Behavior of evoked otoacoustic emission under low-frequency tone exposure: Objective study of the bounce phenomenon in humans

The bounce phenomenon has been investigated in humans, evaluating alterations of click evoked otoacoustic emission (EOAE) after presentation of 250-Hz frequency loud tones during 3 min. EOAE changes were manifested in initial augmentation followed by reduction, peaking at 1 and 3 min of post-exposur...

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Published inHearing research Vol. 222; no. 1; pp. 62 - 69
Main Authors Kevanishvili, Zurab, Hofmann, Gert, Burdzgla, Irina, Pietsch, Markus, Gamgebeli, Zurab, Yarin, Yury, Tushishvili, Michael, Zahnert, Thomas
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier B.V 01.12.2006
Elsevier
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ISSN0378-5955
1878-5891
DOI10.1016/j.heares.2006.05.014

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Abstract The bounce phenomenon has been investigated in humans, evaluating alterations of click evoked otoacoustic emission (EOAE) after presentation of 250-Hz frequency loud tones during 3 min. EOAE changes were manifested in initial augmentation followed by reduction, peaking at 1 and 3 min of post-exposure time, respectively. Recoveries took 5–7 min afterwards. Under linear and nonlinear EOAE acquisition modes both manifestations of bounce appeared similar. At lower exposure intensities, 65–75 dB SPL, augmentations prevailed over reductions. At higher intensities, 80–95 dB SPL, augmentations and reductions were of similar magnitudes. At highest intensity, 100 dB SPL, an obvious EOAE drop has hardly been preceded by any augmentation. Based upon these data, the bounce is considered to be a compound of two opposite events, appearance of each being dependent upon the exposure level. Subjects with high bounce indices in one ear displayed comparable indices in other ear too. Low bounce magnitudes were accordingly typical for particular subjects irrespective of the ears tested. EOAE alterations were observed under ipsilateral, but not contralateral exposures of tones. It has been concluded therefore that the bounce involves peripheral receptor rather than central neural mechanisms. No EOAE shifts were seen under application of clicks without any low-frequency exposure tones. Correspondingly, the bounce is judged to reflect inner-ear processes triggered by low-frequency tones, but not by regular presentations of test-stimuli.
AbstractList The bounce phenomenon has been investigated in humans, evaluating alterations of click evoked otoacoustic emission (EOAE) after presentation of 250-Hz frequency loud tones during 3 min. EOAE changes were manifested in initial augmentation followed by reduction, peaking at 1 and 3 min of post-exposure time, respectively. Recoveries took 5-7 min afterwards. Under linear and nonlinear EOAE acquisition modes both manifestations of bounce appeared similar. At lower exposure intensities, 65-75dB SPL, augmentations prevailed over reductions. At higher intensities, 80-95 dB SPL, augmentations and reductions were of similar magnitudes. At highest intensity, 100 dB SPL, an obvious EOAE drop has hardly been preceded by any augmentation. Based upon these data, the bounce is considered to be a compound of two opposite events, appearance of each being dependent upon the exposure level. Subjects with high bounce indices in one ear displayed comparable indices in other ear too. Low bounce magnitudes were accordingly typical for particular subjects irrespective of the ears tested. EOAE alterations were observed under ipsilateral, but not contralateral exposures of tones. It has been concluded therefore that the bounce involves peripheral receptor rather than central neural mechanisms. No EOAE shifts were seen under application of clicks without any low-frequency exposure tones. Correspondingly, the bounce is judged to reflect inner-ear processes triggered by low-frequency tones, but not by regular presentations of test-stimuli.
The bounce phenomenon has been investigated in humans, evaluating alterations of click evoked otoacoustic emission (EOAE) after presentation of 250-Hz frequency loud tones during 3 min. EOAE changes were manifested in initial augmentation followed by reduction, peaking at 1 and 3 min of post-exposure time, respectively. Recoveries took 5-7 min afterwards. Under linear and nonlinear EOAE acquisition modes both manifestations of bounce appeared similar. At lower exposure intensities, 65-75dB SPL, augmentations prevailed over reductions. At higher intensities, 80-95 dB SPL, augmentations and reductions were of similar magnitudes. At highest intensity, 100 dB SPL, an obvious EOAE drop has hardly been preceded by any augmentation. Based upon these data, the bounce is considered to be a compound of two opposite events, appearance of each being dependent upon the exposure level. Subjects with high bounce indices in one ear displayed comparable indices in other ear too. Low bounce magnitudes were accordingly typical for particular subjects irrespective of the ears tested. EOAE alterations were observed under ipsilateral, but not contralateral exposures of tones. It has been