Background/Objectives: 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 implies that there might be a common origin, such as (hidden) hearing loss, and possibly interrelated neural mechanisms in the pathological development of those two conditions. Here, we propose such interrelated pathological mechanisms. Methods: This is a theoretical work based solely on considerations and published data. Results: We propose a model localized in the dorsal cochlear nucleus (DCN) of the brainstem, based on classical mechanisms of Hebbian and associative plasticity known from classical conditioning. Specifically, our model proposes that hyperacusis results from the synaptic enhancement of cochlear input to the DCN, whereas chronic tinnitus results from the synaptic enhancement of somatosensory input to the DCN. Specific conditions leading to one or the other condition are discussed. Conclusions: Our model predicts that hearing loss leads to chronic tinnitus, while noise exposure (which may also cause hearing loss) leads to hyperacusis. We would like to emphasize that our aim with the proposed model is not to provide a self-contained theoretical construct, but to stimulate thought regarding possible pathological causes of tinnitus and hyperacusis that have not yet been investigated. Individual assumptions that cannot yet be substantiated by the existing literature are intended to provide impetus for future experimental studies.
Schulze et al. (2026) studied this question.