2. Prosper Menière (18 June 1799 – 7
February 1862) was a French doctor
who first identified that the inner ear
could be the source of a condition
combining vertigo, hearing loss and
tinnitus, which is now known as
Ménière's disease (MD)
Menière, P. Mémoire sur les lésions de l’oreille interne donnant
lieu à des symtômes de congestion cérébrale apoplectiforme.
Gaz. Med. Paris 16, 597–601 (in French) (1861).
3. INTRODUCTION
MD is a complex, multifactorial disease of the inner ear that causes
spontaneous episodes of VERTIGO (the sensation that you or your
environment is spinning), FLUCTUATING HEARING LOSS , tinnitus (a
ringing noise in the ears) and AURAL FULLNESS (a feeling of pressure in
the ear).
7. • The membraneous labyrinth contains endolymph and the bony
labyrinth contains perilymph, both in the vestibule and in the cochlea.
• The vestibule includes two otolith organs (the saccule and the
utricle), which are sensitive to linear acceleration, and three
semicircular canals, which are sensitive to rotational acceleration
(head rotation).
• The spiral ganglions and the Scarpa ganglions contain bipolar neurons
connected to sensory cells in the cochlea and the vestibular
apparatus, respectively.
8.
9. • The cochlea consists of the scala vestibuli and scala tympani, which
are filled with perilymph, and the scala media, which is filled with
endolymph.
• The key sensory organ is the organ of Corti, which contains the inner
hair cells, the outer hair cells and supporting cells.
• The stria vascularis produces endolymph. The endolymphatic duct
and sac are thought to be involved in the reabsorption and regulation
of endolymph.
11. A characteristic feature often observed in MD is endolymphatic
hydrops (EH), which is an excessive accumulation of endolymph in the
cochlea and the vestibular system in the inner ear.
A potential explanation for the accumulation of endolymph is disturbed
fluid homeostasis
The cause of EH and the relationship between EH and MD are still
unclear.
Recent evidence suggests that EH has a causal relationship with MD,
but that it requires additional cofactors to become symptomatic.
12. Migraine is considered to be one of the most important cofactors in MD
In most patients, the clinical symptoms of MD present after a considerable
accumulation of endolymph has occurred.
Thus, EH can be symptomatic or asymptomatic, whereas MD is by
definition associated with symptoms.
MD can be unilateral or bilateral. Unilateral MD refers to MD with
symptoms arising from only one ear, although this does not exclude the
possibility that the other ear has asymptomatic EH.
13. • Its diagnosis is complex
• Classification methods have evolved over time and are often based
on a combination of several symptoms
• The diagnostic criteria for MD defined by the American Academy of
Otolaryngology–Head and Neck Surgery (AAOHNS) in 1995.
• This classifies MD into different subtypes: certain, definite, probable
and possible MD.
• The diagnosis of certain MD requires the confirmation of EH by
histopathology of the temporal bone taken after death
14. AAO-HNS DIAGNOSTIC CRITERIA 1995
Certain Menière’s disease
• Definitive Menière’s disease plus histopathologic confirmation
Definite Menière’s disease
• Two or more definitive spontaneous episodes of vertigo lasting 20
minutes or longer
• Audiometrically documented hearing loss on at least one occasion
• Tinnitus or aural fullness in the treated ear
• Other causes excluded
15. Probable Menière’s disease
• 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
Possible Menière’s disease
• Episodic vertigo of the Menière type without documented hearing loss, or
sensorineural hearing loss fluctuating or fixed, with disequilibrium but
without definitive episodes
• Other causes excluded
16. Cochlear and vestibular Meniere’s disease
defined by the AAOO in 1972
• Cochlear Meniere’s disease (MD), or MD without vertigo, is
characterized solely by a fluctuating and progressive sensorineural
deafness with all auditory test results typical of MD.
• Many patients notice a fullness in the ear coincident with a sudden
drop in hearing. Some patients subsequently develop the definitive
dizzy spells and the qualifying term cochlear is discarded.
