Otolaryngology: Open Access
Open Access

Abstract

It is generally accepted that trauma to the cochlea is the most common trigger for tinnitus. The altered input from the cochlea is thought to lead to plasticity in the central auditory system eventually resulting in abnormal patterns of activity in the cortex translating into the perceptual phenomenon that is tinnitus. At that stage, tinnitus is commonly thought to be generated by the brain and independent of cochlear output. However, using an animal model, we have found evidence to suggest the contrary. In our model we use acoustic trauma to induce hearing loss and increased spontaneous activity (hyperactivity) in central auditory structures, which may be involved in the generation of tinnitus. We demonstrated that for some time after trauma, central hyperactivity is due to hyperexcitability and is still dependent on cochlear drive. At later time-points the central hyperactivity becomes generated intrinsically. Our data could explain the mechanism by which furosemide, a loop diuretic known to suppress the spontaneous activity of the auditory nerve, can reduce tinnitus in some patients. It could also be a mechanism by which some forms of cochlear electrical stimulation may affect tinnitus perception. Experiments in our animal model will be discussed showing the effects of such treatments on central hyperactivity and tinnitus. The results show support for the notion that there may be a therapeutic window for recent onset tinnitus for drug or other treatments that target peripheral spontaneous activity.

Biography

Wilhelmina Mulders completed her PhD in 1997 at the University of Nijmegen in The Netherlands and has since then worked at The University of Western Australia. She has published more than 45 papers in international peer-reviewed journals with the majority as first author.