicine, 54(2), 189-205.

Kim, H.-J., Cho, C.-H., Kang, K.-T., Chang, B.-S., Lee, C.-K., & Yeom, J. S. (2015). The significance of pain catastrophizing in clinical manifestations of patients with lumbar spinal stenosis: Mediation analysis with bootstrapping. The Spine Journal, 15(2), 238-246. doi:http://dx.doi.org/10.1016/j.spinee.2014.09.002

Lee, J. H., Choi, T. Y., Lee, M. S., Lee, H., Shin, B. C., & Lee, H. (2013). Acupuncture for acute low back pain: A systematic review. Clinical Journal of Pain, 29(2), 172-185.

Macedo, L. G., Bostick, G. P., & Maher, C. G. (2013). Exercise for prevention of recurrences of nonspecific low back pain. Physical Therapy, 93(12), 1587-1591.

Machado, G. C., Maher, C. G., Ferreira, P. H., Pinheiro, M. B., Lin, C.-W. C., Day, R. O., . . . Ferreira, M. L. (2015). Efficacy and safety of paracetamol for spinal pain and osteoarthritis: Systematic review and meta-analysis of randomised placebo controlled trials. BMJ, 350, h1225.

Mistry, D., Patel, S., Hee, S. W., Stallard, N., & Underwood, M. (2014). Evaluating the quality of subgroup analyses in randomized controlled trials of therapist-delivered interventions for nonspecific low back pain: A systematic review. Spine, 39(7), 618-629.

Oliveira, V. C., Ferreira, P. H., Maher, C. G., Pinto, R. Z., Refshauge, K. M., & Ferreira, M. L. (2012). Effectiveness of self-management of low back pain: Systematic review with meta-analysis. Arthritis care & research, 64(11), 1739-1748.

Saragiotto Bruno, T., Maher Christopher, G., Yamato Tiê, P., Costa Leonardo, O. P., Menezes Costa Luciola, C., Ostelo Raymond, W. J. G., & Macedo Luciana, G. (2016). Motor control exercise for chronic non-specific low-back pain. Cochrane Database of Systematic Reviews, (1).

Schofferman, J. A. (2015). Commentary on the significance of pain catastrophizing in clinical manifestations of patients with lumbar spinal stenosis: Mediation analysis with bootstrapping. The Spine Journal, 15(2), 247-248. doi:http://dx.doi.org/10.1016/j.spinee.2014.11.003

Zarghooni, K., Beyer, F., Siewe, J., & Eysel, P. (2013). The orthotic treatment of acute and chronic disease of the cervical and lumbar spine. Deutsches Arzteblatt International, 110(44), 737-742.