Seminar
Menieres disease
Lancet 2008; 372: 40614
Department of Otolaryngology
Head and Neck Surgery,
Stanford University Medical
Center, San Jose, CA, USA
(H Sajjadi MD); and Department
of Otolaryngology Head Neck
Surgery, University of
Minnesota, Minneapolis, MN,
USA (Prof M M Paparella MD)
Correspondence to:
Dr Hamed Sajjadi, Department of
Otolaryngology Head and Neck
Surgery, Stanford University
Medical Center, 2577 Samaritan
Drive Ste 845, San Jose,
CA 95124, USA
otology@hotmail.com
406
Hamed Sajjadi, Michael M Paparella
Menieres disease is a chronic illness that aects a substantial number of patients every year worldwide. The disease
is characterised by intermittent episodes of vertigo lasting from minutes to hours, with uctuating sensorineural
hearing loss, tinnitus, and aural pressure. Although there is currently no cure, more than 85% of patients with
Menieres disease are helped by either changes in lifestyle and medical treatment, or minimally invasive surgical
procedures such as intratympanic steroid therapy, intratympanic gentamicin therapy, and endolymphatic sac surgery.
Vestibular neurectomy has a very high rate of vertigo control and is available for patients with good hearing who have
failed all other treatments. Labyrinthectomy is undertaken as a last resort and is best reserved for patients with
unilateral disease and deafness.
Introduction Head and Neck Surgery (AAO-HNS) established a
Prosper Mnire rst described this disease in 1861.1 His specic set of criteria for the diagnosis of Menieres
main contribution to its diagnosis was a description of disease (panel).9
the disease entity with episodic vertigo and ringing in the Few articles have been published on the epidemiology
ears; he challenged general terminology at the time that of Menieres disease. In 1973, Stahle and colleagues
named this disease apoplectic cerebral congestion, reported a prevalence of 46 cases per 100 000 population.10
implying a disorder of the brain. Mnire described these From 1975 to 1990, several studies from Japan, which
episodes of vertigo and uctuating hearing loss as being were undertaken for a Research Committee on Menieres
associated with the peripheral end organ of the inner ear Disease and a Committee on Peripheral Vestibular
rather than with the brain. He and other investigators2,3 Disorders, indicated a fairly constant prevalence of
called it glaucoma of the inner ear. 17 cases per 100 000 population.11,12 Kotimaki and
In 1927, Guild4 identied the endolymphatic sac as the colleagues13 analysed the Finnish population of 5 million
site of outow of endolymph in his study of guineapigs. people between 1992 and 1996 with the AAO-HNS
This study was a major insight into the mechanics of recommendations. They reported a prevalence of
endolymphatic ow in the inner ear. Later that same year, 43 per 100 000 and an average yearly incidence of 43 per
Portmann3 described his rst endolymphatic sac surgery 100 000 population.13
for the Menieres disease complex. Endolymphatic sac Most studies suggest a slight female preponderance of
surgery has remained the main non-destructive form of up to 13-times that of men.9 The disease seems to be
surgical treatment for Menieres disease since the much more common in adults in their fourth and fth
early 1900s. 1 year after Portmanns description of sac decade than in younger people, although it has been
surgery, Dandy5 proceeded with vestibular neurectomy, noted in children;14 Meyerho and colleagues15 noted a
trying to isolate the vestibular system from the brain and 3% prevalence of paediatric Menieres disease. A strong
thus cure patients of vertigo. positive family history exists in patients with Menieres
In 1943, Altmann and Fowler6 concluded that problems disease; several studies have indicated that up to 20% of
in production and absorption of endolymph can lead to family members have similar symptoms.14,1618 Menieres
Menieres disease. In a landmark study in 1967, Kimura7 disease also seems to aect more white people of
investigated the rst animal model with guineapigs and northern European descent than it does the African and
showed that blockage of the endolymphatic sac and duct black races.19,20
causes obstruction of endolymphatic outow, leading to
hydrops of the inner ear.
