Hearing loss, tinnitus and the vestibular system

• Hearing is the pathway from sound wave to nerve impulse: auricle and ear canal collect and direct sound, the tympanic membrane and ossicles amplify it, and the cochlea transduces it into neural signals that travel in the vestibulocochlear nerve to the brain.
• Dividing hearing loss into conductive (problem before the cochlea, usually fixable) and sensorineural (problem at or after the cochlea, usually permanent) is the first decision, because the two need completely different action.
• At the bedside, tuning-fork tests (Weber and Rinne) exploit the difference between air and bone conduction to tell which type is present, but an audiogram is needed to confirm and measure it.
• Sudden sensorineural hearing loss is an ear emergency: unilateral loss of at least 30 dB over three contiguous frequencies developing within 72 hours must be referred to be seen within 24 hours and treated without waiting.
• Tinnitus is a symptom, not a disease. Its assessment looks for cause (especially unilateral, pulsatile or distressing tinnitus), impact and associated hearing loss, not for a matching pitch or loudness.
• The inner ear also carries three semicircular canals and two otolithic organs that sense head movement and position; their output drives balance and the vestibulo-ocular reflex that keeps images clear during head motion.

By the end of this page you should be able to:

1. Distinguish conductive from sensorineural hearing loss, name the common causes of each, and choose the first tests.
2. Perform and interpret the Weber and Rinne tests, and say what they can and cannot do.
3. Recognise sudden sensorineural hearing loss as an emergency, state the definition and time windows for referral, and outline initial treatment and cautions.
4. Explain presbycusis, noise-induced hearing loss and ototoxicity, including realistic prevention.
5. Assess tinnitus using the NICE approach (NICE guideline NG155, 2020), including urgent features, questionnaires and imaging.
6. Describe the vestibular organs, the vestibulo-ocular reflex and the commonest peripheral vertigo, and know the central red flags.

Hearing loss is the partial or total inability to detect or understand sound. It is measured in decibels hearing level (dB HL). A useful working definition of disability is a loss that affects communication in everyday settings. Pathologically, hearing loss is either:

• Conductive hearing loss: sound energy fails to reach the cochlea efficiently. The lesion is in the outer ear (auricle, ear canal) or middle ear (tympanic membrane, ossicles, middle-ear cavity). The inner ear and cochlear nerve are intact, so the loss is often reversible with treatment.
• Sensorineural hearing loss: the cochlea, the hair cells, the cochlear nerve (cranial nerve VIII) or the central auditory pathways fail to encode or transmit sound. The loss is usually permanent, although it can fluctuate in a few diseases (for example Meniere disease).
• Mixed hearing loss: both elements are present at the same time, which is common in long-standing middle-ear disease.

Classification drives the whole pathway. Conductive losses need examination of the drum and canal, tympanometry and treatment of the middle ear. Sensorineural losses need an audiogram that separates air and bone conduction, and often further testing for retrocochlear or systemic causes.

On the vestibular side, the same labyrinthine structures that make hearing possible also serve balance. The vestibular (balance) organs share the fluid spaces and the nerve supply, so a single inner-ear insult can produce hearing loss, tinnitus, vertigo and imbalance together. Vestibular disorders are usually classified as peripheral (end organ or vestibular nerve) or central (brainstem or cerebellum).

Sound is collected by the auricle, funnelled down the ear canal and vibrates the tympanic membrane. Three tiny bones (the malleus, incus and stapes) amplify and transmit the vibration through the oval window into the fluid-filled cochlea. Hair cells in the organ of Corti detect shearing forces between the basilar membrane and the tectorial membrane and convert them into electrical signals carried by the vestibulocochlear nerve. High frequencies stimulate the base of the cochlea and low frequencies the apex, which is why high-frequency loss is the earliest sign of most age- and noise-related damage.

The vestibular labyrinth is a separate set of channels in the same temporal bone. Five end organs feed the vestibular nerve: three cristae in the ampullae of the semicircular canals and two maculae in the vestibule (the utricle and the saccule). The semicircular canals sense angular acceleration (rotation of the head). The maculae sense linear acceleration and the position of the head relative to gravity. In an upright person the utricle lies roughly horizontally and the saccule roughly vertically. Their hair cells are embedded in gelatinous membranes (the cupula in the canals, the otoconial membrane in the maculae) that are heavier than endolymph or perilymph, so movement of the head bends the stereocilia and changes firing in the vestibular nerve.

