The Mechanisms Underlying Tinnitus and Hyperacusis: A Comprehensive Overview

Tinnitus and hyperacusis: central noise, gain and variance

Tinnitus is a phantom auditory sensation in the absence of external sounds, while hyperacusis is an atypical sensitivity to external sounds that leads them to be perceived as abnormally loud or even painful. Both conditions may reflect the brain's overcompensation for reduced input from the ear. The present work differentiates between two compensation models: The additive central noise compensates for hearing loss and is likely to generate tinnitus, whereas the multiplicative central gain compensates for hidden hearing loss and is likely to generate hyperacusis. Importantly, both models predict increased variance in central representations of sounds, especially a nonlinear increase in variance by the central gain. The increased central variance limits the amount of central compensation and reduces temporal synchrony, which can explain the insufficient central gain reported in the literature. Future studies need to collect trial-by-trial firing variance data so that the present variance-based model can be falsified.
 

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Tinnitus and hyperacusis: central noise, gain and variance

Tinnitus is a phantom auditory sensation in the absence of external sounds, while hyperacusis is an atypical sensitivity to external sounds that leads them to be perceived as abnormally loud or even painful. Both conditions may reflect the brain's overcompensation for reduced input from the ear. The present work differentiates between two compensation models: The additive central noise compensates for hearing loss and is likely to generate tinnitus, whereas the multiplicative central gain compensates for hidden hearing loss and is likely to generate hyperacusis. Importantly, both models predict increased variance in central representations of sounds, especially a nonlinear increase in variance by the central gain. The increased central variance limits the amount of central compensation and reduces temporal synchrony, which can explain the insufficient central gain reported in the literature. Future studies need to collect trial-by-trial firing variance data so that the present variance-based model can be falsified.
This is an interesting article. I have not seen it discussed much. Conclusion from it:
Conclusion said:
There are two potential mechanisms allowing the central system to compensate for reduced peripheral input: Increasing central noise or increasing central gain. An inevitable consequence of both mechanisms is an increase in central variance, which can help explain both tinnitus and hyperacusis. An additive central noise, which compensates for elevated hearing thresholds like those seen in traditional hearing loss, is more likely to induce tinnitus than hyperacusis. In contrast, an increase in multiplicative central gain, which compensates for hidden hearing loss, is more likely to induce hyperacusis. The effects of compensatory mechanisms on central variance have been ignored in previous studies, but may account for the conflicting results in the generation and behavior of tinnitus and hyperacusis.
In other words:
  • hair cell damage -> tinnitus,
  • synaptopathy -> hyperacusis?
Sucks to have both. I still don't get how hyperacusis can heal. Nerve healing? So like nerves get healed, it does not fix the hearing loss, but somehow reduces/cures hyperacusis. @Jupiterman may find this interesting.
 
This is an interesting article. I have not seen it discussed much. Conclusion from it:

In other words:
  • hair cell damage -> tinnitus,
  • synaptopathy -> hyperacusis?
Sucks to have both. I still don't get how hyperacusis can heal. Nerve healing? So like nerves get healed, it does not fix the hearing loss, but somehow reduces/cures hyperacusis. @Jupiterman may find this interesting.
Yeah, I don't think the problem is hearing loss (some of us with noxacusis don't even have noticeable hearing loss), it's definitely something wired into us specifically that changes our bodies' reaction to sounds.
 

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