Research

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


While a biopsychosocial ‘model’ (or sociopsychobiological framework) has been widely adopted when attempting to understand pain, many critics argue that it just doesn’t give clinicians a clear way to integrate or prioritise clinical information and generate treatments. The ‘model’ itself has been challenged from many angles – it’s too complex, too simplistic, relies on Bertalanffy’s “general systems theory” which has itself been challenged, it’s too “fuzzy”, and of course there are many who think that psychological and sociocultural aspects of human experience are epiphenomena while will ultimately be boiled down to cellular or biological processes. Nevertheless, this framework also has considerable appeal, is widely adopted and I think can provide us with some useful heuristics for thinking about how and why a person presents in the way they do at the time they do – and helps us consider what can be done to reduce distress and disability.

Disclaimer: I work with the “fuzzy” sociopsychological aspects of pain management, and leave a great deal of the biological to those who focus on that – and believe me, the biological is usually done and done to the nth degree in most cases of persistent pain. I rarely see someone who hasn’t had their scans, Xrays, physical examinations, bloods, urine, nerve conduction, surgery, exercise or whatever looked at – but plenty of people who have never once been asked what they think is going on and what their main concern is. Oh and not had their sleep, mood, alcohol and other substance use, daily routines, relationships, work situation, community and spiritual aspects of life ever discussed. So, despite the constant banging on about “don’t forget the bio” – I really do not think this is a thing.

Where do we start with this approach?

The first place I start with my discussions is to ask “Tell me about your problems with pain.” What I’m focusing on in this discussion is when did the person first recognise that there was “something wrong” – and then what did they do about it.

Fabricio Benedetti talks about the neurobiological processes involved in a person detecting that he or she is “unwell”. He writes: “Physiology and neuroscience have a lot to say about feeling sick, for it involves sensory systems that convey different pieces of information related to peripheral organs and apparatuses, as well as brain regions that lead to conscious awareness.” (Benedetti, 2013). To me, this involves biological, psychological and social factors for when does a person recognise that “conscious awareness” means something? Benedetti goes on to say “The second step is what makes a patient “seek relief,” a kind of motivated behavior that is aimed at suppressing discomfort. This behavioral repertoire is not different from that aimed at suppressing hunger or thirst, and the brain reward mechanisms are crucial in this regard” (Benedetti, 2013). Judgements about what internal experiences mean may begin with a reflex response (automatic and based on evolutionary demands to keep safe) but what we DO about those experiences depends a great deal on what we learn from others. The people we most draw from are those around us – mother, father, siblings, people in our immediate family and extended family. And over time, the social nature of humans means we also consider the community in which we live – and wider with social media! Judgements, or appraisals (thoughts and beliefs about the meaning of these internal experiences) are, ‘fraid to say, psychological in nature. While the influences on thoughts and beliefs are – you guessed it – social.

So, how can a clinician use this information? Where’s the research? Come on – science it up woman!!

If it’s not enough to know that there are neurobiological factors underpinning our internal experience, and motivated behaviour is tied up with reward systems, then what else can we use to understand the processes of feeling ill and seeking treatment? To me, the natural first step is to look at learning mechanisms. Yep, very basic Psych 101 classical and operant conditioning mechanisms. Add in a dash of social learning theory (how we learn from watching and talking with others) and we have some rather useful experimentally-validated hypotheses to work with.

What do I mean by this?

Well, at least part of clinical reasoning is a process of recognising potential explanations for the phenomena we see. My take on clinical reasoning is that we can use case formulation to help generate a series of hypotheses to explain why a person is coming to see us in this way at this time – and what might be maintaining their current situation. In case formulation we can use “abductive reasoning” (recognising a potential “rule” or class of behaviour from a specific observation – eg we can postulate that a person’s sleep disturbance might be due to low mood, sleep apnoea, habit, operant conditioning, or a new baby, and we’ll probably collect some more information to test each of these possible explanations before deciding on the most probable reason). If we know a whole bunch of research around what humans do when they’re feeling sore and vulnerable, we are able to come up with a bunch of possible reasons for someone noticing they feel unwell, judging it in a certain way, and then deciding to do something about it.

