WHAT NEUROLOGISTS NEED TO UNDERSTAND OUTSIDE THEIR OWN SPECIALITY
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1
Department of Neurology,
Bashkir State Medical University,
Ufa, Russian Federation
2
Hearing and Balance Research
Unit, Field of Otolaryngology,
School of Medicine, Faculty of
Medicine and Health Technology,
Tampere University, Tampere,
Finland
3
Brain and Mind Centre, The
University of Sydney, Sydney,
Australia
4
Department of
Otorhinolaryngology Head and
Neck Surgery, Klinikum Bielefeld,
Bielefeld, Germany
Accepted 21 October 2020
© Author(s) (or their
employer(s)) 2020. No
commercial re-use. See rights
and permissions. Published by
BMJ.
To cite: Kutlubaev MA,
Pyykko I, Hardy TA, et al.
Pract Neurol Epub ahead of
print: [please include Day
Month Year]. doi:10.1136/
practneurol-2020-002734
Menière’s disease
Mansur Amirovich Kutlubaev ,1 Ilmari Pyykko,2 Todd A Hardy,3
Robert Gürkov4
ABSTRACT
Menière’s disease causes paroxysmal rotatory
vertigo, due to endolymphatic hydrops, an
accumulation of endolymph in the endolymphatic
space of the labyrinth. Its major symptoms are
attacks of rotatory vertigo lasting minutes to hours,
with unilateral hearing loss, tinnitus and aural
fullness. As the disease progresses, attacks happen
less often, but hearing loss and tinnitus gradually
become permanent. Neuro-otological
complications may develop, such as benign
paroxysmal positional vertigo, vestibular drop
attacks and bilateral vestibulopathy. The diagnosis
of Menière’s disease is based on the typical clinical
picture and typical findings on the audiogram.
Furthermore, it is now possible to diagnose it by MR
of the inner ear. Long-term management has
several steps, including diet, diuretics,
intratympanic injection of corticosteroid or
gentamicin and surgery (endolymphatic sac
surgery, grommet insertion, surgical
labyrinthectomy).
EPIDEMIOLOGY
The prevalence of Menière’s disease—
also known as hydropic ear disease—
varies greatly depending on geographic
and ethnic factors as well as setting
where the diagnosis was made. The
UK prevalence is 270 per 100 000
(from BioBank data), while in the
USA, it is 190 per 100 000 (based on
a health claims database). A population-
based study from Finland found a much
higher prevalence of 513 per 100 000
inhabitants. It appears less common in
East Asian countries such as in Japan,
with a prevalence of 3.5 per 100 000.
Menière’s disease symptoms often
start in the fourth and fifth decades of
life. It can manifest earlier but is very
uncommon in children. Some research-
ers have identified a slight female
preponderance.1
PATHOPHYSIOLOGY
The main pathophysiological mechanism
is endolymph accumulation in the
Kutlubaev MA, et al. Pract Neurol 2020;0:1–6. doi:10.1136/practneurol-2020-002734
endolymphatic space of the labyrinth,
known as endolymphatic hydrops.
Although symptoms are usually localised
to one ear, MR shows hydrops in both ears
in about half of cases. The exact cause of
endolymphatic hydrops is unknown, but
different processes may be responsible,
including an abnormal immune reaction,
viral infection, vascular changes and auto-
nomic nervous system dysfunction, lead-
ing to an imbalance in inner-ear
homoeostasis. Allergic hypersensitivity is
three times higher among people with
Menière’s disease than in the general
population, suggesting that an allergic
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reaction may trigger immune-mediated
inner-ear disease that leads to endolym-
phatic hydrops. Genetic factors also play
a role, but culprit genes are yet to be
identified.
Although Menière’s disease is tradition-
ally considered an idiopathic disorder,
endolymphatic hydrops can develop as
a complication of other inner-ear disease,
such as vestibular schwannoma, large ves-
tibular aqueduct syndrome, labyrinthitis,
meningitis, noise-induced hearing loss,
trauma, congenital hearing loss or inner-
ear malformation. These cases of
Menière’s disease are classified as second-
ary, in contrast to primary hydropic ear
disease, where no cause is identified.
