MENIERE’S DISEASE

MENIERE’S DISEASE
Introduction
Also called endolymphatic hydrops.
Ménière’s disease, is a disorder of the inner ear where the endolymphatic system is distended
with endolymph.
It is characterized by
i)Vertigo

ii)sensorineural hearing loss

iii)Tinnitus

iv)aural fullness.
HISTORY
1861: PROSPER MENIERE described a syndrome charaterised by deafness , tinnitus and episodic vertigo.
Linked this condition to a disorder of the inner ear
Knappin (1871): Theorizes dilation of membranous labyrinth.
DR George portmann (1926): documented first endolymphatic sac drainage surgery for the treatment of vertigo in Meniere’s
disease.
Dandy (1928): treated 9 patient of Meniere’s disease by sectioning the 8 th nerve.
HALLPIKE & CAIRNS : first described endo lymphatic hydrops , the principal pathological feature of Meniere’s disease via
temporal bone histology.
PATHOPHYSIOLOGY
The main pathology is distension of endolymphatic system, mainly affecting the cochlear duct (scala media)
and the saccule, and to a lesser extent the utricle and semicircular canals.
The dilatation of cochlear duct is such that it may completely fill the scala vestibule ; there is marked bulging
of Reissner’s membrane, which may even herniate through the helicotrema into the apical part of scala tympani
(Figure 15.1).
The distended saccule may come to lie against the stapes footplate. The utricle and saccule may show
outpouchings into the semicircular canals.
A) Normal cochlear duct.
B) Cochlear duct is distended with endolymph pushing the Reissner’s membrane into scala
vestibuli.
AETIOLOGY
The exact cause of Ménière’s disease is not yet known(i.e idiopathic)
The main pathology in Ménière’s disease is distension of endolymphatic system due to increased volume of
endolymph.
This can result either from increased production of endolymph or its faulty absorption or both.
Normally,endolymph is secreted by stria vascularis, fills the membranouslabyrinth and is absorbed through the
endolymphatic sac (see p. 11 for inner ear fluids).
Various theories have been postulated .
Defective Absorption by Endolymphatic Sac
Vasomotor Disturbance
Allergy
Hypothyroidism
Autoimmune and Viral Aetiologies
1. Defective Absorption by Endolymphatic Sac.
Normally, endolymph is carried by the endolymphatic duct to the sac where it is absorbed.
Defective absorption by the sac may be responsible for raised endolymph pressure.
Experimental obstruction of endolymphatic sac and its duct also produces hydrops.
Ischaemia of sac has been observed in cases of Ménière’s disease undergoing sac surgery, indicating poor
vascularity and thus poor absorption by the sac. Distension of membranous labyrinth leads to rupture of Reissner’s
membrane and thus mixing of perilymph with endolymph, which is thought to bring about an attack of vertigo.
2. Vasomotor Disturbance.
There is sympathetic overactivity resulting in spasm of internal auditory artery and/ or its branches, thus interfering
with the function of cochlear or vestibular sensory neuroepithelium.
This is responsible for deafness and vertigo.
Anoxia of capillaries of stria vascularis also causes increased permeability, with transudation of fluid and increased
production of endolymph.
3. Allergy
The offending allergen may be a foodstuff or an inhalant. In these cases, inner ear acts as the “shock
organ” producing excess of endolymph.
Nearly 50% of patients with Ménière’s disease have concomitant inhalant and/or food allergy.
It is possible that Ménière’s disease is multifactorial, resulting in the common end point of
endolymphatic hydrops with classical presentation.
4. Sodium and Water Retention
Excessive amounts of fluid are retained leading to endolymphatic hydrops.
5. Hypothyroidism
About 3% of cases of Ménière’s disease are due to hypothyroidism. Such cases benefit from thyroid
replacement therapy.
6. Autoimmune and Viral Aetiologies
Have also been suggested on the basis of experimental, laboratory and clinical observations.
EPIDEMIOLOGY
Incidence and prevalence
The exact incidence and prevalence of Meniere’s disease are unknown and in fact difficult to demonstrate in any population because of
inherent difficulties to diagnose this condition after exclusion of all other possible causes.
First-line physicians tend to over diagnose Meniere’s disease in patients with chronic vertigo (with or without recurrent vertigo or any
additional symptoms).
