Acute Unilateral Peripheral Vestibulopathy Research Articles

Accuracy of the Bedside Examination in Patients with suspected Acute Unilateral Peripheral Vestibulopathy.

Acute unilateral peripheral vestibulopathy (AUPVP) is a frequent form of peripheral vestibular vertigo characterized by unilateral vestibular organ dysfunction. Diagnostic challenges in anamnesis and bedside examination can lead to potential misdiagnoses. This study investigated the sensitivity of bedside examinations in diagnosing AUPVP. This retrospective analysis examined 136 AUPVP inpatients at a level 3 university hospital between 2017 and 2019. Demographic data and bedside test results were collected. Instrumental otoneurological tests included caloric testing and video head impulse test (HIT). The sensitivity of each bedside parameter was computed based on the instrumental diagnostics, and statistical analyses were performed. The study included 76 men and 60 women, with a mean age of 59.2 years. Spontaneous nystagmus exhibited a sensitivity of 92%, whereas the absence of skew deviation was identified with a sensitivity of 98%. Abnormal bedside HIT showed a sensitivity of 87%. The combined HINTS (HIT, nystagmus, and test of skew) had a sensitivity of 83%. The Romberg test and Fukuda test demonstrated sensitivities of 26% and 48%, respectively. The sensitivity of bedside tests varied from 26% to 98%. This aligns with previous literature, highlighting the challenge of differentiating AUPVP from vestibular pseudoneuritis solely through bedside examination. Although the tests excel in excluding central causes, they are insufficient for diagnosing AUPVP with certainty. In addition, the bedside examination sensitivities vary widely, and early radiological imaging can be misleading. Therefore, this study underlines the necessity of prompt otoneurological testing for accurate exclusion of vestibular pseudoneuritis and thus improve patient outcomes.

A Case Report of Korean Medicine Treatment Including <i>Samchulgunbi-tang-gagambang</i> in a Patient with Vestibular Neuritis

Background: Vestibular neuritis is a common cause of acute unilateral peripheral vestibulopathy. Vestibular neuritis is the second most common disease among patients with dizziness. Clinical symptoms of vestibular neuritis include the sudden onset of vertigo with spontaneous nystagmus, unsteady gait, nausea, and vomiting that last from days to weeks. However, even after the vertigo disappears, difficulty maintaining balance while walking may persist for weeks to months. Antihistamines, serotonin receptor blockers, and benzodiazepine vestibular suppressants are widely used as symptomatic treatments to reduce the severity of symptoms that occur in the acute phase.Case Summary: A patient diagnosed with acute vestibular neuritis was treated with acupuncture, moxibustion, and herbal medicine. We used the visual analog scale (VAS) to assess each symptom and the vertigo score to observe the effect of treatment. After treatment, the VAS scores for each symptom and the vertigo score decreased, and the severity of nystagmus was reduced.Conclusion: This study suggests that Korean medicine treatments, including <i>Samchulgunbi-tang-gagam</i>, could be effective in improving the clinical symptoms of vestibular neuritis.

Clinical Features and Neurotologic Findings in Patients With Acute Unilateral Peripheral Vestibulopathy Associated With Antiganglioside Antibody.

Anecdotal studies have reported the presence of antiganglioside antibodies in acute unilateral peripheral vestibulopathy (AUPV). This study aimed to determine the prevalence, clinical characteristics, and neurotologic findings of AUPV associated with antiganglioside antibodies. Serum antigangliosides were measured in consecutive patients with AUPV according to the Bárány Society criteria during the acute and recovery phases in a referral-based university hospital in South Korea from September 2019 to January 2023. Clinical characteristics and neurotologic findings were compared between those with and without antiganglioside antibodies. The results of video-oculography, video head impulse and bithermal caloric tests, and other neurotologic evaluations including ocular and cervical vestibular-evoked myogenic potentials and subjective visual vertical were compared between the 2. MRIs dedicated to the inner ear were also conducted when considered necessary. One hundred five patients (mean age ± SD = 60 ± 13 years, 57 male) were included for analyses. During the acute phase, 12 patients (12/105, 11%) were tested positive for serum antiganglioside antibodies, including anti-GQ1b immunoglobulin (Ig) G (n = 5) or IgM (n = 4), anti-GM1 IgM (n = 3), and anti-GD1a IgG (n = 1, including 1 patient with a positive anti-GQ1b antibody). Patients with antiganglioside antibodies showed lesser intensity of spontaneous nystagmus (median [interquartile range] = 1.8 [1.2-2.1] vs 3.4 [1.5-9.5], p = 0.003) and a lesser degree of canal paresis (30 [17-47] vs 58 [34-79], p = 0.028) and gain asymmetry of the vestibulo-ocular reflex for the horizontal semicircular canal during head impulse tests (0.07 [-0.04 to 0.61] vs 0.36 [0.18-0.47], p = 0.032) than those without antibodies. Negative conversion of antibodies and vestibular recovery were observed in most patients (6/8, 75%). Among 30 patients with AUPV with 4-hour delayed 3D fluid-attenuated inversion recovery dedicated to the inner ear, gadolinium enhancement was observed in 18 (18/30, 60%), either in the vestibule (n = 9), semicircular canal (n = 6), or vestibular nerve (n = 5). The positivity rates based on specific antibodies could not be determined due to limited sample sizes. The association between antiganglioside antibodies and AUPV suggests an immune-mediated mechanism in acute vestibular failure and extends the clinical spectrum of antiganglioside antibody syndrome.

