A unified theory for the development of tinnitus and hyperacusis based on associative plasticity in the dorsal cochlear nucleus

TL;DR

This paper presents a unified theoretical model explaining the development of tinnitus and hyperacusis through associative plasticity mechanisms in the dorsal cochlear nucleus, linking hearing loss and noise exposure to these conditions.

Contribution

It introduces a novel model based on Hebbian and associative plasticity in the DCN that explains the distinct neural mechanisms underlying tinnitus and hyperacusis.

Findings

Hearing loss leads to chronic tinnitus via synaptic enhancement of somatosensory input.

Noise exposure causes hyperacusis through synaptic enhancement of cochlear input.

The model predicts specific conditions under which each condition develops.

Abstract

Tinnitus and hyperacusis can occur together or in isolation, with hyperacusis being associated with tinnitus much more frequently than vice versa. This striking correlation between tinnitus and hyperacusis prevalence implicates that there might be a common origin such as a (hidden) hearing loss and possibly interrelated neural mechanisms of pathological development of those two conditions. In this theoretical paper, we propose such interrelated pathological mechanisms, localized in the dorsal cochlear nucleus (DCN) of the brainstem, that are based on classical mechanisms of Hebbian and associative plasticity known from classical conditioning. Specifically, our model proposes that hyperacusis results from synaptic enhancement of cochlear input to the DCN, whereas chronic tinnitus results from synaptic enhancement of somatosensory input to the DCN. Specific conditions leading to one or the other condition are discussed. Our model predicts, that hearing loss leads to chronic tinnitus, while noise exposure (which may also cause hearing loss) leads to hyperacusis.