DPOAE level shifts and ABR threshold shifts compared to detailed analysis of histopathological damage from noise

A detailed comparison of 2f(1)-f(2) distortion product otoacoustic emission (DPOAE) level shifts (LS) and auditory brainstem response (ABR) threshold shifts with noise-induced histopathology was conducted in chinchillas. DPOAE levels (i.e., L(1) and L(2)) at f(1) and f(2), respectively, ranged from 55-75 dB sound pressure level (SPL), with f(2)/f(1)=1.23, 6 points/octave, f(2)=0.41-20 kHz, and ABR thresholds at 0.5-20 kHz, 2 points/octave, were determined pre-exposure. The exposure was a 108 dB SPL octave band of noise centered at 4 kHz (1-1.75 h, n=6) or 80-86 dB SPL (24 h, n=5). DPOAE LSs (magnitude pre- minus post-exposure) and ABR threshold shifts (TS) were determined at 0 days and up to 28 days post-exposure. The cochleae were fixed, embedded in plastic and dissected into flat preparations. The length of the organ of Corti (OC) was measured; missing inner (IHC) and outer (OHC) hair cells counted; stereocilia damage rated; and regions of OC and nerve-fiber loss determined. Cytocochleograms were made showing functional loss and structural damage with the LS and TS overlaid. Some unexpected results were obtained. First, the best correlation of LS with histopathology required plotting the DPOAE data at f(1) with respect to the chinchilla-place map. The best correlation of TS was with IHC and nerve-fiber loss. Second, wide regions of up to 10% scattered OHC loss in the apical half of the OC showed little or no LS. Third, with the 108 dB SPL noise, there was 20-40 dB of recovery for DPOAEs at mid-high frequencies (3-10 kHz) in eight of 12 cochleae where there was 70-100% OHC loss in the basal half of the OC. The largest recovery at mid-high frequencies occurred in regions where the OC was entirely missing. Fourth, with the 80-86 dB SPL noise, there was no LS at small focal lesions (100% loss of OHCs over 0.4 mm) when the frequency place of either f(1) or f(2) was within the lesion but not both. There was no correlation of LS with OHC stereocilia loss, fusion or disarray. These results suggest that, after noise exposure, DPOAEs at mid-high frequencies can originate from or be augmented by generators located at someplace other than the frequency place of f(2), possibly the basal 20% of the OC when this region is intact. Also, noise-induced DPOAE LSs seemed to reflect differing mechanisms for temporary and permanent hearing loss.     

Effect of infrasound on cochlear damage from exposure to a 4 kHz octave band of noise

Infrasound (i.e., <20 Hz for humans; <100 Hz for chinchillas) is not audible, but exposure to high-levels of infrasound will produce large movements of cochlear fluids. We speculated that high-level infrasound might bias the basilar membrane and perhaps be able to minimize noise-induced hearing loss. Chinchillas were simultaneously exposed to a 30 Hz tone at 100 dB SPL and a 4 kHz OBN at either 108 dB SPL for 1.75 h or 86 dB SPL for 24h. For each animal, the tympanic membrane (TM) in one ear was perforated ( approximately 1 mm(2)) prior to exposure to attenuate infrasound transmission to that cochlea by about 50 dB SPL. Controls included animals that were exposed to the infrasound only or the 4 kHz OBN only. ABR threshold shifts (TSs) and DPOAE level shifts (LSs) were determined pre- and post-TM-perforation and immediately post-exposure, just before cochlear fixation. The cochleae were dehydrated, embedded in plastic, and dissected into flat preparations of the organ of Corti (OC). Each dissected segment was evaluated for losses of inner hair cells (IHCs) and outer hair cells (OHCs). For each chinchilla, the magnitude and pattern of functional and hair cell losses were compared between their right and left cochleae. The TM perforation produced no ABR TS across frequency but did produce a 10-21 dB DPOAE LS from 0.6 to 2 kHz. The infrasound exposure alone resulted in a 10-20 dB ABR TS at and below 2 kHz, no DPOAE LS and no IHC or OHC losses. Exposure to the 4 kHz OBN alone at 108 dB produced a 10-50 dB ABR TS for 0.5-12 kHz, a 10-60 dB DPOAE LS for 0.6-16 kHz and severe OHC loss in the middle of the first turn. When infrasound was present during exposure to the 4 kHz OBN at 108 dB, the functional losses and OHC losses extended much further toward the apical and basal tips of the OC than in cochleae exposed to the 4 kHz OBN alone. Exposure to only the 4 kHz OBN at 86 dB produces a 10-40 dB ABR TS for 3-12 kHz and 10-30 dB DPOAE LS for 3-8 kHz but little or no OHC loss in the middle of the first turn. No differences were found in the functional and hair-cell losses from exposure to the 4 kHz OBN at 86 dB in the presence or absence of infrasound. We hypothesize that exposure to infrasound and an intense 4 kHz OBN increases cochlear damage because the large fluid movements from infrasound cause more intermixing of cochlear fluids through the damaged reticular lamina. Simultaneous infrasound and a moderate 4 kHz OBN did not increase cochlear damage because the reticular lamina rarely breaks down during this moderate level exposure.     

