Transcript Meniere`s disease

MENIERE’ DISEASE
PATHOGENESIS & MANAGEMENT
History

1861: Prosper Meniere
described a syndrome
characterized by deafness,
tinnitus, and episodic vertigo.

Linked this condition to a
disorder of the inner ear.

Knappin (1871) :theorizes dilatation of
membranous Labyrinth.

Dr George Portmann (1926) :Documented
first endolymphatic sac drainage surgery
for the treatment of vertigo in meniere’s
ds.
‘AURICULAR GLAUCOMA’

Dandy (1928) : Treated 9 pts of meniere’s
ds by sectioning the 8th nerve.

Hallpike and Cairns (1938) : First
described Endolymphatic hydrops, the
principal pathological feature of Meniere’s
ds via temporal bone histology.

American Academy of Opthalmology &
Otolaryngology Committee on Equilibrium
(1972) described Meniere’s ds :
“A disease of membranous inner ear
characterized by deafness, vertigo & usually
tinnitus, which has as its pathologic correlate
hydropic distension of the endolymphatic
system”

AAO-HNS Committee on Hearing and Equilibrium
revised definition in 1995.

Meniere’s is diagnosed by

Vertigo
Spontaneous, lasting minutes to hours
 Recurrent, must have 2 episodes > 20 min.
 Nystagmus during episodes
Hearing loss :SNHL must be documented at least 1 occasion
 Avg (250, 500, 1000) 15 dB < Avg (1000, 2000, 3000) or
 Avg (500, 1000, 2000, 3000) 20 dB > than other ear
 For bilateral disease Avg (500, 1000, 2000, 3000) > 25 dB in the
studied ear
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Tinnitus
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No guidelines
Aural pressure

No guidelines
AAO-HNS : American Academy of Otolaryngology-Head & Neck Surgery

Possible Meniere's disease


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
Episodic vertigo of the Meniere's type without documented
hearing loss, or
Sensorineural hearing loss, fluctuating or fixed, with
dysequilibrium but without definitive episodes
Other causes excluded
Probable Meniere's disease

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One definitive episode of vertigo
Audiometrically documented hearing loss on at least one
occasion
Tinnitus or aural fullness in the treated ear
Other causes excluded.

Definite Meniere's disease

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Two or more definitive spontaneous episodes of vertigo 20
minutes or longer
Audiometrically documented hearing loss on at least one
occasion
Tinnitus or aural fullness in the treated ear
Other cases excluded
Certain Meniere's disease

Definite Meniere's disease, plus histopathologic confirmation

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
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 budge 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.
Staging of Hearing Loss in Definite/Certain
Meniere’s:
Stage
Four Tone Average dB
1
≤ 25
2
26-40
3
41-70
4
>70
Staging is based on the four-tone average threshold at
500,1000,2000,3000 Hz of the worst audiogram during the interval
6 mths before treatment.
Vertigo control
Numerical Value
Class
0
A
1 to 40
B
41 to 80
C
81-120
D
>120
E
Secondary Treatment
F
Numerical value= (x/y) ×100
X= Av. no of definitive spells/month for the 6 mths 18-24 mths after therapy
Y= Av. no of definitive spells/month for the 6 mths after therapy

Prevalence: varies widely. 50-200/ 100,000

Frequency of bilateral disease : 2-78%
(arenberg,1980)
Family tendency : up to 20% (paparella,1985)
? Aberration in chromosome 7
- Genetic transmission is variable & inheritence is
multifactorial.

Age & Sex disrtibution
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peak incidence:40-50yr
4-90 yr
F:M :: 3:2
1:1 (arenberg,1980)
Physiology

Perilymph – Similar in
composition to CSF


Endolymph – Similar in
compostion to ICF

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
High Na+, Low K+
Low Na+ High K+
Believed to be produced in
Stria Vascularis
Membranous Labyrinth
separates the two
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Difference of 80mV in charge
No difference in pressure
Physiology

Production and flow of
Endolymph - Theories
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Longitudinal – produced in
membranous labyrinth, flows
to endolymphatic sac, then to
dural venous sinuses
Diffuse – produced and
absorbed along the
membranous labyrinth
Periodic Flow – endolymph
flows only with changes in
volume or pressure
Andrews, JC, Intralabyrinthine fluid dynamics: Meniere disease 12(5) Oct 2004 pp408-412
Pathophysiology

