Research

Knee pain – not just a simple case of osteoarthritis


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

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

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

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

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

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

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

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

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

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

 

 

 

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

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

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

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

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

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

Conversations about cannabis for chronic pain


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

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

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

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

Why might I support a change to marijuana laws?

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

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

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

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

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

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

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

My conclusion?

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

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

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

 

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

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

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.

Primary pain disorders


In a move likely to create some havoc in compensation systems around the world (well, at least in my corner of the world!), the International Association for the Study of Pain has worked with the World Health Organisation to develop a way to classify and thus record persistent pain conditions in the new (draft) ICD-11. While primary headache disorder has been in the classification for some years, other forms of persistent pain have not. Recording the presence of a pain disorder is incredibly important step forward for recognising and (fingers crossed) funding research and treatment into the problem of persistent pain. As the IASP website states:

Chronic pain affects an estimated 20 percent of people worldwide and accounts for nearly one-fifth of physician visits. One way to ensure that chronic pain receives greater attention as a global health priority is to improve the International Classification of Diseases (ICD) diagnostic classification.

The classifications are reasonably straightforward, with an overall classification of “chronic pain”, and seven subcategories into which each type of pain can be placed.

Now there will be those who are uncomfortable with labelling a symptom (an experience, aporia, quale) as a separate diagnosis. I can understand this because pain is an experience – but at the same time, just as depression, which is an experience with clinical and subclinical features, so too is pain. There is short-term and useful pain, serving as an alert and warning, and typically an indication of the potential or actual threat to bodily integrity. Just as in depression which has short-term and usually useful episodes of sadness, withdrawal and tearfulness (as in grief). At the same time, there are periods when sadness becomes intractable and unhelpful – and we call this depression. Underlying both of these situations are biological processes, as well as psychological and social contributors. Until now, however, persistent pain has remained invisible.

The definition of chronic pain, at this time, is the IASP one from the 1980’s:

“Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. Often, pain serves as a symptom warning of a medical condition or injury. In these cases, treatment of the underlying medical condition is crucial and may resolve the pain. However, pain may persist despite successful management of the condition that initially caused it, or because the underlying medical condition cannot be treated successfully.

Chronic pain is pain that persists or recurs for longer than three months. Such pain often becomes the sole or predominant clinical problem in some patients. As such it may warrant specific diagnostic evaluation, therapy and rehabilitation. Chronic pain is a frequent condition, affecting an estimated 20% of people worldwide. This code should be used if a pain condition persists or recurs for longer than 3 months.”

Chronic Primary Pain is defined as “…chronic pain in one or more anatomical regions that is characterized by significant emotional distress (anxiety, anger/frustration or depressed mood) and functional disability (interference in daily life activities and reduced participation in social roles). Chronic primary pain is multifactorial: biological psychological and social factors contribute to the pain syndrome. The diagnosis is appropriate independently of identified biological or psychological contributors unless another diagnosis would better account for the presenting symptoms. Other chronic pain diagnoses to be considered are chronic cancer pain, chronic postsurgical or posttraumatic pain, chronic neuropathic pain, chronic headache or orofacial pain, chronic visceral pain and chronic musculoskeletal pain. Patients with chronic primary pain often report increased depressed and anxious mood, as well as anger and frustration. In addition, the pain significantly interferes with daily life activities and participation in social roles. Chronic primary pain is a frequent condition, and treatment should be geared towards the reduction of pain-related distress and disability.” (definition are found here)

The definition doesn’t require identified biological or psychological contributors – so people with primary pain would be those who have fibromyalgia, persistent low back pain, perhaps even “frozen” shoulder. The main requirement is that the person is distressed by it, and that it interferes with life. Now here’s a bit of a problem for those of us who have learned to live well with our persistent pain – I experience widespread pain, but generally I’m not distressed by it, and seeing as I’ve lived with it since my early 20’s, I find it hard to work out whether I’m limited by it, or whether I’ve just adjusted my life around it, so it doesn’t really get in the way of what I want to do. Technically, using the draft definition, I might not be given the label. Does this mean I don’t have chronic primary pain?

Why did I suggest compensation systems might be interested in this new classification? Well, in New Zealand, if a person has a pre-existing condition, for example they have osteoarthritic changes in their spine even if it’s not symptomatic (ie it doesn’t hurt), and then lodges a claim for a personal injury caused by accident, they may well find their claim for cover is declined.  What will happen if someone who has fibromyalgia, has an accident (say a shoulder impingement from lifting something heavy overhead), and the problem fails to settle? I think it’s possible they’ll have their claim declined. Low back pain is probably the most common primary pain disorder. Thousands of people in New Zealand develop low back pain each year. Few will have relevant findings on imaging – and even if imaging shows something, the potential for it to be directly related to the onset of low back pain is open to debate. Especially if we consider low back pain to be a condition that doesn’t just appear once, but re-occurs thereafter (1-7). What will this mean for insurers?

