30 ENT for Entrance Exams

ANSWERS AND EXPLANATIONS

1. (c) 1st and 2nd pharyngeal arch (Ref. Scott Brown, The bony part of EAC and the mastoid tip are not present at
8th ed., Vol 2, page 541) birth.
2. (a) Improper fusion of auricular tubercles (Ref.
Cummings, 6th ed., 2827) • The middle and inner ear structures attain adult
• The failure of fusion of 1st and 2nd arch leads to size well before birth.
the formation of the “PRE-AURICULAR SINUS”. • TM is also of adult size but, in the absence of bony
This is seen in between the tragus (from 1st arch) part of EAC, is horizontally placed.
and the ascending limb of helix (from 2nd arch) 13. (c) Ear ossicles (Ref. Shambaugh, 6th ed., page 5)
most commonly either above the tragus or at the • The tympanic membrane, middle ear and the
root of helix (see the clinical photo in the inner ear structures are fully developed and are
question). of adult size at birth.
3. (a) 1st branchial groove (Ref. Scott Brown, 8th ed., • Orbital structures continue to grow after birth.
Vol 2, page 541) 14. (a) Ear ossicles (Ref. Scott Brown, 8th ed., Vol 2, page
4. (a) 1st branchial cleft anomaly (Ref. Scott Brown, 8th 540)
ed., Vol 2, page 541) • Maxilla and Parietal bone continue to grow after
5. (b) 5–7 years of age (please refer to text) (Ref. birth.
Cummings, 6th ed., 3000) 15. (b) Petrous part of temporal bone (Ref. Shambaugh,
6. (b) and (c) 1st pharyngeal pouch, 2nd pharyngeal 6th ed., page 32) (see the explanation below)
pouch (Ref. Scott Brown, 8th ed., Vol 2, page 540) 16. (b) Cartilaginous bone (Ref. Scott Brown, 8th ed., Vol
2, page 542)
Pharyngeal pouch Structure develops • Cartilaginous bones ossify from a cartilage model
1st and a small part of Middle ear cleft, i.e. Eustachian (endochondral bone formation), e.g. Bony
2nd (also called as tubo- tube, tympanic cavity and labyrinth also called as Otic capsule
tympanic recess) mastoid antrum. • In contrast to cartilaginous bone, membranous
2nd Tonsil bone also called as dermal bone does not form
3rd Inferior parathyroids and the from cartilage that then calcifies. Dermal bone is
thymus formed within the dermis and grows by accretion
only–the outer portion of the bone is deposited
4th Superior parathyroids and
by osteoblasts. Examples of membranous or
some part of the thyroid
dermal bones are clavicle and patella.
7. (b) Pharyngotympanic tube (Ref. Shambaugh, 6th ed., • Inner ear bony labyrinth is present in the petrous
page 7) part of temporal bone. It is known as petrous
8. (a) Tympanic membrane (Ref. Scott Brown, 8th ed., (which means rock like) as it is one of the densest
Vol 2, page 540) bones of the body, though not the strongest. The
• The 1st cleft grows and meet 1st pouch medially strongest bone of the body is the femur.
to form the tympanic membrane. 17. (d) Malleus (Ref. Scott Brown, 8th ed., Vol 2, page 538)
• So the tympanic membrane is made from all the • Pneumatic bones are those bones which contain
3 layers, outer epithelial layer from ectoderm and an air filled cavity within them which make them
inner endothelial layer from endoderm and in light in weight. In humans, they are seen in
between these is the fibrous layer from relation to the nasal cavity, and enclose the
mesoderm. paranasal sinuses. Besides making the skull light
• Retina develops from neuro-ectoderm. in weight, they also help in resonance of sound
Ear

• Dura mater is derived from mesoderm. Pia and and act as air conditioning chambers for the
arachnoid are derived from neural crest. inspired air.
9. (b) 2nd arch (Ref. Scott Brown, 8th ed., Vol 2, page 540) • Pneumatic bones are–maxilla, frontal bone,
10. (b), (d), (e) are true (please refer the text) (Ref. Scott sphenoid and ethmoid.
Brown, 8th ed., Vol 2, page 540) • The mastoid is also most commonly a pneumatic
11. (a) Petrosquamous suture (Ref. Shambaugh, 6th ed., (air filled) bone which encloses numerous air cell
Section I

page 32) spaces giving it a honeycomb appearance.

12. (d) Mastoid (Ref. Shambaugh, 6th ed., page 5) However in some people the mastoid may be
• The mastoid is incompletely developed at birth diploic (marrow filled) or sclerotic (solid bone
and continues to develop till 18 years of age. without air).
• The largest air cell of mastoid called as mastoid 18. (c) Semicircular canal (Ref. Shambaugh, 6th ed., page 42)
antrum is present at birth and is of adult • The posterior and superior semicircular canals
configuration. fuse together to form a common crus called as
 Embryology and Anatomy of Ear 31

“crus commune” which opens into the utricle. • CSF being an extracellular fluid therefore
Because of this the three semicircular canals open perilymph is rich in Na+.
into utricle by five openings instead of six. • Endolymph filling the membranous labyrinth
19. (d) Utriculo saccular duct to endolymphatic sac, and secreted from stria vascularis is rich in
please see the text. (Ref. Shambaugh, 6th ed., page 42) K +.
20. (c) Organ of Corti (it is a part of membranous 33. (b) Scala media (Ref. Scott Brown, 8th ed., Vol 2, page
labyrinth) (Ref. Shambaugh, 6th ed., page 42) 545)
21. (c) 2 ¾, modiolus (Ref. Shambaugh, 6th ed., page 42) • Endolymph is present in the membranous
22. (a) Scala media (Ref. Shambaugh, 6th ed., page 73) labyrinth, whereas perilymph is present in the
bony labyrinth.
23. (b) 20 weeks (Ref. Shambaugh, 6th ed., page 11)
24. (a) Organ of Corti (Ref. Shambaugh, 6th ed., page 73) • Hence scala vestibuli, scala tympani and
their interconnection helicotrema, which are
25. (c) Rotation (Ref. Shambaugh, 6th ed., page 113)
parts of bony labyrinth, are filled with peri-
• Semicircular canals contain cristae which sense lymph.
angular or rotational acceleration.
• Scala media, utricle, saccule and semicircular
• Gravitational movements, head tilt and linear canals, which are parts of membranous labyrinth,
acceleration are sensed by maculae in the utricle are filled with endolymph.
and saccule.
34. (c) Endolymph (Ref. Scott Brown, 8th ed., Vol 2, page
• Sound is sensed by organ of Corti present in
545)
the scala media, situated on the basilar memb-
rane. • Rest are extracellular hence have more of
sodium.
26. (b) Rotational acceleration (Ref. Shambaugh, 6th ed.,
page 113) 35. (a) Connects internal ear with subarachnoid space
(Ref. Scott Brown, 8th ed., Vol 2, page 545)
• The horizontal/lateral semicircular canal along
• The internal ear communicates with the cranium
with posterior and superior semicircular canal
via two openings:
contains cristae which sense angular or rotational
acceleration. 1. Cochlear aqueduct: via this CSF in the
• Horizontal acceleration, i.e. linear acceleration, subarachnoid space enters scala tympani and
gravitational movements and head tilt becomes perilymph which circulates in the
movements are sensed by maculae in the utricle bony labyrinth.
and saccule. 2. Internal acoustic meatus
27. (d) Semicircular canals (Ref. Shambaugh, 6th ed., page • Membranous cochlea is a part of membranous
113) labyrinth which is a closed sac and is not
connected to vestibule which is a part of the bony
28. (b) Oval window (Ref. Shambaugh, 6th ed., page 38)
labyrinth.
• The Oval window is covered by the footplate of
• Endolymphatic sac is a blind pouch responsible
stapes.
for absorption of endolymph and is situated in
• The Round window is covered by secondary between the endosteal and meningeal layer of the
tympanic membrane. dura mater.
• The part of middle ear medial to the descending 36. (a) Cochlear Aqueduct (Ref. Cummings, 6th ed., 2992)
part of facial nerve is called sinus tympani.
• Endolymphatic sac is a closed sac. It does not
• Pyramid is the projection on posterior wall from communicate with CSF.
which originates the stapedius muscle. • The bony canal around the utriculo-saccular duct
29. (c) Scala vestibuli, please refer the text (Ref. and endolymphatic duct is called vestibular
Cummings, 6th ed., 1997) aqueduct
Ear
30. (c) Scala tympani (Ref. Shambaugh, 6th ed., page 599) • Hyrtle fissure is a tympanomeningeal fissure
• The electrodes of cochlear implant are placed into which obliterates by 26 weeks period of gestation.
the Scala tympani by passing through the round If persistent it can lead to a connection between
window. CSF and middle ear.
31. (d) Delivering drug to round window membrane 37. (a) Cochlear Aqueduct (Ref. Cummings, 6th ed., 2992;
Section I

(Ref. Scott Brown, 8th ed., Vol 2, page 580) 2169)

32. (a) Na+ (Ref. Shambaugh, 6th ed., page 79) 38. (c) Scheibe dysplasia (Ref. Cummings, 6th ed., 2982)
• Perilymph is the fluid which fills the bony 39. (b) Loose on medial side (Ref. Scott Brown, 8th ed.,
labyrinth. Vol 2, page 526)
• Perilymph is actually an extension of CSF which • The skin on the lateral side of pinna is firmly
enters from the subarachnoid space into the scala attached because of which any inflammatory
tympani through Cochlear aqueduct. condition on the lateral side is more painful.
 32 ENT for Entrance Exams

40. (b) 24 mm (Ref. Scott Brown, 8th ed., Vol 2, page 527) 51. (a) Vagus (Ref. Shambaugh, 6th ed., page 30)
41. (b) Lateral 1/3 (Ref. Scott Brown, 8th ed., Vol 2, page 52. (d) Greater auricular nerve (Ref. Shambaugh, 6th ed.,
527) page 30)
42. (b) Modified apocrine glands (Ref. Shambaugh, 6th 53. (b) Glossopharyngeal nerve (Ref. Shambaugh, 6th ed.,
ed., page 30) page 30)
• Ceruminous glands are modified sudoriferous • Glossopharyngeal does not supply auricle and
glands (sweat glands) located subcutaneously in external auditory canal. It gives sensory supply
the external auditory canal. They are apocrine to middle ear.
glands, i.e. while discharging the secretions their 54. (c) and (d) (Ref. Current Diagnosis and Treatment
cell’s apical parts are shed off. Otolaryngology, Lalwani, 3rd ed., 600)
• Eccrine or merocrine glands secretions are • Sphenopalatine ganglion is the largest para-
thrown out of the cells by a process of exocytosis, sympathetic ganglion responsible for lacrimation,
the cell remaining intact, e.g. sweat glands. nasal secretion and palatine secretion.
• In some glands the entire cell disintegrates while • The greater superficial petrosal nerve originates
discharging its secretion. These are said to be from the geniculate ganglion of facial nerve. It
holocrine glands, e.g. sebaceous glands. then joins with the deep petrosal nerve to form
• Apocrine, merocrine and holocrine are the the vidian nerve and then through the
descriptions of exocrine glands i.e. the glands sphenopalatine ganglion supplies lacrimal, nasal
which pour their secretions on to an epithelial and palatine glands. See chapter on the anatomy
surface directly or through ducts. of nose.
• Endocrine glands pour their secretions into 55. (c) The Xth cranial nerve (Ref. Shambaugh, 6th ed.,
blood. page 45)
43. (a) Fissure of Santorini (please see the text) (Ref. • The Xth cranial nerve also supplying the larynx
Cummings, 6th ed., 1981) leads to cough on cleaning the ear canal.
• The notch of Rivinus is the upper attachment of 56. (a) Vagus (Ref. Shambaugh, 6th ed., page 45)
pars flaccida. 57. (a), (b) and (e) (Ref. Scott Brown, 8th ed., Vol 2, page
• Petro-tympanic fissure is present on the anterior 529)
wall of middle ear, on which attaches the anterior 58. (b) Glossopharyngeal (Ref. Scott Brown, 8th ed., Vol
malleolar ligament. 2 page 535)
Retropharyngeal fissure does not exist. • The sensory supply of the middle ear is by the
44. (a) Pearly grey (Ref. Scott Brown, 8th ed., Vol 2, page 923) tympanic plexus which is formed by the
Condition of the ear Colour of TM Jacobson’s nerve which is the tympanic branch
Normal Pearly grey of Glossopharyngeal (IX) along with sympathetic
Glue ear or SOM Blue plexus from around the internal carotid.
ASOM Red (congested) 59. (a) IX nerve, i.e. the glossopharyngeal nerve (Ref.
Active otosclerosis Flamingo pink Scott Brown, 8th ed., Vol 2, page 535)
The rest of the nerves do not supply the ear.
45. (b) Shrapnell’s membrane (Ref. Shambaugh, 6th ed.,
page 380) 60. (d) Vestibule of nose (Ref. Shambaugh, 6th ed., page
45)
• Reissner’s membrane separates Scala media from
Scala vestibuli in the inner ear. • Vestibule of nose is supplied by the maxillary
• Basilar membrane separates Scala media or nerve which does not supply the ear.
cochlear duct from Scala tympani in the inner ear. • Pharynx is supplied by the pharyngeal plexus
formed by the vagus and Glossopharyngeal, both
Ear

The organ of Corti rests on the basilar membrane.

• Secondary TM overlies the round window in the of which also supply the ear.
middle ear. • Tongue is supplied by the lingual branch of
46. (b) Peripheral (Ref. Scott Brown, 7th ed., page 3180) mandibular, Glossopharyngeal and vagus, all of
which also supply the ear.
• Peripheral is the best answer here (please refer
to the text). • TM joint is supplied by the Auriculotemporal
Section I

47. (d) 90 mm2 (Ref. Dhingra, 6th ed., page 14) nerve which also supplies the ear.
48. (d) 55 mm2 (Ref. Dhingra, 6th ed., page 14) 61. (d) All of the above (Ref. Shambaugh, 6th ed., page 45)
49. (b) Auriculotemporal (Ref. Scott Brown, 8th ed., Vol • Larynx is supplied by the vagus which also
2, page 526) supplies the ear.
50. (a) Greater occipital nerve (Ref. Shambaugh, 6th ed., • Tongue and oral cavity is supplied by the lingual
page 30) (does not supply pinna, please see text for branch of mandibular, Glossopharyngeal and
the nerve supply of external ear). vagus, all of which also supply the ear.
 Embryology and Anatomy of Ear 33

62. (c) Glossopharyngeal nerve (Ref. Shambaugh 6th ed., • Sinus tympani is the area on the posterior wall
page 45) of mesotympanum medial to the bulge of vertical
• The base of tongue is mainly supplied by the part of facial nerve.
glossopharyngeal nerve which also supplies the • Pyramid is a projection of bone on the posterior
ear. wall from which originates the stapedius muscle.
68. (a) Round window (Ref. Scott Brown, 8th ed., Vol 2,
page 580)
• Anterior 2/3rd of the tongue is supplied by lingual nerve (a 69. (d) All of the above (Ref. Cummings, 6th ed., 509; 2192)
branch of mandibular). Auriculotemporal nerve also a branch • Facial recess is an area on the posterior wall of
of mandibular nerve supplies the ear so in carcinoma anterior middle ear. The facial recess is limited superiorly
2/3rd of tongue pain is referred to ear through mandibular by the fossa incudis, laterally by chorda tympani
nerve. entry and medially by the descending/vertical
• Posterior 1/3rd, i.e. the base of the tongue is mainly supplied facial nerve segment.
by glossopharyngeal nerve and the posterior most part of • The facial recess is the site where opening is made
this posterior 1/3rd tongue is supplied by vagus, both of which on the posterior wall to access the middle ear
also supply the ear, so in carcinoma of this part of tongue,
cavity through the mastoid in “INTACT CANAL
pain will be referred to ear through both glossopharyngeal
WALL” ear surgeries. This is known as the
and vagus.
posterior tympanotomy approach. See chapter on
• But since glossopharyngeal supplies most of the base of the
tongue so in pathologies of base of tongue the pain is referred unsafe CSOM
to the ear mainly through the glossopharyngeal nerve. 70. (a) Facial nerve horizontal part (Ref. Cummings, 6th
ed., 509; 2192)
63. (b) Facial nerve (Ref. Scott Brown, 8th ed., Vol 2, page 580) 71. (b) Medially it is bounded by chorda tympani and
• The stapedius muscle is a second arch derivative laterally by facial nerve (Ref. Cummings, 6th ed., 509)
and therefore is supplied by the nerve of the 2nd • Medially the facial recess is bounded by facial
arch, i.e. facial nerve. nerve and laterally by chorda tympani
64. (a) Anterior part of V nerve (Ref. Shambaugh, 6th ed., 72. (a) Anterior wall (Ref. Shambaugh, 6th ed., page 245)
page 38) 73. (c) 36 mm (Ref. Shambaugh, 6th ed., page 245)
• The tensor tympani muscle is a derivative of 1st 74. (d) and (e) (Ref. Scott Brown, 8th ed., Vol 2, page 537)
arch and is supplied by the nerve of the 1st arch, • The total length of Eustachian tube is about
i.e. mandibular nerve (anterior or motor branch). 36 mm (32–38 mm), the lateral or outer 1/3rd,
65. (b) Basal turn of cochlea (Ref. Shambaugh, 6th ed., i.e. 12 mm is bony, whereas the medial or inner
page 39) 2/3rd, i.e. 24 mm is cartilaginous.
• Promontory is a bulge in the centre of the medial • Eustachian tube normally remains closed and
wall of middle ear, produced by the basal turn opens intermittently during swallowing,
of cochlea. On the promontory, tympanic plexus yawning and sneezing.
is present 75. (a), (c) and (e) (Ref. Shambaugh, 6th ed., page 245)
• The length of Eustachian tube is 32–38 mm, i.e.
• Lateral semicircular canal bulge is present on the
3.2–3.8 cm.
most postero-superior portion of the medial wall
of middle ear just above the horizontal or • Its 1/3rd part is bony and 2/3rd part is
tympanic segment of facial nerve. cartilaginous, just the opposite of EAC.
• Jugular bulb is below the floor of the middle ear • Eustachian tube normally remains closed and
• Body of incus is present in the epitympanum of opens intermittently during swallowing, yawning
middle ear cavity. and sneezing.
• Tensor palati plays the major role in opening the tube
Ear
66. (a) Tendon of tensor tympani (Ref. Shambaugh, 6th
ed. page 38) • The narrowest part of Eustachian tube is the
• Processus Cochleariformis is a hook like structure junction of the bony and cartilaginous parts
present antero-superiorly on the medial wall of known as isthmus.
middle ear. 76. (b) Higher elastin content in adults, refer the text
• The tensor tympani muscle originating from a (Ref. Cummings, 6th ed., 2028)
Section I

canal in the anterior wall of middle ear runs 77. (c) Tensor veli palatini (Ref. Shambaugh, 6th ed., page
medially where its tendon winds around the 245)
processus cochleariformis and then turns 78. (b) Bulb of the internal jugular vein (Ref. Cummings,
laterally to get attached on the upper part of the 6th ed., 1983)
handle of malleus (i.e. just below its neck). • The floor of middle ear cavity is a thin plate of
67. (b) Oval window (Ref. Shambaugh, 6th ed., page 38) bone separating the middle ear from jugular bulb
• Round window is covered by secondary TM. below.
 34 ENT for Entrance Exams

