Abstract
Objectives: Young people are often exposed to high music levels which make them more at risk to develop noise-induced symptoms such as hearing loss, hyperacusis, and tinnitus of which the latter is the symptom perceived the most by young adults. Although, subclinical neural damage was demonstrated in animal experiments, the human correlate remains under debate. Controversy exists on the underlying condition of young adults with normal hearing thresholds and noise-induced tinnitus (NIT) due to leisure noise. The present study aimed to assess differences in audiological characteristics between noise-exposed adolescents with and without NIT.Methods: A group of 87 young adults with a history of recreational noise exposure was investigated by use of the following tests: otoscopy, impedance measurements, pure-tone audiometry including high-frequencies, transient and distortion product otoacoustic emissions, speech-in-noise testing with continuous and modulated noise (amplitude-modulated by 15 Hz), auditory brainstem responses (ABR) and questionnaires.Nineteen students reported NIT due to recreational noise exposure, and their measures were compared to the non-tinnitus subjects.Results: No significant differences between tinnitus and non-tinnitus subjects could be found for hearing thresholds, otoacoustic emissions, and ABR results.Tinnitus subjects had significantly worse speech reception in noise compared to non-tinnitus subjects for sentences embedded in steady-state noise (mean speech reception threshold (SRT) scores, respectively −5.77 and −6.90 dB SNR; p = 0.025) as well as for sentences embedded in 15 Hz AM-noise (mean SRT scores, respectively −13.04 and −15.17 dB SNR; p = 0.013). In both groups speech reception was significantly improved during AM-15 Hz noise compared to the steady-state noise condition (p < 0.001). However, the modulation masking release was not affected by the presence of NIT.Conclusions: Young adults with and without NIT did not differ regarding audiometry, OAE, and ABR.However, tinnitus patients showed decreased speech-in-noise reception. The results are discussed in the light of previous findings suggestion NIT may occur in the absence of measurable peripheral damage as reflected in speech-in-noise deficits in tinnitus subjects.
Highlights
Due to the large amount of social activities in which adolescents are exposed to high music levels such as concerts, night clubs, sports events, pubs, bars, etc., the younger population is at risk to develop noise-induced symptoms such as hearing loss, hyperacusis, and tinnitus (Smith et al, 2000; Serra et al, 2005; Beach et al, 2013) of which noise-induced tinnitus (NIT) is the symptom most frequently reported by adolescents (Widen and Erlandsson, 2004; Gilles A. et al, 2013)
The argument can be made that, ideally, a group of non-exposed students should be included in order to investigate their audiological characteristics and compare them to the subject groups with occasional recreational noise exposure
As recreational noise exposure is an undeniable part of the current society, it is rather impossible to find young subjects who did not have any kind of noise exposure during their lifespan
Summary
Due to the large amount of social activities in which adolescents are exposed to high music levels such as concerts, night clubs, sports events, pubs, bars, etc., the younger population is at risk to develop noise-induced symptoms such as hearing loss, hyperacusis, and tinnitus (Smith et al, 2000; Serra et al, 2005; Beach et al, 2013) of which noise-induced tinnitus (NIT) is the symptom most frequently reported by adolescents (Widen and Erlandsson, 2004; Gilles A. et al, 2013). The ganglion is almost entirely (95%) composed of type I neurons which receive synaptic input from a single inner hair cell. Each inner hair cell forms synapses with 10–30 type I neurons (Davis and Liu, 2011). Spiral ganglion neurons possess tonotopic specializations due to the tonotopically varying soma and axon diameter of putative type I neurons with the largest neurons situated toward the basal regions (Liberman and Oliver, 1984). It was shown that the loss of peripheral terminals of the cochlear neurons occurs almost instantly after noise exposure but that cell death and disappearance of the somata were extremely slow with a decrease of spiral ganglion cells of around 50% over a time period of 2 years (Kujawa and Liberman, 2009)
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.
