Science in practice

Back to basics about psychosocial factors and pain – iv


Part of the definition of pain is that it is “a sensory and emotional experience” – in other words, emotions of the negative kind are integral to the experience of pain. Is it any wonder that poets and authors have written so eloquently about the anguish of unrelieved pain? As I write this, I’ve been pondering the way “psychosocial” has been used when discussing pain, as if those factors aren’t experienced by “normal” people, as if the way we feel about pain and the way people who struggle with their pain feel are two entirely different things.

Chris Eccleston, someone I admire very much, writes about a “normal psychology of chronic pain” and makes some incredibly useful points: that pain is a normal feature of human life. Pain is an everyday occurrence (watch kids playing in a playground – every 20 minutes kids communicate about pain, Fearon et al, 1996). In New Zealand one in five people report experiencing pain lasting six months or longer. Pain really is all around us – and it’s normal and indeed part of the experience itself, to feel negative emotions such as fear, anger, sadness, anxiety, and such when we’re sore.

So why have emotions been lumped in with “other factors” as part of the negative way psychosocial factors are interpreted today? I personally think it’s partly a hangover, in NZ at least, from the way our stoic forebears viewed “weakness”. There wouldn’t be many families in New Zealand who haven’t heard something like “man up”, or “big boys don’t cry”, or “pull yourself together” with great All Blacks who played on despite broken ribs or arms – who didn’t give in when they were injured being held up as examples we should emulate. At the same time pain isn’t given much space in our health professional training programmes – and when it is, it’s primarily viewed in a neuroanatomical way, as we’re taught about spino-thalamic tracts, and nociceptors, and not much else. In fact, I think the gate control theory is still being taught as the main theory in some programmes (despite it being revised and replaced with more sophisticated models).

So what is normal? I really like Acceptance and Commitment Therapy, as you’ve possibly noticed. Amongst one of the many reasons I like it so much is its view of suffering. Within ACT, being psychologically inflexible is the problem – that is, working hard to avoid or control experiences we don’t want, getting caught up in thoughts as if they’re Truth instead of our mind’s opinion of things, being attached to someone’s idea of who and what we are, living in the past or predicting the future, and failing as a result to take actions that line up with what our personal values are. When we get stuck thinking there’s only one way to deal with a situation, and when we forget about what’s important in our lives because we’re working so hard to avoid certain experiences – these aren’t seen as pathological, but instead are just part of the way our mind/language and experience tangle us up. The beauty is that there are ways out of being stuck but they’re counter-intuitive.

What do I mean? Well if we all have negative emotions about pain, why do only some of us struggle with that experience and get stuck? For some people it’s because they’re trying so hard not to feel pain that they spend time and energy doing things to control it and in the process stop doing things that matter. Think of the many appointments and the ups and downs of hope that it will all go away with this magic thing – then despair as it doesn’t work. Just the amount of time people spend waiting for and attending appointments can take time away from being with family, working, living…Now to me, this is not psychopathology. This is what normal minds do – try to fix a problem using strategies that have always worked in the past.

At the same time, given pain is a negative experience, doesn’t it make sense to monitor what went on last time you tried to lift that box, go to work, drive the car… AND doesn’t it make sense to anticipate what might go wrong if you try it again? This isn’t about being depressed, anxious or any other kind of pathology – this is just what we’ve learned to do, and our minds are trying incredibly hard to make it work again.

When I mentioned that a solution might be counter-intuitive, what I mean is recognising that trying to control or avoid an experience that comes with us wherever we go because it’s part of us, can trip us up. Instead, we might do better if we soften our attempts to control or avoid our experience of pain. Maybe spending time exploring pain and doing things alongside pain is possible – especially if the things we want to do are important to us. Don’t believe me? Think about marathon runners – they feel the pain (hit the wall) and still keep running! Why? Because it’s important to them to get to the end.

