Self-motion perception is sensitized in vestibular migraine: pathophysiologic and clinical implications

Self-motion perception is sensitized in vestibular migraine: pathophysiologic and clinical implications
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DOI:
10.1038/s41598-019-50803-y
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发表时间:
2019-10-04
期刊:
影响因子:
4.6
通讯作者:
Lewis, Richard F.
Lewis, Richard F.
中科院分区:
综合性期刊3区
文献类型:
--
作者:
King, Susan;Priesol, Adrian J.;Lewis, Richard F.

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前庭性偏头痛 (VM) 是自发性眩晕的最常见原因,但人们对此仍知之甚少。我们通过测量患者和对照受试者的自我运动知觉阈值,并通过表征前庭眼反射(VOR)以及前庭和头痛症状的严重程度,研究了中枢前庭通路在 VM 中敏感的假设。 VM患者对滚动倾斜异常敏感,滚动倾斜共同调节半规管和耳石器官的活动,但对单独激活耳管或耳石器官的运动不敏感,这意味着耳石整合敏感。当倾斜阈值与前庭症状严重程度或 VOR 动态一起考虑时,VM 患者分为两类。一组中的阈值与症状和 VOR 时间常数呈正相关;第二组中的阈值一致较低并且与症状和时间常数无关。 VM阈值异常表现出与脑干速度存储机制平行的频率依赖性。这些结果支持了一种致病模型,其中前庭症状源自前庭核,前庭核对偏头痛相关的脑干区域敏感,同时受到来自小脑结节和悬雍垂(耳管耳石整合部位)的抑制性反馈的抑制。这一概念框架阐明了 VM 病理生理学,并有可能促进其诊断和治疗。
Vestibular migraine (VM) is the most common cause of spontaneous vertigo but remains poorly understood. We investigated the hypothesis that central vestibular pathways are sensitized in VM by measuring self-motion perceptual thresholds in patients and control subjects and by characterizing the vestibulo-ocular reflex (VOR) and vestibular and headache symptom severity. VM patients were abnormally sensitive to roll tilt, which co-modulates semicircular canal and otolith organ activity, but not to motions that activate the canals or otolith organs in isolation, implying sensitization of canalotolith integration. When tilt thresholds were considered together with vestibular symptom severity or VOR dynamics, VM patients segregated into two clusters. Thresholds in one cluster correlated positively with symptoms and with theVOR time constant; thresholds in the second cluster were uniformly low and independent of symptoms and the time constant. The VM threshold abnormality showed a frequency-dependence that paralleled the brain stem velocity storage mechanism. These results support a pathogenic model where vestibular symptoms emanate from the vestibular nuclei, which are sensitized by migraine-related brainstem regions and simultaneously suppressed by inhibitory feedback from the cerebellar nodulus and uvula, the site of canal-otolith integration. This conceptual framework elucidates VM pathophysiology and could potentially facilitate its diagnosis and treatment.