For many years, the mechanism of
a typical vertigo attack in Menière’s dis-
ease was explained by Schuknecht’s the-
ory of the rupture of Reissner’s membrane
and potassium intoxication of the peri-
lymph. Contemporary research offers an
alternative explanation: the ‘drainage the-
ory’ of Gibson and Arenberg explains epi-
sodes of vertigo as due to a dysfunctional
or blocked endolymphatic sac. This
impairs the longitudinal flow of endo-
lymph, leading to its collection in the
sinus of the endolymphatic duct.
Excessive endolymph refluxes through
the utricular valve of Bast and into the
ampullae of the semicircular canals, result-
ing in rotatory vertigo.
1
 WHAT NEUROLOGISTS NEED TO UNDERSTAND OUTSIDE THEIR OWN SPECIALITY
Long-standing endolymphatic hydrops distends the
basilar membrane and may impair the blood supply to
the neurosensory epithelium. In the early stages of the
disease, the distension comes and goes causing fluctuat-
ing tinnitus and hearing loss, but as degeneration pro-
gresses, the symptoms become permanent. In the long
term, endolymphatic hydrops progresses, and the degree
of endolymphatic hydrops correlates significantly with
abnormalities on audiovestibular function tests (audio-
metry, caloric test, vestibular-evoked myogenic poten-
tials, electrocochleogram, wide-band tympanometry).
However, short-term fluctuations of audiovestibular
symptoms do not correlate with gross endolymphatic
hydrops changes, suggesting that the fluctuations in
hydrops associated with attacks have an amplitude
below the limits of current MR resolution.1
CLINICAL PICTURE
The main symptoms of Menière’s disease are attacks of
rotatory vertigo lasting minutes to hours, associated with
unilateral hearing loss, tinnitus and aural fullness. During
attacks, patients often experience autonomic symptoms,
such as nausea, vomiting, tachycardia and headache. In
the chronic stage, there are often postural and gait pro-
blems. Table 1 shows the current diagnostic criteria for
Menière’s disease (2015). However, they have several
shortcomings and some experts recommend instead
using the 1995 AAO-HNS criteria for clinical practice.
Monosymptomatic forms manifest with either
cochlear (hearing loss) or vestibular (episodes of ver-
tigo) symptoms; these appear to develop if endolym-
phatic hydrops involves only the cochlea or vestibule,
or if lost sensory function in the cochlea or vestibule
‘masks’ the symptoms. Importantly, purely vestibular
attacks in people with long-standing severe hearing loss
are frequently caused by endolymphatic hydrops; this
presentation should prompt clinicians to consider
Menière’s disease. Eventually, the pathological process
underlying endolymphatic hydrops spreads to involve
the whole labyrinth, giving the full clinical picture.
There are also rare atypical forms of Menière’s disease,
Table 1 Diagnostic criteria for Menière’s disease (2015)
Definitive criteria
Two or more spontaneous episodes of vertigo each lasting 20 min to
12 hours
Documented sensorineural hearing loss greater than 30 dB below and
above 2 kHz
Fluctuating aural symptoms (hearing, tinnitus and fullness) in the
affected ear
Not better explained by another vestibular disease
Probable criteria
Two or more episodes of vertigo or dizziness each lasting 20 min to
12 hours
Fluctuating aural symptoms in the affected ear
Not better explained by another vestibular disease
Probable Criteria should be highlighted in the same way as Definitive ones
2 Kutlubaev MA, et al. Pract Neurol 2020;0:1–6. doi:10.1136/practneurol-2020-002734
Pract Neurol: first published as 10.1136/practneurol-2020-002734 on 28 November 2020. Downloaded from http://pn.bmj.com/ on November 28, 2020 at Swets Subscription Service REF:
such as Lermoyez syndrome, characterised by
a transient improvement of hearing and tinnitus during
an attack of vertigo.2
As the disease progresses, attacks become less fre-
quent, but hearing loss and tinnitus gradually become
permanent. In advanced disease, other neuro-
otological complications are more common, such as
benign paroxysmal positional vertigo (BPPV), otolithic
crises of Tumarkin (now known as vestibular drop
attacks) and bilateral vestibulopathy. The prevalence
of BPPV during the disease course may be as high as
38% and it is especially high in advanced disease. This
may be because long-lasting endolymphatic hydrops
leads to otolith membrane degeneration with forma-
tion of free-floating particles (otoconia) in the endo-
lymph. In contrast to idiopathic BPPV, Menière’s
disease-related BPPV more often arises from the hor-
izontal semicircular canal and may require multiple
repositioning manoeuvres.3
Vestibular drop attacks develop when there is an
abrupt loss of muscular tone in the lower limbs from
sudden otolith dysfunction in the sacculus and/or utri-
cle. Typical vestibular drop attacksi lead to a sudden fall
to the ground without loss of consciousness. However,
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recent research has indicated that mild vestibular drop
attacks may result in tripping or near falls; also, vestib-
ular drop attacks may sometimes trigger loss of con-
sciousness, ie, vestibular syncope. Vestibular syncope is
probably mediated by vestibulo-sympathetic reflexes
originating from otolith afferents activating cardio-
inhibitory reflexes and producing postural hypotony.