Visuospatial cognition in acute unilateral peripheral vestibulopathy.

This study aims to investigate the presence of spatial cognitive impairments in patients with acute unilateral peripheral vestibulopathy (vestibular neuritis, AUPV) during both the acute phase and the recovery phase. A total of 72 AUPV patients (37 with right-sided AUPV and 35 with left-sided AUPV; aged 34-80 years, median 60.5; 39 males, 54.2%) and 35 healthy controls (HCs; aged 43-75 years, median 59; 20 males, 57.1%) participated in the study. Patients underwent comprehensive neurotological assessments, including video-oculography, video head impulse and caloric tests, ocular and cervical vestibular-evoked myogenic potentials, and pure-tone audiometry. Additionally, the Visual Object and Space Perception (VOSP) battery was used to evaluate visuospatial perception, while the Block design test and Corsi block-tapping test assessed visuospatial memory within the first 2 days (acute phase) and 4 weeks after symptom onset (recovery phase). Although AUPV patients were able to successfully perform visuospatial perception tasks within normal parameters, they demonstrated statistically worse performance on the visuospatial memory tests compared to HCs during the acute phase. When comparing right versus left AUPV groups, significant decreased scores in visuospatial perception and memory were observed in the right AUPV group relative to the left AUPV group. In the recovery phase, patients showed substantial improvements even in these previously diminished visuospatial cognitive performances. AUPV patients showed different spatial cognition responses, like spatial memory, depending on the affected ear, improving with vestibular compensation over time. We advocate both objective and subjective visuospatial assessments and the development of tests to detect potential cognitive deficits after unilateral vestibular impairments.

Revisiting pathophysiology of benign paroxysmal positional vertigo: a review

Benign paroxysmal positional vertigo (BPPV) is the most common cause of peripheral vertigo. There are several possible underlying causes of BPPV, although the idiopathic form is the most common. BPPV is characterized by brief recurrent episodes of vertigo that are triggered by changes in head position. Although BPPV is a benign vestibular disorder, it can be a severe and disabling problem for some of patients. The pathophysiology of BPPV is still unclear. The pathophysiology for BPPV is complex and the underlying mechanism is related to free-floating debris/otoliths in the semicircular canal (canalolithiasis) or debris/otoliths attached to the cupula (cupulolithiasis). These otolith/debris are originally accumulated after detachment from the neuroepithelium of the utricular macula secondary to degeneration. BPPV can occur following other vestibular disorders. In the majority of cases, the triggering factors are unknown. Some patients of BPPV have a history of previous inner ear diseases such as Meniere’s disease or acute unilateral peripheral vestibulopathy. This clinical entity is well-defined in medical literature and usually effectively treated by certain physical maneuvers. However, the pathophysiology is still obscure and is being critically discussed in this article, which reviews the details pathological mechanism for BPPV. This review article will discuss that aging, trauma, migraine, Meniere’s disease, vestibular neuronitis, and vitamin-D deficiency are the most commonly investigated etiopathological factors resulting in BPPV.

The effects of COVID-19 on the vestibular system.

