[This corrects the article DOI: 10.3389/fneur.2024.1382196.].

Long non-coding RNAs (lncRNAs) have emerged as crucial regulators in the central nervous system, yet their role in vestibular compensation remains elusive. To address this knowledge gap, we employed unilateral labyrinthectomy (UL) in rats to establish animal models of peripheral vestibular dysfunction. Utilizing ribonucleic acid sequencing (RNA-seq), we comprehensively analysed the expression profiles of genes dysregulated in the medial vestibular nucleus (MVN) of these rats at distinct time points: 4 h, 4 days, and 14 days post-UL. Through trans-target prediction analysis integrating differentially co-expressed messenger RNAs (mRNAs) and lncRNAs, we constructed lncRNA-mRNA regulatory networks. Validation of selected mRNAs and lncRNAs was performed using RT-qPCR. Our RNA-seq analysis revealed significant aberrant expression of 3054 lncRNAs and 1135 mRNAs compared to control samples. By applying weighted gene co-expression network analysis (WGCNA), we identified 11 co-expressed modules encompassing all genes. Notably, within the MEmagenta module, we observed an initial upregulation of differentially expressed genes (DEGs) at 4 h, followed by downregulation at 4- and 14-days post-UL. Our findings indicated that 3068 lncRNAs positively regulated 1259 DEGs, while 1482 lncRNAs negatively regulated 433 DEGs in the MVN. The RT-qPCR results corroborated the RNA-seq data, validating our findings. This study offers novel insights into the lncRNA-mRNA expression landscape during vestibular compensation, paving the way for further exploration of lncRNA functions in this context.

Objectives This study aims to evaluate semicircular canal function using video head impulse test (vHIT) in patients with peripheral vestibular disorders without nystagmus. Methods Patients who underwent vHIT were enrolled in this study, and the proportion of abnormal findings on vHIT in patients without nystagmus was investigated. In addition, the results of vestibular testing were investigated in cases in which both vHIT and caloric testing were performed in patients without nystagmus. Results Forty-six patients (23.4%) of 197 patients who had no abnormal findings on the nystagmus tests, including the gaze nystagmus test, positional nystagmus test, and positioning nystagmus test, showed dysfunction in at least one semicircular canal on vHIT. The most frequent diagnosis was vestibular schwannoma (14/46, 30.4%), and cases with bilateral vestibular dysfunction were also included (12/46, 26.1%). A disorganized pattern of catch-up saccade was observed more frequently in patients with subjective symptoms of dizziness/vertigo compared to those without subjective symptoms. Although the sensitivity of vHIT was low compared to caloric testing, vHIT could detect isolated vertical canal dysfunction not detected by caloric testing. Conclusions vHIT is considered to be a useful test for patients without nystagmus, as vHIT could detect abnormalities in approximately one-quarter of patients without nystagmus. vHIT is considered to be one of the first tests to be performed following nystagmus testing, including the gaze nystagmus test, the positional nystagmus test, and the positioning nystagmus test. On the other hand, there are some cases in which vHIT shows no abnormality while caloric testing shows canal paresis. It is necessary to perform vHIT, bearing in mind that there are abnormalities that cannot be detected by vHIT alone.

UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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).
UNASSIGNED: 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.

Objectives: The aim of this study was to evaluate the functional outcomes and balance compensation in patients with severe Meniere\'s disease after vestibular neurectomy. Methods: Pre- and postoperative results were analyzed in twenty patients with unilateral Meniere\'s disease before and two years after vestibular neurectomy. Clinical evaluation was performed using a subjective grading scale proposed by the American Academy of Otolaryngology-Head and Neck Surgery and the Dizziness Handicap Inventory. Sensory organization test results were analyzed to assess the balance system before and after the surgery. Results: All patients reported a complete resolution of vertigo attacks after the vestibular neurectomy; 95% of patients reported functional level improvement according to a scale proposed by the American Academy of Otolaryngology-Head and Neck Surgery, and the average score decreased from 4.5 to 1.6. Clinical improvement, evaluated with the Dizziness Handicap Inventory, was present in all patients, with the average result decreasing from 81.7 to 16.4. Analyzing both grading systems, differences between pre- and postoperative results were statistically significant. No statistically significant differences were found between the sensory organization test results before and after vestibular neurectomy. Significant correlations were found between a patient\'s age and postoperative results of the Dizziness Handicap Inventory and posturography. Conclusions: Vestibular neurectomy is an effective vertigo treatment in patients with severe Meniere\'s disease with no clinical improvement despite conservative treatment. It results in subjective physical, functional, and emotional improvement, enabling patients to return to daily activities and work. An appropriate qualification of patients and comprehensive preoperative evaluation are essential to obtaining satisfactory clinical outcomes.

Despite the high success rate of canalith repositioning maneuvers (CRMs) in the treatment of benign paroxysmal positional vertigo (BPPV), a growing number of patients report residual dizziness symptoms that may last for a significant time. Although the majority of BPPV cases can be explained by canalolithiasis, the etiology is complex. Consideration of the individual patient\'s history and underlying pathophysiology of BPPV may offer the potential for treatment approaches supplementary to CRMs, as well as a promising alternative for patients in whom CRMs are contraindicated. This article provides a summary of the possible underlying causes of BPPV and residual dizziness, along with suggestions for potential management options that may be considered to relieve the burden of residual symptoms.

