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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

Labyrinthitis and vestibular neuritis are sometimes used interchangeably. However, experts in the field now recommend that the term vestibular neuritis be confined to cases in which the vestibular nerve only is involved, whereas labyrinthitis should be used in cases in which the vestibular nerve and the labyrinth are affected.

Labyrinthitis is one of many causes of vertigo. Typically it produces disturbances of balance and hearing to varying degrees and may affect one or both ears.

  • The labyrinth consists of the peripheral sensory organs for balance and hearing, in a delicate membranous network (incorporating the utricle, saccule, semicircular canals and cochlea).
  • Symptoms of labyrinthitis occur when there is inflammation of the membranous labyrinth and when there is damage to the vestibular and auditory end organs.
  • It is possible for a variety of organisms and inflammatory mediators through both local and systemic disease to produce labyrinthitis. Bacteria or viruses can cause labyrinthitis but are sufficiently distinct to be considered as separate disease processes:
    • Bacteria may gain access to the membranous labyrinth through anatomical connections:
      • Between the central nervous system and subarachnoid space via the internal auditory canal and cochlear aqueduct; or
      • Through congenital or acquired defects of the bony labyrinth.
    • Viruses typically spread to labyrinthine structures haematogenously or via the anatomical connections above.
  • Many cases of labyrinthitis appear to be viral in origin and an upper respiratory tract infection precedes the onset of symptoms in about half of cases. It may also be associated with systemic disease. Many factors can cause cochlear trauma, including vertebrobasilar ischaemia, meningitis, Ménière's disease and medication (eg, aminoglycoside)[2].

Viral labyrinthitis is often confused with vestibular neuritis. It is generally accepted that vestibular neuritis is a disorder of the vestibular nerve and is not associated with hearing loss. The cochlea is affected in labyrinthine inflammation and therefore hearing loss is always present to some degree in people with viral labyrinthitis.

It is worth noting that viral infections cause both congenital and acquired hearing loss (rubella and cytomegalovirus are viral causes of prenatal hearing loss). Postnatally, viral-induced hearing loss is usually due to mumps or measles. Viral infections are also implicated in idiopathic sudden sensorineural hearing loss (SNHL).

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  • There is a wide variability in reported prevalence of diseases causing vestibular dysfunction from 3.1% one-year prevalence to 35.4%; however, in all studies the incidence increases with age[4].
  • Viral labyrinthitis is the most common form of labyrinthitis. It is usually observed in adults aged 30-60 years and is rarely observed in children. It is most common in the fourth decade with women outnumbering men by about 2:1.
  • Vestibular migraine is thought to be the most common cause of recurrent spontaneous vertigo attacks. In the general population the lifetime prevalence is about 1% and one-year prevalence of 0.9%[5].
  • Bacterial labyrinthitis is rare in the post-antibiotic era:
    • Meningogenic suppurative labyrinthitis is most often seen in young children (under the age of 2 years), when children are at most risk of meningitis.
    • Otogenic suppurative labyrinthitis can be observed in all ages (with cholesteatoma and in untreated acute otitis media).


Patients may find it difficult to describe their symptoms but clarifying the timing of the vertigo and the triggers, or exacerbating factors if it is continuous, is crucial to making the correct diagnosis.

  • Characteristically, labyrinthitis presents with spontaneous, severe and often incapacitating vertigo:
    • Vertigo is constant and ongoing.
    • It is not triggered by movement but may be exacerbated by movement (vertigo due to benign paroxysmal positional vertigo (BPPV) is episodic and triggered by movement).
  • Nausea and vomiting are frequent.
  • Hearing loss and tinnitus may be complained of in labyrinthitis, although not, by definition, in vestibular neuritis:
    • May be unilateral or bilateral, mild or profound.
    • A feeling of fullness in the ear is more typical of Ménière's disease.
  • 25% of cases have had a single brief prodrome in the week prior to the attack. More than one suggests transient ischaemic attack (TIA) or stroke.
  • Upper respiratory tract infection symptoms (preceding or concurrent) are common and fever may be present, although high fever suggests a more serious cause such as mastoiditis or meningitis.

The following should be sought, as their presence suggests that it may not be labyrinthitis:

  • Otorrhoea is associated with middle ear disease but may also occur following head trauma.
  • Otalgia suggests Ramsay Hunt syndrome, especially if the tympanic membrane is not inflamed.
  • Neck pain/stiffness suggests meningitis or vertebral artery dissection.
  • Facial weakness is not a feature of labyrinthitis but may occur in Ramsay Hunt syndrome and stroke.
  • Cardiovascular risk factors including smoking, diabetes, hypertension and previous stroke all increase the likelihood of the symptoms being due to a TIA or a stroke.
  • Drugs may cause acute vertigo[9]:
    • Aminoglycosides and other ototoxic medications.
    • Antihypertensives, such as amlodipine.
    • Antidepressants. NB: abrupt discontinuation of a selective serotonin reuptake inhibitor (SSRI) may cause vertigo.
    • Tranquilisers, including benzodiazepines.
    • Anti-epileptics.
  • A family history of migraine or Ménière's disease increases the likelihood of these conditions.
  • Carbon monoxide exposure is a rare cause of acute vertigo.


