FIG 1
Diagram illustrating the delay of the otoacoustic emission. Round-trip group delay of the emission measured in the ear canal consists of the delay from speakers to the stapes ( sp-st ), the forward and backward delays in the cochlea ( forward and backward ), and the delay from the stapes to the microphone ( st-mic ).
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It is commonly accepted that the cochlea emits sound by a backward traveling wave along the cochlear partition. This belief is mainly based on an observation that the group delay of the otoacoustic emission measured in the ear canal is twice as long as the forward delay. In this study, the otoacoustic emission was measured in the gerbil under anest...
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... cochlea not only senses a variety of environmental sounds but also generates sounds. Ear-generated sound can be recorded in the external ear canal using a sensitive miniature microphone and is termed an otoacoustic emission (Kemp 1978). When two tones generated by two speakers at frequencies f1 and f2 (f2 f1) are delivered to the ear canal ( Fig. 1), these airborne stimuli vibrate the eardrum and the middle-ear ossicular chain and so propagate into the cochlear fluids. These sounds in the fluid initiate the vibration of the basilar membrane (BM), a spiral membrane structure along the cochlear length (Cooper and Rhode 1997;Robles et al. 1991Robles et al. , 1997. BM vibrations ...
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... the cochlear length (Cooper and Rhode 1997;Robles et al. 1991Robles et al. , 1997. BM vibrations travel to their best-frequency (BF) locations, where the vibration shows the largest amplitude and nonlinearity, i.e., nonproportional growth with stimulus intensity (Rhode 1971;Robles and Ruggero 2001) (f1 and f2 peaks on the right-side plots in Fig. 1). Distortion product otoacoustic emissions (DPOAEs) at frequencies (n 1)f1nf2 and (n 1)f2-nf1 (n 1, 2, 3,. . .) are generated by nonlinear vibration at the f1 and f2 overlapping location (the DP site in Fig. 1) (Cooper and Rhode 1997;Dong and Olson 2005;Kim et al. 1980;Knight and Kemp 2001;Robles et al. 1991Robles et al. , 1997Shera ...
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... i.e., nonproportional growth with stimulus intensity (Rhode 1971;Robles and Ruggero 2001) (f1 and f2 peaks on the right-side plots in Fig. 1). Distortion product otoacoustic emissions (DPOAEs) at frequencies (n 1)f1nf2 and (n 1)f2-nf1 (n 1, 2, 3,. . .) are generated by nonlinear vibration at the f1 and f2 overlapping location (the DP site in Fig. 1) (Cooper and Rhode 1997;Dong and Olson 2005;Kim et al. 1980;Knight and Kemp 2001;Robles et al. 1991Robles et al. , 1997Shera and Guinan 1999;Siegel et al. 1982;Tubis et al. 2000). The DPOAE at the frequency of 2f1f2 has the largest amplitude among different emissions (Lonsbury-Martin et al. 1990;Probst et al. 1991) and is used to study ...
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... emission data in the literature known to us, which show that the emission round-trip delay is twice the forward delay, were measured in the ear canal. Figure 1, however, shows that the group delay of the emission in the ear canal is determined by the delay from the speaker to the stapes ( sp-st ), the forward delay from the stapes to emission-generation site ( forward ), the backward delay from this site to the stapes ( backward ), and the delay from the stapes to the microphone ( sp-mic ). It is impos- sible to calculate backward unless the other delays are known. ...
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... between the results of this study and those of previous studies are due to the delays of the external and middle ears. In contrast to previous studies, the emission was measured as stapes vibration in this study and the external and middle ear delays were not included in the emission round-trip delay. In Fig. 1, the delays of sp-st and sp-mic are determined by the speed of sound in air (about 0.34 mm/s) and the distances between the speaker and the stapes and between the stapes and the microphone. Although the speed of sound in air is relatively constant, the distance can vary dramatically across different studies. The group delay of 2f1-f2 ...
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The thresholds of compound action potentials evoked by tone pips were measured in the cochleae of anesthetized gerbils, both in adults and in neonates aged 14, 16, 18, 20 and 30 days, using round-window electrodes. Stapes vibrations were also measured, using a laser velocimeter, in many of the same ears of adults and neonates aged 14, 16, 18 and 20...