The symptoms and severity of SARS-CoV-2 infection vary greatly across the spectrum, from asymptomatic infection to severe pneumonia with acute respiratory distress syndrome and even death. Dizziness is a frequently reported symptom of SARS-CoV-2 viral infection. However, the extent to which this symptom results from the effect of SARS-CoV-2 on the vestibular system remains unclear. In the present single-center, prospective cohort study, patients with a previous SARS-CoV-2 infection underwent a vestibular assessment consisting of the Dizziness Handicap Inventory to assess dizziness during and after infection, a clinical examination, the video head impulse test, and the subjective visual vertical test. When the subjective visual vertical test result was abnormal, vestibular-evoked myogenic potentials were performed. Vestibular testing results were compared to pre-existing normative data of healthy controls. In addition, we performed a retrospective data analysis of patients admitted to hospital presenting with acute symptoms of dizziness who were also diagnosed with acute SARS-CoV-2 infection. A total of 50 participants have been enrolled. During and after the SARS-CoV-2 infection, women were significantly more likely than men to suffer from dizziness. A significantly reduced semicircular canal or otolith function was not observed in either women or men. Acute SARS-CoV-2 infection was diagnosed in nine patients who presented to the emergency room with acute vestibular syndrome. Six of the patients exhibited acute unilateral peripheral vestibulopathy upon diagnosis. A different patient was diagnosed with vestibular migraine, and two individuals had a posterior inferior cerebellar artery infarct revealed by magnetic resonance imaging. Overall, a persisting structural affection of the vestibular system by SARS-CoV-2 seems to be unlikely and could not be confirmed by vHIT, SVV, and VEMPS in our study. It seems possible but unlikely that SARS-CoV-2 induces acute vestibulopathy. Nevertheless, dizziness is a common symptom in patients with COVID-19, which should be taken and worked through seriously.

Spontaneous nystagmus with an upbeat component: Central or peripheral vestibular disorders?

To determine the topical diagnosis and etiologies of spontaneous nystagmus (SN) with an upbeat component. We retrospectively recruited 43 patients with SN with an upbeat component at a university hospital in China from 2020 to 2022. SN with an upbeat component was divided into pure upbeat nystagmus (UBN), SN with a predominant upbeat component, and SN with a non-predominant upbeat component. We analyzed their clinical and neurotologic findings and the final diagnosis. Fourteen (32.6%) of them showed pure UBN, while 29 (67.4%) exhibited SN mixed with an upbeat component, mixed upbeat-horizontal in 15, mixed upbeat-horizontal-torsional in 13, and upbeat-torsional in the remaining one. Pure UBN and SN with a predominant upbeat component were more common in central than in peripheral vestibular disorders [16 (80.0%) vs. 0 (0%), Chi-Square test, p < 0.001]. Central vestibular disorders were diagnosed in 20 (46.5%) patients, peripheral in 14 (32.6%), and undetermined in nine (20.9%) patients. The underlying causes mainly included acute unilateral peripheral vestibulopathy (n = 11), posterior circulation infarction (n = 9), benign recurrent vertigo (n = 4), vestibular migraine (VM, n = 3), and VM of childhood (n = 2). SN with an upbeat component can be seen in both central and peripheral vestibular disorders. Pure UBN was a characteristic sign of central vestibular dysfunction. Central vestibular disorders should be highly suspected when patients show pure UBN or SN with a predominant upbeat component.

Benign Paroxysmal Positional Vertigo Secondary to Acute Unilateral Peripheral Vestibulopathy: Evaluation of Cardiovascular Risk Factors.

Lindsay-Hemenway syndrome was first described as an acute unilateral peripheral vestibulopathy followed by positional vertigo. A vascular etiology was proposed. An association between cardiovascular risk factors and benign paroxysmal positional vertigo secondary to acute unilateral peripheral vestibulopathy has been described with contradictory evidence. The study aimed to evaluate the prevalence of cardiovascular risk factors in patients with benign paroxysmal positional vertigo secondary to acute unilateral peripheral vestibulopathy and analyze differences in prior history of benign paroxysmal positional vertigo, affected semicircular canals, and response to repositioning maneuvers between patients with idiopathic benign paroxysmal positional vertigo and secondary to acute unilateral peripheral vestibulopathy. We performed a retrospective, descriptive study of all cases of benign paroxysmal positional vertigo between January/2017 and June/2020, with or without a history of acute unilateral peripheral vestibulopathy within the previous year. Cases secondary to trauma or otoneurological causes and acute unilateral peripheral vestibulopathy without confirmatory tests and cases with auditory symptoms were excluded. In total, 242 cases were obtained; 158 idiopathic benign paroxysmal positional vertigo and 84 secondary to acute unilateral peripheral vestibulopathy. No statistically significant differences were found in relation to age: 61.2 ± 14.6 versus 62.4 ± 16.2 years (P=.55), sex: female 78.5% versus 73.8% (P=.41), presence of cardiovascular risk factors: 52.5% versus 54.8% (P=.67), prior history of benign paroxysmal positional vertigo: 22.2% versus 27.7% (P=.43), affected semicircular canals (P=.16) or number of repositioning maneuvers (P=.57). Associations between age, cardiovascular risk factors, and benign paroxysmal positional vertigo secondary to acute unilateral peripheral vestibulopathy have been described with conflicting evidence. This is the first study to evaluate cardiovascular risk factors specifically for Lindsay-Hemenway syndrome, and we did not observe any differences between idiopathic benign paroxysmal positional vertigo cases and those secondary to acute unilateral peripheral vestibulopathy.

