Pain

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.

Advertisements

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 – and central sensitisation


Last week I started to discuss central sensitisation indicators in people with osteoarthritic knees, based on a paper by Lluch, Nijs, Courtney, Rebbeck, Wylde & Baert, et al (2017). I’m going to continue with this topic this week, because with the rise of osteoarthritis in the general population and particularly the impact of an aging population, I think we will all need to think hard about how we conceptualise osteoarthritis, and what we do for management. While efforts within my own Department (CReaTE – tissue engineering) involve developing new ways to remodel knee-joint tissues, we know that it will be some years before this approach is widely available (human trials haven’t started yet), and given the relative lack of funding for joint replacements, I think developing effective assessment and rehabilitation for painful knees is a real area of development.

So last week I discussed using simple measures such as >5 on a 0 – 10 VAS (NRS), pain drawings/maps showing radiating pain or widely distributed pain, the pattern of pain fluctuation (during activity, with an increase after activity), and using a couple of fairly simple questionnaires to help identify those most likely experiencing more than the “simple” OA pain we’ve learned about. And as always, identifying psychosocial factors which can lead to increased disability and distress is important.

Along with the clinical interview, we usually incorporate physical examination or physical performance testing. There are some indicators that might be useful such as inconsistent responses to our usual physical examination (ie testing increases pain even though some of them shouldn’t do so) – this should not be interpreted as a sign that the person is “faking bad” or exaggerating their experience. I can’t emphasise this enough! It’s possible that anxiety on the part of a person can wind the nervous system up – leading to what is usually non-nociceptive input being interpreted as nociceptive (Courtney, Kavchak, Lowry et al, 2010).

Another indicator is the presence of widespread hypersensitivity to mechanical stimuli – it’s a common finding in people who have central sensitisation and includes increased response to pressure and touch. You could, as a clinician, use a pressure algometer both close to the knee, and further away, to establish over-excitability of the nociceptive pathways. Interpreting findings using pressure algometry is not straightforward because there is overlap between those with OA and those without, but it’s possible to use norms from the general population (such as Nesiri, Scaramozzino, Andersen et al, 2011). It’s a bit of a challenge because of the overlap between the two populations, but can add to the clinical picture. Pain (allodynia) on light touch or being stroked with a cottonwool ball around the knee, is definitely a clue that something’s up.

Both thermal hyperalgesia and tactile hypoaesthesia (reduced sensitivity to von Frey fibre testing) have been associated with central sensitisation – if you don’t have formal testing apparatus, the back of a warmed teaspoon placed on the skin for 10 seconds should be experienced as hot but not painful in someone who isn’t tending to central sensitisation, and you can use cottonbuds (or cottonwool) to identify loss of sensation acuity, provided you do so in a systematic way (the authors suggest starting where it’s most painful and stimulating the skin in a wheel spoke pattern, gradually widening out).

Putting it all together

Any single test, on its own, is unlikely to be a good predictor of central sensitisation, but when combined with the information you obtain from the person, along with the relevant questionnaires, should begin to help develop a picture of who is likely to have a less-than-ideal response to planned trauma. What we do about reducing the potential for central sensitisation is still  begin hotly debated but we DO know that giving good information about pain mechanisms, and encouraging graded exposure and graded activity can be helpful. Given that exercise is a good approach for reducing the impact of osteoarthritis in the knee, for those with the additional burden of central sensitisation, I think swimming or hydrotherapy could also be helpful, as could mindfulness and even mindful movement like tai chi, yoga or xi gong.

Conclusion

People living with OA in their knees often spend many years having difficulty managing their pain before they are able to have surgery. From recent research in New Zealand, I don’t think many people are offered a pain “education” approach, and indeed, I’d bet there are a lot of people who don’t get referred for movement-based therapy either. Misunderstanding is rife in OA, with some people uncertain of the difference between osteoarthritis and rheumatoid arthritis, and others very worried that they’re going to “wear the joint out” if they exercise. While OA isn’t as sexy as low back pain, doesn’t have the economic cost of low back pain, and has a reasonable surgical option – it is still a significant problem for many people. Helping those people be more confident to move, helping reduce their uncertainty about the effect of movement on their joints, and giving them an opportunity to think differently about their knee pain would be a real step forward. Surgery, while helpful for many, is either not available or unsuccessful for others, and it’s time we attended to their needs as well.

 

Courtney CA, Kavchak AE, Lowry CD, et al. (2010). Interpreting joint pain: quantitative sensory testing in musculoskeletal management. Journal of Orthopaedic Sports Physical Therapy. 40:818–825.

Lluch Girbes E, Meeus M, Baert I, et al. (2015) Balancing “hands-on” with “hands-off” physical therapy interventions for the treatment of central sensitization pain in osteoarthritis. Manual Therapy. 20:349–352.

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

Neziri AY, Scaramozzino P, Andersen OK, et al. (2011). Reference values of mechanical and thermal pain tests in a pain-free population. European Journal of Pain. 15:376–383.

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

Primary pain disorders


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

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

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

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

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

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

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

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

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

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

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

  1. Dunn, K.M., Hestbaek, L., & Cassidy, J.D. (2013). Low back pain across the life course. Best Practice & Research in Clinical Rheumatology, 27(5), 591-600.
  2. Artus, M., van der Windt, D., Jordan, K.P., & Croft, P.R. (2014). The clinical course of low back pain: A meta-analysis comparing outcomes in randomised clinical trials (rcts) and observational studies. BMC Musculoskeletal Disorders, 15, 68.
  3. Vasseljen, O., Woodhouse, A., Bjorngaard, J.H., & Leivseth, L. (2013). Natural course of acute neck and low back pain in the general population: The HUNT study. Pain, 154(8), 1237-1244.
  4. Hoy, D., March, L., Brooks, P., Blyth, F., Woolf, A., Bain, C., . . . Buchbinder, R. (2014). The global burden of low back pain: Estimates from the global burden of disease 2010 study. Annals of the Rheumatic Diseases, 73(6), 968-974.
  5. Campbell, P., Foster, N.E., Thomas, E., & Dunn, K.M. (2013). Prognostic indicators of low back pain in primary care: Five-year prospective study. Journal of Pain, 14(8), 873-883.
  6. Axén, I., & Leboeuf-Yde, C. (2013). Trajectories of low back pain. Best Practice & Research Clinical Rheumatology, 27(5), 601-612. doi: http://dx.doi.org/10.1016/j.berh.2013.10.004
  7. Hoy, D. G., Smith, E., Cross, M., Sanchez-Riera, L., Buchbinder, R., Blyth, F. M., . . . March, L. M. (2014). The global burden of musculoskeletal conditions for 2010: an overview of methods. Annals of the Rheumatic Diseases, 73(6), 982-989. doi:10.1136/annrheumdis-2013-204344

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


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

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

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

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

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

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

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

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

 

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

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

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

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

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

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

The “Subjective” – and really hearing


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

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

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

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

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

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

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

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

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

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

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

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

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

 

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

Mulling over the pain management vs pain reduction divide


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

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

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

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

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

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

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

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

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

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

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

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

 

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

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

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

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