Getting persistent pain and disability confused

As I read blogs and tweets and posts on social media, and even peer reviewed papers in journals, I often read that what we’re trying to do in sub-acute pain management is to prevent chronic pain from developing (note, when I talk about pain that goes on beyond healing, more than three months, or has no useful function, I may use the term “chronic” or I may use the more recent term “persistent” – they mean the same thing, except persistent has perhaps less baggage…).

I want to take aim at that focus – to prevent pain from persisting – and think carefully about it. Let’s take a 56 year old woman with a painful knee, a knee that’s been diagnosed as having osteoarthritis (OA). Now, although we have surgical management for OA (a knee replacement – uni-compartment or even a total knee replacement), in most cases surgeons are not enthusiastic about doing a knee replacement on a younger person, particularly someone who is active (plays netball, golf, runs, gardens). So if a knee replacement is not a thing – yet – what do we do? Most of us will know about the value of remaining active and fit, losing weight and maintaining good range of movement (see here for the NICE guidelines, 2017). We know that these things will maintain function – but they won’t stop cartilage deterioration (much, if at all), and they won’t stop the pain. No matter what we do – even medications are not always especially helpful – pain is likely to persist. Does that mean we’ve failed? Reading some of these blogs, it certainly seems it does.

Let’s take back pain – most of us will know back pain occurs periodically throughout life, from the time we’re teens, through to old age. In some people a single bout of back pain happens and then they’re fully recovered and never bothered again, but for many of us, we’ll be troubled with repeated bouts throughout our lives. And still others will have one bout than just never ends (Axen & Leboeuf-Yde, 2013; Vasseljen, Woodhouse, Bjorngaard, & Leivseth, 2013).  This is despite our best efforts to prevent the onset of low back pain, and to treat it effectively – pretty much all our treatments provide a small amount of help but only exercise has been shown to prevent a new bout after the first one (Choi, Verbeek, Wai-San Tam & Jiang, 2010) – and even then the evidence was “moderate” and only at one year.

So… when we begin to examine claims that by treating musculoskeletal problems early we can prevent pain from becoming chronic or ongoing, I think we need to stop and pause before letting the blood rush to our head.

If we can’t prevent pain from hanging around, what can we do? What is the aim of all this treatment?

Well, let’s take a quick look at the Global Burden of Disease (Hoy, March, Brooks, Blyth, Woolf, Bain et al, 2014). In this piece of work, “Out of all 291 conditions studied in the Global Burden of Disease 2010 Study, LBP ranked highest in terms of disability (YLDs), and sixth in terms of overall burden (DALYs). The global point prevalence of LBP was 9.4% (95% CI 9.0 to 9.8). DALYs increased from 58.2 million (M) (95% CI 39.9M to 78.1M) in 1990 to 83.0M (95% CI 56.6M to 111.9M) in 2010. Prevalence and burden increased with age.” [emphasis mine].

What this means is that although low back pain is not a fatal disease, that may well be the problem – people don’t die from low back pain, they live with disability all the days of their life. And worse, the burden of low back pain is increasing. And this is despite all the work we (you, me, the entire health system) is putting in.

If we can’t “get rid of” low back pain (and it looks like we don’t yet have the tools to do so), what are we trying to do?

Given our poor outcomes for completely curing low back pain, we need to aim to reduce the impact of pain on people’s lives.

And not just low back pain, but things like tennis elbow, frozen shoulder, neck pain, abdominal pain, pelvic pain, headache, migraine, osteoarthritis…

For a moment, let’s think about the effect on a person going through treatment, being promised that “pain education” will reduce their pain, that exercises will get rid of their pain, that gadget A or B will get rid of their pain, that treatment Y or Z will get rid of their pain. What do you think it feels like to be completely adherent about everything you’re being asked to do, but still feeling a failure because that pain does not go? Think of the language used by some of our colleagues – “failed back syndrome”? Who failed, exactly?

Before I get harangued for breathing the word that, ooops, our treatments don’t work very well, let me address the issue of “pain education” and pain intensity. Don’t forget that the only way we can know how much it hurts someone is by asking them. And our usual tool is that 0 – 10 scale, where 0 = no pain and 10 = most extreme pain imagined. Have you ever tried doing that on yourself? Seriously – how do you rate your own pain? Some of that pain rating is about how much we’re prepared to (capable of) putting up with. Some of that rating is about how bothered (fed up, distressed, frustrated) we are about our pain. Some of it is about “OMG I don’t know what this is and how long it’s going to go on for”.

