Meniere disease

UpToDate

Meniere disease
Authors
Elizabeth A Dinces, MD
Steven D Rauch, MD
Section Editor
Daniel G Deschler, MD, FACS
Deputy Editor
Fenny H Lin, MD
Disclosures
All topics are updated as new evidence becomes available and our peer review
process is complete.
Literature review current through: Oct 2012. | This topic last updated: Sep 28, 2012.

INTRODUCTION Meniere disease is a condition that is thought to arise from

abnormal fluid and ion homeostasis in the inner ear. The disease is named for
Prospere Meniere, a French physician who first reported that the inner ear could be
the source of a syndrome manifesting episodic vertigo, tinnitus, and hearing loss
[1].

The classic pathologic lesion of Meniere disease is termed endolymphatic hydrops.

This lesion can be definitively diagnosed only by postmortem histopathologic
analysis of the temporal bone. However, hydrops has also been identified in
postmortem examination of temporal bones where there was no history of Meniere
symptoms.

Meniere disease refers to presentation of the typical set of symptoms with an

idiopathic etiology. The symptomatic triad may also occur secondary to other inner

ear disorders, in which case it is termed Meniere syndrome. The symptom triad may
be a final common pathway of many different inner ear insults.

This topic will present an overview of the diagnosis and treatment of Meniere
disease. More detailed topics addressing the differential diagnosis of vertigo,
tinnitus, and hearing loss are presented separately. (See "Approach to the patient
with vertigo" and "Pathophysiology, etiology, and differential diagnosis of vertigo"
and "Etiology of hearing loss in adults" and "Sudden sensorineural hearing loss" and
"Etiology and diagnosis of tinnitus".)

EPIDEMIOLOGY Meniere disease can begin at any age but patients typically
present with symptoms between the ages of 20 and 40. Meniere syndrome in
children is most often associated with congenital malformations of the inner ear
[2,3].

The precise incidence of Meniere disease is difficult to determine because of

nonstandard criteria for diagnosis, but the reported incidence ranges from 10 to 150
per 100,000 persons [4]. Bilateral disease occurs in 10 to 50 percent of patients,
with most reports quoting a 25 to 35 percent risk [5-7].

PATHOGENESIS Meniere disease is associated with endolymphatic hydrops with

distortion and distention of the membranous, endolymph-containing portions of the
labyrinthine system. Although most patients have no identifiable other underlying
otologic disease, multiple potential causes of endolymphatic hydrops have been
proposed (table 1).

It is unclear why excess fluid builds up in the endolymphatic spaces of the inner ear.
Several theories have been proposed, but all remain unproven. Lack of a single
etiologic theory for Meniere disease may reflect underlying clinical and genetic
heterogeneity [8].

Proposed etiologies include:

Blockage at the endolymphatic sac or duct One popular theory postulates an

abnormality in the resorption of endolymph at the endolymphatic sac.
Endolymphatic hydrops has been experimentally induced in guinea pigs by blocking
the entrance to the endolymphatic sac [9].
Hypoplasia of the vestibular aqueduct [10].
An immunologic mechanism [11-13].
A genetic predisposition An autosomal dominant inheritance pattern has been
reported, involving 8 to 15 percent of patients with Meniere disease in two studies
[14,15]. Patients with a family history had an earlier age of onset and the
manifestations were more severe in successive generations [14]. A specific gene
marker has not been identified.
A viral etiology [16] Although a viral etiology has been proposed, DNA for
suspected viruses (herpes simplex, varicella zoster, and cytomegalovirus) has not
been detected in endolymphatic samples taken at surgery for patients with Meniere
disease [17].
A vascular etiology Migraine occurs more commonly in patients with Meniere
disease than in the general population, leading to the postulation of a common
vascular pathophysiology for the two disorders [18,19].

The mechanism responsible for symptoms of Meniere disease is also unknown.

While endolymphatic hydrops is present in all patients with Meniere disease, not all
patients with endolymphatic hydrops have symptoms.

The "rupture theory", elaborated 40 to 50 years ago [20,21], proposes that rupture
of the dilated endolymphatic sac allows potassium-rich endolymph into the
perilymphatic space. The resulting biochemical gradient depolarizes the cochlear
and vestibular hair cells, resulting in acute loss of function. Once pressure between
the endolymphatic and perilymphatic space is equalized, the membrane rupture can
seal over. Ion "pumps" restore the normal gradient and hair cell function. Repeated
ionic insults eventually lead to degeneration of the hair cells. Cytologic changes in
hair cells with potassium ion intoxication have been demonstrated [22]. However,
the rupture theory has been called into question [23].

