Abstract
Identifying the multiple contributors to the audiometric loss of a hearing impaired (HI) listener at a particular frequency is becoming gradually more useful as new treatments are developed. Here, we infer the contribution of inner (IHC) and outer hair cell (OHC) dysfunction to the total audiometric loss in a sample of 68 hearing aid candidates with mild-to-severe sensorineural hearing loss, and for test frequencies of 0.5, 1, 2, 4, and 6 kHz. It was assumed that the audiometric loss (HLTOTAL) at each test frequency was due to a combination of cochlear gain loss, or OHC dysfunction (HLOHC), and inefficient IHC processes (HLIHC), all of them in decibels. HLOHC and HLIHC were estimated from cochlear I/O curves inferred psychoacoustically using the temporal masking curve (TMC) method. 325 I/O curves were measured and 59% of them showed a compression threshold (CT). The analysis of these I/O curves suggests that (1) HLOHC and HLIHC account on average for 60–70 and 30–40% of HLTOTAL, respectively; (2) these percentages are roughly constant across frequencies; (3) across-listener variability is large; (4) residual cochlear gain is negatively correlated with hearing loss while residual compression is not correlated with hearing loss. Altogether, the present results support the conclusions from earlier studies and extend them to a wider range of test frequencies and hearing-loss ranges. Twenty-four percent of I/O curves were linear and suggested total cochlear gain loss. The number of linear I/O curves increased gradually with increasing frequency. The remaining 17% I/O curves suggested audiometric losses due mostly to IHC dysfunction and were more frequent at low (≤1 kHz) than at high frequencies. It is argued that in a majority of listeners, hearing loss is due to a common mechanism that concomitantly alters IHC and OHC function and that IHC processes may be more labile in the apex than in the base.
Highlights
Cochlear hearing loss occurs when absolute hearing thresholds for pure tones are higher than normal without signs of middleear or auditory neural pathology (Moore, 2007)
Some authors have assumed that the audiometric loss (HLTOTAL) for a given test frequency may be conveniently expressed as the sum of two contributions: one associated with cochlear mechanical gain loss, or outer hair cell (OHC) dysfunction (HLOHC), and one associated with inefficient inner hair cells (IHCs) transduction, or IHC dysfunction (HLIHC), where HLTOTAL, HLIHC and HLOHC are all in decibels (Moore and Glasberg, 1997; Plack et al, 2004; Moore, 2007; Jepsen and Dau, 2011; Lopez-Poveda and Johannesen, 2012)
With regard to the contribution of IHC and OHC dysfunction to the audiometric loss, the main conclusions are: 1. For cases where a compression threshold (CT) is present, IHC and OHC dysfunction contribute on average to 30–40 and 60–70% to the total audiometric loss, and these contributions are approximately constant across the frequency range from 0.5 to 6 kHz
Summary
Cochlear hearing loss occurs when absolute hearing thresholds for pure tones are higher than normal without signs of middleear or auditory neural pathology (Moore, 2007). Inner hair cells (IHCs) transduce mechanical basilar membrane (BM) vibrations into nerve signals, while outer hair cells (OHCs) amplify BM responses to low-level sounds and are responsible for our high auditory sensitivity (Bacon et al, 2004). A reduction in the number of OHCs or lesions to the OHCs or associated structures can reduce the cochlear gain to low level sounds and cause an audiometric loss. A reduction in IHC count or lesions to the IHCs or their associated structures can increase the BM excitation required for detecting a signal, which may cause an audiometric loss (Moore, 2007). The aim of the present study was to assess HLOHC and HLIHC over the frequency range from 500 Hz to 6 kHz in a large sample of listeners with mild-to-severe sensorineural hearing loss
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
