- Email: [email protected]
Nociception in Kyoto
PAINÒ 143 (2009) 159–160
www.elsevier.com/locate/pain
Letters to the Editor Nociception in Kyoto The letter by Professor Devor [1] and the reply by Professors Loeser and Treede [2] deserve further comment. Loeser and Treede indicate that a ‘‘consensus” was reached by the Taxonomy Committee, but it seemed that the main consensual element was that there was a great deal of disagreement. In my view the broader consultation with the Editorial Board of PAIN confirmed that phenomenon. Council wisely decided not to make changes in the face of a welter of different opinions and different terms, some new and some existing. With respect to allodynia it is true that the first members of the Taxonomy Committee specified the term de novo, and their successors in the Taxonomy Committee would therefore be the appropriate body to revise it. However, revisions should be undertaken with due attention to the original basis for the terms. Allodynia was created, as I indicated in the Committee’s discussions and on the IASP website, at the request of the late Professor William Noordenbos, in order to identify pain occurring on clinical examination or spontaneously in individuals as a result of light touch and in situations where it would not normally be expected. When discussion first emerged about altering the term to describe physiological discoveries Peter Nathan immediately observed that these terms were created by clinicians for clinical usage. The clinical findings were unlikely to change, whereas physiological explanations would change and would advance. In order for them to remain helpful clinical tools it was necessary to keep the clinical terms for the same phenomenon and not to change them in accordance with the changing and improving understanding of physiology. The modifications that have been accepted and agreed in the IASP Definitions of Terms are intended to clarify the expression or application of those ideas, not to gut the primary meaning. For these reasons, I trust that neither the present Taxonomy Committee nor Council will seek to change their support for the essential features of the Terms as they are currently understood and described. As to nociception, Sherrington wrote of nociceptive reflexes and arcs [3]. He introduced the word, one might say obviously, as a term covering both afferent and efferent activity. One must presume that it also comprises the integrative contribution of the neuraxis and brain. If we were to tie nociception to a single set, or even a pair of types of neurons, we would be reversing more than a century of neurophysiological interpretation. Thus, the same objection to changing present definitions exists as with allodynia. We can use nociceptive to cover types of neurons, but neither one afferent neuron nor many afferent neurons alone constitute nociception. Nociception as understood by Sherrington is both an afferent and an efferent phenomenon. It is essentially the whole of the process which deals with both the reception of nervous impulses of a noxious type and the responses intended to prevent or mitigate harm. This is not rocket science nor is it nano-science. It is just using a couple of words that our distinguished predecessors have provided
to us in the way that they intended them to be used. This need not prevent us from appreciating the work of Dr. Devor and Dr. Treede. References [1] Devor M. Nociception in Kyoto. Pain 2008;140:519–20. [2] Loeser JD, Treede RD. Reply to Devor. Pain 2008;140:520–1. [3] Sherrington CS. The integrative action of the nervous system. Reprinted with a new foreword. Cambridge University Press; 1947. p. 255.
Harold Merskey Professor Emeritus of Psychiatry, University of Western Ontario, 71 Logan Avenue, London, ON, Canada N5Y 2P9 Tel.: +1 519 679 1045; fax: +1 519 679 6849. E-mail address: [email protected]
S0304-3959/$36.00 Ó 2009 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.pain.2009.01.032
Does the central nervous system play a role in vitamin D deficiency related chronic pain? The Straube et al. review [8] on vitamin D and chronic pain, and the authors’ call for research to better understand how vitamin D deficiency is associated with chronic pain, is welcomed. As the authors and as others they cite have found, vitamin D does not appear to successfully treat chronic pain in most individuals. One possible role for vitamin D, not mentioned in their review, may include promotion of descending top down central nervous system pathways that inhibit musculoskeletal pain, as proposed elsewhere [6]. Eyles et al. have shown that there are increased numbers of vitamin D receptors in certain human brain areas [2]. One such area is the ventromedial hypothalamus, a known descending pain inhibitory control center [3]. Similarly, there are increased receptors in the anterior cingulate cortex, which has been implicated in descending modulation of endogenous pain control [5]. It is proposed that pain inhibition by the central nervous system is dysfunctional in the vitamin D deficient state, and once ascending pain signaling pathways are engaged, simple vitamin repletion may not extinguish persistent chronic pain. This hypothesis could explain the disparate results in the vitamin D supplementation studies reviewed by the authors. In particular, this concept provides an explanation for results from a study, also reviewed, which showed fibromyalgia pain does not correlate with vitamin D levels [1]. Dysfunctional pain inhibition through descending inhibitory control pathways has been proposed as a mechanism for fibromyalgia pain [4], thereby making adequate vitamin D levels inconsequential. Should this proposed vitamin deficiency induced dysfunction of pain regulation in the central nervous system prove accurate, further research would be needed on how vitamin D prevents the development of chronic pain related conditions. Knowledge of how vitamin D deficiency results in the establish-