In a secondary or tertiary referral balance clinic it is difficult to establish the exact catchment area. In a study on a Finnish population
by Kotimaki et al., a prevalence of 43.2 per 100 000 persons and an incidence of 4.3 definite Meniere’s disease per 100 000 persons
per year was reported (1992–1996).

Age
The age of onset is more commonly reported in the second to sixth decade of life.
Only 1–7% of Meniere’s disease cases are seen in the paediatric population.
Surprisingly, 9% of all patients experience the start of Meniere’s disease at the age of 65 or more, with a higher incidence of
drop attacks.

GENDER
Males are affected more than females.
CLINICAL FEATURES
Vertigo.
It comes in attacks. The onset is sudden. Patient gets a feeling of rotation of himself or his environment.
sometimes, there is feeling of “to and fro” or “up and down” movement.
Attacks come in clusters, with periods of spontaneous remission lasting for weeks, months or years.
Usually, an attack is accompanied by nausea and vomiting with ataxia and nystagmus.
Severe attacks may be accompanied by other symptoms of vagal disturbances such as abdominal cramps, diarrhoea, cold
sweats, pallor and bradycardia.
Usually, there is no warning symptom of an oncoming attack of vertigo but sometimes the patient may feel a sense of fullness in
the ear, change in character of tinnitus or discomfort in the ear which herald an attack.
Some cases of Ménière’s disease show Tullio phenomenon.
It is a condition where loud sounds or noise produce vertigo and is due to the distended saccule lying against the stapes
footplate. This phenomenon is also seen when there are three functioning windows in the ear, e.g. a fenestration of horizontal
canal in the presence of a mobile stapes.
2. Hearing Loss.
It usually accompanies vertigo or may precede it. Hearing improves after the attack and may be
normal during the periods of remission.
This fluctuating nature of hearing loss is quite characteristic of the disease.
With recurrent attacks, improvement in hearing during remission may not be complete; some hearing loss being added in every
attack leading to slow and progressive deterioration of hearing which is permanent.
• Distortion of sound
Some patients complain of distorted hearing.
A tone of a particular frequency may appear normal in one ear and of higher pitch in the other leading to diplacusis. Music
appears discordant.
• Intolerance to loud sounds Patients of Ménière’s disease cannot tolerate amplification of sound due to recruitment
phenomenon. They are poor candidates for hearing aids.
3. Tinnitus
It is low-pitched roaring type and is aggravated during acute attacks.
Sometimes, it has a hissing character. It may persist during periods of remission.
Change in intensity and pitch of tinnitus may be the warning symptom of attack.
4. Sense of Fullness or Pressure
Like other symptoms, it also fluctuates. It may accompany or precede an attack of vertigo.
5. Other Features
Patients of Ménière’s disease often show signs of emotional upset due to apprehension of the repetition of attacks. Earlier, the
emotional stress was considered to be the cause of Ménière’s disease.
VARIANTS OF MÉNIÈRE’S DISEASE
1.Cochlear Hydrops.
Here, only the cochlear symptoms and signs of Ménière’s disease are present.
Vertigo is absent.
It is only after several years that vertigo will make its appearance.
It is believed that in these cases, there is block at the level of ductus reuniens, thereby
confining the increased endolymph pressure to the cochlea only
2. Vestibular Hydrops
Patient gets typical attacks of episodic vertigo while cochlear functions remain normal.
It is only with time that a typical picture of Ménière’s disease will develop. Many of the
cases of vestibular Ménière’s disease are labelled “recurrent vestibulopathy” as
endolymphatic hydrops could not be demonstrated in the study of temporal bones in
such cases.
3. Drop Attacks (Tumarkin’s Otolithic Crisis)
In this, there is a sudden drop attack without loss of consciousness.
There is no vertigo or fluctuations in hearing loss.
Patient gets a feeling of having been pushed to the ground or poleaxed.It is an uncommon manifestation of Ménière’s disease
and occurs either in the early or late course of disease.
Possible mechanism is deformation of the otolithic membrane of the utricle or saccule due to changes in the endolymphatic
pressure.
4. Lermoyez Syndrome
Here symptoms of Ménière’s disease are seen in reverse order.
First there is progressive deterioration of hearing, followed by an attack of vertigo, at which time the hearing recovers.
DIAGNOSIS
Diagnostic criteria for Ménière’s disease
The most recent guidelines for the diagnosis in patients with Meniere’s disease were issued in 2015 by the
Classification Committee of the Barany Society , The Japan Society for Equilibrium Research, The European Academy of
Otology and Neurotology (EAONO), The Equilibrium Committee of the American Academy of Otolaryngology– Head
and Neck Surgery (AAO–HNS) and the Korean Balance Society.