Now I’m not suggesting that ALL people will find this approach helpful, and I’m NOT denying that many people with persistent pain experience depression, anxiety, rotten sleep and generally feel demoralised. What I AM saying is that if we approach everyone with the misguided idea that psychosocial factors exist only in “those people”, we’re wrong. Any one of us will experience negative emotions if pain is present – and even more if pain persists. This is a normal response to a challenging and inherently aversive experience. Of course, if we’ve experienced depression, adverse life events, turmoil in our home and work life, and the stigma of not being believed, the potential to then become angry, depressed, and fed up is only greater. Let’s not make a negative experience worse by stigmatising people with the notion that “psychosocial factors” makes them any different from anyone else.

 

Eccleston, C. (2011). A normal psychology of chronic pain. Psychologist, 24(6), 422-425.

Fearon, I., McGrath, P.J., Achat, H. (1996). ‘Booboos’: The study of everyday pain among young children. Pain, 68, 55-62.

Vowles, K. E., Witkiewitz, K., Levell, J., Sowden, G., & Ashworth, J. (2017). Are reductions in pain intensity and pain-related distress necessary? An analysis of within-treatment change trajectories in relation to improved functioning following interdisciplinary acceptance and commitment therapy for adults with chronic pain. Journal of consulting and clinical psychology, 85(2), 87.

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Back to basics about psychosocial factors and pain – iii


Last week I discussed some of the areas in the brain, and basic principles, that are currently thought to influence our pain experience. This week I thought I’d introduce one of my favourite ways of considering pain mechanisms, mainly because it helps me think through the four main kinds of mechanisms, and can influence our treatment approach. At this stage I want to raise my hand to acknowledge the following:

  • My gratitude to Dr John Alchin, longtime friend and colleague, who first pointed this paper out to me and has shared it with hundreds of people who go to see him at the local tertiary pain management centre.
  • We know this is a simplified, under-developed approach to mechanisms underpinning pain, but it’s helpful nevertheless.
  • Most of our patients will have a combination of mechanisms involved in their experience, not just one.
  • This approach to mechanisms doesn’t include the psychological or social – just the primary biological processes.
  • Throughout this blog, when I use the word “pain” I mean the experience we have once whatever mechanisms involved filter up through to our awareness. So while I talk about peripheral mechanisms, they’re only experienced as pain once we become aware of them – and that process involves a whole lot of what I discussed in my last post .

Clifford Woolf wrote this paper in 2010, and although the research into mechanisms has continued unabated, I think it provides clinicians with a reasonable guide to considering how best to tackle treatment. He begins by dividing the mechanisms into “useful” and “useless” pain – ie pain that is useful for adaptation, survival, warning, alerts. Just as it’s possible to have dysfunction or disease of our cardiac, pulmonary, gastro-intestinal, and skeletal systems, I think it’s just as plausible that we can have something go wrong with our nociceptive system. In fact, because of its complexity, it seems probable to me at least that there are many different ways this system can fail to work properly. But more about that shortly! Let’s begin with the useful pain.

Nociceptive pain – is considered to be pain that is, as Woolf puts it, our “early-warning physiological protective system”. When we touch something super cold, super hot, or a chemical that can harm us (think chilli pepper!), or meet a mechanical force that activates mechano receptors, our high threshold nociceptors are activated – well in advance of tissue damage, I quickly add. This process activates withdrawal – even in simple single-celled animals – and saves us from harm. When combined with behavioural responses including vocalisation, grimaces and other pain behaviours, we signal to everyone around us that we’re in danger, and others shouldn’t do what we’ve just done (Melzack, Dennis, Kosterlitz & Terenius, 1980).  For me, the cool thing about nociceptive pain is that once you’ve removed that stimulus (got rid of the chilli on your lips, let go of the ice-cube or the hot mug of coffee, or shifted in your seat to relieve your butt) the pain simply goes away. Just like that. How cool?!