www.elsevier.com/locate/pain
Letters to the Editor Nociception in Kyoto The letter by Professor Devor [1] and the reply by Professors Loeser and Treede [2] deserve further comment. Loeser and Treede indicate that a ‘‘consensus” was reached by the Taxonomy Committee, but it seemed that the main consensual element was that there was a great deal of disagreement. In my view the broader consultation with the Editorial Board of PAIN confirmed that phenomenon. Council wisely decided not to make changes in the face of a welter of different opinions and different terms, some new and some existing. With respect to allodynia it is true that the first members of the Taxonomy Committee specified the term de novo, and their successors in the Taxonomy Committee would therefore be the appropriate body to revise it. However, revisions should be undertaken with due attention to the original basis for the terms. Allodynia was created, as I indicated in the Committee’s discussions and on the IASP website, at the request of the late Professor William Noordenbos, in order to identify pain occurring on clinical examination or spontaneously in individuals as a result of light touch and in situations where it would not normally be expected. When discussion first emerged about altering the term to describe physiological discoveries Peter Nathan immediately observed that these terms were created by clinicians for clinical usage. The clinical findings were unlikely to change, whereas physiological explanations would change and would advance. In order for them to remain helpful clinical tools it was necessary to keep the clinical terms for the same phenomenon and not to change them in accordance with the changing and improving understanding of physiology. The modifications that have been accepted and agreed in the IASP Definitions of Terms are intended to clarify the expression or application of those ideas, not to gut the primary meaning. For these reasons, I trust that neither the present Taxonomy Committee nor Council will seek to change their support for the essential features of the Terms as they are currently understood and described. As to nociception, Sherrington wrote of nociceptive reflexes and arcs [3]. He introduced the word, one might say obviously, as a term covering both afferent and efferent activity. One must presume that it also comprises the integrative contribution of the neuraxis and brain. If we were to tie nociception to a single set, or even a pair of types of neurons, we would be reversing more than a century of neurophysiological interpretation. Thus, the same objection to changing present definitions exists as with allodynia. We can use nociceptive to cover types of neurons, but neither one afferent neuron nor many afferent neurons alone constitute nociception. Nociception as understood by Sherrington is both an afferent and an efferent phenomenon. It is essentially the whole of the process which deals with both the reception of nervous impulses of a noxious type and the responses intended to prevent or mitigate harm. This is not rocket science nor is it nano-science. It is just using a couple of words that our distinguished predecessors have provided
to us in the way that they intended them to be used. This need not prevent us from appreciating the work of Dr. Devor and Dr. Treede. References [1] Devor M. Nociception in Kyoto. Pain 2008;140:519–20. [2] Loeser JD, Treede RD. Reply to Devor. Pain 2008;140:520–1. [3] Sherrington CS. The integrative action of the nervous system. Reprinted with a new foreword. Cambridge University Press; 1947. p. 255.
Harold Merskey Professor Emeritus of Psychiatry, University of Western Ontario, 71 Logan Avenue, London, ON, Canada N5Y 2P9 Tel.: +1 519 679 1045; fax: +1 519 679 6849. E-mail address: [email protected]
S0304-3959/$36.00 Ó 2009 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.pain.2009.01.032
Does the central nervous system play a role in vitamin D deficiency related chronic pain? The Straube et al. review [8] on vitamin D and chronic pain, and the authors’ call for research to better understand how vitamin D deficiency is associated with chronic pain, is welcomed. As the authors and as others they cite have found, vitamin D does not appear to successfully treat chronic pain in most individuals. One possible role for vitamin D, not mentioned in their review, may include promotion of descending top down central nervous system pathways that inhibit musculoskeletal pain, as proposed elsewhere [6]. Eyles et al. have shown that there are increased numbers of vitamin D receptors in certain human brain areas [2]. One such area is the ventromedial hypothalamus, a known descending pain inhibitory control center [3]. Similarly, there are increased receptors in the anterior cingulate cortex, which has been implicated in descending modulation of endogenous pain control [5]. It is proposed that pain inhibition by the central nervous system is dysfunctional in the vitamin D deficient state, and once ascending pain signaling pathways are engaged, simple vitamin repletion may not extinguish persistent chronic pain. This hypothesis could explain the disparate results in the vitamin D supplementation studies reviewed by the authors. In particular, this concept provides an explanation for results from a study, also reviewed, which showed fibromyalgia pain does not correlate with vitamin D levels [1]. Dysfunctional pain inhibition through descending inhibitory control pathways has been proposed as a mechanism for fibromyalgia pain [4], thereby making adequate vitamin D levels inconsequential. Should this proposed vitamin deficiency induced dysfunction of pain regulation in the central nervous system prove accurate, further research would be needed on how vitamin D prevents the development of chronic pain related conditions. Knowledge of how vitamin D deficiency results in the establish-