• Internal carotid artery is in relation to the anterior 86. (b) Mastoid antrum (Ref. Shambaugh, 6th ed., page 32)
wall of middle ear. • Macewen’s” triangle or suprameatal triangle is a
• Sigmoid sinus is not related directly with middle bony landmark for mastoid antrum. It is
ear cavity. It lies posterior to the mastoid antrum. important while doing mastoid surgeries in
• Round window lies postero-inferiorly on the approaching the mastoid antrum.
medial wall of middle ear. 87. (a) Mastoid antrum (Ref. Shambaugh, 6th ed., page 32)
79. (c) Roof of middle ear (Ref. Cummings, 6th ed., 1983) 88. (a) Mastoid antrum (Ref. Shambaugh, 6th ed., page 32)
• The roof of the middle ear is known as “TEGMEN 89. (a) Squamous temporal (Ref. Scott Brown, 8th ed., Vol
TYMPANI”. It separates the middle ear from the 2, page 543)
middle cranial fossa. • Tegmen Antri forms the roof of antrum.
80. (d) 2 mm (Ref. BD Chaurasia, Human Anatomy 6th ed., • The medial wall of mastoid antrum is related to
Vol 3, page 277) the posterior semicircular canal, which lies in its
Part of the middle ear cavity Distance from lateral to medial wall superior aspect.
90. (c) Promontory (refer the text) (Ref. Shambaugh, 6th
Epitympanum 6 mm (widest)
ed., page 32)
Mesotympanum (centre) 2 mm (narrowest)
Hypotympanum 4 mm 91. (a) Mastoid antrum lies 1.5 cm deep to it (Ref.
Shambaugh, 6th ed., page 32)
81. (a) 2 mm (Ref. BD Chaurasia, Human Anatomy 6th ed., • It is a surgical landmark for the mastoid antrum,
Vol 3, page 277) lying in the postauricular area. It is bounded
• The promontory is present in the centre of medial superiorly by temporal line/supra mastoid crest
wall of middle ear. Its distance from umbo is the which is the posterior extension of suprameatal
narrowest part of the middle ear, i.e. about 2 mm. crest.
82. (d) Mesotympanum–2 mm (Ref. BD Chaurasia, • The suprameatal crest is the superior root of the
Human Anatomy 6th ed., Vol 3, page 277) zygomatic process.
• Epitympanum or attic is widest–6 mm 92. (c) Sinodural angle (Ref. Shambaugh, 6th ed., page 775)
• Hypotympanum–4 mm 93. (b) Mastoid (Ref. Shambaugh, 6th ed., page 773)
83. (a) Epitympanum (Ref. Cummings, 6th ed., 1983) 94. (a) Basilar membrane (Ref. Shambaugh, 6th ed., page
• The space of the epitympanum, lying in between 73)
the Shrapnell’s membrane or pars flaccida and the • Organ of Corti rests on the Basilar membrane
neck of malleus is known as “PRUSSAK’S SPACE”. which separates Scala media from Scala tympani.
• When the retraction pocket on Pars flaccida • Utricle and Saccule contain the sensory end organ
grows medially, it goes into this Prussak’s space of balance for linear acceleration known as
making this the most common site of primary maculae.
cholesteatoma. 95. (b) is secreted by stria vascularis (Ref. Scott Brown,
84. (d) Foot plate of stapes (it is in mesotympanum) (Ref. 8th ed., Vol 2, page 583)
Cummings, 6th ed., 1983) • Endolymph is the fluid that fills in whole of the
Epitympanum contains Mesotympanum contains membranous labyrinth (i.e. the three semicircular
1. Head, neck, anterior and Handle of malleus canals, utricle, saccule and the scala media).
lateral process of malleus • It is secreted by stria vascularis.
2. Body and short process Long process of incus • It is absorbed by the endolymphatic duct.
of incus
96. (a) +80 mV (Ref. Shambaugh, 6th ed., page 79)
3. Incudomalleolar joint (the Incudostapedial joint and
head of malleus articulates the whole of the stapes • The endolymph is rich in K+ which leads to the
with the body of incus) development of an endolymphatic potential of +
Ear

4. The Chorda tympani nerve — 80–85 mV.

5. Prussak’s space — 97. (c) To maintain electric milieu of endolymph (Ref.
Scott Brown, 8th ed., Vol 2, page 561)
• The hypotympanum does not contain anything.
85. (d) Synovial joint (Ref. Scott Brown, 8th ed., Vol 2 page 98. (d) Hair cell (Ref. Scott Brown, 8th ed., Vol 2, page 558)
533) 99. (c) Genu of internal capsule (Ref. Cummings, 6th ed.,
Section I

• The head of malleus articulates with the body of 1991)

incus. This incudomalleolar joint is a saddle type • Genu of internal capsule is not concerned with
of synovial joint. auditory pathway; it is the posterior limb of
• The long process of incus ends in a lentiform internal capsule through which ultimately the
nodule. This lentiform nodule of incus articulates fibres pass through and reach the auditory cortex.
with the head of stapes. This incudostapedial 100. (a) Auditory pathway (Ref. Cummings, 6th ed., 1991)
joint is a ball and socket type of synovial joint. 101. (d) Sound localisation (Ref. Cummings, 6th ed., 1991)
 Embryology and Anatomy of Ear 35

102. (d) Transverse temporal gyrus (Ref. Cummings, 6th 117. (d) Vestibule (Ref. Scott Brown, 8th ed., Vol 2, page
ed., 1991) 531)
103. (c) Linear acceleration (Ref. Shambaugh, 6th ed., page 118. (a) Surface ectoderm (Ref. Shambaugh, 6th ed., page
113) 9)
104. (a) Macula (Ref. Shambaugh, 6th ed., page 113) 119. (b) Michel aplasia (Ref. Cummings, 6th ed., 2983)
• Maculae sense linear acceleration, gravitational 120. (a) One (Ref. Scott Brown, 8th ed., Vol 2, page 526)
(movement either with or against gravity) and 121. (a) IX (Ref. Shambaugh, 6th ed., page 45)
head tilt movements and they also help to 122. (c) Root of helix (Ref. Scott Brown, 8th ed., Vol 2, page
maintain static equilibrium (by facilitating 541)
postural, tonic neck and righting reflexes) 123. (c) Facial recess (Ref. Scott Brown, 8th ed., Vol 2, page
105. (a) Otolith– made up of uric acid crystals (Ref. 531)
Shambaugh, 6th ed., page 113) 124. (c) Jacobson’s nerve (Ref. Shambaugh, 6th ed., page
• Otolith is made up of calcium carbonate. 30)
• They are present in the maculae and stimulated 125. (c) Greater auricular (Ref. Shambaugh, 6th ed., page
by gravity, linear acceleration and head tilt 30)
movements.
126. (c) Greater auricular nerve (Ref. Scott Brown, 8th ed.,
106. (a) Utricle and saccule–cristae (Ref. Shambaugh, 6th Vol 2, page 526)
ed., page 113)
127. (b) Middle and inner (Ref. Scott Brown, 8th ed., Vol 2
• Utricle and saccule contain maculae. page 530)
• Cristae are present in the semicircular canal.
128. (c) Mastoid antrum (Ref. BD Chaurasia, Human
• Foot plate of stapes overlies oval window. Anatomy, 6th ed., Vol 3, 281)
• Macewen’s triangle or suprameatal triangle is the 129. (b) 55 degrees (Ref. Scott Brown, 8th ed., Vol 2, page
bony landmark of mastoid antrum. 529)
• Scala vestibuli is separated from scala media by 130. (d) (Ref. Shambaugh, 6th ed., 599) The middle ear is
Reissner’s membrane. seen here. The marked structure is the round
107. (a) Bill’s bar (Ref. Shambaugh, 6th ed., page 42) window, through which the cochlear implant
• Ponticulus is a ridge which runs from the oval electrodes are introduced into the inner ear.
window to the sinus tympani forming its superior • Stapes foot plate is present on the oval window,
extent. which is seen in the picture above the round
• Cog is a bony projection from the roof of middle window opening
ear, i.e. tegmen tympani to the processus • Intact canal wall surgery is done through the
cochleariformis, serving as an approximate facial recess present on the posterior wall of the
landmark for the facial nerve. middle ear, not visible in the picture
• Falciform crest divides the internal acoustic • ET tube ventilates the middle ear which is present
meatus into a superior and inferior part. on the anterior wall, not visible in the picture
108. (b) Inferior vestibular nerve supplying posterior 131. (a) Facial recess (Ref. Cummings, 6th ed., 2192)
semicircular canal (Please refer the text) (Ref. • In the given picture, the encircled area is the facial
Shambaugh, 6th ed., page 45) recess through which the round window opening
109. (d) Anterior inferior cerebellar artery (Ref. Shambaugh, is visible, also see the schematic picture below.
6th ed., page 47)
• The inner ear is supplied by Labyrinthine artery
which is a branch of Anterior inferior cerebellar
artery or sometimes the basilar artery.
110. (a) Lateral wall of attic (Ref. Scott Brown, 8th ed., Vol
Ear
2, page 529)
111. (a) Connects middle ear to pharynx (Ref. Cummings,
6th ed., 2028)
112. (b) Regulation of distortion activated ion channels
(Ref. Scott Brown, 8th ed., Vol 2, page 554)
Section I

113. (a) Saddle (Ref. BD Chaurasia, Human Anatomy, 6th

ed., Vol 3, page 280) • Facial recess is used to approach the middle ear
114. (a) Postero-lateral part of helix (Ref. Scott Brown, 8th through the mastoid, e.g. in cochlear implanta-
ed., Vol 2, page 525) tion and in intact canal wall surgeries of the
115. (b) Arnolds (Ref. Shambaugh, 6th ed., page 30) mastoid.
116. (c) Downwards, forwards, medially (Ref. Scott Brown, Schematic picture of facial recess, through
8th ed., Vol 2, page 527) which a drill is pointing towards round window:
 36 ENT for Entrance Exams

132. (a) It is the landmark for mastoid antrum (Ref. 145. (c) Utricle (Ref. Shambaugh, 6th ed., page 42)
Shambaugh, 6th ed., page 32) 146. (a) 2.4 cm (Ref. Scott Brown, 8th ed., Vol 2, page 527)
• The marked area is the Macewen’s or suprameatal 147. (a) Petro squamous suture (Ref. Shambaugh, 6th ed.,
triangle. It is the landmark for mastoid antrum. page 32)
• Trautmann’s triangle is present on the medial 148. (a) Malleus (Ref. Scott Brown, 8th ed., Vol 2, page 535)
wall of mastoid antrum and is the landmark to 149. (b) Glossopharyngeal (Ref. Scott Brown, 8th ed., Vol
approach posterior cranial fossa. 2, page 531)
• Prussak’s space is a space in the epitympanum 150. (b) ICF (Ref. Scott Brown, 8th ed., Vol 2, page 545)
lying medial to pars flaccida, please see the text. • Endolymph resembles intracellular fluid as it
• Myringotomy is making an opening on the TM has more of K+.
to remove fluid or pus from the middle ear. • Perilymph resembles intracellular fluid as it has
Mastoid is not opened while doing myringotomy. more of Na+.
133. (d) Otoliths: Semicircular canals (Ref. Cummings, 6th 151. (c) Abducens nerve (Ref. Shambaugh, 6th ed., page 45)
ed., 2014) 152. (c) Sinodural angle (Ref. Shambaugh, 6th ed., page 775)
134. (b) Fissures of Santorini (Ref. Cummings, 6th ed., 153. (d) Anteroinferior (Ref. BD Chaurasia, Human
1981) Anatomy, 6th ed., Vol 3, 276)
135. (a) 7th cranial nerve (Ref. Scott Brown, 8th ed., Vol 2, 154. (c) Valsalva manoeuvre opens ET (Ref. Scott Brown
page 539) 8th ed., Vol 2, page 537)
136. (a) Cochlea (Ref. Shambaugh, 6th ed., page 73)
155. (c) Stapedius (Ref. Scott Brown, 8th ed., Vol 2, page
137. (a) Utricle (Ref. Cummings, 6th ed., 2014) 535)
138. (c) Dysplasia of cochlea and saccule (Ref. Cummings, 156. (b) Fixation of footplate of stapes (Ref. Scott Brown,
6th ed., 2982) 8th ed., Vol 2, page 108)
139. (d) +85 mV (Ref. Scott Brown, 8th ed., Vol 2, page 545) • According to Teunissen and Cremers classifi-
140. (a) Stylomastoid foramen (Ref. Cummings, 6th ed., cation, the most common congenital anomaly of
1985) the middle ear is fixation of footplate of stapes.
141. (a) Superior temporal gyrus (Ref. Cummings, 6th ed., 157. (a) 2 ml (Ref. Scott Brown, 8th ed., Vol 2, page 538)
1991)
158. (c) Eustachian tube (Ref. Cummings 6th ed., 2031)
• The middle and inferior temporal gyrus are
involved in cognitive processes, semantic 159. (a) Semi-circular canal (Ref. Scott Brown, 8th ed., Vol
memory, language process, visual perception and 2, page 529)
integrating information from different senses. 160. (a) Malleus and round window (Ref. Scott Brown,
142. (b) VII (Ref. Cummings, 6th ed., 1985) 8th ed., Vol 2, page 531)
143. (c) Utricle (Ref. Cummings, 6th ed., 2014) 161. (b) Posterior part is more easily assessible (Ref. Scott
144. (c) Vestibulocochlear nerve (Ref. Scott Brown, 8th ed., Brown, 8th ed., Vol 2 page 529)
Vol 2, page 539) 162. (b) Glutamate (Ref. Scott Brown, Vol 2, page 756)
Ear
Section I
 60 ENT for Entrance Exams

ANSWERS AND EXPLANATIONS • Old age (presbycusis) leads to SN hearing loss.

• Loud noise induced hearing loss is associated
1. (b) No alteration of sound intensity. (Ref. Scott with pathological changes in cochlea leading to
Brown, 8th ed., Vol 2; 578) SN hearing loss. Noise trauma, presbycusis and
• Whenever there is a sound of 70–100 dB above ototoxic drugs involve basal turns of cochlea first;
the hearing threshold of the person, the stapedial thereby affect high frequency sounds early.
reflex gets activated which does not allow a high • Cochlear otosclerosis leads to sensory hearing
intensity sound to damage the inner ear thereby loss.
protecting the inner ear from noise trauma. 9. (b) 1000–3000 (Ref. Scott Brown, 8th ed., Vol 2; 578)
• The transformer action of the middle ear reduces 10. (c) 500–2000 Hz (Ref. Dhingra, 6th ed., 15)
the impedance (resistance) and increases the
11. (b) Grant’s test (Ref. Scott Brown, 8th ed., Vol 2; 927)
admittance of sound, thereby amplifying the
sound intensity during normal hearing. (there is no entity in ENT called Grant’s test)
2. (a) Impedance matching (Please refer to text) 12. (a) Better heard (Ref. Cummings 6th ed., 2202)
(Ref. Scott Brown, 8th ed, Vol 2; 578) • The tuning fork tests are most commonly done
3. (b) 1.3:1 (Ref. Cummings, 6th ed., 1996) with 512 Hz (or FPS, i.e. frequency per second)
• The handle of malleus is 1.3 times longer than sound frequency producing forks because these
the long process of incus so that the lever ratio is are better heard.
1.3:1. • Tuning forks with frequency less than 512 have
• 17: 1 is the Areal ratio more of vibration sense and those with frequency
above 512 dampen very fast because of which
• 22 is the total transformer ratio of middle ear
comparison is not possible.
(Areal ratio × lever ratio), see the text
13. (b) 512 Hz (Ref. Cummings, 6th ed., 2202)
4. (a) 17:1 (Ref. Dhingra, 6th ed., 14)
14. (c) Tympanosclerosis (Ref. Cummings, 6th ed., 2203)
5. (a) Difference of surface area of tympanic
membrane and foot plate (Ref. Scott Brown, 8th ed., • Tympanosclerosis being a conductive pathology
Vol 2; 578) so BC > AC so Rinne will be negative.
6. (b) and (c) Helmholtz and Bekesy (Ref. Cummings, All the other options being SN deafness so AC >
6th ed., 1997, 2201) BC so Rinne will be positive.
• Bekesy evolved his travelling-wave theory for 15. (b) CSOM (Ref. Cummings, 6th ed., 2203)
which he received the Nobel Prize. • CSOM being a conductive pathology so BC > AC
• Helmholtz detected the sound amplifying effect so Rinne will be negative.
of the eardrum and the auditory ossicles. All the other options being SN deafness so AC >
Furthermore, he developed the resonance–theory BC so Rinne will be positive.
of the perception of pitch in the inner ear. This 16. (a) 15–20 dB (Ref. Cummings, 6th ed., 2203; Anirban
theory postulates that specific frequencies are Biswas, 5th ed., 27)
displayed on definite locations of the cochlea of 17. (a) AC>BC (Ref. Shambaugh, 6th ed., 181)
the inner ear (place theory of pitch perception). 18. (d) Presbycusis (Ref. Shambaugh, 6th ed., 181)
This was replaced by the travelling wave theory • Presbycusis being a SN pathology so AC > BC so
by Georg v. Békésy Rinne will be positive.
7. (c) Stapes abnormal at oval window (Ref. Scott All the other options being conductive deafness
Brown, 8th ed., Vol 2; 1063) so BC > AC so Rinne will be negative.
• From pinna to foot plate of stapes occurs the 19. (b) Normal individual (Ref. Shambaugh, 6th ed., 181)
conduction of sound. So this is the conductive
• Rinne is said to be positive when AC > BC.
pathway and any defect here will lead to a
Ear

• In normal ear air conduction is more than the

conductive deafness.
bone conduction due to the transformer action
• While travelling in an aeroplane, sudden changes
of the middle ear.
in pressure during descent, leads to forceful
closure of the Eustachian tube and tympanic All the other options are conductive deafness
membrane retraction leading to temporary conditions so BC > AC, i.e. Rinne will be negative.
conductive hearing loss and earache. This can be 20. (d) Placing the tuning fork on the forehead and
Section I

overcome by Valsalva manoeuvre. asking him to report in which ear he hears it better
• Trauma to labyrinth will lead to SN hearing loss. (Ref. Scott Brown, 8th ed., Vol 2; 927)
• Noise induced hearing loss is associated with 21. (a) 5 dB (Ref. Cummings, 6th ed., 2213)
pathological changes in cochlea leading to SN 22. (c) Lateralised to right side (Ref. Scott Brown, 8th ed.,
hearing loss. Vol 2; 928)
8. (d) Rupture of tympanic membrane (leads to • Middle ear pathology indicates conductive
conductive deafness). (Ref. Cummings, 6th ed., 2201) deafness so Weber will be lateralised to the right
 Physiology of Hearing and Audiology 61

side in the right ear pathology, i.e. towards the 31. (d) Do Schwabach test (Ref. Dhingra, 6th ed., 22)
worst side. With Rinne test positive in both ears means either
• Weber is lateralised to the Worst ear in the hearing is normal or there is SN hearing loss in
Conductive hearing loss and Better ear in other words there is no conductive hearing loss.
Sensorineural hearing loss. (Mnemonic: We Since here the Weber lateralizes to the right means
Create–Best Students). that the left ear has a SN hearing loss as it cannot be
23. (b) Sound louder in diseased ear. (Ref. Scott Brown, the conductive hearing loss of the right side, Rinne
8th ed., Vol 2; 928) being positive here. So the diagnosis is left SN
24. (a) Middle ear (Ref. Scott Brown, 8th ed., Vol 2; 927) deafness and Schwabach can confirm this.
• Threshold for bone conduction is normal means 32. (b) Air conduction (AC) in left ear (Ref. Cummings,
that the sensorineural pathway is normal. 6th ed., 2203)
• Threshold for air conduction is increased means • Symbol X or is used to mark air conduction in
conductive hearing loss. left ear in unmasked and masked condition
So this is indicative of middle ear disease. respectively (mnemonic; cross sign indicating
25. (c) Otosclerosis (Gelle’s is negative in Otosclerosis) (crucifixion of) Jesus Christ, (though that is made
([Link] Biswas, 5th ed., 49) differently, we all know) Who will always be in
26. (a) SN deafness (Ref. Scott Brown, 8th ed., Vol 2; 927) our heart (unhidden, i.e. unmasked), and the
heart being on left side.
The other options being conductive pathologies so
show no change in hearing. • After His crucifixion on the day now called Good
Friday (also called God’s Friday/Black Friday),
27. (d) False negative Rinne test (Ref. Scott Brown, 6th
His earthly body was kept in a linen with spices
ed., Vol 2; 2/5/4)
in a coffin ( symbol can be considered for coffin)
• In a patient of suppurative labyrinthitis, positive
and finally 3 days later, on Easter Jesus Christ
Rinne means SN hearing loss.
rose from death). So easy to remember X or is
• Positive fistula test, see chapter on vestibular used for showing AC in left ear in unmasked and
system, suggests that there is a fistula on the masked conditions respectively.
medial wall of middle ear probably this is the
• Air conduction in right ear is marked by symbols
cause of labyrinthitis.
0 (mnemonic; zero sign because the above
• The fistula test becoming negative after two happening was not at all righteous and therefore
weeks in the absence of treatment suggest that we pray to God on Good Friday for our sins to
the ear has become dead and therefore non- The Jesus Christ and vow to become good human
responsive (false negative fistula). So Rinne here beings) and Δ in unmasked and masked
will be false negative because of severe SN conditions respectively.
hearing loss.
• Another mnemonic, for people who do not
28. (a) Weber’s test left lateralised, Rinne-right positive, believe in God, right is right so left will be wrong
BC>AC on left side (Ref. Scott Brown, 6th ed., Vol 2; (X) → simple and clear! (unmasked left AC). For
2/5/4) masked (left AC) let’s change this symbol to ( ),
In this patient there is 30 dB deafness in left ear, the by rearranging the four limbs of X. Now as in a
right ear is normal (so right Rinne positive) and maths equation, right ear being equal to left ear,
Weber’s is lateralised to the left ear indicating left being wrong (zero marks) so right is 0 (zero),
conductive pathology of the left ear (BC > AC on clear, nothing hidden! (unmasked)
left side). • Bone conduction in right ear will be marked by
In left ear the Rinne will be negative. symbols < or [in unmasked and masked
29. (b) Right sided severe sensorineural deafness (Ref. condition respectively and BC in left ear is Ear
Scott Brown, 6th ed., Vol 2; 2/5/4) marked by > or] (same but opposite symbols, the
Here the patient has right sided hearing loss. In opening being towards the respective hand).
the right ear Rinne is negative so there can be • No response in air conduction in right ear and
2 possibilities: left ear will be marked as arrow beneath the
(a) Conductive hearing loss of right ear respective symbols.
(b) Severe SN loss of right ear (false negative Rinne) 33. (a) Air conduction of right ear (Ref. Cummings 6th
Section I

