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Impaired regulation of emotion: neural correlates of reappraisal and distraction in bipolar disorder and unaffected relatives

Deficient emotion regulation has been proposed as a crucial pathological mechanism in bipolar disorder (BD). We therefore investigated emotion regulation impairments in BD, the related neural underpinnings and their etiological relevance for the disorder. Twenty-two euthymic patients with bipolar-I...

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Autores principales: Kanske, P, Schönfelder, S, Forneck, J, Wessa, M
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4312831/
https://www.ncbi.nlm.nih.gov/pubmed/25603413
http://dx.doi.org/10.1038/tp.2014.137
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author Kanske, P
Schönfelder, S
Forneck, J
Wessa, M
author_facet Kanske, P
Schönfelder, S
Forneck, J
Wessa, M
author_sort Kanske, P
collection PubMed
description Deficient emotion regulation has been proposed as a crucial pathological mechanism in bipolar disorder (BD). We therefore investigated emotion regulation impairments in BD, the related neural underpinnings and their etiological relevance for the disorder. Twenty-two euthymic patients with bipolar-I disorder and 17 unaffected first-degree relatives of BD-I patients, as well as two groups of healthy gender-, age- and education-matched controls (N=22/17, respectively) were included. Participants underwent functional magnetic resonance imaging while applying two different emotion regulation techniques, reappraisal and distraction, when presented with emotional images. BD patients and relatives showed impaired downregulation of amygdala activity during reappraisal, but not during distraction, when compared with controls. This deficit was correlated with the habitual use of reappraisal. The negative connectivity of amygdala and orbitofrontal cortex (OFC) observed during reappraisal in controls was reversed in BD patients and relatives. There were no significant differences between BD patients and relatives. As being observed in BD patients and unaffected relatives, deficits in emotion regulation through reappraisal may represent heritable neurobiological abnormalities underlying BD. The neural mechanisms include impaired control of amygdala reactivity to emotional stimuli and dysfunctional connectivity of the amygdala to regulatory control regions in the OFC. These are, thus, important aspects of the neurobiological basis of increased vulnerability for BD.
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spelling pubmed-43128312015-02-09 Impaired regulation of emotion: neural correlates of reappraisal and distraction in bipolar disorder and unaffected relatives Kanske, P Schönfelder, S Forneck, J Wessa, M Transl Psychiatry Original Article Deficient emotion regulation has been proposed as a crucial pathological mechanism in bipolar disorder (BD). We therefore investigated emotion regulation impairments in BD, the related neural underpinnings and their etiological relevance for the disorder. Twenty-two euthymic patients with bipolar-I disorder and 17 unaffected first-degree relatives of BD-I patients, as well as two groups of healthy gender-, age- and education-matched controls (N=22/17, respectively) were included. Participants underwent functional magnetic resonance imaging while applying two different emotion regulation techniques, reappraisal and distraction, when presented with emotional images. BD patients and relatives showed impaired downregulation of amygdala activity during reappraisal, but not during distraction, when compared with controls. This deficit was correlated with the habitual use of reappraisal. The negative connectivity of amygdala and orbitofrontal cortex (OFC) observed during reappraisal in controls was reversed in BD patients and relatives. There were no significant differences between BD patients and relatives. As being observed in BD patients and unaffected relatives, deficits in emotion regulation through reappraisal may represent heritable neurobiological abnormalities underlying BD. The neural mechanisms include impaired control of amygdala reactivity to emotional stimuli and dysfunctional connectivity of the amygdala to regulatory control regions in the OFC. These are, thus, important aspects of the neurobiological basis of increased vulnerability for BD. Nature Publishing Group 2015-01 2015-01-20 /pmc/articles/PMC4312831/ /pubmed/25603413 http://dx.doi.org/10.1038/tp.2014.137 Text en Copyright © 2015 Macmillan Publishers Limited http://creativecommons.org/licenses/by-nc-sa/4.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/
spellingShingle Original Article
Kanske, P
Schönfelder, S
Forneck, J
Wessa, M
Impaired regulation of emotion: neural correlates of reappraisal and distraction in bipolar disorder and unaffected relatives
title Impaired regulation of emotion: neural correlates of reappraisal and distraction in bipolar disorder and unaffected relatives
title_full Impaired regulation of emotion: neural correlates of reappraisal and distraction in bipolar disorder and unaffected relatives
title_fullStr Impaired regulation of emotion: neural correlates of reappraisal and distraction in bipolar disorder and unaffected relatives
title_full_unstemmed Impaired regulation of emotion: neural correlates of reappraisal and distraction in bipolar disorder and unaffected relatives
title_short Impaired regulation of emotion: neural correlates of reappraisal and distraction in bipolar disorder and unaffected relatives
title_sort impaired regulation of emotion: neural correlates of reappraisal and distraction in bipolar disorder and unaffected relatives
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4312831/
https://www.ncbi.nlm.nih.gov/pubmed/25603413
http://dx.doi.org/10.1038/tp.2014.137
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