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ObjectivesTo investigate the possible effects of anxiety and/or depression symptoms on the treatment outcomes and recurrence of benign paroxysmal positional vertigo (BPPV).MethodsThis is a retrospective study conducted at a single institution. 142 consecutive patients diagnosed with idiopathic BPPV at the Department of Otology in Shengjing Hospital of China Medical University between October 2016 and July 2017 were retrospectively reviewed. 127 patients were finally included in this study. Zung self-rating anxiety scale (SAS) and Zung self-rating depression scale (SDS) were used to evaluate the presence of anxiety and/or depression, respectively, in our BPPV patients. A significant score (at or above 50 for SAS and 53 for SDS) represents the presence of clinically significant symptoms. Two-tailed Student’s t-test, χ2 test, and logistic regression analysis were used as appropriate. A p value less than 0.05 was considered statistically significant.ResultsThe prevalence of anxiety and/or depression symptoms in BPPV patients in the present study was 49.61%. The effectiveness of the first time canalith repositioning maneuver (CRM) was 70.08%. With weekly follow-up treatments of CRM, the success rate increased to 97.64% by 1 month. The total recurrence rate at 6-month follow-up post-cure was 14.17%. Holding all other variables constant, patients with psychiatric symptoms (Relative-risk ratio: 3.160; p = 0.027) and patients with non-posterior semicircular canal (PSC) involvement (Relative-risk ratio: 7.828, p = 0.013) were more likely to experience residual dizziness (RD) even after effective CRM treatment. Psychiatric symptoms (Relative-risk ratio: 6.543; p = 0.001) and female gender (Relative-risk ratio: 4.563; p = 0.010) are risk factors for the failure of first time CRM. In addition, BPPV patients with psychiatric symptoms (Odds ratio: 9.184, p = 0.008) were significantly more likely to experience recurrences within the first 6 months after a successful maneuver.ConclusionAnxiety-depression status significantly reduced the efficacy of the first time CRM and increased the risk for recurrence. Other factors, such as female gender and non-PSC involvement are also susceptible risk factors for BPPV patients to require multiple treatments and experience delayed recovery. A screening for psychiatric symptoms in BPPV patients and active treatment of these symptoms would benefit both physicians and patients in understanding and improving the prognosis of the disease and treatment options.

Aminoglycoside-induced ototoxicity can have a major impact on patients' quality of life and social development problems. Oxidative stress affects normal physiologic functions and has been implicated in aminoglycoside-induced inner ear injury. Excessive accumulation of reactive oxygen species (ROS) damages DNA, lipids, and proteins in cells and induces their apoptosis. Dihydromyricetin (DHM) is a natural flavonol with a wide range of health benefits including anti-inflammatory, antitumor, and antioxidant effects; however, its effects and mechanism of action in auditory hair cells are not well understood. The present study investigated the antioxidant mechanism and antiototoxic potential of DHM using House Ear Institute-Organ of Corti (HEI-OC)1 auditory cells and cochlear explant cultures prepared from Kunming mice. We used gentamicin to establish aminoglycoside-induced ototoxicity models. Histological and physiological analyses were carried out to determine DHM's pharmacological effects on gentamicininduced ototoxicity. Results showed DHM contributes to protecting cells from apoptotic cell death by inhibiting ROS accumulation. Western blotting and quantitative RT-PCR analyses revealed that DHM exerted its otoprotective effects by up-regulating levels of peroxisome proliferator activated receptor γ-coactivator (PGC)-1α and Sirtuin (SIRT)3. And the role of PGC-1α and SIRT3 in the protective effects of DHM was evaluated by pharmacologic inhibition of these factors using SR-18292 and 3-(1H-1,2,3-triazol-4-yl) pyridine, respectively, which indicated DHM's protective effect was dependent on activation of the PGC-1α/SIRT3 signaling. Our study is the first report to identify DHM as a potential otoprotective drug and provides a basis for the prevention and treatment of hearing loss caused by aminoglycoside antibiotic-induced oxidative damage to auditory hair cells.

Aminoglycoside antibiotics such as gentamicin could cause ototoxicity in mammalians, by inducing oxidative stress and apoptosis in sensory hair cells of the cochlea. Sodium hydrosulfide (NaHS) is reported to alleviate oxidative stress and apoptosis, but its role in protecting aminoglycoside-induced hearing loss is unclear. In this study, we investigated the anti-oxidant and anti-apoptosis effect of NaHS in in vitro cultured House Ear Institute-Organ of Corti 1 (HEI-OC1) cells and isolated mouse cochlea. Results from cultured HEI-OC1 cells and cochlea consistently indicated that NaHS exhibited protective effects from gentamicin-induced ototoxicity, evident by maintained cell viability, hair cell number and cochlear morphology, reduced reactive oxygen species production and mitochondrial depolarization, as well as apoptosis activation of the intrinsic pathway. Moreover, in the isolated cochlear culture, NaHS was also demonstrated to protect the explant from gentamicin-induced mechanotransduction loss. Our study using multiple in vitro models revealed for the first time, the potential of NaHS as a therapeutic agent in protecting against aminoglycoside-induced hearing loss.

Mitochondrial dysfunction is associated with ototoxicity, which is caused by external factors. Mitophagy plays a key role in maintaining mitochondrial homeostasis and function and is regulated by a series of key mitophagy regulatory proteins and signaling pathways. The results of ototoxicity models indicate the importance of this process in the etiology of ototoxicity. A number of recent investigations of the control of cell fate by mitophagy have enhanced our understanding of the mechanisms by which mitophagy regulates ototoxicity and other hearing-related diseases, providing opportunities for targeting mitochondria to treat ototoxicity.