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

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

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

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

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

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

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

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

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

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

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

Well and good. What does it actually mean?

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

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

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

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


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

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

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

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

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

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

Chronic pain as psychiatric disorder

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

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

“Many people report pain in the absence of tissue damage or any likely pathophysiological cause; usually this happens for psychological reasons…. pain most often has a proximate physical cause (”

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

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

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

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

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

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

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

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

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


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

More discussion on Functional Capacity Evaluations

Some years ago I wrote about Functional Capacity Evaluations and the lack of evidence supporting their use, particularly their use as predictive tools for establishing work “fitness”. 

I’ve received some sharp criticism in the past for my stance on FCE, and I continue to look for evidence that FCE are valid and reliable.  I haven’t found anything recently, and I’m still concerned that FCE are used inappropriately for people with chronic pain.  There is nothing like the demand characteristics of a testing situation for a person with chronic pain to either push themselves – and have a flare-up for some days afterwards but get a “good” report suggesting they have put in “full effort” and that they can manage a full time job of a certain MET demand; or to pace themselves, using pain management strategies – and avoid a flare-up but receive a “bad” report, suggesting they haven’t put in “full effort” and despite this, they can manage a full time job of a certain MET demand.

I can’t understand why FCE providers don’t work alongside people with chronic pain and their vocational counsellors, to help them define their sustainable level of physical demand, and systematically help them to gain confidence that they can find suitable work without exacerbating their pain. 

For the record, I’m not against establishing functional abilities.  And I think having a systematic approach to doing this.  I am against FCE’s being touted as a way to reliably determine work capacity, or to being able to determine “effort” through “consistency”. There simply isn’t published evidence to support these claims.  If someone can provide me with evidence, I’ll gladly change my mind because if there is one thing scientific training teaches, it’s that it’s OK to change your mind – if there’s evidence to do so.

This doesn’t mean that FCE’s would then be fine and dandy – because, as I’ve seen far too many times – HOW they’re used goes often well beyond what any FCE can possibly do, and very often is used as a blunt instrument when some good motivational interviewing and careful vocational counselling would achieve the same.

Here’s my original post, and some very good references are at the end of it.

The Graded Motor Imagery Handbook – a review

I love getting presents, and I love books, so what could be better than getting a book to review as a present!

Graded motor imagery (GMI) has become incredibly popular in pain management, especially for people with unilateral pain.  It’s a treatment that is intensive for patients/participants, but is non-invasive, means the person with pain develops self management skills, and has level B1 evidence.  For those who don’t know – level B1 evidence means there are several RCT’s, and at least one meta-analysis showing support for this approach.

Back to the book.  Like all the NOI books it’s an unusual size, has groovy graphics and an easy-to-use layout. It’s a spiral bound book of over 140 pages with a great index (yay!), logical layout and has room for notes.  The illustrations and photographs are clear and provide excellent guidance for clinicians.  Chapters divide the book into sections of background info including theory and evidence; how to conduct treatment with GMI (clinical reasoning); metaphors (David Butler’s favourite teaching tools); and a whole chapter on how to use the materials available from NOI to support GMI treatment.   Each chapter can stand alone, and it’s not necessary to read from beginning to end – but of course, it does help!

This book isn’t for beginner therapists working in pain management. There are some assumptions about the level of clinical reasoning required and patient selection that are not fully explored, and true psychosocial aspects of managing pain – and the translation into the “real world” – are omitted. This is fine as long as clinicians are aware of the need to identify people who will benefit from the approach and as long as clinicians work within an interdisciplinary team environment.

Patients/participants need to be motivated, committed, and relatively psychologically well, without complex psychosocial contexts such as family/relationship issues, litigation, personality disorders, drug/alcohol problems or other cognitive impairment.  GMI has best application in people with unilateral pain such as CRPS and phantom limb pain – although it has been extended to other pains.  These factors may influence the degree of engagement and time required to carry out GMI, and may influence the outcome.