Clinical examination should include:

  • Assessment of the external ear and tympanic membrane, looking for cholesteatoma or vesicles suggestive of Ramsay Hunt syndrome.
  • Cranial nerve examination for evidence of palsies and hearing loss.
  • Check for mastoid tenderness, nuchal rigidity and high fever.
  • Assessment of gait; inability to stand or walk unassisted is suggestive of ischaemia.
  • A simple hearing test using a 256 Hz (middle C) tuning fork or 512 Hz (top C):
    • Weber's test involves placing a vibrating tuning fork on top the forehead and asking if it is heard louder in either ear. There should be no difference but, in nerve deafness, it is quieter in the affected ear whilst, in conductive deafness, the sound transmitted through the skull is louder in the affected ear.
  • Head impulse test - a sensitive test of peripheral vestibular function - is easy for the non-expert to interpret[10]:
    • Always start by asking the patient to sit upright and to turn their head to either side to assess any limitation of movement and ensure it is safe to proceed.
    • Advise the person to fix their gaze on your nose.
    • Using your hands, turn the head 10-20° and then rapidly turn back to face you and watch the eyes for saccades. Repeat several times randomly to both sides.
    • If the vestibulo-ocular reflex is intact the patient will be able to keep their gaze approximately on your nose; this is normal but will also be the case in central causes of vertigo.
    • If the reflex is impaired, as it is in labyrinthitis, a 'catch-up' reflexive saccade will occur at the end of the head thrust.
  • Nystagmus type:
    • Nystagmus is usually fine horizontal but may be mixed horizontal-torsional.
    • It may be easier to see if sclera are exposed and the movement of scleral blood vessels can be followed.
    • Keeping their head still, ask the patient to look to the right and then to the left. Holding up a blank piece of white paper to the side of their face will help by preventing them from being able to fix their gaze on something.
    • The nystagmus is consistent and unidirectional, even when the head is turned; it will be most obvious when looking towards the direction of the fast phase. It is reduced when the vision is fixed on a point - eg, your nose.
    • Nystagmus that reverses direction with gaze position, ie fast phase to the left when looking to the left that then changes to fast phase to the right on looking to the right, suggests a central cause such as stroke or TIA.
  • Skew deviation:
    • This is tested by using the cover/uncover test.
    • Ask the patient to look at your nose and use your hand to cover one eye then the other. Observe for any vertical movement of the eye as it is uncovered. Movement of the eye suggests a central cause of vertigo.

The HINTS examination, refers to the combination of Head Impulse test, Nystagmus Type and Skew and is used in patients presenting with acute, ongoing vertigo and spontaneous nystagmus, to differentiate vestibular neuritis or labyrinthitis from stroke:

  • An abnormal head impulse test, unidirectional nystagmus and no vertical skew are sensitive markers of vestibular neuritis or labyrinthitis.
  • The combination of a normal head impulse test, the presence of bi-directional nystagmus and vertical skew is more sensitive than an initial MRI for ischaemic stroke detection when patients are seen in the first 48 hours of symptom onset.
  • Including new hearing loss to the HINTS examination makes it an even more sensitive test for stroke; there is increasing evidence that new hearing loss in people with acute vertigo syndrome is more likely if the cause is ischaemic[11].

A patient with labyrinthitis or vestibular neuritis is dizzy at rest, feels worse with any head motion and already has nystagmus. As such, the Dix-Hallpike test, used to confirm posterior canal BPPV, is not indicated.

