Chronic pain

blossom of snow

Deciding when to say when: pain cure? or pain managed?


I think the subject of this post is the singularly most important yet neglected topic in chronic pain research today. When is it time to say “All this looking at pain cure, or reducing your pain isn’t working, it’s time to accept that pain is going to part of your life.” It’s difficult for so many reasons whether you’re the person experiencing the pain, or the clinician trying to help. It’s also incredibly important for everyone including our community.

Cures for pain that persists are not easily found. One possibility is that the underlying disease or dysfunction has not yet been treated – pain in this case is the experience we have when there’s an unresolved threat to body tissues. Find the source of the problem, treat it, and voila! No pain.

Another possibility is that a new or groovy treatment has been developed – something extraordinary, or something that’s being applied to a different problem or something that’s emerging from the experimental phase to clinical practice.  This means clinicians need to have heard about it, maybe will have had to think hard about their clinical reasoning, have developed skills to apply it, and be ready to talk about it with the person they’re treating.

In the case of much chronic pain, pharmacological approaches simply do not work. Machado and colleagues (2009), in a large meta-analysis of placebo-controlled randomised trials, found 76 eligible trials reporting on 34 treatments. Fifty percent of the treatments had statistically significant effects, but for most the effects were small or moderate … the analgesic effects of many treatments for non-specific low back pain are small”, while Machado, Maher and colleagues found that paracetamol was “ineffective” for reducing pain intensity or improving quality of life for people with low back pain, and although there was a statistically significant result for paracetamol on osteoarthritis pain (hip or knee), this was not clinically important (Machado, Maher, Ferreira, Pinheiro, Lin, et al_2015).  Clifford Woolf said “most existing analgesics for persistent pain are relatively ineffective… the number of patients who are needed to be treated to achieve 50% reduction in neuropathic pain in one patient is more than four – a high cost for the three unsuccessfully treated patients and their physicians” (Woolf, 2010).

Woolf’s sentence ends with an important statement: A high cost for the three unsuccessfully treated patients and their physicians. I have emphasised the final three words, because this might be the most difficult to process. It’s hard for clinicians to say “I can’t reduce your pain”, and “there isn’t a cure”. It’s incredibly hard. And it’s perhaps because it’s so hard that I’ve found very little published research looking at the way clinicians go about telling people their pain is likely to be ongoing. It’s like a taboo – let’s not talk about it, let’s pretend it doesn’t happen, after all it doesn’t happen often.  Really?

Amongst allied health (I can’t bear to use the word “non-medical”), and in particular, physiotherapists, there continues to be a push to address pain intensity and (ultimately) to cure pain.  Innovative treatments such as mirror therapy, graded motor imagery, therapeutic pain neuroscience (we used to call it psycho-education in the 1980’s when I first started working in this area), reducing the threat value of the experience have all come into their own over the past 15 years or so. Even long-standing pain problems apparently respond to these approaches – people cured! Who wouldn’t be keen to try them?

Most of these latter treatments are based on the idea that our neurology is plastic; that is, it can change as we change input and thoughts/beliefs about what’s going on.  Unfortunately, the systematic reviews of trials, and at least one “real world” trial of graded motor imagery haven’t shown effects as great as promised from the early research (eg Johnson, Hall, Barnett, Draper, Derbyshire et al, 2012). There are sure to be people who can point to amazing outcomes in the people they treat. I’m certain that it’s not just the “treatment” but an awful lot to do with the person delivering the treatment – and the treatment context – that might make a difference to outcomes.

But where this all leads me to is who makes the decision to stop chasing pain reduction and pain cure? When does it happen? What’s the process? And what if we treatment providers are actually prolonging disability out of the goodness of our hearts to find a cure?

Let me unpack this a little.

In my research, several important factors led to people deciding to begin flexibly persisting (and getting on with life as it is, not as it was, or might be).

  • The first was knowing the diagnosis and that it would not be completely cured but could be managed.
  • The second, that hurting didn’t mean harm (pain is just pain, not a sign of ongoing damage).
  • The third, that there was something important the person wanted or needed to do to be themselves.

There were other things as well, like having a clinician who would stand by the person even if the person didn’t “do as the Doctor ordered”, and developing their own personalised model or explanation for their pain as it fluctuated from day-to-day. BUT the single most important factor was knowing that the problem needed to be managed because there was no cure. Knowing this meant that energy used chasing a cure was redirected towards learning to live well and be the person they were, rather than a patient or being dominated by pain.

Unfortunately, I think that many clinicians confuse the idea of managing pain with that of resignation to a lesser life. Even the wonderful Lorimer Moseley and crew wrote recently that “CBT literature seemed to focus on this idea of ‘pain is now unavoidable so it is now time to learn how to cope with it.’ He goes on to argue that because a CBT approach focuses on thoughts and beliefs (much like Explain Pain does), it’s not incompatible with the idea that the plastic brain can learn to reduce the threat value even further to ultimately “helping them live well with less pain, or perhaps without any pain at all.”

Here’s my concern: Right now there are many people living with chronic pain who have lost their sense of hope. They’ve pursued pain cure after pain cure, and in doing so, they’ve lost normal routines and habits, lost their usual occupations (activities), stopped being around people, stopped working, and have suffered in the true sense of the word – they’ve lost their sense of self. While I applaud the efforts of researchers like Moseley and colleagues, and I think we must continue to seek treatments to reverse the neurobiological underpinnings of pain, at the same time I think we need to look at the psychological and social aspects of our attitudes and expectations towards experiencing pain. And we must think of the negative effects of our emotional response to seeing another person who is experiencing pain.

Is it so terrible to experience pain every day? Speaking as one who does – despite my knowledge of neuroplasticity – my pain doesn’t represent a threat. It’s just an experience. It’s there. I notice it, I can feel it. And the participants in my research similarly acknowledged pain as present – but it didn’t have the emotional primacy that pain can represent before it is explained. In fact, some of the participants said they’d learned important things because they’d had pain. A lot like having a mood disorder (that must be managed), or diabetes (that must be managed), or heart disease (that must be managed), or respiratory disease (that must be managed), perhaps it’s OK to have pain – that must be managed. Because until our research has advanced a LOT further than it has, there are an awful lot of people living with chronic pain, and who will continue to live with chronic pain. And even more sadly, there are an awful lot of people who don’t even get the opportunity to know that it’s possible to live well despite experiencing chronic pain because we (as part of society) still don’t accept that pain can be present without it being a threat.

Sometimes I wonder at our (clinicians and researchers) blind spot. We just don’t seem to be ready to accept persisting pain as something that can be lived with. Is it time to look at our own discomfort with allowing pain to be part of life?

 

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

Cossins, L., Okell, R. W., Cameron, H., Simpson, B., Poole, H. M., & Goebel, A. (2013). Treatment of complex regional pain syndrome in adults: a systematic review of randomized controlled trials published from June 2000 to February 2012. European Journal of Pain, 17(2), 158-173.

Johnson, S., Hall, J., Barnett, S., Draper, M., Derbyshire, G., Haynes, L., . . . Goebel, A. (2012). Using graded motor imagery for complex regional pain syndrome in clinical practice: failure to improve pain. European Journal of Pain, 16(4), 550-561.

Machado, LAC, Kamper, SJ, Herbert, RD, Maher, CG, & McAuley, JH. (2009). Analgesic effects of treatments for non-specific low back pain: a meta-analysis of placebo-controlled randomized trials. Rheumatology, 48(5), 520-527.

