Meniere Disease (Idiopathic Endolymphatic Hydrops) Medication

Updated: Jun 08, 2018
  • Author: John C Li, MD; Chief Editor: Nicholas Lorenzo, MD, MHA, CPE  more...
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Medication

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.

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.

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.

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.

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.

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.

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.

Droperidol

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

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.

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. [30]

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.

Hydrochlorothiazide (Microzide)

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

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.

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.

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.

Ephedrine

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

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