Meniere Disease (Idiopathic Endolymphatic Hydrops) Medication

  • Author: John C Li, MD; Chief Editor: Robert A Egan, MD   more...
 
Updated: Sep 15, 2011
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications. Medication is for both symptomatic and prophylactic use.

Medical treatment of Ménière’s disease is aimed at symptomatic relief. The primary target is relief of vertiginous symptoms. Antiemetics may be used for nausea and vomiting. A trial of intramuscular steroid injection followed by a tapering dose of oral steroids has been recommended. Transtympanic steroid injection has been shown to be beneficial in controlling loss of hearing and the number of vertigo attacks.

Diuretics are often used, but their efficacy has not been established with appropriate clinical trials. Loop diuretics should be used with caution due to the potential for ototoxicity. Vasodilators, such as betahistine, have been used for the treatment of vertigo but are not FDA approved for this indication.

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Vestibulosuppressants

Class Summary

Antiemetics act as vestibulosuppressants to decrease symptoms but generally only mask the vertigo. They dull the brain’s response to the inner ear’s signals. Benzodiazepines act as antiemetics and vestibulosuppressants by binding to specific receptor sites, which apparently potentiates the effects of gamma-aminobutyric acid (GABA) and facilitates inhibitory GABA neurotransmission and other inhibitory transmitters. These effects may offer benefits in the treatment of vertigo and emesis. Examples of vestibulosuppressants include meclizine, dimenhydrinate, droperidol, prochlorperazine, diazepam, lorazepam, alprazolam, and scopolamine.

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Meclizine (Antivert, Bonine, Medi-Meclizine)

 

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

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Dimenhydrinate (Dramamine, Driminate, TripTone)

 

Dimenhydrinate is used for prophylaxis of vestibular disorders that may cause nausea and vomiting. Through its central anticholinergic activity, it diminishes vestibular stimulation and depresses labyrinthine function. It is a 1:1 salt of 8 chlorotheophylline and diphenhydramine.

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Scopolamine (Isopto, Scopace, Transderm Scop)

 

Scoploamine blocks the action of acetylcholine at parasympathetic sites and antagonizes the actions of histamine and serotonin. Transdermal scopolamine may be the most effective agent for motion sickness. Its use in treatment of vestibular neuronitis is limited by its slow onset of action.

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Promethazine (Phenergan, Phenadoz, Promethegan)

 

Promethazine is an antidopaminergic agent that is effective in the treatment of emesis. It blocks postsynaptic mesolimbic dopaminergic receptors in the brain and reduces stimuli to the brainstem reticular system.

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Prochlorperazine (Compro)

 

Prochlorperazine is an antidopaminergic drug that blocks postsynaptic mesolimbic dopamine receptors, has an anticholinergic effect, and can depress the reticular activating system; it may be responsible for relieving nausea and vomiting.

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Metoclopramide (Reglan, Metozolv)

 

Metoclopramide is a dopamine antagonist that stimulates acetylcholine release in the myenteric plexus. It acts centrally on chemoreceptor triggers in the floor of the fourth ventricle, and this action provides important antiemetic activity.

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Droperidol

 

Droperidol may reduce emesis by blocking dopamine stimulation of the chemoreceptor trigger zone.

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Diazepam (Valium, Diastat)

 

Diazepam depresses all levels of the central nervous system (CNS), possibly by increasing the activity of GABA. To avoid adverse effects, individualize the dosage and increase it cautiously.

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Alprazolam (Xanax, Niravam)

 

Alprazolam binds receptors at several sites within the central nervous system, including the limbic system and reticular formation. Effects may be mediated through GABA receptor system.

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Corticosteroids

Class Summary

The anti-inflammatory properties of steroids are helpful in treatment of endolymphatic hydrops, probably by reducing endolymphatic pressure; steroids actually can reverse the vertigo, tinnitus, and hearing loss. No trials evaluating the efficacy of systemic steroids for the treatment of Ménière’s disease have been done.[26]

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Prednisone

 

Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear (PMN) activity.

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Diuretics

Class Summary

Diuretics or diuretic-like medications actually can decrease fluid pressure load in the inner ear. These medications help prevent attacks but are ineffective once an attack is triggered. Examples include hydrochlorothiazide, hydrochlorothiazide/triamterene, acetazolamide, and methazolamide.

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Hydrochlorothiazide (Microzide)

 

Hydrochlorothiazide inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water as well as potassium and hydrogen ions.

