BACKGROUND:This study examines the impact of commonly used disinfectants on hearing and the structural integrity of the inner ear. OBJECTIVE:To evaluate the effects of indophor, alcohol, and chlorhexidine on auditory function and cochlear morphology in mice. METHODS:Sixty-four mice were evenly divided into four groups: saline, indophor, alcohol, and chlorhexidine. Each mouse received a 25 μL injection of the designated liquid into the left ear, while the right ear was remained untreated. Auditory brainstem response (ABR) testing was performed at three intervals: before injection, 24 h post-injection, and one week post-injection. Cochlear tissues from both ears were analyzed using immunofluorescence and scanning electron microscopy to observe morphological changes. RESULTS:Chlorhexidine and alcohol significantly increased ABR thresholds in the left ear 24 h and one week post-injection (p < 0.001). Chlorhexidine caused severe damage to outer hair cells, inner hair cells, and spiral ganglion cells, while alcohol had a milder effect. Iodophor mainly affected outer hair cells, with partial recovery after seven days. In the right ear, only chlorhexidine caused a sustained ABR threshold increase (p < 0.001) and severe damage to outer and inner hair cells. Both alcohol and chlorhexidine induced demyelination of spiral ganglion cells in the left ear, but recovery was seen only in the alcohol group after one week. CONCLUSION:Indophor, alcohol, and chlorhexidine can all affect hearing, with alcohol and chlorhexidine causing more severe and lasting damage. These findings provide crucial insights for selecting disinfectants in ear surgeries. LEVEL OF EVIDENCE:NA Laryngoscope, 135:2154-2163, 2025.

Drug delivery to the inner ear remains a major hurdle to effective therapy, underscoring the importance of precision-based delivery strategies. Diabetes-induced hearing loss (DHL) is a debilitating condition with limited therapeutic options, primarily driven by oxidative stress and microvascular damage in the cochlea. Current treatments are ineffective, highlighting the paramount need for novel strategies. Gelatin methacryloyl (GelMA) hydrogels, owing to their biocompatibility and tunable physicochemical properties, enables in situ crosslinking using ultraviolet (UV) light for precise localization of therapeutic agents. Berberine, renowned for its antioxidant and anti-inflammatory efficacy, has shown potential in mitigating diabetes-related complications and certain types of hearing loss. However, its limited solubility and poor permeability across the blood-labyrinth barrier (BLB) hinder its systemic efficacy. To circumvent this, we designed a localized, injectable, and photo-crosslinked GelMA conjugated berberine chloride hydrate (BCH) hydrogel for sustained cochlear drug delivery. Our results demonstrated that GelMA-BCH hydrogel exhibited excellent biocompatibility, robust adhesion, and prolonged cochlear drug retention, enhancing therapeutic outcomes. Liquid chromatography-mass spectrometry (LC-MS) confirmed higher perilymph BCH concentration following localized GelMA-BCH hydrogel administration compared to systemic free BCH delivery. In streptozotocin (STZ)-induced diabetic mice, GelMA-BCH hydrogel treatment demonstrated significant recovery in auditory function, with improved auditory brainstem responses (ABR) thresholds compared to untreated diabetic controls. Morphological analysis revealed preserved cochlear integrity, particularly through protection of outer hair cells (OHCs) and cochlear synapses. In vitro, GelMA-BCH protected auditory House Ear Institute-Organ of Corti 1 (HEI-OC1) cells by reducing STZ-induced oxidative stress, thereby suppressing inflammatory cytokines and mitochondrial-mediated apoptosis, leading to markedly improved cellular resilience. These findings reinforce the potential application of GelMA-BCH hydrogel as a targeted, bioactive therapeutic strategy for cochlear protection in DHL, offering a novel strategy for future clinical translation and address the urgent unmet need in otology and regenerative medicine.