Search strategy and selection criteria
Epidemiology We searched Medline, ENT Rez, Pubmed, and the Cochrane
Menieres disease remains a dicult disease to diagnose, Library for publications in the past 10 years, with the terms
especially in the early stages when not all its symptoms Menieres disease and Endolymphatic sac, Gentamicin
might be present. Consequently, the incidence and middle ear perfusion, and Steroid middle ear perfusion. We
prevalence of the disease in any population is dicult to largely used materials published within the past 5 years but
ascertain.8 Frequently, patients with Menieres disease did not exclude older publications that were commonly
present to the emergency department with sudden onset referenced and highly regarded. We also searched the
of vertigo and are inaccurately diagnosed as having reference lists of articles identied by this search strategy and
labyrinthitis and discharged home.8 In early stages, selected those that we judged relevant. Several review articles
Menieres disease might present with only cochlear or book chapters were included because they provide
symptoms such as hearing loss and pressure or fullness comprehensive overviews that are beyond the scope of this
in the ear without true vertigo or even ringing in the ears. Seminar. Only references published in English were included.
In 1995, the American Academy of Otolaryngology
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Panel: The American Academy of OtolaryngologyHead
and Neck Surgery criteria for diagnosis of Menieres
disease (1995)
1 Recurrent spontaneous and episodic vertigo. A denitive
spell of vertigo lasting at least 20 min, often prostrating,
accompanied by disequilibrium that can last several days;
usually nausea or vomiting, or both; no loss of
consciousness. Horizontal rotatory nystagmus is always
present
2 Hearing loss (not necessarily uctuating)
3 Either aural fullness or tinnitus, or both
Certain Menieres disease
Denite disease with histopathological conrmation
Denite Menieres disease
Two or more denitive episodes of vertigo with hearing loss,
plus tinnitus, aural fullness, or both
Probable Menieres disease
Only one denitive episode of vertigo and the other
symptoms and signs
Possible Menieres disease
Denitive vertigo with no associated hearing loss or hearing
loss with non-denitive disequilibrium
A study reviewing ve generations of the same family
from Sweden showed a very strong familial trend for
Menieres disease.10 Nine of 25 family members showed
some problems of the inner ear, six of whom satised the
AAO-HNS criteria for diagnosis of Menieres disease.
Morrison21 studied 41 families in which at least one
member had the disorder. Those ndings suggested a
60% penetrance in an autosomal dominant pattern in
families with the disease, with strong anticipation,
meaning that an earlier age of onset and more severe
symptoms are detected in each successive generation
with the disease.
Histocompatibility antigens (HLA) have been
intensively studied by several investigators.22 Arweiler
and colleagues23 investigated 48 patients and detected a
90% prevalence of HLA-A2 in patients with a family
history, and a 75% prevalence in those without a family
history. These investigators propose a multifactorial
aetiology for Menieres disease, combined with a genetic
predisposition caused by mutations of the short arm of
chromosome 6. Furthermore, Paparella16 detected a
20% incidence of positive family history in patients with
Menieres disease in a review of 500 patients.
Pathophysiology
Menieres disease is characterised by intermittent
episodes of vertigo lasting from minutes to hours, with
uctuating sensorineural hearing loss, tinnitus, and
aural pressure.24 It has been classied into typical
Menieres disease, with all the cochlear and vestibular
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Seminar
symptoms, and atypical Menieres disease, with either
cochlear symptoms (eg, hearing loss, tinnitus, aural
pressure) or vestibular symptoms (eg, vertigo alone with
aural pressure but no hearing loss or tinnitus).25 The
primary histopathological correlate is endolymphatic
hydrops. Paparella used the notion of lake-river-pond to
explain the occurrence of malabsorption of endolymph
leading to hydrops.26 This notion describes the
endolymphatic sac as a pond, with the vestibular aqueduct
(the river) connecting it to the endolymphatic uid space
that is like a lake. When there is an obstruction near the
endolymphatic sac or duct, a backlog of endolymphatic
uid is created, leading to hydrops.
