Department of Neurology, Korea University Ansan Hospital, Ansan, South Korea.
Department of Neurology, Chungnam National University Hospital, Daejeon, South Korea.
Ann Clin Transl Neurol. 2022 Oct;9(10):1616-1625. doi: 10.1002/acn3.51661. Epub 2022 Sep 2.
Vestibular syncope is a condition in which vertigo-induced hemodynamic changes cause syncope. This study investigated the clinical and laboratory findings of vestibular syncope and tried to refine our knowledge of the mechanism underlying this newly recognized entity.
This study retrospectively analyzed 53 patients (33 women, median age = 63 years [interquartile range = 54-71 years]) with vestibular syncope from January 2017 to December 2021. To explain the mechanism of vestibular syncope, we incorporated a velocity-storage model into the dual reflex pathways comprising the vestibulo-sympathetic reflex and baroreflex and predicted the cardiovascular responses.
Twenty (37.7%) patients had multiple episodes of vestibular syncope, and seven (13.2%) had potentially life-threatening injuries. Meniere's disease (20.8%) and benign paroxysmal positional vertigo (9.4%) were the most common underlying vestibular disorders. Abnormal vestibular function tests included impaired cervical vestibular-evoked myogenic potentials (57.5%) and positive head impulse tests (31.0%). Orthostatic hypotension was found in 19.5% of patients. Dyslipidemia (30.2%) and hypertension (28.3%) were common medical comorbidities. The dual reflex pathways incorporating the function of the velocity-storage circuit in the brainstem and cerebellum suggest that vestibular syncope is a neurally mediated reflex syncope associated with a sudden hemodynamic change during vertigo. This change can be arterial hypertension triggered by a false downward inertial cue, as suggested previously, or hypotension driven by a false upward inertial cue.
Vestibular syncope is associated with various vestibular disorders and requires careful evaluation and intervention to prevent recurrent falls and significant injuries.
前庭性晕厥是一种由眩晕引起的血液动力学变化导致晕厥的病症。本研究调查了前庭性晕厥的临床和实验室发现，并试图完善我们对这一新认识实体的潜在机制的认识。
本研究回顾性分析了 2017 年 1 月至 2021 年 12 月期间的 53 例（33 例女性，中位年龄 63 岁[四分位距 54-71 岁]）前庭性晕厥患者。为了解释前庭性晕厥的机制，我们将速度存储模型纳入包括前庭-交感反射和压力反射在内的双反射途径中，并预测了心血管反应。
20 例（37.7%）患者有多次前庭性晕厥发作，7 例（13.2%）有潜在危及生命的损伤。梅尼埃病（20.8%）和良性阵发性位置性眩晕（9.4%）是最常见的潜在前庭疾病。异常的前庭功能检查包括颈性前庭诱发肌源性电位受损（57.5%）和阳性头脉冲试验（31.0%）。体位性低血压见于 19.5%的患者。血脂异常（30.2%）和高血压（28.3%）是常见的合并症。纳入脑桥和小脑速度存储回路功能的双反射途径提示，前庭性晕厥是一种与眩晕时突然血液动力学变化相关的神经介导反射性晕厥。这种变化可以是动脉高血压，如前所述，是由虚假向下惯性线索触发的，也可以是低血压，是由虚假向上惯性线索驱动的。
前庭性晕厥与各种前庭疾病相关，需要仔细评估和干预，以防止反复发作和严重损伤。
