Purpose:
Human studies of noise-induced cochlear synaptopathy using physiological indicators identified in animal models (auditory brainstem response [ABR] Wave I amplitude, envelope following response [EFR], and middle ear muscle reflex [MEMR]) have yielded mixed findings. Differences in the population studied may have contributed to the differing results. For example, due to differences in the intensity level of the noise exposure, noise-induced synaptopathy may be easier to detect in a military Veteran population than in populations with recreational noise exposure. We previously demonstrated a reduction in ABR Wave I amplitude and EFR magnitude for young Veterans with normal audiograms reporting high levels of noise exposure compared to non-Veteran controls. In this article, we expand on the previous analysis in the same population to determine if MEMR magnitude is similarly reduced.
Method:
Contralateral MEMR growth functions were obtained in 92 young Veterans and non-Veterans with normal audiograms, and the relationship between noise exposure history and MEMR magnitude was assessed. Associations between MEMR magnitude and distortion product otoacoustic emission, EFR, and ABR measurements collected in the same sample were also evaluated.
Results:
The results of the statistical analysis, although not conventionally statistically significant, suggest a reduction in mean MEMR magnitude for Veterans reporting high noise exposure compared with non-Veteran controls. In addition, the MEMR appears relatively insensitive to subclinical outer hair cell dysfunction, as measured by distortion product otoacoustic emissions, and is not well correlated with ABR and EFR measurements.
Conclusions:
When combined with our previous ABR and EFR findings in the same population, these results suggest that noise-induced synaptopathy occurs in humans. In addition, the findings indicate that the MEMR may be a good candidate for noninvasive diagnosis of cochlear synaptopathy/deafferentation and that the MEMR may reflect the integrity of different neural populations than the ABR and EFR.
Supplemental Material:
https://doi.org/10.23641/asha.18665645