CLINICAL FEATURES The clinical features of Meniere disease include the following:

Episodic vertigo (a true spinning sensation that has an onset and an offset)
Sensorineural hearing loss
Tinnitus

Meniere disease is diagnosed only if patients complain of both episodic vertigo and
sensorineural hearing loss. Aural fullness and nausea may be seen in conjunction
with these symptoms. Affected patients tend to cycle from active symptoms to
prolonged remissions. (See 'Diagnosis' below.)

Vertigo is characteristically rotatory spinning or a rocking sensation and may be

associated with nausea and vomiting, and persists from 20 minutes to 24 hours
duration [24]. Additional sensations of disequilibrium or other patterns of dizziness
are seen in about 15 percent of cases. (See "Approach to the patient with vertigo".)

Hearing loss is sensorineural, usually fluctuating, and often initially affects the lower
frequencies. Hearing loss progresses over time, and often results in permanent
hearing loss at all frequencies in the affected ear over an 8 to 10 year period. (See
"Etiology of hearing loss in adults".)

Downward fluctuations in hearing are typically associated with intense aural fullness
or pressure in the ear or the side of the head [24].

Tinnitus is characteristically low pitch (like listening to a seashell or machinery) and

may be associated with auditory distortion. (See "Etiology and diagnosis of
tinnitus".)

The course of Meniere disease varies among individuals. Some patients have
marked hearing fluctuation and progressive hearing loss with infrequent vestibular
symptoms; some have severe and frequent vertigo with only mild auditory
symptoms; and some manifest both auditory and vestibular symptoms in equal
measure. Approximately two-thirds of patients experience vertigo attacks in
clusters, while one-third have sporadic attacks. The frequency of vertigo episodes
may decline over time [25].

DIAGNOSIS The presumed diagnosis of endolymphatic hydrops is based upon

clinical symptoms. There is no specific diagnostic test for Meniere disease and a
definitive diagnosis can only be made postmortem.

The clinical diagnosis in most patients is based upon the history, neurotologic
evaluation, and clinical response to medical management. Patients usually have
some variable auditory and/or vestibular symptoms for three to five years before
they meet the diagnostic criteria for Meniere disease.

Diagnostic criteria proposed by the American Academy of Otolaryngology and Head

and Neck Surgery (AAO-HNS) stipulate that a "definite" diagnosis of Meniere disease
requires the following [26]:

Two spontaneous episodes of rotational vertigo lasting at least 20 minutes

Audiometric confirmation of sensorineural hearing loss
Tinnitus and/or a perception of aural fullness

Further investigation is also required to rule out other disorders in the differential
diagnosis. (See 'Differential diagnosis' below.)

Audiometry Audiometry should be performed in all patients with suspected

Meniere disease. The most common audiometric pattern in early Meniere disease is
a low frequency or combined low and high frequency sensory loss with normal
hearing in the mid frequencies. Over time the hearing loss "flattens out."

Vestibular testing Vestibular testing may be normal early in the course, but will
eventually be abnormal on the affected side. Testing is primarily useful in
determining candidacy for interventional treatments or identifying possible bilateral
disease.

A standard vestibular evaluation includes electronystagmography (ENG), rotary

chair testing, and computerized dynamic posturography. With progression of
Meniere disease, both the ENG and rotary chair test should show evidence of

declining peripheral vestibular function in the affected ear. The ENG (particularly the
caloric test, in which the ear canals are irrigated with warm and cool water to
stimulate the inner ear) is more sensitive for inner balance dysfunction, but the
rotary chair test is more specific.

Laboratory testing Blood testing includes a search for suspected comorbid

conditions (table 2) and an RPR test for syphilis. (See "Diagnostic testing for
syphilis".)

Tests for antibodies against inner ear antigens have been described [27-29], but are
not considered to be clinically useful and are not part of a routine evaluation for
Meniere disease.

Imaging studies Magnetic resonance imaging (MRI) can identify features that
support a diagnosis of Meniere disease, but the findings are not diagnostic [30].
Nevertheless, MRI is usually indicated to rule out central nervous system (CNS)
lesions that can mimic Meniere disease, including CNS tumors, aneurysms, or
stenosis of the posterior circulation, Arnold-Chiari malformations, and findings
suggesting multiple sclerosis. (See 'Differential diagnosis' below.)

Tests for endolymphatic hydrops Specific tests for endolymphatic hydrops include
glycerine, urea, or sorbitol "stress" tests [31], and electrocochleography [32]. These
tests have low sensitivity and specificity and their role in the diagnosis and
management of Meniere disease is controversial.