Histological studies have suggested that endolymph is
primarily produced in the stria vascularis, and some
production also occurs in the planum semilunatum and
dark vestibular cells.27 Endolymph is then absorbed in the
endolymphatic duct and sac through an active transport
mechanism. Longitudinal ow proceeds slowly, and
radial ow rapidly, into the endolymphatic sac.27 Gibson
and Arenberg28 suggested that because of obstruction of
the endolymphatic sac, hormones such as saccin might
be produced to increase production of endolymph to
overcome the obstruction. Furthermore, the sac might
also produce glycoproteins that osmotically attract
endolymph towards it. As a result of overow of
endolymph behind the obstruction, the obstruction
might be relieved and the sudden outow across the sac
could lead to vertigo. Kimura and colleagues29 devised an
animal study showing that obliteration of the ductus
reuniens causes cochlear hydrops.
Many histological features have been seen in patients
with Menieres disease by use of temporal-bone studies.
These studies include ndings of perisaccular brosis,30
atrophy of the sac and loss of epithelial integrity,27
hypoplasia of the vestibular aqueduct,31 and narrowing of
the lumen of the endolymphatic duct.32 We have shown
that the sigmoid sinus is signicantly anteriorly and
medially displaced in patients with Menieres disease
compared with healthy controls.33 Our study suggested
that the forwardly located lateral sinus can cause vascular
compression of the endolymphatic sac leading to
obstruction and hydrops, which would be a genetic
predisposition of an anatomical abnormality. Revisional
surgery on the endolymphatic sac has shown that surgical
removal of perisaccular brosis can allow patients who
had initially good results with an endolymphatic sac
enhancement (ESE) to improve and reduce their
symptoms.34,35
Revision of ESE surgery has contributed signicantly to
our knowledge of the pathophysiology of this disease.
Revisional ESE is undertaken for patients who have
beneted from the primary endolymphatic surgery for at
least 1 year postoperatively, and then have recurrence of
their symptoms. Several investigators have noted
substantial pathological ndings during repeat surgery,
once ESE has been done.3436 These ndings have included
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 Seminar
a hypoplastic mastoid air-cell system with perisaccular
brosis, discolouration of the silastic sheathing inserted
in the primary procedure, and granulation tissue lling
the mastoid and the perisaccular space, which all create
compression leading to saccular obstruction. Complete
decompression of the sigmoid sinus and the mastoid
cavity is the most important surgical contribution to
correction of the symptoms of Menieres disease.
Diagnosis
The clinical picture of Menieres disease includes
uctuating sensorineural hearing loss accompanied by
aural pressure, tinnitus, and episodic vertigo. The
hallmark of the disease is its uctuation, waxing, and
waning of symptoms. Typical Menieres disease includes
all symptoms; the episodic vertigo lasts from several
minutes to hours, with positional vertigo in between and
during attacks. Furthermore, almost all patients note a
sense of pressure or fullness in the ear and various forms
of tinnitus. Most patients develop unilateral symptoms,
and a large proportion might develop bilateral disease
many years after the onset of the unilateral symptoms.
Several studies have reported the rate of bilateral
Menieres disease to be as high as 50% after many years
of the initial diagnosis.37
The AAO-HNS subcommittee on Hearing and
Equilibrium and Its Measurements has proposed various
consensual statements to reach a denition of Menieres
disease (panel).25 Menieres disease remains a clinical
diagnosis; a detailed history and a complete physical
examination are necessary for a diagnosis to be made.
Once the history and physical examination have been
completed, the essential tests needed to guide clinicians
to make the diagnosis include a full audiometric
assessment and possibly video nystagmography or
electonystagmographic testing with bithermal caloric
evaluation. Electrocochleography is an optional test to
augment the diagnosis of Menieres disease. In all
unilateral cases, MRI of the brain with views of the
internal auditory canal with and without contrast is
needed to rule out retrocochlear pathological disorders
that can present with sensorineural hearing loss, tinnitus,
and vertigo. CT-scanning of temporal bone is of little
value in diagnosis of Menieres disease. Standard lateral
mastoid radiographs could be obtained to aid diagnosis
by documenting the forward location of the sigmoid
sinus, which is seen in almost all patients with this
disease.37
Most patients with Menieres disease present with an
up-sloping low-frequency sensorineural hearing loss
that, with time and after many uctuations, could lead to
a at sensorineural hearing loss. In very few patients, a
slight conductive component to the hearing loss might
also be noted initially.36 This conductive loss is dicult to
explain, but has led to incorrect diagnoses of Eustachian
tubal dysfunction in patients with early presentation of
Menieres disease. Serial audiograms are very helpful in
408
diagnosis, by documenting uctuation of sensorineural
hearing loss. Paparella and several investigators38,39 have
recorded a so-called peak pattern of audiographical
ndings with sensorineural hearing loss of low
frequencies, with better hearing at 2000 Hz and worse
hearing at frequencies greater than 2000 Hz.