Weber’s will help us to differentiate between the two. ed., 2203)

Since it shows lateralisation to left side which is the 34. (b) Ototoxicity (Ref. Anirban Biswas, 5th ed., 27 )
better side it means that there is severe SN hearing High frequency audiometry:
loss on the right side. • Conventional audiometry tests frequencies
30. (b) Right severe sensorineural hearing loss between 250 Hz–8000 Hz, whereas high
(Explanation same as above) (Ref. Scott Brown, 6th frequency audiometry tests frequencies in the
ed., Vol 2; 2/5/4) region of 8000 Hz–20,000 Hz.
 62 ENT for Entrance Exams

• It is used to detect early ototoxicity and early 47. (d) and (e) Otosclerosis reduces compliance, Flat
noise induced hearing loss as these lead to high curve in TM perforation (Ref. Cummings, 6th ed., 2055)
frequency hearing loss initially and therefore if 48. (d) Middle ear fluid causes dome shaped /type B
detected early these conditions can be prevented curve on tympanogram. ([Link] Biswas, 5th ed.,
or minimised. 98)
35. (b) 20–20,000 Hz (Ref. Shambaugh 6th ed. 50) • In Otosclerosis As type curve is seen.
36. (c) 61–80 dB (Ref. Scott Brown, 8th ed., Vol 2; 76) • In ossicular discontinuity Ad type curve is seen.
37. (c) 41–55 dB (Ref. Scott Brown, 8th ed., Vol 2; 76) • In TM perforation Tympanometry cannot be
If WHO not given go with ASHA categories. done as it is not possible to do pressure changes
Please note for moderately severe it is 56–70 dB. hence a flat curve is obtained.
Easy to remember MMS–Moderate and 49. (a) Serous Otitis media (due to Blockade of Eusta-
Moderately Severe; 41–70 dB. chian tube) causes type B curve on tympanogram.
(Ref. Cummings, 6th ed., 2203)
38. (b) 10 times (Ref. Cummings, 6th ed., 1995) please refer 50. (a) Flat (Ref. Cummings, 6th ed., 2055)
the text 51. (b), (c) and (e) Serous Otitis media, Perforation of
39. (a) 10–40 dB (Ref. Cummings, 6th ed., 2201) (refer the ear drum and Safe CSOM
table in the text. Please note in this table, the hearing • In Serous Otitis media when the fluid is so much
loss is in a range in TM perforation only, whereas in that the tympanic membrane cannot move at all,
other conditions it is a stat value). a B type curve with no peak (flat curve) is obtained.
40. (a) Ossicular disruption with intact tympanic 52. (d) Low-compliance (Ref. Shambaugh, 6th ed., 201)
membrane (54 dB-See the Table in the text) (Ref. • Osteogenesis Imperfecta an autosomal dominant
Cummings, 6th ed., 2201) condition is characterised by recurrent fractures
• Ossicular disruption with perforated tympanic due to brittle bones, blue sclera, dental abnor-
membrane will have rather less hearing loss malities and progressive hearing loss due to
(38 dB) because some sound is able to enter Otosclerosis. Therefore, As type of curve, which
the windows directly through the perforated is a low compliance and normal pressure, is seen.
TM. 53. (b) Ad type tympanogram (Ref. Cummings, 6th ed.,
• In Otitis media with effusion the hearing loss is 2201)
never more than 40 dB. Hearing loss with intact TM and normal inner ear
• In otosclerosis the hearing loss increases with (cochlear reserve) following accident suggests that
increasing fixation of foot plate and reaches a the defect is in middle ear.
maximum conductive hearing loss of 60 dB in • 55 dB AB gap suggests ossicular discontinuity.
complete fixation. Hence Ad type of curve on tympanogram.
41. (a) Ossicular disruption with intact tympanic 54. (a) Distortion of ossicular chain (Ref. Cummings, 6th
membrane (Ref. Cummings, 6th ed., 2201) ed., 2055)
42. (c) Complete closure of oval window (it means • Intact TM with increased compliance on impedance
complete fixation of foot plate) (Ref. Cummings, 6th suggests distortion of ossicular chain.
ed., 2201) • Hemotympanum is a possibility following head
43. (a) Congenital SNHL (Ref. Scott Brown, 8th ed. Vol 2; injury leading to conductive deafness but here
712) TM compliance will be reduced.
• Trough shaped or U shaped or cookie bite curve • Tympanosclerosis and otosclerosis do not follow
is seen in congenital SN hearing loss and in head injury and Tympanometry shows reduced
cochlear otosclerosis. compliance.
Ear

44. (b) Middle ear (Ref. Cummings, 6th ed., 2203) 55. (b) It is a protective reflex against loud sound (Ref.
• In impedance audiometry we do tympanometry Cummings, 6th ed., 2055)
which is a measure of the condition of the middle • Whenever there is a loud sound 70–100 dB above
ear at the level of TM. the hearing threshold of a person, the Stapedial
45. (b) Impendence audiometry (Ref. Cummings, 6th ed., reflex gets activated and protects the inner ear
2203) from noise trauma. It is a bilateral reflex.
Section I

• Pure tone audiometry tests the threshold of 56. (d) VII and VIII nerves (Ref. Cummings, 6th ed., 2055)
hearing at various frequencies. It tells about the • The afferent of the Stapedial reflex is the 8th nerve
type and degree of hearing. and the efferent is the 7th nerve.
• Caloric test is a test of vestibular function. 57. (b) Normal sounds heard as loud and painful is
• BERA tests the peripheral and central auditory known as hyperacusis. (Ref. Cummings, 6th ed., 2343)
pathways. • It is because of absence of stapedial reflex in facial
46. (a) 226 Hz (Ref. Shambaugh, 6th ed., 196) nerve palsy.
 Physiology of Hearing and Audiology 63

• Ability to hear better in noisy surroundings is auditory pathway, it is the investigation of choice
Paracusis wilisii phenomenon seen in otoscle- here.
rosis, see Chapter 10. • Impedance audiometry is also objective but it is
58. (c) VIII nerve lesion (Ref. Anirban Biswas, 5th ed. 118; limited to middle ear pathologies which are
Cummings, 6th ed., 2055) usually not the cause of deafness at this age.
• In VIII nerve lesion Stapedial reflex is absent in • In Free field and behavioural audiometry
both ipsilateral and contralateral ears as it is the auditory signals are presented to infants and
afferent of the reflex. children and their change in behaviour is
observed.
59. (a) Right side (Ref. Cummings, 6th ed., 2055)
67. (a) BERA (Ref. Cummings, 6th ed., 2063)
• Since facial nerve forms the efferent of stapedial
reflex, in facial nerve palsy of right side Stapedial • Impedance and pure tone audiometry test the
reflex is absent on the right side only. middle ear.
60. (b) Neural deafness (Ref. Anirban Biswas, 5th ed. 56) 68. (c) Lateral lemniscus (Ref. Cummings, 6th ed., 2063, 2076)
• Tone decay is a function of nerve fatigue. • The wave V is the most prominent and easily
identifiable and hence the most important wave
• If the nerves are fatigued the patient stops
of BERA. Wave V is generated from lateral
hearing a sound given to him continuously before
lemniscus.
the completion of 1 minute.
• Cochlear nucleus gives wave III
• A tone decay of more than 30 dB is suggestive of
retrocochlear or neural deafness • Superior olivary complex gives wave IV
61. (d) Evoked potential generated in cochlea and • Inferior Colliculus gives waves VI and VII
auditory nerve (refer the text) (Ref. Cummings, 6th 69. (a), (e) Can differentiate cochlear and retrocochlear
ed., 2057) lesion, to diagnose brainstem pathology (Ref.
62. (b) Otoacoustic emissions (OAEs). (Ref. Cummings, Cummings, 6th ed., 2063)
6th ed., 2074) • With BERA the exact site of lesion in SN hearing
• OAE is considered to be the best audiometric test loss can be found out by noting the latency and
to screen hearing in neonates. Absent OAE amplitude of the affected wave.
indicate cochlear lesions. • Complete blood cell count (CBC), electrolytes,
• For screening purposes the test has to be easy to BUN, creatinine, and glucose estimations are
do, less time consuming, results should be done to distinguish barbiturate poisoning from
available immediately and cost effective. metabolic causes of coma. Serum Phenobarbital
• For these reasons OAE is better than BERA for levels will confirm barbiturate poisoning.
screening hearing in neonates and children. • OAE is the screening hearing test in infants
• If OAEs are absent, the child is taken up for BERA 70. (b) Auditory neuropathy (since OAEs are present
for confirmation. so pathology is retrocochlear) (Ref. Cummings, 6th
• Electrocochleography is an invasive test. It is ed., 2065)
done for Meniere’s, which is not the pathology, 71. (a) Caloric test is for vestibular assessment (Ref.
at this age. Scott Brown, 8th ed., Vol 2; 795)
• Tympanometry is used to detect middle ear • Rinne, Weber and ABC are tests of hearing, to
lesions which are also unusual at this age. find out conductive and sensorineural hearing
• Developmental anomalies of the cochlea are to loss.
be ruled out at this age, if found, the child can be 72. (b) Impedance audiometry (Ref. Scott Brown, 6th ed.,
taken up for cochlear implantation as early as one Vol 2; 2/12/1)
year of age for proper speech development. • Impedance audiometry is an objective test. It does Ear
63. (b) Otoacoustic Emissions (OAE) (Ref. Scott Brown, not require the cooperation of patient.
8th ed., Vol 2; 60) • Other objective audiometry tests are; OAEs,
64. (b) Outer hair cells (Ref. Cummings, 6th ed., 2071) Electrocochleography and BERA
• Maculae are for balance and not for hearing 73. (a) Pure tone audiometry (Ref. Scott Brown, 6th ed.,
65. (a), (c), (d) Are by-product of outer hair cell, Used Vol 2; 2/12/1)
as a screening test of hearing in newborn infant, Rest are objective.
Section I

Useful in ototoxicity monitoring. (Ref. Cummings, 74. (a) Stenger test (refer to the text) (Ref. Cummings,
6th ed., 2074) 6th ed., 2067)
• Otoacoustic emissions disappear in cochlear • Bing, Weber and Rinne tests are for the detection
pathology. of conductive and SN hearing loss.
66. (b) BERA (Ref. Cummings, 6th ed., 2078) 75. (d) Profound SNHL in right ear, left ear normal
• Since BERA is an objective test and it tests the (Ref. Scott Brown, 6th ed., Vol 2; 2/5/4)
electrical activity occurring in the whole of the Please refer to the text.
 64 ENT for Entrance Exams

76. (c) It needs sound proof room (Ref. Cummings, 6th 94. (d) Early Eustachian tube obstruction (Ref. Cummings,
ed., 2203) 6th ed., 2055)
77. (d) Refer, see text (Ref. Cummings, 6th ed., 2973; 95. (c) Moderately severe (Ref. Scott Brown, 8th ed., Vol
Anirban Biswas, 5th ed., 263) 2; 60)
78. (b) 100–200 msec (Ref. Scott Brown, 8th ed., Vol 2; 76; 96. (c) Non-organic hearing loss ([Link] Biswas, 5th
Anirban Biswas, 5th ed., 126) ed., Vol. 1, 46)
79. (a) Left ear Rinnes +ve; Weber’s lateralised to right 97. (c) Meniere’s disease ([Link] Biswas, 5th ed.,
(Ref. Scott Brown, 6th ed., Vol 2; 2/5/4) 63)
80. (b) CSOM (Ref. Cummings, 6th ed., 2203) 98. (a) Outer hair cells (Ref. Cummings, 6th ed., 2074)
81. (b) Tympanometry ([Link] Biswas, 5th ed., 114) 99. (c) Schwabach test–lengthened 1) (Ref. Dhingra, 6th
82. (b) Vestibulocochlear nerve (Ref. Scott Brown, 6th ed., 22)
ed., Vol 2; 2/12/2)
100. (a) Spontaneous OAE is absent in 50% normal
83. (a) Conductive hearing loss right ear (Ref. Cummings, individuals (Ref. Cummings, 6th ed., 2074)
6th ed., 2053)
101. (a) Sensorineural hearing loss of 45 dB in left ear
In the left ear the AC is 10 dB (average of speech and normal right ear (Ref. Scott Brown, 6th ed., Vol 2;
frequencies) which is normal. Since AC is a measure 2/5/4)
of both conductive and SN pathway and it being
102. (d) 22:1 (Ref. Dhingra, 6th ed., 14)
normal, both conductive and SN pathway are normal.
In the right ear AC is 60dB. Had it been a SN hearing 103. (a) Latency of wave V increased in the affected ear
loss in the right ear, the BC would have been worse ([Link] Biswas, 5th ed., Vol 1, 197)
than AC and would have been shown in the audiogram. 104. (c) Auditory steady state response (ASSR) (Ref.
Since it is not shown here, it should be presumed Cummings, 6th ed., 2081)
that it is normal in the right ear. So the audiogram is 105. (d) 2 times (Ref. Cummings, 6th ed., 2201)
showing conductive hearing loss of the right ear. 106. (d) 34 wk (Ref. Scott Brown, 8th ed., Vol 2; 655)
84. (a) Superior olivary complex (Ref. Anirban Biswas, Prenatally there is a progressive improvement in the
5th ed., 119) detection of waves I, III, and V of BERA with
85. (c) >81 dB in the better ear (Ref. Scott Brown, 8th ed., increasing gestational age due to maturation of
Vol 2; 76) auditory pathway. Since the maximum age given
86. (b) 60 dB (Ref. Scott Brown, 8th ed., Vol 2; 926) among the options is 34 wks so this is the best
• The intensity of sound at 1 metre, in various answer. The wave forms of BERA are of adult
human conversations are as below: configuration by 18 months.
i. Whisper–30 dB 107. (c) In severe SN hearing loss AC > BC (Ref. Cummings,
6th ed., 2203)
ii. Normal conversation–60 dB
iii. Shout–90 dB 108. (b) SOM (Ref. Cummings, 6th ed., 2203)
109. (d) Disappear in 8th nerve pathology (Ref. Cummings,
There occurs Discomfort in the ear at 120 dB
6th ed., 2074)
and pain in the ear at a loudness of 130 dB
110. (b) BERA (Ref. Cummings, 6th ed., 2076, 2975)
87. (a) 30 dB (Ref. Scott Brown, 8th ed ., Vol 2; 926) 111. (d) Phase differential between the two windows
88. (c) Obliteration of oval window (Ref. Cummings, 6th (Ref. Cummings, 6th ed., 2202)
ed., 2201) 112. (b) Left severe SN hearing loss (Ref. Scott Brown,
89. (a) Cochlear sensorineural hearing loss (Ref. Scott 6th ed., Vol 2; 2/5/4). Refer to the text
Brown, 8th ed., Vol 2; 629) 113. (a) During 1st month. It is done within 48 hours of
90. (b) Speech discrimination is highly impaired birth. Refer to the text. (Ref. Anirban Biswas, 5th ed.,
([Link] Biswas, 5th ed., 63) 202)
Ear

91. (a) Meniere’s disease (Ref. Scott Brown, 8th ed., Vol 114. (a) In Utero. Refer to the text. (Ref. Anirban Biswas,
2; 629) 5th ed., 203)
92. (c) Tympanometry (Ref. Shambaugh, 6th ed., 196) 115. (c) B/L CHL (Ref. Scott Brown, 8th ed., Vol 2; 639)
93. (d) BERA (Ref. Scott Brown, 8th ed., Vol 2; 60; 116. (b) 30% (Ref. Dhingra, 6th ed., 39)
Cummings, 6th ed., 2975) 117. (a) As (Ref. Cummings, 6th ed., 2205)
Section I
 74 ENT for Entrance Exams

• In bi-thermal caloric test the normal response is C O

ANSWERS AND EXPLANATIONS
W S, i.e. with Cold water nystagmus is towards the
1. (a) Duration not limited (Ref. Cummings, 6th ed., page Opposite side and with Warm water it is towards
2567; 2551) the Same side.
2. (b) Direction fixed (Ref. Anirban Biswas, 5th ed., Vol • If both meatus are irrigated simultaneously with cold
2; page 98) water the normal response is an up-beating
3. (c) Cochlear disease (Ref. Cummings, 6th ed., page nystagmus with torsion.
2531) 15. (a) Nystagmus to the right side (Ref. Scott Brown,
• Nystagmus and vertigo per se are not the manifes- 8th ed., Vol 2; page 796)
tations of cochlear diseases. Cochlear diseases lead • If the same is done with warm water the nystagmus
to hearing loss. However as mentioned in Table 3.1 will be towards the same side, i.e. left side.
in the text in vestibular pathologies additionally • Direction changing nystagmus is seen in central
there may be tinnitus and deafness when there lesions.
occurs involvement of cochlea. • Positional nystagmus is seen in BPPV.
• In Cerebellar disease the nystagmus is pendular. 16. (d) None (all are true) (Ref. Scott Brown, 8th ed., Vol
• In Vestibular disease the nystagmus is jerky. 2; page 796)
• In the Arnold-Chiari malformation a part of the 17. (a) Vertical upbeat with slow component down-
brainstem and the cerebellum are herniated into the wards (Ref. Scott Brown, 6th ed., Vol 2; page 2/21/20)
cervical vertebral canal. The Arnold-Chiari malfor- • If both meatuses are irrigated simultaneously with
mation is typically associated with vertical downbeat cold water, under normal circumstances the effect
nystagmus. within both horizontal semicircular canals is equal
4. (a) Medulla (Ref. Cummings, 6th ed., page 2531) and self cancelling; this eventually causes an up
5. (b) Left side (Ref. Anirban Biswas, 5th ed., Vol 2; 287) beating vertical nystagmus.
6. (d) Torsional vertical nystagmus (Ref. Cummings, 6th • Vertical upbeat means the fast component is
ed., page 2531; Scott Brown, 8th ed., Vol 2; page 833) upwards, hence the slow component will be
7. (c) Vertebrobasilar insufficiency (Ref. Cummings, 6th downwards.
ed., page 2531) 18. (a) Cold air caloric test (Ref. Dhingra, 6th ed., page
• Vertebrobasilar insufficiency is a central vestibular page 43)
condition. 19. (a) Lateral semicircular canal (Ref. Shambaugh, 6th
• The two vertebral arteries on each side are branches ed., page page 466)
of the subclavian arteries. They enter the skull through 20. (c) Hypermobile footplate of stapes (Ref. Cummings,
the foramen magnum and join at the pontomedullary 6th ed., page 2562)
junction to form the basilar artery which divides into 21. (a) Congenital syphilis (Ref. Cummings, 6th ed., page
two posterior cerebral arteries at the upper pons. 2562)
• The vertebrobasilar arterial system perfuses the 22. (b) Erosion of lateral semicircular canal (Ref.
medulla, cerebellum, pons, midbrain, thalamus, and Shambaugh, 6th ed., page 181)
occipital cortex. 23. (a) Dead ear (Ref. Shambaugh, 6th ed., page 181)
• Therefore vertebrobasilar insufficiency leads to
• If there is a fistula on the medial wall but inner ear is
involvement of the central vestibular system.
dead (not responding to pressure changes), then in
8. (b) and (d) Fistula test, Cold caloric test (Ref. Scott spite of presence of fistula, fistula test will be
Brown, 8th ed., Vol 2; page 795) negative. This is false negative fistula test.
• Acoustic reflex is a part of impedance audiometry • If the footplate of stapes is hypermobile, it results in
which is a test of hearing. false positive fistula test.
9. (a), (c), (e) Galvanic stimulation test, Fistula test,
Ear

