Pain

The “onion ring” model of pain


Clinicians constantly search for a better way to describe the tangled mess that constitutes ways to explore pain. Today I’m hoping to add another way, but hopefully one that might help disentangle certain aspects of pain for ease of learning. And as usual, it’s largely not my own model, but one first developed by Professor John Loeser, eminent neurologist and neurosurgeon and Director of the Multidisciplinary Pain Center from 1982-1997 at the University of Washington.

There are many different versions of the ‘Onion ring’ model – Gordon Waddell, orthopaedic surgeon and contemporary of Loeser also developed one, and more recently we’ve seen a version from Lorimer Moseley and colleagues in NOI publications. I’m going back to Loeser’s one because I think it’s useful – and in the case of conceptual models like this utility is the measure by which we decide to adopt a model or not. You be the judge. This is my public announcement that this is not intended to be a scientific model for generating and testing hypotheses: it’s meant to be an explanatory metaphor, if you like.

OK, so what is this model?

Like any onion, the model has inner to outer layers, but unlike an onion, these layers are permeable, and slightly fuzzy. They interact with one another, and the resultant whole is intended to reflect the experience of pain, along with the aspects that you and I might see – and includes various factors thought to influence the experience. It’s incomplete because much of what is known about pain is incomplete. It can’t explain everything, because no metaphor can – but it does provide some hooks for our minds to grab onto when we’re accessing new information and we want to establish relevance and recognition.

Loeser’s Onion Ring Model (1983)

The purple ring in the centre is all about neurobiology for me. Loeser’s original model labeled this “nociception”, but since 1983 we’ve learned a great deal more about the neurobiology of pain and we know that pain in the absence of nociception is probably a product of something gone awry in the way our nociceptive system is interpreting information. It could be neuropathic pain (where there is an identifiable lesion of the somatosensory system), or it might be nociplastic pain ( “pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain.” – click). At this level of the model this is not pain. This inner ring refers only to biological processes prior to conscious awareness.

The next ring (dark blue) refers to the conscious experience we have of pain. This is the part we personally experience – it’s subjective, unpleasant, sensory and emotional, and we learn to associate this experience with potential or actual tissue damage, or we describe it in similar ways. In many respects this is the quale – the quality of what-it-is-like to experience pain – although others would argue it is an aporia (In philosophy, Aporia means literally ‘impasse, difficulty in passage, lack of resources, puzzlement’). However we like to define it, this part of Loeser’s model refers to the experience once our brain/mind has deemed it relevant to our predicament.

But, as the saying goes, wait! There’s more!

Because this dark blue ring is experiential, we can’t share it, or even know about another’s experience unless we do something about it, and before we do something about it, we appraise or judge it. With some provisos (told you this was a metaphor not a testable model!).

Drawing from cognitive models, Loeser then wraps another ring around the experience “pain” – this is what he described as suffering, but I prefer to describe as “judgement” or “appraisal”. Suffering is a judgement that this experience is threatening our essential self, our future (Cassel, 1999). So while there are certain behaviours that occur prior to awareness or judgement (see this) as soon as we are consciously aware of pain we’re judging that experience. And probably, because brains don’t just sit there waiting for information to come towards it, there is a good deal of permeability between the neurobiology ring, the pain-experience ring, and this ring. But for simplicity’s sake, let’s take it that when we experience “ouch” we typically check it out and interpret the meaning of that ouch in context of where we are, what we’re currently doing, who we’re with, and our past experiences. This interpretation or judgement phase can augment the meaning of pain to increase its threat value, or vice versa (OMG that was a snake bite! or Oh that was a bruise I didn’t need).

Wrapping around that “judgement” ring is a further ring – and this is possibly the one we most need to come to grips with. This ring is the behavioural response to our appraised experience. Pain behaviour or what we do when we recognise and judge our experience of pain is complex. It’s complex because all human behaviour is complex. It’s also complicated because we naively judge one another on the basis of what we see – and our own assumptions about what that behaviour might mean.

Behaviours include nocifensive responses, but don’t stop there. As we develop and mature from babyhood to adulthood, we embroider and alter our behavioural response to pain, just as we do with our appraisals. As babies we’re likely to scream our lungs out at the heel prick test at birth. I hope we don’t do that when we get a flu jab (and I truly hope you DO get a flu jab, and if you’re in Christchurch New Zealand that you get a measles immunisation pronto). We learn what to do from watching others (social learning), from others responses to us (operant conditioning), and from events that occur at the same time as our pain occurs (classical conditioning). Social learning is powerful – within different cultural groups, peer groups and family groups, we learn what is normal and OK to do when we’re sore. We also get rewarded (or not) for the way we behave. Little kids get told “stop that crying, it’s nothing” when they stub a toe, or they might get cuddled instead. Footballers get extra time if they roll around on the ground with an injury during a match; rugby players get adulation when they carry on playing despite a rib fracture or two. And for some people, associating a movement with pain can lead to longstanding limitations and avoiding that same movement in case it brings the pain on.

Pain behaviours include language and even that old “pain rating scale”. We use language and nonverbal behaviour to communicate. So when someone says “my pain is 12/10” what they’re really saying is “this is more than I can bear, help me”. We do not have a pure measure of how intense a pain is – and any measure of intensity is likely filtered through a process of judgement “what does this mean for me?” and communication “what will happen if I say X number?” So stop judging someone if they say their pain is 12/10 – it means they’re freaking out, and need comfort.

If you’re smart you’ll notice that I’ve sneakily been discussing the final onion ring, and to be fair, Loeser didn’t include this in his version – it’s one that Waddell, Main, and others have added and I think it’s integral to understanding what’s going on so I’ve added it too. The outer ring refers to the social context because this influences what people do (pain behaviours) as I’ve just outlined. It also includes social factors such as the workplace and compensation, legislation covering what is and isn’t covered in insurance plans, our community attitudes towards people who are experiencing pain, stigma and social isolation and sense of online community and such.

Loeser’s onion ring provides me with some nice ways to separate parts of my understanding of pain so I can explain how and why we need to examine them and influence them separately. Health professionals are always and inevitably influencing the judgement, behaviour, and social aspects of pain. Sometimes we get to influence the neurobiology and through interactions between all these layers, sometimes the experience of pain is reduced. Other times it is not. At the same time, if we can begin to shift the judgements and what we do about pain and yes, the social contexts in which experiencing weird unexplained pain is viewed as a moral failing or attempt to “get secondary gain”, maybe then we can help people live better lives despite their pain.

