Acute Unilateral Vestibulopathy Research Articles

Systematic Review and Meta-Analysis of the Diagnostic Accuracy of a Graded Gait and Truncal Instability Rating in Acutely Dizzy and Ataxic Patients.

In patients presenting with acute prolonged vertigo and/or gait imbalance, the HINTS [Head-Impulse, Nystagmus, Test-of-Skew] are very valuable. However, their application may be limited by lack of training and absence of vertigo/nystagmus. Alternatively, a graded gait/truncal-instability (GTI, grade 0-3) rating may be applied. We performed a systematic search (MEDLINE/Embase) to identify studies reporting on the diagnostic accuracy of bedside examinations in adults with acute vestibular syndrome. Diagnostic test properties were calculated for findings using a random-effects model. Results were stratified by GTI-rating used. We identified 6515 articles and included 18 studies (n = 1025 patients). Ischemic strokes (n = 665) and acute unilateral vestibulopathy (n = 306) were most frequent. Grade 2/3 GTI had moderate sensitivity (70.8% [95% confidence-interval (CI) = 59.3-82.3%]) and specificity (82.7 [71.6-93.8%]) for predicting a central cause, whereas grade 3 GTI had a lower sensitivity (44.0% [34.3-53.7%] and higher specificity (99.1% [98.0-100.0%]). In comparison, diagnostic accuracy of HINTS (sensitivity = 96.8% [94.8-98.8%]; specificity = 97.6% [95.3-99.9%]) was higher. When combining central nystagmus-patterns and grade 2/3 GTI, sensitivity was increased to 76.4% [71.3-81.6%] and specificity to 90.3% [84.3-96.3%], however, no random effects model could be used. Sensitivity was higher in studies using the GTI rating (grade 2/3) by Lee (2006) compared to the approach by Moon (2009) (73.8% [69.0-78.0%] vs. 57.4% [49.5-64.9%], p = 0.001). In comparison to HINTS, the diagnostic accuracy of GTI is inferior. When combined with central nystagmus-patterns, diagnostic accuracy could be improved based on preliminary findings. GTI can be readily applied in the ED-setting and also in patients with acute imbalance syndrome.

Altered thalamus functional connectivity in patients with acute unilateral vestibulopathy: a resting-state fMRI study.

Acute unilateral vestibulopathy (AUVP) is the second leading cause of peripheral vestibular vertigo. Full recovery of AUVP is related to sufficient central vestibular compensation. It has been confirmed that the vestibular nucleus and vestibular cortex are involved in the process of vestibular compensatory in AUVP patients. However, few studies have focused on the functional compensation of thalamus in patients with AUVP. This study aimed to explore the alterations of resting-state functional connectivity (FC) focused on thalamus using functional magnetic resonance imaging (fMRI) in AUVP patients. Data of 3D-T1 and resting-state fMRI were collected from 40 AUVP patients and 35 healthy controls (HC). Seeds-based (bilateral thalamus) FC was analyzed to investigate the changes in FC between the two groups. Furthermore, we evaluated the associations between altered thalamus FC and clinical features in AUVP patients using Pearson's partial correlation. Compared with HC, AUVP patients showed decreased FC between bilateral thalamus and left insula. We also observed decreased FC between right thalamus and left supramarginal gyrus. Additionally, we found increased FC between left thalamus and right postcentral gyrus (PCG), as well as increased FC between right thalamus and regions of bilateral PCG, right middle frontal gyrus and right middle occipital gyrus in AUVP patients. Furthermore, the FC between left thalamus and left insula was negatively correlated with values of canal paresis in patients with AUVP (p = 0.010, r = -0.434). Our results provided first evidence for the decreased thalamo-vestibular cortex pathway, as well as increased thalamo-somatosensory and thalamo-visual cortex pathway in AUVP patients. These findings help us better understand the underlying mechanisms of central dynamic compensatory following an acute unilateral peripheral vestibular damage.

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.

Evolution of Hyperventilation-Induced Nystagmus in Acute Unilateral Vestibulopathy-Interpretative Model and Etiopathogenetic Hypotheses.

