Why “Centralized” Is Unacceptable As A Descriptor For The Pain Of Fibromyalgia

Why “Centralized” Is Unacceptable As A Descriptor For The Pain Of Fibromyalgia

The search is on for a third pain descriptor for chronic pain that is more appropriate for the large group of people whose pain is not associated with tissue damage (i.e. “nociceptive pain”) or with demonstrable nerve damage (i.e. “neuropathic pain”).

A recent article in the prestigious journal PAIN outlines the need for such a third descriptor and suggests the following candidates: “nociplastic”, “algopathic” and “nocipathic” [Kosek et al. 2016].

It is important to recognise that these descriptors are not diagnoses, just as “pain” itself is not a diagnosis. However they are intended to imply underlying neurophysiological mechanisms.

But another candidate has recently appeared upon the scene – “centralized pain” [Clauw 2014]. In this context, centralized refers to “central nervous system origins or amplification of pain”. Given that pain as an experience always originates from within the nervous system, and that pain is not a “thing” that can amplify itself, this proposition does not make sense.

The term “centralized” can refer only to an anatomical location within the central nervous system. Not only does the word itself not imply a mechanism but also it creates potential for confusion with conditions such as “central post-stroke pain” (which is technically “neuropathic”) and quite different from the phenomena that underlie Fibromyalgia.

Therefore “centralized” has no legitimate place as a descriptor for pain.

 

John Quintner & Milton Cohen

 

References:

Clauw DJ. Fibromyalgia: a clinical review. JAMA 2014; 311(15): 1547-1555,

Kosek E, Cohen M, Baron R, et al. Do we need a third mechanistic descriptor for chronic pain states? Pain 2016; 157(7): 132-186.

13 Comments

    • Thanks for your suggestion. “Maladaptive” is not an adjective I would choose as a descriptor for pain as it has the potential to stigmatise the sufferer. Can you come up with another word that might be more appropriate than any of the three words currently on offer? For the record, my preference is “nociplastic”.

  1. Interesting perspective, thank you. I do not like the term central sensitisation as little as I like the whole concept of implying that once a patient can understand the pathways of pain, that that in itself is somehow supposed to change the pain. Or put simply, by changing a person’s understanding of how their system has become over sensitive to pain they in turn might experience less pain! It doesn’t make sense to me. Pain is the message to tell the patient that they are doing something wrong, that they are either not moving properly or not moving enough or more often a combination of the two. I find that fibromyalgic patients have lost sense of what is the ‘normal’ sensation of movement. They find tiredness or muscle soreness after exercise threatening. There is a psychological process occurring rather than a neuro-physiological one, although the former probably results in the latter. The language that I use in my Physiotherapy approach with my patients reflects my own belief in keeping things simple!I am most interested in this subject and find any conversations around pain useful so thank you again for posting.

    • Louise, I heartily agree with the first part of your comment.

      However, I do not share your belief about “pain” in these patients.

      Since 1993, Milton Cohen and I have foregrounded “central sensitization of nociception” as being a key concept in the understanding of fibromyalgia.

      In 2011, together with Dr Pamela Lyon, we published our hypothesis for Chronic Widespread Pain (aka fibromyalgia).

      Let me quote from our conclusion:

      “Drawing on diverse findings in neurobiology, immunology, physiology, and comparative biology, we suggest that the form of central sensitization that leads to the profound phenomenological features of chronic widespread pain is part of a whole-organism stress response, which is evolutionarily conserved, following a general pattern found in the simplest living systems.”

      Our hypothesis has not been challenged. Of more importance, it has broken out of the circularity that typified the ongoing debate since the 1990 ACR Classification Criteria were first promulgated. Moreover, it transcends the seemingly endless either/or body/mind argument that so coloured the literature and stigmatized so many patients.

      References:

      Cohen ML, Quintner JL. Fibromyalgia syndrome, a problem of tautology. Lancet 1993; 342: 906-909.

