Molecular Mechanism of Tinnitus

Abstract

Tinnitus (phantom noise) is predicted to occur due to a broad variety of etiologies and pathogeneses (Eggermont, 2007; Jastreboff, 2007). In a current common view, tinnitus is primarily linked to damage in the periphery of the auditory system, probably even in cases in which an impairment cannot be assessed by clinical routine audiometry (Shiomi et al., 1997; Lockwood et al., 2002; Saunders, 2007). From animal studies, it is hypothesized that an increased spontaneous discharge rate in subcortical auditory neurons and increased neural synchrony and hyperactivity in the auditory cortex (AC) are correlates of tinnitus (Bauer, 2004; Kaltenbach, 2010; Roberts et al., 2010). The subcortical hyperactivity is currently interpreted as a consequence of the loss of the stimulus-driven activity that triggers centrally compensating synaptic adjustments (Schaette & Kempter, 2009).