Hyperventilation induces metabolic changes that can elicit nystagmus (hyperventilation-induced nystagmus, HVIN) in various vestibular disorders, revealing vestibular imbalance and bringing out central or peripheral asymmetries. In acute unilateral vestibulopathy (AUVP, namely vestibular neuritis), hyperventilation can induce different patterns of nystagmus (excitatory, inhibitory, or negative), disclosing or modifying existing static vestibular asymmetries through its ability to invalidate compensation or increase peripheral excitability. In this context, we followed the evolutionary stages of HVIN in AUVP across 35 consecutive patients, with the goal of assessing alterations in the oculomotor pattern caused by hyperventilation over time. In the acute phase, the incidence of the excitatory pattern (and the strongly excitatory one, consisting of a reversal nystagmus evoked by hyperventilation) was significantly higher compared to the inhibitory pattern; then, a progressive reduction in the incidence of the excitatory pattern and a concomitant gradual increase in the incidence of the inhibitory one were observed in the follow-up period. Assuming the role of the ephaptic effect and the transient loss of vestibular compensation as opposing mechanisms, i.e., excitatory and inhibitory, respectively, the oculomotor pattern evoked by hyperventilation is the result of the interaction of these two factors. The data obtained allowed us to hypothesize an interpretative model regarding the pathogenetic aspects of responses evoked by hyperventilation and the etiologies of the disease: according to our hypotheses, the excitatory pattern implies a neuritic (viral) form of AUVP; instead, the inhibitory (and negative) one can be an expression of both the neuritic (viral) and vascular forms of the disease.

The clinical significance of arterial stiffness in the differential diagnosis of vertigo

Objectives: Pulse wave velocity (PWV) is a known indicator of arterial stiffness reflecting vascular damage. However, there are few reports of the relationship between PWV and dizziness/vertigo of a vascular origin. We investigated whether the PWV value could be useful as an ancillary measurement for identifying the etiology of dizziness/vertigo.Methods: We enrolled dizzy patients from March 2016 to December 2018. The patients with posterior circulation stroke presenting with dizziness/vertigo were categorized as having central vertigo. The patients with vertigo due to benign paroxysmal positional vertigo, Ménière disease, or acute unilateral vestibulopathy were categorized as having peripheral vertigo. The PWV value, ankle-brachial index (ABI), and traditional vascular risk factors were collected.Results: We consecutively enrolled a total of 93 participants. The PWV values were higher in the central vertigo group (p<0.001), but ABI did not differ between the groups. Among the vascular risk factors, the number of patients with diabetes mellitus, dyslipidemia, and male patients was significantly higher in the central vertigo group. The brachial-ankle PWV (baPWV) values were higher in the central vertigo group, even after adjusting for confounding factors (p<0.01). The receiver operating characteristic curve showed that the sensitivity was 74% and specificity was 81% when the mean baPWV value was 14.78 m/sec.Conclusions: Increased baPWV values were observed in patients with dizziness/vertigo due to stroke. Measurement of the baPWV value could be an ancillary test for evaluating the cause of dizziness/vertigo, even though more convincing evidence is still required.

The value of saccade metrics and VOR gain in detecting a vestibular stroke.

A normal video Head Impulse Test is the gold standard in the emergency department to rule-in patients with an acute vestibular syndrome and a stroke. We aimed to compare the diagnostic accuracy of vHIT metrics regarding the vestibulo-ocular reflex gain and the corrective saccades in detecting vestibular strokes. Prospective cross-sectional study (convenience sample) of patients presenting with acute vestibular syndrome in the emergency department of a tertiary referral centre between February 2015 and May 2020. We screened 1677 patients and enrolled 76 patients fulfilling the inclusion criteria of acute vestibular syndrome. All patients underwent video head impulse test with automated and manual data analysis. A delayed MRI served as a gold standard for vestibular stroke confirmation. Out of 76 patients, 52 were diagnosed with acute unilateral vestibulopathy and 24 with vestibular strokes. The overall accuracy of detecting stroke with an automated vestibulo-ocular reflex gain was 86.8%, compared to 77.6% for cumulative saccade amplitude and automatic saccade mean peak velocity measured by an expert and 71% for cumulative saccade amplitude and saccade mean peak velocity measured automatically. Gain misclassified 13.1% of the patients as false positive or false negative, manual cumulative saccade amplitude and saccade mean peak velocity 22.3%, and automated cumulative saccade amplitude and saccade mean peak velocity 28.9% respectively. We found a better accuracy of video head impulse test for the diagnosis of vestibular strokes when using the vestibulo-ocular reflex gain than using saccade metrics. Nevertheless, saccades provide an additional and important information for video head impulse test evaluation. The automated saccade detection algorithm is not yet perfect compared to expert analysis, but it may become a valuable tool for future non-expert video head impulse test evaluations.