Middle-ear sound transmission was evaluated as the middle-ear transfer admittance H(MY) (the ratio of stapes velocity to ear-canal sound pressure near the umbo) in gerbils during closed-field sound stimulation at frequencies from 0.1 to 60 kHz, a range that spans the gerbil's audiometric range. Similar measurements were performed in two laboratorie...
The cochlear travelling wave is fundamental to the ability of the mammalian auditory system to resolve frequency. The seashell-shaped outer bone of the cochlea (the auditory inner ear) contains a spiral of cochlear fluid and the sensory tissue known as the cochlear partition. Sound travels down the ear canal to the eardrum, causing its flexible tym...
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... The steep phase gradient, as well as the group delay, originates from the signal front delay which is the time difference between the onset of the basilar membrane (BM) and stapes, and the filter delay that the BM spends on building the peak of the traveling wave (Ruggero, 2004). The filter delay of the BM, the major portion of the OAE group delay, is a unique physiological parameter closely related to the frequency selectivity of the cochlear tuning, with sharper tuning corresponding to longer group delays (Shera and Guinan, 2003;Ren et al., 2006). If there is no cochlear tuning involved (such as the response in a passive tube), the steep phase gradient would disappear (Figure 3) and the group delay would approach 0 as a consequence. ...
Otoacoustic emissions (OAEs) are low-level sounds generated by the cochlea and widely used as a noninvasive tool to inspect cochlear impairments. However, only the amplitude information of OAE signals is used in current clinical tests, while the OAE phase containing important information about cochlear functions is commonly discarded, due to the insufficient frequency-resolution of existing OAE tests. In this study, swept tones with time-varying frequencies were used to measure stimulus frequency OAEs (SFOAEs) in human subjects, so that high-resolution phase spectra that are not available in existing OAE tests could be obtained and analyzed. The results showed that the phase of swept-tone SFOAEs demonstrated steep gradients as the frequency increased in human subjects with normal hearing. The steep phase gradients were sensitive to auditory functional abnormality caused by cochlear damage and stimulus artifacts introduced by system distortions. At low stimulus levels, the group delays derived from the phase gradients decreased from around 8.5 to 3 ms as the frequency increased from 1 to 10 kHz for subjects with normal hearing, and the pattern of group-delay versus frequency function showed significant difference for subjects with hearing loss. By using the swept-tone technology, the study suggests that the OAE phase gradients could provide highly sensitive information about the cochlear functions and therefore should be integrated into the conventional methods to improve the reliability of auditory health screening.
... They are sensitive to the phenomenon of suppressive masking (Zurek and Clark, 1981) as well as to auditory overstimulation (Evans et al., 1981). The roundtrip delay of these emissions, measured as the phase-frequency slope (i.e., group delay) is twice as large as the forward delay propagation of the cochlear traveling wave (Kimberley et al., 1993;Ren et al., 2006). This has been deemed evidence of a traveling wave propagating backwards and arguably refutes any possible origin from higher neuronal processes. ...
The vertebrate ear is endowed with remarkable perceptual capabilities. The faintest sounds produce vibrations of magnitudes comparable to those generated by thermal noise and can nonetheless be detected through efficient amplification of small acoustic stimuli. Two mechanisms have been proposed to underlie such sound amplification in the mammalian cochlea: somatic electromotility and active hair-bundle motility. These biomechanical mechanisms may work in concert to tune auditory sensitivity. In addition to amplitude sensitivity, the hearing system shows exceptional frequency discrimination allowing mammals to distinguish complex sounds with great accuracy. For instance, although the wide hearing range of humans encompasses frequencies from 20 Hz to 20 kHz, our frequency resolution extends to one-thirtieth of the interval between successive keys on a piano. In this article, we review the different cochlear mechanisms underlying sound encoding in the auditory system, with a particular focus on the frequency decomposition of sounds. The relation between peak frequency of activation and location along the cochlea - known as tonotopy - arises from multiple gradients in biophysical properties of the sensory epithelium. Tonotopic mapping represents a major organizational principle both in the peripheral hearing system and in higher processing levels and permits the spectral decomposition of complex tones. The ribbon synapses connecting sensory hair cells to auditory afferents and the downstream spiral ganglion neurons are also tuned to process periodic stimuli according to their preferred frequency. Though sensory hair cells and neurons necessarily filter signals beyond a few kHz, many animals can hear well beyond this range. We finally describe how the cochlear structure shapes the neural code for further processing in order to send meaningful information to the brain. Both the phase-locked response of auditory nerve fibers and tonotopy are key to decode sound frequency information and place specific constraints on the downstream neuronal network.
