Source of level dependent minima in rabbit distortion product otoacoustic emissions.

Sharp level dependent minima (commonly called nulls or notches) in the distortion product otoacoustic emissions (DPOAEs) have been postulated to be due to two different mechanisms. It is shown here that the level dependent nulls in rabbit 2f(1)-f(2) DPOAEs carry the signature of the mixing of a third order nonlinear term with a fifth order nonlinear term. This suggests that the minima are not due to the mixing of signals from two different physical sites of origin, but rather are due to the nature of the nonlinearity itself. Model simulations show that null production is indifferent to several properties of nonlinear input/output functions.

Mechanism for bandpass frequency characteristic in distortion product otoacoustic emission generation.

It is commonly observed that the levels of the 2f1-f2 and the other mf1-nf2 (m = n + 1 = integer) distortion product otoacoustic emissions (DPOAEs) initially increase in level for fixed f2 as fl -->f2, starting at f1

Susceptibility of DPOAEs to sound overexposure in inbred mice with AHL.

The notion that three inbred strains of mice, i.e., C57BL/6J (C57), BALB/cByJ (BALB), and WB/ReJ (WB), which exhibit differential rates of age-related hearing loss (AHL), may also exhibit differential susceptibility to noise-induced hearing loss was tested by comparing the effects of sound overexposure on these strains. The aftereffects of noise overstimulation on the distortion-product otoacoustic emissions (DPOAEs) of these three strains were compared and contrasted to those for the CBA/CaJ (CBA) strain, which does not show changes in hearing threshold sensitivity up to 15 months of age. Two cohorts of mice, one at 2.5 and the other at 6 months of age, were first exposed to a tonal overstimulation paradigm, were allowed to recover, and then were later re-exposed to an octave band noise (OBN), at 3 or 7 months of age, respectively. The two sound exposure episodes were designed to produce either a temporary (tonal exposure) or permanent (OBN exposure) reduction in the levels of the 2f1 - f2 DPOAE in the WB strain, which exhibited the fastest rate of AHL. Although the tonal paradigm resulted in a temporary decrease in DPOAE levels for all strains at both ages, the 2.5-month BALBs showed the greatest susceptibility to this overexposure, while the 2.5-month WBs exhibited the least effects on DPOAEs. At the older age of 6 months, tonal overexposure produced essentially the same reduction in DPOAE levels for all four strains. In addition, there were no differences noted between CBAs and C57s, at either of the two ages. The OBN paradigm resulted in a permanent decrease in DPOAE levels in all the strains exhibiting early AHL, i.e., the C57, BALB, and WB mice, for frequencies about one-half to an octave higher than the exposure frequency, regardless of age. In contrast, the CBA strain was not significantly affected by the OBN overexposure.

Nonlinear interactions that could explain distortion product interference response areas.

Suppression and/or enhancement of third- and fifth-order distortion products by a third tone that can have a frequency more than an octave above and a level more than 40 dB below the primary tones have recently been measured by Martin et al. [Hear. Res. 136, 105-123 (1999)]. Contours of iso-suppression and iso-enhancement that are plotted as a function of third-tone frequency and level are called interference response areas. After ruling out order aliasing, two possible mechanisms for this effect have been developed, a harmonic mechanism and a catalyst mechanism. The harmonic mechanism produces distortion products by mixing a harmonic of one of the primary tones with the other primary tone. The catalyst mechanism produces distortion products by mixing one or more intermediate distortion products that are produced by the third tone with one or more of the input tones. The harmonic mechanism does not need a third tone and the catalyst mechanism does. Because the basilar membrane frequency response is predicted to affect each of these mechanisms differently, it is concluded that the catalyst mechanism will be dominant in the high-frequency regions of the cochlea and the harmonic mechanism will have significant strength in the low-frequency regions of the cochlea. The mechanisms are dependent on the existence of both even- and odd-order distortion, and significant even- and odd-order distortion have been measured in the experimental animals. Furthermore, the nonlinear part of the cochlear mechanical response must be well into saturation when input tones are 50 or more dB SPL.