Inflammatory pain – is also a useful pain to have. Unlike nociceptive pain, inflammation involves disruption to the tissues, triggering a release of a whole bunch of neurochemicals and cells that quickly lower the point at which nociceptors will fire (making you much more sensitive to mechanical, chemical and temperature input), and increasing the blood supply to allow foreign material, dead cells and spent neurochemicals to be whisked away. Inflammation is reasonably easy to see in the periphery (though not so easy in the internal organs because the innervation is more diffuse) and you’ll all have had it – think sunburn (I know you’re not meant to, but everyone gets sunburned at least once, especially in our NZ sun). With sunburn you’re red, hot and often swollen, and you really know it when you step into the shower! That experience of ouch! to your usual shower temperature (and the ouch! when you towel down) is allodynia, or the experience of pain when a usually comfortable stimulus is applied. You’ll experience hyperalgesia if your mate comes along and slaps you on your sunburned shoulders!

Now both of these mechanisms are useful because they alert us to threat, they make it more difficult to move around, and we often respond to them with changes in our behaviour that act as a signal to others around us. Let’s turn the attention to two mechanisms where there is something gone awry with the nervous system – in other words, useless pain.

Neuropathic pain – is defined by IASP as “pain caused by a lesion or disease of the somatosensory nervous system.” What this means is that there must be an identifiable lesion in the nervous system somewhere – something that can be imaged or tested to demonstrate damage. This could be in the periphery – think of radial nerve entrapment with its characteristic tingling, deep aching and burning over the distribution of the nerve. It could be in the spinal cord itself – think of a complete spinal cord injury where the person is unable to move from the lesion down, and who also gets the same tingling, aching, burning and electric shock pain over the same area. A simple example would be radicular pain where the nerve root is compressed – and this can be seen on imaging, and where the pain is experienced over the same nerve distribution. The final group in this nasty set of neuropathies is when someone has a stroke, where part of the brain is damaged leading to intractable, deep, aching pain with electric shock-like pain just to make it nastier. For a great paper reviewing neuropathic pain, Finnerup and colleagues wrote one published in 2016 (see below), describing a grading system to indicate possible, probable and confirmed neuropathic pain. The hallmark of this pain is that it doesn’t represent tissue damage except in the area of the nervous system where the lesion is located. In other words, that pain down the leg is not where the problem lies in radicular pain – it’s near the spinal cord. So this pain doesn’t have a function for survival – it’s just a horrid nuisance.

The final mechanism is poorly understood – even less well understood than neuropathic pain. This is where ostensibly the nervous system appears intact. The pain experience might be in multiple parts of the body, it could be just in the head (migraine, for example), or it could be just in the shoulder (frozen shoulder maybe?), or it might be everywhere (fibromyalgia). The name isn’t even completely determined – it’s called “dysfunctional” by Woolf, and he collapsed this and neuropathic pain into one mechanism, but I prefer to keep it separate because it’s more helpful for management especially when a neuropathy might be amenable to surgery. Another term, and one I like, is nociplastic – referring to the idea that it’s the unhelpful neuroplasticity of our nervous system that has over-responded to potential threat (Kosek, Cohen, Baron et al, 2016). Some would argue that this mechanism is partly a general tendency to a lower nociceptive threshold, maybe genetic, maybe behavioural (ie we’ve learned to monitor and respond to threat perhaps because of early life experiences), perhaps a diathesis-stress where the predisposition exists but it’s not brought into expression until a stressor, perhaps a virus or an injury, exerts an influence on homeostasis.

Ultimately, pain is an experience that we’ve all had, and one that has individual meaning for each of us based on our previous experiences, predictions for the future, current goals, culture and biology. What a mechanisms-based approach to pain management might mean is better and more accurate management for each one. So we’d be looking to remove that bunion so people can walk more easily; reduce the inflammation in an auto-immune disease; decompress a squished nerve in neuropathic pain and look to altering plasticity in nociplastic pain. But pain is weird and as I said at the very beginning, it’s entirely possible to have more than one mechanism involved – and because pain is not just biology, we’d be foolhardy to think that just by down-tuning the intensity, everyone so treated will go “back to normal”. More on that next week!

