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Vestibular compensation is the natural process of recovery that occurs with acute peripheral vestibular lesion. Here, we summarize the current understanding of the mechanisms underlying vestibular compensation, focusing on the role of the medial vestibular nucleus (MVN), the central hub of the vestibular system, and its associated neural networks. The disruption of neural activity balance between the bilateral MVNs underlies the vestibular symptoms after unilateral vestibular damage, and this balance disruption can be partially reversed by the mutual inhibitory projections between the bilateral MVNs, and their top‐down regulation by other brain regions via different neurotransmitters. However, the detailed mechanism of how MVN is involved in vestibular compensation and regulated remains largely unknown. A deeper understanding of the vestibular neural network and the neurotransmitter systems involved in vestibular compensation holds promise for improving treatment outcomes and developing more effective interventions for vestibular disorders. The mechanism of vestibular compensation.11 The MVN receive afferent signals from the peripheral vestibular system and other brain regions, such as the cerebellum, the neuronal activity is balanced between the bilateral vestibular nuclei. After the unilateral peripheral injury, this loss of afferent leads to down‐regulation of neuronal activity in the ipsilateral vestibular nucleus, while up‐regulation in the contralateral side. This imbalance is believed leading to the symptoms of vestibular disorders. CNS can partially rebalance the neural activity between bilateral MVN, and reverse the vestibular symptoms. In contrast to the ipsilateral side, the contralateral MVN neurons become more active, which might be due to the reduced inhibitory input from the ipsilateral vestibular nucleus. Besides the inhibitory commissural projections between the bilateral MVN, the cerebellum and other brain region inputs are also critical for vestibular compensation. Green dashed line with arrowheads: Excitatory transmission; Brown dashed line with arrowheads: Inhibitory transmission. CNS, Central nervous system; MVN, Medial Vestibular Nucleus.

The vestibular system has been shown to play a role in the integration of spatial sensory information. For instance, vestibular perturbations induce significant shifts in spatial tactile tasks, but results have been contradictory regarding auditory modality. This observation may be because some of the previous vestibular stimulation methods (i.e., stochastic GVS) did not reliably induce a self-motion effect. This study aims to evaluate the importance of directional illusory motion on auditory localization mechanism, using direct current GVS. Twenty young healthy participants performed a sound localization task under earphones with 9 positions in the azimuth plane divided into three quadrants 7Left (45°;− 30°;− 20°), Center (− 10°;0°;10°), and Right (20°;30°;45)]. Participants were asked to verbally identify the exact position of the sound source under 3 conditions: (1) Without GVS (2) GVS with anode on the right mastoid (3) GVS with anode on the left mastoid. Results were analyzed using the non-parametric Friedman test and Wilcoxon rank-sum post-hoc test with a Bonferroni correction applied to account for multiple comparisons. Compared to baseline, left anodal stimulation caused a greater error ratio for sounds in all quadrants. Moreover, for sounds in the right quadrant, a significantly greater error ratio was observed for anode left compared to the anode right condition. Right anodal condition caused a greater error ratio for sounds in the left and the center quadrants compared to the baseline condition. This study demonstrates for the first time, that sound source localization can be influenced by direct current GVS and is modulated according to the anode position.

•Galvanic vestibular stimulation (GVS) and fear conditioning show a considerable overlap in cerebral representation.•Fear conditioning shows increased fMRI-activation in anterior insula, bilateral thalamus and periaqueductal grey.•Intensity of perceived movement during GVS was associated with ventrolateral PFC activation.•Those participants with high trait fear showed higher anterior insula activation during the extinction phase of fear conditioning. Clinical and meta-analytic imaging data suggest a considerable overlap between vestibular-sensory and anxiety-emotional processing networks. We therefore examined functional MRI activation using galvanic vestibular stimulation (GVS) and a fear conditioning paradigm in the same 28 healthy individuals. This study was to proof the effects of both stimulations in the same individual whereas our earlier meta-analytical analysis compared groups of participants who had received only one or the other stimulation. In the actual study we further assessed subjective experience (expectancy ratings, questionnaires) and autonomic arousal (skin conductance response; SCR). Activation patterns during vestibular stimulation confirmed previous findings showing highest fMRI-activation in the parieto-insular vestibular cortex. Fear conditioning activated the anterior insula, secondary somatosensory cortex (S2) and thalamus. A conjunction of fMRI-activation maps for both stimulation paradigms revealed bilateral anterior and posterior insula, dorsolateral prefrontal cortex and S2 as well as cerebellar hemisphere fMRI-activation. Regression analyses showed a high positive association of left anterior insular activation during the fear extinction period with trait anxiety. The vestibular intensity during GVS was positively associated with right ventro-lateral prefrontal cortex (PFC) fMRI-activation. This is compatible with the earlier hypothesized top-down regulation of vestibular perception which involves the PFC beneficial for suppression of unusual vestibular excitation or vertigo related to vestibular disorders.

