A longitudinal study of changes in evoked otoacoustic emissions and pure-tone thresholds as measured in a hearing conservation program

Non-linear transient-evoked otoacoustic emissions (TEOAEs) at 74dB pSPL, distortion-product otoacoustic emissions (DPOAEs) at 65/45dB SPL and pure-tone audiometry were used to detect noise-induced, inner car changes in a longitudinal study. Repeated-measures ANOVAs were made on the Noise (n=69) and Quiet (n=42) groups. The Noise group's hearing thresholds increased by 1.2 dB and DPOAE amplitude decreased by -0.9 dB. For both groups, TEOAE amplitude decreased by approximately -0.6 dB. Eight of 12 ears with permanent threshold shift (PTS) and 10 of 13 ears with temporary threshold shift (TTS) showed TEOAE decrements or low baseline TEOAE amplitudes. Fewer TTS and PTS ears also showed DPOAE decrements, and there was never a DPOAE decrement without a corresponding TEOAE decrement or low TEOAE baseline. Some TTS ears showed permanent emission decrements. Although otoacoustic emissions show promise in detecting noise-induced inner ear changes, it is premature to use them in hearing conservation programs.     

Effects of repeated "benign" noise exposures in young CBA mice: shedding light on age-related hearing loss

Temporary hearing threshold shift (TTS) resulting from a "benign" noise exposure can cause irreversible auditory nerve afferent terminal damage and retraction. While hearing thresholds and acute tissue injury recover within 1-2 weeks after a noise overexposure, it is not clear if multiple TTS noise exposures would result in cumulative damage even though sufficient TTS recovery time is provided. Here, we tested whether repeated TTS noise exposures affected permanent hearing thresholds and examined how that related to inner ear histopathology. Despite a peak 35-40 dB TTS 24 hours after each noise exposure, a double dose (2 weeks apart) of 100 dB noise (8-16 kHz) exposures to young (4-week-old) CBA mice resulted in no permanent threshold shifts (PTS) and abnormal distortion product otoacoustic emissions (DPOAE). However, although auditory brainstem response (ABR) thresholds recovered fully in once- and twice-exposed animals, the growth function of ABR wave 1( p-p ) amplitude (synchronized spiral ganglion cell activity) was significantly reduced to a similar extent, suggesting that damage resulting from a second dose of the exposure was not proportional to that observed after the initial exposure. Estimate of surviving inner hair cell afferent terminals using immunostaining of presynaptic ribbons revealed ribbon loss of ～ 40 % at the ～ 23 kHz region after the first round of noise exposure, but no additional loss of ribbons after the second exposure. In contrast, a third dose of the same noise exposure resulted in not only TTS, but also PTS even in regions where DPOAEs were not affected. The pattern of PTS seen was not entirely tonotopically related to the noise band used. Instead, it resembled more to that of age-related hearing loss, i.e., high frequency hearing impairment towards the base of the cochlea. Interestingly, after a 3rd dose of the noise exposure, additional loss of ribbons (another ≈ 25 %) was observed, suggesting a cumulative detrimental effect from individual "benign" noise exposures, which should result in a significant deficit in central temporal processing.     

Diplacusis, hearing threshold and otoacoustic emissions in an episode of sudden, unilateral cochlear hearing loss

Limited data are available on the relationship between diplacusis and otoacoustic emissions and sudden hearing threshold changes, and the detail of the mechanism underlying diplacusis is not well understood. Data are presented here from an intensively studied single episode of sudden, non-conductive, mild hearing loss with associated binaural diplacusis, probably due to a viral infection. Treatment with steroids was administered for 1 week. This paper examines the relationships between the hearing loss, diplacusis and otoacoustic emissions during recovery on a day-by-day basis. The hearing thresholds were elevated by up to 20 dB at 4kHz and upwards, and there was an interaural pitch difference up to 12% at 4 and 8 kHz. There was also a frequency-specific change in transient evoked otoacoustic emission (TEOAE) and distortion-product otoacoustic emission (DPOAE) level. DPOAE level was reduced by up to 20 dB. with the greatest change seen when a stimulus with a wide stimulus frequency ratio was used. Frequency shifts in the 2f2-fi DPOAE fine structure corresponded to changes in the diplacusis. Complete recovery to previous levels was observed for TEOAE, DPOAE and hearing threshold. The diplacusis recovered to within normal limits after 4 weeks. The frequency shift seen in the DPOAE fine structure did not quite resolve, suggesting a very slight permanent change. The time-courses of TEOAE. diplacusis and hearing threshold were significantly different: most notably, the hearing threshold was stable over a period when the diplacusis deteriorated. This suggests that the cochlear mechanisms involved in diplacusis, hearing threshold and OAE may not be identical.     

