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Convergent clinical and neuroimaging evidence suggests that higher vestibular function is subserved by a distributed network including visuospatial, cognitive–affective, proprioceptive, and integrative brain regions. Clinical vestibular syndromes may perturb this network, resulting in deficits across a variety of functional domains. Here, we leverage structural and functional neuroimaging to characterize this extended network in healthy control participants and patients with post‐concussive vestibular dysfunction (PCVD). Then, 27 healthy control subjects (15 females) and 18 patients with subacute PCVD (12 female) were selected for participation. Eighty‐two regions of interest (network nodes) were identified based on previous publications, group‐wise differences in BOLD signal amplitude and connectivity, and multivariate pattern analysis on affective tests. Group‐specific “core” networks, as well as a “consensus” network comprised of connections common to all participants, were then generated based on probabilistic tractography and functional connectivity between the 82 nodes and subjected to analyses of node centrality and community structure. Whereas the consensus network was comprised of affective, integrative, and vestibular nodes, PCVD participants exhibited diminished integration and centrality among vestibular and affective nodes and increased centrality of visual, supplementary motor, and frontal and cingulate eye field nodes. Clinical outcomes, derived from dynamic posturography, were associated with approximately 62% of all connections but best predicted by amygdalar, prefrontal, and cingulate connectivity. No group‐wise differences in diffusion metrics or tractography were noted. These findings indicate that cognitive, affective, and proprioceptive substrates contribute to vestibular processing and performance and highlight the need to consider these domains during clinical diagnosis and treatment planning. Convergent clinical and neuroimaging evidence suggests that higher vestibular function is subserved by a distributed network including visuospatial, cognitive–affective, proprioceptive, and integrative brain regions. In this article, we leverage structural and functional neuroimaging to characterize an extended vestibular‐cognitive network in twenty‐seven healthy control participants and eighteen patients with post‐concussive vestibular dysfunction (PCVD), determine commonalities between control and PCVD patients as a “consensus” network, and describe network differences corresponding to clinical outcomes.

Ménière's disease (MD), a chronic inflammatory disorder with age‐related increased incidence, exhibits poorly understood pathogenesis and limited therapeutic options. Here, we demonstrate that cellular senescence, marked by mitochondrial damage, reactive oxygen species accumulation, and senescence‐associated secretory phenotype (SASP), is prevalent in the vestibular tissue of MD patients and an endolymphatic hydrops mouse model. The transcription factor GATA4 is upregulated in MD and mice, and its genetic deletion in hair cells alleviates LPS‐induced audio‐vestibular dysfunction and cellular senescence in mice and HEI‐OC1 cells. Mechanistically, HDAC6 interacts with GATA4 and restrains its nuclear transport, while RNA‐seq and ChIP‐seq identify HtrA1, a serine protease, as a direct transcriptional target of GATA4. Inhibition of HDAC6 or AAV‐mediated HtrA1 overexpression exacerbates MD‐like symptoms, whereas inhibition of HtrA1 by Galegenimab ameliorates these phenotypes in mice. In aged mice, GATA4 deletion reduces age‐related audio‐vestibular deficits and senescence markers. Collectively, our findings establish GATA4 as a critical regulator of cellular senescence and inflammaging in inner ear pathologies, providing promising therapeutic targets for MD and age‐related audio‐vestibular disorders. This study identifies the HDAC6/GATA4/HtrA1 axis as a critical driver of cellular senescence in the inner ear. GATA4 nuclear translocation, facilitated by HDAC6 downregulation, transcriptionally activates HtrA1, promoting hair cell senescence, SASP, and audio‐vestibular dysfunction in models of Ménière's disease and age‐related audio‐vestibular dysfunction. Targeting this axis with an HtrA1‐inhibiting antibody ameliorates pathology, revealing a novel therapeutic strategy.

The vestibular system may have a critical role in the integration of sensory information and the maintenance of cognitive function. A dysfunction in the vestibular system has a significant impact on quality of life. Recent research has provided evidence of a connection between vestibular information and cognitive functions, such as spatial memory, navigation and attention. Although the exact mechanisms linking the vestibular system to cognition remain elusive, researchers have identified various pathways. Vestibular dysfunction may lead to the degeneration of cortical vestibular network regions and adversely affect synaptic plasticity and neurogenesis in the hippocampus, ultimately contributing to neuronal atrophy and cell death, resulting in memory and visuospatial deficits. Furthermore, the extent of cognitive impairment varies depending on the specific type of vestibular disease. In the present study, the current literature was reviewed, potential causal relationships between vestibular dysfunction and cognitive performance were discussed and directions for future research were proposed.

