Altered cerebellar gray matter and cerebellar-cortex resting-state functional connectivity in patients with bipolar disorder Ⅰ

小脑 基于体素的形态计量学 神经科学 心理学 中央后回 双相情感障碍 磁共振成像 医学 解剖 功能磁共振成像 白质 放射科 认知
作者
Liqian Cui,Hao Li,Jin Biao Li,Huixing Zeng,Yizhi Zhang,Wenhao Deng,Wenjin Zhou,Liping Cao
出处
期刊:Journal of Affective Disorders [Elsevier]
卷期号:302: 50-57 被引量:14
标识
DOI:10.1016/j.jad.2022.01.073
摘要

Bipolar disorder (BP) is a common psychiatric disorder characterized by extreme fluctuations in mood. Recent studies have indicated the involvement of cerebellum in the pathogenesis of BP. However, no study has focused on the precise role of cerebellum exclusively in patients with bipolar I disorder (BP-I).Forty-five patients with BP-I and 40 healthy controls were recruited. All subjects underwent clinical evaluation and Magnetic Resonance diffusion Tension Imaging scans. For structural images, we used a spatially unbiased infratentorial template toolbox to isolate the cerebellum and then preformed voxel-based morphometry (VBM) analyses to assess the difference in cerebellar gray matter volume (GMV) between the two groups. For the functional images, we chose the clusters that survived from VBM analysis as seeds and performed functional connectivity (FC) analysis. Between-group differences were assessed using the independent Students t test or the nonparametric Mann-Whitney U Test. For multiple comparisons, the results were further corrected with Gaussian random field (GRF) approach (voxel-level P < 0.001, cluster-level P < 0.05).Compared with healthy controls, BP-I patients showed significantly decreased GMV in left lobule V and left lobule VI (P < 0.05, GRF corrected). The FC of cerebellum with bilateral superior temporal gyrus, bilateral insula, bilateral rolandic operculum, right putamen, and left precentral gyrus was disrupted in BP-I patients (P < 0.05, GRF corrected).BP-I patients showed decreased cerebellar GMV and disrupted cerebellar-cortex resting-state FC. This suggests that cerebellar abnormalities may play an important role in the pathogenesis of BP-I.
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