For example, we know from research studies that people who have had adverse experiences in early childhood have a greater risk of developing post-traumatic stress disorder and chronic pain (eg Afari, Ahumada, Wright, Lostoufi, Golnari, Reis & Cuneo, 2014; Jones, Power & Macfarlane, 2009). We also know that those people may develop weaker attachments to others and so feel vulnerable in relationships where high levels of trust are needed – also linked to the presence of persistent pain – and adversely affecting outcomes from multidisciplinary pain management programmes (Anno, Shibata, Ninomiya, Iwaki, Kawata, Sawamoto et al., 2015; Kowal, McWilliams, Peloquin, Wilson, Henderson & Fergusson, 2015).

These factors might mean that when we ask someone about their theory for why they have persistent pain, or what they think is going on, we might keep an ear open to listen for threats to relationships around the time of the onset of the problem dealing with pain (especially if the pain has been present for a while but the person hasn’t been looking for treatment until just now). We might also be thinking hard about the neurobiological effects of relationship breakups and how this might impinge on either coping (eg accessing strategies to manage effectively during painful experiences) or on stress responses (eg heightened vigilance to threat).

Two things: (1) This doesn’t mean persistent pain is “psychological” – it’s not, but these experiences might set the scene for neurobiological changes, both in “set-point” for threat and in resilience for dealing with threat. (2) This also doesn’t mean that we need to deal with the response to relationship stress ourselves – it might mean we listen respectfully, and bear this vulnerability in mind during our interactions, being careful not to threaten trust, and work hard to retain a sense of warmth/empathy as well as competence for this person.

Next time: More on learning theory and how these might influence the way we look at why someone seeks treatment with us, and why at this time, and what may be maintaining the behaviours we see.

 

Afari N, Ahumada SM, Wright LJ, Mostoufi S, Golnari G, Reis V, Cuneo JG., (2014). Psychological trauma and functional somatic syndromes: A systematic review and meta-analysis. Psychosomatic Medicine, 76, 2-11.

Anno, K., Shibata, M., Ninomiya, T., Iwaki, R., Kawata, H., Sawamoto, R., . . . Hosoi, M. (2015). Paternal and maternal bonding styles in childhood are associated with the prevalence of chronic pain in a general adult population: The hisayama study. BMC Psychiatry, 15(1), 181. doi:10.1186/s12888-015-0574-y

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

Jones GT, Power C, Macfarlane GJ, (2009). Adverse events in childhood and chronic widespread pain in adult life: Results from the 1958 British Birth Cohort Study. Pain 143:92-96.

Kowal, J., McWilliams, L. A., Péloquin, K., Wilson, K. G., Henderson, P. R., & Fergusson, D. A. (2015). Attachment insecurity predicts responses to an interdisciplinary chronic pain rehabilitation program. Journal of Behavioral Medicine, 38(3), 518-526. doi:10.1007/s10865-015-9623-8

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What should healthcare professionals learn?


I was lucky enough to spend two days attending the Placebo Symposium in Sydney in November this year – what an experience! A lineup of the cream of researchers exploring placebo and contextual responses (meaning responses) – all were excellent speakers and the focus was on both research and what this means to clinicians. If you’re keen to watch all you can for free over the next two weeks – click here: www.placebo.armchairmedical.tv.

At the end of the symposium, the speakers were asked a question by artist Eugenie Lee what subjects they would want taught if they had all the facilities and students with top class skills attending. This is what they said (it’s the Lennox Thompson translation, any mis-translations are entirely my responsibility):

  • Inform students about the contextual effects of every single clinical encounter and treatment
  • Help them focus on supporting patients to develop helpful expectations about treatments
  • Read Stanislovski (A good doctor [healthcare professional] is about being a good actor)
  • Always remember: we’re treating people not tissues
  • Use words wisely (they can heal – and harm)
  • Listen to your patients (and show them you’re listening)
  • Interprofessionalism is a thing
  • Talk with your patients not at them
  • Train together with your allied health colleagues
  • Ignore “placebo” or contextual effects at your peril
  • “Placebo” will eventually die – but the effect of context lives on in every treatment
  • Communication skills training needs more than a taste – to learn these skills takes time and intensity
  • Emphasise not just empathy – but also competence – these two factors contribute enormously to the “meet the therapist moment” (generating a sense of trustworthiness)
  • Introduce neurobiology from the beginning of the course
  • Learn [much much much more] about pain throughout the programme – not just the neurobiological systems but the psychological and social
  • Develop greater understanding of research methodologies for studying treatments and their effects

What were my take-away points from this whole conference?