Back to the book again!   I love the chapter written by Lorimer Moseley on the neuroscience underpinning GMI.  His writing is clear and provides an excellent scientific basis for the approach.  He doesn’t extend his writing into psychological aspects of pain beyond the concepts of what he calls “neurotags”, or “interconnected neurones … that produce an output”.  Neurotags involve areas across the whole brain and, when activated, produce, for example, the experience of a whiff of fresh bread (along with the scent, the associated emotions and cognitions from past learning and the anticipation of future action).  I have learned these associations as just that – associations between various aspects of learning and anticipation, and have called them the neuromatrix – but NOI have used the term neurotag, and I guess it’s as good a name as any.

The chapter on conducting GMI treatment written by Tim Beames is extremely clear and well written.  While it’s possible to use this as a sort of cook-book to treatment, with the information from other chapters such as Lorimer’s neuroscience, and Butler’s metaphors, it becomes far more flexible.  I like this.  It is a chapter that I think many clinicians will turn to regularly – but as is emphasised throughout this handbook, patients/participants should read this stuff too.

Worth getting? Yes, I think so. 

My caution lies in over-interpreting the application of GMI beyond the evidence-base.  If you intend to try it with a patient/person with pain, please explain that this is an experiment that you and the person are conducting to see how this treatment works for him or her.  Select patients appropriately, checking for motivation, factors that could distract from engagement in treatment, and type of pain.  Record a baseline. Monitor progress. And involve the other members of your treatment team (particularly occupational therapists) to help transfer what is practiced out into the wide, wide world.  After all, the most complex context of all is being engaged in occupations like grocery shopping, driving, cooking a meal, playing a sport – where the environment is always changing, contains all those triggers, and where the brain is involved in multiple decisions moment-by-moment.

Where to get it? Go here – and let ’em know I sent you.

What is this thing called pain?
As I’m busy writing up research papers for publications to “count” towards my research productivity, I’m reminded of one reason I keep on blogging – and it’s this: blogs are open to anyone.  People can comment on what I write.  When someone comments, whether they agree, disagree, or simply pose a question, it’s an opportunity for dialogue and reflection. That’s not nearly as easy to do in a peer-reviewed journal!

As a result of comments from my post yesterday, I’m musing on ways to explain the distinction between acute and chronic pain that will make sense to someone who experiences fluctuations in pain intensity. I think I’m clear in my own mind between the two, but perhaps things are not as distinct as I’ve made them – or maybe I haven’t explained things well.

There are several ways that acute pain can be distinguished from chronic pain, none of them particularly satisfactory except, maybe, one.  We can think of the association between pain and tissue damage or threat of tissue damage.  In acute pain, tissue damage or the potential to damage tissue is often present – but not always.  Think of a typical “tension” headache.  It’s usually short term, but not associated with muscle damage.

We can consider duration – how long does this pain persist?  Acute pain is typically short-term, it does end at some point – sometimes well after the need for a “warning” alarm is necessary – but what about chronic hip osteoarthritis?

Some of the other factors I see used to distinguish acute pain from chronic include – quality of the sensation, how quickly the pain comes on, whether psychosocial factors are relevant, whether disability or illness behaviour is present, even the location or specificity of the pain can be used as an identifying factor.

We can also think of usefulness – acute pain is usually useful.  It tells we need to do something, take action to reduce the threat to our body’s integrity.  I think this is probably the most useful definition of the lot, even in the case of a “tension” headache – when it  might simply be an indication we need to have some time out, drink more water or get some new glasses.

Chronic pain has a bad rap.  There are many clinicians who consider that chronic pain is almost entirely influenced by psychosocial factors – therefore the person with pain needs to simply “get over it” and they’ll recover.  Then there are those who think chronic pain is simply pain that hasn’t had the “source” of the pain identified yet – find that source, burn it or cut it or otherwise remove it, and the pain will be gone.  And for some kinds of ongoing pain, like an osteoarthritic hip, that’s the case.

Over the years I’ve worked in chronic pain management, I think I can confidently say that chronic pain can be sharp, stabbing, dull, burning, deep, aching – all the same kinds of sensations that acute pain can be.  Its onset can be pretty rapid, but also insidious or gradualBoth acute and chronic pain are strongly influenced by psychosocial factors – things like attention, general alertness level, “threat value” or beliefs about what the pain means, attention from others, past learning – all of these things influence our experience of both acute and chronic pain, although it’s probably true to say that as pain persists, many of these psychosocial factors play an increasingly important role in the disability associated with pain.

