In July this year a group of researchers published a paper (open access) in Pain asking if we need a third mechanistic descriptor for chronic pain states. It was an interesting read, and here are some of their main points …
A bit of history
Currently the IASP taxonomy provides two classifications of pain states:
Neuropathic pain – pain caused by a lesion or disease of the somatosensory nervous system
Nociceptive pain – pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors.
This definition of neuropathic pain is relatively new, amended in 2011. The previous 19994 definition included ‘pain initiated or caused by a primary lesion, dysfunction, or transitory perturbation of the peripheral or central nervous system’. Notably, the word dysfunction has been removed and the system is now referred to as the somatosensory nervous system. It was thought that the previous definition was limited in its ability to distinguish neuropathic pain conditions in a clinically meaningful way.
‘The clinical challenge is to identify and ameliorate the cause(s) of the pain, which may be tissue damage, damage to the body’s warning system, both, or neither. We are not doing the patients any good by giving them a diagnostic label for which there is no basis.’
So what’s the problem?
Not everyone is happy. This new definition has left a large group of patients without a valid pathophysiological descriptor for their experience of pain.
Not only does it miss those with lesions in areas outside the somatosensory nervous system (i.e. the cerebellum or frontal cortices) but notably it also misses those whose pain is not due to neuropathy but for whom activation of nociceptors also cannot be confidently established – i.e. fibromyalgia, musculoskeletal pain (such as non-specific back pain) and visceral pain disorders (such as irritable bowel syndrome, bladder pain syndrome).
What to do with the gap
This gap has led to the pain of some groups being termed ‘idiopathic’ or ‘pain of unknown origin’, and some are calling to reinstate the 1994 definition, saying that this new definition of neuropathic pain is too restrictive and has the potential to suffocate new research. However, others don’t agree. They are happy to accept the new definition, but believe it warrants a third category to fill this caveat.
Some interesting suggestions come from a 2016 paper by Kosek et al.
‘It is proposed that a new term be introduced to describe pain states characterised by clinical and psychophysical findings that suggest altered nociception, despite there being no clear evidence of actual or threatened tissue damage causing the activation of nociceptors or evidence for disease or lesion of the somatosensory system causing the chronic pain.’
So here are their suggestions:
Nociplastic: arising from ‘nociceptive plasticity’ to reflect change in function of nociceptive pathways.
Algopathic: which combines ‘algos’ (Greek for pain) with ‘pathic’ (Greek for suffering) to reflect a pathological sensation of pain not generated by injury.
Nocipathic: from ‘nociceptive pathology’ to reflect a pathological (ie. not “normal”) state of nociception.
Note: The terms are intended for clinical usage and are neither a diagnosis nor a synonym for ‘central sensitisation of nociception,’ which is a neurophysiological concept.
So do we need a third descriptor? Although these pain conditions have unexplained mechanisms, should we still provide them a mechanistic category more defind then ‘idiopathic‘? And if so, do any of these suggestions float your boat?
– Hayley Leake
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Yes, it is obvious to me that we do need a third pain descriptor. I favour the term “nociplastic”.
I like “nociplastic” too. The others are a bit scary and the “plastic” in it suggests changeability
I think narrowing pain down to the somatosensory NS and nociceptive signaling might be reflective of overlooking a few things:
Pain and Stress in a Systems Perspective
Reciprocal Neural, Endocrine and Immune Interactions
C. Richard Chapman et al
J Pain. 2008 Feb; 9(2): 122–145.
Published online 2007 Dec 21. doi: 10.1016/j.jpain.2007.09.006
If you missed this article:
I’ve been having a debate in my head about these classifications for a while and I don’t think any of them are really appropriate as the previous comment says, they narrow the issues down. Also pain is such an individual experience.
Pain is what a person says it is. You could argue that giving it a label such has neuropathic or nociceptive could increase the threat. Why can’t we just call it pain? Given that nerves transmit a danger signal, not a specific pain signal, are any of these categorisations still valid? Forgive my naivety here but are there different types of danger signal that the brain interprets differently? It’s surely a lot more complex than any of these categorisations suggest?
Are we talking about having a different classification for acute and long-term pain perhaps? In terms of long-term pain couldn’t we describe it all as (technically) neuropathic as it is down to changes in the nervous system? In this respect I would prefer to use ‘neuroplastic pain’. As David says, including the term ‘plastic’ gives hope whereas ‘pathic’ doesn’t.
As part of this ongoing debate with myself I’ve been asking why does the brain make different types of pain – does the pain we get from putting our hand on a hot plate feel like a ‘burning’ pain because the brain sees the hot plate as ‘hot’? The influence of language, perhaps?
The pain of a MSK injury is generally different from that of a ‘tweaked’ nerve but why? Why do we need different types of pain? If it’s to get a more accurate message across having weighed up the whole scenario how come we humans have similar pain experiences when we put our hands on something hot or after intensive exercise for example? Could that be down to expectation, anticipation, learning or conditioning into thinking pain of this kind ‘should’ feel like this?
If we need different types of pain in order to get a more accurate message and each of us has individual, diverse experience bases to draw on in the process of creating this experience, it is pretty miraculous that we, in general, describe different pains reasonably consistently. Perhaps it is these classifications themselves that have shaped these experiences/descriptions?
I have to admit I rarely take notice of these classifications anyway. I would rather listen to the individual’s story and take it from there. Personally I don’t see the point in having them.
I could go around and around for a long time on this! 🙂
I think such reductionist descriptors are probably inevitable and useful, as long as they are accurate and ‘functional.’ The basic reasoning would be for directing research, education, communication and directing treatment/rehabilitation, as examples.
Having said that, I would tend to agree with Marcel above. One only need to glance at the content of the reference he provides, and perhaps sense a bit of a gap between our level of knowledge regarding pain and the current definitions?
If we are moving to a predictive processing model of pain through the SNH, as Tim has argued previously and I suspect he is right, these definitions are likely to keep undergoing further revisions?
“Centralized” has been nominated as yet another potential third descriptor to be used in the context of fibromyalgia. Here is the link to the discussion on this topic: http://www.fmperplex.com/2016/08/23/why-centralized-is-unacceptable-as-a-descriptor-for-the-pain-of-fibromyalgia/
For those interested.
From Nature Outlook: free access to 10 recent articles on pain including some words of L. Moseley in the art. Biomedicine. Patient centered views in ”
Neuropathy: A name for their pain” and more.
“Nature Outlook is available free online for six months and provides clear, concise articles on pain research. It tackles the hottest areas of scientific, clinical and societal research, giving you an inside view of the latest developments within the field of pain.”
“Central pain disorders ” might be an option?
Pain hypersensitivity mechanisms at a glance
Vijayan Gangadharan, Rohini Kuner
Disease Models & Mechanisms 2013 6: 889-895; doi: 10.1242/dmm.011502
Marcel, the term “central” refers to an anatomical site. But we now know that there is no such “pain centre” within the brain (or within the body). Nevertheless, how would you operationalise your suggested third descriptor for clinical purposes?
John, I know. Actually I realise now, that term from the ref. “Central pain disorders (: conditions caused by damage to or dysfunction of the CNS)” isn’t a good one.
Just found this extensive publication in Neuron you might be interested in, that’s if you haven’t read it already.
“Nociception, Pain, Negative Moods, and Behavior Selection”
Marwan N. Baliki, Vania Apkarian
Thought this applies here (from the article) :
quote Christof Koch: “We must resist the hypnotic appeal of hot spots in brain scans with their naive phrenological interpretation: the perception of faces is computed over here, pain over there, and consciousness just yonder. Consciousness does not arise from regions but from highly networked neurons within and across regions”