@Emgee
Just wanted to add that Liberman's research points towards loudness hyperacusis being caused by damage to specific A1 synaptic nerve fibers.
But even if that's the not the case there are a limited number of structures that can be damaged.
OHC, IHC, and A1 fibers are being addressed. The EF-MOC fibers are extremely well protected against noise and idiopathic injury. The EF-LOC system is less studied but from what I can find these synapses are also very difficult to damage. A2 fibers are involved with pain hyperacusis (noxacusis) instead so not really relevant.
I know people are worried because these regen med companies aren't specifically testing for loudness hyperacusis, but imo it doesn't really matter as long as the structure or inflammation is fixed. It has to originate somewhere and current research points to loudness hyperacusis and reactive tinnitus being solved much in the same way as normal tinnitus.
I do think noxacusis folks might have to wait a bit longer, but they're making huge strides with that condition as well.