Summary
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.
Definition
- 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 [1][2]
- Labyrinthitis: ipsilateral sensorineural hearing loss associated with features of vestibular neuritis [1]
- Acute vestibular syndrome: acute-onset vertigo, nausea, vomiting, and gait instability (with or without hearing loss) [3]
- Acute peripheral vestibulopathy: a term used to encompass peripheral causes of acute vestibular syndrome (i.e., vestibular neuritis and labyrinthitis) [4]
- Dizziness: an umbrella term commonly used by patients to describe a variety of sensations, including vertigo, presyncope, imbalance, and confusion [5]
- 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
Epidemiology
- Second most common cause of vertigo (after BPPV) [6]
- Age: peak incidence at 30–50 years of age
- Sex: ♀ = ♂ [2]
Epidemiological data refers to the US, unless otherwise specified.
Etiology
- Idiopathic inflammation of the vestibular nerve
- Tends to occur more often after upper airway infections [2][7]
Clinical features
-
Acute or subacute onset of the following symptoms: [1][6]
- Severe vertigo: persistent and continuous, often exacerbated by head motion
- Nausea and vomiting
- Gait instability
- Nystagmus (spontaneous horizontal unilateral)
- Oscillopsia
- Increased risk of falling toward the affected side
- 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.
- Examination
- Characteristic findings on HINTS examination
- Neurological examination is otherwise normal.
Cochlear symptoms (e.g., hearing loss, tinnitus) are usually absent in vestibular neuritis.
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).
Diagnostics
Approach [1][3][8]
- 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.
Head impulse, nystagmus, test of skew [3][9]
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.
The HINTS examination should be performed in all patients with features of acute vestibular syndrome. [3]
| Head impulse, nystagmus, test of skew (HINTS) [3][9] | |||
|---|---|---|---|
| Test | Procedure | Findings | |
| Peripheral cause | Central cause [3] | ||
| Head impulse test [2] |
|
|
|
| Nystagmus [2] |
|
|
|
| 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 [3][9]
Spontaneous unidirectional nystagmus is characteristic of a peripheral cause of acute vestibular syndrome. Direction-changing nystagmus is indicative of a central cause.
Neuroimaging [3][8]
-
Indication: suspected central cause of acute vestibular syndrome [1]
- Focal neurological deficit
- Concurrent severe headache
- Findings suggestive of a central cause on any part of the HINTS exam
- Risk factors for ischemic stroke.
- 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).
Additional tests
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 [3][11]
-
Caloric testing (with electronystagmography): unilateral assessment of the vestibuloocular reflex [1][12]
- 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 [1]
The direction of the fast component of the physiological nystagmus elicited with caloric testing can be remembered with the term COWS: Cold Opposite; Warm Same.
Differential diagnosis of vertigo
Differential diagnosis of peripheral vertigo [6]
| Causes of peripheral vertigo | ||||
|---|---|---|---|---|
| Characteristics | Vestibular neuritis | Ménière disease | Benign paroxysmal positional vertigo | Persistent postural-perceptual dizziness |
| Vertigo |
|
| ||
| Temporality and triggers [6] |
|
|
|
|
| Other symptoms |
|
|
|
|
Differentiating peripheral vertigo from central vertigo
| Peripheral vs. central vertigo [3] | ||
|---|---|---|
| Characteristics | Peripheral vertigo | Central vertigo |
| Etiology |
|
|
| Location of the underlying disorder | ||
| HINTS |
|
|
| Associated cerebellar symptoms (e.g., ataxia, dysmetria) |
|
|
| Sense of motion |
|
|
| Associated hearing loss and/or tinnitus |
|
|
| Associated focal neurological findings (e.g., diplopia) |
|
|
References:[13][14][15]
Treatment
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. [2][3]
Medical therapy [13][16][17]
-
Supportive medical treatment
- Indication: severe symptoms (e.g., severe nausea and/or vomiting) during the acute phase (first ∼ 48 hours)
- Options
- Antihistamines (e.g., dimenhydrinate )
- Antiemetics; (e.g., metoclopramide, or ondansetron) and other vestibular suppressants (e.g., benzodiazepines) [10]
- Important consideration: short-term use recommended; prolonged use may interfere with central vestibular compensation and delay recovery
-
Corticosteroids (e.g., prednisone ) [18]
- Not routinely recommended [16]
- There is evidence they improve recovery at the one-month mark, but long-term benefits are uncertain. [19]
- If considered , they should be started within 72 hours of symptom onset. [20]
- Antiviral therapy: not routinely recommended [6][20]
Vestibular rehabilitation therapy [1][2]
- 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 [21]
- Overview: reduce or eliminate sensory information output to the brain to allow for central compensation
- Indication: consider in patients with refractory symptoms
-
Procedures
- Chemical labyrinthectomy: transtympanic gentamicin infusion [22]
- Surgery: vestibular neurectomy or labyrinthectomy
Complications
- BPPV: In about 10–15% of patients, BPPV develops within weeks of vestibular neuritis onset. [2]
- Persistent postural perceptual dizziness: fear of falling or unsteadiness without actual falls or vestibular dysfunction to explain the symptoms [2]
We list the most important complications. The selection is not exhaustive.
Prognosis
- Spontaneous recovery or central vestibular compensation and habituation within a few weeks is common (good prognosis). [23][24][25]
- Vertigo symptoms usually improve within 24–48 hours of onset in most patients. [2]
- Vestibular rehabilitation can speed up recovery. [2]
- Recurrence is uncommon (2–11%). [2]