The vestibulo-ocular reflex uses this information: when the head turns, the eyes move in the opposite direction by an equal amount so that the image stays stable on the retina. It works even in darkness. That reflex is what clinicians test with caloric irrigation, the head impulse test and the Dix-Hallpike manoeuvre. The vestibular nuclei (superior, lateral, medial and inferior) integrate input and connect to the eye-movement nuclei, the cerebellum, the thalamus and the spinal cord.

Hearing loss is the commonest sensory impairment worldwide. It becomes much more prevalent with age (see presbycusis below), rises with noise exposure in industry and leisure, and is commoner where aminoglycoside antibiotics and platinum-based chemotherapy are used without monitoring.

• Sudden sensorineural hearing loss (SSNHL) affects 5 to 27 per 100,000 people per year, with about 60,000 new cases annually in the United States. It is typically unilateral, and bilateral involvement occurs in less than 2% of cases. ^[2]
• Presbycusis (age-related hearing loss) affects approximately one third of people over the age of 65, and by 2025 there will be 1.2 billion people over 60 worldwide, with more than 500 million suffering significant impairment. ^[3]
• Occupational noise exposure is still the commonest preventable cause of adult hearing loss. Noise-induced permanent loss accumulates with repeated or prolonged exposure above safe levels. ^[5]

Regional note on worldwide practice: any patient who can be spoken to at arm's length only if the speaker shouts, who has tinnitus after noise, or who works in noise (industry, construction, music, farming) should have hearing protection and periodic testing; this is as true in low-resource settings as in high-income ones.

Conductive loss

• Wax impacted in the canal, foreign bodies, otitis externa.
• Acute otitis media, glue ear (otitis media with effusion), chronic suppurative otitis media, cholesteatoma.
• Perforation of the tympanic membrane, ossicular fixation (otosclerosis) or erosion.

Sensorineural loss

• Age (presbycusis).
• Noise trauma, acute acoustic trauma.
• Ototoxic drugs (aminoglycosides, cisplatin and carboplatin, loop diuretics, macrolides, antimalarials). ^[4]
• Viral and other infections, meningitis, mumps, congenital cytomegalovirus.
• Meniere disease, vestibular schwannoma, autoimmune inner-ear disease.
• Head injury with temporal bone fracture, barotrauma.

Risk factors that are modifiable are the most important for prevention: noise exposure (including recreational music at unsafe levels), unmonitored ototoxic drug use, and untreated middle-ear disease in children.

Conductive loss reduces the energy that reaches the cochlea. The path is mechanical: obstruction, inflammation, fluid or ossicular immobility. The sensory apparatus remains intact, so once the mechanical problem is cleared, hearing returns. Some conductive losses also mimic sensorineural loss clinically, which is why tuning-fork tests and audiometry are needed.

Sensorineural loss reflects damage to the irreplaceable hair cells of the organ of Corti or to the nerve fibres. Inner hair cells are the actual sensory transducers; outer hair cells are the cochlear amplifier. Most age-, noise- and drug-related loss preferentially damages the outer hair cells of the basal (high-frequency) turn of the cochlea. That explains the classic early finding: loss of high frequencies, difficulty hearing speech in noise, and relatively preserved low-tone thresholds.

Hair cells do not regenerate in humans, so the loss is permanent. A notable complication is "hidden hearing loss": synapses between inner hair cells and auditory nerve fibres can be lost even when the audiometric threshold is still normal, so a patient may complain of difficulty hearing in noise with a normal audiogram. Noise-, age- and drug-related synapse loss converge on this pathway. ^[3]

Tinnitus arises when there is abnormal spontaneous neural activity anywhere along the auditory pathway, usually in the setting of reduced peripheral input. The brain increases central gain in response to missing input, and the result is a phantom sound. Because the mechanism is central, tinnitus can persist even when the peripheral problem is removed. Subjective tinnitus is heard only by the patient and is by far the common form. Objective tinnitus is sound generated in the ear or vessels that an examiner can hear and is much rarer; it is a pointer to vascular, muscular or middle-ear causes and needs investigation. ^[6]

Vertigo is the false sensation of movement and reflects a mismatch or imbalance in vestibular input. Normal balance needs agreement between the vestibular organs, vision and proprioception. A sudden unilateral vestibular loss creates a difference in firing between the two sides even at rest, and the brain interprets that as movement.

