Reduced Dynamic Interactions Within Intrinsic Functional Brain Networks in Early Blind Patients
Reduced Dynamic Interactions Within Intrinsic Functional Brain Networks in Early Blind Patients
复制标题
早期失明患者内在功能性大脑网络内的动态相互作用减少
DOI:
10.3389/fnins.2019.00268
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发表时间:
2019-03
影响因子:
4.3
通讯作者:
Tian Jie
中科院分区:
文献类型:
--
作者:
Li Xianglin;Wang Ailing;Xu Junhai;Sun Zhenbo;Xia Jikai;Wang Peiyuan;Wang Bin;Zhang Ming;Tian Jie
Neuroimaging studies in early blind (EB) patients have shown altered connections or brain networks. However, it remains unclear how the causal relationships are disrupted within intrinsic brain networks. In our study, we used spectral dynamic causal modeling (DCM) to estimate the causal interactions using resting-state data in a group of 20 EB patients and 20 healthy controls (HC). Coupling parameters in specific regions were estimated, including the medial prefrontal cortex (mPFC), posterior cingulate cortex (PCC), and inferior parietal lobule (IPC) in the default mode network (DMN); dorsal anterior cingulate cortex (dACC) and bilateral anterior insulae (AI) in the salience network (SN), and bilateral frontal eye fields (FEF) and superior parietal lobes (SPL) within the dorsal attention network (DAN). Statistical analyses found that all endogenous connections and the connections from the mPFC to bilateral IPCs in EB patients were significantly reduced within the DMN, and the effective connectivity from the PCC and lIPC to the mPFC, and from the mPFC to the PCC were enhanced. For the SN, all significant connections in EB patients were significantly decreased, except the intrinsic right AI connections. Within the DAN, more significant effective connections were observed to be reduced between the EB and HC groups, while only the connections from the right SPL to the left SPL and the intrinsic connection in the left SPL were significantly enhanced. Furthermore, discovery of more decreased effective connections in the EB subjects suggested that the disrupted causal interactions between specific regions are responsive to the compensatory brain plasticity in early deprivation.
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