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Background and purpose: Tolosa-Hunt Syndrome (THS) is a rare disorder, and detailed clinical information and treatment outcomes have yet to be fully elucidated. This study aims to investigate the clinical features and factors associated with the treatment outcomes of THS, as defined by the established diagnostic criteria. Methods: This study retrospectively recruited 91 patients with a diagnosis of THS from 2003 to 2020. We analyzed the clinical features and outcomes, the initial treatment response, recurrences, and the final treatment response. Results: Isolated ocular motor nerve palsy was the most common (82.4%) finding of ophthalmoplegia, involving the oculomotor nerve in more than half of the cases (52.0%). The MRI lesions were mostly observed in the cavernous sinus (94.5%) with an extracavernous extension in about one-third of them. Five patients showed only extracavernous lesions. A total of 25 (27.5%) patients experienced recurrence. Recurrence occurred during steroid tapering as part of the initial treatment in seven, while in 18 patients, it happened after the successful termination of the initial treatment. However, all patients achieved complete remission at the final. Age was associated with a decrease in initial symptom duration (HR = 1.023, CI = 1.004–1.044) as well as an increase in recurrence-free duration (HR = 0.944, CI = 0.911–0.978). High-dose corticosteroid treatment was associated with a decrease in initial symptom duration (HR = 1.642, CI = 1.001–2.695) and total treatment duration (HR = 2.203 CI = 1.302–3.730). Conclusions: THS can recur frequently especially in younger but have a favorable prognosis. High-dose corticosteroids can be an effective initial treatment and reduce the total treatment duration. [ABSTRACT FROM AUTHOR]

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]

Purpose: To delineate the association between otolith function and changes in mean orthostatic blood pressure (BP) and heart rate (HR) in patients with postural orthostatic tachycardia syndrome (POTS). Methods: Forty-nine patients with POTS were prospectively recruited. We analyzed the results of ocular vestibular-evoked myogenic potentials (oVEMPs) and cervical vestibular-evoked myogenic potentials (cVEMPs), as well as head-up tilt table tests using a Finometer. The oVEMP and cVEMP responses were obtained using tapping stimuli and 110 dB tone-burst sounds, respectively. We measured maximal changes in 5-s averaged systolic BP (SBP), diastolic BP (DBP), and heart rate (HR) within 15 s and during 10 min after tilting. We compared the results with those of 20 age- and sex-matched healthy participants. Results: The n1–p1 amplitude of oVEMPs was larger in patients with POTS than in healthy participants (p = 0.001), whereas the n1 latency (p = 0.280) and interaural difference (p = 0.199) did not differ between the two. The n1–p1 amplitude was a positive predictor for POTS (odds ratio 1.07, 95% confidence interval 1.01–1.13, p = 0.025). Body weight (p = 0.007) and n1–p1 amplitude of oVEMP (p = 0.019) were positive predictors for ΔSBP15s in POTS, whereas aging was a negative predictor (p = 0.005). These findings were not observed in healthy participants. Conclusions: Augmented utricular inputs may be associated with a relative predominance of sympathetic over vagal control of BP and HR, especially for an early response during orthostasis in patients with POTS. Overt sympathoexcitation due to exaggerated utricular input and lack of readaptation may be associated with the pathomechanism of POTS. [ABSTRACT FROM AUTHOR]

Differentiation of spinocerebellar ataxia type 17 (SCA17) from Huntington's disease (HD) is often challenging since they share the clinical features of chorea, parkinsonism, and dystonia. The ocular motor findings remain to be elucidated in SCA17, and may help differentiating SCA17 from HD. We retrospectively compared the ocular motor findings of 11 patients with SCA17 with those of 10 patients with HD. In SCA17, abnormal ocular motor findings included impaired smooth pursuit (9/11, 82%), dysmetric saccades (9/11, 82%), central positional nystagmus (CPN, 7/11, 64%), abnormal head-impulse tests (4/11, 36%), and horizontal gaze-evoked nystagmus (GEN, 3/11, 27%). Among these, CPN was more frequently observed in SCA17 than in HD (7/11 (64%) vs. 0/10 (0%), p = 0.004) while saccadic slowing was more frequently observed in HD than in SCA17 (8/10 (80%) vs. 2/11 (18%), p = 0.009). Of six patients with follow-up evaluation, five later developed bilateral saccadic hypermetria (n = 4), GEN (n = 1), CPN (n = 1), bilaterally abnormal smooth pursuit (n = 1), and hyperactive head-impulse responses (n = 1) along with a clinical decline. Ocular motor abnormalities can be utilized as a diagnostic marker for differentiation of SCA17 from HD as well as a surrogate marker for clinical decline in SCA17. [ABSTRACT FROM AUTHOR]

