Low back pain

Wait and see…when do we “escalate” care for low back pain?


Prompted by reading a paper by Linton, Nicholas and Shaw (in press), today’s post is about various service delivery models for low back pain and not the content of back pain treatment.

Service delivery in New Zealand is assumed to be based on getting most bang for the buck: we have a mainly socialised healthcare system, along with a unique “no fault, 24 hour” insurance model for accidents whether at work or elsewhere, which means market forces existing in other countries are less dominant. There are, however, many other influences on what gets delivered and to whom.

Back to most bang for buck. With a limited healthcare budget, and seriously when is there ever NOT a limited budget in health, it would make sense to a thinking woman for healthcare to focus on high value treatments. Treatments that have large impact and are low cost. In low back pain, the techno-fix has limited application. Things like costly surgical approaches (synthetic disc replacements, fusions to stop vertebral movement) should be reserved for only those with clear indications for the procedure, and given on the basis of clinical need rather than in response to a distressed person. The outcomes just are not all that great (see Maher, Underwood & Buchbinder (2017) for a good review of nonspecific low back pain).

High value and low cost treatments are typically delivered by low status clinicians. Those “nonmedical” people like occupational therapists, physiotherapists, osteopaths, chiropractors and the like. Maybe it’s for this reason that these treatments are relatively poorly funded. We lack lobby power.

Back to service delivery models. Currently in Christchurch, where I live, there is a health pathway (in other words, a service delivery model) developed in collaboration with GP’s, physiotherapists, osteopaths and secondary care. The model adopted applies to ALL episodes of low back pain, and uses the STarTBack tool to triage those who may need more intensive treatment under a biopsychosocial model (mainly because of the additional risk psychosocial factors pose for these people), and to continue with treatment as usual for those with lower risk as measured by this tool.

After about six weeks, if the person hasn’t responded to treatment, clinicians are meant to refer the person to a team for review and to see whether additional treatments or another pathway might be appropriate. Unfortunately, there is no indication of the makeup of that team, and no obligation for the clinician to send the person to it. I’m not sure about clinical audit of this pathway, and again this isn’t clear.

One of the problems (amongst many) with this approach is that six weeks without responding to treatment and the time needed after this to review the file, then be referred elsewhere is a very long time to someone experiencing back pain. A very long time. By six weeks it wouldn’t be surprising if the person’s sick leave is gone. If they’re receiving ACC the processes will have kicked in, but for the person who has typical grumpy back symptoms without an “accident” initiating it, there may be nothing.

Linton, Nicholas and Shaw point out that all of the triaging approaches for low back pain hold assumptions. The three are stepped care (begin with low intensity, once that hasn’t helped progress to more intensive and so on); stratified (triage those with high risk, and treat them accordingly, while low risk get lower intensity treatment); and matched care (treatments are administered according to an algorithm based on grouping people with similar characteristics).

Stepped care

The assumptions of stepped care include that people with basic acute low back pain will recover relatively easily, while those who need more help will be fine waiting for that additional level of care. There’s an assumption that factors leading to chronic disability occur in stages – the longer a person waits the more risk factors will appear – but this isn’t actually the case. Many people present with risk factors from the very beginning (and they can be identified), while waiting only allows those problems to be cemented in place. At the same time, we know acute low back pain is quite a rare thing: most people will have their first bout of back pain in adolescence, and will have learned good and not so good habits and attitudes from that experience. Another assumption is that duration of back pain doesn’t harm, but we know delayed attention to risk factors for chronicity is harmful. Stepped care can be useful because it’s efficient, easy to implement and overtreatment is less likely – but what about the person who appears with all the risk factors evident from the beginning? These people may not get adequate or appropriate treatment from the outset.

Stratified care

In stratified care, treatment is provided according to the category of risk the person presents with, maybe circumventing some of the problems from stepped care. Stratified care assumes we’re able to identify risk factors, and that they are stable from the outset rather than changing over time. It also assumes that risk factors exert a cumulative effect with more risk factors meaning greater risk. BUT while screening can identify some risks, and those at low risk get more adequate treatment while higher intensity treatment is given to those with more risk, this approach doesn’t identify underlying mechanisms, and more comprehensive treatments addressing specific issues may not be provided. This approach may not even consider the impact of workplace factors, family dynamics, social and recreational issues. It’s also pretty challenging to implement as I think the Christchurch example demonstrates.

Matched care

In matched care risk factors are identified and treatments are matched to the person’s needs, and like stratified care it assumes that risk factors can be identified, are stable, and that they can form a “profile” or subtype. This approach also assumes that tailoring interventions to individual risk will be more efficient than alternatives. There’s some support that screening can identify some risks, and that profiles can be constructed – but this continues to be a work under progress. Some of the limitations are the emerging nature of research into grouping people according to multiple indicators is complex, particularly at the beginning of treatment, and treatments matching profiles are therefore also under development. It’s a very complex approach to implement so I can understand why local health authorities may be reluctant to embark on this strategy. It’s also back to the problem of assuming that people’s risk profiles are stable over time.

What do we do?

One part of me thinks, well it doesn’t matter really because as a lowly nonmedical person I have very little influence over health systems, the perverse incentives that drive them, and absolutely no political clout whatsoever. BUT I know that the “wait and see” six weeks before reviewing progress is not helping. And the current considerations fail to integrate those important workplace, family, socio-economic and contextual factors that are hard to quantify.

We already know that low back pain guidelines are routinely ignored by most clinicians in favour of “what I do” and “it’s worked before” and “the guidelines are biased so I won’t follow them”. There’s also the fear that by identifying psychosocial risk factors we’re condemning people to the “back pain is really in your head” meme (it’s even something I’ve been accused of. FWIW I think low back pain is far more complex and is multifactorial. Psychosocial factors are certainly more useful at predicting disability than biomechanical or diagnostic ones, but this doesn’t mean the problem is purely psychological. <steps off soapbox>). Furthermore, it’s clear that not only do physiotherapists feel poorly-prepared to identify and work with psychosocial factors (Singla, Jones, Edwards & Kumar, 2015; Zangoni & Thomson, 2017), so also do medical practitioners although for different reasons (Coudeyre, Rannou, Tubach, Baron, Coriat, Brin et al, 2006). It’s difficult to open Pandora’s box when you only have 10 minutes with a patient.

As Linton, Nicholas and Shaw (in press) point out, training is needed before clinicians can feel both confident and efficient at screening and then managing low back pain via an integrated multidimensional model. “Role” delineation (who can contribute to the various aspects of treatment?) and the paucity of funding for allied health within primary care, especially in New Zealand makes this approach an aspiration. 

