A meta-analysis of cognitive deficits in first-episode Major Depressive Disorder

2012 ◽  
Vol 140 (2) ◽  
pp. 113-124 ◽  
Author(s):  
Rico S.C. Lee ◽  
Daniel F. Hermens ◽  
Melanie A. Porter ◽  
M. Antoinette Redoblado-Hodge
2021 ◽  
Vol 12 ◽  
Author(s):  
Jin Liu ◽  
Bangshan Liu ◽  
Mi Wang ◽  
Yumeng Ju ◽  
Qiangli Dong ◽  
...  

Background: Cognitive deficits have shown progressive feature in major depressive disorder (MDD). However, it remains unknown which component of cognitive function is progressively impaired across episodes of MDD. Here we aim to identify the progressively impaired cognitive components in patients with MDD.Methods: A comprehensive neurocognitive test battery was used to assess the cognitive components (executive function, attention, processing speed, memory, working memory, inhibition, shifting, and verbal fluency) in 35 patients with first-episode MDD (FED), 60 patients with recurrent MDD (RD) and 111 matched healthy controls (HCs). After 6 months of treatment with antidepressant, 20 FED and 36 RD patients achieved clinical remission and completed their second-time neurocognitive tests. Statistical analyses were conducted to identify the impaired cognitive components in the FED and RD groups before and after treatment, and to assess the relationship between the cognitive components and the number of episodes and total illness duration in the MDD patient group.Results: At baseline, both the FED and RD groups showed impairments in all of the cognitive components; the FED and RD groups showed no significant difference in all of the components except for shifting. After remission, only shifting in the RD group showed no significant improvement and remained in an impaired status. Furthermore, shifting was the only component negatively correlated with the number of episodes as well as the total illness duration.Conclusions: Shifting may serve as the progressive cognitive deficit across episodes of MDD.Clinical Trials Registration: Registry name: HPA function and MRI study of trauma-related depression; Registration number: ChiCTR1800014591; URL: http://www.chictr.org.cn/edit.aspx?pid=24669&htm=4.


2019 ◽  
Vol 45 (Supplement_2) ◽  
pp. S192-S193
Author(s):  
Nuray Çakici ◽  
Arjen L Sutterland ◽  
Brenda W ◽  
J H Penninx ◽  
Lieuwe de Haan ◽  
...  

2012 ◽  
Vol 43 (10) ◽  
pp. 2017-2026 ◽  
Author(s):  
E. Bora ◽  
B. J. Harrison ◽  
M. Yücel ◽  
C. Pantelis

BackgroundThere is evidence to suggest that cognitive deficits might persist beyond the acute stages of illness in major depressive disorder (MDD). However, the findings are somewhat inconsistent across the individual studies conducted to date. Our aim was to conduct a systematic review and meta-analysis of existing studies that have examined cognition in euthymic MDD patients.MethodFollowing a systematic search across several publication databases, meta-analyses were conducted for 27 empirical studies that compared euthymic adult MDD patients (895 participants) and healthy controls (997 participants) across a range of cognitive domains. The influence of demographic variables and confounding factors, including age of onset and recurrent episodes, was examined.ResultsCompared with healthy controls, euthymic MDD patients were characterized by significantly poorer cognitive functions. However, the magnitude of observed deficits, with the exception of inhibitory control, were generally modest when late-onset cases were excuded. Late-onset cases demonstrated significantly more pronounced deficits in verbal memory, speed of information processing and some executive functions.ConclusionsCognitive deficits, especially poor response inhibition, are likely to be persistent features, at least of some forms, of adult-onset MDD. More studies are necessary to examine cognitive dysfunction in remitted psychotic, melancholic and bipolar spectrum MDD. Cognitive deficits overall appear to be more common among patients with late-onset depression, supporting the theories suggesting that possible vascular and neurodegenerative factors play a role in a substantial number of these patients.


2020 ◽  
Vol 88 ◽  
pp. 547-558 ◽  
Author(s):  
Nuray Çakici ◽  
Arjen L. Sutterland ◽  
Brenda W.J.H. Penninx ◽  
Virgil A. Dalm ◽  
Lieuwe de Haan ◽  
...  

2019 ◽  
Author(s):  
Tiffany C. Ho ◽  
Boris Gutman ◽  
Elena Pozzi ◽  
Hans J. Grabe ◽  
Norbert Hosten ◽  
...  

AbstractAlterations in regional subcortical brain volumes have been widely investigated as part of the efforts of an international consortium, ENIGMA, to determine reliable structural brain signatures for Major Depressive Disorder (MDD). Given that subcortical structures are comprised of distinct subfields, we sought to build significantly from prior work to precisely map localized MDD-related differences in subcortical regions using shape analysis. In this meta-analysis of subcortical shape from the ENIGMA-MDD working group, we compared 1,781 patients with MDD and 2,953 healthy controls (CTL) on individual measures of shape metrics (thickness and surface area) on the surface of seven bilateral subcortical structures: nucleus accumbens, amygdala, caudate, hippocampus, pallidum, putamen, and thalamus. Harmonized data processing and statistical analyses were conducted locally at each site, and findings were aggregated by meta-analysis. Relative to CTL, patients with MDD had lower surface area in the subiculum of the hippocampus, the basolateral amygdala, and the nucleus accumbens shell. Relative to CTL, patients with adolescent-onset MDD (≤ 21 years) had lower thickness and surface area of the subiculum of the hippocampus and the basolateral amygdala. Relative to first-episode MDD, recurrent MDD patients had lower thickness and surface area in the CA1 of the hippocampus and the basolateral amygdala. Our results suggest that previously reported MDD-associated volumetric differences may be localized to specific subfields of these structures that have been shown to be sensitive to the effects of stress, with important implications for mapping treatments to patients based on specific neural targets and key clinical features.


Sign in / Sign up

Export Citation Format

Share Document