Search

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]

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]

Isolated vestibular syndrome may occur all along the vestibular pathways from the peripheral labyrinth to the brain. By virtue of recent developments in clinical neurotology and neuroimaging, however, diagnosis of isolated central vestibulopathy is increasing. Here, we review five distinct syndromes of isolated central vestibular syndrome from lesions restricted to the vestibular nuclei, the nucleus prepositus hypoglossi, the flocculus, the tonsil, and the nodulus, and introduce a new vestibular syndrome from isolated involvement of the inferior cerebellar peduncle. Decreased responses to head impulses do not exclude a central lesion as a cause of isolated vestibular syndrome. Brain imaging, including diffusion-weighted magnetic resonance imaging (MRI), may be falsely negative during the acute phase in patients with isolated vestibular syndrome because of a stroke. Central signs should be sought carefully in patients with isolated vertigo, even when the patients show the features of peripheral vestibulopathy and negative MRIs. Recognition of these isolated central vestibular syndromes would aid in defining the lesions responsible for various vestibular manifestations in central vestibulopathy. [ABSTRACT FROM AUTHOR]