D-methionine (D-met) significantly rescues noise-induced hearing loss: timing studies

We have previously reported rescue from noise-induced auditory brainstem response (ABR) threshold shifts with d-methionine (d-met) administration 1?h after noise exposure. The present study investigated further d-met rescue intervals at 3, 5 and 7?h post-noise exposure. Chinchillas laniger were exposed to a 6?h 105?dB sound pressure level (dB SPL) octave band noise (OBN) and then administered d-met i.p. starting 3, 5, or 7?h after noise exposure; controls received saline i.p. immediately after noise exposure. ABR assessments were performed at baseline and on post-exposure days 1 and 21. Outer hair cell (OHC) loss was measured in cochleae obtained at sacrifice 21 days post-exposure. Administration of d-met starting at any of the delay times of 3-7?h post-noise exposure significantly reduced day 21 ABR threshold shift at 2 and 4?kHz and OHC loss at all hair cell regions measured (2, 4, 6 and 8?kHz). ABR threshold shifts in the control group at 6 and 8?kHz were only 8 and 11?dB respectively allowing little opportunity to observe protection at those 2 frequencies.     

Fine alterations of distortion-product otoacoustic emissions after moderate acoustic overexposure in guinea pigs

Guinea pigs were exposed to a pure tone at 6 kHz and 80 dB SPL for 30 minutes in order to induce mild reversible auditory fatigue over the 4 hours following exposure. Cochlear monitoring aimed to compare the shifts in round-window compound action potentials (CAP) thresholds to those of 2f1-f2 distortion-product otoacoustic emissions (DPOAE, frequency of stimuli f1 and f2). Both responses were evaluated every 1/10th octave between 6 and 12 kHz for CAP thresholds, and from 4 to about 14 kHz for DPOAEs in response to 50- and 70-dB SPL stimuli. The auditory fatigue turned out to be sufficiently mild that DPOAEs remained present, so that their microstructure could be followed up while the stimulus frequency ratio f2/f1 was swept from 1.06 to 1.30 (fixed f2) so as to derive DPOAE level profiles against f2/f1 and group latencies. CAP thresholds decreased by about 10 dB above 7.2 kHz, whereas DPOAE amplitudes decreased at most f2 frequencies from 6.6 kHz to 15.2 kHz, with the range of decrease being slightly narrower at higher stimulus intensities. While the mean DPOAE shift after 1 hour was around 5 dB irrespective of stimulus intensity, it tended to increase slightly after 2 hours despite stable CAP thresholds. DPOAE profiles against f2/f1 were slightly modified by the auditory fatigue, so that the maximum tended to be reached at lower ratio. No significant variation of DPOAE latencies was found after acoustic overstimulation. These experiments show that complex DPOAE changes were induced by auditory fatigue and their relationship to CAP threshold changes does not seem to be straight-forward. Nonetheless, fine DPOAE recordings might be useful to detect early changes in cochlear mechanics.     

