Vestibular Neuritis

Vestibular neuritis is an inflammation of the balance nerve running from one ear to the brain. The body, often after a cold or viral infection, mistakenly attacks part of this nerve. The result is a sudden onset of intense vertigo that lasts several days, with nausea and unsteadiness, and a strong urge to lie completely still.

Hearing is not affected — this is the key feature that distinguishes it from inner-ear infections that involve the cochlea too.

The symptoms typically peak within a day and gradually improve over one to two weeks, although a slight feeling of imbalance can persist for months. Most patients recover completely, helped along by vestibular rehabilitation exercises.

Vestibular neuritis is one of the most common causes of acute vestibular syndrome (AVS): sudden-onset, persistent, continuous vertigo lasting at least 24 hours, with associated nausea, head-motion intolerance, and unsteady gait. Estimated annual incidence is around 3.5 per 100,000.1

The Bárány Society's 2022 consensus criteria prefer the term acute unilateral vestibulopathy(AUVP), reflecting uncertainty about whether every case is genuinely inflammatory — but the older "vestibular neuritis" remains widespread in clinical practice and the two are used interchangeably.4

The diagnostic challenge is not making the diagnosis — the history and bedside examination are stereotyped — but making it safely. Posterior circulation stroke (PICA, AICA) can present identically, and missing such a stroke is the single most consequential vestibular error in emergency medicine. Most of this module is about the bedside discriminators.

Vestibular neuritis preferentially affects the superior division of the vestibular nerve — the bundle that carries afferents from the anterior and lateral canals and the utricle. The inferior division (posterior canal, saccule) is usually spared. This anatomical selectivity is a clinical fingerprint: the head impulse is abnormal in the horizontal plane (lateral canal failure), oVEMP amplitudes are reduced (utricular failure), but cVEMPamplitudes are preserved (saccular sparing), and posterior-canal BPPV may develop in the aftermath as the dependent canal's otoconia are liberated by inflammation.1,2

The aetiology is most commonly proposed as reactivation of latent herpes simplex virus type 1 in Scarpa's ganglion. HSV-1 DNA has been demonstrated in postmortem vestibular ganglia, and the geographical and seasonal patterns of neuritis cluster with viral epidemics.3 Alternative aetiologies — autoimmune, microvascular, post-vaccination — have been proposed but lack consistent evidence. Bilateral simultaneous neuritis is exceedingly rare and should prompt consideration of ototoxicity, autoimmune inner ear disease, or central pathology.

The three parts of HINTS each test something slightly different about how the brain and inner ear interact. The head impulse tests whether the inner ear can keep the eyes locked on a target while the head is suddenly turned. The nystagmus test looks for an abnormal pattern of eye jerking. The skew test looks for one eye drifting up while the other drifts down — a sign of brainstem trouble.

Used together, these three tests reliably separate the common inner-ear problem (vestibular neuritis) from the rarer but dangerous brain stroke. The key teaching point: an abnormal head impulse test is reassuring — it means the inner ear is at fault, not the brain.

Each HINTS component has a specific peripheral and central signature. The head impulse, first described as a bedside sign by Halmagyi and Curthoys in 1988,5tests the high-acceleration horizontal VOR by rapidly rotating the head while the patient fixates on the examiner's nose. A working VOR keeps the eyes locked on the target; a failed VOR produces a corrective saccade as the eyes catch up. In vestibular neuritis, the head impulse is abnormal when the head is rotated toward the affected ear. In posterior fossa stroke, the head impulse is typically normal — because the labyrinth itself is intact.7

The video head impulse test (vHIT) is the instrumented refinement, using lightweight goggles with high-frame-rate cameras to quantify VOR gain and detect covert saccades. Sensitivities exceed 90% for canal-specific paresis in experienced hands.6

Nystagmus in vestibular neuritis is unidirectional, mostly horizontal with a torsional component, beating toward the healthy ear, enhanced by removing fixation (Frenzel glasses). It obeys Alexander's law — intensity rises when looking toward the fast phase. Central nystagmus, by contrast, often changes direction with gaze, may be purely vertical or torsional, and is not suppressed by fixation.

Skew deviation is the rarest of the three components but the most specific for central pathology. Detected with alternate cover testing: the uncovered eye refixates vertically as it takes up fixation. It reflects an ocular tilt reaction from disruption of the graviceptive pathways in the brainstem.

The discriminating power of HINTS depends entirely on operator skill and on careful patient selection. The original Kattah cohort comprised patients with continuous vertigo lasting at least 24 hours and at least one stroke risk factor — exactly the AVS population where HINTS performs as advertised.8 Applied to patients with episodic or positional vertigo, or to patients without persistent spontaneous nystagmus, HINTS loses sensitivity and specificity dramatically. Do not test HINTS in a patient without nystagmus — the test is built on the asymmetry of spontaneous vestibular tone.