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.

The suppression head impulse paradigm (SHIMP) involves suppression of the vestibulo-ocular reflex (VOR) and anticompensatory saccades generated thereof. SHIMP is gaining importance to understand vestibular compensation with its different parameters (VOR gain/peak saccadic velocity PSV/latency of saccades). SHIMP studies are emerging in adults, but pediatric studies have hardly been performed. This study is a retrospective case note audit over a period of 2 months in a tertiary pediatric vestibular center in the United Kingdom to investigate whether SHIMP is safe/robust to be used in children conforming to existing standards/norms in normal children and whether it yields any meaningful inferences in pediatric vestibular hypofunction. This is the largest pediatric SHIMP study to date. A total of 44 referred children (6-18 years, female children>male children) with a range of complaints from dizziness, imbalance, motor incoordination, postural instability, and hearing loss were included, and their SHIMP parameters were measured. All children underwent comprehensive functional/objective audiovestibular assessments. Two groups were defined-Group A with normal vestibular function and Group B with abnormal vestibular function. The normal population showed an average SHIMP VOR gain of 0.98+/-0.08 and latency of overt saccades at 215.68+/-46.16 milliseconds agreeing with published evidence. The PSV of overt saccades was 315.39+/-56.30/s, and there was a gain asymmetry of 7.42+/-4.68 between the sides. Statistically significant differences with moderate/large effect sizes were observed between the groups in terms of VOR gain and PSV but not in saccade latencies. Covert saccades were rare in SHIMP, while overt saccades were observed in 100% of children. VOR gain difference between the head impulse paradigm (HIMP) and the SHIMP was significant as well. We observed statistically significant differences in side asymmetry of VOR gain between the groups. Furthermore, we identified a group of children with cerebellar lesions where overt saccades in SHIMP were rather low in number. Further research is recommended to investigate pediatric PSV, asymmetry, and inability to generate overt saccades that may suggest useful means to assess compensation and central function. We conclude that SHIMP yields valuable information and is a safe, easy to perform, and a reliable test that should be used in children to supplement HIMP.

OBJECTIVE: To evaluate pre- and post-operative semicircular canal function in patients with vestibular schwannoma (VS) by the video Head Impulse Test (vHIT).
METHODS: Nineteen patients with VS who underwent surgery were enrolled in this study. The gain in vestibulo-ocular reflex (VOR) and the degree of scatter in catch-up saccades were examined pre- and post-operatively for the semicircular canals in VS patients.
RESULTS: Ten of 19 cases (52.6 %) with VS were defined as demonstrating both superior vestibular nerve (SVN) and inferior vestibular nerve (IVN) impairment from the results of pre-operative vHIT. Hearing level and subjective vestibular symptoms showed significant correlations with pre-operative semicircular canal function. Compared to pre-operative vHIT results, VOR gains within 1 month after surgery were significantly reduced in all three canals; however, significant differences had disappeared in the anterior and posterior semicircular canals at 6 months after surgery. Cases of unknown origin had a significantly greater reduction in posterior semicircular canal function after surgery compared with those with disease of IVN origin.
CONCLUSIONS: As vHIT could evaluate pre-operative vestibular nerve impairment, post-operative VOR gain reduction and the degree of vestibular compensation, semicircular canal function evaluated by vHIT provides a good deal of useful information regarding VS patients undergoing surgery compared to caloric testing, and vHIT should be performed pre- and post-operatively for patients with VS.

Unlike other sensory systems, since the vestibular system maintains the tension balance of the entire system in a\"push-pull\" mode, local dysfunction in the system will cause the balance of the entire system to collapse. Unilateral peripheral vestibular dysfunction will cause severe vestibular symptoms, but it can recover spontaneously within a few days to several weeks. This phenomenon is called \"vestibular compensation\"（VC）. Since the peripheral vestibular impact in most cases is irreversible, it is widely believed that the central mechanism plays a key role in the vestibular compensation process. Static symptom is fully compensated within a few weeks, which is in parallel with the restored balance in the resting discharge of the vestibular nucleus on both sides; the incomplete compensation of dynamic deficits takes longer and is achieved mainly through the mechanism of sensory substitution and behavioral substitution. Here we briefly reviewed the mechanism of vestibular compensation and treatment in order to provide an insight into further study and clinical treatment strategies.
摘要: 与其他感觉系统不同，前庭系统通过“推-拉”的模式维持整个系统的张力平衡，局部功能异常增强或减弱都将导致整个系统的功能障碍。单侧外周前庭受损将引起显著的前庭症状，但其可在数日至数周内逐步自行缓解，该现象被称为“前庭代偿”。由于多数情况下的前庭外周损伤为不可逆性，因此广泛认为中枢机制是前庭代偿的主因。其中，静态症状在数周内消失，代偿较为完全，推测是前庭核团放电再平衡的结果；动态症状的代偿需要更长时间，通过感觉替代、行为替代等方式实现，且代偿不完全。本文简要综述了前庭代偿及治疗机制的研究进展以期为未来的研究工作和临床治疗策略提供参考。.