Hearing and balance
Hearing and balance: middle ear, cochlea, hair cells, hearing tests and vestibular system
How the middle ear amplifies sound, how cochlear hair cells code pitch, and how Rinne and Weber separate types of deafness, for FCPS Part 1. Also covers the vestibular organs, noise and age-related loss, glue ear, BPPV and Ménière disease.
Sound
- Human hearing ranges from about 20 to 20,000 Hz and is most sensitive at 1,000–4,000 Hz, the speech range.
- Loudness is measured in decibels (logarithmic; each 10 dB is a tenfold rise in intensity). Conversation is about 60 dB; sustained exposure above 85 dB damages hearing; pain begins around 130 dB.
External and middle ear
- The tympanic membrane is about 17 times larger than the stapes footplate, and the ossicular lever adds about 1.3 times, giving about 22-fold pressure gain. This impedance matching overcomes the loss of energy when sound passes from air into cochlear fluid; without it about 99.9% would be reflected.
- Tensor tympani (mandibular nerve) and stapedius (facial nerve) contract to loud sound (attenuation reflex), damping low-frequency transmission. Stapedius paralysis in Bell palsy causes hyperacusis.
- The Eustachian tube equalises middle ear pressure. In young children it is short, horizontal and easily blocked by adenoids and colds; air in the middle ear is absorbed, pressure falls, and fluid transudes: otitis media with effusion (glue ear), with a dull retracted drum, flat tympanogram, conductive loss and speech delay. A persistent one-sided effusion in an adult needs nasopharyngeal examination.
- Barotrauma in divers and fliers occurs when the tube fails to equalise; unequal middle ear pressures on the two sides can cause alternobaric vertigo.
- Otosclerosis: new bone fixes the stapes footplate, causing progressive conductive loss in young adults, often worse in pregnancy. Patients may hear better in noise (paracusis), because others raise their voices over background noise that the patient cannot hear.
Cochlea
- Scala vestibuli and scala tympani contain perilymph (high Na⁺, like extracellular fluid). Scala media contains endolymph: high K⁺, low Na⁺, secreted by the stria vascularis, which also creates the endocochlear potential of about +80 mV.
- The organ of Corti sits on the basilar membrane. Inner hair cells (about 3,500 in one row) carry about 95% of afferent signals. Outer hair cells (about 12,000 in three rows) change length when stimulated (electromotility), amplifying basilar membrane movement and producing otoacoustic emissions, used for newborn screening.
- Transduction: bending of stereocilia towards the tallest row pulls tip links that open mechanically gated channels; K⁺ flows in from endolymph (driven by the large electrical gradient), depolarising the cell. Ca²⁺ entry triggers glutamate release onto cochlear nerve fibres.
- Tonotopy (travelling wave): the basilar membrane is narrow and stiff at the base (near the oval window), where high frequencies peak, and wide and floppy at the apex, where low frequencies peak.
Causes of sensorineural loss
| Cause | Site and mechanism | Clue |
|---|---|---|
| Presbycusis | Loss of hair cells at the basal turn first | Bilateral, symmetrical, high-frequency; trouble in noisy places |
| Noise exposure | Outer hair cells, around the 4 kHz region | Notch at 4 kHz on audiogram (soldiers, jet engineers) |
| Ototoxic drugs | Hair cells (aminoglycosides, cisplatin) or stria vascularis (loop diuretics) | Bilateral loss, often with tinnitus |
| Bacterial meningitis | Infection spreads to the cochlea (labyrinthitis), later ossification | Profound bilateral loss; test early for cochlear implant |
| Ménière disease | Endolymphatic hydrops | Fluctuating low-frequency loss, vertigo, tinnitus, fullness |
| Vestibular schwannoma | Cochlear nerve in the cerebellopontine angle | Unilateral loss; later facial numbness (V), facial weakness (VII) |
| Congenital rubella, Alport syndrome | Cochlear development; type IV collagen | Cataract and heart defect; nephritis |
- Paget disease of bone (thick skull, raised ALP, normal calcium) causes mixed hearing loss by compressing the cochlear nerve and affecting the ossicles.
- Sudden sensorineural hearing loss with a normal ear canal and drum is an emergency: give urgent high-dose oral steroids and arrange audiometry and MRI.
Hearing tests
| Result | Conductive loss in left ear | Sensorineural loss in left ear |
|---|---|---|
| Rinne (left) | Negative (bone louder than air) | Positive (air louder than bone), both reduced |
| Weber | Lateralises to the left (affected ear) | Lateralises to the right (better ear) |
- Rinne negative on the right with Weber to the left is a dead (severely sensorineural) right ear: bone-conducted sound is heard by the left cochlea, giving a false-negative Rinne.
