Otoacoustic Emission Testing measures an acoustic response that is produced by the inner ear (cochlea), which in essence bounces back out of the ear in response to a sound stimulus. The test is performed by placing a small probe, which contains a microphone and speaker into the ear. During testing, sounds are generated in the probe and responses that come back from the cochlea are recorded. OAEs are clinically important because they are a simple, non-invasive, test for hearing defects in newborn babies and in children who are too young to cooperate in conventional hearing tests.
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.
Two types of Otoacoustic Emission Testing
Transient otoacoustic emissions (TOAEs) or transient evoked otoacoustic emissions (TEOAEs) – Sounds emitted in response to an acoustic stimuli of very short duration; usually clicks but can be tone-bursts
Distortion product otoacoustic emissions (DPOAEs) – Sounds emitted in response to 2 simultaneous tones of different frequencies
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.
OAE’s are not suppressed by certain inhaled anesthetics, and from this observation, it would seem possible that they might be useful to detect damage to the hearing organ during surgery.
Otoacoustic Emission Testing is 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 Otoacoustic Emission Testing one needs an unobstructed outer ear canal, absence of significant middle ear pathology, and functioning cochlear outer hair cells.
The elements in the pathway for the OAE include the sound source, the ear drum, ossicular chain, inner ear, and outer hair cells. The same structures transmit sound coming out of the outer hair cells. OAEs can be affected by anything in the chain – -if sound doesn’t get in or out — no OAE. If there is a resonance or filter between the sound source and microphone this will cause altered frequency spectrum of OAEs (Grenner, 2012). Thus, OAEs “reflect” a combination of inner ear and external/middle ear function. Individuals with small ear canals (such as infants) are different than adults due to the difference in external and middle ear size.
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.
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. Our clinical experience with OAE’s, is that they do not discriminate well between causes of hearing loss. In other words, we would expect someone with an intact cochlea (including their outer hair cells), perhaps due to an acoustic tumor, to be equally likely to have absent OAE’s as someone with cochlear damage due to noise. Kagova and others have observed that OAE’s are generally reduced by acoustic neuromas.
Otoacoustic Emission Testing is 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.
For the very young group, Trosman et al (2016) suggested that OAE+tymps were more cost effective than audiograms, because of the “questionable reliablity” of behavioral audiometry in very young children.
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.
One would think that OAE’s might be a better method of screening for occupational hearing loss, generally caused by noise, than conventional hearing testing. OAE’s are based on objective measurements rather than patient responses that are subject to misdirection. Contrary to this common sense hypothesis, Wooles et al (2015) reported that there was “no evidence of a robust relationship” between DPOAE’s and pure tone audiometry. We think that this comparison of apples: oranges — an objective measurement to a subjective measurement in a setting where there is motivation to exaggerate, is fraught with peril due to bias, and that the “jury is still out”.
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.
Cisplatin ototoxicity. Cisplatin is the most widely used anticancer drug currently and unfortunately, it is cochleotoxic. The toxicity begins in the outer hair cells (Reavis et al, 2011), and affects high frequencies first, the same area as age and noise. Because of the outer hair cell toxicity, DPOAE’s have been suggested to be a reasonable method of detecting toxicity (Reavis et al, 2011). It would seem to us that this use would be greatly limited by the propensity of normal people to loose their OAE’s at high frequency as they age.
Elevated intracranial pressure. There are some possible changes to the frequency distribution of OAE’s as a result of changes in pressure in the inner ear as a result of intracranial pressure alterations. So far, this idea has not “panned out” due to variability.
Migraine — There is a small effect on OAE’s on DPOAE (less) and less contralateral suppression. (Bolay et al, 2006; Murdin et al, 2010). This observation may eventually develop into a useful clinical test for phonophobia.
OAE’s are not very helpful in Meniere’s disease. This is probably 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. This is an odd thing about Meniere’s disease – – conventional dogma would make one expect that high-frequency outer hair cells would go first as they are metabolically very active and therefore more vulnerable. It suggests that conventional dogma (about the mechanism of Meniere’s disease) is just wrong.
DPOAE’s are probably not useful in detecting aminoglycoside ototoxicity, or for that matter, cisplatin ototoxicity (except perhaps in young people). Fausti and associates have suggested a possible use for DPOAE in ototoxicity as ototoxicity 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 left 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.
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