In the patient's own words:

• "I can't hear people against background noise" (early high-frequency loss, presbycusis, noise, early ototoxicity).
• "It sounds as if people are mumbling." (high-frequency consonants are lost.)
• "My ear feels blocked or full" (wax, middle-ear effusion, sudden SNHL, early Meniere). Always exclude wax first.
• "It came on over a few hours" (sudden sensorineural hearing loss, an emergency).
• "Ringing, buzzing, hissing in the ear" (tinnitus, common with most hearing losses).
• "The room spins when I lie down, turn over or look up" (benign paroxysmal positional vertigo).
• "I feel unsteady, especially with rapid head movements" (vestibular hypofunction, compensation).

Ask about noise exposure at work and in leisure, recurrent ear infections, otorrhoea, pain, previous ear surgery, aural fullness, vertigo and its triggers, familial hearing loss, drug history (aminoglycosides, cisplatin, loop diuretics, macrolides), and any neurological symptoms (facial weakness, double vision, ataxia).

• Inspection: pinna, pre- and post-auricular skin, scalp, mastoid tenderness.
• Otoscopy: wax, discharge, perforation, retraction pockets, cholesteatoma debris, a bulging drum, fluid levels, a white mass behind the drum (glomus), vascular pulsation.
• Hearing at the bedside: whisper test (a few words from about an arm's length, with the opposite ear masked), tuning forks, free-field voice.
• Vestibular: nystagmus (direction, fixation suppression), head impulse test, Dix-Hallpike, gait and Romberg (with vision and without), coordination.
• Cranial nerves and cerebellar signs if central disease is possible.

Tuning fork tests (Weber and Rinne) are the classic bedside tools. Weber places the base of a tuning fork on the midline of the skull and asks where the sound is heard. Rinne compares air conduction with bone conduction at the mastoid. They are quick and require no equipment beyond a fork, but they are operator-dependent and can mislead; they must be confirmed with an audiogram.

For a patient with hearing difficulty, separate by type:

Red flags that suggest a specific cause rather than ordinary hearing loss:

• Unilateral or asymmetrical sensorineural loss: consider vestibular schwannoma, Meniere disease, autoimmune inner-ear disease, previous noise in one ear. NICE suggests MRI of the internal auditory meati when there is an asymmetry of 15 dB or more at any two adjacent test frequencies (0.5, 1, 2, 4 and 8 kHz) in sensorineural loss without localising signs, and always when localising signs exist. ^[1]
• Pulsatile tinnitus: vascular, glomus tumour, dehiscent superior semicircular canal, intracranial hypertension.
• Vertigo with a completely normal examination and no hearing loss: consider vestibular migraine or persistent postural-perceptual dizziness, which are diagnoses of exclusion after structural causes are ruled out.
• Unilateral hearing loss with ipsilateral facial droop or altered facial sensation: refer immediately, because this can be stroke. ^[1]

1. Exclude reversible external and middle-ear causes first: wax, otitis externa, acute infection. ^[1]
2. Tuning forks (Weber and Rinne) as above.
3. Pure-tone audiometry with air and bone conduction, usually with speech audiometry: the gold standard. It confirms type and degree, lateralises asymmetry, and is needed before any management decision. NICE audiological assessment in adults also records history (symptoms, comorbidities, cognition, mobility and dexterity), hearing and communication needs, psychosocial impact, expectations and motivation, and otoscopy. ^[1]
4. Tympanometry when middle-ear fluid or Eustachian tube dysfunction is suspected. ^[6]
5. MRI of the internal auditory meati for localising signs, asymmetry as above, or tinnitus with neurological, otological or head and neck signs. ^[1][6]
6. Blood tests do not diagnose ordinary hearing loss. Send cultures if infection of a mass is suspected and consider autoimmune serology when an autoimmune inner-ear disease is plausible. Routine blood work in SSNHL is discouraged: results are usually normal, do not change initial management, and false positives can drive unnecessary testing. ^[2]
7. Vestibular tests when balance is the presenting problem: head impulse test, video head impulse, caloric testing, rotary chair and posturography. These map the gain and symmetry of the vestibulo-ocular reflex.

