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The TW envelope represents the excitation intensity applied to the organ of Corti as a function of distance along the length of the cochlea. The tonotopic re-distribution of stimulus energy achieved by the TW is essential in the mammalian cochlea because it facilitates the neural representation of stimulus frequencies well above the maximum nerve fibre firing rate of around 2 kHz.

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This follows because acoustic radiation efficiency is strongly related to the size of the radiating object, with sound from large objects tending to be dominated by low frequencies and peaking near the apex and with sounds from small objects tending to be dominated by high frequencies, peaking at the base. The functional significance of this is obvious. He found the travelling wave peak in response to a pure tone stimulus to extend over a third or more of the entire cochlear length see Fig. In the healthy living cochlea, the TW peak for low-level pure tone stimulation is much sharper 17 , The TW peak covers less than 1 mm and a shift in frequency of just one-third of an octave moves the TW peak to stimulate an entirely different set of sensory cells see Ashmore, this volume.

The reason for the poor imaging quality of a dead or deaf cochlea Fig. If viscous damping is low, then the TW peak will be sharp and its amplitude will be large. Hearing will be more sensitive and cochlear frequency resolution and selectivity will be more acute in a cochlea with less damping. These viscous losses are physically inevitable because: i sensory cells must absorb stimulus energy to operate; and ii in order to reach the inner hair cells, cochlear fluid motion must take place in the extremely constricted sub-tectorial space Fig.

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The energy lost from the TW due to viscous fluid drag in the subtectorial space plus energy absorbed by the hair cell themselves is very substantial. In fact the majority of the incident stimulus energy is actually lost before reaching its appropriate frequency place. Under purely mechanical forces, the cochlea cannot develop a strong and sharp TW image. The mammalian cochlea has evolved a unique mechanism for replacing TW energy lost by viscosity, at least for weak stimuli.

It was revived following the discovery of OAEs 3 ,20 , but became a credible possibility only after the discovery of hair cell motility by Brownell Electro-motility Ashmore, this volume is the only known functional characteristic of the outer hair cells, which out-number the inner hair cells by Fig. If OHC forces exceed that necessary to overcome viscosity, then excitation will be increased above that delivered by the stimulus, providing the possibility of amplification — as implied in Figure 5B.

This process of TW enhancement in the cochlea by stimulated mechanical energy release parallels with what happens to light inside the laser. They arrive in the ear canal as a result of BM disturbances that escape from the cochlear amplifier mechanism and travel away from the sensory cells back to the base of the cochlea. OAEs can only be generated if the cochlear amplifier mechanism is present and to some degree operational. But, paradoxically, the reasons why vibrations are sent back to the base to form OAEs all relate to natural imperfections in this mechanism.

What kind of amplifier imperfections result in OAEs?

An Overview of OAEs and Normative Data for DPOAEs

In a travelling wave amplifier, any lack of uniformity in construction or function places an upper limit on the level of stable amplification. By scattering amplified energy back to the base of the cochlea, energy is wasted and appears as stimulus frequency OAEs. It is not only spatial imperfections that can generate OAEs.

In the cochlea, most energy travels apically and is absorbed, but any energy that escapes basally to reach the base can be partially reflected back, forming a new forward TW. This can re-stimulate the OHC mechanism. Under conditions of high amplification, endless recirculation of the TW leads to sustained oscillation inside the cochlea and to spontaneous OAE of one or more pure tones into the ear canal.

To what extent can the functional status of a cochlea be characterised and quantified using OAEs? OAEs are only a by-product of cochlear function. Also, several different cochlear locations may contribute to a single frequency component of an OAE and these may fortuitously summate or interfere with each other Fig.

The transmission back to the ear canal also depends on individual middle ear characteristics. The interplay of all these factors cannot yet be accurately modelled, not least because most parameters are unknown. It is not surprising, therefore, that individual healthy ears differ greatly in the level and the spectrum of the OAEs they exhibit. Stimuli of slightly differing frequency or spectral composition can give rise to quite different OAE patterns.

OAEs are frequency-specific responses and tend to emerge only in frequency bands where hearing is near normal. This provides a useful pointer to normally and abnormally functioning parts of a cochlea. In any non-linear system, intermodulation distortion is always strongest when the two interacting signals have similar levels at the non-linearity. Making the lower-frequency stimulus relatively more intense than f2 at the input will shift the place of greatest intermodulation towards the f2 peak of the TW and so enhance DP production.

Increasing the f1 level too much will be counter-productive. Therefore, for each stimulus level, there is an optimum stimulus intensity ratio for maximum DP production. DP production does not ensure DP emission, which is governed by the second rule. This depends on the relative travelling wave velocities of f1 and f2 at the non-linearity.

As Figure 3 illustrates, many different DPOAEs co-exist and their generation is intimately linked to the operating characteristics of the outer hair cells. Strong TW amplification must co-exist with irregularities to cause a strong wave to be returned to the base and the proportion reflected back into the cochlea by the middle ear must, after re-amplification and re-emission, be sufficient to sustain a continuous oscillation of the middle ear and along a substantial section of the BM.

