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 cochlear outer hair cells (see image above). This youtube link shows a movie of one moving.
There are 2 types of otoacoustic emissions in clinical use:
|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).
OAE's are not suppressed by certain inhaled anesthetics (Gungor et al, 2014), and from this observation, it would seem possible that they might be useful to detect damage to the hearing organ during surgery.
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.
Most tests of the inner ear get worse with age. This is also the case with OAE's. Konrad-Martin et al (2017) repoorted that "Across a wide range of f2's, DPOAE level decreases by 3 to 4 dB from 1 to 13 months of age followed by a more gradual decline of <1 dB/year. An f2 of 6 kHz shows the smallest decrease during the early rapid maturation period. "
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.
|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.
|Sweep 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.|
In our practice at Chicago Dizziness and Hearing, we use a far better OAE device than the ones discussed above. More detailed output can be obtained from sweep OAE devices. The one used above can scan the entire spectrum of OAEs, possibly finding areas of drop-out which might go undetected otherwise. This may have some special utility in Tinnitus. A comparison between the two techniques is discussed in this poster.
In this variant one presents another sound to the opposite ear being tested. This is the reduction of amplitude of TEOEs in the opposite ear to the masking sound. This effect is attributed to alteration of cochlear micromechanics via the medial superior olivary complex neurons. Kumar et al (2012) suggested that the contralateral suppression test was not sufficiently reliable for clinical use.
The clinical significance of OAEs 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. OAEs decline with age.(Gates et al. 2002; Cilento et al. 2003). Our clinical experience with OAEs, 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 OAEs as someone with cochlear damage due to noise. Kagova and others (2012) have observed that OAEs are generally reduced by acoustic neuromas.
OAEs 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.
For the very young group, Trosman et al (2016) suggested that OAE+tymps were more cost effective than audiograms, because of the "questionable reliability" of behavioral audiometry in very young children.
In adults, we feel that OAEs 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, OAEs are very sensitive to noise and age related hearing disturbances.
One would think that OAEs might be a better method of screening for occupational hearing loss, generally caused by noise, than conventional hearing testing. OAEs 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).
OAEs 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 OAEs at high frequency as they age.
Elevated intracranial pressure. There are some possible changes to the frequency distribution of OAEs 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 OAEs 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.
OAEs are not very helpful in Meniere's disease. This is probably because OAEs 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 OAEs 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.