There are other definitions of chronic pain.  One is duration – pain that persists beyond “normal healing time” (whatever this is).  Alternatively, pain that has been present for three to six months.  My problem with this definition is that it’s common for people to have pain around a fracture site for up to 12 months even when bony union is progressing normally.  Is this chronic pain?  What about instances where the pain is intermittent – migraine? Noncardiac chest pain? Abdominal pain?

So, what about chronic pain that fluctuates?  This seems to be the case more often than not.  It’s very very rare for me to hear someone say their chronic pain is at exactly the same intensity day in, day out.  When I do hear it, I like to spend some time exploring this experience in more detail.  Without fail, with gentle enquiry, fluctuations of pain intensity are there but may be subtle.

Why is recognising this so important?  Well, let me first put to bed any idea that I think people with chronic pain are immune to acute pain – that’s so not true.  What is arguable is whether fluctuations in pain, particularly when they’re the “same old, same old” pain, need to be managed using acute pain treatments.

And this is important because

  • so many acute pain treatments are passive,
  • take time away from living,
  • put the person getting the treatment at risk of yet another diagnosis or explanation,
  • reduce the opportunity to gain confidence with using self management strategies,
  • in the case of medication can put the person at risk of addiction or inappropriate use of this,
  • and, often unrecognised, can train the person to begin to fear (& then avoid) experiencing pain – leading to increased distress and continued treatment seeking

Am I advocating never using adjuntive intervention? See yesterday’s post in answer to that! But at the same time, I’d suggest that it’s pretty important to be aware of the risks.

So far, in answer to the question posed in my title, one of the best descriptions of the various types of pain and of the distinction between “normal” pain and “pathological” pain there is, Clifford Woolf’s paper is my choice.  Actually, the whole issue of this journal (which is – fabulously! – completely open access online!) could be required reading for anyone wanting to be informed about advances in our knowledge of pain.  I particularly love the examples he provides for each type of pain problem and how they arise.  That’s great stuff.

But even this set of wonderful papers doesn’t really explore some of the aspects of pain that don’t really get mentioned – disability and the effects of social, family, community attitudes and responses.  Yes, I know they’re messy to research.  They’re complex. They differ across countries, cities, villages and families.  But oh how powerful they are in our experience of pain.

Woolf, C. (2010). What is this thing called pain? Journal of Clinical Investigation, 120 (11), 3742-3744 DOI: 10.1172/JCI45178

Black and white thinking must be abolished

Black and white thinking, for those readers unfamiliar with cognitive distortions, refers to the tendency to reduce complex ideas and situations into simple, dichotomous, and mutually exclusive categories.

Think of good or bad, yes or no, all correct or all wrong, acute pain or chronic pain, neuromatrix or peripheral mechanisms, cure the pain or manage the pain.

It’s a way of simplifying arguments or decisions that can work well when the situation requires very fast decision-making, or where the options are very limited.

It doesn’t work at all in the messy and complicated worlds of clinical reasoning, theory development, or in discussions to broaden understanding.

I’m pondering this because of the way various aspects of pain management and the science of pain are misrepresented as opposed to each other, when maybe it’s not quite so simple.

I hope (crossing fingers and toes) that I’m not doing prone to doing it too often on the pages of this blog, or elsewhere for that matter!

There are multiple strands of research into pain at present. 

There are the reductionists who focus exhaustively on smaller and smaller elements of biology to explain the processes involved in nociception and transmission from noxious input to the perception of pain and back to the responses as a result. 

There are the phenomenologists who focus on the ‘lived experience’ of the individuals who have pain.

There are those who are furiously investigating laterality and cortical processing.

There are others feverishly working on ways to abolish all pain, and those who are equally enthusiastically researching why so many people are unbothered by their pain even though it’s severe.

Can you see all those opportunities for opposing views? for argument and debate?  It’s common for any of us to think mainly in terms of our own orientation, and there are many factors in human cognitive bias and group decision-making that get in the way of us working towards consensus – or even hearing each other.  And that can lead to trouble within teams, especially multi- or inter-disciplinary teams.