Naturally I’d like to see a range of different health professionals involved in developing health pathways. Not just professionals, but people well-versed in understanding the research literature and those with effective knowledge translation skills. I’d love to see high value and low cost treatments provided rather than techno-fix approaches, especially when the high value treatments are significantly safer and develop personal self efficacy and locus of control. Wouldn’t that be a thing to see?

  • Coudeyre, E., Rannou, F., Tubach, F., Baron, G., Coriat, F., Brin, S., … & Poiraudeau, S. (2006). General practitioners’ fear-avoidance beliefs influence their management of patients with low back pain. Pain, 124(3), 330-337.
  • Linton, S. J., Nicholas, M., & Shaw, W. Why wait to address high-risk cases of acute low back pain? A comparison of stepped, stratified, and matched care. Pain. in press
  • Maher, C., Underwood, M., & Buchbinder, R. (2017). Non-specific low back pain. The Lancet, 389(10070), 736-747.
  • Singla, M., Jones, M., Edwards, I., & Kumar, S. (2015). Physiotherapists’ assessment of patients’ psychosocial status: are we standing on thin ice? A qualitative descriptive study. Manual Therapy, 20(2), 328-334.
  • Zangoni, G., & Thomson, O. P. (2017). ‘I need to do another course’-Italian physiotherapists’ knowledge and beliefs when assessing psychosocial factors in patients presenting with chronic low back pain. Musculoskeletal Science and Practice, 27, 71-77.
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The dynasty of the disc! More history in pain management


Low back pain, despite the multitude of explanations and increasing disability associated with it, has been with humans since forever. Who knows why and I’m not about to conjecture. What’s interesting is that despite ergonomic solutions (fail), increased fitness amongst many people (also a fail), surgical solutions (fail), hands on solutions (fail, fail), and a whole bunch of “special” exercises (fail, fail, fail) we still don’t have a handle on how to reduce disability from it.

I don’t think there will be many people who haven’t seen this:
I’ve never quite worked out why, when you search for imagines of disc bulges (or rather, prolapse of the nucleus pulposus – herniated or ruptured disc was the term preferred by Mixter and Ayer (1935) who proposed the notion of disc prolapse being the cause of “injuries to the spine” (Allan & Waddell, 1989), you end up with these nasty red glowing areas (see below). I think it’s because how else do you convey the idea that this is meant to be “the source of pain”.

Let’s dig back a little into history. Allan and Waddell (1989) describe the “modern” concept of the disc based on four papers: Goldthwaite (1911); Middleton & Teacher (1911); Dandy (1929) and Mixter and Barr (1934). Pathologists had described the presence of these prolapses when conducting postmortem examinations – but their patients couldn’t tell them whether they hurt, and neither was there any clinical awareness of any relationship between pain and disc prolapse. In 1911, two papers described patients with massive disc prolapses – one was a fatal case of paraplegia after a disc prolapse followed by Middleton and Teacher conducting lab experiments to see whether injury (force applied to the disc) could produce a prolapse (Middleton & Teacher, 1911). Goldthwaite described a case of paresis (not pain) after manipulation of the back, presuming that a “displaced sacroiliac joint” was responsible and identified that the nerve at the lumbosacral joint could be compressed – this was supported by later authors.

Cushing, a surgeon, performed a laminectomy which didn’t turn out well – but identified that “narrowing of the canal” might be responsible for the person’s pain, and from there the disc was blamed as the cause of “many cases of lumbago, sciatica and paraplegia”.  This narrative was followed up by other clinicians, and Mixter and Barr (1934) increased the attention given to these theories. Ultimately this led to a meeting of the minds where Mixter and Barr (Mixter being a neurologist, Barr an orthopaedic surgeon) carried out an investigation into enchondromas and and normal discs. What were thought to be tumours were mainly “normal cartilage”.  Mixter and Ayer (1935) went on to pursue the idea of disc prolapse being involved in not only cases where neurological changes were evident, but also low back pain.

Mixter and Ayer (1935) found that surgical responses were not very good – while leg pain was fixed patients still complained of a painful back. Their paper, however, emphasised that lesions of the disc were caused by “trauma” (even though history of even minor trauma was only found in 14 of their 23 cases). Canny men that they were, they noted that if trauma was involved it would “open up an interesting problem in industrial medicine”: who caused the trauma?

Well, like many ideas of the time, this one took root in an exciting climate of medical and surgical discovery – detailed descriptions of the techniques and procedures used were published, but even at that time outcome measures were not reported because, in their words “the question of liability, compensation and insurance loom large on the horizon and add complications compounded to an already knotty problem”. The meme of physical trauma to the back causing disc prolapse and subsequent back pain caught hold of the imagination, and although initially diagnosed using a myelogram, very quickly became replaced (in the name of avoiding complications, cost, discomfort and potentially missing ‘concealed’ discs) by clinical history and neurological examination.

Over the years 1930 – 1950, anaesthetics and surgery became safer and more routine – and accepted, after all look at how these surgeons patched up the brave soldiers! But by the 1970’s the enthusiasm began to wane as more patients reported adverse outcomes, and continued to experience pain.  So… it was decided disc prolapses should only be surgically managed in the case of sciatica rather than simply low back pain – but what about disc degeneration? Surely that could be the “cause”! And yes, we know that even though normal age-related changes were present, these were ignored, along with the somewhat tenuous relationship between disc changes and pain… Instead cadaver biomechanical studies were used to confirm that the disc could bulge with certain forces, and because the problem was now “degenerative” there was no cure – it would ‘inevitably’ progress. Thus the surgical fusion was brought in to play to reduce the “wear and tear” on the disc to “stabilise” the joint (though instability hadn’t been found, and fusion didn’t produce great results).

What was really striking was the move during this period towards rest as treatment. Previously bonesetters (predecessors of osteopathy and chiropractic and manual medicine) manipulated and then quickly mobilised people with low back pain. The hands-on treatment provided short-term relief but the real cure was to keep doing. Orthopaedics, however, based both on knowledge of fracture and tissue healing and ongoing use of surgery for low back pain, emphasised rest to allow “inflammation” to heal. Whether there was any inflammation is moot – what took root in the minds of medical and other practitioners was the need to rest until the pain was gone.

And that, dear ones, is how the epidemic of disability (the effect on function, limitations on what people can do, on participation) was born. It’s called iatrogenesis, or what health professionals can do to increase harm, inadvertently or not. And it’s still happening today.