According to these guidelines, the diagnosis of Meniere’s disease in a vertigo patient is based on clinical symptoms and
exclusion of identifiable other etiologies, rendering Meniere’s disease idiopathic.
They provide 2 degrees of certitude: definite and probable Meniere’s disease.
EXAMINATION
1. Otoscopy
No abnormality is seen in the tympanicmembrane.
2. Nystagmus.
It is seen only during acute attack. The quick component of nystagmus is towards the unaffected ear.
3. Tuning Fork Tests
They indicate sensorineural hearing loss.
Rinne test is positive, absolute bone conduction is reduced in the affected ear and Weber is lateralized to the
better ear.

INVESTIGATIONS
Pure Tone Audiometry
There is sensorineural hearing loss. In early stages, lower frequencies are affected and the curve is of rising type.
When higher frequencies are involved curve becomes flat or a falling type
2. Speech Audiometry.
Discrimination score is usually55–85% between the attacks but discrimination ability is much impaired during and immediately
following an attack.
3. Special Audiometry Tests.
They indicate the cochlear nature of disease and thus help to differentiate from retrocochlear lesions, e.g. acoustic neuroma
(a) Recruitment test is positive.
(b) SISI (short increment sensitivity index) test. SISI score is better than 70% in two-thirds of the patients (normal 15%).
(c) Tone decay test. Normally, there is decay of less than 20 dB.
4. Electrocochleography
It shows changes diagnostic of Ménière’s disease. Normally, ratio of summating potential (SP) to action potential (AP) is 30%.
In Ménière’s disease, SP/AP ratio is greater than 30%.
5. Caloric Test.
It shows reduced response on the affected side in 75% of cases.
Often, it reveals a canal paresis on the affected side (most common) but sometimes there is directional preponderance to healthy
side or a combination of both canal paresis on the affected side and directional preponderance on the opposite side.
6. Glycerol Test.
Glycerol is a dehydrating agent.
When given orally, it reduces endolymph pressure and thus causes an improvement in hearing.
Patient is given glycerol (1.5 mL/kg) with an equal amount of water and a little flavouring agent or lemon
juice.
Audiogram and speech discrimination scores are recorded before and 1–2 h after ingestion of glycerol. An improvement of 10
dB in two or more adjacent octaves or gain of 10% in discrimination score makes the test positive.
There is also improvement in tinnitus and in the sense of fullness in the ear. The test has a diagnostic and prognostic value.
These days, glycerol test is combined with electrocochleography.
(A) Audiogram in early Meniere’s disease. Note: Hearing Electrocochleography.
loss is sensorineural and more in lower frequencies—the rising (A) Normal ear.
curve. (B) Ear with Meniere’s disease. Voltage of summating
As the disease progresses, middle and higher frequencies get potential (SP) is compared with that of action potential
involved and audiogram becomes flat or falling type (B & C). (AP).
Normally SP is 30% of AP.
This ratio is enhanced in Meniere’s disease.
TREATMENT
A. GENERAL MEASURES
1. Reassurance
Patient anxiety can be relieved by reassurance and by explaining the true nature of disease. This is particularly important in acute attack.

2. Cessation of smoking
Nicotine causes vasospasm so Smoking should be completely stopped.
For some patients, this may be the only treatment necessary.
3. Low salt diet
Patient should take salt-free diet as far as possible.
No extra salt should be permitted. Salt intake should not exceed 1.5–2.0 g/day.
4. Avoid excessive intake of water.
5. Avoid over-indulgence in coffee, tea and alcohol.
6. Avoid stress and bring a change in lifestyle. Mental relaxation exercises and yoga are helpful to decrease stress.
7. Avoid activities requiring good body balance. As the attack of Ménière’s disease is abrupt, sometimes with no warning symptom, professions such as
flying, underwater diving or working at great heights should be avoided.
B. MANAGEMENT OF ACUTE ATTACK
During the acute attack, there is severe vertigo with nausea and vomiting. Patient is apprehensive. Head movements provoke
giddiness.
