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. 2013 Jan:295:172-9.
doi: 10.1016/j.heares.2012.05.009. Epub 2012 May 26.

An active loudness model suggesting tinnitus as increased central noise and hyperacusis as increased nonlinear gain

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An active loudness model suggesting tinnitus as increased central noise and hyperacusis as increased nonlinear gain

Fan-Gang Zeng. Hear Res. 2013 Jan.

Abstract

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.

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Figures

Fig. 1
Fig. 1
Loudness growth function in normal hearing (solid diagonal line in panel A) and hearing loss (dashed line in panel D, I0’ denotes the elevated threshold). Loudness function changes with tinnitus (shallower line intercepting the y-axis in panel B) and concomitant hearing loss (panel C). Loudness function changes with hyperacusis (steeper line intercepting the dotted top horizontal line in panel E, Im’ denotes the reduced sound level that reaches the maximal loudness level) and concomitant hearing loss (panel F).
Fig. 2
Fig. 2
A. Passive brain loudness model. The power transformation occurs in the ear, while only linear addition of loudness occurs in the brain. B. Active brain loudness model. The power transformation is achieved by combining a logarithmic function in the ear with an exponential function in the brain. See text for details.
Fig. 3
Fig. 3
An active loudness model incorporating additive noise and gain before (N0 and g) and after (S0 and α) the nonlinear exponentiation process. Both gains can be adjusted by a feedback loop. The output of this active loudness model (La) can be modeled by three parameters, including a linear gain (G), a nonlinear gain (g) and a central noise (L0). See text for details.
Fig. 4
Fig. 4
Normal loudness growth (panel A) and altered loudness growth as a function of central noise (panel B), linear gain (panel C), nonlinear gain (panel D), or a combination of these three factors (bottom panels from E to H). See text for details.
Fig. 5
Fig. 5
Hearing-impaired loudness growth (steeper dashed line in panel A) and altered loudness growth as a function of central noise (panel B), linear gain (panel C), nonlinear gain (panel D), or a combination of these three factors (bottom panels from E to H). See text for details.
Fig. 6
Fig. 6
Peripheral (bottom up) or central (top-down) origin of tinnitus and hyperacusis. The peripheral origin: Hearing loss reduces input, leading to increased nonlinear gain in the form of steepened loudness growth as either loudness recruitment or hyperacusis; the increased gain causes an imbalance state in the brain, which requires increased central noise to restore balance, thus generating tinnitus. The central origin: An imbalanced state in the brain increases the central noise, namely, generating tinnitus. If the tinnitus interferes with sound detection, then the nonlinear gain may be increased, producing hyperacusis; If not, then tinnitus occurs without hyperacusis or hearing loss.

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