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Objective: Conventionally, MRI aids in differentiating acute unilateral peripheral vestibulopathy/vestibular neuritis (AUPV/VN) from mimickers. Meanwhile, the diagnostic utility of MRIs dedicated to the inner ear remains to be elucidated for diagnosing AUPV/VN. Methods: We prospectively recruited 53 patients with AUPV/VN (mean age ± SD = 60 ± 15 years, 29 men). Initial MRIs were performed with a standard protocol, and an additional axial 3D‐fluid‐attenuated inversion recovery (3D‐FLAIR) sequence was obtained 4 h after intravenous injection of gadoterate meglumine. Abnormal enhancement was defined as a signal intensity that exceeded the mean + 2SD value on the healthy side. The findings of neurotologic evaluation and MRIs were compared. Results: Overall, the inter‐rater agreement for gadolinium enhancement was 0.886 (Cohen's kappa coefficient). Enhancement was observed in 26 patients (49%), most frequently in the vestibule (n = 20), followed by the anterior (n = 12), horizontal (HC, n = 8), posterior canal (n = 5), and superior (n = 3) and inferior (n = 1) vestibular nerves. In multivariable logistic regression analysis, the enhancement was associated with decreased HC gain in video head‐impulse tests (p = 0.036), increased interaural difference in ocular vestibular‐evoked myogenic potentials (p = 0.001), and a longer onset‐to‐MRI time span (p = 0.024). The sensitivity and specificity were 92.3% and 81.5%, respectively, with an area under the curve of 0.90 for predicting gadolinium enhancement. Interpretation: Robust gadolinium enhancement was observed on 4‐hour‐delayed 3D‐FLAIR images in nearly half of the patients with AUPV/VN, with a good correlation with the results of neurotologic evaluation. The positivity may be determined by the extent of vestibular deficit, timing of imaging acquisition, and possibly by the underlying etiology causing AUPV/VN. MRIs may aid in delineating the involved structures in AUPV/VN. [ABSTRACT FROM AUTHOR]

Background and purpose: Diagnosis of lymphoma involving the central nervous system (CNS) is challenging. This study aimed to explore the abnormal vestibular and ocular motor findings in CNS lymphoma. Methods: A retrospective search of the medical records identified 30 patients with CNS lymphoma presenting ocular motor and vestibular abnormalities from four neurology clinics of university hospitals in South Korea (22 men, age range 14–81 years, mean 60.6 ± 15.2). The demographic and clinical features and the results of laboratory, radiological and pathological evaluation were analyzed. Results: Patients presented with diplopia (13/30, 43%), vestibular symptoms (15/30, 50%) or both (2/30, 7%). In 15 patients with diplopia, abnormal ocular motor findings included ocular motor nerve palsy (n = 10, 67%), internuclear ophthalmoplegia (n = 2, 13%), external ophthalmoplegia (n = 2, 13%) and exophoria (n = 1, 7%). The vestibular abnormalities were isolated in 14 (82%) of 17 patients with vestibular symptoms and included combined unilateral peripheral and central vestibulopathy in three from lesions involving the vestibular nuclei. CNS lymphoma involved the brainstem (53%), cerebellum (33%), leptomeninges (30%), deep gray nuclei (23%) or cranial nerves (17%). Two patients showed the "double‐panda" sign by involving the midbrain. Conclusions: This study expands the clinical and radiological spectra of CNS lymphoma. Neuro‐ophthalmological and neuro‐otological evaluation may guide the early diagnosis of CNS lymphoma. [ABSTRACT FROM AUTHOR]

Thus, the preferential saccadic impairments and truncal ataxia observed in our patient may corroborate the cerebellar midline lesion observed in most patients. Indeed, metronidazole-associated peripheral neuropathy is found in one-third of patients with metronidazole CNS toxicity [[1]]. C Fluid-attenuated inversion recovery (FLAIR) images show high-signal-intensity lesions involving the dentate nuclei (yellow arrows), superior colliculi (yellow arrowheads), and splenium of the corpus callosum. Notably, a characteristic reversible dentate nuclei lesion is found in 90% of patients [[1], [4]]. [Extracted from the article]