Therefore, treatment would consist of:
1. Reassurance and psychological support to allay worry and anxiety.
2. Bed rest with head supported on pillows to prevent excessive movements.
3. Intravenous fluids and electrolyte administration to combat their loss due to vomiting.
4. Vestibular sedatives to relieve vertigo. They should be administered intramuscularly or intravenously, if vomiting precludes
oral administration. Drugs useful in acute attack are dimenhydrinate (Dramamine), promethazine theoclate (Avomine) or
prochlorperazine (Stemetil).
Diazepam (Valium or Calmpose) 5–10 mg may be given intravenously.
It has a tranquillizing effect and also suppresses the activity of medial vestibular nucleus.
In some patients, acute attack can be stopped by atropine, 0.4 mg, given subcutaneously.
5. Vasodilators: Carbogen (5% CO2 with 95% O2) is a good cerebral vasodilator and its inhalation improves
labyrinthine circulation.
C. MANAGEMENT OF CHRONIC PHASE
When patient presents after the acute attack, the treatment consists of:
1. Vestibular sedatives: Prochlorperazine (Stemetil)10 mg, thrice a day, orally for two months and then reduced to 5 mg
thrice a day for another month.
2. Vasodilators: Betahistine (Vertin) 8–16 mg, thrice a day, given orally, also increases labyrinthine blood flow by releasing
histamine in the body.
3. Diuretics: Sometimes, diuretic furosemide, 40 mg tablet, taken on alternate days with potassium supplement helps to control
recurrent attacks, if not controlled by vasodilators or vestibular sedatives. Thiazide diuretics (hydrochlorothiazide), 12.5 mg
daily can also be used.
4. Propantheline bromide (Probanthine), 15 mg, thrice a day, can be given alone or in combination with vasodilator and is
quite effective. However, they are not preferred by many due to side effects.
5. Elimination of allergen: Sometimes, a food or inhalant allergen is responsible for such attacks. It should be found and
eliminated or desensitization done.
6. Hormones: Investigations should be directed to find any endocrinal disorder such as hypothyroidism, and
appropriate replacement therapy given. Control of stress by change in lifestyle is important to prevent recurrent attacks.
About 80% of the patients can be effectively managed by medical therapy alone.
Intratympanic gentamicin therapy(chemical labyrinthectomy)
Gentamicin is mainly vestibulotoxic.
It has been used in daily or biweekly injections into the middle ear.
Drug is absorbed through the round window and causes destruction of the vestibular labyrinth.
Total control of vertigo spells has been reported in 60–80% of patients with some relief from symptoms in others. Hearing loss,
sometimes severe and profound, has been reported in 4–30% of patients treated with this mode of therapy.
Microwick
It is a small wick made of polyvinyl acetate and measures 1 mm × 9 mm.
It is meant to deliver drugs from external canal to the inner ear and thus avoid repeated intratympanic injections.
it requires a tympanostomy tube (grommet) to be inserted into the tympanic membrane and the wick is passed through it.
When soaked with a drug, the wick delivers the drug to the round window to be absorbed into the inner ear.
It has been used to deliver steroids in sudden deafness and gentamicin to destroy vestibular labyrinth in Ménière’s disease.
D. SURGICAL TREATMENT
It is used only when medical treatment fails.
1.Conservative Procedures: They are used in cases where vertigo is disabling but hearing is still useful and needs to be preserved.
They are:
(a) Decompression of endolymphatic sac.
(b) Endolymphatic shunt operation: A tube is put, connecting endolymphatic sac with subarachnoid space, to drain excess endolymph.
(c) Sacculotomy (Fick’s operation) : It is puncturing the saccule with a needle through stapes footplate.
A distended saccule lies close to stapes footplate and can be easily penetrated.
Cody’s tack procedure consists of placing a stainless steel tack through the stapes footplate.
The tack would cause periodic decompression of the saccule when it gets distended. Both these operations were claimed to have shown good results but they could not be
reproduced by others and thus abandoned.
Cochleosacculotomy is another similar procedure in which, instead of saccule, cochlear duct is punctured and drained into the perilymph (oticperioticshunt).
The procedure is performed with a curved needle passed through the round window to puncture cochlear duct.
(d) Section of vestibular nerve : The nerve is exposed by retrosigmoid or middle cranial fossa approach and selectively sectioned.
It controls vertigo but preserves hearing.
(e) Ultrasonic destruction of vestibular labyrinth : Cochlear function is preserved.
2. Destructive Procedures : They totally destroy cochlear and vestibular function and are thus used only when cochlear
function is not serviceable.