I don’t know where this classification will lead insurers, but from my perspective, I can only hope that by incorporating chronic pain into the ICD-11 we will at least begin to show just how pervasive this problem is, and how many people need help because of it. And maybe, just maybe, governments like the New Zealand government, will begin to take persistent pain seriously and make it a national health priority.

  1. 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.
  2. 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.
  3. 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.
  4. Hoy, D., March, L., Brooks, P., Blyth, F., Woolf, A., Bain, C., . . . Buchbinder, R. (2014). The global burden of low back pain: Estimates from the global burden of disease 2010 study. Annals of the Rheumatic Diseases, 73(6), 968-974.
  5. Campbell, P., Foster, N.E., Thomas, E., & Dunn, K.M. (2013). Prognostic indicators of low back pain in primary care: Five-year prospective study. Journal of Pain, 14(8), 873-883.
  6. 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
  7. Hoy, D. G., Smith, E., Cross, M., Sanchez-Riera, L., Buchbinder, R., Blyth, F. M., . . . March, L. M. (2014). The global burden of musculoskeletal conditions for 2010: an overview of methods. Annals of the Rheumatic Diseases, 73(6), 982-989. doi:10.1136/annrheumdis-2013-204344

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


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

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

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

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

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

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

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

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

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

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

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

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

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

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

The take-home messages from this study are these:

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

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

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

…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.

Is central sensitisation really a thing?


It seems odd to me that there’s much argument about central sensitisation in pain circles. I thought the idea of central sensitisation was well-established based on research from some years ago – but apparently there are still arguments about its relevance, and lots of debate about how to identify it clinically. This post is based mainly on a presentation by Jo Nijs from Pain in Motion, at the recent NZ Pain Society meeting in Nelson. In this post I want to briefly review the material presented by Jo suggesting that central sensitisation is a thing. I’ll write more about assessment in a future blog, or this post will be the longest ever!

Firstly, what is it and why should it matter? Researchers have long been aware that when a nerve is repeatedly stimulated, in future stimulation it will respond for longer and with more intensity – this is called long-term potentiation. Recently, the contribution of glial cells to this situation has been identified (remember glia? Those little cells whose purpose no-one really knew? Turns out they release gliotransmitters that circulate throughout the spinal cord and allow information to be transmitted widely, far from the original source of stimulation – see Kronschlager, Drdla-Schutting, Gassner, Honsek et al, (2016). Glial cells occur widely throughout the central nervous system, and while LTP is a process we’ve known about in the CNS for some time – we’ve known because this is how “memories” are formed (remember “nerves that fire together wire together”? Pathways that frequently activate develop the tendency to continue to activate together) – we’ve perhaps not been aware that this occurs in the spinal cord as well. So, LTP occurs in both the spinal cord and the brain, and there is more than one way this process is facilitated. Glial cells are one. Central sensitisation involves this process of long-term potentiation across and amongst pathways within our nervous system – it means information from peripheral regions like your big toe are more likely to be transmitted to areas in the brain responsible for attending and responding to threatening information.

Why does this matter? Well, if we think of ourselves as a finely tuned homeostatic machine, one that wants to remain in a stable state, we can think of two systems balanced with one another. One system works to facilitate information transmission (nociceptive facilitation), while the other works to reduce or modulate this transmission (endogenous hypoalgesia). If we continue with the machine analogy, we want to know about “trouble” as soon as possible – so our nociceptive facilitatory system is like an accelerator, working promptly to make sure we know about the state of play very quickly. If you’ve ever driven a race car, you’ll know how twitchy the accelerators are! The brakes on this system is our endogenous opioid system which reduces the influence of the nociceptive system so we can keep moving forward. If the brakes fail, for whatever reason, in a race car we’ll burst forward! Similarly, if the endogenous modulatory system fails, for whatever reason, far more information ascends to relevant regions in the brain for interpretation – and ouch.

What sorts of things enhance connectivity between areas of the brain that deal with nociceptive information? Well, this is where things get all woolly and psychosocial for a while (sorry guys!). From many fMRI studies, it’s possible to establish that “pain catastrophising” or the tendency to brood on pain, feel helpless about it, and regard the pain as seriously intense activates brain areas like the dorsolateral prefrontal cortex, the anterior cingulate cortex, and the insula, which in term reduces the efficiency of the opioid analgesic system (that endogenous opioid system), makes it harder to distract attention from the pain, and increases facilitation (ie the transmission of nociceptive information from lower CNS to higher). In other words, this very psychological construct has a biological component to it.