This document, titled "Ocular Flutter Evoked by Vestibular Stimulation," discusses a case study of a 26-year-old woman who experienced ocular flutter, a condition characterized by spontaneous bursts of eye movements, exclusively during head motion and vestibular stimulation. The patient presented with oscillopsia (the perception of objects moving) and other symptoms such as clumsiness and headache. Various tests and examinations were conducted, including video-oculography, which revealed the presence of ocular flutter during specific stimuli. The authors propose several mechanisms that may explain the occurrence of ocular flutter in this case, involving the interaction between the vestibular and saccadic systems. The patient's symptoms improved after receiving treatment with intravenous immunoglobulin and methylprednisolone. The study suggests that vestibular stimulation may play a role in generating ocular flutter. [Extracted from the article]

Given that exyclodeviation and prominent adduction hypertropia, hyperdeviation may be ascribed to bilateral trochlear nerve palsy in association with combined skew deviation [as a constellation of ocular tilt reaction (OTR)] in our patient. Therefore, a combination of an OTR to the right with bilateral trochlear nerve palsy (more severely affected in the right eye) would explain the missing SVV tilt to the left on the left eye in association with the excyclotropia. As in our patient, patients often compound the problem of distinguishing bilateral trochlear nerve palsy from skew deviation. Keywords: Strabismus; Diplopia; Skew deviation; Trochlear nerve palsy EN Strabismus Diplopia Skew deviation Trochlear nerve palsy 1781 1783 3 03/01/23 20230301 NES 230301 Dear Sirs, Superior oblique palsy is a common cause of acquired hyperdeviation, mostly caused by traumatic injury of the trochlear nerve [[1]]. [Extracted from the article]

The article discusses a case study of a 57-year-old man with multiple system atrophy (MSA) presenting with ocular flutter triggered specifically by vestibular stimulation, alongside various neurological symptoms including gait difficulty, oscillopsia, and dysarthria. It highlights the diagnostic challenges and neurological manifestations associated with MSA, emphasizing the role of vestibular and ocular motor deficits in differentiating this condition from other neurodegenerative disorders.

Similarly, cerebral lesions can also present with spontaneous or positional nystagmus especially when the lesions involve the hippocampus and parahippocampal gyrus that are part of the multisensory vestibular cortices [[3]-[5]]. Dear Sirs, A small punctuate lesion in the hippocampus can cause acute amnesia, confabulation, and altered consciousness, and it represents a typical radiologic finding of transient global amnesia (TGA). Accordingly, 40% of patients having a punctuate lesion in this area reported vertigo and dizziness in an MRI-based patient series [[1]]. [Extracted from the article]

Research Background: Vitamin D insufficiency/deficiency is known to be related to occurrences and recurrences of benign paroxysmal positional vertigo (BPPV). However, the efficacy of vitamin D supplementation in reducing recurrences of BPPV remains to be established. We performed a meta-analysis to determine the therapeutic effects of vitamin D supplementation, with or without calcium, for preventing recurrences of BPPV. Methods: We searched the PubMed, the Embase, the Web of Science and the reference lists of the articles. We included randomized or non-randomized trials that determined the efficacy of supplementing vitamin D or related compounds, alone or with calcium, in comparison to placebo or no intervention in preventing recurrences of BPPV. The primary outcome was the number of patients with BPPV recurrences. Data were collected and pooled using a weighted relative risk (RR) with corresponding 95% CIs, where possible, by adopting the fixed-effect or random-effect model according to the heterogeneity among the studies. The between-study heterogeneity was tested using the χ2 test and the I2 statistic, and funnel plots were used to evaluate any publication bias. Results: We included five trials (four non-randomized trials and one randomized controlled trial) with a total of 1250 participants. The analyses showed a significant preventive effect on the recurrences of BPPV (RR = 0.37; 95% CI = 0.18–0.76; p = 0.007 with the random-effects model) with supplementation of vitamin D. Although a considerable heterogeneity was detected among the studies, the sensitivity analyses showed the reliability and stability of our results. Conclusions: Vitamin D supplementation provides a benefit for secondary prevention of BPPV. Supplementation of vitamin D should be considered in patients with frequent attacks of BPPV, especially when serum vitamin D is subnormal. [ABSTRACT FROM AUTHOR]