• Labyrinthectomy: Membranous labyrinth is completely destroyed either by opening through the lateral semicircular canal by
transmastoid route or through the oval window by a transcanal approach.
This gives relief from the attacks of vertigo.

3. Intermittent Low-Pressure Pulse Therapy [Meniett Device Therapy]

It is observed that intermittent positive pressure delivered to inner ear fluids brings relief from the symptoms of Ménière’s
disease.
Not only there is improvement in vertigo, tinnitus and ear fullness, but hearing may also improve. Intermittent positive pressure
waves can be delivered through an instrument called Meniett device which has been approved by FDA.
A prerequisite for such a therapy is to perform a myringotomy and insert a ventilation tube so that the device when coupled to
the external ear canal can deliver pressure waves to the round window membrane via the ventilation tube.
Pressure waves pass through the perilymph and cause reduction in endolymph pressure by redistributing it through various
communication channels such as the endolymphatic sac or the blood vessels.
Some believe they regulate secretion of endolymph by the stria vascularis.
Patient can self-administer the treatment at home. It may require a few months before complete remission
of disease is obtained.
Meniett device therapy has been recommended for patients who have failed medical treatment
and the surgical options are being considered.

Mechanism of intermittent low pressure pulse therapy.

Pressure waves pass through ventilation tube(1) to round window membrane (2) and transmitted to perilymph
(yellow) and compress endolymphatic labyrinth (blue) to redistribute endolymph pressure to sac
(3) And blood vessels (4).
MENIETT DEVICE IN MENIÈRE’S DISEASE:
RANDOMIZED, DOUBLE-BLIND, PLACEBO-
CONTROLLED MULTICENTER TRIAL
FRANCESCA
Francesca Yoshie Russo, Yann Nguyen, Daniele de Seta, Didier
Bouccara, Olivier Sterkers, Evelyne Ferrary, Daniele
Bernardeschi
ABSTRACT
OBJECTIVE : To evaluate the efficacy of Meniett® low-pressure pulse generator in Menière’s disease.
STUDY DESIGN: Randomized, double-blind, placebo-controlled, multicenter trial carried out in seventeen academic medical
centers.
METHODS: One hundred twenty-nine adults presenting Menière’s disease (AAO-HNS criteria) not controlled by conventional
medical treatment were included. The protocol included three phases: 1) placement of a transtympanic tube and evaluation of its
effect; if resolution of symptoms, the patient was excluded; 2) randomization: 6-weeks treatment with Meniett® or placebo
device; 3) removal of the device and 6-weeks follow-up period. The evaluation criteria were: the number of vertigo episodes (at
least 20 minutes with a 12 hours free interval), and the impact on daily life assessed by self-questionnaires.
RESULTS: Ninety-seven patients passed to the second phase of the study, 49 and 48 patients received the Meniett® device or
the placebo device, respectively. In the placebo group, the number of vertigo episodes decreased from 4.3 ± 0.6 (mean ± SEM)
during the first phase to 2.6 ± 0.5 after 6 weeks of treatment, and to 1.8 ± 0.8 after the removal of the device. Similar results
were observed in the Meniett® group: 3.2 ± 0.4 episodes during the first phase, 2.5 ± after 6 weeks of Meniett® treatment, and
1.5 ± 0.2 after the third phase.
CONCLUSION: An improvement of symptoms is evidenced in all patients, with no difference between the Meniett® and the
placebo groups. The decrease in number of vertigo episodes could be explained by an effect of the medical care.
KEYWORDS: Transtympanic tube; inner ear; placebo; endolymphatic hydrops; vertigo
Meniett® low-pressure pulse generator
INTRODUCTION
Menière’s disease is a chronic illness that affects approximately 0.2% of the world’s population. The estimated annual incidence of the disease is 2/1000
Its origin is an imbalance in inner ear hydrodynamics. Of as yet poorly understood physiopathology, this syndrome is characterized by sudden and
repeated vertigos, hearing loss, feeling of pressure in the ear, and tinnitus .
Vertigo can last hours or even days, during which time the patient is often bedridden. The disease can have a significant effect on quality of life including
a not insignificant risk of workplace injury
Because of the natural history of Menière’s disease, benefit of each treatment should be compared to a spontaneous improvement, and to the well-known
placebo effect. Symptoms have for long time been treated by medications such as Betahistine, steroids and diuretics, and yet their effect on hearing loss
and on the long-term evolution of the disease has not been established.
