science

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 (ii)


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

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

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

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

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

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

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

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

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

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

Next time – delving into mechanisms!

What are the implications of the complexity of central processing?

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

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

 

 

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

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

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

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

Knee pain – and central sensitisation


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

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

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

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

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

Putting it all together

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

Conclusion

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

 

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

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

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

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

Getting stuck with language


In my last post I talked about the ways in which humans learn to relate abstract concepts and experiences together (symbolic relations). I pointed out that we learn to take another person’s point of view as part of developing empathy, and that by interacting with our world we become aware of our place (here) and someone or something else’s place (there). We also learn “me” and “you” (not me), along with near and far, now and then and myriad other abstract concepts that our language can allow us to understand. I suggested that the flexibility of symbolic relations and the relational framing we develop as a result of this skill can be both a help and a hindrance.

Yes, we can remember that a pot can be used to cook, but we also can’t unlearn that relationship. And in being unable to unlearn a relationship we can find it difficult to consider alternative relationships between that pot and whatever else we could do with it. The pot will always be recognised as “something to cook with” although it might also become associated with a receptacle for water, a paperweight, a hat, and even a weapon – but when we’re first asked “what do you use a pot for?” we’ll almost always come up with “cooking”.

In relational frame theory, we develop the ability to empathise or adopt the view of another person based on perspective taking and contextual cues. Contextual cues help us learn the concepts of “I” and “you”  by moving from “here” to “there” to take the place of the other person. If a pen is here, and paper is there, when I go to the paper, it becomes “here” and the pen is “there”. In technical terms this is called deictic framing and this is how kids learn that some concepts only make sense from a given point of view – and here and there are two of those concepts.

How does this relate to pain?

Well, to enjoy being with others, you need to have sufficient deictic framing skills to “stand in another person’s moccasins”, to empathise with their feelings and to be willing to feel those feelings (Villatte, Villatte & Hayes, 2016, p. 32). The thing is, we don’t always want to feel what another person is feeling, especially if we’re angry with them, or they’re feeling sad or some other negative emotional state. We learn to put our ability to empathise on hold to avoid experiencing those feelings. We do this with our own emotions and experiences we’d rather not have. And it’s an adaptive thing – we don’t want to be completely immersed in another person’s experience all the time because it’s difficult to know what our own feelings are vs those of another. We also don’t want to experience all the negative things around us – we learn from them, true, but we don’t really want to feel them all the time. So we develop a skill called “experiential avoidance”. That is, we learn not avoid experiences we’d rather not have.

Experiential avoidance is a cool skill, it’s definitely helpful – it is a process that we use to avoid personal injury, unpleasant people, or situations we don’t feel comfortable in. BUT there’s a catch. Because we relate concepts to one another, we associate words with experiences and memories as well. This is also useful – we can recall the lovely feeling of summer even in the middle of a grey old winter! But at the same time, our most potent learning is often associated with unpleasant experiences, and so for me the sound of a rumbling truck can bring back all the memories of my house being jolted and struck by an earthquake. And because that experience is associated with feeling out of control, helpless, worried and unsettled, those emotions come back along with the memory of the earthquakes. All brought about by hearing a truck rumbling past! And talking about the earthquakes, for some people, is enough to bring back all those same memories.

No wonder, then, for some of the people we work with, just seeing someone walking by is enough to generate the memories, emotions and concerns they experience when they try to walk on a painful foot.

Because of our tendency to avoid experiences that don’t feel good, we naturally try to avoid coming into contact with those stimuli that evoke those negative feelings etc. For some people this can mean avoiding watching images on TV – I remember avoiding watching the tsunami in Japan that happened just after the quakes here in Christchurch. To me the emotions were too raw, I felt too overwhelmed by my own situation to feel I could empathise with those people in Japan.  In some of our clients, just talking about their own painful body can be overwhelming, bringing back unpleasant emotions, memories and thoughts. And indeed for some people, just seeing others doing the things they believe will hurt if they did them is enough to provoke both a negative emotional response AND an flare-up of their pain.