Dear Sirs, Although mydriasis is a red flag sign that indicates possible compressive oculomotor nerve palsy [[1]], pupils can be spared when the lesion resides in the cavernous sinus [[2]]: The accompanied oculosympathetic disruption can mask the cholinergic denervation from the compressive oculomotor nerve palsy. We present a patient with oculomotor nerve palsy due to a compressive aneurysm, although not showing evident mydriasis complicating the diagnosis. C Schematic illustration of the neural structures responsible for the ocular motor finding in our patient Our patient presented with painful ophthalmoplegia showing trochlear and oculomotor nerve palsy with Horner syndrome. [Extracted from the article]

Dear Sirs, Although ventriculitis is usually secondary to neurosurgical trauma or catheter infection, it may be primary with diverse clinical presentation [[1]-[4]]. Our patient implicates that primary ventriculitis can be considered as a differential diagnosis among those presenting with acute vestibular syndrome in association with headache and fever. [Extracted from the article]

Bilateral vestibular dysfunction (BVD) refers to hypofunction of the vestibular nerves or labyrinths on both sides. Patients with BVD present with dizziness, oscillopsia, and unsteadiness, mostly during locomotion, which worsen in darkness or on uneven ground. Although aminoglycoside ototoxicity, Meniere's disease, infection, and genetic disorders frequently cause BVD, the etiology remains undetermined in up to 50% of the patients. The diagnosis of BVD requires both symptoms and documentation of deficient vestibulo-ocular reflex function using head-impulse, bithermal caloric, and rotatory chair tests. Since various neurologic and systemic disorders may present with BVD, clinicians should be cautious not to overlook the symptoms and signs of central nervous system and systemic involvements. Vestibular rehabilitation, application of vibrotactile and auditory feedbacks, and vestibular prosthesis can aid the patients with BVD along with the correction of the underlying causes. [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]

Objectives/hypothesis: To aid in diagnosis of Meniere's disease (MD) during the attacks using caloric and head-impulse tests (HITs).Study Design: Retrospective case series review.Methods: We analyzed the results of bithermal caloric and HITs during the attacks in 16 patients with MD. Quantitative analyses of HITs were conducted using a magnetic search coil technique.Results: In unilateral MD (14 patients, 42 semicircular canals), the head impulse gain of the vestibulo-ocular reflex (VOR) was either normal (28 of 42, 67%), decreased (8 of 42, 19%), or increased (6 of 42, 14%) for each semicircular canal in the affected ear. Likewise, the head impulse VOR gain was either normal (29 of 42, 69%), increased (11 of 42, 26%), or decreased (2 of 42, 5%) in the intact ear. The VOR gain for the horizontal canal was significantly lower on the affected side (P = 0.013). However, the VOR gains for the anterior and posterior canals did not differ between the sides (P = 0.270, P = 0.282). In bilateral MD (two patients, 12 semicircular canals), the VOR gain was either decreased (6 of 12, 50%) or normal (6 of 12, 50%) in either ear. In contrast, the caloric responses were usually decreased in the affected ear (7 of 11, 64%, including one with bilateral MD).Conclusion: During the attacks of MD, HITs showed varied results between the ears and among the canals, although the caloric responses were usually decreased in the involved ear. These dissociations suggest a frequency-dependent impairment of canal function or mechanical property of the endolymphatic hydrops during the attacks of MD.Level Of Evidence: 4. Laryngoscope, 127:702-708, 2017. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 45-year-old woman presented with spontaneous vertigo for a day, who had suffered from cough and myalgia for a week before the presentation. Topics include features of acute unilateral peripheral vestibulopathy mimicking vestibular neuritis (VN) in the patient, signs of decreased ocular vestibular-evoked myogenic potentials (VEMPs), and diagnosis of anti-ganglioside antibody-associated acute unilateral peripheral vestibulopathy.