As a longtime convert to Dan Moerman’s re-labeling to meaning response of what we often call “placebo effect”, the key points I took away were these (and you’ll see them pop up again and again in my blogs I’m sure):

  • Every healthcare encounter involves four things: a person seeking help, a person hoping to deliver help, a treatment ritual, and a social context. These can’t be divided if we hope to understand the outcome of treatment.
    • We need to understand the person seeking help – how they identify their illness, how they frame recovery, what their main concern is, and the context in which they are experiencing their illness.
    • We need to understand the person hoping to deliver help – how they view their contribution, how they view the person seeking help, the way they frame their treatment, the context in which they’re given the authority to help, and how they frame recovery.
    • We need to explore the treatment ritual – from the packaging, the meaning (to both parties) of the artifacts, the procedures, the words and actions – all of these have meaning, as marketing companies undoubtedly know (and exploit).
    • We need to examine the social context – the communities in which we live, the way illness and wellbeing are defined, the way healing is understood, how treatments are recognised, the impact of language and interpretation of that language and the way language evolves over time, how communities view treatment seekers and treatment givers, historical understanding and how this influences who, what, why and how therapeutic interactions are enacted.
  • The psychological is underpinned [as much as we can detect for now] by neurobiology, at one level of analysis. Neurobiological processes are incredibly complex and we don’t understand them very well. As we do, many of the influences decried as “woolly” or “fluffy” by some of my colleagues are, I think, going to be uncovered and found to be extraordinarily complex interactions between neurobiological systems. And yes, they will be complex – beyond most mortal’s understanding. This doesn’t mean they’re woo, or that they can be disregarded.
  • A other levels of analysis, sociopsychological processes are incredibly important contributors to the way treatments are sought – and treatments have effects. This means we’re unlikely to understand them in any simplistic sense. So to deride these processes as irrelevant or “unscientific” simply because they don’t fit in with an existing model of cause and effect (particularly if they don’t fit with a simple 1+2+3=6 model) probably means there’s a lot of learning needed. Simply because an empirical basic science or RCT doesn’t show “what’s going on” does not mean the concept under study is “not science” – it just means a scientific methodology that accommodates these complexities is needed. Not everything can be reduced to an experimental design – qualitative research is valid for some very important questions.
  • Communication – what and how we express meaning to another, and how this is interpreted and responded to by that other – occurs everywhere and all the time. Whether we attend to it or not. Meaning-making is something humans just do. So maybe as health professionals we should invest rather more than we do in training ourselves to be skilled at communicating. This means recording our interactions, reviewing them, getting to know the effect of what we communicate and training ourselves to be just as careful with our communication as we are with prescribing anything else. Because it could be that our communication is the most potent ingredient in our treatment.

“A good listener is not only popular everywhere, but after a while he knows something.” —Wilson Mizner

What’s the biggest barrier to learning more?


Reading and engaging with clinicians online and face-to-face, it’s clear to me that effectively integrating psychosocial factors into daily clinical reasoning, especially amongst physical or manual therapists, is a real challenge. There’s enough research around showing how poorly these factors are identified and then factored in to change what we do and how we do it for me to be convinced of this. What intrigues me, though, is why – given psychosocial risk factors have, in NZ, been around since 1997 – it’s still a problem.

It’s not ignorance. It’s not holding an alternative viewpoint. It’s not just that clinical reasoning models don’t seem to integrate these factors, or that our original training kinda partitioned the various “bits” of being human off – I think that it’s probably that we think we’re already doing well enough.

Image result for dunning kruger effect

This effect has a name – Dunning-Kruger effect. Now, don’t be put off by this term, because I know in some social media circles it’s used to bash people who are  maybe naive, or haven’t realised their lack of knowledge, and it can feel really awful to be told “well actually you’re ignorant”, or “you’re inflating your skill level”.  The thing is, it’s a common experience – we all probably think we’re great car drivers – but in reality we’re all pretty average.