Suppression of the 2f1-f2 otoacoustic emission in humans.

Suppression of the 2f1-f2 distortion-product otoacoustic emission (DPOAE), stimulated with primaries, f1 and f2, in the frequency regions of 1, 2, and 4 kHz was measured in one ear of 14 human subjects with normal hearing. Suppression rate functions were generated with a suppressor at either 1, 2, or 4 kHz increasing in level from 30 to 76 dB SPL for the corresponding f1 and f2 combinations. Stimulus levels for DPOAEs were L1 = 70 dB SPL and L2 adjusted to produce the highest amplitude DPOAE for each ear (range, 0 to 6 dB below L1). Results indicated that DPOAEs were reduced 3 dB in amplitude for a mean suppressor level of 61 dB SPL. Maximum amplitude reduction occurred at a mean suppressor level of 69 dB SPL. These levels varied little for the three stimulus frequency regions. Mean slopes of the rate functions decreased as stimulus frequency region increased. Suppression tuning curves (STCs) were generated in the same three frequency regions and with L1 at either 70 or 55 dB SPL and L2 adjusted individually for each ear. The tips of the STCs were at frequencies associated with f1 and f2. The tip regions of the STCs for the 4-kHz stimulus condition were more complex in that they contained more multiple minima than did those for the 1- and 2-kHz regions. Results confirm that optimal suppression of the 2f1-f2 DPOAE occurs for frequencies in the vicinity of f1 and f2 rather than at 2f1-f2.     

An anatomically based frequency-place map for the mouse cochlea

An anatomically based frequency-place map was created for the mouse using C57BL/CBA F1 hybrids by matching noise-induced lesions in the organ of Corti with permanent hearing losses as determined by auditory brainstem response (ABR) thresholds. Twenty-six mice developed 'notched' ABR threshold shifts after exposure to an octave band of noise with a center frequency of 2 kHz at 120 dB SPL for 24 h, 4 kHz at 110 dB SPL for 4 h or 8 kHz at 100 dB SPL for 1 or 2 h. ABR thresholds were determined at several intervals post-exposure until thresholds stabilized (14-27 days). Once thresholds had stabilized, the mice were killed and their cochleas were prepared for phase-contrast microscopic examination as plastic-embedded flat preparations. Hair cell loss, stereocilia damage, and myelinated nerve fiber degeneration as a function of percentage distance from the cochlear apex were determined. Frequency-position matches could be made for 22 of the 26 mice by correlating areas of hair cell loss/stereocilia damage with permanent changes in ABR thresholds. These frequency-position data were fitted with the equation: % Distance from apex=56.6 log (f(Hz))-179.1; r(2)=0.810. This frequency-place function agrees well with Ehret's (1975) theoretical function based on critical bands and masked auditory thresholds.     

Suppression and enhancement of distortion-product otoacoustic emissions by interference tones above f(2). II. Findings in humans