Potentiation of noise-induced hearing loss by amikacin in guinea pigs.

Noise and aminoglycosides initially attack cochlear outer hair cells (OHCs). Distortion product otoacoustic emissions (DPOAEs) are used for the early diagnosis of damage to OHCs. The effects of sub-damaging doses of amikacin, an aminoglycoside antibiotic agent, on noise-induced hearing loss (NIHL) were examined in guinea pigs. Animals were grouped by gender and exposed to broadband noise at 105 dB SPL for 12 h and/or injected i.m. with either amikacin (100 mg/kg/day) or saline for 10 days. Auditory brainstem response (ABR) thresholds, along with DPOAE amplitudes, were measured serially before and after noise exposure. DPOAE amplitudes decreased and ABR thresholds elevated immediately after noise exposure and then gradually recovered. At all frequencies, the emission amplitudes recovered completely to pre-exposure baseline values by 4 days after noise exposure. There was no effect of amikacin on either the ABR threshold or DPOAE amplitudes, in animals treated with amikacin only. However, amikacin significantly prolonged the effect of noise exposure on DPOAE amplitude but not on the noise-induced temporary threshold shift (TTS) of the ABR. In animals treated with a combination of noise and amikacin, significant changes in DPOAE amplitudes were still observed at 4 weeks after cessation of noise exposure. No gender difference in the responses to noise and/or amikacin could be demonstrated. The present findings indicate that even sub-damaging dosages of amikacin might impair recovery from NIHL in guinea pigs.     

Diplacusis,hearing threshold and otoacoustic emissions in an episode of sudden,unilateral cochlear hearing loss

Limited data are available on the relationship between diplacusis and otoacoustic emissions and sudden hearing threshold changes, and the detail of the mechanism underlying diplacusis is not well understood. Data are presented here from an intensively studied single episode of sudden, non-conductive, mild hearing loss with associated binaural diplacusis, probably due to a viral infection. Treatment with steroids was administered for 1 week. This paper examines the relationships between the hearing loss, diplacusis and oto-acoustic emissions during recovery on a day-by-day basis. The hearing thresholds were elevated by up to 20 dB at 4 kHz and upwards, and there was an interaural pitch difference up to 12% at 4 and 8 kHz. There was also a frequency-specific change in transient evoked otoacoustic emission ( TEOAE) and distortion-product otoacoustic emission (DPOAE) level. DPOAE level was reduced by up to 20 dB, with the greatest change seen when a stimulus with a wide stimulus frequency ratio was used. Frequency shifts in the 2f2 – f1 DPOAE fine structure corresponded to changes in the diplacusis. Complete recovery to previous levels was observed for TEOAE, DPOAE and hearing threshold. The diplacusis recovered to within normal limits after 4 weeks. The frequency shift seen in the DPOAE fine structure did not quite resolve, suggesting a very slight permanent change. The timecourses of TEOAE, diplacusis and hearing threshold were significantly different; most notably, the hearing threshold was stable over a period when the diplacusis deteriorated. This suggests that the cochlear mechanisms involved in diplacusis, hearing threshold and OAE may not be identical.     