We should not lay the blame for ongoing harm at the feet of orthopaedic surgeons and neurologists of the day. It was a perfect storm of media attention, community fascination with technology and miracles performed as a result of the war, the heroic soldiers and their equally heroic surgeons, the courts (in the case of industry as responsible for trauma to civilians), and of course the insurers – all over the period between 1880 – and until even today.  While outcomes are being more widely reported in orthopaedic surgery (and other treatments), changing clinical behaviour, community attitudes and the legacy of our history is slow. Cognitive dissonance is a thing… and even though 1965 saw gate control theory revolutionise our thinking about the way pain is produced, the implications are not yet fully accepted.

 

Allan, D. B., & Waddell, G. (1989). An historical perspective on low back pain and disability. Acta Orthopaedica Scandinavica, 60(sup234), 1-23.

Learning from old research (digging into history)


I recently submitted a manuscript to a journal. After the usual delay as the reviewers commented on my draft, I received the feedback – one comment stood out to me: “the references are quite old”. I scurried around to find some more recent references and resubmitted, but as I did, I started pondering this drive to continually draw on recent research even if the findings of the older references had not been superseded. There is a sense that maybe journal editors and perhaps people reading the journals think that old research has no merit.

As someone who relishes reading about the history of pain and pain management (If you haven’t yet read Melanie Thernstrom’s The Pain Chronicles or Joanna Bourke’s The Story of Pain, it’s time to do so!), and because some of the best and most revolutionary papers in pain and pain management were published in the 1980’s (Fordyce, W. E. (1988). Pain and suffering: A reappraisal. American Psychologist, 43(4), 276-283. ; Waddell, G. (1987). 1987 volvo award in clinical sciences: A new clinical model for the treatment of low-back pain. Spine, 12(7), 632-644. ; Waddell, G., Main, C. J., Morris, E. W., Paola, M. D. I., & Gray, I. C. (1984). Chronic low-back pain, psychologic distress, and illness behavior. Spine, 9(2), 209-213.), I find it extraordinary that some of the concepts being discussed today as New! Improved! Radical! are pretty much the same as those introduced waaaay back then…

Examples? Well one is the whole notion of helping people understand something of what’s know about neurobiology of pain. The “Pain Neuro Education” or “Explain Pain” thing. I’ve read several papers touting the idea that before Lorimer Moseley and colleagues published their paper on “intensive neurophysiology education in chronic low back pain” we never included information about what we knew about distinctions between acute and chronic pain. There’s this really weird disconnect between the practice discussed in the 1970’s and 1980’s where at the very least the Gate Control Theory was integral to helping people distinguish between hurt and harm – and this New! Improved! Radical! pain ‘education’. Seriously, incorporating what’s know about pain neurobiology has been part of a cognitive behavioural approach to pain management since the 1970’s if not earlier. It was even provided to me when I first developed chronic pain, and that was the mid-1980’s.

What can we learn from old research, and why does history matter?

Well, one of the things that strikes me about learning from history is that in the general population, and possibly even more so in the health professional population, there are “legacy models” of pain hanging on. Most of us will have encountered someone we’re treating/working with who holds a really strong belief that if there’s a problem with a disc (it’s degenerated, bulging, or otherwise misbehaving), then it just needs to be removed and maybe a new one put in, and everything will be just fine. Where does that come from? And some of us will point to our orthopaedic colleagues and suggest that it’s something “they’ve” encouraged. But perhaps if we take a closer look at the things that contributed to a shift away from “oh I can live with this aching back” to “it must be fixed” we might learn something about how to help shift beliefs back towards a more accommodating and accepting view of the problem.

The history of low back pain

Gordon Waddell, orthopaedic surgeon (Sept 21 1942 – April 20 2017) was, amongst many other things, a keen historian. His fascination came from his desire to understand how it was that low back pain went from being something most people experienced but were not troubled by, to the epidemic of disability that it had become – and still is.

David Allan and Gordon Waddell wrote a paper in 1989 for Acta Orthopaedica Scandinavica, called An historical perspective on low back pain and disability.  The paper was written to try to outline the genesis of the increasing epidemic of low back disability since World War II. In it, Allan and Waddell detail historic understandings of backache from as early as 1500 BC (Egypt) through Greek times (Galen, ~150AD) when back pain was described as “one of the fleeting pains that affected joints and muscles. Treatment was symptomatic. Spas, soothing local applications and counter irritants were used.” (p. 1). Back pain was not often talked about, possibly because it was so common and settled mainly by itself. Over the period 1493 (Paracelsus) to 1642 (Baillou) back pain was gradually classified as one of the diseases of “rheumatism” – a watery discharge or evil humour which flowed from the brain to cause pain in the joints or other parts of the body. Rheumatism was thought to be caused by damp and cold but not trauma – note that well!

By 1800, said Allan and Waddell, doctors started to seek a cause of low back pain itself. Maybe it was “rheumatic phlegm” – let’s rub the area, let’s heat it, let’s blister the area, let’s use cupping… And in 1828 a doctor from Glasgow (Brown) described “spinal irritation” and the vertebral column and nervous system could be the source of low back pain. This radical notion “swept Europe and had a profound effect on medical thinking for nearly thirty years”. The exact nature of “spinal irritation” was never shown… and the specific diagnosis faded away but by then and until today the idea that a painful spine “must somehow be irritable” remains.

Back pain and trauma

Chronic low back pain was not thought due to injury until the latter half of the 19th century. In other words – not all that long ago. And we can blame the industrial revolution and railways for the development of an association between back pain and trauma. In the fear that often arises during the introduction of new technology (remember RSI in the 1980’s and 1990’s? due to all these new-fangled computers we were using… and maybe, just maybe “text neck” could go the same way…) people attributed back pain and a number of other ailments on “minor injuries and cumulative trauma” to the spine because of the speed of early railway travel. This was when trauma and back pain became firmly linked.

But wait – there’s much more to come! Next week I’ll talk about the rise of the “Dynasty of the Disc” and why orthopaedic surgeons got in on the act…

 

Allan, D. B., & Waddell, G. (1989). An historical perspective on low back pain and disability. Acta Orthopaedica Scandinavica, 60(sup234), 1-23.

Moseley, G., Nicholas, M. K., & Hodges, P. W. (2004). A randomized controlled trial of intensive neurophysiology education in chronic low back pain. The Clinical Journal of Pain, 20(5), 324-330. doi:http://dx.doi.org/10.1097/00002508-200409000-00007

Clinical reasoning and why models of low back pain need to be integrated


Clinical reasoning has been defined as “the process by which a therapist interacts with a patient, collecting information, generating and testing hypotheses, and determining optimal diagnosis and treatment based on the information obtained.” (thanks to https://www.physio-pedia.com/Clinical_Reasoning#cite_note-Higgs-1). The model or lens through which we do these processes naturally has a major influence on our relationship with the person, the information we think is relevant, the hypotheses we develop, and ultimately the problems we identify and how we treat them. No arguments so far, yes?