Distortion-product otoacoustic emission (DPOAE) suppression tuning curves (STCs) can be obtained in a variety of laboratory animals and humans by sweeping the frequencies and levels of a third tone (f(3)) around a set of f(1) and f(2) primaries. In small laboratory animals, it was previously observed that, when the suppressor tone (f(3)) is above f(2), substantial suppression and or enhancement (suppression/enhancement) could be obtained. In the present study, it was of interest to determine if similar suppression/enhancement phenomena could be observed in humans and to what extent this might influence the interpretation of STC results reported in the literature. To this end, STCs were measured for DPOAEs at 2f(1)-f(2) and 2f(2)-f(1) in human subjects at geometric-mean frequencies (GM) of 1, 2, 3, and 4 kHz, and primary-tone equilevels of 80/80 and 75/75 dB SPL and unequal levels of 65/55 dB SPL. Overall, STC parameters were found to be comparable to those reported in the literature. For the 2f(1)-f(2) DPOAE, STC tip frequencies tuned to the region of the primaries, and tip frequencies were slightly influenced by primary-tone level. STC tip thresholds were typically within 10 dB of the level of L(2), and Q(10dB) values ranged from 1.0 to 2.5, which was consistent with the higher-level primaries employed. The 2f(1)-f(2) DPOAE showed consistent regions of suppression that were approximately an octave above the GM for the 1-kHz, 65/55-dB SPL condition. The 2f(2)-f(1) DPOAE tuned to its characteristic place above f(2) and showed reliable enhancement above the STC tip region for the 1-kHz, 75/75-dB SPL primaries. Overall, the results clearly revealed that human ears also display suppression/enhancement phenomena when f(3) reaches frequencies considerably above f(2). If suppression/enhancement phenomena reflect secondary DPOAE sources, then these sources are present in the ear-canal signal from humans as well as small laboratory animals.     

Otoacoustic emission, evoked potential, and behavioral auditory thresholds in the rhesus monkey (Macaca mulatta).

Distortion product otoacoustic emission (DPOAE), auditory brainstem evoked response (ABR), and behavioral thresholds were recorded in a group of 15 adult rhesus monkeys with normal auditory function. DPOAE thresholds were recorded with stimulus parameters selected to maximize signal-to-noise ratio. Additional averaging at the lowest frequencies ensured comparable noise levels across frequencies. DPOAE thresholds decreased with increasing frequency (f(2)=0.5-16 kHz) and at 16 kHz were close to 0 dB SPL. ABR thresholds were best from 1 through 16 kHz (32-38 dB peSPL); higher at 0.5 (45 dB peSPL), 24 (39 dB peSPL), and 30 kHz (49 dB peSPL). At all levels including threshold, the early ABR waves (II and I) were more prominent at the high frequencies while the later waves (IV and V) were more prominent at the low frequencies. The behavioral thresholds recorded were similar to those reported by other researchers although elevated by about 10 dB presumably because of the complexity of the threshold task. DPOAE and ABR thresholds can be reliably and efficiently recorded in the rhesus monkey and provide information concerning site of processing in the auditory pathway not directly available from behavioral data.     

Olivocochlear activity and temporary threshold shift-susceptibility in humans

STUDY OBJECTIVES: Animal studies (guinea pig, cat, chinchilla) have shown that activity of the medial olivocochlear efferents can exert noise-protective effects on the cochlea. It is not yet known whether such effects are also existent in humans. Olivocochlear activity can be estimated indirectly by contralateral suppression (CS) of otoacoustic emissions (OAE). MATERIAL AND METHODS: We measured Input/Output functions of distortion products of OAE (DPOAE), with and without contralateral acoustic stimulation by white noise, in 94 normal hearing young male subjects. Seven stimuli with L2 between 20 and 60 dB SPL and L1 = 39 dB + 0.4 L2 ("scissor paradigm") were used at f2 = 2, 3, 4, 5, and 6 kHz. The measurement was repeated 2 weeks later. In 83 subjects of the same group, pure tone audiometry was registered before and 6 minutes after shooting exercises to evaluate individual susceptibility to develop a temporary threshold shift (TTS). RESULTS: Test-retest repeatability of CS was generally good. CS averaged 0.98 dB SPL (SD 1.19 dB, median 0.56 dB). As expected, CS was greatest at low stimulus levels (median 1.06 dB at L2 = 20 dB, as compared with 0.33 dB at L2 = 60 dB). The smallest average CS was found at 4 kHz, and the greatest CS appeared at 2 kHz. A TTS occurred in 7 of 83 (8.5%) subjects. Statistical analysis did not reveal any correlation between the amount of CS and individual TTS susceptibility. CONCLUSIONS AND OUTLOOK: 1) Measurement of CS of DPOAE using an extensive measurement paradigm revealed good test-retest repeatability, confirming the reliability of this audiologic tool. 2) CS of DPOAE does not predict individual susceptibility to mild TTS induced by impulse noise in humans. Possible explanations for the missing association are discussed. Future perspectives include longitudinal studies to further elucidate the association between medial olivocochlear bundle-activity and permanent threshold shift in humans. The goal is to develop a diagnostic tool for the prediction of individual noise vulnerability in humans, thereby preventing noise-induced hearing loss.     