Cassell, E. J. (1999). Diagnosing Suffering: A Perspective. Annals of Internal Medicine, 131(7), 531-534. doi:10.7326/0003-4819-131-7-199910050-00009

Loeser JD, Ford WE. Chronic Pain. In: Carr JE, Dengerink HA, (eds). Behavioral Science in the Practice of Medicine. New York: Elsevier Biomedical:1983:331-345

Five things I learned about pain this year


  1. Our definitions of pain matter more to researchers and people who like to philosophise about pain than to people experiencing pain. At the same time, definitions do matter because when the IASP definition of pain was first established, the distinction between the neurobiological underpinnings of pain – and the experience – was clear. And this matters because neurobiology is only part of the picture. (Chekka & Benzon, 2018; Cohen, Quintner & van Rysewyk, 2018; Reuter, Sienhold & Sytsma, 2018; Tesarz & Eich, 2017; Williams & Craig, 2016)
  2. The idea of “tribes” in pain and pain management is a misinterpretation of our need to work together as clinicians because pain is complex. The old argument that we’ve omitted “the bio” because we use a biopsychosocial framework for understanding pain is, frankly, ignorant. It’s also destructive because we need one another when we try to help people who are seeking our help. And even if someone has a straightforward sprain, fracture, or whatever – that sprain is happening to a living, breathing, thinking, emoting, motivated person. If we are to break down the silo thinking in pain management, we also need to learn how to work together within an interprofessional team. This means learning to speak a common language. This also means including the person with the pain as part of the team. To think that we can ignore the person and focus only on “the tissues” means we also must agree that our contribution as health professionals could be replaced by an algorithm (Gordon, Watt-Watson & Hogans, 2018; Lötsch & Ultsch, 2018; Shluzas & Pickham, 2018 .
  3. The gap between what is investigated in research institutions and both the concerns of clinicians and patients, and implementing research findings is enormous. Accusing researchers of ‘living in ivory towers’ fails to recognise that most of our active pain researchers in rehabilitation still continue in clinical practice. The gap seems to be between funding agencies (valuing high tech, high impact research) and the concerns of clinicians (often about high value, low tech, and low cost research). There are very active discussions about “how do I use this study” on social media across the board – Twitter, Facebook, LinkedIn, blogging – and these represent possibly the most important vehicles for clinicians, policy-developers, researchers and people living with pain to break down silo thinking and begin to address the factors that contribute to the knowledge translation gap. Many discussions on Exploring Pain: Research and Meaning (Facebook group) end with acknowledgement that funding systems simply do not support collaborative evidence based teamwork (Arumugam, MacDermid, Walton & Grewal, 2018; Bérubé, Poitras, Bastien, Laliberté, Lacharité & Gross, 2018; Chen, Tsoy, Upadhye & Chan, 2018; Romney, Salbach, Parrott & Deutsch, 2018; Tougas, Chambers, Corkum, Robillard, Gruzd, Howard,… & Hundert et al., 2018).
  4. The social part of pain is receiving increased research and clinical attention – and it’s a messy area of study. Social isn’t well-defined – it can mean social psychology, sociology, culture, health systems, media, feminism, political science, legislation – anything where people interact. Social psychology studies investigate things like trustworthiness, gender effects in interactions, stigma (Naushad, Dunn, Muñoz & Leykin, 2018; Sherman, Walker, Saunders, Shortreed, Parchman, Hansen, … & Von Korff, 2018; Wesolowicz, Clark, Boissoneault & Robinson, 2018), while sociology examines diagnoses and power relationships in healthcare – things like being “too young” for a diagnosis of arthritis (Kirkpatrick, Locock, Farre, Ryan, Salisbury & McDonagh, 2018) or validating the pain of menstruation (Wright, 2018) or a diagnosis of fibromyalgia (Mengshoel, Sim, Ahlsen & Madden, 2018). It seems no accident that many of the pain problems needing “validation” occur more often in women, and fail to have “objective” signs. But social means more than labeling and interacting, it’s also about community values and ideas – and how pain is portrayed by people experiencing pain, and in the media (Kugelmann, Watson & Frisby, 2018). The way WE talk about pain, and how we talk about people living with pain. How people living with pain are portrayed and how they portray themselves (ourselves). I suspect the social aspects of our experience with pain are amongst the most complex and most potent in determining suffering (loss of sense of “who am I?”) and disability (“what can I still do?”).
  5. Finally, I am encouraged by the wealth of information being shared freely, discussed passionately, and applied in many different forms around the world. I am proud to have been associated with many different groups as we – you, me, people living with pain, us – keep this topic alive and up-front. While I am no great productive scholar, I publish few peer-reviewed articles, and in the eyes of University hierarchy I am insignificant, I believe the conversations had on social media and into the real world have an impact on how we work in the clinic. If we can achieve the things we talk about, even if we achieve only a fraction of those things, we will have helped more people than we can ever imagine. I feel so privileged to have got to know some of the greatest “lived experience” advocates for greater ‘patient’ involvement in our conversations about pain. Isn’t it time we remembered the old adage “nothing about us without us”? Social media allows us to break the code of silence – and the distinction between “us” and “them” in the world of pain. After all, many of “us” are also living well with persistent pain.


Arumugam, V., MacDermid, J. C., Walton, D., & Grewal, R. (2018). Attitudes, knowledge and behaviors related to evidence-based practice in health professionals involved in pain management. International journal of evidence-based healthcare, 16(2), 107-118.

Bérubé, M. È., Poitras, S., Bastien, M., Laliberté, L. A., Lacharité, A., & Gross, D. P. (2018). Strategies to translate knowledge related to common musculoskeletal conditions into physiotherapy practice: a systematic review. Physiotherapy, 104(1), 1-8.

Chen, E., Tsoy, D., Upadhye, S., & Chan, T. M. (2018). The Acute Care of Chronic Pain Study: Perceptions of Acute Care Providers on Chronic Pain, a Social Media-based Investigation. Cureus, 10(3).

Chekka, K., & Benzon, H. T. (2018). Taxonomy: definition of pain terms and chronic pain syndromes. In Essentials of Pain Medicine (Fourth Edition) (pp. 21-24).

Cohen, M., Quintner, J., & van Rysewyk, S. (2018). Reconsidering the International Association for the Study of Pain definition of pain. Pain reports, 3(2).

Gordon, D. B., Watt-Watson, J., & Hogans, B. B. (2018). Interprofessional pain education—with, from, and about competent, collaborative practice teams to transform pain care. Pain Reports, 3(3).

Kirkpatrick, S., Locock, L., Farre, A., Ryan, S., Salisbury, H., & McDonagh, J. E. (2018). Untimely illness: When diagnosis does not match age‐related expectations. Health Expectations.

Kugelmann, R., Watson, K., Frisby, G (2018). Social representations of chronic pain in newspapers, online media, and film. Pain, in press.

Lötsch, J., & Ultsch, A. (2018). Machine learning in pain research. Pain, 159(4), 623.

Mengshoel, A. M., Sim, J., Ahlsen, B., & Madden, S. (2018). Diagnostic experience of patients with fibromyalgia–A meta-ethnography. Chronic illness, 14(3), 194-211.

Naushad, N., Dunn, L. B., Muñoz, R. F., & Leykin, Y. (2018). Depression increases subjective stigma of chronic pain. Journal of affective disorders, 229, 456-462.

Reuter, K., Sienhold, M., & Sytsma, J. (2018). Putting pain in its proper place. Analysis.