ObjectiveTo investigate the effects of Zexie decoction on vestibular and auditory function in guinea pigs with endolymphatic hydrolysis induced by desmopressin. Methods: Sixty guinea pigs were randomly and evenly divided into four groups, each group has 15 guinea pigs: normal control group, DDAVP group, DDAVP modeling combined with Zexie Decoction group, and DDAVP combined with Double Zexie group. At 7 and 14 days, bone-conducted cervical vestibular evoked myogenic potential tests, auditory brainstem responses, and distortion-product otoacoustic emissions were conducted on each group of guinea pigs to evaluate their vestibular and auditory function quantitatively. After functional testing, the outer hair cells were observed by scanning electron microscope. On day 14, one guinea pig was randomly selected from both the normal control group and DDAVP group to verify the successful establishment of the model using gadolinium-enhanced magnetic resonance imaging of the inner ear.ResultsWe conducted BC-cVEMP, ABR, and DPOAE tests on guinea pigs, and the results showed that DDAVP did affect vestibular function and hearing in guinea pigs. Analyses were performed from those results that were statistically significant, Zexie Decoction improved DDAVP-induced vestibular dysfunction and hearing loss dose-dependently, though complete reversal was not achieved. About scanning electron microscopy, outer hair cells of the DDAVP group showed significant loss and cilia lodging, however, treatment with Zexie decoction can alleviate the loss of outer hair cells and the lodging of cilia. When the outer hair cells were exposed to DDAVP for a long time, the improvement effect of Zexie decoction was not as obvious as before.ConclusionThe extent of improvement correlates with the concentration and dosage of Zexie Decoction. Even at double the dosage, Zexie Decoction only partially mitigates the decline in vestibular and auditory function induced by DDAVP, falling short of complete reversal.

BackgroundInner ear disorders, such as EH, commonly lead to hearing loss and vestibular dysfunction. EH is particularly prevalent in various inner ear diseases, including Meniere’s disease. We aimed to evaluate the effects of EH on WAI and OAEs.ObjectiveThis study explores the potential of wideband acoustic immittance (WAI) and otoacoustic emissions (OAEs) for the early detection of changes in acoustic transmission associated with vasopressin-induced endolymphatic hydrops (EH) in a guinea pig model.MethodsWe induced EH in guinea pigs via daily intraperitoneal injections of arginine vasopressin over 14 consecutive days. Auditory function was assessed using Auditory Brainstem Responses (ABR), while changes in sound energy transmission were measured using WAI and Distortion Products Otoacoustic Emissions (DPOAE).ResultsIncreased ABR thresholds in EH models were statistically significant (p < 0.05). After 14 days of EH induction, absorbance at 1 kHz significantly increased, whereas it significantly decreased at 4 kHz and 6 kHz (p < 0.05). DPOAE measures, both magnitude and phase, showed no significant changes (p > 0.05).ConclusionWAI demonstrates greater sensitivity than DPOAE in the early detection of acoustic transmission alterations in EH models, suggesting its utility as a diagnostic tool in early-stage inner ear disorders.

OBJECTIVE:To evaluate the clinical significance of WAI as a predictive marker for MD and LVAS among adults. METHODS:Participants included 110 ears with MD, 18 ears with LVAS, and 92 normal ears (control group) recruited from clinical audiology settings. The outcome measures included Wideband Energy Absorbance (WBA), Resonance Frequency (RF), admittance Magnitude (YM), and phase Angle (YA). Propensity Score Matching (PSM) was conducted to treat the group imbalance. RESULTS:Compared with the control group, The MD group exhibited significantly lower WBA between 1587 and 4000 Hz (p < 0.05), while the LVAS group showed lower WBA between 1000 and 2520 Hz (p < 0.05). The MD and LVAS groups had lower RF (p < 0.05), while they had higher YM at low frequencies (226 and 678 Hz for MD, and 1000 Hz for LVAS, p < 0.05). CONCLUSIONS:This study showed that LVAS has a lower WBA at middle frequencies, whereas MD has a lower WBA at middle and high frequencies. These findings suggest that WAI may serve as a predictive marker for MD and LVAS. However, further studies are needed to explore its diagnostic utility in Third Mobile Window Abnormalities (TMWA). LEVEL OF EVIDENCE:IV: Retrospective cohort study.

Noise-induced hearing loss (NIHL) results from prolonged exposure to intense noise, causing damage to sensory outer hair cells (OHCs) and spiral ganglion neurons (SGNs). The blood labyrinth barrier (BLB) hinders systemic drug delivery to the inner ear. This study applied a retro-auricular round window membrane (RWM) method to bypass the BLB, enabling the transport of macromolecular proteins into the inner ear. Pigment epithelium-derived factor (PEDF), which has anti-inflammatory and neuroprotective properties, is conjugated to a prestin-targeting peptide 2 (PrTP2) using N-succinimidyl-3-maleimidopropionate (SMP) to form PrTP2-SMP/PEDF. This compound specifically targeted Prestin and accumulated around OHCs for sustained release, effectively reducing OHC and SGN loss. Functional and structural tests, including auditory brainstem response (ABR), confocal microscopy, and scanning electron microscopy (SEM), revealed significant hearing restoration and cellular protection. Additionally, the results of enzyme-linked immunosorbent assay (ELISA), Annexin V and propidium iodide (PI) staining and immunoblotting show that noise exposure may induce pyroptosis in the cochlea by activating the NOD-like receptor protein 3 (NLRP3)-apoptosis-associated speck-like protein containing a CARD (ASC) - cysteinyl aspartate specific proteinase (Caspase-1) pathway and PrTP2-SMP/PEDF alleviates the inflammatory response by inhibiting pyroptosis. Toxicity analysis indicates no adverse effects, suggesting that PrTP2-SMP/PEDF has a promising therapeutic prospective for NIHL.