 

 

Finnerup NB, Haroutounian S, Kamerman P, et al. Neuropathic pain: an updated grading system for research and clinical practice. Pain. 2016;157(8):1599-1606. doi:10.1097/j.pain.0000000000000492.
Kosek, E., Cohen, M., Baron, R., Gebhart, G. F., Mico, J. A., Rice, A. S., … & Sluka, A. K. (2016). Do we need a third mechanistic descriptor for chronic pain states?. Pain, 157(7), 1382-1386.

Melzack, R., Dennis, S. G., Kosterlitz, H. W., & Terenius, L. Y. (1980). Phylogenetic evolution of pain-expression in animals. Pain and Society, 13-26.

Woolf CJ. What is this thing called pain? The Journal of Clinical Investigation. 2010;120(11):3742-3744. doi:10.1172/JCI45178.

Back to basics about psychosocial factors and pain (ii)


But what about the bio? No, not the biographical, the biological! It’s something I often get asked – like “if you think pain is psychological/psychosocial factors play a part then you’re obviously not including the biological” – oh woe is me, for no, pain definitely involves the biological. But it’s not quite as simple as we’ve come to believe.

Let’s begin at the very beginning. Can we have pain – and not know about it?

The answer is – no, and that’s exactly why anaesthetics are used. The distinction between pain and nociception is that it’s entirely possible for nociception to be occurring all the time, even while unconscious, whereas pain can only be experienced by a conscious person. What this means is nociception is about activity in the nociceptive system right up until the point at which we become conscious of it. And the point at which we become conscious of the ouch shifts depending on a bunch of things, one of which is how much attention we have available, our current goals, whether we’ve had this experience before, what we think the experience is about, and what we’ve learned about this experience from our community.

So, I’m going to discuss pain biology from the brain down instead of nociceptive fibres because our brains are not just blank pages waiting for information to hit it – but actively filter, select and augment information to (a) keep us alive and safe, and (b) help us reach our goals. Louis Gifford put this nicely – our brain is sampling from our context, cognitive set, mood, chemical and structural inputs (neurodegeneration, metabolic changes and plasticity) as well as our current sensory input (which is the bit we usually start from). What the brain then does is generate outputs – the experience of pain, movements, immune response, endocrine responses, and what goes on in our somatosensory system (Gifford, 1998).

What parts of the brain are active when we feel pain?

Well, there are at least three parallel cortical processes – one is essentially about where we hurt and involves the S1 or somatosensory cortex, the parietal operculum, the cingulate cortex and the posterior insula. The second is about attention or salience and involves the anterior cingulate cortex, the amygdala and the anterior insula. The third is about generating and integrating a behavioural response – and involves the frontal cortex (orbitofrontal, anterolateral and prefrontal), the middle cingulate cortex, and the posterior cingulate cortex. (Fenton, Shih, & Zoltan, 2015).

Now before I go any further, I want to point out that our understanding of these networks is based on various brain imaging studies – and brain imaging studies do not show the “what it is like” to experience pain. Our understanding is incomplete still because imaging technology is still evolving (see Borsook, Sava & Becerra (2010) for more information). But it is from the studies that we begin to  get an understanding of the complexity of the processes and networks involved in producing our experience – no wonder some feel overwhelmed by the sheer volume of information we could explore when trying to understand pain! Especially if our focus has traditionally been on peripheral to spinal nociceptive processing – by the time we get to the brain we’re overloaded and it just seems a bit hard to comprehend.

