Acute peripheral vestibulopathy from inflammation of the vestibular nerve (neuritis) or whole inner ear (labyrinthitis), producing prolonged vertigo.
Also known as: vestibular neuritis, labyrinthitis, vestibular neuronitis, acute peripheral vestibulopathy, AUVS
Overview
Acute Vestibular Syndrome (AVS) characterized by rapid-onset, prolonged (days), continuous vertigo, nausea/vomiting, gait instability, and spontaneous nystagmus, lasting more than 24 hours. Vestibular neuritis spares hearing; labyrinthitis adds sensorineural hearing loss and/or tinnitus by involving the cochlea.
Epidemiology
Annual incidence 3-15 per 100,000. Peak age 30-60. No clear sex predilection. Vestibular neuritis is the third most common cause of peripheral vertigo after BPPV and Ménière disease.
Try two board-style Vestibular Neuritis and Labyrinthitis questions
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Question 1EENTMedium
A 42-year-old woman presents with 2 days of severe continuous vertigo, nausea, and vomiting following a recent upper respiratory infection. She also reports decreased hearing and tinnitus in the left ear. She denies focal weakness, dysarthria, or diplopia. On exam, she has horizontal nystagmus with the fast phase to the right, an abnormal head-impulse test toward the left, and a sensorineural hearing loss on the left by Weber and Rinne testing. Neurologic exam is otherwise nonfocal. Which of the following is the most likely diagnosis?
ALabyrinthitis
BMeniere disease
CBenign paroxysmal positional vertigo
DVestibular neuritis
EVestibular schwannoma
Reveal answer & full explanation
Correct answer: A — Labyrinthitis
ALabyrinthitis✓
BMeniere disease
CBenign paroxysmal positional vertigo
DVestibular neuritis
EVestibular schwannoma
Why Labyrinthitis is correct
Labyrinthitis is inflammation of both the vestibular and cochlear portions of the inner ear, most often viral and following a recent upper respiratory infection.
Hallmark: acute, continuous vertigo lasting days accompanied by unilateral sensorineural hearing loss and tinnitus, with peripheral signs (unidirectional horizontal nystagmus, abnormal head-impulse test toward the affected side) and an otherwise normal neurologic exam — all present here.
Why the others are wrong
Vestibular neuritis — presents identically except hearing is preserved, because only the vestibular nerve is involved; this patient's clear sensorineural hearing loss makes labyrinthitis the more accurate diagnosis.
Benign paroxysmal positional vertigo — causes brief episodes (seconds) of vertigo provoked by head position changes with a positive Dix-Hallpike; not days of continuous symptoms with hearing loss.
Meniere disease — causes recurrent episodes of vertigo lasting minutes to hours with fluctuating low-frequency hearing loss, aural fullness, and tinnitus; not a single prolonged postviral episode.
Vestibular schwannoma — shares unilateral sensorineural hearing loss and tinnitus, but it is a slow-growing tumor that typically causes gradually progressive hearing loss with mild imbalance, not days of severe continuous vertigo with vomiting following a recent URI.
Additional high-yield points
The combination of continuous vertigo, unilateral sensorineural hearing loss, and recent URI is the defining triad of labyrinthitis.
Question 2NeurologyMedium
A 44-year-old man presents with the sudden onset of severe, constant spinning vertigo that began 18 hours ago and has not let up, along with nausea, vomiting, and inability to walk without veering to the left. He reports a head cold about 10 days ago but denies any hearing change, tinnitus, ear pain, or facial weakness. On exam he has spontaneous right-beating horizontal-torsional nystagmus that worsens when fixation is removed, an abnormal head impulse test to the left with a corrective catch-up saccade, and no skew deviation. There is no dysarthria, limb dysmetria, or focal weakness, and hearing is normal bilaterally. Which of the following is the most likely diagnosis?
AVestibular neuritis
BVestibular migraine
CBenign positional vertigo
DViral labyrinthitis
ECerebellar infarction
Reveal answer & full explanation
Correct answer: A — Vestibular neuritis
AVestibular neuritis✓
BVestibular migraine
CBenign positional vertigo
DViral labyrinthitis
ECerebellar infarction
Why Vestibular neuritis is correct
This is an acute vestibular syndrome: rapid-onset, continuous vertigo that persists for hours to days and is still ongoing, with nausea, vomiting, and gait instability, classically preceded by a viral URI 1-2 weeks earlier (attributed to HSV-1 reactivation in the vestibular ganglion).