Objectives: This study aimed to assess the clinical significance of Wideband Absorbance (WBA) in children with Large Vestibular Aqueduct Syndrome (LVAS), which could potentially serve as diagnostic and predictive markers for LVAS in children. Design: This was a single-center retrospective case-control study. Audiological measurements and Wideband Acoustic Immittance (WAI) were performed. Propensity score matching (PSM) was considered to treat group imbalance. The Receiver Operating Characteristic (ROC) curves and area under the ROC curve (AUC) were used to evaluate the sensitivity and specificity of WBA. Study sample: Participants included 42 children with LVAS and 163 normal children aged 6 months -11 years recruited from clinical audiology settings between 2019 and 2021. Results: The WBA at Tympanometric Peak Pressure (WBA(TPP)) and Ambient Pressure (WBA(A)) in the LVAS group were significantly lower than those of the control group at 1259-2000 Hz but higher at 4000-6349 Hz (p < 0.05, power >0.8). The WBA(A (1587 Hz)) AUC value was 0.805, identifying a score <= 0.565 as indicative of a LVAS risk. Conclusions: WBA holds promise in distinguishing LVAS from the normal condition and warrants further exploration as a tool to examine the influence of inner ear pressure on acoustic energy transmission in the middle ear.

Objective: To explore whether Cyclic Adenosine Monophosphate (cAMP)-Epac1 signaling is acti-vated in 1-Desamino-8-D-arginine-Vasopressin-induced Endolymphatic Hydrops (DDAVP-induced EH) and to provide new insight for further in-depth study of DDAVP-induced EH.Methods: Eighteen healthy, red-eyed guinea pigs (36 ears) weighing 200-350 g were randomly divided into three groups: the control group, which received intraperitoneal injection of sterile saline (same volume as that in the other two groups) for 7 consecutive days; the DDAVP-7d group, which received intraperitoneal injection of 10 mg/mL/kg DDAVP for 7 consecutive days; and the DDAVP-14d group, which received intraperitoneal injection of 10 mu g/mL/kg DDAVP for 14 consecutive days. After successful modeling, all animals were sacrificed, and cochlea tissues were collected to detect the mRNA and protein expression of the exchange protein directly activated by cAMP-1 and 2 (Epac1, Epac2), and Repressor Activator Protein-1 (Rap1) by Reverse Transcription (RT)-PCR and western blotting, respectively.Results: Compared to the control group, the relative mRNA expression of Epac1, Epac2, Rap1A, and Rap1B in the cochlea tissue of the DDAVP-7d group was significantly higher (p < 0.05), while no significant difference in Rap1 GTPase activating protein (Rap1gap) mRNA expression was found between the two groups. The relative mRNA expression of Epac1, Rap1A, Rap1B, and Rap1gap in the cochlea tissue of the DDAVP-14d group was significantly higher than that of the control group (p < 0.05), while no significant difference in Epac2 mRNA expression was found between the DDAVP-14d and control groups. Comparison between the DDAVP-14d and DDAVP-7d groups showed that the DDAVP-14d group had significantly lower Epac2 and Rap1A (p < 0.05) and higher Rap1gap (p < 0.05) mRNA expression in the cochlea tissue than that of the DDAVP-7d group, while no significant differences in Epac1 and Rap1B mRNA expression were found between the two groups. Western blotting showed that Epac1 protein expression in the cochlea tissue was the highest in the DDAVP-14d group, followed by that in the DDAVP-7d group, and was the lowest in the control group, showing significant differences between groups (p < 0.05); Rap1 protein expression in the cochlea tissue was the highest in the DDAVP-7d group, followed by the DDAVP-14d group, and was the lowest in the control group, showing significant differences between groups (p < 0.05); no significant differences in Epac2 protein expression in the cochlea tissue were found among the three groups.Conclusion: DDAVP upregulated Epac1 protein expression in the guinea pig cochlea, leading to activation of the inner ear cAMP-Epac1 signaling pathway. This may be an important mechanism by which DDAVP regulates endolymphatic metabolism to induce EH and affect inner ear function. Oxford Centre for Evidence-Based Medicine 2011 Levels of Evidence: Level 5.(c) 2023 Associacao Brasileira de Otorrinolaringologia e Cirurgia C ' ervico-Facial. Published by Elsevier Espan similar to a, S.L.U. This is an open access article under the CC BY license (http:// creativecommons.org/licenses/by/4.0/).