What this means is that when someone gives an explanation it can –

• make the experience less frightening,
• less distressing,
• more understandable,
• less bothersome

and as a result, when we’re then asked for our pain intensity rating on that darned scale, we reduce the score we give our pain. It does not necessarily mean the pain has reduced in intensity – a pain scale is a means of communicating something about our experience, thus it’s a pain-associated behaviour with the purpose of communicating something. So if a person isn’t ‘convinced’ by our pain education, you know they’ll keep their score pretty high.

So, there are some people for whom we cannot reduce or get rid of their pain. It’s likely to persist. And it’s these people who can be viewed as “heartsink” patients, who hang around not getting better. Well, unless we begin looking at their experience and examine what they’re looking for (and believe me, it’s not pain reduction – it’s what pain reduction means they can do) we’re going to be stuck. And so will they. Let’s get it into our heads that pain reduction is not achievable for all, but reducing the impact of pain on life is something we can all help with. Let’s stop demonising the person who has to live with pain that doesn’t respond to all our ministrations and begin looking deeply at ourselves and why we avoid recognising that we can’t win ’em all. And let’s get on with the business of helping people do what’s important in their lives, irrespective of pain.

 

 

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

Choi, B. K. L., Verbeek, J. H., Wai-San Tam, W., & Jiang, J. Y. (2010). Exercises for prevention of recurrences of low-back pain. Occupational and Environmental Medicine, 67(11), 795-796. doi:10.1136/oem.2010.059873

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. doi:10.1136/annrheumdis-2013-204428

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.

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Back to basics about psychosocial factors and pain – v

I’ve been writing about psychosocial factors and pain but I realise that I haven’t actually defined what I mean by psychosocial factors. The strange thing about this term is that it’s often conflated with “psychological” or “psychopathological” when it’s actually not. So… where to begin?

The Collins English Dictionary defines psychosocial as: “of or relating to processes or factors that are both social and psychological in origin”, while the Oxford English Dictionary defines it as “Of or relating to the interrelation of social factors and individual thought and behaviour.” According to the Oxford, it first appeared in the American Journal of Psychology in 1890 when it was used to describe the factors associated with the increase of alcoholism. An 1899 journal used it to describe “… psycho-social phenomena, such as language, customs, rights, religion etc., arising from the action of social elements with or upon the individual mind.”

So, the term is fairly recent but seems to have always been associated with broader influences on thoughts and behaviour – that is, a reciprocal response between what individuals think and do, and what helps to shape (and also responds to) what happens in the community.

When we think about pain, the most common “psychosocial” factors seem to be psychological – things like attention (vigilance), catastrophising (thinking the worst), negative affect (low mood), treatment seeking (behaviours associated with looking for help), avoidance (not doing, not approaching). What is lacking in clinical practice, in my humble opinion, is the relationship between how these factors develop and are maintained, and how those around an individual (both family and the wider community) respond to these factors. It’s not that there is no research into these relationships – it’s that research is complex, it’s tough to conduct experiments in this field, and effecting change once relationships are identified is pretty hard. More than that, health professionals typically see individuals, not people-in-context.

BUT here are some of the areas currently being explored.

Clinician behaviour – there would be few readers of this blog who are unfamiliar with Ben Darlow’s work on the power of what clinicians say (Darlow, Dowell, Baxter, Mathieson, Perry & Dean, 2013), though he’s not the first research to begin to look at this – Tamar Pincus and others have also reviewed the influence of practitioners beliefs on what they do for people with persistent pain (Parsons, Harding, Breen, Foster, Pincus, Vogel & Underwood, 2007).  The broad conclusions from this body of work, of which these two are tiny tips of a very large iceberg, is that what clinicians believe about pain and chronicity and hurt/harm influences both their treatment recommendations and their attitude towards people experiencing persistent pain, and has a direct effect on chronicity in the acute stages of a pain problem.