Romney, W., Salbach, N., Parrott, J. S., & Deutsch, J. E. (2018). A knowledge translation intervention designed using audit and feedback and the Theoretical Domains Framework for physical therapists working in inpatient rehabilitation: A case report. Physiotherapy theory and practice, 1-17.

Sherman, K. J., Walker, R. L., Saunders, K., Shortreed, S. M., Parchman, M., Hansen, R. N., … & Von Korff, M. (2018). Doctor-patient trust among chronic pain patients on chronic opioid therapy after opioid risk reduction initiatives: A Survey. The Journal of the American Board of Family Medicine, 31(4), 578-587.

Shluzas, L. A., & Pickham, D. (2018). Human Technology Teamwork: Enhancing the Communication of Pain Between Patients and Providers. In Design Thinking Research (pp. 313-325). Springer, Cham.

Tesarz, J., & Eich, W. (2017). A conceptual framework for “updating the definition of pain”. Pain, 158(6), 1177-1178.

Tougas, M. E., Chambers, C. T., Corkum, P., Robillard, J. M., Gruzd, A., Howard, V., … & Hundert, A. S. (2018). Social Media Content About Children’s Pain and Sleep: Content and Network Analysis. JMIR Pediatrics and Parenting, 1(2), e11193.

Wesolowicz, D. M., Clark, J. F., Boissoneault, J., & Robinson, M. E. (2018). The roles of gender and profession on gender role expectations of pain in health care professionals. Journal of Pain Research, 11, 1121.

Williams, A. C. D. C., & Craig, K. D. (2016). Updating the definition of pain. Pain, 157(11), 2420-2423.

Wright, K. O. (2018). “You have Endometriosis”: Making Menstruation-Related Pain Legitimate in a Biomedical World. Health communication, 1-4.

Pain science is not a thing


Today’s post is occasioned by reading several discussions on various forums where the term “pain science” and various adjectives to describe this kind of practice. For those who don’t want to read the rest of my ramblings: no, it’s not a thing, science is an approach to understanding phenomena, and I would have thought all health professionals would use a science-based approach to treatment.

I went on to Google, as you do, to find out when this term began its rise in popularity. Google wasn’t particularly helpful but did show that it’s been around since 2004 at least, and seems to have been centred around the US, UK and Australia in roughly May 2004. I can’t grab data from earlier than this, sadly, but I think it’s interesting to take a look at the popularity peaks and troughs…

So, what does “pain science” mean to commentators? I haven’t delved in too deeply to the social media use of the term, but given I’m a social animal and have written my blog since 2007 (which is mainly on “pain science”) I’ve encountered it many times. It seems to be related to using a neurobiological explanation for pain as an experience (referring to the phenomenon and the underlying biological processes involved) rather than focusing purely on biomechanics or tissue damage/nociception as the key force. And it does seem to tie in with the emergence of “Explain pain” as one way of helping people reconceptualise their experience as something they can influence rather than something other people need to “fix”.

Commentators who aren’t in love with the “explain pain” thing have said things like “the pain science camp” or as one person put it “There’s your manual PTs, your pain science PTs, and your just load it PTs etc”

I went on to Twitter and the hashtag #painscience was paired with #BPSModel and #PT and #physicaltherapy (or variations), #chronicpain #exercise #lowbackpain – and so on.

So what do I think pain science means if it’s not a neurobiological approach to pain management? Well – pain science is a lot like cardio-respiratory science, and neurological science, and psychological science – it’s about applying a scientific approach to understanding pain. Science has been defined as “the intellectual and practical activity encompassing the systematic study of the structure and behaviour of the physical and natural world through observation and experiment.” In this instance, Google is your friend. So science is about systematically studying phenomena through observation and experimenting. If we apply this to pain – it’s the systematic study of structure and behaviour of the phenomenon we call ‘pain’ through observation and experiment. For what it’s worth, scientific study of pain has been going on since… oh at least Descartes, but probably much earlier given that pain is a ubiquitous and essential part of human experience.

To me, understanding pain involves multiple disciplines: yes to biology, and especially neurobiology because the experience (as we understand it now) involves neurobiological processing. But it’s also about psychology
the scientific study of the human mind and its functions, especially those affecting behaviour in a given context; sociology – the study of the development, structure, and functioning of human society; the humanities – the study of how people process and document the human experience; politics – the activities associated with the governance of a country or area, especially the debate between parties having power; and Anthropology –  the study of humans and human behavior and societies in the past and present. Social anthropology and cultural anthropology study the norms and values of societies. Linguistic anthropology studies how language affects social life.

So to describe an entire approach to understanding a phenomenon as if it’s a “movement” or “camp” or “dogma” or even “tribe” suggests serious  misunderstanding of both science and of an intervention.

What is “explain pain” then, or pain neurobiology education? – it’s an explanation of some of the biological elements of our nociceptive system as they combine to produce the experience we know as pain. For some people it’s the first time anyone took the trouble to explain why the pain of a papercut feels so bad compared with, for example, the pain of a sprained ankle; and why they still experience pain despite having no “damage” as visible on imaging. It’s an attempt to give people a frame of reference from which to understand their own journey towards recovering from a painful injury/disease/problem. In itself it’s not new: explanations for pain have been used in pain management programmes since the 1970’s (and earlier, if we consider that Fordyce used explanations in his behavioural approaches to pain management), and have routinely drawn on current pain research to help provide explanations that make sense to both the person and the clinician. The distinction between earlier explanations which drew heavily on the gate control theory, and this latest iteration is that the explanations are more complex, pain is considered to be an “output” that emerges from multiple interactions between brain and body, and that’s about it. Oh and it’s been picked up and enthusiastically used by physiotherapists (and other primarily body therapists) around the world.

What’s the evidence for this approach? Well, IMHO it’s not intended to be a stand-alone “treatment” for most people experiencing pain. I see giving an explanation as integral to usual practice, just as we do when we explain why it’s not a good idea to go running on a newly sprained ankle or why we’re suggesting a mindfulness to someone with a panic disorder. So far there have been a lot of studies examining variants of “explaining pain” alone or in combination with a number of other treatments including exercise. A recent systematic review and meta-analsyis of “pain neuroscience education” for chronic low back pain found eight papers (with 615 participants) showing that in the short-term, this kind of education reduces disability (by 2.28 points on the Roland-Morris Disability Questionnaire which is a 24 point scale) in the short-term and a slightly lesser effect in the long-term  (2.18). There were greater effects when this was combined with physiotherapy, though we often don’t know exactly what is included in “physiotherapy”.  There was some evidence that this kind of education helps reduce pain scores (by 1.32) but only in combination with other physiotherapy interventions. The authors pointed out that the strength of evidence for education on pain in the short term was low to moderate, but that it doesn’t have much of an impact on pain-related fear and avoidance, or on pain catastrophising (Wood & Hendrick, in press).