Impact of infrasound on the human cochlea

Low-frequency tones were reported to modulate the amplitude of distortion product otoacoustic emissions (DPOAEs) indicating periodic changes of the operating point of the cochlear amplifier. The present study investigates potential differences between infrasound and low-frequency sounds in their ability to modulate human DPOAEs. DPOAEs were recorded in 12 normally hearing subjects in the presence of a biasing tone with f(B)=6Hz and a level L(B)=130dB SPL. Primary frequencies were fixed at f(1)=1.6 and f(2)=2.0kHz with fixed levels L(1)=51 and L(2)=30dB SPL. A new measure, the modulation index (MI), was devised to characterise the degree of DPOAE modulation. In subsequent measurements with biasing tones of f(B) = 12, 24 and 50Hz, L(B) was adjusted to maintain the MI as obtained individually at 6Hz. Modulation patterns lagged with increasing f(B). The necessary L(B) decreased by 12dB/octave with increasing f(B) and ran almost parallel to the published infrasound detection threshold. No signs of an abrupt change in transmission into the cochlea were found between infra- and low-frequency sounds. The results show clearly that infrasound enters the inner ear, and can alter cochlear processing.     

Altered susceptibility of 2f1-f2 acoustic-distortion products to the effects of repeated noise exposure in rabbits

Hearing sensitivity and the generation of acoustic-distortion products at 2f1-f2 were examined systematically in behaviorally trained rabbits, before, during, and following regular exposure to a 95-dB SPL octave band of noise, centered at 1 kHz. During the exposure period, the octave-band noise was interrupted once every 24 h in order to monitor the progressive loss in auditory function using tests of behavioral threshold and distortion-product otoacoustic emissions (DPOAEs). When low-frequency DPOAEs from 1-4 kHz diminished to noise-floor levels, i.e., when their amplitudes were reduced by about 20-30 dB, the exposure was terminated. Subsequent recovery of behavioral thresholds and DPOAE amplitudes and detection 'thresholds' was evaluated at regular intervals over a 3-week post-exposure period. Following the recovery period, the rabbits again received the identical exposure/recovery treatment until a permanent 10 dB or greater loss in DPOAE amplitudes was achieved for any point of measurement between 2-10 kHz. The primary result was that the number of days of overstimulation required for rabbits to reach the criterion loss in DPOAE amplitudes increased for each successive exposure session. In addition, DPOAEs accurately tracked the frequency pattern described by the behavioral threshold shifts during both the development and recovery stages of exposure.     

Contralateral suppression of DPOAE measured in real time

The aim of this study was to measure contralateral suppression of distortion product otoacoustic emissions (DPOAE) in real time. A total of 10 human subjects were studied with a novel device to record DPOAE without signal time averaging, using digital narrow band pass filtering. Real time DPOAE levels were recorded at 2f1-f2 using primary tone settings of f2/f1 = 1.22 and L1 = 70 dB SPL, L2 = 65 dB SPL, at five values of f2 between 2.2 and 7.7 kHz. An acoustic stimulus was applied intermittently to the contralateral ear to cause DPOAE suppression. Characteristic features of contralateral suppression were identified and distinguished from small spontaneous variations in the real time DPOAE signal. Magnitude of suppression increased with contralateral stimulus intensity. Onset latency of suppression was around 43 ms (31-95 ms). Potential clinical applications are discussed in the light of these findings, including a role in improving the specificity of neonatal hearing screening.     