So. Experiential avoidance can help us avoid feeling overwhelmed…but it also stops us experiencing what is happening right now. And I think you can see how it can stop us learning, and it can limit the range of things we’re happy to do – not because there’s any threat right here and now, but because we remember what has happened, and we make predictions of what might happen in the future. The things that might happen – might not happen too! And the things that have happened have already occurred… but our brains are good at joining the dots and being a bit over-protective.

What this means for us as clinicians (and for us as people, too), is that we might need to be gentle but firm, and help people be present here and now. And gradually show people how to be OK with experiencing things that remind us of unpleasant events in the pursuit of something far more useful – flexible responses in a world that is always changing.

Villatte, M., Viullatte, J., & Hayes, S. (2016). Mastering the clinical conversation: Language as intervention. The Guilford Press: New York. ISBN: 9781462523061

Faking pain – Is there a test for it?


One of the weird things about pain is that no-one knows if you’re faking. To date there hasn’t been a test that can tell whether you’re really in pain, or just faking it. Well, that’s about to change according to researchers in Israel and Canada.

While there have been a whole range of approaches to checking out faking such as facial expression, responses to questionnaires, physical testing and physical examinations, none of these have been without serious criticism. And the implications are pretty important to the person being tested – if you’re sincere, but someone says you’re not, how on earth do you prove that you’re really in pain? For clinicians, the problem is very troubling because allegations of faking can strain a working relationship with a person, and hardly lead to a sense of trust. Yet insurance companies routinely ask clinicians to make determinations about fraudulent access to insurance money – and worst of all, clinicians often feel they have little choice other than to participate.

In this study by Kucyi, Sheinman and Defrin, three hypotheses were tested: 1) Whether feigned performance could be detected using warmth and pain threshold measurements; 2) whether there were changes in the statistical properties of performance when participants were faking; and 3) whether an “interference” or distractor presented during testing interferes with the ability to fake and therefore provide a clue to when someone is being sincere or not.

Using university students (I hope they got course credits for participating!) who were not health science students, and were otherwise healthy, the investigators gave very little information about the procedure or hypotheses to minimise expectancy bias. Participants were then tested using a thermal stimulator to obtain “warmth sensation threshold” and “heat-pain thresholds” – this is a form of quantitative sensory testing (QST). TENS was used as a distractor in the experimental case, applied for 2 minutes before measuring the pain threshold, and during the heat pain threshold test. This was repeated with first the threshold test, then TENS. Participants were asked to pretend they were in an insurance office, being tested to establish whether they were experiencing genuine pain, after being told the test would be able to tell whether their pain was real.

What did they find out?

Well in situation one, where both threshold and warmth detection were used, and participants were asked to fake the pain intensity, respondents gave higher warmth detection ratings than normal. Not only this, but the ability to repeat the same response with the same temperature was poorer.  Heat pain threshold was also consistently different between the sincere and faked conditions, with heat pain threshold lower when people were faking (to around 3 degrees).

When the second testing option was carried out (using TENS to distract), heat pain threshold was significant lower when participants were faking, and the variance of the feigned + interference condition was three times that of the sincere condition, and the CV of the feigned + interference condition was twice that of the sincere condition.

What does this mean?

Well first of all, it means there are some consistent effects of faking in response to tests of warmth and heat-pain threshold when a distractor like TENS is used. Increased reports of warmth threshold and reduced heat pain threshold were observed, and where statistically significant. Interestingly, it was only when a distractor was used that the variability of reports were found – these authors suggest that people are pretty skilled at giving consistent reports when they’re not being distracted by an additional sensory stimulus.

Now here’s where I begin to pull this apart from a clinical and practical perspective. The authors, to give them credit, indicate that the research is both new and that it may identify some people who do have pain as malingerers. My concerns are that people with chronic pain may not look at all like healthy young university students.

