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The incidence and characteristics of acute vestibular symptoms, responsible structures, and lateralization of the causative lesions in supratentorial stroke remain unknown. This study aimed to determine the incidence, clinical features, and anatomical correlation of acute vestibular symptoms in supratentorial stroke. We performed a prospective, multicenter, observational study that had recruited patients with supratentorial stroke from the neurology clinics of referral-based four university hospitals in Korea. All patients received a constructed neuro-otological evaluations, and neuroimaging. We analyzed the incidence of acute vestibular symptoms, abnormal ocular motor and vestibular function tests, and stroke lesions. Of 1301 patients with supratentorial stroke, 48 (3.7%) presented with acute vestibular symptoms, and 13 of them (1%) had the vestibular symptoms in isolation. In patients with acute vestibular symptoms, abnormal findings included spontaneous nystagmus (5%), impaired horizontal smooth pursuit (41%), and abnormal tilt of the subjective visual vertical (SVV) (20%). Video head impulse and caloric tests were normal in all the patients. There was no clear correlation between acute vestibular symptoms and involvement of specific vestibular cortex. In patients with unilateral stroke, there was also no lateralization of the causative lesions of acute vestibular symptoms (left vs. right; 52 vs. 48%), even in patients with vertigo (left vs. right; 58 vs. 42%). This study demonstrates that the incidence of acute vestibular symptoms in supratentorial stroke is 3.7%, with being isolated in 1%. The widespread lesions responsible for acute vestibular symptoms implicate diffuse multisensory cortical–subcortical networks in the cerebral hemispheres without a lateralization. [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]

Caloric tests are useful for disease surveillance of Meniere's disease (MD), although the interpretation of caloric tests remains controversial during the attacks of MD. Therefore, we aimed to characterize the findings of caloric tests during the attacks of MD. We analyzed the results of bithermal caloric tests during and between the attacks in 43 patients with unilateral definite MD. Evaluation was performed during the irritative/recovery phase in 22 and during the paretic phase in 26 patients. During the irritative/recovery phase, less than half of patients (10/22, 45%) showed a caloric asymmetry of more than 25%, lesser responses in the affected ear in six and in the healthy ear in the other four. In contrast, patients usually showed a caloric asymmetry of more than 25% during the paretic phase (19/26, 73%) with a decreased response almost always in the affected ear (18/19, 95%). Between the attacks, caloric asymmetry was found in less than half of the patients (20/43, 47%) with a decreased response almost always in the affected ear (19/20, 95%) when observed. The caloric asymmetry was less during the irritative/recovery phases than between the attacks (p = 0.007). In contrast, the caloric asymmetry was larger during the paretic phase than between the attacks (p = 0.041). The caloric asymmetry decreased during the irritative/recovery phases with an estimated mean difference of 34% (adjusted 95% CI 16–53%, p < 0.001) and 23% (adjusted 95% CI 8–38%, p = 0.002) compared to the paretic and interictal phases. Caloric responses fluctuate during and between the attacks of MD depending on the electrophysiologic status of the vestibular afferents. The results of caloric tests in MD, thus should be interpreted with consideration of each phase when the evaluation was done. [ABSTRACT FROM AUTHOR]