When we investigate what Melzack calls the “neuromatrix” we need to remember that our understanding is incomplete. What we do know is there is no “pain matrix” but instead there is a salience matrix where simultaneous processing across multiple locations in the brain occur. These locations include areas generally associated with emotions, areas associated with cognitions, and with location and response generation. And importantly, there is never a time when these areas are completely inactive – there is constant activity throughout the networks, meaning that when a stimulus arrives from the periphery, it arrives into an active “salience” network – always determining the question “compared with what is happening right now (goals and alertness) how dangerous/important is this really?”

For a lovely image showing the various areas of the brain involved in processing this experience – click here for the full article – take a look at this image from Denk, McMahon & Tracey (2014)

Now if you’re wondering why I haven’t covered the brainstem and spinal cord etc – do not worry, these will be coming soon! But I won’t be discussing nociception because this is usually discussed in undergraduate training and is often the focus and only aspect of pain covered!

Next time – delving into mechanisms!

What are the implications of the complexity of central processing?

  1. The brain is not simply waiting for information – it actively seeks information relevant to survival
  2. Psychological processes such as attention, emotion and decision-making are biological
  3. The point at which we become aware of pain shifts depending on inputs (bottom up) as well as salience, emotions and consciousness (top down) and contextual factors including what we learn from our socio-cultural environment

And what this means is that psychosocial factors are integral to a biopsychosocial framework for understanding pain. In other words – it is not possible to divide the experience of pain into biological, psychological or social only, except for teaching/learning purposes.

 

 

Borsook, D., Sava, S., & Becerra, L. (2010). The pain imaging revolution: advancing pain into the 21st century. Neuroscientist, 16(2), 171-185. doi:10.1177/1073858409349902

Denk, F., McMahon, S. B., & Tracey, I. (2014). Pain vulnerability: A neurobiological perspective. Nat Neurosci, 17(2), 192-200. doi:10.1038/nn.3628

Fenton, B. W., Shih, E., & Zolton, J. (2015). The neurobiology of pain perception in normal and persistent pain. Pain Management, 5(4), 297-317.

Gifford, L. (1998). Pain, the Tissues and the Nervous System: A conceptual model. Physiotherapy, 84(1), 27-36. doi:10.1016/S0031-9406(05)65900-7

Back to basics about psychosocial factors in pain (i)


From time to time I see a flurry of tweets or Facebook posts about pain and psychosocial factors. Many of them are informative, intriguing and empathic, but some are just plain wrong. The ones I most get upset about are those arguing that because someone has “psychosocial factors” their pain must be psychological in origin, followed closely by the idea that psychosocial factors equate to psychopathology. This is a series of back to basics posts where I hope to set these things right.

Pain, according to the current definition, is

“an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”[7] is derived from a 1964 definition by Harold Merskey,[8] and it was first published in 1979 by IASP in PAIN, number 6, page 250.

An associated note, which should be read alongside this definition is:

Note: The inability to communicate verbally does not negate the possibility that an individual is experiencing pain and is in need of appropriate pain-relieving treatment. Pain is always subjective. Each individual learns the application of the word through experiences related to injury in early life. Biologists recognize that those stimuli which cause pain are liable to damage tissue. Accordingly, pain is that experience we associate with actual or potential tissue damage. It is unquestionably a sensation in a part or parts of the body, but it is also always unpleasant and therefore also an emotional experience. Experiences which resemble pain but are not unpleasant, e.g., pricking, should not be called pain. Unpleasant abnormal experiences (dysesthesias) may also be pain but are not necessarily so because, subjectively, they may not have the usual sensory qualities of pain. Many people report pain in the absence of tissue damage or any likely pathophysiological cause; usually this happens for psychological reasons. There is usually no way to distinguish their experience from that due to tissue damage if we take the subjective report. If they regard their experience as pain, and if they report it in the same ways as pain caused by tissue damage, it should be accepted as pain. This definition avoids tying pain to the stimulus. Activity induced in the nociceptor and nociceptive pathways by a noxious stimulus is not pain, which is always a psychological state, even though we may well appreciate that pain most often has a proximate physical cause.

