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Purpose of review This review considers recent observations on vestibular syncope in terms of clinical features, laboratory findings, and potential mechanisms. Recent findings Vestibular syncope, potentially associated with severe fall-related injuries, may develop multiple times in about one-third of patients. Meniere's disease and benign paroxysmal positional vertigo are the most common causes of vestibular syncope, but the underlying disorders remain elusive in 62% of cases with vestibular syncope. The postictal orthostatic blood pressure test exhibits a lower diagnostic yield. Vestibular function tests, such as cervical vestibular-evoked myogenic potentials and video head impulse tests, can reveal one or more abnormal findings, suggesting compensated or ongoing minor vestibular dysfunctions. The pathomechanism of syncope is assumed to be the erroneous interaction between the vestibulo-sympathetic reflex and the baroreflex that have different operating mechanisms and action latencies. The central vestibular system, which estimates gravity orientation and inertia motion may also play an important role in abnormal vestibulo-sympathetic reflex. Summary Vestibular disorders elicit erroneous cardiovascular responses by providing false vestibular information. The results include vertigo-induced hypertension or hypotension, which can ultimately lead to syncope in susceptible patients.
Purpose of review This review considers recent observations on vestibular syncope in terms of clinical features, laboratory findings, and potential mechanisms. Recent findings Vestibular syncope, potentially associated with severe fall-related injuries, may develop multiple times in about one-third of patients. Meniere's disease and benign paroxysmal positional vertigo are the most common causes of vestibular syncope, but the underlying disorders remain elusive in 62% of cases with vestibular syncope. The postictal orthostatic blood pressure test exhibits a lower diagnostic yield. Vestibular function tests, such as cervical vestibular-evoked myogenic potentials and video head impulse tests, can reveal one or more abnormal findings, suggesting compensated or ongoing minor vestibular dysfunctions. The pathomechanism of syncope is assumed to be the erroneous interaction between the vestibulo-sympathetic reflex and the baroreflex that have different operating mechanisms and action latencies. The central vestibular system, which estimates gravity orientation and inertia motion may also play an important role in abnormal vestibulo-sympathetic reflex. Summary Vestibular disorders elicit erroneous cardiovascular responses by providing false vestibular information. The results include vertigo-induced hypertension or hypotension, which can ultimately lead to syncope in susceptible patients.
Objective Vestibular-evoked myogenic potentials (VEMPs) can help in assessing otolithic neural pathway in the brainstem, which may also contribute to the cardiovascular autonomic function. Parkinson’s disease (PD) is associated with altered VEMP responses; however, the associations between VEMP abnormalities and multiple system atrophy (MSA) remain unknown. Therefore, we compared the extent of otolith dysfunction using ocular (oVEMP) and cervical VEMPs between patients with MSA and PD.Methods We analyzed the clinical features, VEMP, and head-up tilt table test (HUT) findings using the Finometer in 24 patients with MSA and 52 with de novo PD who had undergone neurotologic evaluation at a referral-based university hospital in South Korea from January 2021 to March 2023.Results MSA was associated with bilateral oVEMP abnormalities (odds ratio [95% confidence interval] = 9.19 [1.77–47.76], <i>p</i> = 0.008). The n1–p1 amplitude was negatively correlated with the Unified Multiple System Atrophy Rating Scale I-II score in patients with MSA (<i>r</i> = -0.571, <i>p</i> = 0.033), whereas it did not correlate with the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale-III score in patients with PD (<i>r</i> = -0.051, <i>p</i> = 0.687). The n1 latency was negatively correlated with maximum changes in systolic blood pressure within 15 s during HUT in patients with PD (<i>r</i> = -0.335, <i>p</i> = 0.040) but not in those with MSA (<i>r</i> = 0.277, <i>p</i> = 0.299).Conclusion Bilaterally abnormal oVEMP responses may indicate the extent of brainstem dysfunction in MSA. oVEMP reflects the integrity of otolith-autonomic interplay, reliably assists in differentiating between MSA and PD, and helps infer clinical decline.
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