• SSNHL is defined as rapid-onset hearing loss of at least 30 dB HL across three contiguous frequencies, developing in 72 hours or less. It can develop instantaneously or over hours, and aural fullness and tinnitus almost always accompany it; some patients also have vertigo. Treatment is more effective the sooner it starts; some studies report significantly better hearing outcomes when treatment begins within 7 days of onset. ^[2]
• Severity of hearing loss is conventionally graded by pure-tone average into mild, moderate, severe and profound; band limits vary between classification systems, so quote the scale and its source whenever you grade a loss.
• Disabling hearing loss as used by WHO underlies the presbycusis prevalence figure quoted above. ^[3]
• Pure-tone asymmetry thresholds for imaging are given above (15 dB at two adjacent frequencies). ^[1]

Sudden or rapid-onset hearing loss is a red-flag presentation:

• Hearing loss that developed suddenly (over 3 days or less) within the last 30 days: refer immediately (to be seen within 24 hours) to an ear, nose and throat service or an emergency department. ^[1]
• Hearing loss that developed suddenly more than 30 days ago: refer urgently (to be seen within 2 weeks). ^[1]
• Hearing loss that worsened rapidly (over 4 to 90 days): refer urgently (to be seen within 2 weeks). ^[1]
• If tinnitus accompanies a sudden loss: refer within 24 hours. ^[6]

On arrival at secondary care, the priority is to confirm that the loss is sensorineural with tuning forks and then an urgent audiogram, and to exclude conductive causes (the AAO-HNSF stresses that differentiating conductive from sensorineural loss is the crucial first step, because management differs completely). ^[2]

Initial treatment: the standard is a tapered course of oral corticosteroids. ^[2] NICE says consider a steroid to treat idiopathic sudden sensorineural hearing loss in adults. ^[1] Corticosteroids started early give a greater chance of recovery; treatment initiated within 7 days of onset has been associated with significantly better hearing outcomes. ^[2] Intratympanic steroids and hyperbaric oxygen are arranged by the otolaryngologist; follow local dosing protocols. Antivirals should not be prescribed: reviews found no statistically significant benefit, and they add side effects. ^[2] Acute management also needs urgent MRI of the brain, brainstem and internal auditory canal with gadolinium when retrocochlear pathology is a possibility; CT is relatively insensitive and delivers radiation, while routine bloods are discouraged. ^[2]

Contraindications to systemic corticosteroids (list them explicitly before prescribing): diabetes, labile hypertension, glaucoma, tuberculosis, peptic ulcer disease, and prior psychiatric reactions to corticosteroids. ^[2] Be very careful in a patient with an upper respiratory infection who may have Eustachian or middle-ear disease rather than true SSNHL. Short courses of 10 to 14 days (as quoted in the review) usually have reversible side effects, while serious events are rare.

Counselling: 32 to 65% of cases recover spontaneously, but these figures may be overestimated and the consequence of missing an effective treatment is permanent loss, so do not wait for spontaneous recovery. ^[2] Successful treatment also usually improves the associated tinnitus. ^[2]

• Conductive loss: remove wax (electronic irrigation, microsuction, manual removal after softening; not syringing); treat infection; drain middle-ear effusion; repair perforation; refer for ossicular surgery or for a specialist opinion on otosclerosis. ^[1]
• Hearing rehabilitation: NICE recommends offering hearing aids to adults whose loss affects communication, awareness of warning sounds or enjoyment of music, with two aids where both ears have aidable loss, and cochlear or bone-conduction implants where appropriate. ^[1] Follow-up is at 6 to 12 weeks, then reassessment. ^[1]
• Single-sided deafness and asymmetric loss need specialist discussion (CROS hearing aids, bone-anchored devices, cochlear implantation).
• Presbycusis: no drug reverses it. Rehabilitation is hearing aids, assistive listening devices, communication tactics and environmental modification (quiet rooms, face-to-face seating, good lighting). Annual reassessment. Treat concomitant wax promptly. Screen older adults with concern, and refer for implant evaluation when aids are no longer sufficient. Because untreated presbycusis contributes to social isolation, depression and cognitive decline, identification is worthwhile. ^[3]
• Noise-induced loss: there is no curative treatment; the emphasis is prevention (below) and rehabilitation once loss is present.
• Ototoxicity (see below).
• Meniere disease, vestibular schwannoma and other specific causes: specialist referral; beyond the scope of this page but must be excluded in unilateral or progressive sensorineural loss.

• Counselling, reassurance and tinnitus information (below).
• Wax removal only by trained staff with the right equipment. ^[1]
• Vestibular rehabilitation (see vestibular section).

