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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]

Benign paroxysmal positional vertigo (BPPV) is the most common cause of vertigo worldwide. This review considers recent advances in the diagnosis and management of BPPV including the use of web-based technology and artificial intelligence as well as the evidence supporting the use of vitamin D supplements for patients with BPPV and subnormal serum vitamin D. [ABSTRACT FROM AUTHOR]

This study aimed to determine the etiologic distribution of dizziness and vertigo in a referral-based dizziness clinic in South Korea. We analyzed the diagnoses of 21,166 consecutive dizzy patients (12,691 women, mean age = 57.9 ± 15.7, age range = 3–97) seen from 2003 to 2019 using a registry and medical records. Overall, dizziness and vertigo were more common in women (60.0%, CI 0.59–0.61) than in men without a difference in age (57.7 ± 15.5 vs. 58.1 ± 16.1, p = 0.094). Benign paroxysmal positional vertigo (BPPV, 24.1%) was the most common cause of dizziness/vertigo, followed by psychiatric or persistent postural perceptual dizziness (20.8%), vascular disorders (12.9%), vestibular migraine (10.2%), Meniere's disease (7.2%), and vestibular neuritis (5.4%). These six disorders comprised more than 80% of all disorders. The etiology could not be determined in 5.0%, and more than one etiology was found in 14.1%. Vestibular migraine was the most common disorder in children and adolescents (< 19 years), psychiatric or persistent postural perceptual dizziness (26.3%) in the adults (19–64 years), and BPPV (28.2%) in the elderly (≥ 65 years). This etiologic distribution is similar to that reported in another country, and indicates no significant differences in the proportion of diseases causing dizziness and vertigo across different ethnic groups. This study provides valuable information to establish healthcare policy for dizziness and vertigo. [ABSTRACT FROM AUTHOR]

Since the positional nystagmus did not respond to repeated canalith-repositioning maneuvers (CRMs), he took brain MRIs without gadolinium-enhancement twice, both reported as normal (Fig. Apogeotropic nystagmus was induced during supine roll test, and the left beating nystagmus in the rightward head-turned position was greater than the right beating apogeotropic nystagmus (Fig. Nystagmus in apogeotropic HC-BPPV and apogeotropic CPN shares some common characteristics in addition to triggering positions and nystagmus direction. [Extracted from the article]

Ophthalmoplegia is the diagnostic hallmark of anti-GQ1b antibody syndrome. This study aimed to define the patterns of acute comitant strabismus in patients with anti-GQ1b antibody syndromes. We retrospectively analyzed the ocular motor findings in 84 patients with anti-GQ1b antibody-associated ophthalmoplegia during the acute phases. Of the 84 patients, 11 (13%) showed acute comitant strabismus. Compared to those without, patients with acute comitant strabismus frequently showed abnormal ocular motor findings that included gaze-evoked (n = 8), spontaneous (n = 4) and positional nystagmus (n = 4), saccadic hypermetria (n = 3), head-shaking nystagmus (n = 2), pulse-step mismatch (n = 1), and impaired visual cancellation of the vestibulo-ocular reflex (n = 1, p < 0.001). On the contrary, iridoplegia (p = 0.029) and ptosis (p = 0.001) were more commonly observed in patients with paralytic (incomitant) strabismus than in those with acute comitant strabismus. Comitant strabismus can manifest during the acute phase of anti-GQ1b antibody syndromes in association with other central ocular motor abnormalities. These findings implicate that the cerebellum and/or brainstem can be the primary target of the anti-GQ1b antibodies. [ABSTRACT FROM AUTHOR]

The original version of this article unfortunately contained a mistake. Second author's affiliation was incorrect. [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]

These corrective saccades were only noticeable during the bedside HITs and had been interpreted as back-up saccades. Herein, we describe overt back-up saccades during HITs due to hypermetric covert saccades in a patient with an acute circumscribed lesion involving the cerebellum, which were misinterpreted as reversed corrective saccades due to the hyperactive VOR during bedside examination. When these corrective saccades are hypermetric due to cerebellar dysfunction, the eyes would overshoot the target with corrective saccades in the opposite direction. (MP4 15487 KB) Graph: Supplementary file3 Video-head impulse tests show hypermetric covert corrective (red arrowhead) and overt back-up saccades (red arrow) during stimulation of the left horizontal semicircular canal and covert corrective saccades (blue arrowhead) during stimulation of the right horizontal canal. [Extracted from the article]