Machado, Gustavo C, Maher, Chris G, Ferreira, Paulo H, Pinheiro, Marina B, Lin, Chung-Wei Christine, Day, Richard O, . . . Ferreira, Manuela L. (2015). Efficacy and safety of paracetamol for spinal pain and osteoarthritis: systematic review and meta-analysis of randomised placebo controlled trials (Vol. 350).

Woolf, Clifford J. (2010). Overcoming obstacles to developing new analgesics. Nature Medical, 16(11), 1241-1247. doi: doi:10.1038/nm.2230

chilly lake

“Sleep is my drug, my bed is the dealer, and my alarm clock the police.”


Sleep.  The “little death”, the “golden chain that binds health and our bodies together”, “sleep is a hint of lovely oblivion”.

There’s no doubt that having pain and sleeping well just don’t go together – having trouble with sleep is a common problem for people living with pain.  One study reports that over a period of 26 months, 67% of people living with chronic low back pain experienced poor sleep (Axen, 2015). More than this, in the same study one single day of bothersome pain increased the risk of reporting 2 to 7 nights with disturbed sleep by two, and people with chronic low back pain were more likely to report poor sleep than those with acute low back pain.

In another study, (Harrison, Wilson & Munafo, 2015) teenagers from a large cohort study in the UK were surveyed to identify the presence of sleep problems, mood problems and pain problems. 21% of the population reported trouble with sleep, 5.5% reported pain problems, and 2.8% experienced both pain and sleep problems.

And in yet another study, participants with fibromyalgia had significantly shorter and more frequent wake bouts than those with primary insomnia, and the researchers argue that sleep disruption in fibromyalgia does not lead to prolonged periods of wakefulness, but seems to be a disorder of the sleep system whereby internal or external events repeatedly disturb and fragment sleep, and suggest the resulting increased frequency of awakenings may be, at least in part, due to pain, as studies have shown that reducing pain also improves sleep.

These researchers also considered that there is a relatively intact homeostatic drive in participants with fibromyalgia that causes them to quickly return to sleep after an awakening. This is evidenced by shorter initial sleep latency (LPS) and increased slow wave sleep, in addition to shorter duration of wake bouts compared with individuals with primary insomnia (Roth, Brown, Pitman, Roehrs & Resnick, 2015).
People who experience chronic pain can often experience depression, while those who have depression commonly experience sleep disturbance. There are suggestions that common neurobiological pathways exist between all three states.  Atrophy of the hippocampus and increased limbic area activation has been reported across all three conditions, while increased limbic activation occurs in all three conditions as well. Neurochemical changes are also found in all three conditions: HPA-axis hyperactivity has been found, with subsequent alteration to glucocorticoid receptor downregulation, monoaminergic neurons are inhibited as a result of glucocorticoid-induced monoamine depletion, thus reducing inhibitory drive and therefore increasing pain.
Slow wave sleep has been found to inhibit the HPA axis and cortisol secretion, with wakefulness associated with increased cortisol which could lead to increased HPA activation and subsequent elevation of pain (Boakye, Olechowski, Rashiq, Verrier, Kerr, Witmans, Baker, Joyce and Dick, 2015).
Essentially it seems clear that there are neurobiological factors that are implicated in chronic pain, depression and poor sleep.
The importance of this finding shouldn’t be under-estimated. In qualitative studies, participants report that one of the most challenging aspects of dealing with chronic pain is handling fatigue and sleep-related problems (Turk, Dworkin, Revicki, Harding et al, 2008). Pain not only affects sleep quality, but because it intrudes on cognitive processing, there is perceived effort involved in just handling day-to-day situations.
What to do about it…
Well, here’s the thing. Most of the ways GP’s manage sleep problems is through short-term prescriptions of hypnotics such as zopiclone and occasionally benzodiazepines. While there are some useful short-term effects from these drugs, chronic pain is not a short-term problem. Sleep disturbance associated with chronic pain is thus less likely to be helped by simply increasing the length of prescription – these drugs are not intended to be taken long-term. Other medications are used primarily for their pain reducing effects (such as gabapentin and the tricyclic antidepressants), but happily, also possess sedative effects.  These can be taken long-term – but may not work for everyone.
Alternatives include using cognitive behavioural therapy for insomnia. Actually, there are two alternatives – CBTi and sleep restriction, and in some cases, both together.
CBTi is a brief form of cognitive behavioural therapy that has been shown to be highly effective, and focuses on the thoughts and beliefs people hold about sleep, the habits people have associated with sleeping, and associations between habits, thoughts and sleep onset.  Sleep restriction, on the other hand, reduces the amount of time people are actually in bed overall, with the aim to consolidate sleep, and reduce the amount of time spent awake while in bed. Sleep restriction also influences the sleep architecture, so that people can descend into deep sleep more quickly, while reducing the amount of time in REM sleep and lighter levels of sleep.
A final alternative is to use mindfulness to help people become aware of their thoughts and habits about sleep, but instead of challenging or refuting them, learning to attend to them with curiosity and kindness, while at the same time reducing the amount of time awake while in bed.
As a long-time insomniac (now recovered!), I am well familiar with being awake when all else is silent, and on the troubles of trying to get off to sleep while my bed partner snoozes. I also know how hard it is to get back off to sleep after waking in the middle of the night.
Here’s what I did:
  1. Used deep relaxation hypnosis to help establish the association between being relaxed and being in bed. I used this every night for ages, then I realised that I could do the hypnosis “in my head” rather than having someone else’s voice do it for me.
  2. I got out of bed if I hadn’t been to sleep in about 30 minutes. Especially during the middle of the night! Not easy, but worthwhile so I didn’t lie there trying hard not to fidget and wake my partner. I found that if I tried to stay in bed I’d end up being so aware of my fidgeting and so strung out by trying NOT to fidget that I’d be wide awake and stressed. Not the best way to sleep!
  3. Keeping the lights down low, and reading a book I’d already read was the next step once I’d got out of bed. That way I didn’t need to read every word, and it didn’t matter if I snoozed a little.
  4. After about 30 minutes or so, I’d slide back into bed with my mind full of the story rather than being frazzled by not sleeping. And I’d return to my relaxation and breathing and gradually slip off to sleep.
  5. More recently I’ve kicked the mental hypnosis/relaxation habit, and I now go to bed and simply roll over and slow my breathing and fall asleep. Learning to do this without using the hypnosis has been fabulous so I no longer need to worry about being awake at 3.00 in the morning! If I do wake, I head to the toilet, do my business, then slide back into bed and roll over and slow my breathing.

What I’ve learned from this is that the main habit I needed to learn was how to put myself to sleep. I also learned to remind myself that the occasional night with poor sleep is OK, I can handle. And if my sleep really turns to custard I have the skills to manage it myself.

I can’t stop the fact that fibromyalgia means there are some changes to the way my brain processes information, and that this means I’m likely to have poorer sleep than many other people. What I can change is how much I allow that to affect me. And by learning how to go off to sleep by myself, without the external aids, has meant I actually do fall asleep more quickly and don’t feel the effects of disrupted sleep to the same extent as I used to.

 

 

Canada

More than something to blame when the treatment doesn’t work


A friend of mine told me that during her physiotherapy training when they discussed “psychosocial” factors it was usually in the context of explaining why a treatment didn’t work.  This still happens. Even well-informed and scientifically savvy people can unintentionally “blame” those pesky psychosocial factors for getting in the way of complete recovery. What do I mean? Well, let’s think about it: when we’ve done the “explaining” or “educating” – and the person still doesn’t understand and/or their pain doesn’t reduce, what’s our explanation?