Aims: Noise damage to auditory hair cells is associated with oxidative stress and mitochondrial dysfunction. This study aimed to investigate the possible effect of sestrin 2 (SESN2), an endogenous antioxidant protein, on noise-induced hearing loss (NIHL) and the underlying mechanisms.Results: We identified SESN2 as a protective factor against oxidative stress in NIHL through activation of Parkin-mediated mitophagy. Consistently, SESN2 expression was increased and mitophagy was induced during the early stage after a temporary threshold shift due to noise exposure or hydrogen peroxide(H2O2) stimulation; conversely, SESN2 deficiency blocked mitophagy and exacerbated acoustic trauma. Mechanistically, SESN2 interacted with Unc-51-like protein kinase 1(ULK1), promoting ULK1 protein-level stabilization by interfering with its proteasomal degradation. This stabilization is essential for mitophagy initiation, since restoring ULK1 expression in SESN2-silenced cells rescued mitophagy defects.Innovation and Conclusion: Our results provide novel insights regarding SESN2 as a therapeutic target against noise-induced cochlear injury, possibly through improved mitophagy.

OBJECTIVE:To detect the expression of Epac1 and Epac2 in the inner ear of guinea pigs and its association with microcirculation in the inner ear. METHODS:The temporal bones of 30 healthy red-eye guinea pigs (60 ears) weighing 200-350 g were collected, then the surrounding bone wall of the cochlea was removed under a dissection microscope. Real-time quantitative PCR (RT-qPCR) and Western blot were used to detect mRNA and protein expression, respectively, of Epac1 and Epac2 in the inner ear and to compare their expression in heart, liver, kidney, intestine, and lung tissues. The specimens of the cochlea included the stria vascularis, basilar membrane, saccule, and utricles isolated under a microscope to detect the localization of Epac1 and Epac2 proteins in various parts of the inner ear through immunofluorescence staining. RESULTS:The RT-qPCR and Western blot results showed that Epac1 mRNA was universally expressed in the inner ear, heart, liver, kidneys, intestines, and lungs, and was highly expressed in the liver, kidneys, and intestines (p < 0.05 vs heart, liver, kidney, intestine; p > 0.05 vs lung). Epac2 mRNA was expressed in the inner ear and heart, but not in the liver, kidneys, intestines, or lungs (p < 0.05 vs Heart). Epac1 and Epac2 proteins were both expressed in the inner ear, heart, liver, kidneys, intestines, and lungs. The relative expression of Epac1 proteins in the inner ear was significantly different from the liver, kidneys, intestines, and lungs (p < 0.05). The relative expression of Epac2 proteins in the inner ear was significantly different from the liver, kidneys, and lungs (p < 0.05), but not from the heart (p = 0.127) or intestines (p = 0.274). Immunofluorescence staining observed under confocal microscopy indicated that Epac1 and Epac2 proteins were expressed in the stria vascularis, basilar membrane, saccule, and utricles of the inner ear. They were expressed in maginal cells, intermediate cells, and basal cells of the stria vascularis, and highly expressed in capillary endothelial cells. CONCLUSIONS:Epac1 and Epac2 mRNA and proteins were both expressed in the inner ear of guinea pigs and evenly expressed in the spiral ganglion, basilar membrane, saccule, and utricles. However, their expression in capillary endothelial cells of the stria vascularis was more obvious, suggesting that cyclic adenosine monophosphate-Epac1 signaling may play an important role in maintaining the function of the blood-labyrinth barrier and regulating the stability of microcirculation in the inner ear.

