According to a recent epidemiological survey, the incidence of sudden sensorineural hearing loss (SSNHL) is increasing yearly. The cause of SSNHL is of great interest in research. To date, viral infection, vascular occlusion, abnormal cellular stress responses within the cochlea, and immune-mediated mechanisms are considered the most likely etiologies of this disease. Among these etiologies, the relationship between viral infection and sudden deafness has been unclear. In this review, we mainly discuss the viral hypothesis of SSNHL. There is little research proving or clearly indicating the pathogenesis of this disease. Further research is needed to elucidate the precise etiopathogenesis to better understand SSNHL and establish more suitable treatment to help restore hearing in affected patients.

Lesion-induced cochlear damage can result in synaptic outgrowth in the ventral cochlear nucleus (VCN). Tinnitus may be associated with the synaptic outgrowth and hyperactivity in the VCN. However, it remains unclear how hearing loss triggers structural synaptic modifications in the VCN of rats subjected to salicylate-induced tinnitus. To address this issue, we evaluated tinnitus-like behavior in rats after salicylate treatment and compared the amplitude of the distortion product evoked otoacoustic emission (DPOAE) and auditory brainstem response (ABR) between control and treated rats. Moreover, we observed the changes in the synaptic ultrastructure and in the expression levels of growth-associated protein (GAP-43), brain-derived neurotrophic factor (BDNF), the microglial marker Iba-1 and glial fibrillary acidic protein (GFAP) in the VCN. After salicylate treatment (300 mg/kg/day for 4 and 8 days), analysis of the gap prepulse inhibition of the acoustic startle showed that the rats were experiencing tinnitus. The changes in the DPOAE and ABR amplitude indicated an improvement in cochlear sensitivity and a reduction in auditory input following salicylate treatment. The treated rats displayed more synaptic vesicles and longer postsynaptic density in the VCN than the control rats. We observed that the GAP-43 expression, predominantly from medial olivocochlear (MOC) neurons, was significantly up-regulated, and that BDNF- and Iba-1-immunoreactive cells were persistently decreased after salicylate administration. Furthermore, GFAP-immunoreactive astrocytes, which is associated with synaptic regrowth, was significantly increased in the treated groups. Our study revealed that reduced auditory nerve activity triggers synaptic outgrowth and hyperactivity in the VCN via a MOC neural feedback circuit. Structural synaptic modifications may be a reflexive process that compensates for the reduced auditory input after salicylate administration. However, massive increases in excitatory synapses in the VCN may represent a detrimental process that causes central hyperactivity, leading to tinnitus.

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Meatoplasty with canalplasty and tympanoplasty in individuals with CAS can yield reliable and lasting positive hearing results with a low incidence of severe complications. The existence and preoperative condition of patients' TM and EAC skin helped improve hearing results and decrease the incidence of complications. However, the final hearing results and complications required stricter indications for CAA patients.