eMedicine Specialties > Emergency Medicine > Neurology

Vestibular Neuronitis

Keith A Marill, MD, Faculty, Department of Emergency Medicine, Massachusetts General Hospital

Updated: Nov 6, 2009

Introduction

Background

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.

Pathophysiology

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.

Frequency

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

Mortality/Morbidity

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

Sex

Studies have shown no consistent male or female predominance.³

Age

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

Clinical

History

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

Physical

• Spontaneous, unidirectional, horizontal nystagmus is the most important physical finding.⁴
  • 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.^5,6

Causes

• 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

Benign Positional Vertigo
Central Vertigo
Labyrinthitis
Migraine Headache
Stroke, Hemorrhagic
Stroke, Ischemic

Other Problems to Be Considered

Cerebellopontine angle tumors

Workup

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.⁷

Procedures

• 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.

Treatment

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.

Consultations

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

Medication

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. However, recent data 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.⁸

H1-receptor antagonists

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 (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.

Dosing

Adult

50-100 mg PO q4-6h not to exceed 400 mg/24 h
50 mg IV in 10 mL NaCl given over 2 min; do not inject intra-arterially
50 mg IM prn

Pediatric

<2 years: Not established
2-5 years: Up to 12.5-25 mg q6-8h; not to exceed 75 mg/d
6-12 years: 25-50 mg PO q6-8h; not to exceed 150 mg/d
1.25 mg/kg or 37.5 mg/m² IM qid; not to exceed 300 mg/d

Interactions

Alcohol or other CNS depressants may have additive effect; take concurrently with antibiotics that may cause ototoxicity, may mask ototoxic symptoms and irreversible damage may result

Contraindications

Documented hypersensitivity; do not administer to neonates; IV products may contain benzyl alcohol, which has been associated with fatal "gasping syndrome" in premature infants and low-birth-weight infants

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Do not treat severe emesis with antiemetic drugs alone; may contain either sulfites or tartrazine, which may cause allergic-type reactions in susceptible persons; may impede diagnosis of conditions such as brain tumors, intestinal obstruction, and appendicitis; may obscure signs of toxicity from overdosage of other drugs

Diphenhydramine (Benadryl, Bydramine, Hyrexin)

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

Dosing

Adult

25-50 mg PO q6-8h prn; not to exceed 400 mg/d
10-100 mg IV/IM if required; not to exceed 400 mg/d

Pediatric

12.5-25 mg PO divided tid/qid, or 5 mg/kg/d, or 150 mg/m²/d; 5 mg/kg/d or 150 mg/m²/d IV/IM divided qid; not to exceed 300 mg/d

Interactions

Potentiates effects of CNS depressants; alcohol in syrup form—do not give to patients taking medications that can cause disulfiramlike reactions

Contraindications

Documented hypersensitivity; MAOIs

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction

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.

Dosing

Adult

25-50 mg PO q12-24h; not to exceed 100 mg/d

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

May increase toxicity of CNS depressants, neuroleptics, and anticholinergics

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in angle-closure glaucoma, prostatic hypertrophy, pyloric or duodenal obstruction, and bladder neck obstruction

Promethazine (Phenergan)

For symptomatic treatment of nausea in vestibular dysfunction.

Dosing

Adult

12.5 mg PO/PR tid and 25 mg hs
25 mg IV/IM, repeat in 2 h prn; switch to PO as soon as possible

Pediatric

<2 years: Contraindicated
0.25-1 mg/kg PO/IV/IM/PR 4-6 times/d prn

Interactions

CNS depressants or anticonvulsants; epinephrine may cause hypotension

Contraindications

Documented hypersensitivity; children <2 y (incidences of death due to respiratory depression)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiovascular disease, impaired liver function, seizures, sleep apnea, and asthma; not to administer SC or intra-arterially since necrotic lesions may develop; causes sedation and may have anticholinergic adverse effects

Benzodiazepines

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.

