Offset analgesia is not affected by cold pressor induced analgesia

Thomas Dahl Nissen; Carsten Dahl Mørch; Lars Arendt-Nielsen; Asbjørn Mohr Drewes; Anne Estrup Olesen

doi:10.1515/sjpain-2018-0082

Offset analgesia is not affected by cold pressor induced analgesia

Thomas Dahl Nissen, Carsten Dahl Mørch, Lars Arendt-Nielsen, Asbjørn Mohr Drewes, Anne Estrup Olesen^*

^*Corresponding author for this work

2 Citations (Scopus)

Abstract

Background and aims: Offset analgesia (OA) is a pain modulating mechanism described as a disproportionately large decrease in pain intensity evoked by a minor decrease in stimulus intensity. Precise mechanisms of OA are still not elucidated and studies are needed to evaluate factors modulating OA. The aim of this study was to investigate OA before and during tonic cold pain (thought to induce descending inhibition), in a group of healthy volunteers. Methods: A randomized, crossover study was performed in 17 healthy participants (8 males and 9 females). The OA paradigm lasted 35 s and was induced by the traditional method using thermal stimulation applied to the forearm. A constant control heat stimulus (CTL) paradigm was used as control to assess adaptation. Pain intensity was assessed continuously. For induction of tonic cold pain, the participants immersed their hand into 2 °C water for 2 min. After 1 min and 25 s, the heat stimulation (OA or CTL paradigm) was repeated to assess the modulatory effect of the cold pressor test. Results: It was possible to induce OA both before and during the cold pressor test. Tonic cold pain modulated the peak pain reported during both the OA (p = 0.015) and CTL paradigms (p = 0.001) reflecting endogenous pain modulation. However, the magnitude of OA was not modulated by tonic cold pain (p > 0.05). Conclusions: The offset analgesia magnitude was not modulated by simultaneously tonic cold pain, thought to reflect another endogenous pain modulation mechanism. Implications: Neither offset analgesia magnitude nor adaptation were modulated by cold pressor induced endogenous analgesia. This could be explained by the fact, that offset analgesia was already at maximum in healthy participants. Hence, offset analgesia may not be a suitable assessment tool to investigate modulation induced by experimental methods or pharmacology in healthy participants.

Original language	English
Journal	Scandinavian Journal of Pain
Volume	18
Issue number	4
Pages (from-to)	695-701
ISSN	1877-8860
DOIs	https://doi.org/10.1515/sjpain-2018-0082
Publication status	Published - 2018

Keywords

cold-pressor
conditioned pain modulation
offset analgesia
pain

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10.1515/sjpain-2018-0082

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@article{892c727d54a24c9b9e4b50a363eaba2a,

title = "Offset analgesia is not affected by cold pressor induced analgesia",

abstract = "Background and aims: Offset analgesia (OA) is a pain modulating mechanism described as a disproportionately large decrease in pain intensity evoked by a minor decrease in stimulus intensity. Precise mechanisms of OA are still not elucidated and studies are needed to evaluate factors modulating OA. The aim of this study was to investigate OA before and during tonic cold pain (thought to induce descending inhibition), in a group of healthy volunteers. Methods: A randomized, crossover study was performed in 17 healthy participants (8 males and 9 females). The OA paradigm lasted 35 s and was induced by the traditional method using thermal stimulation applied to the forearm. A constant control heat stimulus (CTL) paradigm was used as control to assess adaptation. Pain intensity was assessed continuously. For induction of tonic cold pain, the participants immersed their hand into 2 °C water for 2 min. After 1 min and 25 s, the heat stimulation (OA or CTL paradigm) was repeated to assess the modulatory effect of the cold pressor test. Results: It was possible to induce OA both before and during the cold pressor test. Tonic cold pain modulated the peak pain reported during both the OA (p = 0.015) and CTL paradigms (p = 0.001) reflecting endogenous pain modulation. However, the magnitude of OA was not modulated by tonic cold pain (p > 0.05). Conclusions: The offset analgesia magnitude was not modulated by simultaneously tonic cold pain, thought to reflect another endogenous pain modulation mechanism. Implications: Neither offset analgesia magnitude nor adaptation were modulated by cold pressor induced endogenous analgesia. This could be explained by the fact, that offset analgesia was already at maximum in healthy participants. Hence, offset analgesia may not be a suitable assessment tool to investigate modulation induced by experimental methods or pharmacology in healthy participants. ",

keywords = "cold-pressor, conditioned pain modulation, offset analgesia, pain",

author = "Nissen, {Thomas Dahl} and M{\o}rch, {Carsten Dahl} and Lars Arendt-Nielsen and Drewes, {Asbj{\o}rn Mohr} and Olesen, {Anne Estrup}",

