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Specific neurophysiological mechanisms underlie cognitive inflexibility in inflammatory bowel disease

Inflammatory bowel disease (IBD) is highly prevalent. While the pathophysiological mechanisms of IBD are increasingly understood, there is a lack of knowledge concerning cognitive dysfunctions in IBD. This is all the more the case concerning the underlying neurophysiological mechanisms. In the curre...

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Autores principales: Petruo, Vanessa A, Zeißig, Sebastian, Schmelz, Renate, Hampe, Jochen, Beste, Christian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5655331/
https://www.ncbi.nlm.nih.gov/pubmed/29066846
http://dx.doi.org/10.1038/s41598-017-14345-5
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author Petruo, Vanessa A
Zeißig, Sebastian
Schmelz, Renate
Hampe, Jochen
Beste, Christian
author_facet Petruo, Vanessa A
Zeißig, Sebastian
Schmelz, Renate
Hampe, Jochen
Beste, Christian
author_sort Petruo, Vanessa A
collection PubMed
description Inflammatory bowel disease (IBD) is highly prevalent. While the pathophysiological mechanisms of IBD are increasingly understood, there is a lack of knowledge concerning cognitive dysfunctions in IBD. This is all the more the case concerning the underlying neurophysiological mechanisms. In the current study we focus on possible dysfunctions of cognitive flexibility (task switching) processes in IBD patients using a system neurophysiological approach combining event-related potential (ERP) recordings with source localization analyses. We show that there are task switching deficits (i.e. increased switch costs) in IBD patients. The neurophysiological data show that even though the pathophysiology of IBD is diverse and wide-spread, only specific cognitive subprocesses are altered: There was a selective dysfunction at the response selection level (N2 ERP) associated with functional alterations in the anterior cingulate cortex and the right inferior frontal gyrus. Attentional selection processes (N1 ERP), perceptual categorization processes (P1 ERP), or mechanisms related to the flexible implementation of task sets and related working memory processes (P3 ERP) do not contribute to cognitive inflexibility in IBD patients and were unchanged. It seems that pathophysiological processes in IBD strongly compromise cognitive-neurophysiological subprocesses related to fronto-striatal networks. These circuits may become overstrained in IBD when cognitive flexibility is required.
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spelling pubmed-56553312017-10-31 Specific neurophysiological mechanisms underlie cognitive inflexibility in inflammatory bowel disease Petruo, Vanessa A Zeißig, Sebastian Schmelz, Renate Hampe, Jochen Beste, Christian Sci Rep Article Inflammatory bowel disease (IBD) is highly prevalent. While the pathophysiological mechanisms of IBD are increasingly understood, there is a lack of knowledge concerning cognitive dysfunctions in IBD. This is all the more the case concerning the underlying neurophysiological mechanisms. In the current study we focus on possible dysfunctions of cognitive flexibility (task switching) processes in IBD patients using a system neurophysiological approach combining event-related potential (ERP) recordings with source localization analyses. We show that there are task switching deficits (i.e. increased switch costs) in IBD patients. The neurophysiological data show that even though the pathophysiology of IBD is diverse and wide-spread, only specific cognitive subprocesses are altered: There was a selective dysfunction at the response selection level (N2 ERP) associated with functional alterations in the anterior cingulate cortex and the right inferior frontal gyrus. Attentional selection processes (N1 ERP), perceptual categorization processes (P1 ERP), or mechanisms related to the flexible implementation of task sets and related working memory processes (P3 ERP) do not contribute to cognitive inflexibility in IBD patients and were unchanged. It seems that pathophysiological processes in IBD strongly compromise cognitive-neurophysiological subprocesses related to fronto-striatal networks. These circuits may become overstrained in IBD when cognitive flexibility is required. Nature Publishing Group UK 2017-10-24 /pmc/articles/PMC5655331/ /pubmed/29066846 http://dx.doi.org/10.1038/s41598-017-14345-5 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
Petruo, Vanessa A
Zeißig, Sebastian
Schmelz, Renate
Hampe, Jochen
Beste, Christian
Specific neurophysiological mechanisms underlie cognitive inflexibility in inflammatory bowel disease
title Specific neurophysiological mechanisms underlie cognitive inflexibility in inflammatory bowel disease
title_full Specific neurophysiological mechanisms underlie cognitive inflexibility in inflammatory bowel disease
title_fullStr Specific neurophysiological mechanisms underlie cognitive inflexibility in inflammatory bowel disease
title_full_unstemmed Specific neurophysiological mechanisms underlie cognitive inflexibility in inflammatory bowel disease
title_short Specific neurophysiological mechanisms underlie cognitive inflexibility in inflammatory bowel disease
title_sort specific neurophysiological mechanisms underlie cognitive inflexibility in inflammatory bowel disease
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5655331/
https://www.ncbi.nlm.nih.gov/pubmed/29066846
http://dx.doi.org/10.1038/s41598-017-14345-5
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