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Triamterene (Dyrenium)

 

Triamterene is a potassium-sparing diuretic with relatively weak natriuretic properties. It exerts a diuretic effect on the distal renal tubule to inhibit reabsorption of sodium in exchange for potassium and hydrogen. It increases sodium excretion and reduces excessive loss of potassium and hydrogen associated with hydrochlorothiazide. It is not a competitive antagonist of mineralocorticoids, and its potassium-conserving effect is observed in patients with Addison disease (ie, without aldosterone). Triamterene's onset and duration of activity is similar to hydrochlorothiazide.

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Acetazolamide (Diamox)

 

Acetazolamide is a carbonic anhydrase inhibitor that acts by inhibiting the conversion of carbon dioxide to bicarbonate, thus it may decrease vertiginous symptoms.

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Methazolamide (Neptazane)

 

Methazolamide reduces aqueous humor formation by inhibiting the carbonic anhydrase enzyme, which results in decreased vertiginous symptoms.

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Adrenergic Agonists

Class Summary

Adrenergic agonists are useful in treating vertigo, but their mechanism of action is unclear.

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Ephedrine

 

Ephedrine stimulates the release of epinephrine stores, producing alpha- and beta-adrenergic

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Contributor Information and Disclosures
Author

John C Li, MD  Private Practice in Otology and Neurotology; Medical Director, Balance Center

John C Li, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, American Neurotology Society, American Tinnitus Association, Florida Medical Association, and North American Skull Base Society

Disclosure: Nothing to disclose.

Coauthor(s)

Christopher I Doty, MD, FACEP, FAAEM  Assistant Professor of Emergency Medicine, Residency Program Director, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate Medical Center

Christopher I Doty, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Gerard J Gianoli, MD  Clinical Associate Professor, Department of Otolaryngology-Head and Neck Surgery, Tulane University School of Medicine; Vice President, The Ear and Balance Institute; Chief Executive Officer, Ponchartrain Surgery Center

Gerard J Gianoli, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Neurotology Society, American Otological Society, Society of University Otolaryngologists-Head and Neck Surgeons, and Triological Society

Disclosure: Vesticon, Inc. None Board membership

Michael E Hoffer, MD  Director, Spatial Orientation Center, Department of Otolaryngology, Naval Medical Center of San Diego

Michael E Hoffer, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery

Disclosure: American biloogical group Royalty Other

J Stephen Huff, MD  Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

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.

Nicholas Lorenzo, MD  Consulting Staff, Neurology Specialists and Consultants

Nicholas Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, and American College of Physician Executives

Disclosure: Nothing to disclose.

Arlen D Meyers, MD, MBA  Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine

Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society

Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation Unrestricted gift Unknown; Axis Three Corporation Ownership interest Consulting; Omni Biosciences Ownership interest Consulting; Sentegra Ownership interest Board membership; Syndicom Ownership interest Consulting; Oxlo Consulting; Medvoy Ownership interest Management position; Cerescan Imaging Honoraria Consulting; GYRUS ACMI Honoraria Consulting

Mark S Slabinski, MD, FACEP, FAAEM  Vice President, EMP Medical Group

Mark S Slabinski, MD, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Ohio State Medical Association

Disclosure: Nothing to disclose.

R Gentry Wilkerson, MD  Assistant Professor, Director of Research, Emergency Medicine Residency Program, University of South Florida College of Medicine, Tampa General Hospital

R Gentry Wilkerson, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Spiros Manolidis, MD  Associate Professor of Otolaryngology and Neurological Surgery, Columbia University

Spiros Manolidis, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Auditory Society, American Head and Neck Society, American Medical Association, Canadian Society of Otolaryngology-Head & Neck Surgery, Society of University Otolaryngologists-Head and Neck Surgeons, and Texas Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Glenn Lopate, MD  Associate Professor, Department of Neurology, Division of Neuromuscular Diseases, Washington University School of Medicine; Director of Neurology Clinic, St Louis ConnectCare; Consulting Staff, Department of Neurology, Barnes-Jewish Hospital

Glenn Lopate, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and Phi Beta Kappa

Disclosure: Baxter Grant/research funds Other; Amgen Grant/research funds None

Chief Editor

Robert A Egan, MD  Director of Neuro-Ophthalmology, St Helena Hospital

Robert A Egan, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, North American Neuro-Ophthalmology Society, and Oregon Medical Association

Disclosure: Nothing to disclose.

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Transtympanic instillation device is used to administer drugs to inner ear.
Intraoperative view of the left ear treated with labyrinthectomy; endolymphatic sac can be seen in this view.
Tinnitus model. Two phenomena in auditory cortex are associated with peripheral deafferentation: (1) hyperactivity in lesion projection zone and (2) increased cortical representation of lesion-edge frequencies (here, C6) in lesion projection zone. These 2 phenomena are presumed to be neurophysiologic correlates of tinnitus. Red letters correspond to octave intervals of fundamental frequency.
 
 
 
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