An fMRI study of visuo-vestibular interactions following vestibular neuritis.
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ABSTRACT:
SUBMITTER: Roberts RE
PROVIDER: S-EPMC6197146 | biostudies-literature | 2018
REPOSITORIES: biostudies-literature
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Project description:Vestibular neuritis (VN) mostly involves the superior vestibular nerve. Isolated inferior vestibular neuritis (IVN) has been more rarely described. The diagnosis of IVN is based on an abnormal head impulse test (HIT) for the posterior semicircular canal (PSC), pathological cervical vestibular-evoked myogenic potentials (C-VEMPs), and spontaneous downbeat nystagmus consistent with acute functional loss of inner ear sensors lying within the inferior part of the labyrinth. HIT for both lateral and superior semicircular canals is normal, as are ocular VEMPs and bithermal caloric irrigations. The etiology of IVN is debated since peripheral acute vestibular loss with a similar lesion pattern can often be associated with ipsilesional sudden hearing loss (HL). Viral inflammation of vestibular nerves is considered the most likely cause, although reports suggest that VN usually spares the inferior division. On the other hand, an ischemic lesion involving the terminal branches of the common cochlear artery has been hypothesized in cases with concurrent HL. Debated is also the lesion site in the case of IVN without HL since different instrumental patterns have been documented. Either isolated posterior ampullary nerve involvement presenting with selective PSC functional loss on video-HIT, or only saccular lesion with isolated ipsilesional C-VEMPs impairment, or inferior vestibular nerve damage (including both saccular and posterior ampullary afferents) exhibiting an impairment of both C-VEMPs and PSC-HIT. We report an interesting case of a patient with an acute vestibular loss consistent with IVN without HL who developed a PSC ossification on follow-up, questioning the viral origin of the lesion and rather orienting toward an occlusion of the posterior vestibular artery. To the best of our knowledge, this is the first report of PSC ossification after a clinical picture consistent with IVN.
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Project description:Vestibular schwannoma (VS) is commonly accompanied by hearing loss, tinnitus, and dizziness and tends to be chronically progressive in nature. We report a case of VS presenting as left vestibular neuritis (VN) in a previously healthy 57-year-old patient. Right-beating horizontal-torsional spontaneous nystagmus was observed, and the bedside head impulse test revealed a left catch-up saccade. The bithermal caloric test showed left canal paresis, and pure-tone audiometry revealed an average threshold of 22.5 dB bilaterally. Brain magnetic resonance imaging (MRI) demonstrated a 0.7-cm enhancing mass in the left internal auditory canal, consistent with VS. The patient was administered with high-dose systemic corticosteroids and vestibular suppressants with antiemetic, which relieved acute vertigo. Although dizziness in VS is chronically progressive in nature, VS may present as an acute vestibular syndrome that mimics VN. VS should be considered a potential cause of acute vestibular syndrome, and thorough neurological examination with MRI may be helpful for accurate diagnosis.
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Project description:We sought to identify predictors of symptomatic recovery in vestibular neuritis. Forty VN patients were prospectively studied in the acute phase (median = 2 days) and 32 in the recovery phase (median = 10 weeks) with vestibulo-ocular reflex, vestibular-perceptual, and visual dependence tests and psychological questionnaires. Clinical outcome was Dizziness Handicap Inventory score at recovery phase. Acute visual dependency and autonomic arousal predicted outcome. Worse recovery was associated with a combination of increased visual dependence, autonomic arousal, anxiety/depression, and fear of bodily sensations, but not with vestibular variables. Findings highlight the importance of early identification of abnormal visual dependency and concurrent anxiety.
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Project description:Symptomatic recovery after acute vestibular neuritis (VN) is variable, with around 50% of patients reporting long term vestibular symptoms; hence, it is essential to identify factors related to poor clinical outcome. Here we investigated whether excessive reliance on visual input for spatial orientation (visual dependence) was associated with long term vestibular symptoms following acute VN. Twenty-eight patients with VN and 25 normal control subjects were included. Patients were enrolled at least 6 months after acute illness. Recovery status was not a criterion for study entry, allowing recruitment of patients with a full range of persistent symptoms. We measured visual dependence with a laptop-based Rod-and-Disk Test and severity of symptoms with the Dizziness Handicap Inventory (DHI). The third of patients showing the worst clinical outcomes (mean DHI score 36-80) had significantly greater visual dependence than normal subjects (6.35° error vs. 3.39° respectively, p?=?0.03). Asymptomatic patients and those with minor residual symptoms did not differ from controls. Visual dependence was associated with high levels of persistent vestibular symptoms after acute VN. Over-reliance on visual information for spatial orientation is one characteristic of poorly recovered vestibular neuritis patients. The finding may be clinically useful given that visual dependence may be modified through rehabilitation desensitization techniques.