The HINTS exam shows a peripheral pattern: an ABNORMAL head impulse with a catch-up saccade, UNIDIRECTIONAL (right-beating) nystagmus suppressed by fixation, and NO skew. Preserved hearing makes this vestibular neuritis rather than labyrinthitis.
Falls toward the affected side and the absence of any brainstem or cerebellar signs further support a peripheral lesion.
Why the others are wrong
Viral labyrinthitis — inflammation of the whole membranous labyrinth, including the cochlea, produces this same acute vestibular syndrome PLUS new unilateral sensorineural hearing loss or tinnitus; he denies any hearing change or tinnitus and hearing is normal bilaterally, which is the finding that separates the two.
Cerebellar infarction — the critical central mimic, but it produces a central HINTS pattern (NORMAL head impulse, direction-changing nystagmus, or skew deviation) and is suggested by vascular risk factors and gait failure out of proportion to the nystagmus; this patient has a reassuring peripheral pattern and no cerebellar signs.
Vestibular migraine — causes recurrent episodes of vertigo with migraine features such as headache, photophobia, or aura, not a single first prolonged event after a recent URI with a peripheral HINTS pattern.
Benign positional vertigo — the most common cause of vertigo overall, but BPPV causes brief spells lasting under a minute that are triggered by head-position changes and are diagnosed with the Dix-Hallpike maneuver; it does not produce 18 hours of continuous vertigo with spontaneous nystagmus and an abnormal head impulse test.
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Preceding upper respiratory viral illness (1-2 weeks prior in many cases)
Reactivation of latent HSV-1 within Scarpa's ganglion (leading hypothesis)
Recent ear infection (bacterial labyrinthitis)
Cholesteatoma or chronic otitis media (suppurative labyrinthitis)
Autoimmune disorders
Vascular risk factors (raise suspicion for stroke mimics)
Pathophysiology
Vestibular neuritis is most often attributed to viral (HSV-1) reactivation within the vestibular ganglion or post-infectious immune-mediated demyelination of the superior vestibular nerve (which supplies the horizontal and anterior semicircular canals and utricle). Labyrinthitis involves both vestibular and cochlear structures and may be viral (post-URI) or bacterial (from acute otitis media, meningitis, or cholesteatoma — a true emergency).
Clinical presentation
Symptoms
Sudden severe constant vertigo lasting hours to days, often peaking on day 1-2
Nausea, vomiting, profuse diaphoresis
Gait instability and falls toward the affected side
Hearing loss and tinnitus only in labyrinthitis (NOT in neuritis)
Often preceded by viral URI symptoms 1-2 weeks earlier
Symptoms gradually improve over 1-2 weeks; chronic mild imbalance may persist for months
Signs / physical exam
Spontaneous unidirectional horizontal-torsional nystagmus with fast phase AWAY from the affected ear (peripheral pattern)
Nystagmus suppressed by visual fixation, intensifies with fixation removed (Frenzel goggles)
HINTS exam (Head Impulse, Nystagmus, Test of Skew) — peripheral pattern: abnormal/catch-up saccade on head impulse, unidirectional nystagmus, no skew
Positive Romberg, falls toward affected ear
Hearing preserved (neuritis) or unilateral SNHL (labyrinthitis)
No focal weakness, dysarthria, dysmetria, or other brainstem/cerebellar findings
Classic findings
AVS with peripheral HINTS pattern + recent URI + unidirectional nystagmus suppressed by fixation.
Differential diagnosis
Posterior circulation stroke (especially PICA/AICA) — CRITICAL mimic — central HINTS pattern (normal head impulse, direction-changing nystagmus, skew deviation), other brainstem/cerebellar signs, vascular risk factors; MRI with DWI to exclude
Ménière disease — Recurrent episodes 20 min-12 h with low-frequency hearing loss, tinnitus, aural fullness; not a single prolonged event
Bárány Society 2022 (acute unilateral vestibulopathy/vestibular neuritis): acute or subacute sustained spinning or non-spinning vertigo lasting at least 24 h; spontaneous direction-fixed, generally horizontal-torsional peripheral nystagmus enhanced by removing fixation; reduced VOR function (head impulse or caloric) on the side opposite the fast phase; no acute central neurologic, audiologic, or otologic symptoms or signs. Labyrinthitis (the same picture plus cochlear involvement) is not covered by these criteria.
