title: Cochlear-motor, transduction and signal-transfer tinnitus: models for three types of cochlear tinnitus.
abstract: The present paper reviews possible molecular and cellular mechanisms in the cochlea that might contribute to tinnitus. They constitute a part of a highly integrated network in cochlear sound processing and are divided for easier understanding into three different models, i.e. active motor tinnitus, transduction tinnitus and signal-transfer tinnitus. Some of the steps of the pathophysiological models can even be pharmacologically influenced (as exemplified by experimental applications of lidocaine, calcium channel blocker, benzodiazepine, glutamate and atropine). This provides a rationale for the efficient suppression of tinnitus in some patients by these drugs. The most evident problem of all models in tinnitus, including the ones proposed in this paper, is the lack of objective verification by measurement. Thus, the well-defined clinical situation of each patient is hardly attributable to one of the models suggested. In addition, adequate therapy--perhaps one of the drugs considered--still cannot be based upon a reliable clinical finding.
authors.affiliation: Department of Otolaryngology, University of Tübingen, Federal Republic of Germany.
authors.forename: H P
authors.initials: HP
authors.lastname: Zenner
authors.forename: A
authors.initials: A
authors.lastname: Ernst
mesh_terms: D000818:Animals; D002118:Calcium / Q000502:physiology; D003051:Cochlea / Q000503:physiopathology*; D004594:Electrophysiology; D006198:Hair Cells, Auditory / Q000503:physiopathology; D006801:Humans; D007473:Ion Channels / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000502:physiology; D014012:Tinnitus / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D007473:Ion Channels; D018377:Neurotransmitter Agents; D002118:Calcium