17. • Vestibular MD, or MD without deafness, is characterized solely by
the definitive spells of vertigo.
• This is more difficult to diagnose as there is no objective finding
between spells. The diagnosis may be accepted on the exclusion of
other diseases. Some patients subsequently develop deafness and
the qualifying ‘vestibular’ is dropped.
18. 2015 proposed criteria of Meniere’s disease
Criteria proposed by the Classification Committee of the Barany Society, the Japan Society for Equilibrium Research, the European Academy of
Otology and Neurotology, the Equilibrium Committee of the American Academy of Otolaryngology–Head and Neck Surgery and the Korean
Definite Meniere’s disease
• At least two spontaneous episodes of vertigo, each lasting from 20
minutes to 12 hours
• Audiometrically documented low-frequency to medium-frequency
sensorineural hearing loss in one ear, defining the affected ear on at
least one occasion before, during or after one of the episodes of
vertigo
• Fluctuating aural symptoms (hearing, tinnitus or fullness) in the
affected ear
• Not better accounted for by another vestibular diagnosis
19. Probable Meniere’s disease
• At least two episodes of vertigo or dizziness, each lasting from 20
minutes to 24 hours
• Fluctuating aural symptoms (hearing, tinnitus or fullness) in the
affected ear
• Not better accounted for by another vestibular diagnosis
20. Epidemiology
• The prevalence of MD was estimated as 0.27% in the United Kingdom
• A study in the United States reported an estimated prevalence of
0.19%
• In earlier studies, the estimated prevalence varied from 17 to 513
cases per 100,000
• MD is regarded as a disease of middle age. The mean age of onset of
MD peaks at 40–50 years; 10% of patients with MD had a disease
onset at ≥65 years of age
21. Cumulative age
distribution of
onset of
symptoms in
patients with
Meniere’s
disease. The
mean age at
onset of
symptoms was
estimated to be
44.0 years on the
basis of data from
22. Mechanisms / pathophysiology
• MD is a complex, heterogeneous disorder in which numerous
underlying factors interact, including anatomical variations in the
temporal bone, genetics, autoimmunity, migraine, altered
intralabyrinthine fluid dynamics and cellular and molecular
mechanisms.
24. • Endolymphatic hydrops
• EH is characterized by an accumulation of fluid (endolymph), leading
to an expansion of the endolymphatic space.
• The progression of Meniere’s disease is associated with the
advancement of EH.
• The thin membrane bordering the endolymph and the perilymph is
flaccid.
• When a rupture of the membraneous labyrinth and subsequent
collapse of the endolymphatic space is observed at some point in the
inner ear, EH is usually observed in other parts inside the inner ear.
25. • One of the earliest and most important findings IS that of gross
distension of the endolymphatic system in the inner ear in patients
with MD.
• Studies assessing the distribution of EH in specimens obtained after
death from patients with MD revealed the universal involvement of
structures of the inferior parts of the inner ear (the saccule and the
cochlea), with less-frequent involvement of the superior sections
(the utricle and the semicircular canals)
26. • Exaggerated narrowing of the isthmus of the endolymphatic duct is a
histopathological feature more commonly observed in the temporal
bone of patients with MD.
• it remains unclear whether EH results from the overproduction or
under-resorption of endolymphatic fluid.
• Histopathological evaluation of the diseased cochlea shows distension
of the scala media with ballooning of Reissner’s membrane into the
scala vestibuli
27. • damage to ganglion cells rather than damage to sensory hair cells is
directly associated with the initiation and progression of symptoms.
• the scarcity of samples from patients with confirmed clinical MD has
propelled the scientific community to develop animal models to study
the pathogenesis of this disease.
28. Experimental models of MD
• Guinea pig models of EH mirror the human condition in that a vast
decrease in the diameter of the eighth cranial nerve occurs, suggesting
that MD is primarily a neuronal pathology.