The most important nding in vestibular testing of
patients for Menieres disease is the unilateral vestibular
hypofunction seen on bithermal caloric testing.40
However, up to 50% of patients with Menieres disease
might still have completely normal nystagmography and
bithermal caloric assessments, even with incapacitating
vertigo.41 In patients who are unable to undergo MRI
because of installation of a pacemaker or other reasons,
auditory brainstem response audiometry can provide a
less accurate alternative to rule out retrocochlear
pathological disorders.41
Patients who present with incapacitating vertigo,
sensorineural hearing loss, and all the symptoms
suggestive of Menieres disease should still undergo
routine haematological tests to rule out more common
causes of vertigo and ill feeling. These tests include a
complete blood count to rule out anaemia, leukaemia, and
other disorders, as well as a sedimentation rate to check
for any occult inammatory processes. Tests of the thyroid
functions; cholesterol, lipids, and triglycerides; a fasting
blood glucose; and haemoglobin A1C are suggested to rule
out diabetes and other lipid and cholesterol abnormalities.
All patients should have a uorescent Treponema
antibody-absorption test for syphilis. These tests are
helpful to assess the general health of patients presenting
with such incapacitating symptoms, and to avoid missing
other medical problems that are correctable.42
Migraine-associated dizziness is a fairly new diagnosis
that has several clinical similarities to Menieres disease,
especially to the vestibular Menieres variant. 43 A detailed
history of headaches with and without concomitant
dizziness is very important for dierentiation between
these illnesses. Patients with migraines frequently have
an aura with their headaches, as well as nausea,
photophobia, phonophobia, and visual scintillating
scotoma. Patients with migraine-associated dizziness
usually have normal hearing or symmetrical, incidental,
non-uctuating hearing loss.44 Aural pressure, which is a
hallmark of patients with Menieres disease, is mostly
absent in those with migraines. Previously, many patients
with migraine-associated dizziness might have been
inadvertently diagnosed as having Menieres disease,
thus aecting results of treatment outcome. Migraine
associated dizziness should be recognised and
dierentiated from Menieres disease early in the clinical
work-up phase.
Medical and surgical management
Several medical and surgical remedies have been
oered to patients with Menieres disease over the past
150 years. The plethora of medical and surgical therapies
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Diagnosis conrmed
All patients
Low salt diet,
avoidance of caeine,
chocolate, alcohol,
tobacco products
36 month trial Acute attacks
Diuretics Oral, intramuscular, or
intratympanic steroids
Treatment failure
Meniett device
Treatment failure
Endolymphatic sac enhancement surgery
Treatment failure
Gentamicin perfusion
Treatment failure
Vesticular neurectomy
Treatment failure
Labyrinthectomy
Figure: Treatment algorithm for Menieres disease
signies that no one eective treatment is available for
these patients. However, most will be helped by a
combination of medical therapy, psychological
counselling and reassurance, and lifestyle and dietary
changes.
The cure for this disease is yet to be discovered; it
could lie in genetic re-engineering that might need a
functioning labyrinth for an eective outcome.
Therefore, destructive procedures that might preclude
implementation of a possible cure for patients in the
future should be avoided. For us to continue to be
conservative by preserving the structures of the inner
ear both chemically and physically and working at
alleviation of the patients symptoms without destroying
these structures, as much as possible, would be
prudent.
The medical and surgical options available to treat
patients with Menieres disease should be oered
according to the severity of the patients symptoms and
failure to respond to appropriate therapy. The following
options are listed in order of disease severity, and the
gure gives a treatment algorithm.