The relationship between auditory threshold and evoked otoacoustic emissions

The aim of this study was to compare transiently evoked otoacoustic emissions (TEOAE) and distortion product otoacoustic emissions (DPOAE) in normal hearing ears (n = 44) and ears with cochlear hearing loss (HL) to obtain defined data on qualitative and quantitative correlations. In addition, we wanted to determine the reliability with which a clinical examiner could predict a typical, idealized audiometric configuration from TEOAE measurements. In the hearing-impaired subjects (n = 149), a 50% reduction of OAE incidence was caused by a mean HL of 10.5 dB for TEOAE compared to 27 dB SPL for DPOAE. A 90% incidence reduction was found at a mean threshold elevation of 33 dB for TEOAE and 51 dB for DPOAE. Correlation between TEOAE amplitudes and HL was in general rather low (r = –0.1 to –0.5), while DPOAE amplitudes showed a slightly better correlation with HL (r = –0.3 to –0.6). In general, efforts to derive an audiogram from evoked OAE have been more promising for DPOAE than for TEOAE. However, our studies showed that approximately 40% of the ears with HL could be categorized correctly into one of five typical audiometric patterns from TEOAE measurements. Additionally, a cochlear HL in or near the medium frequency range was much more likely to cause a reduction in TEOAE than an isolated low- or high-frequency lesion. Accordingly, TEOAE were often preserved in ears with isolated HL in the high or low frequencies. Received: 7 May 1998 / Accepted: 25 September 1998     

Distortion-product otoacoustic emissions in humans with high frequency sensorineural hearing loss

Distortion-product otoacoustic emissions (DPOAEs) and pure-tone behavioral thresholds were compared in 20 ears with normal hearing and in 20 ears with high-frequency sensorineural hearing loss. The purpose was to determine if DPOAE amplitude is associated with pure-tone behavioral threshold. Comparison of results from the two groups of ears indicated that DPOAEs were reduced in amplitude or were absent in ears with high-frequency hearing loss. The differences occurred at frequencies above 1,500 Hz. Comparing results from 750 to 8,000 Hz within the same ear revealed a frequency-related correspondence of elevated behavioral threshold to reduced DPOAE amplitude. When behavioral thresholds were better than 20 dB HL, DPOAE amplitude was within the range (+/- 2 SDs) determined for the ears with normal hearing. When pure-tone threshold was greater than 50 dB HL, DPOAEs were absent or were significantly attenuated in 16/17 subjects (94%). The association of emission level with behavioral threshold level was variable when threshold was between these two extremes. Results imply that the measurement of DPOAEs has clinical potential as a means of detecting hearing loss by frequency.     

Susceptibility of young adult and old rats to noise-induced hearing loss

This study was designed to test whether old rats show signs of presbyacusis and whether they would be either similarly or more or less susceptible to noise-induced hearing loss than young adult rats. Old (24 months) and young adult (3-4 months) Wistar rats were exposed to a broad-band noise of 113 dB SPL for a duration of 1 h (producing temporary threshold shifts) or 3 days (12 h noise/12 h quiet; permanent shifts). Auditory brainstem response (ABR), distortion product otoacoustic emissions (DPOAEs) and transient evoked otoacoustic emissions (TEOAEs) were measured before and after exposure. At the initial recording (before exposure), old rats demonstrated a small mean ABR threshold elevation, a reduction in amplitude of wave I (WI), a shortening of WI latency and a prolongation of the interpeak interval between WI and WIV, as compared to the young rats. The old rats also demonstrated a small DPOAE amplitude reduction and a reduction of peak-to-peak amplitude in the TEOAE response 2 ms after stimulus, but no reduction in TEOAE energy content between 2 and 4 kHz. These are signs of presbyacusis in the old rats. The noise exposures caused elevations in ABR threshold and reductions in DPOAE amplitude and TEOAE energy content that were similar in both the old and young rats. Their recovery from the noise-induced loss was also similar. Thus, the results of this study show that old and young adult rats, at least when considering clinically relevant intensities and durations of noise exposure, are equally susceptible to the effects of the exposure.     