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]

In central as well as peripheral vestibular lesions, right-beating horizontal nystagmus is almost always associated with clockwise (top poles of the eyes beating to the right ear) torsional nystagmus when observed and vice versa (concordant nystagmus). This study aimed to determine the etiologies and mechanisms of horizontal and torsional nystagmus beating in the opposite directions (discordant nystagmus). We reviewed the medical records of 16 consecutive patients with discordant horizontal–torsional nystagmus who had been evaluated at the dizziness clinics of Seoul National University Bundang Hospital (n = 11, from March 2003 to March 2021) and Korea University Medical Center (n = 5, from March 2019 to March 2021). The underlying etiologies included inferior vestibular neuritis (n = 7), Meniere's disease (n = 4), internuclear ophthalmoplegia (n = 3), medullary hemorrhage (n = 1), and normal pressure hydrocephalus (n = 1). The torsional nystagmus decreased during the gaze in the same direction (for instance, during rightward gaze in clockwise nystagmus) and increased during the gaze in the opposite direction. Head-impulse tests (HITs) were positive for the ipsilesional posterior canal (PC) in all 11 patients with unilateral peripheral vestibulopathy and two of the three patients with unilateral central vestibulopathy. Discordant horizontal–torsional nystagmus may be observed in peripheral as well as central lesions. Given the findings of HITs and modulation of spontaneous nystagmus during lateral gazes, discordant horizontal–torsional nystagmus may be ascribed to selective damage of the excitatory or inhibitory pathway from the PC that innervates the ipsilateral superior oblique and contralateral inferior rectus muscles. [ABSTRACT FROM AUTHOR]

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.

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]

Objective Methods Results Interpretation 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.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.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.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]

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]

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]

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]

LH horizontal position of the left eye, LT torsional position of the left eye, LV vertical position of the left eye, RH horizontal position of the right eye, RT torsional position of the right eye, RV vertical position of the right eye One week later, the patient also developed sudden hearing loss in the left ear. Pure tone audiometry and speech discrimination showed a profound hearing loss in the right ear (Fig. Pure tone audiometry documented profound hearing loss in the left ear at this time (Fig. Our patient adds an evidence that protein S deficiency can cause SSNHL, and anticoagulation may not be sufficient to prevent recurrences in the setting of a comorbid cardioembolic source of stroke. [Extracted from the article]

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]

Dear Sirs, Systemic lupus erythematosus (SLE) is a chronic, relapsing inflammatory disease that typically involves the skin, joints, bone marrow, and central nervous system [[1]]. The patient also showed persistent geotropic nystagmus after turning the head to either side while supine. As in our patient, various neurotologic findings can be observed in SLE, including gaze-evoked, positional nystagmus, unilateral canal paresis, or abnormal saccades [[4]-[6]]. [Extracted from the article]

Evolution of vestibular function requires further elucidation in spinocerebellar ataxia (SCA). This study aimed to determine temporal evolution in the findings of head impulse tests (HITs) in SCA type 6 (SCA6). We serially evaluated HITs in 12 patients with SCA6 using video-oculography for 3 months to 5 years [median = 12 months, interquartile range (IQR) = 9–50] at two university hospitals in South Korea. Patients (8/12, 67%) usually showed abnormal responses at least for one semicircular canal during video-HITs. The gains of the vestibulo-ocular reflex (VOR) for the anterior canals (ACs) were larger than those for the posterior canals (PCs, p = 0.005) at initial presentation. During the follow-up, the VOR gains decreased for the horizontal canals (HCs, p = 0.008) and ACs (p = 0.021), but those for the PCs remained unchanged (p = 0.212). Perverted HITs were observed in seven patients (7/12, 58%). The differences in the head impulse VOR gains were larger between the ACs and PCs (ΔACs − PCs) in those with perverted HITs than in those without (p = 0.003). The gains for each semicircular canal showed a negative correlation with the Scale for the Assessment and Rating of Ataxia (HCs, Spearman's coefficient = − 0.675, p = 0.003; ACs, − 0.637, p = 0.006; PCs, − 0.605, p = 0.010). The head impulse gain of the VOR may serve a marker for clinical decline in SCA6. The dissociation in the temporal evolution of the VOR gain indicates dissimilar cerebellar modulation of the vestibular signals from each semicircular canal. [ABSTRACT FROM AUTHOR]