What causes hydrops?
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Obstruction of endolymphatic duct/sac
Alteration of absorption of endolymph
Immunologic insult to inner ear

Elevated levels of IG’s in endolymph
Pathophysiology

Endolymphatic hydrops leads to distortion of
membranous labyrinth
Normal membranous labyrinth
Dilated membranous labyrinth
in Meniere's disease (Hydrops)
Pathophysiology

Build up in pressure may lead to microruptures of membranous labyrinth (Minor
et al)
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Ruptures are confirmed by various histologic
studies
May responsible for episodic nature of attacks
Healing of ruptures may account for return of
hearing
Review Article: Minor, Lloyd et al, Meniere’s Disease, Current Opinion in Neurology 17(1) Feb2004
Pathophysiology

Hydrops role in causation of Meniere’s is
not entirely clear

Rauche et al 1998 – Study of 19 temporal
bone histologies with hydrops13/19 patients with hydrops by histology showed
Meniere’s symptoms
 6/19 showed no Meniere’s symptoms

Rauch SD, et al Meniere’s syndrome and endolymphatic hydrops: double blind temporal
bone study. Ann Otol Rhinol Laryngol 1989; 98:873-883
Aetiological factors

Meniere’s disease :
1.
7.
Genetic
Anatomical
Traumatic
Viral infection
Allergy
Autoimmunity
Psychosomatic & personality features.

Secondary endolymphatic hydrops :
1.
Developmental insult
Abnormal metabolic & endocrine states
Syphilis
Chronic otitis media
Viral infections
Autoimmunity
Otosclerosis
Abnormal fluid balance
Leukemia
2.
3.
4.
5.
6.
2.
3.
4.
5.
6.
7.
8.
9.
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Genetic : possible locus lying between the HLA-C &

HLA-A loci on the short arm of chromosome 6.(Xenellis
et al 1986)
HLA-DR2 locus (Koyama et al.1993)

Anatomical : small vestibular aqueduct.

(Clemis et al.1968)
Smaller endolymphatic sac & duct.
(Tanioka et al 1992)

Trauma : may produce biochemical dysfunction
in the cells of the membranous labyrinth or
cause release of debris into the endolymph.

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Viral infections : Damage to endolymphatic
sac & duct by viral infection. (Schuknecht,1986)
Neurotropic viruses are more likely offenders.
HSV type I
Group specific protein of enterovirus.VP1
Role of Allergy

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
High incidence of associated allergy in pts of meniere’s
ds.(Pulec.1972)
Both food & inhalent allergy were implicated.
Relief in symptoms with immunotherapy in 62% cases. (Derebery et
al.1992)
Autoimmunity
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Immunological abnormalities noted.
Endolymphatic sac capable of generating a humoral or cellular
immune response.
Igs seen deposited in walls & luminal fluid of endolymphatic sacs of
patient.
↑ed serum Ig, ESR, complements in 16% cases.(Suzuki et al 1992)
↑ed circulating immune complexes
(Brookes.1986)
Antibodies against type-2 collegen
(tomada et al.1993)
What damage is done by Meniere's Disease?
1. Hair cell death: Repeated attacks of Meniere's kills


hair cells in the inner ear.
Frequently resulting in unilateral functional deafness.
Cochlear (hearing) hair cells are the most sensitive.
What damage is done by
Meniere's Disease?
2. Mechanical changes to
the ear.



Dilation of the utricle and
saccule.
The saccule may dilate so that
in later stages, it is adherent to
the underside of the stapes
footplate.
mechanical disruption and
distortion of normal inner ear
structures may result in the
gradual onset of a chronic
unsteadiness.
Variants of meniere’s disease



Cochlear hydrops : only cochlear symptoms.
Vertigo absent.
Vestibular hydrops : cochlear function normal
Lermoyez syndrome :characterised by
attacks of tinnitus and diminished
hearing/deafness followed by vertigo after
which hearing improves.
Otolithic crisis of Tumarkin



dangerous variant causing
abrupt fall.
attributed to sudden
mechanical deformation of
the otolith organs(utricle
and saccule), causing a
sudden activation of
vestibular reflexes.
Often surgical
management required.
Physical Examination

During an acute attack
 severe vertigo
 diaphoresis and pallor
 hypertension, tachycardia, tachypnoea
 spontaneous nystagmus with fast component
towards the affected ear
Physical Examination

A complete neurologic examination is necessary.
New-onset vertigo might be an early sign of stroke,
migraine, or brainstem compression.

