A possible new tinnitus therapy based on Stochastic Resonance phenomena

Subjective tinnitus is generally assumed to be a consequence of hearing loss. In animal studies it has been demonstrated that acoustic trauma induced cochlear damage can lead to behavioral signs of tinnitus. In addition it was shown that noise trauma may lead to deafferentation of cochlear inner hair cells even in the absence of elevated hearing thresholds, and it seems conceivable that such hidden hearing loss may be sufficient to cause tinnitus. Numerous studies have indicated that tinnitus is correlated with pathologically increased spontaneous firing rates and hyperactivity of neurons along the auditory pathway. It has been proposed that this hyperactivity is the consequence of a mechanism aiming to compensate for reduced input to the auditory system by increasing central neuronal gain. We here propose an alternative model for tinnitus development based on Stochastic Resonance (SR).

This new approach was implemented and tested in a phenomenological computational model.

We could demonstrate that SR might be a major processing principle of the auditory system that serves to partially compensate for acute or chronic hearing loss, e.g. due to cochlear damage. Hereby the noise necessary for SR to work corresponds to increased spontaneous neuronal firing rates in early processing stages of the auditory brainstem. In the light of the model tinnitus is a side effect of a mechanisms that improves hearing thresholds after hearing loss.

We propose the possibility of superseding the internally generated neuronal noise by adding external noise, thereby extinguishing the tinnitus percept. Recently published results validated our model by confirming this crucial prediction in mice. Hence, our model and its implicated prediction indicate a possible new tinnitus therapy.

Publication History

Publication Date:
18 April 2018 (online)