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]

This study aimed to define the clinical features and involved structures that aid in differentiation of neuromyelitis optica spectrum disorder (NMOSD) from multiple sclerosis (MS) involving the brainstem and cerebellum. We analyzed the clinical and ocular motor findings, and lesion distribution on brain MRIs in 42 patients with MS (17 men, mean age ± SD = 37 ± 12) and 26 with NMOSD (3 men, mean age ± SD = 43 ± 15) that were recruited from two university hospitals in South Korea (whole study population). An additional subgroup analysis was also conducted in 41 patients presenting acute brainstem or vestibular syndrome (brainstem syndrome population). Logistic regression analysis showed that bilaterality of the lesions (p = 0.012) and presence of horizontal gaze-evoked nystagmus (hGEN, p = 0.041) were more frequently associated with NMOSD than with MS in the whole study population. In the brainstem syndrome population, only hGEN (p = 0.017) was more frequent in NMOSD than in MS. The lesions specific for NMOSD were overlapped in the medial vestibular nucleus (MVN) and nucleus prepositus hypoglossi (NPH) at the pontomedullary junction. In conclusion, presence of hGEN and bilateral lesions involving the MVN and NPH favor the diagnosis of NMOSD rather than MS. [ABSTRACT FROM AUTHOR]

The eye then drifts back to the previous position with a slow glissadic eye motion with a decreasing slow-phase velocity, consistent with single saccadic pulse. b Dissociated adducting nystagmus is observed during lateral gazes. c Horizontal saccades are hypermetric to overshoot the target, and then the eyes slowly drift back to the target (glissades) after each saccade especially to the right, which is consistent with a pulse-step mismatch. Video-oculography (SMI, Teltow, Germany) documented alternating monocular adducting saccades in both eyes which were followed by a slow glissadic eye movement to the primary position (Fig. Graph: Video 2 The patient shows alternating monocular adducting saccades in both eyes followed by glissadic eye movements (MP4 1768 kb) Graph: Video 3 The patient shows a pulse-step mismatch, especially in the adducting eye, and dissociated adducting nystagmus during horizontal saccades. [Extracted from the article]

Opsoclonus often presents with other neurological symptoms and signs such as dizziness, myoclonus, ataxia, and mental confusion [[3]]. In this study, we report vestibular hyperreflexia in a patient with opsoclonus-myoclonus syndrome as a rare complication of acute hepatitis A virus (HAV) infection. Based on the clinical presentation, laboratory results, and response to the immune-modulating treatments, the patient was finally diagnosed with opsoclonus-myoclonus syndrome due to HAV-associated autoimmune encephalitis. Opsoclonus-myoclonus syndrome associated with mumps virus infection. [Extracted from the article]

We sought to determine the cerebellar structures responsible for tilt suppression of post-rotatory nystagmus. We investigated ocular motor findings and MRI lesions in 73 patients with isolated cerebellar lesions who underwent recording of the vestibulo-ocular reflex (VOR) using rotatory chair tests. Tilt suppression of post-rotatory nystagmus was diminished in 27 patients (27/73, 37.0 %). The gains of the VOR and the TCs of per- and post-rotatory nystagmus did not differ between the patients with diminished and with normal tilt suppression. The patients with impaired tilt suppression showed perverted ('cross-coupled') head-shaking nystagmus (pHSN) and central positional nystagmus (CPN) more frequently than those with normal responses. Tilt suppression was impaired in five (71.4 %) of the seven patients with isolated nodulus and uvular infarction. Probabilistic lesion-mapping analysis showed that the nodulus and uvula are responsible for tilt suppression. Impaired tilt suppression may be ascribed to disruption of cerebellar contribution to the vestibular velocity-storage mechanism, which integrates information from the semicircular canals and otolith organs to help derive the brain's estimate of the head orientation relative to the pull of gravity. [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.

The article presents a case study of a 47-year-old man who was referred for further evaluation of progressive visual loss in both eyes for 3 months. It mentions that video-oculography documented intermittent windmill nystagmus with a counter-clockwise rotation of the beating direction. It informs that genetic analysis for Leber’s hereditary optic neuropathy was negative for mitochondrial DNAs. It states that Windmill nystagmus resembles periodic alternating nystagmus (PAN).