Romberg test reveals significant instability during acute
attacks.

Hennebert sign is nystagmus owing to applied pressure
in the external auditory canal.

Tullio phenomenon is sound-induced vertigo or
nystagmus or both.
Historically associated with syphilis but has been
described in Ménière disease

Dix-Hallpike positional test
Lab Studies
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Complete blood cell count
Electrolyte level
Sedimentation rate
C-reactive protein
Urinalysis
Thyroid panel
Fluorescent treponemal antibody
Hearing Evaluation
Audiogram typical of early Meniere's
disease on the right side .
Audiogram typical of middle-stage
Meniere's disease on the right side
.
Hearing Evaluation
•Early ds : characterstic pattern is of one of a low frequency
flucuant hearing loss.
•Second early pattern is one of the low frequency hearing loss in
concert with a high frequency hearing loss, resulting in a
‘Inverted V’ shape audiogram.
•Downward sloping less likely.
•Dysacusis : sounds are perceived to have an abnormal tinny
nature.
•Displacusis : A tone of particular frequency may appear normal
in one ear & of higher pitch in another.

Speech audiometry : Discrimation score is
usually 55-85% between attacks.
much impaired during & immediately after
an attack.

SISI test (short increment sensitivity
index): >70% (Normal<15%)

Recruitment test is positive.
Glycerol dehydration test




Dehydrating agent.
1.5ml/kg with equal amt of water
Audiogram & speech discrimination scores
before & 2 hr after ingestion
Positive test : Improvement of 10 db in 2
or more adjacent octaves or gain of 10%
in discrimination score.
Transtympanic electrocochleography
(ECOG)


Specifically detects
distortion of the neural
membranes of the inner
ear.
This is presumably due to
perilymph pressure
fluctuations and can show
evidence of cochlear
involvement.
Transtympanic electrocochleography
(ECOG)


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Silver ball electrode placed
on the promontory.
Sounds stimuli are
produced from a
loudspeaker in earphones
usually in form of clicks.
An averaging computer is
used to average out the
background electrical
activity & produce the clear
electrophysiological
potentials.
Summating potential : complex, multicomponent response representing the
sum of various electrical event occuring within the cochlea.
Evoked action potential : compound action potential representing the
synchronus firing of multiple cochlear neurons derived mainly from the basal
turn of cochlea.
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


Typical transtympanic
ECoG findings in
meniere’s ds are :
Small distorted
cochlear microphonic
Widened AP/SP
waveform.
SP/AP >.45
Electronystagmography (ENG)



Test of the inner ear function (particularly the
semicircular canals).
Tests central and peripheral function and can
help localize the site of lesion.
Reduced vestibular response in the affected
ear in menieres, although response may be
increased secondary to an irritative lesion.
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
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Auditory brain stem evoked responses
Otoacoustic emissions
VEMP
Imaging Studies

MRI : to detect abnormal inner ear anatomy,
masses, and lesions such as multiple sclerosis
and Arnold-Chiari malformations.

CT : to detect dehiscence of the superior
semicircular canals, widened cochlear and
vestibular aqueducts, and subarachnoid
hemorrhage.
Differential Diagnosis

Benign Positional Vertigo
Headache, Migraine
Hypothyroidism and Myxedema Coma
Labyrinthitis
Multiple Sclerosis
Otitis Media
Stroke, Ischemic
Subarachnoid Hemorrhage
Temporal Lobe Epilepsy
Toxicity, Salicylate
Transient Ischemic Attack
Vestibular Neuronitis
TREATMENT
“Natural History”

Silverstein et al (1989)
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1985 AAO criteria
Studied a group of patients who failed medical
treatment and declined surgery
Vertigo
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Hearing
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57-60% complete control in 2 years
71% complete control at 8 years (average)
43% unchanged in unoperated patients
45% unchanged in operated patients
Conclusion

“Given sufficient length of follow-up, a large proportion of
patients will have a spontaneous ‘cure’ of vertigo.”
Placebo Effect

Multiple studies of both medical and surgical therapies
have shown high levels of improvement with placebo.

