Tinnitus, is the sensation of sound in the absence of an external auditory stimulus (“phantom sound”).
The pathophysiology of different forms of tinnitus varies, but if triggered by an external sound, it is defined as noise-induced tinnitus.
Noise-induced tinnitus is believed to involve glutamate and NMDA receptors in the synapses between the inner hair cells and the spiral ganglion cells.
In the early phase following the acoustic trauma this translates to a state of cochlear overstimulation believed to be perceived the patient as tinnitus.
As times passes, the origin of sound-induced tinnitus undergoes a gradual relocation from the cochlea to the auditory brain, a process termed neural plasticity involving a form of re-programming of the brain.
This has implications for the timing of interventional treatments following noise-induced tinnitus. While the tinnitus is still of peripheral and cochlear origin it may still be amenable to treatment via intratympanic injection of drugs stabilizing the cochlear signaling. This may prevent the permanent plasticity changes occurring in the auditory brain which could translate into chronic tinnitus.