Objective: This study aims to estimate the incidence of Vestibular neuritis (VN) in three different districts in Italy, its epidemiological features, and the prevalence of comorbidities associated with it.
Methods: An observational prospective study of 198 patients referred to ENT departments in Siena, Grosseto, and Cuneo was carried out over a 2-year period. Each patient underwent a complete otoneurologic examination in the first 48 h from the onset of symptoms and a brain MRI in the early stages of the disease. The follow-up lasted for 1 year.
Results: The total VN incidence rate of the three municipalities was 48.497 (95% CI: 48.395–48.598) and its standardized value was 53.564 (95% CI: 53.463–53.666). The total VN incidence rate for the whole sample (municipality and district of the three centers) was 18.218 (95% CI: 18.164–18.272), and its standardized value was 20.185 (95% CI: 20.129–20.241). A significant difference was highlighted between patients living in the city compared to those living in the surrounding area (p < 0.000), this may be due to the ease of reaching the otoneurological referral center.
Conclusion: The total incidence rate for the three municipalities was 48.497. This result is higher than previously reported studies.
Introduction: Predicting hearing outcome in sudden sensorineural hearing loss (SSNHL) is challenging, as well as detecting the underlying pathomechanisms. SSNHL could be associated with vestibular damage since cochleo-vestibular structures share the same vascularization, along with being in close anatomical proximity. Whereas viral inflammations and autoimmune/vascular disorders most likely represent the involved aetiologies, early-stage Menière's disease (MD) can also present with SSNHL. Since an early treatment could beneficially influence hearing outcome, understanding the possible etiology plays a pivotal role in orienting the most appropriate treatment. We aimed to evaluate the extent of vestibular damage in patients presenting with SSNHL with or without vertigo, investigate the prognostic role of vestibular dysfunctions on hearing recovery and detect specific lesion patterns related to the underlying pathomechanisms.
Methods: We prospectively evaluated 86 patients with SSNHL. Audio-vestibular investigation included pure-tone/speech/impedance audiometry, cervical/ocular-VEMPs, vHIT and video-Frenzel examination. White matter lesions (WML) were evaluated on brain-MRI. Patients were followed-up and divided into “SSNHL-no-vertigo,” “SSNHL+vertigo” and “MD” subgroups.
Results: Hearing was more impaired in “SSNHL+vertigo” patients who exhibited either down-sloping or flat-type audiograms, and was less impaired in “MD” where low frequencies were mostly impaired (p < 0.001). Otolith receptors were more frequently involved than semicircular canals (SCs). Although the “SSNHL-no-vertigo” subgroup exhibited the lowest vestibular impairment (p < 0.001), 52% of patients developed otolith dysfunctions and 72% developed nystagmus. Only “MD” subjects showed anterior SC impairment and upbeating spontaneous/positional nystagmus. They more frequently exhibited cervical-VEMPs frequency tuning (p = 0.036) and ipsilesional spontaneous nystagmus (p < 0.001). “SSNHL+vertigo” subjects presented with more frequently impaired cervical-VEMPs and posterior SC and with higher number of impaired receptors (p < 0.001). They mainly exhibited contralesional spontaneous and vibration-induced nystagmus (p < 0.05) and only they showed the highest WML score and “vascular” lesion patterns (p < 0.001). Concerning the outcomes, hearing was better in “MD” and worse in “SSNHL+vertigo” (p < 0.001). Hearing recovery was mostly affected by cervical-VEMPs impairment and the number of involved receptors (p < 0.05). Patients with “vascular” lesion patterns presented with the highest HL degree and WML score (p ≤ 0.001), while none of them exhibited a complete hearing recovery (p = 0.026).
Conclusions: Our data suggest that vestibular evaluation in SSNHL can provide useful information on hearing recovery and underlying aetiologies.
Introduction: Acute unilateral vestibular hypofunction is characterized by sudden onset of vertigo or dizziness, vomiting/nausea, gait instability, and nystagmus. This is commonly described as an acute vestibular syndrome and usually attributed to vestibular neuritis; however, up to 25% of acute vestibular syndrome is caused by a stroke of posterior circulations. The video head impulse test is a recent tool in the vestibular test battery that assesses the vestibule-ocular reflex by measuring the VOR gain and recording overt and covert saccades, these findings have been found to be helpful in the diagnosis of various vestibular disorders.
Method: A literature search was conducted in databases, including PubMed Central, PubMed, and Web of Science. All the articles that define video head impulse test (vHIT), acute vestibular hypofunction, and vestibular neuritis were considered for the preliminary search. No limits were placed on the date of publication. The searches were limited to studies with full-text availability, published in English, and including human subjects. Search words such as “head impulse test,” “video head impulse test,” “vestibular ocular reflex,” “acute vestibular syndrome,” “acute vestibular hypofunction,” “vestibular neuritis,” and “vHIT in central vestibular disorders” were entered into different databases in different combinations using boolean operators such as AND, OR, and NOT.
