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Vestibular neuritis

Last updated: September 23, 2021

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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.

Epidemiological data refers to the US, unless otherwise specified.

  • Acute or subacute onset of the following symptoms: [1][6]
  • 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

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).

Approach [1][3][8]

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]

  • Ask the patient to maintain a fixed central gaze.
  • Rapidly rotate the patient's head from the center to one side and observe the patient's eye movements.
  • Repeat the rapid rotation of the patient's head to the contralateral side.
  • Positive head impulse test (impaired VOR) : inability to maintain central fixed gaze during head rotation followed by a corrective shift of the eyes back to the target [1]
  • Negative head impulse test (normal VOR) : central fixed gaze is maintained during head rotation. [3]
Nystagmus [2]
  • Spontaneous horizontal nystagmus [10]
  • Unidirectional nystagmus
  • Fast component beats away from the side of the lesion
  • Intensity increases with gaze toward the fast phase, decreases with gaze toward the slow phase (Alexander law)
  • Nystagmus is inhibited by visual fixation.
Test of skew
  • Ask the patient to maintain a fixed central gaze and keep both eyes open during the examination.
  • Alternate between covering and uncovering each eye.
  • Observe for a deviation from the central gaze on uncovering the eye.

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]

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) [1][12]
    • Normal reaction to cold water: nystagmus with the fast phase away from the stimulated ear
    • Normal reaction to warm water: nystagmus with the fast phase toward the stimulated ear
    • Supportive of vestibular neuritis: unilaterally reduced or absent caloric response in the affected side
  • 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 peripheral vertigo [6]

Causes of peripheral vertigo
Characteristics Vestibular neuritis Ménière disease Benign paroxysmal positional vertigo Persistent postural-perceptual dizziness
Vertigo
  • Severe vertigo for 1–2 days
  • Mild symptoms (e.g., nausea) may persist for weeks or months.
  • Vertigo lasts for minutes to hours.
  • Vertigo for only a few seconds.
  • Vertigo is always triggered by movement (e.g., lying down, reclining).
  • Not actually vertigo, but a sensation of dizziness that lasts for at least 3 months
Temporality and triggers [6]
  • Continuous
  • Spontaneous
  • Episodic
  • Spontaneous
  • Episodic
  • Triggered by movement
  • Episodic
  • Spontaneous
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)
  • Absent or mild
  • Marked
Sense of motion
  • Severe
  • Mild
Associated hearing loss and/or tinnitus
  • Rare
Associated focal neurological findings (e.g., diplopia)
  • Rare
  • Common

References:[13][14][15]

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
  • 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]

Interventional therapy [21]

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). [23][24][25]
  • Recurrence is uncommon (2–11%). [2]
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