The article describes the case of a 63-year-old woman with diabetes mellitus and hypertension for two years who presented acute spontaneous vertigo and headache for ten days. Topics discussed include findings on the medical examination conducted on the patient, the bilaterally abnormal cervical vestibular-evoked myogenic potential (VEMPs) shown by the patient in the presence of normal ocular VEMPs, and dissociated VEMP results.

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]

Internuclear ophthalmoplegia (INO) indicates a lesion involving the medial longitudinal fasciculus (MLF) that interconnects the abducens nucleus and medial rectus subnucleus of the oculomotor nuclear complex. In fact, rostral-caudal localization value of the INO is often limited except when it accompanies symptoms and signs owing to involvement of nearby structures. Ataxia is often observed in lesions involving the cerebellum or the fibers to and from it anywhere in the brainstem. Herein, we sought to determine the localizing value of INO plus ataxia in the rostrocaudal axis of the brainstem. Thirty patients with INO plus limb or truncal ataxia were subjected to analyses. For comparison, 20 patients with isolated INO without any ataxia served as the control. We determined the lesion extent in the MRIs responsible for INO plus ataxia using a probabilistic lesion mapping and subtraction analysis and analyzed the neuro-otologic findings using video-oculography. In patients with INO with limb or truncal ataxia, the responsible lesions were mostly restricted to the paramedian tegmentum at the pontomesencephalic junction. In contrast, the lesions causing isolated INO without ataxia were mostly located in the caudal or mid-pontine area. The rostro-caudal distribution of the lesions was similar among the patients with only limb ataxia ( n = 3), both limb and truncal ataxia ( n = 10), and only truncal ataxia ( n = 17). INO plus ataxia indicates a lesion involving the MLF at the pontomesencephalic junction. Damage to the brachium conjunctivum or mesencephalic locomotor region may explain the ataxia in association with INO in lesions involving this area. [ABSTRACT FROM AUTHOR]

A 3D cubic structure of mesoporous graphitic carbon nitride (3D-g-CN) was fabricated by nano casting using the mesoporous silica hard template KIT-6. The abundant intrinsic amine functionalities of 3D-g-CN were applied as a selective adsorbent for silver ions using the unique affinity of silver and amine functionalities. The large surface area of 3D-g-CN resulted in increased amine functionalities at the surface and enabled it to form complexes with silver ions. As a result, almost 400 mg/g of silver ion could be removed from 100 mM of initial solution at 293.15 K. The isotherm of silver ion adsorption onto 3D-g-CN was described by the Freundlich and Sips models and indicated heterogeneity of the adsorbent surface. Thermodynamic parameters determined from temperature dependent isotherms were verified by the endothermic silver ion adsorption process of 3D-g-CN. The adsorption capacity of silver ion on 3D-g-CN was maintained during several reuses without a significant decrease in capacity. Overall, the results indicate that 3D-g-CN has intrinsic amine functional groups with a large surface area and could therefore be utilized as an efficient selective adsorbent of silver ions for water purification. [ABSTRACT FROM AUTHOR]

Purpose: To delineate the association between otolithic dysfunction and orthostatic hypotension (OH). Methods: We retrospectively reviewed the medical records of 382 patients who presented with orthostatic dizziness at a tertiary dizziness center between July 2017 and December 2021. Patients were included for analyses when they had completed ocular (oVEMP) and/or cervical vestibular-evoked myogenic potentials (cVEMP), and head-up tilt table test with a Finometer (n = 155). We compared the results between the patients with OH (n = 38) and those with NOI (normal head-up tilt table test despite orthostatic intolerance, n = 117). Results: Thirty-eight patients with OH were further categorized as either classic (n = 30), delayed (n = 7), or initial (n = 1) types. Multivariable logistic regression showed that OH was associated with high baseline systolic BP (p = 0.046), presence of heart failure (p = 0.016), and unilateral oVEMP abnormalities (p = 0.016). n1 latency of oVEMP were negatively correlated with the maximal changes of systolic blood pressure (BP) in 15 s (Δ SBP15s, p = 0.013), 3 min (Δ SBP3min, p = 0.005) and 10 min (Δ SBP10min, p = 0.002). In contrast, the n1-p1 amplitude was positively correlated with Δ SBP15s (p = 0.029). Meanwhile, p13 latency of cVEMP was negatively correlated with Δ SBP10min (p = 0.018). Conclusions: Our study provides evidence of utricular dysfunction related to OH. [ABSTRACT FROM AUTHOR]

The original version of this article unfortunately contained a mistake. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 49-year-old man who was taken to the emergency room due to left ear tinnitus and vertigo. Medical diagnosis of the patient with the use of magnetic imaging resonance for the Meniere disease (MD) and response of the vestibular-evoked myogenic potentials (VEMPs) was performed. The article discusses the effect of the VEMPs leading to the labyrinthine ischemia in the patient.