The same thing occurs when we consider our ability to be:

  • empathetic
  • responsive
  • good listeners
  • client-centred
  • collaborative

Another important effect found in clinicians is that we believe our experience as clinicians means we’re better at aspects of clinical care, and especially at clinical reasoning. Over time we get better at recognising patterns – but this can actually be a problem for us. Humans are excellent at detecting patterns but as a result we can jump to conclusions, have trouble stopping ourselves from fixating on the first conclusion we draw, begin looking for things to confirm our hunch, overlook things that don’t fit with the pattern we’ve identified, and basically we begin to use stereotypes rather than really looking at the unique person sitting in front of us (see Croskerry, Singhal & Mamede, 2013a, b).

The effect of these biases, and especially our bias towards thinking we do better than we actually do (especially regarding communication skills and psychosocial factors) means we’re often completely unaware of HOW we communicate, and HOW poorly we pick up on psychosocial factors.

So often I’ve heard people say “Oh I use intuition, I just pick up on these psychosocial issues” – but the problem is that (a) we’re likely to over-estimate how well we pick up on them and (b) our intuition is poor. The risk for our patients is that we don’t identify something important, or alternatively, that we label something as a psychosocial risk factor when it’s actually irrelevant to this person’s problem.

Clinical reasoning is difficult. While recognising patterns becomes easier over time because we have a far broader range of patterns we’ve seen before, at the same time

  • research is expanding all the time (we can be out of date)
  • we can get stuck prematurely identifying something that isn’t relevant
  • we get hooked in on things we’ve just read about, things that happen rarely, things that remind us of something or someone else

Hypothetico-deductive reasoning is an alternative approach to clinical reasoning. It’s an approach that suggests we hold some ideas about what’s going on in our mind while collecting more information to test whether this is the case. The problem here is that we look for information to confirm what we think is happening – rather than looking for something to disconfirm, or test, the hypothesis we hold. So, for example, we might observe someone’s pain behaviour and think to ourselves “oh that person is doing that movement because of a ‘dysfunctional movement pattern’. We can assume that the reason for this movement pattern is because of underlying dysfunction of some sort – but we fail to test that assumption out to see whether it might in fact be a movement pattern developed because someone told the person “this is the way you should move”, or the person is moving that way because of their beliefs about what might happen if they move differently.

The problem with intuition and these other cognitive biases is that they simplify our clinical reasoning, and they reduce effort, so they’re easy traps to fall into. What seems to help is slowing down. Deliberately putting a delay in between collecting information and making a decision. Holding off before deciding what to do. Concurrently, we probably need to rely less on finding “confirming” information – and FAR more on collecting information across a range of domains, some of which we may not think are relevant.

That’s the tough bit. What we think is relevant helps us narrow down our thinking – great for reducing the amount of information we need to collect, but not so great for testing whether we’ve arrived at a reasonable conclusion. My suggested alternative is to systematically collect information across all the relevant domains of knowledge (based on what’s been found in our research), wait a bit and let it settle – then and only then begin to put those bits and pieces together.

Why doesn’t it happen? Well, we over-estimate how well we do this assessment process. We do jump to conclusions and sometimes we’re right – but we wouldn’t know whether we were right or not because we don’t check out alternative explanations. We’re pushed by expectations from funders – and our clients – to “set goals” or “do something” at the very first assessment. We feel guilty if we don’t give our clients something to take away after our initial assessment. We want to look effective and efficient.

Great quote?

For every problem, there is a solution that is simple, elegant, and wrong. H.L. Mencken.

If you’d like to question your own practice, try this: Record your session – and transcribe that recording. Notice every time you jump in to give advice before you’ve really heard your client. Notice how quickly you form an impression. Examine how often you look for disconfirmation rather than confirmation. See how often you ask about, and explore, those psychosocial factors. It’s tough to do – and sobering – but oh how much you’ll learn.

Croskerry, P., Singhal, G., & Mamede, S. (2013). Cognitive debiasing 1: origins of bias and theory of debiasing. BMJ Quality & Safety, 22(Suppl 2), ii58-ii64. doi:10.1136/bmjqs-2012-001712

Croskerry, P., Singhal, G., & Mamede, S. (2013). Cognitive debiasing 2: impediments to and strategies for change. BMJ Quality & Safety, 22(Suppl 2), ii65-ii72. doi:10.1136/bmjqs-2012-001713

The gap in managing pain


If you’ve read my blog for any period of time you’ll know that I like practical research, and research that helps clinicians do what they do with humanity, compassion and evidence. One really enormous gap in the field is rarely mentioned: how do clinicians pull their assessment findings together and use them for clinical reasoning? Especially if you’re part of an interprofessional team (or work in a biopsychosocial framework). The silence in the pain literature is deafening!