Cardiovascular risk factors among patients with acute unilateral inner ear hypofunction: A case-control study.

To assess the prevalence of cardiovascular risk factors (CVRFs) and their impact on acute unilateral inner ear hypofunction (AUIEH), including acute unilateral peripheral vestibulopathy (AUPVP), sudden sensorineural hearing loss (SSNHL) and acute unilateral audiovestibular hypofunction (AUAVH). One hundred and twenty-five patients consecutively diagnosed with AUPVP, SSNHL or AUAVH and 250 sex- and age-matched controls were included. Cases presented a mean age of 58.6 ± 14.7 years and included 59 women and 66 men. The correlation between CVRFs (high blood pressure [HBP], diabetes mellitus [DM], dyslipidemia [DLP], cardiocerebrovascular disease [CCVD]) and AUIEH was assessed by multivariate conditional logistic regression analysis. A higher prevalence of CVRFs was identified in patients than in controls (30 individuals with DM, 53 with HBP, 45 with DLP and 14 with a previous history of CCVD, p < .05). A significantly elevated risk of AUIEH was found in patients with two or more CVRFs (adjusted odds ratio [OR] 5.11; 95% CI 2.23-11.70). Previous CCVD individually predicted AUIEH (OR 8.41; 95% CI 2.36-29.88). Subgroup analysis showed the same tendency for AUPVP and SSNHL. Acute unilateral inner ear hypofunction patients presented significantly more CVRFs than controls, and the presence of two or more CVRFs was associated with AUIEH. Future studies evaluating vascular risk in AUIEH may include AUPVP and SSNHL patients from the same source population to better characterize risk profiles that can indicate a vascular origin. 3b.

Retrospective Study on the Outcome After Acute Unilateral Peripheral Vestibulopathy in 197 Patients

Retrospective Study on the Outcome After Acute Unilateral Peripheral Vestibulopathy in 197 Patients

Acute Unilateral Peripheral Vestibulopathy After COVID-19 Vaccination: Initial Experience in a Tertiary Neurotology Center.

ObjectiveThe aim of the present study was to identify patients who developed acute unilateral peripheral vestibulopathy (AUPVP) after COVID-19 vaccination.MethodsFor this single-center, retrospective study, we screened the medical records of our tertiary interdisciplinary neurotology center for patients who had presented with AUPVP within 30 days after COVID-19 vaccination (study period: 1 June−31 December 2021). The initial diagnosis of AUPVP was based on a comprehensive bedside neurotological examination. Laboratory vestibular testing (video head impulse test, cervical and ocular vestibular evoked myogenic potentials, dynamic visual acuity, subjective visual vertical, video-oculography, caloric testing) was performed 1–5 months later.ResultsTwenty-six patients were diagnosed with AUPVP within the study period. Of those, n = 8 (31%) had developed acute vestibular symptoms within 30 days after COVID-19 vaccination (mean interval: 11.9 days, SD: 4.8, range: 6–20) and were thus included in the study. The mean age of the patients (two females, six males) was 46 years (SD: 11.7). Seven patients had received the Moderna mRNA vaccine and one the Pfizer/BioNTech mRNA vaccine. All patients displayed a horizontal(-torsional) spontaneous nystagmus toward the unaffected ear and a pathological clinical head impulse test toward the affected ear on initial clinical examination. Receptor-specific laboratory vestibular testing performed 1–5 months later revealed recovery of vestibular function in two patients, and heterogeneous lesion patterns of vestibular endorgans in the remaining six patients.Discussion and ConclusionsThe present study should raise clinicians' awareness for AUPVP after COVID-19 vaccination. The relatively high fraction of such cases among our AUPVP patients may be due to a certain selection bias at a tertiary neurotology center. Patients presenting with acute vestibular symptoms should be questioned about their vaccination status and the date of the last vaccination dose. Furthermore, cases of AUPVP occurring shortly after a COVID-19 vaccination should be reported to the health authorities to help determining a possible causal relationship.

