Hemispatial neglect is thought to result from disruption of interhemispheric equilibrium. Right hemisphere lesions deactivate the right frontoparietal network and hyperactivate the left via release from interhemispheric inhibition. Support for this putative mechanism comes from neuropsychological evidence as well as transcranial magnetic stimulation (TMS) studies in healthy subjects, in whom right posterior parietal cortex (PPC) inhibition causes neglect-like, rightward, visuospatial bias. Concurrent TMS and fMRI after right PPC TMS show task-dependent changes but may fail to identify effects of stimulation in areas not directly activated by the specific task, complicating interpretations. We used resting-state functional connectivity (RSFC) after inhibitory TMS over the right PPC to examine changes in the networks underlying visuospatial attention and used diffusion-weighted imaging to measure the structural properties of relevant white matter pathways. In a crossover experiment in healthy individuals, we delivered continuous theta burst TMS to the right PPC and vertex as control condition. We hypothesized that PPC inhibitory stimulation would result in: a rightward visuospatial bias, decrease frontoparietal RSFC, and increase the PPC RSFC with the attentional network in the left hemisphere. We also expected that individual differences in fractional anisotropy (FA) of the frontoparietal network and the callosal pathway between the PPCs would account for variability of the TMS-induced RSFC changes. As hypothesized, TMS over the right PPC caused a rightward shift in line bisection judgment and increased RSFC between the right PPC and the left superior temporal gyrus. This effect was inversely related to FA in the posterior corpus callosum. Local inhibition of the right PPC reshapes connectivity in the attentional network and depends significantly on interhemispheric connections.

中文翻译：

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胼胝体各向异性预测顶叶抑制刺激后的注意网络变化

半空间忽视被认为是由于半球间平衡的破坏造成的。右半球病变使右额顶网络失活，并通过解除半球间抑制而过度激活左侧。对这种假定机制的支持来自神经心理学证据以及对健康受试者的经颅磁刺激 (TMS) 研究，在这些受试者中，右后顶叶皮层 (PPC) 抑制会导致类似忽视的向右视觉空间偏差。右 PPC TMS 后并发 TMS 和 fMRI 显示任务相关的变化，但可能无法识别未由特定任务直接激活的区域的刺激效果，使解释复杂化。我们在右侧 PPC 上使用抑制性 TMS 后的静息状态功能连接 (RSFC) 来检查视觉空间注意力基础网络的变化，并使用弥散加权成像来测量相关白质通路的结构特性。在健康个体的交叉实验中，我们将连续的 theta 脉冲 TMS 传递到正确的 PPC 和顶点作为控制条件。我们假设 PPC 抑制性刺激会导致：向右的视觉空间偏差，减少额顶 RSFC，并通过左半球的注意网络增加 PPC RSFC。我们还预计额顶叶网络的分数各向异性 (FA) 和 PPC 之间的胼胝体通路的个体差异将解释 TMS 诱导的 RSFC 变化的变异性。正如假设的那样，右侧 PPC 上的 TMS 导致线平分判断向右移动，并增加右侧 PPC 和左侧颞上回之间的 RSFC。这种效果与后胼胝体中的 FA 呈负相关。对正确 PPC 的局部抑制重塑了注意力网络中的连接性，并且在很大程度上取决于半球间的连接。