Central sensitisation has been identified in many different pain problems, ranging from osteoarthritis in the knee (Akinci, Al Shaker, Chang, et al, 2016), post-cancer pain (Lam, 2016), shoulder pain (Sanchis, lluch, Nijs, Struyf & Kangasperko, 2015), and yes, those messy complicated ones like whiplash (Coppieters, Ickmans, Cagnie, Nijs, et al, 2015), low back pain (Sanzarello, Merlini, Rosa, Perrone et al, 2016) and fibromyalgia (Walitt, Ceko, Gracely & Gracely, 2016). Rates of central sensitisation vary from 10% in shoulder pain to 100% in fibromyalgia. For some good reading on central sensitisation in these disorders, take a look at the references I’ve cited.

So yes, central sensitisation is a thing, and it results in increased pain experiences that last longer and spread. Why do some people experience while others don’t? Now we’re venturing into rather more speculative areas, but some findings seem clinically useful. People who have, in their early years, experienced physical and/or psychological trauma, those who tend to catastrophise or have unhelpful beliefs (often inaccurate beliefs) about their pain,  those who have poor sleep, and those who have an elevated stress response seem more likely to have pain that fits with what we’d expect with central sensitisation (See Nijs & Ickmans, 2014).

Why does this occur? Well, stress increases release of glutamate and this in turn increases CNS excitability (makes sense – let’s react faster to everything, at least for a short time). At the same time, stress reduces GABA and serotonin, and as a result inhibition is reduced (the brakes come off). If we add microglial activity to the mix (remember that’s going to increase the connectivity between neurones), and if we add ongoing release of adrenaline in because the stress has been continuing for a while, we’re going to end up with activated glial activity in the prefrontal cortex, amygdala and hippocampus, all important areas for detecting salience and making decisions to act. These glial cells release chemicals known to increase neuroinflammation, reducing hippocampal activity (ultimately reducing volume of neurones in this area), increasing the size of the amygdala (which means it’s more capable of responding to threat), and reducing the prefrontal cortex size, reducing the capacity to make considered decisions (Kregel, Meeus, Malfliet et al, 2015). Ew… nasty! In longterm stressful situations, it seems our brains adapt – and not in a helpful way when it comes to experiencing pain. Whatever you do DON’T say to your patients  “Oh and by the way, your back pain means your brain is inflamed and parts of your brain are shrinking” – this is NOT helpful!

Next post I’ll discuss assessing for central sensitisation – but before I do, remember that central sensitisation is not the only factor at play in ongoing pain. In fact, some people don’t seem to develop central sensitisation even with ongoing nociception from either disease processes, or inflammation. We don’t really know why. What we do know is that simply treating peripheral nociceptive input when central sensitisation is present may fail to help the person – so keeping an eye out for it is important.

 

Akinci, A., Al Shaker, M., Chang, M. H., Cheung, C. W., Danilov, A., Jose Duenas, H., . . . Wang, Y. (2016). Predictive factors and clinical biomarkers for treatment in patients with chronic pain caused by osteoarthritis with a central sensitisation component. International Journal of Clinical Practice, 70(1), 31-44.

Coppieters, I., Ickmans, K., Cagnie, B., Nijs, J., De Pauw, R., Noten, S., & Meeus, M. (2015). Cognitive performance is related to central sensitization and health-related quality of life in patients with chronic whiplash-associated disorders and fibromyalgia. Pain Physician, 18(3), E389-401.

Kregel, J., Meeus, M., Malfliet, A., Dolphens, M., Danneels, L., Nijs, J., & Cagnie, B. (2015). Structural and functional brain abnormalities in chronic low back pain: A systematic review☆. Paper presented at the Seminars in arthritis and rheumatism.

Kronschläger, M. T., Drdla-Schutting, R., Gassner, M., Honsek, S. D., Teuchmann, H. L., & Sandkühler, J. (2016). Gliogenic ltp spreads widely in nociceptive pathways. Science, 354(6316), 1144-1148. doi:10.1126/science.aah5715

Lam, D. K. (2016). Emerging factors in the progression of cancer-related pain. Pain Management, 6(5), 487-496.

Nijs, J., & Ickmans, K. (2014). Chronic whiplash-associated disorders: To exercise or not? The Lancet, 384(9938), 109-111.

Sanchis, M. N., Lluch, E., Nijs, J., Struyf, F., & Kangasperko, M. (2015). The role of central sensitization in shoulder pain: A systematic literature review. Seminars in Arthritis & Rheumatism, 44(6), 710-716.

