SLPOtherEar and hearing2022

AudioChip: A Deep Phenotyping Approach for Deconstructing and Quantifying Audiological Phenotypes of Self-Reported Speech Perception Difficulties.

Ishan Sunilkumar Bhatt, Raquel Dias, Nathan Wineinger and 6 others

PMID 34860719

WHAT IT FOUND

Normal-hearing young adults with speech-in-noise complaints showed varied physiological profiles.

Brainstem response timing and amplitude correlated with self-reported difficulty, but noise exposure history did not predict these neural measures in this small, female-only sample.

Key findings

01Self-reported hearing difficulty scores were significantly associated with specific auditory brainstem response measures, including wave I amplitude and complex ABR offset latency.

02The study found no statistically significant association between estimated noise exposure background and ABR Wave I amplitude, a common proxy for cochlear synaptopathy.

03Participants with high versus low self-reported difficulty scores differed significantly in extended high-frequency hearing thresholds at 16 kHz in the right ear.

STILL TO COME

How it was doneWhat they foundWhat it means for SLPs

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What it does not show

The sample consisted only of young women, so results cannot be generalized to men or older adults. The study was cross-sectional, providing only a snapshot of hearing status rather than tracking changes over time. The sample size was small (70 participants), limiting the power of the statistical models. The proposed 'AudioChipping' method is not yet validated for clinical use and remains a research framework. The lack of association between noise exposure and brainstem measures contradicts some previous animal and human studies, possibly due to the low noise exposure levels in this specific cohort.

Declared interests

The authors declare no conflicts of interest. The study was approved by the Institutional Review Board of Northern Arizona University.

The easy way to misread this

Do not interpret the lack of association between noise exposure and Wave I amplitude as evidence that noise-induced cochlear synaptopathy does not exist in humans. This null finding occurred in a small, low-noise-exposure group of young women and may reflect the limitations of the proxy measures or the sample characteristics rather than a true absence of the effect.

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