Vasospasm of the internal auditory artery: significance in cerebellopontine angle surgery.

BACKGROUND: Cochlear ischemia is likely involved in sensorineural hearing loss after cerebellopontine angle (CPA) surgery. OBJECTIVE: To demonstrate the type of vascular damage to the cochlea, apart from arterial section, that can be induced by CPA surgery. METHODS: The effects on measures of both cochlear blood flow (CBF) and distortion-product otoacoustic emissions (DPOAEs) of partial or total mechanical compressions of the internal auditory artery (IAA) were compared in young adult rabbits. RESULTS: When preocclusion baseline activity was compared with postocclusion CBF and DPOAEs, it was clear in the majority of cases that total compressions lasting < or =7 minutes produced the same full recoveries for both measures as did the shorter obstructions of only a few minutes. By contrast, both short and long partial occlusions in which ischemia was interrupted by periods of poor reperfusion (<50% of the initial CBF value) resulted in delayed and prolonged recoveries. In addition, at times, full recovery was not achieved, particularly for DPOAEs, because of vasospasm-like activity. CONCLUSION: Vasospasm of the IAA was induced by a systematic series of IAA compressions and releases that did not provide for full reperfusion. These data support the concept that vasospasm should be prevented whenever hearing preservation is attempted in CPA surgery.

Effects of cis-platinum chemotherapy on otoacoustic emissions: the development of an objective screening protocol. Third place--Resident Clinical Science Award 1998.

To develop an objective, fast, and simply performed screening protocol for cis -platinum (CP) ototoxicity, we compared the efficacy of screening with distortion-product otoacoustic emissions (DPOAEs) with the outcome of both conventional and ultra-high-frequency (UHF) audiometry. Baseline audiometric and DPOAE testing was performed in 66 patients, 33 of whom met criteria for inclusion in the final database. Comparisons were made between baseline measurements and those recorded before subsequent CP infusions. Outcomes were analyzed clinically and with paired repeated-measures analysis of variance. Results indicated that DPOAEs and UHF were better measures than conventional audiometry. Further, DPOAEs may be better suited for screening older patients receiving CP chemotherapy because DPOAEs are as sensitive as UHF and are present in a greater number of these patients. Screening with DPOAEs may be enhanced by testing only in the 3- to 5.2-kHz range, thus decreasing testing time. Higher time averages to increase the signal-to-noise ratio and use of this narrower bandwidth might also allow for accurate bedside testing.

Age-related loss of distortion product otoacoustic emissions in four mouse strains.

Changes in cochlear function in four inbred strains of mice, CBA/CaJ (CBA), C57BL/6J (C57), BALB/cByJ (BALB), and WB/ReJ (WB), previously used to study age-related hearing loss, were evaluated serially as a function of age with 2f(1)-f(2) distortion-product otoacoustic emissions (DPOAEs). DPOAE levels in response to equilevel primary tones for geometric-mean (GM) frequencies from 5.6 to 48.5 kHz were recorded systematically as DP-grams and response/growth or input/output (I/O) functions at monthly intervals from about 2 to 15 months of age. Over the approximate 13-month measurement period, CBAs showed robust and unchanged DPOAEs for all tested frequencies, while BALBs, C57s, and WBs showed strain-specific, age-related decreases in DPOAEs that progressed systematically from the high to low frequencies. Specifically, for the youngest WBs at 2 months of age, no DPOAEs were recordable for GM frequencies > or = 32 kHz, while C57s and BALBs reached the identical stage of cochlear dysfunction by 5 and 8 months, respectively. The differential decline in DPOAE activity shown for WB, C57, and BALB mice supports the notion that they represent unique animal models of age-related changes in cochlear function. In contrast, the unchanging DPOAEs for CBAs over the same time period indicate that this strain makes an effective control for normal cochlear function in the mouse, at least, up to 15 months of age.