I wonder if it’s time to apply some of the cognitive techniques we can use with patients to ourselves as clinicians.  Let’s take a quick look at some of the basics.

Firstly, why do we use black and white thinking?  Well, it simplifies things.  If we’re feeling a little bit sad, we’re more likely to tell a loved one that we’re feeling “terrible”.  We don’t mean to exaggerate, we’re aiming to get empathy from the person we’re talking to, so we unintentionally use dichotomous language – we think in terms of feeling “amazing” vs feeling “terrible”.   Humans like to identify patterns, and to group similar things together so we can generalise.  We like to reduce an argument into “either – or”.  And when we do this, once again because of our tendency to look for information that confirms our own position, we often fail to recognise other alternatives, or information that doesn’t fit with our own views.

What we can do is step back and carry out some metacognition – thinking about our own thinking.

Some questions we can use to challenge our own position are:

  • How did I come to that conclusion?
  • What’s the evidence for the other position?
  • Is it possible to use “and” instead of “either/or”?
  • What are the other options?
  • Are there parts of my argument that can’t explain something the other position can explain?
  • This idea is only an idea – not my personal possession
  • Consider saying things like “at the moment my position is…”, “I’m attracted to this idea currently…”

I’ve personally found it useful to relax a little and recognise that in the end, the data will speak for itself.  So, for example, I was initially not keen on mirrorbox and laterality training for CRPS.  The studies, especially in the early stages, weren’t carried out in people with the degree of chronicity and complex psychosocial background that I saw.   Over time, and as the evidence has been gathering, I’ve changed my position.  I don’t mind acknowledging this change – in the end, it’s not my ego that’s important, nor “my” ideas – it’s what helps this person at this time with this particular problem.

Having said this, developing critical thinking skills, and in particular, being able to unpack and delve into how a study has been conducted and whether the conclusions drawn are supported by the data is vital.  Cherry picking, or selecting studies that support one view or another while ignoring or failing to account for studies with conflicting findings, just doesn’t do – again I try to relax a little, because in the end the balance of evidence does fall one way or another.  Or, in the case of chronic pain management, maybe there is so much to learn that what we know now is not even beginning to find answers.

If you’re keen to learn more about how to develop critical thinking, Foundation for Critical Thinking has a wealth of information.

What to do about catastrophising even when you’re not a psychologist
OK, it’s time I stopped the suspense.  This post is about what to do about catastrophising even when you’re a physiotherapist, massage therapist, acupuncturist, nurse, occupational therapist, social worker – oh just about anyone working with people who have pain!

Catastrophising is “an exaggerated negative “mental set” brought to bear during actual or anticipated pain experience” (Sullivan, Thorn, Haythornthwaite, Keefe, Martin, Bradley and Lefebvre, 2001).  It’s demonstrated when people describe their pain in highly vivid and negative terms “My muscles feel like they are tearing away from the bone”, “I can’t cope with this any more”, “I keep on thinking about the pain all the time” and so on.  Catastrophising is associated with greater distress, lower mood, greater disability and poorer prognosis (Sullivan MJ, Thorn B, Haythornthwaite JA, Keefe F, Martin M, Bradley LA, & Lefebvre JC, 2001).

A recent study of army troops found that catastrophising is present even in young, healthy people (Ciccon, Chandler and Kline, 2010).  In this study, 25.9% of those reporting acute pain, and 51.3% of those reporting chronic pain endorsed catastrophising beliefs.  And this group of people were not seeking treatment (as an aside, this is one of few studies to look at non-treatment-seeking people)!  The study also found that in those with high levels of catastrophising, mental health problems were more prevalent, and that catastrophising explained a good proportion of work disability.  In other words, even in this very healthy group of people, catastrophising was associated with greater vulnerability to having difficult managing pain and keeping mentally healthy.  If this finding is identified in other non-treatment-seeking people, I think we can confidently draw the conclusion that catastrophising may be one of the more prevalent unhelpful cognitive biases around.

