5Otoacoustic Emissions (and SOAEs)

FEchoes from the cochlear amplifier

Outer hair cells (OHCs) do not just detect sound — they actively amplify it, and a by-product of that motility is faint sound radiated back out through the ossicles into the ear canal, where a sensitive microphone can record it. These otoacoustic emissions (OAEs) are therefore a direct, non-invasive read-out of OHC function. Because OHCs are the cochlea’s most vulnerable element, OAEs often fail before the pure-tone audiogram moves.

Two evoked forms dominate clinical use. Transient-evoked OAEs (TEOAEs) are elicited by a click and give a broadband ‘is the cochlea working?’ answer. Distortion-product OAEs (DPOAEs) use two simultaneous tones and produce frequency-specific output, mapping OHC integrity across the cochlea — the more useful tool when you want to localise damage [2013].

TOAEs in tinnitus with a normal audiogram

Many tinnitus patients have an audiogram read as ‘normal’, yet their cochleae are not. When such patients are tested, reduced or absent emissions — especially DPOAEs in the high frequencies — frequently appear, betraying focal OHC loss that the behavioural audiogram averages out. This makes OAEs the practical bedside way to demonstrate ‘hidden’ cochlear pathology and to reassure both clinician and patient that the tinnitus has a peripheral substrate [2015].

The finding fits the dominant model: loss of OHC output reduces afferent drive at specific frequencies, the central auditory system raises its gain to compensate, and that increased spontaneous activity is heard as tinnitus — commonly pitched near the region of greatest emission loss [2015]. Long-term follow-up of normal-hearing tinnitus patients shows these cochlear differences are stable rather than artefactual [2022].

CThe efferent brake: contralateral suppression

The medial olivocochlear (MOC) efferent system feeds back onto the OHCs and damps their gain; sound presented to the opposite ear activates this reflex and measurably reduces the OAE amplitude. The size of that reduction — contralateral suppression of OAEs — indexes how strong the efferent brake is.

In tinnitus patients, particularly the normal-hearing subgroup, this suppression is often weaker than in controls, suggesting that a deficient efferent ‘brake’ lets cochlear and central activity run unchecked. The degree of reduced suppression has even been related to how annoying patients find their tinnitus, hinting at a mechanistic link between efferent dysfunction and tinnitus distress rather than mere presence [2015].

TSpontaneous OAEs versus true objective tinnitus

Spontaneous OAEs (SOAEs) are narrow-band emissions the cochlea produces with no external stimulus. They are common — present in a large minority of normal ears, more often in women and in right ears — and the great majority are silent: the patient does not hear them, and they are emphatically not the source of ordinary subjective tinnitus, which is a central phantom percept.

Very rarely, however, a high-level SOAE becomes audible to the patient and can even be recorded in the canal, producing a genuine, measurable objective tinnitus. This is the exception that proves the rule: most tinnitus has no detectable acoustic correlate, so the routine task of SOAE testing is to exclude, not assume, an emission origin [2013].

CWhere OAEs fit in the work-up

OAEs are quick, objective and need no patient response, which makes them an efficient second-tier test once audiometry is done. Their highest-value use is the normal-audiogram tinnitus patient, where demonstrating reduced DPOAEs reframes ‘idiopathic’ tinnitus as cochlear in origin and informs counselling about noise protection and realistic expectations.

OAEs also help triage neural cases: emissions that are preserved alongside an absent or grossly abnormal ABR raise the possibility of auditory neuropathy or synaptopathy — an OHC-sparing, neural pattern that changes management entirely. Read together, OAE and ABR results separate cochlear from neural tinnitus far better than either does alone [2013].