Vascular mechanisms in acute unilateral peripheral vestibulopathy: a systematic review.

SUMMARYAcute unilateral peripheral vestibulopathy (AUPVP) is a frequent cause of vestibular loss. Several aetiologies have been proposed, but the exact mechanism remains unknown. The aim of this study is a systematic analysis of the literature evaluating the vascular aetiology of AUPVP. A systematic literature search was performed in PubMed, Cochrane Library and Embase, including articles published from January 1st, 2010 to November 30th, 2020. Two reviewers independently selected articles investigating a link between AUPVP and vascular disease. The following information was extracted: year of publication, country, level of evidence, assessed vascular risk factors and number of patients. A total of 450 articles was obtained. Eleven articles were retained with 100% agreement between the two reviewers. In a pooled population of 805 patients, the main results were the higher neutrophil to lymphocyte ratio and higher prevalence of vascular risk factors among AUPVP patients. A meta-analysis was not performed because the studies were too heterogeneous in terms of methodology. Indirect arguments for vascular mechanisms in AUPVP were found. These findings indicate that larger prospective well-controlled studies are needed to clarify the vascular aetiology of AUPVP.

Modern approaches to drug treatment for vestibular vertigo

In recent years, some progress has been achieved in elaborating the algorithms and standards for the treatment of many conditions accompanied by vertigo. The current possibilities of treating vestibular vertigo consist of a gradually expanding arsenal of symptomatic and pathogenetic drugs. Among the drugs used for the symptomatic treatment of vestibular vertigo, there are vestibular suppressants (antihistamines, benzodiazepines, and calcium antagonists) and antiemetics (dopamine antagonists and serotonin 5-HT3 receptor antagonists). The paper discusses the possibilities of using betahistine and vitamin D as pathogenetic agents for recurrent benign paroxysmal positional vertigo; diuretics, betahistine (including the new prolonged release formulation Betaserc® Long), glucocorticoids, and gentamicin for Meniere's disease; triptans, beta-blockers, tricyclic antidepressants, and anticonvulsants for vestibular migraine; glucocorticoids, antiviral agents, and drugs that accelerate vestibular compensation for acute unilateral peripheral vestibulopathy (vestibular neuritis and Ramsey Hunt syndrome).The emergence of new drugs, as well as the design of new dosage forms that enhance patient adherence to the prescribed treatment, can improve quality of life in patients suffering from diseases that have recently led to long-term disability or even incapacitation.

Quantitative Evaluation of a New Posturo-Locomotor Phenotype in a Rodent Model of Acute Unilateral Vestibulopathy.

Vestibular pathologies are difficult to diagnose. Existing devices make it possible to quantify and follow the evolution of posturo-locomotor symptoms following vestibular loss in static conditions. However, today, there are no diagnostic tools allowing the quantitative and spontaneous analysis of these symptoms in dynamic situations. With this in mind, we used an open-field video tracking test aiming at identifying specific posturo-locomotor markers in a rodent model of vestibular pathology. Using Ethovision XT 14 software (Noldus), we identified and quantified several behavioral parameters typical of unilateral vestibular lesions in a rat model of vestibular pathology. The unilateral vestibular neurectomy (UVN) rat model reproduces the symptoms of acute unilateral peripheral vestibulopathy in humans. Our data show deficits in locomotion velocity, distance traveled and animal mobility in the first day after the injury. We also highlighted alterations in several parameters, such as head and body acceleration, locomotor pattern, and position of the body, as well as “circling” behavior after vestibular loss. Here, we provide an enriched posturo-locomotor phenotype specific to full and irreversible unilateral vestibular loss. This test helps to strengthen the quantitative evaluation of vestibular disorders in unilateral vestibular lesion rat model. It may also be useful for testing pharmacological compounds promoting the restoration of balance. Transfer of these novel evaluation parameters to human pathology may improve the diagnosis of acute unilateral vestibulopathies and could better follow the evolution of the symptoms upon pharmacological and physical rehabilitation.