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Project description:ObjectiveThis 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.MethodsAn 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.ResultsThe 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.ConclusionThe total incidence rate for the three municipalities was 48.497. This result is higher than previously reported studies.
| S-EPMC10232831 | biostudies-literature
Project description:Gaze stabilization compensates for movements of the head or external environment to minimize image blurring. Multisensory information stabilizes the scene on the retina via the vestibulo-ocular (VOR) and optokinetic (OKR) reflexes. While the organization of neuronal circuits underlying VOR is well-described across vertebrates, less is known about the contribution and evolution of the OKR and the basic structures allowing visuo-vestibular integration. To analyze these neuronal pathways underlying visuo-vestibular integration, we developed a setup using a lamprey eye-brain-labyrinth preparation, which allowed coordinating electrophysiological recordings, vestibular stimulation with a moving platform, and visual stimulation via screens. Lampreys exhibit robust visuo-vestibular integration, with optokinetic information processed in the pretectum that can be downregulated from tectum. Visual and vestibular inputs are integrated at several subcortical levels. Additionally, saccades are present in the form of nystagmus. Thus, all basic components of the visuo-vestibular control of gaze were present already at the dawn of vertebrate evolution.
| S-EPMC9365791 | biostudies-literature
Project description:Previous studies have shown that illusory ownership over a mannequin's body can be induced through synchronous visuo-tactile stimulation as well as through synchronous visuo-vestibular stimulation. The current study aimed to elucidate how three-way combinations of correlated visual, tactile and vestibular signals contribute to the senses of body ownership and self-motion. Visuo-tactile temporal congruence was manipulated by touching the mannequin's body and the participant's unseen real body on the trunk with a small object either synchronously or asynchronously. Visuo-vestibular temporal congruence was manipulated by synchronous or asynchronous presentation of a visual motion cue (the background rotating around the mannequin in one direction) and galvanic stimulation of the vestibular nerve generating a rotation sensation (in the same direction). The illusory experiences were quantified using a questionnaire; threat-evoked skin-conductance responses (SCRs) provided complementary indirect physiological evidence for the illusion. Ratings on the illusion questionnaire statement showed significant main effects of synchronous visuo-vestibular and synchronous visuo-tactile stimulations, suggesting that both of these pairs of bimodal correlations contribute to the ownership illusion. Interestingly, visuo-tactile synchrony dominated because synchronous visuo-tactile stimulation combined with asynchronous visuo-vestibular stimulation elicited a body ownership illusion of similar strength as when both bimodal combinations were synchronous. Moreover, both visuo-tactile and visuo-vestibular synchrony were associated with enhanced self-motion perception; self-motion sensations were even triggered when visuo-tactile synchrony was combined with visuo-vestibular asynchrony, suggesting that ownership enhanced the relevance of visual information as a self-motion cue. Finally, the SCR results suggest that synchronous stimulation of either modality pair led to a stronger illusion compared to the asynchronous conditions. Collectively, the results suggest that visuo-tactile temporal correlations have a stronger influence on body ownership than visuo-vestibular correlations and that ownership boosts self-motion perception. We present a Bayesian causal inference model that can explain how visuo-vestibular and visuo-tactile information are combined in multisensory own-body perception.
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Project description:Herpesvirus is a prevalent pathogen that primarily infects human epithelial cells and has the ability to reside in neurons. In the field of otolaryngology, herpesvirus infection primarily leads to hearing loss and vestibular neuritis and is considered the primary hypothesis regarding the pathogenesis of vestibular neuritis. In this review, we provide a summary of the effects of the herpes virus on cellular processes in both host cells and immune cells, with a focus on HSV-1 as illustrative examples.
| S-EPMC10819745 | biostudies-literature
Project description:Vestibular information about self-motion is combined with other sensory signals. Previous research described both visuo-vestibular and vestibular-tactile bilateral interactions, but the simultaneous interaction between all three sensory modalities has not been explored. Here we exploit a previously reported visuo-vestibular integration to investigate multisensory effects on tactile sensitivity in humans. Tactile sensitivity was measured during passive whole body rotations alone or in conjunction with optic flow, creating either purely vestibular or visuo-vestibular sensations of self-motion. Our results demonstrate that tactile sensitivity is modulated by perceived self-motion, as provided by a combined visuo-vestibular percept, and not by the visual and vestibular cues independently. We propose a hierarchical multisensory interaction that underpins somatosensory modulation: visual and vestibular cues are first combined to produce a multisensory self-motion percept. Somatosensory processing is then enhanced according to the degree of perceived self-motion.
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Project description:Objective: In order to identify genetic variants associated with vestibular neuritis, a common cause of peripheral vertigo with a potential causative link to the reactivation of herpes simplex type 1 (HSV-1), we conducted a genome-wide association study. Methods: Association was assessed using approximately 8 million variants. 131 patients with vestibular neuritis and 2,609 controls of European ancestry were included. Results: Genome-wide associations with vestibular neuritis were detected in 4 regions containing protein coding genes assignable to two functional groups: virus hypothesis and insulin metabolism. Genes of set 1 are related to viral processes: nuclear receptor subfamily 3 group C member 2 (NR3C2) is a receptor for mineralocorticoids and glucocorticoids and was shown to be a host factor for HSV-1 replication. Ankyrin repeat domain 30A (ANKRD30A) encodes a host factor for human immunodeficiency virus-1 (HIV-1) infection. It shows rapid evolution and is induced by interferon stimulation. Mediator complex 30 (MED30), an important member of the mediator complex, has been shown to be involved in replication of HIV-1, a knockdown leading to impaired viral replication. The second set of genes LIM homeobox transcription factor 1 alpha (LMX1A), solute carrier family 30 member 8 (SLC30A8) is associated with insulin metabolism and resistance, a feature of some patients in whom type 2 diabetes is an accompanying comorbidity of vestibular neuritis. Conclusions: Using a GWAS approach to evaluate the etiology of vestibular neuritis these findings provide another piece of evidence that it may be caused by a viral inflammation.
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