Family responses – Herta Flor and colleagues explored the impact of persistent pain on family relationships way back in the 1980’s, while much more recently,  Burns, Post, Smith, Porter et al (in press) investigated the interaction between spouse criticism and the effect on pain intensity and behaviour in people with persistent low back pain. Chan, Connelly & Wallace (2017) established that poor peer relationships influenced both emotional functioning and persistent pain amongst adolescents, while treatment seeking amongst adolescents was found to be associated with elevated treatment seeking in their parents (Stone & Wilson, 2016). Whether the relationships are genetic (in family patterns of persistent pain and disability), or learned (social learning theory) or a mix of both – it looks like how others respond and behave in relation to pain and disability has a strong influence on persistent pain in an individual.

Work – This, naturally, has been the place of many a study trying to establish a relationship between biomechanical factors and the onset and maintenance of pain, but it has also been the location for studies examining social relationships like supervisory responses, peer relationships, employer flexibility along with the personal effects of workplace stress on the body. I’m not going to review the myriad studies, but point you to a good systematic review of prognostic factors for return to work by Steenstra, Munhall, Irvin, Oranye, Passmore et al (2016) to demonstrate just how many factors have already been identified.

I’ve barely touched the surface of the social aspects influencing our experience of pain and disability. It’s evident that these factors have been identified – but let me ask you this: How often do you identify and then provide an intervention for these social factors? And if not, why not? And if not you – who?

 

Burns, J. W., Post, K. M., Smith, D. A., Porter, L. S., Buvanendran, A., Fras, A. M., & Keefe, F. J. (2017). Spouse criticism and hostility during marital interaction: effects on pain intensity and behaviors among individuals with chronic low back pain. Pain.

Chan, S. F., Connelly, M., & Wallace, D. P. (2017). The Relationship Between Pain Characteristics, Peer Difficulties, and Emotional Functioning Among Adolescents Seeking Treatment for Chronic Pain: A Test of Mediational Models. Journal of Pediatric Psychology, jsx074.

Darlow, B., Dowell, A., Baxter, G. D., Mathieson, F., Perry, M., & Dean, S. (2013). The enduring impact of what clinicians say to people with low back pain. The Annals of Family Medicine, 11(6), 527-534.

Flor, H., Turk, D. C., & Scholz, O. B. (1987). Impact of chronic pain on the spouse: marital, emotional and physical consequences. Journal of psychosomatic research, 31(1), 63-71.

Parsons, S., Harding, G., Breen, A., Foster, N., Pincus, T., Vogel, S., & Underwood, M. (2007). The influence of patients’ and primary care practitioners’ beliefs and expectations about chronic musculoskeletal pain on the process of care: a systematic review of qualitative studies. The Clinical journal of pain, 23(1), 91-98.

Steenstra, I. A., Munhall, C., Irvin, E., Oranye, N., Passmore, S., Van Eerd, D., … & Hogg-Johnson, S. (2016). Systematic review of prognostic factors for return to work in workers with sub acute and chronic low back pain. Journal of occupational rehabilitation, 1-13.

Stone, A. L., & Wilson, A. C. (2016). Transmission of risk from parents with chronic pain to offspring: An integrative conceptual model. Pain, 157(12), 2628-2639.

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.

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.

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

Great expectations – and low back pain

Have you ever wondered why there are so many treatments for low back pain? Like there are actually hundreds of different ways to “treat” back pain… yet the truth is, none of them work for everyone. Actually, most of them seem to help pass the time until low back pain settles of its own accord. Until it’s back again (no pun intended!).

This post is prompted after reading a string of general news articles discussing the common non-specific low back pain – under various guises of “dead butt syndrome“, “Dr Tom: Ouch I’ve hurt my back” and the like – I think it’s time for a frank discussion about the natural history of low back pain, as found in large epidemiological studies. There’s no doubt that low back pain is a problem around the world, and I think it’s partly due to unmet expectations (along with a whole lot of other variables). The Global Burden of Disease found low back pain to be the most common reason for days lived with disability around the world – that’s more than anaemia, depression, hearing loss, migraine!

Low back pain is common in every single country in the world.