• Fenestration operation is an iatrogenic cause of

Cold caloric test (Ref. Scott Brown, 8th ed., Vol 2; page positive fistula test.
795)
24. (d) Posterior semicircular canal (Ref. Cummings, 6th
• Acoustic reflex and Impedance audiometry are tests ed., page 2550)
of hearing.
25. (a) Vestibular function (Ref. Cummings, 6th ed., page
10. (b) Lateral semicircular canal (Ref. Cummings, 6th 2551)
Section I

ed., page 2537)

• DIX-Hallpike manoeuvre is a manoeuvre to rule out
11. (b) 30° (Ref. Cummings, 6th ed., page 2537) BPPV (benign paroxysmal positional vertigo) in any
12. (a) 30° and 44° (Ref. Cummings, 6th ed., page 2538) patient presenting with vertigo.
13. (c) Both slow and fast components (Ref. Cummings, 26. (d) Canalith repositioning procedure (Ref. Cummings,
6th ed., page 2510) 6th ed., page 2552)
14. (a) Towards the opposite side (Ref. Cummings, 6th • Canalith repositioning procedure or the Epley’s
ed., page 2510) manoeuvre is the treatment for benign positional
 Vestibular Physiology and Assessment of Vestibular Function 75

vertigo. In this manoeuvre the patient’s head is 33. (d) Multiple sclerosis (Ref. Scott Brown, 8th ed., Vol
moved into different positions in a sequence that will 2; page 833)
move the debris from the posterior semicircular 34. (a) Assess vestibular function (Ref. Scott Brown, 8th
canal back into the utricle. ed., Vol 2; page 800)
• When the vestibular organs are damaged with 35. (b) Spinning of world around sensation (Ref. Scott
disease or injury, the brain can no longer rely on Brown, 8th ed., Vol 2; page 774)
them for accurate information about equilibrium and • Cerebellar pathologies present with ataxia and
motion. dysarthria
Vestibular exercises promote CNS compensation • Central causes of vertigo lead to deficits of cranial
for these permanent or fixed deficits. nerves III to XII which are closely associated with
• In Benign positional vertigo vestibular exercises are the brainstem.
not required, as the cause of BPPV gets treated by 36. (b) Testing vestibulo-ocular reflex by injecting cold
Canalith repositioning procedure or the Epley’s water (Ref. Scott Brown, 8th ed., Vol 2; page 795)
manoeuvre. • Vestibulo-ocular reflex or caloric test is a test to
• Vestibular sedatives and antihistamines may be used evaluate the vestibular system and hence the
to control the severe symptoms, though they are not brainstem functioning. One of the utility of this test
of much benefit and repositioning or Epley’s is to confirm brain death.
manoeuvre is the treatment of choice in BPPV. • Syringing is never done in a patient of CSOM.
27. (d) Epley’s manoeuvre or the repositioning mano- • Politzerisation is for endotracheal tube function.
euvre (Ref. Cummings, 6th ed., page 2552) 37. (a) Hearing loss is often present (Ref. Cummings, 6th
28. (a) Positional vertigo (Ref. Cummings, 6th ed., page 2552) ed., page 2551)
29. (c) Inferior Vestibular Nerve (Ref. Scott Brown, 8th 38. (c) BPPV (Ref. Scott Brown, 8th ed., Vol 2; page 835)
ed., Vol 2; page 829) 39. (d) Stimulates Posterior Semicircular Canal (Ref.
30. (a) Fistula test positive without fistula (Ref. Shambaugh, Scott Brown, 8th ed., Vol 2; page 796)
6th ed., page 181) • It stimulates horizontal/lateral semicircular canal
31. (a) Towards the opposite side (Ref. Scott Brown, 8th 40. (c) Injury to SCC and Vestibulo-ocular tract (Ref.
ed., Vol 2; page 796) Anirban Biswas, 5th ed., Vol 2; page 446)
32. (a) Diagnose benign paroxysmal positional vertigo 41. (a) Fast component is to left (Ref. Cummings, 6th ed.,
(Ref. Scott Brown, 8th ed., Vol 2; page 833) page 2510)

Ear
Section I
 86 ENT for Entrance Exams

ANSWERS AND EXPLANATIONS up by the osteoclasts and osteoblasts and indicates

the bony erosion during the malignant Otitis externa.
1. (b) Hematoma of pinna in boxers (Ref. Scott Brown, • Malignancy of the EAC usually follows long standing
8th ed., Vol 2; 1102) ear discharge which has not been mentioned in the
2. (a) Haematoma (Ref. Scott Brown, 8th ed., Vol 2; 1102) above question. A biopsy will be diagnostic of
3. (b) Pseudomonas (Ref. Scott Brown, 8th ed., Vol 2; 959) malignancy and Tc99 scan is not required here.
4. (a) Aspergillus niger (Ref. Scott Brown, 8th ed., Vol 1; • Nasopharyngeal carcinoma with ET blockade
206) presents with upper deep cervical lymphadenopathy
5. (b) Candida (Ref. Scott Brown, 8th ed., Vol 2; 956) with U/L serous otitis media.
• MC organism causing otomycosis is Aspergillus 20. (a) Influenza (Ref. Scott Brown, 8th ed., Vol 2; 936)
followed by Candida. Since Aspergillus is not given 21. (c) Bacteria (Ref. Scott Brown, 8th ed., Vol 2; 936)
in the choice, the next most common is Candida. 22. (b) Posterosuperior (Ref. Scott Brown, 8th ed., Vol 2;
6. (c) Both (Ref. Scott Brown, 8th ed., Vol 2; 956) 235)
7. (c) Swimmer’s ear (Ref. Cummings, 6th ed., 2116) 23. (a) Normal ‘cone of light’ (Ref. Dhingra, 6th ed., 55)
8. (a), (c), (d) Aspergillus, Candida, Pseudomonas (Ref. 24. (d) Shiny pearly grey tympanic membrane (Ref.
Cummings, 6th ed., 2116) Dhingra, 6th ed., 55)
• Infections of the EAC (external auditory canal) are • Retracted tympanic membrane appears dull and
known as Otitis externa. These can be bacterial, lustreless due to absent or interrupted cone of
fungal or viral, please refer the text. light.
9. (c) P. aeruginosa (Ref. Scott Brown, 8th ed., Vol 2; 1421) 25. (c) Healed perforation has 3 layers (Ref. Scott Brown,
10. (c) Diabetes (Ref. Scott Brown, 8th ed., Vol 2; 1420) 8th ed., Vol 2; 529)
11. (d) Pseudomonas infection in diabetic patient (Ref. • The TM membrane which heals by itself does not
Cummings, 6th ed., 2118) have the fibrous layer. It has 2 layers only, the outer
12. (b) Common in diabetics and old age (Ref. Cummings, epithelial and the inner endothelial.
6th ed., 2118) Rest are true, see the chapter on anatomy of ear
• Malignant Otitis externa is extremely painful. It is 26. (c) Tympanosclerosis (Ref. Cummings, 6th ed., 2151)
caused by Pseudomonas. 27. (b) Desquamated epithelial cells (Ref. Scott Brown,
13. (c) Mitotic figures are high (Ref. Scott Brown, 8th ed., 8th ed., Vol 2; 942)
Vol 2; 1420) 28. (a) Keratosis obturans (Ref. Scott Brown, 8th ed., Vol
• High mitotic figures are suggestive of a malignant 2; 942)
condition. Malignant Otitis externa is not a • Since the TM is intact so it cannot be CSOM
malignancy but an infective and locally invasive • Otitis externa is an acute condition
condition. • Carcinoma of EAC of such a long duration will not
14. (a), (c) and (e) (Ref. Cummings, 6th ed., 2119) remain localised
15. (c) Malignant Otitis externa (Ref. Scott Brown, 8th 29. (c) 250 mm (Ref. Dhingra, 6th ed., 374)
ed., Vol 2; 1420) 30. (c) 9 cm (Ref. Dhingra, 6th ed., 374)
• Malignant Otitis externa can lead to granulations and • The diameter of the mirror is 3.5 inch/9 cm/90 mm
bony erosion leading to facial nerve palsy. 31. (c) Removal of foreign body from the ear (Ref.
The other options do not cause bony erosion and Dhingra, 6th ed., 374)
facial nerve palsy. • Removal of foreign body of ear is done by syringing
16. (b) Surgery never done (Ref. Scott Brown, 8th ed., Vol or instrumentation.
2; 1422) 32. (d) Pseudomonas (Ref. Cummings, 6th ed., 2118)
17. (a) Ciprofloxacin (Ref. Scott Brown, 8th ed., Vol 2; 1422) 33. (d), (e), Vegetable matter, Lead battery (Ref. Scott
Ear

• Old diabetic with rapidly spreading infection and Brown, 8th ed., Vol 2; 386)
granulations, the diagnosis is malignant Otitis 34. (b) Sensory hearing loss is common presentation
externa. The cause is pseudomonas. (Ref. Cummings, 6th ed., 2118)
• Antipseudomonal antibiotics (e.g. Ciprofloxacin, 35. (b) Local release of chemical from battery and
Ceftazidime, Piperacillin/Ticarcillin, Meropenem, etc.) destruction of tissue (Ref. Scott Brown, 8th ed., Vol 2;
for 3–6 weeks are given and debridement of necrotic 386)
Section I

material is done. 36. (b) Softening followed by syringing (Ref. Scott

18. (a) Malignant otitis externa (Ref. Cummings, 6th ed., Brown, 8th ed., Vol 2; 921)
2118) 37. (c) Parotitis (Ref. Scott Brown, 8th ed., Vol 2; 1421)
19. (c) Malignant otitis externa (Ref. Scott Brown, 8th ed., 38. (b) Bacterial infection (Ref. Cummings, 6th ed., 2116)
Vol 2; 1422) 39. (c) Post-traumatic (Ref. Scott Brown, 8th ed., Vol 2; 1102)
• This is a clear cut case of malignant Otitis externa. • This is the picture of hematoma of pinna showing
For early diagnosis Tc99 scan is used. Tc99 is taken the typical cauliflower appearance
 Diseases of External Ear 87

40. (c) 3 (Ref. Shambaugh, 6th ed., 395) can be picked up early (it being an external condition
41. (b) Pseudomonas aeruginosa (Ref. Scott Brown, 8th and therefore early management here), it is the least
ed., Vol 2; 1420) life threatening among the rest of the choices.
42. (c) Syringing uses room temperature water directed Emphysematous infections in a diabetic are caused
at ear drum (Ref. Scott Brown, 8th ed., Vol 2; 386) by fermentation of glucose by bacterial and fungal
• Syringing uses body temperature water (37°C) and pathogens. Also due to immunocompromised state
not room temperature. in D/M, these infections of the internal organs may
lead to perforation leading to high mortality.
• There is a chance of vegetative F B to get swollen up
Mucormycosis being angio-invasive therefore
and therefore get stuck up. Therefore syringing is
spreads rapidly from nose to orbits to CNS and thus
avoided here.
fatal. Malignant otitis externa may also lead to death,
43. (d) Adhesive otitis media (Ref. Shambaugh, 6th ed.,
but for the reason mentioned, it is the least likely
395)
cause.
44. (b) Sensorineural hearing loss is common
47. (d) Most common organism is Staph. aureus and
presentation (Ref. Cummings, 6th ed., 2118)
Proteus mirabilis (Ref. Cummings, 6th ed., 2119)
Invasion of inner ear to result into SN hearing loss is
48. (c)VII (Ref. Scott Brown, 8th ed., Vol 2; 1420)
unusual and if it all occurs, will be a very late feature.
45. (c) Infective condition (Ref. Scott Brown, 8th ed., Vol 49. (b) Clotrimazole ear drops (Ref. Scott Brown, 8th ed.,
2; 1419) Vol 2; 956)
46. (c) Malignant otitis externa (Ref. Scott Brown, 8th ed., 50. (a) Ear pulled up and backwards, syringe jet
Vol 2; 1419) posterosuperiorly (Ref. Dhingra, 6th ed., 53)
Though all are life threatening complications in a 51. (b) Maggots of the ear (Ref. Dhingra, 6th ed., 161)
diabetic patient but since Malignant otitis externa 52. (c) 37° (Ref. Dhingra, 6th ed., 53)

Ear
Section I
 Acute Infections of Middle Ear 91

11. (d) Postero-inferior (Ref. Hazarika, 3rd ed., 202)

ANSWERS AND EXPLANATIONS
• In ASOM myringotomy is done in the postero-
1. (b) Eustachian tube (Ref. Scott Brown, 8th ed., Vol 2; 140) inferior quadrant by a curvilinear J-shaped incision.
2. (a) Pneumococcus (Ref. Scott Brown, 8th ed., Vol 2; 139) • In serous Otitis media myringotomy along with
• The MC organism causing AOM is Streptococcus grommet insertion is done in the antero-inferior
pneumoniae (pneumococcus) followed by Haemophilus quadrant by a radial incision (refer to chapter on
influenzae. serous Otitis media for the reason for these preferred
• In the ear Staphylococcus is the most common sites of incision in the said two conditions).
causative organism in furuncle of the EAC 12. (c) Oral antibiotics and decongestants (Ref. Scott
• Beta-hemolytic Streptococcus is the causative Brown, 8th ed., Vol 2; 142)
organism in ANOM and acute mastoiditis. • The slight bulge of TM may regress with antibiotics
3. (b) Streptococcus pneumoniae (Ref. Scott Brown, 8th alone. Myringotomy being an invasive procedure is
ed., Vol 2; 139) done only when the TM is full and bulging.
• Irrespective of the age of the patient suffering from • Myringotomy with grommet insertion is the
AOM, the MC organism is Streptococcus pneumoniae treatment modality in serous Otitis media
followed by Haemophilus influenzae. 13. (c) Myringotomy (please see the explanation to the
• In the ear Pseudomonas causes perichondritis, above question) (Ref. Scott Brown, 8th ed., Vol 2; 143)
diffuse Otitis externa and malignant Otitis externa • Ciprofloxacin is given in pseudomonal and other
and it is also the main organism in unsafe CSOM. Gram-negative infections.
4. (a) ASOM (Ref. Hazarika, 3rd ed., 149) • Cortical mastoidectomy is done in acute mastoiditis
• In Glomus “rising sun sign” or “red reflex” is seen. • In ASOM steroids are not used
• In Otitis media with effusion (OME) TM appears 14. (c) Streptomycin (Ref. Scott Brown, 8th ed., Vol 2; 142)
dull, retracted and sometimes bluish. • Streptomycin—an aminoglycoside is used in anti-
• In CSOM the TM will be perforated (please refer the tubercular treatment.
respective chapters) • The MC organism causing ASOM is Streptococcus
5. (a) Antero-inferior (Ref. Shambaugh, 6th ed., 437; Scott pneumoniae followed by Haemophilus influenzae. So
Brown, 8th ed., Vol 2; 147). beta-lactum, macrolides and fluro-quinolones active
However this answer is controversial as according against these bacteria, are the antibiotics of choice.
to Shambaugh it is most commonly anteroinferior 15. (a) Most frequently it resolves without sequelae
but Scott Brown says it is the posterior half of pars (Ref. Scott Brown, 8th ed., Vol 2; 141)
tensa. • ASOM usually resolves completely without
6. (a) ASOM (Ref. Hazarika, 3rd ed., 150) complications.
7. (c) ASOM (Ref. Hazarika, 3rd ed., 150) • ASOM commonly follows infection in the naso or
8. (a) Stage of suppuration (Ref. Shambaugh, 6th ed., 426; oro-pharynx via Eustachian tube.
Hazarika, 3rd ed., 150) • Most common organism causing ASOM is
9. (b) Surgical opening in tympanic membrane (Ref. Streptococcus pneumoniae.
Scott Brown, 8th ed., Vol 2; 974) • Myringotomy may be required to be done in ASOM.
10. (c) ASOM (Ref. Scott Brown, 8th ed., Vol 2; 143) 16. (c) Myringotomy (Ref. Dhingra, 6th ed., 63)
• Myringotomy is indicated in ASOM. Another 17. (b) Oral antibiotics (Ref. Cummings, 6th ed., 3020)
indication of doing Myringotomy is in serous Otitis • Grommet insertion is not done in ASOM. It is put in
media (SOM). Here in SOM Myringotomy along SOM
with grommet insertion is done. 18. (a) ASOM (Ref. Hazarika, 3rd ed., 202)
Ear
Section I
 100 ENT for Entrance Exams

7. (b) Nasopharyngeal carcinoma (Ref. Cummings, 6th

ANSWERS AND EXPLANATIONS
ed., 2035)
1. (b) Is painless (Ref. Scott Brown, 8th ed., Vol 2; 115) • CSOM and Mastoiditis do not lead to Serous Otitis
• Unlike ASOM Glue ear being a non-infective media.
condition (or the biofilm aggregated bacteria being • Foreign body of external ear will not lead to fluid
sequestered), is therefore painless. collection in middle ear.
• Radical mastoidectomy is done in unsafe CSOM. In 8. (a) and (d) Impedance audiometry, otoscopy (Ref.
Glue ear if medical management does not help then Cummings, 6th ed., 3020)
the best management is Myringotomy with • A patient presenting with painless blocked feeling
Grommet insertion along with Adenoidectomy/ of ear in a sub-acute fashion and on otoscopy TM
tonsillectomy. appearing dull and retracted and showing fluid
• Na F is given in active Otosclerosis. levels or air bubbles, a diagnosis of SOM is
2. (b) Secretory otitis media (Ref. Cummings, 6th ed., considered. The diagnostic investigation is
2139) impedance audiometry which shows B type curve.
• This is a case of SOM developing over ASOM • Pure tone audiometry shows conductive hearing loss
probably due to Biofilms formation, (please see the of approximately 20–35 dB which can also be seen
text) so some symptoms of ASOM, i.e. pain and fever in complete obstruction of EAC or in TM perforation,
have subsided but due to persistence of fluid see Chapter 2.
deafness is persisting. • X-ray of the mastoid may show clouding which can
• Penicillin is not an ototoxic drug, see Chapter 12 for also be seen in ASOM and mastoiditis.
ototoxic drugs. 9. (c) Tympanostomy tubes are usually required for
• Adhesive Otitis media is a late complication of treatment (Ref. Cummings, 6th ed., 3031)
chronic serous Otitis media where adhesions form • SOM leads to conductive deafness of approximately
between the TM and middle ear structures leading 20–35 dB.
to conductive hearing loss. • SOM does not lead to intracranial complications.
• Tympanosclerosis is also a late complication of • If medical management does not help, then the best
chronic serous Otitis media. It can also follow CSOM. management of SOM is surgical, i.e. Myringotomy
Here there is hyalinisation and calcification of (to remove the collected fluid) with tympanostomy
tympanic membrane seen as thickened white patches tube (or Grommet or ventilation tube) insertion (to
on the TM. In most patients, these plaques are provide ventilation to middle ear for the time being
clinically insignificant and cause a little or no hearing till Eustachian tube opens up) along with treatment
impairment. of causative factor (Adenoidectomy/tonsillectomy).
3. (a) Serous otitis media (Ref. Cummings, 6th ed., • SOM being non-infective or the biofilm aggregated
3020) bacteria being sequestered, there are no organisms
4. (d) Malignancy (Ref. Scott Brown, 8th ed., Vol 2; 973) in the fluid.
• Any adult presenting with U/L non-suppurative 10. (b), (c) and (d) (Ref. Scott Brown, 8th ed., Vol 2; 121)
Otitis media should be investigated for nasopharyn- • The initial management of otitis media with effusion
geal carcinoma which might be obstructing that consists of Antiallergics and Decongestants.
particular side Eustachian tube. Myringotomy is done in patients not responding to
• If serous Otitis media occurs because of overproduc- medical management after a duration of 3 months
tion of middle ear fluid due to allergy, it will be and an associated hearing loss of > 25 dB in both
bilateral. the ears.
• URTI may lead to ASOM. 11. (c) Myringotomy with ventilation tube insertion
• Trauma does not lead to Serous Otitis media. (Ref. Scott Brown, 8th ed., Vol 2; 125)
Ear