• these studies have shown that EH causes a profound loss of spiral ganglion
cells in the apical region of the cochlea; the magnitude of the loss is
correlated with the severity of EH.
• These studies suggest that early functional or biochemical disturbances
lead to progressive cochlear and vestibular dysfunction, but the exact
mechanisms are currently unknown
29. • Quantitative studies show a topographical pattern of spiral ganglion
cell loss (that is, starting at the apex of the cochlea and moving
towards the base); this pattern mirrors the progression of EH (apex to
base) .
• Targeting neurotoxicity might be a promising avenue for the
treatment of MD. For example, systemic treatment with riluzole (a
glutamate release inhibitor) and dimethyl sulfoxide (a free radical
scavenger) slowed hearing loss in the surgical model of MD in guinea
pigs
30. • One other potential mechanism of EH progression is linked with the
vasopressin type 2 receptor (V2R), a water channel protein regulated
by vasopressin that controls fluid homeostasis in the inner ear.
• Some studies have shown that patients with MD have increased
plasma levels of vasopressin as well as increased V2R mRNA
expression in the endolymphatic sac
31. Clinical symptoms
• Symptoms can evolve during the course of the EH disease, either
spontaneously or as a response to treatment.
• Although hearing loss is correlated with the extent of EH in most
patients, this relationship is complex as hearing can be relatively well
preserved despite prominent EH.
• The association of tinnitus and vertigo with EH is not evident owing to
insufficient data.
32. • The occurrence of recurring episodes of spontaneous vertigo is the main
feature of MD and it is present in 96.2% of patients (Paparella and Mancini,
1985).
• Vertigo is the most disabling symptom, commonly described as spinning,
exacerbated by head movements, and accompanied by nausea, vomiting,
and sweating.
• Spells of vertigo last several hours, and when they subside patients
complain of unsteadiness for several days. These spells are often
preceded by tinnitus, aural fullness, and a decrease in hearing in the
affected ear.
• Some patients report sudden falls with no previous warning or provocative
factor, and without vertigo, loss of consciousness, or other neurologic
symptoms. These episodes are named otolithic crises of Tumarkin
33. • Hearing loss is associated with vertigo attacks in 77% of patients
(Lopez-Escamez et al., 2014)
• The basilar membrane is wider and softer in the apex than in the
base of the cochlea. As a consequence, distension of the membranes
in EH start within the apex, as does hearing loss.
• Hearing loss associated with MD thus begins with low frequencies.
The threshold of low-tone and middle-tone hearing can indirectly
reflect the severity of EH in the cochlea.
• It is fluctuating in the first years.
34. • as the disease progresses, hearing worsens with each crisis and it
does not return to the previous level.
• Eventually, deafness becomes permanent and no longer fluctuates.
• Lermoyez’s syndrome is a rare phenomenon in some patients with
MD. It consists of a transient improvement of hearing during the
onset of a vertigo attack. Tinnitus may also improve.
• A possible explanation for Lermoyez syndrome is the movement of
endolymph from the cochlea towards the semicircular canals,
resulting in a reduction of EH in the cochlea, but an increase in EH in
the semicircular canals
35. Some patients report a previous history of hearing loss, often since
childhood, preceding the onset of the episodes of vertigo.
Tinnitus may be the initial symptom of MD, preceding
the full picture by months. It is commonly described
as low-pitched, as a harsh, roaring, machine-like sound
or a hollow seashell sound.
At the onset of the disease,
tinnitus is intermittent and appears during the attacks
in 83% of patients and disappears afterward
36. • Vertigo in MD arises because of the abnormal excitability or cessation
of sensory input from the affected ear as a result of fluid disturbance
in the inner ear
• Once initiated, vertigo attacks persist for up to several hours.