There are any number of articles on what can be included in an initial assessment, most of them based on the idea that if factor X is an important predictor, it oughta be assessed. So we have a proliferation of assessments across (mainly) the biopsychological spectrum, with a teeny tiny bit of social (family relationships) thrown in, if you’re lucky. There are numerous papers proposing treatments for aspects of pain – anything from medications, to movement treatments, to cognitive treatments (yes, pain education), and behavioural treatments – but after reading them it almost feels like authors think anyone with pain that’s going on longer than we’d hope “should” have That Treatment, and then of course the person will be just fine.

Except that – there are just as many people with persistent pain today as there were 20 years ago, perhaps more (given the global burden of disease shows that low back pain is The Most Common problem associated with years lived with disability). In other words, all our treatments across all our specialties don’t seem to be having the impact that the research papers suggest they ought to. What gives?

I think it’s time to take a leaf from some of the better-conducted pharmacological studies. Yes, I said that! What I mean is that given our treatments especially for low back pain seem to have broadly the same or similar effects, maybe we need to look beyond the grouped analyses where individual differences are lost within the grouped data, and head to some of the sub-analyses proposed and used by Moore, Derry, Eccleston & Kalso (2013). In this paper, they advocate using responder analysis – who, exactly, gets a good result?

At the same time, I think we need to get much better at assembling, integrating and using the multitude of assessments people complete for us when we start treating them. Several points here: yes, we all carry out assessment but how well do we put them together to “tell the story” or generate a set of hypotheses to explain the crucial questions:

Why is this person presenting in this way at this time? And what can be done to reduce distress and disability?

I think case formulations may take us a step towards better use of our assessments, better clinical reasoning, better teamwork, and, most of all, better collaboration with the person we hope to help.

Case formulations are not new in psychology. They’re really a cornerstone of clinical psychological reasoning – assembling the information gathered during assessment into some sort of explanatory framework that will help the therapist generate possibly hypotheses about predisposing factors, what precipitated the problem, what perpetuates the problem, and any protective factors. Psychologists are no less prone to arguing about whether this approach works than anyone else – except they do some cool studies looking at whether they’re consistent when generating their formulations, and sadly, formulations are not super-consistent with each other (Ridley, Jeffrey & Robertson, 2017).

BUT here’s why I think it might be a useful approach, especially for people with complex problems associated with their pain:

  1. Case formulations slow our clinical reasoning down. “Huh?” you say, “Why would that be good?” Well because rapid clinical judgements on the basis of incomplete information tend to lead us towards some important cognitive biases – anchoring on the first possible idea, discounting information that doesn’t fit with that idea, we notice weird stuff more than the commonplace, we fill in information based on stereotypes, generalities and past histories, and we don’t shift from our first conclusion very easily. By taking time to assemble our information, we can delay drawing a conclusion until we have more information.
  2. By completing a consistent set of assessments (instead of choosing an ad hoc set based on “the subjective”) we reduce the tendency to look for confirmation of our initial hunch. I know this isn’t usual practice in some professions because that “subjective” history is used to guide assessments which are then used to determine a diagnosis – but the risk is that we’ll look for assessments that confirm our suspicions, meanwhile being blinded to possible alternative explanations (or hypotheses or diagnoses).
  3. Working together with the expert on their own situation (ie the person seeking help!) we build collaboration, a shared understanding of the person’s situation, and we can develop an effective working relationship without any hint of “one-up, one-down” that I can see appeals to “experts” who like to point out the “problems” with, for example, posture, gait, motor control and so on – all which may have little to do with the patient’s pain, and a whole lot more to do with creating a “listen to me because I Know Things” situation.
  4. Other team members can contribute their assessments, creating a common understanding of the various factors associated with the person’s situation. Common goals can be developed, common language about what might be going on, common treatment aims and enhanced understanding of what each profession contributes can happen when a formulation includes all the wonderful information collected across the team.
  5. If one of the treatments doesn’t work (ie the hypothesis doesn’t hold up to testing) there are other options to draw on – we’re not stuck within our own clinical repertoire, we can think across disciplines and across individual clinical models and become far more confident about knowing when to refer on, and how we can support our colleagues.