So when we come to thinking about pain, particularly where a “diagnosis” can’t be readily established – or where the treatment doesn’t directly address a proposed causal factor – clinical reasoning should be led by some sort of model, but how explicit is our model, really? And, what’s more, how well does the research support our model, and the relationships between variables?

I’m thinking about my approach as an occupational therapist where my interest in assessment is to identify why this person is presenting in this way at this time, and what might be maintaining their current predicament; and my aim is to identify what can be done to reduce distress and disability, while promoting participation in daily occupations (activities, things that need to be done or the person wants to do). For many years now I’ve used a cognitive behavioural model first developed by Dr Tim Sharp who has now moved into Positive Psychology. His reformulation of the cognitive behavioural model works from the “experience” of pain through to responses to that experience, but incorporates some of the cyclical interactions between constructs. The model doesn’t include inputs to the “experience” component from the nociceptive system – but it could.

Many other models exist. Some of them are quite recent – the STarT Back Tool, for example, provides a very simplified screening approach to low back pain that some people have identified as a clinical reasoning model. Another is by Tousignant-Laflamme, Martel, Joshi & Cook (2017), and is a model aimed at pulling all the various approaches together – and does so with a beautifully-coloured diagram.

But.

You knew there would be one! What I think these two models omit is to generate some relationships between the constructs, particularly the psychological ones. You see, while it’s a cyclical interaction, there are some relationships that we can identify.  And over the next few weeks I’ll be writing about some of the known associations, just to begin to build a picture of the relationships we can assess before we begin generating hypotheses.

For example, we know that the nervous system, and in particular our mind/brain, is never inactive and is therefore never a completely blank slate just waiting for information to come into it, but we also know there are relationships between the intensity/salience/novelty of a stimulus that attract attention, and that this competes with whatever cognitive set we have operating at the time (Legrain, Van Damme, Eccleston, Davis, Seminowicz & Crombez, 2009). So one relationship we need to assess is current contexts (and there are always many), and the times when a person is more or less aware of their pain.

Now, what increases the salience of a stimulus? For humans it’s all about meaning. We attribute meaning to even random patterns (ever seen dragons and horses in the clouds?!), so it’s unsurprising that as we experience something (or watch someone else experiencing something) we make meaning of it. And we generate meanings by relating concepts to other concepts – for a really good introduction to a very geeky subject, head here to read about relational frame theory. Relational frame theory is used to explain how we generate language and meanings by relating events with one another (The Bronnie translation! – for an easier version go here). Wicksell and Vowles (2015) describe this, and I’m going to quote it in full:

As described by relational frame theory, the theoretical framework underlying ACT, stimulus functions are continuously acquired via direct experiences, but also through their relations with other stimuli [5]. This implies that a behavioral response is not due to just one stimuli but rather the relational network of stimuli. Pain as an interoceptive stimulus is associated with a large number of other stimuli, and the actions taken depend on the psychological function(s) of that relational network of stimuli. A seemingly trivial situation may therefore elicit very strong reactions due to the associations being made: a relatively modest pain sensation from the neck trigger thoughts like “pain in the neck is bad,” which in turn are related to ideas such as “it may be a fragile disk,” and “something is terribly wrong,” that eventually lead to fatalistic conclusions like “I will end up in a wheelchair.” Thus, even if the initial stimulus is modest, it may activate a relational network of stimuli with very aversive psychological functions.

In other words, we develop these networks of meaning from the time we’re little until we die, and these mean any experience (situation, context, stimulus, event, action) holds meaning unique and particular to the individual. And these networks of meaning are constructed effortlessly and usually without any overt awareness. Each event/experience (yeah and the rest) then has further influence on how we experience any subsequent event/experience. So if you’ve learned that back pain is a Very Bad Thing, and you’ve done so since you were a kid because your Mother had back pain and took herself to the doctor and then stopped playing with you, you may have a very strong network of relationships built between low back pain, resting, healthcare, abandonment, sadness, anger, loneliness, fear, mother, father, pills, treatment – and the this goes on.

So when we’re beginning to construct a clinical reasoning model for something like low back pain we cannot exclude the “what does it mean” relationship. Every time someone experiences “ouch!” they’re processing a network of associations and relationships and behaviours that go on to influence their response to that experience – and affect attention to it and subsequent response to it.

Over 1000 words and I’ve not even started on emotions and pain!

Take home message: Even if we think we’re not addressing “psychological” stuff – we ARE. Omitting the “what does it mean to you?” and failing to factor that in to our clinical reasoning and subsequent treatment means we’re walking uphill on a scree slope. Oh, and telling someone they’re safe does not change those associations, especially if they’re longstanding. There’s more needed.

 

Legrain V, Damme SV, Eccleston C, Davis KD, Seminowicz DA, & Crombez G (2009). A neurocognitive model of attention to pain: behavioral and neuroimaging evidence. Pain, 144 (3), 230-2 PMID: 19376654

Sharp, T. J. (2001). Chronic pain: A reformulation of the cognitive-behavioural model. Behaviour Research and Therapy, 39(7), 787-800. doi:http://dx.doi.org/10.1016/S0005-7967(00)00061-9

Tousignant-Laflamme, Y., Martel, M. O., Joshi, A. B., & Cook, C. E. (2017). Rehabilitation management of low back pain – it’s time to pull it all together! Journal of Pain Research, 10, 2373-2385. doi:10.2147/JPR.S146485

Wicksell, R. K., & Vowles, K. E. (2015). The role and function of acceptance and commitment therapy and behavioral flexibility in pain management. Pain Management, 5(5), 319-322. doi:10.2217/pmt.15.32

One way of using a biopsychosocial framework in pain management – vi


I could write about a BPS (biopsychosocial) model in every single post, but it’s time for me to explore other things happening in the pain management world, so this is my last post in this series for a while. But it’s a doozy! And thanks to Eric Bowman for sharing an incredibly relevant paper just in time for this post…

One of the problems in pain management is that there are so many assessments carried out by the professionals seeing a person – but very little discussed about pulling this information together to create an overall picture of the person we’re seeing. And it’s this aspect I want to look at today.