• The rupture of Reissner’s membrane or the membranous labyrinth
has been suggested as a cause of vertigo attacks mediated by the
leakage of high-potassium endolymph into the perilymph, which can
depolarize and activate auditory nerve fibres into pathological firing
37. • drop attacks or Tumarkin attacks — a sudden fall without loss of
consciousness that can be potentially life-threatening — are caused
by disorders of the otolith organs in the utricle and the saccule.
• Serious drop attacks occur in 6% of patients with MD and some
milder types of drop attack in 72% of patients with MD
• Drop attacks are generally difficult to treat compared with the typical
vertigo attacks, but can resolve spontaneously
38. Disease progression.
• Initial symptoms include only one of the typical features (vertigo,
hearing loss, tinnitus or aural fullness)
• Symptoms often start with vertigo (in 41.2% of patients) with or
without tinnitus and aural fullness, whereas hearing loss as the sole
symptom occurs considerably less frequently (in 15% of patients).
• MRI has shown that EH can progress during the disease course and its
severity is correlated with the deterioration of cochlear, saccular and
horizontal semicircular canal function. Considering the frequency of
EH in asymptomatic and symptomatic ears, it is thought that
symptomatic MD is always preceded by asymptomatic EH
39. • Of all the symptoms of MD, hyperacousis (an increased sensitivity to
certain frequency or volume ranges), drop attacks, tinnitus and
moving difficulties have been associated with increased aural
pressure.
• Drop attacks seem to be associated with gait difficulties, intense
tinnitus and anxiety
• Nausea associated with vertigo was most common among patients
with a long history of disease
40. FUNCTIONAL TESTS
• PURE-TONE AUDIOMETRY
• The AAO-HNS established a hearing staging system, according to the
pure-tone thresholds at 0.5, 1, 2, and 3 kHz obtained in the
audiogram.
• Audiometrically documented fluctuating low-tone unilateral SNHL is
the key to the diagnosis of MD when facing patients with an episodic
vestibular syndrome. With follow-up, it is easy to document
fluctuation when recovery is appreciated, thus supporting the
diagnosis of MD.
41. • A shift in pure-tone thresholds for bone conduction by at least 30 dB
hearing level at each of two adjacent frequencies below 2000 Hz is
required for unilateral MD.
• The low frequencies (250 and 500 Hz) are typically affected at the
earlier stages
42. Staging should be applied only to
cases of definite or certain
Menie`re’s disease
43. ELECTROCOCHLEOGRAPHY (ECoG)
• ECoG is a neurophysiologic technique in which an auditory evoked
potential is obtained in response to brief sound stimuli and recorded
by an intratympanic or extratympanic (noninvasive) electrode.
• The cochlear microphonic and the summating potential (SP) are
generated by the hair cells of the organ of Corti, whereas the
compound action potential (AP) of the auditory nerve represents the
summed synchronized response of many individual nerve fibers.
• Testing parameters include latencies and amplitudes of SP and AP,
and SP/AP amplitude ratio, and area under the curve of SP/AP ratio.
44. • Changes in the SP response can reflect pressure differences between
the scala media and the scala vestibuli, indicating excessive fluid
pressure, thus deforming the basilar membrane toward the scala
tympani, so that enhanced-amplitude SP is thought to reflect EH.
SP/AP ratio is the most common parameter for diagnosis of EH.
• Increases in SP amplitude with an enlarged SP/AP ratio and a
prolongedAPlatency shift have been observed in patients with MD
(Ge and Shea, 2002; Ferraro and Durrant, 2006)
45. • When hearing thresholds reach 60 dB, EcoG cannot be used. ECoG
has been performed for determining hearing outcome (Moon et al.,
2012) and to monitor the response to intratympanic steroid therapy
(Martin-Sanz et al., 2013a).