Evaluating cochlear function and the effects of noise exposure in the B6.CAST+Ahl mouse with distortion product otoacoustic emissions

Cochlear function and susceptibility to noise over-exposure were examined in the congenic mouse strain B6.CAST+Ahl (B6.CAST) and compared to these same features in the CAST/Ei (CAST) and C57BL/6J (C57) parental strains. For both types of comparisons, the primary measure was the distortion-product otoacoustic emissions (DPOAE) at 2f1-2f2. Our assumption was that the B6.CAST mouse was corrected for the early onset age-related hearing loss (AHL) exhibited by one of its parental strains (C57) by the age-resistant properties of its other parental strain (CAST), and thus would exhibit neither AHL nor susceptibility to noise overstimulation effects. With respect to cochlear function, for 2.5-month mice, there was a tendency for DPOAEs to be slightly lower for mid-frequency primary tones for both C57 and B6.CAST mice, while the former mice showed clear AHL effects at the highest test frequency. However, by 5 months of age, the B6.CAST mice, like the CAST mice, displayed robust DPOAE levels that were significantly larger than DPOAE levels for the C57 mice, which were essentially absent for frequencies above about 30 kHz. To investigate the role of the Ahl gene in the susceptibility of the cochlea to the effects of noise over-exposure, two distinct paradigms consisting of temporary (TTS: 1-min, 105-dB SPL, 10-kHz pure tone) and permanent (PTS: 1-h, 105-dB SPL, 10-kHz octave band noise) threshold-shift protocols were used. The brief TTS exposure produced reversible reductions in DPOAEs that for both the B6.CAST and CAST mice recovered to within a few dB of their baseline levels by 3 min post-exposure. In contrast, the C57 mice recovered somewhat slower and, by 5 min post-exposure, emission levels were still 5 dB or more below their corresponding pre-exposure values. At 3 months of age, the TTS mice along with another group of na?ve subjects representing the same three mouse strains were exposed to the PTS paradigm. By 4 days post-exposure, for B6.CAST and CAST mice, DPOAE levels had recovered to their pre-exposure control levels. However, DPOAEs for the C57 mice at most of the measurable frequencies were at least 10-30 dB lower than their counterpart baseline levels. Together these data suggest that the Ahl allele in the C57 strain contributes to both the early onset AHL exhibited by these mice as well as their susceptibility to both TTS and PTS over-exposures.     

短时纯音暴露对畸变产物耳声发射的影响

畸变产物耳声发射（ＤＰＯＡＥ）测试所采用的参数可以对测试结果有明显影响，为研究改变ＤＰＯＡＥ测试参数对反映耳蜗功能变化是否有影响，使１０只大白兔（１６耳）接触短时（３分钟）、中等强度（８２ｄＢ ＳＰＬ）的纯音暴露后发现，以等强原始音（Ｌ１＝Ｌ２）诱发的ＤＰＯＡＥ的幅度变化小于以差强原始音（Ｌ２＝Ｌ１－１２ｄＢ）诱发的ＤＰＯＡＥ（相差１０．１１ｄＢ），而其恢复过程也短于后者（相差１００．７１秒）。这     

Contralateral suppression of distortion product otoacoustic emissions: effect of the primary frequency in Dpgrams