      Lyon P, Cohen ML, Quintner JL. An evolutionary stress-response hypothesis for chronic widespread pain (Fibromyalgia Syndrome). Pain Medicine 2011; 12: 1167-1178.

  2. A vigorous debate is now taking place in the journal PAIN over the choice of a third pain descriptor. Here are the views of those who champion “centralized”:

    Title: “We agree with the need for a new term but disagree with the proposed terms”

    Letter To Editor:

    We applaud Kosek et al. for their article entitled “Do we need a third mechanistic descriptor for chronic pain states?” The article does a very nice job of laying out the reasons why such a category is needed and why previous terms such as “idiopathic” or “functional” are inappropriate and even misleading.
    However, we strongly disagree with the terms they propose. As a research group that has been studying these conditions and this phenomenon for several decades, we feel it would be far better to consider terms that are already in widespread use and that give clinicians a sense of where this pain originates. Such terms that are now being widely used include “centralized pain” (our preferred term), central sensitization, and central hypersensitivity—none contain the pejorative tone that previous terms have conveyed. Some pain researchers might understand the terms that these authors propose (ie, nociplastic/ algopathic/nocipathic), but these terms are entirely new and have no precedence. Even more troubling, they share the same mechanistic vagueness of the terms they are meant to replace. It just does not seem necessary to invent new jargon when almost any descriptor that includes the word “central” will be much more likely to be understood by nonpain specialists. The authors encourage discussion about this topic—let the debate begin.

    Conflict of interest statement: The authors have no conflicts of interest to declare.

    Chad Brummett Daniel Clauw Richard Harris Steve Harte Afton Hassett David Williams
    Department of Anesthesiology, University of Michigan,
    University of Michigan Chronic Pain and Fatigue Research Center, Ann Arbor, MI, USA
    E-mail address: dclauw@umich.edu (D. Clauw)

    Reference
    Kosek E, Cohen M, Baron R, Gebhart GF, Mico J-A, Rice ASC, Rief W, Sluka KA. Do we need a third mechanistic descriptor for chronic pain states? PAIN 2016;157:1382–6.

  3. Reply by Kosek et al. (2016)

    Letter To Editor:

    We welcome the positive engagement with this issue from Dr Brummett et al., especially their concurrence with our proposition that a third mechanistic descriptor for chronic pain states is indeed required.

    We take the point made by Dr Brummett and colleagues that they would prefer terms already in circulation to the ones we suggested. Our first comment in response is to note that consistent with the precedent set by “nociceptive” and “neuropathic,” a descriptor must be an adjective. That would exclude “central sensitization” and “central hypersensitivity” which are qualified nouns.

    Their preferred term is “centralized pain” or, to be consistent, the descriptor “centralized.” Our problem with this is that “centralized” is in a different category from “nociceptive” and “neuropathic.” Both of these latter 2 descriptors incorporate hypotheses of causation that are physiological-based, one referring to activation of nociceptors and the second identifying altered nerve function caused by a lesion or a disease of the somatosensory nervous system.

    By contrast, “centralized” is an anatomically based term and does not incorporate a hypothesis of pathogenesis. Furthermore, the term “central” would imply that all “nociplastic/ algopathic/nocipathic” pains were only central in origin, an assumption that is not justified.

    Having said this, we do not dispute that the underlying mechanism of most cases of the category of chronic pain in question is likely to be central sensitization (or central hypersensitivity) of nociception or nociceptive pathways. The quest then becomes etymological, namely to find an adjective that incorporates this hypothesis of causation. Given that central sensitization of nociception is considered to reflect plasticity in nociceptive pathways, the challenge is to find a word that indicates the specificity of this change in function.

    In the absence of existing alternatives, especially words in the same category as “nociceptive” and “neuropathic,” the search for a term led us to explore neologisms, the derivation of which is described in our article.

    Drs Brummett et al. are concerned that this has “no precedence,” but it is not unprecedented for new phenomena to require new words, “television” springs to mind.