But, you know, I looked in the pain journals, searched far and wide – and I found few examples of case formulation for persistent pain. The best paper I’ve found so far is from a textbook – so not readily accessible. It’s Linton & Nicholas (2008) “After assessment, then what? Integrating findings for successful case formulation and treatment tailoring”. Where is the rest of the research?!!

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

Moore, A., Derry, S., Eccleston, C., & Kalso, E. (2013). Expect analgesic failure; pursue analgesic success. BMJ: British Medical Journal (Online), 346.

Ridley, C. R., Jeffrey, C. E. and Roberson, R. B. (2017), Case Mis-Conceptualization in Psychological Treatment: An Enduring Clinical Problem. J. Clin. Psychol., 73: 359–375. doi:10.1002/jclp.22354

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 – iii


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

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

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

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

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

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

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

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

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

 

 

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

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

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

Back to basics about psychosocial factors and pain (ii)


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

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

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

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

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

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

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

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

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

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

Next time – delving into mechanisms!

What are the implications of the complexity of central processing?

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

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

 

 

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

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

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

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

Knee pain – and central sensitisation


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

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

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

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

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

Putting it all together

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

Conclusion

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

 

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

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

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

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

Knee pain – not just a simple case of osteoarthritis


Knee osteoarthritis is, like so many chronic pain problems, a bit of a weird one. While most of us learned that osteoarthritis is a fairly benign disease, one that we can’t do a whole lot about but one that plagues many of us, the disability associated with a painful knee is pretty high – and we still don’t have much of a clue about how the pain we experience is actually generated.  Cartilage doesn’t have nociceptive fibres, yet deterioration of cartilage is the hallmark of osteoarthritis, though there are other structures capable of producing nociceptive input around the knee joint. Perhaps, as some authors argue, knee osteoarthritis is a “whole organ disease with a complex and multifactorial pathophysiology involving structural, psychosocial and neurophysiological factors” (Arendt-Nielsen, Skou, Nielsen et al, 2015).

Central sensitisation, or the process in which spinal cord and the brain become “wound up” or more responsive to input than normal, and seems to be a factor in the pain some people experience when they have osteoarthritic knees (Fingleton, Smart, Moloney et al, 2015; Finan, Buenaver, Bounds, Hussain, Park, Haque et al, 2013), particularly in women (Bartley, King, Sibille, et al, 2016). The problem is, few people are routinely screened for central sensitisation before they receive surgical treatment (a good question is whether pain-related research is a factor in orthopaedic assessment). Why should we think about screening? Well, outcomes for joint replacements in knee OA are not as good as they are for hip OA, and a good proportion of people have more than one surgery to attempt to revise the joint but ultimately don’t obtain a satisfactory resolution of their pain.

The authors of this very useful clinically-relevant paper “Clinical descriptors for the recognition of central sensitization pain in patients with knee osteoarthritis” (Lluch, Nijs, Courtney, Rebbeck, Wylde, Baert, Wideman, Howells and Skou, 2017) openly acknowledge that although the idea of central sensitisation in humans is appealing, and seems to answer a number of important questions, the actual term “central sensitisation” can, at this time, only be measured in animal models. The use of the term in humans is not yet agreed upon, and a term I find appealing is “nociplastic”, or in other words, plasticity of the nervous system underpinning an increase in responsiveness to “actual or potential tissue damage” (to quote from the IASP definition of pain). They argue that central sensitisation may not exist in a dichotomous “yes you have it” or “no you don’t”, but instead may from a continuum from a lot to a little, and they note that pain sensitivity also exists on a continuum (a bell-shaped curve).

So what’s a good clinician to do? We can’t all go out and get involved in conditioned pain modulation or in using brain imaging, yet it seems important to establish who might respond well to joint replacement vs who might need additional input so they get a good outcome. And something that’s not going to add too much expense or complexity to an assessment process that, at least in New Zealand, is rationed because of cost. (oops, sorry not “rationed” just “waitlist management”).

