Abstract
Tinnitus is one of the most common clinical symptoms of otology, and its pathogenesis is still unclear. The mechanism of tinnitus has been studied through a cognitive progress from the periphery （cochlea） to auditory center to the limbic system. Auditory peripheral lesions, such as damages to ribbon synapses, may form excitatory deafferentation, then it induces the auditory center to start the compensatory gain, leading to an increase in excitatory response; If the damage is further aggravated, it may cause continuous enhancement of central gain effect, hyperexcitability may occur and leading to tinnitus. Besides, the limbic system may be involved in the maintenance or exacerbation of tinnitus symptoms. This paper reviews the recent researches on tinnitus mechanism and auditory center plasticity.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology, head, and neck surgery
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