We know that pain is an experience, not a separate thing to be treated, but the experience an individual has when his or her brain determines there is a threat to the body (and that threat is more important than other competing goals). We also know there are numerous mechanisms underpinning this experience, many of which are biological. But what we are always left with is the fact that we cannot know anything about this other person’s world except through (1) their behaviour and (2) our interpretation of their behaviour.

I’ve emphasised this because recently I’ve heard one registration board suggesting that a profession should not talk about pain, nor consider psychosocial factors because their domain of influence is bodily tissues.

I’ve also emphasised this because in our efforts to become all sciencey and sound (at least) like we know what we’re talking about, I think we may have forgotten that the only reason we know someone is sore is because they are doing something that we interpret as a signal that they’re sore. And that this occurs within a social setting that has emerged from a combination of historical practices and assumptions, and we are part of that social setting.

The biological substrates for our experience of pain have received the lion’s share of research attention and funds. What has received rather less is understanding some of the social aspects – what individuals learn throughout their life, including the assumptions we develop about what is “normal” and what is not. Unique family and cultural factors influence each individual’s experience – what does this person pay attention to? What does this person ignore? When this person recognises something as “not normal” what is the usual way of dealing with it? Who does this person first see for treatment?

More than this, what about the research looking at treatment provider’s decoding and response to the social communication of the person seeking treatment? We know, for example, that healthcare providers who view video vignettes of people displaying pain behaviour with no medical evidence but with psychosocial factors rate those individuals as experiencing less pain and interference, they have less sympathy, expect medication effectiveness to be less, and those individuals were more likely to be rated as potentially trying to deceive the treatment providers (De Ruddere, Goubert, Stevens, Deveugele, Craig & Crombez, 2014). These responses appear to use both automatic (unintentional, reflexive) and controlled (intentional, purposive) neuroregulatory systems. Observers (ie health professionals) also incorporate automatic (unintentional, reflexive) and controlled (intentional, reflective) reactions. We seem more likely to demonstrate instant ‘‘visceral’’ emotional reactions to unintentional, reflexive expression, while controlled expression characterised by purposive (deliberate) behaviour appears more likely to suggest to health professionals (or observers) that we should think a little about the purpose behind that individual’s pain expression (Craig, Versloot, Goubert, Vervoort & Crombez, 2010). The point is: this occurs even when we know about it, and even if the individual is experiencing pain, and even though the individual is only trying to get the treatment provider’s attention!

Pain behaviour as independent from the individual’s experience of pain is one of the key features of the behavioural model of pain. Pain behaviours were what Fordyce and Loeser and Turk and the very great original thinkers about chronic pain management first thought could and should be dealt with. The reason? Because despite all the surgical and pharmacological treatments available in the late 1960’s, 70’s and 80’s,  many people were still left experiencing pain and were also highly disabled by it. By helping people reduce their pain behaviour (eg stop guarding that body part, start moving more quickly and fluidly, be more relaxed, groan less) they noticed that people were also reporting that their pain bothered them less.

Cognitive behavioural therapy (or a cognitive behavioural approach, to be more accurate) incorporated more “education”, or helping people understand the mechanisms involved in their experience of pain, helping them understand the difference between hurting vs doing damage. A CBT approach meant people were acknowledged as being able to think differently about their pain, reduce their distress and begin to do more. A CBT approach combined education with behavioural experiments and encouraged people to get on with life.

Much more recently we have physiotherapists deciding that giving people pain neurobiology education (sounds almost exactly like the CBT education/explanation to me) is really good and reduces the threat value of the experience. And combined with graded reactivation, exposure to doing things that have been avoided, using methods to reduce distress and by avoiding flare-ups of pain, people are helped.

Two or three important points for me:

  1. Health professionals need to be aware of their own psychosocial responses/background/biases when they observe another person who is indicating they are sore.
  2. If we are two people interacting, all the messy psychosocial factors are immediately present – whether we attend to them, or not.
  3. Given how important those factors are in both our response to another person and their response to treatment (eg placebo, expectancy) it is critical that we integrate effective communication skills into every clinical interaction.

And probably another important point:

In the enthusiasm for pain neurobiology education and the potential for the person to no longer experience pain, we need to remember that reducing disability is arguably more relevant than reducing pain. Despite the impressive results reported by clinicians and some researchers there are many many people who continue to live with chronic pain. As clinicians we may even inadvertently delay recovery if our focus is inappropriately on pain reduction. I say this because there is SUCH clear evidence that pain intensity is less of a factor in ongoing disability than unhelpful beliefs and avoidance (Froud, Patterson, Eldridge, Seale, Pincus, Rajendran et al, 2014; Shaw, Campbell, Nelson, Main & Linton, 2013; Wilkens, Scheel, Grundnes, Hellum & Storheim, 2013).

To conclude, it seems to me that it’s high time for health professionals to take a hard look at what they consider to be “their” domain of concern. Not only must we avoid “blaming” psychosocial factors for poor outcomes from treatments we provide, we also must begin to recognise our own biases as we work with people living with pain. One of these biases is the temptation to believe that we are not influenced by our own psychosocial factors. Another is to recognise that delicate moment when it’s time to take our attention away from reducing pain and towards reducing disability. We need to elevate the status of effective communication – not just “can I make myself understood” and “can I establish rapport”, but that much more nuanced scope of implementing reflective listening, truly hearing our clients, and responding in a way that upholds client choice and self efficacy. I think this belongs to all health professions, not simply those tasked with dealing with “psychosocial” factors.

 

Craig, K.D. (2015). Social communication model of pain. Pain, 156(7), 1198-1199.

Craig, K.D., Versloot, J., Goubert, L., Vervoort, T., & Crombez, G. (2010). Perceiving pain in others: Automatic and controlled mechanisms. The Journal of Pain, 11(2), 101-108. doi: http://dx.doi.org/10.1016/j.jpain.2009.08.008

De Ruddere, L., Goubert, L., Stevens, M.A.L., Deveugele, M., Craig, K.D., & Crombez, G. (2014). Health care professionals’ reactions to patient pain: Impact of knowledge about medical evidence and psychosocial influences. The Journal of Pain, 15(3), 262-270. doi: http://dx.doi.org/10.1016/j.jpain.2013.11.002

Froud, R., Patterson, S., Eldridge, S., Seale, C., Pincus, T., Rajendran, D., . . . Underwood, M. (2014). A systematic review and meta-synthesis of the impact of low back pain on people’s lives. BMC Musculoskeletal Disorders, 15, 50.

Shaw, W.S., Campbell, P., Nelson, C.C., Main, C.J., & Linton, S.J. (2013). Effects of workplace, family and cultural influences on low back pain: What opportunities exist to address social factors in general consultations? Best Practice & Research in Clinical Rheumatology, 27(5), 637-648.

Wilkens, P., Scheel, I.B., Grundnes, O., Hellum, C., & Storheim, K. (2013). Prognostic factors of prolonged disability in patients with chronic low back pain and lumbar degeneration in primary care: A cohort study. Spine, 38(1), 65-74.

forest walk

Life seems but a succession of busy nothings – Jane Austin


We hold some very contradictory opinions about being busy. On the one hand, Socrates is reported to have said “Beware the barrenness of a busy life”, and on the other Dale Carnegie is quoted as saying “Inaction breeds doubt and fear. Action breeds confidence and courage. If you want to conquer fear, do not sit home and think about it. Go out and get busy.”