The amplitude of the 2f1-f2 distortion product otoacoustic emission (DPOAE) can be suppressed by presenting contralateral acoustic stimulation. To test the hypothesis that DPOAE contralateral suppression is influenced by the primary frequency in DPgrams, DPgrams were recorded at resolutions of 1, 8, and 17 pts/octave, in the absence and presence of contralateral broadband noise (BBN). Participants were 20 normal-hearing human adults. In DPgrams with higher frequency resolutions, DPOAE suppression at amplitude peaks in DPgrams (8 pts/octave: Mean = - 0.92 dB, SD = 0.71 for BBN at 60 dB SPL; 17 pts/octave: Mean = - 0.25 to -1.44 dB, SD = 0.51 to 0.86 for BBN at 40 to 70 dB SPL, respectively) was larger than the suppression at the dips in DPgrams (8 pts/octave: Mean = - 0.13 dB, SD = 1.00; 17 pts/octave: Mean = - 0.03 to -0.73 dB, SD = 0.55 to 0.91). A larger intersubject variability in DPOAE contralateral suppression was observed at the dips. The results suggest that measuring DPOAE contralateral suppression at the primary frequencies corresponding to the peaks in DPgrams with higher frequency resolutions may improve the assessment of the efferent system function.     

Detection of hearing loss using 2f2-f1 and 2f1-f2 distortion-product otoacoustic emissions.

Although many distortion-product otoacoustic emissions (DPOAEs) may be measured in the ear canal in response to 2 pure tone stimuli, the majority of clinical studies have focused exclusively on the DPOAE at the frequency 2f1-f2. This study investigated another DPOAE, 2f2-f1, in an attempt to determine the following: (a) the optimal stimulus parameters for its clinical measurement and (b) its utility in differentiating between normal-hearing and hearing-impaired ears at low-to-mid frequencies (相似文献   

Human efferent adaptation of DPOAEs in the L1,L2 space

The adaptive properties of distortion product otoacoustic emissions (DPOAEs) at 2f(1)-f2 were investigated in 12 ears of normally hearing adults aged 18-30 years using long-lasting 1-s primary-tone on-times. In this manner, DPOAE adaptation at a single f2 of 1.55 kHz (f2/f1=1.21) was evaluated as a function of the levels of the primary tones in a matrix of L1, L2 settings, which varied from 45 to 80 dB SPL, in 5-dB steps. DPOAEs were elicited under both monaural and binaural stimulus-presentation conditions. Adaptation was defined as the difference in DPOAE levels between the initial 92-ms baseline measure using a standard protocol and one obtained during the final 92 ms of the prolonged 1-s primary-tones. These differences were averaged across subjects to create contour plots of mean adaptation in the L1,L2 space. The 2f(1)-f2 DPOAE revealed consistent regions of suppression (-0.5 dB difference) or enhancement (+0.5 dB difference) with respect to baseline measures within the L(1),L(2) matrix for both acoustic-stimulation conditions. Specifically, 2f(1)-f2 DPOAE suppressions of 1-2 dB occurred for both monaural and binaural presentations, typically at level combinations in which L1>L2. In contrast, larger 2f(1)-f2 DPOAE enhancements of 3-4 dB occurred for only the binaural condition, at primary-tone level combinations where L1相似文献   

Protection against acoustic trauma by forward and backward sound conditioning

The purpose of the present study was to determine if short-term sound conditioning provides protection when delivered either before (forward sound conditioning) or after (backward sound conditioning) a traumatic exposure in the guinea pig. Two different sound conditioning paradigms were studied (1 kHz, 81 dB SPL, 24 h; 6.3 kHz, 78 dB SPL, 24 h). The 1-kHz forward sound conditioning paradigm (81 dB SPL, 24 h) protected distortion product otoacoustic emissions (DPOAEs) against a short-duration acoustic trauma (2.7 kHz, 103 dB SPL, 5 min) compared to the group exposed to the acoustic trauma alone. The 1-kHz forward sound conditioning paradigm (81 dB SPL, 24 h) also protected both the auditory brainstem response (ABR) thresholds and DPOAEs against a longer-duration acoustic trauma (2.7 kHz, 103 dB SPL, 30 min). The group exposed to the acoustic trauma alone showed ABR threshold shifts between 15 and 24 dB, and DPOAE amplitude shifts between 11 and 24 dB, while the group with 1-kHz forward sound conditioning showed statistically significant protection at all ABR frequencies and at all DPOAE frequencies. The 1-kHz backward sound conditioning paradigm protected against acoustic trauma (2.7 kHz, 103 dB SPL, 30 min). The ABR thresholds were protected at 1, 2 and 4 kHz, and DPOAEs at all frequencies (except 8 kHz) when compared to the group exposed only to the acoustic trauma. The 6.3-kHz forward sound conditioning paradigm protected against acoustic trauma (5.5 kHz, 109 dB SPL, 30 min) at 6.3, 8 and 10 kHz. The 6.3-kHz backward sound conditioning paradigm showed no protection against acoustic trauma at any DPOAE frequency. Taken together, these findings are important for understanding how the auditory system can be modulated by acoustic stimulation and highlights the importance of the acoustic environment during the recovery process of the auditory system.     

