Vestibular Neuronitis 

Updated: Jul 16, 2018
Author: Keith A Marill, MD; Chief Editor: Gil Z Shlamovitz, MD, FACEP 



Vestibular neuronitis may be described as acute, sustained dysfunction of the peripheral vestibular system with secondary nausea, vomiting, and vertigo. As this condition is not clearly inflammatory in nature, neurologists often refer to it as vestibular neuropathy.

Although vestibular neuronitis and labyrinthitis may be closely related in some cases, vestibular neuronitis is generally distinguished from labyrinthitis by preserved auditory function.


Its etiology remains largely unknown, yet vestibular neuronitis appears to be a sudden disruption of afferent neuronal input from 1 of the 2 vestibular apparatuses. This imbalance in vestibular neurologic input to the central nervous system (CNS) causes symptoms of vertigo. At least some cases are thought to be due to reactivation of latent herpes simplex virus type 1 in the vestibular ganglia.



United States

Dizziness is the primary ED complaint in 3.3% of US ED visits, and approximately 5.6% of these patients are diagnosed with vestibular neuritis or labyrinthitis. Thus, the annual incidence of these two diagnoses in US EDs is approximately 150,000 patients.[1]


Most patients experience complete recovery within a few weeks. A minority have recurrent vertiginous episodes following rapid head movement for years after onset.[2]


Studies have shown no consistent male or female predominance.[3]


This syndrome occurs most commonly in middle-aged adults; mean age of onset is 41 years.[3]




Patients usually complain of abrupt onset of severe, debilitating vertigo with associated unsteadiness, nausea, and vomiting.[4] They often describe their vertigo as a sense that either they or their surroundings are spinning. Vertigo increases with head movement.


Spontaneous, unidirectional, horizontal nystagmus is the most important physical finding.[5, 6] Fast phase oscillations beat toward the healthy ear. Nystagmus may be positional and apparent only when gazing toward the healthy ear, or during Hallpike maneuvers. Patients may suppress their nystagmus by visual fixation.

Patient tends to fall toward his or her affected side when attempting ambulation or during Romberg tests.

Affected side has either unilaterally impaired or no response to caloric stimulation.

Vestibular neuronitis is unlikely if any of the following findings are present. The following symptoms should be absent:

  • Multidirectional, nonfatiguing nystagmus suggesting vertigo of central origin

  • Hearing loss

  • Other cranial nerve deficits

  • Truncal ataxia (suggests cerebellar disease or another CNS process)

  • Inflamed tympanic membrane

  • Mastoid tenderness

  • High fever

  • Nuchal rigidity

The head impulse test is a test for normal ocular fixation in association with rapid passive head rotation. An abnormal response is indicated by an inability to maintain fixation during head rotation with a corrective gaze shift after the head stops moving. An abnormal test seems to be sensitive, but not perfectly specific, for a peripheral vestibular disorder.[7, 8]

One group has combined the head impulse test with an assessment of nystagmus type and a test of skew to form the HINTS test, a three component eye movement battery of tests.[8, 9, 10] This clinical battery of tests appears helpful in differentiating vestibular neuritis from a more dangerous central process such as cerebellar stroke, though it awaits further independent confirmation.[8, 9]


Viral infection of the vestibular nerve and/or labyrinth is believed to be the most common cause of vestibular neuronitis.

Acute localized ischemia of these structures also may be an important cause.

Especially in children, vestibular neuritis may be preceded by symptoms of a common cold. However, the causative mechanism remains uncertain.



Differential Diagnoses



Laboratory Studies

Laboratory studies generally do not help determine the etiology or type of vertigo.

However, laboratory studies may be useful to help distinguish between vertigo and other types of dizziness such as light-headedness.

Consider abnormal serum glucose, anemia, or any ongoing cardiac dysrhythmia when patients report feeling light-headed.

Imaging Studies

Cerebral imaging may be necessary to assess causes of central vertigo.

