Vestibular neuritis and labyrinthitis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Vestibular neuritis is an acute loss of vestibular nerve function that commonly produces prolonged vertigo, nausea, spontaneous nystagmus and imbalance. Labyrinthitis describes inflammation involving the labyrinth, including its auditory structures, so hearing loss or tinnitus may accompany the vestibular illness. These labels are often used loosely in practice. Precise documentation of hearing, neurological findings and symptom timing prevents the phrase inner-ear infection from becoming an unsupported diagnosis.

The most disabling spinning usually eases over days, while head-motion sensitivity and imbalance may take weeks to settle. Recovery involves both peripheral function and central compensation. A recent respiratory illness may support an inflammatory context but cannot exclude stroke. Similarly, hearing change helps distinguish neuritis from an audiovestibular disorder, yet it does not establish the cause of that disorder. New sensorineural hearing loss needs timely specialist evaluation because potentially useful treatment may be time-sensitive.

Key points

Vestibular neuritis affects balance without causing new hearing loss or tinnitus.
Labyrinthitis involves the inner ear and may include hearing impairment.
Continuous symptoms differ from the brief triggered episodes of BPPV.
Exclude stroke before accepting a peripheral acute vestibular diagnosis.
Use vestibular suppressants for up to three days during the disabling acute phase.
Resume supported movement as nausea settles rather than maintaining prolonged bed rest.
Persistent disequilibrium benefits from reassessment and specialist vestibular rehabilitation.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Vestibular nerve inflammation

An inflammatory or post-infectious process may impair vestibular nerve function. A preceding viral illness is common in histories but does not prove an individual cause.

Labyrinthine inflammation

Inflammation involving the sensory structures of the inner ear can affect both balance and hearing. Bacterial spread is less common but carries different urgency.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Acute unilateral imbalance
Unequal resting vestibular signals generate a false sense of motion and spontaneous eye movements, even when the head remains stationary in bed.
2
Auditory involvement
Cochlear injury adds hearing impairment or tinnitus to the vestibular syndrome. The presence of these symptoms indicates an audiovestibular problem rather than isolated nerve neuritis.
3
Central compensation
Brainstem and cerebellar adaptation gradually reduces the mismatch between sensory inputs. Movement and task practice help recovery, while the speed of compensation varies between individuals.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

An acute sustained syndrome

Symptoms begin abruptly and remain present over hours or days, although moving or opening the eyes may intensify them. Ask whether vertigo genuinely disappears between movements. Continuous illness is inconsistent with ordinary isolated posterior-canal BPPV.

Peripheral vestibular pattern

In an appropriately selected patient, expert examination may show unidirectional horizontal-torsional nystagmus and a corrective saccade on head impulse towards the impaired side without skew. The entire clinical picture must support this interpretation, including the absence of unexplained central signs.

Hearing separates the syndromes

Vestibular neuritis does not itself produce new tinnitus or hearing loss. Ask about telephone hearing, a blocked sensation and new sound distortion, and compare the ears. A normal-looking tympanic membrane does not exclude sensorineural loss.

Possible bacterial disease

Severe otalgia, otorrhoea, mastoid signs, fever or meningeal symptoms may accompany bacterial middle-ear or intracranial infection with inner-ear involvement. This is a different clinical problem from a self-limiting post-viral vestibular illness and may need admission.

Red flags requiring action

New deafness with acute vertigo, neurological signs or profound gait instability must not be dismissed as uncomplicated labyrinthitis.
Fever, severe ear pain, mastoid swelling, meningism or systemic illness suggests an infective complication requiring urgent hospital assessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Acute neurological and vestibular assessmentFirst step
Why
Determine whether the presentation can safely be managed as peripheral dysfunction.
Interpretation and limitations
Evaluate cranial nerves, eye movements, limb coordination and gait. A trained clinician may use HINTS in continuous acute vestibular syndrome with spontaneous nystagmus. If appropriate expertise is absent and no benign explanation accounts for the syndrome, NICE advises immediate stroke-pathway referral.
02
Otoscopy and bedside hearing comparison
Why
Detect ear disease and identify an auditory component requiring escalation.
Interpretation and limitations
Inspect the canal, tympanic membrane and mastoid region. Tuning-fork tests may help distinguish conductive from sensorineural patterns, but bedside testing cannot quantify loss reliably. Do not postpone the urgent hearing-loss pathway while awaiting an audiology appointment.
03
Formal audiometry
Why
Measure suspected hearing impairment and guide specialist auditory management.
Interpretation and limitations
Audiometry can document sensorineural loss and provide a baseline for recovery. Sudden unexplained loss over three days or less within the preceding thirty days warrants assessment within twenty-four hours under NG98, whether or not vertigo is present.
04
Selective blood tests and imaging
Why
Assess complications or investigate a central or bacterial alternative.
Interpretation and limitations
Renal function and electrolytes are useful with dehydration or before relevant medicines. Infection testing and imaging follow the suspected complication. Routine blood tests do not confirm vestibular neuritis, and an early negative brain scan must be interpreted alongside persistent clinical concern.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Posterior circulation ischaemia

Brainstem, cerebellar or labyrinthine vascular injury can closely resemble peripheral inflammation. A hearing deficit or preserved limb power cannot reliably exclude it.

Ménière disease

Recurrent spontaneous attacks with fluctuating hearing, tinnitus and fullness suggest an episodic inner-ear disorder rather than one sustained inflammatory vestibular event.