不同环境对正常青年人诱发性耳声发射检测的影响

目的 研究正常青年人在隔音和非隔音环境下的瞬态诱发耳声发射（TEOAE）和畸变产物耳声发射（DPOAE）,探讨环境噪声对耳声发射的影响,为临床应用提供参考。方法 应用Capella耳声发射仪对正常听力青年人102耳分别在隔音和非隔音环境下记录DPOAE和TEOAE。结果 两种环境下DPOAE的幅值无显著差异,信噪比（S/N－ratio）、叠加次数、扫描时间有显著性差异;ＴＥＯＡＥ的幅值、信噪比、相关系数（Ｃorr)、叠加次数、扫描时间均有显著性差异;隔音和非隔音环境下的ＤＰＯＡＥ、ＴＥＯＡＥ的通过率有显著性差异。结论 环境噪声（５５－６５dBSpL)对ＤＰＯＡＥ幅值（除０.5kHz外）无明显影响,对ＴＥＯＡＥ有显著影响;在听力筛选时,尤其是在非隔音环境下应用ＤＰＯＡＥ较ＴＥＯＡＥ准确率高;不但具有频率特异性,且可明显降低假阳性率。     

Maturation of the auditory system: 1. Transient otoacoustic emissions as an index of inner ear maturation

The transiently evoked otoacoustic emission amplitude of 42 preterm babies (84 ears; post-conceptional age [PCA] 30–36 weeks) was compared with the TEOAE amplitude of 39 full-term babies (78 ears; PCA 37–45 weeks) in order to trace the inner ear maturation characteristics. An ILO-92 otoacoustic emission recording system was used with linear clicks of 70 dB peak equivalent SPL. The results obtained indicated: (1) There was no statistically significant difference between preterm and full-term ears; (2) There was no significant difference between males and females; (3) There was a significant difference between left and right ear TEOAE amplitude; (4) The interaction of ear with age in relation to TEOAE amplitude was statistically significant; (5) Noise and stimulus parameters did not reveal any significant differences between right and left ears; (6) A positive correlation existed between birthweight and TEOAE amplitude; and (7) A negative correlation existed between aminoglycoside treatment and TEOAE amplitude. The results indicate subtle changes in TEOAE amplitude over time, showing a natural development of the inner ear function during the process of maturation.     

Clinical investigation on spontaneous otoacoustic emission (SOAE) in 447 ears

OBJECTIVES: It is known that spontaneous otoacoustic emission (SOAE) is often observed in normal hearing ears, but concrete clinical application of SOAE test has been rarely reported, compared with transiently evoked otoacoustic emission (TEOAE) and distortion product otoacoustic emission (DPOAE) tests. In addition, there have been a variety of opinions concerning laterality of SOAE, and influence of gender and hearing on SOAE. The reason for this may be that each report has the small number of subjects and lacks in statistical power. Therefore, in the present study, SOAE, TEOAE and DPOAE were measured in 447 ears of subjects at various ages with different hearing level, and statistical analysis was performed to investigate the clinical significance of SOAE. MATERIALS AND METHODS: The subjects were 447 ears in 268 patients (268 ears in females, and 179 ears in males). The age of subjects ranged from 0 to 75 years (mean: 30.8 years), and there were 222 left and 225 right ears. The subjects of schoolchildren or older (414 ears) received pure-tone audiometry, and infants (33 ears) received auditory brain-stem response (ABR). SOAE and TEOAE were measured using ILO88 (Otodynamics, Version 4.20). DPOAE was measured using ILO92 (Otodynamics, Version 1.32). RESULTS: Incidence of SOAE and the number of SOAE per ear were high in the subjects at age of 50 years or younger, in those with hearing level of not more than 30 dB, in the right ear, and in females. Incidence of SOAE in the whole of normal hearing ears was approximately 38%, but the ears with SOAE had almost normal hearing of not more than 30 dB. CONCLUSIONS: SOAE is useful for objective hearing assessment. Moreover, SOAE sometimes appeared in the ears in which TEOAE or DPOAE could not be confirmed, and it might be useful for definite diagnosis of disease state to measure SOAE in addition to TEOAE or DPOAE.     