We know very little about the responses to QST by people with different forms of chronic pain. We already know that people with impaired descending noxious inhibitory control respond differently to some forms of QST. We also know that contextual factors including motivation can influence how nervous systems respond to input. But my concerns are far more about the potential harm to those who are tested and found to be malingering when they’re not.

What do you do if you think a person is faking? How do you deal with this? What good does it do to suggest to someone their pain is not real, or isn’t nearly as bad as they make out? Once the words are out of your mouth (or written in a report) any chance of a therapeutic relationship has just flown right out the door. And you’re still left with a person who says they’re having trouble – but now you have an angry, resentful person who has a strong need to prove that they DO have pain.

You see, I think it might be more fruitful to ask why is this person faking pain? If it’s simply for money, surely there are far easier ways to get money than pretending to be disabled by pain? If it’s the case that a person is off out fishing or playing golf or living it up when “supposed” to be in pain, wouldn’t it make more sense to reframe their response as either recovering well (doing what’s healthy) and therefore get on with returning to work; or use a private investigator to demonstrate that he or she is actually capable of doing more than they indicate?

The presence or absence of pain is not really the problem, IMHO. To me we need to address the degree of disability that’s being attributed to pain and work on that. Maybe a greater focus on reducing disability rather than on expensive procedures to remove pain or otherwise get rid of pain is in order?

Kucyi, A., Sheinman, A., Defrin, R. (in press). Distinguishing feigned from sincere performance in psychophysical pain testing. The Journal of Pain.

Relax… if you text, your head won’t fall off & you won’t damage your spine!


You can’t have missed it – headlines in newspapers, all over the internet here and here.

https://i0.wp.com/www.kewosteo.com.au/uploads/2/4/1/3/24132050/6043934_orig.png

“Text neck” is a thing: 5 frightening maladies of the digital era

We’re all addicted to our electronic devices. Few of us realize the physical toll they’re taking on our bodies

“14 year old diagnosed with ‘text neck'”

Texting creating ‘text neck’ epidemic, doctor warns

The headlines are enough to make anyone just a bit worried – but do we need to, really?

Let’s begin with some anatomy and physiology. Necks and heads are supported by a wonderful array of ligaments and tendons (you know those tough fibrous bands you usually want to cut out of that piece of steak?), loads of muscles developed for strength, flexbility and subtle adjustment, and plenty of blood supply. The skull, although weighing about 5 1/2 kg, is supported by these muscles (and yes, there are a lot of them!), as well as balanced on strong but interlocking vertebrae.

https://i1.wp.com/padayogi.com/wp-content/uploads/2013/12/posterior_neck.gif

The thing is, that even though you’ll have seen the calculations, these are quite misleading. For one thing, the biomechanical equations used in these calculations are often based on a single point about which the head/neck rotate – and this just isn’t the case.

You can see that there are seven or more vertebrae involved in the movement, meaning the weight of your skull is distributed along each one of them – as well as that, if you take a look at the illustration above on the left, you’ll see two things: one is the strong and inelastic attachment (in white/grey) along the base of the skull and the vertebrae, and the second is just how long that trapezius muscle is. If you know much about physics, you’ll know that when there’s a long and strong anchor to an upright, it can withstand far greater forces than if it’s a short upright without any anchor. So, the weight of your skull is cantilevered (almost) forward with this muscle (and that criss-cross set of muscles you can see in the cutaway section of the image on the left above) and guess what? It’s designed so you can look forward, to the left, to the right, look up – and yes, look down.  What’s even more important to know is that calculations based on this weird equation don’t factor in living, adaptive tissue and the effects of goals, attention, beliefs and your fabulously adaptive nervous system.

This range of movement is really important: it’s so that our forward facing eyes can see all that’s needed to be seen. And most importantly, given that humans are tool-users, our necks allow our heads to bend forwards so we can see our hands as we use tools.

So, when we look down at things for ages, what’s the pain about ?