Lifestyle changes
A strong association with seasonal allergies and
circulating immune-complexes exists in patients with
known diagnoses of Menieres disease.45,46 Simple
allergy-avoidance and changes in lifestyle could alleviate
some of the allergy symptoms associated with this disease
and allow for improved quality of life for patients. Some
studies have reported a signicant reduction (up to 62%)
in both frequency and severity of attacks of vertigo in
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patients with Menieres disease after starting
immunotherapy for allergies.47
Patients with symptoms of Menieres disease react
adversely to consumption of large quantities of caeine,
chocolate, alcohol, and salt. However, the actual
mechanism and pathophysiology of this adverse reaction
is unknown. Some patients might actually have an allergy
to some of these items. Therefore, food allergies should
be investigated in patients with Menieres disease and
should be treated and avoided as much as possible.
All patients with Menieres disease are encouraged to
reduce their salt intake to a maximum of 2 g per day, and
to 15 g per day if tolerated. They are also asked to avoid
all sources of caeinated products, to reduce their intake
of chocolate, and to avoid all tobacco and alcoholic
products as much as possible. As early as 1934,
Furstenberg showed the relation between sodium
retention and Menieres disease, and recommended a
substantial reduction in intake of sodium.48 Several other
investigators have also reported this relation and shown
the ecacy of diuretics for reduction of these
symptoms.49,50
Diuretics
Recent studies have suggested no relation between use of
diuretics and Menieres disease; however, we believe that
most of the time diuretics are a fairly safe option and are
oered to all patients.51 Once diuretics are used, a repeat
blood test should be done a week later to ensure that the
concentration of potassium in the blood has not
decreased; even though potassium-sparing diuretics are
frequently used, there is always a slight chance of loss of
potassium because of diuretic use. The most commonly
used diuretic is a combination of hydrochlorothiazide
and triamterene. Patients who are allergic to sulpha could
use acetazolamide or chlorthalidone.42,52
Steroids
Steroid therapy has been used in treatment of acute and
chronic symptoms of Menieres diseaseboth oral
steroids and intratympanic steroid injections have been
tried. Trials of steroids could be of substantial value to
most patients since a large number with Menieres
disease have allergies and also because of problems with
immune-mediated occurrences. For acute attacks,
intramuscular or intravenous methylprednisolone can be
used to control the severe hearing loss and vertigo
followed by oral prednisone at a dose of 1 mg/kg, given
on a daily basis for 1014 days before a slow tapering dose
can take eect for the next 2 weeks.
If patients do not respond to the oral steroids and their
hearing continues to deteriorate, intratympanic methyl-
prednisolone or dexamethasone injections can be given.
Patients who have a pronounced response to oral or
intratympanic steroids might have other immune-
mediated inner-ear diseases and should have a complete
work-up for autoimmune problems. Consultation with a
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 Seminar
rheumatologist who is interested in taking care of such
patients can be very benecial.42 In a randomised and
blinded controlled trial at a tertiary referral centre,
Morales and colleagues53 randomly assigned patients to
oral acetazolamide or oral acetazolamide and prednisone
and assessed their responses. The investigators ndings
suggested a signicant reduction in patients refractory
vertigo and tinnitus with oral prednisone therapy, but
they noted no change in patients aural fullness or
hearing.53
Intratympanic dexamethasone injection has been used
by several investigators to control symptoms of vertigo
and hearing loss in patients with Menieres disease. In a
2-year prospective placebo-controlled double-blinded
randomised trial, Garduno-Anaya and colleagues54
studied the eect of dexamethasone perfusion of the
inner ear in patients with unilateral Menieres disease.
They concluded that dexamethasone at 4 g/L injected
into the ear transtympanically under local anaesthesia
showed an 82% complete control of vertigo compared
with 57% control in the placebo group. They noted a
48% subjective improvement in tinnitus, 35% improve-
ment in hearing loss, and 48% improvement in aural
fullness compared with signicantly lower proportions
in the control group.54
Since most patients with Menieres disease can present
with sudden hearing loss, intratympanic steroids might
also be of benet to those with sudden hearing loss in
Menieres disease.5559 In a study to assess the results of
intratympanic steroid therapy with dexamethasone in
patients with cochlear hydrops, Hillman and colleagues60
concluded that hearing improved in 40% of patients, was
worse in only 4%, and did not change in 56% who
received intratympanic steroids for hydrops.