Depression and anxiety affect up to half of people
with Menière’s disease, and so clinicians should screen
patients for affective disorders. Timely treatment with
antidepressants, such as selective serotonin reuptake
inhibitors, may positively affect the disease course.
Fatigue is another common associated symptom.
Although, in most cases, this probably results from the
distressing paroxysmal symptoms, it has been proposed
that psychiatric disorders might also trigger endolym-
phatic hydrops (although with no clearly identified
mechanism hitherto.4)
Patients with advanced Menière’s disease may
develop a bilateral vestibulopathy. At this stage, vertigo
attacks subside, and there is prominent hearing loss.
Major complaints include movement-dependent pos-
tural dizziness and unsteadiness, which is worse in
darkness and when on uneven ground.
DIAGNOSIS
In early-stage disease, the clinical examination between
attacks may be normal. However, during or immedi-
ately after a vertigo attack, there may be signs of
i
Recording of the typical vestibular drop attacks has been published recently:
Chen Z, Zhang Y, Zhang Q. Tumarkin Drop Attack Recorded by Video
Surveillance. JAMA Neurol. 2020;77(7):897–898. doi:10.1001/
jamaneurol.2020.0884.
 WHAT NEUROLOGISTS NEED TO UNDERSTAND OUTSIDE THEIR OWN SPECIALITY

Pract Neurol: first published as 10.1136/practneurol-2020-002734 on 28 November 2020. Downloaded from http://pn.bmj.com/ on November 28, 2020 at Swets Subscription Service REF:
asymmetric vestibular dysfunction. Nystagmus is always 125 250 500 1000 2000 4000 8000
-10
unidirectional but may change direction during an
attack. First, it beats towards the affected ear for 0
a short time (irritative nystagmus) before changing
direction (paralytic nystagmus, usually present at the X X X
30
time of clinical examination), and finally again beats
towards the affected ear (recovery nystagmus). The X X
head-impulse test is often positive on the affected side 60 X X
and patients also tend to fall to the affected side. Caloric
testing usually confirms the vestibular asymmetry.
Pure-tone audiogram is a widely available test of 90
hearing function. It helps to assess the impact of the
disease and may reveal changes typical of Menière’s
disease. In the early stages of the disease, hearing loss 120

occurs only during attacks and recovers completely

after the attack subsides. Later, a permanent sensori- A.
neural hearing loss develops, affecting low frequencies 250 500 1000 2000 4000 8000
125
(125–1000 kHz), giving a rising configuration on the -10
audiogram from low to high frequency. This low- 0
frequency hearing loss is the most important diagnostic
audiometric feature. As the disease progresses, hearing
loss also involves higher frequencies (2000–8000 kHz) 30
and the audiogram flattens due to hearing loss across
both low and high frequencies (figure 1).

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A dehydration test increases the diagnostic value of 60 X X X X X
a pure-tone audiogram in diagnosing Menière’s disease.
For the test, patients undergo baseline pure-tone audio- X
gram and then take glycerol 1 mL/kg body weight (or less 90 X
often furosemide, or urea). The patient has a second and
third audiogram at 1.5 hours and 3 hours, respectively.
The test is positive if the pure-tone hearing thresholds 120

increase by 10 dB or more. The sensitivity of the dehydra-

tion test is 66%. It is more useful in the early stages of the
disease when there is fluctuating hearing loss; in more
advanced disease, there can be false negatives.
More sophisticated investigations include vestibular-
evoked myogenic potentials, electrocochleogram and
imaging techniques. A transtympanic electrocochleo-
gram usually identifies high summating potential/
action potential ratio reflecting endolymphatic
hydrops. Vestibular-evoked myogenic potential ampli-
tudes show vestibular asymmetry, but this finding is not
specific for Menière’s disease. Other results of vestibu-
lar-evoked myogenic potential test (such an increased
sensitivity to higher frequencies of the acoustic stimu-
lus) can provide a diagnostic hint.