- Other tests: pure tone audiometry, tympanometry (flat in effusion), otoacoustic emissions, auditory brainstem responses.
Auditory pathway
Cochlear nerve, cochlear nuclei (ipsilateral only), superior olivary complex (first binaural comparison for localisation by timing and intensity), lateral lemniscus, inferior colliculus, medial geniculate body, primary auditory cortex (Heschl gyrus, areas 41 and 42). Above the cochlear nuclei each ear is represented on both sides, so a unilateral central lesion rarely causes one-sided deafness; one-sided deafness implies the ear, cochlear nerve or cochlear nucleus.
Vestibular system
| Organ | Detects | Receptor |
|---|---|---|
| Semicircular canals | Angular (rotational) acceleration | Crista ampullaris: hair cells in a gelatinous cupula moved by endolymph flow |
| Utricle | Horizontal linear acceleration, head tilt | Macula with otoconia (calcium carbonate crystals) |
| Saccule | Vertical linear acceleration | Macula with otoconia |
- Each hair cell has stereocilia and one kinocilium; bending towards the kinocilium depolarises it, away hyperpolarises.
- Vestibulo-ocular reflex keeps gaze stable as the head turns (doll's eye movements show an intact brainstem in coma).
- Nystagmus is a slow drift followed by a fast corrective phase, named by the fast phase. Caloric test: cold water produces fast phase to the opposite side, warm to the same side.
- Motion sickness arises from mismatch between vestibular and visual input (hyoscine, antihistamines).
Vestibular disorders
- BPPV: loose otoconia from the utricle drift into a semicircular canal (usually posterior), so the canal responds to gravity. Brief vertigo (under a minute) on rolling in bed or looking up; Dix–Hallpike reproduces torsional nystagmus; cured by the Epley repositioning manoeuvre, not sedatives.
- Ménière disease: episodes of vertigo lasting hours with fluctuating hearing loss.
- Vestibular neuritis: vertigo for days without hearing loss.
Remember Base hears high, apex hears low; endolymph is rich in potassium and K⁺ entry excites hair cells.
Exam trap Semicircular canals sense angular acceleration; utricle and saccule sense linear acceleration and gravity.
Exam trap In sensorineural loss Weber goes to the better ear; in conductive loss it goes to the affected ear.
How FCPS asks about this
- Where high frequencies are detected: base of the cochlea, near the oval window.
- Endolymph composition: high K⁺, low Na⁺, made by the stria vascularis; hair cells depolarise by K⁺ entry.
- Noise-induced deafness: outer hair cell damage with a 4 kHz notch; presbycusis begins at the basal turn.
- Rinne negative and Weber to the affected ear in a child with retracted drum: conductive loss from glue ear (Eustachian tube dysfunction).
- Deafness after meningitis: infection spreading into the cochlea.
- Brief positional vertigo: BPPV from loose otoconia; treat with Epley.
- Sudden unilateral sensorineural loss: urgent oral steroids.
Test yourself on this topic
5 of the 28 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
What is the ionic composition of endolymph in the cochlear duct?
Answer: High potassium, low sodium
Endolymph, made by the stria vascularis, is rich in potassium and poor in sodium, like intracellular fluid. It sits at about +80 mV (endocochlear potential). When stereocilia bend, potassium flows into hair cells and depolarises them. Perilymph, around the membranous labyrinth, resembles CSF and plasma (high sodium). Excess endolymph causes Ménière's disease.
Inner ear fluids
- Endolymph: high K⁺, low Na⁺
- Made by stria vascularis
- Endocochlear potential +80 mV
- Perilymph: like CSF
- Excess endolymph: Ménière's
Remember Endolymph is potassium-rich, like the inside of a cell.
Exam trap Hair cells depolarise by potassium inflow, not sodium.
Why the other options are wrong
- High sodium, low potassium That describes perilymph.
- High calcium, high protein Not correct.
- Identical to cerebrospinal fluid Perilymph resembles CSF; endolymph does not.
- High glucose, low chloride Not correct.
When the stereocilia of a cochlear hair cell bend towards the tallest row, the cell depolarises. Which ion movement mainly causes this?
