AUTHOR INFORMATION

Section 1 of 11

Authored by 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, American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine

Edited by 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; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; J Stephen Huff, MD, Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health System; John Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; and Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital

Author's Email:	Keith A Marill, MD
Editor's Email:	Peter MC DeBlieux, MD

eMedicine Journal, May 3 2006, VOLUME 7, Number 5

INTRODUCTION

Section 2 of 11

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 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.

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.

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

CLINICAL

Section 3 of 11

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.

• 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

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.

DIFFERENTIALS

Section 4 of 11

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

Other Problems to be Considered:

Cerebellopontine angle tumors

WORKUP

Section 5 of 11

Lab Studies:

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

• Lab studies may be useful, however, 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.

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

Section 6 of 11

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

Section 7 of 11

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.

Drug Category: 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.

Drug Name	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.
Adult Dose	50-100 mg q4-6h PO 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 Dose	<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
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
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
Pregnancy	B - Usually safe but benefits must outweigh the risks.
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

Drug Name	Diphenhydramine (Benadryl, Bydramine, Hyrexin) -- For treatment and prophylaxis of vestibular disorders that may cause nausea and vomiting.
Adult Dose	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 Dose	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
Contraindications	Documented hypersensitivity; MAOIs
Interactions	Potentiates effects of CNS depressants; alcohol in syrup form—do not give to patients taking medications that can cause disulfiramlike reactions
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction

Drug Name	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.
Adult Dose	25-50 mg PO q12-24h; not to exceed 100 mg/d
Pediatric Dose	<12 years: Not established >12 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	May increase toxicity of CNS depressants, neuroleptics, and anticholinergics
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Caution in angle-closure glaucoma, prostatic hypertrophy, pyloric or duodenal obstruction, and bladder neck obstruction

Drug Name	Promethazine (Phenergan) -- For symptomatic treatment of nausea in vestibular dysfunction.
Adult Dose	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 Dose	<2 years: Contraindicated 0.25-1 mg/kg PO/IV/IM/PR 4-6 times/d prn
Contraindications	Documented hypersensitivity; children younger than 2 y (incidences of death due to respiratory depression)
Interactions	CNS depressants or anticonvulsants; epinephrine may cause hypotension
Pregnancy	C - Safety for use during pregnancy has not been established.
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

Drug Category: Benzodiazepines -- These agents centrally inhibit vestibular responses, presumably by potentiating inhibitory GABA receptors.

Drug Name	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.
Adult Dose	5-10 mg PO/IV/IM q3-4h; not to exceed 30 mg in 8 h; repeat q2-4h prn
Pediatric Dose	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
Contraindications	Documented hypersensitivity; narrow-angle glaucoma
Interactions	Phenothiazines, barbiturates, alcohol, and MAOIs increase toxicity in CNS
Pregnancy	D - Unsafe in pregnancy
Precautions	Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)

Drug Name	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.
Adult Dose	1-10 mg/d PO/IV/IM divided bid/tid
Pediatric Dose	0.05 mg/kg/dose PO/IV/IM q4-8h
Contraindications	Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma
Interactions	Alcohol, phenothiazines, barbiturates, and MAOIs increase toxicity in CNS
Pregnancy	D - Unsafe in pregnancy
Precautions	Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease

Drug Category: Anticholinergics -- These agents are thought to work centrally by suppressing conduction in vestibular cerebellar pathways.

Drug Name	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.
Adult Dose	0.3-0.65 mg IM/SC/IV and repeat q4-6h 2.5 cm2 transdermal patch to hairless area behind ear qod
Pediatric Dose	6 mcg/kg/dose IM/SC/IV; not to exceed 0.3 mg/dose or 0.2 mg/m2/ dose; repeat q6-8h
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
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)
Pregnancy	C - Safety for use during pregnancy has not been established.
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

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

Drug Name	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.
Adult Dose	100 mg per day PO tapered down to 10 mg per day PO over a three week period
Pediatric Dose	Uncertain for this condition
Contraindications	Documented hypersensitivity; viral infection, peptic ulcer disease, hepatic dysfunction, connective tissue infections, fungal or tubercular skin infections; GI disease
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
Pregnancy	B - Usually safe but benefits must outweigh the risks.
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

Section 8 of 11

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.

In/Out Patient Meds:

• 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.

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

Section 9 of 11

Medical/Legal 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 brain-stem can be life threatening and always must be considered

• Failure to exclude other cranial nerve deficits, which exclude a 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. Possibility of bacterial infection increases. Admission or consultation for diagnostic assistance and further treatment is recommended. Consider empiric parenteral antibiotics as well as possible CNS infection.

TEST QUESTIONS

Section 10 of 11

CME Question 1: A 35-year-old man with no medical history presents with acute onset of sustained vertigo and unilateral hearing loss. What is the most likely diagnosis?

A: Benign positional vertigo
B: Labyrinthitis
C: Vestibular neuronitis
D: Cerebellar hemorrhage
E: Multiple sclerosis

The correct answer is B: While all of these conditions may present with vertigo, only labyrinthitis is associated characteristically with hearing loss.