Dunn, Hestbaek & Cassidy (2013) examined the prevalence of low back pain across the life span – they found that many of us view low back pain as a simple “yes/no” question – do you have it, or don’t you. They point out that people with no back pain at the time of a survey are not all the same: some might never have had a bout ever, while some might have had several bouts but just don’t have one right now. These presentations are not the same! Those who have had a previous episode will have developed an understanding of back pain on the basis of what happened, and this will influence their expectations, and subsequent response, to treatments.

Dunn, Hestbaek & Cassidy found that children/adolescents have a point prevalence (ie at the time of the survey, they reported they had back pain) of 12%. As people get older the prevalence continues to be around 12%. The elderly, those over 60 (that doesn’t really feel old to me!), seem to have a prevalence similar to people in middle age, and activities affected by low back pain seem to increase as we age.

Given the lifetime prevalence of low back pain is around 80% (or more), following people up over time seems to paint a different picture from the point prevalence studies: it’s not the same 12% of people that has low back pain all the time. Some studies show that at least 40% of people do recover within a year of an episode (see Hestbaek, Leboeuf-Yde, & Manniche, 2003). A Danish study with 5 year follow-up found around 23% of people consistently reported no pain days during the previous year (during the study) but around 10% reported more than 30 days of back pain every time they were asked. So, while long-term low back pain isn’t common in the adult population, most people do have a couple of bouts over long periods of time.

What are the risk factors? Well one clear risk factor is having had a previous episode, although this isn’t a consistent predictor for long-term back pain. Perhaps we should take a look more closely at the natural course of acute neck and low back pain – from the Norwegian longitudinal studies. From one city in Norway, these researchers screened 9056 people between 20 – 67 years old to identify those with a brand new bout of neck or back pain in the previous month – 219 people were identified, then followed for 12 months. What these researchers found was pain decreasing rapidly in the first month, irrespective of treatment, thereafter though, back pain didn’t change for the rest of the year especially for those with pain in the neck as well as the back at the first assessment, and for those who had 4 or more pain sites in the beginning.

Now what’s really interesting about this study is that the pain reduction people experienced, particularly in low back pain, was pretty close to the pain reduction people achieved whether they had treatment, or not. Hmmmm. Next question: what if we look at all the treatments people get, and those who are in the control group, and pooled that information to find out what happens? Artus, van der Windt, Jordan & Croft examined whether just taking part in a study on low back pain might influence outcomes – so they pooled 70 RCTs and 19 cohort studies, and both sets of data showed “a rapid improvement in the first six weeks followed by a smaller further improvement until 52 weeks. there was no statistically significant different in pooled standardised mean change (a measure used to compared the pooled within-group change in pain in RCTs with cohort studies) – get this, at any time point.

But wait, there’s more!

Axen & Leboeuf-Yde (2013) looked at the trajectories of low back pain over time. They summarised four studies in primary care or the general population, finding that over the course of between 12 weeks and 12 months, participants could be divided into two to four groups: one group remained uncomfortable, perhaps staying that way over the whole 12 months (around 10 – 21%); one group also remained uncomfortable but they reported their pain as “moderate” or “mild” – around 36%; another approximately 30% experienced fluctuating or intermittent low back pain; and finally, the group we love – those who recovered and remained that way, around 30 – 58%.

This is not the picture we hear in the media. This is not what we were taught. And yes, I know there are problems with pooled data because individualised responses get ironed out. But what all this says to me is – our patients come to us expecting that low back pain should completely resolve. The reality is that for a lot of people, back pain will come and go throughout the lifetime.

What does this mean to me?

Isn’t it time to give people an idea that if they have a bout of back pain, chances are high they’ll have another. Complete resolution of low back pain may not occur for a large number of people. A new bout of low back pain may not mean a new “injury” (given we don’t know why many people develop back pain in the first place). Learning to self-manage a bout of back pain is likely to save people a load of heartache, not to mention a lot of money. And maybe it’s the latter that means it’s very hard to find clear, effective messages about just how safe a painful back is. It’s far easier to sell a message of vulnerability, of the need for treatment for that “unhappy spine” as a chiropractor in Christchurch calls it. And of course, if we continue to allow the expectation that all pain should be gone, we’re going to be in business for a very long time…

 

Artus, M., van der Windt, D., Jordan, K.P., & Croft, P.R. (2014). The clinical course of low back pain: A meta-analysis comparing outcomes in randomised clinical trials (rcts) and observational studies. BMC Musculoskeletal Disorders, 15, 68.

