Hostname: page-component-586b7cd67f-g8jcs Total loading time: 0 Render date: 2024-11-28T04:31:36.507Z Has data issue: false hasContentIssue false

Mechanisms in noise-induced permanent hearing loss: an evoked otoacoustic emission and auditory brainstem response study

Published online by Cambridge University Press:  29 June 2007

Zheng-Min Xu*
Affiliation:
Department of Otolaryngology, University Hospital Ghent, Ghent, Belgium.
Bart Vinck
Affiliation:
Department of Otolaryngology, University Hospital Ghent, Ghent, Belgium.
Eddy De Vel
Affiliation:
Department of Otolaryngology, University Hospital Ghent, Ghent, Belgium.
Paul van Cauwenberge
Affiliation:
Department of Otolaryngology, University Hospital Ghent, Ghent, Belgium.
*
Address for correspondence: Zheng-Min Xu, M.D., Ph.D., Department of Otolaryngology, University Hospital Ghent, De Pintelaan 185 B–9000 Ghent, Belgium.

Abstract

In this study 22 patients (44 ears) with noise-induced permanent hearing loss were audiologically evaluated using transient-evoked otoacoustic emissions (TEOAE) and auditory brain-stem response (ABR). Twenty-one normal subjects (42 ears) without exposure to occupational noise were used as controls. Based upon the hearing loss at 4, 3, 2 and 1 kHz on the pure-tone audiogram, they were classified into four groups. In group 1 (eight ears), emissions were present in all ears but their TEOAE-noise level and their reproducibility (percentage) proved to be weak. The auditory brain-stem response (ABR) indicated that the I/V amplitude ratio, the latency values of wave V and the I–V intervals fell within the normal range in all ears. In Group 2 (14 ears), 40 per cent had no emissions, whereas the remaining ears showed weak emissions. The ABR revealed that in all ears the I/V amplitude ratio became small while wave V peak latency as well as I–V intervals were within the normal range. In Group 3 (10 ears), emissions were absent in 50 per cent, while in the other ears the emissions were very weak. The ABR revealed that the I/V amplitude ratio, which could be calculated in the 60 per cent in which wave I was present, was smaller than in Group 2. Wave V latency as well as I–V intervals were within the normal range. In Group 4 (12 ears), none of the ears showed emissions. The ABR indicated that the I/V amplitude ratio was much smaller when wave I was present (27 per cent) as well as I–V interval values being within the normal range. Wave V absolute latency value (δV index) indicated a positive index in 17 per cent of this group (two ears) when wave I was absent. In the present study a dynamic process from cochlear outer hair cells to cochlear neurons was seen, correlating with an increasing hearing loss.

Type
Main Articles
Copyright
Copyright © JLO (1984) Limited 1998

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Almadori, G., Ottaviani, F., Paludett, G., Rosignoli, L., Gallucci, L., Alatri, D., Vergoni, G. (1988) Auditory brainstem responses in noise-induced permanent hearing loss. Audiology 27: 3641.CrossRefGoogle ScholarPubMed
Bess, F. H., Humes, L. E. (1995) Pathologies of the auditory system. In Audiology: The Fundamentals. 2nd Edition, (Bass, F. H., Humes, L. E., eds.) Williams and Wilkins, Baltimore, pp 155196.Google Scholar
Bredberg, G. (1968) Cellular pattern and nerve supply of the human organ of Corti. Acta Otolaryngologica (Stockholm) (Suppl 236): 1135.Google ScholarPubMed
Kemp, D. T. (1980) Towards a model for the origin of cochlear echoes. Hearing Research 2: 533548.CrossRefGoogle Scholar
Lim, D. J. (1986) Functional structure of the organ of Corti: a review. Hearing Research 22: 117146.CrossRefGoogle ScholarPubMed
Moore, E. J., Hall, D. B., Narahashi, T. (1996) Sodium and potassium currents of type I spiral ganglion cells from rat. Acta Otolaryngologica (Stockholm) 116: 552560.CrossRefGoogle ScholarPubMed
Morest, D. K., Bohne, A. (1983) Noise-induced degeneration in the brain and representation of inner and outer hair cells. Hearing Research 9: 145151.CrossRefGoogle ScholarPubMed
Musiek, F. E., Kibbe, K., Rackliffe, L., Weider, D. J. (1984) The auditory brain stem response I-V amplitude ratio in normal, cochlear and retrocochlear ears. Ear Hearing 2: 5255.CrossRefGoogle Scholar
Prasher, D. K., Tun, T., Brookes, G. B., Luxon, L. M. (1995) Mechanisms of hearing loss in acoustic neuroma: an otoacoustic emission study. Acta Otolaryngologica (Stockholm) 115: 375381.CrossRefGoogle ScholarPubMed
Prosser, S., Arslan, E. (1987) Predication of auditory brainstem wave V latency as a diagnostic tool of sensor-ineural hearing loss. Audiology 26: 179187.CrossRefGoogle Scholar
Rop, I., Raber, A., Fischer, G. H. (1979) Study of the hearing losses of industrial workers with occupational noise exposure, using statistical methods for the analysis of qualitative data. Audiology 18: 181196.CrossRefGoogle ScholarPubMed
Saunders, J. C., Rhyne, R. L. (1970) Cochlear nucleus activity and threshold shift in cat. Brain Research 24: 336339.CrossRefGoogle ScholarPubMed
Spoendlin, H. (1971) Primary structural changes in the organ of Corti after acoustic overstimulation. Acta Otolaryngologica (Stockholm) 71: 166176.CrossRefGoogle ScholarPubMed
Vinck, B., De Vel, E., Xu, Z. M., Van Cauwenberge, P. (1996) Distortion product otoacoustic emissions: a normative study. Audiology 35: 231245.CrossRefGoogle ScholarPubMed
Xu, Z. M., Van Cauwenberge, P., Vinck, B., De Vel, E. (1998) Sensitive detection of noise-induced damage in human subjects using transiently evoked otoacoustic emissions. Acta Otolaryngologica Belgica 52: 1924.Google ScholarPubMed
Ward, W. D., Sanit, P. A., Duvall, A. J., Turner, C. W. (1981) Total energy and critical intensity concepts in noise damage. Annals of Otology, Rhinology and Laryngology 90: 584590.CrossRefGoogle ScholarPubMed