Possible causes of central vertigo include the following:

  • Cerebellar bleeds

  • Infarcts and tumors

  • Lesions of the brain stem

  • Cerebellopontine angle tumors

  • Multiple sclerosis

Because significant bony artifacts degrade CT images of the posterior fossa, MRI is the preferred imaging modality when available.

Imaging generally is not indicated in patients with isolated vertigo, in those with no history or physical findings that suggest any diagnosis other than vestibular neuronitis, and in those without cerebrovascular disease risk factors. A lower threshold for imaging should be maintained for elderly patients or those with risk factors for cerebrovascular disease. These patients have a higher risk for a central cause of vertigo, even when no other symptoms manifest. In one study, 10% of patients with cerebellar infarction presented with isolated prolonged vertigo suggestive of vestibular neuronitis.[11]


Perform the Hallpike maneuver on all patients who complain of vertigo but do not exhibit nystagmus on routine examination of the extraocular muscles.

Hallpike maneuver requires patient to lie back from sitting to supine position 3 times. The first time, have the patient lie back with the head facing forward and the neck slightly extended; repeat this movement with the patient's head turned 45 degrees to the right and a third time with the head turned 45 degrees to the left.

Instruct patient to keep both eyes open each time he or she lies back.

Check for nystagmus and ask patient about any symptoms of vertigo.

Among the characteristics of an elicited nystagmus that would suggest disease of peripheral origin are a pause before nystagmus appears (latency), unidirectional nystagmus, and fatiguing of nystagmus after approximately 1 minute or repeated inductions.

Failure either to observe or to provoke unidirectional nystagmus casts doubt on whether the process is localized to the peripheral vestibular system. Either finding suggests a need to consider other diagnostic alternatives.



Emergency Department Care

ED physicians must first distinguish true vertigo from other types of dizziness. Then, after determining that the patient truly has vertigo, central vertigo must be ruled out through a careful history, physical examination, and, if still uncertain, imaging studies.

Regardless of the vertigo's etiology, ED physicians should attempt to alleviate patient suffering. An intravenous (IV) line often is started to rehydrate the patient, who should be allowed to lie still in bed as desired. Parenteral medicines then are administered.


In cases refractory to acute medical treatment, ED physicians may wish to consult with a neurologist or otolaryngologist.



Medication Summary

Several types of medications have been used to treat vestibular neuronitis. Treatment generally has been based on responses of patients with motion sickness, a related condition. Few controlled studies exist; treatment is often empiric. The results from one trial suggest a 3-week course of methylprednisolone tapered from 100 mg down to 10 mg daily may reduce long-term loss of vestibular function. Despite the evidence of viral infection in at least some patients, valacyclovir was found not to be helpful alone or in combination with methylprednisolone in the same study.[12] Conversely, other small outpatient trials suggested possible enhancement of early recovery but no long-term benefit from a course of steroid therapy.[13, 14, 15, 16] A rigorous Cochrane review that included four trials found no significant difference in the symptomatic resolution of vertigo at 24 hours, and no clear benefit in long-term recovery, though the sparsity of high quality data was noted.[17]

H1-receptor antagonists

Class Summary

These agents may suppress vestibular responses through an effect on the CNS, although their mechanism remains unknown. Some investigators believe this action is mediated primarily by central anticholinergic activity. Dimenhydrinate appears to be more effective and less sedating than lorazepam at the doses tested for the relief of acute vertigo.[18]

Dimenhydrinate (Dramamine, Dimetabs, Dymenate)

A 1:1 salt of 8 chlorotheophylline and diphenhydramine thought to be useful in treatment of vertigo. Diminishes vestibular stimulation and depresses labyrinthine function through central anticholinergic effects. However, prolonged treatment may decrease rate of recovery of vestibular injuries.

Diphenhydramine (Benadryl, Bydramine, Hyrexin)

For treatment and prophylaxis of vestibular disorders that may cause nausea and vomiting.

Meclizine (Antivert)

Decreases excitability of middle ear labyrinth and blocks conduction in middle ear vestibular-cerebellar pathways. These effects associated with relief of nausea and vomiting.

Promethazine (Phenergan)

For symptomatic treatment of nausea in vestibular dysfunction.