Results: Searches across different databases, including Web of Science, PubMed Central, and PubMed, resulted in a total of 1,790 articles. Title screening was done for all the articles. Out of the 1,790 articles, we found that 245 articles were related to vestibular hypofunction i.e., 1,545 articles were removed at this stage. A further 56 duplicate articles were removed. This led to a final screening of 189 articles. The exclusion criteria included unavailability of full text, studies reported in languages other than English, case reports, reviews, and articles including participants having other comorbid conditions. This final screening led to 133 articles being excluded, which led to the full-text screening of 56 articles. After screening the full-text articles as per the eligibility criteria, 21 articles were found to be eligible for the systematic review. Among the remaining studies, six articles were excluded due to different specific reasons. A total of 15 articles were included in this systematic review. The mean VOR gain for the patients with vestibular neuritis was 0.48 ± 0.14 for the ipsilesional ear, whereas the mean VOR gain was > 0.80 in the contralesional ear for all the patients with acute vestibular neuritis. In patients with PICA lesions, the VOR gain for the ipsilesional ear was 0.90 (range 0.87–0.94) and for the contralesional ear was 0.88 (range 0.84–0.93). In patients with AICA lesions, the mean VOR gain was variable. Based on the above mean VOR gain findings, the authors propose the following adjective description scale of VOR of the lateral canal using vHIT: normal VOR gain above 0.80, mild VOR gain loss for 0.70–0.79, moderate loss for 0.69–0.4, severe loss for 0.39–0.2, and profound loss for < 0.2.
Purpose: We aimed to assess the ability of a head-shaking test (HST) to reflect vestibular compensation in patients after unilateral peripheral vestibular loss and to provide missing evidence and new insights into the features of head-shaking-induced nystagmus (HSN) over a 2-year follow-up.
Background: HSN may occur after a prolonged sinusoidal oscillation of the head. HSN is frequently observed in subjects with vestibular function asymmetry; it usually beats toward the functionally intact or “stronger” ear and can be followed by a reversal of its direction.
Study design: A prospective observational case-control study.
Settings: A tertiary academic referral center.
Methods: A total of 38 patients after acute unilateral vestibular loss (22 patients with vestibular neuronitis and 16 patients after vestibular neurectomy) and 28 healthy controls were followed for four consecutive visits over a 2-year period. A complex vestibular assessment was performed on all participants, which included spontaneous nystagmus (SPN), the caloric test, the head-shaking test (HST), the video head impulse test (vHIT), the Timed Up and Go (TUG) test, and the Dizziness Handicap Inventory (DHI) questionnaire. We established the criteria for the poorly compensated group to assess different compensatory behaviors and results.
Results: We found a time-related decrease in HSN (ρ < −0.84, p < 0.001) after unilateral vestibular loss. After 2 years of follow-up, HSN intensity in compensated patients reached the level of the control group; TUG and DHI also improved to normal; however, the caloric and vHIT tests remained abnormal throughout all follow-ups, indicating a chronic vestibular deficit. Besides, poorly compensated patients had a well-detectable HSN throughout all follow-ups; TUG remained abnormal, and DHI showed at least a moderate deficit.
Conclusions: Our study showed that, after a unilateral peripheral vestibular loss, the intensity of HSN decreased exponentially over time, reflecting an improvement in dynamic ability and self-perceived deficit. HSN tended to decline to the value of the control group once vestibular compensation was satisfactory and sufficient for a patient's everyday life. In contrast, well-detectable HSN in poorly compensated patients with insufficient clinical recovery confirmed the potential of HSN to reflect and distinguish between adequate and insufficient dynamic compensation. HSN could serve as an objective indicator of stable unilateral vestibular loss.
Acute vestibular syndrome (AVS) represents a clinical picture that involves urgent management due to the important procession of symptoms accompanying the event, which can be positively or negatively influenced by therapeutic choices and intervention timing. This forces a differential diagnosis and therapeutic choices to be made in conditions that are not always favorable and often not in the specialist field. In this work, we will examine in detail the pharmacological therapeutic possibilities, correlating them to the differential and, as far as possible, to the etiological diagnosis. In particular, the pharmacological possibilities for the two main conditions we can face will be investigated, namely, vestibular neuritis and posterior circulation stroke.
Objective: The aim of the present study was to identify patients who developed acute unilateral peripheral vestibulopathy (AUPVP) after COVID-19 vaccination.
Methods: For 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.
Results: Twenty-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 Conclusions: The 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.
Benign paroxysmal positional vertigo (BPPV) is amongst the most common causes of episodic vestibular syndrome. It can be classified as idiopathic and secondary types according to the causative factors, and the underlying mechanism between idiopathic (i-BPPV) and secondary BPPV (s-BPPV) may differ. Idiopathic sudden sensorineural hearing loss (ISSNHL) has been considered as a common inner ear disease that precipitates s-BPPV. Yet, few studies have addressed the functional impairment of the semicircular canal (SCC) system in patients with s-BPPV associated with ISSNHL. Our purpose was to explore the pathophysiological mechanism and investigate the clinical implications of video head impulse test (vHIT) in these patients. Here, the clinical and laboratory data of patients with BPPV secondary to ISSNHL, including the results of vHIT, were retrospectively reviewed, and compared with those of patients with i-BPPV. Pathological vHIT findings (low vestibulo-ocular reflex gain and re-fixation saccade), which mainly affected the posterior SCC, were more common in the s-BPPV group than in the i-BPPV group (41.9 and 0%, respectively). The incidence of horizontal SCC involvement was also higher in the s-BPPV group (45.16 and 16.67%, respectively). Furthermore, patients with s-BPPV showed lower vHIT gains of the posterior and horizontal SCCs in affected ears than in unaffected ears. Compared to i-BPPV, posterior SCC paresis detected by vHIT is more prevalent in BPPV secondary to ISSNHL. This dysfunction may be associated mainly with vestibular impairments caused by ISSNHL, and not with BPPV per se.
Frontiers in Neuroscience
Translational Side of Emerging Invasive and Non-Invasive Stimulation Therapies, Volume I