Maturation of the auditory system: 1. Transient otoacoustic emissions as an index of inner ear maturation

The transiently evoked otoacoustic emission amplitude of 42 preterm babies (84 ears; post-conceptional age [PCA] 30-36 weeks) was compared with the TEOAE amplitude of 39 full-term babies (78 ears; PCA 37-45 weeks) in order to trace the inner ear maturation characteristics. An ILO-92 otoacoustic emission recording system was used with linear clicks of 70 dB peak equivalent SPL. The results obtained indicated: (1) There was no statistically significant difference between preterm and full-term ears; (2) There was no significant difference between males and females; (3) There was a significant difference between left and right ear TEOAE amplitude; (4) The interaction of ear with age in relation to TEOAE amplitude was statistically significant; (5) Noise and stimulus parameters did not reveal any significant differences between right and left ears; (6) A positive correlation existed between birthweight and TEOAE amplitude; and (7) A negative correlation existed between aminoglycoside treatment and TEOAE amplitude. The results indicate subtle changes in TEOAE amplitude over time, showing a natural development of the inner ear function during the process of maturation.     

Correlations among evoked potential thresholds, distortion product otoacoustic emissions and hair cell loss following various noise exposures in the chinchilla

Changes in cubic distortion product otoacoustic emissions (ΔDPOAEs), evoked potential threshold shifts (TSs) and outer hair cell (OHC) losses were measured in a population of 95 noise-exposed chinchillas. Each animal was exposed to one of 23 different noises in an asymptotic threshold shift (ATS) producing paradigm or an interrupted noise paradigm which typically produced a toughening effect. Noises were narrow band (400 Hz) impacts with center frequencies of 0.5, 1.0, 2.0, 4.0 or 8.0 kHz presented 1 impact/s at peak SPLs of 109, 115, 121 or 127 dB. The duration of the exposures was 24 h/day for 5 days (ATS paradigm) or 6 h/day for 20 days (toughening paradigm). Based on a linear regression analysis of individual subject and group mean data, correlations among the following dependent variables were made: ΔDPOAEs, ATS, toughening or TS recovery (TS_r), permanent threshold shift (PTS) and OHC loss. Correlations among these metrics were generally highest for DPOAE primary frequency levels, L₁=L₂=70 dB. Correlation between ΔDPOAE and TS_r was typically low, while a considerably higher correlation was found between ΔDPOAE and ATS. Correlations among the permanent measures of noise-induced effects, i.e. for ΔDPOAE/PTS and ΔDPOAE/OHC loss were typically poor when there was only a small or a moderate noise-induced effect (PTS<25 dB and ΔDPOAE<20 dB). However, for PTS<25 dB the correlation between PTS and OHC loss was considerably better than the correlation between ΔDPOAE and OHC loss. For more severe noise-induced changes there was generally a good correspondence between OHC loss, PTS and ΔDPOAE metrics.     

