Vestibular neuritis (VN) is the idiopathic inflammation of the vestibular nerve. Although the etiology is unclear, it is thought to be viral in origin because it commonly occurs after upper airway infections. The disorder manifests as acute vestibular syndrome with persistent, acute-onset vertigo, nausea and vomiting, and gait instability in otherwise healthy patients. When hearing loss is present, it is sometimes referred to as labyrinthitis. Diagnosis is clinical and should include a complete otoneurological examination to exclude a central cause of acute vestibular syndrome, such as cerebellar stroke or lateral medullary syndrome. Vestibular rehabilitation therapy is the most important aspect of treatment and should be initiated as soon as possible. Symptomatic therapy with vestibular suppressants may be considered during the acute phase. Glucocorticoids are no longer routinely recommended as there is insufficient evidence regarding their long-term efficacy The acute phase of severe vertigo usually lasts a few days and symptoms typically resolve in 2–3 weeks with treatment. In refractory cases, which are rare, vestibular ablation therapy or surgery involving the inner ear may be necessary.
- Vestibular neuritis: inflammation of the vestibular nerve that typically manifests with features of vestibular hypofunction, such as vertigo, nausea, vomiting, and gait instability, usually without hearing loss 
- Labyrinthitis: ipsilateral sensorineural hearing loss associated with features of vestibular neuritis 
- Acute vestibular syndrome: acute-onset vertigo, nausea, vomiting, and gait instability (with or without hearing loss) 
- Acute peripheral vestibulopathy: a term used to encompass peripheral causes of acute vestibular syndrome (i.e., vestibular neuritis and labyrinthitis) 
- Dizziness: an umbrella term commonly used by patients to describe a variety of sensations, including vertigo, presyncope, imbalance, and confusion 
- Vertigo: the sensation of spinning or swaying of oneself (internal vertigo) or of one's surroundings (external vertigo) while stationary
- Presyncope (lightheadedness): near loss of consciousness; most commonly due to a drop in systemic blood pressure or hypoxia
- Second most common cause of vertigo (after BPPV) 
- Age: peak incidence at 30–50 years of age
- Sex: ♀ = ♂ 
Epidemiological data refers to the US, unless otherwise specified.
- Acute or subacute onset of the following symptoms: 
- Progression and duration of symptoms
- Usually develop over several hours
- Severe symptoms usually last for 1–2 days
- Mild symptoms may persist for weeks or even months.
- Characteristic findings on
- Neurological examination is otherwise normal.
The presence of neurological abnormalities (e.g., truncal ataxia) in a patient with acute vestibular syndrome should raise suspicion for a central cause (e.g., cerebellar stroke, lateral medullary syndrome).
- Vestibular neuritis is a clinical diagnosis.
- Perform a complete otoneurological examination to distinguish between peripheral and central causes of acute vestibular syndrome in all patients.
- Urgent neuroimaging is indicated if otoneurological examination findings indicate a central cause and in patients with risk factors for ischemic stroke.
A three-step bedside oculomotor examination used to distinguish between peripheral (acute vestibular neuritis) and central causes (cerebellar stroke, lateral medullary syndrome) of acute vestibular syndrome.
|Head impulse, nystagmus, test of skew (HINTS) |
Central cause 
Head impulse test 
|Test of skew|
Head impulse test has a high sensitivity and specificity for detecting stroke in patients with acute vestibular syndrome. Test of skew has a high specificity for predicting brainstem involvement in central etiologies of acute vestibular syndrome 
- Indication: suspected central cause of acute vestibular syndrome 
- Modality: MRI head with or without MRA
- Supportive findings: Typically normal in vestibular neuritis
Neuroimaging is indicated if clinical findings raise suspicion for a central cause of acute vestibular syndrome (e.g., cerebellar stroke, lateral medullary syndrome), especially in patients at increased risk for stroke (e.g., age ≥ 65 years, multiple comorbidities).
The following tests are not routinely indicated but can be used to evaluate additional findings (e.g., hearing loss) or further assess vestibular hypofunction.
- Audiogram: to objectively evaluate a suspected loss of hearing; typically normal in vestibular neuritis 
Caloric testing (with electronystagmography): unilateral assessment of the vestibuloocular reflex 
- Procedure: Infuse cold water and, subsequently, warm water into each ear and document the elicited nystagmus.
- Findings and interpretation
- Viral testing (culture or serology): not routinely recommended 
Differential diagnosis of peripheral vertigo 
|Causes of peripheral vertigo|
|Vertigo|| || |
|Temporality and triggers || || || || |
|Other symptoms|| || |
Differentiating peripheral vertigo from central vertigo
|Peripheral vs. central vertigo |
|Characteristics||Peripheral vertigo||Central vertigo|
|Location of the underlying disorder|
|Associated cerebellar symptoms (e.g., ataxia, dysmetria)|| || |
|Sense of motion|| || |
|Associated hearing loss and/or tinnitus|| || |
|Associated focal neurological findings (e.g., diplopia)|| || |
Therapy is supportive. Antiemetics and vestibular suppressants are only indicated in the acute setting. Vestibular rehabilitation therapy facilitates central vestibular compensation and accelerates recovery. Hospital admission may be necessary in patients with severe symptoms or if there is any concern for a central etiology of symptoms. 
Medical therapy 
Supportive medical treatment
- Indication: severe symptoms (e.g., severe nausea and/or vomiting) during the acute phase (first ∼ 48 hours)
- Important consideration: short-term use recommended; prolonged use may interfere with central vestibular compensation and delay recovery
Corticosteroids (e.g., prednisone ) 
- Not routinely recommended 
- There is evidence they improve recovery at the one-month mark, but long-term benefits are uncertain. 
- If considered , they should be started within 72 hours of symptom onset. 
- Antiviral therapy: not routinely recommended 
Vestibular rehabilitation therapy 
- Definition: a set of exercises facilitating vestibular habituation and central vestibular compensation
- Indication: all patients with vestibular neuritis; also used in the management of other causes of peripheral vertigo (e.g., BPPV, Meniere disease)
- Important consideration: Counsel patients to start vestibular rehabilitation as soon as possible and to repeat the exercises several times a day (for at least 30 minutes).
Exercises (e.g., Cawthorne-Cooksey exercises, Brandt-Daroff exercises)
- Active head movements
- Controlled eye movements
- Walking and balance exercises
Interventional therapy 
- BPPV: In about 10–15% of patients, BPPV develops within weeks of vestibular neuritis onset. 
- Persistent postural perceptual dizziness: fear of falling or unsteadiness without actual falls or vestibular dysfunction to explain the symptoms 
We list the most important complications. The selection is not exhaustive.
- Spontaneous recovery or central vestibular compensation and habituation within a few weeks is common (good prognosis). 
- Recurrence is uncommon (2–11%).