Hearing Physiology
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Direct answer
Hearing is a transformer problem: air-borne sound must reach the fluid-filled cochlea without losing nearly all its energy to reflection, and the middle ear solves this by impedance matching, gaining roughly 20-25 decibels through the area ratio of tympanic membrane to oval window plus the lever ratio of the ossicles. Inside the cochlea, von Bekesy's travelling wave peaks at the base for high frequencies and near the apex for low frequencies — the place principle — while low frequencies also use frequency coding through phase locking of nerve fibres. Inner hair cells transduce (they carry about 95 per cent of the afferents); outer hair cells amplify, powered by the protein prestin, and their activity is what otoacoustic emissions record. Endolymph's positive potential of about +80 millivolts, with a high potassium concentration, drives transduction through tip links when stereocilia deflect.
What you must remember
- Frequency range: the young human ear detects 20 to 20,000 hertz; conversational speech concentrates between about 500 and 4,000 hertz, which is why pure tone averages use 500, 1000 and 2000 hertz.
- External canal resonance: the canal resonates around 3,000-4,000 hertz, adding roughly 10 decibels — and explaining why noise-induced notches appear first at 4,000 hertz.
- Middle ear transformer: area ratio (drum to oval window) around 14-17 to 1, ossicular lever ratio about 1.3 to 1, net gain roughly 22-25 decibels; disruption of the chain produces the 60-decibel conductive drop of an absent reflex.
- Middle ear muscles: the stapedial reflex contracts bilaterally at about 70-90 decibels above threshold, damping low frequencies and protecting against sustained loud sound.
- Travelling wave: passive mechanics deliver high frequencies to the stiff basal turn and low frequencies to the compliant apex; each point has a characteristic frequency.
- Hair cell division of labour: inner hair cells are the true transducers (afferent type I fibres); outer hair cells lengthen and shorten through prestin to sharpen tuning — the cochlear amplifier, measurable clinically as otoacoustic emissions.
- Coding below about 4,000-5,000 hertz: volley principle or phase locking supplements the place principle; above it, place coding alone operates.
- Clinical physiology signatures: loudness recruitment points to cochlear (outer hair cell) disease; abnormal tone decay and reflex decay point to retrocochlear disease — the single most examinable application of this topic.
Worked example: two ears, one complaint
A 30-year-old finds gunfire makes one ear dull and ringing for hours, and words blur in crowds. Audiometry shows a mild high-frequency loss, but speech discrimination falls disproportionately and loudness discomfort arrives early — recruitment. Outer hair cells at the basal cochlea, damaged by noise, no longer amplify soft sounds, so thresholds rise; intact inner hair cells still fire once sound is intense, so loudness grows abnormally fast and dynamic range collapses — why hearing aids frustrate recruiting ears without compression.
Contrast a vestibular schwannoma squeezing the nerve: thresholds stay near normal, but the nerve cannot sustain firing — tone decay is abnormal, the stapedial reflex decays, speech scores collapse below what the audiogram predicts. Same complaint of hearing without understanding, two mechanisms: hair cell disease recruits, nerve disease adapts. Every special test — reflex decay, Bekesy type III and IV patterns, otoacoustic emissions present in early neural but absent in cochlear disease — applies this split, and most questions are answerable by asking which compartment is broken.
How the exam frames it
Questions rarely describe the travelling wave; they ask why the ear needs ossicles, why noise notches appear at 4,000 hertz, or which emission disappears first. The physics answer examiners reward is reflection at the air-fluid interface: without the transformer, most airborne energy reflects and roughly 30 decibels are lost, which is also the logic of bone-conduction testing and Rinne interpretation. Candidates who confuse middle ear effusion (transformer ablated, cochlea intact) with sensorineural disease lose the easy mixed-loss marks.
Frequently asked questions
Why does the middle ear amplify sound, and by how much?
By impedance matching — the tympanic membrane-to-oval window area ratio plus the ossicular lever convert a large low-pressure movement into a small high-pressure push, gaining roughly 22-25 decibels.
Where in the cochlea are high frequencies represented?
At the basal turn, because the basilar membrane there is stiff and narrow; low frequencies travel to the wide, compliant apex, per the travelling wave.
What is the role of outer hair cells in hearing?
Through prestin-driven length changes they amplify and sharpen tuning of the travelling wave; their dysfunction causes loss of sensitivity, cochlear-type loudness recruitment and absent otoacoustic emissions.
What is loudness recruitment and what does it indicate?
Abnormally rapid growth of loudness once threshold is crossed, indicating cochlear outer hair cell damage — characteristic of Meniere disease and noise-induced loss, not retrocochlear lesions.
Which ion and potential characterise endolymph?
Endolymph has a high potassium concentration and a positive endocochlear potential of about +80 millivolts generated by the stria vascularis, driving current through the hair cells during transduction.