Class Summary

These agents centrally inhibit vestibular responses, presumably by potentiating inhibitory GABA receptors.

Diazepam (Valium, Diastat, Diazemuls)

Probably most commonly used benzodiazepine to treat vertigo, its CNS duration is relatively short as it is highly lipophilic and undergoes rapid redistribution after administration.

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life. By increasing action of GABA, which is major inhibitory neurotransmitter in brain, may depress all levels of CNS, including limbic and reticular formation.


Class Summary

These agents are thought to work centrally by suppressing conduction in vestibular cerebellar pathways.

Scopolamine (Scopace, Transderm Scop)

Blocks action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands, and CNS. Antagonizes histamine and serotonin action. Transdermal scopolamine may be most effective agent for motion sickness. Use in vestibular neuronitis limited by its slow onset of action.


Class Summary

Have anti-inflammatory properties and cause profound and varied metabolic effects. Modify the body's immune response to diverse stimuli.

Prednisone (Deltasone, Orasone)

Anti-inflammatory properties may reduce inflammation and edema of the vestibular nerve and associated apparatus, leading to faster recovery and less permanent damage.



Further Outpatient Care

Refer patients for rapid follow-up to their primary care physician, a neurologist, or ear, nose, and throat specialist.

Further Inpatient Care

Consider admission for patients who have persistent vomiting despite treatment and for patients unable to walk satisfactorily.

Inpatient & Outpatient Medications

Outpatient treatment usually continues after discharge.

Multiple oral medicines are available.

In most cases, the brain rapidly compensates and adjusts to the new vestibular deficit, or the inflammatory process resolves.

Evidence indicates many sedating medicines commonly used for this condition may slow recovery. Thus, medical treatment may reduce symptoms but prolong recovery.


Most patients recover from severe vertigo and imbalance within 1 week.

A minority have recurrent, less severe attacks or persistent symptoms. The likelihood of incomplete long-term recovery can be predicted based on initial bedside testing.[19]

Patient Education

In general, movement and activity, to the extent they can be tolerated by the patient, may hasten cerebral compensation and recovery. Eventually, patients can be taught exercises of the eyes and neck to hasten cerebral compensation and recovery. Exercises are seldom practical during the acute episode because of patient discomfort.


Questions & Answers


What is vestibular neuronitis?

What is the pathophysiology of vestibular neuronitis?

What is the prevalence of vestibular neuronitis in the US?

What is the mortality and morbidity associated with vestibular neuronitis?

What is the sexual predilection for vestibular neuronitis?

Which age groups have the highest prevalence of vestibular neuronitis?


Which clinical history findings are characteristic of vestibular neuronitis?

Which physical findings are characteristic of vestibular neuronitis?

Which physical findings help to exclude a diagnosis of vestibular neuronitis?

What is the role of the head impulse test in the evaluation of vestibular neuronitis?

What causes vestibular neuronitis?


What are the differential diagnoses for Vestibular Neuronitis?


What is the role of lab studies in the workup of vestibular neuronitis?

What is the role of cerebral imaging studies in the workup of vestibular neuronitis?

What is the Hallpike maneuver and how is it used in the workup of vestibular neuronitis?


What is included in emergency department (ED) care of vestibular neuronitis?

Which specialist consultations are beneficial to patients with vestibular neuronitis?


Which medications are used in the treatment of vestibular neuronitis?

Which medications in the drug class Corticosteroids are used in the treatment of Vestibular Neuronitis?

Which medications in the drug class Anticholinergics are used in the treatment of Vestibular Neuronitis?

Which medications in the drug class Benzodiazepines are used in the treatment of Vestibular Neuronitis?

Which medications in the drug class H1-receptor antagonists are used in the treatment of Vestibular Neuronitis?


Who should provide follow-up care for patients with vestibular neuronitis?

When is inpatient care indicated for the treatment of vestibular neuronitis?

What is the role of medications in the treatment of vestibular neuronitis?

What is the prognosis of vestibular neuronitis?

Which activity modifications are used in the treatment of vestibular neuronitis?