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Functional Brain Network Mechanism of Hypersensitivity in Chronic Pain

Fibromyalgia (FM) is a chronic widespread pain condition characterized by augmented multi-modal sensory sensitivity. Although the mechanisms underlying this sensitivity are thought to involve an imbalance in excitatory and inhibitory activity throughout the brain, the underlying neural network prope...

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Autores principales: Lee, UnCheol, Kim, Minkyung, Lee, KyoungEun, Kaplan, Chelsea M., Clauw, Daniel J., Kim, Seunghwan, Mashour, George A., Harris, Richard E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5762762/
https://www.ncbi.nlm.nih.gov/pubmed/29321621
http://dx.doi.org/10.1038/s41598-017-18657-4
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author Lee, UnCheol
Kim, Minkyung
Lee, KyoungEun
Kaplan, Chelsea M.
Clauw, Daniel J.
Kim, Seunghwan
Mashour, George A.
Harris, Richard E.
author_facet Lee, UnCheol
Kim, Minkyung
Lee, KyoungEun
Kaplan, Chelsea M.
Clauw, Daniel J.
Kim, Seunghwan
Mashour, George A.
Harris, Richard E.
author_sort Lee, UnCheol
collection PubMed
description Fibromyalgia (FM) is a chronic widespread pain condition characterized by augmented multi-modal sensory sensitivity. Although the mechanisms underlying this sensitivity are thought to involve an imbalance in excitatory and inhibitory activity throughout the brain, the underlying neural network properties associated with hypersensitivity to pain stimuli are largely unknown. In network science, explosive synchronization (ES) was introduced as a mechanism of hypersensitivity in diverse biological and physical systems that display explosive and global propagations with small perturbations. We hypothesized that ES may also be a mechanism of the hypersensitivity in FM brains. To test this hypothesis, we analyzed resting state electroencephalogram (EEG) of 10 FM patients. First, we examined theoretically well-known ES conditions within functional brain networks reconstructed from EEG, then tested whether a brain network model with ES conditions identified in the EEG data is sensitive to an external perturbation. We demonstrate for the first time that the FM brain displays characteristics of ES conditions, and that these factors significantly correlate with chronic pain intensity. The simulation data support the conclusion that networks with ES conditions are more sensitive to perturbation compared to non-ES network. The model and empirical data analysis provide convergent evidence that ES may be a network mechanism of FM hypersensitivity.
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spelling pubmed-57627622018-01-17 Functional Brain Network Mechanism of Hypersensitivity in Chronic Pain Lee, UnCheol Kim, Minkyung Lee, KyoungEun Kaplan, Chelsea M. Clauw, Daniel J. Kim, Seunghwan Mashour, George A. Harris, Richard E. Sci Rep Article Fibromyalgia (FM) is a chronic widespread pain condition characterized by augmented multi-modal sensory sensitivity. Although the mechanisms underlying this sensitivity are thought to involve an imbalance in excitatory and inhibitory activity throughout the brain, the underlying neural network properties associated with hypersensitivity to pain stimuli are largely unknown. In network science, explosive synchronization (ES) was introduced as a mechanism of hypersensitivity in diverse biological and physical systems that display explosive and global propagations with small perturbations. We hypothesized that ES may also be a mechanism of the hypersensitivity in FM brains. To test this hypothesis, we analyzed resting state electroencephalogram (EEG) of 10 FM patients. First, we examined theoretically well-known ES conditions within functional brain networks reconstructed from EEG, then tested whether a brain network model with ES conditions identified in the EEG data is sensitive to an external perturbation. We demonstrate for the first time that the FM brain displays characteristics of ES conditions, and that these factors significantly correlate with chronic pain intensity. The simulation data support the conclusion that networks with ES conditions are more sensitive to perturbation compared to non-ES network. The model and empirical data analysis provide convergent evidence that ES may be a network mechanism of FM hypersensitivity. Nature Publishing Group UK 2018-01-10 /pmc/articles/PMC5762762/ /pubmed/29321621 http://dx.doi.org/10.1038/s41598-017-18657-4 Text en © The Author(s) 2017 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
Lee, UnCheol
Kim, Minkyung
Lee, KyoungEun
Kaplan, Chelsea M.
Clauw, Daniel J.
Kim, Seunghwan
Mashour, George A.
Harris, Richard E.
Functional Brain Network Mechanism of Hypersensitivity in Chronic Pain
title Functional Brain Network Mechanism of Hypersensitivity in Chronic Pain
title_full Functional Brain Network Mechanism of Hypersensitivity in Chronic Pain
title_fullStr Functional Brain Network Mechanism of Hypersensitivity in Chronic Pain
title_full_unstemmed Functional Brain Network Mechanism of Hypersensitivity in Chronic Pain
title_short Functional Brain Network Mechanism of Hypersensitivity in Chronic Pain
title_sort functional brain network mechanism of hypersensitivity in chronic pain
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5762762/
https://www.ncbi.nlm.nih.gov/pubmed/29321621
http://dx.doi.org/10.1038/s41598-017-18657-4
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