Peripheral vestibular disorders: an update.

To provide an update on the most frequent peripheral vestibular disorders. The on-going classification of vestibular disorders by the Bárány Society represents major progress. The diagnosis of bilateral vestibulopathy (BVP) requires quantitative testing of vestibular function. 'Acute unilateral peripheral vestibulopathy' (AUPVP) is now preferred over 'vestibular neuritis.' Menière's disease is a set of disorders with a significant genetic contribution. The apogeotropic variant of horizontal canal benign paroxysmal positional vertigo (hcBPPV) and anterior canal BPPV (acBPPV) can be distinguished from a central vestibular lesion. Vestibular paroxysmia is now an internationally accepted clinical entity. The diagnosis of SCDS is based on conclusive findings. Diagnosis of BVP requires significantly reduced vestibular function. The clinical picture of AUPVP depends on how much the vestibular end organs or their innervation are affected. Menière's disease phenotype is a constellation of symptoms. Although diagnostic and therapeutic criteria for pc and hcBPPV are well defined, a number of less frequent and controversial are increasingly diagnosed and can be treated. Diagnosis of vestibular paroxysmia requires that a patient responds to treatment with a sodium channel blocker. The diagnosis of SCDS requires conclusive findings with various methods. There is still a great need for state-of-the-art randomized controlled treatment trials in most peripheral vestibular disorders.

The Clinical Efficacy of Vestibular Function Tests in Patients with Acute Unilateral Vestibulopathy

Objectives Aim of this study is to investigate the clinical efficacy of the vestibular function tests (VFTs) and the predictability of lesion side of vestibular asymmetry parameters in acute unilateral peripheral vestibulopathy. Methods Medical records and results of VFTs (caloric, rotatory chair, and head impulse tests) of 57 patients with acute unilateral vestibulopathy were reviewed retrospectively. The VFTs were examined within 7 days after the clinical onset. Results For the caloric test, 74% showed significant canal paresis and the predictability of lesion side was 88%. For the sinusoidal harmonic acceleration test, 91% had low gain in at least 1 Hz, phase lead showed 70%, 89% showed phase asymmetry and the predictability of lesion side was 90%. For velocity step test, 67% had abnormal Tc asymmetry and the predictability of lesion side was 95%. In bedside head impulse test (HIT), abnormal catch up saccades were observed in 89% and the predictability of lesion side was 100%. For the video HIT, cover or overt catch-up saccades were observed in 95% and the predictability of lesion side was 100%. One hundred percent (100%) had low gain on the video HIT, but the lesion sides were uncertain because of bilateral involvements or artifacts. Conclusions The most important things in the diagnosis of acute unilateral vestibulopathy are typical clinical symptoms and spontaneous nystagmus. A combination of rotatory, caloric, and HITs will result in a more complete examination of the vestibular system. Among them, HIT is recommended as the best tool in acute unilateral vestibulopathy. Keywords: Acute unilateral vestibulopathy; Vestibular function tests; Caloric test; Rotatory chair test; Head impulse test 중심 단어: ì¼ì¸¡ì„±ì „ì •ìž¥ì• , ì „ì •ê¸°ëŠ¥ê²€ì‚¬

Prediction of Vestibular Imbalance in Acute Peripheral Vestibulopathy by Measuring Horizontal Ocular Deviation on Magnetic Resonance Imaging.

The aim of the study is to evaluate whether horizontal ocular deviation (OD) from MR imaging in the emergency room (ER) reflects vestibular imbalance, by comparing the horizontal OD in patients with acute vestibulopathy to controls. Retrospective review. A total of 69 patients with acute unilateral peripheral vestibulopathy and 30 healthy subjects were included. Horizontal OD was quantified by using the axial T2-weighted fast-spin echo (FSE) images of the brain at 1.5 T. In the study group, the results of VFTs (videonystagmography [VNG], caloric test, rotary chair test, and cervical vestibular evoked myogenic potentials [cVEMP]) were also reviewed. The averaged angle of right and left horizontal ODs was compared between patients with acute unilateral vestibulopathy and healthy controls. Also, the correlation between horizontal OD and results of VFTs was analyzed in the study group. The averaged angle of horizontal OD in study group (23.7° ± 11.6°) was significantly greater than that of control group (4.27° ± 3.7°) (p < 0.05). Horizontal OD significantly correlated with slow phase velocity of spontaneous nystagmus (SN), the value of caloric paresis (CP) on caloric testing, rotary chair gain, asymmetry ratio of rotary chair test and interaural difference (IAD) of cVEMP, regardless of time intervals between magnetic resonance imaging (MRI) and VFTs. Horizontal OD significantly correlated with parameters of VFT which reflect the vestibular imbalance. Therefore, horizontal OD can be used as an indicator of unilateral peripheral vestibular weakness.

