Latency of tone-burst-evoked auditory brain stem responses and otoacoustic emissions: Level, frequency, and rise-time effects

Rasetshwane, Daniel M.; Argenyi, Michael S; Neely, Stephen T.; Kopun, Judy G.; Gorga, Michael P.

doi:10.1121/1.4798666

Cited by 33 publications

(83 citation statements)

References 38 publications

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“…Although basilar membrane data are not available for humans and mice, there also seems to be break in SFOAE group delays around 1-2 and 10-15 kHz, respectively (Siegel 2008;Shera et al 2010). In agreement with the human SFOAE data, Rasetshwane et al (2013) reported that latencies of TEOAEs were shorter than forward travel times extracted from auditory brainstem responses at frequencies below 1.5 kHz, while the opposite trend was observed at higher frequencies. It has been proposed that this break in SFOAE group delays marks a transition between basal-and apical-like behaviors (Shera and Guinan 2003;Shera et al 2010).…”

Section: Differences In Low-versus High-frequency Cochlear Responses supporting

confidence: 86%

Tuning of SFOAEs Evoked by Low-Frequency Tones Is Not Compatible with Localized Emission Generation

Charaziak

Siegel

2015

JARO

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Stimulus-frequency otoacoustic emissions (SFOAEs) appear to be well suited for assessing frequency selectivity because, at least on theoretical grounds, they originate over a restricted region of the cochlea near the characteristic place of the evoking tone. In support of this view, we previously found good agreement between SFOAE suppression tuning curves (SF-STCs) and a control measure of frequency selectivity (compound action potential suppression tuning curves (CAP-STC)) for frequencies above 3 kHz in chinchillas. For lower frequencies, however, SF-STCs and were over five times broader than the CAP-STCs and demonstrated more high-pass rather than narrow band-pass filter characteristics. Here, we test the hypothesis that the broad tuning of low-frequency SF-STCs is because emissions originate over a broad region of the cochlea extending basal to the characteristic place of the evoking tone. We removed contributions of the hypothesized basally located SFOAE sources by either pre-suppressing them with a high-frequency interference tone (IT; 4.2, 6.2, or 9.2 kHz at 75 dB sound pressure level (SPL)) or by inducing acoustic trauma at high frequencies (exposures to 8, 5, and lastly 3-kHz tones at 110-115 dB SPL). The 1-kHz SF-STCs and CAP-STCs were measured for baseline, IT present and following the acoustic trauma conditions in anesthetized chinchillas. The IT and acoustic trauma affected SF-STCs in an almost indistinguishable way. The SF-STCs changed progressively from a broad high-pass to narrow band-pass shape as the frequency of the IT was lowered and for subsequent exposures to lowerfrequency tones. Both results were in agreement with the Bbasal sources^hypothesis. In contrast, CAP-STCs were not changed by either manipulation, indicating that neither the IT nor acoustic trauma affected the 1-kHz characteristic place. Thus, unlike CAPs, SFOAEs cannot be considered as a place-specific measure of cochlear function at low frequencies, at least in chinchillas.

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Section: Differences In Low-versus High-frequency Cochlear Responses supporting

confidence: 86%

Tuning of SFOAEs Evoked by Low-Frequency Tones Is Not Compatible with Localized Emission Generation

Charaziak

Siegel

2015

JARO

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“…Leveldependent changes in the latencies of physiological measures including otoacoustic emissions (Shera et al, 2002;Sisto and Moleti, 2007;Shera et al, 2010), the compound action potential (Eggermont, 1979;Rutten, 1986;Henry et al, 2011), and wave V of the auditory brainstem response (ABR; Neely et al, 1988;Don et al, 1998;Dau, 2003;Elberling and Don, 2008;Strelcyk et al, 2009;Elberling et al, 2010;Rønne et al, 2012;Rasetshwane et al, 2013;Verhulst et al, 2013) have also been attributed to effects mediated at the level of the cochlea. The present study examined the effect of stimulus level on ABR wave V latencies in NH and HL ears.…”

Section: Introductionmentioning

confidence: 99%

“…Wave V presumably originates from the lateral-lemniscal pathway (Møller et al, 1995) in the brainstem, but depends on peripheral processes at the levels of the auditory nerve and cochlea. For instance, wave V latency decreases with increasing frequency (e.g., Gorga et al, 1988;Dau, 2003;Rasetshwane et al, 2013), reflecting the shorter travel time required by the traveling wave to excite more basal (higher-frequency) regions of the cochlea. Additionally, when evoked by rising-frequency chirps designed to compensate for traveling-wave dispersion, the amplitude of wave V is larger than it is for both clicks and falling-frequency chirps (Dau et al, 2000;Elberling and Don, 2008; wave I amplitude exhibits similar behavior- Shore and Nuttall, 1985;Chertoff et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