Hopefully I’ve made the point that catastrophising is something that needs to be identified because of the profound effect it has on how people can live well despite having pain.  The argument is that by addressing catastrophising, people will be more able to cope with their pain, feel less helpless and distressed, and live lives less hampered by their pain.

What do we do about catastrophising?

I think (watch out – soapbox time!) that anyone who works with people who have pain and tend to catastrophise must help those people develop coping strategies to help them cope effectively.   It’s not enough to think that psychologists alone need to do this job.  This is because, as the Ciccone and colleagues study shows, catastrophising is very prevalent even in those people who are relatively well.  The people in that study weren’t likely to seek treatment from a psychologist for their pain – they’re far more likely to see a physiotherapist, an osteopath or chiropractor, an acupuncturist, a massage therapist.

Furthermore, in groups of people who do see a psychologist about their pain, at least in New Zealand, they’ll also most commonly be seeing other clinicians such as physiotherapists or occupational therapists – and a consistent approach is vital.  It only takes one clinician to reinforce an unhelpful belief for the work of the team to be undermined.

I also argue that the best time and place to work on reality testing unhelpful thoughts and beliefs is when people are doing things they’re worried about – in other words, when they’re working on movements, discussing work, developing an exercise programme, working on how they might do household activities, sports and so on.

Yes, psychologists have specialist training in working with thoughts, beliefs and emotions.  Occupational therapists, physiotherapists and other allied health clinicians are always influencing thoughts, beliefs and emotions.  To think we don’t is to ignore the incredibly powerful influence we wield almost because we tend to do it indirectly.

I argue that if we have an influence on people, we need to develop that skill so we can influence positively and helpfully.  In the case of catastrophising, I don’t think we need to become psychologists – that would devalue the other aspects of our various professions.  I do think we need to look at what we say, how we say it, and how we work with people within our professional scopes to maximise the benefit of our input.

What can we do to influence catastrophising?

Here’s another Healthskills Advice for Non-Psychologists working with people who tend to catastrophise!

  1. Find out what the person thinks is going on, and how they’ve arrived at this belief – listen well and with empathy.
  2. Empathise – say something like “It sounds like this is really scary/worrying/hard to handle.”
  3. Ask if it’s OK to give them your perspective – most of the time people will say yes, but asking gives you their permission to provide new information, and they’ll be more willing to listen.
  4. Use calm, neutral language to give an evidence-based explanation – keep it simple, and beware technical language that can be misinterpreted!  For example, an “unstable back” might be your technojargon for poor recruitment of muscles, but your patient may well have an image of their back breaking or collapsing if they move. Don’t you DARE give them a theoretical explanation that has no evidence in the peer-reviewed literature. EVER.
  5. Check out what they’ve heard.  You can ask them “Can you tell me how what I’ve just gone through might mean to you?” or “Can you let me know how that might apply to you?”.
  6. Listen to their response.  Reflect back to them your understanding of their interpretation.  This may seem repetitive, but it’s so important for people to know that you’re listening to them.
  7. Check if they have questions or doubts.  Listen to these without interrupting or saying they’re wrong.  These are their beliefs!
  8. Ask them if they’re willing to test your interpretation out, or how they might test their own interpretation.  You can ask them “how likely is it that this is true?”, “what makes you think this will happen?”, “what’s the most likely thing that will happen?”, “what does it mean if this happens?”.
  9. Set up an opportunity to test their interpretation (or your new one, if they’re prepared to).  This is in the nature of a mini-experiment – so if they think they will get stuck on the ground if they try to get down, see if they’ll do so while you’re there.  Be prepared for qualifiers – “oh but it didn’t happen because you were there”, so make sure you point out what they did to manage.
  10. Finally, make sure you convey confidence that, even though they are worried about “the worse thing happening” – you know they will get by.  They’re not asked to enjoy the process of getting by – but they can manage, and the catastrophe is averted. If pain increase is their personal catastrophe, it’s likely the belief that they “can’t cope”, or not liking the negative consequences of having an increase in pain (feeling irritable, wanting to rest, having to work with pain the rest of the day) that is the problem.  And managing that is for my next post!

It’s worth remembering Mark Twain’s comment: “I’ve had a lot of problems in my life and most of them never happened.”