To compare this with another active treatment, exposure therapy for fear of movement/reinjury in chronic low back pain, de Jong, Vlaeyen, Onghena, Goossens, Geilen & Mulder (2005) performed a careful study of six individuals, using a single case experimental design. (If you’re not familiar with this approach to research – it’s extremely rigorous and useful in a clinical setting, this link takes you to a chapter discussing its use).  The aim was to establish which part of treatment “did the work” to change behaviour, but also measured pain intensity, and fear of pain and movement.  The treatments were information about pain and mechanisms, and the activities were those the person particularly wanted to be able to do. Their findings identified that explanations do little to pain intensity, avoidance or fear – but what actually worked was doing graded exposure. In other words, experiencing something different, DOING that something different in the real world, was more effective than talking about why someone shouldn’t be afraid. A much more recent replication of this study was conducted by Schemer, Vlaeyen, Doerr, Skoluda, Nater, Rief & Glombiewski (2018) and shows the same result: doing trumps talking about doing.

When we sit down and take a cold hard look at what we do in pain management we can see that the field has to draw on a huge range of disciplines and fields of study to understand the problems people experiencing pain have. This is, in fact, why Bonica and colleagues first established the International Association for the Study of Pain, and why multidisciplinary (and now interprofessional) pain management teams and approaches were established. None of us can possibly hold all the knowledge needed to work effectively in the area. At the same time, as health professionals working with people, we do need to have some foundation knowledge about biology, disease, illness, psychology, sociology and anthropology. These areas of study inform us as we work hard to help people get their heads around their pain. Do we need to be experts in all of these fields? Yes – if you work completely in isolation. No – if you work within an extended team (whether co-located or otherwise). Pain research will continue to push our understanding ahead – and to be responsible health professionals, we must incorporate new understandings into our practice or we risk being unprofessional and irrelevant. I would go as far as to say we’re irresponsible and harming patients if we fail to incorporate what is known about pain as a multidimensional experience. It’s time to back away from temporary guruism and move towards a far more nuanced, and perhaps less flighty approach to understanding pain.

Pain science. No, it’s not a thing. Pain being examined through multiple scientific lenses: definitely a thing.

NB for the avoidance of doubt: pain is never a “thing” but examining pain through multiple scientific lenses involves many “things”. (Merriam-Webster – click)


de Jong, J. R. M., Vlaeyen, J. W. S. P., Onghena, P. P., Goossens, M. E. J. B. P., Geilen, M. P. T., & Mulder, H. O. T. (2005). Fear of Movement/(Re)injury in Chronic Low Back Pain: Education or Exposure In Vivo as Mediator to Fear Reduction? [Article]. Clinical Journal of Pain Special Topic Series: Cognitive Behavioral Treatment for Chronic Pain January/February, 21(1), 9-17.

Schemer, L., Vlaeyen, J. W., Doerr, J. M., Skoluda, N., Nater, U. M., Rief, W., & Glombiewski, J. A. (2018). Treatment processes during exposure and cognitive-behavioral therapy for chronic back pain: A single-case experimental design with multiple baselines. Behaviour Research and Therapy, 108, 58-67.

Wood, L., & Hendrick, P. A. A systematic review and meta-analysis of pain neuroscience education for chronic low back pain: Short-and long-term outcomes of pain and disability. European Journal of Pain, 0(0). doi:doi:10.1002/ejp.1314


Wandering back from the IASP World Congress


Meetings, meanderings, mind-expansions

I’ve been away for abut 10 days, attending the World Congress of the International Association for the Study of Pain. It was a time of meetings with wonderful people I’ve met via the interwebs, with researchers and clinicians, and most importantly, with people living with pain.

It was also a time for meanderings – around the very walkable city of Boston, embracing history and looking towards the future, and mind meanderings as well.

And because it was a conference, it was also mind-expanding. New ideas, new ways of investigating this human experience of pain, new discoveries, and new applications.

… and expanding the way we help people who live with pain.

What struck me between the eyeballs?

Good things: for the first time, people living with pain were included in the proceedings. I’m reminded of the old saying from the disabilities movement “Nothing about us without us” – well, it’s finally arrived at the World Congress! There are some concerns about this move amongst clinicians, and there’s no doubt that some of the people I’ve seen for whom the experience of being seen about their pain has been disheartening, stigmatising and frustrating, are very angry. I think, though, that continuing to avoid meeting with people who are in this space serves only to fuel their rage, and perhaps it’s time for us as clinicians to learn what it is about their experiences that we can learn from.

Professor Fiona Blyth talking about the Global Burden of Disability – 21%

Another “between the eyeballs” moment was when Professor Fiona Blyth discussed the knowledge that 21% of the total global burden of disability, and that this is increasing more quickly in developing countries because of the rapidly increasing percentage of older people (with multiple MSK comorbidities) – but here’s the kicker: There has been little-to-no change in funding policies to reflect this increasing burden of disease. You read that right. Funding goes to diseases that can kill you – but very little goes to the diseases that simply leave you disabled for the rest of your days.

Not so good things: Well, much of the research shows that change is incremental and that while strategies like exercise have reasonably good research support what actually matters is that exercise gets done: the form of exercise for persistent pain is a whole lot less more important than issues of adherence (Professor Kathleen Sluka’s plenary lecture showed this).

There was a good focus on behavioural science and pain, disability and response to treatment. And plenty of emphasis on sharing the responsibility for using psychologically-informed treatments with all health professionals, not just psychologists.

Why have I included this in my “not so good things”? Because a very recent Twitter discussion suggests that there continues to be a misperception that by using a psychologically-informed treatment, the aetiology of a pain problem is therefore assumed to be psychological.

There continues to be tussling over whether a biopsychosocial (or sociopsychobiological) model has sufficient emphasis on “the bio”, along with misinterpreting the historic origins of Engel’s thinking. Various people argue that “all is bio” or “but it’s reductionist” – yet readers of Engel’s original writings will recognise an interactional systems approach, where an effect in one factor will likely have flow-on effects everywhere else.

The final “not so good” for me was the dearth of discussion about occupational therapy’s historic and ongoing involvement in pain and pain management. There were at least 20 occupational therapists at the meeting, and despite Fordyce including occupational therapists in his original behavioural approach to disability (Fordyce, Fowler & Delateur, 1968), scant evidence of occupational therapy’s important contribution to this field over the years.

This is important because occupational therapy is one of the few professions to have adopted, retained and integrated a sociopsychobiological approach to healthcare. If you’re ever thinking about asking “how does one profession use the BPS model?” maybe talking with an occupational therapist will help you.

I was lucky to have a chance to offer a piece of research conducted by Brian Rutledge and me, looking at the function of an online discussion group (yes! Facebook!). The purpose was to establish whether the group Exploring Pain Science functions as a “Community of Practice“. The answer is a resounding Yes! and you can review the poster here – click

There will be a paper forthcoming, and some further analysis of the processes used in this group.

…Why look at Facebook groups?

Well, one reason is that there was a resounding call for knowledge translation – and all manner of ways thought to be useful in this pursuit. But as far as I am aware, using Facebook groups (especially ones that have emerged “organically”) is both a popular strategy – and one that has been under-examined in pain research – for people trying to implement what they’ve read or heard from research into their daily practice.