In severe cases, resistant to medical treatment, chemical or surgical labyrinthectomy is considered, but a debate on the risk-benefit ratio still exist.
Therefore, effective, less invasive, treatments are eagerly awaited.
In this context, it has long been shown that changes in local pressure in the middle ear could have a positive effect on Menière’s disease. In vivo studies
showed that the insertion of a transtympanic tube could reduce the development of endolymphatic hydrops, resulting in an improvement of symptoms. A
similar effect was also noticed in patients with Menière’s disease, where it has been shown that the inner ear hydrodynamic system balance could be
corrected with low-pressure air pulses in the middle ear. The development of the miniaturized, portable device Meniett® may provide the accessibility of
this treatment. The results of an initial placebo-controlled study with the Meniett® device developed by Medtronic Xomed, have been positive and the
trial was able to document the ease of use and safety of the device .
The present prospective, multicenter, double-blind placebo controlled study aims to validate the effectiveness, and to assess the
benefits of the Meniett® device on number of vertigos, and on quality of life of patients affected by Menière’s disease.
Additionally, the introduction of a run-out period should permit to estimate the possible residual effects of this method.
Considering both the spontaneous and unpredictable occurrence of Menière’s disease and the difficulty in predicting its natural
evolution over a given period, a controlled trial is crucial.
Moreover, as the use of the Meniett® device requires the insertion of a transtympanic tube, it is necessary to demonstrate that
its effectiveness is not a result of the only transtympanic tube effect.
MATERIALS AND METHODS
This study was a multicenter (17 centers), randomized, double-blind, placebo controlled study.The protocol was approved by
the local institutional boards.
Patients’ selection
An analysis with power calculation was performed for the study design.Given the lack of published data concerning the
evolution of vertigos following placement of a t-tube, the calculation was made considering the percentage of subjects who are
free of symptom. Based on the results of previous studies, the percentage of patients that no longer experience vertigo following
drain placement was estimated between 50 and 66. Thus, the number of 47 patients per group was adapted to detect a possible
variation of 30% of the Meniett® over the placebo device (alpha risk 5%, beta risk 20%, two sided test).
After giving their written consent, all patients underwent complete ENT examination, audiometry, and videonystagmometry
were realized to confirm the diagnosis. All patients were adults over 18 years old age, affected by a stage 2, or greater, unilateral
definite Menière’s disease, according to the AAO-NHS criteria 2. They were included if they experienced at least two episodes
of rotatory vertigo in the preceding two months (vertigo lasting at least 20 minutes, with a free interval of 12 hours), with or
without associated tinnitus, and/or a sensation of fullness in the ear. Moreover, the impact of vertigo on the patient’s daily life
had to be at level 3 at least on the functionality level according to AAO-HNS criteria. Patients having undergone surgical
treatment or chemical labyrinthectomy for Menière’s disease were excluded.
Phases of the protocol
The clinical protocol comprised three phases
First phase: Placement of the transtympanic tube associated to the complete withdrawn of any anti-vertigo treatment,
afterwards a period of eight weeks maximum (56 days), with recording of the number of vertigo episodes. The objective was to
ensure the washout of any earlier anti-vertigo treatment, and to document the onset of at least two episodes of vertigo. This
phase had a mean duration of 33 days (median: 28 and 29 days, in placebo and Meniett® groups, respectively). If patients had at
least two episodes of vertigo, they were included in the second phase.
Second phase: In this phase of the duration of six weeks (45 days) the patients were randomly assigned under double-blind
conditions to receive either the Meniett® device or a placebo device. Randomization was performed by blocks of four. Each
center received a block of four devices (2 Meniett® and 2 Placebo). If necessary, according to the rate of inclusion in a given
center, more blocks of four devices were attributed to the center. The boxes were randomly numerated and the physician did not
know their content, and had to distribute them to the patients. The placebo was identical in all aspects to the active device, but
did not generate pressure pulses. The patients were instructed to use the device three times daily for 15 minutes each, the
pressure pulsed waves were at a frequency of 6 Hz and a maximum pressure of 12 cm/H20. Patients were seen at 3 weeks (day
21 ± 3), and at the end of the six weeks period (day 42 ± 3).
Third phase: At the end of second phase, the Meniett® or the placebo devices were removed and the evolution of the number
of vertigo attacks was observed for an additional six-week period. Also in this phase the patients were seen at 3 weeks (day 21 ±
3), and at the end of the six weeks period (day 42 ± 3).