year = "2018",

doi = "10.1515/sjpain-2018-0082",

language = "English",

volume = "18",

pages = "695--701",

journal = "Scandinavian Journal of Pain",

issn = "1877-8860",

publisher = "De Gruyter",

number = "4",

}

TY - JOUR

T1 - Offset analgesia is not affected by cold pressor induced analgesia

AU - Nissen, Thomas Dahl

AU - Mørch, Carsten Dahl

AU - Arendt-Nielsen, Lars

AU - Drewes, Asbjørn Mohr

AU - Olesen, Anne Estrup

PY - 2018

Y1 - 2018

N2 - Background and aims: Offset analgesia (OA) is a pain modulating mechanism described as a disproportionately large decrease in pain intensity evoked by a minor decrease in stimulus intensity. Precise mechanisms of OA are still not elucidated and studies are needed to evaluate factors modulating OA. The aim of this study was to investigate OA before and during tonic cold pain (thought to induce descending inhibition), in a group of healthy volunteers. Methods: A randomized, crossover study was performed in 17 healthy participants (8 males and 9 females). The OA paradigm lasted 35 s and was induced by the traditional method using thermal stimulation applied to the forearm. A constant control heat stimulus (CTL) paradigm was used as control to assess adaptation. Pain intensity was assessed continuously. For induction of tonic cold pain, the participants immersed their hand into 2 °C water for 2 min. After 1 min and 25 s, the heat stimulation (OA or CTL paradigm) was repeated to assess the modulatory effect of the cold pressor test. Results: It was possible to induce OA both before and during the cold pressor test. Tonic cold pain modulated the peak pain reported during both the OA (p = 0.015) and CTL paradigms (p = 0.001) reflecting endogenous pain modulation. However, the magnitude of OA was not modulated by tonic cold pain (p > 0.05). Conclusions: The offset analgesia magnitude was not modulated by simultaneously tonic cold pain, thought to reflect another endogenous pain modulation mechanism. Implications: Neither offset analgesia magnitude nor adaptation were modulated by cold pressor induced endogenous analgesia. This could be explained by the fact, that offset analgesia was already at maximum in healthy participants. Hence, offset analgesia may not be a suitable assessment tool to investigate modulation induced by experimental methods or pharmacology in healthy participants.

AB - Background and aims: Offset analgesia (OA) is a pain modulating mechanism described as a disproportionately large decrease in pain intensity evoked by a minor decrease in stimulus intensity. Precise mechanisms of OA are still not elucidated and studies are needed to evaluate factors modulating OA. The aim of this study was to investigate OA before and during tonic cold pain (thought to induce descending inhibition), in a group of healthy volunteers. Methods: A randomized, crossover study was performed in 17 healthy participants (8 males and 9 females). The OA paradigm lasted 35 s and was induced by the traditional method using thermal stimulation applied to the forearm. A constant control heat stimulus (CTL) paradigm was used as control to assess adaptation. Pain intensity was assessed continuously. For induction of tonic cold pain, the participants immersed their hand into 2 °C water for 2 min. After 1 min and 25 s, the heat stimulation (OA or CTL paradigm) was repeated to assess the modulatory effect of the cold pressor test. Results: It was possible to induce OA both before and during the cold pressor test. Tonic cold pain modulated the peak pain reported during both the OA (p = 0.015) and CTL paradigms (p = 0.001) reflecting endogenous pain modulation. However, the magnitude of OA was not modulated by tonic cold pain (p > 0.05). Conclusions: The offset analgesia magnitude was not modulated by simultaneously tonic cold pain, thought to reflect another endogenous pain modulation mechanism. Implications: Neither offset analgesia magnitude nor adaptation were modulated by cold pressor induced endogenous analgesia. This could be explained by the fact, that offset analgesia was already at maximum in healthy participants. Hence, offset analgesia may not be a suitable assessment tool to investigate modulation induced by experimental methods or pharmacology in healthy participants.

KW - cold-pressor

KW - conditioned pain modulation

KW - offset analgesia

KW - pain

U2 - 10.1515/sjpain-2018-0082

DO - 10.1515/sjpain-2018-0082

M3 - Journal article

C2 - 30307901

AN - SCOPUS:85049758176

SN - 1877-8860

VL - 18

SP - 695

EP - 701

JO - Scandinavian Journal of Pain

JF - Scandinavian Journal of Pain

IS - 4

ER -

Offset analgesia is not affected by cold pressor induced analgesia

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