Axén, I., & Leboeuf-Yde, C. (2013). Trajectories of low back pain. Best Practice & Research Clinical Rheumatology, 27(5), 601-612. doi: http://dx.doi.org/10.1016/j.berh.2013.10.004

Dunn, K.M., Hestbaek, L., & Cassidy, J.D. (2013). Low back pain across the life course. Best Practice & Research in Clinical Rheumatology, 27(5), 591-600.

Hestbaek L, Leboeuf-Yde C, Engberg M, Lauritzen T, Bruun NH, Manniche C. (2003). The course of low back pain in a general population. Results from a 5-year prospective study. Journal of Manipulative & Physiological Therapeutics, 26(4):213–9.

Hestbaek L, Leboeuf-Yde C, Manniche C. (2003). Low back pain: what is the long-term course? A review of studies of general patient populations. European Spine Journal, 12(2):149–65.

Vasseljen, O., Woodhouse, A., Bjorngaard, J.H., & Leivseth, L. (2013). Natural course of acute neck and low back pain in the general population: The HUNT study. Pain, 154(8), 1237-1244.

Primary pain disorders

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

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

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

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

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

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

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

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

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

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

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

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

Clinical reasoning in persistent pain management

I think we need to take a cold hard look at clinical reasoning in pain management and especially at how we can integrate all the various factors influencing the person sitting in front of us. There are too few papers really addressing how different professions can put their assessment findings together to generate a truly multi-faceted model of why this person is having trouble with their pain. I could find only one paper detailing interprofessional clinical reasoning for chronic pain – and it’s inside a textbook dates from 2008 (Linton & Nicholas, 2008). So it’s no wonder, when a team gets together, that we collectively find it difficult to work together.

The approach discussed by Linton and Nicholas was the way I was trained to work, so I’m biased. Nevertheless I think this is a practical and useful way of putting the jigsaw puzzle together to see how each factor influences every other factor. I’m not suggesting that every case should be formulated this way – but I do find myself using the same strategy for every person I see.

We all do a bunch of assessments when we first see a person. But then what do we do with all that material? As Linton and Nicholas say, most assessments are used to document the intensity of the problem. Case formulations try to identify the main problems experienced by the person – and then generate hypotheses about the mechanisms supporting those problems for this person sitting in front of me.

So here’s a question for y’all – if you have information on the person’s pain intensity, how much it is interfering in their life, how depressed they are, as well as understanding their fear-avoidance beliefs and catastrophising; and if you know how their family responds to them, should we simply provide our standard treatment package ( e.g. analgesic medication, home exercises, and relaxation training)?

Wouldn’t it make more sense to only target catastrophising if they seem to add to the person’s problems? And wouldn’t it be better to add home exercises only if the person seems to be avoiding activities?

Or have we got to the place where everyone gets exactly the same solutions to what, for them, is a very unique and individual problem?

A key part of case formulation is involving the individual in the process. I think it’s crucial to actively be putting their perspective into generating the hypotheses about the factors maintaining their problem – this helps them see the relevance of each piece of the treatment puzzle, and ensures we don’t over-interpret (or under-interpret) factors.

Another really good reason for case formulation is to counter our cognitive biases. We know we jump to conclusions, find patterns where there aren’t any, look for things that confirm our own beliefs, look for simple options and ignore complex and ambiguous options – and so on, and case formulation can buy us time to avoid some of these really significant problems.

So, how do they work. Linton and Nicholas use a “spaghetti diagram” – looks like a bunch of arrows connecting various factors together. It looks a bit like this:

I personally use something that looks a bit different because I like Tim Sharp’s reformulation of a CBT model.

Whatever the approach, having a structure, taking time to “fill in the gaps”, including the person living with pain, and understanding the literature that clarifies those factors important in pain and disability, will allow us to avoid some of the major cognitive bias traps. Using a common formulation across all the clinicians involved really helps all of the team know why they’re doing what they’re doing – and why the other members of the team are so important. That means we can support one another!

