| 王玮,钱绍文,刘锴,李勃,辛阔林,孙钢.广泛性焦虑障碍发病机制的静息态功能磁共振成像[J].中国医学影像技术,2016,32(3):358~362 |
| 广泛性焦虑障碍发病机制的静息态功能磁共振成像 |
| Resting-state functional magnetic resonance imaging in neural mechanism of generalized anxiety disorder |
| 投稿时间：2015-07-24 修订日期：2015-12-11 |
| DOI：10.13929/j.1003-3289.2016.03.010 |
| 中文关键词: 广泛性焦虑障碍 磁共振成像 静息态 功能连接 |
| 英文关键词:Generalized anxiety disorder Magznetic resonance imaging Resting state Functional connectivity |
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| 中文摘要: |
| 目的 应用静息态功能磁共振成像(rs-fMRI)观察广泛性焦虑障碍(GAD)患者全脑活动及网络连接的变化,探索其与临床焦虑症状的相关性。方法 对28例GAD患者(GAD组)、28名健康对照(HC)组进行fMRI扫描。逐体素对比分析两组低频振幅(ALFF)和种子点静息态功能连接(FC)的差异,采用Pearson相关分析研究其与焦虑自评量表、汉密尔顿焦虑量表(HAM-A)、GAD-7项量表和汉密尔顿抑郁量表等评分的相关性。结果 GAD组双侧背内侧前额叶、左楔前叶/后扣带回和双侧背外侧前额叶ALFF值明显高于HC组(P均<0.05)。GAD组右侧眶额叶/岛叶-背内侧前额叶、左侧眶额叶/岛叶-背内侧前额叶、左侧背外侧前额叶皮层-右侧海马的功能连接与HAM-A评分和GAD-7评分均有相关性。结论 背侧前额叶皮层及楔前叶/后扣带回脑活动、前额叶-边缘组织回路异常可能是GAD重要的发病机制。 |
| 英文摘要: |
| Objective To observe regional and network-level neural function abnormalities in generalized anxiety disorder(GAD) with resting-state functional MR imaging(rs-fMRI), and to assess the relationships between these alterations and clinical symptom scores. Methods Twenty-eight GAD patients(GAD group) and 28 matched healthy controls(HC, HC group) underwent rs-fMRI. Amplitude of low-frequency fluctuation(ALFF) and seed-based resting-state functional connectivity(RSFC) were compared between the two groups using voxel-wise two-sample t test to explore the regional neural function and RSFC integration, and Pearson correlation analysis was performed to explore their correlations with self-rating anxiety scale, Hamilton anxiety rating scale(HAM-A), GAD-7 items scale and Hamilton depression rating scale scores. Results Compared to HC group, ALFF was higher in the bilateral dorsomedial prefrontal cortex(DMPFC), bilateral dorsolateral prefrontal cortex(DLPFC) and left precuneus/posterior cingulate cortex(PCU/PCC) in GAD group(all P<0.05). RSFC between right orbitofrontal cortices(OFC)/insula and DMPFC, left OFC/insula and DMPFC, left DLPFC and right hippocampus significantly correlated with both HAM-A scores and GAD-7 items scores. Conclusion Abnormal neural activities in dorsal prefrontal cortices and precunes/posterior cingulate cortex, and aberrant prefrontal-limbic circuit may be important pathogenesis of GAD. |
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