Suppression and enhancement of distortion-product otoacoustic emissions by interference tones above f(2). I. Basic findings in rabbits.

The present study measured interference-response areas (IRAs) for distortion-product otoacoustic emissions (DPOAEs) at 2f(1)-f(2), 3f(1)-2f(2), and 2f(2)-f(1). The IRAs were obtained in either awake or anesthetized rabbits, or in anesthetized guinea pigs and mice, by sweeping the frequencies and levels of an interference tone (IT) around a set of f(1) and f(2) primary tones, at several fixed frequencies and levels, while plotting the effects of the IT on DPOAE level. An unexpected outcome was the occurrence of regions of suppression and/or enhancement of DPOAE level when the IT was at a frequency slightly less than to more than an octave above f(2). The IRA of the 2f(1)-f(2) DPOAE typically displayed a high-frequency (HF) lobe of suppression, while the 2f(2)-f(1) emission often exhibited considerable amounts of enhancement. Moreover, for the 2f(2)-f(1) DPOAE, when enhancement was absent, its IRA usually tuned to a region above f(2). Whether or not suppression/enhancement was observed depended upon primary-tone level and frequency separation, as well as on the relative levels of the two primaries. Various physiological manipulations involving anesthesia, eighth-nerve section, diuretic administration, or pure-tone overstimulation showed that these phenomena were of cochlear origin, and were not dependent upon the acoustic reflex or cochlear-efferent activity. The aftereffects of applying diuretics or over-exposures revealed that suppression/enhancement required the presence of sensitive, low-level DPOAE-generator sources. Additionally, suppression/enhancement were general effects in that, in addition to rabbits, they were also observed in mice and guinea pigs. Further, corresponding plots of DPOAE phase often revealed areas of differing phase change in the vicinity of the primary tones as compared to regions above f(2). These findings, along with the effects of tonal exposures designed to fatigue regions above f(2), and instances in which DPOAE level was dependent upon the amount of suppression/enhancement, suggested that the interactions of two DPOAE-generator sources contributed, in some manner, to these phenomena.

Comparison of the auditory-evoked brainstem response wave I to distortion-product otoacoustic emissions resulting from changes to inner ear blood flow.

OBJECTIVE/HYPOTHESIS: Examine and compare in detail the time courses of the auditory brainstem response (ABR) wave I amplitude and latency to the distortion-product otoacoustic emission (DPOAE) amplitude and phase measured in the rabbit model following deliberate obstruction of cochlear blood flow (CBF). METHODS: Using a posterior fossa craniotomy in five rabbits, the internal auditory artery (IAA) was compressed with a probe. ABR and otoacoustic emission were continuously monitored before, during, and after the compressions. RESULTS: ABR wave I amplitudes demonstrated measurable decreases at a mean of 28.3 s after IAA compression, whereas DPOAE amplitudes decreased after a mean of 14.8 s. Wave I latencies began to increase at a mean of 18.3 s after occlusion, while DPOAE phase measures changed after a mean of only 4.8 s following IAA compression. The time-course patterns were similar for the amplitudes of both ABR wave I and DPOAE. CONCLUSIONS: ABR wave I amplitude follows a similar, though delayed (by approximately 10 s) time-course pattern to that of the DPOAE following IAA compression. The implication of these findings for intraoperative auditory monitoring is that changes in many currently employed measures will lag actual surgically induced alterations in CBF by at least 20 to 30 s.

Effects of loop diuretics on the suppression tuning of distortion-product otoacoustic emissions in rabbits.