Assessment parameters
At each visit the permeability of the transtympanic tube was verified.
During the three phases, the patients were asked to record on a journal all the attacks that they had during the day, and their
duration, the patients had to score the vertigo attacks by mean of a visual analog scale (VAS) going from 1: very weak vertigo,
to 10: unbearable vertigo attack.
The main assessment criteria of the therapeutic impact of the Meniett® device were the total number of vertigo episodes lasting
at least 20 minutes during each study phase.
Two successive episodes were considered as distinct if they occurred at a minimum asymptomatic interval of 12 hours,
otherwise they were considered as a single episode.
The second parameter was the evolution of the impact of vertigo on daily life evaluated with the AAO-HNS scale.
RESULTS
Characteristics of the population
One hundred twenty-nine patients were enrolled and had a transtympanic tube insertion. Among them, 32 patients (26%)
showed the complete absence of vertigo during the first phase of six weeks.
Therefore, 97 patients were included in the second phase: after the randomization 49 were treated with the Meniett® device, and
48 with the placebo device. Considering the clinical data of the population (sex ratio, age, weight, height, body mass index,
blood pressure), the two groups were homogeneous.
The duration of Menière’s disease ranged from 0.22 to 24.5 months (mean 5 ± 0.81 months), and from 0.15 to 26.5 months
(mean: 7 ± 0.97 months), in placebo and Meniett® groups, respectively.
The number of vertigo episodes, including dizziness, during the previous six months was comparable in the Meniett® group (36
± 4.6, range: 4-180, median: 30) and in the placebo group (28 ± 3.0, range: 3-72, median: 23). The impact of vertigo estimated
by the patient on the AAO-HNS scale, was 4.3 ± 0.10 (range: 3-5, median: 4) in the placebo group, and 4.5 ± 0.093 (range 3-5,
median: 5) in the Meniett® group.
Evolution of the number of vertigo episodes > 20 minutes during the different phases
A decrease of the number of the vertigo lasting more than 20 min occurred in both groups in the second phase compared to the
first one, and persisted during the third phase when the devices were removed . In the placebo group the number of vertigo
episodes decreased from 4.3 ± 0.6 during the first phase, to 2.6 ± 0.5 after 6 weeks of treatment, and to 1.8 ± 0.8 after the third
phase.
Similar results were observed in the Meniett® group: 3.2 ± 0.4 episodes during the first phase, 2.5 ± after 6 weeks of Meniett®
treatment, and 1.5 ± 0.2 after the third phase.
A decrease of vertigo episodes was observed in both group if comparing the first phase to the end of the second phase, and if
comparing the episodes recorded after the first 21 days of the second phase and the third phase (Figure 2, Tukeys’s HSD post-
hoc test).
However, there was no significant difference between the 2 study groups at all the phases of the study (Two-ways ANOVA,
F=2.57 p=0.11).
Considering the individual evolution, a decrease of the number of vertigo episodes, was observed in both groups during the
second and the third phase, compared to the first phase. shows the number of patients that have improved, worsened, or that
were stable for each period of 21 days. No difference was found between the two groups (Fisher’s exact test), and overall the
10% of patients aggravated their symptoms, the 30% were stable, and the 60 % improved their symptoms. It should be noticed
that fivepatients interrupted the treatment after the end of the second phase (3 placebo, 2 Meniett®), and 15 during the third
phase (9 placebo, 6 Meniett®).
Evolution of short duration vertigo and dizziness
The number of the short duration vertigos (5-20 min), and the number of dizziness episodes (vertigos of less than 5 min
duration) remained stable in both groups during the three phases (Table 3). The decrease of the number of 20 min lasting vertigo
during the treatment and the run-out periods was clearly not associated to an increase in shorter vertigos or dizziness.
Impact of vertigo in daily life
Concerning the impact of vertigo on quality of life, whatever the treatment, Meniett® or placebo, the quality of life of the
patient was improved, and this, even after the treatment was removed, with no significant difference between the two groups of
patients.
DISCUSSION
This study demonstrates that patients with Menière’s disease could be improved in terms of number of vertigo episodes after placement
of transtympanic tube, and after Meniett or placebo treatment without significant difference between these two later groups.