But the bit missing, for me, is the “what do you do when you see these patterns?” To me, it’s about identifying the person’s main concerns – what are they primarily concerned about? Often it’s not the pain intensity, but instead it’s whether they’ll be able to still work, or their sleep, or their family reactions, or loss of roles. So we need to look for factors that are influencing these aspects of their situation so we actually address the problems that the person identified (rather than our own preference!). Shock and horror ensues! That might mean the person doesn’t need to see a physio for an exercise programme – they might prefer to work on sleep management, or work.

And if the person doesn’t avoid because they’re not too bothered by their pain, why would we need to give them “pain education”? Perhaps we’d do better to treat their depression, or help with their sleep. Similarly, if someone isn’t distressed, isn’t avoiding and just needs some medication – shouldn’t they get just that? Do we seriously need them to see a psychologist, occupational therapist, physiotherapist and go to the gym four days a week? Maybe less can be more.

I guess some of my frustration lies with the fact that despite all this talk of integrating the various parts of pain management, what we often end up with is a formulaic “education, exercise and mindfulness” for everyone – irrespective of their actual needs. Is it time to talk about what we might do differently for the person who might have a tendency to catastrophise but isn’t avoiding, or for the person who is very fit but doesn’t want to sit, or the person who is having such trouble sleeping because of their pain? Let’s be a bit nuanced, folks!

Linton, S. J., & Nicholas, M. K. (2008). After assessment, then what? Integrating findings for successful case formulation and treatment tailoring. Clinical Pain Management Second Edition: Practice and Procedures, 4, 1095.

Everyday hassles of fibromyalgia

This post has been on my mind for a while now. I live with fibromyalgia (FM) and want to share some of the everyday hassles I face. This isn’t a “oh woe is me” kind of post, it’s more of a “if you’re a clinician working with someone who has fibromyalgia, these are some things to ponder”.

Diagnosis

I worked in chronic pain management for almost 20 years before I recognised that the pains I’d been experiencing most of my adult life actually added up to “…a syndrome of diffuse body pain with associations of fatigue, sleep disturbance, cognitive changes, mood disturbance, and other variable somatic symptoms”(Fitzcharles, Ste-Marie, Goldenberg et al, 2012). I’d hurt my back in my early 20’s, thankfully been seen by Dr Mike Butler and given the Melzack & Wall book “The Challenge of Chronic Pain” to read, so I wasn’t afraid of my pain and just accepted it as part of life. What I hadn’t really recognised was that not only was the pain in my lower back part of the picture, so too was the pain in my neck, shoulders, arms, hips, legs, feet, and the irritable bowel, and the gastro discomfort, and the migraines and the dysmenorrhoea. Not to mention the fatigue, rotten sleep, foggy thoughts, and low mood.

Diagnosis for people living with fibromyalgia is often delayed.  People with fibromyalgia may resist going to the GP for what seem to be short-term but painful bouts in various parts of the body. There for a couple of weeks, then shifting to another part of the body. As one person said to me “You feel a fool going to see a Dr about a pain that’s not consistent to say ‘Oh Doctor and I have pain here, and here and here and last week I had one here…especially when it might be gone next week, and that other one has already gone.'”. This experience is echoed in qualitative research where, for example in a study by Undeland and Malterud (2007) people said that although having a label was reassuring (it’s not something that will kill you!), the label itself was often difficult to obtain (doctors not being keen to label something so nebulous as FM), and even with a label health professionals and the general public “pay no attention to the name, or blatantly regard them as too cheerful or healthy looking” (Undeland & Malterud, 2007).

Treatment

One of the problems with getting the diagnosis is that very few people get relief from medication. Those that do may find their pain settles almost completely, but many others have no effective analgesia despite trying numerous combinations. I’m one of them. What this means is that “self management” is the order of the day – yet in many places this is not even considered, let alone having services to help people develop such skills.

I’ve learned that my body feels best when I maintain a consistent level of activity irrespective of the day of the week. I enjoy stretching, walking, cycling and dancing, but I also love gardening, fishing, walking the dog – and I guess I can add in doing the housework and working as part of the mix. New activities are bound to give me aches and pains that last for weeks, while stopping my usual routine also brings me aches and pains that last for weeks. So boring consistency is the name of the game. And as I’ve previously blogged that means I look for a variety of different movement options in my repertoire.