Pacing, one of the cornerstones of “traditional” pain management, is intended to moderate both under-activity (avoidance) and over-activity so that important things can get done without running out of puff – or having an enormous flare-up of pain with subsequent crash into a jellied lump. Yet people who cope well with pain, and ourselves if we’re honest, are often guilty of doing more when we are highly  motivated to do something (or want to achieve a specific goal), and doing less afterwards so we can recuperate.

What is an optimal level of activity for a person living with chronic pain and why might this be important?

I’ll address the second question first. Fatigue is experienced by many people living with chronic pain. Fatigue is a term “used to describe a period of extreme tiredness, as a result of emotional strain, physical exertion, boredom or a general lack of rest and sleep” (Psychology dictionary) People living with chronic pain often develop a sense of fatigue as part of their pain, and some authors believe that not only is it because of disruption to the delta sleep phase (the deepest sleep we achieve), but also because some brain activity continues all the time as the neuromatrix processes potential threat from the painful parts of the body. This activity may result in changes to brain structure, although brain structures may actually cause some of this effect (Baliki, Geha, Apkarian & Chialvo, 2008; Wiech, Ploner & Tracey, 2008). The practical impact of experiencing fatigue is to reduce cognitive efficiency: it takes longer to solve problems, and even boring tasks can feel very difficult.

Some interesting facts: the effect of fatigue on performance differs depending on an individual’s beliefs about fatigue – there is a thing called “fatigue catastrophising” which, like pain catastrophising, means individuals unduly and negatively assess the effect of fatigue on their ability to do things. Being fatigued influences the ability to switch tasks from one task to another, fatigue reduces the ability to ‘change tack’. Interestingly, being bored increases the likelihood of experiencing fatigue. There is an optimal level of stimulation in which we operate. Stress, while initially increasing alertness, over time results in increased fatigue.

So in terms of the importance of identifying and developing an optimal level of activity, it seems that for people living with chronic pain, there might be a need to carefully work out just what level of activity is sufficient to avoid boredom but not so much as to stimulate unhealthy levels of fatigue.

And now, what is an optimal level of activity for a person living with chronic pain?

This question is a much more difficult question to answer, not only because “optimal” will depend a great deal on an individual’s satisfaction with his or her activity level, but also because it’s difficult to measure, definitions about activity level are unclear, and because there are many assumptions about activity levels that have been retained since the early operant conditioning model of pain was proposed by Fordyce. In this model, avoidance develops by reducing activity levels as a way to reduce pain (or prevent it from increasing), while over-activity is thought to occur when activity increases pain resulting in avoidance. Some research suggests that over-activity is an ongoing habit used by individuals who have always tended to be those that work long hours and remain highly engaged in activities they value.

There has been a lot of interest in the notion of over-activity, in part because of the recent interest in “pacing”, but also because people who “over-do” exhibit some features inconsistent with the old avoidance model. For some reason people who over-do engage in activity that will increase their pain – and yet they continue doing so, despite the need to “recover” or do less on the days following their high activity days. Something is overriding the (expected or usual) sense of concern about experiencing pain at the time of their over-activity.

A study by Andrews, Strong and Meredith (in press) looks at activity patterns and particularly over-activity and avoidance patterns and has been able to validate the construct of “over-activity” as a pattern of activity that increases pain – but inconsistent findings relating to avoidance and over-activity. While pain is known to increase, the effect of this on future activity levels is not yet known.

What I wonder is whether these patterns relate to contextual aspects of activity carried out by people living lives. We all know that we push ourselves some days and chill out a little on others. We know that sometimes we’ll do things that will be either fatiguing or actually generate pain (like when you need to move house, dig the garden in spring, do a fun run, have a Christmas dinner at our place), and for most of us this is something we accommodate by being a little less busy for a couple of days afterwards. If we take actigraph recordings over a week or two (Jawbone anyone?), I’m sure it will also show a pattern of high activity and then lower activity, so that over time the activity levels probably flatten out around a mean level of activity. When we do something we value very much, the perceived sense of effort (fatigue) may be lower – we feel energised and enthused although we are tired. When we do something we don’t value (for me it has to be vacuuming!), it feels more tiring and time goes very slowly.

I wonder if people living with pain need additional time to “recover” because of both increased pain, and also the feeling of fatigue. And whether perhaps we need to also study what it is about the tasks being undertaken that is valued rather than simply the task activity level. Busyness may depend on the value of what is being done.

 

Andrews, N.E., Strong, J., & Meredith, P.J. Overactivity in chronic pain: Is it a valid construct? Pain.

Baliki, M.N., Geha, P.Y., Apkarian, A., & Chialvo, D.R. (2008). Beyond feeling: Chronic pain hurts the brain, disrupting the default-mode network dynamics. The Journal of Neuroscience, 28(6), 1398-1403. doi: http://dx.doi.org/10.1523/JNEUROSCI.4123-07.2008

Wiech, K., Ploner, M., & Tracey, I. (2008). Neurocognitive aspects of pain perception. Trends in Cognitive Sciences, 12(8), 306-313. doi: doi:10.1016/j.tics.2008.05.005

headlands

“Failed back surgery” syndrome – who or what failed?


It’s a term I thought had died a natural death. Failed back surgery syndrome. I used to hear it in the late 1980’s when people with low back pain often had five or six surgeries to try to “fix” whatever wasn’t working in the back. I hadn’t heard it for a while and I really thought it had gone the way it should have – into that great rubbish bin diagnosis pile in the sky, along with “somatisation” and “functional pain” and trigger points. But, to my astonishment, there it is, now a separate MeSH title when you search through Ovid or Medline.

The question I always ask is “Who or what has failed?”

Is it the patient who dares to carry on saying that they have pain, sometimes even more pain than before surgery?

Is it the surgeon for choosing the wrong surgery, or perhaps for doing surgery at all?

Is it the nervous system, already sensitised, now subject to more sensitisation through the planned trauma of the surgical scalpel?

Is it the system for funding surgery?

In a paper written by Shapiro (2015), the rate of “failed back surgery syndrome” is reported as being between 10 – 40%. It seems to increase when the surgery is complex, and it hasn’t improved despite developing less invasive surgical techniques.  Shapiro goes so far as to define FBSS as  “a multidimensional chronic pain syndrome that has significant myofascial and psychosocial components that are directly related to the high incidence of lumbar surgeries in the United States.” Sorry to say, but it’s not just present in the US.

These are the psychosocial risk factors, as identified by Chan and Peng :

  • significant levels of depression,
  • anxiety,
  • poor coping,
  • somatisation
  • hypochondriasis

To be honest, I think these indications would be risk factors for ANY surgery (and probably ANY invasive procedure, including dry needling). But there’s more than this – preoperative risks such as having had prior surgery (spinal instability seems to become worse with repeated revisions); surgery carried out when imaging results suggest there may be good reason, but there is no corresponding clinical correlation; nonsurgical cases of radiculopathy and neuropathy (eg diabetes, viruses, inflammation, vascular disease). And intra-operative risks such as difficult radiographic imaging, inadequate decompression – this paper uses the term “pain generator” for the potential source of nociception, but you and I know that pain only occurs as an output of the brain within a biopsychosocial system; lots of other surgical issues including bleeding, fragments of tissue, “battered root syndrome” (!) where the nerve root is damaged during discectomy; and finally, there are a load of post-operative issues as well – such as haematoma, pseudoarthritis, fibrosis, irritation of the nerve roots, spinal instability, loss of disc height and the list goes on.