... The estimates were based on the assumption that the DPOAE group delays for f2 or f1 sweeps amount to twice the CF group delay of the BM traveling wave. However, other researchers showed on experimental animals this to be not the case [53,66]. ...
To date, objective measurements and psychophysical experiments have been used to measure frequency dependent basilar membrane (BM) delays in humans; however, in vivo measurements have not been made. This study aimed to measure BM delays by performing intracochlear electrocochleography in cochlear implant recipients. Sixteen subjects with various degrees of hearing abilities were selected. Postoperative Computer Tomography was performed to determine electrode locations. Electrical potentials in response to acoustic tone pips at 0.25, 0.5, 1, 2, and 4 kHz and clicks were recorded with electrodes at the frequency specific region. The electrode array was inserted up to the characteristic cochlear frequency region of 250 Hz for 6 subjects. Furthermore, the array was inserted in the region of 500 Hz for 15 subjects, and 1, 2, and 4 kHz were reached in all subjects. Intracochlear electrocochleography for each frequency-specific tone pip and clicks showed detectable responses in all subjects. The latencies differed among the cochlear location and the cochlear microphonic (CM) onset latency increased with decreasing frequency and were consistent with click derived band technique. Accordingly, BM delays in humans could be derived. The BM delays increased systematically along the cochlea from basal to apical end and were in accordance with Ruggero and Temchin, 2007.
... The backward traveling wave theory, which postulates that OAE-induced waves travel slowly along the basilar membrane (BM), is widely accepted as an explanation of the propagation of the OAE [1,2]. However, this predominant backward slow-wave theory cannot explain some experimental phenomena [3][4][5][6] favoring the fast compression wave theory that would exist in the lymph fluids surrounding the BM. In the compression wave theory, the slow-speed propagation of the backward transversal wave motion of the BM is replaced by a fast-fluidic compression wave and experimental time/phase differences are accounted for by mechanisms independent of the wave. ...
... where d is the differential operator, φ is the phase in radius, and f is the frequency. Group delay has been used in most OAE studies [2,5,15,16,24] to quantify the delay for determining the direction of the wave propagation. ...
... However, this influence is minimal considering that the speed of the compression wave is two orders of magnitude higher than that of the traveling wave. The BM vibration measurement method used in this study is also essentially the same as that used by He et al. and Ren et al. [3][4][5]. Therefore, if the compression wave does exist in this preparation, we should be able to observe its effect, as a transverse wave in the forward direction in our experiments. ...
The discovery that an apparent forward-propagating otoacoustic emission (OAE) induced basilar membrane vibration has created a serious debate in the field of cochlear mechanics. The traditional theory predicts that OAE will propagate to the ear canal via a backward traveling wave on the basilar membrane, while the opponent theory proposed that the OAE will reach the ear canal via a compression wave. Although accepted by most people, the basic phenomenon of the backward traveling wave theory has not been experimentally demonstrated. In this study, for the first time, we showed the backward traveling wave by measuring the phase spectra of the basilar membrane vibration at multiple longitudinal locations of the basal turn of the cochlea. A local vibration source with a unique and precise location on the cochlear partition was created to avoid the ambiguity of the vibration source in most previous studies. We also measured the vibration pattern at different places of a mechanical cochlear model. A slow backward traveling wave pattern was demonstrated by the time-domain sequence of the measured data. In addition to the wave propagation study, a transmission line mathematical model was used to interpret why no tonotopicity was observed in the backward traveling wave.
... An alternative concept referred to as the fast compression wave (CW) hypothesis recently gained new attention based on the results of a series of studies by Ren and colleagues (Ren 2004;Ren et al. 2006;He et al. 2007;He et al. 2008;He et al. 2010;He and Ren 2013). According to their interpretation, twotone evoked distortion products (DPs) appear to travel back to the stapes via cochlear fluids as a CW, where motion of the stapes then initiates a forward-TW along the cochlear partition. ...