  • Routine blood tests are not helpful; neither are viral antibody tests. However, if a systemic infection is suspected, FBC and blood cultures are indicated.
  • Perform culture and sensitivity testing of middle ear effusions if present.
  • Most patients do not require imaging. However:
    • A CT scan can help rule out mastoiditis.
    • A temporal bone CT scan may help in patients with cholesteatoma and labyrinthitis, although gadolinum MRI is more useful in the early stages of suppurative labyrinthitis[12].
    • If a sinister cause is suspected, MRI scan can be helpful. Compared with CT, it provides much better pictures of the posterior fossa and VIII nerve course, although still has a low sensitivity for ischaemic stroke in dizziness, especially in the first 24-48 hours[6].
  • Pure tone audiometry may be indicated in hearing loss.
  • Vestibular function testing:
    • Caloric testing and an electronystagmogram may help in diagnosing difficult cases and in determining the prognosis for recovery.
    • Vestibular-evoked myogenic potentials have been developed to assess vestibular activity[13].
  • Portable video-oculography is available which measures eye movements so as to quantify the vestibulo-ocular reflex.
  • Ramsay Hunt syndrome (herpes zoster oticus):
    • Occurs when varicella-zoster virus is reactivated in the facial nerve.
    • It causes facial paralysis, loss of taste, vestibulocochlear dysfunction and pain.
  • Suppurative labyrinthitis:
    • It is almost always associated with cholesteatoma.
    • Profound hearing loss, severe vertigo, ataxia, nausea and vomiting are common symptoms.
    • Tinnitus was universal in one cohort study[12].
  • Serous labyrinthitis:
    • Is associated with acute or chronic middle ear disease and is a common complication of otitis media.
    • An audiogram reveals mixed hearing loss when a middle ear effusion is present.
    • Vestibular symptoms may occur but are less common.
    • The hearing loss is usually transient but may persist if the otitis is left untreated.
    • Treatment is aimed at the underlying infection and clearing the middle ear effusion.
  • Vestibular neuronitis or neuritis:
    • Presentation is as for labyrinthitis but with no hearing loss.
    • The treatment of vestibular neuritis and viral labyrinthitis is similar.
  • BPPV:
    • The characteristic nystagmus and vertigo are brief and triggered by changes of position but between movements they may have few or no symptoms.
    • Onset is sudden and severity very variable.
  • Vestibular migraine[5, 14]:
    • Vertigo lasts from five minutes to 72 hours.
    • Vertigo can precede, accompany or occur after the headache but there will be one or more migraine features with at least 50% of episodes.
    • However, in about 6% the symptoms alternate between episodes.
    • Hearing is only mildly and transiently affected.
    • During an attack patients may develop either central or peripheral vestibular dysfunction.
    • Interictal ocular motor abnormalities may be present and appear to increase over time.
    • The cause may be enhanced vestibular excitability inducing interactions in the vestibular and pain pathways from the inner ear to the thalamus and cortex.
  • Consider admission to hospital or an emergency referral to an ENT specialist:
    • If the patient presents with sudden-onset unilateral hearing loss. Hearing loss can be indicative of acute ischaemia of the labyrinth or brain stem.
    • Emergency treatment in such cases can restore the patient's hearing if seen within 12 hours of the onset of symptoms.
  • Otherwise, the patient can usually be managed at home. During an acute attack the patient will want to lie still with their eyes closed.
  • Encourage the patient to be active as soon as they can, even if it worsens the vertigo, as this is thought to speed up the development of vestibular compensation.
  • Patients should be advised to seek further medical care for worsening symptoms - especially neurological symptoms (such as diplopia, slurred speech, gait disturbances, localised weakness or numbness)[15].
  • Medication:
    • Vertigo, nausea and vomiting may be helped by prochlorperazine or antihistamines.
    • Medication should be taken for the minimum time possible, as it may interfere with the body's compensatory mechanisms and delay recovery.
    • Consider buccal or deep intramuscular injection of prochlorperazine if symptoms are severe.
    • Antivirals or benzodiazepines are not recommended.
    • Corticosteroids show no improvement in symptoms compared with placebo and are also not recommended[16].
  • Surgical treatment may be necessary - eg, myringotomy and evacuation of effusion in labyrinthitis secondary to otitis media, and mastoidectomy for mastoiditis or cholesteatoma.
  • Vestibular rehabilitation, consisting of physical manoeuvres and exercise regimes, is safe and effective and improves functioning in the medium term in unilateral vestibular dysfunction[17].

NB: always advise patients not to drive or operate machinery when experiencing symptoms of vertigo or taking medication for symptoms.

Labyrinthitis is generally benign and self-limiting.

  • Falls.
  • Unilateral hearing loss.
  • Chronic or recurrent cases merit referral to exclude sinister aetiology.
  • The acute symptoms of vertigo, nausea and vomiting resolve after several days to a few weeks in the majority of all of the different types of labyrinthitis.
  • Recovery of hearing loss is more variable:
    • Suppurative labyrinthitis usually leaves permanent and profound hearing loss.
    • Hearing loss associated with viral labyrinthitis may recover. Disequilibrium or positional vertigo may be present long-term following resolution of the acute infection.
  • Anxiety, phobic disorders and depression have previously been thought to be common comorbidities with labyrinthitis and vestibular neuritis but a study of 68 patients with organic vertigo syndromes has challenged this[18]:
    • Psychiatric comorbidity rates for those with vestibular neuritis corresponded roughly with those in the general population.
    • However, anxiety, phobic disorders and depression are increased in people with vestibular migraine and those with Ménière's disease; the reasons for this may be neuro-anatomical and neuro-biological.