The suppression tuning of distortion-product otoacoustic emissions (DPOAEs) is commonly assumed to measure frequency selectivity, because the dominant features of suppression-tuning curves (STCs) are similar to the principal properties of the neural-tuning curves (NTCs) of single auditory-nerve fibers. In the present study, several common loop diuretics were used to affect the DPOAE-generation process to determine if reversible ototoxicity could adversely modify the characteristics of STCs, in a manner similar to that shown previously for NTCs. Contour plots of DPOAE level in the presence of a series of variable-level suppressor tones were obtained before and after administering diuretic drugs that reversibly reduced or eliminated DPOAEs. Primary-tone pairs were centered at 2.8 or 4 kHz, with L1 = L2, or L2 < L1. From the resulting plots, STC parameters including tip frequency, threshold at the tip frequency, and Q10 dB measures of tuning were extracted for four suppression criteria of 3, 6, 9, and 12 dB. In the pre-drug nonototoxic state, suppression tuning depended on both primary-tone level (L1, L2), and the relative levels of the primaries (L1-L2), with tuning being sharper for lower- than for higher-level equilevel primaries, and sharpest for offset-level primary tones. Following drug injection, the expected decrease in sharpness of tuning evidenced by changes in Q10 dB as well as the dramatically elevated tip thresholds normally seen for NTCs under similar conditions, were not observed. Overall, Q10 dB increased or decreased more or less randomly, with a slight tendency for STCs to become sharper than prior to drug dosing, for the two highest suppression criteria. The STC-tip frequencies demonstrated significant decreases following diuretic administration that were weakly correlated with the associated decreases in DPOAE amplitude. The most consistent changes in response to the drug-induced reduction in DPOAE level were increases in the STC-tip thresholds. However, these changes were relatively small and rarely exceeded 10 dB. In the absence of notable changes in overall STC shape, a major finding was a change in the effectiveness of suppression following ototoxic insult. However, when the amount of suppression was expressed as a percentage of the DPOAE remaining, the effects of diuretic dosing were often almost completely obscured. Overall, the results demonstrated that when the generation of DPOAEs was interfered with by the introduction of a suppressor tone to produce STCs that resemble NTCs, STCs behaved quite differently following reversible cochlear insult than their previously documented neural counterparts. These findings imply that STCs do not assess the frequency-selective aspects of the cochlear amplification process in a manner similar to NTCs.

Locus of generation for the 2f1-f2 vs 2f2-f1 distortion-product otoacoustic emissions in normal-hearing humans revealed by suppression tuning, onset latencies, and amplitude correlations.

The present study used distortion-product otoacoustic emission (DPOAE) suppression tuning curves (STCs), DPOAE onset latencies (OLs), and DPOAE amplitude correlations to investigate the locus of generation of the 2f1-f2 DPOAE versus the 2f2-f1 DPOAE in humans. The results of the tuning study revealed that, for the 2f1-f2 DPOAE, the tips of the STCs tuned consistently below the geometric-mean (GM) frequency of the primary tones. In contrast, for the 2f2-f1 DPOAE, STCs tuned above the GM of the primaries, with 50% of the tip frequencies at, or above, the 2f2-f1 frequency place. When the average ratio of the 2f2-f1 to the 2f1-f2 tip frequencies was computed, a factor of 1.44 provided an estimate of the frequency shift needed to align the two DPOAE generation sites. Other results showed that OLs for the 2f2-f1 DPOAE were uniformly shorter than those for the 2f1-f2, with differences at the low frequencies amounting to as much as 6-7 ms. Further, for both DPOAEs, curves describing latency decreases as a function of increasing GM frequencies were best fit by power functions. Shifting the GM frequency producing the 2f2-f1 DPOAE by a factor of 1.6 caused the latency distributions for both DPOAEs to overlap thus resulting in a single function that described cochlear delay as a function of GM frequency. Finally, for each GM frequency in the DP-gram, sliding correlations from 108 normal ears were performed on both DPOAEs by holding the primaries producing the 2f1-f2 DPOAE constant, while all 2f2-f1 DPOAE amplitudes were successively correlated with the 2f1-f2 amplitudes. This procedure demonstrated that, for a given GM frequency producing the 2f1-f2, the correlations between the two DPOAEs peaked when the primaries of the 2f2-f1 were at a GM frequency that positioned the 2f2-f1 frequency place near the GM of the primaries that produced the 2f1-f2 DPOAE. As a whole, the above findings strongly suggest that the 2f2-f1 DPOAE in humans is generated basal to the primary-tone place on the basilar membrane.