Well, the first thing is that feeling sore in the muscles around the neck is common – not only do those muscles support our head and neck, they’re also responsible for lifting and moving our shoulders. And if you hold any muscle in one position for long enough it will probably be uncomfortable. This discomfort is great! I’m not kidding, it’s a good thing to feel uncomfortable not because you’re doing any damage to the area, but because it means you’ll move. So we often sit with shoulders elevated, perhaps while writing, holding something, and most often, being tense or stressed. It’s a protective position we can get into because it makes us look a bit smaller and less threatening (blame that on our ancestors).

The second thing is that feeling sore doesn’t mean you’re doing any damage – pain in this instance is all about giving you an alert that it could be worth moving, provided your current goal isn’t more important than doing so.

What are the long-term problems with looking down a lot?

Well, this is where the research gets a bit murky. Perhaps, over time, the muscles that are usually elongated but have to work hard to support your head and neck, get used to being in that position. Perhaps the bones (vertebrae) start to reshape to conform to that position. Perhaps we feel more uncomfortable when looking up, or straight ahead even, so we avoid it. The truth is, the research literature isn’t very clear at all – and in the absence of clear evidence that looking down is bad (and I mean looking down all the time) I think we can relax a bit.

The cure for getting comfortable again? You’ve probably all done it yourselves – shrugged your shoulders, looked around (up, down, left, right), stretched your arms up and out, and perhaps – OMG – gone for a walk.

For a far more detailed analysis of posture and pain, you don’t need to look any further than Paul Ingraham’s article on Posture correction. Paul has so many other amazing and well-referenced articles on pain science that you really do need to go take a look (just remember to get up and move a little now and then, OK?)

Todd Hargrove also writes very clearly about pain and posture – this time about back pain (but include neck and shoulder pain too).

Tony Ingram has over 100 articles on pain science, so take a look at them too.

Finally, Nick Ng wrote this article: click

You might be asking why on earth am I writing about text neck when so many others have written clearly about it before.

Well, over the last week I was attending an occupational therapy conference where I was astonished to find clinicians and educators warning us about the health effects of too much screen time. Text neck was mentioned. Add to this, a recent occupational therapy newsletter featured an article by a physiotherapist arguing that we need to protect our necks from the ills of text neck. I don’t want to diss the person who said it, or the person who wrote that article, but I do think it’s critical to point out that the basis for this information is outdated pain science. It’s unnecessary scaremongering, it creates fear and concern about normal aches and pains that we all experience, it can begin a process of “medicalising” (or perhaps “pathologising” is a better word) experiences that we can self manage very easily. We simply need to know that moving is good, holding any constrained posture (even so-called “good posture”) gets uncomfortable after a while, and that it’s OK to feel pain and then do something about it. It does not mean an injury or long-term pathology has been uncovered.

Why no references? Well, the three sites I’ve posted have summarised the research very well, so I figure it’s best to go read what they’ve written rather than rehash a lot of literature that I’m not especially familiar with (I like to deal with people rather than muscles and bones and nerves).

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


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

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

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

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

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

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

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

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

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

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

Well and good. What does it actually mean?

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

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

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

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

 

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

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

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

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

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

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

Chronic pain as psychiatric disorder


For years I’ve taken a stance that chronic pain is not a psychiatric disorder. Yes, it’s associated with depression, anxiety and a host of other problems, but in itself it’s not primarily a mental health problem. I was taken to task for this the other day. The argument went like this:

“Pain disorder”: chronic pain…thought to be caused by psychological stress.  I argued that I didn’t like the label, and have met more people with psychological problems after they’ve developed chronic pain, rather than chronic pain initiated through psychological stress. The International Association for the Study of Pain notes accompanying the definition of pain states:

“Many people report pain in the absence of tissue damage or any likely pathophysiological cause; usually this happens for psychological reasons…. pain most often has a proximate physical cause (http://www.iasp-pain.org/Taxonomy?navItemNumber=576).”

Some people argue that this set of statements doesn’t consider central sensitisation (it was written before there were ways to examine living brain function) – but the end result was, as intended, to equate the experience of pain with only the experience of pain, rather than nociception or tissue damage. The person who disagreed with me suggested I was denigrating those with a mental health diagnosis – I hope I’m not, because illness affects people whether it’s so-called “physical” or “mental”.

