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Vestibular neuronitis

SNOMED: 1084691000119100707 wordsUpdated 03/03/2026
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Exam Tips

  • In OSCEs, the key discriminator is continuous acute vertigo without hearing loss plus peripheral nystagmus and a positive head impulse test.
  • Always state red flags that mandate urgent stroke assessment: focal neurological signs, direction-changing/vertical nystagmus, severe truncal ataxia, or normal head impulse in a patient with continuous acute vertigo.
  • Do not use vestibular suppressants for prolonged periods; examiners often ask this because overuse can delay central compensation.
  • Head impulse test safety point: screen neck movement first and avoid forceful manoeuvres in cervical spine pathology.
  • If vertigo recurs after initial recovery, mention secondary BPPV as a common post-neuronitis complication.

Definition

Vestibular neuronitis (vestibular neuritis, also termed acute unilateral vestibulopathy) is an acute peripheral vestibular syndrome causing sudden-onset, continuous rotational vertigo with nausea, vomiting, and gait unsteadiness, but without hearing loss. It is a clinical diagnosis based on a compatible history and peripheral vestibular signs (for example unidirectional horizontal-torsional nystagmus and an abnormal head impulse test), after excluding central causes such as posterior circulation stroke.

Pathophysiology

The disorder is most commonly explained by acute dysfunction of one vestibular nerve, usually presumed inflammatory (often post-viral), leading to asymmetrical vestibular input from the two labyrinths. This asymmetry causes spontaneous nystagmus, vertigo, autonomic symptoms, and postural lateropulsion toward the affected side; alternative mechanisms include ischaemia of the anterior vestibular artery. Recovery over weeks reflects central vestibular compensation (cerebellar/brainstem recalibration of vestibulo-ocular and vestibulospinal reflexes), which can be slowed by prolonged vestibular-suppressant use. See Figure: vestibulo-ocular reflex pathway and unilateral vestibular loss model.

Risk Factors

  • Recent viral prodrome (especially upper respiratory tract infection) or sick contacts with viral illness
  • Age 30-60 years (most common age band at presentation)
  • Seasonal pattern (reported more often in spring/early summer)
  • Possible rare temporal association after COVID-19 vaccination (causality not established)

Clinical Features

Symptoms

  • Acute spontaneous rotational vertigo, typically constant initially and worsened by head movement
  • Nausea and often vomiting, with autonomic symptoms (sweating, pallor, malaise)
  • Marked imbalance/unsteadiness, sometimes veering or falling toward the affected side
  • No cochlear symptoms: hearing loss and tinnitus are typically absent
  • No focal brainstem/cerebellar symptoms (for example diplopia, dysarthria, limb weakness)

Signs

  • Spontaneous unidirectional horizontal or horizontal-torsional nystagmus, fast phase away from affected ear
  • Nystagmus suppresses with visual fixation (peripheral pattern)
  • Positive head impulse test toward affected side with corrective saccade
  • Normal otoscopy and bedside hearing assessment
  • Broad-based gait imbalance/lateropulsion toward affected side

Investigations

Clinical bedside diagnosis (history + neuro-otological examination):Typical acute vestibular syndrome with peripheral features and no focal neurological deficit; usually sufficient without routine imaging
Head impulse test:Corrective saccade when head is rapidly turned toward affected side, indicating reduced ipsilateral vestibulo-ocular reflex
HINTS bedside assessment in continuous acute vertigo:Peripheral pattern supports vestibular neuronitis (abnormal head impulse, unidirectional nystagmus, no skew); central pattern warrants urgent stroke evaluation
MRI brain/internal auditory meatus (if atypical or red flags):Usually normal for vestibular neuronitis; used to exclude posterior circulation stroke, demyelination, or structural lesions

Management

Lifestyle Modifications

  • Give clear safety-netting: seek urgent care for new neurological deficits, severe occipital headache, inability to stand, or new hearing loss
  • Falls-risk advice (avoid driving/heights during acute phase, mobilise with support initially)
  • Encourage early graded mobilisation and vestibular rehabilitation exercises once vomiting settles to promote central compensation
  • Avoid prolonged bed rest and avoid long-term vestibular suppressants

Pharmacological Treatment

Short-term vestibular suppressants/antiemetics (acute phase only)

  • Prochlorperazine 5-10 mg orally 3-4 times daily as needed (or buccal 3 mg twice daily) for up to 7 days
  • Cyclizine 50 mg orally up to 3 times daily as needed (short course)
  • Promethazine 25 mg at night, then 10-20 mg twice daily if needed (short course)

Use the lowest effective dose for the shortest duration (typically 24-72 hours, max about 1 week) because longer use may delay vestibular compensation. Prochlorperazine: caution/exclude Parkinson's disease, seizure disorders, prolonged QT risk, and extrapyramidal adverse effects. Cyclizine/promethazine: anticholinergic sedation (falls, confusion), caution in angle-closure glaucoma, urinary retention, and older adults; avoid alcohol and driving if drowsy.

Corticosteroids

  • Prednisolone 50 mg orally once daily for 5 days, then taper over 5 days (specialist-guided, selected cases)

Evidence for routine use is mixed; may be considered early in severe presentations after specialist discussion. Check contraindications and risks (hyperglycaemia, infection risk, GI irritation, psychiatric effects); use caution in diabetes, peptic ulcer disease, and immunosuppression.

Complications

  • Benign paroxysmal positional vertigo (often posterior canal on affected side) developing weeks after the acute episode
  • Persistent postural-perceptual dizziness (chronic dizziness/visual dependence)
  • Oscillopsia due to incomplete vestibulo-ocular compensation
  • Falls, reduced independence, and impaired quality of life/employment

Prognosis

Symptoms usually peak in the first 24 hours, improve over 48-72 hours, and continue to settle over 2-6 weeks; many patients feel substantially recovered by around 6 weeks. A minority develop persistent dizziness or visual-motion sensitivity despite peripheral recovery. Recurrence should prompt reassessment for alternative diagnoses (especially BPPV, vestibular migraine, or central causes), although recurrent episodes can occur in some patients.

Sources & References

NICE Guidelines(1)

📖Textbook References(8)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 942)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 273)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 942)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 631)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1846)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 495)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 495)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 477)[context]

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