Chapter 5 — Otoacoustic emissions

TEOAE, DPOAE, and the cochlear amplifier as clinical signal.

Until 1978 the cochlea was understood as a fundamentally passive device — air pressure went in, neural spikes came out. David Kemp’s discovery, published in JASA that year, was that this picture is wrong. A working cochlea is actively generating sound. Place a sensitive microphone in the sealed ear canal, present a brief click, and the microphone records first the click itself and then — a few milliseconds later — a faint, frequency-dispersed echo coming back out of the ear. The echo is not a reflection; it is a re-emission, produced by the outer hair cells of a living cochlea. It exists in normal-hearing ears, vanishes when the outer hair cells die, and lets us measure cochlear health without the patient’s behavioural cooperation.

This chapter develops the otoacoustic emission as a clinical signal: the underlying physics (the cochlear amplifier as a nonlinear active element, see Hearing 4.5 refresher →), the two clinical implementations (transient-evoked vs distortion-product), and the screening protocols that have made OAE testing the universal first test in every birthing hospital in the developed world. Newborn hearing screening — driven entirely by OAEs and AABR — has lowered the average age at which congenital sensorineural loss is identified from 24 months in the 1990s to under 6 months in 2026.

Three lessons:

• 5.1 The cochlear amplifier as clinical signal source — outer hair cells as active elements; reverse traveling waves; why the OAE exists at all.
• 5.2 Transient-evoked OAEs and newborn screening — the click stimulus, latency-dispersed band response, and pass/refer screening criteria. Includes a TEOAE waveform interactive.
• 5.3 Distortion-product OAEs and the DP-gram — two-tone primaries, the 2f₁−f₂ cubic distortion product, and the DPOAE clinical analogue of the audiogram. Includes a DPOAE spectrum interactive.