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Official reprint from UpToDatewww.uptodate.com

2010 UpToDate

AuthorsElizabeth A Dinces, MD

Steven D Rauch, MD

Section EditorDaniel G Deschler, MD, FACS

Deputy EditorPracha Eamranond, MD, MPH

Meniere's disease

Last literature review version 18.1:January 2010 | This topic last updated:November 9, 2009

INTRODUCTION Meniere's 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'sdisease 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's disease refers to presentation of the typical set of symptoms with an idiopathic etiology. Th

symptomatic triad may also occur secondary to other inner ear disorders, in which case it is termed

Meniere's 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's disease. More detailed

topics addressing the differential diagnosis of vertigo, tinnitus, and hearing loss are presented

separately. (See "Evaluation of vertigo"and "Pathophysiology, etiology, and differential diagnosis ofvertigo"and "Etiology of hearing loss in adults"and "Sudden sensorineural hearing loss"and

"Pathogenesis and diagnosis of tinnitus".)

EPIDEMIOLOGY Meniere's disease can begin at any age but patients typically present with

symptoms between the ages of 20 and 40. Meniere's syndrome in children is most often associated

with congenital malformations of the inner ear [2,3].

The precise incidence of Meniere's diseaseis difficult to determine because of nonstandard criteria for

diagnosis, but the reported incidence ranges from 10 to 150 per 100,000 persons [4]. Bilateral diseas

occurs in 10 to 50 percent of patients, with most reports quoting a 25 to 35 percent risk [5-7].

PATHOGENESIS Meniere's disease is associated with endolymphatic hydrops with distortion anddistention 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's disease

may reflect underlying clinical and genetic heterogeneity [8].
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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's disease in two studies [14,15]. Patients with a family histor

had an earlier age of onset and the manifestations were more severe in successive generations [14].

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's disease [17].

A vascular etiology Migraine occurs more commonly in patients with Meniere's 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's disease is also unknown. While endolymphatic

hydrops is present in all patients with Meniere's 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's disease include the following:

Episodic vertigo (a true spinning sensation that has an onset and an offset)

Sensorineural hearing loss

Tinnitus

Meniere's 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 nause

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 "Evaluation o

vertigo".)

Hearing loss is sensorineural, usually fluctuating, and often initially affects the lower frequencies.
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Hearing loss progresses over time, and often results in permanent hearing loss at all frequencies in th

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 "Pathogenesis and diagnosis of tinnitus".)

The course of Meniere's 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's disease and a definitive diagnosis can only be made

postmortem.

The clinical diagnosis in most patients is based upon the history, neurotologic evaluation, and clinicalresponse 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's disease.

Diagnostic criteria proposed by the American Academy of Otolaryngology and Head and Neck Surgery

(AAO-HNS) stipulate that a "definite" diagnosis of Meniere's 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's disease. The

most common audiometric pattern in early Meniere's 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's 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) an
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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 t

be clinically useful and are not part of a routine evaluation for Meniere's disease.

Imaging studies Magnetic resonance imaging (MRI) can identify features that support a diagnosis

of Meniere's disease, but the findings are not diagnostic [30]. Nevertheless, MRI is usually indicated t

rule out central nervous system (CNS) lesions that can mimic Meniere's disease, including CNS tumor

aneurysms, or stenosis of the posterior circulation, Arnold-Chiari malformations, and findingssuggesting 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's disease is controversial.

The vestibular evoked myogenic potential (VEMP) is a newer test that shows promise for diagnosis and

monitoring [33]. VEMP 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 o

classic Meniere's symptoms [34]. In addition to diagnosis, VEMP may be useful for monitoring patient

for disease progression, and to identify the active ear in patients with bilateral disease.

DIFFERENTIAL DIAGNOSIS Conditions that need to be considered when Meniere's 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's 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's 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 tha

Meniere's 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 [35]. 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's disease in the US population [36]. Migraine must always

be considered as an alternative or confounding illness.
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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's 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 vertiginou

episodes [37]. (See "Migrainous vertigo".)

Successful treatment with tryptans 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 wit

Meniere's 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 an

can include vestibuloauditory symptoms that are similar to Meniere's disease. The diagnosis is typicall

raised by the constellation of symptoms associated with Cogan's syndrome, including eye disease and

systemic vasculitis. (See "Cogan's syndrome".)

PRINCIPLES OF TREATMENT Meniere's 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's disease are able to maintain normal daily activities with medical management.

Determining the optimal treatment for Meniere's disease is limited by the lack of randomized,

controlled trials [8,38]. 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's

disease should be referred at a relatively early stage to an otologist/otolaryngologist.

NONINTERVENTIONAL TREATMENT Noninterventional treatment for Meniere's disease include

lifestyle adjustments, medical therapies, and rehabilitation.

Lifestyle adjustments Patients with Meniere's disease are more vulnerable to dietary and

environmental factors that can impact hearing and balance. Triggers for Meniere's disease may includ
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high salt intake, caffeine, alcohol, nicotine, stress, monosodium glutamate (MSG), and allergies.

Avoidance for patients with identified triggers may alleviate or ameliorate symptoms.