Studies have shown that some people do develop chronic pain after being exposed to workplace stress – but haven’t been able to demonstrate that this is a direct stress —> pain relationship. Instead there could be any number of mediating and moderating factors, such as genetic predisposition to chronic pain, tendency to respond to stress with fatigue and increased risk of making errors, response from within the workplace system, working faster and harder because of stress, limited attention to recovery and so on. To show a direct relationship between stress and developing chronic pain, we’d need to see clear evidence of an impact on biological systems that are involved with both stress and pain, and we’d need to see a dose-response relationship and so on. There’s some suggestion that chronic stress may influence the HPA axis, particularly during childhood development, but the main hypothesis about stress and cortisol and neuroinflammation (the glucocorticoid cascade hypothesis) doesn’t appear to have translated well from animal studies to humans (Frodl & O’Keane, 2013).  Quintner and colleagues have suggested fibromyalgia may be the outcome of long-term adaptation to stress, but this hypothesis has not yet been rigorously tested (Lyon, Cohen & Quintner, 2011).

My stance on stress and chronic pain is that having chronic pain is extremely stressful. When a person experiences pain it disrupts and interferes with usual bodily experience during movement and rest. Being unable to do what’s important in life is frustrating, and can lead to social rejection – social rejection itself activates a number of neural pathways that are very similar to those active in chronic pain (MacDonald & Leary, 2005). There’s no doubt that for some people, the demoralising effect of trying time after time for a diagnosis, and the search for effective treatment is stressful enough to produce depression and/or anxiety, and certainly a sense of hopelessness and helplessness. If you happen to be vulnerable to mood problems, or to the effects of stress on a sensitive nervous system, then I’m certain there is a relationship between the two. But not in every case, and not all the time. And the jury is still out on which came first: the mood problem or the chronic pain.

Whatever, I have other reasons for not wanting chronic pain to be labelled a psychiatric disorder. Like it or not, mental health problems are not as well accepted socially as say, breaking a leg or having the flu. Despite the vigorous efforts of many people to raise awareness about depression and anxiety, it’s not anywhere near as easy to announce to people “I’ve got depression” than it is to say “I’ve got the flu”. It’s more difficult if you have chronic pain. Not only is there a really strong belief in the general community that pain should be associated with some sort of visible tissue insult, this belief carries through to many health professionals. Hopefully that’s changing, but far too slowly. What’s worse, many insurers and much compensation law identifies that if there’s no tissue damage, or the problem can’t be imaged, then pain is not a compensable condition. This places the person experiencing pain in an incredibly difficult position – how to demonstrate to people around them that they have a problem that isn’t imaginary and can’t be shrugged off.

Now add another layer of complexity to the argument. By labeling chronic pain a psychiatric disorder, the person being thus labelled experiences a double-whammy. Their pain may be real but not acknowledged, their suffering may be acknowledged but labelled a psychiatric problem. And very often treatment for psychiatric conditions is poorly funded, with limited attention to a biopsychosocial model or to an interdisciplinary approach.

A person given a diagnosis of “somatic symptom and related disorder” (according to DSM 5) is meant to mean they have “somatic symptoms associated with significant distress and impairment.”  The diagnosis is to be made “on the basis of positive symptoms and signs (distressing somatic symptoms plus abnormal thoughts, feelings, and behaviors in response to these symptoms) rather than the absence of a medical explanation for somatic complaints.” (See DSM-5, p. 309.)

I wonder, what are “abnormal” thoughts, feelings and behaviours in response to pain?  How is this judged? Who does the judging? What’s normal? Simply having pain that no-one can explain is, in itself, distressing. I’d have thought this was a pretty normal response.

