tanglewood

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


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

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

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

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

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

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

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

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

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

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

Well and good. What does it actually mean?

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

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

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

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

 

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

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

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

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

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

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

One comment

  1. CS is a loaded expression, with most practitioners reaching for a copy of the DSM and implications of somatisation. It is however far more than a subjectively amplified response – exemplified by the second most likely manifestation of headache/jaw pain. TMJD is visible, the bruxism which breaks teeth isn’t anxiety. Think of the clenching induced by MDMA/eccys and the association with catecholamines reported by Vanderas.
    Medicine has a problem with spectral disorders involving dysregulated endocrines and HPA axis, loosely described as syndromes. Hierarchial taxonomies are less favoured than diagnostic definitions for disease – even when pathognomonic exactness is under challenge! ACR Editor Gary Firestein’s 2014 article ‘The disease formally known as RA’ reflects these changes. The patients also dislike being boxed into a category that devalues their symptom reports.

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