The final sentence in the note is important, distinguishing between the experience of pain and the biological apparatus transmitting information from the nociceptors, ending in a bunch of places in the brain. I personally dispute the sentence “many people report pain in the absence of tissue damage or any likely pathophysiological cause; usually this happens for psychological reasons” because (recall when it was first written) science has moved on and we now have good evidence supporting the notion that abnormal processing is involved in cases such as migraine (Iyengar, Ossipov & Johnson, 2017; Pietrobon, 2017) and fibromyalgia (Schmidt-Wilcke & Diers, 2017; Tour, Lofgren, Mannerkorpi, Gerdle, Larsson, Palstam et al, 2017). As a side note, I love science because we can revisit beliefs and revise our understanding as more information is collected – whether we’ll ever get to the “truth” is debatable, but we can get closer and closer as we continue learning (see Bhaskar).

Back to basics. It’s evident that ALL pain is a psychological experience and therefore will be influenced by our current goals, past experiences and predictions for the future. And these aspects of attention, motivation, memory and decision-making are present in all of us and for every sensory experience. Take sound, for example. I’m sitting at home listening to a large truck rumbling away, dumping construction materials in the section two doors down. That sound is so like the deep rumble and thud of an earthquake that I’m aware I’m on edge because, after more than 10,000 earthquakes since the first one in the Canterbury region this day seven years ago, my nervous system has learned to be on high alert – who knows what could happen next?

Seven years of learning, 10,000 earthquakes-worth of learning, lots of emotions and lots of very real and scary outcomes. It affects people. In the same way, pain, which we learn about from birth, is influenced by personal experience, by other people’s experiences, and by prevailing community attitudes. This is not psychopathology – at least, not for me though some people have experienced PTSD as a result of the earthquakes we’ve been through. You’d likely do that if you were trapped in a building with no way out, and countless aftershocks continuing while rescuers try to get to you. Most people in Christchurch, however, have simply learned to be aware of sights and sounds that signal a quake – and quickly get back to usual once the sounds have gone. Similarly, most people who experience pain, don’t have a mental health problem – they’ve learned, as we all do, that pain is unpleasant, and learn to avoid situations where pain is likely to occur. In our society, experiencing pain is not viewed as “normal” and indeed, some people have called us “algophobic” – afraid of pain (Kugelmann, 2016). This means we’ve learned to look for ways to get rid of our pain, even if it’s not very intense – because pain means something is “not right” with us.

And one of the functions of pain is to alert us to the potential that something is threatening our bodily integrity, and withdraw or avoid such situations (ie, to learn from them). And as a species we’re designed to be social, so we also display behaviour when we’re hurt that others can see – thus helping spread the word “don’t do that dumb thing!” (Steinkopf, 2016).

To summarise: pain is an experience we’ve all had, and yet it remains something we don’t fully understand. Irrespective of the modality of sensory experience, humans are hard-wired to make sense of, and act upon, experiences based on prior learning, current goals and future predictions, within a context that is inherently social. We’re actively engaged in making sense of our experiences so we can remain safe and give and receive support from those around us. While the experience is psychological, the apparatus producing that experience is biological, filtered through our social and contextual experiences. Like taste, sound, and colour – pain is inherently subjective.

Next post – does this mean the biological is redundant?

Iyengar, S., Ossipov, M. H., & Johnson, K. W. (2017). The role of calcitonin gene–related peptide in peripheral and central pain mechanisms including migraine. Pain, 158(4), 543.
Kugelmann, R. (2016). Constructing Pain: Historical, psychological and critical perspectives. Taylor & Francis.
Pietrobon, D. (2017). Lessons from familial hemiplegic migraine and cortical spreading depression. Neurobiological Basis of Migraine.
Schmidt-Wilcke, T., & Diers, M. (2017). New Insights into the Pathophysiology and Treatment of Fibromyalgia. Biomedicines, 5(2), 22.
Steinkopf, L. (2016). An evolutionary perspective on pain communication. Evolutionary Psychology, 14(2), 1474704916653964. doi:doi:10.1177/1474704916653964
Tour, J., Löfgren, M., Mannerkorpi, K., Gerdle, B., Larsson, A., Palstam, A., … & Schalling, M. (2017). Gene-to-gene interactions regulate endogenous pain modulation in fibromyalgia patients and healthy controls—antagonistic effects between opioid and serotonin-related genes. Pain, 158(7), 1194.