Acute unilateral peripheral vestibulopathy in neurosyphilis

IntroductionNeurosyphilis producing basal meningitis presenting as sequential transient cranial nerve palsies was well recognized before the antibiotic era. ObjectiveTo report two patients presenting with acute unilateral peripheral vestibulopathy due to syphilitic basal meningitis. ResultsIn Case 1 basal meningitis occurred early in the secondary phase of the infection, in Case 2 in the late latent phase. The diagnosis was not made immediately in either case; in Case 1 after previous presentation with increasing hearing loss and then with facial palsy and then a subsequent presentation with optic neuritis; in Case 2 after investigation for possible lymphoma. ConclusionSyphilitic basal meningitis in either the secondary or in the latent phase can present as acute unilateral peripheral vestibulopathy with transient involvement of the facial or auditory nerve.

About the pathophysiology of acute unilateral vestibular deficit – vestibular neuritis (VN) or peripheral vestibulopathy (PVP)?

To determine whether patients with acute unilateral peripheral vestibulopathy (PVP), often called "vestibular neuritis/neuronitis or neuropathy" (VN) have a vestibular lesion pattern consistent with the distribution of the neurological afferents. Much is known about the clinical nature of PVP, however less so about its etiology and pathogenesis. Due to the frequency with which VN is used to describe the syndrome, an inflammation of the vestibular nerve or of one of its branches is often assumed to be the cause of PVP, though there is insufficient data so far to support this assumption. We conducted a retrospective study of 25 patients who had presented to our clinic with PVP and had all vestibular receptor organs tested shortly after start of symptoms. We analysed their vestibular lesion patterns in order to determine whether they were consistent with the neuritis hypothesis (NH). The lesion patterns varied conspicuously. 76% did not follow an innervation pattern, thereby contradicting the NH and only 24% had a lesion pattern that either definitely (16%) or probably (8%) supported the NH. These results should remind us to be careful before jumping to quick conclusions about the pathogenetic nature of PVP. With any reason to question VN as the only cause of PVP, we should reconsider the treatment approach to PVP. If the cause probably or even possibly lies inside the vestibular labyrinth, an intratympanic steroid injection might prove to be a more effective measure, even in first-line treatment. If the etiology is unsure, a combination of systemic and intratympanic steroid treatment may be adequate.

Mastication-induced vertigo and nystagmus

Even though trigeminovestibular connections are well established in animals, mastication-induced dizziness has been described only as a vascular steal phenomenon in humans. We determined induction or modulation of nystagmus in two index patients with mastication-induced vertigo, 12 normal controls, and 52 additional patients with peripheral (n = 38, 26 with vestibular neuritis/labyrinthitis and 12 with Meniere's disease) or central (n = 14, 11 with Wallenberg syndrome, two with cerebellar infarction, and one with pontine infarction) vestibulopathy during their acute or compensated phase. Both index patients developed mastication-induced vertigo after near complete resolution of the spontaneous vertigo from presumed acute unilateral peripheral vestibulopathy. The nystagmus and vertigo gradually built up during mastication and dissipated slowly after cessation of mastication. Brain MRI and cerebral angiography were normal in these patients. Mastication did not induce nystagmus in normal controls. However, mastication induced nystagmus in five (24 %) of the 21 patients without spontaneous nystagmus (SN) but with a previous history of a vestibular syndrome, and either increased (21/31, 68 %) or decreased (7/31, 23 %) the SN in almost all the patients (28/31, 90 %) with SN. Mastication may induce significant vertigo and nystagmus in patients with a prior history of acute vestibulopathy. The induction or modulation of nystagmus by mastication in both peripheral and central vestibulopathies supports trigeminal modulation of the vestibular system in human. The gradual build-up and dissipation suggest a role of the velocity storage mechanism in the generation of mastication-induced vertigo and nystagmus.