Torok (1977)


“… the ultimate results, whatever course of medication or
surgery was applied. Recovery varies from about 60% to 80%
…improved are 20% to 30% and …failure is between 10% and
25%.”
Jongkees (1964)

“Result of treatment depends more upon the personality of the
doctor and the belief he has in his treatment.”
Medical Management


Acute Therapy
Maintenance Therapy
Medical Management
Medical Management

Maintenance Therapy

No conclusive studies show efficacy of drugs
intended to alter disease course of Meniere’s
Medical Management

Diuretics and Salt restriction

? Alter fluid balance in inner ear leading to
depletion of endolymph

Osmotic Diuretics (Urea, Glycerol)




Unpleasant taste
Have been consistently shown to reduce symptoms in a
proportion of patients, but the effects only last for a few hours
Objective data includes alteration of the SP:AP ratio on
electrocochleography
Acetazolamide



IV adminisration has been shown to worsen hydrops and
hearing loss (Brookes)
Oral administration may improve hydrops
Side effects encountered include metabolic acidosis and renal
calculi
Vasodilators

Vasodilators

Thought to work by decreasing
ischemia in the inner ear and
allowing better metabolism of
endolymph

Betahistine
Papaverine, isoxpurine, nylidrin,
dipyradamole, amyl nitrate, nitro
glycerine, nicotinic acid, Co2

Beta histine
Betahistine

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A popular choice
studies showing decreased
vertigo
partial agonist against
cerebral H1 receptors
potent H3 receptor
antagonist
increases histamine release
Side effects :worsening
asthma, GI upset.
Water Therapy

Naganuma et al (2006)
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Prospective study
Patients: 18 test, 29 control
Test group: 35 mL/kg/day water x 2 years
Control group: Diuretics and salt restriction
Timeline: 2 years
Results:
Low frequency PTA’s significantly improved in the
water therapy group
 Vertigo resolved in both groups

Laryngoscope. 116(8), August 2006, pp 1455-1460
Meniett Device

Transtympanic “Micropressure”
Treatment


Treatment self-administered
Requires a tympanostomy tube
Meniett Device

Principle :The excess fluid
of the inner ear, can be
restored to normal levels by the
application of low-pressure
pulses to the outer ear which
are then transmitted to the inner
ear through an opening in the
eardrum.
 Each treatment is three 1minute cycles
 Applies intermittent,
alternating pressure 0-20 cm
H20
Meniett Device

Gates GA, Green JD. (2002)



Design: Prospective study, 10
patients, 3-10 months
Criteria: “active symptoms of
vestibular or cochleovestibular
hydrops”
Vertigo



90% Complete control
(presumed level A)
10% with “50%” reduction
(response level C)
Functional Level

Improved 1-3 levels in all cases
Problems
Tube otorrhea, blockage, extrusion
Recurrence of disease after therapy cessation
Meniett Device

Thomsen et al (2005)
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Prospective, randomized, placebo control trial of
“overpressure” device in 40 patients
Placebo device did not generate pressure
AAO-HNS 1995 standards were used
Definite Meniere’s patients only
Functional levels monitored
Vertigo



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Both groups had large decreases in the number of attacks
No statistical significance between active and placebo, although
“there was a trend … toward a reduction”
Significant improvement over the placebo was found in patient
perception of vertigo control.
Functional Level

Statistical significance in the improvement of functional level
between placebo and overpressure
Intratympanic Therapy
Intratympanic Therapy
Goal is to maximize local effects in inner ear while
minimizing systemic effects
Intratympanic Ablation

Fowler (1948) and Schuknecht (1957)
established role of aminoglycoside therapy.

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Streptomicin used initially
Vertigo eliminated in all patients
Profound hearing loss in all patients
Gentamicin treatment now preferred

Theoretical targets of therapy are


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Dark cells of the stria vascularis
Planum semilunatum of the semicircular canals
Higher doses destroy the hair cells of the cochlea
Intratympanic Gentamicin

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Gentamicin is preferred because it is more vestibuloselective
Side effects can include:

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Many methods of delivery exist

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Temporary imbalance or nystagmus
Hearing loss
Tinnitus
Injection
Gelfoam placement
Microwick
Multiple dosing schedules have been proposed

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Low dose
Weekly
Multiple Daily
Continuous
Titration
Intratympanic Gentamicin
Low dose therapy

Harner et al (2001)
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Retrospective study
Patients: 51
Dosing: 1 dose of 40mg/mL injection, re-evaluated at
1 month and given another if needed
Vertigo: 86% Class A/B (2 yrs)
Hearing