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

Lluch, E., Nijs, J., Courtney, C. A., Rebbeck, T., Wylde, V., Baert, I., . . . Skou, S. T. (2017). Clinical descriptors for the recognition of central sensitization pain in patients with knee osteoarthritis. Disability and Rehabilitation, 1-10. doi:10.1080/09638288.2017.1358770

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

Conversations about cannabis for chronic pain


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

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

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

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

Why might I support a change to marijuana laws?

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

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

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

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

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

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

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

My conclusion?

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

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

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

 

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

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

Exercise? Who me? Yoga or physiotherapy or education…


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

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

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

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

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

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

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

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

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

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

 

 

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

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

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


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

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

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

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

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

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

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

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

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

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

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

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

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

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

The take-home messages from this study are these:

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

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

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

Being mindful about mindfulness


I’m generally a supporter of mindfulness practice. It’s been a great discipline for me as I deal with everyday life and everything. I don’t admit to being incredibly disciplined about “making time for meditation” every day – that is, I don’t sit down and do the whole thing at a set time each day – but I do dip in and out of mindfulness throughout my day. While I’m brushing my teeth, slurping on a coffee, driving, sitting in the sun, looking at the leaves on the trees, cuddling my Sheba-dog I’ll bring myself to the present moment and take a couple of minutes to be fully present. Oddly enough I don’t do this nearly as often when I’m cold (like this morning when it’s about 8 degrees in my office!), or when I’m eating parsnip (ewwwww!), or waiting to see a dentist. Or perhaps that’s not odd at all, because I wonder if we have a skewed view on mindfulness and what it’s about.

My reason for writing this post comes from reading Anhever, Haller, Barth, Lauche, Dobos & Cramer (2017) recent review of mindfulness-based stress reduction for treating low back pain. In it, they found “MBSR was associated with short-term improvements in pain intensity (4 RCTs; mean difference [MD], −0.96 point on a numerical rating scale [95% CI, −1.64 to −0.34 point]; standardized mean difference [SMD], −0.48 point [CI, −0.82 to −0.14 point]) and physical functioning (2 RCTs; MD, 2.50 [CI, 0.90 to 4.10 point]; SMD, 0.25 [CI, 0.09 to 0.41 point]) that were not sustained in the long term.” There were only seven RCTs included in the study, with a total of only 864 participants, and many of the studies had no active control groups, so my interpretation is that there are flaws in many of the studies examining MBSR, and that it’s difficult to draw any conclusions, let alone strong conclusions.

Where do we go wrong with mindfulness? The first point about the studies included in Anhever and colleagues paper is that there is a difference between mindfulness in general and mindfulness based stress reduction – and although the difference may be minimal, it’s nevertheless worth understanding. MBSR is a full programme that includes mindfulness as one element (Kabat-Zinn, 1982). Mindfulness is a key component, yes, but the programmes include other elements.  The second point is that perhaps we’re assuming mindfulness to be something that it isn’t –  I suspect, from reading numerous articles in both the popular media and research papers, that mindfulness is being applied as another form of relaxation.

Relaxation training was introduced as part of a behavioural approach to managing stress. In pain management it’s been part of programmes since the 1970’s, particularly using forms of progressive muscle relaxation (See Dawn & Seers, 1998). The intention is to provide an experience that is incompatible with tension, and to develop the capability to down-regulate the body and mind to mitigate the stress response that is so often part of persistent pain.

