Munich Neuroscience Calendar

Event:

28.01.2019, 18:00 Graduate School of Neuroscience

Event Type: Talk
Speaker: Prof. Dr. Sarah Verhulst
Institute: Hearing Technology, Ghent University, Belgium

Title: Supra-threshold psychoacoustics and envelope-following response relations: Normal-hearing, synaptopathy and cochlear gain loss

Location:
B01.019
GroƟhaderner Str. 2
82152 Martinsried

Host: Miguel Obando Leiton
Host Email: miguel.obando@tum.de
Abstract:
The perceptual consequences of cochlear synaptopathy are presently not well understood as a direct quantification of synaptopathy is not possible in humans. To circumvent this problem and to study its role for human hearing, recent studies have correlated individual differences in subcortical EEG responses, as a proxy measure for synaptopathy, to changes in basic supra-threshold psychoacoustic tasks. However, it is not clear whether the reported missing relationships between EEG and psychoacoustic quantities are due to the adopted methods, or to a minor role of synaptopathy for sound perception.

To address this issue, we investigated the theoretical relationship between subcortical EEG and psychoacoustic methods for different sensorineural hearing deficits. We use a computational model of the human auditory periphery calibrated for auditory brainstem (ABR) and envelope following responses (EFRs) and simulate how different sensorineural hearing deficits impact EFRs and psychoacoustic cues important for amplitude-modulation (AM) and tone-in-noise (TiN) detection. Simulated synaptopathy can reduce EFR magnitudes and detection task performance by up to 15 dB, corroborating expectations from animal studies of synaptopathy. OHC loss was seen to impact the EFRs and psychoacoustic tasks to a much smaller degree, as these measures mostly rely on robust encoding of supra-threshold envelope cues. In fact, OHC deficits had a negligible role when OHC deficits and synaptopathy co-occurred. Our simulations show that individual differences in the considered metrics are explained by individual differences in the synaptopathy degree, irrespective of whether OHC deficits were also present. This finding is further supported by synaptopathy driving the regression between the EFR magnitude and AM/TiN detection thresholds across models with mixtures of OHC loss and synaptopathy.


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