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Cortical activity evoked by an acute painful tissue-damaging stimulus in healthy adult volunteers
Everyday painful experiences are usually single events accompanied by tissue damage, and yet most experimental studies of cutaneous nociceptive processing in the brain use repeated laser, thermal, or electrical stimulations that do not damage the skin. In this study the nociceptive activity in the b...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Physiological Society
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652217/ https://www.ncbi.nlm.nih.gov/pubmed/23427303 http://dx.doi.org/10.1152/jn.00990.2012 |
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author | Fabrizi, Lorenzo Williams, Gemma Lee, Amy Meek, Judith Slater, Rebeccah Olhede, Sofia Fitzgerald, Maria |
author_facet | Fabrizi, Lorenzo Williams, Gemma Lee, Amy Meek, Judith Slater, Rebeccah Olhede, Sofia Fitzgerald, Maria |
author_sort | Fabrizi, Lorenzo |
collection | PubMed |
description | Everyday painful experiences are usually single events accompanied by tissue damage, and yet most experimental studies of cutaneous nociceptive processing in the brain use repeated laser, thermal, or electrical stimulations that do not damage the skin. In this study the nociceptive activity in the brain evoked by tissue-damaging skin lance was analyzed with electroencephalography (EEG) in 20 healthy adult volunteers (13 men and 7 women) aged 21–40 yr. Time-frequency analysis of the evoked activity revealed a distinct late event-related vertex potential (lance event-related potential, LERP) at 100–300 ms consisting of a phase-locked energy increase between 1 and 20 Hz (delta-beta bands). A pairwise comparison between lance and sham control stimulation also revealed a period of ultralate stronger desynchronization after lance in the delta band (1–5 Hz). Skin application of mustard oil before lancing, which sensitizes a subpopulation of nociceptors expressing the cation channel TRPA1, did not affect the ultralate desynchronization but reduced the phase-locked energy increase in delta and beta bands, suggesting a central interaction between different modalities of nociceptive inputs. Verbal descriptor screening of individual pain experience revealed that lance pain is predominantly due to Aδ fiber activation, but when individuals describe lances as C fiber mediated, an ultralate delta band event-related desynchronization occurs in the brain-evoked activity. We conclude that pain evoked by acute tissue damage is associated with distinct Aδ and C fiber-mediated patterns of synchronization and desynchronization of EEG oscillations in the brain. |
format | Online Article Text |
id | pubmed-3652217 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | American Physiological Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-36522172014-05-01 Cortical activity evoked by an acute painful tissue-damaging stimulus in healthy adult volunteers Fabrizi, Lorenzo Williams, Gemma Lee, Amy Meek, Judith Slater, Rebeccah Olhede, Sofia Fitzgerald, Maria J Neurophysiol Articles Everyday painful experiences are usually single events accompanied by tissue damage, and yet most experimental studies of cutaneous nociceptive processing in the brain use repeated laser, thermal, or electrical stimulations that do not damage the skin. In this study the nociceptive activity in the brain evoked by tissue-damaging skin lance was analyzed with electroencephalography (EEG) in 20 healthy adult volunteers (13 men and 7 women) aged 21–40 yr. Time-frequency analysis of the evoked activity revealed a distinct late event-related vertex potential (lance event-related potential, LERP) at 100–300 ms consisting of a phase-locked energy increase between 1 and 20 Hz (delta-beta bands). A pairwise comparison between lance and sham control stimulation also revealed a period of ultralate stronger desynchronization after lance in the delta band (1–5 Hz). Skin application of mustard oil before lancing, which sensitizes a subpopulation of nociceptors expressing the cation channel TRPA1, did not affect the ultralate desynchronization but reduced the phase-locked energy increase in delta and beta bands, suggesting a central interaction between different modalities of nociceptive inputs. Verbal descriptor screening of individual pain experience revealed that lance pain is predominantly due to Aδ fiber activation, but when individuals describe lances as C fiber mediated, an ultralate delta band event-related desynchronization occurs in the brain-evoked activity. We conclude that pain evoked by acute tissue damage is associated with distinct Aδ and C fiber-mediated patterns of synchronization and desynchronization of EEG oscillations in the brain. American Physiological Society 2013-05-01 2013-02-20 /pmc/articles/PMC3652217/ /pubmed/23427303 http://dx.doi.org/10.1152/jn.00990.2012 Text en Copyright © 2013 the American Physiological Society Licensed under Creative Commons Attribution CC-BY 3.0 (http://creativecommons.org/licenses/by/3.0/deed.en_US) : the American Physiological Society. |
spellingShingle | Articles Fabrizi, Lorenzo Williams, Gemma Lee, Amy Meek, Judith Slater, Rebeccah Olhede, Sofia Fitzgerald, Maria Cortical activity evoked by an acute painful tissue-damaging stimulus in healthy adult volunteers |
title | Cortical activity evoked by an acute painful tissue-damaging stimulus in healthy adult volunteers |
title_full | Cortical activity evoked by an acute painful tissue-damaging stimulus in healthy adult volunteers |
title_fullStr | Cortical activity evoked by an acute painful tissue-damaging stimulus in healthy adult volunteers |
title_full_unstemmed | Cortical activity evoked by an acute painful tissue-damaging stimulus in healthy adult volunteers |
title_short | Cortical activity evoked by an acute painful tissue-damaging stimulus in healthy adult volunteers |
title_sort | cortical activity evoked by an acute painful tissue-damaging stimulus in healthy adult volunteers |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652217/ https://www.ncbi.nlm.nih.gov/pubmed/23427303 http://dx.doi.org/10.1152/jn.00990.2012 |
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