Relaxation training can take many forms, and breath control is a common component. I use it often for myself, and when working with clients – I’m aiming to show people that although they may not be able to control heart rate or blood pressure, they can control breath and muscle tension. It’s useful especially as part of sleep management.

The thing with relaxation training is it’s entire purpose is to help downregulate an upregulated nervous system. Mindfulness, on the other hand, is not.

What is mindfulness about if it’s not about relaxation? Well, mindfulness has been defined in many different ways, but the one I especially like is by Kabat-Zinn (1990) “a process of bringing a certain quality of attention to moment-by-moment experience”.  This definition can be further unpacked by examining its components: “Mindfulness begins by bringing awareness to current experience—observing and attending to the changing field of thoughts, feelings, and sensations from moment to moment—by regulating the focus of attention.” (italics are mine) –  this quote is from Bishop, Lau, Shapiro and colleagues (2004) and is from a paper looking at defining mindfulness in an operational way (so we can be aware of what it means in practice, or as we teach others). These authors go on to say that this process leads to a feeling of being very alert to what is occurring in the here and now. I like to remind people that it’s about being here rather than remembering or anticipating what might.

So at least one part of mindfulness is learning how to attend to what YOU want to attend to, rather than being dragged back to memories, or forward to predictions, or to experiences or moments that you don’t want to notice at that moment.  The definition also points to noticing and experiencing what is happening, rather than thoughts or ruminations about what you’re experiencing. For people living with persistent pain, I think this is an invaluable tool for dealing with the interruptive effects of pain on attention.

A second aspect of mindfulness is an attitude – one of curiosity. When being mindful, you’re not trying to produce any particular state, instead you’re being curious about what you are experiencing, whether it’s something you’d ordinarily want to experience – or not. This approach to experience is really similar to what we’re aiming for in persistent pain management – acknowledging and being willing to experience what is, rather than attempting to avoid that experience, or quickly change it to something more palatable.

Now this aspect of mindfulness is often brought to bear on new and pleasant experiences – sometimes people are asked to mindfully eat a raisin, or mindfully examine a ballpoint pen (one of my favourites). But it’s also just as valid to bring this attitude to bear on less than pleasant experiences like my cold fingers and legs (it’s cold in my office this morning). Or to pain and where it is – and where it isn’t.

So I wonder if part of our approach to using mindfulness in pain management is incorrect. If we’re intending people to come away from mindfulness feeling relaxed and calm, perhaps we’re doing it wrong. If we think people should feel better after mindfulness, again, perhaps we’re doing it wrong. Sometimes, yes, these are the effects we’ll have. Other times, not so much. What we will always develop, over time, however, is better ability to focus attention where we want it to go, and more openness to being present to what is rather than struggling against it. And I think those are incredibly valuable tools in life, not just persistent pain management. And perhaps, just perhaps, if we began viewing our use of mindfulness in these ways, the outcomes from RCTs of mindfulness might show more of what it can do.

 

Anheyer, D., Haller, H., Barth, J., Lauche, R., Dobos, G., & Cramer, H. (2017). Mindfulness-based stress reduction for treating low back pain: A systematic review and meta-analysis. Annals of Internal Medicine, 1-9. doi:10.7326/M16-1997

Dawn, Carroll, and Kate Seers. “Relaxation for the relief of chronic pain: a systematic review.” Journal of advanced nursing 27.3 (1998): 476-487.

Kabat-Zinn, J. (1990). Full catastrophe living: Using the wisdom of your mind to face stress, pain and illness. New York:Dell.

Kabat-Zinn, J. (1982). An outpatient program in behavioral medicine for chronic pain patients based on the practice of mindfulness meditation: Theoretical considerations and preliminary results. General hospital psychiatry, 4(1), 33-47. doi:http://dx.doi.org/10.1016/0163-8343(82)90026-3

…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.