• vestibular neuritis (vestibular neuronitis) probably results from inflammation of the vestibular portion of the eighth cranial nerve
  • typical presentation includes vertigo, nausea, and gait imbalance; symptoms typically last several days
  • it is the 3rd most common cause of peripheral vertigo after Meniere disease and benign paroxysmal positional vertigo (BPPV)
  • central causes, such as stroke, must be differentiated (vestibular neuritis belongs to potential stroke mimics)


  • several etiologies are discussed
  • most probable is inflammatory disorder (viral)
    • commonly associated with viral infections
    • linked to the reactivation of latent herpes virus in the vestibular ganglion
    • inflammatory changes in the vestibular nerve on MRI support this theory
  • vascular lesion – reduced blood flow to the vestibular nerve.
  • autoimmune disorder – inflammation following an upper respiratory tract infection

Clinical Presentation

  • mostly younger individuals are affected (30-40 years)
  • acute/subacute onset of rotational vertigo without hearing impairment
    • symptoms develop within hours and last for several days
    • sometimes preceded by a viral infection
  • vegetative symptoms (nausea and vomiting)
  • anxiety
  • oscillopsia corresponding to spontaneous nystagmus
  • nystagmus is unidirectional, conjugate, II-III degree, beating (fast component) towards the unaffected ear
    • eye fixation inhibits peripheral nystagmus (Frenzel glasses enhance nystagmus)
  • tonic deviations of the head, trunk, and limbs in the direction opposite to the prominent, fast component ⇒ “harmonic” vestibular syndrome
  • exclude symptoms that do not fit the diagnosis
    • hearing impairment (labyrinthitis, Meniere’s disease)
    • visual disturbances
    • headache
    • sensory and motor disturbances
    • gait disturbances
    • ataxia, dysmetria
    • dysarthria, dysphonia, dysphagia
  • distinguish between the stage of static vestibular imbalance (dominant nystagmus, first 2-3 days) and the stage of dynamic vestibular imbalance (compensated lesion, characterized by the positive head pulse test)

Diagnostic evaluation

  • diagnosis is based on key signs and symptoms
  • medical history + neurological examination + ENT examination
    • the typical signs of the peripheral vestibular lesion are detected (HINTS)  → examination of vestibular functions
      • positive head impulse test (HI)
      • “peripheral” type of nystagmus (N)
      • negative test of skew (TS)
      • tonic deviation of arms + tendency to lean toward the affected side (opposite to the fast phase of nystagmus ⇒ harmonic vestibular syndrome)
    • patients with vestibular neuritis otherwise have a normal physical exam and neurological exam (no signs of central lesion – negative skew test, no dysarthria, diplopia, etc.)
  • in case of additional unilateral hearing loss, the condition is called labyrinthitis
  • in doubt, imaging studies such as MRI may be used to rule out central causes such as PICA and AICA ischemic syndrome or cerebellar hemorrhage → vertebrobasilar stroke
  • a test that reveals asymmetry in vestibular system function
  • the subject, preferably wearing Frenzel glasses, slightly tilts their head anteriorly to bring the lateral semicircular canal into the horizontal plane (~ 30° tilt)
  • with closed eyes, the subject rapidly rotates their head from side to side, performing this movement 30 times
  • upon stopping the head shaking, the subject opens their eyes
  • search for the presence of nystagmus or any abnormal eye movement
  • a healthy individual with symmetrical vestibular function shows no nystagmus; occasionally, 1-2 eye jerks may be observed
  • in individuals with impaired symmetry of vestibular function, regardless of the origin, nystagmus is observed; based on its character, we can estimate whether it has a peripheral or central origin
    • peripheral lesions – nystagmus is horizontal, with the slow phase directed toward the hypoactive side
    • vertical response after movement in the horizontal plane indicates central involvement
  • the direction of nystagmus is determined by the fast component (which represents a compensatory movement)
  • nystagmus follows a rule termed Alexander’s law, which states that the intensity of nystagmus increases when the patient looks toward the direction of the fast phase. The slow phase of the nystagmus beats towards the injured side (healthy vestibular system prevails)
  • unidirectional, horizontal beating or horizontal-torsional nystagmus (fast phase beats towards one direction regardless of the orientation of gaze) is typically peripheral

Differential diagnosis

Peripheral causes
  • BPPV  (typically episodic, lasts seconds to tens of seconds, predictable head movements trigger symptoms
  • Meniere’s disease – hearing impairment, tinnitus, attacks last minutes to hours (up to 12 hours)
  • vestibular paroxysmia
  • bilateral vestibulopathy (ototoxic drugs, autoimmune diseases, spinocerebellar degeneration, MSA)
  • labyrinthitis (concurrent hearing impairment, lasts days to weeks)
  • focal labyrinth ischemia
  • post-traumatic labyrinth lesions (concussion, labyrinth contusion)
  • perilymphatic fistula (concurrent hearing impairment)
  • acoustic schwannoma (neuroma)
Central causes
  • vertebrobasilar stroke
    • associated focal symptoms (brainstem syndromes)
  • brainstem or cerebellar hemorrhages
    • associated focal symptoms (brainstem syndromes)
    • headache
  • vestibular migraine (concurrent headache, no hearing impairment, recurrent episodes lasting minutes to hours)
Hearing Loss Absent Hearing Loss Present
benign positional paroxysmal vertigo (BPPV)
vertebrobasilar stroke
vestibular neuronitis
central nervous system disorders
Lyme disease
multiple sclerosis
perilymphatic fistula
Meniere disease
acoustic neuroma
autoimmune processes



  • antiemetics – should be used in the acute stage to control nausea and vomiting (usually in the first 3 days)
    • ondansetron
    • promethazine
    • metoclopramide
  • antihistamines
    • meclizine (ANTIVERT)
    • diphenhydramine (Benadril, Dicopanol)
  • benzodiazepines (diazepam, lorazepam)
  • PREDNISONE 100 mg daily for 3 days followed by taper over 2-3 weeks (~ 10 mg/day)
    • insufficient evidence to recommend their use in those with acute vestibular dysfunction [Fishman, 2011]
    • use of valacyclovir either alone or combined with a glucocorticoid has not been shown to be effective  (Vroomen, 2004)

Rehabilitation and supportive care

  • supportive care
    • adequate hydration
    • bed rest during the acute phase
    • avoidance of triggers such as sudden head movements
  • early rehabilitation
    • start immediately after the resolution of severe vegetative symptoms; mild discomfort is acceptable
    • vestibular rehabilitation therapy (VRT)  – customized exercises to improve balance and reduce vertigo
    • rehabilitation supports the vestibular compensation mechanism


  • most commonly benign course with a complete recovery; ~ 15% have persistent problems even at one year (Furman, 1999)
  • some patients have a higher risk of developing:
    • BPPV (benign paroxysmal positional vertigo)
    • PPPD (persistent postural-perceptual dizziness) → see here [Popkirov, 2018]
      • non-spinning vertigo and unsteadiness exacerbated by upright posture, active or passive motion, and complex visual stimuli
      • symptoms persist for > 3 months
      • management includes vestibular rehabilitation, cognitive-behavioral therapy, and SSRIs or SNRIs
    • chronic postural vertigo (CPV) involves a sensation of spinning related to certain positions or movements
  • estimated recurrence risk of neuronitis is low (2-11%) [Mandalá, 2010]

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Vestibular neuritis
link: https://www.stroke-manual.com/vestibular-neuritis/