Vestibular migraine

Migraine-related episodes can last hours or days and include motion sensitivity. The history of recurrent migraine features and previous attacks helps distinguish the pattern.

Additional chapter-specific clues

Recovery versus deterioration

Gradual improvement in nausea and ability to walk supports recovery, but evolving focal deficits, worsening headache or a new auditory symptom requires renewed diagnostic assessment. Persistent vomiting and inability to manage fluids can require hospital support even with a supported peripheral diagnosis.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01InitialEstablish a safe diagnosisFirst stepAn adult presents for the first time with sustained disabling vertigo.

1Assess immediate stability, onset, neurological findings, hearing and the ability to mobilise before accepting a peripheral label.
2Refer urgently through stroke or ENT pathways when central features, sudden hearing loss or an infective complication is suspected.
3Explain what supports the working diagnosis and which changes should trigger immediate reassessment, using a written plan when vomiting or distress limits recall.

02Acute careBrief symptomatic supportAssessment supports peripheral vestibular illness with troublesome nausea or vomiting.

1Encourage small frequent drinks when safe, provide assistance for transfers and use hospital care if oral hydration or safe mobility cannot be maintained.
2Consider a short course of an appropriate antiemetic or vestibular suppressant, generally for no more than three days in this acute illness.
3Review contraindications, sedative interactions and the risk of falls before prescribing; stop once the disabling nausea settles.
4Do not prescribe routine antibiotics for a presumed viral illness or present corticosteroids as an established universal treatment for neuritis.

03RecoveryRebuild movement and balanceThe severe spinning is easing but motion sensitivity or functional imbalance remains.

1Encourage gradual walking and ordinary head movement within tolerable limits, initially with another person available for support.
2Avoid alcohol and driving, cycling or machinery while dizzy, sedated or unable to react safely.
3Arrange review if symptoms worsen, fail to improve after several days or remain unimproved after a week of treatment.
4Refer persistent vestibular disability for an individual rehabilitation programme while checking for BPPV, migraine, hearing problems or another diagnosis.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

May reduce disabling vertigo-associated nausea during the early illness while hydration and safe mobilisation are restored.

Prochlorperazine: Stemetil 5 mg oral tablets

For an adult with acute vestibular vertigo, the product starting dose is 5 mg orally three times daily. Restrict symptomatic use in neuritis or labyrinthitis to up to three days, then stop or reassess; older adults need a lower initial dose.

Avoid with phenothiazine hypersensitivity, liver or renal dysfunction, Parkinson disease, hypothyroidism, cardiac failure, phaeochromocytoma, myasthenia, prostatic hypertrophy or a history of narrow-angle glaucoma or agranulocytosis. Review seizure risk, QT-prolonging medicines and electrolyte disturbance. Sedation, hypotension and dystonia can occur; avoid alcohol and driving. Pregnancy requires benefit-risk assessment, and this SmPC advises suspending breastfeeding during treatment.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Dehydration and electrolyte loss

Repeated vomiting can cause reduced oral intake and electrolyte disturbance, increasing orthostatic symptoms and the adverse-effect risk of some antiemetic medicines.

Persistent vestibular hypofunction

Incomplete compensation may leave oscillopsia, gait insecurity and difficulty in visually busy places. These limitations can persist after the initial spinning has resolved.

Auditory disability

Inner-ear disease with cochlear involvement can leave lasting hearing loss or tinnitus, requiring audiological follow-up and communication support alongside balance recovery.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Monitor hydration, vomiting frequency and ability to walk independently, rather than relying only on a numerical dizziness score.
Check new or worsening hearing symptoms promptly; auditory recovery and vestibular compensation are separate outcomes and may follow different courses.
Review any antiemetic use at the end of the short acute course, particularly when imbalance, restlessness or unusual eye movements may be adverse effects.
Ask about return to ordinary activity, falls, visual blurring during movement and avoidance behaviour; persistent limitations can identify a need for vestibular rehabilitation.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Steroids are a separate decision

Evidence for routine corticosteroids in isolated vestibular neuritis is uncertain. Discuss selected use with a specialist rather than implying inevitable benefit. NICE separately advises considering a steroid for idiopathic sudden sensorineural hearing loss; that recommendation should not be transferred indiscriminately to neuritis.

Suppressants and compensation

The nervous system needs movement-related sensory information to recalibrate after vestibular loss. Prolonged suppression and inactivity can delay this process. A short prescription should therefore have a clear stop point and be linked to a recovery plan.

Later positional vertigo

BPPV can follow labyrinthitis or another vestibular illness. A later pattern of brief bed-turning spins may need positional testing even if the original problem was continuous vertigo. Repeating antiemetics misses a potentially treatable mechanical component.

Auditory symptoms remain important

A patient may initially focus on severe vomiting and only later notice deafness. Ask again when the acute distress settles. Hearing loss with ipsilateral facial weakness or sensory change is another reason for immediate specialist assessment.

11Common pitfallsFrequent interpretation and management errors.

01
Using a preceding cold as sufficient proof of neuritis overlooks central disease that can occur at the same time.
02
Renewing prochlorperazine for weeks without reassessment may perpetuate sedation and interfere with vestibular compensation.
03
Treating all labyrinthitis with oral antibiotics fails to distinguish presumed viral inflammation from serious bacterial ear or intracranial disease.
04
Interpreting residual imbalance as permanent damage too early may discourage graded activity and delay useful rehabilitation.