This document discusses the history, presentation, diagnosis and management of Meniere's disease. Some key points: - Meniere's disease was first described in 1861 and is characterized by hearing loss, tinnitus, and vertigo due to endolymphatic hydrops (fluid buildup) in the inner ear. - Diagnosis is based on recurrent vertigo spells lasting 20 minutes to 24 hours, fluctuating hearing loss, tinnitus and aural fullness. Tests like electrocochleography and VEMPs can provide supportive evidence. - Treatment includes dietary sodium restriction, diuretics, medications and surgical options like intratympanic injections if conservative measures fail. The

1. Humra shamim

2.  In 1861 Prosper
Meniere described
a syndrome
characterized by
deafness, tinnitus,
and episodic
vertigo. He linked
this condition to a
disorder of the
inner ear.

3.  In 1871 Knapp advanced the hypothesis that
hydrops was similar to ocular glaucoma :
aural glaucoma
 In 1938 Hallpike and Cairns described the
underlying pathology of Meniere’s disease as
being endolymphatic hydrops but the precise
etiology still remains elusive

4.  In 1902, Parry performed a CN VIII division
for vertigo in a patient with suspected
Meniere’s disease.
 Portman did endolymphatic sac
decompression via a transmastoid approach
in 1926.
 In 1931,McKenzie performed a selective
vestibular neurectomy.

5. Ménière’s disease, also called endolymphatic
hydrops, is a disorder of the inner ear where
the endolymphatic system is distended with
endolymph. It is characterized by
(i) Vertigo,
(ii) Sensorineural hearing loss,
(iii) Tinnitus and
(iv) Aural fullness.

6.  The disease seems to be more prevalent
among whites, with a variable female-to-
male ratio ( ranging from 1:1, 1.3:1, 2:1 ;
female preponderance ).
 The peak age at onset is in the fourth and
fifth decades of life, although presentation
can be at almost any age.
 The incidence of bilateral disease probably is
in the range of 19% to 24%.

7.  Familial occurrence of Meniere’s disease has
been reported in 10% to 20% (An AD mode)
Migraine is strongly associated in such cases.
 The incidence is elevated in persons with
specific major histocompatability complexes
(MHCs).
 Human leukocyte antigens (HLA) B8/DR3 and
Cw7 have been associated with Meniere’s
disease.

8. Review of anatomy

10.  Resorption of the water content of endolymph
 Ability to participate in some ionic exchanges with
endolymph
 Removal of metabolic and cellular debris, including
otoconia
 Immunodefense function ( perisaccular )
 Inactivation and removal of viruses
 Secretion of Glycoproteins to attract extra fluid
(Glycoproteins act as a driving force for longitudinal
flow)

12. The main pathology is
distension of endolymphatic
system,mainly affecting the
cochlear duct (scala media)
and the saccule, and to a
lesser extent the utricle
and semicircularcanals. The
dilatation of cochlear duct
is such that it may
completely fill the scala
vestibuli; there is marked
bulging of Reissner’s
membrane, which may even
herniate through the
helicotrema into the apical
part of scala tympani

13.  Endolymphatic hydrops causes distortion of
membranous labyrinth
 Pressure building up in the scala media may
cause mirco ruptures of membranous
labyrinth
 This would account for the episodic nature
of the attacks
 Healing of these ruptures causes resolution
of the disorder

14.  Main pathology here is distention of
endolymphatic system due to increased
volume of endolymph
1. Increased production of endolymph
2. Faulty absorption
3. Both

15. Exact cause not known
1. Defective absorption by endolymphatic sac
2. Vasomotor disturbances: there is
sympathetic over-activity resulting the
spasm of internal auditory artery and/or
its branches intefering with the function of
cochlear or ventibular sensory
neuroepithelium.
3. Allergy
4. Sodium and water retention
5. Hypothyroidism(3% of cases)
6. Autoimmune and viral aetiologies

16.  Anatomical-abnormalities
 Genetic- AD
 Immunological - immune complex deposition
 Viral-serum IgE to herpes simples virus types
I and II, Epstein-Barr virus and CMV
 Vascular-associated with migraines
 Metabolic-potassium intoxication

17. Meniere’s disease
Autoimmune
process
Viral infection
(herpes family)
stress
Sodium and water
retention
tinnitus
Episodic vertigo
Aural fullness
Endocrinal
(hypothyroidism)
Defective
absorption by sac
Food or
inhalant
allergen
Fluctuating hearing
loss