5. (b) B-shaped tympanogram (Ref. Shambaugh, 6th ed., 12. (a) Antero-inferior quadrant (Ref. Scott Brown, 8th
427) ed., Vol 2; 126)
• In SOM Tympanic membrane is dull and retracted 13. (c) Serous otitis media (Ref. Scott Brown, 8th ed., Vol
and may appear bluish. Perforation is not seen here 2; 126)
and Rinne test is –ve. 14. (c) Myringotomy (Ref. Scott Brown, 8th ed., Vol 2; 125)
6. (b) Evaluation for Nasopharyngeal Mass (Ref. • Tympanoplasty constitutes surgical repair of the TM,
Section I

Cummings, 6th ed., 2035) i.e. myringoplasty along with replacement of

• This man is suffering from U/L SOM. Any adult ossicles, i.e. ossiculoplasty and is the procedure for
presenting with U/L SOM should be investigated CSOM.
for nasopharyngeal carcinoma. If this is ruled out, 15. (d) It is the least vascular region (Ref. Scott Brown,
then initially conservative management in the form 8th ed., Vol 2; 126)
of antihistaminics and decongestants and later if no 16. (a) Secretory otitis media (Ref. Scott Brown, 8th ed.,
relief Myringotomy with grommet insertion is done. Vol 2; 125)
 Serous Otitis Media, Functions of Eustachian Tube, Otitic Barotrauma 101

17. (a) Grommet insertion (Ref. Scott Brown, 8th ed., Vol 20. (c) Patulous Eustachian tube (Ref. Scott Brown, 8th
2; 125) ed., Vol 2; 1041)
• Since Eustachian tube function takes time to come 21. (b) Fistula test (Ref. Cummings, 6th ed., 2036)
back to normal Myringotomy with grommet should Fistula test is a test of vestibular function, see Chapter 3.
have been done along with adenoidectomy in the 22. (d) 90 mm H2O (Ref. Scott Brown, 8th ed., Vol 2; 1119)
mentioned child. 23. (b) 90 mm of H2O (Ref. Scott Brown, 8th ed., Vol 2;
18. (d) Adenoidectomy with grommet insertion (Ref. 1119)
Scott Brown, 8th ed., Vol 2; 125) 24. (b) Descent in air (Ref. Scott Brown, 8th ed., Vol 2; 1121)
• This child is suffering from adenotonsillar hyper- 25. (c) Supportive (Ref. Scott Brown, 8th ed., Vol 2; 1123)
trophy which is causing recurrent URTI, mouth
26. (b) 3 months (Ref. Scott Brown, 8th ed., Vol 2; 130)
breathing, failure to grow and high-arched palate,
27. (b) Caloric test (Ref. Cummings, 6th ed., 2036)
refer the chapter on adenoids.
28. (c) Serous otitis media (Ref. Scott Brown, 8th ed., Vol
• Hypertrophied adenoids may have led to Eustachian
2; 125)
tube blockade with a resultant SOM which explains
impaired hearing. 29. (b) Descent (Ref. Scott Brown, 8th ed., Vol 2; 1121)
• So the treatment is adenoidectomy with grommet 30. (a) Serous otitis media (Ref. Scott Brown, 8th ed., Vol
insertion. It is understood that the grommet has to 2; 115)
be put by radial Myringotomy in the antero-inferior 31. (c) Myringotomy and grommet (Ref. Scott Brown, 8th
quadrant. ed., Vol 2; 125)
19. (a), (b), (c) and (d) (Ref. Scott Brown, 8th ed., Vol 2; 32. (c) Tympanostomy tubes are usually required for
126) treatment (Ref. Scott Brown, 8th ed., Vol 2; 125)
• This child is probably suffering from adenotonsillar 33. (b) Tympanometry (Ref. Cummings, 6th ed., 2036)
hypertrophy which is causing recurrent respiratory 34. (b) 20–40 dB (Ref. Scott Brown, 8th ed., Vol 2; 122)
tract infections and mouth breathing. 35. (d) Tympanometry (Ref. Scott Brown, 8th ed., Vol 2; 120)
• Hypertrophied adenoids/tonsils might have led to 36. (a), (c) and (d) Small plastic tube aerating middle
Eustachian tube blockade with a resultant SOM ear. Healing occurs spontaneously after extrusion.
which explains decreased hearing. It is placed anteriorly on tympanic membrane (Ref.
• So the treatment is Myringotomy with grommet Scott Brown, 8th ed., Vol 2; 126)
insertion along with Adeno-tonsillectomy in the 37. (b) Decongestants and antiallergics (Ref. Scott
same sitting. Brown, 8th ed., Vol 2; 126)
• Myringoplasty is the surgical repair of TM and is 38. (c) SOM (Ref. Scott Brown, 8th ed., Vol 2; 126)
done in CSOM. 39. (c) SOM (Ref. Scott Brown, 8th ed., Vol 2; 126)

Ear
Section I
 Tubotympanic or Chronic Mucosal Otitis Media 107

ANSWERS AND EXPLANATIONS 7. (a) Eradication of middle ear disease with

reconstruction of tympanic membrane and ossicles
1. (a) Aetiology is multiple bacteria (Ref. Scott Brown, (Ref. Shambaugh, 6th ed., 465)
8th ed., Vol 2; 1001) 8. (a) Tympanoplasty (Ref. Shambaugh, 6th ed., 491)
• CSOM is caused by mixed aerobic and anaerobic 9. (c) Type III (Ref. Shambaugh, 6th ed., 491) (mnemonic-
organisms. MC aerobic organism being Pseudomonas, Collumela, letter C is the IIIrd alphabet). This is the
others include Proteus, E. coli and Staph. aureus. MC type of tympanoplasty done.
Bacteroids are the anaerobic bacteria here. 10. (a) Temporalis fascia (Ref. Scott Brown, 8th ed., Vol
• Oral antibiotics and antibiotic ear drops are given to 2; 1025)
control the infection and once the ear is dry for 11. (a), (b) Temporalis fascia, Cartilage (Ref. Scott Brown,
6 weeks without antibiotics surgical repair is taken up. 8th ed., Vol 2; 997)
• Otic hydrocephalus is a complication of unsafe 12. (b) Malleus handle and stapes suprastructure (Ref.
CSOM, see next Chapter. Scott Brown, 8th ed., Vol 2; 1030)
• Resorption of bony ossicles in safe CSOM is due to 13. (b) CSOM (Ref. Cummings, 6th ed., 2177)
repeated infections with resultant local inflammatory • Active otosclerosis is managed by Na F, whereas
cytokines and local acidosis mainly in the area of mature otosclerosis is managed by stapedotomy.
low blood supply (most commonly long process of
• ASOM responds to antibiotics, antihistaminics,
incus and incudo-stapedial joint).
decongestants and analgesics.
2. (b) Tympanoplasty (Ref. Scott Brown, 8th ed., Vol 2; 14. (d) Tympanic membrane (Ref. Scott Brown, 8th ed.,
997) Vol 2; 1021)
• Surgical repair of TM is known as myringoplasty. If 15. (d) If required malleus is also reconstructed (Ref.
while doing the surgery any ossicle is found to be Shambaugh, 6th ed., 491)
necrosed, then ossiculoplasty is also done.
16. (a) In underlay graft is placed medial to the annulus
• This repair of the TM (myringoplasty) with
(Ref. Scott Brown, 8th ed., Vol 2; 1026)
ossiculoplasty is together known as tympanoplasty.
• In both underlay and overlay, a portion of the graft
• Since here the ossicular status has not been is placed medial to the malleus.
mentioned the preferable answer is tympanoplasty
• In underlay, graft is placed medial to the annulus,
because myringoplasty is type 1 tympanoplasty.
whereas in overlay graft is placed lateral to the annulus.
• Modified mastoidectomy is done in unsafe CSOM.
17. (c) Long process of incus (Ref. Scott Brown, 8th ed.,
• Conservative management is the strategy in acute
Vol 2; 1023)
perforations following trauma and ASOM.
18. (a) Autograft (i.e. from the same individual) (Ref.
3. (b) Long process of incus (Ref. Scott Brown, 8th ed., Scott Brown, 8th ed., Vol 2; 1025)
Vol 2; 997) • Allograft or homograft is a graft from another human
• Ossicle most commonly involved in CSOM is long being, i.e. from the same species.
process of incus because of its poor blood supply. • Xenograft is a graft from a different species, e.g. animals
4. (d) Tympanoplasty (Ref. Scott Brown, 8th ed., Vol 2; • Isograft is a graft from an identical/monozygotic
997) twin.
• Management of tubo-tympanic CSOM is tympano- 19. (c) Marginal Perforation (it is a feature of atticoantral
plasty CSOM) (Ref. Scott Brown, 8th ed., Vol 2; 989)
• Radical and modified radical mastoidectomy are 20. (c) Myringostapediopexy (Ref. Shambaugh, 6th ed.,
done for unsafe CSOM. 491)
• Simple mastoidectomy or Schwartze operation is 21. (c) Mastoidectomy (Ref. Scott Brown, 8th ed., Vol 2;
done for acute and coalescent mastoiditis. 1022)
5. (a) Operative microscope (Ref. Shambaugh, 6th ed.,
Ear
• Non-foul smelling discharge of 6 months duration
508; Scott Brown, 8th ed., Vol 2; 1021) suggests that the above is a case of safe CSOM. Hence
6. (c) 250 mm (Ref. Dhingra, 6th ed., 374) management is ear toileting, local and systemic
• Also remember that the focal length of the lens used antibiotics and once the ear is dry for 6 weeks without
in microscopic laryngeal surgeries is 400 mm. antibiotics, surgical repair by tympanoplasty.
Section I
 116 ENT for Entrance Exams

• Keratosis obturans is the collection of desquamated

ANSWERS AND EXPLANATIONS
keratin debris in the external auditory canal. This
1. (b) Associated with cholesteatoma (Ref. Scott Brown, keratin debris comes from the external auditory canal
8th ed. Vol 2; 989) stratified squamous epithelium.
• Any perforation of pars flaccida is unsafe CSOM 10. (b) Cholesteatoma (Ref. Cummings, 6th ed., 2141)
because it is associated with cholesteatoma. • In cholesteatoma the ear discharge is due to bone
2. (b) Marginal (Ref. Scott Brown, 8th ed. Vol 2; 989) erosion, hence it is scanty and foul smelling. It is
• Perforation of a part of pars tensa with destruction painless.
of tympanic annulus is called marginal perforation. • In central perforation, i.e. safe CSOM the ear discharge
• Attic perforation is perforation of the pars flaccida. is painless, on and off and is mucopurulent, non-foul
• Subtotal perforation is a perforation when a small smelling and moderate in amount.
margin of pars tensa all around is still there. • In ASOM following rupture of TM, there is relief of
• Total perforation is perforation of whole of the pars pain and the ear discharge is profuse, mucopurulent
tensa along with its annulus. and non-foul smelling.
3. (d) Acute necrotising Otitis media (Ref. Cummings, • In Otitis externa, e.g. furuncle, the ear discharge is
6th ed., 2146) only purulent and characteristically lacks the mucoid
• The MC route of secondary cholesteatoma is component which indicates that it is not coming from
migration of keratinising stratified squamous the middle ear. It is associated with pain.
epithelium through marginal perforation of TM. 11. (a), (d) and (e) (Ref. Cummings, 6th ed., 2141)
• This marginal perforation follows ANOM. • Unsafe CSOM (atticoantral) presents with scant foul
• Rest of the choices are not associated with cholesteatoma. smelling discharge (because of osteitis and bone
4. (a), (b), (d) (Ref. Shambaugh, 6th ed. 429) erosion) and deafness.
5. (c) Migration of squamous epithelium (Ref. Cummings, • The patient can also present with any of the
6th ed., 2146) complications of CSOM. Convulsions can be due to
• The MC route of secondary cholesteatoma is migration temporal lobe abscess, see next Chapter.
of keratinising stratified squamous epithelium through • Ossicular necrosis is seen in both unsafe and safe
marginal perforation of TM (Habermann’s theory). CSOM. In unsafe CSOM it is mainly due to eroding
• Congenital cholesteatoma is due to the presence of cholesteatoma and in safe CSOM ossicular necrosis
congenital cell rests which later on form stratified is due to repeated infections. The MC ossicle to get
squamous epithelium in any part of temporal bone. necrosed is long process of incus because of its pre-
• Squamous metaplasia and retraction pocket are carious blood supply.
theories for primary cholesteatoma. • Central perforation is a feature of tubo-tympanic safe
6. (a) Sensorineural hearing loss (Ref. Cummings, 6th CSOM.
ed., 2143) • Otalgia is a feature of ASOM not CSOM.
• A postero-superior retraction pocket, if allowed to 12. (d) Erodes the bone (Ref. Cummings, 6th ed., 2148)
progress, will lead to primary cholesteatoma which • Cholesteatoma word is misnomer. It does not contain
in turn can lead to sensorineural hearing loss. cholesterol. It is not a malignant tumour and therefore
• Secondary cholesteatoma is migration of keratinising does not metastasise. It is also not a benign tumour;
stratified squamous epithelium through marginal however, its bone eroding property justifies the
perforation of TM. suffix ‘oma’.
• Tympanosclerosis is hyalinisation and calcification 13. (b) Erodes bone (Ref. Shambaugh, 6th ed. 453)
of the fibrous layer of tympanic membrane. 14. (d) Lymphatic permeation (Ref. Cummings, 6th ed.,
There is no condition called tertiary cholesteatoma. 2143)
7. (c) Attic region (Ref. Cummings, 6th ed., 2143) • Cholesteatoma spreads by eroding bone and not by
• Most common site of primary cholesteatoma is attic lymphatics.
• The most common site of marginal perforation 15. (b) CSOM (Ref. Cummings, 6th ed., 2141)
through which migration occurs leading to secondary • Cholesteatoma formation is characteristic of unsafe
Ear

cholesteatoma is postero-superior marginal. CSOM.

• Congenital cholesteatoma is most commonly present • The other mentioned options are not associated with
in Anterosuperior quadrant of middle ear. cholesteatoma.
8. (a) Attic perforation (Ref. Cummings, 6th ed., 2143) 16. (a) Surgery (Ref. Cummings, 6th ed., 2145)
• Central perforation of the TM leads to safe CSOM, • The main management of cholesteatoma, i.e. unsafe
i.e. Tubo-tympanic disease and is not associated with CSOM is surgery.
Section I

cholesteatoma. • The main aim of the surgery is to give the patient a

• Meniere’s disease is endolymphatic hydrops. safe, dry and hearing ear.
9. (a) Atticoantral CSOM (Ref. Scott Brown, 8th ed. Vol • Discharge in unsafe CSOM is mainly because of bony
2; 989) erosion so medical management with local and
• Tympanosclerosis is hyalinisation and calcification systemic antibiotics is indicated only in superimposed
of the fibrous layer of tympanic membrane. It is not acute infection or infection causing extra or
associated with cholesteatoma. Foreign body in ear intracranial complications assisted by erosion due
does not lead to cholesteatoma formation. to cholesteatoma, see next chapter.
 Atticoantral or Squamous Chronic Otitis Media 117

17. (a) Mastoidectomy (Ref. Cummings, 6th ed., 2145) • In secretory Otitis media initially the treatment is
• The main management of unsafe CSOM is mastoid medical for 3 months and if not responding treatment
exploration by mastoidectomy which can be intact is surgical, i.e. myringotomy with grommet
canal wall or canal wall down procedure (please refer insertion. Also it is not a suppurative Otitis media.
the text for details of these procedures). • Of the remaining 3 options of suppurative Otitis
• Initial medical management of atticoantral CSOM media CSOM being characterised by permanent
with local and systemic antibiotics is indicated only perforation requires surgical treatment. Tympano-
in superimposed acute infection or complication. plasty is for safe CSOM and MRM for unsafe CSOM.
• Underlay myringoplasty is done in tubo-tympanic • Tubercular Otitis media responds to ATT and
CSOM. antibiotics are the treatment modality in ASOM.
• Ventilation tube or grommet is inserted in serous 25. (a) Safe CSOM (Ref. Cummings, 6th ed., 2148)
Otitis media. • In Safe CSOM tympanoplasty is done.
18. (b) Modified radical mastoidectomy (Ref. Cummings, 26. (c) Atticoantral cholesteatoma (Ref. Cummings, 6th
6th ed., 2145) ed., 2190)
• Since reconstruction of hearing is not done in radical • These days MRM is preferred over radical
mastoidectomy, so MRM is preferred over radical mastoidectomy in the management of unsafe CSOM
mastoidectomy in the treatment of unsafe CSOM to with or without complications except for a few areas,
give the patient a hearing ear besides making the please see the text.
ear safe and dry, please refer the text. 27. (d) Maintenance of patency of Eustachian tube (Ref.
19. (a) Cutting drill over the bleeding area, please see Shambaugh, 6th ed. 516)
the text (Ref. Shambaugh, 6th ed., 511) 28. (c) Cochlea removed (Ref. Shambaugh, 6th ed. 516)
20. (d) Tympanomastoid exploration (Ref. Cummings, 29. (d) Radical mastoidectomy (Ref. Cummings, 6th ed.,
6th ed., 2145) 2190)
• Foul smelling discharge and perforation in the pars 30. (a) Facial (Ref. Shambaugh, 6th ed. 518)
flaccida of the tympanic membrane indicates that it 31. (c) Pain (Ref. Cummings, 6th ed., 2303)
is an unsafe CSOM patient. So the management is • Tubercular otitis media is a painless condition. Rest
Tympanomastoid exploration. are true, refer the text
• Tympanoplasty is done as a part of Modified radical 32. (d) Multiple perforation (Ref. Cummings, 6th ed.,
mastoidectomy in unsafe CSOM and per se is not 2304)
the primary management. It is the primary 33. (b) Mastoid air cells (Ref. Cummings, 6th ed., 105)
management of tubo-tympanic disease or safe CSOM. • Schuller’s view and Law’s view are lateral oblique
21. (d) Myringoplasty (Ref. Cummings, 6th ed., 2145) views of mastoid to see the extent of pneumatisation
• Any retraction pocket of the pars flaccida or postero- and destruction, and the dural and sinus plate.
superior part of TM has to be considered as unsafe • X-ray of the ear was formerly the standard method
CSOM and has to be treated by mastoid exploration of diagnosing diseases of mastoid but now HRCT
with tympanoplasty (MRM). scan shows a much clearer picture of the mastoid
• Audiometry is done pre- and post-operatively to and other structures and thus is of greater utility in
assess the improvement in hearing. assessing the various conditions of the ear and their
• Myringoplasty alone is done in safe CSOM. complications. Therefore the use of standard X-rays
22. (b) Mastoid segment of facial nerve (Ref. Cummings, has now declined.
6th ed., 2193) 34. (a) Temporal bone (Ref. Cummings, 6th ed., 105)
• The sinus tympani area is the hidden area of the • Stenver’s view is to see the whole of the petrous
middle ear and is the most common site of residual pyramid (internal acoustic meatus, labyrinth,
cholesteatoma. It lies medial to the bulge of the cochlea, mastoid antrum). Nowadays HRCT is done
vertical part of fallopian canal, i.e. mastoid segment to assess temporal bone pathologies.
of facial nerve. It being a hidden area, it is the most 35. (d) Modified radial mastoidectomy (Ref. Cummings,
difficult site to remove cholesteatoma. 6th ed., 2145) Ear
• It can be visualised through the posterior tympano- 36. (d) Stapes footplate (Ref. Cummings, 6th ed., 2190)
tomy approach. Please see the text. 37. (d) Pressure of keratin (Ref. Cummings, 6th ed., 2144)
23. (c) Canal wall down mastoidectomy (Ref. Cummings, 38. (b) Stapes footplate (Ref. Cummings, 6th ed., 2190)
6th ed., 2175) 39. (a) CSOM with attic perforation and cholesteatoma
• Intact canal wall mastoidectomy is done in unsafe (Ref. Cummings, 6th ed., 2143)
CSOM with limited and minimal disease. 40. (b) Modified radical mastoidectomy (Ref.
Section I