Hope this very brief tour through just a couple of the things I’ve been pondering since this World Congress will encourage YOU and others to join IASP. It truly represents the only global organisation that is transprofessional, wedded to a biopsychosocial model of pain, and one that is progressing our understanding of pain so much.


Fordyce, W. E., Fowler, R. S., & Delateur, B. (1968). An Application of Behavior Modification Technique to a Problem of Chronic Pain. Behaviour Research and Therapy, 6(1), 105-107.


Myths about exposure therapy


Exposure therapy is an effective approach for pain-related anxiety, fear and avoidance, but exposure therapy is used less often than other evidence-based treatments, there is a great deal of confusion about graded exposure, and when it is used, it is not always well-conducted. It’s not a treatment to be used by every therapist – some of us need to challenge our own beliefs about pain, and whether it’s OK to go “into” the pain a little, or even slightly increase pain temporarily!

Below are some common misconceptions and suggestions for how to overcome them:

Misconception: Exposure therapy causes clients undue distress and has adverse consequences.

Suggestions: Although exposure therapy can lead to temporary increases in anxiety and pain, it is important to remember that these symptoms are not dangerous, and that exposure is generally carried out in a very gradual and predictable way. Exposure very rarely causes clients harm, but it is important to know your clients’ medical histories. For example, a client with a respiratory condition would not be asked to complete an exposure designed to elicit hyperventilation.

I usually begin with a really clear explanation for using this approach, basing my explanation on what the person has already said to me. By using Socratic or guided discovery, I try to understand the logic behind the person’s fear: what is it the person is most worried about? Often it’s not hurt or harm, it’s worrying that they won’t sleep, or they’ll have a flare-up that will last a looooong time – and they won’t be able to handle it. These are fundamental fears about having pain and vital to work through if the person is going to need to live with persistent pain for any length of time.

Once I’ve understood the person’s reasons for being bothered by the movements and pain, then I work on developing some coping strategies. These must be carefully carried out because it’s so easy to inadvertently coach people into using “safety behaviours” or “cues” that work to limit their contact with the full experience. Things like breath control, positive self-statements, any special ways of moving, or even ways of recovering after completing the task may serve to control or reduce contact with both anxiety and pain. I typically draw on mindfulness because it helps people focus on what IS happening, not what may have happened in the past – or may happen in the future. By really noticing what comes up before, during and after a graded exposure task, and being willing to experience them as they are, people can recognise that anticipating what might happen is often far worse than what does happen.

Finally, I’ll work through the scenario’s – either pictures of movements and activities, or descriptions of the same things. I prefer photographs (based on the Photographs of Daily Activity), because these elicit all the contextual details such as the other people, weather, flooring or surface and so on that are often factors increasing a person’s concerns. We begin with the activity that least bothers the person and consistently work up from there, with practice in the real world between sessions. I’ll go out to the places the person is most concerned about, we’ll do it together at first, then the person can carry on by themselves afterwards.

Misconception: Exposure therapy undermines the therapeutic relationship and leads to high dropout.

Suggestions: If you give your person a clear reason for using this approach and deliver it well,  the person is more likely to achieve success – and this in turn strengthens your relationship. Additionally, there is evidence that dropout rates for exposure are comparable to other treatments.

There is something about achieving a difficult thing that bonds us humans, and if you approach graded exposure with compassion, curiosity, and celebration, you may find your relationship is far more rewarding and deeper than if you simply prescribe the same old same old.

Misconception: Exposure therapy can lead to lawsuits against therapists.

Suggestions: Survey data suggest that lawsuits against therapists using exposure are extremely rare. As with any kind of therapy, you can take several steps to protect yourself from a legal standpoint. Don’t forget to obtain informed consent, ensure your treatment is delivered with competency, professionalism, and ethical consideration.

The best book/resource by far for graded exposure is Pain-Related Fear: Exposure-Based Treatment for Chronic Pain, (click) by Johan W.S. Vlaeyen, Stephen J. Morley, Steven J. Linton, Katja Boersma, and Jeroen de Jong.

Before you begin carrying out this kind of treatment, check you have these skills (from the book I’ve referenced):

Vlaeyen, Johan, Morley, Stephen, Linton, Steven, Boersma, Katja, & de Jong, Jeroen. (2012a). Pain-related Fear. Seattle: IASP Press.

What it means to be a therapist


I wrote the following response to a discussion held recently on a Facebook group Exploring Pain Science – about the term “catastrophising”. It’s a term that elicits great anger and frustration from people living with persistent pain, and I see the term used poorly by clinicians as a judgement about another’s experience. There’s certainly plenty of research showing relationships between high levels of “thinking the worst” about pain, and poorer outcomes – but HOW we as clinicians respond to someone in distress may be more of a problem than the act of a person describing their fears and worries about the future. This is what I wrote:

I’ve been pondering – I think I see people as doing the absolute best they can to make the best decisions they can based on what they know at the time. And “knowing” means all the messy uncertainty, lack of logic, emotion and coercion from others! So whatever a person is doing to manage is the best they can do. All I can do is offer some options that I’ve seen other people use, maybe provide some more information, maybe even more accurate information, support people to be guided by what they see as important (usually values), and be there for them as they make their own minds up about what to do next. I’m a cheerleader, encyclopaedia, visualiser (lay out the options in a way that makes sense), perhaps a guide but only in so far as helping people notice things they hadn’t before.

To me, if someone is thinking the worst, it could be that they don’t have all the information about their resilience that they need, it might be misinformation about what’s happening in their body, it could be conclusions that over-estimate the threat and under-estimate resilience. It might also be difficulty pulling the mind away from sticky thoughts that stop clear thinking, or as one researcher called it “misdirected problem solving” – a way for the mind to remind the person that there’s an unresolved situation. It might also be feelings of helplessness, feeling like there is no point in trying anything new because nothing works anyway, a sense of not having enough energy to keep trying…

Those aren’t necessarily inaccurate thoughts, but they’re certainly not helpful thoughts, especially at 3.00am! So temporarily at least it seems helpful to bear witness to that person’s distress, to make room to be present, not to judge or dismiss but to allow those worst fears to be recognised. Sometimes bringing the worst fears out into the light shows that they can be managed better than expected, sometimes they fade into nothing, and sometimes they allow someone else to be there and support when the person’s run out of puff.

While I can understand how the language of uninvolved clinicians hurts because so often they fail to acknowledge the real distress of the person, I can still recognise that many of the contents of thoughts and beliefs won’t happen, – those scenarios are there wanting recognition, but they may not happen. If they do there will be things to do then – but mostly, when I catastrophise, I use it as energy to recognise how lacking I feel. And that’s not a nice place to be, but it’s simultaneously true (I lack) and untrue (others have what I need).