In the last 5 years, there has been a surge in evidence that hearing loss (HL) may be a risk factor for cognitive dysfunction, including dementia. At the same time, there has been an increase in the number of studies implicating vestibular loss in cognitive dysfunction. Due to the fact that vestibular disorders often present with HL and other auditory disorders such as tinnitus, it has been suggested that, in many cases, what appears to be vestibular-related cognitive dysfunction may be due to HL (e.g., Dobbels et al. Front Neurol 11:710, 2020). This review analyses the studies of vestibular-related cognitive dysfunction which have controlled HL. It is suggested that despite the fact that many studies in the area have not controlled HL, many other studies have (~ 19/44 studies or 43%). Therefore, although there is certainly a need for further studies controlling HL, there is evidence to suggest that vestibular loss is associated with cognitive dysfunction, especially related to spatial memory. This is consistent with the overwhelming evidence from animal studies that the vestibular system transmits specific types of information about self-motion to structures such as the hippocampus.

Despite numerous anticoagulants available, warfarin is widely used due to its efficacy and cost-effectiveness in treating thromboembolic diseases. However, its potential impact on vestibular function remains unexplored. This study investigates the association between warfarin use and vestibular dysfunction using data from the NHANES database and examines underlying mechanisms through network pharmacology, Mendelian randomization (MR), and molecular docking. We conducted a cross-sectional analysis of NHANES data (1999–2004) to evaluate the prevalence of vestibular dysfunction among warfarin users. Network pharmacology identified overlapping genes between warfarin targets and vestibular dysfunction-related genes. MR analysis assessed the causal relationship, and molecular docking examined interactions between warfarin and significant genes. The study included 1681 participants, revealing a higher prevalence of vestibular dysfunction in warfarin users. Multiple regression analysis confirmed a significant association between warfarin use and vestibular dysfunction. Network pharmacology identified 31 overlapping genes, with MAPK8 emerging as a key gene through MR analysis. Molecular docking showed a strong binding affinity between warfarin and MAPK8. Findings suggest that warfarin use is significantly associated with vestibular dysfunction, potentially through interactions with MAPK8. This highlights the importance of monitoring vestibular function in patients on warfarin therapy and considering genetic factors to personalize treatment. Future research should explore these mechanisms further and validate findings in broader populations.

Vestibular compensation is a physiological response of the vestibular organs within the inner ear. This adaptation manifests during consistent exposure to acceleration or deceleration, with the vestibular organs incrementally adjusting to such changes. The molecular underpinnings of vestibular compensation remain to be fully elucidated, yet emerging studies implicate associations with neuroplasticity and signal transduction pathways. Throughout the compensation process, the vestibular sensory neurons maintain signal transmission to the central equilibrium system, facilitating adaptability through alterations in synaptic transmission and neuronal excitability. Notable molecular candidates implicated in this process include variations in ion channels and neurotransmitter profiles, as well as neuronal and synaptic plasticity, metabolic processes, and electrophysiological modifications. This study consolidates the current understanding of the molecular events in vestibular compensation, augments the existing research landscape, and evaluates contemporary therapeutic strategies. Furthermore, this review posits potential avenues for future research that could enhance our comprehension of vestibular compensation mechanisms.

Background Vestibular dysfunction is closely associated with the pathophysiology of Parkinson’s disease (PD) accompanied by freezing of gait (FOG); however, evidence supporting this clinical association is lacking. Vestibular-evoked myogenic potentials (VEMPs) have been widely acknowledged as a crucial electrophysiological parameter in the clinical evaluation of vestibular function. Objective The present study investigated the possible correlation of FOG occurrence with VEMP observations in patients diagnosed with PD. Methods Altogether, 95 idiopathic PD patients were recruited into the present cross-sectional study. All patients underwent motor and non-motor assessments using serial scales. In addition, the electrophysiological vestibular evaluation was conducted, which included cervical (cVEMP) and ocular VEMP (oVEMP) assessments. Furthermore, the correlations of bilateral c/oVEMP absence with clinical phenotypes, especially FOG, among the PD patients were analyzed. Results Among the 95 patients with PD, 44 (46.3%) had bilateral oVEMP absence and 23 (24.2%) had bilateral cVEMP absence, respectively. The proportions of patients with bilateral oVEMP absence (77.8% vs 30.9%, p  = 0.004) and bilateral cVEMP absence (44.4% vs 19.5%, p  = 0.035) were higher in the patient group exhibiting FOG than in the group without FOG. Following the adjustment of confounding variables, bilateral oVEMP absence (OR = 8.544, p  = 0.007), rather than bilateral cVEMP absence, was shown to independently predict FOG occurrence in patients with PD. Conclusion The close correlation between bilateral oVEMP absence and FOG in PD patients sheds new light on the possible role of central vestibular/upper brainstem dysfunction in FOG development in patients with PD.

