Role of the Insula and Vestibular System in Patients with Chronic Subjective Dizziness: An fMRI Study Using Sound-Evoked Vestibular Stimulation.
Role of the Insula and Vestibular System in Patients with Chronic Subjective Dizziness: An fMRI Study Using Sound-Evoked Vestibular Stimulation.
复制标题
DOI：
10.3389/fnbeh.2015.00334
复制
发表时间：
2015
影响因子：
3
通讯作者：
Passamonti L
中科院分区：
文献类型：
--
作者：
Indovina I;Riccelli R;Chiarella G;Petrolo C;Augimeri A;Giofrè L;Lacquaniti F;Staab JP;Passamonti L
慢性主观性眩晕(CSD)是一种常见的前庭疾病，其特征是持续的非眩晕、不稳定，以及对运动刺激的高度敏感，在导致急性前庭症状或平衡障碍的事件后可能持续数月至数年。CSD与基本前庭或动眼反射的异常无关。相反，它被认为是由于持续使用高威胁的姿势控制策略，以及在触发事件解决很长时间后，更多地依赖视觉线索来确定空间方向(即视觉依赖)。与焦虑相关的人格特征使人更容易患上慢性精神障碍。中央前庭系统和与焦虑相关的神经结构之间的异常相互作用可能会维持这种状态。前庭和焦虑相关的过程在大脑中重叠，特别是在脑岛和海马体。这些脑区对前庭刺激的活动和连通性的改变可能是CSD的神经基础。我们通过比较18名CSD患者和18名健康对照的大脑活动来验证这一假设，这些大脑活动是通过功能磁共振成像测量的，在响亮的短音脉冲期间，这是可以唤起强烈前庭反应的听觉刺激。与对照组相比，CSD患者在顶岛前庭皮质(PIVC)，包括后岛、前岛、额下回、海马体和前扣带回对声音诱发前庭刺激的激活减少。CSD患者前岛叶与PIVC、前岛叶与枕中皮质、海马与PIVC、前扣带回皮质与PIVC之间的连通性也发生改变。我们的结论是，PIVC、海马体、前脑岛、额叶下回和前扣带回的激活减少，以及这些区域之间的连通性改变，可能与CSD患者的长期前庭症状有关。此外，与对照组相比，CSD患者前脑岛和枕中皮质之间的连通性改变可能是更多地依赖视觉线索进行空间定向的基础。
Chronic subjective dizziness (CSD) is a common vestibular disorder characterized by persistent non-vertiginous dizziness, unsteadiness, and heightened sensitivity to motion stimuli that may last for months to years after events that cause acute vestibular symptoms or disrupt balance. CSD is not associated with abnormalities of basic vestibular or oculomotor reflexes. Rather, it is thought to arise from persistent use of high-threat postural control strategies and greater reliance on visual cues for spatial orientation (i.e., visual dependence), long after triggering events resolve. Anxiety-related personality traits confer vulnerability to CSD. Anomalous interactions between the central vestibular system and neural structures related to anxiety may sustain it. Vestibular- and anxiety-related processes overlap in the brain, particularly in the insula and hippocampus. Alterations in activity and connectivity in these brain regions in response to vestibular stimuli may be the neural basis of CSD. We examined this hypothesis by comparing brain activity from 18 patients with CSD and 18 healthy controls measured by functional magnetic resonance imaging during loud short tone bursts, which are auditory stimuli that evoke robust vestibular responses. Relative to controls, patients with CSD showed reduced activations to sound-evoked vestibular stimulation in the parieto-insular vestibular cortex (PIVC) including the posterior insula, and in the anterior insula, inferior frontal gyrus, hippocampus, and anterior cingulate cortex. Patients with CSD also showed altered connectivity between the anterior insula and PIVC, anterior insula and middle occipital cortex, hippocampus and PIVC, and anterior cingulate cortex and PIVC. We conclude that reduced activation in PIVC, hippocampus, anterior insula, inferior frontal gyrus, and anterior cingulate cortex, as well as connectivity changes among these regions, may be linked to long-term vestibular symptoms in patients with CSD. Furthermore, altered connectivity between the anterior insula and middle occipital cortex may underlie the greater reliance on visual cues for spatial orientation in CSD patients relative to controls.