Update: I have received a reply from Paul Fuchs! I thought it would be appropriate to post the reply I received here since it pertains more to Retigabine. He replied really promptly and gave quite a lengthy response - he's also taken note of Retigabine as a potential therapy. Also great to hear that there is an ongoing doctoral thesis on this.
"Thanks for your note, but most sorry to know you are among those suffering from these paradoxical ear pathologies. I'm not a physician so please take what follows as informational only, not prescriptive.
As I'm sure you're aware from your research, tinnitus and hyperacusis both follow some degree of peripheral damage. Tinnitus is complicated by central nervous system changes, but hyperacusis in particular seems more akin to peripheral somatic neuropathies. We have been struck by the potential of potassium channel openers to diminish the excitability of type 2 cochlear afferents, putative damage sensors, and have been told about retigabine use by by some. Our work to date has only involved cochlear tissue excised from rats or mice. Our next steps are to employ genetically-modified mice in which type 2 cochlear afferents can be selectively modulated by systemic drug delivery. We need this experimental model to determine whether type 2 cochlear afferents really act as nociceptors. So for example, we would 'chemogenetically' activate type 2 cochlear afferents to evoke avoidance behavior, then treat with retigabine or other drugs to see if effective. Other avenues include the use of magnetic nanoparticles for drug delivery specifically to the inner ear (avoiding systemic effects).
So in short, yes, we will continue our efforts to develop informative animal models in which to test hypotheses of disease, and potential therapies. We've spent some years now pursuing the idea that type 2 cochlear afferents are nociceptors responsible for 'noxacusis', painful hyperacusis. We speculate that these neurons and/or the surrounding tissue, become hyperexcitable after peripheral trauma (ongoing doctoral thesis of Nate Nowak), by analogy to the hyperalgesia of somatosensory afferents. Postdoctoral fellow Dr. Megan Wood is exploring the impact of cochlear inflammation and type 2 activity as additional factors in the prolonged pain response to sound."