concluded therefore that the bounce involves peripheral receptor rather than central neural mechanisms. No EOAE shifts were seen under application of clicks without any low-frequency exposure tones. Correspondingly, the bounce is judged to reflect inner-ear processes triggered by low-frequency tones, but not by regular presentations of test-stimuli.The bounce phenomenon has been investigated in humans, evaluating alterations of click evoked otoacoustic emission (EOAE) after presentation of 250-Hz frequency loud tones during 3 min. EOAE changes were manifested in initial augmentation followed by reduction, peaking at 1 and 3 min of post-exposure time, respectively. Recoveries took 5-7 min afterwards. Under linear and nonlinear EOAE acquisition modes both manifestations of bounce appeared similar. At lower exposure intensities, 65-75dB SPL, augmentations prevailed over reductions. At higher intensities, 80-95 dB SPL, augmentations and reductions were of similar magnitudes. At highest intensity, 100 dB SPL, an obvious EOAE drop has hardly been preceded by any augmentation. Based upon these data, the bounce is considered to be a compound of two opposite events, appearance of each being dependent upon the exposure level. Subjects with high bounce indices in one ear displayed comparable indices in other ear too. Low bounce magnitudes were accordingly typical for particular subjects irrespective of the ears tested. EOAE alterations were observed under ipsilateral, but not contralateral exposures of tones. It has been concluded therefore that the bounce involves peripheral receptor rather than central neural mechanisms. No EOAE shifts were seen under application of clicks without any low-frequency exposure tones. Correspondingly, the bounce is judged to reflect inner-ear processes triggered by low-frequency tones, but not by regular presentations of test-stimuli.
The bounce phenomenon has been investigated in humans, evaluating alterations of click evoked otoacoustic emission (EOAE) after presentation of 250-Hz frequency loud tones during 3 min. EOAE changes were manifested in initial augmentation followed by reduction, peaking at 1 and 3 min of post-exposure time, respectively. Recoveries took 5–7 min afterwards. Under linear and nonlinear EOAE acquisition modes both manifestations of bounce appeared similar. At lower exposure intensities, 65–75 dB SPL, augmentations prevailed over reductions. At higher intensities, 80–95 dB SPL, augmentations and reductions were of similar magnitudes. At highest intensity, 100 dB SPL, an obvious EOAE drop has hardly been preceded by any augmentation. Based upon these data, the bounce is considered to be a compound of two opposite events, appearance of each being dependent upon the exposure level. Subjects with high bounce indices in one ear displayed comparable indices in other ear too. Low bounce magnitudes were accordingly typical for particular subjects irrespective of the ears tested. EOAE alterations were observed under ipsilateral, but not contralateral exposures of tones. It has been concluded therefore that the bounce involves peripheral receptor rather than central neural mechanisms. No EOAE shifts were seen under application of clicks without any low-frequency exposure tones. Correspondingly, the bounce is judged to reflect inner-ear processes triggered by low-frequency tones, but not by regular presentations of test-stimuli.
Author Kevanishvili, Zurab
Tushishvili, Michael
Burdzgla, Irina
Pietsch, Markus
Hofmann, Gert
Yarin, Yury
Gamgebeli, Zurab
Zahnert, Thomas
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Issue 1
Keywords Exposure intensity dependence
Acquisition dependence
Ipsilateral vs. contralateral effects
EOAE
N
p
SD
TTS
EOAE effects
min
dB SPL
cont
Bounce phenomenon
Human
Alteration
Click
Evoked otoacoustic emission
Low frequency
Recovery
Inner ear
Organ of hearing
Ipsilateral
Nonlinearity
Biological receptor
Language English
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Snippet The bounce phenomenon has been investigated in humans, evaluating alterations of click evoked otoacoustic emission (EOAE) after presentation of 250-Hz...
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StartPage 62
SubjectTerms Acoustic Stimulation - methods
Acquisition dependence
Adult
Auditory Threshold
Biological and medical sciences
Bounce phenomenon
Ear - physiology
Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation
Ear, auditive nerve, cochleovestibular tract, facial nerve: diseases, semeiology
EOAE effects
Exposure intensity dependence
Female
Fundamental and applied biological sciences. Psychology
Hearing - physiology
Humans
Ipsilateral vs. contralateral effects
Male
Medical sciences
Non tumoral diseases
Otoacoustic Emissions, Spontaneous
Otorhinolaryngology. Stomatology
Vertebrates: nervous system and sense organs
Title Behavior of evoked otoacoustic emission under low-frequency tone exposure: Objective study of the bounce phenomenon in humans
URI https://dx.doi.org/10.1016/j.heares.2006.05.014
https://www.ncbi.nlm.nih.gov/pubmed/17052872
https://www.proquest.com/docview/68139428
https://www.proquest.com/docview/85396344
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