Further reading & references

  1. Thompson TL, Amedee R; Vertigo: a review of common peripheral and central vestibular disorders. Ochsner J. 2009 Spring;9(1):20-6.
  2. Lee AT; Diagnosing the cause of vertigo: a practical approach. Hong Kong Med J. 2012 Aug;18(4):327-32.
  3. Neuhauser HK; Epidemiology of vertigo. Curr Opin Neurol. 2007 Feb;20(1):40-6.
  4. Koo JW, Chang MY, Woo SY, et al; Prevalence of vestibular dysfunction and associated factors in South Korea. BMJ Open. 2015 Oct 26;5(10):e008224. doi: 10.1136/bmjopen-2015-008224.
  5. Dieterich M, Obermann M, Celebisoy N; Vestibular migraine: the most frequent entity of episodic vertigo. J Neurol. 2016 Apr;263 Suppl 1:S82-9. doi: 10.1007/s00415-015-7905-2. Epub 2016 Apr 15.
  6. Newman-Toker DE, Edlow JA; TiTrATE: A Novel, Evidence-Based Approach to Diagnosing Acute Dizziness and Vertigo. Neurol Clin. 2015 Aug;33(3):577-99, viii. doi: 10.1016/j.ncl.2015.04.011.
  7. Vertigo; NICE CKS, April 2010 (UK access only)
  8. Vestibular neuronitis; NICE CKS, February 2011 (UK access only)
  9. Chimirri S, Aiello R, Mazzitello C, et al; Vertigo/dizziness as a Drugs' adverse reaction. J Pharmacol Pharmacother. 2013 Dec;4(Suppl 1):S104-9. doi: 10.4103/0976-500X.120969.
  10. Jorns-Haderli M, Straumann D, Palla A; Accuracy of the bedside head impulse test in detecting vestibular hypofunction. J Neurol Neurosurg Psychiatry. 2007 Oct;78(10):1113-8. Epub 2007 Jan 12.
  11. Newman-Toker DE, Kerber KA, Hsieh YH, et al; HINTS outperforms ABCD2 to screen for stroke in acute continuous vertigo and dizziness. Acad Emerg Med. 2013 Oct;20(10):986-96. doi: 10.1111/acem.12223.
  12. Maranhao AS, Godofredo VR, Penido Nde O; Suppurative labyrinthitis associated with otitis media: 26 years' experience. Braz J Otorhinolaryngol. 2016 Jan-Feb;82(1):82-7. doi: 10.1016/j.bjorl.2014.12.012. Epub 2015 Dec 11.
  13. Agrawal Y, Bremova T, Kremmyda O, et al; Semicircular canal, saccular and utricular function in patients with bilateral vestibulopathy: analysis based on etiology. J Neurol. 2013 Mar;260(3):876-83. doi: 10.1007/s00415-012-6724-y. Epub 2012 Oct 27.
  14. Radtke A, Neuhauser H, von Brevern M, et al; Vestibular migraine - validity of clinical diagnostic criteria. Cephalalgia. 2011 Jun;31(8):906-13. doi: 10.1177/0333102411405228. Epub 2011 Apr 20.
  15. Seemungal BM, Bronstein AM; A practical approach to acute vertigo. Pract Neurol. 2008 Aug;8(4):211-21. doi: 10.1136/jnnp.2008.154799.
  16. Fishman JM, Burgess C, Waddell A; Corticosteroids for the treatment of idiopathic acute vestibular dysfunction (vestibular neuritis). Cochrane Database Syst Rev. 2011 May 11;(5):CD008607. doi: 10.1002/14651858.CD008607.pub2.
  17. McDonnell MN, Hillier SL; Vestibular rehabilitation for unilateral peripheral vestibular dysfunction. Cochrane Database Syst Rev. 2015 Jan 13;1:CD005397. doi: 10.1002/14651858.CD005397.pub4.
  18. Eckhardt-Henn A, Best C, Bense S, et al; Psychiatric comorbidity in different organic vertigo syndromes. J Neurol. 2008 Mar;255(3):420-8. doi: 10.1007/s00415-008-0697-x. Epub 2008 Mar 14.

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 makes no warranty as to its accuracy. Consult a doctor or other healthcare professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Richard Draper
Current Version:
Peer Reviewer:
Dr Laurence Knott
Document ID:
2367 (v24)
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