TY - JOUR

T1 - The trajectory of emotional and non-emotional cognitive function in newly diagnosed patients with bipolar disorder and their unaffected relatives

T2 - A 16-month follow-up study

AU - Kjærstad, Hanne Lie

AU - Søhol, Kristine

AU - Vinberg, Maj

AU - Kessing, Lars Vedel

AU - Miskowiak, Kamilla Woznica

N1 - Publisher Copyright: © 2022 The Author(s)

PY - 2023

Y1 - 2023

N2 - Cognitive impairments are evident in remitted patients with bipolar disorder (BD) and their unaffected relatives (UR) compared to healthy controls (HC). However, the temporal course of cognition, and whether cognition is marked by neuroprogressive changes, remain unclear. In a large prospective study of newly diagnosed patients with BD, we assessed patients with BD (n = 266), UR (n = 105) and HC (n = 190) using an extensive cognitive battery of non-emotional and emotional cognition at baseline and 16-months follow-up. Cognitive change across groups was examined with linear mixed-model analyses. Results showed no evidence of trajectory differences between patients with BD, UR, and HC in neurocognition and emotional cognition (ps≥.10). Patients with BD showed stable impairments in global neurocognitive functioning over time, as well as within the domains of ‘working memory and executive function’ and ‘attention and psychomotor speed’, compared to HC. Patients who relapsed during the follow-up time were less successful at down-regulating emotions in positive social scenarios compared to HC. Unaffected relatives also displayed stable deficits in ‘working memory and executive function’ over time, with performance at intermediate levels between BD probands and HC. Finally, poorer neurocognition and positive emotion regulation were associated with more subsyndromal symptoms and functional impairments. In conclusion, we found no evidence of a neuroprogressive origin of cognitive impairments in the newly diagnosed BD or in their UR. Patients’ and UR's impairments in working memory and executive function may reflect a stable cognitive trait-marker of familial risk. Difficulties with positive emotion regulation may be associated with illness progression in BD.

AB - Cognitive impairments are evident in remitted patients with bipolar disorder (BD) and their unaffected relatives (UR) compared to healthy controls (HC). However, the temporal course of cognition, and whether cognition is marked by neuroprogressive changes, remain unclear. In a large prospective study of newly diagnosed patients with BD, we assessed patients with BD (n = 266), UR (n = 105) and HC (n = 190) using an extensive cognitive battery of non-emotional and emotional cognition at baseline and 16-months follow-up. Cognitive change across groups was examined with linear mixed-model analyses. Results showed no evidence of trajectory differences between patients with BD, UR, and HC in neurocognition and emotional cognition (ps≥.10). Patients with BD showed stable impairments in global neurocognitive functioning over time, as well as within the domains of ‘working memory and executive function’ and ‘attention and psychomotor speed’, compared to HC. Patients who relapsed during the follow-up time were less successful at down-regulating emotions in positive social scenarios compared to HC. Unaffected relatives also displayed stable deficits in ‘working memory and executive function’ over time, with performance at intermediate levels between BD probands and HC. Finally, poorer neurocognition and positive emotion regulation were associated with more subsyndromal symptoms and functional impairments. In conclusion, we found no evidence of a neuroprogressive origin of cognitive impairments in the newly diagnosed BD or in their UR. Patients’ and UR's impairments in working memory and executive function may reflect a stable cognitive trait-marker of familial risk. Difficulties with positive emotion regulation may be associated with illness progression in BD.

KW - Bipolar disorder

KW - Cognition

KW - Emotional cognition

KW - Endophenotypes

KW - Longitudinal

KW - Unaffected relatives

U2 - 10.1016/j.euroneuro.2022.11.004

DO - 10.1016/j.euroneuro.2022.11.004

M3 - Journal article

C2 - 36462414

AN - SCOPUS:85145579618

VL - 67

SP - 4

EP - 21

JO - European Neuropsychopharmacology

JF - European Neuropsychopharmacology

SN - 0924-977X

ER -