The vestibular evoked myogenic potential (VEMP) is a newer test that shows
promise for diagnosis and monitoring [33]. Cervical VEMP (cVEMP) is an inhibitory
sacculocollic reflex test that shows characteristic changes in symptomatic ears of
Meniere patients [33], and may detect early saccular hydrops before the onset of
classic Meniere symptoms [34]. Ocular VEMP (oVEMP) engages both utricular and
saccular afferent nerve fibers and may also be useful in assessment of Meniere
patients [35]. In addition to diagnosis, VEMP may be useful for monitoring patients
for disease progression, and to identify the active ear in patients with bilateral
disease. VEMP is an emerging technology that has not yet been standardized or
fully validated clinically.

DIFFERENTIAL DIAGNOSIS Conditions that need to be considered when Meniere

disease is suspected include (table 3):

Vestibular schwannoma Patients with vestibular schwannoma (acoustic

neuroma) typically present with progressive asymmetric hearing loss but can
sometimes have fluctuating hearing loss. Such patients rarely have true vertigo but
may complain of imbalance. Occasional patients will have tinnitus and imbalance
with normal hearing. Auditory brainstem response (auditory evoked response)
testing and MRI in patients with vestibular schwannoma show abnormalities
indicating compression of the eighth nerve complex. (See "Vestibular schwannoma
(acoustic neuroma)".)
Multiple sclerosis Multiple sclerosis (MS) can present with symptoms identical
to those of Meniere disease. However, the observed nystagmus during an attack of
MS is typically more severe and longer lasting, and the patients may have other
neurologic complaints. Central abnormalities are seen on electronystagmogram
testing (which is typically normal in early Meniere disease). White matter lesions
may be seen on MRI and cerebrospinal fluid abnormalities may be detected. (See
"Diagnosis of multiple sclerosis in adults".)
Transient ischemic attack Transient ischemic attacks (TIAs) are typically of
shorter duration than Meniere attacks. In addition, patients with TIAs rarely
experience simultaneous vestibular and cochlear symptoms, and TIAs do not cause
persistent tinnitus or objective hearing loss. (See "Initial evaluation and
management of transient ischemic attack and minor stroke".)
Migraine Migraine-associated vertigo is an important consideration, especially
those with a history of migraine headache and in young patients with new onset of
episodic vertigo [36]. The prevalence of migrainous vertigo is approximately 3 to 5
percent in the general population, far higher than the 0.2 percent prevalence of
Meniere disease in the US population [37]. Migraine must always be considered as
an alternative or confounding illness.

Headache is usually present with migrainous vertigo, either during the episode or
afterwards (when vertigo or tinnitus is a migraine aura). Migrainous vertigo is often
accompanied by photophobia or phonophobia, symptoms not seen in vertigo
episodes associated with Meniere disease. Diagnostic criteria include episodic
vestibular symptoms, and at least two migraine symptoms (migrainous headache,
photophobia, phonophobia, or visual or other aura) occurring during at least two
vertiginous episodes [38]. (See "Migrainous vertigo".)

Successful treatment with triptans during an attack is generally diagnostic,

although migrainous vertigo is less responsive than headaches. A decrease in the
frequency of events with migraine prophylaxis supports the diagnosis of migrainous
vertigo. (See "Pathophysiology, clinical manifestations, and diagnosis of migraine in
adults".)
Other Diabetes and thyroid disease can sometimes cause symptoms that have
some overlap with Meniere disease. Hearing complaints and/or tinnitus are usually
bilateral in these conditions and the patients often have chronic imbalance instead
of attacks of true vertigo. Similar symptoms may occur in patients with severe
anemia. Appropriate testing can diagnose these conditions.

Cogan's syndrome is a chronic inflammatory condition that occurs most commonly

in young adults and can include vestibuloauditory symptoms that are similar to
Meniere disease. The diagnosis is typically raised by the constellation of symptoms
associated with Cogan's syndrome, including eye disease and systemic vasculitis.
(See "Cogans syndrome".)

PRINCIPLES OF TREATMENT Meniere disease should be considered a chronic

condition; treatment may successfully relieve symptoms but does not address the
underlying abnormal pathophysiology.

The goals of treatment are to [8]:

Reduce the frequency and severity of vertigo attacks

Reduce or eliminate hearing loss and tinnitus associated with attacks
Alleviate chronic symptoms (tinnitus and balance issues)
Minimize disability
Prevent disease progression, particularly hearing loss and imbalance

Patient education is an important part of conservative management, and includes

outlining an explanation of the disease, expectations for response, and treatment
options. Up to 90 percent of patients with Meniere disease are able to maintain
normal daily activities with medical management.