Objective The aim of this study is to investigate the differences in vestibular organ function tests and the temporal bone computed tomography (CT) findings between healthy individuals and patients with motion sickness (MS), providing a basis for establishing functional and imaging diagnostic criteria for MS. Method Vestibular organ function tests and temporal bone CT imaging were performed on patients in the MS group ( n  = 50) and healthy individuals in the control group ( n  = 50). Functional and imaging anomalies of the vestibular organ were identified and their features and patterns were analyzed. Patients with MS were further stratified based on severity to examine whether temporal bone CT findings varied across severity grade, and indexes of diagnostic significance were identified. Results Comparisons of vestibular function tests revealed significantly lower bilateral vestibular evoked myogenic potential (VEMP) amplitudes in the MS group compared to the control group, with statistical significance ( P  < 0.05). The severity of MS demonstrated a positive correlation with reductions in bilateral cervical VEMP (cVEMP) amplitudes ( P  < 0.05). Video head impulse test (v-HIT) results indicated statistically significant differences in the gains of the left anterior, right horizontal, and left posterior semicircular canals ( P  < 0.05). There were significant differences in the bilateral vestibular caloric test (CT) values ( P  < 0.05). In terms of the temporal bone CT findings in the two groups, the detection rate of high jugular bulb combined with sinusitis, poor mastoid pneumatization, diploetic mastoid, or sclerotic mastoid was higher in patients with MS than in the healthy control group. Additionally, the detection rate of temporal bone anomalies in CT scans was significantly higher in the very severe and severe MS groups compared to the mild and moderate MS groups. Conclusion In this study, we found that patients with MS exhibited functional and structural anomalies in vestibular function and temporal bone CT findings, which were correlated with the severity of MS. These findings suggest that vestibular function tests and temporal bone CT imaging can be used as objective reference indexes for the diagnosis of MS and assessment of its severity.

Fragmented and piecemeal evidence from animal and human studies suggests that vestibular information is transmitted to the striatum, a part of the basal ganglia that degenerates in Parkinson’s Disease. Nonetheless, surprisingly little is known about the precise effects of activation of the vestibular system on the striatum. Electrophysiological studies have yielded inconsistent results, with many studies reporting only sparse responses to vestibular stimulation in the dorsomedial striatum. In this study, we sought to elucidate the effects of electrical stimulation of the peripheral vestibular system on electrophysiological responses in the tail of the rat striatum, a newly discovered region for sensory input. Rats were anaesthetised with urethane and a bipolar stimulating electrode was placed in the round window in order to activate the peripheral vestibular system. A recording electrode was positioned in the tail of the striatum. Local field potentials (LFPs) were recorded ipsilaterally and contralaterally to the stimulation using a range of current parameters. In order to confirm that the vestibular system was activated, video-oculography was used to monitor vestibular nystagmus. At current amplitudes that evoked vestibular nystagmus, clear triphasic LFPs were evoked in the bilateral tail of the striatum, with the first phase of the waveform exhibiting latencies of less than 22 ms. The LFP amplitude increased with increasing current amplitude (P ≤ 0.0001). In order to exclude the possibility that the LFPs were evoked by the activation of the auditory system, the cochlea was surgically lesioned in some animals. In these animals the LFPs persisted despite the cochlear lesions, which were verified histologically. Overall, the results obtained suggest that there are vestibular projections to the tail of the striatum, which could possibly arise from projections via the vestibular nucleus or cerebellum and the parafasicular nucleus of the thalamus.

Hypoxia has been found to adversely affect sensory function at altitudes above 3000 m, but sensory decrements have not been reported in peer-reviewed literature at or below 2400 m nor has research focused on the impact of hypoxia on human vestibular thresholds. These knowledge gaps are problematic, because the vestibular system has high metabolic needs and makes fundamental behavioral contributions. We hypothesized that mild hypoxia would impact vestibular function, which we tested by having participants breathe air with 15.4% O 2 to simulate an altitude of 2400 m (8000 ft)—mimicking the oxygen available on commercial aircraft. We measured earth-vertical translation thresholds and arterial oxygen saturation (SpO 2 ) and found that the average threshold increased by over 20% relative to thresholds measured while breathing air with 20.9% O 2 , and that these threshold changes negatively correlated with changes in SpO 2 . These findings suggest that vestibular changes provide a harbinger of hypoxia.

Benign Paroxysmal Positional Vertigo (BPPV) is one of the most prevalent peripheral vestibular disorders seen in specialized dizziness clinics. Despite being a well-understood condition with effective treatment options, BPPV remains associated with significant diagnostic delays and healthcare costs. If proven reliable, telemedicine approaches could help address these challenges by improving diagnostic accessibility and efficiency. To investigate the interobserver agreement in BPPV diagnosis, when using eye movement recordings. Six vestibular medicine specialists (Specialist 1, 2, 3, 4, 5, 6) were recruited to participate in this study. The specialists were asked to evaluate the recordings of 240 patient cases who underwent assessment for BPPV (first assessment). After viewing the recordings of each case, they were required to make a BPPV diagnosis. Five specialists (2, 3, 4, 5, 6) agreed to repeat the procedure twice, to additionally evaluate the intraobserver agreement (second assessment). The proportion of agreement and Cohen’s kappa were calculated for both interobserver and intraobserver agreement. Furthermore, agreement with the original diagnoses was evaluated. The interobserver agreement between experts was fair to moderate with a Cohen’s kappa value of 0.40 (CI 95% [0.35, 0.45]) and a proportion of agreement of 60% (CI 95% [54, 67]). Specialists 2, 4, and 5 exhibited substantial intraobserver agreement. In contrast, Specialist 3 demonstrated fair intraobserver agreement, while Specialist 6 showed almost perfect intraobserver agreement. Regarding the first assessment, agreement with the original diagnoses ranged from fair to substantial, with kappa values between 0.40 and 0.70, and corresponding percentages between 58 and 78%. Similar results were observed for the second assessment. The interobserver agreement between specialists diagnosing BPPV using eye movement recordings, was fair to moderate. The suboptimal agreement could be related to missing clinical information (e.g. patient history and symptoms during positional maneuvers). Future studies should incorporate this information and reassess interobserver agreement.