My view is that a BPS approach provides us with an orientation towards the multiple factors involved in why this person is presenting in this way at this time (and what is maintaining their presentation), and by integrating the factors involved, we’re able to establish a way to reduce both distress and disability. A BPS approach is like a large-scale framework, and then, based on scientific studies that postulate mechanisms thought to be involved, a clinician or team can generate some useful hypotheses through abductive reasoning, begin testing these – and then arrive at a plausible set of explanations for the person’s situation. By doing so, multiple different options for treatment can be integrated so the person can begin to find their way out of the complex mess that pain and disability can bring.

The “mechanisms” involved range from the biological (yes, all that cellular, genetic, biomechanical, muscle/nerve/brain research that some people think is omitted from a BPS approach IS included!), to the psychological (all the attention, emotion, behavioural, cognitive material that has possibly become the hallmark of a BPS approach), and eventually, to the social (interactions with family, friends, community, healthcare, people in the workplace, the way legislation is written, insurers, cultural factors and so on). That’s one mess of stuff to evaluate!

We do have a framework already for a BPS approach: the ICF (or International Classification of Functioning, Disability and Health) provides one way of viewing what’s going on, although I can empathise with those who argue that it doesn’t provide a way to integrate these domains. I think that’s OK because, in pain and disability at least, we have research into each one of these domains although the social is still the most under-developed.

Tousignant-Laflamme, Martel, Joshi & Cook (2017) provide an approach to help structure the initial domains to explore – and a way to direct where attention needs to be paid to address both pain and disability.

What I like about this model (and I urge you to read the whole paper, please!) is that it triages the level of complexity and therefore the intervention needed without dividing the problem into “physical” and “psychosocial”. This is important because any contributing factor could be The One to most strongly influence outcome – and often an integrated approach is needed, rather than thinking “oh but the biological needs to be addressed separately”.

Another feature I like about this model is the attention paid to both pain and disability.

Beginning from the centre, each of the items in the area “A” is something that is either pretty common, and/or easily modified. So, for example, someone with low back pain that’s eased by flexion, maybe has some osteoarthritis, is feeling a bit demoralised and worries the pain is going to continue, has a job that’s not readily modified (and they’re not keen on returning) might need a physiotherapist to help work through movement patterns, some good information about pain to allay their worries, an occupational therapist to help with returning to work and sleeping, and maybe some medication if it helps.

If that same person has progressed to become quite slow to move and deconditioned, they’re experiencing allodynia and hyperalgesia, they have a history of migraine and irritable bowel, their sleep is pretty rotten, and they’re avoiding movements that “might” hurt – and their employer is pretty unhappy about them returning to work – then they may need a much more assertive approach, perhaps an intensive pain management programme, a review by a psychiatrist or psychologist, and probably some occupational therapy intervention at work plus a graded exposure to activities so they gain confidence despite pain persisting. Maybe they need medications to quieten the nervous system, perhaps some help with family relationships, and definitely the whole team must be on board with the same model of healthcare.

Some aspects are, I think, missing from this model. I’d like to see more attention paid to family and friends, social and leisure activities, and the person’s own values – because we know that values can be used to help a person be more willing to engage in things that are challenging. And I think the model is entirely deficits-based meaning the strengths a person brings to his or her situation aren’t incorporated.  Of course, too, this model hasn’t been tested in practice – and there are lots of gaps in terms of the measures that can be used to assess each of these domains. But as a heuristic or a template, this model seems to be practical, relatively simple to understand – and might stop us continuing to sub-type back pain on the basis of either psychosocial risk factors or not.

Clinicians pondering this model might now be wondering how to assess each of these domains – the paper provides some useful ideas, and if the framework gains traction, I think many others will add their tuppence-worth to it. I’m curious now to see how people who experience low back pain might view an assessment and management plan based on this: would it be acceptable? Does it help explain some of the difficulties people face? Would it be useful to people living with pain so they can explore the factors that are getting in the way of recovery?

Tousignant-Laflamme, Y., Martel, M. O., Joshi, A. B., & Cook, C. E. (2017). Rehabilitation management of low back pain – it’s time to pull it all together! Journal of Pain Research, 10, 2373-2385. doi:10.2147/JPR.S146485

One way of using a biopsychosocial framework in pain management – iv


And yes! There’s more to this series of posts on how I use a biopsychosocial model in practice!

Today’s post is about moving from a conceptual model to a practical model, or how we can use research in our clinical reasoning.

A biopsychosocial model (BPSM) as envisaged by Engel was a framework for clinicians to think about why this person is presenting in this way at this time (and what may be maintaining their situation), as well as what could be done to reduce distress and disability. Engel wanted clinicians to go beyond disease processes, isolated from the people experiencing them, and to explore aspects of how the person coped with everyday challenges (including health), the factors that influenced their decision that their health problem was indeed a problem, and the context of seeking healthcare.  He wanted clinicians to be scientific about how they generated hypotheses which could then be tested in clinical practice, and ultimately confirm or disconfirm the contribution of that factor.

The “bio” aspect of pain (which is a contentious word – I’ll comment in a bit) involves disease processes, trauma, all the biological aspects prior to conscious awareness of the “ouch” we know as pain. Theoretical developments in this area include all the work being conducted in terms of understanding anatomy and physiology of the human body, from molecular study (information transmission from one neurone to another); detailed understanding of spinal cord mechanisms; of the role of glia; of inflammatory processes; of genetic and epigenetic changes; of relationships between blood flow to and from various parts of the brain; of biomechanics; of normal healing processes – and so on. There’s no lack of information being generated by researchers undertaking basic science about the biological mechanisms involved in our experience of pain. Because I typically see people with persistent pain that has been present for maybe 12 months or more (usually much longer than that), I rely on the work of my colleagues to make a good diagnosis. Most people have had more investigation than is probably helpful for them, and I think we can use Clifford Woolf’s broad mechanisms as a reasonable stance when considering an underlying mechanism involved in a person’s pain. Essentially he identifies four main mechanisms: nociceptive, inflammatory, neuropathic and what is now known as “nociplastic” (where the nociceptive system appears to have a problem with processing information).

Yes, we can argue that our current state of understanding is incomplete and there is more to learn, but by working from these basic mechanisms I think we can begin to work on the “bio” part of a biopsychosocial model with a degree of confidence. For my work, anyway, these mechanisms seem to provide a reasonable framework from which the “bio” part of management can begin.

But this is where many clinicians start – and stop. Directly treating, for example, inflammation, certainly provides a reduction in pain – for example, my partner who takes Humera for his ankylosing spondylitis. He no longer experiences inflammatory pain and as his CRP levels reduced, so too did his pain. We can see similar effects when someone has a grotty old hip joint replaced, which removes nociceptive input, ultimately leaving them with a shiny new and painfree hip (in most cases). But as my partner found out, having no pain doesn’t immediately change old habits.