46. Electrocochleography in a patient with left Meniere’s disease. The SP/AP ratio is normal in the
asymptomatic ear (right ear (R); that is, 0.250 (trial I) and 0.222 (trial II) (norm <0.42); part a), whereas those of
the symptomatic ear (left ear (L)) are higher (0.729 (trial I) and 0.776 (trial II); part b). This finding suggests that
an abnormal electrical potential is generated by the symptomatic inner ear, which might be an indication for
endolymphatic hydrops. Two consecutive trials (I and II) confirm the reproducibility
47. Vestibular testing
• CALORIC TESTS
• Bithermal caloric irrigation with computerized electronystagmography
or videonystagmography has been the main laboratory test to
evaluate vestibulo-ocular reflex (VOR) function.
• Caloric tests assess horizontal semi-circular canal function, with the
percentage of unilateral caloric weakness or canal paresis as the main
outcome measure. Unilateral vestibular hypofunction on caloric
testing is observed in up to 75% of unilateral MD patients (Wang et
al., 2012),
• a normal bithermal caloric response has been reported in up to 50%
of patients in some series.
48. VIDEO-HEAD IMPULSE TEST (vHIT)
• This is a video-oculography device that allows assessment of the VOR
at high frequencies during HIT.
• The equipment may provide an objective measurement of VOR gain
when head impulses are performed in the plane of each of the six
semicircular canals.
• It has been reported that 67% of patients with MD show a reduced
VOR gain in at least one semicircular canal when the six canals are
tested; the posterior semicircular canal of the affected ear is the
most frequently involved canal (Zulueta-Santos et al., 2014).
49. VESTIBULAR-EVOKED MYOGENIC POTENTIALS
(VEMPS)
• These are otolith-mediated, middle-latency reflexes that are
recorded from sternocleidomastoid (cVEMPs) or infraocular
(oVEMPs) electromyography in response to high-intensity auditory
stimuli (air conduction) or high-frequency vibratory stimulation (bone
conduction).
• Air conduction is preferred for cVEMPs, while bone conducted
vibration is mostly used in oVEMPs. VEMPs show a biphasic waveform
with a positive and a negative peak.
50. • It is widely accepted that cVEMPs evaluate the integrity of the
sacculus and the inferior vestibular nerve, whereas oVEMPs primarily
evaluate contralateral utriculus and superior vestibular nerve.
• Patients with unilateral MD usually show abnormalities in VEMPs
with reduced or absent responses, although at the initial stage an
augmented response is sometimes registered.
• The sensitivity and specificity of VEMPs in diagnosing MD are as low
as 50% and 49%, respectively.
51. Visualization of endolymphatic
hydrops using MRI and
intratympanic gadolinium-based
contrast agent.
after the intratympanic administration of an
eightfold diluted gadolinium-based contrast
agent (GBCA). The diluted solution is
injected, usually intratympanically,
through the tympanic membrane.
Because the GBCA moves into the
perilymph, but not into the endolymph, the
perilymph looks white and the
endolymph looks black. The image
shows a profoundly enlarged
endolymphatic space (EH) in the
52. Visualization of endolymphatic hydrops using MRI and intravenous
gadolinium-based contrast agent
A The affected ear has an enlarged endolymphatic space (endolymphatic hydrops; black) within the white
perilymph, which contains GBCA, in the cochlea (thin arrows) and the vestibule (thick arrows).
b | The unaffected ear shows no or only a very small endolymphatic space.
53. Differential diagnosis of Menie`re’s disease
• Autosomal-dominant sensorineural hearing loss type 9 (DFNA9)
caused by COCH gene
• Autoimmune inner-ear disease
• Cerebrovascular disease (transient ischemic attack/infarction/
hemorrhage in the vertebrobasilar system)
• Cogan’s syndrome
• Endolymphatic sac tumor
• Meningiomas and other masses of the cerebellopontine angle
• Neuroborreliosis
55. PROGNOSIS
• The clinical course of MD is variable, with episodes occurring at
irregular intervals. Usually as the disease progresses, attacks decrease
in frequency, and hearing loss becomes permanent, as does the
tinnitus (Perez-Garrigues et al., 2008).