The autonomic nervous system maintains homeostasis, with the vestibulosympathetic reflex playing a key role in regulating blood pressure during postural changes. Benign paroxysmal positional vertigo (BPPV), a common vestibular disorder, has been linked to autonomic dysfunction, but the impact of vestibular-autonomic interactions on BPPV recurrence remains unclear. This prospective study investigated whether changes in diastolic blood pressure (DBP) responses during head-up tilt tests before and after treatment are associated with BPPV recurrence in 370 patients with idiopathic BPPV. DBP responses were recorded at 1 and 2 min after tilting, and patients were categorized into three groups based on DBP changes. At 6 months, the high-response group in the 1-minute DBP category had a 1.98-fold higher recurrence rate than the low-response group ( p  = 0.029). At 12 months, this group showed a 9.8-fold higher multiple recurrence rate ( p  = 0.033), while the high-response group in the 2-minute category had a 14.3-fold higher rate ( p  = 0.012). These results suggest that elevated DBP responses during vestibulosympathetic reflex activation are significantly associated with BPPV recurrence. Monitoring DBP through head-up tilt tests could provide valuable insights into recurrence risk, highlighting the role of vestibular-autonomic interactions in BPPV.

Spatial normalization of multisubject inner ear imaging data is challenging, due to both substantial intraindividual differences and the small size of the organ compared to other intracranial structures. Automatic whole brain co-registration to standard space can only roughly co-align the peripheral vestibular endorgan, and complemental manual registration is highly time-consuming. Here, we compared the accuracy of four geometry-maintaining co-registration methods (one semi-manual method and three automatic methods). High-resolution structural T2-MRI of 153 inner ears from patients and healthy participants were co-registered to an inner-ear atlas. The semi-manual method used a three-point landmark-based approach (3P), two automatic methods were based on unassisted standard algorithms (Advanced Normalization Tools (ANTs), Elastix (EL)), while the fourth automatic method utilized a volumetrically dilated, atlas-based mask (thick inner ear, TIE) for probabilistic inner ear masking. Registration accuracy was evaluated by neurotologists blinded to the respective registration paradigm, and the resulting median volumes were quantified using colocalization analyses. The mask-aided automatic approach showed the best ratings, followed by the semi-manual three-point landmark-based registration (mean ratings (lower: better) TIE 2.21 ± 1.15; 3P 2.58 ± 0.61; EL 3.42 ± 1.06; ANTs 3.49 ± 1.26). The semi-manual method had the lowest rate of insufficient registrations, followed by TIE (3P: 3.70%; TIE: 8.28%; EL: 22.66%; ANTs: 27.02%). TIE showed the highest colocalization metrics with the atlas. Only TIE and 3P allowed for sufficient semicircular canal visualization in method-wise average volumes. Overall, geometry-preserving spatial normalization of multisubject inner ear imaging data is possible and could allow groupwise examinations of the bony labyrinth or temporal bone morphology in the future.

Amblyopia is a developmental disorder of the central nervous system resulting in visual impairment, with potential impacts on cognitive and motor functions. This study evaluated the risk of benign paroxysmal positional vertigo (BPPV) in patients with amblyopia over a 9-year follow-up. Data from the National Health Insurance Service-National Sample Cohort (NHIS-NSC) was used. Amblyopia ( n  = 2,660) and non-amblyopia ( n  = 2,660) groups were matched by Propensity Score. The primary endpoint was the diagnosis of BPPV. Amblyopia was associated with a higher BPPV risk (HR 2.25, 95% CI: 1.49–3.41). The risk was lower in men (HR 0.47, 95% CI: 0.31–0.73) but increased with age (20–39 years: HR 3.35 [95% CI: 1.93–5.83]; 40–59 years: HR 9.92 [95% CI: 6.05–16.28]; ≥60 years: HR 14.80 [95% CI: 7.65–28.69]). In this long-term study, individuals with amblyopia had a 2.25-fold increased risk of developing BPPV compared to controls. These findings suggest that visual and vestibular functions are more closely linked than previously recognized, indicating that sensory disorders such as amblyopia may have broader neurological implications beyond vision alone. Nevertheless, the findings should be interpreted with caution and considered exploratory, providing population-level evidence for potential visual–vestibular associations that require validation in future prospective studies.