CME Question 2: A 40-year-old woman is diagnosed with vestibular neuronitis. What is the optimal medical therapy?

A: Dimenhydrinate (Dramamine)
B: Diazepam (Valium)
C: Meclizine (Antivert)
D: Unknown
E: None of the above

The correct answer is D: While all of these medicines are thought to ameliorate symptoms of vestibular neuronitis, optimal medication is unknown.

Pearl Question 1 (T/F): Middle-aged adults are the age group most commonly affected with vestibular neuronitis.

The correct answer is True: The mean age of onset is 41 years.

Pearl Question 2 (T/F): Nystagmus seen in vestibular neuronitis generally has the following characteristics: horizontal, fatigable, and not suppressed by ocular fixation.

The correct answer is False: Nystagmus seen in vestibular neuronitis is horizontal, fatigable, and can be suppressed with ocular fixation.

Pearl Question 3 (T/F): Viral infection of the vestibular nerve and/or labyrinth is the most likely etiology of vestibular neuronitis.

The correct answer is True: Acute localized ischemia of these structures also may be an important cause.

Pearl Question 4 (T/F): Clinicians should recommend that patients with vestibular neuronitis resume normal activities, as tolerated.

The correct answer is True: Clinician should recommend that their patients resume activities, as safely tolerated. Movement in general is thought to facilitate cerebral compensation to the acute unilateral loss of vestibular input.

BIBLIOGRAPHY

Section 11 of 11

• Babe KS, Jr., Serafin WE: Histamine, bradykinin, and their antagonists. In: Goodman & Gilman's The Pharmacological Basis of Therapeutics 1996: 581-600.
• Baloh RW, Lopez I, Ishiyana A: Vestibular neuritis: Clinical-pathologic correlation. Otolaryngol Head Neck Surg 1996; 114: 586-92[Medline].
• Baloh RW: Vestibular Neuritis. N Engl J Med 2003; 348: 1027-32.
• Bohmer A: Acute Unilateral Peripheral Vestibulopathy. In: Disorders of the Vestibular System 1996: 318-27.
• Cohen B, Vianney deJong JMB: Meclizine and Placebo in Treating Vertigo of Vestibular Origin. Arch Neurol 1972; 27: 129-35[Medline].
• Division of Drugs and Toxicology: Drugs used for motion disorders and vomiting. Drug Evaluations Annual 1995: 465-92.
• El-Kashlan HK, Telian SA: Diagnosis and initiating treatment for peripheral system disorders: imbalance and dizziness with normal hearing. Otolaryngol Clin North Am 2000; 33: 563-78[Medline].
• Froehling DA, Silverstein MD, Mohr DN: Does this dizzy patient have a serious form of vertigo? JAMA 1994 Feb 2; 271(5): 385-8[Medline].
• Gizzi M, Riley E, Molinari S: The diagnostic value of imaging the patient with dizziness. A Bayesian approach. Arch Neurol 1996 Dec; 53(12): 1299-304[Medline].
• Hotson JR, Baloh RW: Acute vestibular syndrome. N Engl J Med 1998 Sep 3; 339(10): 680-5[Medline].
• Marill KA, Walsh MJ, Nelson BK: Intravenous lorazepam versus dimenhydrinate for treatment of vertigo in the emergency department: A randomized clinical trial. Ann Emerg Med 2000; 36: 310-9[Medline].
• Peppard SB: Effect of drug therapy on compensation from vestibular injury. Laryngoscope 1986 Aug; 96(8): 878-98[Medline].
• Philpot SJ, Archer JS: Herpes encephalitis preceded by ipsilateral vestibular neuronitis. J Clin Neurosci 2005 Nov; 12(8): 958-9[Medline].
• Rascol O, Hain TC, Brefel C: Antivertigo medications and drug-induced vertigo. A pharmacological review. Drugs 1995 Nov; 50(5): 777-91[Medline].
• Ryu JH, McCabe BF: effects of diazepam and dimenhydrinate on the resting activity of the vestibular neuron. Aerosp Med 1974 Oct; 45(10): 1177-9[Medline].
• Schwaber MK: Vestibular Disorders. Clinical Otology 1997: 345-65.
• Strupp M, Zingler VC, Arbusow V: Methylprednisolone, Valacyclovir, or the Combination for Vestibular Neuritis. N Engl J Med 2004; 351: 354-61.
• Troost BT: Dizziness and Vertigo. Neurology in Clinical Practice 1996; 1: 219-32.
• Troost BT, Waller MA: Neuro-Otology. Neurology in Clinical Practice 1996; 1: 647-57.

eMedicine Journals > Emergency Medicine > Neurology > Vestibular Neuronitis

Please email us with any comments you have on our new chapter format.

Author Information | Introduction | Clinical | Differentials | Workup | Treatment | Medication | Follow-up | Miscellaneous | Test Questions | Bibliography