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EEG Beta functional connectivity decrease in the left amygdala correlates with the affective pain in fibromyalgia: A pilot study

Fibromyalgia (FM) is a major chronic pain disease with prominent affective disturbances, and pain-associated changes in neurotransmitters activity and in brain connectivity. However, correlates of affective pain dimension lack. The primary goal of this correlational cross-sectional case-control pilo...

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Detalles Bibliográficos
Autores principales: Makowka, Soline, Mory, Lliure-Naima, Mouthon, Michael, Mancini, Christian, Guggisberg, Adrian G., Chabwine, Joelle Nsimire
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9943002/
https://www.ncbi.nlm.nih.gov/pubmed/36802404
http://dx.doi.org/10.1371/journal.pone.0281986
Descripción
Sumario:Fibromyalgia (FM) is a major chronic pain disease with prominent affective disturbances, and pain-associated changes in neurotransmitters activity and in brain connectivity. However, correlates of affective pain dimension lack. The primary goal of this correlational cross-sectional case-control pilot study was to find electrophysiological correlates of the affective pain component in FM. We examined the resting-state EEG spectral power and imaginary coherence in the beta (β) band (supposedly indexing the GABAergic neurotransmission) in 16 female patients with FM and 11 age-adjusted female controls. FM patients displayed lower functional connectivity in the High β (Hβ, 20–30 Hz) sub-band than controls (p = 0.039) in the left basolateral complex of the amygdala (p = 0.039) within the left mesiotemporal area, in particular, in correlation with a higher affective pain component level (r = 0.50, p = 0.049). Patients showed higher Low β (Lβ, 13–20 Hz) relative power than controls in the left prefrontal cortex (p = 0.001), correlated with ongoing pain intensity (r = 0.54, p = 0.032). For the first time, GABA-related connectivity changes correlated with the affective pain component are shown in the amygdala, a region highly involved in the affective regulation of pain. The β power increase in the prefrontal cortex could be compensatory to pain-related GABAergic dysfunction.