Effects of intense pure tones on auditory temporal acuity

Gap detection thresholds (GDTs) were obtained from human listeners before and after exposure to a brief 0.4- or 1.7-kHz tone. The temporary threshold shift (TTS) produced 2 min after an exposure was approximately 10 dB. GDT stimuli were octave-band noises centered at one of three frequencies: the exposure frequency, one-half octave above the exposure frequency or one octave above the exposure frequency. GDTs were obtained at 35, 55, and 75 dB SPL at each center frequency. GDT and TTS recovery were monitored at logarithmically-spaced time intervals after the exposures. Following the 1.7-kHz exposure, shifts in post-exposure GDT were only obtained with the low-level stimulus conditions--the magnitude of GDT shift was correlated with the size of the TTS, and the shifts in GDT and absolute threshold required similar amounts of time to recover. Significant post-exposure shifts in GDT were also observed following the 0.4-kHz exposure. However, shifts were found at frequencies where there was no measurable TTS, and they required longer periods of time to recover than did absolute threshold.     

The 2f1-f2 DPOAE amplitudes and latencies in the groups of older people with presbyacusis and young people with normal hearing

Otoacoustic emissions have been shown to be useful as indicators of the cochlear function. One of the most valuable techniques is distortion product otoacoustic emission recording (DPOAE), mostly 2f1-f2 distortion, which is described as being present regularly and indicating the strongest connection with hearing level. DPOAE amplitudes are analysed as relating to the frequency (DP-gram) or to the signal levels (input-output function). Another feature of DPOAE providing many details with regard to cochlear mechanics seems to be the assessment of 2f1-f2 DPOAE latencies. In the present study 2f1-f2 DPOAE amplitudes and latencies were analysed and compared in two groups: the elderly with presbyacousis and the young with normal hearing level. All measurements were taken using Otodynamics ILO 92 system. DPOAE latencies were recorded by phase gradient method with fixed-f1 and swept-f2 signal. The following signal parameters were used: f2 ranging from 732 to 6396 Hz, signal levels L1 = L2 = 70 dB SPL, f2/f1 ratio ranging from 1.18 to 1.25. According to the mathematical formula y = 1.412 + exp(7.685-0.7698*ln(f2)) 2f1-f2 DPOAE latencies were calculated in the group of young people at f2 = 1.0 kHz; 2.0 kHz; 3.0 kHz; 4.0 kHz; 5.0 kHz; 6.0 kHz as follows: 12.08 ms; 7.67 ms; 5.99 ms; 5.08 ms; 4.50 ms; 4.10 ms. The analogous analysis revealed the following results in the group of the elderly: y = 2.402 + exp(9.293-1.019*ln(f2)) and calculated latencies--11.9 ms; 7.09 ms; 5.50 ms; 4.71 ms; 4.24 ms; 3.93 ms. The greater differentiation of the latencies measured in low frequency band was observed in the elderly while in the young subjects in mid and high frequency bands. The 2f1-f2 DPOAE amplitudes recorded for the whole frequency band were significantly higher in the young people than in the elderly. No correlation was observed between latencies and amplitudes in both investigated groups.