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Neural and behavioral changes driven by observationally-induced hypoalgesia

Observing successful pain treatment in others can induce anticipatory neural processes that, in turn, relieve pain. Previous studies have suggested that social learning and observation influence placebo hypoalgesia. Here, we used electroencephalography (EEG) to determine the neurophysiological chang...

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Autores principales: Raghuraman, Nandini, Wang, Yang, Schenk, Lieven A., Furman, Andrew J., Tricou, Christina, Seminowicz, David A., Colloca, Luana
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6930247/
https://www.ncbi.nlm.nih.gov/pubmed/31874985
http://dx.doi.org/10.1038/s41598-019-56188-2
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author Raghuraman, Nandini
Wang, Yang
Schenk, Lieven A.
Furman, Andrew J.
Tricou, Christina
Seminowicz, David A.
Colloca, Luana
author_facet Raghuraman, Nandini
Wang, Yang
Schenk, Lieven A.
Furman, Andrew J.
Tricou, Christina
Seminowicz, David A.
Colloca, Luana
author_sort Raghuraman, Nandini
collection PubMed
description Observing successful pain treatment in others can induce anticipatory neural processes that, in turn, relieve pain. Previous studies have suggested that social learning and observation influence placebo hypoalgesia. Here, we used electroencephalography (EEG) to determine the neurophysiological changes associated with pain relief acquired through the observation. Thirty-one participants observed a demonstrator undergo painful heat stimulations paired with a “control” cream and non-painful ones paired with a “treatment” cream, which actually were both Vanicreams. After their observation, the participants then received the same creams and stimulations. We found that the treatment cream led to lower self-reported pain intensity ratings than the control cream. Anticipatory treatment cues elicited smaller P2 in electrodes F1, Fz, FC1, and FCz than the control condition. The P2 component localization indicated a higher current density in the right middle frontal gyrus, a region associated with attentional engagement. In placebo responders, the sensorimotor cortex activity captured in electrodes C3, Cz, and C4 indicated that hypoalgesia was positively correlated with resting state peak alpha frequency (PAF). These results suggest that observationally-induced placebo hypoalgesia may be driven by anticipatory mechanisms that modulate frontal attentional processes. Furthermore, resting state PAF could serve as a predictor of observationally-induced hypoalgesia.
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spelling pubmed-69302472019-12-27 Neural and behavioral changes driven by observationally-induced hypoalgesia Raghuraman, Nandini Wang, Yang Schenk, Lieven A. Furman, Andrew J. Tricou, Christina Seminowicz, David A. Colloca, Luana Sci Rep Article Observing successful pain treatment in others can induce anticipatory neural processes that, in turn, relieve pain. Previous studies have suggested that social learning and observation influence placebo hypoalgesia. Here, we used electroencephalography (EEG) to determine the neurophysiological changes associated with pain relief acquired through the observation. Thirty-one participants observed a demonstrator undergo painful heat stimulations paired with a “control” cream and non-painful ones paired with a “treatment” cream, which actually were both Vanicreams. After their observation, the participants then received the same creams and stimulations. We found that the treatment cream led to lower self-reported pain intensity ratings than the control cream. Anticipatory treatment cues elicited smaller P2 in electrodes F1, Fz, FC1, and FCz than the control condition. The P2 component localization indicated a higher current density in the right middle frontal gyrus, a region associated with attentional engagement. In placebo responders, the sensorimotor cortex activity captured in electrodes C3, Cz, and C4 indicated that hypoalgesia was positively correlated with resting state peak alpha frequency (PAF). These results suggest that observationally-induced placebo hypoalgesia may be driven by anticipatory mechanisms that modulate frontal attentional processes. Furthermore, resting state PAF could serve as a predictor of observationally-induced hypoalgesia. Nature Publishing Group UK 2019-12-24 /pmc/articles/PMC6930247/ /pubmed/31874985 http://dx.doi.org/10.1038/s41598-019-56188-2 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Raghuraman, Nandini
Wang, Yang
Schenk, Lieven A.
Furman, Andrew J.
Tricou, Christina
Seminowicz, David A.
Colloca, Luana
Neural and behavioral changes driven by observationally-induced hypoalgesia
title Neural and behavioral changes driven by observationally-induced hypoalgesia
title_full Neural and behavioral changes driven by observationally-induced hypoalgesia
title_fullStr Neural and behavioral changes driven by observationally-induced hypoalgesia
title_full_unstemmed Neural and behavioral changes driven by observationally-induced hypoalgesia
title_short Neural and behavioral changes driven by observationally-induced hypoalgesia
title_sort neural and behavioral changes driven by observationally-induced hypoalgesia
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6930247/
https://www.ncbi.nlm.nih.gov/pubmed/31874985
http://dx.doi.org/10.1038/s41598-019-56188-2
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