18. Normal membranous labyrinth Dilated membranous labyrinth
in Meniere's disease (Hydrops)

19.  Classical Meniere’s disease
 Vestibular Meniere’s disease – vestibular
symptoms and aural pressure
 Cochlear Meniere’s disease – cochlear
symptoms and aural pressure
 Lermoyez syndrome – Reverse Meniere’s
 Tumarkin’s crisis – Utricular Meniere’s

20.  variant of Meniere’s disease
 sudden sensorineural hearing loss, which
improves during or immediately after the
attack of vertigo.
 Cause is sudden spasm of the labyrinthine
artery followed by immediate dilatation
 TBD showed hydrops and membrane rupture
typically in basal cochlea and saccule

21.  AKA Tumarkin’s drop attacks
 abrupt falling attacks of brief
duration without loss of
consciousness.
 due to an enlarging utricle due to
excess endolymphatic volume
 an erroneous vertical gravity
reference occurs as a consequence
of an abrupt change in otolithic
input. This in turn generates an
inappropriate postural adjustment
via the vestibulospinal pathway,
which results in a sudden fall.

22.  The typical history consists of recurring attacks
of vertigo (96.2%) with tinnitus (91.1%) and
ipsilateral hearing loss (87.7%).
 Attacks often are preceded by an aura
consisting of a sense of fullness in the ear,
increasing tinnitus, and a decrease in hearing.
 The classic presentation is not always detailed
by the patient. This is particularly true early in
the disease presentation. the disease seems to
manifest with a predominance of either
vestibular or auditory complaints, 50% of
patients came to medical attention with vertigo
and hearing loss together, 19% with vertigo only,
and 26% with only deafness.

23. • Sensorineural hearing loss is fluctuating and progressive, with the
sensation of fullness or pressure in the ear.
• In only 1% to 2% of patients does the hearing loss progress to
profound deafness.
• Additional features include diplacusis, a difference in the
perception of pitch between the ears (43.6%) and recruitment (56%)
.
• Tinnitus tends to be nonpulsatile and variously described as
whistling or roaring. It may be continuous or intermittent. Tinnitus
often begins, gets louder, or changes pitch as an attack approaches.
Frequently a period of improvement follows the attack.

24. • The Romberg test generally shows significant instability
and worsening when the eyes are closed.
• The Weber tuning fork test usually lateralizes away from
the affected ear.
• The Rinne test usually indicates that air conduction
remains better than bone conduction.
• Complete neurologic evaluation is important. New-onset
vertigo might be an early sign of stroke, migraine, or
brainstem compression that may require emergent
evaluation and care.

25. Particularly helpful to document present hearing acuity
and to detect future change.
-The patient may not notice a loss at specific
frequencies. Low-frequency or mixed low- and high-
frequency insufficiency may be observed.
- Typically, the lower frequencies are affected
more severely. This is due to preferential sensitivity of
the apex to the hydrops.
- Multiple hearing tests, which document
fluctuating hearing loss, are helpful in diagnosing
Ménière.

26.  The diagnosis of Meniere disease is made
based on a careful history and physical
exam.
 If the work-up is normal and the classic
symptoms continue, the diagnosis of
Meniere disease is made.

30.  This is abnormal
growth in the
perceived intensity
of sound
 This is usually
positive in patients
with Meniere’s
disease
 ABLB is the test
used to look for the
presence of
recruitment

31.  Ratio of amplitudes of the SP
and the 8th cranial nerve
action potential (AP), the
SP/AP ratio.
 The SP becomes relatively
larger in hydrops;
accordingly, the SP/AP ratio
increases; SP:AP > 0.45
 The summating potential (SP)
is larger and more negative
due to distention of the
basilar membrane into the
scala tympani, causing an
increase in the normal
asymmetry of its vibration

32.  No single test makes the diagnosis of Meniere
disease. Rather a complete history that
includes a detailed description of the pattern
of disease presentation, supported by
quantitative testing, is required. The most
recent definition of the disease has been
established by the Committee on Hearing and
Equilibrium of the American Academy of
Otolaryngology– Head and Neck Surgery
(AAO-HNS); this is summarized as follows:

33. Major Symptoms
1.Vertigo
 Recurrent, well-defined episodes of spinning or rotation • Duration from 20
minutes to 24 hours.
 Nystagmus associated with attacks
 Nausea and vomiting during vertigo spells common
 No neurologic symptoms with vertigo
2.Deafness
 Hearing deficits fluctuate
 Sensorineural hearing loss
 Hearing loss progressive, usually unilateral
3.Tinnitus
 Variable, often low-pitched and louder during attacks
 Usually unilateral
 Subjective

34.  Possible Meniere’s disease
1. Episodic vertigo without hearing loss or
2. Sensorineural hearing loss, fluctuating or fixed, with dysequilibrium,
but without definite episodes
3. Other causes excluded
 Probable Meniere’s disease
1. One definitive episode of vertigo
2. Hearing loss documented by audiogram at least once
3. Tinnitus or sense of aural fullness in the presumed affected ear
4. Other causes excluded
 Definite Meniere’s disease
1. Two or more definitive spontaneous episodes of vertigo lasting at
least 20 minutes
2. Audiometrically documented hearing loss on at least one occasion
3. Tinnitus or sense of aural fullness in the presumed affected ear
4. Other causes excluded
 Certain Meniere’s disease
 Definite Meniere’s disease, plus histopathologic confirmation

35. Vertigo
a. Any treatment should be evaluated after at least 24 months.
b. Formula to obtain numeric value for vertigo:
ratio of average number of definitive spells per month after therapy
divided by definitive spells per month before therapy (averaged over a
24-month period) × 100 = numeric value.
Numeric value scale Control Class
0 Complete control of
definitive spells
A
0-40 Limited control of definitive
spells
B
41-80 Insignificant control of
definitive spells
C
81-120 D
>120 Secondary treatment
initiated
E

36. Disability
a. No disability
b. Mild disability: intermittent or continuous
dizziness/unsteadiness that precludes working
in a hazardous environment.
c. Moderate disability: intermittent or
continuous dizziness that results in a
sedentary occupation
d. Severe disability: symptoms so severe as to
exclude gainful employment

37.  Hearing is measured using a four-frequency pure-tone
average (PTA) of 500 Hz, 1 kHz, 2 kHz, and 3 kHz.
• Pretreatment hearing level: worst hearing level during 6 months
before therapy
• Post-treatment hearing level: poorest hearing level measured 18-
24 months after institution of therapy
 Hearing classification:
i. Unchanged: ≤10-dB PTA improvement or worsening or ≤15%
speech discrimination improvement or worsening.
ii. Improved: >10-dB PTA improvement or >15% discrimination
improvement
iii. Worse: >10-dB PTA worsening or >15% discrimination worsening

38.  In 1996, the Committee on Hearing and Equilibrium
reaffirmed and clarified the guidelines, adding
initial staging and reporting guidelines:
 Initial Hearing Level
Stage Four tone
average(dB)
1 < 25
2 26-40
3 41-70
4 >70

39.  Therapy is aimed at the reduction of
symptoms, and the optimal curative
treatment should stop vertigo, abolish
tinnitus, and reverse hearing loss..

40.  Electrocochleography
 Dehydrating Agents
 Vestibular evoked Myopotentials

41.  Vestibular evoked myogenic potential
 Measures the relaxation of sternomastoid muscle
in response to ipsilateral click stimulus
 Brief high intensity ipsilateral clicks produce
large short latency inhibitory potentials (VEMP)
in the toncially contracted Ipsilateral
sternomastoid muscle
 Afferent arises from sound responsive cells in
the saccule, conducted via the inferior
vestibular nerve.
 Efferent is via vestibulo spinal tract
 Normal responses are composed of biphasic
(positive-negative) waves
 VEMP reveals saccular dysfunction

42.  Glycerol
 Mannitol
 Frusemide
 Isosorbide
 These tests involve the subject ingesting
glycerol or mannitol and observing for a
change in symptoms and a measurable
improvement in hearing
Tests are positive if there is pure tone
improvement of 10dB or more at two / more
frequencies between 200-2000Hz

43.  First introduced by Klockhoff and Lindblom –
1966
 Glycerol is administered in doses of 1.5 mg/kg
body wt in empty stomach
 Serum osmolality should increase at least by 10
mos/kg
 Side effects include Headache, Nausea,
vomiting, drowsiness
 PTA is performed 2-3 hours after administration
 False positivity is rare
 Positivity depends on the phase of the disease