Clinical Significance of Neutrophil-to-Lymphocyte Ratio and Platelet-to-Lymphocyte Ratio in Acute Unilateral Vestibulopathy.

The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) have been identified as useful biomarkers for assessing the inflammatory response and for predicting the prognosis of various diseases. This study aimed to determine the clinical significance and effects on prognostic prediction of NLR and PLR in acute unilateral vestibulopathy (AUV). We retrospectively recruited 128 patients who were diagnosed with AUV from July 2016 to April 2021, and compared NLR and PLR values between these patients with AUV and age- and sex-matched healthy subjects. We also analyzed the correlations of various clinical parameters with NLR and PLR. NLR and PLR in the AUV group were 3.41±2.80 (mean±standard deviation) and 128.86±67.06, respectively, with only NLR being significantly higher than that in the control group (1.55±0.60, p<0.001). The gain asymmetry of the horizontal vestibulo-ocular reflex (VOR) was slightly larger in patients with high NLR (n=52) than in those with normal NLR (n=76) (41.9%±20.2% vs. 33.6%±17.4%, p=0.048). However, the hospitalization period, preceding infection, canal paresis, and absolute horizontal VOR gain did not differ between patients with high and normal NLR and PLR values. The correlation analyses also revealed that none of the clinical parameters were significantly correlated with NLR or PLR. At 3-month follow-up examinations, NLR and PLR did not differ significantly between patients with and without function recovery of the horizontal VOR. This study found a high NLR in AUV, suggesting an acute inflammatory status in the vestibular organ. However, the usefulness of NLR and PLR as prognostic markers remains unclear.

The six most frequent peripheral vestibular syndromes

Three forms of peripheral vestibular disorders, each with its typical symptoms and clinical signs, can be differentiated functionally, anatomically and pathophysiologically: 1. inadequate unilateral paroxysmal stimulation or rarely inhibition of the peripheral vestibular system, e. g., BPPV, Menière's disease, vestibular paroxysmia or syndrome of the third mobile windows; 2. acute unilateral vestibulopathy leading to an acute vestibular tone imbalance manifesting as an acute peripheral vestibular syndrome; and 3. loss or impairment of function of the vestibular nerve and/or labyrinth: bilateral vestibulopathy. For all of these diseases, current diagnostic criteria by the Bárány-Society are available with a high clinical and scientific impact, also for clinical trials. The treatment depends on the underlying disease. It basically consists of 5 principles: 1. Explaining the symptoms and signs, pathophysiology, aetiology and treatment options to the patient; this is important for compliance, adherence and persistence. 2. Physical therapy: A) For BPPV specific liberatory maneuvers, depending on canal involved. Posterior canal: The new SémontPLUS maneuver is superior to the regular Sémont and Epley maneuvers; horizontal canal: the modified roll-maneuver; anterior canal the modified Yacovino-maneuver; 3. Symptomatic or causative drug therapy. There is still a deficit of placebo-controlled clinical trials so that the level of evidence for pharmacotherapy is most often low. 4. Surgery, mainly for the syndrome of the third mobile windows. 5. Psychotherapeutic measures for secondary functional dizziness.

