Tinnitus is the perception of sound in the absence of an external sound source and, in most cases, occurs with a hearing loss. Clinically, there are many tinnitus symptoms, and because of its subjective nature, it is not well understood.
This page covers tinnitus generation linked to cochlear pathology, which could account for a number of tinnitus types - notably after noise trauma, or linked to presbycusis.
Note that saying that tinnitus has a cochlear origin does not take into account its evolution over time: it is possible that it can 'centralise' and still remain after the cochlea has been destroyed or the cochlear nerve has been sectioned! In this way, it is similar to chronic phantom pain.
Finally, there is a completely different tinnitus category caused by the perception of internal sounds.
Tinnitus and cochlear synapses
Two main cochlear pathologies could be at the origin of tinnitus: malfunction of the glutamatergic synapse between the inner hair cell and the auditory nerve, and the disruption of the outer hair cells' active mechanisms.
Research (such as that by Puel et al. in Montpellier) is providing more and more findings to support the first of these hypotheses, relating tinnitus to an 'epileptic' reaction in the auditory nerve.
It could be that an imbalance in the glutamateric synapse between the inner hair cells and the auditory nerve is caused by excitotoxic shock (ischema and/or acoustic trauma). Overexpression of NMDA receptors in the spiral ganglion neurons after excitotoxiticy leads to an increase in the spontaneous activity in certain nerve fibers, which is, in turn, interpreted in the central auditory system as a sound.
In experimental animals, it is possible to block the abnormal activity in the auditory nerve with an NMDA antagonist. In this way, tinnitus can be stopped as it starts! Pharmacological treatment of tinnitus, notably after acoustic trauma, could therefore be developed in the future based on the trans-tympanic application of active molecules.
Tinnitus and outer hair cells?
Spontaneous activation of the outer hair cells (OHCs), producing active mechanisms without acoustic stimulation, could be followed by physiological effects: i.e. the activation of the inner hair cells and auditory nerve fibers. The signal that would be be sent in this case would be as 'real' as a natural sound, and the subject would hear a whistling noise with a frequency corresponding to the frequency range of the damaged OHCs.
Some researchers have suggested a role for the efferent system in the generation of spontaneous OHC activation, and therefore tinnitus. However, it is rare that such activation can be characterised as spontaneous otoacoustic emissions corresponding to the frequency of the subject's tinnitus...
Note that imbalance in the cochlear glutamatergic synapses can also give rise to similar imbalance along the primary auditory pathway which uses this neurotransmitter: in this case, central tinnitus generator is possible. This may explain, for example, the fact that, in some cases, tinnitus remains after the auditory nerve has been sectioned.
A variant of the synaptic hypothesis implicates GABA: this neurotransmitter inhibits the activity of central glutamatergic synapses, but may be unable to moderate this activity in the case of abnormal glutamatergic synapses.
Internal noise transmitted to the ear
Also known as objective tinnitus, this type of tinnitus is caused by sounds generated by the body and perceived by the patient. Objective tinnitus is generally perceived as characteristic pulsatile sounds that are synchronous to the person's heart beat, sound like the ticking of a watch, or a crackling sound. Rarely, objective tinnitus can be perceived as a whistling sound.
The most common causes of objective tinnitus are: vascular abnormalities close to the inner ear; abnormally rhythmic muscle contractions (myoclonus); or abnormalities associated with jaw motion.
The cause of most of these types of objective tinnitus can be accurately diagnosed, and, for many cases, there is an appropriate therapy.