No routine drugs for conductive or sensorineural loss. Ototoxic drugs should be monitored or avoided where alternatives exist. Betahistine is not recommended for tinnitus (below).

• Myringoplasty or tympanoplasty for perforation, ossiculoplasty, stapedotomy for otosclerosis.
• Drainage, ventilation tubes or adenoidectomy in appropriate children with glue ear (not covered in detail here).
• Cochlear implantation or bone-anchored hearing devices for suitable severe-to-profound loss. ^[1]

Audiological follow-up at 6 to 12 weeks after first fitting, then regular reassessment, and a clear route back to service if hearing changes, tinnitus worsens or vertigo develops. ^[1]

Refer urgently as above. Also refer (consider referral, in NICE's words) for non-acute problems such as unilateral or asymmetric loss as a primary concern, fluctuating loss not linked to an upper respiratory infection, hyperacusis, persistent unilateral or pulsatile tinnitus, recurrent or unresolved vertigo, and any loss not explained by age. ^[1] Refer immediately (within 24 hours) for acquired unilateral loss with ipsilateral facial droop or altered sensation, or for immunocompromised patients with otalgia and otorrhoea unresponsive to 72 hours of treatment. ^[1]

• Permanent hearing loss with social, educational and occupational impact.
• Tinnitus and hyperacusis.
• Falls and isolation in older adults with untreated loss.
• After middle-ear surgery: infection, worsening of hearing, facial nerve injury (rare).
• Vestibular hypofunction and compensation failure after inner-ear insults.

• SSNHL: variable. Even with prompt treatment, some patients do not recover, while up to two thirds may recover spontaneously. Greater initial loss, flat or down-sloping audiogram and vertigo at onset predict worse recovery. ^[2]
• Presbycusis: progressive; management restores communication rather than reverses loss. ^[3]
• Ototoxicity: often permanent; recovery is more likely if the drug is stopped early and hearing is already being monitored. ^[4]

• Noise: follow the NIOSH recommended exposure limit of 85 A-weighted decibels as an eight-hour time-weighted average, reducing exposure duration by half for each 3 dB increase above that. Use hearing protection (earplugs or muffs, correctly inserted) where noise is loud, and prefer quiet hobbies and lower volumes through headphones. ^[5]
• Drugs: whenever possible avoid ototoxic drugs; if they are necessary, monitor hearing and vestibular function, agree an ototoxicity monitoring plan with oncology and audiology, and consider alternatives. ^[4]
• Infection control and immunisation where available, and prompt treatment of middle-ear disease in children to prevent permanent conductive loss.
• Wax: advise against putting cotton buds or small objects in the ear canal. ^[1]
• Hearing checks for older adults and for anyone with concern; hearing aids improve quality of life and are under-used.

• Older adults: presbycusis is the norm, not the exception. Examine ears, remove wax, and consider aids, with regular reassessment; take cognition and dexterity into account when choosing devices. NICE advises considering referral of adults with diagnosed or suspected dementia or mild cognitive impairment to an audiology service for hearing assessment. ^[1]
• Children: congenital and acquired loss needs a different pathway (newborn hearing screening, paediatric audiology); avoid ototoxic drug exposure in children, whose ears are more vulnerable. Up to 60% of cisplatin-treated children develop ototoxicity. ^[4]
• Pregnancy: no specific recommendations in our sources; manage SSNHL and tinnitus on their merits and avoid teratogenic drugs.
• Immunocompromised patients: refer immediately if hearing loss with ear pain and discharge does not respond within 72 hours. ^[1]

Ototoxicity is injury to the cochlea, the vestibular labyrinth or the auditory nerve caused by drugs. Aminoglycoside antibiotics, platinum-based chemotherapeutics, loop diuretics, macrolide antibiotics and antimalarials are the commonly used agents with well-documented efficacy. ^[4]

Prevalence estimates vary, which shows why monitoring matters rather than relying on a single number:

• cisplatin: 23 to 50% in adults and up to 60% in children, with some studies reporting elevated thresholds in all treated patients; ^[4]
• aminoglycosides: around 63%; ^[4]
• furosemide: around 6 to 7%. ^[4]

Onset is usually in the high frequencies (above 8,000 Hz), progresses to the speech frequencies, and is dose-dependent and cumulative. It may be reversible (for example with some loop-diuretic or macrolide effects) or permanent. Risk rises with renal impairment, age, concurrent noise, pre-existing loss and genetic susceptibility: the mitochondrial A1555G mutation in particular increases aminoglycoside susceptibility. ^[4]