Dural Arteriovenous Fistula Presenting as Acute Unilateral Vestibulopathy

Intracranial dural arteriovenous fistula (dAVF) is characterized by an abnormal connection between branches of arteries and veins in the dura mater. Clinical manifestations of dAVF vary depending on their location, feeder arterial supply, amount of shunting, and most importantly, their venous drainage pattern. Acute vertigo has been rarely reported as an initial presentation of dAVF due to venous congestion in the brainstem. We report a patient who presented with acute right vestibulopathy without any brainstem signs in dAVF involving the transversesigmoid sinus. The patient showed abnormal caloric response but normal head impulse in the affected ear. Without any treatment, the patient’s symptoms gradually improved with a normalization of right canal paresis. Follow-up cerebral angiography also revealed a spontaneous regression of the shunt flow and reduction of venous drainage at the right transverse-sigmoid sinus. Based on the results of vestibular function tests and cerebral angiography, acute vertigo in our patient may be ascribed to impaired reabsorption of endolymph by focal venous congestion.

Acute unilateral vestibulopathy: a practical diagnostic approach and new insight on management

Acute unilateral vestibulopathy: a practical diagnostic approach and new insight on management

Pharmacological Treatment of Acute Unilateral Vestibulopathy: A Review.

There have been few investigations on the epidemiology, etiology, and medical management of acute unilateral vestibulopathy (AUV). Short-term pharmaceutical resolutions include vestibular symptomatic suppressants, anti-emetics, and some cause-based therapies. Anticholinergics, phenothiazines, antihistamines, antidopaminergics, benzodiazepines, and calcium channel antagonists are examples of vestibular suppressants. Some of these medications may show their effects through multiple mechanisms. In contrast, N-acetyl-L-leucine, Ginkgo biloba, and betahistine improve central vestibular compensation. Currently, AUV pathophysiology is poorly understood. Diverse hypotheses have previously been identified which have brought about some causal treatments presently used. According to some publications, acute administration of anti-inflammatory medications may have a deleterious impact on both post-lesional functional recovery and endogenous adaptive plasticity processes. Thus, some authors do not recommend the use of corticosteroids in AUV. Antivirals are even more contentious in the context of AUV treatment. Although vascular theories have been presented, no verified investigations employing anti-clotting or vasodilator medications have been conducted. There are no standardized treatment protocols for AUV to date, and the pharmacological treatment of AUV is still questionable. This review addresses the most current developments and controversies in AUV medical treatment.

A Case Report of Korean Medicine Treatment Including &lt;i&gt;Samchulgunbi-tang-gagambang&lt;/i&gt; 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 &lt;i&gt;Samchulgunbi-tang-gagam&lt;/i&gt;, 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.

A Case of Delayed Audiovestibulopathy after Posterior Circulation Ischemic Stroke

Distinguishing central and peripheral causes of dizziness is vital. A case is presented where a 42-year-old man with a history of posterior circulation ischemic stroke developed acute unilateral vestibulopathy with hearing loss. Clinical examination revealed signs of vestibular dysfunction on the left side. Audiometry confirmed deafness on the left, but imaging ruled out new central issues. The patient was diagnosed with audiovestibulopathy and treated with steroids, antiviral agents, intratympanic injections, and hyperbaric oxygen therapy. Hearing loss persisted, but dizziness improved with vestibular rehabilitation. Poststroke patients should be closely monitored for peripheral complications. Further research should explore the benefits of antiplatelet therapy in vascular-related conditions, even without clear central lesions.

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.

Vestibular rehabilitation improves spontaneous nystagmus normalization in patients with acute unilateral vestibulopathy.

Spontaneous nystagmus (SN) can be observed after acute unilateral vestibulopathy (AUVP). The slow phase eye velocity of the SN progressively decreases in darkness as the result of rebalanced neurophysiological activity between both vestibular nuclei, a process that can take several months. Although this compensatory process can occur spontaneously, there is poor evidence that vestibular rehabilitation (VR) can facilitate the process. We documented the natural time course of SN reduction in patients with AUVP, as well as the effects of VR by means of a unilateral rotation paradigm. In a retrospective study (Study 1: n = 126 AUVP patients), we compared the time course of the SN reduction in patients with VR (n = 33) and without VR (n = 93). In a prospective study (Study 2: n = 42 AUVP patients), we compared the effects of early VR (n = 22; initiated within the first two weeks of symptoms onset) or late VR (n = 20; initiated after the second week of symptoms onset) on the time course of the SN reduction. Study 1 showed shorter median time of SN normalization in patients with VR compared to patients without VR (14 days and 90 days, respectively). Study 2 showed that AUVP patients with early and late VR had a similar median time of SN normalization. The SN slow phase eye velocity was significantly decreased as early as the end of the first VR session in both groups, and kept decreasing at each subsequent VR session. In the early VR group, 38% of the patients had slow phase eye velocity below 2°/s after the first VR session, 100% after the fifth session. Similar findings were observed in the late VR group. Taken together, these results indicate that VR with a unidirectional rotation paradigm speeds up the normalization of SN. This effect seems independent of the time between symptoms onset and commencement of VR, but early intervention is recommended to speed up the SN reduction.