Antioxidant treatment reduces blast-induced cochlear damage and hearing loss

Exposure to blast overpressure has become one of the hazards of both military and civilian life in many parts of the world due to war and terrorist activity. Auditory damage is one of the primary sequela of blast trauma, affecting immediate situational awareness and causing permanent hearing loss. Protecting against blast exposure is limited by the inability to anticipate the timing of these exposures, particularly those caused by terrorists. Therefore a therapeutic regimen is desirable that is able to ameliorate auditory damage when administered after a blast exposure has occurred. The purpose of this study was to determine if administration of a combination of antioxidants 2,4-disulfonyl α-phenyl tertiary butyl nitrone (HPN-07) and N-acetylcysteine (NAC) beginning 1 h after blast exposure could reduce both temporary and permanent hearing loss. To this end, a blast simulator was developed and the operational conditions established for exposing rats to blast overpressures comparable to those encountered in an open-field blast of 14 pounds per square inch (psi). This blast model produced reproducible blast overpressures that resulted in physiological and physical damage to the auditory system that was proportional to the number and amplitude of the blasts. After exposure to 3 consecutive 14 psi blasts 100% of anesthetized rats had permanent hearing loss as determined at 21 days post exposure by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE) testing. Animals treated with HPN-07 and NAC after blast exposure showed a significant reduction in ABR threshold shifts and DPOAE level shifts at 2-16 kHz with significant reduction in inner hair cell (IHC) and outer hair cell (OHC) loss across the 5-36 kHz region of the cochlea compared with control animals. The time course of changes in the auditory system was documented at 3 h, 24 h, 7 day and 21 day after blast exposure. At 3 h after blast exposure the auditory brainstem response (ABR) threshold shifts were elevated by 60 dB in both treated and control groups. A partial recovery of to 35 dB was observed at 24 h in the controls, indicative of a temporary threshold shift (TTS) and there was essentially no further recovery by 21 days representing a permanent threshold shift (PTS) of about 30 dB. Antioxidant treatment increased the amount of both TTS and PTS recovery relative to controls by 10 and 20 dB respectively. Distortion product otoacoustic emission (DPOAE) reached a maximum level shift of 25-30 dB measured in both control and treated groups at 3 h after blast exposure. These levels did not change by day 21 in the control group but in the treatment group the level shifts began to decline at 24 h until by day 21 they were 10-20 dB below that of the controls. Loss of cochlear hair cells measured at 21 day after blast exposure was mostly in the outer hair cells (OHC) and broadly distributed across the basilar membrane, consistent with the distribution of loss of frequency responses as measured by ABR and DPOAE analysis and typical of blast-induced damage. OHC loss progressively increased after blast exposure reaching an average loss of 32% in the control group and 10% in the treated group at 21 days. These findings provide the first evidence that a combination of antioxidants, HPN-07 and NAC, can both enhance TTS recovery and prevent PTS by reducing damage to the mechanical and neural components of the auditory system when administered shortly after blast exposure.     

自发性耳声发射与耳蜗传出调控的关系探讨

OBJECTIVE: To study the relationship between spontaneous otoacoustic emissions(SOAE) and efferent control of cochlea and their clinical significance. METHODS: SOAE, transient evoked otoacoustic emissions (TEOAE), distortion product otoacoustic emissions (DPOAE) and contralateral white noise (60 dB SPL) suppression of TEOAE and DPOAE experiments were conducted in 312 ears of 95 patients with retrocochlear impairment and/or MOCS dysfunction and 64 normal young adults. RESULTS: MOCS dysfunction was shown in 126 ears of 65 patients (130 ears) with auditory neuropathy, 2 ears of 2 patients with unilateral acoustic neuroma, 4 ears of 2 patients with hyperacusis, 14 ears of 26 patients(48 ears) with normal hearing level in unilateral or bilateral tinnitus. Stronger EOAE could be recorded in total 146 ears with MOCS dysfunction at any pure tone hearing level. SOAE could be recorded in 126 of 146 ears (86.3%) with MOCS dysfunction and 44 of 128 ears (34.3%) with normal hearing. SOAE of ears with MOCS dysfunction was mainly at frequencies from 0.693 to 3.055 kHz and SOAE of normal ears was at frequencies from 1.135 to 2.746 kHz. Average value of maximum amplitude of SOAE spectrum (-3.4 +/- 6.4) dB SPL was significantly greater than that in normal ears (-6.8 +/- 7.8) dB SPL (P < 0.01). The major frequency range of SOAE (0.693-3.055 kHz) in MOCS dysfunction ears was essentially consistent with that of efferent suppression in normal ears (0.7-3 kHz). CONCLUSION: The modulation of the cochlear active mechanisms by MOCS mainly presents in the low- and mid-frequency regions, these frequencies correspond to the frequency range of SOAE. Stronger SOAE indicates pathophysiological significance. There is a clear clinical relationship between SOAE and the efferent modulation of the cochlea.     

Evaluation of Hearing Loss after Spinal Anesthesia with Otoacoustic Emissions

The aim of this study was to determine the degree and reversibility of hearing loss (HL) following spinal anesthesia with an objective audiometric test: otoacoustic emissions (OAE). Eleven patients (22 ears) who were undergoing surgery under spinal anesthesia were included in this study. Transient-evoked otoacoustic emissions (TEOAE) and distortion product otoacoustic emissions (DPOAE) were evaluated 1 day before the operation and postoperative day 1, 2, and 15. DPOAE were recorded as DPgram and input/output functions (I/O). The emission amplitudes of the TEOAE and DPOAE of right and left ears were found to be affected immediately after the surgery and progressive improvement detected with full recovery within postoperative 15 days. These changes were mainly at around 1,500–3,000 Hz. None of the patients had permanent OAE amplitude deterioration. Transient HL may occur more often than it is generally assumed, and the symptoms might not be recognized. OAE is an effective and objective way of evaluating the HL in this particular group of patients. We suggest informing patients about this transient HL for medicolegal issues.     

