National Institute of Neurological Disorders and Stroke, Bethesda, USA; Department of Psychology, George Washington University, Washington DC, USA.
National Institute of Neurological Disorders and Stroke, Bethesda, USA.
Neuroimage. 2021 Feb 1;226:117559. doi: 10.1016/j.neuroimage.2020.117559. Epub 2020 Nov 13.
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.
半侧空间忽略被认为是由于大脑两半球间平衡破坏所致。右侧大脑半球损伤通过解除两半球间抑制作用使右侧额顶网络失活，并使左侧网络过度活跃。这一假说机制的证据来自神经心理学以及健康被试的经颅磁刺激（TMS）研究，在后顶叶皮质（PPC）的右侧给予 TMS 抑制可引起类似忽略的、右偏的、视空间偏向。右侧 PPC 给予 TMS 后进行 TMS 与 fMRI 的同步研究显示出任务相关的变化，但可能无法识别出刺激对未直接被特定任务激活的区域的影响，从而使解释复杂化。我们使用右侧 PPC 抑制性 TMS 后的静息态功能连接（RSFC）来研究视空间注意的基础网络的变化，并使用弥散加权成像来测量相关白质通路的结构特性。在一项健康个体的交叉实验中，我们连续给予右侧 PPC 和顶点 theta 爆发 TMS 作为对照条件。我们假设 PPC 抑制性刺激会导致视空间偏向右侧，减少额顶 RSFC，并增加左半球注意网络的 PPC RSFC。我们还预计，PPC 之间额顶网络和胼胝体通路的各向异性分数（FA）的个体差异将解释 TMS 诱导的 RSFC 变化的可变性。正如假设的那样，右侧 PPC 的 TMS 导致线二分判断向右偏移，并增加了右侧 PPC 与左颞上回之间的 RSFC。这种效应与后胼胝体的 FA 呈负相关。右侧 PPC 的局部抑制重塑了注意网络的连接，并且显著依赖于两半球间的连接。