• Without treatment, 57%of patients had complete control of vertigo at
2 years, and 71% had complete control after an average of 8.3 years.
• The functional scale developed by the AAO-HNS is useful to monitor
the impact of MD on daily activities.
56. Functional level scale
• Regarding your current state of overall functioning, 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
57. • 4. I am able to work, drive, travel, take care of a family, or engage in
most essential activities, but I must exert a great deal of effort to do
so. I must constantly make adjustments in my activities and budget
my energies. I am barely making it
• 5. I am unable to work, drive, or take care of a family. I am unable to
do most of the active things that I used to. Even essential activities
must be limited. I am disabled
• 6. I have been disabled for 1 year or longer and/or I receive
compensation (money) because of my dizziness or balance problem
58. MANAGEMENT
• The goal of the management of MD is to provide relief during acute
attacks of vertigo, to prevent recurrent attacks and to eliminate the
progressive damage to hearing and vestibular function in the affected
ear.
• the elimination of the progressive damage to hearing and vestibular
function has proved elusive.
59. Treatment of acute vertigo attacks
• Several drugs are used to reduce the asymmetry in neuronal input to
the brainstem during vertigo attacks. Drugs that are used to treat
motion sickness are useful for acute attacks of MD.
• Centrally acting antihistamines with anticholinergic effects have the
dual effect of suppressing the vestibular system while also acting as
anti-emetics.
• dimenhydrinate has the shortest onset, meclizine is the least
sedating and promethazine is the most sedating but is available as a
rectal suppository, which is useful if vomiting prevents the use of oral
medication.
60. • Benzodiazepines (for example, diazepam, lorazepam and
clonazepam) are also often used for their γ-aminobutyric acid (GABA)
agonist effect.
• GABA is the main central inhibitory neurotransmitter, therefore
agonists cause a decrease in neuronal firing throughout the brain and
in the vestibular nuclei.
• Daily use should be avoided because it can result in addiction and
withdrawal symptoms. In this class, lorazepam has the fastest onset
and its duration best matches that of the typical MD vertigo attack.
61. Prophylactic treatments
• Because attacks cannot be aborted once initiated, the prevention of
MD vertigo attacks provides the most effective relief of vertigo.
• Some medical and surgical treatments have the potential to slow the
progression of hearing loss and vestibular injury; however, this has
not yet been unequivocally proven for any therapy.
• As MD is a multifactorial disorder, no single treatment will provide
relief in all patients. The first step in medical management is to
delineate correctable factors that might be contributing to the
attacks.
62. • Management of risk factors:
• Based on the association between MD and disorders such as
migraine, sleep apnoea, autoimmune diseases, coagulopathies and
vasculopathies, it has been suggested that cerebrovascular ischaemia
contributes to attacks.
• A rigorous search for vascular risk factors should be undertaken and
treatment should be initiated.
• In people <50 years of age, migraine is the most common cofactor of
MD. Drugs that are prophylactic in migraine, such as topiramate,
calcium channel blockers (verapamil, nimodipine, flunarizine and
lomerizine), β-blockers and acetazolamide can be used
63. • In patients >50 years of age, traditional vascular risk factors, such as
hypertension, increased levels of cholesterol or a history of stroke or
myocardial infarction,
• can be managed medically with antihypertensive drugs, including
diuretics, calcium channel blockers and β-blockers, along with low
doses of aspirin and statins.
64. Preventive treatment
The main goal of preventive treatment is to improve
patients’ quality of life. This may be achieved by reducing
the frequency, duration, and severity of vertigo spells.
Preventive treatment includes lifestyle and dietary modifications,
pharmacologic therapy, and in some cases surgical
procedures
65. Lifestyle and dietary modifications
Patients with MD are counseled to follow a regular daily
routine, and avoid triggers such as stress, barometric
pressure change, fatigue, or sleep deprivation.
Alcohol, coffee, and tobacco are traditionally restricted, although
the efficacy of these measures has not been demonstrated
in randomized controlled trials (Luxford et al., 2013).