Autophagy plays a pathogenic role in neurodegenerative disease. However, the involvement of autophagy in the pathogenesis of age-related hearing loss (ARHL) remains obscure. Naturally aged C57BL/6J mice were used to identify the role of autophagy in ARHL, and rapamycin, a mammalian target of rapamycin (mTOR) inhibitor, was administered for 34 weeks to explore the potential therapeutic effect of rapamycin in ARHL. We found that the number of autophagosomes and the expression of microtubule-associated protein 1 light chain 3B (LC3B) decreased as the mice aged. The expression of autophagy-related (Atg) proteins, including Beclin1 and Atg5, and the ratio of LC3-II/I was reduced in aged mice, while mTOR activity in aged mice gradually increased. Rapamycin improved the auditory brainstem response (ABR) threshold (at 8, 12, and 24 kHz). Further exploration demonstrated that spiral ganglion neuron (SGN) density was enhanced in response to administration of rapamycin. The rate of apoptosis in the basal turn SGNs was decreased, whereas autophagy activity was increased in the experimental group. Meanwhile, mTOR activity in the experimental group was decreased. Our findings indicate that age-related deficiency in autophagy may lead to increased apoptosis of aged SGNs. Rapamycin enhances autophagy of SGNs by inhibiting mTOR activation, resulting in amelioration of ARHL. Therapeutic strategy targeting autophagy may provide a potential approach for treating ARHL.

Overproduction of reactive oxygen species (ROS) and inflammation are two key pathogeneses of noise-induced hearing loss (NIHL), which leads to outer hair cell (OHC) damage and hearing loss. In this work, we successfully developed ROS-responsive nanoparticles as berberine (BBR) carriers (PL-PPS/BBR) for OHC-targeted therapy of NIHL: Prestin-targeting peptide 2 (PrTP2)-modified nanoparticles (PL-PPS/BBR), which effectively accumulated in OHC areas, and poly(propylene sulfide)120 (PPS120), which scavenged ROS and converted to poly(propylene sulfoxide)120 in a ROS environment to disintegrate and provoke the rapid release of BBR with anti-inflammatory and antioxidant effects. In this study, satisfactory anti-inflammatory and antioxidant effects of PL-PPS/BBR were confirmed. Immunofluorescence and scanning electron microscopy (SEM) images showed that PL-PPS/BBR effectively accumulated in OHCs and protected the morphological integrity of OHCs. The auditory brainstem response (ABR) results demonstrated that PL-PPS/BBR significantly improved hearing in NIHL guinea pigs after noise exposure. This work suggested that PL-PPS/BBR may be a new potential treatment for noise-associated injury with clinical application.

目的 探讨乙状窦还纳术对乙状窦憩室或骨壁缺损引起搏动性耳鸣的疗效,并分析特殊病例特点及原因.方法 回顾性分析35例乙状窦还纳术治疗搏动性耳鸣患者临床资料,在术前、术后1月、3月、6月进行耳鸣量表THI评分及统计分析.结果 无效0例、显效18例、痊愈16例、失访1例.显效组THI量表术前:65.78±5.40,术后6月:28.11±4.52,统计学差异显著.结论 对乙状窦憩室或骨壁缺损引起的搏动性耳鸣进行乙状窦还纳术疗效确切,局麻手术有利于进行术中评估.

INTRODUCTION:Meniere's disease is associated with impaired hearing, tinnitus, vertigo, and aural fullness. Many anatomical studies have suggested idiopathic endolymphatic hydrops as the pathological basis of Meniere's disease, which now can be visualized by using gadolinium -enhanced magnetic resonance imaging of the inner ear.OBJECTIVE:To investigate the development of endolymphatic hydrops in Meniere's disease by monitoring the vestibules and cochleae of affected patients.METHODS:Inner ears of 178 patients with definite unilateral Meniere's disease diagnosis were visualized by 3-dimensional fluid-attenuated inversion recovery and three-dimensional real inversion recovery magnetic resonance imaging following bilateral gadolinium intratympanic injection. The scans were used to evaluate the presence and degree of endolymphatic hydrops in the vestibules and cochlear structures, including the cochlear apical turn, the cochlear middle turn, and the cochlear basal turn. The correlation of endolymphatic hydrops occurrence between the various parts of the inner ear was determined.RESULTS:Symptomatic endolymphatic hydrops was detected on the affected side in all patients, whereas asymptomatic endolymphatic hydrops was detected on the unaffected contra-lateral side in 32 patients (18.0%). On the affected side, the cochlear apical turn and the cochlear middle turn demonstrated significantly higher rates of endolymphatic hydrops than the cochlear basal turn and the vestibule. The severity of endolymphatic hydrops gradually decreased from the cochlear apical turn to the cochlear basal turn. On the contra lateral side, the incidence and degree of the detected asymptomatic endolymphatic hydrops were significantly greater in the cochleae than in the vestibules (p<0.05), with no significant difference detected between the cochlear turns.CONCLUSION:Progression of endolymphatic hydrops appears to be directional, initiated in the cochlea. The order of endolymphatic hydrops severity gradually decreases from the cochlear apical turn to the cochlear basal turn and then to the vestibule. Endolymphatic hydrops in the vestibule is associated with symptomatic Meniere's disease.

