Background: It is well-known that ocular vestibular evoked myogenic potentials (oVEMPs) predominantly reflect utricular function whilst cervical vestibular evoked myogenic potentials (cVEMPs) reflect saccular function. To date, there are no published reports on the systemic evaluation of utricular and saccular function in benign paroxysmal positional vertigo (BPPV), nor are there any reports on the differences in VEMPs between patients with recurrent and non-recurrent BPPV. The aim of this study was to evaluate the difference in cervical and ocular (c/o)VEMPs between patients with BPPV and normal controls, as well as between patients with recurrent and non-recurrent BPPV. Methods: Thirty patients with posterior canal BPPV and 30 healthy subjects (as normal controls) were prospectively enrolled. cVEMP and oVEMP testing using 500 Hz tone-burst stimuli were performed on all. VEMP tests were repeated 3 times on each subject to ensure reliability and reproducibility of responses. VEMPs were defined as present or absent. Abnormal VEMP was defined by lack of VEMP response. Results: In the control group, abnormal cVEMPs responses were detected in 6.67 % and abnormal oVEMPs responses were detected in 3.34 %. In BPPV patients (10 with recurrent BPPV, 20 with non-recurrent BPPV), abnormal cVEMPs responses were detected in 30 % and abnormal oVEMPs responses were detected in 56.7 %. More patients with BPPV showed abnormal responses in c/oVEMPs as compared to the control group ( p < 0.05). oVEMPs was more often abnormal as compared to cVEMPs in BPPV patients ( p < 0.05). There was no statistical difference between abnormal cVEMP responses in non-recurrent BPPV patients (25 %) and recurrent BPPV patients (40 %) ( p > 0.05). Differences in abnormal oVEMP responses (non-recurrent BPPV, 40 %; recurrent BPPV, 90 %) were significant ( p < 0.05). Conclusion: An increased occurrence of abnormal c/oVEMP recordings appeared in BPPV patients, possibly as a result of degeneration of the otolith macula. oVEMPs were more often abnormal in BPPV patients as compared to cVEMPs, suggesting that utricular dysfunction may be more common than saccular dysfunction. Furthermore, oVEMP abnormalities in the recurrent BPPV group were significantly higher than those in the non-recurrent BPPV group. Assessment of c/oVEMPs in BPPV patients may therefore be of prognostic value in predicting likelihood of BPPV recurrence.

Sensorineural hearing loss (SNHL) is a category of hearing loss that often leads to difficulty in understanding speech and other sounds. Auditory system dysfunction, including deafness and auditory trauma, results in cognitive deficits via neuroplasticity. Cognitive impairment (CI) refers to an abnormality in the brain’s higher intellectual processes related to learning, memory, thinking and judgment that can lead to severe learning and memory deficits. Studies have established a strong correlation between SNHL and CI, but it remains unclear how SNHL contributes to CI. The purpose of this article is to describe three hypotheses regarding this relationship, the mainstream cognitive load hypothesis, the co-morbidity hypothesis, and the sensory deprivation hypothesis, as well as the latest research progress related to each hypothesis.

Background: Cervical and ocular vestibular evoked myogenic potentials (c/oVEMPs) reflect otolith function. Up-to-date, there are no published reports on the systemic evaluation of otolith function in Ménière's Disease (MD) nor are there any reports on the differences in VEMPs between patients with early and late stage MD. The aim of this study was to evaluate the difference in c/oVEMPs between patients with MD and normal controls, as well as between patients with early and late stage MD. Methods: Thirty patients with unilateral MD and thirty healthy subjects (as normal controls) were prospectively enrolled. c/oVEMPs using 500 Hz tone-burst stimuli were performed. VEMP tests were repeated 3 times on each subject to ensure reliability and reproducibility of responses. VEMPs were defined as present or absent. Abnormal VEMP was defined by lack of VEMP response. Results: In the control group, abnormal cVEMPs and oVEMPs responses were detected in 6.67 and 3.34 % respectively. In MD patients (20 with early stage MD [ES-MD], 10 with late stage MD [LS-MD]), abnormal cVEMPs and oVEMPs responses were detected in 40 and 16.7 % respectively. More patients with MD showed abnormal responses in c/oVEMPs as compared to the control group ( p < 0.05). cVEMPs was more often abnormal as compared to oVEMPs in MD patients ( p < 0.05). There was a significant difference in abnormal cVEMP responses between ES-MD patients (25 %) and LS-MD patients (70 %) ( p < 0.05). Difference in abnormal oVEMP responses (ES-MD, 5 %; LS-MD, 40 %) was significant ( p < 0.05). Conclusion: An increased occurrence of abnormal c/oVEMP recordings appeared in MD patients, possibly as a result of hydrops of the otolith. cVEMPs were more often abnormal in MD patients as compared to oVEMPs, suggesting that saccular dysfunction may be more common than utricular dysfunction. Furthermore, o/cVEMP abnormalities in the LS-MD group were significantly higher than those in the ES-MD group, suggesting the trend that otolith damage is gradually increasing with the aggravation of cochlear injury in MD.