There’s a process I use for myself called creative catastrophising. I write down my worst fears, get them out on paper, make them visible. Sometimes that’s all I need to do. Other times I begin planning “what if X disaster happened, what would I do” – and when I’m in the right frame of mind, I can figure out a way to get by. I can’t tell anyone else to do that – but it’s a strategy that’s stood me in good stead as I’ve gone through the ups and downs of my life. It’s one way I cope.

Clinicians, if you can bear witness to another’s distress, without wanting to change, fix, judge or DO anything apart from being fully present, you’ll be doing the very best thing you can. The time for doing something “to help” is just around the corner – whatever you do, do NOT tell the person “you’re catastrophising” because this immediately means you’ve moved from being with to judging.

The dynasty of the disc! More history in pain management


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

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

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

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

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

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

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

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

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

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

 

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

Each time we face our fear, we gain strength, courage, and confidence in the doing – Theodore Roosevelt


I’m not certain Theodore Roosevelt actually said that – but who cares?! It’s a great statement. For the person living with persistent pain, though, it can be the last thing you want to hear. After all, it’s tough enough getting up and just doing the normal things let alone challenge yourself! So… how can a health professional help?

Let’s briefly recap. Self efficacy is the confidence I can do something successfully if I wanted to. It’s a robust predictor of many health behaviours including exercise, stopping smoking, eating healthily and coping well with persistent pain (Jackson, Wang, Wang & Fan, 2014; Williams & Rhodes, 2016). It was first introduced as a concept by Bandura as part of his theoretical model of behaviour change, and further discussed in an experimental study in a paper investigating systematic desensitisation processes, arguing that this approach to treatment created and strengthened expectations of personal efficacy (Bandura & Adams, 1977). Bandura argued that people develop a sense (expectation) of self efficacy from their own performance, watching others succeed, being persuaded by someone that yes indeed you have the skills to achieve, and also awareness of physiological arousal from which people can judge their own level of anxiety.

Self efficacy is more than a simple “general confidence” construct, however. It’s far more selective than this. For example, although I believe I can successfully dance in my lounge with no-one there and the curtains closed, this does not translate to me dancing on a stage on my own in the spotlights with an audience watching! Self efficacy refers to confidence to succeed and produce the outcome I desire in a given context – and that’s extremely important for pain management, and in particular, exercise for people experiencing pain.

How does self efficacy improve outcomes? There are at least two ways: (1) through the actions taken to manage or control pain (for example, gradually increasing activity levels but not doing too much) and (2) managing the situations associated with pain (for example, people with low self efficacy may avoid activities that increase pain, or cope by using more medication (Jackson, Wang, Wang & Fan, 2014).

To examine how self efficacy affects outcomes, Jackson and colleagues (2014) conducted a meta-analysis of papers examining this variable along with other important outcomes. Overall effect sizes for relationships between self efficacy and all chronic pain outcomes were medium and highly significant. This is really important stuff – we don’t find all that many studies where a single variable has this much predictive power!

As a moderator, the adjusted overall effect size (r=.50) of self efficacy and impairment was larger than the average effect sizes of meta-analyses on relations between disability and fear-avoidance beliefs, and pain as a threat for future damage and challenge for future opportunities. Self efficacy has stronger links with impairment than cognitive factors such as fear-avoidance beliefs and primary appraisals of pain (Jackson, Wang, Wang & Fan, 2014).  Age and duration of pain were the strongest moderators of these associations and suggest that reduced self-efficacy can become entrenched over time. In other words – as time passes, people experience fewer opportunities for success and begin to expect they won’t ever manage their pain well.

An important point is made by these authors: how we measure self efficacy matters. They found that self efficacy measures tapping “confidence in the capacity to function despite pain” had
stronger associations with impairment than did those assessing confidence in controlling pain or managing other symptoms.

Bolstering self efficacy – not just about telling people they can do it!

Given that self efficacy is domain-specific, or a construct that refers to confidence to do actions that lead to success in specified situations, here are a few of my questions:

  • Why are most people attending pain management programmes provided with gym-based programmes that don’t look at lot like the kinds of things people have to do in daily life? It’s like there’s an expectation that “doing exercise” – any exercise – is enough to improve a person’s capabilities.

    BUT while this might increase my confidence to (a) do exercise and (b) do it in a gym – but does it mean I’ll be more confident to return to work? Or do my housework?

  • How often are people attending gyms told to “push on”, or to “stop if it hurts”? And what effect does this have on people?

If their confidence is low, being told “just do it” is NOT likely to work. People need to experience that it’s possible to do things despite pain – and I think, to be able to handle a flare-up successfully. Now this is not going to happen if we adopt the line that getting rid of all pain is the aim, and that flare-ups should be avoided. If we want people to deal successfully with the inevitable flare-ups that occur, especially with low back pain, then we need to (a) be gentle, and grade the activities in an appropriate way (b) have some “ways of coping” we can introduce to people rather than simply telling them they can cope or reducing the demands (c) have other people around them also coping well (and that includes us health professionals)

  • Ensure we attribute change to the person, not to us.

That’s right: not to our sparkling personality, not to our special exercises, not to the machines we use, not to the techniques we have – you get the drift? Progress must be attributed to the person and his or her skills and perseverance. Because, seriously, all this arguing over which exercise regime is best doesn’t stack up when it’s actually self efficacy that predicts a good outcome.

And for case managers who may read this: just because someone has successfully completed an exercise programme, or a vocational programme with exercise as a component, this does not mean the person can manage successfully at work. Well, they may manage – but they may utterly lack confidence that they can. Context matters.

 

Bandura, A., & Adams, N. E. (1977). Analysis of self-efficacy theory of behavioral change. Cognitive Therapy and Research, 1(4), 287-310.

Estlander AM, Takala EP, Viikari-Juntura E., (1998). Do psychological factors predict changes in musculoskeletal pain? A prospective, two-year follow-up study of a working population. Journal of Occupational and Environmental Medicine 40:445-453

Jackson, T., Wang, Y., Wang, Y., & Fan, H. (2014). Self-efficacy and chronic pain outcomes: A meta-analytic review. The Journal of Pain, 15(8), 800-814.

Williams, D. M., & Rhodes, R. E. (2016). The confounded self-efficacy construct: Conceptual analysis and recommendations for future research. Health Psychology Review, 10(2), 113-128.

Managing sleep problems – a medication-free approach (i)


I’ve recently completed two posts on assessing sleep problems in people experiencing persistent pain, and today I turn my attention to strategies for managing sleep problems – without medication. Why without medication? Because to date there are no medications for insomnia that don’t require a ‘weaning off’ period, during which time people often find their original sleep problems emerge once again… I’m not completely against medications for sleep or pain – but I think they need to be used with care and full disclosure about the effects, side-effects, and the need to eventually withdraw from them.

The approach I’m advocating is a modified form of cognitive behavioural therapy for insomnia (CBTi). CBTi is a form of treatment that is now considered to be first line therapy by both the British Association for Psychopharmacology (Wilson, Nutt, Alford, Argyropoulos, Baldwin, Bateson et al, 2010), and the American College of Physicians (Qaseem, Kansagara, Forciea, Cooke, Denberg et al, 2016). It includes sleep hygiene, cognitive therapy for the thoughts and beliefs associated with sleep, and sleep restriction for those who clinically need it. The modified version I advocate is based on Dr Guy Meadows ACT-based approach and I’ll cover that next week, but I’ll describe the classical CBT approach first.