Shapiro suggests that some types of ongoing pain after surgery are misdiagnosed myofascial pain, stirring up or producing trigger points. He does add that central sensitisation in the dorsal horn could also play a part, expanding receptive fields in the spinal cord and amplifying “perception” (once again, think of this as amplifying nociceptive input reaching the brain). He also favours the notion of motor control problems following surgery, again compounding the problems that occur with movement after surgery and feeding back into the ongoing pain experienced by the individual.

Shapiro also goes on to suggest various ways the problems could be ameliorated, primarily through careful imaging and then possible surgical management.  The overall management, however, he argues should be pharmacological, “with the goal of increasing physical activity and community involvement”.  Interestingly, Shapiro says “FBSS patients are often pushed aside and told that their surgeons have little to offer them after their surgeries were unsuccessful. These patients are generally managed by community-based physicians, including primary care physicians, anesthesiologists, physiatrists, and neurologists.”  He goes on to say “Treatment of FBSS demands recognition that it is a chronic pain syndrome. One reason that FBSS is a difficult-to-treat syndrome and a public health problem is that the antecedent back pain did not respond to intervention and was often augmented with additional pain complaints caused by the surgery. The psychosocial burden for individuals is huge, especially if there is job loss or loss of function physically. Many of the immediate postoperative pharmacologic strategies complicate the situation further by altering the patient sensorium, mood, affect, and even libido. Opioid-induced hyperalgesia is probably under-recognized and under-reported.”

What does this mean to me?

It must be terribly distressing to be offered a treatment for low back pain and leg pain that is both invasive and expensive – only to find that it hasn’t helped one bit. And even more distressing to then be advised that “there is nothing more I can do, it’s a risk of having surgery”. Worse, then to be advised that the options for managing this pain are quite limited – and for many people, means repeated surgery, perhaps even to the point of having a spinal cord stimulator implanted (with all the known complications of this kind of intervention). Shapiro describes people being offered facet joint radiofrequency neurotomy, but even he acknowledges that “it does not offer a permanent fix to facet-mediated pain, which should raise concern with regard to overutilisation”.

What astonishes me, but probably shouldn’t, is that interdisciplinary pain management approaches continue to be seen as costly, yet there is ample research showing these programmes achieve clinical and cost-effective improvements in patient function.  I’ll let you draw your own conclusions from the following paragraph snipped from Shapiro’s paper:

The cost for this individually tailored 20-day outpatient program, including physical therapy, occupational therapy, and psychological support, is approximately $15,000 (Pain SolutionsNetwork, personal communication, 2013). This is similar to the cost for a single-level laminectomy not requiring a hospital stay and is substantially less costly than the direct costs for lumbar fusion when hospital, hardware, surgeon, and anesthesia costs are added up. [and I’d go even further to add that the 30% risk of a poor outcome is even more expensive…]

I think the health system has failed the people who undergo surgery for low back pain. With a failure rate quoted by Shapiro as approximately 30%, and an increase in epidural injections and facet joint injections of over 250% without any similar improvement in health status, something is going wrong. Very wrong.

Allied health professionals can and do provide cost-effective interdisciplinary pain management for people living with so-called “failed” back surgery syndrome. I think it’s time for allied health professionals to begin agitating, and perhaps even advertising direct to people who have pain – we can help. Our treatments don’t have the risks of invasive procedures. We are focused on helping you DO despite your pain. And what we do can hardly make your pain worse – unlike some of the very sad stories I’ve read.

 

 

Chan C, Peng P. (2011). Failed back surgery syndrome. Pain Medicine 12:577–606.

Shapiro, C.M. (2014). The failed back surgery syndrome: Pitfalls surrounding evaluation and treatment. Physical Medicine & Rehabilitation Clinics of North America, 25(2), 319-340.

Rhodin, A. (2014). A case of severe low back pain after surgery. Journal of Pain & Palliative Care Pharmacotherapy, 28(2), 167-168; discussion 168-169.

tanglewood

Central sensitisation – can a questionnaire help find out who is, and who isn’t?


My orthopaedic colleagues have been asking for a way to identify which surgical candidate is unlikely to have a good outcome after major joint surgery. They know that between 10 – 50% of people undergoing surgery will have chronic pain.  5 – 10% of those people experiencing pain that’s rated >5/10 on a numeric rating scale where 0 = no pain, and 10 = most severe pain you can imagine ( Kehlet, Jensen, & Woolf, 2006). The people with severe pain are the kind of people who hear “well the surgery I did went well…” and can be left wondering why they ever decided to go ahead with their surgery.

Two main factors seem to be important in postsurgical chronic pain: the presence of central sensitisation (usually indicated by reporting chronic pain in at least two other areas of the body) and catastrophising. I’ve discussed catastrophising a great deal here and here .

What I haven’t talked about is central sensitisation. Now, the idea that people can experience chronic pain associated with changes in the way the nervous system responds to stimuli isn’t new, but the neurobiology of it is still slowly being unravelled.  I’m not going to get into definitions or whether having changes in the nervous system equates with “chronic pain” (because pain is an experience and the neurobiology is just the scaffolding that seems present, the two are not equivalent). I want to talk about the measurement of this “sensitisation” and whether a pen and paper tool might be one way of screening people who are at greatest risk of developing problems if they proceed with surgery.

First of all, what symptoms come under this broad heading of “response to an abnormally sensitised nervous system”? Well, Yunus (2007) proposed that because there are similarities between several so-called “medically unexplained symptoms” such as fibromyalgia, chronic fatigue, irritable bowel disorder and so on, perhaps there is a common aetiology for them. Based on evidence that central sensitisation involves enhanced processing of many sensory experiences, Yunus proposed the term “central sensitivity syndrome” – basically a disorder of the nociceptive system. Obviously it’s pretty complicated, but various researchers have proposed that “dysregulation in both ascending and descending central nervous system pathways as a result of physical trauma and sustained pain impulses, and the chronic release of pro-inflammatory cytokines by the immune system, as a result of physical trauma or viral infection… including a dysfunction of the stress system, including the hypothalamic–pituitary–adrenal axis (Mayer, Neblett, Cohen, Howard, Choi et al, 2012, p. 277)”. (what are “pain impulses”?!)

By proposing this mechanism, various researchers have been able to pull together a number of symptoms that people experience, and their premise is that the more symptoms individuals endorse, the more likely it is that they have an underlying central sensitisation disorder.

The authors completed a literature review to identify symptoms and comorbidities associated with fibromyalgia and the other disorders they believe indicate a sensitised central nervous system. they then develop a self-report instrument and asked people with these problems to complete it, and compared their results with a group of people who wouldn’t usually be thought to have any sensitisation problems (students and staff at a University – we could argue this, but let’s not!).

What they found, after much statistical analysis, is a four factor measure:

Factor 1 – Physical Symptoms (30.9%)
Factor 2 – Emotional Distress (7.2%)
Factor 3 – Headache/Jaw Symptoms (10.1%)
Factor 4 – Urological Symptoms (5.2%)

Test-retest reliability was established, and because the questionnaire could discriminate between those who reported widespread pain (aka fibromyalgia) and those who had no pain, it’s thought to have discriminant validity as well. (BTW a copy of this measure is included in the appendix of the Mayer, Neblett, Cohen, Howard, Choi, Williams et al (2012) paper – go get it!)