Answer: K⁺ entry from endolymph
Bending towards the tallest stereocilia stretches the tip links and opens mechanotransduction channels at the tips. Endolymph is rich in K⁺ and held at about +80 mV by the stria vascularis, so K⁺ flows into the hair cell down a large electrical gradient and depolarises it. Depolarisation opens voltage-gated Ca²⁺ channels at the base, triggering glutamate release onto auditory nerve fibres. K⁺ then leaves through the basolateral membrane into the low-K⁺ perilymph.
Hair cell transduction
- Tip links open channels
- K⁺ enters from endolymph
- Endocochlear potential +80 mV
- Base: Ca²⁺ in, glutamate out
Remember In the ear, potassium depolarises.
Exam trap Damage to the stria vascularis, as with loop diuretics, reduces the endocochlear potential.
Why the other options are wrong
- Na⁺ entry from perilymph The stereocilia tips are bathed in endolymph, which is low in sodium.
- Cl⁻ entry from endolymph Chloride does not cause depolarisation here.
- Ca²⁺ release from the stria Calcium enters at the base after depolarisation.
- K⁺ exit into perilymph This repolarises the cell.
A newborn has automated otoacoustic emission testing before discharge from the maternity ward. Which cells produce the response being recorded?
Answer: Outer hair cells of the cochlea
Outer hair cells contain the motor protein prestin and change length in response to sound, amplifying vibration of the basilar membrane; this is the cochlear amplifier. Their movement also sends faint sounds back out through the middle ear, which a probe in the ear canal can detect as otoacoustic emissions. Inner hair cells are the main sensory cells that drive auditory nerve fibres, so a baby with auditory neuropathy can have normal emissions but absent brainstem responses.
Otoacoustic emissions
- From outer hair cells
- Prestin: cochlear amplifier
- Absent in most sensorineural loss
- Normal in auditory neuropathy
Remember OAE tests outer hair cells.
Exam trap Middle ear fluid in the first days can block emissions and give a false refer result.
Why the other options are wrong
- Inner hair cells of the cochlea They are the main sensory receptors but do not generate emissions.
- Spiral ganglion neurons Neural loss does not abolish emissions.
- Cells of the stria vascularis Makes endolymph and the endocochlear potential.
- Hair cells of the utricle Vestibular cells, not tested here.
In the auditory pathway, which midbrain structure is an obligatory relay before the medial geniculate body?
Answer: Inferior colliculus
Auditory pathway: cochlear nerve to cochlear nuclei (medulla), superior olivary complex (pons, sound localisation), lateral lemniscus, inferior colliculus (midbrain), medial geniculate body (thalamus) and primary auditory cortex (Heschl's gyrus, superior temporal). Because fibres cross at several levels, a unilateral lesion above the cochlear nuclei does not cause deafness in one ear. The superior colliculus serves visual reflexes.
Auditory pathway
- Cochlear nuclei → superior olive
- Lateral lemniscus → inferior colliculus
- → medial geniculate
- → Heschl's gyrus
Remember Inferior for ears, superior for eyes.
Exam trap Central lesions above the cochlear nuclei rarely cause one-sided deafness.
Why the other options are wrong
- Superior colliculus Visual reflexes and eye movements.
- Red nucleus Motor coordination.
- Substantia nigra Dopaminergic motor control.
- Periaqueductal grey Pain modulation.
A 30-year-old woman with otosclerosis says she hears conversation better on a noisy bus than in a quiet room. Which of the following explains this?
Answer: Others speak louder above noise she cannot hear
This is paracusis Willisii, typical of conductive deafness such as otosclerosis. In a noisy place, people with normal hearing speak much louder to be heard over the background. The woman's conductive loss filters out much of the low-frequency background noise, but the raised voices are now loud enough to cross her threshold. People with sensorineural loss do worse in noise, because their cochlear frequency discrimination is impaired.
Paracusis Willisii
- Seen in conductive loss
- Others speak louder in noise
- Her loss filters background
- SNHL is worse in noise
Remember Better in noise: think otosclerosis.
Exam trap Otosclerosis often worsens in pregnancy.
Why the other options are wrong
- Noise opens her Eustachian tubes Eustachian tube function is not the issue in otosclerosis.
- Loud sound loosens the fixed stapes The stapes stays fixed.
- Noise triggers a stronger stapedius reflex The stapedius reflex reduces, not increases, transmission.
- Background noise improves cochlear tuning Noise worsens, not improves, cochlear discrimination.
Where this sits in the CPSP syllabus
- Paper 1: Special senses, Hearing and balance
- Surgery & Allied, Paper 2: Special senses, Hearing and balance
- Medicine & Allied, Paper 2: Special senses, Hearing and balance