His situation is a nice illustration of the interaction between a disease process which responded really well to a drug that eliminates inflammation, and his beliefs and behaviour which wasn’t changed. Let me explain – once his drug kicked in and he had no pain, he found it odd not to have to think about his pain when climbing hills. It took him about a month or two to fully return to hill climbing in the way he’d done before his anky spond started. That’s right – no pain for a month or two, but that long before he felt confident to go about his activities. And he’s not a man who worries much about his pain!

To add some theory to this, his beliefs (that if he climbed hills a full speed he would inevitably end up with a very sore back) led to him having learned not to go a full pace (through both classical and operant conditioning). We could call this “pain-related fear and avoidance” – or “fear avoidance”. This is one theory that has been extensively researched, and we can integrate the hypotheses generated from this theory into our understanding of why my partner initially had some hesitation about climbing hills. Flowing on from this, we can consider treatments that have been found useful to address his hesitation.

The first treatment could be “explaining pain” to him. Now that wasn’t useful in this case because – oh yeah – his pain had gone! And although he knew his inflammatory pain wasn’t going to harm him (otherwise he’d never have been a high country fire fighter for 20 years despite his anky spond!), he didn’t like the after-effects of aggravating his pain. What helped was addressing his anxiety about the potential for a big flare-up – and this was primarily about beginning at a level that was just beyond his “normal” hill climb, and gradually progressing.

This superficially looks like “exercise” – but it’s exercise with a twist. My partner is as fit as a buck rat. His cardiovascular fitness was fine. Gradually increasing his hill walking wasn’t about increasing fitness – it was about helping him approach an activity that he was a tad concerned might flare his pain up, leading to a rotten night’s sleep (as it had in the past). In fact, this “treatment” was almost all about reducing avoidance by exposing him to things that increased his anxiety just a bit – enough for him to establish that the rotten sleep consequence didn’t happen.

So a biopsychosocial approach to his recovery involved the biological which quickly resolved his pain but left him with some concerns (reasonable ones I think) about pushing himself too hard. Addressing those concerns by taking a theory developed originally from phobia research, applying it to his situation and developing a treatment based on this theory, has led to his return to full participation. Using research-based information to address another part of “why is this person presenting in this way at this time, and what might be maintaining this situation” involves thinking beyond the disease process, and into understanding the problems the person identifies. It means thinking beyond a single discipline. It means reading widely and thinking creatively. That was a good part of Engel’s original proposition.

 

One way of using a biopsychosocial framework in pain management – ii


Last week I discussed case formulation as one way of using a biopsychosocial framework in pain management, and I reviewed Benedetti’s description of the process of becoming aware that something’s wrong, seeking relief from that discomfort, then the “meet the therapist moment”, and finally the “receiving the therapy” steps along the way. Benedetti considers this within a neurobiological model (Benedetti, 2013), while Engel (1977) used general systems theory to frame his critique of the original biomedical model.

This week I want to look at a behavioural model. I do this partly because I think it’s been a long time since this model was brought into our discussions about pain and pain behaviour, and I do it because I think we can understand a great deal about why different people respond differently to their pain when we look at behaviour alone – before we even begin to look at beliefs or attitudes about pain.

Let’s do a little revision (Psych 101). In a behavioural model, we’re looking at two main forms of conditioning: Pavlovian or classical conditioning, and operant or instrumental conditioning. In the case of pain, we also need to revisit the distinction made between the experience (pain), and our behavioural response to that experience (pain behaviours). Pain behaviours are typically filtered or influenced by what we think is going on (judgements about the meaning of pain – eg super-scary crumbling back, or I just did too much gardening), what we’ve learned to do, and the context in which we’re experiencing pain. That context can be current (eg I’m in Church and it’s very quiet so I’d better not swear as I hit my toe against the pew!), or past (eg last time I kicked my toe against the pew and swore, everyone looked at me – how embarrassing!), or even future (eg if I swear when I kick my toe against the pew, I’ll never be able to show my face here again!). It’s the learned part I want to discuss today.

Pain behaviours range from reflex withdrawal responses (lifting the foot up while straightening the other leg to support me when I stand on a tack), to quite complex behaviours we’ve learned are relevant in our environment (filling out a claim form for compensation and treatment).

We probably developed pain behaviours as part of our evolutionary development: the reflex withdrawal behaviours don’t require conscious thought, so they begin in infancy (actually, before), and rely on spinal mechanisms (eg Rohrbach, Zeiter, Andersen, Wieling & Spadavecchia, 2014), with various parts of the brain becoming involved as part of strategies to avoid threat (see Damasio and Damasio (2016) for some insights into evolutionary aspects of withdrawal reflex). But because we have a developed cortex, we’ve learned ways of suppressing our responses, depending on social context – and on responses from others around us.

Reflexive responses are those associated with classical conditioning – and lead us to learn relationships between previously non-threatening stimuli and both withdrawal responses and the physiological arousal that goes with them. For example, if I bend over to make the bed and OUCH! my back suddenly gets really sore. I straighten up very carefully – and I’ve learned something: next time I bend over to make the bed, I’ll be remembering and preparing for that OUCH! to happen once again. The bed and bending forward movement become associated, in my mind, with that OUCH! Of course, for most of us, once we make the bed a few more times (make that many times), we’ll learn that OUCH! doesn’t inevitably follow the bend, so we gain confidence to repeat that movement without preparing for the OUCH! Now what do you think might happen if I never had an opportunity to make the bed again? Say, if I have a really protective person in my life who stopped me every time I go to do it – will that association I have in my mind persist, or will it reduce? This is, in essence, what is thought to happen when someone develops so-called “fear avoidance”. Note: the experience of pain does not have to re-occur for me to avoid bending and begin to rev my nervous system up. What needs to happen is for the first instance to be pretty strong, and for me to not test my belief again. It’s the behaviour that persists (avoidance) because by avoiding something I believe will be OUCH! I avoid experiencing OUCH! And by avoiding that experience, I never test whether OUCH! happens every time, or just that once.

