eMedicine Specialties > Emergency Medicine > Neurology

Vestibular Neuronitis: Treatment & Medication

Author: Keith A Marill, MD, Faculty, Department of Emergency Medicine, Massachusetts General Hospital
Contributor Information and Disclosures

Updated: Nov 6, 2009

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.

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

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

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

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.

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

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

Documented hypersensitivity; MAOIs

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.

Adult

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

Pediatric

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

May increase toxicity of CNS depressants, neuroleptics, and anticholinergics

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.

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

CNS depressants or anticonvulsants; epinephrine may cause hypotension

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

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.

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

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

Documented hypersensitivity; narrow-angle glaucoma

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.

Adult

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

Pediatric

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

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

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

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.

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

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)

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

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.

Adult

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

Pediatric

Uncertain for this condition

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

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

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

More on Vestibular Neuronitis

Overview: Vestibular Neuronitis
Differential Diagnoses & Workup: Vestibular Neuronitis
Treatment & Medication: Vestibular Neuronitis
Follow-up: Vestibular Neuronitis
References

References

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Further Reading

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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