Tinnitus affects 10 to 15% of the population. Consensus exists on hearing loss as a frequent cause of it. The exact mechanism of development is still under debate.
In our group we propose a new model of tinnitus development: The brain constantly optimizes information transmission into the hearing system by physiological neuronal processes (stochastic resonance, SR) which can diminish hearing loss. Tinnitus develops as a side product. This hypothesis is supported by animal model data as well as by data from a collective of more than 40.000 patients with and without tinnitus.
In this study anamnesis of 575 tinnitus patients (1150 ears) of different ages from that collective have been investigated if the patient came to the ENT hospital Erlangen explicitly because of the percept (n = 132, Te) or because of another disease (n = 443, Ta). Multifactorial ANOVAs revealed independent on age the worst hearing thresholds at/above tinnitus frequency. This fits to the correlation of tinnitus development and cochlear synaptopathy in our animal model. Additionally, the hearing thresholds of Te patients are significantly better than those of Ta patients and their tinnitus loudness is significantly higher. This suggests a correlation of higher tinnitus intensity and better hearing thresholds already shown in the animal model.
Summarized, human data supports the animal model data and strengthen the hypothesis, that by SR a physiological mechanism for rescuing thresholds after hearing loss takes place along the auditory pathway that produces tinnitus as a side product.