The results of video head impulse tests (video-HITs) may be confounded by data artifacts of various origins, including pupil size and eyelid obstruction of the pupil. This study aimed to determine the effect of these factors on the results of video-HITs. We simulated ptosis by adopting pharmacological dilatation of the pupil in 21 healthy participants (11 women; age 24–58 years). Each participant underwent video-HITs before and after pupillary dilatation using 0.5% tropicamide. We assessed the changes in the vestibulo-ocular reflex (VOR) gain, corrective saccade amplitude, and frequency of eyelid flicks. After pupillary dilatation, the VOR gain decreased for both right (RAC; 1.12 ± 0.12 vs. 1.01 ± 0.16, p = 0.011) and left anterior canals (LACs; 1.15 ± 0.13 vs. 0.96 ± 0.14, p < 0.001), and right posterior canal (RPC, 1.10 ± 0.13 vs. 0.98 ± 0.09, p = 0.001). The corrective saccade amplitudes also decreased significantly for all four vertical canals. The frequency of eyelid flicks, however, did not change. The changes of VOR gain were positively correlated with the lid excursion in RPC (r = 0.629, p = 0.002) and LPC (r = 0.549, p = 0.010). Our study indicates that eyelid position and pupil size should be considered when interpreting the results of video-HITs, especially for the vertical canals. Pupils should be shrunk in a very well-lit room, and artifacts should be prevented by taping or lifting the eyelids as required during video-HITs. [ABSTRACT FROM AUTHOR]

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 integrity of the vestibulo-ocular reflex (VOR) remains to be delineated in patients with parkinsonism. We aimed to define the findings of the VOR using head-impulse tests (HITs) and their differential diagnostic value in patients with Parkinson's disease (PD) and multiple system atrophy (MSA). From December 2019 to January 2021, 30 patients with PD and 23 patients with MSA (17 with cerebellar-type MSA and 6 with parkinsonian-type MSA) had a video-oculographic recording of HITs at two university hospitals in South Korea. Reversed (p = 0.034) and perverted (p = 0.015) catch-up saccades were more frequently observed in MSA than in PD during HITs. The gain difference between the ACs and the PCs were larger in MSA than in PD (p = 0.031), and positively correlated with the disease duration in patients with MSA (Spearman's coefficient = 0.512, p = 0.012). Multivariate logistic regression analysis showed that reversed (p = 0.044) and perverted (p = 0.039) catch-up saccades were more frequently associated with MSA than with PD during HITs. In conclusion, HITs aid in differentiation of MSA from PD, and may serve as a surrogate marker for the clinical decline. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 59-year-old woman who had suffered from recurrent vertigo for 2 months and later found out to have cerebellopontine angle (CPA) meningioma that mimicked vestibular paroxysmia. The meningioma originating from the CPA has showed recurrent paroxysmal spontaneous vertigo that mimicked vestibular paroxysmia. The patient was placed on carbamazepine per day and discharged 4 days later.

The clinical features of a lesion confined to the superior cerebellar peduncle (SCP) have not been defined well in human. A 92-year-old woman suddenly developed mild dysarthria and severe imbalance from an isolated unilateral SCP infarction, and examination showed ipsiversive ocular torsion, severe ipsilesional limb ataxia, and truncal ipsipulsion. These findings are well consistent with those observed in monkeys when the SCP was severed. In addition to the dentate-rubro-thalamic projections, the SCP appears to contain the fibers involved in the control of eye motion in the roll plane. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented which discusses the case of a patient with vertigo and downbeat nystagmus (DBM) induced by swallowing.

