The Atlas · Chapter 1

Anatomy & Physiology

Otoacoustic emissions arise from the active, energy-producing machinery of the cochlea. Understanding where they come from — the outer hair cells and the amplifier they drive — explains both what the test measures and what it can never see.

From ear canal to cochlea

Sound entering the ear travels through the canal, vibrates the eardrum, and is carried by three small bones to the cochlea — the coiled, fluid-filled organ of hearing. Inside the cochlea sit two kinds of sensory cells: inner hair cells, which send hearing signals to the brain, and outer hair cells, which act as tiny biological amplifiers.

basilar membranetectorial membraneinner hair cellsends signal to brainOHC1OHC2OHC3outer hair cells — electromotile amplifiers (prestin)length change
The organ of Corti in cross-section. A single row of inner hair cells transduces sound for the auditory nerve; three rows of outer hair cells, driven by the motor protein prestin, change length cycle-by-cycle to amplify the traveling wave. That active movement is the source of otoacoustic emissions. Schematic — not to scale.

Otoacoustic emissions come from those outer hair cells. When they are healthy, they actively move — and that movement produces a faint sound that travels back out of the ear. Recording that sound tells us the outer hair cells are working.

The cochlear amplifier

Outer hair cells are electromotile: they change length in response to changes in membrane voltage, driven by the motor protein prestin in their lateral wall[4]. This length change feeds mechanical energy back into the travelling wave on the basilar membrane on a cycle-by-cycle basis, sharpening the wave's peak and boosting low-level sounds by 40–60 dB. The by-product of this active process — energy radiating backward through the middle ear — is the otoacoustic emission [1].

The cochlea is tonotopic: the stiff basal end responds to high frequencies, the floppy apical end to low frequencies. Because of this, the high-frequency components of a transient emission return to the ear canal first, and the low-frequency components arrive later — the latency dispersion that distributes each frequency to its own characteristic place along the membrane.

base · high freqapex · low freqcharacteristic place · 2000 Hzouter hair cells pump
A 2000 Hz tone sets up a traveling wave that grows as it moves apically, peaks at the tonotopic place tuned to that frequency, then dies away sharply. Outer hair cells at the peak change length cycle-by-cycle to amplify it — the active process whose by-product is the otoacoustic emission. Simplified model (Greenwood map + asymmetric envelope) — not to scale.

Two physical mechanisms generate the emissions we record, and they map onto how each emission is evoked. Linear reflection from fixed irregularities along the cochlear partition produces the place-fixed component, while a nonlinear distortion mechanism in the region of overlap between two stimulus tones produces a wave-fixed component [2]. This dual origin explains why distortion-product and reflection-based emissions can behave differently even in the same ear [3].

The medial olivocochlear efferent system

Outer hair cell gain is not fixed. The medial olivocochlear (MOC) bundle projects from the brainstem onto the outer hair cells and, when activated — for example by contralateral noise — reduces their gain. This efferent suppression measurably lowers emission amplitude and is itself a probe of brainstem-level auditory function[7].

test earother ear (noise)OHCsemissionbrainstemMOC efferent · activecontralateral noise 54 dB · emission −2.1 dBsuppression vs contralateral level3.50suppression (dB)threshold0306090contralateral level (dB SPL) →
Outer-hair-cell gain is adjustable. Noise in the opposite ear drives the medial olivocochlear reflex through the brainstem, which turns the cochlear amplifier down a little — so the recorded emission shrinks by up to a few decibels, more as the contralateral level rises, then saturates. The size of that drop is itself a probe of efferent, brainstem-level function. Simplified educational model (a saturating reflex layered on the amplifier) — not calibrated data.

Clinically, the key consequence of this anatomy: emissions test the pre-neural cochlea only. A normal emission with an abnormal auditory brainstem response is the signature of auditory neuropathy spectrum disorder — outer hair cells intact, neural transmission impaired [6]. This dissociation is the reason emissions and the brainstem response are read together rather than in isolation.

The cochlea in summary.Sound → eardrum → ossicles → cochlea → outer hair cells amplify the travelling wave (prestin) → a by-product sound radiates back out as the otoacoustic emission. The amplifier is pre-neural and under efferent control — which is exactly why a normal emission cannot rule out a neural lesion.