Saltrestriction is commonly recommended as part of initial therapy [39,40], although data supporting

its efficacy are not available [8]. An appropriate salt-restricted diet will have approximately 2 to 3 g o

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".)

Caffeineand nicotineare vasoconstrictors that may reduce microvascular flow in the labyrinthinesystem. Alcohol also causes fluid and electrolyte shifts that can stress a fragile ear. Limiting caffeine t

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 (meclizineand dimenhydrinate), and anticholinergics (scopolamine).Promethazineand prochlorperazinemay be used for the acute treatment of severe nausea and

vomiting and are available in suppository form. Lorazepamhas 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's 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 [41].

Diuretics and betahistinehave been thought to reduce the degree of endolymphatic hydrops [39,42].

Betahistine, a vasodilator available in Europe, is reported to act by improving microvascular circulation

in the stria vascularis of the cochlea [43] or by inhibiting vestibular nuclei activity [44].

One review found that diuretics and betahistinehydrochloride were the only drugs with demonstrated

efficacy for long-term control of vertigo in double-blind studies [42]. However, two subsequent

systematic literature reviews found methodologic flaws in all trials, with no trials of either diuretics

[45] or betahistine [46] being of sufficient quality to meet the review standard for use. In the absenc

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's 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 wit

Meniere's disease [47]. Similarly, definitive studies are needed before immunosuppressive therapy wit

low dose methotrexate[48] or etanercept[49] 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].
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Rehabilitation Patients with Meniere's 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 tertiar

referral center demonstrated a composite 25 percent improvement on four tests of disequilibrium [50

Vestibular rehabilitation may also be considered for untreated patients with Meniere's 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 du

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's 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's Disease Functional Level Scale (tabl

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's 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's disease include

intratympanic gentamicininjection, surgical labyrinthectomy, and vestibular nerve section. In general,

destructive techniques should 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
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inner ear. (See "Pathogenesis and prevention of aminoglycoside nephrotoxicity and ototoxicity".)

Gentamicindelivered 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 semicircula

canals, ablating labyrinthine function on the treated side without adverse systemic effects.

Multiple applications of gentamicincontrol vertiginous symptoms of Meniere's disease in 80 to 90

percent of patients [51-54]. However, this therapy does not affect hydrops and the associated fullnes

hearing fluctuations, and sensory loss. Treatment is associated with a moderate risk of sensorineuralloss (up to 30 percent of patients) that is irreversible [55].

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 [56]. A

second injection was required in 15 to 20 percent of patients.

There is little consensus of the optimal protocol for intratympanic gentamicinadministration. One

meta-analysis found that titrating repeated gentamicin doses until a vestibular response is achieved is

superior to other treatment regimens [57], while another meta-analysis found no difference in

effectiveness for fixed dose or titration regimens, but noted significant quality issues in all trials

evaluated [58].

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 [59]. 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 i

associated with a low risk (10 to 20 percent) of sensorineural hearing loss [59].

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's was not altered [59].

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's disease in patients with intac

hearing, despite concerns that effectiveness may be due to placebo effect [60].

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
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plausible [61].

Control of vertigo has been reported in 75 to 80 percent of patients in uncontrolled case series [62-

66]. Symptomatic improvement in hearing and tinnitus have also been reported with apparent

longterm maintenance of benefits [65-67]. 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 [65].

The only trial of endolymphatic shunt surgery that used sham surgery as a control concluded nodifference in effectiveness for the sham or interventional procedure [68]. These results have been

called into question with reanalysis that challenged both study design and statistical analysis [69].

Intratympanic glucocorticoids The possible immunologic basis for Meniere's 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's disease.

In a prospective study of 21 patients, complete relief of vertigo was maintained in 9 patients (43

percent) at six months [70]. 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

[71].

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 patient

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 shortterm efficacy and safety

of overpressure pulsing in the treatment of refractory Meniere's disease [72-74]. Longterm efficacy ha

also been demonstrated in two small studies with 67 percent [75] and 92 percent [76] 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].

SUMMARY AND RECOMMENDATIONS

Meniere's disease is a clinical diagnosis, associated with hearing loss, episodic vertigo, and tinnitus

(See 'Introduction'above.)

Patients with Meniere's 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.)
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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's 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 vestibula

evoked myogenic potential (VEMP) test may be useful for monitoring disease progression. (See'Diagnosis'above.)

Meniere's disease is a chronic condition; patients should be given reasonable expectations of

treatment, which include symptom relief but not cure. Patients with suspected Meniere's disease shou

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 rehabilitationmay 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 beenimplicated. Intratympanic glucocorticoids may improve vertigo symptoms, but await controlled trials. A

positive pressure pulse generator has demonstrated longterm effectiveness but requires a patent

tympanostomy and is expensive. (See 'Interventional treatment'above.)

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GRAPHICS


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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.


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Conditions that may cause symptoms of Meniere's syndrome

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


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Differential diagnosis for Meniere's 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


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Medications used to treat Meniere's 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 withautoimmune 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


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Gentamicin

Streptomycin

Others

Betahistine

Scopolamine


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Functional level scale

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 withoutrestriction. 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 Otolaryngology-

Head 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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