Herein, we report a patient with isolated disc edema and positive serum anti-GQ1b antibody. Our patient implicates that anti-GQ1b antibody can play a role for atypical optic disc edema that do not readily fit into the typical idiopathic intracranial hypertension which mostly affects young, obese woman with a prominent increment of the CSF opening pressure. Dear Sirs, Anti-GQ1b antibody has been associated with constellation of symptom of ophthalmoplegia, ataxia, and areflexia [[1]]. [Extracted from the article]

A clinical scale fully dedicated to evaluating ocular motor abnormalities is required for now. We investigated the utility of a recently developed Scale for Ocular motor Disorders in Ataxia (SODA) in patients with multiple system atrophy (MSA). We prospectively assessed SODA in consecutive patients with MSA between August 2021 and August 2023 at the Korea University Medical Center. The results of the clinical exam-based SODA were compared with those measured using video-oculography (VOG-guided SODA). We also compared the findings with other established clinical scales targeting patients with MSA, including the Unified Multiple System Atrophy Rating Scale (UMSARS) I-II, Movement Disorder Society-Unified Parkinson’s Disease Rating Scale motor part (UPDRS-III), Scale for Assessment of Rating of Ataxia (SARA), Composite Autonomic Symptom Score-31 (COMPASS-31), and Composite Autonomic Severity Score (CASS). Twenty patients were enrolled in our study (17 with cerebellar-type MSA and three with Parkinson-type MSA). Scores ranged from 1 to 14 (median [interquartile range (IQR)] = 8 [5−10]). Among the subscales, saccades had a median score of 2.5 (IQR = 1–3), followed by ocular pursuit (1 [0–1]), nystagmus (1 [0–2]), saccadic intrusions (1 [0–1]), vestibulo-ocular reflex (VOR) (0.5 [0–1]), ocular alignment (0 [0–1]), and VOR cancellation (1 [0–1]). The clinical-exam-based SODA (p = 0.020) and VOG-guided SODA (p = 0.034) positively correlated with disease duration. No correlation was found between clinical exam-based SODA and other scales. Skew deviation, gaze-evoked nystagmus, VOR cancellation, and smooth pursuit had the highest precision among the items. Ocular misalignment and spontaneous and positional nystagmus were frequently false positive and were poorly detected with clinical exam-based SODA. Six patients with repeated evaluation exhibited higher scores, along with deterioration documented on other clinical scales. The SODA can reliably predict neurodegeneration as an additional clinical surrogate in MSA. [ABSTRACT FROM AUTHOR]

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]

Impaired tilt suppression of post-rotatory nystagmus and cross-coupled head-shaking nystagmus in cerebellar lesions: image mapping study. Lesions involving the ION have mostly been reported as a form of pseudo-hypertrophic olivary degeneration (HOD) that refers to vacuolar degeneration of the enlarged neurons in the ION and mostly develops several months after damage to the dentato-rubro-olivary tract (the Guillain-Mollaret triangle) [[2]]. The inferior olivary nucleus (ION) receives signals from the spinal cord and cerebellum, and regulates coordination and motor learning [[1]]. [Extracted from the article]

Video head impulse tests (video-HITs) are commonly used for vestibular evaluation; however, the results can be contaminated by various artifacts, including technical errors, recording problems, and participant factors. Although video-HITs can be used in patients with Parkinson’s disease (PD), the effect of neck rigidity has not been systematically investigated. This study aimed to investigate the effect of neck rigidity on video-HIT results in patients with PD. We prospectively recruited 140 consecutive patients with PD (mean age ± standard deviation = 68 ± 10 years, 69 men) between September 2021 and April 2024 at Korea University Medical Center. The video-HIT results were compared with those of 19 age- and sex-matched healthy participants. Neck rigidity was stratified as a subdomain of the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale motor part (MDS-UPDRS-III). In 59 patients, the vestibulo-ocular reflex (VOR) gain was overestimated in at least one canal plane (58/140, 41%), mostly in the anterior canal (AC, n = 44), followed by the horizontal (HC, n = 15) and posterior canals (PC, n = 7). VOR gain overestimation was also observed in patients with no (18/58, 35%), subtle (20/58, 34%), or mild (17/58, 29%) neck rigidity. Multivariable logistic regression analysis showed that VOR overestimation was positively associated with neck rigidity (odds ratio [OR] [95% confidence interval] = 1.51 [1.01–2.25], p = 0.043). The head velocities of patients decreased during head impulses for the AC (p = 0.033 for the right AC; p = 0.014 for the left AC), whereas eye velocities were similar to those of healthy participants. Our findings suggest that neck rigidity may be a confounder that can contaminate video-HIT results. Thus, the results of video-HITs, especially for the AC, should be interpreted with the context of head velocity during head impulses in patients with neck rigidity. [ABSTRACT FROM AUTHOR]

• Falls were not associated with cVEMP or oVEMP abnormalities. • Falls were associated with higher MDS-UPDRS-III scores. • cVEMP and oVEMP amplitudes were not associated with disease duration or disease severity. [ABSTRACT FROM AUTHOR]