It's a great question. We know that cochlear damage is almost always the initiator of tinnitus. We also know that a compensatory plasticity process in the brain that has run amok is almost certain the direct cause of tinnitus. But you are wise to question the gray area in between. Does the haywire plasticity process that generates the phantom tinnitus percept depend on the ongoing abnormal input from the ear or, once initiated, is it sustained independent of the ear? A) we don't really know for sure. B) Alas, the answer is almost certainly both. C) we researchers should really figure that out ASAP.
Most research findings suggest the following scenario: when the input coming through the auditory nerve suddenly drops, neurons in the auditory brainstem (e.g., the dorsal cochlear nucleus) detect the loss of input as a drop in intracellular calcium. This drop initiates a sequence of HOMEOstatatic changes that allow those brainstem neurons to become more sensitive to whatever input remains. The excitability of neurons at these earliest stages of auditory processing is so tightly linked to input from the cochlear nerve that if the damage is severe enough they may never ever be able to recover to their set point of intracellular calcium. They keep turning their amplifiers up and up and up but there just isn't enough drive from the cochlear nerve that would allow them to fully recover to their set point. In that sense, yes, the central pathology is sustained by the abnormal input from the ear.
The situation is different at higher stages of central auditory processing (e.g., the auditory cortex), where the activity of neurons more directly sculpts our perception of sound (both real or imagined). The loss of input from the ear initiates the same homeostatic processes, but these neurons receive a far greater set of inputs than do neurons at the earliest stages of processing. Unlike the brainstem centers, which are more 'hardwired' it is possible to supplant the missing input from the damaged region of the cochlea with other viable inputs through HEBBIAN plasticity mechanisms. This is what companies like MicroTransponder are trying to do with their vagus nerve trial. In effect, we should be able to reprogram the activity set point of higher auditory neurons and effectively turn off the cellular "distress signal" that causes the tinnitus sound. Even when the input from the ear remains abnormal. At least that is the hope.
I see. I believe this is also the research Susan Shore is involved in, if I'm not wrong. I read a few studies about the hyper-excited neurons reacting to other senses (like touch) because of the lack of auditory input. I did notice that gently pressing the intraorbital foramen on the left side (the area just below the eye) causes a tone-like percept in the left ear (the affected ear for me). Might this be an explanation for this phenomena?
I wonder; what are those "other viable inputs" you mention to compensate for the lost auditory input? And if the day comes auditory input can be restored due to inner-ear hair cell regeneration or restoring synaptic function by providing the ear with e.g. neurotrophins, are we able to re-route these inputs to the auditory ones? I suppose the answer will be "yes", seeing this part of the brain is considered plastic, but I wonder if there will be any difficulty in this and hence, any argument against taking a treatment like the one developed by MicroTransponder.
Thank you for your informative replies. It is much appreciated.