Visualization of the onset of distortion-product otoacoustic emissions, and measurement of their latency.

This paper describes a method for visualization of the onset of distortion-product otoacoustic emission (DPOAE) waveforms in the time domain. The DPOAE waveforms are obtained using ensemble averaging of samples of microphone output. A rectangular sample window is used, and the primary tones are turned on within the sample window. The phases of the primary tones (f1 and f2) are varied systematically between samples in such a way that the primary tones, and all DPOAEs (e.g., 2f2-f1, 3f1-2f2, 2f1), except the DPOAE of interest (e.g., 2f1-f2), are cancelled in the ensemble average. Visualization of the DPOAE onset allows measurement of the onset latency (OSL) of the DPOAE. These direct measurements of OSL are compared to phase-gradient latencies (PGLs) in the same ears determined by measuring the phase change of the DPOAE as a function of DPOAE frequency. The direct measures of OSL vary from > 10 to < 1 ms, decrease with increasing frequency and increasing stimulus level, and are shorter in rabbits than humans. The direct measures of OSL are, in general, quantitatively similar to PGL estimates, but there are exceptions. Visualization of DPOAE onset also allows quantification of DPOAE rise times, and reveals phase and amplitude changes of the DPOAE that occur several milliseconds after onset in rabbits and humans. It is proposed that the phase and amplitude changes result from vector summation of multiple components of the DPOAE signal, each with a different latency.

Effects of ear-canal standing waves on measurements of distortion-product otoacoustic emissions.

At frequencies above 3 kHz, standing waves in the ear canal complicate calibration of stimulus sound-pressure levels (SPLs) for measurements of distortion-product otoacoustic emissions (DPOAEs). In the literature, two stimulus-presentation strategies have been used for DPOAE measurements. In the "in-the-ear adjustment" strategy, the voltage command to the speakers is adjusted to maintain a constant stimulus SPL across frequency at the DPOAE-measurement microphone. In the "iso-voltage" strategy, the voltage presented to the speakers is held constant across frequency, on the basis of the assumption that the frequency response of the speakers is approximately flat at the eardrum in the average human ear canal. Because of standing-wave effects, there are large, systematic but idiosyncratic differences of stimulus SPL between the two strategies. DPOAE-versus-frequency functions ("DPOAE audiograms") obtained using both stimulus-presentation strategies in the same ears are presented. The differences of stimulus SPL between the two strategies, and the associated differences of DPOAE amplitude, are described and quantified. Around frequencies of standing-wave minima at the DPOAE probe, the in-the-ear adjustment strategy resulted in smaller DPOAEs at high L1 = L2, but much larger DPOAEs at low L1 = L2, than did the iso-voltage strategy. For any L1, the DPOAE-amplitude differences between the two strategies varied systematically with L1-L2. At the stimulus levels used to construct previously published population norms for clinical applications (i.e., L1 > or = 65 dB SPL), there are only small differences of mean DPOAE amplitudes, and of the standard deviations of these means, between the two strategies.

Time-windowing of click-evoked otoacoustic emissions to increase signal-to-noise ratio.

