Relations between cochlear synaptopathy and auditory deficits in humans with normal audiograms

UoM administered thesis: Phd

Abstract

In animals, noise exposure can destroy synapses between inner hair cells and auditory nerve fibres, without widespread loss of hair cells. This 'cochlear synaptopathy' does not permanently elevate cochlear thresholds, but does permanently reduce brainstem-response amplitudes at medium-to-high stimulus levels. If this pathophysiology manifests in humans, it might constitute a 'hidden' hearing loss, leading to auditory deficits despite normal audiometric thresholds. We recruited a cohort of adults with tinnitus and normal audiograms, and compared them with controls matched for age, sex, and audiometric thresholds. We also conducted a parallel study in adults with impaired speech perception in noise (SPiN) and normal audiograms. Measures of synaptopathy in both studies were the auditory brainstem response (ABR) and envelope-following response (EFR). Lifetime noise exposure was estimated using a detailed structured interview, which has since been developed into an instrument for use by other researchers. Neither study revealed any association of auditory deficits with measures of synaptopathy, although tinnitus was associated with greater lifetime noise exposure. Finally, we conducted a study assessing the reliability and interrelations of seven proxy measures of synaptopathy. Raw amplitude and threshold measures were highly reliable, but likely reflect myriad factors besides synaptopathy. Differential ABR and EFR measures were unreliable, and purported measures of synaptopathy did not correlate. Taken together, the results of the project provide no evidence that cochlear synaptopathy is a significant aetiology of tinnitus or impaired SPiN in humans with normal audiograms. However, in light of the uncertain validity of measures of synaptopathy, absence of evidence cannot be taken as evidence of absence.

Details

Original languageEnglish
Awarding Institution
Supervisors/Advisors
Award date31 Dec 2018

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