Determining the optimal treatment for Meniere disease is limited by the lack of
randomized, controlled trials [8,39]. In addition, drug therapy has been associated
with a significant placebo effect, and the relapsing remitting nature of the disorder
has made evaluation of various treatments difficult.

Vertigo attacks can be controlled in 90 to 95 percent of patients by conservative

medical treatment, although progressive hearing loss rarely responds to treatment.
Patients with suspected Meniere disease should be referred at a relatively early
stage to an otologist/otolaryngologist.

NONINTERVENTIONAL TREATMENT Noninterventional treatment for Meniere

disease includes lifestyle adjustments, medical therapies, and rehabilitation.

Lifestyle adjustments Patients with Meniere disease are more vulnerable to

dietary and environmental factors that can impact hearing and balance. Triggers for
Meniere disease may include high salt intake, caffeine, alcohol, nicotine, stress,
monosodium glutamate (MSG), and allergies. Avoidance for patients with identified
triggers may alleviate or ameliorate symptoms.

Salt restriction is commonly recommended as part of initial therapy [40,41],

although data supporting its efficacy are not available [8]. An appropriate saltrestricted diet will have approximately 2 to 3 g of sodium per day. The daily sodium
intake should be evenly spread across meals to avoid a large bolus at any time.
(See "Patient information: Low sodium diet (Beyond the Basics)".)

Caffeine and nicotine are vasoconstrictors that may reduce microvascular flow in
the labyrinthine system. Alcohol also causes fluid and electrolyte shifts that can
stress a fragile ear. Limiting caffeine to one caffeinated beverage (coffee, tea, or
cola) daily and limiting alcohol to one drink daily is typically recommended.

Medical management

Acute episodes Acute episodes of vertigo should be managed with vestibular

suppressants and antiemetics (table 4). Doses should be started low and increased
to positive effect or side effects. (See "Treatment of vertigo".)

Vestibular suppressants include benzodiazepines, that have the advantage of

anxiolytic properties for short-term use, antihistamines (meclizine and
dimenhydrinate), and anticholinergics (scopolamine). Promethazine and
prochlorperazine may be used for the acute treatment of severe nausea and
vomiting and are available in suppository form. Lorazepam has been administered
sublingually in "off-label" usage. Although this has not been studied in clinical trials,
otologists have found that a dose of 0.5 to 1 mg administered up to four times daily
may achieve relief of acute vertigo attacks.

Rest and, if appropriate, volume repletion are important adjuvant therapies in the
acute setting.

Drug therapy A number of medications have been used to treat Meniere disease
(table 5). Diuretics and as-needed vestibular suppressants/antiemetics are typically
used when diet alone does not adequately control the episodes. Combinations of
these agents control episodes of vertigo in the majority of patients, although they
have not been shown to affect hearing loss [42].

Diuretics and betahistine have been thought to reduce the degree of endolymphatic
hydrops [40,43]. Betahistine, a vasodilator available in Europe, is reported to act by
improving microvascular circulation in the stria vascularis of the cochlea [44] or by
inhibiting vestibular nuclei activity [45].

One review found that diuretics and betahistine hydrochloride were the only drugs
with demonstrated efficacy for long-term control of vertigo in double-blind trials
[43]. However, two subsequent systematic literature reviews found methodologic
flaws in all trials, with no trials of either diuretics [46] or betahistine [47] being of
sufficient quality to meet the review standard for use. In the absence of better data
and the low risk of adverse effects, we suggest use of diuretics when diet alone
does not adequately control episodes.

Use of systemic glucocorticoid therapy for Meniere disease has been considered,
based on the possible immunologic etiology, and the role of steroids in patients with
sudden sensorineural hearing loss [8]. However, there are no randomized or
prospective trials of oral glucocorticoids in patients with Meniere disease [48].
Similarly, definitive studies are needed before immunosuppressive therapy with low
dose methotrexate [49] or etanercept [50] can be recommended.

Patients have reported improvement with vitamin regimens, herbal remedies, and
vasodilators. However, these treatments are not supported by evidence of efficacy
[8].

Rehabilitation Patients with Meniere disease may be candidates for hearing aid
use, vestibular rehabilitation therapy, or other types of rehabilitation. Vestibular
rehabilitation uses exercise activities to maximize balance and central nervous
system compensation for disequilibrium.