• Simple mastoidectomy is done for acute and Cummings, 6th ed., 2145)
coalescent mastoiditis, see next Chapter. 41. (a) Primary acquired cholesteatoma (Ref. Cummings,
• Cavity obliteration and canal wall reconstruction is 6th ed., 2143)
carried out in cases of unsafe CSOM without 42. (b) Primary cholesteatoma (Ref. Cummings, 6th ed.,
complications. 2145)
24. (d) Chronic suppurative Otitis media (Ref. Cummings, • The picture shows attic retraction pocket with
6th ed., 2145) whitish cholesteatoma flakes.
 128 ENT for Entrance Exams

medial wall of middle ear (lateral semicircular canal,

ANSWERS AND EXPLANATIONS
promontory, oval window) is causing facial nerve
1. (d) Lymphatic spread (Ref. Shambaugh, 6th ed., 453) palsy and vertigo respectively. So the management
2. (b) Mastoiditis (Ref. Cummings, 6th ed., 2157; Scott is immediate mastoid exploration to remove
Brown, 8th ed., Vol 2; 972) cholesteatoma.
• This is the most common complication following 18. (a), (c) and (d) (Ref. Cummings, 6th ed., 2167)
ASOM. • Cholesteatoma most commonly erodes Lateral
• Facial nerve palsy is an uncommon complication of semicircular canal.
ASOM • It can also erode the oval window and promon-
• Deafness (along with Pain and ear discharge) is the tory.
presenting feature of ASOM • All these structures are on the medial wall of the
• Cholesteatoma is not associated with ASOM. middle ear and erosion of these leads to a fistula on
3. (b) and (d) Facial nerve palsy, labyrinthitis (Ref. the medial wall leading to vertigo on external
Cummings, 6th ed., 2157) pressure changes and positive fistula test.
• Hearing loss is the presentation of CSOM. • The bulge of superior semi-circular canal is present
• Epidural abscess and sigmoid (lateral) sinus on the anterior slant of the petrous part of temporal
thrombosis are intracranial complications, please see bone and not on the medial wall. Hence a middle
the text. ear cholesteatoma does not erode it.
4. (a), (c) and (d) Labyrinthitis, Bezold abscess, facial 19. (a), (b) V, VI (Ref. Cummings, 6th ed., 2165)
nerve palsy (Ref. Cummings, 6th ed., 2157) 20. (a) Gradenigo syndrome (Ref. Scott Brown, 8th ed.,
5. (c) Mastoiditis (Ref. Cummings, 6th ed., 2157) Vol 2; 1318)
6. (c) Vertigo (Ref. Cummings, 6th ed., 2160) 21. (d) Petrositis (Ref. Scott Brown, 8th ed., Vol 2; 1318)
7. (b) Clouding of air cells of mastoid (Ref. Cummings, The given patient has developed petrositis which
6th ed., 2161) explains fever, ear discharge, diplopia (due to
• X-ray mastoid and CT scan shows clouding of air involvement of VI nerve) and pain side of head (in
cells because of the collection of exudates in them. the distribution of the ophthalmic division of
Later on mastoid pneumatisation is lost and a single trigeminal).
mastoid cavity may be seen. The rest of the choices are clearly not the considera-
8. (a) Bezold abscess, please refer the text (Ref. tions, see the text for their presentation.
Cummings, 6th ed., 2163) 22. (a) It is associated with jugular vein tenderness (Ref.
9. (b) Sternocleidomastoid muscle (Ref. Cummings, 6th Scott Brown, 8th ed., Vol 2; 1318)
ed., 2164) 23. (b) V, VI (Ref. Cummings, 6th ed. 2165)
10. (d) Coalescent mastoiditis, (Ref. Dhingra, 6th ed. 78) 24. (c) VII nerve palsy (Ref. Cummings, 6th ed. 2165)
please refer the text 25. (b), (c) and (d) (Ref. Scott Brown, 8th ed., Vol 2; 1318)
11. (a) Cortical mastoidectomy (Ref. Shambaugh, 6th ed., • The Gradenigo triad is caused by petrositis (or
501) abscess of petrous apex) and constitutes:
12. (d) Acute mastoiditis (Ref. Shambaugh, 6th ed., 501) i. VI nerve involvement leading to diplopia
13. (a) Acute mastoiditis (Ref. Shambaugh, 6th ed., 509) ii. V nerve involvement (ophthalmic division)
14. (b) Coalescent mastoiditis (Ref. Cummings, 6th ed. leading to retro-orbital pain
2161) iii. Ear discharge
15. (b) VII (Ref. Shambaugh, 6th ed., 512) • Conductive deafness is also seen in petrositis (or
• Most common nerve to be damaged in CSOM is the abscess petrous apex) as petrositis follows otitis
facial nerve as it passes through the middle ear. media but it is not a part of the triad.
Ear

• Rest of the nerves mentioned are not related to the 26. (c) Petrositis (Ref. Cummings, 6th ed., 2165)
ear. • Since the air cells of the petrous bone communicate
16. (b) Immediate mastoidectomy (Ref. Cummings, 6th with the mastoid, in any patient, if there is persistent
ed., 2169) ear discharge following cortical or modified radical
• In a patient of unsafe CSOM the cholesteatoma mastoidectomy, petrositis should be ruled out by CT
may erode the fallopian canal and cause facial and MRI. Also retroorbital pain is suggestive of
Section I

nerve paresis. So here immediate mastoidectomy petrositis (due to involvement of ophthalmic division
is done to remove the disease. There is no role of of trigeminal).
antibiotics. • Labyrinthitis per se does not lead to ear discharge
17. (c) Immediate mastoid exploration (Ref. Shambaugh, once the middle ear and mastoid disease has been
6th ed., 448) cleared by surgery. Moreover, in labyrinthitis there
• This is an unsafe CSOM. Here cholesteatoma eroding will be vertigo along with hearing loss. So this is not
fallopian canal and causing fistula formation on the the complication in the given case.
 Complications of Suppurative Otitis Media 129

• Latent mastoiditis or masked mastoiditis can be a • Acute subarachnoid haemorrhage is due to rupture
consequence of inadequate medical management; of intracranial aneurysm or head trauma. It presents
but there is no question of it arising after modified with sudden loss of consciousness. It may also
radical mastoidectomy. present with sudden onset very severe headache
27. (a) Labyrinthitis (Ref. Cummings, 6th ed., 2169) described as worst ever headache.
• Following mastoidectomy deafness along with • Lateral sinus thrombosis presents with fever,
vertigo is suggestive of labyrinthitis. tenderness over jugular vein and oedema over the
28. (a) Extradural abscess (Ref. Shambaugh, 6th ed., 447) mastoid.
• Extradural abscess is most often a silent complication 34. (b) Brainstem evoked response audiometry (Ref.
and is detected accidently during mastoid exploration. Cummings, 6th ed., 2076)
29. (c) Immediate mastoid exploration (Ref. Cummings, Meningitis can lead to labyrinthitis and thereby
6th ed., 2169) deafness which an infant will not report and if
• This is an unsafe CSOM with labyrinthitis. So the diagnosed early, cochlear implantation will have
management is immediate mastoid exploration to good results, so BERA needs to be done.
remove cholesteatoma. 35. (a) Streptococcus pneumoniae (Ref. Cummings, 6th
30. (a) Meningitis (Ref. Cummings, 6th ed., 2157) ed., 2171)
• The most common intracranial complication of chronic MC cause of otogenic meningitis was H. influenzae
suppurative Otitis media is meningitis followed by but after the introduction of Hib vaccine in the
intracerebral abscess (temporal lobe abscess) universal immunisation programme, it is
• Cholesteatoma promotes the above complications in Streptococcus pneumoniae now.
unsafe CSOM. 36. (b) CSOM with lateral sinus thrombosis in turn can
• Conductive deafness is one of the presenting features cause brain abscess (Ref. Cummings, 6th ed., 2172)
of CSOM. (please refer to the spreading pathways for
complications of CSOM in the beginning of the
31. (d) Meningitis (Ref. Cummings, 6th ed., 2157)
chapter)
• The most common intracranial complication of
chronic suppurative Otitis media is meningitis • H. influenzae which was previously the most common
followed by brain abscess (temporal lobe abscess). cause of otogenic meningitis is rarely found in
otogenic brain abscess, refer the text for organisms
• Mastoiditis is the most common extracranial
causing brain abscess.
complication.
• Most common intracranial complication of CSOM
• Subperiosteal or postauricular abscess is the most
is meningitis.
common abscess following mastoiditis.
• Personality changes are associated with Frontal lobe
32. (a) Cochlear aqueduct (Ref. Cummings, 6th ed., 2169;
abscess.
Scott Brown, 8th ed., Vol 2; 1012)
37. (b) Gradenigo triad (Ref. Cummings, 6th ed., 2165)
• Most potential route for transmission of labyrinthitis
• Gradenigo triad is seen in association with abscess
leading to meningitis or vice versa is through
of petrous apex or petrositis. Rest all are seen in
cochlear aqueduct. From the inner ear the infection
lateral sinus thrombosis.
can spread to the cranium via.
i. Cochlear aqueduct (which connects the CSF to 38. (a) Lateral sinus thrombosis (Ref. Shambaugh, 6th ed.,
the scala tympani and is the site of entry of CSF 459)
leading to the formation of perilymph) 39. (a) Lateral sinus thrombosis (Ref. Shambaugh, 6th ed.,
ii. Internal acoustic meatus. 459)
• Endolymphatic sac is a part of membranous 40. (c) Canal wall down mastoidectomy (Ref. Cummings,
labyrinth. It is a closed sac, present extradurally and 6th ed., 2175) Ear
responsible for absorption of endolymph. • Intact canal wall down mastoidectomy is done when
• Vestibular aqueduct is the part of bony labyrinth there is limited disease in the mastoid.
which surrounds the endolymphatic duct. • Simple mastoidectomy also known as cortical
Hyrtle fissure is the tympanomeningeal hiatus mastoidectomy is done for acute and coalescent
present at 16–18 week stage during fetal life. It mastoiditis.
connects round window to the posterior cranial • Following any canal wall down procedure the big
Section I

fossa. It fuses and disappears by 26 weeks. mastoid cavity can be obliterated to prevent cavity
33. (b) Pyogenic meningitis (Ref. Scott Brown, 8th ed., related problems but if the unsafe CSOM is associated
Vol 2; 1012) with complications this is postponed to a next stage.
• Focal neurological deficits being not mentioned so 41. (b) Griesinger’s sign (Ref. Shambaugh, 6th ed., 459)
brain abscess is not the right choice. Also • Battle’s sign represents ecchymosis around the
meningismus causing neck rigidity is generally not mastoid process from head trauma that has caused
present in brain abscess. a temporal bone fracture.
 130 ENT for Entrance Exams

• Irwin Moore sign: On pressure of anterior pillar there CSOM. Intracranial complication has to be managed
is expression of cheesy material from the tonsil. It is first.
a feature of chronic tonsillitis. 47. (d) Hitzelberger sign (Ref. Shambaugh, 6th ed., 647)
• Hennebert’s sign is False positive fistula test. 48. (a) Gradenigo syndrome (Ref. Cummings, 6th ed.,
42. (b) Lateral sinus thrombophlebitis (Ref. Shambaugh, 2165)
6th ed., 459) Diplopia is causing compensatory head tilt in the
43. (b) Lateral sinus thrombophlebitis (Ref. Cummings, said patient.
6th ed., 2175) 49. (a) Upper part of neck (Ref. Cummings, 6th ed., 2164)
44. (d) Jugular vein thrombosis (Ref. Shambaugh, 6th ed., 459) (along the sternocleidomastoid muscle)
45. (a) Mastoid bone edema (Ref. Shambaugh, 6th ed., 459) 50. (a) Schwartze operation (Ref. Cummings, 6th ed.,
46. (a) Abscess drainage followed by MRM (Ref. 2160)
Cummings, 6th ed., 2172) 51. (c) Palatal palsy (Ref. Scott Brown, 8th ed., Vol 2; 1318)
The ring enhancing lesion that is being seen 52. (c) Surgical repair (Ref. Cummings, 6th ed., 2169)
here is temporal lobe abscess following unsafe 53. (c) Facial palsy (Ref. Scott Brown, 8th ed., Vol 2; 1318)
Ear
Section I
 Otosclerosis 137

ANSWERS AND EXPLANATIONS 9. (b) Otosclerosis (Ref. Cummings, 6th ed., 2213)
• The patient of otosclerosis gives the typical history
1. (c) Fissula ante-fenestrum (Ref. Cummings, 6th ed., of hearing better in noisy surrounding which is
2212) known as Paracusis Willisii.
• Though otosclerosis ultimately results in the fixation • Hyalinisation and calcification of the fibrous layer
of the footplate and margins of stapes which is lying of TM is known as tympanosclerosis. Here a very
over the oval window, it actually gets initiated most mild conductive hearing loss is present.
commonly in the immature cartilaginous area of the • Meniere’s disease being a U/L condition leads to
bony labyrinth which lies anterior to the fenestra of distortion of sound which is known as diplacusis,
oval window and hence called fissula ante i.e. both the cochleas sense the same sound as
fenestrum. different.
• Fissula post-fenestrum area of the bony labyrinth is • Presbycusis is the age related B/L SN hearing loss.
also cartilaginous but otosclerosis is uncommon here. 10. (d) Paracusis (Ref. Cummings, 6th ed., 2213)
2. (a) Oval window (Ref. Cummings, 6th ed., 2211) See the explanation to the above question
• Since the most common site of origin of otosclerosis • Hyperacusis is because of absence of stapedial reflex
is fissula ante fenestrum, the overgrowth from here seen in facial nerve palsy. Here normal sounds
comes over the footplate of stapes lying over the oval appear abnormally loud.
window. So the part most commonly involved in 11. (d) All (Ref. Scott Brown, 8th ed., Vol 2; 755)
otosclerosis is oval window.
Tinnitus in otosclerosis is not common; if present it
3. (c) 20–30 yrs (Ref. Cummings, 6th ed., 2211) is due to:
4. (a) Autosomal dominant (Ref. Cummings, 6th ed., i. Active otosclerosis because of increased vascularity
2211)
ii. Cochlear otosclerosis
5. (a), (d) and (e) are correct (Ref. Cummings, 6th ed., 2211)
• Any hearing loss condition, be it conductive or SN
6. (a) Otosclerosis (Ref. Cummings, 6th ed., 2211) can as such lead to tinnitus. So all are possible
30-yr-old woman with family history of hearing loss, mechanisms.
presenting with B/L hearing loss during pregnancy, 12. (a) Normal (Ref. Shambaugh, 6th ed., 531)
pure tone audiometry showing an apparent bone
• In 90% patients of otosclerosis the tympanic
conduction hearing loss at 2000 Hz, i.e. Carhartz
membrane appears normal, i.e. pearly white.
notch is diagnostic of otosclerosis.
• In 10% cases which are active tympanic membrane
• Acoustic neuroma is seen in the age group of
is flamingo pink.
40–70 yrs and presents with U/L SN hearing loss
• Blue TM is a feature of glue ear because of cholesterol
and tinnitus.
granuloma.
• Otitis media with effusion or glue ear is seen most
• Yellow TM is not seen in any condition
commonly in children and presents with B/L
conductive hearing loss. Tympanic membrane here 13. (a) Otosclerosis (Ref. Cummings, 6th ed., 2213)
is dull retracted with fluid level and air bubbles seen • In active otosclerosis the TM appears pink known
behind. as flamingo (a bird) pink, though 90% cases are
• Sigmoid sinus thrombosis is a complication of unsafe mature otosclerosis where TM is pearly white.
CSOM and presents with hectic fever, jugular vein • In Glomus the vascular mass abutting on TM gives
area tenderness, oedema of the mastoid and features it a red reflex.
of unsafe CSOM, i.e. ear discharge, cholesteatoma, • In acute otitis media the increased vascularity on the
and hearing loss. TM makes it appear red.
7. (b) B/L conductive deafness (Ref. Cummings, 6th ed., • In serous otitis media or glue ear the TM is blue.
2213) 14. (b) Otosclerosis (Ref. Cummings, 6th ed., 2213) Ear
• Otospongiosis causing fixation of foot plate of stapes • 10% cases of otosclerosis are active. In these the active
is a conductive pathology. division is taking place on the medial wall of middle
• Uncommonly when there occurs cochlear otosclerosis ear leading to increased vascularity. This appears
(please refer to the text) it leads to, B/L SN hearing pinkish through the intact tympanic membrane
loss along with conductive, i.e. mixed hearing loss. leading to flamingo pink appearance of TM also
8. (b) Otospongiosis (Ref. Cummings, 6th ed., 2211) known as Schwartze sign.
Section I

• Otosclerosis is the most common cause of B/L • In Glomus jugulare the vascular tumour coming
progressive conductive hearing loss in adults. from the floor of the middle ear gives a rising sun
• Meniere’s disease presents with U/L SN hearing appearance on the TM. This is also known as red reflex.
loss, vertigo and tinnitus. • In Meniere’s and Acoustic neuroma the TM appears
• With the kind of presentation mentioned the no3rmal, i.e. pearly white.
remaining two options of conductive hearing loss 15. (b) Normal tympanic membrane (Ref. Cummings 6th
are less common than otosclerosis. ed., 2213)
 138 ENT for Entrance Exams