CT scanning can exclude inner-ear structural pathol-
ogy, such as third-window syndromes (perilymph fis-
tula, canal dehiscence, enlarged vestibular aqueduct)
but cannot visualise endolymphatic hydrops.
However, MR can identify endolymphatic hydrops
and so helps to confirm the diagnosis in difficult-to-
diagnose cases and in those being considered for inva-
sive or ablative treatment options. The best MR technique
to evaluate endolymphatic hydrops is 24-hour delayed
three-dimensional fluid-attenuated inversion recovery
(3D-FLAIR) following intratympanic contrast. If this is
not available, a 4-hour delayed 3D-FLAIR sequence after
B.
Figure 1 (A) Rising audiometric curve showing low-tone hear-
ing loss in the left ear in early-stage Menière’s disease. (B) Almost
flat audiometric curve showing pan-tonal hearing loss in left ear
in late-stage Menière’s disease. The reduced hearing at higher
frequencies reflects age-related hearing loss.
intravenous gadolinium could be used. With either
method, the perilymphatic, but not endolymphatic,
space enhances with gadolinium (figure 2). This
enables imaging either of an enlarged scala media (in
cochlear hydrops) or an enlarged saccule (in vestibular
hydrops). In late-stage Menière’s disease, this imaging
may show almost complete obliteration of the peri-
lymphatic space. MR of the inner ear is mostly used in
suspected Menière’s disease, where asymmetry of
perilymph enhancement can contribute to its diagno-
sis. MR scan of brain with gadolinium is important to
exclude structural brain lesions such as brainstem
ischaemia or meningeal disease.2
Clinicians should use appropriate history taking and
serological tests help to distinguish Menière’s disease
from its mimics, including autoimmune diseases, or
infections such as syphilis and borreliosis.

Kutlubaev MA, et al. Pract Neurol 2020;0:1–6. doi:10.1136/practneurol-2020-002734 3

 WHAT NEUROLOGISTS NEED TO UNDERSTAND OUTSIDE THEIR OWN SPECIALITY
A symptoms can also manifest in the brain and eye, includ-
B restricted diffusion, together with clustering of lesions
Figure 2 MR scan of the left inner ear with contrast enhance-
ment. (A) Normal labyrinth. (B) Endolymphatic hydrops (dilated
endolymphatic space in black).
Differential diagnosis
Several inner-ear and brain diseases may have audio-
vestibular symptoms that can mimic Menière’s disease.
Vestibular migraine shares several of the early symp-
toms of Menière’s disease, before the typical hearing
loss has developed. People with Menière’s disease may
also have migraine, making a definitive diagnosis diffi-
cult. Helpful differentiating features are the duration of
vertigo attacks beyond 24 hours and the presence of
photophobia. Patients with vestibular migraine often
report long-standing motion intolerance and a history
of childhood benign positional vertigo; attacks of ves-
tibular migraine in women may correlate strongly with
the menstrual cycle. As Menière’s disease progresses,
and as low-frequency sensorineural hearing loss devel-
ops, the diagnosis becomes more assured. Cochlear
otosclerosis is also a potential cause, since there can
be associated endolymphatic hydrops with symptoms
resembling Menière’s disease.
Especially in a first attack of vertigo, it is important to
exclude stroke and posterior circulation transient
4 Kutlubaev MA, et al. Pract Neurol 2020;0:1–6. doi:10.1136/practneurol-2020-002734
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ischaemic attack. A set of signs named HINTS-plus allows
clinicians to distinguish peripheral from central vestibu-
lopathy better than diffusion-weighted MR can.
However, rarely, anterior inferior cerebellar artery occlu-
sion may cause labyrinthine infarction presenting as
a peripheral vestibular syndrome, but almost always
there are other neurological signs. Once typical attacks
of vertigo recur, then the diagnosis of Menière’s disease
becomes clearer.
Psychogenic disorders can cause dizziness attacks
resembling early Menière’s disease. Spontaneous nys-
tagmus during attacks is important for distinguishing
these disorders.