Introduction: Meniere’s disease is associated with impaired hearing, tinnitus, vertigo, and aural fullness. Many anatomical studies have suggested idiopathic endolymphatic hydrops as the pathological basis of Meniere’s disease, which now can be visualized by using gadolinium -enhanced magnetic resonance imaging of the inner ear. Objective: To investigate the development of endolymphatic hydrops in Meniere’s disease by monitoring the vestibules and cochleae of affected patients. Methods: Inner ears of 178 patients with definite unilateral Meniere’s disease diagnosis were visualized by 3-dimensional fluid-attenuated inversion recovery and three-dimensional real inversion recovery magnetic resonance imaging following bilateral gadolinium intratympanic injection. The scans were used to evaluate the presence and degree of endolymphatic hydrops in the vestibules and cochlear structures, including the cochlear apical turn, the cochlear middle turn, and the cochlear basal turn. The correlation of endolymphatic hydrops occurrence between the various parts of the inner ear was determined. Results: Symptomatic endolymphatic hydrops was detected on the affected side in all patients, whereas asymptomatic endolymphatic hydrops was detected on the unaffec-ted contra-lateral side in 32 patients (18.0%). On the affected side, the cochlear apical turn and the cochlear middle turn demonstrated significantly higher rates of endolymphatic hydrops than the cochlear basal turn and the vestibule. The severity of endolymphatic hydrops gradually decreased from the cochlear apical turn to the cochlear basal turn. On the contra lateral side, the incidence and degree of the detected asymptomatic endolymphatic hydrops were significantly greater in the cochleae than in the vestibules ( p < 0.05), with no significant difference detected between the cochlear turns. Conclusion: Progression of endolymphatic hydrops appears to be directional, initiated in the cochlea. The order of endolymphatic hydrops severity gradually decreases from the cochlear apical turn to the cochlear basal turn and then to the vestibule. Endolymphatic hydrops in the vestibule is associated with symptomatic Meniere’s disease.

PurposeThe aims of the present study are to investigate the variations in clinical features, including medical history, hearing function, vestibular function, and degree of endolymphatic hydrops (EH), in Meniere's disease (MD) patients with and without drop attacks (DAs), and to examine the efficacy of intratympanic gentamicin (ITG) treatment in alleviating DAs.MethodsIn total, 177 unilateral definite MD patients, including 16 patients with DAs and 161 patients without DAs, were enrolled. The results of hearing test, vestibular-evoked myogenic potentials (VEMPs), and magnetic resonance imaging (MRI) were analyzed. Thirteen patients with DAs received a single ITG treatment and were followed up.ResultsThe disease course of MD in the DA group was significantly longer than that in the control group (p=0.007). MD patients with DAs had significantly greater hearing loss and worse EH than MD patients without DAs (p<0.05). However, there was no between-group difference in vestibular function. In the study, 92.31% of refractory definite MD patients with DAs achieved satisfactory control of DAs after ITG treatment.ConclusionsMD patients with DAs tend to suffer from severe hearing loss and a significant degree of EH in the inner ear. However, the vestibular function of MD patients with DAs may not be completely abolished, but be sensitive to stimulating signals. ITG treatment, which helps to decrease vestibular sensitivity, was an effective treatment to control DAs.

梅尼埃病是耳科门诊中常见的眩晕疾病,发病率为200/100 000～500/100 000.其临床特点为反复发作眩晕,多数同时伴有患耳听力减退、耳鸣和耳闷胀感.每次眩晕发作持续时间一般为20 min～12 h.听力一般早期呈波动性低频听力下降,在疾病的间隙期可改善甚至恢复至正常.病情反复发作后逐渐累及中高频,最终为平坦型的重度聋[1].并非所有的梅尼埃病患者均会有梅尼埃病的特征性临床表现.既往研究认为仅50％的患者有梅尼埃病的特征性临床表现,即同时有听力下降、眩晕和耳鸣耳闷的临床特点,19％的患者仅有眩晕出现,26％的患者仅反复发作听力下降而没有眩晕发生[2].