“…The decrease in wave V latency that occurs with increasing stimulus level Neely et al, 1988;Rasetshwane et al, 2013) may also be due, at least in part, to cochlear processing. As level increases for tonal stimulation, the basilar-membrane excitation pattern broadens and the place of maximum excitation shifts toward the cochlear base (Rose et al, 1971;Ruggero et al, 1997;Rhode and Recio, 2000;Ren and Nuttall, 2001;Moore et al, 2002;Ren, 2002;Lopez-Poveda et al, 2007;Rhode, 2007), presumably resulting in shorter response latencies.…”

Section: Introductionmentioning

confidence: 99%

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Tone-burst auditory brainstem response wave V latencies in normal-hearing and hearing-impaired ears

Lewis

Kopun

Neely

et al. 2015

The Journal of the Acoustical Society of America

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The metric used to equate stimulus level [sound pressure level (SPL) or sensation level (SL)] between ears with normal hearing (NH) and ears with hearing loss (HL) in comparisons of auditory function can influence interpretation of results. When stimulus level is equated in dB SL, higher SPLs are presented to ears with HL due to their reduced sensitivity. As a result, it may be difficult to determine if differences between ears with NH and ears with HL are due to cochlear pathology or level-dependent changes in cochlear mechanics. To the extent that level-dependent changes in cochlear mechanics contribute to auditory brainstem response latencies, comparisons between normal and pathologic ears may depend on the stimulus levels at which comparisons are made. To test this hypothesis, wave V latencies were measured in 16 NH ears and 15 ears with mild-to-moderate HL. When stimulus levels were equated in SL, latencies were shorter in HL ears. However, latencies were similar for NH and HL ears when stimulus levels were equated in SPL. These observations demonstrate that the effect of stimulus level on wave V latency is large relative to the effect of HL, at least in cases of mild-to-moderate HL.

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“…The latencies of the different components are approximately level invariant and separated in time by a factor of 1.6 (Carvalho et al 2003;Goodman et al 2011;Moleti et al 2012). The difference in component latencies and leveldependent contributions to the total TEOAE underlies the decrease in the total TEOAE's latency with increasing stimulus level (Moleti et al 2012;Rasetshwane et al 2013;Lewis and Goodman 2014). Contributions to the stimulus-frequency (SF) OAE from different-latency components analogous to those in the TEOAE may similarly underlie the level-dependency of SFOAE latency and account for non-monotonicity in SFOAE input/ output (I/O) functions (e.g., Schairer et al 2003;Choi et al 2008;Lewis and Goodman 2014).…”

Section: Introductionmentioning

confidence: 99%

Basal Contributions to Short-Latency Transient-Evoked Otoacoustic Emission Components

Lewis

Goodman

2014

JARO

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The presence of short-latency (SL), less compressivegrowing components in bandpass-filtered transientevoked otoacoustic emission (TEOAE) waveforms may implicate contributions from cochlear regions basal to the tonotopic place. Recent empirical work suggests a region of SL generation between ∼1/5 and 1/10-octave basal to the TEOAE frequency's tonotopic place. However, this estimate may be biased to regions closer to the tonotopic place as the TEOAE extraction technique precluded measurement of components with latencies shorter than ∼5 ms. Using a variant of the non-linear, double-evoked extraction paradigm that permitted extraction of components with latencies as early as 1 ms, the current study empirically estimated the spatial-extent of the cochlear region contributing to 2 kHz SL TEOAE components. TEOAEs were evoked during simultaneous presentation of a suppressor stimulus, in order to suppress contributions to the TEOAE from different places along the cochlear partition. Three or four different-latency components of similar frequency content (∼2 kHz) were identified for most subjects. Component latencies ranged from 1.4 to 9.6 ms; latency was predictive of the component's growth rate and the suppressor frequency to which the component's magnitude was most sensitive to change. As component latency decreased, growth became less compressive and suppressor-frequency sensitivity shifted to higher frequencies. The shortest-latency components were most sensitive to suppressors approximately 3/5-octave higher than their nominal frequency of 2 kHz. These results are consistent with a distributed region of generation extending to approximately 3/5-octave basal to the TEOAE frequency's tonotopic place. The empirical estimates of TEOAE generation are similar to model-based estimates where generation of the different-latency components occurs through linear reflection from impedance discontinuities distributed across the cochlear partition.

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Latency of tone-burst-evoked auditory brain stem responses and otoacoustic emissions: Level, frequency, and rise-time effects

Cited by 33 publications

References 38 publications

Tuning of SFOAEs Evoked by Low-Frequency Tones Is Not Compatible with Localized Emission Generation

Tuning of SFOAEs Evoked by Low-Frequency Tones Is Not Compatible with Localized Emission Generation

Tone-burst auditory brainstem response wave V latencies in normal-hearing and hearing-impaired ears

Basal Contributions to Short-Latency Transient-Evoked Otoacoustic Emission Components

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