• Sounds are rather better heard in noisy environment, 25. (d) Radical mastoidectomy (Ref. Cummings, 6th ed., 2213)
the Paracusis Willisii phenomenon. 26. (d) Otosclerosis (Ref. Scott Brown, 8th ed., Vol 2 page 1070)
• Otosclerosis is seen more commonly in females. 27. (c) Irreversible loss of hearing (Ref. Cummings, 6th
• The ossicle affected is Stapes. ed., 1071)
16. (b) and (d) (Ref. Scott Brown, 8th ed., Vol 2 page 1068) • Since the hearing loss in otosclerosis is due to fixation
• In 70–85% of patients otosclerosis is a bilateral of footplate of stapes so the mobilisation of stapes
condition. by stapedotomy reverses the hearing loss.
• The audiogram of a patient of otosclerosis shows an • Largely there occurs conductive deafness but when
A-B gap >15 dB and typical dip at 2000 Hz in the bone there is involvement of cochlea, i.e. cochlear otosclerosis
conduction curve. This dip is known as “Carhart’s SN deafness is also seen.
notch”. Rest options have been discussed previously.
• Fluctuating conductive hearing loss is seen in serous 28. (c) Fluorides (Ref. Cummings, 6th ed., 2218)
Otitis media, whereas fluctuating SN hearing loss is • In active otosclerosis cases, i.e. when Schwartz sign
seen in Meniere’s disease. is present medical management with sodium fluoride
• Due to progressive fixation of the footplate of stapes, (Na F) decreases the progression by accelerating the
there is progressive conductive hearing loss in maturation and inhibiting proteolytic enzymes. Please
otosclerosis. see text.
17. (b) Positive Rinne test (Ref. Cummings, 6th ed., 2213) • As per the pathogenesis of otosclerosis steroids,
• Since otosclerosis majorly leads to conductive antibiotics and vitamins have no role in the
deafness so Rinne test is negative. management of otosclerosis.
18. (b) Vertigo present (Ref. Cummings, 6th ed., 2213) 29. (b) Acts by inhibiting osteoblastic activity (Ref.
• Vertigo is not a feature of otosclerosis Cummings, 6th ed., 2218)
19. (a) Otosclerosis (Ref. Dhingra, 6th ed., 22) 30. (d) Gentamicin (Ref. Cummings, 6th ed., 2213)
• Gelle’s is negative in otosclerosis, i.e. change in the The given tympanogram shows As type of curve and
pressure of EAC does not produce any change in as per the description the diagnosis is clearly
hearing as Ossicular chain is already fixed. otosclerosis.
Please refer to Gelle’s test in audiometry chapter. Gentamicin is a vestibulotoxic drug given in Meniere’s
20. (b) As (Ref. Cummings, 6th ed., 2213) to relieve vertigo. It has no role in otosclerosis.
Lady with B/L hearing loss with history of worsening 31. (c) Stapedotomy (Ref. Cummings, 6th ed., 2213)
during pregnancy is suggestive of otosclerosis. • In mature otosclerosis when the footplate is fixed
• Impedance audiometry shows As type curve (normal and active division has stopped the treatment
middle ear pressure with reduced compliance). This consists of mobilisation of footplate of stapes. This
is diagnostic of otosclerosis. can be done either by Stapedectomy or Stapedotomy.
• Ad type curve is seen in ossicular discontinuity. Fenestration operation is no longer done now.
• B type curve is seen in serous Otitis media. • Previously Sacculotomy used to be done in Meniere’s
to decompress the endolymph. It is no longer done now.
• C curve is seen in early stages of Eustachian tube
obstruction. 32. (a) Teflon piston (Ref. Cummings, 6th ed., 2215)
21. (a) Low compliance (Ref. Scott Brown, 8th ed., Vol 2 1071) • Grommet insertion is required in serous Otitis media.
• The As type of curve in otosclerosis is low • Total ossicular replacement prosthesis (TORP) is
compliance and normal pressure type. used when it is required to reconstruct whole of the
ossicular chain, for example, in unsafe CSOM when
• High compliance, normal pressure type of curve is
there occurs complete necrosis of all the three ossicles.
Ad, seen in ossicular discontinuity.
• Normal compliance, normal pressure is A type, i.e. 33. (d) Lenticular process of Incus (Ref. Cummings, 6th
Ear

normal curve. ed., 2213)

22. (d) 2000 Hz in BC (Ref. Shambaugh, 6th ed., 532) Please refer to the text.
34. (c) It quickens the maturity of the active focus and
In otosclerosis the dip at 2000 Hz is seen in bone
reduces osteoclastic resorption (Ref. Scott Brown, 8th
conduction curve which is known as Carhart’s notch.
ed., Vol 2 1074)
Mnemonic: Carhart’s in Bone Conduction, CBC.
23. (b) 2 kHz or 2000 Hz (Ref. Scott Brown, 8th ed., Vol 2 35. (a) White races (Ref. Cummings, 6th ed., 2211)
Section I

1070) 36. (d) Otosclerosis (Ref. Cummings, 6th ed., 2213)

• In otosclerosis there is an increase in BC threshold 37. (b) Carhart’s notch (Ref. Scott Brown, 8th ed., Vol 2 1070)
of approx. 5 dB, 10 dB and 15 dB at 500, 1000, 38. (c) Stapedotomy and piston insertion (Ref. Scott
2000 Hz respectively. So the deepest dip is at 2 kHz Brown, 8th ed., Vol 2 1086)
which is known as Carhart’s notch. 39. (d) As graph with loss of stapedial reflex (Ref.
• At 4 or 8 kHz, there is no hearing loss in otosclerosis. Anirban Biswas 5th ed., 118)
24. (c) Otosclerosis (Ref. Shambaugh, 6th ed., 532) 40. (d) Ad (Ref. Anirban Biswas, 5th ed., 90)
 Facial Nerve and its Disorders 151

at the Geniculate ganglion) which is responsible for

ANSWERS AND EXPLANATIONS
lacrimation there will be dry eye on the same side.
1. (d) Paralysis of lower facial muscles on left side • Tympanic segment, Vertical segment and Chorda
(Ref. Scott Brown, 6th ed., 1639) tympani all are beyond the geniculate ganglion.
2. (a) Horizontal part, refer the text (Ref. Scott Brown, 8. (a) Geniculate ganglion (Ref. Cummings, 6th ed., 2606)
6th ed., 1386) • Mastoid segment and Stylomastoid foramen are
3. (a) Greater petrosal nerve (Ref. Scott Brown, 6th ed., beyond the geniculate ganglion.
1385) • Otic ganglion is for the parasympathetic supply to
• The greater superficial petrosal nerve arises from the the parotid.
geniculate ganglion at the first genu. This is the first 9. (a) Loss of corneal reflex at side of lesion. (Ref.
branch. Cummings, 6th ed., 2606)
• The 2nd branch is the nerve to the stapedius given • When the injury is at the stylomastoid foramen, the
at the pyramid. extracranial motor part of facial is affected leading
• The 3rd is the chorda tympani given 4–6 mm before to loss of corneal reflex, see the text above.
the exit of facial nerve from stylomastoid foramen. • The branches of facial before the stylomastoid
• Lesser superficial petrosal nerve is not a branch of foramen, i.e. greater superficial petrosal, nerve to
facial. It arises from tympanic plexus and supplies stapedius and Chorda tympani will all be preserved
the Otic ganglion. Otic ganglion is for the therefore there won’t be any loss of lacrimation,
parasympathetic supply to the parotid. Secretomotor hyperacusis and loss of taste respectively
fibres to the parotid arise from glossopharyngeal 10. (a) The nasolabial fold is obliterated on same side
nerve, reach the otic ganglion through the lesser (Ref. Scott Brown, 6th ed., 1370)
superficial petrosal nerve via the tympanic plexus • In facial nerve palsy, the motor supply of the facial
and then reach the parotid through the muscles on the same side will be affected leading to
auriculotemporal nerve arising from the otic obliteration of nasolabial fold, loss of facial movements
ganglion. and incomplete closure of the eye on the affected side.
4. (a) Chorda tympani nerve (Ref. Scott Brown, 6th ed., • The face deviates to the opposite side because of the
1934) pull of the normal side facial muscles.
• Chorda tympani nerve gives taste to the anterior 11. (b) Loss of taste sensations from anterior 2/3rd of
2/3rd of the tongue and parasympathetic supply to tongue (Ref. Scott Brown, 6th ed., 1387)
the sublingual and submandibular salivary glands. • The innervation of most of the posterior 1/3rd of
Here in this question since the Stapedial reflex is tongue and circumvallate papillae is by glossopharyn-
normal so injury is beyond the nerve to stapedius, geal nerve.
i.e. at or before Chorda tympani but after the • Secretomotor fibres to the parotid arise from
pyramid and will lead to loss of taste from anterior glossopharyngeal nerve; reach the otic ganglion
2/3rd of tongue and reduced salivary flow leading through the lesser petrosal nerve and then reach the
to some dryness of mouth. parotid through the auriculotemporal nerve.
• Stapedial reflex will also be absent with facial nerve 12. (d) Proximal to geniculate ganglion (Ref. Cummings,
injury at CP angle and geniculate ganglion. 6th ed., 2606)
5. (a) Facial nerve (Ref. Cummings, 6th ed., 2620) • Since all the intratemporal branches of facial are
6. (a) Deviation of angle of mouth towards opposite involved, the injury should be before the 1st branch
site. (Ref. Scott Brown, 6th ed., 1387) (i.e. greater superficial petrosal) which is given off
• When there is lesion at the outlet of stylomastoid at the geniculate ganglion.
foramen the motor fibres which supply the facial 13. (a) Below the processus cochleariformis (Ref. Scott
muscles on the same side are affected leading to Brown, 6th ed., 1386, 1387) Ear
deviation of angle of mouth towards opposite side • The first genu of facial nerve lies antero-superior to
due to the pull of the normal side facial muscles. the Processes cochleariformis.
• The chorda tympani originates before the 14. (c) and (e) labyrinthine artery, stylomastoid artery,
stylomastoid foramen so taste sensation in anterior (Ref. Scott Brown, 6th ed., 1388) please refer the text.
2/3rd of tongue is preserved here. 15. (a) Otosclerosis (Ref. Scott Brown 6th ed., 1401)
Section I

• Sensation over cheek is by trigeminal nerve and the 16. (d) All (Ref. Scott Brown, 6th ed., 1401)
motor supply of tongue is by hypoglossal, both of 17. (c) Malignant Otitis externa (Ref. Cummings, 6th ed., 2618)
which will not be affected in facial nerve palsy. • Among the given options Malignant Otitis externa
7. (d) Geniculate ganglion (Ref. Cummings, 6th ed., is locally invasive infective condition and leads to
2606) facial nerve palsy. It is seen in immunocompromised
• Whenever there is injury before or at the origin of patients and is caused most commonly by
the greater superficial petrosal nerve (i.e. before or pseudomonas.
 152 ENT for Entrance Exams

18. (d) Bell’s palsy (Ref. Scott Brown, 6th ed., 1400) • In Bell’s palsy facial palsy may be associated with
• The MC cause of facial nerve palsy is idiopathic. The other cranial nerve neuropathies which are Vth,
MC idiopathic facial nerve palsy is Bell’s palsy. VIIIth, IXth and Xth.
• The second most common cause of facial nerve palsy • Facial nerve paralysis with uveitis and parotid
is iatrogenic. The most common iatrogenic cause of enlargement constitutes Heerfordt’s syndrome.
facial nerve palsy is parotid surgery followed by 29. (c) Oral steroids + Acyclovir is the best answer. (Ref.
mastoid surgery. Cummings, 6th ed., 2621)
• Non iatrogenic trauma causing temporal bone • Antiviral has to be started within 3 days. Since the
fractures can lead to facial nerve palsy. Here patient has presented on the 3rd day, acyclovir
transverse fractures leads to facial nerve palsy more should also be started here along with the steroids.
commonly than the longitudinal fractures. • If the patient comes after 3 days he should be given
• Ramsay Hunt syndrome is an infective cause of facial only the steroid and vitamin B.
nerve palsy due to Herpes zoster. • Intratympanic steroids and vasodilators are not used
19. (c) Bell’s palsy (Ref. Scott Brown, 6th ed., 1400) for Bell’s palsy. Please refer the text.
20. (d) LMN VIIth nerve (Ref. Cummings, 6th ed., 2619) 30. (d) Electrophysiological nerve testing. (Ref. Cummings,
• In LMN VIIth nerve palsy (Most common being 6th ed., 2622)
Bell’s palsy) the complete half of the ipsilateral side • If on electrophysiological tests the signs of regenera-
of face gets involved. tion are not present surgical decompression is
• In UMN VIIth nerve palsy the lower half of the indicated.
opposite side of face gets involved. Vasodilators and ACTH have no role.
21. (a) Immediate surgical decompression, (Ref. • Physiotherapy is started from the 1st day itself while
Cummings, 6th ed., 2621) please refer to text. treating Bell’s palsy.
• Steroids in Bell’s palsy are given in the dosage of 1 mg/
22. (d) I/L ptosis (Ref. Scott Brown, 6th ed., 1370)
kg body weight and gradually tapered. If there is no
• In Bell’s palsy because of involvement of the facial
response electrophysiological nerve testing is done.
nerve, the muscles of the ipsilateral face are
31. (b) H. zoster (Ref. Cummings, 6th ed., 2622)
paralysed which leads to incomplete closure of the
eye but not ptosis. • Herpes Zoster of external ear with facial palsy is
known as Ramsay Hunt syndrome.
• Ptosis is seen in 3rd nerve palsy.
• H. simplex is being reported to be associated with
23. (d) Stapedius (Ref. Cummings, 6th ed., 2620)
Bell’s palsy.
• Hyperacusis is normal sounds perceived as
• Facial nerve palsy can also be caused by other
abnormally loud. This is due to loss of Stapedial
viruses, for example HIV, influenza, polio, EBV, etc.
reflex. In Bell’s palsy this is due to paralysis of the
32. (a) Herpes zoster (Ref. Cummings, 6th ed., 2622)
facial nerve which supplies the stapedius.
Ramsay Hunt syndrome is the underlying condition.
• Tensor tympani which also helps in protecting the ear
• H. simplex is found to be associated with Bell’s palsy
from loud noise, is supplied by the mandibular nerve.
in some patients but there are no vesicular eruptions
• The other muscles in the options are not involved in
in Bell’s palsy.
hyperacusis.
33. (c) Surgical treatment gives excellent prognosis
24. (b) Always recurrent (Ref. Scott Brown, 6th ed., 1400) (Ref. Scott Brown, 6th ed., 1403)
• Recurrence is uncommon. There may occur • Treatment is steroids and acyclovir like Bell’s palsy.
spontaneous remission but steroids are very Rest are true please refer the text.
important in the management, please see the text. 34. (d) Results of spontaneous recovery are excellent
25. (a), (c), (e) (Ref. Scott Brown, 6th ed., 1400) (Ref. Cummings, 6th ed., 2622)
26. (a) Spontaneous recovery (please refer the text) (Ref. 35. (c) Mastoidectomy (Ref. Scott Brown, 6th ed., 1405)
Ear

Cummings, 6th ed., 2621) • The most common iatrogenic cause of facial nerve
27. (a), (b), (c), (d), (e) (Ref. Scott Brown, 6th ed., 1394, palsy is parotid surgery.
1400) all are true • The next common iatrogenic cause of facial nerve
28. (c) Bell’s palsy is idiopathic LMN palsy of facial palsy is mastoid exploration.
nerve causing ipsilateral paralysis of face. (Ref. Scott • It may also occur following rest of the options.
Brown, 6th ed., 1400) 36. (b) Transverse fractures (Ref. Scott Brown, 6th ed.,
Section I

• Ipsilateral Facial nerve paralysis and contralateral 1404) please refer the text.
Hemiparesis along with ipsilateral VI nerve palsy 37. (a) More common with transverse fractures (Ref.
constitutes Millard Gubler syndrome. It is a form of Scott Brown, 6th ed., 1404)
“crossed hemiplegia,” as the paralysis of muscles Facial nerve palsy is usually of immediate onset.
controlled by the facial nerve occurs on the same side Mnemonic: Transverse fracture Traumatises the
as the lesion, while the hemiplegia of muscles below facial nerve whereas Longitudinal fracture Leaves
the neck occurs on the opposite side from the lesion it usually.
 Facial Nerve and its Disorders 153

38. (d) Fracture of petrous temporal bone (Ref. Scott 49. (c) Sphenopalatine ganglion (Ref. Shambaugh, 6th ed.,
Brown, 6th ed., 1110) 621)
39. (b) Fracture of petrous ridge (Ref. Scott Brown, 6th 50. (a) Horizontal segment (Ref. Scott Brown, 6th ed.,
ed., 1110) 1394)
40. (a) Nerve decompression (Ref. Scott Brown, 6th ed., 51. (a) Tympanic neurectomy is contraindicated (Ref.
1404) Cummings, 6th ed., 1257)
• In sudden onset complete palsy following fracture 52. (a) Prednisolone (Ref. Cummings, 6th ed., 2621)
(which is the common presentation) early exploration
53. (d) Auriculotemporal nerve (Ref. Cummings, 6th ed.,
and decompression of facial nerve or nerve repair
3107)
should be carried out.
54. (a) Sympathetic cholinergic fibres (Ref. Cummings,
• Delayed onset palsy, which might be because of
6th ed., 3107)
surrounding edema, should be treated with steroids
and watchful waiting. 55. (c) Gustatory sweating (Ref. Cummings, 6th ed., 1257)
41. (b) Facial nerve repair (Ref. Scott Brown, 6th ed., 1404) 56. (b) Primary repair (Ref. Scott Brown, 6th ed., 1403)
• Since generally following trauma the facial nerve • Any sudden onset palsy following injury (iatrogenic
injury occurs as sudden onset. Facial decompression or non iatrogenic trauma), should be managed by
should be the best option. immediate exploration and repair.
42. (a) Immediate decompression (Ref. Scott Brown, 6th 57. (b) Posterior wall (Ref. Shambaugh, 6th ed., 621)
ed., 1404) 58. (b) Greater auricular nerve (Ref. Cummings, 6th ed.,
43. (a) Cross innervations of facial nerve fibres. (Ref. 1254)
Scott Brown, 6th ed., 1370) • The nerve that supplies skin over the angle of
44. (a) aberrant reinnervation of parasympathetic mandible is Greater auricular Nerve. Sometimes
fibres of auriculotemporal nerve with sympathetic during parotid surgeries, Greater auricular Nerve
sweat glands (Ref. Cummings, 6th ed., 1257) also gets injured along with the Auriculotemporal
45. (a) Before greater superficial petrosal (Ref. Scott Nerve. In this situation with the aberrant regeneration
Brown, 6th ed., 1370) of the Auriculotemporal Nerve, the parasympathetic
46. (c) Injection Botulinum toxin in lacrimal gland (Ref. fibres (of the auriculotemporal nerve) to salivary
Scott Brown, 6th ed., 1408) glands become aberrantly connected with the sympa-
47. (c) HRCT (Ref. Scott Brown, 6th ed., 1399) thetic cholinergic fibres to sweat glands of the skin
48. (b) Parotid gland (Ref. Cummings, 6th ed., 2606) overlying the parotid as well as overlying the angle
• lacrimal and nasal mucosal glands are supplied by of mandible (the territory of Greater auricular nerve).
greater superficial petrosal nerve. Submandibular 59. (c) Oral steroids + Acyclovir (Ref. Cummings, 6th ed.,
and sublingual glands are supplied by Chorda 2621)
tympani. Parotid is supplied by the otic ganglion 60. (b) Due to reactivation of Herpes zoster virus in
through the Auriculotemporal nerve. the geniculate ganglion (Ref. Cummings, 6th ed., 2622)

Ear
Section I
 168 ENT for Entrance Exams

10. (All) (Ref. Cummings, 6th ed., 2556)

ANSWERS AND EXPLANATIONS
• Diarrhoea and vomiting along with diaphoresis,
1. (b) Endolymphatic hydrops (Ref. Cummings, 6th ed., pallor, nausea, abdominal cramps, and bradycardia
2331) may occur as vagal manifestations associated with
• Meniere’s is also known as endolymphatic hydrops. vertigo in Meniere.
• There is no condition called Perilymphatic hydrops. 11. (a) and (b), (Ref. Cummings, 6th ed., 2556) Refer the text
• Otospongiosis also known as otosclerosis is fixation 12. (c) Low frequency sensorineural deafness is often
of foot plate of stapes. seen in pure tone audiogram (Ref. Cummings, 6th
• Coalescent mastoiditis is infection of the mastoid air ed., 2331)
cells and is a complication following ASOM/ unsafe • Meniere is characterised by endolymphatic hydrops.
CSOM. This dilatation of the membranous labyrinth starts
2. (a) Meniere’s disease (Ref. Cummings, 6th ed., 2331) from the apex of membranous cochlea going down,
3. (a) 6 (refer to text) (Ref. Cummings, 6th ed., 2554) so low frequency sensorineural deafness is seen in
• In this regard it is worth mentioning that some pure tone audiogram in the early stages.
authors relate Meniere’s disease to the COCH gene • Carhart’s notch, which is a dip at 2000 Hz in BC, is a
(“cochlin” gene) located on chromosome no. 14 q. characteristic feature in pure tone audiogram in
But studies have proven that the Mutations in the otosclerosis.
COCH gene are a frequent cause of autosomal • Schwartze’s sign or flamingo pink appearance of the
dominant progressive cochleovestibular dysfunction, tympanic membrane is seen in active otosclerosis.
but not of Meniere’s disease. • Decompression of fallopian canal is the treatment of
4. (d) Vertigo, hearing loss and tinnitus (Ref. choice in facial nerve palsy, see chapter on facial nerve
Cummings, 6th ed., 2331) palsy. Endolymphatic sac decompression is done in
• The presenting triad of Meniere is vertigo followed Meniere when the medical management fails.
by deafness (SN) and tinnitus. 13. (b) Meniere’s disease (Ref. Cummings, 6th ed., 2556)
5. (d) Otorrhoea (Ref. Scott Brown, 8th ed., Vol 2, 819) • Recruitment phenomenon, i.e. abnormal growth of
• Meniere is manifested as vertigo followed by loudness on increasing the level of loudness (refer
deafness (SN), tinnitus and a sensation of fullness in to audiology chapter) is seen in cochlear pathologies
the ear but no discharge. like Meniere.
6. (d) Loss of consciousness (Ref. Scott Brown, 8th ed., • Otosclerosis and Otitis media with effusion are
Vol 2, 819) middle ear pathologies.
• The patient is fully conscious and oriented during • Acoustic nerve schwannoma is retro cochlear.
an attack of Meniere. 14. (c) Tullios phenomenon seen (Ref. Scott Brown, 8th
• Meniere being a disturbance of peripheral vestibular ed., Vol 2, 819)
system is therefore not characterised by any focal 15. (c) Increase endolymph reabsorption (Ref.
(such as diplopia, dysarthria, paresthesia, etc.) or Cummings, 6th ed., 2558)
generalised neurological symptoms like loss of 16. (a) Nicotinic acid (Ref. Cummings, 6th ed., 2558)
consciousness, seizures, etc. 17. (d) Delivering drug to the round membrane (Ref.
• The neurological symptoms accompany a central Cummings, 6th ed., 2558)
vestibular disturbance. 18. (c) Meniere’s disease (Ref. Cummings, 6th ed., 2559)
• However, vertigo of Meniere may be associated with • Meniere’s disease being characterised by endolympha-
vagal symptoms i.e. diaphoresis, pallor, nausea, tic hydrops so here endolymphatic sac decompression
vomiting, abdominal cramps, diarrhoea and is done when the medical management fails.
bradycardia. • Tinnitus is treated as per the underlying cause.
7. (a) Diplopia (see the explanation above) (Ref.
Ear

