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

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.