The researchers then went on to look at some norms for the measure and found that amongst people with chronic pain, referred to an outpatient multidisciplinary pain centre, those with more diagnosed “central sensitisation syndromes” scored more highly on this measure, and that a score of 40 on the measure was able to discriminate between those who didn’t have sensitisation and those who did (Neblett, Cohen, Choi, Hartzell, Williams, Mayer & Gatchel, 2013).

Well and good. What does it actually mean?

This is where I think this measure can come unstuck. I like the idea of people being asked about their pain and associated symptoms. We often don’t have time in a clinical interview to ask about the enormous range of symptoms people experience, so being able to get people to fill out a pen and paper measure to take stock of the different things people know about themselves is a good thing.

What this measure doesn’t yet do is indicate whether there is any underlying common causal link between these experiences. It’s tautological to list the symptoms people might experience with central sensitisation based on the literature, then ask them to indicate which ones they experience and then conclude “oh yes! this means they have central sensitisation!” All it means is that these people report similar symptoms.

What needs to happen, and is now beginning to occur, are studies examining central nervous system processing and the scores individuals obtain on this measure. That, and establishing whether, by completing this questionnaire, it is possible to predict who is more or less likely to develop things like post-surgical chronic pain. Now that would be a really good measure, and very likely to be used by my orthopaedic colleagues.

In the meantime, whatever this measure indicates, it seems to be able to differentiate between people who are more likely to report “medically unexplained symptoms” and people who don’t. This might be useful as we begin to look at targeting treatment to suit different types of persistent pain. At this point in time, though, I think this measure is more useful in research than clinical practice.

 

Kehlet H, Jensen TS, Woolf CJ. Persistent postsurgical pain: risk factors and prevention. Lancet. 2006;367:1618–1625

Mayer, T.G., Neblett, R., Cohen, H., Howard, K.J., Choi, Y.H., Williams, M.J., . . . Gatchel, R.J. (2012). The development and psychometric validation of the central sensitization inventory. Pain Practice, 12(4), 276-285. doi: 10.1111/j.1533-2500.2011.00493.x

Neblett, R., Cohen, H., Choi, Y., Hartzell, M.M., Williams, M., Mayer, T.G., & Gatchel, R.J. (2013). The central sensitization inventory (csi): Establishing clinically significant values for identifying central sensitivity syndromes in an outpatient chronic pain sample. The Journal of Pain, 14(5), 438-445. doi: http://dx.doi.org/10.1016/j.jpain.2012.11.012

Roussel, N.A., Nijs, J., Meeus, M., Mylius, V., Fayt, C., & Oostendorp, R. (2013). Central sensitization and altered central pain processing in chronic low back pain: Fact or myth? Clin J Pain, 29, 625-638. doi: 10.1097/AJP.0b013e31826f9a71

Van Oosterwijck, J., Nijs, J., Meeus, M., & Paul, L. (2013). Evidence for central sensitization in chronic whiplash: A systematic literature review. European Journal of Pain, 17(3), 299-312. doi: 10.1002/j.1532-2149.2012.00193.x

Yunus, M.B. (2007). Fibromyalgia and overlapping disorders: The unifying concept of central sensitivity syndromes. Seminars in Arthritis & Rheumatism, 36(6), 339-356.

BFT poster

My North American Tour!! #Bronnie2015


It’s fast coming up – my wonderful North American tour!! Thanks to some amazing friends who have organised the details, I’m going to be in North America from the end of May to mid-June at the following places:

11 June – one day workshop on graded exposure!
13/14 June
What am I doing?
This is a two-day workshop on integrating biopsychosocial factors into clinical assessment, clinical reasoning and treatment planning. It’s about taking pain management from the clinic into the real world. It’s a time to learn more about the practical aspects of integrating these messy concepts – without breaching your scope of practice!
By the end of the two days you’ll have some tools you can use on Monday, gained confidence and had fun.
Come and join me and the fabulous team who have done all the arranging for these workshops!
silent angel comfort me

What does using a biopsychosocial framework mean in practice?


A good friend of mine told me that during her training (as a physiotherapist), psychosocial factors were “what you blame when your treatment doesn’t work”. It’s something I’ve heard more than once. I’ve also been asked many times “…but are you sure you’re not doing something outside your scope of practice?” when I talk about using cognitive behavioural principles and ACT (Acceptance and Commitment Therapy) and other psychological strategies. And some of you might have seen earlier posts of mine where I ask “How social is your biopsychosocial model?”

Today’s medical students are trained in using a biopsychosocial framework in their undergraduate years. They leave medical school, begin their hospital and advanced training, and I guess I wouldn’t be alone in asking “what happened to the psychosocial?” when we see them working.

So today’s post is a bit of a reflection and a musing on what I think using a BPS approach might mean in pain practice.

BPS is, I think, less of a “model” than a way of thinking. Thinking that is based on a systems approach – every factor affects and is affected by every other factor. In fact, Engel, the originator of this way of viewing human health, was strongly influenced by general systems theory which was developed by Ludwig von Bertalanffy, a biologist who lived between 1901 – 1972. General systems theory was a model describing processes thought to be common in many different fields of knowledge. General systems theory is based on these five beliefs:

(1)  There is a general tendency towards integration in the various sciences, natural and social.

(2)  Such integration seems to be centred in a general theory of systems.

(3)  Such theory may be an important means of aiming at exact theory in the nonphysical fields of science.

(4)  Developing unifying principles running ‘vertically’ through the universe of the individual sciences, this theory brings us nearer to the goal of the unity of science.

(5)  This can lead to a much-needed integration in scientific education.

Engel then applied this to a model of the influences on human health. At the time he wrote his seminal article (Engel, 1977), psychiatrists were being challenged by reductionism on the one hand, particularly around approaches to mental health – the distinction between “diseases” where biological causal factors are influential, such as neurological disorders, and “problems of living” such as alcoholism, where the relevance of biology was, at the time, hotly debated; and concern that psychiatrists might lose ground to nonmedical practitioners such as psychologists. It’s an argument that continues today: should, for example, nonspecific low back pain be the domain of medical practitioners or should physiotherapists, occupational therapists, psychologists and others pick up primary responsibility for its management? (For a very interesting discussion of socio-political debates about this, read Wilson, N., Pope, C., Roberts, L., & Crouch, R. (2014). Governing healthcare: Finding meaning in a clinical practice guideline for the management of non-specific low back pain. Social Science & Medicine, 102(0), 138-145. doi: http://dx.doi.org/10.1016/j.socscimed.2013.11.055)

Back to the story. The broad BPS “model” can’t be tested, and to some, was never intended to be a “scientific” model but rather a discussion tool. A way of shaping a dialogue between the person seeking help, and the clinician wanting to understand what was influencing how and why this person was presenting in this way at this time. I like to think of it as a way to remember that the person seeing you is a person-in-context.

We can argue the toss about exactly which factors belong in which “bit” of a biopsychosocial approach, but broadly speaking, we want to understand biological influences on health. Some of these are genetic (a bit hard to investigate for most of us), some of these are environmental (rickets? Vit D deficiency?), some are other organisms (M. leprae and M. lepromatosis? – Leprosy to you and me). Some are associated with what people do – tripping, jumping off things; while some are associated with what people don’t do – manage diabetes, exercise. The bio part is far more readily assessed and addressed than the other messy bits and pieces, so I won’t deal with that any further.

The psychosocial, on the other hand, is messy. It’s muddled and hard to measure and changes over time and geography and culture.

