An active loudness model suggesting tinnitus as increased central noise and hyperacusis as increased nonlinear gain.
The present study uses a systems engineering approach to delineate the relationship between tinnitus and hyperacusis as a result of either hearing loss in the ear or an imbalanced state in the brain. Specifically examined is the input-output function, or loudness growth as a function of intensity in both normal and pathological conditions. Tinnitus reduces the output dynamic range by raising the floor, while hyperacusis reduces the input dynamic range by lowering the ceiling or sound tolerance level. Tinnitus does not necessarily steepen the loudness growth function but hyperacusis always does. An active loudness model that consists of an expansion stage following a compression stage can account for these key properties in tinnitus and hyperacusis loudness functions. The active loudness model suggests that tinnitus is a result of increased central noise, while hyperacusis is due to increased nonlinear gain. The active loudness model also generates specific predictions on loudness growth in tinnitus, hyperacusis, hearing loss or any combinations of the three conditions. These predictions need to be verified by experimental data and have explicit implications for treatment of tinnitus and hyperacusis.
Department of Anatomy and Neurobiology, University of California, Irvine, CA 92697-5320, USA. fzeng@uci.edu
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D000818:Animals; D001309:Auditory Threshold / Q000502:physiology; D001698:Biomedical Engineering; D034381:Hearing Loss / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D012001:Hyperacusis / Q000209:etiology* / Q000503:physiopathology*; D008144:Loudness Perception / Q000502:physiology*; D008954:Models, Biological; D009622:Noise; D017711:Nonlinear Dynamics; D049490:Systems Biology; D014012:Tinnitus / Q000209:etiology* / Q000503:physiopathology* / Q000628:therapy