Towards the end of 2017, IASP put forward a new mechanistic classification: nociplastic pain. The definition is: “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.
Note: Patients can have a combination of nociceptive and nociplastic pain”.
This was great news! Prior to this, the term “central sensitisation” was used and abused to describe processes involved in ongoing pain that wasn’t inflammatory or neuropathic. Problem with that term is that it’s apparent in nociceptive mechanisms, as well as both inflammatory and neuropathic…. When the way people used the term was more akin to “well, the pain hasn’t settled down, so ‘something weird’ is going on and it must be in the central nervous system so we’ll adopt this term seeing as Clifford Woolf described it in the spinal cord” (Woolf, 1996, 2007).
In other words, any pain that seemed to radiate, hang around, and no respond to treatment was “centrally sensitised”. Perhaps so. Perhaps not. Suffice to say, people got confused because most of the typical central sensitisation from nociceptive/inflammatory processes subsides over time, but these “centrally sensitised” pains did not.
I, for one, am glad there’s a group in which weird pains that don’t appear to involve typical nociceptive, inflammatory or neuropathic mechanisms can be put.
Problem is: how do we know what fits into this group? We can be pretty certain when it comes to neuropathic pain, because the definition is very clear (though not so clear in the clinic) – “Pain caused by a lesion or disease of the somatosensory nervous system.” The notes go on to say that “neuropathic pain is a description, not a diagnosis” and I’d say the same about nociplastic pains (which is why I use the plural…). I also step out to say that I don’t think ALL nociplastic pains will be found to have the same biological mechanisms, especially given how widely variable neuropathic pains are.
Nevertheless, we need some way to decide which pains are in, and which are out of this group.
This table comes from Kosek et al., (2021) and summarises the findings from a consensus process within an expert group. They make the point that acute pain isn’t helpfully included in this group, and instead it should be used for pains that persist for 3 months or longer. They also point out that regional pain is included while discrete pain is typically not because of the central sensitisation processes involved (note: this is the correct use of the term! Confused? CS is a neurophysiological phenomenon, associated with more than nociplastic pain).
Looking at the above criteria, possible nociplastic pain is present if the person has criteria 1, and criteria 4. Probable nociplastic is present if the person has all the above.
There are some notes, of course: regional means the musculoskeletal pain is deep, regional or in several places or even widespread (not localised to one place), and each condition eg frozen shoulder and OA knee needs to be assessed separately. If there is an identifiable nociceptive source (or neuropathic source) then the pain needs to be more widespread than “usual” for that pathology. Finally, because nociplastic pain unlike neuropathic pain, has no definitive test currently, there is no “definite nociplastic” category – but once there is, this will be added.
What does this mean for us as clinicians?
Firstly it ought to stop people being thought as faking, malingering or otherwise not being believed. That should be a given but unsurprisingly because of legal and health systems and our own frustration at not being able to “fix” people, people with pain get that impression more often than they should. It also ought to stop psychopathologising people who have this kind of pain: we can’t distinguish between people with nociplastic pain and the DSM5 “Somatic Disorder” – so let’s just not add another unhelpful mental health label to what is already a stigmatised situation.
Then it ought to stop clinicians using treatments that simply don’t help – such as opioids for fibromyalgia. It might help clinicians pause before prescribing movement therapies at a level that is too intense for the person, because this only revs the nervous system up even more making the whole process unpleasant. Beginning at the level the person can manage and gradually increasing is crucial to success. And it ought to stop clinicians from administering “explanations” or “education” and expecting that alone to reduce pain. Because while cortical processes are part and parcel of every pain there is, it’s in this group of pains that some people think “top down” by thinking yourself out of pain is a thing. FWIW pain reduction is lovely and part of treatment, but shouldn’t ever be the only outcome (Ballantyne, 2015), and many times in this group of pains, may not even be an outcome.
Finally, it should stimulate helpful discussion about what “whole person” approaches to managing these pains looks like. The authors say “patients with nociplastic pain are likely to respond better to centrally than peripherally targeted therapies” and this does not mean talk therapy alone, or exercise alone, or indeed medications such as gabapentin or nortriptyline alone. To me, it means individualised, tailored, and integrated strategies to moving, managing daily life, restoring sleep, enjoying an intimate relationship, managing mood and memory, and these might best be offered by pain coaches rather than siloed “therapies” of physical, psychological or whatever other stripe there is.
Ballantyne, J. C., & Sullivan, M. D. (2015). Intensity of Chronic Pain — The Wrong Metric? New England Journal of Medicine, 373(22), 2098-2099. https://doi.org/10.1056/NEJMp1507136
Kosek, E., Clauw, D., Nijs, J., Baron, R., Gilron, I., Harris, R. E., Mico, J.-A., Rice, A. S. C., & Sterling, M. (2021). Chronic nociplastic pain affecting the musculoskeletal system: clinical criteria and grading system. Pain, 162(11), 2629-2634. https://doi.org/10.1097/j.pain.0000000000002324
Woolf, C. J. (1996). Windup and central sensitization are not equivalent. Pain, 66(2), 105-108.
Woolf, C. J. (2007). Central sensitization: uncovering the relation between pain and plasticity. The Journal of the American Society of Anesthesiologists, 106(4), 864-867.