Vestibular rehabilitation has been used primarily in patients whose vertigo

responded to medical or surgical treatment, but who had residual disequilibrium. In
a series of 26 patients who had responded to treatment for vertigo prior to study
inclusion, an eight week vestibular therapy program in a tertiary referral center
demonstrated a composite 25 percent improvement on four tests of disequilibrium
[51]. Vestibular rehabilitation may also be considered for untreated patients with
Meniere disease who experience significant balance and disequilibrium symptoms
between acute spells of vertigo [8]. However, there is no evidence of a reduction in
the frequency or severity of vertigo attacks.

Hearing aids should be considered for patients with significant binaural hearing loss,
but frustration due to hearing fluctuation leads to poor patient compliance in this
disorder.

INTERVENTIONAL TREATMENT Approximately 10 percent of patients have

intractable or progressive, unremitting symptoms that significantly impair their
quality of life, despite medical therapy. These individuals are candidates for invasive
treatments.

The American Academy of Otolaryngology-Head and Neck Foundation (AAO-HNS)

has set forth criteria for Meniere disease disability [26]:

Mild intermittent or continuous dizziness/unsteadiness that precludes working

in a hazardous environment.
Moderate intermittent or continuous dizziness that results in a sedentary
occupation.
Severe disability symptoms so severe as to exclude gainful employment.

A self-assessment tool developed by the AAO-HNS, the Meniere Disease Functional

Level Scale (table 6), is useful in identifying patients who are candidates for
interventional treatment to control vertigo, and in assessing efficacy of therapy.

Interventional treatments for Meniere syndrome include:

Destructive therapies, which act to reduce or eliminate signals from the affected
labyrinthine system to the brain
Nondestructive surgical treatments, whose mechanisms of action are unknown,
but perhaps reduce the accumulation of fluid in the endolymphatic spaces, or
otherwise alter fluid and electrolyte physiology.

There is no agreement on which procedures are first line therapy. The degree of
labyrinthine function and the level of hearing determine the best initial
interventional treatment for an individual patient.

Destructive procedures Destructive procedures for the treatment of Meniere

disease include intratympanic gentamicin injection, surgical labyrinthectomy, and
vestibular nerve section. In general, destructive techniques are better suited to
patients who have failed medical therapy and who have unilateral disease.
However, in cases of severe bilateral disease or intractable vertigo, labyrinthine
ablation must still be considered.

Intratympanic gentamicin Aminoglycosides are toxic to the sensory

neuroepithelium of the inner ear. (See "Pathogenesis and prevention of
aminoglycoside nephrotoxicity and ototoxicity".)

Gentamicin delivered into the middle ear space, by injection or cannula, allows the
drug to locally penetrate the labyrinth through the round window membrane and
destroy hair cells in the semicircular canals, ablating labyrinthine function on the
treated side without adverse systemic effects.

Multiple cohort studies have found that applications of gentamicin control

vertiginous symptoms of Meniere disease in 80 to 90 percent of patients [52-55].
One systematic review including two randomized trials of patients with Meniere
disease found that intratympanic gentamicin was effective in reducing symptoms of
vertigo, compared to placebo [56]. However, this therapy does not affect hydrops
and the associated fullness, hearing fluctuations, and sensory loss. Treatment is
associated with a moderate risk of sensorineural loss (up to 30 percent of patients)
that is irreversible [57].

A newer technique uses a minimal dose of gentamicin (0.5 to 0.75 mL of a 40

mg/mL solution of gentamicin) injected into the middle ear, with the intent to
impact vestibular function without affecting cochlear function. In one study, one
transtympanic gentamicin injection resulted in good control of vertigo in 76 percent
of patients followed for four or more years, with minimal cochlear loss [58]. A
second injection was required in 15 to 20 percent of patients. An open randomized
trial compared low-dose intratympanic gentamicin (2.0 mL of a 40.0 mg/mL solution
of gentamicin, maximum of two injections) with intratympanic dexamethasone (4
mg/mL, three injections over seven days) [59]. Complete and substantial vertigo
control (81.0 and 12.5 percent, respectively) was greater in the gentamicin group
compared with the dexamethasone group (43 and 18 percent, respectively).
Significant hearing loss (>10 dB) occurred in 4 of 32 patients in the gentamicin
group.

There is little consensus of the optimal protocol for intratympanic gentamicin

administration. One meta-analysis found that titrating repeated gentamicin doses
until a vestibular response is achieved is superior to other treatment regimens [60],
while another meta-analysis found no difference in effectiveness for fixed dose or
titration regimens, but noted significant quality issues in all trials evaluated [61].
Intratympanic gentamicin is now widely accepted as the treatment of choice for

most patients with intractable vertigo who have failed diet and diuretic therapy and
have significant hearing loss in the affected ear.