Everyday hassles

The one thing that makes my life difficult is when I develop a new pain in a part of my body that doesn’t usually feel uncomfortable. Like most people living with persistent pain, I’ve developed an awareness of “my normal” (see this study by Strong & Large, 1995, for a nice description of this aspect of living with pain, one that is not often discussed). I know the usual pattern of my pains – bellyache, low back pain, neck and upper back pain, wrists and fingers, and often, knees, headaches and facial pain. These are my normal – but when should I seek help for a new pain? After all, it could be simply a manifestation of my fibromyalgia (ie there is nothing medically to be found, and no real change in management). At the same time, these are new pains – one in my shoulder that feels like an impingement (painful arc), and one that’s possibly an adductor tendon thing that’s very localised and hasn’t moved for over 7 months.

The question that keeps coming back to me is whether I’m overlooking something that can be treated, or whether it’ll just settle down like most of my pains do. Essentially I’ve just kept doing what I do and ignoring it.

The difference between my situation and those of people who are not painiacs, who don’t know that their pain is largely unrelated to the state of the tissues, is that I’m immersed in pain research all day, every day. I’m not overly bothered by these new pains. I’m continuing to exercise as normal and these pains aren’t interfering with what I need and want to do in daily life (well, perhaps a little…).

I can understand why someone might ask for help for a new pain. There are no rules saying that just because you have a persistent pain disorder you’re immune from acute musculoskeletal disorders. And sometimes by treating a new pain as an acute pain, it will vanish. Though, it must be said that outcomes for people with more than 3 or 4 persistent areas of pain with low back pain are not as good as those who only have one or two (Nordstoga, Nilsen, Vasseljen et al, 2017), nor of recovery and benefit from total hip and knee replacement (Wylde, Sayers, Odutola, Gooberman-Hill et al, 2017).

Points to ponder

So how do we as clinicians help people who must live with persistent pain?

• Do we consider the meaning of the labels we give? And do we read around the experiences of those who have been given the diagnosis? Or do we, instead, rely on our own beliefs and biases when thinking about the way we handle diagnosis?
• Do we give people an explanation for their pain that they can understand, or do we rely on currently favoured language and models without really considering what this means to the person? And do we ever check out how they’ve interpreted our explanations?
• Do we ever discuss how to self-manage pain? Do we think about the practical implications of needing to learn to modify every aspect of life in the face of pain that will not just go away? When I compare the tasks of living well with persistent pain against those needed to cope with other disorders, pain can interfere with everything – do we talk about the impact on sex? on relaxation? on having a holiday?
• Do we talk about what to do when a new pain turns up? Do we think about how someone can decide whether their pain is worth seeing someone about, or one they can handle? And do we even talk about the effect of having a persistent pain problem and then going on to have surgery? Do we teach people to recognise their “normal” pain, or are we afraid to teach people this because it might focus their attention on their pain?

I don’t have researched answers to these questions. I have my experience. And I’ve been working in this field a long time – yet somehow the voices of people living successfully with this pain are rarely heard.

 

Fitzcharles, M.-A., Ste-Marie, P. A., Goldenberg, D. L., Pereira, J. X., Abbey, S., Choinière, M., . . . Proulx, J. 2012 canadian guidelines for the diagnosis and management of fibromyalgia syndrome. http://fmguidelines.ca/

Nordstoga, A. L., Nilsen, T. I. L., Vasseljen, O., Unsgaard-Tøndel, M., & Mork, P. J. (2017). The influence of multisite pain and psychological comorbidity on prognosis of chronic low back pain: Longitudinal data from the norwegian hunt study. BMJ open, 7(5). doi:10.1136/bmjopen-2016-015312

Strong, J., & Large, R. (1995). Coping with chronic low back pain: An idiographic exploration through focus groups. The International Journal of Psychiatry in Medicine, 25(4), 371-387. doi:10.2190/H4P9-U5NB-2KJU-4TBN

Undeland, M., & Malterud, K. (2007). The fibromyalgia diagnosis – hardly helpful for the patients? Scandinavian Journal of Primary Health Care, 25(4), 250-255. doi:10.1080/02813430701706568

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