    The phenomenon of a clinical state in urgent need for a rational descriptor required a bold venture, which generated “nociplastic,” “algopathic,” and “nocipathic,” specifically to describe pain states characterized by clinical and psychophysical findings that suggest altered nociception and in which “nociceptive” or “neuropathic” are not applicable.

    We would assert further that any of these proposed terms stands in stark contrast to the “mechanistic vagueness” of terms such as “idiopathic” or “functional.” In agreement with Dr Brummett et al., we regard the latter as inappropriate and misleading if not also pejorative and stigmatizing.

    As Dr Brummett and colleagues invite – let the debate continue.

    Conflict of interest statement: The authors have no conflicts of interest to declare.

  4. For the purpose of advancing this debate, I have endeavoured to “unpack” the thinking behind the recommendation that “centralized” becomes the third pain descriptor.

    In the context of chronic widespread pain, the term “centralized” refers to “central nervous system origins of or amplification of pain” [Clauw 2014]. Elsewhere in his article, Professor Clauw suggests that the term implies “peripheral nociceptive input might be responsible for some of a patient’s pain but central nervous system factors likely amplify the pain.”

    Thus it appears that peripheral nociceptive input is not a necessary contributor to a patient’s pain. But should it happen to be the case, Clauw [2014] proposes that the patient feels “more pain than would normally be expected based on the degree of nociceptive input.” But he does not disclose how a clinician/observer is able to make such a determination with any degree of confidence! It sounds to me like a lot of guesswork is involved.

    When discussing amplification of pain, Clauw uses the analogy of an electronic device, i.e. the amplifier. Apparently, the levels of neurotransmitters that can either facilitate or reduce “pain transmission” determine where the dial is set for a particular patient. Of course, the belief that pain is “transmitted” along “pain pathways” (as claimed by Clauw) is epistemologically flawed and outdated. Nerves transmit electrical impulses rather than a “thing” called pain.

    Furthermore, given that the brain produces the lived experience that we call “pain,” it seems impossible to conceive of a brain being able to amplify an experience for which it is primarily responsible.

    According to Clauw (2014), “Fibromyalgia and other centralized pain states are much better understood now than ever before.”

    But he gives the game away when he suggests that on the one hand fibromyalgia can be considered as a “discrete diagnosis” whilst on the other hand it can be considered as “a constellation of symptoms characterized by central nervous system pain amplification with concomitant fatigue, memory problems, and sleep and mood disturbances.” According to his formulation, clinicians are permitted to choose either possibility.

    Far from there being a “better understanding” of fibromyalgia, it seems to me that an appreciable element of diagnostic confusion and circularity still exists.

    Reference: Clauw DJ. Fibromyalgia: a clinical review. JAMA 2014; 311(15): 1547-1555.

  5. Dear John,

    Thank you for your thoughtful work on this. You say:

    “Having said this, we do not dispute that the underlying mechanism of most cases of the category of chronic pain in question is likely to be central sensitization (or central hypersensitivity) of nociception or nociceptive pathways. The quest then becomes etymological, namely to find an adjective that incorporates this hypothesis of causation. Given that central sensitization of nociception is considered to reflect plasticity in nociceptive pathways, the challenge is to find a word that indicates the specificity of this change in function.”

    Given this, would you be comfortable saying that this group of patients in question have central sensitization? Is that a fair label to apply, in your eyes? Can we call this 3rd group the “central sensitization” group?

    Thanks

    • Dear Yoni,

      “Central sensitisation of nociception” is an inference as to an underlying neurophysiological process. However, a third descriptor should incorporate an hypothesis of causation.

      Does this help?

      John

      • Hi John,

        I believe that central sensitization is one link in the causal pathway of chronic pain in this 3rd group. Do you agree with that? You are right that its not a complete description of causation, but I do think it describes part of the causal pathway. I read your posts above with great interest and am keen to better understand your position. Thank you.

        Yoni

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