Journal of affective disorders · 2018
Analysis of voxel-mirrored homotopic connectivity in medication-free, current major depressive disorder.
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Fan Huanhuan, Yang Xiao, Zhang Jian, Chen Yayun, Li Tao, Ma Xiaohong
Аннотация
BACKGROUND: Recent neuroimaging studies suggest that abnormal function connectivity exists in patients with major depressive disorder (MDD). The aim of this study was to further analyze the underlying neural mechanism of MDD and explore whether clinical characteristics are correlated with the alerted homotopic connectivity in patients with MDD.
METHODS: Using voxel-mirrored homotopic connectivity (VMHC) during resting state, we compared 80 medication-free patients having current episodes of MDD and 124 never-depressed healthy controls (HCs) matched for age and gender.
RESULTS: We found decreased VMHC in patients with MDD in bilateral posterior cingulate cortex (PCC) extending to precuneus (Pre) compared with the HCs, which provided strong support for the potential role of PCC/Pre in recognizing interhemispheric connectivity deficits of MDD. Negative correlation between illness course and VMHC in PCC was observed as well.
LIMITATIONS: First, we just compared the functional connectivity at a rest state but not under a specific task. Second, we did not mitigate the delayed effect on the measurable alterations in homotopic brain activity. Third, we did not make a longitudinal comparison after patients receiving therapeutic drugs.
CONCLUSIONS: These findings that linking illness course with functional brain changes in depression help us understand the neural architecture of MDD.
METHODS: Using voxel-mirrored homotopic connectivity (VMHC) during resting state, we compared 80 medication-free patients having current episodes of MDD and 124 never-depressed healthy controls (HCs) matched for age and gender.
RESULTS: We found decreased VMHC in patients with MDD in bilateral posterior cingulate cortex (PCC) extending to precuneus (Pre) compared with the HCs, which provided strong support for the potential role of PCC/Pre in recognizing interhemispheric connectivity deficits of MDD. Negative correlation between illness course and VMHC in PCC was observed as well.
LIMITATIONS: First, we just compared the functional connectivity at a rest state but not under a specific task. Second, we did not mitigate the delayed effect on the measurable alterations in homotopic brain activity. Third, we did not make a longitudinal comparison after patients receiving therapeutic drugs.
CONCLUSIONS: These findings that linking illness course with functional brain changes in depression help us understand the neural architecture of MDD.