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eMedicine - Vestibular Neuronitis : Article by

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Stroke, Ischemic




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AUTHOR AND EDITOR INFORMATION

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

Keith A Marill is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Editors: 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 Sciences Center; 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; Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital

Author and Editor Disclosure

Synonyms and related 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  

INTRODUCTION

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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.

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.

Sex

Studies have shown no consistent male or female predominance.

Age

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


CLINICAL

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


DIFFERENTIALS

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

Other Problems to be Considered

Cerebellopontine angle tumors


WORKUP

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Lab 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 who are at higher risk for a central cause of vertigo, even when no other symptoms manifest.

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

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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

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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 NameDimenhydrinate (Dramamine, Dimetabs, Dymenate)
DescriptionA 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 Dose50-100 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 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
ContraindicationsDocumented 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
InteractionsAlcohol 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
PregnancyB - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
PrecautionsDo 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 NameDiphenhydramine (Benadryl, Bydramine, Hyrexin)
DescriptionFor treatment and prophylaxis of vestibular disorders that may cause nausea and vomiting.
Adult Dose25-50 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 Dose12.5-25 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
ContraindicationsDocumented hypersensitivity; MAOIs
InteractionsPotentiates effects of CNS depressants; alcohol in syrup form—do not give to patients taking medications that can cause disulfiramlike reactions
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsMay exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction

Drug NameMeclizine (Antivert)
DescriptionDecreases excitability of middle ear labyrinth and blocks conduction in middle ear vestibular-cerebellar pathways. These effects associated with relief of nausea and vomiting.
Adult Dose25-50 mg PO q12-24h; not to exceed 100 mg/d
Pediatric Dose<12 years: Not established
>12 years: Administer as in adults
ContraindicationsDocumented hypersensitivity
InteractionsMay increase toxicity of CNS depressants, neuroleptics, and anticholinergics
PregnancyB - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
PrecautionsCaution in angle-closure glaucoma, prostatic hypertrophy, pyloric or duodenal obstruction, and bladder neck obstruction

Drug NamePromethazine (Phenergan)
DescriptionFor symptomatic treatment of nausea in vestibular dysfunction.
Adult Dose12.5 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
ContraindicationsDocumented hypersensitivity; children <2 y (incidences of death due to respiratory depression)
InteractionsCNS depressants or anticonvulsants; epinephrine may cause hypotension
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCaution 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 NameDiazepam (Valium, Diastat, Diazemuls)
DescriptionProbably 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 Dose5-10 mg PO/IV/IM q3-4h; not to exceed 30 mg in 8 h; repeat q2-4h prn
Pediatric Dose0.12-0.8 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
ContraindicationsDocumented hypersensitivity; narrow-angle glaucoma
InteractionsPhenothiazines, barbiturates, alcohol, and MAOIs increase toxicity in CNS
PregnancyD - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
PrecautionsCaution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)

Drug NameLorazepam (Ativan)
DescriptionSedative 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 Dose1-10 mg/d PO/IV/IM divided bid/tid
Pediatric Dose0.05 mg/kg/dose PO/IV/IM q4-8h
ContraindicationsDocumented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma
InteractionsAlcohol, phenothiazines, barbiturates, and MAOIs increase toxicity in CNS
PregnancyD - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
PrecautionsCaution 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 NameScopolamine (Scopace, Transderm Scop)
DescriptionBlocks 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 Dose0.3-0.65 mg IM/SC/IV and repeat q4-6h
2.5 cm2 transdermal patch to hairless area behind ear qod
Pediatric Dose6 mcg/kg/dose IM/SC/IV; not to exceed 0.3 mg/dose or 0.2 mg/m2/ dose; repeat q6-8h
ContraindicationsDocumented hypersensitivity; primary glaucoma (including initial stages); pyloric obstruction; toxic megacolon; hepatic disease; paralytic ileus; severe ulcerative colitis; renal disease; obstructive uropathy; myasthenia gravis
InteractionsMay 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)
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCaution 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 NamePrednisone (Deltasone, Orasone)
DescriptionAnti-inflammatory properties may reduce inflammation and edema of the vestibular nerve and associated apparatus, leading to faster recovery and less permanent damage.
Adult Dose100 mg per day PO tapered down to 10 mg per day PO over a 3-wk period
Pediatric DoseUncertain for this condition
ContraindicationsDocumented hypersensitivity; viral, fungal, tubercular skin, or connective tissue infections; peptic ulcer disease; hepatic dysfunction; GI disease
InteractionsCoadministration 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
PregnancyB - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
PrecautionsAbrupt 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

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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

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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. 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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Vestibular Neuronitis excerpt

Article Last Updated: Mar 3, 2008