Dosing

Adult

5-10 mg PO/IV/IM q3-4h; not to exceed 30 mg in 8 h; repeat q2-4h prn

Pediatric

0.12-0.8 PO mg/kg/d divided q6-8h
0.05-0.3 mg/kg/dose IV/IM over 2-3 min; not to exceed 10 mg/dose; repeat q2-4h prn

Interactions

Phenothiazines, barbiturates, alcohol, and MAOIs increase toxicity in CNS

Contraindications

Documented hypersensitivity; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)

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.

Dosing

Adult

1-10 mg/d PO/IV/IM divided bid/tid

Pediatric

0.05 mg/kg/dose PO/IV/IM q4-8h

Interactions

Alcohol, phenothiazines, barbiturates, and MAOIs increase toxicity in CNS

Contraindications

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease

Anticholinergics

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.

Dosing

Adult

0.3-0.65 mg IM/SC/IV and repeat q4-6h
2.5 cm² transdermal patch to hairless area behind ear qod

Pediatric

6 mcg/kg/dose IM/SC/IV; not to exceed 0.3 mg/dose or 0.2 mg/m²/ dose; repeat q6-8h

Interactions

May decrease antipsychotic effectiveness of phenothiazines; may increase anticholinergic adverse effects of phenothiazines (adjust dose as necessary); TCAs may increase anticholinergic adverse effects (eg, dry mouth, constipation, urinary retention) due to additive effect (TCAs with less anticholinergic activity may be beneficial)

Contraindications

Documented hypersensitivity; primary glaucoma (including initial stages); pyloric obstruction; toxic megacolon; hepatic disease; paralytic ileus; severe ulcerative colitis; renal disease; obstructive uropathy; myasthenia gravis

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in elderly because of increased incidence of glaucoma; large doses may suppress intestinal motility and precipitate or aggravate toxic megacolon; may aggravate hiatal hernia associated with reflux esophagitis; patients with prostatism can have dysuria and may require catheterization; use cautiously in patients with asthma or allergies; reduction in bronchial secretions can lead to inspissation and formation of bronchial plugs

Corticosteroids

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.

Dosing

Adult

100 mg per day PO tapered down to 10 mg per day PO over a 3-wk period

Pediatric

Uncertain for this condition

Interactions

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Contraindications

Documented hypersensitivity; viral, fungal, tubercular skin, or connective tissue infections; peptic ulcer disease; hepatic dysfunction; GI disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

Follow-up

Further Inpatient Care

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

Further Outpatient Care

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

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.

Prognosis

• 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.⁹

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.

Miscellaneous

Medicolegal Pitfalls

• Failure to consider vertigo of central origin is the most important diagnostic error a clinician can make. Vestibular neuronitis generally is a benign and self-limited condition. Diseases involving the cerebellum and brainstem can be life threatening and always must be considered.^10,7
• Failure to exclude other cranial nerve deficits. The presence of other cranial nerve deficits essentially excludes the diagnosis of vestibular neuronitis
• Failure to note presence of hearing loss, which suggests involvement of the cochlea and other inner ear structures, a condition described as labyrinthitis. The possibility of bacterial infection increases with this finding. Admission or consultation for diagnostic assistance and further treatment is recommended. Consider empiric parenteral antibiotics as well if possible CNS infection.

References

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Keywords

vestibular neuronitis, vestibular neuropathy, inflammation of the vestibular nerve, vertigo, dizziness, reactivation of latent herpes simplex virus type 1, herpes simplex virus, vertiginous episodes, rapid head movement  

Contributor Information and Disclosures

Author

Keith A Marill, MD, Faculty, Department of Emergency Medicine, Massachusetts General Hospital
Keith A Marill, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Medtronic Ownership interest None; Cambridge Heart, Inc. Ownership interest None

Medical Editor

Peter MC DeBlieux, MD, Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University Health Sciences Center
Peter MC DeBlieux, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Radiological Society of North America, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

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