Basic principles

The basic idea behind a CBT approach to insomnia is that although the initiating event may be out of our control, it’s unlikely to be maintaining the problem – and the factors maintaining the problem are typically the habits people have, and the thoughts and beliefs about their sleep problem.

Sleep is a behaviour that is infinitely malleable, as anyone who has travelled far enough on long-haul flights will know (and parents of small babies as well!). There are cues we use to decide when we should head to bed, and how long we should stay asleep. Bodies in turn respond to these cues and modify automatic processes such as digestion, urine production, and body temperature to ensure we stay asleep for as long as needed. When those cues change – for example, we’re in a new time zone when it’s light at the “wrong” time, and we’re hungry at the “wrong” time, we have trouble staying asleep until the body adjusts. Some people say we can manage a two-hour time zone shift every 24 hours, but in some sensitive people even a one-hour daylight savings change can upset the apple-cart!

If sleep is a habitual behaviour, then we can manipulate the cues to our benefit when sleep is elusive. We learn to associate things like the routine we follow prior to going to bed, light in the room, the “winding down” process we use, and even the timing of our snacks and drinks as a way to signal to the body/mind that we’re sleepy/tired.

There are three basic steps in CBTi: stimulus control (aka sleep hygiene), cognitive therapy, and sleep restriction – with the usual relapse prevention steps an essential part as well.

Sleep hygiene (stimulus control)

The basis of sleep hygiene is to control the stimuli associated with going to sleep so that we clearly indicate to the body/mind that it’s time to get to sleep. That means some basic “rules” around what we do in the time preceding getting into bed, and what we do when in bed trying to sleep.

The golden rule is that the bed is for sleep and sex – not for worrying in, not for watching TV or using the computer or phone or tablet, not for arguing in, not for talking on the phone. If you’re awake in bed for longer than 20 minutes, it’s time to get out of bed until you’re sleepy/tired (more on this in a moment), keeping the lights down low, doing something tedious or boring, then returning to bed to actually sleep.

Simple, commonsense things like keeping the room dark and warm, blocking out the worst of the noise, NOT using a TV or radio or any other noise-making device to go to sleep, ensuring caffeine intake is limited, having a regular bedtime and wake-up time, not taking naps through the day and timing when exercise and relaxation are undertaken are all part of sleep hygiene and most of us are aware of these steps. If they’re not familiar to you, this site is a good one – click.

Cognitive therapy

The cognitive therapy part is about managing the thoughts and attitudes that can exacerbate the sleep problem – things like having a busy mind, worrying about not being able to sleep, believing that it’s crucial to have a certain number of hours of sleep or the next day will be awful, getting that sinking dread as bedtime approaches, following any number of almost (and sometimes actual) obsessive rituals to achieve sleep – and so on…

As usual, with any conventional CBT, dealing with these thoughts involves firstly reality testing – Is it true that you must have a certain number of hours of sleep or the next day will inevitably be terrible? Must the room be absolutely silent or sleep will elude you? Then challenging or disputing those thoughts – “It’s possible I’ll feel tired tomorrow, but I can still function even if I’m not at my best”, “It might take me longer to fall asleep but I’ll get to sleep even though I can hear a clock ticking”.

These simple approaches are reasonably easy to implement – and they are effective. But if sleep is still a problem, and the person isn’t getting more than 4 hours sleep a night, it’s time to bring in the big guns.

Sleep restriction

There are two parts of altering sleep habits that are particularly challenging: getting out of bed after 20 minutes of being awake (especially in the wee hours of the morning!); and using sleep restriction. Neither are easy, yet both are effective.

The idea behind sleep restriction is to reduce the amount of time being in bed while not actually being asleep. Simple huh? So that period from when you first hop into bed and until you actually fall asleep is called sleep latency – and the longer your sleep latency, the less sleep you actually get. You become inefficient at sleeping, and worst, your body/mind learns that it’s OK to be in bed wide awake, and as I mentioned earlier, people begin to associate even going into the bedroom as a negative thing which revs up the autonomic nervous system making it even more difficult to fall asleep.

The nuts and bolts are to work out what time you actually fall asleep, and only go to bed at that time. So if you stay awake until 2.00 or 3.00am, you only go to bed at 2.00am. And you keep your morning wake-up time the same as normal. Yes, this means you end up being only able to sleep for the time between 2.00am and 7.00am! Ouch!

The idea is to extinguish the “habit” of being awake while in bed, reducing the association between being in bed and wide awake, while getting you absolutely tired and sleepy that you fall asleep into a deep sleep quickly. Once this falling asleep part happens regularly (usually for a week or so) then it’s possible to begin a very gradual process of bringing the bedtime back to a more reasonable hour – I usually suggest 15 minute increments, returning to the previous step if falling asleep begins to be difficult.

The process is reasonably difficult – not because it’s hard to stay awake (after all, the person has been practicing it for some time!) but because of the mind chatter. It’s truly tough when your mind starts having a go at you, suggesting you can’t sleep, or you’ll be so incredibly tired you won’t cope, or you’ll be cranky and that it’s dangerous and how on earth  will you go at work without any sleep? And this is where having access to a really good clinician can be helpful, although there are apps that provide a pretty good alternative if a human isn’t available.

For a detailed examination of the literature on sleep restriction therapy, Kyle, Aquino, Miller, Henry, Crawford, Espie & Spielman (2015) provide a really good systematic analysis of how sleep restriction is employed in research trials.  For a plain language version of CBTi, this is a good description – click

As I mentioned above, I’ll be going through a slightly different version of CBTi – an Acceptance and Commitment Therapy approach to insomnia that is also gaining popularity and an evidence base. Come right on back next week for that exciting episode!

 

Kyle, S. D., Aquino, M. R. J., Miller, C. B., Henry, A. L., Crawford, M. R., Espie, C. A., & Spielman, A. J. (2015). Towards standardisation and improved understanding of sleep restriction therapy for insomnia disorder: A systematic examination of cbt-i trial content. Sleep Medicine Reviews, 23, 83-88.

Manber, R., Simpson, N. S., & Bootzin, R. R. (2015). A step towards stepped care: Delivery of cbt-i with reduced clinician time. Sleep Medicine Reviews, 19, 3-5.

