Separate auditory pathways for the induction and maintenance of tinnitus and hyperacusis?

Tinnitus and hyperacusis often occur together, however tinnitus may occur without hyperacusis or hyperacusis without tinnitus. Based on animal research one could argue that hyperacusis results from noise exposures that increase central gain in the lemniscal, tonotopically organized, pathways, whereas tinnitus requires increased burst firing and neural synchrony in the extra-lemniscal pathway. However, these substrates are not sufficient and require involvement of the central nervous system. The dominant factors in changing cortical networks in tinnitus patients are foremost the degree and type of hearing loss, and comorbidities such as distress and mood. So far, no definite changes have been established for tinnitus proper, albeit that changes in connectivity between the dorsal attention network and the parahippocampal area, as well as the default-mode network-precuneus decoupling, appear to be strong candidates. I conclude that there is still a strong need for further integrating animal and human research into tinnitus and hyperacusis.