Gong JiaYing, Chen Guanmao, Jia Yanbin, Zhong Shuming, Zhao Lianping, Luo Xiaomei, Qiu Shaojuan, Lai Shunkai, Qi Zhangzhang, Huang Li, Wang Ying
Medical Imaging Center, First Affiliated Hospital of Jinan University, Guangzhou 510630, China; Department of Radiology, Six Affiliated Hospital of Sun Yat-sen University, Guangzhou 510655, China.
Medical Imaging Center, First Affiliated Hospital of Jinan University, Guangzhou 510630, China.
Prog Neuropsychopharmacol Biol Psychiatry. 2019 Jan 10;88:11-18. doi: 10.1016/j.pnpbp.2018.06.012. Epub 2018 Jun 26.
Recent studies demonstrate that functional disruption in resting-state networks contributes to cognitive and affective symptoms of bipolar disorder (BD), however, the functional connectivity (FC) pattern underlying BD II depression within the default mode network (DMN), salience network (SN), and frontoparietal network (FPN) is still not well understood. The primary aim of this study was to explore whether the pathophysiology of BD II derived from the pattern of FC within the DMN, SN, and FPN by using seed-based FC approach of resting-state functional magnetic resonance imaging (rs-fMRI).
Ninety-six BD II patients and 100 HCs underwent rs-fMRI and three-dimensional structural data acquisition. All patients were either drug naive or unmedicated for at least 6 months. The following four regions of interest were used to conduct seed-based FC: the left posterior cingulate cortex (PCC) seed to probe the DMN, the left subgenual anterior cingulate cortex (sgACC) and amygdala seeds to probe the SN, the left dorsal lateral prefrontal cortex (dlPFC) seed to probe the FPN.
Compared with HCs, patients with BD II demonstrated hypoconnectivity of the left PCC to the bilateral medial prefrontal cortex (mPFC) and bilateral precuneus/PCC, and of the left sgACC to the right inferior temporal gyrus (ITG); nevertheless, the left amygdala and dlPFC had no within-network hypo- or hyperconnectivity to any other SN and FPN regions.
Our findings suggest that disrupted FC is located in the DMN and SN, especially in the PCC-mPFC and precuneus/PCC, and sgACC-ITG connectivity in BD II patients.
近期研究表明，静息态网络中的功能破坏会导致双相情感障碍（BD）的认知和情感症状，然而，目前对于II型双相抑郁在默认模式网络（DMN）、突显网络（SN）和额顶叶网络（FPN）中的功能连接（FC）模式仍了解不足。本研究的主要目的是通过使用基于种子点的静息态功能磁共振成像（rs-fMRI）方法，探讨II型双相障碍的病理生理学是否源于DMN、SN和FPN内的FC模式。
96例II型双相障碍患者和100名健康对照者接受了rs-fMRI和三维结构数据采集。所有患者均未用药或至少6个月未接受药物治疗。使用以下四个感兴趣区域进行基于种子点的FC分析：以左侧后扣带回皮质（PCC）为种子点探测DMN，以左侧膝下前扣带回皮质（sgACC）和杏仁核为种子点探测SN，以左侧背外侧前额叶皮质（dlPFC）为种子点探测FPN。
与健康对照者相比，II型双相障碍患者左侧PCC与双侧内侧前额叶皮质（mPFC）及双侧楔前叶/PCC之间的连接减弱，左侧sgACC与右侧颞下回（ITG）之间的连接减弱；然而，左侧杏仁核和dlPFC与SN和FPN的其他任何区域之间在网络内均未出现连接减弱或增强。
我们的研究结果表明，II型双相障碍患者的FC破坏位于DMN和SN，尤其是PCC-mPFC、楔前叶/PCC以及sgACC-ITG连接。