OBJECTIVE: To investigate the effects of decreasing the response-window duration on the signal-to-noise ratio (S/N) of click-evoked otoacoustic emissions (CEOAEs). DESIGN: The ILO88 (Otodynamics, Ltd.) was used to measure CEOAEs from 149 normal adult ears, and 75 adult ears with high-frequency sensorineural hearing loss. Data were collected using the default response window of 2.5 to 20.5 msec post-click. Each response was rewindowed, post-hoc, from 2.5 to 7.5 msec, 2.5 to 9 msec, 7.75 to 14.25 msec, and 13 to 19.5 msec post-click. For each window, spectra of the CEOAE and of the background noise were determined. The S/N was estimated by subtracting the noise level from the CEOAE amplitude. RESULTS: The 13- to 19.5-msec window contained little CEOAE energy relative to earlier windows. Relative to the 2.5- to 20.5-msec window, the 2.5- to 7.5- and 2.5- to 9-msec windows reduced noise levels more than CEOAE amplitudes, yielding increased S/N, and greater "reproducibility" values. The increased S/N of the 2.5- to 7.5- and 2.5- to 9-msec windows allowed measurement of greater CEOAE-amplitude reductions in the impaired ears relative to the normal ears. With short-duration windows, click-presentation rate could be increased, allowing more responses to be averaged in a given time, thus further decreasing noise levels. Although click rate was not varied in the present study, the decrease of noise levels is predictable. Accounting for this factor, it is expected that a specified S/N would be obtained about five times faster using the 2.5- to 7.5-msec window with a 7.5-msec interstimulus interval, than when using the default window. CONCLUSIONS: Decreasing the response-window duration substantially increases the measurement efficiency of CEOAEs in adults, and thus may enhance clinical-test performance.

Patterns of evoked otoacoustic emissions associated with acoustic neuromas.

Evoked otoacoustic emissions (OAEs) are assumed to reflect healthy outer hair cell function. Over the past few years, evoked OAEs have been shown to be useful as indicators of cochlear hearing loss. Because basic studies have shown that OAEs are extremely sensitive to cochlear anoxia and hypoxia, as well as to the adverse effects of many inner ear diseases, it is possible that these objective tests can provide some insight into the fundamental basis of the hearing loss exhibited by patients with acoustic neuromas. The primary aim of the present study was to examine the effects of acoustic neuromas on the amplitudes of evoked OAEs and to compare these findings with tumor-induced hearing levels. To this end, tests of behavioral audiometry, distortion-product otoacoustic emissions and transiently evoked otoacoustic emissions were performed on 44 patients with verified acoustic neuromas. The results demonstrated that the majority of ears with acoustic neuromas displayed one of two distinct patterns of evoked OAEs: a cochlear pattern or a noncochlear pattern. Although behavioral hearing thresholds were higher with larger tumors, OAE levels exhibited no clear relationship to tumor size. The present findings support the notion that acoustic neuromas may cause hearing impairment according to two types of influence that act at different levels of the peripheral auditory system. The tumor's cochlear effect on evoked OAE activity is most likely caused by an indirectly mediated compromise of the organ of Corti's vascular supply. It is probable that the direct pressure of the tumor on the eighth cranial nerve is responsible for the observed noncochlear effects.

Dependence of distortion-product otoacoustic emissions on primary levels in normal and impaired ears. II. Asymmetry in L1,L2 space.

