Vestibular Neuritis

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Labyrinthitis and Vestibular Neuritis written for patients

Synonym: vestibular neuronitis

Strictly speaking the term means inflammation of the vestibular nerve but the aetiology is thought to be a vestibular neuropathy. A theory gaining support is that a significant proportion of cases are caused by a reactivation of herpes simplex virus that affects the vestibular ganglion, vestibular nerve, labyrinth, or a combination of these.[1][2] There is sudden disruption of afferent neural input so that acute vertigo results.

Vestibular neuritis affects both adults and children but has a peak age of onset of 40 to 50 years.[3] The incidence has been quoted as 3.5 cases per 100,000.[4] 

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  • Onset is usually very abrupt.
  • There is unsteadiness, nausea and vomiting.
  • They feel as if the room is rotating.
  • Moving the head aggravates symptoms.
  • Distinguish between true rotational vertigo and giddiness, faintness or weakness. Patients are often very vague in the terms they use and may attempt medical terminology but get it wrong.


  • Spontaneous, unidirectional, horizontal nystagmus is characteristic.The fast direction is towards the healthy ear. The fast direction may be the more obvious but it is really the correction of the pathological slow direction.
  • Nystagmus may be apparent only on gazing away from the affected side or it may be suppressed by optic fixation.
  • On walking or during the Romberg's test, the patient tends to fall towards the affected side.

The following should be sought, as their presence suggests that it is not vestibular neuritis:

  • Nystagmus is multidirectional and does not become fatigued on repetitive testing.
  • Hearing loss.
  • Abnormalities of cranial nerves other than VIII.
  • Red tympanic membrane.
  • Cerebellar ataxia.
  • Mastoid tenderness, nuchal rigidity or high fever.

If it was not possible to demonstrate the vertigo, the Hallpike manoeuvre may be employed (although provocative tests such as these will be unpleasant for the patient and so may not be appropriate):[5]

  • The patient sits on the couch with the head end flat.
  • The patient should lie back from sitting to supine three times. The first time the head faces forward with the neck slightly extended. The second time the head is turned 45° to one side and the third time to the other side.
  • The patient should keep both eyes open all the time. Each time check for signs of nystagmus and ask about feelings of vertigo.

There is usually a slight latent period of just seconds between the manoeuvre and the onset of symptoms and signs. There is also a tendency for them to fatigue with repeated testing. If these features are not present it suggests that the aetiology might be central, in the brain, rather than peripheral in the vestibular apparatus.

Another helpful test to differentiate vestibular neuritis from stroke is the head impulse test. The patient is asked to fix their gaze on a point and the head is rapidly rotated. If the eyes do a corrective shift once the head stops moving rather than maintaining contact throughout the movement, this is deemed suggestive of a vestibular disorder. An enhancement using a video recorder is considered to be more accurate.[6] 

  • The diagnosis can usually be made clinically and blood tests are usually unhelpful.
  • Imaging studies (eg, brain MRI or CT scanning) may demonstrate tumours, haemorrhage or ischaemic stroke or demyelination. Imaging tends to be reserved for cases where more sinister pathology is suspected. With respect to stroke, MRI is much more sensitive than CT scanning but is not often a pragmatic option.
  • Reassure the patient that the symptoms usually settle within a few weeks, even with no treatment. Alcohol, tiredness and intercurrent illness can aggravate symptoms.
  • Advise about safety risks - driving, hazards at work (eg, heavy machinery, ladders) and falls at home during attacks.
  • Bed rest may be necessary if symptoms are severe but early activity should be encouraged to promote vestibular compensation.
  • If the patient has marked vertigo with vomiting, an anti-emetic is useful and it may suppress the vertigo too. Nausea will retard gastric emptying and an injection may be required.
  • A vestibular suppressant such as prochlorperazine (buccal or intramuscular if vomiting is severe) may be beneficial but should be stopped within a few days of onset, as prolonged use may impede the process of central vestibular compensation. This may best be achieved by taking oral medication as necessary rather than regularly after the first three days.
  • Buccal prochlorperazine may be appropriate if the patient has recurrent attacks and needs self-administered medication.
  • Promethazine and domperidone may be effective.
  • Antiviral drugs and steroids are not recommended.
  • A Cochrane review found moderate evidence that vestibular rehabilitation (exercises to promote central nervous system compensation) was effective in reducing dizziness in vestibular neuritis in the medium term.[11] 

In most patients, symptoms resolve within a few weeks, with or without symptomatic treatment.[10] Another study found a persistence of dizziness related to anxiety in one third of patients one year after the initial episode.[12]

Further reading & references

  • Strupp M, Dieterich M, Brandt T; The treatment and natural course of peripheral and central vertigo. Dtsch Arztebl Int. 2013 Jul;110(29-30):505-16. doi: 10.3238/arztebl.2013.0505. Epub 2013 Jul 22.
  • Gacek RR; A perspective on recurrent vertigo. ORL J Otorhinolaryngol Relat Spec. 2013;75(2):91-107. doi: 10.1159/000348710. Epub 2013 Jun 21.
  1. Walker MF; Treatment of vestibular neuritis. Curr Treat Options Neurol. 2009 Jan;11(1):41-5.
  2. Jeong SH, Kim HJ, Kim JS; Vestibular neuritis. Semin Neurol. 2013 Jul;33(3):185-94. doi: 10.1055/s-0033-1354598. Epub 2013 Sep 21.
  3. Agrup C, Gleeson M, Rudge P; The inner ear and the neurologist. J Neurol Neurosurg Psychiatry. 2007 Feb;78(2):114-22.
  4. Strupp M, Brandt T; Current treatment of vestibular, ocular motor disorders and nystagmus. Ther Adv Neurol Disord. 2009 Jul;2(4):223-39. doi: 10.1177/1756285609103120.
  5. Labuguen R; Initial Evaluation of Vertigo, American Family Physician, January 2006
  6. Mahringer A, Rambold HA; Caloric test and video-head-impulse: a study of vertigo/dizziness patients in a community hospital. Eur Arch Otorhinolaryngol. 2013 Mar 15.
  7. Kerber KA; Vertigo and dizziness in the emergency department. Emerg Med Clin North Am. 2009 Feb;27(1):39-50, viii. doi: 10.1016/j.emc.2008.09.002.
  8. Thompson TL, Amedee R; Vertigo: a review of common peripheral and central vestibular disorders. Ochsner J. 2009 Spring;9(1):20-6.
  9. Cunningham S et al; Infections of the Labyrinth, University of Texas Medical Branch, 2004
  10. Vestibular neuronitis; NICE CKS, February 2011
  11. Hillier SL, McDonnell M; Vestibular rehabilitation for unilateral peripheral vestibular dysfunction. Cochrane Database Syst Rev. 2011 Feb 16;(2):CD005397.
  12. Neuhauser HK; Epidemiology of vertigo. Curr Opin Neurol. 2007 Feb;20(1):40-6.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Laurence Knott
Current Version:
Peer Reviewer:
Dr Helen Huins
Document ID:
2919 (v22)
Last Checked:
Next Review:

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