The Onset-Offset N1-P2 Cortical Auditory Evoked Response in Individuals With High-Frequency Sensorineural Hearing Loss: Responses to High- and Low-Frequency Narrowband Noise.

Purpose: This study aimed to determine whether onset-offset N1-P2 auditory evoked responses differ in amplitude, latency, and offset-to-onset trough-to-peak N1-P2 amplitude ratios (OOAR) between normal hearing (NH) sensitivity and moderate high-frequency sensorineural hearing loss (HFSNHL) groups when stimuli target regions of peripheral hearing sensitivity where the groups are in the normal range (i.e., 500 Hz) versus where they differ regarding presence of hearing loss (i.e., 4000 Hz).

Method: Onset-offset N1-P2 auditory evoked responses were measured from 10 participants with normal hearing sensitivity and seven participants with moderate HFSNHL using 500-Hz and 4000-Hz narrowband noise (NBN) stimuli. Stimuli were 2000 ms with 40-ms rise-fall times presented at 50 dB SL referenced to stimulus behavioral thresholds. Amplitudes and latencies were analyzed for N1 and P2 onset and offset components via repeated measures analysis of variance (ANOVA). OOARs were compared between groups using one-way ANOVA and across stimuli per group using paired samples tests.

Results: Despite dB SPL stimulus presentation differences between groups, there were no significant differences in individual/absolute amplitude and latency waveform components between groups for either stimulus. Derived comparative calculations of OOAR for 4000-Hz NBN were significantly larger ( < .025; NH: .39; HFSNHL: .62) for the group with HFSNHL than the group with NH sensitivity; 500-Hz NBN OOAR did not reach significance. OOARs revealed no significant difference between stimuli for the group with normal hearing sensitivity, with .38 OOAR for both stimuli ( = .961). OOAR comparisons for the HFSNHL group across stimuli were significant ( = .012), with the 4000-Hz NBN OOAR being nearly double the size of the 500-Hz NBN OOAR.

Conclusions: OOARs may provide insight to the balance of excitatory and inhibitory neural firing in the central auditory nervous system (CANS). Larger OOARs may be a biomarker of reduced CANS inhibition, perhaps indicative of a homeostatic central auditory gain mechanism.