Ciccone DS, Chandler HK, & Kline A (2010). Catastrophic appraisal of acute and chronic pain in a population sample of new jersey national guard troops. The Clinical journal of pain, 26 (8), 712-21 PMID: 20664336

Pain behaviours persist…
I’m taking a tiny detour from the world of catastrophising – but only a tiny one because catastrophising is associated with greater levels of pain behaviour, and of course, discussion about pain behaviour is how I came to begin my exploration of catastrophising anyway!

There have been several schools of thought, or models of treatment, for people with pain.  While the current focus and the one over the past five to ten years or so has been strongly cognitive in focus (let’s help people understand their thoughts about pain and how these influence emotions and subsequently affect behaviour), well before then in the origins of pain management, a behavioural approach dominated.  Wilbert Fordyce is credited with developing the first pain management programme based on modifying what people do in response to pain rather than working to reduce pain itself.  (Here’s a link to one of his papers)

I’m a bit of a fan of behavioural approaches because to me the true test of a treatment is whether the person begins to do “normal” things again – go out and have fun, return to work, be with family and so on.  They also seem to be effective – for example, graded exposure is very effective for pain-related anxiety and avoidance.

In this study by Martel, Thibault and Sullivan (2010), people with back pain were recorded on two separate occasions (on averge 22 days apart) while carrying out two lifting tasks designed to elicit pain behaviours.  These recordings were reviewed by trained observers who recorded the number of pain behaviours in each segment of film using a standardised coding scheme (developed by Keefe and Block, 1982).  Participants in the lifting tasks also completed a range of questionnaires – the Tampa Scale for Kinesiophobia, the McGill Pain Questionnaire, and the Pain Catastrophising Scale.

Before I describe the findings, in this study two different forms of pain behaviour were identified – communicative behaviours are things like grimacing, speaking, sighing, moaning and so on; while protective behaviours are things like guarding, holding, touching, or rubbing.

What the researchers found was that pain behaviours are pretty stable irrespective of sex, pain severity or psychological characteristics, but that different forms of pain behaviour demonstrated different degrees of stability.

  • Pain behaviours identified as primarily about communicating were more stable from time one to time two than those identified as being mainly about protecting the body part.
  • Women’s protective pain behaviour varied more than men’s protective pain behaviour, while both men and women demonstrated stable communicative pain behaviour.
  • Pain severity and the number of pain behaviours varied consistently – but, interestingly, individuals with higher levels of pain behaviour at time one also demonstrated higher levels of pain behaviour at time two irrespective of pain intensity.
  • Significant positive relationships were found between psychological variables such as catastrophising and fear of movement and pain behaviours.  Even more interesting was that even when changes in catastrophising and fear of movement reduced over time, pain behaviours remained consistent.

What do these findings mean?I think they suggest that giving information, educating or even working hard on cognitive aspects of coping may not change the behaviours that signal to other people “Hey! I’m sore!”.

This could be because of long-standing motor patterns that take a while to change, or actually need to be deliberately replaced with new or different patterns.

It could also be because behaviours are reinforced by other people – and as a result of intermittent reinforcement being so effective at strengthening behaviour, pain behaviours may persist.

Whatever the underlying reason for this finding, I’m sure we need to direct our focus more on specifically addressing pain behaviours in the future.

Martel, M., Thibault, P., & Sullivan, M. (2010). The persistence of pain behaviors in patients with chronic back pain is independent of pain and psychological factors Pain, 151 (2), 330-336 DOI: 10.1016/j.pain.2010.07.004

Catastrophising and pain (i)
One reason I love blogging is the discussion between me and readers. I wrote about the language of pain recently, and out of that discussion I’ve spent a few days digging around the literature to look at what is known about the relationship between language, pain and catastrophising. I’d argued in my post that metaphoric language can reflect distress both in the communicator and the listener, and that this is supported by fMRI studies in which various parts of the brain are activated when emotion-laden communication about pain is being carried out, while one of my readers thought I might be taking this interpretation too far.