Labyrinthectomy Surgical destruction of the bony and membranous labyrinth by

removal of all of the neuroepithelium from the treated side relieves vertigo in
virtually all patients but also causes irreversible hearing loss in all patients [62].
Thus, it is only indicated in individuals with intractable symptoms despite medical
therapy who already have poor or complete hearing loss on the affected side.

The concern of many physicians is that patients may have subclinical disease in the
opposite ear that will ultimately progress and cause total deafness. We do not
believe that treatment should be withheld in patients with disabling vertigo or drop
attacks, for a potential and unpredictable future event.

Vestibular neurectomy Vestibular neurectomy involves surgical lysis of the

vestibular nerve bundle as it enters the internal auditory canal. It relieves vertigo in
90 to 95 percent of patients and is associated with a low risk (10 to 20 percent) of
sensorineural hearing loss [62].

However, vestibular neurectomy requires general anesthesia with craniotomy and

overnight monitoring in an intensive care unit, and is associated with significantly
more morbidity than labyrinthectomy. Up to 25 percent of patients experience
postoperative headache, and 7 percent have a leak of cerebrospinal fluid. In one
series, hearing was preserved in 82 percent of patients undergoing this procedure,
although the gradual progression of deafness due to Meniere was not altered [62].
Since the widespread adoption of intratympanic gentamicin treatment for patients
who fail non-invasive therapies, vestibular neurectomy has become a very
infrequent treatment choice. It is reserved for those patients who have failed noninvasive therapies and who still have a level of hearing in the affected ear that they
are unwilling to risk to intratympanic gentamicin. (See 'Intratympanic gentamicin'
above.)

Nondestructive procedures

Surgical The nondestructive surgical procedures include endolymphatic sac

procedures (enhancement or shunting or both) and sacculotomy. These procedures

are associated with a low risk of sensorineural hearing loss and are commonly
performed for Meniere disease in patients with intact hearing, despite concerns that
effectiveness may be due to placebo effect [63].

These procedures expose the endolymphatic sac and duct, with the aim to improve
drainage of endolymph. However, anatomic studies of the endolymphatic sac
indicate that such drainage is not plausible [64].

Control of vertigo has been reported in 75 to 80 percent of patients in uncontrolled

case series [65-69]. Symptomatic improvement in hearing and tinnitus have also
been reported with apparent long-term maintenance of benefits [68-70]. Installation
of steroids into the endolymphatic sac following drainage, in a controlled trial, did
not affect the response rate for relief of vertigo symptoms but increased the percent
of patients who had some hearing improvement [68].

The only trial of endolymphatic shunt surgery that used sham surgery as a control
concluded no difference in effectiveness for the sham or interventional procedure
[71]. These results have been called into question with reanalysis that challenged
both study design and statistical analysis [72].

Intratympanic glucocorticoids The possible immunologic basis for Meniere

disease and use of intratympanic glucocorticoids in treatment of sudden
sensorineural hearing loss and in tinnitus has led to studies of intratympanic
steroids in patients with intractable Meniere disease that have found some benefit:

In a randomized trial of 22 patients with Meniere disease, patients randomly

assigned to intratympanic dexamethasone (4 mg/ml daily for five consecutive days)
had improvement in symptoms and functional scores compared to those assigned
to placebo [73].
In a prospective cohort study of 21 patients, complete relief of vertigo was
maintained in 9 patients (43 percent) at six months [74]. The complication rate was
low, although repeated injection was often necessary and the efficacy of the
injection appeared to decrease over time.
A retrospective review of over 120 patients with two year follow-up showed that
vertigo symptoms could be controlled to a level that obviated need for destructive
therapy in approximately 90 percent [75].

In a randomized trial comparing intratympanic low-dose gentamicin and

intratympanic dexamethasone, control of vertigo was significantly greater for the
gentamicin group, but 43 percent of patients in the dexamethasone group did
achieve complete vertigo control with no loss and even slight improvement in
hearing for those whose vertigo improved [59].

Most studies have shown that vertigo symptoms may improve, without change in
hearing or tinnitus [8]. Optimal regimens for intratympanic glucocorticoids have not
been developed, and further studies are indicated.

Positive pressure pulse generator (Meniett) Positive pressure applied to the

middle ear may improve fluid exchange in the inner ear. Overpressure treatment, in
which a device (Meniett pulse generator) applies pulses of pressure to the middle
ear via a ventilation tube, is an option for patients who fail medical therapy or as an
adjunct to medical therapy in patients with functional level 3 or greater (table 6).