Labs
Generally clinical diagnosis; labs as needed to exclude metabolic mimics
CBC, BMP for hydration assessment
Imaging
HINTS exam at bedside is more sensitive than early MRI for posterior stroke in AVS when performed by a trained examiner in a patient with spontaneous nystagmus; without a trained examiner, obtain MRI with DWI (CT does not rule out posterior stroke) (GRACE-3 2023)
MRI brain with DWI within 24-72 h if any central features, vascular risk factors, age >60, severe imbalance disproportionate to nystagmus, or any HINTS findings suggesting central etiology (INFARCT mnemonic — Impulse Normal, Fast-phase Alternating, Refixation on Cover Test)
Audiometry to characterize hearing loss in labyrinthitis
Caloric testing or video head impulse test (vHIT) — unilateral vestibular weakness in neuritis
Temporal bone CT if cholesteatoma or suppurative labyrinthitis suspected
Treatment
First-line
Acute symptomatic relief (24-72 h only, then taper): meclizine 25-50 mg q6-8h, dimenhydrinate, promethazine, lorazepam, ondansetron
Hydration — IV fluids if vomiting precludes oral intake
Vestibular rehabilitation therapy starting within 48-72 h — improves central compensation; the single most important long-term intervention
Antivirals (valacyclovir) — not shown to improve outcomes; not routinely recommended
Viral labyrinthitis
Same supportive care as vestibular neuritis
Audiology evaluation for hearing loss; consider intratympanic or oral steroids for sudden SNHL
Hearing aid or cochlear implant for permanent severe loss
Bacterial / suppurative labyrinthitis
Otolaryngology consultation urgently
IV antibiotics covering AOM/meningitis pathogens (ceftriaxone ± vancomycin)
Surgical drainage if cholesteatoma or mastoiditis
Steroids to reduce inflammation
Meningitis precautions
Ramsay Hunt syndrome
Valacyclovir or acyclovir + prednisone
Eye protection if facial palsy
Second-line / adjunct
Vestibular rehabilitation (gaze stabilization, balance exercises) — outpatient or home program
Address driving and fall risk during recovery
Counseling — anxiety often complicates recovery
Corticosteroids (e.g., methylprednisolone 100 mg/day PO tapered over 3 weeks) — optional adjunct if started within ~3 days of onset (GRACE-3 2023: consider a short course); improve caloric (vestibular function) recovery but have no proven long-term symptomatic benefit (Strupp NEJM 2004; Cochrane 2011)
Complications
Persistent unilateral vestibular hypofunction with chronic imbalance
Permanent hearing loss (labyrinthitis)
Secondary BPPV (debris dislodged into posterior canal during acute event) — Dix-Hallpike at follow-up
The most important task in AVS is to distinguish vestibular neuritis from a posterior circulation stroke — use HINTS (head impulse, nystagmus direction, test of skew), not MRI alone (MRI DWI may be falsely negative in the first 24-48 h for posterior strokes).
Peripheral pattern (consistent with neuritis): ABNORMAL head impulse (corrective catch-up saccade after a rapid head turn toward the affected side), UNIDIRECTIONAL nystagmus, NO skew deviation.
Central pattern (consistent with stroke): normal head impulse, direction-CHANGING nystagmus, or skew deviation — refer urgently for stroke evaluation.
Limit vestibular suppressants to ~3 days — chronic use impairs central compensation.
Steroids started within ~3 days improve caloric (vestibular function) recovery in vestibular neuritis (Strupp NEJM 2004) but have no proven long-term symptomatic benefit, so they are an optional adjunct; antivirals do not help.
Pure hearing loss without vertigo is NOT labyrinthitis — consider sudden sensorineural hearing loss (SSNHL), an emergency requiring high-dose steroids.
HINTS plus: new unilateral hearing loss in acute vestibular syndrome can signal AICA (labyrinthine artery) infarction, which may show a peripheral-appearing head impulse; obtain MRI with DWI before calling it labyrinthitis.
References
Bárány Society 2022 — Strupp M et al. Acute unilateral vestibulopathy/vestibular neuritis: Diagnostic criteria. J Vestib Res 2022;32:389-406.
Strupp 2004 — Strupp M et al. Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. NEJM 2004;351:354-361.
HINTS — Kattah JC et al. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI DWI. Stroke 2009;40:3504-3510.
GRACE-3 2023 — Edlow JA et al. Guidelines for reasonable and appropriate care in the emergency department 3 (GRACE-3): Acute dizziness and vertigo in the emergency department. Acad Emerg Med 2023;30:442-486.
Cochrane 2011 — Fishman JM, Burgess C, Waddell A. Corticosteroids for the treatment of idiopathic acute vestibular dysfunction (vestibular neuritis). Cochrane Database Syst Rev 2011;(5):CD008607.
HINTS plus — Newman-Toker DE et al. HINTS outperforms ABCD2 to screen for stroke in acute continuous vertigo and dizziness. Acad Emerg Med 2013;20(10):986-996.
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