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.
HealthSkills Blog 
Bronnie, as one who was present at the birth of the term “nociplastic”, I am well qualified to comment on your blog.
Unfortunately, “nociplastic” has been high-jacked.
If you are wondering how this happened, the details can be found by following this link:
Language, words, classifications all have a life of their own. I’m well aware of the controversy over this term, having read Cohen’s position. Nevertheless, the term is in use and clarifying how it might be fruitfully employed is my intention in this blog. As ever, I am a pragmatist.
Bronnie, it was indeed our intention that the term “nociplastic” be fruitfully employed.
But, as you correctly point out, “language, words and classifications all have a life of their own”.
In fact, in our recently published paper – Pain is not a “thing”: how that error affects language and logic in Pain Medicine – we identified a need to clarify much of the language used in Pain Medicine.
The sooner this is done, the better it will be for all concerned.
At the moment, John Bonica’s analogy of the “Tower of Babel” holds true.
I will add, though, that none of the mechanistic descriptors are diagnoses. They simply collect together a number of different pains that appear to have similar underlying mechanisms – eg neuropathic pain is not a diagnosis, but neuropathic pains have “an identifiable lesion or disease of the somatosensory system”.
I’m not calling pains that have as-yet unexplained mechanisms “syndromes” and neither do I agree with the language identifying “nociceptive pain” is not present – or the “out of proportion with” because these not only use “pain” as a “thing” but also suggest that there is some kind of direct relationship between mechanisms in the tissues and the “proportionate” response we describe as pain.
BUT for simple folks, such as me and many other clinicians, these terms are in common use and won’t die out. Let’s make the most of what they do offer us, and let the semantic debates occur outside of this forum (my blog) and where they might influence more important commentators – such as the journal Pain.
Another great post, yet the proposed algorithm builds on false assumptions about the uniqueness of symptoms to a thought-to-exist mechanism (Letter to the editor in PAIN in press). I would suggest not to apply it since it creates an arbitrary separation between patients. Instead I suggest to treat all patients like you describe.
They do acknowledge the need for validity/reliability etc and I agree also that ALL people with pain should have individualised treatment from a multidisciplinary team (preferably interprofessional team). I don’t know that the authors think there is a single mechanism (pretty much as there isn’t a single mechanism for neuropathic or inflammatory pains), and the bit I don’t like is that assumption that cognitive fog/sleep disorders/sensory sensitivity are always part of this group, and I don’t know that this is so. We don’t have data to show this.
I’ve articulated the two things I hope it will stop – or the ICD-11 Chronic Primary Pain diagnosis should. And I really do hope QST shows more promise than it currently does (or there are some alternative testing procedures that will be developed).
It’s challenging because we all know there are people experiencing pain that doesn’t follow the rules of nociceptive, inflammatory, or neuropathic pain – and this descriptor isn’t clear or parsimonious – I’m just hoping to clarify something about it for the clinicians who will be reading about it, getting utterly confused, and possibly making the mistake of “blaming” the person who hasn’t got better when they “ought to”.
I know you know this!
Thanks for stopping by!
I agree (as you know 😉) and trying to make nociplastic the new “CS-syndrome” is unhelpful at best. The mechanisms behind nociceptive and neuropathic pain are quite well understood and still we cannot fully predict what the look like clinically. So, let’s be realistic and just say that nociplastic is a way to acknowledge that we don’t know it all, and that this should not stop us from understanding the patients.
Best, Morten
Absolutely – using CS as a comprehensive explanation isn’t helpful. Clarifying exactly what we mean by CS (as Woolf did so well) is crucial – and then distinguishing between one mechanistic group and another are two crucial steps. The other thing that worries me (there are a few!) is whether the criteria are exclusive to this group. I doubt they are.
Wait for the next exciting instalment on the blog!
Morten, in the interests of fairness, I have extracted the following paragraphs from Professor Milton Cohen’s Letter to the Editor of PAIN in response to the paper by Kosek et al. 2021. Milton was a member of this IASP taxonomy committee but withdrew his name when he was unable to accept what was then the consensus view. His objections were as follows:
In the introductory paragraph, the authors seek to distinguish between “nociplastic pain,” “central sensitisation of nociception,” and “chronic primary pain”4 but succeed only in conflating them.
There are 2 classic examples of the fallacy of begging the question:
• (1) “Chronic pain conditions such as fibromyalgia, CRPS type 1, and irritable bowel syndrome are examples of pain conditions where nociplastic pain is typically present.”
• (2) “The latter is reflected in the ICD-11 classification of chronic pain into primary, pain as a disease, and secondary, pain as a symptom, where most, if not all, of the primary pain subgroups consist of conditions with nociplastic pain.”
Hence, even before the clinical features that might lead to the identification of presumed nociplastic pain have been proposed, let alone settled, it is asserted that one can identify conditions in which it occurs typically and that “chronic primary pain” is essentially synonymous with “nociplastic pain.”
To be fair, the authors do state, “However, it must be recognized that the terms reflect different dimensions as ‘nociplastic’ is a mechanistic term, while ‘primary pain’ is a diagnostic concept, therefore they cannot be regarded as synonyms.”
Nonetheless they ignore their own admonition by claiming to diagnose “typical” examples of nociplastic pain by invoking features that are not related to nociception.
This would be analogous to defining angina pectoris by invoking the presence of anxiety.
Such conflation of a taxonomic concept (primary pain), a hypothesis of mechanism (nociplastic), and clinical diagnosis (“typical” conditions) is unacceptable logically, biologically, and clinically and serves only to confuse the main issue.
That issue is, how can one clinically infer that altered nociceptive function has occurred, in the absence of evidence of nociceptive pain (as defined) and of neuropathic pain (as defined)?
This can be achieved only by reference to features of the pain and associated phenomena directly related to nociception. These are found in the authors’ other 3 sets of criteria:
• (1) The pain is chronic, regional in distribution, and not explainable by a nociceptive or neuropathic process.
• “(2) There is a history of pain hypersensitivity in the region of pain.”
• “(4) Evoked pain hypersensitivity phenomena can be elicited clinically in the region of pain.”
Regarding “pain hypersensitivity,” the key criterion is #4, although why it is demoted in the list is strange.
New concepts in the science underpinning nociception and the practice of pain medicine require careful explication and step-wise logical development, not conflation and circular argument. To include clinical features that are unrelated to nociception in the identification of a descriptor of pain is a major epistemological error.
Reference: Cohen ML. Proposed clinical criteria for nociplastic pain in the musculoskeletal system are flawed. Pain 2022;163(4):e606-e607. doi: 10.1097/j.pain.0000000000002505
Absolutely, John Q – the next instalment on this blog will attempt to tackle this for clinicians. We can’t unring a bell and both the term central sensitisation AND nociplastic exist in clinical conversations right now. I think the best we can do is argue for caution about what these terms mean for treatment, and to be wary of assuming anything. We simply don’t know the mechanisms involved, and we need to be humble about this. We can conjecture – but this doesn’t help clinicians who are meeting people with “weird” pain every day.
Pragmatically, my strategy is helping clinicians reconsider the utility of “diagnosis” and “classification”. Case formulations help people tease out what matters to people with pain, the hypothesised antecedents and consequences, and offers options for helping the person, in the context of a therapeutic relationship built on trust and empathy. Something I’ve been hammering on about in this blog for many years.
Diagnoses, unless there’s a known causal mechanism (or set of) with a known response to treatment, offer more to clinicians in terms of shared language than anything else. And in most persistent pains, diagnoses don’t offer even this.