The round trip travel time also has to be exactly right for this to occur and so can happen only at one precise frequency, just as in the laser. The precise frequency of an SOAE does not imply an origin at a precise place in the cochlea, but only a particular co-incidence of travel time and reflection from an ill-defined region of high OHC activity.

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But, because of their intrinsic stability and critical dependence on cochlear status, SOAEs are, when present, particularly sensitive indicators of metabolic and physiological changes in the cochlea. All OAE forms show a high degree of sensitivity to changes in cochlear status. Changes in cerebrospinal fluid pressure induced by posture changes affect SOAE frequency and evoked OAE intensity — probably by their influence on cochlear fluid pressure and stapedial position Drugs known to depress hearing, including aspirin and quinine, also depress OAEs, and loop diuretics known to depress the endocochlear potential also depress OAEs 33 , This may indicate that some forms of masking originate preneurally in the cochlea.

The sharpness of such curves confirms the close association between OAEs and auditory function, and demonstrates that sharp mechanical tuning is present at the cochlear level. Perhaps the most interesting suppression effect is the slight depression of OAE level by 0. First discovered by Collet et al in , this effect has been identified as being largely due to the influence of the medial cochlear efferent system.

This terminates directly on the OHC bodies and presumably normally plays a role in the day-to-day maintenance of effective OHC status. The neural mechanism and function remain somewhat obscure. Absence of a contralateral OAE suppression effect can be the result of a brain stem lesion, but Collet has also reported it in certain stages of sleep, and it can be absent in some healthy individuals. It has even been suggested that absence of contralateral OAE suppression may correlate with autism and dyslexia 40 — The phenomenon of contralateral OAE suppression is not well understood.

In general, OAE responses carry a large amount of information about the status, activity and environment of OHCs, which we are currently unable to interpret.

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OAEs tend to be dominated by microscopic details of little relevance to hearing. Nevertheless, OAEs provide the only detailed non-invasive window on the cochlea and by their very presence confirm normal presynaptic cochlear function. Although useful today, if we can learn how to extract definitive data on OHC status from OAE data, then their clinical importance will be greatly enhanced.

OAEs are already an essential part of the audiological diagnostic test battery Key points for clinical use are summarised below. Background room noise levels of 40 dB or below are recommended. A good probe fit helps block out external noise, although this effect is minimal with neonate ears. Short bursts of more intense noise e. Patient movement is also not a problem with OAEs provided it does not result in cable-rub noise. Jaw action, swallowing and vocalisations cause ear canal noises, which can prevent good OAE recordings.

Patency of the ear canal is essential for successful recordings. Obstruction by wax in older patients, or by fluid or birth debris in neonates, or by collapse of the canal in the latter, prevent OAEs from reaching the ear canal and are major causes of OAE recording failure.

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Sleep and sedation have minimal effects on OAEs Waveform-based TEOAE measurements, as originally used in universal new-born hearing screening programmes, are also useful as a sensitive initial screen prior to full clinical examination. DPOAE instruments can be used for screening with an appropriately low stimulus level e. OAE detection is affected by conductive losses and OAEs will be absent if there is effusion, glue, otosclerosis or ossicular dislocation.

Grommets do not greatly affect OAEs. Absent OAEs can re-appear following effective middle ear treatment or surgery if the residual conductive loss is very small and the cochlea is normal. This does not arise with neonates, but their ear canals are extremely small and this needs to be accommodated in the selection of probe size and stimulation intensity. OAEs come exclusively from outer hair cells which do not themselves activate primary auditory nerve fibres, yet a strong relationship exists between the absence of OAEs and hearing loss. Inefficient transmission of excitation to the IHCs causes loss of hearing sensitivity and frequency selectivity.

Since there remains a pathway for stimulation to reach the IHCs, profound hearing loss cannot be caused by OHC dysfunction alone. Total OHC failure is estimated to cause no more than 60 dB hearing loss. Loss of OAEs with a normal middle ear indicates sensory transmissive loss.

This could give rise to any degree of hearing loss from mild to profound since the auditory nerves themselves have no sensitivity to sound simulation. Loss of frequency selectivity would not necessarily accompany threshold elevation in a pure sensory transductive loss, and OAEs would be normal.

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It is clear from the high correlation between sensory loss and OAE absence that most sensory losses are of the sensory transmissive type. This makes sense, as the outer hair cell mechanism is both highly specialised and highly vulnerable to degradation by excessive noise, anoxia or ototoxic agents. OHCs selectively amplify weak stimuli which would otherwise fall below the threshold for IHCs to trigger a neural response and as a consequence the symptoms of sensory transmissive loss necessarily include loudness recruitment in addition to threshold elevation and reduced frequency selectivity see BJM Moore, this volume The presence of robust evokeable OAEs across the key speech frequency range 1.

For clinical purposes, it is useful to record OAE status as a function of frequency, averaged over one-half or one-third octave frequency bands.