Management:

• Treat the underlying condition; avoid the drug when an alternative exists.
• Before treatment, take a baseline history (noise exposure, prior ototoxic drugs, family history) and a baseline audiogram including high frequencies from 9,000 to 20,000 Hz if available. ^[4]
• Baseline testing within 24 hours of chemotherapy and within 72 hours of starting an aminoglycoside. ^[4]
• Monitor with pure-tone audiometry from 250 to 8,000 Hz, high-frequency audiometry, distortion-product otoacoustic emissions and tympanometry; ASHA criteria flag a 20 dB drop at any test frequency or a 10 dB drop at two adjacent frequencies. ^[4]
• Watch for tinnitus, aural fullness, vertigo and oscillospia, which patients should report immediately.
• Vestibulotoxicity: aminoglycosides are the classic cause. There is no single test; bedside screening includes dynamic visual acuity and the head impulse test, with the Dizziness Handicap Inventory. ^[4]
• No drug is FDA-approved to prevent drug-induced ototoxicity in adults, and the only such approval is sodium thiosulfate (Pedmark) for children aged 1 month or older with localized, non-metastatic solid tumors receiving cisplatin; for everything else, detection with the monitoring above and dose adjustment remain the main protections. ^[4]

Noise damages both cochlear hair cells and their synapses. The characteristic audiogram is a dip in the mid-high frequencies with recovery at the top end, though long exposure flattens this into a general high-frequency loss. Rock concerts, nightclubs, firearms, power tools and personal audio at unsafe volume all contribute, not just heavy industry.

Practical advice worth giving every patient: take breaks from noise every hour; wear properly fitted earplugs or earmuffs (a proper fit matters more than the rating); never stand directly in front of loudspeakers; protect children, who cannot judge loudness themselves. Screening should be considered after loud occupational or recreational exposure. There is no medication or supplement with solid evidence for prevention.

Presbycusis is the progressive, usually bilateral and symmetrical sensorineural loss of older age. It is the commonest sensory impairment of later life. ^[3]

• It affects about one third of people over 65 and 500 million people over 60 by 2025. ^[3]
• Loss begins in the high frequencies and spreads to lower frequencies; speech in noise and sound localisation suffer early. ^[3]
• Men are generally more severely affected than women. ^[3]
• It is irreversible and can contribute to social isolation, depression and cognitive decline. ^[3]

Schuknecht's three forms are a useful framework (recognising that most older ears have mixed pathology):

1. Sensory: abrupt high-frequency loss, outer hair-cell loss at the base of the cochlea.
2. Strial (metabolic): a flat or gently sloping audiogram, strial atrophy.
3. Neural: loss of cochlear neurons throughout, disproportionate difficulty understanding speech.

Risk factors overlap with noise and vascular disease; the balance between biological ageing and lifelong noise exposure explains why hearing varies so much at the same age. General health (hypertension, diabetes, smoking) is relevant. Management is rehabilitation (aids, assistive devices, communication tactics) plus active treatment of reversible contributors such as wax and middle-ear disease.

Tinnitus is the perception of sound without an external source. It is very common and for most people is intermittent and mild. NICE guideline NG155 (2020) frames assessment around impact and cause, not around matching pitch or loudness.

Assessment:

• Take a full history: onset (sudden or gradual), laterality, quality, pulsatility, severity, sleep disturbance, mood, associated hearing loss, vertigo, headache, jaw symptoms and noise exposure.
• Examine ears and perform Rinne and Weber when hearing loss is present.
• All patients should receive information and reassurance: tinnitus is common, may be temporary, is not usually associated with serious physical disease, and has manageable strategies. ^[6]
• Assess impact with the Tinnitus Functional Index in adults; use visual analogue scales if questionnaires are not suitable (language or cognitive problems), and age-appropriate measures in children. ^[6]
• Ask directly about sleep. Screen for depression and anxiety when concerned. ^[6]
• An audiological assessment is offered to everyone with tinnitus. ^[6]
• Tympanometry is used when middle-ear or Eustachian tube dysfunction or other conductive causes are suspected. ^[6]
• Do not offer acoustic reflex testing, uncomfortable loudness level testing, otoacoustic emissions (unless other signs), or psychoacoustic tests such as pitch and loudness matching. ^[6]

Imaging:

• Non-pulsatile tinnitus: MRI of the internal auditory meati for those with neurological, otological or head and neck signs; consider MRI for unilateral or asymmetrical tinnitus without signs; no imaging if symmetrical and unaccompanied by signs. ^[6]
• Pulsatile tinnitus needs imaging (see choices in NICE). ^[6]

Management (NICE NG155):

• Urgent referral is the same as for sudden hearing loss: within 24 hours when tinnitus with sudden loss in the last 30 days; within 2 weeks for distress affecting daily life despite initial support, or for sudden loss more than 30 days ago; immediately for suicide risk, sudden neurological signs, acute uncontrolled vestibular symptoms or suspected stroke. ^[6]
• Refer for routine tinnitus assessment when it bothers the patient, when it is persistent and objective, or when it accompanies unilateral or asymmetric hearing loss; consider referral for persistent pulsatile or persistent unilateral tinnitus. ^[6]
• Offer amplification (hearing aids) when tinnitus coexists with communication-affecting hearing loss; consider aids when there is loss but no communication difficulty; do not offer aids for tinnitus with normal hearing. ^[6]
• Provide tinnitus support: information, reassurance, self-help, relaxation and a jointly agreed management plan.
• For distress that persists, a stepped psychological approach: digital CBT first, then group-based mindfulness/ACT/CBT, then individual CBT. ^[6]
• Do not offer betahistine. ^[6]
• Sound therapy and neuromodulation did not attract routine recommendations (research is ongoing). ^[6]

Low-resource note: in most primary care settings worldwide, the most useful interventions are hearing aids when loss is present, tinnitus information and reassurance, and structured follow-up. The stepped psychology recommendations require access that many systems will not have; telehealth and guided self-help can partly close the gap.

Balance integrates vestibular, visual and proprioceptive input. The peripheral vestibular system has five end organs: three semicircular canals (sensing angular acceleration, i.e. rotation) and two otolith organs (the utricle and saccule, sensing linear acceleration and gravity). ^[7] The semicircular canals are wrapped in fluid and their crista hair cells project into gelatinous cupulae; the utricle is predominantly horizontal and the saccule predominantly vertical, their hair cells covered by otoconial membranes. ^[7] Each end organ is oriented so that every direction of head motion is detected by at least one, and ears work in complementary pairs: when one is excited, its paired organ on the other side is inhibited. ^[7]

The vestibulo-ocular reflex keeps gaze stable during head movement by moving the eyes in the opposite direction; it works even in darkness. Clinicians use it directly: caloric testing, active and passive head movements, positioning tests (Dix-Hallpike) and rotary chair. ^[7]

• Benign paroxysmal positional vertigo (BPPV): the commonest cause of vertigo. Dislodged otoconia fall into a semicircular canal (most often the posterior, accounting for 75 to 95% of cases; the horizontal canal in about 5%). Short bursts of vertigo triggered by lying down, turning over, or looking up. Diagnosis with the Dix-Hallpike manoeuvre; treatment is canalith repositioning (Epley for posterior canal, barbecue roll for horizontal). ^[7]
• Vestibular neuritis: acute prolonged vertigo (days) after a viral-type illness, horizontal nystagmus, no hearing loss, with gradual central compensation. Management is symptomatic (anti-emetics and, variably, steroids in the first 3 days), then vestibular rehabilitation.
• Meniere disease: episodic vertigo with fluctuating low-frequency sensorineural hearing loss, tinnitus and aural fullness. Management: low-salt diet, betahistine is used in some countries (NICE does not recommend it for tinnitus specifically), diuretics, intratympanic therapy, and surgery in refractory cases.
• Vestibular migraine: vertigo associated with migraine; a clinical diagnosis.
• Central causes (stroke, tumour, multiple sclerosis, cerebellar lesions): vertigo with neurological signs (double vision, dysarthria, limb ataxia, new headache, inability to walk or stand), direction-changing nystagmus that does not suppress with fixation, or acute severe vertigo in a vascular risk-factor patient. Refer urgently.