This letter, published in the Journal of Neurology, presents a case report and literature review on central paroxysmal positional nystagmus (CPN) mimicking posterior canal benign paroxysmal positional vertigo (BPPV) in pontine infarction. The report describes a 67-year-old man who presented with acute vertigo and nystagmus, initially diagnosed as right acute unilateral peripheral vestibulopathy with posterior canal BPPV. However, further examination revealed features of central vestibulopathy, and brain MRI confirmed an acute infarction in the lateral pontine tegmentum. The patient's symptoms resolved after two days, and follow-up showed no positional nystagmus. The authors discuss the characteristics of CPN and differentiate it from BPPV based on nystagmus patterns and response to treatment. [Extracted from the article]

Objectives: This study aimed to define the factors affecting accuracy of bedside determination of the involved side in HC-BPPV. Interventions: We developed 44 video clips including the nystagmus induced during supine head-roll test from patients with apogeotropic (n = 23) or geotropic (n = 21) HC-BPPV. The intensity of nystagmus was also quantified using video-oculography. Each video clip was presented twice to 25 participants, 14 medical students, and 11 medical personnel trained in neurology or neurotology, and the participants reported the lesion side using an evaluation sheet after each presentation. From the quantified video-oculographic data, absolute difference and asymmetry (absolute difference divided by the sum) of nystagmus intensity were calculated. Main outcomes and measures: The accuracy of bedside lateralization of HC-BPPV was 83.5% after the first presentation, and 86.0% after the second presentation, and was not different between the medical students and trained personnel after the second presentation. The accuracy was more closely correlated with the asymmetry than the absolute difference (Spearman's ρ = 0.627, p < 0.001). With a cut-off for the asymmetry at 30.8%, the accuracy was estimated at 93.8% with a sensitivity of 92.9%, and the area under the ROC curve of 0.779. Conclusions and relevance: The accuracy of bedside lateralization of the affected side is acceptable in HC-BPPV when the nystagmus asymmetry is more than 30%. [ABSTRACT FROM AUTHOR]

The diagnostic criteria were established for benign paroxysmal positional vertigo (BPPV), the most common vestibular disorder worldwide, by the Barany Society in 2015. This marked an important milestone in the diagnosis and treatment of BPPV. However, there still remain uncertainties and ambiguities regarding the clinical features and pathophysiology of BPPV, and its clinical variants. In this manuscript, we will discuss 1) the emerging and controversial syndromes of BPPV (i.e., canalolithiasis of the anterior canal, cupulolthiasis of the posterior canal, and lithiasis of multiple canals) with updates, 2) atypical nystagmus according to the canal involved (e.g., nystagmus induced by head position changes in the pitch plane in horizontal canal BPPV, and positional downbeat nystagmus in posterior canal BPPV), 3) persistent geotropic positional nystagmus. Consideration of these uncommon types and manifestations of BPPV would broaden our understanding of BPPV pathomechanisms and allow differentiation from central vertigo and nystagmus. • Recognition of the variant forms of benign paroxysmal positional vertigo (BPPV) is essential for differentiation of BPPV from central positional nystagmus. • The patterns of pitch plane nystagmus, and presence of 'null point' aid in lateralization of horizontal-canal BPPV. • Downbeat nystagmus may be observed during Dix-Hallpike maneuver when the otoliths are located in the non-ampullary arm of the posterior canal or in the canal side of the anterior canal. • In cupulolithiatic posterior canal-BPPV, a 'half Dix-Hallpike maneuver' may be more effective in inducing positional nystagmus than the conventional Dix-Hallpike maneuver. • The 'light cupula' may generate persistent geotropic nystagmus, which should be differentiated from canalolithiatic horizontal canal-BPPV. [ABSTRACT FROM AUTHOR]

A correction is presented to the article correcting errors in Table 1 of a case report and literature review discussing central paroxysmal positional nystagmus mimicking posterior canal benign paroxysmal positional vertigo in pontine infarction.

This study aimed to determine the prevalence and mechanism of linear vertigo reported by the patients during the attacks of benign paroxysmal positional vertigo (BPPV). We prospectively evaluated the characteristics (rotational vs. linear) of positional vertigo in 70 patients with posterior and horizontal canal BPPV using a questionnaire allowing multiple choices. In patients with linear vertigo, we further assessed the directionality of linear vertigo. We adopted the velocity-storage model to explain the occurrence and direction of linear vertigo in these patients with BPPV. Patients reported only rotational vertigo in 46 (46/70, 65.7%), only linear vertigo in 10 (14.3%), and both rotational and linear vertigo in 14 (20%). The patients experienced fear from rotational vertigo in 54 (54/70, 77.1%) and from linear vertigo in 20 (20/70, 28.6%). The direction of linear vertigo was concordant with the direction of inertial acceleration predicted by the velocity-storage model. Patients with BPPV may experience linear as well as rotational vertigo during the attacks. This linear vertigo may be ascribed to centrally estimated inertial acceleration. [ABSTRACT FROM AUTHOR]