Sound energy propagates in the cochlea through a forward-traveling or slow wave supported by the cochlear partition and fluid inertia. Additionally, cochlear models support traveling wave propagation in the reverse direction as the expected mechanism for conveying otoacoustic emissions out of the cochlea. Recently, however, this hypothesis has been questioned, casting doubt on the process by which otoacoustic emissions travel back out through the cochlea. The proposed alternative reverse travel path for emissions is directly through the fluids of the cochlea as a compression pressure in the form of a fast wave. In the present study, a custom-made micro-pressure sensor was used in vivo in the gerbil cochlea to map two-tone-evoked pressure responses at distinct longitudinal and vertical locations in both the scala tympani and scala vestibuli. Analyses of the magnitude and phase of intracochlear pressure responses at the primary tone and distortion product frequencies were used to distinguish between fast and slow waves in both the forward- and reverse-propagation directions. Results demonstrated that distortion products may travel in both forward and reverse directions post-generation and the existence of both traveling and compression waves. The forward-traveling component appeared to duplicate the process of any external tone, tuned to the local characteristic-frequency place, as it increased compressively and nonlinearly with primary-tone levels. A compression wave was evidenced at frequencies above the cutoff of the recording site. In the opposite direction, a reverse-traveling wave played the major role in driving the stapes reversely and contributed to the distortion product otoacoustic emission. The compression wave may also play a role in reverse propagation when distortion products are generated at a region close to the stapes.
... If, however, the degree of asymmetry is increased so that the net force on the BM is increased, an additional wave packet at 2t g will become more evident. In a healthy cochlea, a net force on the partition can potentially be generated from various physiological process, such as the distortion product that is hypothesized to arise from the interaction of two primary tones in a region near the best place of the higher tone [27]. In an experiment reported by He et al. [28], the BM only had a group delay t g when it was stimulated by such forces. ...
In a sensitive cochlea, the basilar membrane response to transient excitation of any kind-normal acoustic or artificial intracochlear excitation-consists of not only a primary impulse but also a coda of delayed secondary responses with varying amplitudes but similar spectral content around the characteristic frequency of the measurement location. The coda, sometimes referred to as echoes or ringing, has been described as a form of local, short term memory which may influence the ability of the auditory system to detect gaps in an acoustic stimulus such as speech. Depending on the individual cochlea, the temporal gap between the primary impulse and the following coda ranges from once to thrice the group delay of the primary impulse (the group delay of the primary impulse is on the order of a few hundred microseconds). The coda is physiologically vulnerable, disappearing when the cochlea is compromised even slightly. The multicomponent sensitive response is not yet completely understood. We use a physiologically-based, mathematical model to investigate (i) the generation of the primary impulse response and the dependence of the group delay on the various stimulation methods, (ii) the effect of spatial perturbations in the properties of mechanically sensitive ion channels on the generation and separation of delayed secondary responses. The model suggests that the presence of the secondary responses depends on the wavenumber content of a perturbation and the activity level of the cochlea. In addition, the model shows that the varying temporal gaps between adjacent coda seen in experiments depend on the individual profiles of perturbations. Implications for non-invasive cochlear diagnosis are also discussed.
... There is no phase difference between the reticular lamina and basilar membrane vibration (Fig. 2B). The large phase lag resulted mainly from the propagation delays of the sound system, external and middle ears [15]. ...
Mechanical coupling between the tectorial membrane and the hair bundles of outer hair cells is crucial for stimulating mechanoelectrical transduction channels, which convert sound-induced vibrations into electrical signal, and for transmitting outer hair cell-generated force back to the basilar membrane to boost hearing sensitivity. It has been demonstrated that the detached tectorial membrane in mice with C1509G alpha tectorin mutation caused hearing loss, but enhanced electrically evoked otoacoustic emissions. To understand how the mutated cochlea emits sounds, the reticular lamina and basilar membrane vibrations were measured in the electrically stimulated cochlea in this study. The results showed that the electrically evoked basilar membrane vibration decreased dramatically while the reticular lamina vibration and otoacoustic emissions exhibited no significant change in C1509G mutation mice. This result indicates that a functional cochlear amplifier and a normal basilar membrane vibration are not required for the outer hair cell-generated sound to exit the cochlea.
... Two opposing hypotheses have been put forward to explain backward propagation. According to the slow travelling wave hypothesis, the vibration backpropagates as a travelling wave using the BM as a medium [248][249][250][251], while in the other one, OAE exits the cochlea by a fast compression wave in the cochlear fluid [247,[252][253][254][255][256][257]. A wide variety of experiments and models have been devised for demonstrating the validity of both hypotheses and it has been shown that the original results of He et al. [258] can be reproduced in models without fast waves [259,260]. ...