Previous research suggests that patients with peripheral vestibular dysfunction (PVD) suffer from nonspatial cognitive problems, including executive impairments. However, previous studies that assessed executive functions are conflicting, limited to single executive components, and assessments are confounded by other cognitive functions. We compared performance in a comprehensive executive test battery in a large sample of 83 patients with several conditions of PVD (34 bilateral, 29 chronic unilateral, 20 acute unilateral) to healthy controls who were pairwise matched to patients regarding age, sex, and education. We assessed basic and complex executive functions with validated neuropsychological tests. Patients with bilateral PVD performed worse than controls in verbal initiation and working memory span, while other executive functions were preserved. Patients with chronic unilateral PVD had equal executive performance as controls. Patients with acute unilateral PVD performed worse than controls in the exact same tests as patients with bilateral PVD (verbal initiation, working memory span); however, this effect in patients with acute PVD diminished after correcting for multiple comparisons. Hearing loss and affective disorders did not influence our results. Vestibular related variables (disease duration, symptoms, dizziness handicap, deafferentation degree, and compensation) did not predict verbal initiation or working memory span in patients with bilateral PVD. The results suggest that bilateral PVD not only manifests in difficulties when solving spatial tasks but leads to more general neurocognitive deficits. This understanding is important for multidisciplinary workgroups (e.g., neurotologists, neurologists, audiologists) that are involved in diagnosing and treating patients with PVD. We recommend screening patients with PVD for executive impairments and if indicated providing them with cognitive training or psychoeducational support.

The vestibular system plays an important role in maintaining balance and posture. It also contributes to vertical perception, body awareness and spatial navigation. In addition to its sensory function, the vestibular system has direct connections to key areas responsible for higher cognitive functions, such as the prefrontal cortex, insula and hippocampus. Several studies have reported that vestibular dysfunction, in particular bilateral vestibulopathy, is associated with an increased risk of cognitive impairment and the development of dementias such as Alzheimer’s disease. However, it is still controversial whether there is a causal relationship between vestibular damage and cognitive dysfunction. In this mini-review, we will explore the relationship between the vestibular system, cognitive dysfunction and dementia, hypotheses about the hypothesis and causes that may explain this phenomenon and also some potential confounders that may also lead to cognitive impairment. We will also review multimodal neuroimaging approaches that have investigated structural and functional effects on the cortico-vestibular network and finally, describe some approaches to the management of patients with vestibular damage who have shown some cognitive impairment.

People with Parkinson’s disease (PD) have increased visual dependency for balance and suspected vestibular dysfunction. Immersive virtual reality (VR) allows graded manipulation of visual sensory inputs during balance tasks, and hence VR coupled with portable force platforms have emerged as feasible, affordable, and validated tools for assessing sensory-motor integration of balance. This study aims to determine (i) how people with PD perform on a VR-based visual perturbation standing balance task compared to healthy controls (HC), and (ii) whether balance performance is influenced by vestibular function, when other known factors are controlled for. This prospective observational study compared the balance performance under varying sensory conditions in 40 people with mild to moderate PD with 40 age-matched HC. Vestibular function was assessed via Head Impulse Test (HIMP), cervical and ocular vestibular evoked myogenic potentials (cVEMPs and oVEMPs) and subjective visual vertical (SVV). Regression analyses were used to determine associations between VR balance performance on firm and foam surfaces with age, group, vestibular function, and lower limb proprioception. PD failed at significantly lower levels of visual perturbation than HC on both surfaces. In PD, greater disease severity was significantly associated with lower fall thresholds on both surfaces. Multiple PD participants failed prior to visual perturbation on foam. On firm, PD had a greater visual dependency. Increasing age, impaired proprioception, impaired SVV, abnormal HIMP and cVEMP scores were associated with worse balance performance. The multivariate model containing these factors explained 29% of the variability in balance performance on both surfaces. Quantitative VR-based balance assessment is safe and feasible in PD. Balance performance on both surfaces was associated with age, HIMP abnormality and proprioception.