44. • Dietary modifications and diuretics
• Vasodilators
• Symptomatic treatment
– Antiverginous medications
– Antiemetics
– Sedatives
– Antidepressants
– Psychiatric treament
• Local overpressure therapy

45.  Salt restriction and diuresis may be the best
initial therapy for Meniere disease. The goal of
salt restriction and use of diuretics is to reduce
endolymph volume by fluid removal and/or
reduced production.
 Carbonic anhydrase inhibitors such as
acetazolamide were recommended based on the
localization of carbonic anhydrase in the dark
cells and the stria vascularis
 Despite the lack of hard evidence of their
efficacy, we feel that a low-salt diet combined
with diuresis is an appropriate and effective
treatment for Meniere disease that has a low risk
of side effects.

46. • Salt wasting diuretic such as diazide (1 month
trial)
• Betahistine (2 week trial, often combined with
verapamil)
– Relaxes the precapillary sphincters and thus improves
the microcirculation of inner ear
– Antivertigo action due to imhibition of massive
impulses to the polysynaptic lateral vestibular
nucleus)
• Lipoflavins and vitamins ( hypothetical
importance )

47.  Since 2000, the Meniett
device has been approved
for use by the U.S. Food
and Drug Administration
(FDA). The device is a
handheld air-pressure
generator that the patient
can use to self-administer
therapeutic pressure
pulses. The pressure is
delivered in complex
pulses of up to 20 cm of
water delivered over 5
minutes, and the device
requires a ventilation tube
to be placed in the
tympanic membrane prior
to starting therapy

48.  Restoring balance in the hydrodynamic
system of the inner ear by applying low-
pressure pulses to the middle ear
 A randomized controlled trial
demonstrated that patients using the
Meniett device experienced a significant
decrease in vertigo symptoms for the first
3 months of therapy but that findings
afterward were similar to those with
placebo.

49. 1. Classic unilateral Meniere’s disease
2. Intense vestibular / cochlear symptoms
3. Failed medical therapy
4. Over 65 years of age
5. Imbalance / aural fullness / tinnitus after
gentamycin treatment

50.  Intratympanic injection
 Endolymphatic sac surgery
 Nerve section
 Labyrinthectomy

51.  To be offered when vertigo is intractable but the patient still
has some functional hearing.
 The risk of hearing loss or other complications from the
steroid injection appears to be low.
 A small randomized trial has shown complete resolution of
vertigo symptoms in 82% of patients receiving
dexamethasone, compared with 57% receiving saline
injection.
 Dexamethasone injections may need to be repeated every 3
months to maintain the patient free of vertigo symptoms,
although the optimal dosing frequency is variable and
unknown.
 Concentrations used have varied from 2 to 24 mg/mL.

52.  After giving puncture in the TM, with needle
being just above the round window 0.5ml of
hyaluronidase & 1 ml of 16mg dexamethasone
mixed together; injected in ME
 Pt instructed to lie down for 3 hrs with injected
ear up, entire process repeated 3 consecutive
days

53.  Has a vestibulotoxicity that is high relative to its
cochleotoxicity; accordingly, it can be used to control
vestibular symptoms while sparing hearing.
 The gentamicin can be administered through either a
tympanostomy tube or directly injected through the
tympanic membrane.
 Peripheral vestibular deficits are evident on head thrust
testing after even a single dose of gentamicin

54. • 40 mg/ml gentamycin is buffered with soda bicarb (pH6.4) final
concentration 26.7mg/ml.
• 0.7ml of gentamicin injection mixed with 0.3ml of sodium bicarbonate
solution
• Three injections are given per day in outpatient setting
• Injections are given for 4 days
• After injection patient should lie supine with the infiltrated ear up for 30
mins

55.  The ideal procedure for Meniere disease
would restore normal function, or at least
preserve residual function, while stabilizing
the ear. As discussed next, two operative
procedures have been proposed to achieve
this goal:
 Cochleosacculotomy and
 Endolymphatic sac surgery(ELS) surgery.
 Vestibular neurectomy

56.  Cochleosacculotomy aims to create a
fracture dislocation of the osseous spiral
lamina (and hence a permanent fistulization
of the endolymph-containing cochlear duct)
by inserting a hook through the round
window metnbrane.