The cochlea plays a crucial role in mammal hearing. The basic function of the cochlea is to map sounds of different frequencies onto corresponding characteristic positions on the basilar membrane (BM). Sounds enter the fluid-filled cochlea and cause deflection of the BM due to pressure differences between the cochlear fluid chambers. These deflections travel along the cochlea, increasing in amplitude, until a frequency-dependent characteristic position and then decay away rapidly. The hair cells can detect these deflections and encode them as neural signals. Modelling the mechanics of the cochlea is of help in interpreting experimental observations and also can provide predictions of the results of experiments that cannot currently be performed due to technical limitations. This paper focuses on reviewing the numerical modelling of the mechanical and electrical processes in the cochlea, which include fluid coupling, micromechanics, the cochlear amplifier, nonlinearity, and electrical coupling.
... It is still unknown if this discrepancy is due to measurement limitations in recording low-level SOAEs or due to an additional mechanism that is related to evoked OAEs and threshold microstructure but not to SOAEs. Numerous empirical studies reported evidence that OAE related intracochlear backward transmission toward the stapes occurs via fast compressional sound waves, and not via slow backward traveling waves (Ren 2004; Ren et al. 2006; Ruggero 2004; Siegel et al. 2005, He et al. 2008 He et al. 2010 ). These results are consistent with the LOT, because the LOT does not require a backward traveling wave, and local oscillator-generated emissions can reach the stapes through the cochlear fluids. ...
Understanding the origin of spontaneous otoacoustic emissions (SOAEs) in mammals has been a challenge for more than three decades. Right from the beginning two mutually exclusive concepts were explored. After 30 years this has now resulted in two well established but incompatible theories, the global standing-wave theory and the local oscillator theory. The outcome of this controversy will be important for our understanding of inner ear functions, because local tuned oscillators in the cochlea would indicate the possibility of frequency analysis via local resonance also in mammals. A previously unexploited opportunity to gain further information on this matter lies in the occasional cases of high-multiple SOAEs in human ears, which present a large number of adjacent small frequency intervals. Here, eight healthy ears of four subjects (12 to 32 SOAEs per ear) are compared with individually simulated ears where frequency spacing was random-generated by two different techniques. Further, a group of 1000 ears was simulated presenting a mean of 21.3 SOAEs per ear. The simulations indicate that the typical frequency spacing of human SOAEs may be due to random distribution of emitters along the cochlea plus a graded probability of mutual close-range suppression between adjacent emitters. It was found that the distribution of frequency intervals of SOAEs shows no above-chance probability of multiples of the preferred minimum distance (PMD) between SOAEs and that the size of PMD is related to SOAE density. The variation in size between adjacent small intervals is not significantly different in random-generated than in measured data. These three results are not in agreement with the global standing-wave theory but are in line with the local oscillator theory. In conclusion, the results are consistent with intrinsic tuning of cochlear outer hair cells.
... Either special methods utilizing interrupted stimuli allow DPOAE onset latency to be visualized directly (293), or the frequency dependence of the phase of DPOAEs reveals their so-called group delays (see sect. IVF) (130,185,186,221,231). ...
To enhance weak sounds while compressing the dynamic intensity range, auditory sensory cells amplify sound-induced vibrations in a nonlinear, intensity-dependent manner. In the course of this process, instantaneous waveform distortion is produced, with two conspicuous kinds of interwoven consequences, the introduction of new sound frequencies absent from the original stimuli, which are audible and detectable in the ear canal as otoacoustic emissions, and the possibility for an interfering sound to suppress the response to a probe tone, thereby enhancing contrast among frequency components. We review how the diverse manifestations of auditory nonlinearity originate in the gating principle of their mechanoelectrical transduction channels; how they depend on the coordinated opening of these ion channels ensured by connecting elements; and their links to the dynamic behavior of auditory sensory cells. This paper also reviews how the complex properties of waves traveling through the cochlea shape the manifestations of auditory nonlinearity. Examination methods based on the detection of distortions open noninvasive windows on the modes of activity of mechanosensitive structures in auditory sensory cells and on the distribution of sites of nonlinearity along the cochlear tonotopic axis, helpful for deciphering cochlear molecular physiology in hearing-impaired animal models. Otoacoustic emissions enable fast tests of peripheral sound processing in patients. The study of auditory distortions also contributes to the understanding of the perception of complex sounds.
