On the pathophysiology of tinnitus; a review and a peripheral model.

In this paper I investigate the consequences of the assumption that tinnitus is the result of correlated neural activity in auditory nerve fibers under 'no sound' conditions. Two possible pathological conditions capable of causing this correlation are ephaptic excitation of one nerve fiber by neighboring nerve fibers and synchronization of the various synapses in individual hair cells. The first condition is likely to be found in cases suffering from acoustic neuroma where the myelin sheath of the auditory neurons is damaged. The second condition is attributed to a spontaneous excess influx of K+ or Ca2(+)-ions into the hair cell resulting in transient hair cell depolarizations causing synchronous transmitter release at all hair cell synapses. This condition is postulated in noise trauma and ototoxic drug damage of the inner hair cell membrane. The model produces the excess of short interspike intervals found in auditory nerve fiber recordings in animal models of tinnitus as well as the theoretically required correlation in the activity of neighboring neurons.