• Head impulse test: rapid passive horizontal head thrust; a catch-up saccade indicates a peripheral vestibular deficit on the side of thrust (high sensitivity for unilateral peripheral loss). ^[7]
• Dix-Hallpike: position provokes posterior-canal BPPV with appropriate nystagmus.
• Caloric testing: irrigates the ear with warm and cool water or air; asymmetry quantifies each labyrinth's function. ^[7]
• Gait and Romberg with eyes open and closed, sit-to-stand; look for veering or falling.
• Nystagmus characteristics: spontaneous unidirectional horizontal nystagmus that suppresses with fixation favours a peripheral lesion; vertical, pure torsional or direction-changing nystagmus, or nystagmus that fails to suppress, points centrally. ^[7]

Compensation is the brain's recalibration of balance responses after peripheral loss. Static symptoms (spontaneous nystagmus, tilting) settle over days; dynamic deficits (gaze stability during head movement) take weeks to months. Vestibular rehabilitation (gaze-stabilisation exercises, habituation, balance retraining) and early mobilisation promote compensation; Cawthorne-Cooksey exercises are the classic example. ^[7] Compensation can be incomplete, especially after bilateral loss, and symptoms may persist; stress, poor sleep and visual over-reliance (anxiety) worsen them.

• Use a tuning fork and an otoscope: these alone separate most conductive from sensorineural loss and cost almost nothing. ^[2]
• Hearing aids, wax removal tools and a quiet room are high-yield and cheap.
• For SSNHL, the referral time windows (within 24 hours) and a single course of oral corticosteroids are affordable and well-supported; the critical step is recognising it early.
• Vestibular rehabilitation needs only a trained therapist and practice, not equipment.
• Tinnitus support can be delivered by trained nurses or community workers with written materials.

• Divide every hearing loss into conductive, sensorineural or mixed first; this single decision sets the rest of the pathway.
• Conductive loss is mechanical and often reversible; sensorineural loss is usually permanent but often rehabilitable.
• Weber: conductive loss makes the affected ear louder; sensorineural loss makes the unaffected ear louder. Rinne: conductive gives bone at least as loud as air; sensorineural gives air louder than bone.
• SSNHL: at least 30 dB across three contiguous frequencies within 72 hours, usually unilateral (bilateral under 2%). Refer within 24 hours if within the last 30 days. Oral corticosteroids started early (within 7 days best) are the standard; avoid antivirals. ^[2]
• NICE time windows: sudden loss within 30 days -> 24 hours; sudden loss older than 30 days -> 2 weeks; rapidly worsening over 4 to 90 days -> 2 weeks. ^[1]
• NICE recommends MRI of the internal auditory meati for asymmetry of 15 dB or more at two adjacent frequencies (0.5, 1, 2, 4, 8 kHz) in sensorineural loss. ^[1]
• Ototoxic drugs: cisplatin 23 to 50% in adults (up to 60% in children); aminoglycosides about 63%; furosemide about 6 to 7%. Monitor high-frequency hearing; no FDA-approved preventive drug. ^[4]
• Presbycusis affects about one third over 65 and contributes to isolation, depression and cognitive decline; rehabilitation, not reversal, is the goal. ^[3]
• Noise: NIOSH recommended exposure limit is 85 dBA over an eight-hour day, halving time for each 3 dB rise. ^[5]
• Tinnitus is a symptom, not a diagnosis: reassure, assess impact with the Tinnitus Functional Index, examine ears, offer aids when there is hearing loss that affects communication, and avoid betahistine; refer routinely or urgently by features. ^[6]
• The vestibular labyrinth has 5 end organs (3 semicircular canals for rotation, utricle and saccule for linear acceleration and gravity) that drive the vestibulo-ocular reflex and balance. ^[7]
• BPPV is the commonest vertigo; posterior canal in 75 to 95% of cases and horizontal in about 5%; diagnosed with Dix-Hallpike and treated with repositioning manoeuvres. ^[7]
• Central red flags: vertical or direction-changing nystagmus, failure to suppress with fixation, focal neurological signs, acute vascular risk, inability to stand or walk.

Related topics (as plain text): vestibular migraine and headache; stroke and transient ischaemic attack assessment; aural rehabilitation; Meniere disease; acoustic neuroma; middle-ear disease in children; dementia and cognitive impairment; depression and anxiety. No linked topics are published yet in this library for direct cross-linking.

This page summarises current guidelines that were open at the time of writing: NICE guideline NG98 (last updated 02 October 2023) and NICE guideline NG155 (published 11 March 2020), together with the AAO-HNSF Clinical Practice Guideline: Sudden Hearing Loss (Update, 2019) and the AAO-HNSF tinnitus guideline as reported through the review and sources cited above. Recommendations change; check the guidelines for the latest version before applying them.