Several conditions causing hearing loss and vestibular
ing inflammatory and granulomatous disorders of cen-
tral nervous system (CNS). The rising configuration of
low-frequency to high-frequency hearing loss character-
istic of Menière’s disease also occurs in Susac’s syndrome
and less often in Cogan’s syndrome; all three of these
conditions can cause severe pan-tonal hearing loss. An
important message is that if audiovestibular symptoms
suggesting Menière’s disease are associated with other
neurological signs or visual symptoms, it is important to
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exclude brain, eye and ear conditions. An MR scan of
brain helps to exclude most of these conditions, but an
ophthalmology review can also provide important clues.
In Susac’s syndrome, MR scan of brain typically shows
widespread supratentorial and infratentorial T2/FLAIR
hyperintensities, associated, in acute cases, with
in the corpus callosum, including classic ‘snowball’
lesions. Branch retinal artery occlusions may be best
appreciated with a fluorescein angiogram. In Cogan’s
syndrome, the characteristic ophthalmological finding is
of non-syphilitic interstitial keratitis.5
MANAGEMENT AND VESTIBULAR
REHABILITATION
Short-term management of acute vertigo attacks in
Menière’s disease is with vestibular suppressants and
antiemetics to reduce vertigo and nausea. Several medica-
tions are believed to suppress vestibular function: H1-
blockers, anticholinergics, benzodiazepines and neurolep-
tics. However, recent data show that they act mostly as
antiemetics. When nausea and vomiting are only mild or
moderate, metoclopramide or prochlorperazine can help.
In more severe cases, the options include 5-HT3 antago-
nists, such as ondansetron, or neuroleptics. Patients with
continued vomiting require rehydration.1
Long-term management has several steps, taken one
after another.
The first step involves lifestyle and initial medication.
Patients should be reassured that Menière’s disease is
not a brain disease but an inner-ear disorder, and they
must appreciate the importance of lifestyle modifica-
tion. Although the evidence is weak, clinicians usually
advise patients to restrict dietary salt intake and to
 WHAT NEUROLOGISTS NEED TO UNDERSTAND OUTSIDE THEIR OWN SPECIALITY
increase the amount of water they drink. Reducing salt
intake to 1000–1500 mg daily may prevent vertigo
attacks. Diet appears important in controlling attacks,
and patients might be advised to avoid caffeine, sugar
and alcohol. Some case reports also advocate that those
with food allergies modify their diet accordingly.
Physical exercise leading to sweating, a good night’s
sleep lasting 8 hours/day and proper stress management
are also important in its long-term management.
The most popular medications prescribed to prevent
vertigo attacks of Menière’s disease are diuretics and/or
betahistine. There are several low evidence-level studies
reporting efficacy of diuretics in its medical manage-
ment. Osmotic diuretics are often used as an urgent
treatment of frequent attacks, given as a brief course
over several days. Widely used osmotic diuretics include
mannitol, glycerol and isosorbitol, the latter mostly pre-
scribed in Japan. Historically, urea was also used as an
osmotic diuretic, but patients often find it unpalatable,
limiting its use nowadays. Other diuretics such as acet-
azolamide, chlorthalidone and hydrochlorothiazide
could be used for longer courses. Potassium-sparing
agents such as triamterene can be prescribed alongside.
Betahistine is a strong H3 antagonist and a weak H1
agonist, increasing cochlear blood flow and improving
vestibular compensation in animal models. It is widely
used in Europe and Japan, but it has never been
approved by the Food and Drug Administration in the
USA due to weak efficacy evidence. Its recommended
dose is 48 mg/day, but some experts advocate doses as
high as 480 mg/day. The results of some smaller clinical
trials were inconclusive. In 2016, the BEMED trial pro-
vided high-quality evidence in a trial of 220 patients
with Menière’s disease that high-dose or regular-dose
betahistine was no better than placebo. Calcium-channel
blockers such as nimodipine and cinnarizine may
improve labyrinthine circulation, but their potential
benefits have never been tested in randomised con-
trolled trials. In severe cases, corticosteroids can alleviate
the symptoms, a favoured regimen being oral predniso-
lone 1 mg/kg body weight for a week with gradual dose
tapering over 1–2 weeks. Patients with Menière’s disease
and migraine may benefit from additional therapy for
migraine. Depressed patients with Menière’s disease
should be treated along standard guidelines.
The second step in longer-term management is intra-
tympanic injections of corticosteroid. Dexamethasone
(4 mg/mL) daily for 5 consecutive days or once a week
for 1–4 weeks is effective in many refractory cases.
Alternatively, methylprednisolone (62.5 mg/mL) given
2 weeks apart is as effective as gentamicin, but without
the risk of ototoxicity.