Background: Gentamicin is a commonly used aminoglycoside antibiotic, with ototoxicity as a significant side effect. Ferroptosis, an iron-dependent form of cell death, has been implicated in a variety of disorders. Whether ferroptosis impacts gentamicin ototoxicity is not yet known. The current work used an in-vitro model to examine the influence of gentamicin-induced ferroptosis on cochlear hair cell damage and probable molecular biological pathways. Methods: House Ear Institute-Organ of Corti 1 (HEI-OC1) cells were treated with different concentrations of gentamicin for 24 hours, with or without ferrostatin-1 pretreatment, to observe gentamicin-induced ferroptosis. The role of p53/solute carrier family 7 member 11 (SLC7A11)/glutathione peroxidase 4 (GPX4) signaling in gentamicin-induced ferroptosis was explored by pretreating cells with the p53 inhibitor pifithrin-α (PFT-α). We investigated the effect of gentamicin on cells by assessing cell viability. Cellular proteins were isolated and Western blots were performed to detect changes in the expression of p53, SLC7A11, and GPX4. Fluorescence staining was used to assess levels of reactive oxygen species. An enzymatic detection kit was used to detect glutathione, Fe, and malondialdehyde markers. Results: Gentamicin reduced cell viability, glutathione content, and SLC7A11 and GPX4 protein levels, and increased levels of p53 protein, reactive oxygen species, malondialdehyde, and Fe. These effects were largely blocked by pretreatment with ferrostatin-1. Pretreatment with the p53 inhibitor PFT-α prevented the gentamicin-induced reduction in SLC7A11 and GPX4, which alleviated several features of ferroptosis including glutathione depletion, iron overload, and lipid peroxidation build-up. Conclusion: Gentamicin induces ferroptosis in the HEI-OC1 cell line, and the mechanism may be related to the p53/SLC7A11/GPX4 signaling pathway.

Hypothesis The stress hormone cortisol affects aminoglycoside-induced ototoxicity. Background: The widespread use of aminoglycosides is a prevalent cause of sensorineural hearing loss. Patients receiving aminoglycosides usually have elevated levels of circulating stress hormones due to disease or physiological stress; however, whether the stress hormone cortisol impacts aminoglycoside-mediated injury of cochlear hair cells has not been fully investigated. Methods: House Ear Institute-Organ of Corti 1 (HEI-OC1) cells with or without cortisol pretreatment were exposed to gentamicin, we investigated the effect of cortisol pretreatment on gentamicin ototoxicity by assessing cell viability. Molecular pathogenesis was explored by detecting apoptosis and oxidative stress. Meanwhile, by inhibiting glucocorticoid receptors (GR) and mineralocorticoid receptors (MR), the potential roles of receptor types in cortisol-mediated sensitization were evaluated. Results: Cortisol concentrations below 75 μmol/l did not affect cell viability. However, pretreatment with 50 μmol/l cortisol for 24 hours sensitized hair cells to gentamicin-induced apoptosis. Further mechanistic studies revealed that cortisol significantly increased hair cell apoptosis and oxidative stress, and altered apoptosis-related protein expressions induced by gentamicin. In addition, blockade of either GR or MR attenuated cortisol-induced hair cell sensitization to gentamicin toxicity. Conclusion: Cortisol pretreatment increased mammalian hair cell susceptibility to gentamicin toxicity. Sensitization was related to the activation of the intrinsic apoptotic pathway and excessive generation of reactive oxygen species. Cortisol may exacerbate aminoglycoside ototoxicity.

Age-related hearing loss (ARHL) is a prevalent neurodegenerative condition commonly linked to aging and chronic inflammation. However, there is currently a lack of substantial proteomic evidence elucidating the underlying mechanisms within the brain. The study employed proteomic techniques to identify proteins as biomarkers for ARHL and to investigate and predict their underlying pathogenic mechanisms and potential intervention targets. In studying the impact of aging on ARHL, we found significant expression of 7 hearing-related proteins. including Mbp, Mag, Plp1, Orm1, Orm2, Tubb2b, Tuba3aa, and Tuba4a. These proteins were enriched in the ceramide-related pathway (CAMS), sphingolipid pathway, and microtubule transport pathway. Further investigations into the impact of chronic neuroinflammation, particularly reflecting the activation of microglial, revealed an improvement in hearing following the inhibition of microglial activation. Additionally, two proteins significantly associated with hearing were discovered to be expressed in the cochlear nucleus. Mag, Orm1, enriched in CAMs and sphingolipid pathways. In conclusion, we predict that aging may hinder the microtubule transport pathway, affect the CAMS and acidic glycoprotein pathways, influence the differential expression of proteins, thereby leading to the occurrence and development of ARHL. After the inhibition of microglia, key proteins of the CAMS and acidic glycoprotein pathways appeared among the differentially expressed proteins, which suggests that aging may induce ARHL by affecting myelin stripping in microglia, ultimately promoting the development of ARHL.