Age dependence of otoacoustic emissions: the loss of amplitude is primarily caused by age-related hearing loss and not by aging alone

The amplitude of otoacoustic emissions (OAE) is known to decrease with increasing age, but it is still unclear whether this is due to aging alone or to age-related hearing loss. This study describes the exploration of a large database (5,142 patients from 0.4 to 89.8 years) collected in a routine clinical testing. Reliable pure tone audiograms, transitory evoked otoacoustic emissions (TEOAE) and distortion product otoacoustic emissions (DPOAE) recordings were available from 5,424 ears without conductive loss, acute sudden deafness or retrocochlear disorder. From this database, group 1 with behavioral thresholds of 10 dB HL or better at all frequencies from 1 to 4 kHz and group 2 with age-accordant thresholds after ISO 7029 were formed. In both groups, the OAE amplitude decreased with increasing age, but in group 1, the effect was significant only for DPOAE recorded at 3 and 4 kHz. In group 2, the loss of amplitude was steeper and highly significant for TEOAE as well as DPOAE at all frequencies, but most pronounced at high frequencies. These findings support the hypothesis that the reduction of OAE amplitude with increasing age is primarily caused by age-linked hearing loss and not by aging alone.     

外耳道压力改变对耳声发射幅值的影响

目的了解外耳道压力改变对耳声发射幅值的影响，进而探讨外耳道压力因素对耳功能状态的影响。方法用ＧＳＩ３３型声导抗仪和ＩＬ０９２型耳声发射仪，对２３例（４６耳）正常人进行不同外耳道压力状态下的ＴＥＯＡＥ和ＤＰＯＡＥ测试。结果外耳道正、负压越大，ＴＥＯＡＥ的平均反应幅值越低，低频区频谱幅值下降明显，高频区无明显改变，Ｆ２在６９６～２００２Ｈｚ之间时，ＤＰＯＡＥ幅值降低明显，Ｆ２为３００３、５００５、６００６Ｈｚ时，ＤＰＯＡＥ幅值无明显改变，Ｆ２为４００４Ｈｚ时，ＤＰＯＡＥ幅值增高。结论正常的耳声发射幅值依赖于正常的耳功能状态。外耳道压力改变可使中耳和内耳的传音功能发生改变，主要表现为低频声的传导被阻滞。     

Increased Sensitivity to Noise-Induced Hearing Loss by Blockade of Endogenous PI3K/Akt Signaling

The PI3K/Akt signaling pathway is involved in mediating survival of sensory hair cells. Here, we investigated the involvement of PI3K/Akt in noise-induced hearing loss in both temporary and permanent threshold shift noise models. The PI3K regulatory subunit p85α and phosphorylation of Akt on serine 473 (p-Akt S473) are downregulated in sensory hair cells, including both outer and inner hair cells, and supporting cells of the mouse organ of Corti 1 h after exposure to permanent-threshold-shift-inducing noise (PTS noise), but not with temporary-threshold-shift-inducing noise (TTS noise). In contrast, the PI3K catalytic subunit p110α and phosphorylation of Akt on threonine 308 (p-Akt T308) do not change with PTS or TTS noise. Additionally, mice pretreated with p85α small interfering RNA (siRNA) have decreased expression of p-Akt1 (S473) in their sensory hair cells and increased sensitivity to TTS noise-induced hearing loss. Finally, Akt1-knockout mice also have enhanced sensitivity to TTS noise-induced hearing loss. In conclusion, this study suggests that endogenous PI3K/Akt signaling is an intrinsic protective mechanism of the inner ear. Blockade of PI3K/Akt signaling pathways increases sensitivity to TTS noise-induced hearing loss.     

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.