The improvement of the symptoms was evidenced immediately after the placement of the transtympanic tube, indeed after the first
phase the 26% of patients were excluded from the study for absence of vertigo episodes. A transtympanic tube effect has been first
evidenced in guinea pigs , where the middle ear ventilation reduced the development of endolymphatic hydrops induced by the blockage
of the endolymphatic duct. The authors proposed that the inhibition of hydrops was due to pressure release into the middle ear and/or
improved oxygenation of the middle and inner ears. In patients with Menière’s disease, Barbara et al. evidenced a major effect of the
transtympanic tube, the number of vertigo decreasing from 9 to 1 after a 40-day period.
During the subsequent phase of the study an overall improvement in the number of vertigo episodes was evidenced, without difference
between the group treated with middle ear pressure therapy by Meniett®, and the group that received a placebo device. Moreover, this
improvement persisted about one month and half after the end of the treatment, and after the third phase, the 60% of all the patients
showed an improvement in symptoms, suggesting a positive effect of the transtympanic tube, and/or of the medical care in general.
These observations lead to pose some questions concerning the diagnosis of Menière’s disease. The clinical diagnosis of Meniere’s
disease is universally accepted to be based on the AOS-HNS criteria. Nevertheless an instrumental diagnosis of endolymphatic hydrops
can be realized by mean of electrocochleography (ECoG). Although for some authors the only reliable diagnosis of Meniere’s disease is
clinical , the symptoms of the disease are very variable and heterogeneous, and to assess the effectiveness of a device, an objective
instrumental finding concerning the condition of the inner ear appears to be necessary.
A weakness of the present study is the lack of an objective assessment of inner ear status at the inclusion phase, for example by
means of ECoG. Indeed the diagnosis of Menière’s disease was defined only by clinical parameters as recommended by AAO-
NHS, and we can hypothesize that some patients did not have an active endolymphatic hydrops.
Considering the whole population at the end of the protocol, 60% of them had a decrease in the number of long duration vertigo
episodes. This percentage can be considered high and may raise some issues for the patients’ selection.
The relationship between the middle ear, easily accessible, and the inner ear pressures changes in connection with
endolymphatic approaches has been the subject of several experimental and clinical studies. Most of them support the
hypothesis that continuous or intermittent pressure to the middle ear could prevent the development of endolymphatic hydrops
(in animal), or improve both the clinical symptoms and the electrophysiological hearing parameters in patients with Menière’s
disease. Nevertheless, the evaluation of the effectiveness of treatments for Menière’s disease incurs in considerable difficulties
because of the natural course of the disease, characterized by spontaneous remissions and placebo effect. This may explain the
different conclusion of several literature reviews concerning the Meniett® device, some of them assessing a positive effect of
this treatment, others the inefficacy of it.
Many randomized controlled studies were realized, in order to investigate the expected placebo effect. The first published study
reported improvement concerning frequency and intensity of vertigo and also hearing and electrocochleographic recordings in
31 patients compared to 25 who had a placebo device. Unfortunately, these very encouraging results were not reproduced in the
following studies. Gates et al studied 67 patients and reported less severe vertigo, fewer days with definite vertigo, and fewer
days lost from work, but no difference in hearing and electrocochleographic results between the two groups of patients.
One year later, Thomsen at al evidenced an improved functionality level in the 20 treated patients compared to the 20 who
received the placebo, but the difference in the frequency of the vertiginous attacks was clearly not significant. However, the
central issue is the selection criteria of the patients.
Gates et al. included medical treatment resistant patients and with a median duration of treatment of 4.5 years. The patients in
Thomsen’s study had variable disease duration, ranging from less than one year to 37 years with a median between 5 and 10. In
the present study, the patients had disease duration much shorter, less than two years.
One suggestion could be that local pressure treatment should be indicated, and effective, in case of well-established and resistant
disease, at an early stage.
CONCLUSION
The benefit of the treatment assessed in about the 60% of the patients of both study groups, Meniett® or placebo, strongly
suggests a positive effect of the medical management in patients suffering from Meniere’s disease, independently from the
treatment.
Nevertheless, because this effect persisted at the end of the active treatment phase, a pressure effect of the transtympanic tube
can be suspected.
Moreover, this effect has been rapidly evidenced in 32 patients who were not included after the first phase.
Further studies are needed to investigate this beneficial effect of the transtympanic tube and to determine patients that would
improve their symptomatology by this procedure.
Special attention is needed considering the heterogeneity of this disease in order to define the hydrops evolutivity.
Indeed, it is clear from this study that the clinical classification is not sufficient, electrophysiological data (ECoG, for example)
would be needed to more precisely select the patients.
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