Several randomized double-blind placebo-controlled studies have shown short-term

efficacy and safety of overpressure pulsing in the treatment of refractory Meniere
disease [76-78]. Long-term efficacy has also been demonstrated in two small
studies with 67 percent [79] and 92 percent [80] of patients maintaining
improvement in vertigo symptoms at two-year follow-up. Maintenance of a patent
tympanostomy tube is required for overpressure treatment. The device is
expensive, and does not improve subjective hearing [8].

INFORMATION FOR PATIENTS UpToDate offers two types of patient education

materials, The Basics and Beyond the Basics. The Basics patient education
pieces are written in plain language, at the 5th to 6th grade reading level, and they
answer the four or five key questions a patient might have about a given condition.
These articles are best for patients who want a general overview and who prefer
short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at the 10th
to 12th grade reading level and are best for patients who want in-depth information
and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage
you to print or e-mail these topics to your patients. (You can also locate patient

education articles on a variety of subjects by searching on patient info and the

keyword(s) of interest.)

Basics topic (see "Patient information: Meniere disease (The Basics)")

Beyond the Basics topics (see "Patient information: Dizziness and vertigo (Beyond
the Basics)")

SUMMARY AND RECOMMENDATIONS

Meniere disease is a clinical diagnosis, associated with hearing loss, episodic

vertigo, and tinnitus. (See 'Introduction' above.)
Patients with Meniere disease have endolymphatic hydrops in the labyrinthine
system of the affected ear. The etiology is unknown, but may be related to
anatomic, immunologic, genetic, and/or vascular factors. (See 'Pathogenesis'
above.)
Sensorineural hearing loss is fluctuating and progressive. Vertigo episodes last
from 20 minutes to 24 hours and typically occur in clusters. Aural fullness and
nausea may be associated with other symptoms. Symptoms are cyclical and
prolonged periods of remission are typical. (See 'Clinical features' above.)
Meniere disease is a clinical diagnosis. Although not diagnostic, patients should
undergo audiometry, vestibular testing, and MRI to rule out other causes of
symptoms (table 2). The vestibular evoked myogenic potential (VEMP) test may be
useful for monitoring disease progression. (See 'Diagnosis' above.)
Meniere disease is a chronic condition; patients should be given reasonable
expectations of treatment, which include symptom relief but not cure. Patients with
suspected Meniere disease should be referred at a relatively early stage to an
otologist/otolaryngologist. (See 'Principles of treatment' above.)
We suggest that patients limit intake of salt, caffeine, nicotine, and alcohol
(Grade 2C). Acute symptoms of vertigo should be managed with appropriate
medication (table 4). We suggest use of diuretics when diet alone does not
adequately control episodes (Grade 2C). Vestibular rehabilitation may help patients
with residual disequilibrium, and hearing aids can improve hearing in compliant
patients. (See 'Noninterventional treatment' above.)
Interventional therapy may be indicated in the 5 to 10 percent of patients who
have intractable vertigo symptoms that significantly impair quality of life despite

aggressive medical management. The degree of labyrinthine function and level of

hearing determine the best initial interventional treatment for an individual patient.
Interventional techniques include destructive procedures (intratympanic
gentamicin, labyrinthectomy, and vestibular neurectomy) and nondestructive
procedures. Endolymphatic sac surgery has been effective for patients with intact
hearing in prospective series, although a placebo response has been implicated.
Intratympanic glucocorticoids may improve vertigo symptoms, but await controlled
trials. A positive-pressure pulse generator has demonstrated long-term
effectiveness but requires a patent tympanostomy and is expensive. (See
'Interventional treatment' above.)

Causes of endolymphatic hydrops

2012 UpToDate
Causes of endolymphatic hydrops*
Acoustic trauma
Autoimmune inner ear disease
Chronic otitis media
Cogan's syndrome
Congenital deafness
Endolymphatic sac tumors
Fenestration of the otic capsule
Labyrinthine concussion
Letterer-Siwe disease
Leukemic infiltrates
Mondini dysplasia
Otosclerosis
Paget's disease
Serous labyrinthitis
Surgical trauma to inner ear
Syphilis
Temporal bone/head trauma
Viral labyrinthitis
* Endolymphatic hydrops determined at autopsy.
Adapted from Jackler, RK, Brackmann, DE, Eds, Neurotology, Mosby Year Book Inc, Missouri
1994, p. 635.
Causes Meniere disease
2012 UpToDate
Conditions that may cause symptoms of Meniere disease
Hyper/hypothyroidism
Diabetes

