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Cerebellar nodulus and uvula and their connections with the vestibular nuclei form the so‐called velocity‐storage circuit. Lesions involving the velocity‐storage circuit give rise to positional vertigo and nystagmus. Herein, we present a 32‐year‐old man with cerebellar nodulus and uvular hemorrhage who showed periodic vertigo and downbeat nystagmus in the supine position. To explain this unusual pattern, we adopted velocity‐storage model with a lesion on the neural connection between the gravity and inertia estimators, resulting in periodic neural impulses and a gravity bias in a specific position. This report expands the spectrum of central positional nystagmus due to dysfunction of the velocity‐storage mechanism. [ABSTRACT FROM AUTHOR]

Background and purpose: The temporal characteristics of stroke risks were evaluated in emergency department patients who had a diagnosis of peripheral vertigo. It was also attempted to reveal the stroke risk factor amongst those with peripheral vertigo. Methods: This is a parallel‐group cohort study in a tertiary referral hospital. After assigning each of 4367 matched patients to the comparative set of peripheral vertigo and appendicitis‐ureterolithiasis groups and each of 4911 matched patients to the comparative set of peripheral vertigo and ischaemic stroke groups, the relative stroke risk was evaluated. In addition, to predict the individual stroke risk in patients with peripheral vertigo, any association between the demographic factors and stroke events was evaluated in the peripheral vertigo group. Results: The peripheral vertigo group had a higher stroke risk than the appendicitis‐ureterolithiasis group (hazard ratio 1.73, 95% confidence interval 1.18–2.55) but a lower risk than the ischaemic stroke group (hazard ratio 0.30, 95% confidence interval 0.24–0.37). The stroke risk of the peripheral vertigo group was just below that of small vessel stroke. The stroke risk of the peripheral vertigo group differed markedly by time: higher within 7 days, moderate between 7 days and 1 year, and diminished thereafter. Old age (>65 years), male gender and diabetes mellitus were the risk factors for stroke in the peripheral vertigo group. Conclusion: Patients with a diagnosis of peripheral vertigo in the emergency department showed a moderate future stroke risk and so a stroke preventive strategy tailored to the timing of symptom onset and individual risk is required. [ABSTRACT FROM AUTHOR]

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]

Objectives: To elucidate the mechanism of paroxysmal central positional nystagmus (CPN) by determining the effects of head rotation velocity on the intensity of paroxysmal downbeat nystagmus induced during straight head hanging (SHH). Methods: We recruited 21 patients with paroxysmal downbeat CPN induced during SHH at the Dizziness Center of Seoul National University Bundang Hospital from September 2018 to July 2019. Twenty-one patients had manual SHH at two different lying velocities, the fast (routine) and slow, and they also underwent SHH at different rotation velocities of 10, 20, 30, and 40 °/s using a motorized rotation chair. Induced nystagmus was recorded using video-oculography and the maximum slow phase velocity (SPV) and time constant (TC) of the induced paroxysmal nystagmus were analyzed. Results: During manual SHH, paroxysmal downbeat nystagmus was invariably induced during routine SHH (fast lying down), but absent or minimal during slow positioning. During motorized SHH, the median of maximum intensity of downbeat nystagmus increased from 7.6 °/s (0–16.9) to 14.0 °/s (0–32.5), 16.5 °/s (0–44.6), and 19.1 °/s (0–55.2) as the rotation velocity increased from 10 to 20, 30, and 40°/s (P < 0.001, P < 0.001, P = 0.004; linear mixed models). In contrast, the TCs of paroxysmal downbeat CPN remained unchanged (P = 0.558, P = 0.881, P = 0.384, linear mixed models). Conclusions: The dependence of nystagmus intensity on head rotation velocity supports a disinhibited and exaggerated inhibitory rebound of the canal signals as the mechanism of paroxysmal CPN. [ABSTRACT FROM AUTHOR]

Objectives: The aim of this study was to delineate the clinical and laboratory features suggestive of intralabyrinthine schwannoma (ILS). Methods: We compared the clinical features of 16 patients with ILS, who had been diagnosed at the Seoul National University Bundang Hospital from 2003 to 2018, with those of 18 patients with symptomatic unilateral intracanalicular schwannoma and randomly selected 20 patients with definite or probable unilateral Meniere's disease (MD). Results: Patients with ILS presented with either recurrent spontaneous dizziness/vertigo combined with auditory symptoms (n = 8), isolated auditory symptoms without dizziness/vertigo (n = 7), or recurrent spontaneous dizziness/vertigo without auditory symptoms (n = 1). Most patients reported no improvement (n = 11) or worsening (n = 1) of the symptoms despite medical treatments including intratympanic (n = 5) or intravenous steroids (n = 2). Conventional brain MRIs failed to detect ILS in about a half of the patients (7/16, 44%). However, ILS showed a filling defect on 3-dimensional (3D) heavily T2-weighted MRIs (n = 12), and nodular enhancement on 3D contrast-enhanced T1 (n = 15) or FLAIR MRIs (n = 13) targeted for the inner ear. Compared to MD or intracanalicular schwannoma, ILS showed mostly abnormal head-impulse tests (HITs, p = 0.001). In contrast, the incidence of canal paresis did not differ among the groups (p = 0.513). Conclusion: ILS may mimic MD by presenting recurrent dizziness/vertigo and auditory symptoms. ILS should be suspected in patients with recurrent audiovestibulopathy especially when (1) the duration of the dizziness is not typical for MD, (2) the patients do not respond to medical treatments, or (3) HITs are abnormal. [ABSTRACT FROM AUTHOR]

Introduction: Labyrinthine infarction is a cause of acute audiovestibulopathy, but can be diagnosed only in association with other infarctions involving the brainstem or cerebellar areas supplied by the anterior inferior cerebellar artery (AICA) since current imaging techniques cannot visualize an infarction confined to the labyrinth. This case series aimed to establish embolic labyrinthine infarction as a mechanism of isolated acute audiovestibulopathy. Methods: We analyzed clinical features, imaging findings, and mechanisms of embolism in 10 patients (8 men, age range: 38-76) who had developed acute audiovestibulopathy in association with an obvious source of embolism and concurrent acute embolic infarctions in the non-anterior inferior cerebellar artery territories. The presence of audiovestibulopathy was defined when bedside or laboratory evaluation documented unilateral vestibular (head-impulse tests or caloric tests) or auditory loss (audiometry). Results: Six patients showed combined audiovestibulopathy while three had isolated vestibulopathy. One patient presented isolated hearing loss. Audiovestibular findings were the only abnormalities observed in nine patients. In all patients, MRIs documented single or multiple infarctions in the cerebellum (n = 5) or cerebral hemispheres (n = 5). Especially three patients showed single or scattered foci of tiny acute infarctions only in the cerebral hemispheres. Cardiac sources of embolism were found in eight, and artery-to-artery embolism was presumed in two patients. Conclusion: Selective embolism to the labyrinth may be considered in patients with acute unilateral audiovestibulopathy and concurrent acute infarctions in the non-AICA territories. [ABSTRACT FROM AUTHOR]