Pain

Knee pain – not just a simple case of osteoarthritis


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

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

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

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

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

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

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

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

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

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

 

 

 

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

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

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

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

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

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

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

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


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

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

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

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

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

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

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

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

 

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

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

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

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

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

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

The “Subjective” – and really hearing


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

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

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

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

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

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

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

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

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

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

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

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

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

 

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

Mulling over the pain management vs pain reduction divide


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

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

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

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

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

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

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

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

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

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

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

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

 

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

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

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

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

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


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

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

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

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

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

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

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

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

Three strategies to consider:

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

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

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

 

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

 

Does central sensitisation matter?


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

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

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

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

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

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

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

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

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

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

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

 

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

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

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

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

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

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

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.

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 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)