Worldwide Survey on the Treatment of Peripheral Vestibular Disorders (P3-9.002)

<h3>Objective:</h3> The aim of this world wide survey was to evaluate the currently used treatment options of the six most frequent peripheral vestibular disorders: benign paroxysmal positional vertigo (BPPV), acute unilateral vestibulopathy (AUVP)/vestibular neuritis, Menière’s disease, bilateral vestibulopathy (BVP), vestibular paroxysmia and superior canal deshiscence syndrome (SCDS). <h3>Background:</h3> For the therapy of vestibular disorders, there are basically four treatment options: physiotherapy (liberatory maneuvers or balance training), pharmacotherapy, surgery and psychotherapy. Since there are very few state-of-the-art RCTs, the treatment of vestibular disorders is so far not standardized and various methods are applied with heterogeneous efficacy. <h3>Design/Methods:</h3> A web-based standardized survey questionnaire on the treatment of the six most frequent peripheral vestibular disorders was used to collect data. <h3>Results:</h3> 234 replies from five continents, 47 countries, 162 cities and 188 centers were received: (% from all 234 replies; multiple answers possible): BPPV: posterior canal: 71% Epley, 40% Sémont, and 12% others. Horizontal canal BPPV canalithiasis: 58% roll-maneuver, 33% Gufoni, 7% prolonged rest, and 9% others. Horizontal canal cupulolithiasis: 35% Gufoni, 27% roll-maneuver, 9% Zuma, and 7% head shaking: AUVP: 79% pharmacotherapy, namely 47% glucocorticoids, 39% antiemetics, and 24% betahistine; 67% physiotherapy. Menière’s disease: 85% pharmacotherapy, namely 65% betahistine, 21% diuretics, 20% steroids, 16% antiemetics, 14% gentamicin; 37% surgery. Vestibular paroxysmia: 65% pharmacotherapy, namely 57% anticonvulsants; 7% surgery. BVP: 77% physiotherapy. SCDS: 50% Surgery, namely 19% canal plugging, 12% capping, and 8% resurfacing. <h3>Conclusions:</h3> In this world wide survey with 234 replies from 188 centers widely heterogeneous applied treatment options were reported for the six most frequent peripheral vestibular disorders. For example, medication use is often not supported by evidence. Namely in AUVP, Menière’s disease and vestibular paroxysmia well designed controlled trials are needed with clinically meaningful endpoints are needed. <b>Disclosure:</b> Dr. Strupp has received personal compensation in the range of $10,000-$49,999 for serving as a Consultant for IntraBio. Dr. Strupp has received personal compensation in the range of $0-$499 for serving as a Consultant for AurisMedical. Dr. Strupp has received personal compensation in the range of $10,000-$49,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Springer. Dr. Strupp has received personal compensation in the range of $5,000-$9,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Frontiers. Dr. Strupp has stock in IntraBio. Mr. Kern has nothing to disclose. Prof. Laurell has nothing to disclose. Eva Grill has received personal compensation in the range of $500-$4,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for ELSEVIER. The institution of Eva Grill has received research support from German Federal Ministry of Education and Research. The institution of Eva Grill has received research support from AOK Bayern. Eva Grill has received personal compensation in the range of $500-$4,999 for serving as a Speaker with Apothekerkammer Bayern. Ralf Strobl has nothing to disclose.

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.