Gentamicin transtympanic perfusion
Destructive treatments can be used in patients with
intractable vertigo. One such treatment, with intra-
tympanic aminoglycosides, was rst used to treat unilateral
intractable Menieres disease more than 30 years ago.61
The present drug of choice seems to be gentamicin, which
causes direct damage to both the sensorineural epithelium
and the dark cells of the labyrinth, thus aecting vestibular
function and cochlear function. Nedzelski and col-
leagues62 presented his preliminary report on 33 patients
given intratympanic gentamicin between 1988 and 1989
for intractable vertigo. Hearing improved in 36% of
these patients, was unchanged in 39%, and worsened
in 25%. He reported an 897% control of vertigo. Parnes
and Ridell61 also showed a similar proportion of hearing
loss in their preliminary series of patients.
Driscoll and colleagues63 proposed a low-dose single
treatment with gentamicin for Menieres disease. He
concluded that low-dose intratympanic gentamicin was a
safe and simple procedure that was eective in the
control of denitive episodes of vertigo in most patients
with unilateral Menieres disease; control of vertigo was
410
obtained in 84% of patients with a low incidence of
hearing loss. McFeely and colleagues64 studied
25 consecutive patients given intratympanic gentamicin
for Menieres disease between 1992 and 1996 and
reported a 20% prevalence of pronounced sensorineural
hearing loss and 8% prevalence of total deafness after
gentamicin treatment. They also reported an
88% complete control of vertiginous spells with another
12% substantially controlled. Kaasinen and colleagues65
investigated 93 patients with intractable Menieres
disease who were given serial injections of intra-
tympanic gentamicin and followed up for 2 years. They
reported a complete resolution of vertigo in 81% of
patients, with an 11% prevalence of total sensorineural
hearing loss. The investigators concluded that this
method was a safe and eective way to treat vertiginous
attacks in patients with Menieres disease.
Minor66 devised a protocol using transtympanic
gentamicin injections for patients with vertigo in
Menieres disease, titrating it to development of signs of
unilateral vestibular hypofunction, as shown by total
loss of caloric stimulation response on video
nystagmagraphy or electrode nystagmagraphy tests. He
reported a very low prevalence of sensorineural hearing
loss in only one patient (3%) and a 91% control of
vertigo.66 Initial studies had recommended a complete
ablation of vestibular function with gentamicin to obtain
successful results in patients with vertigo.67 However,
results from studies now recommend that a partial
ablation could be just as eective with less risk of
sensorineural hearing loss.68 The main risk of
intratympanic gentamicin treatment for vertigo is the
sensorineural hearing loss and associated disequilibrium,
which are common complaints after this treatment.
Many studies suggest that a complete ablation of
function is not necessary for control of vertigo, and that
partial ablation could reduce the risk of hearing loss to
just 2021%.68
An important indicator for intratympanic gentamicin
therapy seems to be the control of vertigo in non-
serviceable earsie, speech reception threshold worse
than 50 db and speech discrimination score of less than
50%or in patients who have failed endolymphatic sac
surgery.63 Transmastoid labyrinthectomy has traditionally
been oered for non-serviceable ears in patients with
Menieres disease. This method has been the gold
standard, and it is very eective in eradication of vertigo
in more than 94% of patients. However, transtympanic
gentamicin therapy can provide a minimally-invasive
ambulatory means with low morbidity and few
side-eects, which is very cost eective for management
of vertigo in these patients with non-serviceable ears.69
Marzo and Leonetti70 have also shown the ecacy of
intratympanic gentamicin therapy for patients who have
failed endolymphatic sac surgery, thus reducing the need
for vestibular neurectomy in those with intractable
disease.
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Colletti and colleagues71 reported auditory results after
209 patients had undergone vestibular nerve section and
compared these ndings with 24 patients who had
received intratympanic gentamicin injections. The
auditory data indicated a slight drop in scores for speech
discrimination in those who had vestibular nerve
sections, from 85% to 82% postoperatively. However, in
the group who received gentamicin, scores dropped
from 87% to 65% after treatment. This signicant
dierence between the two groups suggested a much
higher rate of sensorineural hearing loss in the
gentamicin group than in those who had vestibular
neurectomy. The control of vertigo in patients who had
vestibular neurectomy was 958% compared with 75% in
those who received gentamicin. Patients have to be
counselled about the substantial risk of sensorineural
hearing loss and disequilibrium that might result after
gentamicin therapy. Furthermore, they should be
informed that intratympanic gentamicin therapy is a
chemical ablation of the vestibular system, and as such it
remains a destructive procedure.