PTA minimal change
SRT some drop
Authors claim better hearing preservation
Harner, Stephen et al: Long-term follow-up of transtympanic gentamicin
for Meniere’s Syndrome. Otology & Neurotol 22:210-214, 2001
Intratympanic Gentamicin

Ablation via Multiple Daily Dosing

Jackson and Silverstein – Study on 92
patients who underwent myringotomy and
wick placement through to round window
niche.
Pts. self-administered gentamicin drops TID until
100% reduction on ENG of vestibular response
 85% relief of vertigo, 67% improvement in aural
pressure
 36% hearing loss

Jackson, LE; Silverstein, H: Chemical perfusion of the inner ear. Otolaryngol Clin North
Am 2002, 35:639-653
Intratympanic Gentamicin

Titration Therapy

Martin and Perez 2003 (prospective study,
n=71)
Serial daily injections of buffered (pH 6.4)
26.7mg/cc gentamicin solution via 27 gauge
needle into middle ear
 Injections repeated until vestibular symptoms
developed (spontaneous or evoked nystagmus)
 At 2 years, 69% had Class A vertigo control,
14.1% had Class B
 32.4% had hearing loss

Martin E, Perez N: Hearing loss after intratympanic gentamicin therapy for unilateral
Meniere’s Disease. Otol Neurotol 2003, 24:800-806
Intratympanic Gentamicin

Other methods of delivery

Weekly administration


Single dose of gentamicin once a week for four
treatments
Continuous administration
Microcatheter delivery of gentamicin using a
continuous perfusion method
 Results in extremely variable amount of
gentamicin delivery
 Better perfusion techniques may be needed

Intratympanic Gentamicin

Chia et al performed a meta-analysis of different
modalities of application in 2004
Class A or B
Vertigo Control
Chia, Stanley H, et al Intratympanic Gentamicin Therapy for Meniere’s Disease: a MetaAnalysis. Otology&Neurotol 25(4) July 2004 pp 544-552
Intratympanic Gentamicin


Hearing loss was greatest for multiple
daily dosing
Hearing loss was least for titration therapy
Intratympanic steroid


An attempt to control symptoms without
vestibular ablation
least invasive, least destructive surgery
Intratympanic steroid

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

Barr et al (2001)
21 patients
Intratympanic injections of 4 mg/mL
dexamethasone over a period of 4 wks
Complete relief of vertigo 11 /21 (52%) at 3
months
9 /21 (43%) at 6 months.
Laryngoscope,111(12), 2001, pp 2100-2104
Surgical Therapy

Reserved for medical treatment failures
and is otherwise controversial.

Surgical procedures are divided into 2 major
classifications as follows:
Destructive surgical procedures
 Nondestructive surgical procedures

surgical procedures Cont’d

Destructive surgical procedures



Rationale to control vertigo: Fluid pressure
accumulation within the inner ear→ temporary
malfunction and misfiring of the vestibular
nerve. → vertigo.
Destruction of the inner ear and/or the
vestibular nerve prevents these abnormal
signals.
As long as the opposite inner ear and
vestibular apparatus function normally, the
brain eventually will compensate for the loss
of one labyrinth.
Destructive surgical procedures Cont’d

Problems with destructive procedures:




Destruction of one inner ear depends on the
adequate function of the opposite ear.
Meniere’s disease can be bilateral (7-50%), in
which case this method is contraindicated.
destruction of the balance portion carries a
high risk of hearing loss.
irreversible and reserved for severe cases.
surgical procedures Cont’d

Nondestructive surgical procedures:



Directed toward improving the state of the inner ear
Less invasive
Do not preclude the use of other treatment
modalities.
1.
2.
3.
4.
endolymphatic sac decompression or shunt
vestibular nerve section
Sacculotomy
Ultrasonic destruction of vestibular labyrinth
Endolymphatic Sac Surgery

Purported to address the
site of obstruction causing
hydrops

4 types:




Decompression – removal of
bone around the sac
Shunting – placement of
synthetic shunt to drain
endolymph into mastoid
Drainage – incision of the sac
to allow drainage
Removal of sac
Endolymphatic Sac Surgery

Jens Thomsen et al (1981)




Double-blinded placebo-control study
Patients: 30
Procedure: Cortical mastoidectomy without
decompression vs. endolymphatic shunt placemen
Results:




