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dc.contributor.authorCaseras Vives, Francesc Xavier
dc.contributor.authorMurphy, Kevin
dc.contributor.authorLawrence, Natalia S.
dc.contributor.authorFuentes-Claramonte, Paola
dc.contributor.authorWatts, Jessica
dc.contributor.authorJones, Derek K.
dc.contributor.authorPhillips, Mary L.
dc.date.accessioned2016-04-05T10:39:36Z
dc.date.available2016-04-05T10:39:36Z
dc.date.issued2015-03-15
dc.identifier.citationCASERAS, Xavier, et al. Emotion regulation deficits in euthymic bipolar I versus bipolar II disorder: a functional and diffusion‐tensor imaging study. Bipolar disorders, 2015, vol. 17, no 5, p. 461-470.ca_CA
dc.identifier.issn1398-5647
dc.identifier.urihttp://hdl.handle.net/10234/156087
dc.description.abstractObjectives Emotion regulation deficits are a core feature of bipolar disorder. However, their potential neurobiological underpinnings and existence beyond bipolar I disorder remain unexplored. Our main goal was to investigate whether both individuals with bipolar I and bipolar II disorder show deficits in emotion regulation during an attention control task, and to explore the neurophysiological underpinnings of this potential deficit. Methods Twenty healthy controls, 16 euthymic participants with bipolar I disorder, and 19 euthymic participants with bipolar II disorder completed psychometric and clinical assessments, a neuroimaging emotion regulation paradigm, and an anatomical diffusion-weighted scan. Groups were matched for age, gender, and verbal IQ. Results During the presence of emotional distracters, subjects with bipolar I disorder showed slowed reaction times to targets, and increased blood oxygenation level-dependent (BOLD) responses in the amygdala, accumbens, and dorsolateral prefrontal cortex, but not increased inverse functional connectivity between these prefrontal and subcortical areas, and altered white matter microstructure organization in the right uncinate fasciculus. Subjects with bipolar II disorder showed no altered reaction times, increased BOLD responses in the same brain areas, increased inverse functional connectivity between the prefrontal cortex and amygdala, and no abnormalities in white matter organization. Conclusions Participants with bipolar I disorder showed abnormalities in functional and anatomical connectivity between prefrontal cortices and subcortical structures in emotion regulation circuitry. However, these deficits did not extend to subjects with bipolar II disorder, suggesting fundamental differences in the pathophysiology of bipolar disorder subtypes.ca_CA
dc.description.sponsorShipThis research project was supported by grants from the Welsh Institute of Cognitive Neurosciences (WCS034) and Seed Corn funding from the MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University. KM is supported by a fellowship from the Wellcome Trust, DKJ by a Wellcome Trust New Investigator Award and MLP by the Pittsburgh Foundation. The authors thank the Bipolar Disorder Research Network (BDRN) and the National Centre for Mental Health (NCMH) for their help with the recruitment of participants.ca_CA
dc.format.extent10 p.ca_CA
dc.format.mimetypeapplication/pdfca_CA
dc.language.isoengca_CA
dc.publisherJohn Wiley & Sons Ltd.ca_CA
dc.relation.isPartOfBipolar disorders, 2015, vol. 17, no 5ca_CA
dc.rights© 2015 The Authors. Bipolar Disorders This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.ca_CA
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/*
dc.subjectbipolar disorderca_CA
dc.subjectBOLDca_CA
dc.subjectDTIca_CA
dc.subjectemotion regulationca_CA
dc.subjectfMRIca_CA
dc.titleEmotion regulation deficits in euthymic bipolar I versus bipolar II disorder: a functional and diffusion-tensor imaging studyca_CA
dc.typeinfo:eu-repo/semantics/articleca_CA
dc.identifier.doihttp://dx.doi.org/10.1111/bdi.12292
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_CA
dc.relation.publisherVersionhttp://onlinelibrary.wiley.com/doi/10.1111/bdi.12292/abstractca_CA
dc.type.versioninfo:eu-repo/semantics/publishedVersionca_CA


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