Three failure modes deserve specific mention. First, AICA infarction can disrupt the labyrinth's own blood supply and produce an abnormal head impulse alongside the central signs — so an "abnormal HI" in a patient with new hearing loss is a red flag, not a green light. Second, small cerebellar infarcts of the posterior inferior cerebellar artery territory may produce HINTS findings indistinguishable from neuritis on one or two components but typically violate the rule on the third. Third, skew deviation can be subtle — an experienced examiner will pick up minor vertical refixation that is missed on inspection alone.

The HINTS'Plus' modification adds bedside finger-rub hearing as a fourth component; new unilateral hearing loss in AVS classifies the case as central. This increases sensitivity for AICA strokes (which involve the labyrinthine artery) at the cost of a few additional "central" calls in labyrinthitis patients.9,10

A normal hearing test is part of confirming the diagnosis of vestibular neuritis. If hearing has dropped on one side, the problem is more likely to be in the inner ear itself (a condition called labyrinthitis) or, more worryingly, a small stroke affecting both the balance nerve and the hearing supply at the same time.

Audiometric assessment is recommended in every AVS workup, not because vestibular neuritis affects hearing but because hearing changes redirect the differential. Acute SNHL with persistent vertigo is concerning for AICA infarction — the labyrinthine artery is a terminal branch — and warrants vascular imaging regardless of an otherwise "peripheral" HINTS.10 A conductive hearing loss in the same context should prompt examination for tympanic membrane pathology and consideration of acute otitis media with secondary labyrinthitis.

Beyond the audiogram, supportive evidence for the diagnosis of vestibular neuritis includes a unilateral caloric paresis on bithermal caloric testing, reduced VOR gain on vHIT for the affected horizontal canal, and reduced or absent oVEMPs with preserved cVEMPs (reflecting selective superior-division involvement). None of these are required for diagnosis under the Bárány criteria, but they aid localisation and have medicolegal value when stroke must be definitively excluded.4

Treatment focuses on symptom control, prevention of long-term imbalance, and recovery. Anti-nausea medications are used for the first few days; longer-term use slows recovery and is discouraged. Once the worst of the vertigo has passed, the patient should be encouraged to get up and move — staying still actually makes recovery slower. Vestibular rehabilitation, a programme of head and eye exercises supervised by a physiotherapist, accelerates recovery.

Corticosteroids may be used in the first week to limit inflammation; the evidence is suggestive but not definitive. Most patients are substantially better at one month and back to normal by three.

The Bárány Society's 2022 diagnostic criteria for acute unilateral vestibulopathy require:4

1. Acute or subacute onset of sustained spinning or non-spinning vertigo (an acute vestibular syndrome) of moderate to severe intensity, lasting at least 24 hours.
2. Spontaneous peripheral vestibular nystagmus — direction-fixed, enhanced by removing fixation, with a trajectory appropriate to the involved canal afferents (generally horizontal-torsional).
3. Unambiguous evidence of a reduced VOR function on the affected side (clinical head impulse test, vHIT, calorics, or rotational testing).
4. No accompanying acute audiological or central neurological signs.
5. Not better accounted for by another disease or disorder.

Management proceeds along three axes. Symptomatic relief with anti-emetics and vestibular suppressants (e.g. prochlorperazine, antihistamines) is appropriate in the first 72 hours but should be discontinued promptly thereafter — prolonged use suppresses the central compensation process.1Corticosteroids (typically methylprednisolone) within the first 72 hours improved caloric recovery at 12 months in the Strupp 2004 RCT, although a follow-up Cochrane review considered the overall evidence inconclusive.11Antiviral therapy alone or in combination with steroids has not been shown to add benefit. Vestibular rehabilitation started early significantly shortens functional disability and is the best-evidenced intervention.12

Three management decisions in vestibular neuritis warrant deliberate consideration in every case. First, the safety workup. Even after a peripheral HINTS, patients with stroke risk factors and an unconvincing examination should have MRI/MRA — the cost of missing a small posterior fossa stroke in a patient who later deteriorates is high enough to justify imaging liberally. Second, the steroid decision. The Strupp 2004 trial demonstrated improved vestibular recovery on caloric testing at 12 months but did not show improved subjective recovery — many neurologists offer steroids within 72 hours by default, others reserve them, and the evidence supports either practice. Third, the vestibular rehabilitation referral. Early VR halves the time to symptom resolution and is the only intervention with consistently strong evidence; arrange it before the patient leaves the acute setting if practicable.12,11

Long-term outcomes: most patients recover to a functional state but maintain a measurable canal paresis on caloric testing indefinitely. Persistent imbalance — particularly visual-vestibular mismatch in busy visual environments — is common at three to six months and usually resolves with continued vestibular rehabilitation. Failure to compensate after six months should prompt consideration of persistent postural-perceptual dizziness (PPPD) as a secondary diagnosis, with cognitive behavioural therapy and SSRIs as additional management options.

Recurrence is uncommon (around 2% per year) and should prompt reconsideration of the diagnosis — recurrent acute vestibular syndrome is more often vestibular migraine, Ménière's, or vestibular paroxysmia than recurrent neuritis.