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Page last modified: June 13, 2008
OAE or otoacoustic emission testing is the recording of sounds that the ear produces itself. Otoacoustic emissions were first reported by Kemp in 1978. They appear to be generated by motile elements in the cochlear outer hair cells (see image above).
There are 2 types of otoacoustic emissions in clinical use:
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| Figure 1: Method of recording an OAE or ABR in an infant (Bio-logic) | OAE test in an adult (Bio-logic) |
OAE's can be partially suppressed centrally via the superior olivary complex. Axons of the lateral and medial olivocochlear bundles extend from the superior olive and leave the brainstem as a ventral component to the inferior vestibular nerve. They join the cochlear nerve as Oort's vestibulocochlear anastemosis. Axons of the lateral olivocochlear bundle synapses with afferent neurons from the cochlea. Axons of the medial olivocochlear bundle terminate a the base of cell bodies of the outer hair cells. It is generally believed that the medial efferents counteract the amplifying effects of the outer hair cells. It is probably mediated by acetylcholine. (Bolay et al, 2006)
OAEs are measured by presenting a series of sounds to the ear through a probe that is inserted in the ear canal. The probe contains a loudspeaker that generates the sounds and a microphone that measures the resulting OAEs that are produced in the cochlea and are transmitted through the middle ear into the outer ear canal. The resulting sound that is picked up by the microphone is digitized and processed using signal averaging methodology.
To obtain an OAE one needs an unobstructed outer ear canal, absence of significant middle ear pathology, and functioning cochlear outer hair cells.
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| Test result for DP-OAE produced by the Bio-Logic "Scout". This device can test up to 10 frequencies on each ear. It produces a tabular format on a label that can be inserted into the chart. |
The OAE devices used in most clinics are "screeners". The typically check 5-10 frequencies and report whether the signal/noise ratio exceeds a preset limit, in which it indicates that the ear is a "pass", or if not, a "refer". This "go/no-go" type of output is often helpful in deciding whether there is any hearing problem -- people who "pass" at all frequencies are unlikely to have anything seriously wrong with their inner ear. OAE's are quick and not bothersome to patients.
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| Research OAE -- This device, used in our clinic in Chicago, plots the difference between the noise floor and response continously. This normal person had good OAE's at all frequences up to roughly 4500 Hz. |
Full spectrum OAE
More detailed output can be obtained from research OAE devices. The one used above can scan the entire spectrum of OAE's, possibly finding areas of drop-out which might go undetected otherwise. This may have some special utility in Tinnitus.
Contralateral suppression.
In this variant one presents another sound to the opposite ear being tested. This is the reduction of amplitude of TOAE's in the opposite ear to the masking sound. This effect is attributed to alteration of cochlear micromechanics via the medial superior olivary complex neurons.
The clinical significance of OAE's is that they only occur in a normal cochlea with normal or near normal hearing. If there is damage to the outer hair cells producing mild hearing loss, then OAEs are not evoked. A rule of thumb is that OAEs are present if hearing is 35 dB or better. Because OAEs are evoked by transient signals that have a wide frequency response, a broad region of the cochlea responds, providing information on the frequency range from 1000 Hz to 4000 Hz. OAE's decline with age.(Gates et al. 2002; Cilento et al. 2003)
OAE's are appropriate for use in difficult-to-test patients: newborn infants, young children, patients who are attempting to feign a hearing loss (i.e. malingering), and developmentally delayed populations. OAEs primarily provide information about the activity of the cochlea, and do not assess the status of the rest of the auditory pathway, except for crossed responses mediated through the cochlear efferent system.
In adults, we feel that OAE's are most helpful in persons who may financially benefit from being diagnosed with hearing loss, and also as a cross-check on audiometry. In our experience, OAE's are very sensitive to noise and age related hearing disturbances.
TOAE's are commonly used to screen infant hearing, to validate auditory thresholds obtained via other techniques, and to assess the cochlear contribution to hearing.
DPOAE's are also used for infant screening. They can be obtained in persons in whom TOAE's cannot be obtained, and they can be obtained at higher frequencies than TOAE's (i.e. over 1000 hz).
OAE's have a special utility in auditory neuropathy. This is a condition, primarily of children, in which hearing is impaired but cochlear function is presumed intact. This is rather rare.
Migraine -- There is a small effect on OAE's on DPOAE (less) and less contralateral suppression. (Bolay et al, 2006). This observation may eventually develop into a useful clinical test for photophobia.
OAE's are not very helpful in Meniere's disease. This is because OAE's mainly test high frequencies, and Meniere's disease usually starts with low-frequency hearing loss. It appears that Meniere's must not selectively damage outer hair cells, as one would expect that OAE's would go earlier than conventional hearing testing -- and this is not the case.
DPOAE's may are probably not useful in detecting aminoglycoside ototoxicity. Some have suggested a possible use as this condition usually affects high-frequency hair cells first, and DPOE's are readily available at higher frequencies than are standard hearing testing. The problem with this idea is that high-frequency hearing usually declines with age, and thus there is nothing to measure. Some have also suggested that gentamicin (an aminoglycoside) selectively impairs responses mediated through the cochlear efferents, and that this might be a method of detecting ototoxicity. At this writing (4-07), to us this appears to be an unproven conjecture, without much support from our clinical data.
| © Copyright June 13, 2008 , Timothy C. Hain, M.D. All rights reserved. Last saved on June 13, 2008 |