Pain behaviour
My reason for being interested in how we communicate about pain is that talking about pain (including describing it) is a pain behaviour. Pain behaviours are a range of behaviours that occur when we are sore and seeking help, and can include voluntary and involuntary actions. There can be an assumption that people are fully aware of the behaviours they do in relation to pain, so when a person demonstrates a lot of pain behaviour some clinicians believe the person “must” know that this is what they’re doing. This is sometimes the case, but there are numerous factors that can influence the behavioural responses we have to an experience of pain.

Pain behaviours occur on a continuum, however, from involuntary such as the withdrawal reflex, through more voluntary actions such as swearing (yes, it does seem to help!) and ultimately to very complex behaviour such as seeking treatment for pain.  And from an evolutionary point of view, pain behaviours are there primarily to communicate to others that we need or want help.

Pain behaviour and catastrophising
There is a relationship between catastrophising, or “an exaggerated negative “mental set” brought to bear during actual or anticipated pain experience” (Sullivan, Thorn, Haythornthwaite, Keefe, Martin, Bradley and Lefebvre, 2001), and pain behaviours – including verbal reports of pain intensity, seeking treatment including hospital stays, use of medications, and has been posited as one reason health professionals may pursue more intensive and invasive approaches to pain assessment and treatment.  Catastrophising is thought to influence the ways in which people interpret their pain – there are several theories identifying how this might occur.  But first, let’s have a look at how catastrophising is identified.

Measuring catastrophising
As I’ve mentioned in an earlier post, there are several pen and paper measures of catastrophising.  Questionnaires are simply standardised, or repeatable sets of questions that have been tested and thought to measure some underlying concept – they’re not “x-rays of the mind” and while they’re helpful and allow researchers and clinicians to do statistics on the findings and establish how similar or different one person’s answers are from “the rest”, they are based on language.  The words and phrases that people use reflect the way they interpret a situation, and while the actual wording differs depending on the vocabulary the person commonly uses, the way the person appraises or judges a situation underpins what they say.

There are several problems levelled at questionnaire measurement of catastrophising.  Because catastrophising as a concept is “invisible” – we can’t measure it directly and have to use statements that are believed to be associated with it – some critics have identified that the Coping Strategies Questionnaire, for example, might confuse measurement of catastrophising with measurement of depression.  Others have suggested that catastrophising is so closely related to fear of pain or anxiety or even perceived disability that it might not be worth measuring it as a distinct entity.  The conclusion currently, however, is that catastrophising is a distinct concept, and the most favoured assessment tool is the Pain Catastrophising Scale.

This scale has been found to have three subscales – rumination (or “repetitively (and passively) focusing on the symptoms of distress, and on its possible causes and consequences” – thanks to Wikipedia), magnification, and helplessness.

Three possible theories
Appraisals – Lazarus and Folkman proposed a general model of the ways people respond to situations. Primary appraisal involves determining whether a situation represents a threat, positive or irrelevant. Secondary appraisal involves determining coping options and likelihood of success. The PCS magnification and rumination subscales might form part of primary appraisal, while helplessness might be related to secondary appraisal.
Attention – People who demonstrate elevated levels of catastrophising also seem to focus on pain more than those with lower levels. This suggests that one of the pathways from catastrophising to the experience of pain might be via hypervigilance, or increased tendency to quickly attend to pain – and from there to negatively appraise pain as something difficult to deal with.
Coping – One form of coping is to obtain help from other people. A model that could explain the usefulness of catastrophising might be that by communicating distress, help might be obtained from other people, so that the individual doesn’t have to cope alone. The experimental and clinical evidence supporting this function of catastrophising, as demonstrated through pain behaviour and verbalisations, seems to be reasonably compelling – and my thoughts are that one way in which catastrophising language “works” is through empathy, which itself seems to be related to those darned mirror neurones.

The question nonpsychologists might have is – so do I need to use the PCS to identify people who catastrophise? And if I know someone tends to catastrophise, what does it have to do with me?

And that is for another post, so y’all come back now!

Sullivan MJ, Thorn B, Haythornthwaite JA, Keefe F, Martin M, Bradley LA, & Lefebvre JC (2001). Theoretical perspectives on the relation between catastrophizing and pain. The Clinical journal of pain, 17 (1), 52-64 PMID: 11289089