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Background and Objectives: 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. Methods: 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. Results: 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. Conclusions: Vestibular syncope is associated with various vestibular disorders and requires careful evaluation and intervention to prevent recurrent falls and significant injuries. [ABSTRACT FROM AUTHOR]

Fixation nystagmus refers to the nystagmus that appears or markedly increases with fixation. While relatively common in infantile (congenital) nystagmus, acquired fixation nystagmus is unusual and has been ascribed to lesions involving the cerebellar nuclei or the fibers projecting from the cerebellum to the brainstem. We aimed to report the clinical features of patients with acquired fixation nystagmus and discuss possible mechanisms using a model simulation and diagnostic significance. We describe four patients with acquired fixation nystagmus that appears or markedly increases with visual fixation. All patients had lesions involving the cerebellum or dorsal medulla. All patients showed direction-changing gaze-evoked nystagmus, impaired smooth pursuit, and decreased vestibular responses on head-impulse tests. The clinical implication of fixation nystagmus is that it may occur in central lesions that impair both smooth pursuit and the vestibulo-ocular reflex (VOR) but without creating a spontaneous nystagmus in the dark. We develop a mathematical model that hypothesizes that fixation nystagmus reflects a central tone imbalance due to abnormal function in cerebellar circuits that normally optimize the interaction between visual following (pursuit) and VOR during attempted fixation. Patients with fixation nystagmus have central lesions involving the cerebellar circuits that are involved in visual–vestibular interactions and normally eliminate biases that cause a spontaneous nystagmus. [ABSTRACT FROM AUTHOR]

We aimed to characterize the central positional nystagmus (CPN) observed in lesions involving the inferior cerebellar peduncle (ICP). We analyzed the clinical and neurotologic findings in six patients with an isolated unilateral ICP infarction that had been diagnosed at a university hospital in South Korea from 2003 to 2019. Patients usually presented with acute vestibular syndrome in isolation (4/6, 67%). Ipsilesional spontaneous nystagmus was observed in five while supine (5/6, 83%). Four (4/6, 67%) patients showed CPN which included apogeotropic (n = 3) or geotropic (n = 1) during head turning to either side while supine, and vertical nystagmus during straight-head hanging, Dix-Hallpike maneuvers, or up-righting (n = 3). Four patients showed contraversive ocular tilt reaction or tilt of the subjective visual vertical. Bedside and video head-impulse tests were normal in all patients. CPN is a usual finding in ICP lesions, and may be ascribed to damage of the fibers running from the nodulus/uvula onto the vestibular nucleus via the ICP. [ABSTRACT FROM AUTHOR]