Let’s look at the other really powerful learning mechanism: operant conditioning. In this situation, the likelihood of me repeating my behaviour is increased or reduced, depending on responses in the environment. So, let’s take my bending forward and experiencing OUCH! If my partner (bless him) then decided to fuss over me, make me a cup of tea and tell me not to worry about making the bed ever again – AND if I liked that idea – my response is likely to be to avoid making the bed. I might even go as far as wincing a bit when walking, so he makes me another cup of tea and fusses over me. I might talk about my back pain because he’s so concerned about me (or I really want him to be concerned about me) and if he carries on fussing, I’m likely to carry on with these behaviours. Now picture that in a two-year-old kid – every time the kid trips and cries, some concerned parent comes picks him up, something the kid likes, it’s probable that kid will learn that this is normal, and something to do when he hurts. For more on learning theory, Johan Vlaeyen summarises the state of play in a review paper from 2015 (Vlaeyen, 2015).

We’re smart, us humans. We learn to predict and remember patterns even from imprecise data – it doesn’t take much for us to put two and two together, particularly when it’s something relevant to surviving! Whenever I’m listening to someone telling me their story about why they’re presenting in this way at this time, and what is maintaining their situation, I keep thinking about the various learning mechanisms involved. Social context and the people around us and how they respond to us exert a powerful force on what we do – and many times we’re not even aware of why we do what we do.  Knowing this stuff means that when I’m listening to someone’s story I try very hard to factor in those things that may have influenced what the person does, rather than just thinking the person is aware of doing all they are doing.

 

Benedetti, F. (2013). Placebo and the new physiology of the doctor-patient relationship. Physiological Reviews, 93(3), 1207-1246. doi:10.1152/physrev.00043.2012

Damasio, A., & Damasio, H. (2016). Pain and other feelings in humans and animals. Animal Sentience: An Interdisciplinary Journal on Animal Feeling, 1(3), 33.

Engel, G. L. (1977). The need for a new medical model: A challenge for biomedicine. Science, 196(4286), 129-136.

Rohrbach, H., Zeiter, S., Andersen, O. K., Wieling, R., & Spadavecchia, C. (2014). Quantitative assessment of the nociceptive withdrawal reflex in healthy, non-medicated experimental sheep. Physiology & behavior, 129, 181-185.
Vlaeyen, J. W. (2015). Learning to predict and control harmful events: Chronic pain and conditioning. Pain, 156, S86-S93.

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.

What should we do about acute low back pain?


There’s no doubt that low back pain presents a major healthcare problem in all parts of the world. It’s probably the most common form of musculoskeletal pain around, it can be highly disabling – and its management is one of the most contentious imaginable. As someone once said “if there was an effective treatment for low back pain, there wouldn’t be such a range of treatments available!”

I want to take a step back and consider people living with nonspecific low back pain only, it’s by far the most prevalent, and while no-one would say there is a single diagnosis that can be applied to all forms of back pain, there seem to be some similarities in how this kind of pain responds.

What we’ve learned over the past year is that acetaminophen hardly touches the pain of nonspecific low back pain Machado, Maher, Ferreira, Pinheiro et al, 2015). This means anti-inflammatory medications (NSAIDs) are the most likely group of medications to be prescribed, or perhaps codeine. Exercise was the recommended treatment for osteoarthritis of the hip and knee, suggesting that this approach might also be recommended for low back pain.

Turning to exercise, it seems that there is no clear indication that any particular type of exercise is any better than any other exercise for low back pain (not even motor control exercise)(Saragiotto, Maher, Yamato Tie, Costa et al, 2016), and all exercise improves pain and disability – and even recurrences (Machado, Bostick & Maher, 2013). What seems important is that people get moving again, and do so quickly after the onset of their back pain.

Graded exposure has also been in the news, latest being a study using graded exposure for elderly people living with chronic low back pain, where it was found to not only improve function (reduce disability) but also found to reduce pain (Leonhardt, Kuss, Becker, Basler et al, in press). OK, pain reduction wasn’t reduced a great deal, but neither have many treatments – and at least this one has few adverse effects and improves disability.

Where am I going with this?

Well, recently I made some apparently radical suggestions: I said that

  1. sub-typing low back pain doesn’t yet seem to be consistent;
  2. that no particular exercise type seems better than anything else;
  3. that ongoing disability is predicted more by psychosocial factors than by physical findings – even when injection treatments are used (van Wijk, Geurts, Lousberg,Wynne, Hammink, et al, 2008).
  4. that people with low back pain seem to get better for a while, and often find their back pain returns or grumbles along without any particular provocation;
  5. and that perhaps treatment should focus LESS on reducing pain (which doesn’t seem to be very effective) and LESS on trying to identify particular types of exercise that will suit particular people and MORE simply on graded return to normal activity.
  6. Along with really good information about what we know about low back pain (which isn’t much in terms of mechanics or anatomy, but quite a lot about what’s harmful and what doesn’t help at all), maybe all we need to do is help people get back to their usual activities.

For my sins I was asked not to remain involved in the group planning health system pathways (I also suggested maybe osteopaths, chiropractors, massage therapists and both occupational therapists and psychologists might also be good to be involved – maybe that was the radical part because I can’t see an awful lot radical about my other suggestions!).

Here’s my suggestion – when one of the most difficult aspects of low back pain management is helping people return to normal activities within their own environment (work, home, leisure), why not call in the experts in this area? I’m talking about YOU, occupational therapists! So far I haven’t been able to find a randomised controlled trial of occupational therapy graded exposure for low back pain. I’m sorry about this – it’s possibly a reflection of the difficulty there is in even suggesting that DOING NOTHING (ie not attempting to change the tissues, just helping people return to normal activity) might be an active form of treatment, and one that could work.

I don’t want to denigrate the wonderful work many clinicians do in the field of low back pain, but I suspect much of what seems to work is “meaning response” – well-meaning clinicians who believe in their treatments, patients who believe in their therapists, treatments that appear plausible within the general zeitgeist of “why we have low back pain”, all leading to a ritual in which people feel helped and begin to do things again.

Many of us have read Ben Darlow’s paper on The Enduring Impact of What Clinicians Say to People with Low Back Pain (Darlow, Dowell, Baxter, Mathieson, Perry & Dean, 2013). We have yet to count the cost of well-meaning clinicians feeding misinformed and unhelpful beliefs (and behaviours) to people with acute low back pain. I think the cost will be extremely high.

I just wonder if we might not be able to cut out much of the palaver about low back pain if we went directly to the “feeling helped and begin to do things again” without the misinformation and cost of the rituals involved. While other clinicians can contribute – the process of doing in the context of daily life is where occupational therapy research, experience and models have focused for the discipline’s history. That’s the professional magic of occupational therapy.

