Coulborn Sean, Taylor Chris, Naci Lorina, Owen Adrian M, Fernández-Espejo Davinia
Centre for Human Brain Health and School of Psychology, University of Birmingham, Birmingham B15 2TT, UK.
Trinity College Institute of Neuroscience, School of Psychology, Trinity College Dublin, D02 PN40 Dublin, Ireland.
Brain Sci. 2021 Jun 4;11(6):749. doi: 10.3390/brainsci11060749.
Recent research indicates prolonged disorders of consciousness (PDOC) result from structural and functional impairments to key cortical and subcortical networks, including the default mode network (DMN) and the anterior forebrain mesocircuit (AFM). However, the specific mechanisms which underpin such impairments remain unknown. It is known that disruptions in the striatal-pallidal pathway can result in the over inhibition of the thalamus and lack of excitation to the cortex that characterizes PDOC. Here, we used spectral dynamic causal modelling and parametric empirical Bayes on rs-fMRI data to assess whether DMN changes in PDOC are caused by disruptions in the AFM. PDOC patients displayed overall reduced coupling within the AFM, and specifically, decreased self-inhibition of the striatum, paired with reduced coupling from striatum to thalamus. This led to loss of inhibition from AFM to DMN, mostly driven by posterior areas including the precuneus and inferior parietal cortex. In turn, the DMN showed disruptions in self-inhibition of the precuneus and medial prefrontal cortex. Our results provide support for the anterior mesocircuit model at the subcortical level but highlight an inhibitory role for the AFM over the DMN, which is disrupted in PDOC.
近期研究表明，长期意识障碍（PDOC）是由关键皮质和皮质下网络的结构和功能损伤所致，包括默认模式网络（DMN）和前脑内侧中环路（AFM）。然而，导致此类损伤的具体机制仍不清楚。已知纹状体 - 苍白球通路的破坏可导致丘脑过度抑制以及对皮质缺乏兴奋，这是PDOC的特征。在此，我们对静息态功能磁共振成像（rs - fMRI）数据使用频谱动态因果模型和参数经验贝叶斯方法，以评估PDOC中DMN的变化是否由AFM的破坏引起。PDOC患者在AFM内的整体耦合减少，具体而言，纹状体的自我抑制降低，同时纹状体到丘脑的耦合减少。这导致从AFM到DMN的抑制丧失，主要由包括楔前叶和顶下小叶在内的后部区域驱动。反过来，DMN在楔前叶和内侧前额叶皮质的自我抑制方面出现破坏。我们的结果在皮质下水平为前脑内侧中环路模型提供了支持，但突出了AFM对DMN的抑制作用，而这种作用在PDOC中受到破坏。