Both surgery and placebo showed statistically significant
improvements over pre-treatment status
Physician evaluation showed good results in 73% of shunts
vs. 80% of placebo
Patient subjective evaluation showed good results in 73% of
shunts vs. 67% of placebo
Conclusion:

Impact of surgery on the symptoms of Meniere’s disease is
nonspecific and unrelated to the actual shunt procedure.”
Endolymphatic Sac Surgery

Silverstein et al (1989)



Compared different surgical interventions to unoperated
Meniere’s patients
Patients: 89 operated ears, 50 unoperated ears
Vertigo




Hearing


No difference between ELS and “natural history”
Nerve section significantly better than no surgery
ELS procedures resulted in 40% complete control vs. 91-100%
complete control in nerve section patients
No difference in operated (all types) vs. unoperated ears
Conclusion

Endolymphatic sac shunt surgery should not be recommended to
patients with Meniere’s disease.
Vestibular Nerve Section



Direct method of functional vestibular ablation
Single step procedure
Approaches:




Middle Fossa
Retrolabyrinthine/Retrosigmoid
Transcanal
Complications



Damage to facial nerve
Damage to cochlear nerve
CSF leak (about 13%)
Vestibular Nerve Section

Hillman et al (2004)




Retrospective comparison of VNS to IT Gentamicin
High level of vertigo with minimal hearing change
Low rate of complications (12.8% CSF leak)
Conclude that both Gent and VNS are appropriate alternatives

Labyrinthectomy


Useful in patients with no serviceable hearing
and those who cannot tolerate intracranial
procedure
Similar in efficacy to vestibular nerve section
Dietary Modifications

Distribute food and fluid intake evenly throughout the day and
from day to day.

Avoid eating foods or fluids which have a high salt content.

Consult with a nutritionist to establish a rigid salt-restricted diet
(1.5 g sodium per day).

Drink adequate amounts of fluid daily.

Avoid caffeine-containing fluids and foods (such as coffee, tea
and chocolate).
Limit alcohol intake.
Avoid foods containing MSG (monosodium glutamate). prepackaged food products.



Avoid aspirin,ibuprofen or naproxen

Activity:



Endolymphatic hydrops does not preclude
regular activity.
Exercise is recommended in moderation.
Because of the unpredictable nature of the
disease, balance-intensive, dangerous tasks
(eg, especially climbing ladders) should be
avoided.
Overview


Acute Therapy


Non-invastive medical treatments
Lifestyle modification
Alternative options
Alternative Therapies
Meniett
Non-Destructive Therapy



Diuretics
Salt Restriction
Vasodilators
? Water Therapy
Long-Term Stabilization


Vestibular
Suppressants
Medical: IT Steroids
Surgical: Mastoid shunt
Intratympanic
Steroid Therapy
Destructive Therapy


Medical: IT Gentamicin
Surgical


Nerve section
Labyrinthectomy
Shunt surgery
Intratympanic
Gentamicin Therapy
Surgical Ablation
Nerve Section
Labyrinthectomy
Disease progression



Most bothersome in early stages.
In later stages, the hydrops fills the vestibule
so completely that no further room is available
for pressure fluctuation and the vertigo spells
disappear.
Acute attacks are replaced by constant
imbalance and progressive hearing loss.
Medical Management

Diuretics and Salt Restriction


Ruckenstein et al evaluated data from two double
blind studies
Showed no difference in Diuretics vs. placebo
Ruckenstein M.J., Rutka J.A.
& Hawke M. (1991) The
treatment of Meniere's
disease: Torok revisited.
Laryngoscope101, 211-218
Normal electrocochleogram from the tympanic
membrane to clicks presented in alternating polarity at
80 dB HL. The amplitudes of the Summating Potential
(SP) and Action Potential (AP) can be measured from
peak-to-trough (left panel), or with reference to a
baseline value (right panel).
Ginkgo Biloba Extract



70 patients with vertiginous
syndrome
3 month therapy
Ginko group :47%
Placebo group :18%
Prognosis

Variable, since the disease pattern of
exacerbation and remission makes
evaluation of treatment and prognosis
difficult to predict.



In general, meniere’s symptoms tend to
stabilize spontaneously with time.
With regard to vertigo, about half of patients
stabilize over several years.
Patients tend to "burn out" over time and with
residual poor balance and hearing.