 

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. Annals of Family Medicine, 11(6), 527-534. doi:10.1370/afm.1518

Leonhardt C, Kuss K, Becker A, Basler HD, de Jong J, Flatau B, Laekeman M, Mattenklodt P, Schuler M, Vlaeyen J, Quint S.(in press). Graded Exposure for Chronic Low Back Pain in Older Adults: A Pilot Study. Journal of Geriatric Physical Therapy.

Macedo, L. G., Bostick, G. P., & Maher, C. G. (2013). Exercise for prevention of recurrences of nonspecific low back pain. Physical Therapy, 93(12), 1587-1591.

Machado, G. C., Maher, C. G., Ferreira, P. H., Pinheiro, M. B., Lin, C.-W. C., Day, R. O., . . . Ferreira, M. L. (2015). Efficacy and safety of paracetamol for spinal pain and osteoarthritis: Systematic review and meta-analysis of randomised placebo controlled trials (Vol. 350).

Saragiotto Bruno, T., Maher Christopher, G., Yamato Tiê, P., Costa Leonardo, O. P., Menezes Costa Luciola, C., Ostelo Raymond, W. J. G., & Macedo Luciana, G. (2016). Motor control exercise for chronic non-specific low-back pain. Cochrane Database of Systematic Reviews, (1). http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD012004/abstract doi:10.1002/14651858.CD012004

van Wijk, R. M. A. W., Geurts, J. W. M., Lousberg, R., Wynne, H. J., Hammink, E., Knape, J. T. A., & Groen, G. J. (2008). Psychological predictors of substantial pain reduction after minimally invasive radiofrequency and injection treatments for chronic low back pain. Pain Medicine, 9(2), 212-221.

Using a new avoidance measure in the clinic


A new measure of avoidance is a pretty good thing. Until now we’ve used self report questionnaires (such as the Tampa Scale for Kinesiophobia, or the Pain Catastrophising Scale), often combined with a measure of disability like the Oswestry Disability Index to determine who might be unnecessarily restricting daily activities out of fear of pain or injury. These are useful instruments, but don’t give us the full picture because many people with back pain don’t see that their avoidance might be because of pain-related fear – after all, it makes sense to not do movements that hurt or could be harmful, right?

Behavioural avoidance tests (BAT) are measures developed to assess observable avoidance behaviour. They’ve been used for many years for things like OCD and phobias for both assessments and treatments. The person is asked to approach a feared stimulus in a standardised environment to generate fear-related behaviours without the biases that arise from self-report (like not wanting to look bad, or being unaware of a fear).

This new measure involves asking a person to carry out 10 repetitions of certain movements designed to provoke avoidance. The link for the full instructions for this test is this: click

Essentially, the person is shown how to carry out the movements (demonstrated by the examiner/clinician), then they are asked to do the same set of movements ten times.  Each set of movements is rated 0 = performs exactly as the clinician does; 1 = movement is performed but the client uses safety behaviours such as holding the breath, taking medication before doing the task, asking for help, or motor behaviours such as keeping the back straight (rotation and bending movements are involved); 2 = the person avoids doing the movement, and if the person performs fewer than 10 repetitions, those that are not completed are also coded 2. The range of scores obtainable are 0 – 60.

How and when would you use this test?

It’s tempting to rush in and use a new test simply because it’s new and groovy, so some caution is required.

My questions are: (1) does it help me (or the person) obtain a deeper understanding of the contributing factors to their problem? (2) Is it more reliable or more valid than other tests? (3) Is it able to be used in a clinical setting? (4) Does it help me generate better hypotheses as to what’s going on for this person? (5) I also ask about cost, time required, scoring and whether special training is required.

This test is very useful for answering question (1). It provides me with a greater opportunity to review the thoughts, beliefs and behaviours of a person in the moment. This means I can very quickly identify even the subtle safety behaviours, and obtain the “what’s going through your mind” of the person. If I record the movements, I can show the person what’s going on. NB This is NOT intended to be a test of biomechanical efficiency, or to identify “flaws” in movement patterns. This is NOT a physical performance test, it’s a test of behaviour and belief. Don’t even try to use it as a traditional performance test, or I will find you and I will kill (oops, wrong story).

It is more valid than other tests – the authors indicate it is more strongly associated with measures of disability than measures of pain-related fear and avoidance behaviour. This is expected, because it’s possible to be afraid of something but actually do it (public speaking anyone?), and measures of disability don’t consider the cause of that disability (it could be wonky knees, or a dicky ticker!).

It’s easy to do in a clinical setting – A crate of water bottles (~8 kg) and a table (heights ~68 cm) are needed to conduct the BAT-Back. The crate weighed  7.8 kg including six one-litre plastic bottles. One could argue that people might find doing this test in a clinic is less threatening than doing it in real life, and this is quite correct. The setting is contained, there’s a health professional around, the load won’t break and there’s no time pressure, so it’s not ecologically valid for many real world settings – but it’s better than doing a ROM assessment, or just asking the person!

Does it help me generate better hypotheses? Yes it certainly does, provided I take my biomechanical hat off and don’t mix up a BAT with a physical performance assessment. We know that biomechanics are important in some instances, but when it comes to low back pain it doesn’t seem to have as much influence as a person’s thoughts and beliefs – and more importantly, their tendency to just not do certain movements. This test allows me to go through the thoughts that flash through a person’s mind as they do the movement, thus helping me and the person more accurately identify what it is about the movement that’s bothering them. Then we can go on to test their belief and establish whether the consequences are, in fact, worse than the effects of avoidance.

Finally, is it cost-effective? Overall I’d say yes – with a caveat. You need to be very good at spotting safety behaviours, and you need to have a very clear understanding about the purpose of this test, and you may need training to develop these skills and the underlying conceptual understanding of behavioural analysis.

When would I use it? Any time I suspect a person is profoundly disabled as a result of their back pain, but does not present with depression, other tissue changes (limb fracture, wonky knees or ankles etc) that would influence the level of disability. If a person has elevated scores on the TSK or PCS. If they have elevated scores on measures of disability. If I think they may respond to a behavioural approach.

Oh, the authors say very clearly that one of the confounds of this test is when a person has biological factors such as bony changes to the vertebrae, shortened muscles, arthritic knees and so on. So you can put your biomechanical hat on – but remember the overall purpose of this test is to understand what’s going on in the person’s mind when they perform these movements.

Scoring and normative data has not yet been compiled. Perhaps that’s a Masters research project for someone?

Holzapfel, S., Riecke, J., Rief, W., Schneider, J., & Glombiewski, J. A. (in press). Development and validation of the behavioral avoidance test – back pain (bat-back) for patients with chronic low back pain. Clinical Journal of Pain.