Test–retest reliability of Wave I amplitude and latency was assessed in 30 healthy adults (18–25 years, 19 women) with normal hearing and speech-in-noise performance, along with potential sources of variability (head size, cardiorespiratory parameters, tester effects)
We repurpose the click-evoked otoacoustic emissions paradigm to monitor the brainstem reflexes and aid in the differential diagnosis of auditory neuropathy.
Misophonia demonstrated steeper N1–P2 slopes alongside shallower categorical loudness scaling compared to controls.
This study demonstrates that individuals with misophonia exhibit altered auditory cortical processing.
In the same animals, single-unit recordings from IC neurons revealed that old mice show degraded tone detection in noise, with fewer units responding selectively to the embedded tone, a shift toward more sustained response types, and heterogeneous spiking responses to tone-in-noise stimuli compared to young animals.
Statistical learning may be the mechanism that improves listening in quiet during a cortical speech tracking experiment.
Individuals with misophonia show significantly shorter MLR latencies but no amplitude differences compared to controls, pointing to enhanced thalamocortical neural transmission as a neurophysiological correlate of misophonia.
Multi-response deconvolution preserves pABR estimation quality under increasing response overlap, whereas conventional averaging reduces SNR but has minimal practical impact on ABR morphology.
Quantitative facial videography and physiological tracking reveal that misophonia triggers produce distinct, measurable signatures.
Alignment of measured DPOAE growth functions with simulated level maps enables quantitative inference of cochlear amplifier gain and reveals pronounced gain-dependent changes in DPOAE responses.
Individuals with misophonia demonstrated a significantly delayed FFR offset peak, suggesting abnormal subcortical auditory encoding that may underlie their heightened sensitivity to trigger sounds.