The third step is surgical non-destructive treatment,
including endolymphatic sac surgery, aiming to reduce
the pressure of the endolymph in the sac. Grommet inser-
tion or mastoidectomy can also be considered. There is
only weak evidence for the efficacy of these interventions
and some studies have failed to show benefit over placebo.
Kutlubaev MA, et al. Pract Neurol 2020;0:1–6. doi:10.1136/practneurol-2020-002734
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The fourth step is a medical destructive procedure,
intratympanic injection of gentamicin (40 mg/mL).
Although it is the most effective conservative method
of treatment of vertigo attacks as well as vestibular drop
attacks, there is a serious risk of hearing loss. For this
reason, the procedure is recommended for those with
frequent vertigo attacks, impaired hearing function and
preserved vestibular function on the contralateral side.
Importantly, carriers of a mutation in the mitochondrial
gene MTRNR1 develop complete deafness even after
single injection of aminoglycoside and so patients need
appropriate patient screening before the injection.
The fifth step is destructive surgery (surgical labyr-
inthectomy and vestibular neurectomy), recommended
only if other treatments have failed. In order to avoid
bilateral vestibulopathy, only those with preserved con-
tralateral vestibular function should undergo such treat-
ment. Patients who have bilateral profound hearing loss
can benefit from cochlear implantation, which can be
performed simultaneously with labyrinthectomy.
Vestibular rehabilitation promotes vestibular adap-
tation and substitution by enhancing gaze and pos-
tural stability, ultimately improving activities of
daily living. It has a limited role in early Menière’s
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disease due to its fluctuating course, but becomes
important in the later stages, especially in those who
underwent ablative treatments or who have
Menière’s disease affecting both ears complicated
by bilateral vestibulopathy.
Key points
► Menière’s disease presents with episodic rotatory vertigo,
unilateral hearing loss, tinnitus and aural fullness lasting
30 min to 12 hours; permanent sensorineural low-tone
hearing loss develops later and may progress to deafness.
► In advanced disease, neuro-otological complications, such
as benign paroxysmal positional vertigo, otolithic
Tumarkin crises and bilateral vestibulopathy, may
develop.
► Menière’s disease is diagnosed using clinical findings with
low-frequency sensorineural hearing loss on pure-tone
audiometry; complex cases may require investigation
with electrocochleography, vestibular-evoked myogenic
potentials and MR scan of the inner ear.
► Vertigo attacks resembling Menière’s disease may
occur with vestibular migraine, CNS inflammatory
disorders, transient ischaemic attacks and some
inner-ear diseases.
► Conservative management of Menière’s disease includes
lifestyle modification, including reduced salt intake and
medication such as diuretics and betahistine. If
conservative measures are ineffective, surgical options
include intratympanic injections of corticosteroid and
gentamicin, endolymphatic sac decompression and
labyrinthectomy.
5
 WHAT NEUROLOGISTS NEED TO UNDERSTAND OUTSIDE THEIR OWN SPECIALITY
FURTHER READING
1. Nakashima T, Pyykkö I, Arroll MA, Casselbrant ML,
Foster CA, Manzoor NF, Megerian CA, Naganawa S,
Young YH. Menière’s disease. Nat Rev Dis Primers
12 May 2016;2:16028. doi: 10.1038/nrdp.2016.28.
PMID: 27170253.
2. Liu Y, Yang J, Duan M. Current status on researches of
Meniere’s disease: a review. Acta Otolaryngol 2020
Oct;140(10):808–812. doi: 10.1080/00016489.2020.
1776385. Epub 21 June 2020. PMID: 32564698.
Contributors MAK prepared the first draft. IP, TH and RG
reviewed the manuscript for intellectual content.
Funding The authors have not declared a specific grant for this
research from any funding agency in the public, commercial or
not-for-profit sectors.
Competing interests MAK reports signing contracts to receive
fees for lectures with Abbot Laboratories.
Patient consent for publication Not required.
Provenance and peer review Commissioned. Externally peer
reviewed by Diego Kaski, London, UK.
6 Kutlubaev MA, et al. Pract Neurol 2020;0:1–6. doi:10.1136/practneurol-2020-002734
Pract Neurol: first published as 10.1136/practneurol-2020-002734 on 28 November 2020. Downloaded from http://pn.bmj.com/ on November 28, 2020 at Swets Subscription Service REF:
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