The first step as described by Lluch and colleagues involves the “subjective” assessment – I loathe the word “subjective” because this is the person’s own experience, and doesn’t need to be tainted with any suggestion that it’s inaccurate or can’t be trusted. ‘Nuff said. During an interview portion of an assessment, the authors suggest using some simple measures: reports of pain above 5/10 on a numeric rating scale where 0 – no pain, 10 – extreme pain. They add increased weight to this report if there is little significant found on simple imaging of the knee, because central sensitisation is thought to be less relevant where there is severe structural changes in the knee joint.

A pain drawing can be helpful – radiating pain, pain on the contralateral leg, and pain in other body sites can be an indication of central sensitisation, while pain that is localised just to the joint itself may be an indication that a surgical approach will be more likely to help. Using the Widespread Pain Index score >7 and painDETECT score >19 (seeVisser, et al, 2016) may be a relatively simple process for clinicians to use to identify those with troublesome pain.

The behaviour of pain with/without movement may be a useful indicator: those that find movement painful, or who report increased pain after engaging in physical activity might be responding to central sensitisation, given that OA pain is usually associated with rest. Add to this a discussion about what relieves the pain and what doesn’t (where easing up on mechanical demands should reduce pain while with central sensitisation, this may not occur), and those with pain that continues after movement may need more help with central sensitisation than those who don’t.

The authors also suggest two questionnaires that may help to spot the person experiencing central sensitisation – the painDETECT or the Central Sensitisation Inventory. At this point I’m not entirely certain that the CSI measures only central sensitisation (it may simply measure somatic attention, or distress), so I’d interpret the findings carefully and make sure the clinical picture confirms or doesn’t… while the painDETECT has been used to identify those with neuropathic pain, and may be appropriate though it hasn’t been strongly confirmed for use with knee OA (it was developed for low back pain). While you’re at it, you should also assess for psychosocial factors such as the tendency to think the worse, low mood, feeling helpless, and perhaps factors such as not liking your job, having limited family support, and maybe self-medicating with alcohol and tobacco or other substances.

Finally, for today’s post (yes I’ll carry on to the clinical tests next week!), response to pharmacology may also be a useful approach to identifying those with central sensitisation. Poor response to NSAIDs (the mainstay for knee OA in NZ), weak opioids (like codeine), and perhaps not responding to things like heat or joint mobilisation, may also be useful predictors.

In summary, there are numerous indicators one can use to help establish who might not respond well to a peripheral-only treatment. While some of these measures are used routinely by enlightened clinicians, there are plenty of people who think of these responses as an indication of “poor coping” or someone who REALLY needs surgery. Unless surgeons and those who work with people with knee OA begin to examine the literature on pain in knee OA, I think we’ll continue to have patients who receive surgery when perhaps it’s not the best thing for them. More on this next week.

 

 

 

Arendt-Nielsen L, Skou ST, Nielsen TA, et al. (2015). Altered central sensitization and pain modulation in the CNS in chronic joint pain. Current Osteoporosis Reports, 13:225–234.

Bartley EJ, King CD, Sibille KT, et al. (2016) Enhanced pain sensitivity among individuals with symptomatic knee osteoarthritis: potential sex differences in central sensitization. Arthritis Care Research (Hoboken). ;68:472–480.

Finan PH, Buenaver LF, Bounds SC, Hussain S, Park RJ, Haque UJ, et al. (2013). Discordance between pain and radiographic severity in knee osteoarthritis: findings from quantitative sensory testing of central sensitization.  Arthritis & Rheumatism, 65, 363-72. doi:10.1002/art.34646

Fingleton C, Smart K, Moloney N, et al. (2015). Pain sensitization in people with knee osteoarthritis: a systematic review and meta-analysis. Osteoarthritis and Cartilage, 23:1043–1056.

Kim SH, Yoon KB, Yoon DM, Yoo JH & Ahn KR. (2015). Influence of Centrally Mediated Symptoms on Postoperative Pain in Osteoarthritis Patients Undergoing Total Knee Arthroplasty: A Prospective Observational Evaluation.  Pain Practice, 15, E46-53. doi:10.1111/papr.12311

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

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

Conversations about cannabis for chronic pain


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

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

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

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

Why might I support a change to marijuana laws?

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

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

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

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

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

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

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

My conclusion?

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

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

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

 

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

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