Previous studies indicate that the amplitude of 2f1-f2 distortion-product otoacoustic emissions (DPOAEs), evoked by two tones of frequencies f1 < f2, demonstrates a complex dependence on the levels (L1 and L2) of the primary tones. In the present study, 2f1-f2 DPOAE amplitudes were measured over a wide range of L1 and L2 in normal human ears, allowing a systematic, level-dependent asymmetry of DPOAE amplitude in L1,L2 space to be characterized. The L1,L2 at which DPOAEs were largest was close to L1 = L2 at high stimulus levels, but moved monotonically toward L1 > L2 as stimulus levels decreased. A related observation was that DPOAE amplitude had a greater dependence on L1 and on L2. These asymmetries were quantified in normal human ears, and compared to the corresponding asymmetries apparent in data from animal models. Recent studies have demonstrated that the reduction of DPOAE amplitude by cochlear trauma is greater when L1 > L2 than when L1 = L2, suggesting that the reduction of DPOAEs by trauma demonstrates an asymmetry in L1,L2 space that is qualitatively similar to that of normative DPOAE amplitude. To investigate this issue, 2f1-f2 DPOAE amplitudes were measured over a wide range of L1 and L2 in rabbit ears pre- and postinjection of the ototoxic loop-diuretic ethacrynic acid. The results indicate that the asymmetry in L1,L2 space of the reduction of DPOAEs by trauma is both qualitatively and quantitatively similar to the asymmetry in L1,L2 space of normative DPOAE amplitude. Specifically, the L1 values that maximized normative DPOAE amplitudes for any specified L2 (or, equivalently, the L1 values that allowed L2 to be minimized for any specified normative DPOAE amplitude) also yielded the greatest reduction of DPOAEs by the diuretic. In humans, the L1 values that maximize normative DPOAE amplitudes for any specified L2 are well approximated by a simple equation, with parameters that vary with frequency and f2/f1. It is suggested that the L1,L2 values defined by this equation may be optimum for use in clinical applications.

Early effects of cerebellopontine angle compression on rabbit distortion-product otoacoustic emissions: a model for monitoring cochlear function during acoustic neuroma surgery.

A rabbit model was developed to simulate the effects of ischemia that may occur during surgical removal of tumors involving the cerebellopontine angle or internal auditory canal. Specifically, the internal auditory artery was visualized through a posterior craniotomy and mechanically compressed for repetitive 1-minute intervals with a micromanipulator-controlled glass pipet terminating in a smooth bead. The 2f1-f2 distortion-product otoacoustic emissions were used to monitor the susceptibility of cochlear function to compressive effects. Distortion-product otoacoustic emissions were measured during discrete preblock, block, and postblock periods to determine the time course of distortion-product otoacoustic emission reduction and its return to baseline levels after rapid obstruction and resumption, respectively, of the cochlear vascular supply. Comparisons during these times indicated that preblock distortion-product otoacoustic emission levels were very stable, often varying by less than 1 dB. Additionally, distortion-product otoacoustic emissions were very sensitive to brief vascular occlusions in that, within approximately 25 seconds of blockage onset, emission levels at all frequencies decreased at rates of about -1.5 dB/second. On alleviation of the occlusion, distortion-product otoacoustic emissions rapidly and completely returned to preblock levels with a delay of about 4 seconds and recovery slopes of about 10.5 dB/second. A notable finding in some animals was that early and reproducible variations in distortion-product otoacoustic emission levels occurred within 5 to 8 seconds of internal auditory artery compression. When present, these transitory changes in distortion-product otoacoustic emission levels acted as early warning signs for vascular compromise of cochlear function.

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.

Distortion product emissions in humans. II. Relations to acoustic immittance and stimulus frequency and spontaneous otoacoustic emissions in normally hearing subjects.

Multifrequency and multicomponent evaluations of aural acoustic immittance, including tympanometry and acoustic reflex testing, were performed on 44 normal ears to examine the influence of middle ear functioning on the generation and detection of distortion product otoacoustic emissions (DPEs). In the same ears, the prevalence and parametric features of spontaneous and stimulus frequency emissions were also assessed so that their relationship to the detection "thresholds" and amplitudes of corresponding DPEs could be determined. The general outcome was that none of the examined features of acoustic immittance provided an explanation for the discrete, low-amplitude DPE regions observed in about one third of normal ears. Moreover, the presence of typical spontaneous and stimulus frequency emissions in these same "irregular" ears indicated that emission generation and reverse cochlear transmission were also operating normally within these regions of reduced DPEs. Consequently, other, as yet undetermined influences appear to contribute to the DPE variability noted in some ears. Finally, the simultaneous presence of stimulus frequency emissions, but not spontaneous emissions, appeared to reduce the detection "thresholds" and increase the amplitudes of low-frequency DPEs.