PP509 - Brainstem Representation of Rapid Tonal Sweeps Among Marching Band Participants with Normal Hearing

Abstract:
Loud sound exposure is shown to cause cochlear synaptopathy (hidden hearing loss). The studies employed to characterize HHL in humans have yielded confounding results. This project attempted to measure neural encoding of time-varying stimuli (rapid rate of frequency change) among participants of the marching band (high-risk group) and non-marching band (low-risk group). The results indicate that the neural encoding of frequency change was larger for the high-risk group, particularly at the later window for faster rates. This pattern of results suggests the complex interaction of music experience, sound over-exposure, and homeostatic central compensation when comparing low-risk and high-risk groups.

Summary:
Rationale/

Purpose:
Recent animal studies suggest that even moderate noise exposure levels can damage synaptic ribbons between the inner hair cells and auditory nerve fibers without affecting audiometric thresholds, giving rise to the term "hidden hearing loss" (HHL). Given the pervasive exposure to occupational and recreational noise in the general population, it is likely that individuals afflicted with HHL will go unidentified unless sensitive clinical measures are developed to diagnose this condition. The studies employed to characterize HHL in humans have yielded confounding results. This project attempted to measure neural encoding of time-varying stimuli (rapid rate of frequency change) to answer whether loud sound exposure history disrupts precise neural phase-locking needed to encode rapid tonal sweeps.

Hypothesis:
Using a mice model, Shaheen et al. (2015) demonstrated that frequency following responses (FFR) might be a more sensitive marker than the auditory brainstem response (ABR) to detect changes in neural activity associated with noise-induced synaptopathy. Considering this, we hypothesize that the temporal pattern of neural activity reflected in the FFRs in the high-risk group (marching band) may be disrupted for encoding rapid tonal sweeps. Contrarily, there is compelling evidence suggesting music experience (notwithstanding exposure to loud music) dependent enhancement of neural representation of speech and musical stimuli. Given this, we hypothesize that the high-risk group may show an experience-dependent enhancement of neural representation of rapid tonal sweeps. There could also be a complex interaction of many factors (music experience, sound over-exposure, homeostatic central compensation), resulting in a complex pattern of results emerging when comparing low-risk and high-risk groups.

Methods:
We evaluated the FFR elicited by linear frequency-changing stimuli of 150 ms duration. The three rates of frequency change, 1333Hz/sec (slow rate), 2666Hz/sec (medium rate), and 3999 Hz/sec (fast rate) was considered. These rates of change are based on what is found in English formant transitions (Basu et al., 2010; Plyler & Krishnan, 2001). Participants were 22 young normal-hearing individuals who participated in the marching band for at least five years (high-risk group) and 22 non-marching band groups with low noise-exposure history (low-risk group).

Results:
There is a decrement in the amplitude of FFR with an increasing rate. The peak of the spectral slices shifted systematically following the stimulus's frequency shift. The neural encoding of frequency change reflected in the sustained phase-locked FFRs was larger for the high-risk group, particularly at the later window for faster rates.


Conclusions:
The tonal sweeps employed in this study are similar to musical glides associated with dynamic musical notes. Playing music (including marching band) involves accurate perception and fine-tuning one's musical instrument to the ensemble. It is possible that the enhancement we observe here in the high-risk group may reflect a music experience-dependent plasticity. Overall, the pattern of results suggests the complex interaction of many factors (music experience, sound over-exposure, homeostatic central compensation). To better understand the complex nature of sound over-exposure in normal-hearing individuals, larger-scale datasets with different noise exposure backgrounds and longitudinal measurements with an array of behavioral and electrophysiological tests are needed.