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1.
  • Abé, Christoph, et al. (författare)
  • Manic episodes are related to changes in frontal cortex: a longitudinal neuroimaging study of bipolar disorder 1.
  • 2015
  • Ingår i: Brain : a journal of neurology. - 1460-2156. ; 138:Pt 11, s. 3440-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Higher numbers of manic episodes in bipolar patients has, in cross-sectional studies, been associated with less grey matter volume in prefrontal brain areas. Longitudinal studies are needed to determine if manic episodes set off progressive cortical changes, or if the association is better explained by premorbid brain conditions that increase risk for mania. We followed patients with bipolar disorder type 1 for 6 years. Structural brain magnetic resonance imaging scans were performed at baseline and follow-up. We compared patients who had at least one manic episode between baseline and follow-up (Mania group, n = 13) with those who had no manic episodes (No-Mania group, n = 18). We used measures of cortical volume, thickness, and area to assess grey matter changes between baseline and follow-up. We found significantly decreased frontal cortical volume (dorsolateral prefrontal and inferior frontal cortex) in the Mania group, but no volume changes in the No-Mania group. Our results indicate that volume decrease in frontal brain regions can be attributed to the incidence of manic episodes.
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  • Anders, Silke, et al. (författare)
  • When seeing outweighs feeling : a role for prefrontal cortex in passive control of negative affect in blindsight
  • 2009
  • Ingår i: Brain. - Oxford : Oxford University Press. - 0006-8950 .- 1460-2156. ; 132:11, s. 3021-3031
  • Tidskriftsartikel (refereegranskat)abstract
    • Affective neuroscience has been strongly influenced by the viewthat a ‘feeling’ is the perception of somatic changesand has consequently often neglected the neural mechanisms thatunderlie the integration of somatic and other information inaffective experience. Here, we investigate affective processingby means of functional magnetic resonance imaging in nine corticallyblind patients. In these patients, unilateral postgeniculatelesions prevent primary cortical visual processing in part ofthe visual field which, as a result, becomes subjectively blind.Residual subcortical processing of visual information, however,is assumed to occur in the entire visual field. As we have reportedearlier, these patients show significant startle reflex potentiationwhen a threat-related visual stimulus is shown in their blindvisual field. Critically, this was associated with an increaseof brain activity in somatosensory-related areas, and an increasein experienced negative affect. Here, we investigated the patients’response when the visual stimulus was shown in the sighted visualfield, that is, when it was visible and cortically processed.Despite the fact that startle reflex potentiation was similarin the blind and sighted visual field, patients reported significantlyless negative affect during stimulation of the sighted visualfield. In other words, when the visual stimulus was visibleand received full cortical processing, the patients’ phenomenalexperience of affect did not closely reflect somatic changes.This decoupling of phenomenal affective experience and somaticchanges was associated with an increase of activity in the leftventrolateral prefrontal cortex and a decrease of affect-relatedsomatosensory activity. Moreover, patients who showed strongerleft ventrolateral prefrontal cortex activity tended to showa stronger decrease of affect-related somatosensory activity.Our findings show that similar affective somatic changes canbe associated with different phenomenal experiences of affect,depending on the depth of cortical processing. They are in linewith a model in which the left ventrolateral prefrontal cortexis a relay station that integrates information about subcorticallytriggered somatic responses and information resulting from in-depthcortical stimulus processing. Tentatively, we suggest that theobserved decoupling of somatic responses and experienced affect,and the reduction of negative phenomenal experience, can beexplained by a left ventrolateral prefrontal cortex-mediatedinhibition of affect-related somatosensory activity.
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  • Aoki, Y, et al. (författare)
  • Corrigendum
  • 2018
  • Ingår i: Brain : a journal of neurology. - 1460-2156. ; 141:5, s. e42-
  • Tidskriftsartikel (refereegranskat)
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