Tinnitus compensation: a proposed 'noise cancellation' model in tinnitus. Initially, a tinnitus signal results from peripheral deafferentiation (loss of hair cells from injury, age, noise exposure) and subsequent lesion‐induced reorganisation of central auditory structures. The nucleus accumbens and the associated paralimbic networks in the prefrontal cortex play an important role in long‐term habituation to continuous unpleasant sounds. As long as the NAc‐system is intact (A: "Compensated tinnitus"), the tinnitus signal is filtered out and will not be relayed to the auditory cortex. If the NAc‐system becomes compromised (B: Tinnitus), cancellation of the tinnitus signal at the thalamic level is no longer possible, long‐term reorganisation of auditory cortex sets in and tinnitus perception becomes potentially chronic. Structures with serotoninergic innervation are shown by hatching; inhibitory structures are shown in red: yellow indicates presence of tinnitus signal. NAc = nucleus accumbens; vmPFC = ventromedial prefrontal cortex; MGN = thalamus; TRN = talamic reticular nucleus.

Reprinted from Rauschecker JP, Leaver AN, Muhlau M. Turning out the noise: limbic‐auditory interactions in tinnitus. Neuron 2010;66:819‐25, with permission from Elsevier (Rauschecker 2010).

The Prevalence of Tinnitus (Panel A) and Hearing Impairment (Panel B). From: Lockwood AH, Salvi RJ, Burkard RF. Tinnitus. New England Journal of Medicine 2002; 347(12):904‐10. Values are based on responses to the question "Do you have tinnitus (or) ringing in the ears or deafness (or) other trouble hearing?" Included in the National Center for Health Statistics Survey of noninstitutionalized Americans, 1999.

Study flow diagram: detail of literature review for the 2012 update.

Comparison 1 Trazodone versus placebo, Outcome 1 Tinnitus intensity.

Comparison 1 Trazodone versus placebo, Outcome 2 Tinnitus discomfort.