57.  Sacculotomy was proposed by Fick in 1964,
and consisted of using a needle to puncture
the saccule through the stapes footplate. A
later variation on this technique involved
leaving a sharp prosthesis in the footplate
that ruptured the saccule each time it
expanded.Long-term follow-up of patients so
treated has shown an unacceptable degree of
hearing loss

58. •Cochleosacculotomy creates a
fracture dislocation of osseous spiral
lamina, this procedures have
highdegree of hearing loss
• Helpful in treating debilitated
patients
• Involves disruption of osseous
spiral lamina
• Angular pick introduced via round
window towards oval window. It
will accommodate 3 mm long pick
• After perforation the pick is
withdrawn and the round window
is sealed by fat

59.  Endolynmphatic sac
surgery begins with
simple
mastoidectomy and
identification of the
tegmen, sigmoid
sinus, and facial
ridge.

60.  Once these
landmarks are
established, the
horizontal and
posterior canals
should be
skeletonized and
the bone over the
posterior fossa
thinned

61.  The last shell of
bone covering the
sigmoid sinus (SS)
and the posterior
fossa dura (PFD) is
being removed

62. The superior edge of the
endolymphatic sac
is identified; it usually lies
at or below
Donaldson's line, which
extends posteriorly
along the plane of the
horizontal canal and
bisects the posterior canal.

63. After the sigmoid
sinus (SS) and the
posterior fossa
dura(PFD) have been
uncovered, retraction
of the dura
posteriorly reveals
the endolymphatic
duct (<) exiting
medial to the
posterior semicircular
canal (PSC)

64.  The procedure from
this point varies
according to which
endolymphatic
surgery is
planned.Decompress
ion of the sac
requires only that
the bone of the
posterior fossa plate
be removed

65.  Using microscissors,
the lateral wall of
the endolymphatic
sac(<) is separated
from its medial wall
(^). PSC Posterior
semicircular canal

66.  Endolymphatic shunting is
most simply performed by
incising the exposed sac
and placing a stent to
keep the incision open.
 The popular Paparella and
Hanson technique involves
opening the edge of the
sac, lysing any
intraluminal adhesions,
and probing the duct to
insure that it is patent. A
piece of Silastic" is placed
through the incision in the
sac allowing long-term
drainage
A T-shaped piece of silicone is coiled
and placed into a lateral incision in
the endolymphatic sac to create a
drainage path to the mastoid cavity.

67.  Endolymphatic-subarachnoid
shunt. After exposing and
opening the lateral wall of the
endolymphatic sac, the medial
wall of the sac is incised to
open the lateral prolongation
of the basal cistern. Dissection
in the cistern is carried out
bluntly to avoid venous injury.
A silicone (Silastic®) shunt is
inserted to maintain drainage
path between the
endolymphatic sac and the
basal cistern.The lateral
endolymphatic sac is carefully
closed with a fascia graft to
prevent cerebrospinal fluid
leak.

68.  Several approaches to the vestibular nerve
have been described.
 The earliest approach was the retrosigmoid
 The term retrosigmoid and suboccipital are
now used interchangeably.
 The middle fossa approach to the internal
auditory canal and superior vestibular nerve
was developed by William House in the early
1960s and was later modified to include
inferior vestibular nerve section.

69. The skin incision is made as shown.

70.  An extended
mastoidectomy has been
achieved in a left
temporal bone

71. oThe dura has been uncovered from
the overlying bone.

72.  A 5 × 5-cm
craniotomy flap
(CT) has been
created. Note that
the craniotomy
should be located
posterior to the
sigmoid sinus (SS)
and inferior to the
transverse sinus

73.  A septal raspatory is
used to detach the
craniotomy flap
(CT) from the
underlying posterior
fossa dura

74.  The craniotomy flap
is separated from
the dura.

75.  An anteriorly based
flap (F) is created in
the posterior fossa
dura (PFD) and fixed
anteriorly using
sutures. TS
Transverse sinus

76.  Through the
craniotomy, the
acousticofacial
bundle (AFB)can be
seen entering the
internal auditory
canal (^). IX
Glossopharyngeal
nerve
The vestibular, cochlear, and facial
nerves are identified, and then the
superior and inferior vestibular
nerves can be sectioned .
Afterward the dura is
reapproximated, and the bone flap
is replaced and covered as the
wound is closed.