Sanzarello, I., Merlini, L., Rosa, M. A., Perrone, M., Frugiuele, J., Borghi, R., & Faldini, C. (2016). Central sensitization in chronic low back pain: A narrative review. Journal of Back & Musculoskeletal Rehabilitation, 29(4), 625-633.
Walitt, B., Ceko, M., Gracely, J. L., & Gracely, R. H. (2016). Neuroimaging of central sensitivity syndromes: Key insights from the scientific literature. Current Rheumatology Reviews, 12(1), 55-87.

A surfeit of learning


It’s been a busy few weeks as I’ve been at the San Diego Pain Summit and then the New Zealand Pain Society meeting where wonderful speakers presented on topics like exercise for pain, cognitive functional therapy, central sensitisation, opioid use in New Zealand, sensory profiles and other such topics. The chance to meet and spend time with clinicians who are passionate to not only learn about pain, but apply what they’ve learned in clinical practice is something I can’t miss.

What’s difficult, though, is deciding what to apply on Monday morning after having been to meetings or events where there’s so much new material to absorb. And that’s one of the problems, I think, in our clinical practice today. The years when it was relatively easy to do the same old, same old, have (thankfully!) gone – but in its place is the challenge of sifting through that new information and deciding what and how to do it.

So today I thought I’d go through some of the practices I’ve used – maybe it will help someone else?

Firstly, I try to take just one thing away from a meeting. If I absorb more than this, it’s fine, but one new thing is usually quite enough for me! Someone made the point that changing habits is hard – and, just for a moment, think about what we expect the people we treat to do, and then think about that last conference and what you intended to do, but just didn’t… Without  intention, planning and support to change what you do, you’ll carry on doing what’s easy, what’s worked before, and what feels “comfortable”. So be kind to yourself and pick just one thing. For me, that one thing is to feel OK about teaching people to ask “and what does that mean to you?” when someone is telling me their story about their pain.

Next, I let the rest of the information I heard just sit and percolate a while. This means I might casually read something related, or I might review the speaker’s slides or recordings, but I don’t do this in a way that I’m madly trying to cram in action points. This is because I’ve chosen one thing to do, and that’s enough. The rest of the information won’t just disappear because I’m letting it rest, it’s just going to connect with other concepts and pop out later when I stumble on it while reading something else.

To apply what I’ve learned, I plan. Yep, you heard it, I plan! Just like our clients, we need to make specific action plans if we’re going to do things differently. I think there are two factors to apply: the first is how important I think the concept/action is to me, the second is how confident I am to make a change.

  1. Importance: While simply selecting the single thing I take away from a meeting implies that I think it’s important, it’s worth considering why I decided it’s so important. So I list a few reasons I valued that concept. For me, it was the idea that we can uncover more of the real concerns of a person if we ask what it means to them, we can be more able to hear what the person really wants. I also took the idea that anyone: PT, OT, MT, Osteo, Chiro, Doc, Nurse ANYONE can ask this question. This is important to me because if that question isn’t asked, the person may go on fearing the worst even if they appear to be “doing well”. And we cannot rely on “someone else” asking this question. Even if we’re not psychologists, and so think that beliefs and attitudes are out of scope, we ARE experts in how the human body works. We know structure and function. This means we have a responsibility to help people understand what’s going on their body rather than living in ignorance or confusion.
  2. Confidence: It’s not enough to think that something is important. We need to make it easy to make a change. This means identifying what might get in the way of change and planning around that. It also means identifying what might make it easy to change and structuring life so it’s not hard. It could mean writing some “cheat sheets” giving brief phrases to use (Alison Sim and I used this approach in our recent workshop), or it might mean a poster in a prominent place to act as a reminder. It might mean removing something from the environment so you don’t use it as easily. It could mean simplifying for a couple of times. For me it will mean working through possible arguments people make against asking those questions about meaning, using open-ended questions. Often the questions relate to time available in clinic, scope of practice questions, “opening Pandora’s box” questions, “what do I say next” questions, or the “it’s not my focus” questions. I’ll work on responses to these in advance so I can explore what these mean to the clinician before asking if it’s OK to explain my perspective.

I ask myself “what would it look like if I applied this new strategy?”, or “how would I know I was using this strategy?”. I also take time to review how I’ve gone using that new strategy – recording myself, asking someone to sit in on a session, even just reviewing against the “cheat sheet” to see what I used, and what I could have used.

If you take a moment to review my process, hopefully you’ll see the elements of a motivational approach to behaviour change. I’ve written quite a bit about motivation – hope this helps you too!

 

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)