66. The most important dietary recommendation is a high
water intake and a very low sodium diet.
Sodium restriction is supported by the hypothesis that
an increase of endolymphatic pressure can lead to the
rupture of membranes in the scala media.
An increase in water intake is presumed to reduce the
severity of MD symptoms by decreasing the systemic
AVP arginine vasopressin level (Naganuma et al., 2006).
67. Betahistine
This drug is broadly used worldwide, except for the USA, since it has not
been approved by the US Food and Drug Administration.
Betahistine is a structural analog of histamine that acts as a weak partial
postsynaptic histamine H1 receptor agonist and presynaptic H3 receptor
antagonist, with no effect on postsynaptic H2 receptors (Gbahou et al.,
2010).
The mechanism of action of the drug appears to depend mainly on its
action on H3 receptors mediated by two metabolites,
aminoethylpyridine and hydroxyethylpyridine
68. • Experimental studies in animals demonstrate that betahistine
improves labyrinthine microcirculation by vasodilation of the
arterioles of the stria vascularis, and also in the posterior semicircular
canal ampulla.
• betahistine would reduce endolymphatic pressure by achieving a
reduction in the production of, and an increment in the re-
absorption of, endolymph
69. Diuretics
Diuretics are commonly used in MD patients, especially in the USA, where
they are the primary mode of therapy.
Diuretics act by diminishing sodium reabsorption at differen sites in the
nephron, thereby increasing urinar sodium and water loss.
This reduction of extracellular volume is supposed to decrease
endolymphatic pressure
and volume, either by increased drainage of endolymph or a reduction in its
production at the stria vascularis.
• Thiazides, such as hydrochlorothiazide, are the most frequently used
diuretics in patients with MD
70. Intratympanic gentamicin therapy (IGT)
The aminoglycoside antibiotics are used in the management
of MD at low dosage to produce a partial vestibular ablation.
The aim of IGT is to obtain a long-lasting, nonfluctuating,
peripheral vestibular hypofunction capable of
being centrally compensated. As compared with systemic
administration, intratympanic therapy has many
advantages: it is an office-based procedure that avoids
toxicity in the contralateral ear or other organs and yields
a higher concentration of drug in the inner ear.
71. GUIDELINE FORCONSERVATIVE TREATMENT
OF MD
Lifestyle modifications and medical therapy are able to control
vestibular symptoms in most patients, although they have no effect on
progression of hearing loss or tinnitus.
1. low-sodium diet (around 1800 mg/day) and high water intake (2000
mL/day), considered as baseline therapy
2. betahistine 24 mg/8 hours for at least 6 months
3. prednisone 1 mg/kg for 15 days if multiple episodes of vertigo with
longer duration are observed in consecutive weeks or a sudden drop in
hearing level is found. If no response is observed, prednisone is
stopped in 4 weeks
72. 4. intratympanic gentamicin, if there are six episodes in the last 3
months. The most studied dosage is 0.3–0.5 mL gentamicin sulfate
using a concentration of 26.4 mg/mL. It can be repeated up to four
times.
Gentamicin should not be used in patients with bilateral disease, since
they can develop bilateral vestibular hypofunction and persistent
vestibular ataxia.
74. OTHER TREATMENT MODALITIES
• Endolymphatic sac surgery
• Semicircular canal occlusion
• Vestibular neurectomy
• Labyrinthectomy
• Cochlear implantation
• Transtympanic ventilation tube insertion
• Hearing aids
75. Interesting fact
• Dr. William House had developed a surgical treatment to relieve the
symptoms of Meniere's disease. Astronaut Alan Shepard, the first
American in space, and 5th man to walk on moon, developed the
disease and consulted House for a fix. Without it, he couldn't fly to
the moon.
• In 1971 The astronaut called Dr. William House when he was en route
to the moon and three quarters away from moon, to thank Dr. House
