Downregulation of early visual cortex excitability mediates oscillopsia suppression.
Downregulation of early visual cortex excitability mediates oscillopsia suppression.
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DOI：
10.1212/wnl.0000000000004360
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发表时间：
2017-09-12
期刊：
影响因子：
9.9
通讯作者：
Bronstein A
中科院分区：
文献类型：
--
作者：
Ahmad H;Roberts RE;Patel M;Lobo R;Seemungal B;Arshad Q;Bronstein A
在一项观察性研究中，确定介导双侧前庭功能衰竭（BVF）患者对失视适应的神经生理学机制。我们直接探讨的假设，介导视错觉抑制的适应性变化牵连早期视觉皮层（V1/V2）。因此，我们调查了V1/V2兴奋性使用经颅磁刺激（TMS）在12个avestibular患者和12名健康对照。具体来说，我们评估了TMS诱导的光幻视阈值在基线和皮质兴奋性的变化，同时在以下条件下进行视觉运动适应范例：基线测量（即，静态），在视觉运动期间（即，适应前的运动），以及在单向视觉运动适应5分钟后的视觉运动期间（即，运动适应）。患者的基线光幻视阈值显著较高，反映了潜在的适应机制。个体阈值与幻视症状负荷相关。在视觉运动适应条件下，没有观察到基线兴奋性的差异，但在适应前的运动和运动适应条件下，我们观察到显着减弱患者的皮层兴奋性。同样，这种兴奋性的衰减在症状较轻的患者中更强。我们的研究结果提供了神经生理学证据，V1/V2的皮质介导的适应机制在抑制BVF患者的视觉障碍中起着至关重要的作用。
To identify in an observational study the neurophysiologic mechanisms that mediate adaptation to oscillopsia in patients with bilateral vestibular failure (BVF). We directly probe the hypothesis that adaptive changes that mediate oscillopsia suppression implicate the early visual-cortex (V1/V2). Accordingly, we investigated V1/V2 excitability using transcranial magnetic stimulation (TMS) in 12 avestibular patients and 12 healthy controls. Specifically, we assessed TMS-induced phosphene thresholds at baseline and cortical excitability changes while performing a visual motion adaptation paradigm during the following conditions: baseline measures (i.e., static), during visual motion (i.e., motion before adaptation), and during visual motion after 5 minutes of unidirectional visual motion adaptation (i.e., motion adapted). Patients had significantly higher baseline phosphene thresholds, reflecting an underlying adaptive mechanism. Individual thresholds were correlated with oscillopsia symptom load. During the visual motion adaptation condition, no differences in excitability at baseline were observed, but during both the motion before adaptation and motion adapted conditions, we observed significantly attenuated cortical excitability in patients. Again, this attenuation in excitability was stronger in less symptomatic patients. Our findings provide neurophysiologic evidence that cortically mediated adaptive mechanisms in V1/V2 play a critical role in suppressing oscillopsia in patients with BVF.