77. Retrosigmoid approach to vestibular nerve section. The cerebellum is
retracted medially giving a view of the superior and inferior
vestibular nerves. A, The posterior fossa is exposed and nerves are
identified.B, The superior vestibular nerve is separated from the
more anterior facial nerve. C, The superior vestibular nerve has been
sectioned

78. The skin incision is made as shown.
The site of the craniotomy (CT) carried
out for the middle cranial fossa approach.

79.  After the
craniotomy flap
(CT) has been
created in a left
temporal bone, a
septal raspatory is
carefully used to
separate the bony
flap from the
middle fossa dura.

80.  The craniotomy is
successfully elevated from
the middle fossa dura
(MFD). EAC External
auditory canal, ZP Base of
the zygomatic process

81.  The sharp bony
edges are smoothed
using a diamond
burr while the
middle fossa dura
(MFD) is being
retracted using the
suction tube. MFP
Middle fossa plate,
ZP Base of the
zygomatic process

82.  Elevation of the
middle fossa dura
(MFD) from the
middle fossa plate
(MFP).

83.  The first landmark to be
identified is the arcuate
eminence(AE)

84.  As dural elevation
advances anteriorly,
the middle
meningeal artery
(MMA) is identified
next.

85.  The greater petrosal
nerve (GPN) is
identified next

86.  The middle fossa
retractor is fixed at
the petrous ridge
(PR).

87.  The expected
location of the
internal auditory
canal (IAC).
 The bar-shaded
areas are the
locations for
drilling.

88.  A closer view shows
that the location of
the internal
auditory
 canal (IAC) has been
identified

89.  Further drilling
identifies the
posterior fossa dura
(PFD) under
the thin bone
covering.

90.  The bony covering
of the posterior
fossa dura (*) is
being removed.

91.  The bony covering
of the internal
auditory canal and
the posterior fossa
dura anterior to the
canal (*) is being
removed

92.  A hook is used to
create a hole in the
posterior fossa dura.
This step is useful in
live surgery, to
reduce intracranial
pressure

93.  The dura of the
internal auditory
canal (IAC) is being
opened.

94.  The acousticofacial
bundle (AFP) can be
seen within the
opened internal
auditory canal.

95.  The dura of the
internal auditory
canal has been
further removed.
 Bill’s bar (BB) can
be seen at the level
of the fundus.

96.  A small hook is used
carefully to dislodge
the superior
vestibular nerve

97.  The superior
vestibular nerve
(SV) has been
dissected away,
 and the hook now is
being used to
dissect the inferior
vestibular nerve

98.  Vestibular nerve section has a complete
vertigo control rate of about 85 to 95% with
80 to 90%of patients maintaining their
preoperative hearing immediately
postoperatively. The procedure offers much
greater vertigo control rates than
endolymphatic shunt procedures, but is also
a more invasive and technically challenging
procedure.

99.  Labyrinthectomy is the most destructive
procedure in the treatment of Meniere's as it
destroys both hearing and vestibular function
 Ideal candidate is a patient with no
functional hearing and in whom all more
consevative treatment like gentamycin
injection have failed
 There are two approaches:
Transcanal and
Transmastoid approach affords much better
exposure and is more popular.

100. Transcanal labyrinthectomy. A,
Removal of promontory bone and
stapes provides wide exposure of the
vestibule. B, The utricular
neuroepithelium (UN) is removed
from the elliptical recess of the
vestibule.

101.  The limitation of the transcanal approach is
the poor access it yields to the posterior
canal, located medial to the facial nerve;
thus, complete ablation may not be
achieved. The limited exposure also makes
the procedure more technically difficult than
the transmastoid approach.

102.  The transmastoid approach to
labyrinthectomy is more commonly
performed and has the advantage of allowing
direct visualization of the vestibular end
organs as they are removed

103. The approach begins with a standard postauricular incision.The mastoid cavity is
opened with identification of the three semicircular canals and the facial nerve. C,
The three semicircular canals are blue lined and traced to their ampullated ends. D,
The ampullae and neuroepithelium of the three semicircular canals are exposed, along
with the otolithic organs (the saccule and the utricle)

104.  CUMMINGS OTOLARYNGOLOGY HEAD &NECK
SURGERY 6TH EDITION
 Glasscock-Shambaugh surgery of ear 6th
edition
 The Temporal Bone A Manual for Dissection
and Surgical Approaches Mario Sanna, M.D.