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Abnormal Auditory Gain in Hyperacusis: Investigation with a Computational Model.

Diehl PU, Schaette R - Front Neurol (2015)

Bottom Line: Assuming that perceived loudness is proportional to the summed activity of all auditory nerve (AN) fibers, the model was tuned to reproduce normal loudness perception.Good fits to the average patient LDLs were obtained for a general increase in gain that affected all frequency channels to the same degree, and also for a frequency-specific gain increase in the high-frequency range.Moreover, the gain needed to be applied after subtraction of spontaneous activity of the AN, which is in contrast to current theories of tinnitus generation based on amplification of spontaneous activity.

View Article: PubMed Central - PubMed

Affiliation: Bernstein Center for Computational Neuroscience , Berlin , Germany.

ABSTRACT
Hyperacusis is a frequent auditory disorder that is characterized by abnormal loudness perception where sounds of relatively normal volume are perceived as too loud or even painfully loud. As hyperacusis patients show decreased loudness discomfort levels (LDLs) and steeper loudness growth functions, it has been hypothesized that hyperacusis might be caused by an increase in neuronal response gain in the auditory system. Moreover, since about 85% of hyperacusis patients also experience tinnitus, the conditions might be caused by a common mechanism. However, the mechanisms that give rise to hyperacusis have remained unclear. Here, we have used a computational model of the auditory system to investigate candidate mechanisms for hyperacusis. Assuming that perceived loudness is proportional to the summed activity of all auditory nerve (AN) fibers, the model was tuned to reproduce normal loudness perception. We then evaluated a variety of potential hyperacusis gain mechanisms by determining their effects on model equal-loudness contours and comparing the results to the LDLs of hyperacusis patients with normal hearing thresholds. Hyperacusis was best accounted for by an increase in non-linear gain in the central auditory system. Good fits to the average patient LDLs were obtained for a general increase in gain that affected all frequency channels to the same degree, and also for a frequency-specific gain increase in the high-frequency range. Moreover, the gain needed to be applied after subtraction of spontaneous activity of the AN, which is in contrast to current theories of tinnitus generation based on amplification of spontaneous activity. Hyperacusis and tinnitus might therefore be caused by different changes in neuronal processing in the central auditory system.

No MeSH data available.


Related in: MedlinePlus

Hearing thresholds (dashed lines) and loudness discomfort levels (LDLs, solid lines) of normal-hearing control subjects (green) and hyperacusis patients (red). Hyperacusis patient data are from a subgroup of patients with clinically normal HTs, the complete patient data set is presented in Sheldrake et al. (4).
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Figure 1: Hearing thresholds (dashed lines) and loudness discomfort levels (LDLs, solid lines) of normal-hearing control subjects (green) and hyperacusis patients (red). Hyperacusis patient data are from a subgroup of patients with clinically normal HTs, the complete patient data set is presented in Sheldrake et al. (4).

Mentions: The mean audiograms and loudness discomfort levels of the hyperacusis and the control group are shown in Figure 1.


Abnormal Auditory Gain in Hyperacusis: Investigation with a Computational Model.

Diehl PU, Schaette R - Front Neurol (2015)

Hearing thresholds (dashed lines) and loudness discomfort levels (LDLs, solid lines) of normal-hearing control subjects (green) and hyperacusis patients (red). Hyperacusis patient data are from a subgroup of patients with clinically normal HTs, the complete patient data set is presented in Sheldrake et al. (4).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4502361&req=5

Figure 1: Hearing thresholds (dashed lines) and loudness discomfort levels (LDLs, solid lines) of normal-hearing control subjects (green) and hyperacusis patients (red). Hyperacusis patient data are from a subgroup of patients with clinically normal HTs, the complete patient data set is presented in Sheldrake et al. (4).
Mentions: The mean audiograms and loudness discomfort levels of the hyperacusis and the control group are shown in Figure 1.

Bottom Line: Assuming that perceived loudness is proportional to the summed activity of all auditory nerve (AN) fibers, the model was tuned to reproduce normal loudness perception.Good fits to the average patient LDLs were obtained for a general increase in gain that affected all frequency channels to the same degree, and also for a frequency-specific gain increase in the high-frequency range.Moreover, the gain needed to be applied after subtraction of spontaneous activity of the AN, which is in contrast to current theories of tinnitus generation based on amplification of spontaneous activity.

View Article: PubMed Central - PubMed

Affiliation: Bernstein Center for Computational Neuroscience , Berlin , Germany.

ABSTRACT
Hyperacusis is a frequent auditory disorder that is characterized by abnormal loudness perception where sounds of relatively normal volume are perceived as too loud or even painfully loud. As hyperacusis patients show decreased loudness discomfort levels (LDLs) and steeper loudness growth functions, it has been hypothesized that hyperacusis might be caused by an increase in neuronal response gain in the auditory system. Moreover, since about 85% of hyperacusis patients also experience tinnitus, the conditions might be caused by a common mechanism. However, the mechanisms that give rise to hyperacusis have remained unclear. Here, we have used a computational model of the auditory system to investigate candidate mechanisms for hyperacusis. Assuming that perceived loudness is proportional to the summed activity of all auditory nerve (AN) fibers, the model was tuned to reproduce normal loudness perception. We then evaluated a variety of potential hyperacusis gain mechanisms by determining their effects on model equal-loudness contours and comparing the results to the LDLs of hyperacusis patients with normal hearing thresholds. Hyperacusis was best accounted for by an increase in non-linear gain in the central auditory system. Good fits to the average patient LDLs were obtained for a general increase in gain that affected all frequency channels to the same degree, and also for a frequency-specific gain increase in the high-frequency range. Moreover, the gain needed to be applied after subtraction of spontaneous activity of the AN, which is in contrast to current theories of tinnitus generation based on amplification of spontaneous activity. Hyperacusis and tinnitus might therefore be caused by different changes in neuronal processing in the central auditory system.

No MeSH data available.


Related in: MedlinePlus