To me, it means remembering that when two people get together, it’s not just about the words we use, it’s about what we both bring to the setting in terms of experience, habits, expectations, vulnerabilities. It’s about where we meet. It’s about the purpose of meeting. It’s about recognising that everything we say and do is imbued with meaning – but it’s also about not necessarily knowing what we know, or what we don’t know.

So if I’m practicing in a biopsychosocial framework, I’m going to have to know a great deal about myself and my assumptions, my attitudes, habits, how others see me, and even what I don’t know. And the same applies to my knowledge about the person I’m seeing – only because I’m usually the “treatment provider”, I need to shape my conversation so that it’s OK for that person to tell me about this stuff, and this means knowing a bit about how people tick. I especially need to know how to hear what the person coming to me is saying – and not saying.

I see much that is called “psychological” as being about how we communicate and what we know about helping people change behaviour. I’m not “doing psychology” when I teach my child how to tie shoelaces, yet I’m using psychological techniques – modeling, reinforcement, verbal instructions and so on. Likewise when I’m helping someone feel OK about driving their car when they have back pain, I’m using psychological techniques such as verbal instruction, grading the difficulty, encouraging, supporting and so on. To suggest we can’t use psychological techniques to enable normal function is unthinkable.

Using CBT or ACT or motivation interviewing simply means refining my interpersonal skills so that I can optimise the chances that the person feels heard, can understand what I’m on about, and begins to feel OK about taking steps towards the life they want and being themselves. It’s about learning ways of explaining things, learning how to show that I’m listening, learning about the right level of support and challenge that will enhance the chances of success. Most people who live with chronic pain probably don’t need to see a psychologist – they need someone to help them make sense of pain, to show they’re there as they find their way through, and celebrate when they’re doing what’s important in their lives. I think all health professionals should be doing this.

Engel, G.L. (1977). The need for a new medical model: A challenge for biomedicine. Science, 196(4286), 129-136. doi: http://dx.doi.org/10.1126/science.847460

Rarotonga

How much do you really need to deal with catastrophising?


Catastrophising is a popular concept in pain management. It’s been associated with poor outcomes in major joint replacement (Riddle, Wade, Jiranek and Kong, 2010); spinal fusion (Abbott, Tyni-Lenne & Hedlund, (2010); in experimental pain modulation (Bartley & Rhudy, 2008); in cancer pain (Bishop & Warr, 2003); and influences interpersonal relationships (Buenaver, Edwards & Haythornthwaite, 2007).

I’m often asked: so, what do I do about it? Can it be treated? What does it really mean? Should I (any kind of non-psychologist) try to treat it, or should I leave it to the psychologists?

The short answer is, I think, yes we need to be aware of catastrophising, yes we can do something to help people become less likely to catastrophise, and yes I firmly believe any and all health professionals have a contribution to make to reduce the tendency to catastrophise simply because it can be so influential for distress, function and disability.

What does catastrophising really mean?

Catastrophising is, basically, the tendency to think the worst about a situation. It probably has some adaptive function in that it helps people identify all the things that can go wrong so they can do something to reduce that risk. On the other hand, it’s not such a wonderful thing when it leads to ruminating (brooding), feeling helpless, and to magnify (or emphasise) all the disasters that could happen, when the probability is really quite low (Sullivan, Bishop & Pivik, 1995).

It’s likely that most of us will have, at one time or another, anticipated the worst. Most of the time the worst doesn’t happen, and we go our way, reassured that we’ve planned for, and managed the situation more effectively than if we’d carried out regardless. But for people who tend to catastrophise about their pain, the risk is fairly high that they’ll experience more distress, depression and disability than those who don’t.

I want to point out that identifying that someone tends to catastrophise does not mean their fears should be dismissed out of hand.  The person who tends to catastrophise is likely to disagree with you, feel their concerns are being trivialised, feel rejected and less likely to talk to you about their concerns. Not the way to maintain a therapeutic relationship!

How can you tell if someone’s catastrophising?

The main assessment measure of catastrophising is Sullivan, Bishop & Pivik’s “Pain Catastrophising Scale“.  It’s not the only measure, but it’s one of the most well-known. It’s relatively brief, and has excellent psychometric properties. But if you’re not comfortable using a pen and paper measure, how else can you decide if someone’s tending to think this way?

Some good questions to ask are:

“What do you think is the most likely outcome of this [procedure/painful event]?”

“How are you feeling about this pain?”

“What can you do to help yourself when your pain is like this?”

“How much can you distract yourself from the pain?”

“What do you think this pain means? What’s your theory about this pain?”

If the person answers negatively – for example, they say they can’t even think about an outcome it’s so bad, or they don’t think it’s ever going to get better, or it’s “terrible”, or “awful”; if they say they can’t distract themselves from the pain, they keep thinking about it all the time; and if they think there’s nothing they can do to help themselves, they feel helpless or hopeless; and if they think the pain means something sinister or bad – then you’re likely to have identified someone who is appraising their situation more fearfully than is helpful.

If the person says “Oh but it really is that bad!”

Remember when you were a kid and were terrified of the dark, or bugs, or things under the toilet lid? or when you were really upset and someone said “Calm down!” – remember that flash of anger that the other person was just not aware of how terrified you were? Simply disagreeing or correcting someone is not going to reduce their anxiety.

I find that first of all it’s important to reflect to the person that you understand they are really worried by their pain. Saying something like “It seems that your pain is really bothering you, and you’re really worried about what it means now and might mean in the future. Have I understood you correctly?”

I then find it useful to unpack the specifics of what the person is really worried about. I might ask “When you say the pain is terrible, what does that mean? What do you think might happen?”

What I’m trying to do is reduce the global appraisal the “everything” is “awful”. I want to find out the details, the underlying beliefs that are underneath the fearful appraisal. So, for example, if the answer to the question above is “I feel like I’m going to die, I can’t breathe and it’s frightening” or “I think it’s never going to end, it’s going to be there all the time, forever”, I can begin to gently reality test these beliefs and also provide some skills to help the person get through them.  I firstly reflect what I’ve heard: “It sounds so scary, not to be able to breathe – no wonder you’re feeling afraid” or “I’d be worried too, if I thought my pain was going to be there all the time, forever”.

Then I might begin suggesting we work on ways to handle the emotions associated with this belief (it’s very hard to reality test if the person is very distressed). “I wonder if we could just spend a minute looking at some ways to help you deal with your feelings, so they don’t wind your nervous system up more? Even if it’s frightening, it’s hard to deal with when your body is getting very stressed, so tell me, what do you find works well to help you calm down?” I might either use what the person says, or teach some diaphragmatic breathing and mindfulness.

Then it’s often a good time to work through a nonthreatening explanation of pain. There are so many ways to present this – YouTube videos of Lorimer Moseley “explain pain”, or Mike Stewart “Know Pain”, or the 5 minute pain video by Hunter Integrated Pain Service. Or you can use your own explanations and metaphors that are meaningful to the person. A case formulation can be helpful too.

When should you refer to a psychologist?

I think most people with chronic pain are fine just learning simple skills like breathing, mindfulness and gently approaching movements that they’ve been worried about doing. Even better if this is carried out with a strong eye to what the person can do and wants to be able to do in their everyday life. Success does breed success.