Pressure pulse treatment
A fairly new non-invasive method for treatment of
intractable vertigo in patients with Menieres disease has
been positive pressure provided through a pulse-generator
into the ear canal.72,73 The device for this procedure is
called a Meniett (Medtronic Inc, Jacksonville, FL, USA).
Odkvist and colleagues74 compared the Meniett device
with a placebo (a similar device without any pressure
delivered). They noted a signicant reduction in the
frequency and intensity of vertigo, tinnitus, and aural
pressure in the group using the Meniett device compared
with the placebo group.
Densert and Sass75 studied 37 patients with a diagnosis
of denitive Menieres disease and active vestibular
symptoms. They concluded that the pressure treatment
provided by the Meniett device was eective in control of
vertigo in a large number of patients with intractable
Menieres disease. No signicant side-eects were
associated with use of the Meniett. However, Boudewyns
and colleagues76 have shown that the long-term ecacy
of the Meniett device is poor.
Endolymphatic sac surgery
Endolymphatic sac surgery for Menieres disease was
rst proposed by Portmann3 80 years ago; it has stood the
test of time and continues to be oered to patients with
Menieres disease, who receive substantial improvement
in hearing and attacks of vertigo. The endolymphatic
subarachnoid shunt procedure was made common
practice by William House77 in 1962, and the
endolymphatic mastoid sac-enhancement surgery by
Paparella and co-workers78 in 1980. The endolymphatic
sac to mastoid enhancement operation has proven safe
and eective in alleviation of intractable vertigo in more
than 76% of patients.79,80 Paparella and Fina81 reported
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75% total elimination of vertigo and 90% improvement
of vertigo after sac enhancement surgery.
The main technical feature of endolymphatic sac
surgery has been a wide decompression of the sigmoid
sinus, localisation of the endolymphatic sac, and
insertion of a custom-made Silastic sheeting along with
Silastic spacers in the sac and perisaccular area. The
risk of sensorineural hearing loss after endolymphatic
sac decompression is less than 2%. Paparella and Fina81
investigated more than 2000 ESE surgeries that were
undertaken over 35 years and noted an incidence of
revision of only 5%, usually 34 years later. Preservation
of hearing was maintained in more than 98% of
patients, and up to 40% of patients had better hearing
outcomes after ESE than they did before the procedure.
Only 2% of patients sustained serious sensorineural
hearing loss after ESE.
However, Thomsen and colleagues82 concluded that
ESE surgery had no advantages compared with a placebo
operation.82 Although the research has been cited by
sceptics of ESE surgery extensively, the investigators
conclusion was that both the ESE surgery group and the
placebo group had 70% success in controlling vertigo
attacks. Their follow-up study in 1986 stated the same
conclusion.83 In our opinion this study was awed in
several areas. First, it was a very small study of only
30 patients. Second, patients in the placebo group had a
complete mastoidectomy under general anaesthesia.
Many factors during general anaesthesia can aect body
haemodynamics and uid balance, thus aecting the
composition of inner-ear uid in patients with Menieres
disease. Furthermore, a complete mastoidectomy is not a
placebo treatment, since this procedure might have
inadvertently decompressed the tight Trautmanns
triangle and improved endolymphatic sac aeration and
function. We have shown that the main feature of ESE
surgery is the decompression of the sigmoid sinus, which
leads to improved endolymphatic sac decompression.80
The most important part of ESE surgery is a successful
complete mastoidectomy, which was oered to patients
in the placebo group in Thomsens study.
Ostrowski and Kartush84 investigated the long-term
ecacy of ESE-vein decompression surgery on patients
with classic Menieres disease. The investigators reported
a 72% long-term improvement in control of vertigo and
concluded that benecial long-term outcome of this
method supports its continued use as a rst-line treatment
option in patients with intractable Menieres disease.
Huangs study85 of more than 3000 cases indicated a
90% chance of achieving complete or substantial control
of vertigo in the short term (over 3 years).