Qaseem, A., Kansagara, D., Forciea, M., Cooke, M., Denberg, T. D., & for the Clinical Guidelines Committee of the American College of, P. (2016). Management of chronic insomnia disorder in adults: A clinical practice guideline from the american college of physicians. Annals of Internal Medicine, 165(2), 125-133. doi:10.7326/M15-2175

Wilson, S., Nutt, D., Alford, C., Argyropoulos, S., Baldwin, D., Bateson, A., . . . Wade, A. (2010). British association for psychopharmacology consensus statement on evidence-based treatment of insomnia, parasomnias and circadian rhythm disorders. Journal of Psychopharmacology, 24(11), 1577-1601. doi:10.1177/0269881110379307

Assessing problems with sleep and pain – ii


Last week I wrote about my approach to assessing sleep problems in those with persistent pain. As an ex-insomniac I’ve spent a while learning about sleep so I can understand what’s going on, and why sleep can be such a problem. In this week’s post I want to dig a little deeper into what’s going on with poor sleep, as well as some of the unique features of sleep in people experiencing persistent pain.

Having reviewed the five main areas that are fundamental (and can/should be assessed by anyone working with people who experience persistent pain), the next area I want to look at with people is mood. There are two primary psychopathological contributors to poor sleep: the first we’ve dealt with last week (Question 4 – what’s going through your mind…) which is by far and away the most common initiator and maintainer of insomnia, and it doesn’t even need to be a diagnosable anxiety disorder! The second, you’ll probably have guessed, is depression.

Depression is common in people with both rotten sleep and ongoing pain (Boakye, Olechowski, Rashiq, Verrier, Kerr, Witmans et al, 2016), and there are some suggestions that pain and depression may be related and similar neurobiological processes may be involved for both (increased limbic activity being one of them). In depression, there is increased activity in the HPA Axis, reduced BDNF (brain-derived neurotrophic factor), and reduced 5HT with increased pro-inflammatory cytokines . In persistent pain, there may be activity in the HPA Axis, there is certainly reduced BDNF except in the spinal cord, and reduced 5HT, along with increased pro-inflammatory cytokines. And in sleep disturbances there is also increased activity in the HPA Axis, redced BDNF, reduced 5HT and guess what… increased pro-inflammatory cytokines. And all three interact with one another so that if you happen to be depressed, you’re more likely to experience pain that goes on, and your sleep will also reduce your mood and increase your pain. And the reverse. All very messy indeed!.

What this means is that assessing for low mood and the impact on sleep is important – if someone’s describing waking well before they usually do, in the wee small hours (anywhere from 3 – 5am if they usually wake at 7.00am) I’m ready to screen for low mood. To be honest I always assess for that anyway! Depression is also associated with low motivation and loss of “get up and go” so this is likely to interact with poor sleep, creating a very tired person.

There are three other very important aspects of sleep I like to assess for: sleep apnoea, where someone stops breathing for seconds to minutes at a time, often snorting awake, and this may be associated with snoring and daytime sleepiness. Often the person won’t be aware of their sleep apnoea, so it can be helpful for a bed-partner to let you know whether this is a feature of your patient’s sleep.

The next are a group of movement disorders of sleep, many of which are associated with the third area I assess, which are medications.

Movement disorders of sleep include restless leg syndrome – that feeling of absolutely having to move the legs, usually at night, and relieved by getting up to walk around, but in doing so, making it difficult to sleep. Another is periodic limb movement disorder of sleep, which can be every 5 – 30 seconds of leg twitching all night long, and in some cases, whole body twitching though this is less frequent and less rhythmic. This latter problem may not be noticed by the person – but their bed-mate will know about it! – and this problem may be associated with both sleep apnoea and restless leg, AND some doses of antidepressants. Another common contributor to these problems is low iron levels – worth checking both iron and medications!

Finally with medications, I like to understand not only what the person is taking, but also when they’re taking them. Several points are important here: some medications are usually sedating such as tricyclic antidepressants but in some people nortriptyline can paradoxically increase alertness! If that’s the case, timing the dose is really important and should be discussed with either the prescribing doctor, or a clinical pharmacist. Opioids depress respiration (ie slow breathing down) so can be problematic if the person has sleep apnoea AND is taking opioids, the drive to inhale may be less, causing more frequent and deeper periods without breathing normally. For restless legs and periodic limb movement disorder, some antidepressants (venlafaxine is one of them) in high doses can cause the twitching and once the dose is reduced, this fades away, at least a bit.  There is a very small amount of research suggesting that NSAIDs can influence sleep quality in some people also.

The effects of poor sleep are many: anything from micro-sleeps during the day (problematic while driving or operating machinery!), to more irritability, sluggish responses, less concentration and more difficulty solving problems. Pain is associated with more frequent micro-wakenings during the night (Bjurstrom & Irwin, 2016) but findings with respect to whether deep sleep, REM sleep or light sleep were consistently more affected weren’t clear.

Having completed my assessment, more or less, I can also use a few pen and paper measures: Wolff’s Morning Questions (Wolff, 1974), Kryger’s Subjective Measurements (1991), Pittsburgh Sleep Quality Index (Bysse, Reynolds, Monk et al, 1989) and the Sleep Disturbance Questionnaire (Domino, Blair,& Bridges, 1984) are all useful. Speaking to the partner is an excellent idea because I don’t know about you but I never snore but my partner swears I do! Who do you believe?!

People experiencing insomnia are not very reliable when describing their own sleep habits – we’re terrible at noticing when we’re actually asleep or awake in those early stages of sleep, so we typically think we’ve slept less than we actually have. We also do a whole lot of things to avoid not sleeping – and these can actually prolong and extend our sleeplessness!

We’ll discuss what to do about the factors you may have identified in your sleep assessment in next week’s instalment, but you can rest assured it’s not crucial for you to do anything yourself about some things. For example, if someone has sleep apnoea, referring for a sleep study is important, but not something YOU need to do! But please make sure a referral is suggested to someone who can make it happen. Similarly with medications and sleep movement disorders, it’s not something you should tackle on your own – please discuss managing these with a specialist sleep consultant, psychiatrist, or the person’s own GP. Mood problems – treat as you would any time you find someone with a mood problem.

Next week – off to the Land of Nod: A roadmap?!

 

Boakye, P. A., Olechowski, C., Rashiq, S., Verrier, M. J., Kerr, B., Witmans, M., . . . Dick, B. D. (2016). A critical review of neurobiological factors involved in the interactions between chronic pain, depression, and sleep disruption. The Clinical Journal of Pain, 32(4), 327-336.

Buysse DJ, Reynolds CF 3rd, Monk TH, et al. The Pittsburgh Sleep Quality Index: a new instrument for psychiatric practice and research. Psychiatry Res 1989; 28(2):193–213.

Domino G, Blair G, Bridges A. Subjective assessment of sleep by Sleep Questionnaire. Percept Mot Skills 1984;59(1):163–70.

Kryger MH, Steljes D, Pouliot Z, et al. Subjective versus objective evaluation of hypnotic efficacy: experience with zolpidem. Sleep 1991;14(5):399–407.

Moul DE, Hall M, Pilkonis PA, et al. Self-report measures of insomnia in adults: rationales, choices, and needs. Sleep Medicine Reviews, 2004;8(3):177–98.

Wolff BB. Evaluation of hypnotics in outpatients with insomnia using a questionnaire and a self-rating technique. Clin Pharmacol Ther 1974;15(2):130–40.