The American Psychiatric Association states that the DSM 5 Pain Disorder diagnosis “takes a different approach to the important clinical realm of individuals with pain”. They go on to say “In DSM-IV, the pain disorder diagnoses assume that some pains are associated solely with psychological factors, some with medical diseases or injuries, and some with both. There is a lack of evidence that such distinctions can be made with reliability and validity, and a large body of research has demonstrated that psychological factors influence all forms of pain. Most individuals with chronic pain attribute their pain to a combination of factors, including somatic, psychological, and environmental influences. In DSM-5, some individuals with chronic pain would be appropriately diagnosed as having somatic symptom disorder, with predominant pain. For others, psychological factors affecting other medical conditions or an adjustment disorder would be more appropriate.”(click here for the document)

By acknowledging that it’s not possible to distinguish between pain associated with psychological, medical, injury or both, I think this category is a catch-all. I think it’s acknowledging that chronic pain is a problem that many people with mental health problems experience, and it recognises that clinicians working with those who have mental health problems need a box to tick to enable them to address the issues and be paid for it. This isn’t attacking those clinicians who use DSM V to justify their involvement with people who experience chronic pain. But I think it’s a clumsy way of addressing the underlying issue that means insurers and legislators STILL believe there has to be tissue damage, or something we can “see” before a person can have real pain.

 

Frodl, Thomas, & O’Keane, Veronica. (2013). How does the brain deal with cumulative stress? A review with focus on developmental stress, HPA axis function and hippocampal structure in humans. Neurobiology of Disease, 52(0), 24-37. doi: http://dx.doi.org/10.1016/j.nbd.2012.03.012

Lyon, Pamela, Cohen, Milton, & Quintner, John. (2011). An evolutionary stress-response hypothesis for chronic widespread pain (fibromyalgia syndrome). Pain Medicine, 12(8), 1167-1178.

MacDonald, Geoff, & Leary, Mark R. (2005). Why does social exclusion hurt? The relationship between social and physical pain. Psychological bulletin, 131(2), 202.

…but I thought a new knee would fix my pain!


ResearchBlogging.org
Working in an orthopaedic surgery department is quite enlightening. Along with discussions about ceramic vs metal implants and cartilage regeneration (I work with a team of researchers looking at how to create replacement cartilage), the topic of what counts as a surgical success in knee surgery also comes up from time to time. Knee joint replacement isn’t as successful as hip joint replacement for a number of reasons including the complex nature of the joint, the way the joint capsule is disrupted during surgery, and the knee can apparently feel quite different from the original knee.

What this means is there can be quite a mismatch of expectations for people who believe very strongly that there should be no pain and they should have a completely normal knee joint after surgery. In fact, in the NZ National Joint Registry, the main reason recorded for knee joint revision is pain.

Naturally, the problem of pain after surgery is something surgeons and researchers are also interested in. Many studies have shown psychological factors such as catastrophising (thinking the worst) and low mood are associated with poorer outcomes (Riddle, Wade. Jiranek, & Kong, 2010; Roth, Tripp, Harrison, Sullivan & Carson, 2007; Shelby, Somers, Keefe, Pells, Dixon & Blumenthal, 2008).  The outcomes looked at so far include length of stay in hospital at the time of surgery, analgesia use during surgery, increased disability after surgery and revision rates.

Now, one solution to this problem could be simply not performing joint replacement surgery in people who are depressed and tend to think the worst. The problem is that two of the strongest predictors for looking for treatment are – you guessed it: low mood and catastrophising (and disability). Another solution is to provide intervention after surgery to target the people who tend to become fearful – perhaps an enhanced level of physiotherapy for this group, while the less vulnerable may even require less. Some studies have also looked at giving better education about what the surgery entails and the expected outcomes, and doing this before the person undergoes surgery, while another study has looked at providing a pain coping skills training course prior to surgery (Riddle, Wade, Jiranek & Kong, 2011). The outcomes from this last approach were promising, although it was a very small sample size, and the follow-up was for only two months.