But there are a percentage of people who really struggle with catastrophising. If you find that the person you’re working with can’t use breathing to calm down, finds it really difficult to stop brooding (especially if this is going on all night!), or finds it very hard to accept a different way of viewing pain, then it’s time to work together with a psychologist to develop an approach that combines what you do (restoring occupational engagement or function) with cognitive therapy or ACT (Acceptance and Commitment Therapy). I personally find it’s people who have very rigid beliefs about their pain, about how the world works, and who find it difficult to experiment and try new things that need this kind of input.

So – should we think about catastrophising in our clinical work? Definitely yes. It’s too important to omit. Should we help people who tend to think this way? Definitely yes, it’s not necessarily the remit only of a psychologist, and I’d argue that we ALL need to contribute.

 

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

Bartley, E.J., Rhudy, J.L. (2008). The influence of pain catastrophizing on experimentally induced emotion and emotional modulation of nociception. Journal of Pain, 9(5), 388-396.

Bishop, S.R., & Warr, D. (2003). Coping, catastrophizing and chronic pain in breast cancer. Journal of Behavioral Medicine, 26(3), 265-281.

Buenaver, L.F., Edwards, R.R., & Haythornthwaite, J.A. (2007). Pain-related catastrophizing and perceived social responses: Inter-relationships in the context of chronic pain. Pain, 127(3), 234-242.

Riddle, D.L., Wade, J.B., Jiranek, W.A., & Kong, X. (2010). Preoperative pain catastrophizing predicts pain outcome after knee arthroplasty. Clinical Orthopaedics & Related Research, 468(3), 798-806.

Sullivan, M.J., Bishop, S.R., & Pivik, J. (1995). The pain catastrophizing scale: Development and validation. Psychological Assessment, 7(4), 524. doi: dx.doi.org/10.1037//1040-3590.7.4.524

calm still afternoon

Accepting pain – or are we measuring something else?


Acceptance. Ask a person living with chronic pain whether they accept their pain and the answer is highly probably a resounding “No!”. It’s a word that evokes resignation, feeling helpless and giving up. Or at least that’s what many qualitative papers seem to show (Afrell, Biguet, Rudebeck, 2007; Baker, Gallois, Driedger & Santesso, 2011; Budge, Carryer & Boddy, 2012; Clarke & Iphofen, 2007; Lachapelle, Lavoie & Boudreau, 2008; Risdon, Eccleston, Crombez & McCracken, 2003). I remember when hearing a person tell me “Oh I accept my pain” thinking that this was often a clear indication that underneath it all, the person was pretty angry about the unfairness of pain impacting on their life.

Acceptance is defined in Acceptance and Commitment Therapy (ACT) as “a willingness to remain in contact with and to actively experience particular private experiences (Hayes, Jacobson, Follette, Dougher, 1994) (eds): Acceptance and Change: Content and Context in Psychotherapy. Reno, Context Press, 1994), and from this Lance McCracken and colleagues developed the Chronic Pain Acceptance Questionnaire. This measure has two dimensions: willingness to experience pain and engaging in values-directed activity despite pain.  The other way acceptance has been defined draws from self-regulation, and argues that withdrawing from goals that can’t be achieved, in order to turn to goals that can be achieved is a positive way to cope with life – acceptance is defined as disengaging from a goal to get rid of pain and instead, re-engaging in other goals that aren’t affected as much by pain.

Lauwerier, Caes, Van Damme, Goubert and Rosseel (2015) have recently published a paper reviewing the various instruments that purport to measure pain acceptance. In their analysis, a coding scheme was developed consisting of the three main aspects of acceptance that seem to represent the concept: disengaging from controlling pain, pain willingness (in certain circumstances), and engaging in other valued activities. These three concepts were drawn from the literature – and then there were the left-over concepts that were also present in measures of acceptance. These are the interesting ones!

The addition five codes were: controlling pain, pain costs, pain benefits, unclear and no fit.

They identified 18 difference instruments, of which five didn’t specifically measure acceptance of chronic pain or illness and were therefore excluded from the study, leaving 13 measures to review. The one mentioned the most in the studies reviewed was the Chronic Pain Acceptance Questionnaire-2o.

Moving on to the results, what did these researchers find? And of course, why does it matter

Well, most of the instruments were measuring aspects of acceptance – the Brief Pain Coping Inventory, Chronic Pain Acceptance Questionnaire-A and CPAQ-20, and the Pain Solutions Questionnaire. The original CPAQ and the PASOL were the only two measures with moderate (but the highest percentage) of items with all three acceptance features (disengagement from pain control, pain willingness, and engaging in activity other than pain control), and interestingly, most instruments included “engaging in activities other than pain control”, while the other two factors were less well-represented.

Even more interesting is that many of the items in these instruments were classified as “controlling pain” – in other words, measuring how willing individuals are to carry on with life without trying to control pain. At the same time, many of the instruments also measured “pain costs” – such as “because of my illness, I miss the things I like to do best”.

Then these researchers did some pretty fancy analysis, looking at dimensions contained within all the items from all the measures. What they found was a 2-dimensional solution, with one dimension going from “fully engaged in valued activities” (my description!) to “pain costs”, and the other axis going from “pain willingness” to “controlling pain”.

Conclusions and why this is important

Most of the assessment measures contained some of the concepts thought to be important in pain acceptance, but the aspect most commonly found was engaging in activities other than controlling pain. Items measuring disengaging from trying to control pain, and pain willingness were found less often, while many measures incorporate pain control, and some that reflected pain costs or were unclear. This research seems to show that engagement in activities other than pain control and pain willingness are key features of items measuring acceptance, but at the same time show that not many measures look at both of these concepts together.  Additionally, this research shows that many supposedly “acceptance” instruments actually measure attempts to control pain but then reverse score these items – this can mean that people using these measures interpret them as avoidance measures rather than willingness to experience pain – appealing to quite a different theoretical model (the avoidance or fear-avoidance model) rather than a pain acceptance model.

Why is this research important? Well, acceptance is still a relatively new concept in pain research and clinical practice. While it has been talked about a great deal, and there are numerous studies of acceptance, the instruments developed for such research have not been around very long, and as we can see, don’t always adequately represent the fullness of the theoretical domains. Some aspects are not well-represented or are at risk of being misinterpreted. What works in a research setting may not always be accurately transferred to a clinical setting, especially if clinicians pick up a new measure without reading the theoretical basis for its development.

I also argue on the basis of my research that “disengaging from trying to control pain” doesn’t only need to be represented by items suggesting that people no longer seek treatment. From my findings based on people who live well with chronic pain, treatment is still a feature – but the investment in the outcome of treatment is far less. It’s less important that the pain is removed, treatment is “an option” rather than a necessary part of “returning to normal”.

I also argue that pain willingness is conditional upon the values placed on the activities the individual wants to do. So, if the activity is boring, unpleasant, hard work or doesn’t have rewards to the individual, the person is more than likely to avoid it, but if it’s highly valued then pain becomes a less dominant factor in the decision to do it.

Why should clinicians care? Because acceptance is an exciting and fruitful aspect of living well with pain that we can incorporate into our treatments. Acceptance is about learning to live well, “being with” or “making space” for the presence of pain, so that the other aspects of life are able to be engaged in. That’s important given how few people can have their pain completely reduced.

 

 
Lauwerier, E., Caes, L., Van Damme, S., Goubert, L., Rosseel, Y., & Crombez, G. (2015). Acceptance: What’s in a Name? A Content Analysis of Acceptance Instruments in Individuals With Chronic Pain The Journal of Pain, 16 (4), 306-317 DOI: 10.1016/j.jpain.2015.01.001

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