Central nervous system disease (eg, cerebral vascular insufficiency, aneurysm, multiple
sclerosis, concussive syndrome, tumor, pseudotumor cerebri)
Recurrent vestibular neuronitis
Autoimmune disease
Neurosyphilis
Diff diagnosis Meniere disease
2012 UpToDate
Differential diagnosis for Meniere disease
Central nervous system
Acoustic neuroma
Multiple sclerosis
Vascular loop compression of eighth nerve
Basilar/vertebral artery insufficiency
Arnold-Chiari malformation
Cerebellar tumors
Transient ischemic attacks
Peripheral vestibular system
Benign positional vertigo
Syphilitic endolymphatic hydrops
Post-concussive hydrops
Post-infectious hydrops (history of sudden sensorineural hearing loss, chronic otitis media, or
labyrinthitis)
Autoimmune inner ear disease
Perilymphatic fistula
Otosclerosis
Migraine induced vertigo
Other
Diabetes
Thyroid disease
Cogan's syndrome
Anemia

Antivertigo drugs
2012 UpToDate
Drugs for acute vertigo
Drug
Antihistamines
Dimenhydrinate
Diphenhydramine

Dose
50 mg every four to six hours
25 to 50 mg every four to six hours

Meclizine
25 to 50 mg every six hours
Benzodiazepines
Alprazolam
0.5 mg immediate release every eight hours
Clonazepam
0.25 to 0.5 mg every eight hours
Diazepam
5 to 10 mg every twelve hours
Lorazepam
1 to 2 mg every eight hours
Antiemetics
Domperidone
10 to 20 mg every six to eight hours
Metoclopramide
5 to 10 mg every six hours
Ondansetron
8 mg every twelve hours
Prochlorperazine
5 to 10 mg every six hours
For acute emergency ward use:
Antihistamines
Diphenhydramine
10 to 50 mg IM or IV
Antiemetics
Metoclopramide
10 to 20 mg IM
Ondansetron
4 mg IM or IV
Prochlorperazine
5 to 10 mg IM or IV
Promethazine
10 to 50 mg IM or IV
IM: intramuscular; IV: intravenous.

Meds for Meniere disease

2012 UpToDate
Medications used to treat Meniere disease
Diuretics
Hydrochlorthiazide
Hydrochlorthiazide and triamterene (Maxzide, Dyazide)
Acetazolamide (Diamox)
Methazolamide (Neptazane)
Antiemetics
Meclizine
Dimenhydrinate (Dramamine)
Prochlorperazine (Compazine)
Promethazine (Phenergan)
Anxiolytics (suppress the central vestibular response)
Diazepam (Valium)
Lorazepam (Ativan)
Alprazolam (Xanax)
Thorazine
Chlorpromazine

Immunomodulators (for acute severe exacerbations and patients with autoimmune antibodies)
Prednisone
Dexamethasone
Methotrexate
Antihistamines (in patients with concomittant allergy or food allergy)
Diphenhydramine (Benadryl)
Loratadine (Claritin)
Fexofenadrine (Allegra)
Ceftirizine (Zyrtec)
Hydroxyzine (Vistaril)
Ototoxic antibiotics
Gentamicin
Streptomycin
Others
Betahistine
Scopolamine
Funct level scale for Meniere disease
2012 UpToDate
Functional level scale for Meniere disease
Regarding my current state of overall function, not just during attacks (check the ONE that best
applies):
1. My dizziness has no effect on my activities at all.
2. When I am dizzy I have to stop what I am doing for a while, but it soon passes and I can
resume activities. I continue to work, drive, and engage in any activity I choose without
restriction. I have not changed any plans or activities to accommodate my dizziness.
3. When I am dizzy I have to stop what I am doing for a while, but it does pass and I can
resume activities. I continue to work, drive, and engage in most activities I choose, but I have
had to change some plans and make some allowance for my dizziness.
4. I am able to work, drive, travel, take care of a family, or engage in most essential activities,
but I must exert a great deal of effort to do so. I must constantly make adjustments in my
activities and budget my energies. I am barely making it.
5. I am unable to work, drive, or take care of a family. I am unable to do most of the active
things that I used to. Even essential activities must be limited. I am disabled.
6. I have been disabled for 1 year or longer and/or I receive compensation (money) because of
my dizziness or balance problem.
Reproduced with permission from: Committee on Hearing and Equilibrium guidelines for the
diagnosis and evaluation of therapy in Meniere's disease. American Academy of OtolaryngologyHead and Neck Foundation, Inc. Otolaryngol Head Neck Surg 1995; 113:181. Copyright
1995 American Academy of Otolaryngology-Head and Neck Surgery.

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Topic 6859 Version 14.0