There are a number of problems with implementing any of these approaches in clinical practice, at least in the system I’m most familiar with (NZ):

  1. Many orthopaedic surgeons still discount the importance of psychological factors, and consider the information they provide completely adequate for presurgical preparation
  2. It’s difficult to give someone different or special treatment based on psychological factors within a usual clinical setting without also inadvertently giving people a label that may change how they are responded to
  3. Any additional intervention will have an up-front cost (not good for cost accountants!)
  4. These treatments need specially trained clinicians who understand the measures being used, the rationale for treatment, and the type of treatment needed – and because these are psychological factors and surgery is conducted in a “physical” hospital, this is unfamiliar territory for many
  5. Patients may not be very comfortable with a treatment that focuses on thoughts, emotions and pain

It seems to me, and from the results from a recent study looking at analgesic use after surgery, that an argument simply based on the cost of failing to go ahead with effective management of psychosocial factors would make sense. Here’s the detail:

Fuzier, Serres, Bourrel, Palmaro, Montastruc and Lapeyre-Mestre (2014) conducted a large study of patients in the Midi-Pyrenees region of France. They examined the medical records of all 1939 patients who had knee arthroplasty, and compared the drug use (what was dispensed) at four times – 12 months before surgery, 2 months before surgery, and 10 months before and after the knee surgery.  What they found was an increase in analgesic, antineuropathic and opioid drug use in the 12 months after surgery. The actual percentage of patients requiring more medication is astonishing: 47% of people needed more analgesia, 8.6% needed more antineuropathic medications, and 5.6% needed more opioids. That’s a whole lot of drugs!

These researchers also analysed a number of other variables associated with the medication changes, and made some more understandable findings:

  • people having total knee replacement surgery were at a greater risk of using more medication than those having unicompartmental surgery (half a joint)
  • people with high levels of preoperative pain along with “psychiatric vulnerability” were at greater risk of having increased neuropathic medications prescribed
  • but older people were less likely to be prescribed additional medications

Unfortunately, this study didn’t identify the particular “psychiatric vulnerabilities” of the patients who participated – from the paper it looks like data was extracted from clinical records, so psychiatric disorders such as depression, anxiety and so on are the likely culprits. We don’t therefore know whether catastrophising contributed to the medication use – but given the results from at least 20 studies I have in my database, I think it’s probably likely.

Medications are not cheap. While they’re quick to prescribe, dispense and take, they cost not only in fiscal terms (which is a serious consideration, nevertheless), but also in side effects – and more importantly, in loss of personal locus of control. What I mean by this is that these are people who haven’t been given the opportunity to develop pain self management skills. They will continue to catastrophise, and perhaps even more so after surgery because their fears have been confirmed. Maybe it’s cheaper and more humane to bite the bullet and begin giving people appropriate psychosocial treatment before, during and after surgery.

Fuzier, R., Serres, I., Bourrel, R., Palmaro, A., Montastruc, J., & Lapeyre-Mestre, M. (2014). Analgesic drug consumption increases after knee arthroplasty: A pharmacoepidemiological study investigating postoperative pain PAIN®, 155 (7), 1339-1345 DOI: 10.1016/j.pain.2014.04.010

Riddle, D. L., Keefe, F. J., Nay, W. T., McKee, D., Attarian, D. E., & Jensen, M. P. (2011). Pain coping skills training for patients with elevated pain catastrophizing who are scheduled for knee arthroplasty: a quasi-experimental study. Archives of Physical Medicine & Rehabilitation, 92(6), 859-865.

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

Roth, M. L., Tripp, D. A., Harrison, M. H., Sullivan, M., & Carson, P. (2007). Demographic and psychosocial predictors of acute perioperative pain for total knee arthroplasty. Pain Research & Management, 12(3), 185-194.

Shelby, Rebecca A., Somers, Tamara J., Keefe, Francis J., Pells, Jennifer J., Dixon, Kim E., & Blumenthal, James A. (2008). Domain specific self-efficacy mediates the impact of pain catastrophizing on pain and disability in overweight and obese osteoarthritis patients. Journal of Pain, 9(10), 912-919.