Revision of endolymphatic sac surgery has been done
on patients who have initial successful results after
primary endolymphatic sac surgery. In 1988, we reported
an incidence of revised cases of endolymphatic sac
surgery of 7%.86 A further study by Paparella87 also
corroborated that revision of this procedure is rarely
411
 Seminar
needed and that ESE surgery has excellent results in
control of recurrent attacks of vertigo in patients who
have initial successful results from the primary surgery
complete control of vertigo was reported in 21 of
22 patients who underwent revision of ESE, with the
remaining patient needing a vestibular neurectomy.
The safety of ESE surgery has also been established in
elderly patients with Menieres disease.88 In 62 patients
aged 65 years and older who underwent a total of 78 ESE
surgeries, no signicant complications, sequelae, or
perioperative deaths were recorded. The investigators
recorded a prevalence of 16% of major complications,
mainly cardiac arrhythmia. 77% of the elderly patients
undergoing ESE had complete resolution of their vertigo
for up to 2 years after surgery.
Vestibular nerve section
Jackler and Whinneys review89 of surgery on the
VIII cranial nerve indicated signicant uctuations in the
degree of interest in vestibular nerve section during the
20th century. In the mid-1900s, section of the VIII nerve
that was made common practice by Dandy90 was largely
replaced by the endolymphatic sac procedure and
labyrinthectomy.91 There was renewed interest in
vestibular nerve section after House introduced the
middle-fossa vestibular neurectomy in 1961.92 Investi-
gators such as Fisch and Glasscock and colleagues9395
modied Houses middle-fossa approach to include
inferior vestibular neurectomy for improved control of
vertigo. Silverstein and Norrell96,97 described the rst
retrolabyrinthine vestibular nerve section for Menieres
disease. However, the retrolabyrinthine approach proved
to be dicult because of the forward location of the
sigmoid sinus and diculty in accessing the lateral aspect
of the internal auditory canal for patients who had poor
cleavage between the vestibular and cochlear nerves.
Silverstein and others98 modied the vestibular nerve
section to include a retrosigmoid/internal auditory canal
approach, in 1985. This modication proved to be
eective in exposure of the vestibule-cochlear cleavage
and in providing access to the cerebellopontine angle,
and later this technique replaced the retrolabyrinthine
method. Silverstein proposed a combined retrosigmoid-
retrolabyrinthine vestibular nerve section that ensured a
complete cure of vertigo in about 85% of patients and a
substantial improvement in another 7%.99 Preservation
of hearing remained excellent, with only 20% of patients
showing a slight change in levels of hearing compared
with levels before surgery, and up to 4% showing
signicant hearing loss. Combined retrolabyrinthine/
retrosigmoid vestibular nerve section has remained the
gold standard in vestibular neurectomy procedures.99
However, at most otological centres, vestibular
neurectomy is undertaken far less now than it was in the
mid-1980s. Eective medical treatment and dietary
control, combined with intermittent use of oral steroids
and middle-ear perfusion of steroids or gentamicin has
412
substantially reduced the number of patients with
intractable vertigo needing vestibular neurectomy.
Vestibular rehabilitation
Vestibular rehabilitation is a form of physical therapy
designed to improve vestibular function and mechanisms
of central adaptation and compensation. It can be quite
successful in helping patients prevent the signicant
sequelae of vestibular loss and vertigo; vestibular adapta-
tion exercises to prevent falls have proven to be particularly
eective. However, the treatment is only successful for
patients who have stable, non-uctuating vestibular loss.100
Conclusion
Menieres disease continues to aict hundreds of
thousands of patients every year on a global scale. Patients
of all ethnic and racial backgrounds have been aicted
with this chronic illness. It is true that we still do not
have a cure for this disease, as with many other illnesses
in medicine. However, substantial improvements have
been made over the centuries in dealing with this illness,
especially in the past decade, and several safe and eective
medical and surgical therapies are now available to help
patients cope with the disorders sequelae. Physicians
treating patients who have Menieres disease need to
remain optimistic and convey a positive attitude when
dealing with patients aicted with this illness.
Conict of interest statement
We declare that we have no conict of interest.
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