• Treatment modality of Acoustic neuroma is surgical

Cummings, 6th ed., 2331) excision.
8. (b) Pulsatile tinnitus (Ref. Cummings, 6th ed., 2331) • Perilymph fistula is repaired by grafting the fistula.
• The tinnitus in Meniere is subjective (i.e. only the 19. (d) Suppurative otitis media (Ref. Scott Brown, 8th
patient can hear). ed., Vol 2, 833)
• Pulsatile tinnitus is an objective tinnitus (i.e. the • The presenting symptom of Meniere is vertigo. So
Section I

examiner also can hear the tinnitus). Pulsatile therefore CNS disease, labyrinthitis and Acoustic
tinnitus is seen in vascular conditions like Glomus neuroma are among the differentials.
jugulare and aneurysm of internal carotid artery. • Suppurative otitis media is clearly characterised by
9. (b) Meniere’s disease (Ref. Cummings, 6th ed., 2331) ear discharge and perforation of tympanic membrane.
• In otosclerosis there occurs progressive deafness. 20. (c) Meniere’s disease (Ref. Cummings, 6th ed., 2557)
AOM shows temporary deafness. There is no 21. (c), (e) Vestibular neurectomy, Labyrinthectomy
deafness in BPPV. (Ref. Cummings, 6th ed., 2559)
 Meniere’s Disease and Disorders of Vestibular System 169

• Fick’s procedure and Cody tack procedure were 29. (a) Caloric test shows diminished response (Ref.
procedures for decreasing the endolymph pressure Cummings, 6th ed., 2553)
by doing a sacculotomy (puncturing the saccule 30. (b) 120–130 dB 1) (Ref. Dhingra, 6th ed., 19)
through the stapes footplate. They are no longer 31. (b) 85 dB for 8 hours(Ref. Cummings, 6th ed., 2357)
performed now. 32. (b) Noise trauma (Ref. Cummings, 6th ed., 2346)
• Endolymphatic sac decompression is not an organ • In noise trauma the earliest change seen in a
destructive surgery. conventional pure tone audiogram is a dip at 4000 Hz
22. (b) Dehiscent superior semicircular canal (Ref. in both AC and BC which is known as ‘acoustic dip.’
Cummings, 6th ed., 2560) • In otosclerosis the dip is characteristically seen at
23. (b), (c), (d) Positive Tullio phenomenon, Positive 2000 Hz in bone conduction and is known as
Hennebert’s sign, Oscillopsia (Ref. Scott Brown, 8th “Carhartz notch”.
ed., Vol 2, 845) • In Meniere, the low frequency hearing loss leading
• Romberg’s sign is positive when the patient is able to up sloping kind of audiogram is seen in early
to stand with his feet together while his eyes are stages with no particular dip.
open, but sways or falls when they are closed; it is • In presbycusis high frequency hearing loss leading
one of the earliest signs of posterior column disease. to down sloping audiogram is seen with no
• Oscillopsia: patients with nystagmus may notice a particular dip.
constant movement of the objects within the visual 33. (a), (c) and (e) All these lead to vertigo and can follow
field. This subjective manifestation is known as trauma. (Ref. Scott Brown, 8th ed., Vol 2 817, 832, 1124)
oscillopsia. • Perilymphatic fistula can follow iatrogenic
• Positive Dix-Hallpike manoeuvre is indicative of (stapedectomy) or non iatrogenic trauma (fractures)
BPPV. and can lead to vertigo, SN deafness and tinnitus.
24. (d) Posterior semicircular canal (Ref. Scott Brown, Fistula test is positive.
8th ed., Vol 2, 832) • Secondary endolymphatic hydrops as the name is
• Benign paroxysmal positional vertigo (BPPV) is a Meniere’s disease secondary to trauma, viral
condition in which there is dislodged otoconia/ infection, allergy, autoimmune pathology etc. It
debris in the posterior semicircular canal. Movement presents with vertigo, SN deafness, tinnitus and
of these particles in certain head positions stimulates fullness in the ear.
the posterior semicircular canal and leads to vertigo.
• In Benign paroxysmal positional vertigo (BPPV)
25. (d) Canalith repositioning procedure (Ref. Scott
history of head trauma may be present which leads
Brown, 8th ed., Vol 2, 834)
to dislodgment of otoconia/debris in the posterior
• Canalith repositioning procedure or the Epley’s semicircular canal. Movement of these particles in
manoeuvre is the treatment for Benign Paroxysmal certain head positions stimulates the posterior
Positional Vertigo (BPPV). semicircular canal and leads to vertigo.
• When the vestibular organs are permanently
• Vestibular neuronitis is characterised by acute onset
damaged with disease or injury, the brain can no
vertigo with nausea and vomiting but the cause is
longer rely on them for accurate information about
viral infection.
equilibrium and motion. Vestibular exercises promote
• Ossicular discontinuity follows trauma but does not
CNS compensation for these fixed deficits.
lead to vertigo.
• In Benign positional vertigo vestibular exercises are
not required, as the cause of BPPV gets treated by 34. (c) Perilymphatic fistula (Ref. Scott Brown, 8th ed.,
Canalith repositioning procedure or the Epley’s Vol 2; 1085)
manoeuvre. • Serous otitis media can lead to Fluctuating conduc-
• Vestibular sedatives and antihistamines may be used tive deafness.
to control the severe symptoms, though they are not • In hemotympanum and Cholesteatoma the hearing Ear
of much benefit and repositioning or Epley’s loss is mainly conductive and not fluctuating.
manoeuvre is the treatment of choice in BPPV. 35. (d) Propranolol (Ref. Cummings, 6th ed., 2378)
26. (d) Epley’s manoeuvre (Ref. Scott Brown, 8th ed., Vol 2, 36. (c) Streptomycin (Ref. Cummings, 6th ed., 2371)
834) • Streptomycin is predominantly vestibulotoxic. In
27. (a) Positional vertigo (Ref. Scott Brown, 8th ed., Vol 2, very high doses they can affect the cochlear system
834) also, leading to hearing loss and tinnitus.
Section I

28. (c) Vestibular neuritis (Ref. Scott Brown, 8th ed., Vol 2, 37. (d) 4000–5000 Hz (Ref. Cummings, 6th ed., 2370)
850) 38. (d) Atropine (Ref. Scott Brown, 8th ed., Vol 2; 722)
• Vestibular neuritis is a viral infection involving the 39. (d) Stria vascularis (Ref. Cummings, 6th ed., 2378)
vestibular nerve. The cochlear part is not involved 40. (a), (c), (e) Streptomycin is predominantly vestibulo-
so the hearing remains normal. toxic, Salicylates cause reversible deafness, Cisplatin
• In both Acoustic neuroma and Meniere’s disease causes irreversible deafness (Ref. Scott Brown, 8th
hearing is affected. ed., Vol 2; 723)
 170 ENT for Entrance Exams

41. (b) Presbycusis (Ref. Cummings, 6th ed., 2331) 47. (b) NIHL (Ref. Cummings, 6th ed., 2346)
• Presbycusis, Noise induced hearing loss and ototoxic 48. (a) Surgery is the mainstay of treatment (Ref.
drugs all can lead to B/L SN hearing loss (mainly Cummings, 6th ed., 2558). See Chapter 3 for fistula test
high frequency) with proportionate decrease in 49. (b) Neural (Ref. Scott Brown, 8th ed., Vol 2 695)
speech discrimination as all affect the cochlea. The 50. (c) Pulsatile tinnitus (Ref. Cummings, 6th ed., 2556)
speech discrimination/word recognition scores are 51. (d) Amoxycillin (Ref. Scott Brown, 8th ed., Vol 2, 722)
far worse than would be predicted from that ear’s 52. (a) Surgery is mainstay (Ref. Cummings, 6th ed., 2395)
pure tone findings in retrocochlear deafness (acoustic 53. (a) Meniere’s disease (Ref. Cummings, 6th ed., 2356)
neuroma). Moreover acoustic neuroma is U/L.
54. (b) Gentamicin (Ref. Cummings, 6th ed., 2558)
• In the above question no history of noise exposure
55. (a) Fluctuating SNHL (Ref. Cummings, 6th ed., 2556)
or ototoxic drug intake has been mentioned, ruling
56. (a) Diplacusis (Ref. Cummings, 6th ed., 2556)
out acoustic trauma or ototoxicity. The age here is
also suggesting Presbycusis. • Paracusis Willisii is paradoxical hearing better in
42. (a), (b) and (c) Varicella, Measles and Mumps (Ref. noisy surroundings and is a feature of otosclerosis
Cummings, 6th ed., 2332) • Presbycusis is age related hearing loss
43. (a), (b), (d) and (e) (Ref. Scott Brown, 8th ed., Vol 2, 84) • Hyperacusis is normal sounds appearing louder and
is a feature of facial nerve palsy
• Alport syndrome, most commonly an X-linked
dominant condition, is the most common hereditary 57. (c) Metronidazole (Ref. Cummings, 6th ed., 2379)
glomerulonephritis. The most common extra-renal 58. (a) Meniere’s disease (Ref. Cummings, 6th ed., 2556)
manifestation in Alport syndrome is high tone The typical triad of vertigo, deafness and tinnitus in
progressive SN hearing loss. this case is suggestive of Meniere. Acoustic neuroma
• Pendred syndrome is autosomal recessive condition does not present with vertigo. There is no hearing
characterised by non toxic goitre and SN hearing loss. loss in Migraine. Multiple sclerosis will have other
• Treacher–Collins syndrome is autosomal dominant intracranial manifestations also.
condition characterised by hypoplasia of the first 59. (c) Ototoxicity (Ref. Scott Brown, 8th ed., Vol 2; 725)
branchial arch which leads to the formation of facial 60. (b) Presbycusis (Ref. Cummings, 6th ed., 2330)
bones. Therefore, this is also known as maxillo- 61. (d) Disorder of posterior semicircular canal (Ref.
mandibular hypoplasia. In the ear it is associated Scott Brown, 8th ed., Vol 2; 832)
with malformation of first arch derivatives, i.e. 62. (a) Meniere (Ref. Scott Brown, 8th ed., Vol 2; 819)
malleus, incus, pinna and meatal atresia. Hence this The given audiogram shows low frequency
leads to conductive hearing loss. sensorineural hearing loss (up sloping audiogram).
• Crouzon syndrome is autosomal dominant condition • In otosclerosis there is conductive hearing loss.
characterised by craniofacial dysostosis. It is • Ototoxicity and Noise induced hearing loss lead to
associated with mixed hearing loss. high frequency hearing loss (downsloping
• Michel aplasia is a total non-development of inner audiogram).
ear and therefore is associated with SN hearing loss. 63. (c) Meniere’s disease (Ref. Cummings, 6th ed., 2556)
44. (a) Presents as unilateral SNHL mostly (Ref. Scott • Vertebrobasilar (posterior) circulation constitutes the
Brown, 8th ed., Vol 2; 695) arterial supply to the brainstem, cerebellum, and
45. (a), (c), (d) (Ref. Cummings, 6th ed., 2556) occipital cortex.
46. (d) Inactivates (Na, K-ATPase) channels of type I • Along with vertigo, nausea and vomiting, the patient
and type II hair cells (Ref. Cummings, 6th ed., 2370) presents with loss of vision in one or both eyes,
• Gentamicin in the doses given in trans-tympanic double vision, numbness or tingling in the hands or
injection, affects only the vestibular type I and type feet, slurred speech and changes in mental status.
II hair cells, sparing the cochlear inner and outer hair • In labyrinthitis the vertigo and hearing loss last for
Ear

cells, it being preferentially a vestibulotoxic drug. a few weeks and not for 4 hours
The first three choices are about damage to the outer • In Benign paroxysmal vertigo there is only vertigo
hair cells and stria vascularis in the cochlea so they and no hearing loss
cannot be the answer. 64. (b) Noise trauma (Ref. Cummings, 6th ed., 2346)
• Gentamicin through the transport channels (Na, K- 65. (c) Recruitment negative (Ref. Cummings, 6th ed., 2556)
ATPase) on the vestibular hair cells, gets concentra-
Section I

66. (b), (d), (e) (Ref. Scott Brown, 8th ed., Vol 2; 739)
ted in these cells leading to their death and ultimately
relieving the patient from vertigo, while at the same 67. (b) CMV (Ref. Scott Brown, 8th ed., Vol 2; 78)
time preserving hearing as it does not affect the inner 68. (a) Labyrinthectomy (Ref. Cummings 6th ed., 2559)
and outer hair cells or stria vascularis. 69. (a) Superior semi-circular canal dehiscence (Ref.
• In this regard it is also worth mentioning that it is Scott Brown, 8th ed., Vol 2; 844)
the type 1 hair vestibular hair cells which are more 70. (d) Rinnes is falsely positive (Ref. Scott Brown, 8th
prone to damage by Gentamicin. ed., Vol 2; 739)
 Tumours of External and Middle Ear 175

ANSWERS AND EXPLANATIONS SN deafness and vertigo occur late with labyrinthine
spread.
1. (a) Exostosis (Ref. Scott Brown, 8th ed., Vol 2 page 964) 9. (d) Usually invades epitympanum (Ref. Cummings,
2. (c) Glomus tumour (Ref. Cummings, 6th ed., 2738) 6th ed., 2738)
• Most common benign tumour of middle ear is From the floor of middle ear glomus jugulare invades
glomus tumour. into the hypotympanum.
• Acoustic neuroma is the most common benign
10. (a) Glomus jugulare (Ref. Cummings, 6th ed., 2739)
tumour of the CP angle.
11. (a) Glomus tumour (Ref. Scott Brown, 8th ed., Vol 2
• Squamous cell carcinoma is the most common
page 1215, Dhingra 6th ed., 109)
carcinoma of the middle ear.
• Adenocarcinoma is an occasional glandular tumour 12. (a) Glomus jugulare (Ref. Shambaugh, 6th ed., 733)
of the middle ear. 13. (a) MR angiography (Ref. Cummings, 6th ed.,
3. (c) It is a disease of infancy (Ref. Scott Brown, 8th 2756)
ed., Vol 2 page 1303) • Magnetic resonance angiography is used to evaluate
• Glomus is seen most commonly in middle age (40– for compression of internal carotid artery.
50 yrs) usually in females. It presents with • CECT is diagnostic of Glomus jugulare.
conductive deafness and pulsatile tinnitus. • X-ray has no role in the assessment of Glomus
• It is a benign but locally invasive tumour and can jugulare.
invade mastoid, labyrinth, petrous pyramid, jugular • MR venography is useful to assess collateral
foramen, Eustachian tube and middle/posterior circulation within the dural sinuses of the skull as
cranial fossa. the tumour blocks the blood flow in the internal
4. (b), (d) and (e) (Ref. Cummings, 6th ed., 2739) jugular vein and in turn leads to blockade of the
• Since Glomus jugulare is a benign tumour lymph sigmoid sinus.
node metastasis is not seen. • Jugular venography is no longer used because
5. (d) Glomus tumour (Ref. Cummings, 6th ed., 2739) intravenous tumour extension can be seen with MR
6. (b) Hypotympanum (Ref. Cummings, 6th ed., 2738) venography.
• Glomus jugulare arises from the paraganglionic cells 14. (d) Glomus tumour (Ref. Stell and Maran's, 5th ed.,
in relation to the jugular bulb which is related to the 261)
floor of the middle ear. Therefore from the floor it
15. (c) Interferon (Ref. Cummings, 6th ed., 2738)
comes into the hypotympanum.
The clinical description suggests Glomus tumour.
• Less commonly Glomus may arise from promontory
Please refer the text for its management
and is called Glomus tympanicum.
Since it is locally invasive Glomus may later on reach 16. (c) Type C2 (Ref. Current Diagnosis and Treatment
epitympanum, mastoid and other nearby areas. Otolaryngology-Lalwani, 3rd ed., 814)
7. (d) Glomus jugulare tumour (Ref. Scott Brown, 8th 17. (a) Glomus tumour (Ref. Stell & Maran's, 5th ed.,
ed., Vol 2 page 1283) 263)
• For the tinnitus to be pulsatile the cause has to be 18. (d) Fluctuating conductive type of hearing loss is
vascular. Vascular causes to tinnitus are Glomus seen (Ref. Stell and Maran’s, 5th ed., 263)
jugulare and internal carotid aneurysms. 19. (b) Geniculate ganglion (Ref. Cummings, 6th ed.,
8. (a) Pulsatile tinnitus (Ref. Cummings, 6th ed., 2738) 2738)
• Earliest presenting symptoms of Glomus tumour 20. (a) Glomus tumour (Ref. Stell & Maran's, 5th ed.,
are conductive hearing loss and pulsatile tinnitus. 263)
Ear
Section I
 Acoustic Neuroma/Vestibular Schwannoma 181

cranial nerve disorders) in sharp contrast to acoustic

ANSWERS AND EXPLANATIONS
neuroma where these usually occur at last.
1. (a) Acoustic neuroma is the most common benign Depending upon the area of brain involved in
tumour of the CP angle. (Ref. Cummings, 6th ed., gliomas, there are focal neurological symptoms, e.g.
2748) seizures, hemiparesis, visual field defects, etc.
• The next most common tumour here is meningioma 13. (a) Vestibular schwannoma (Ref. Shambaugh, 6th ed.,
followed by epidermoid, i.e. cholesteatoma. 647)
2. (a) CP angle (Ref. Cummings, 6th ed., 2748) • In vestibular schwannoma the involvement of
3. (a) Vestibular part of VIII nerve (Ref. Shambaugh, sensory fibres of facial (i.e. nervus intermedius or
6th ed., 644) nerve of Wrisberg) leads to anaesthesia over the
• Rarely it may originate from the other mentioned postero-superior part of external auditory meatus
options in the question and canal. This is known as ‘Hitselberger sign’. But
4. (b) Inferior vestibular nerve (Ref. Shambaugh, 6th ed., this ‘Hitselberger sign’ is present only in 25% of
644) patients.
5. (a) Sensorineural hearing loss (Ref. Scott Brown, 8th • Mastoiditis shows “reservoir sign”, see Chapter on
ed., Vol 2 page 1371) complications of CSOM.
• Mild vertigo and Facial weakness occur late. • Bell’s palsy is acute idiopathic lower motor neuron
• There is no ear discharge in Acoustic neuroma. palsy of facial nerve.
6. (c) Reduced corneal reflex (Ref. Scott Brown, 8th ed., • Cholesteatoma is the presence of keratinising
Vol 2 page 1371) stratified squamous epithelium in any part of
• Facial weakness and cerebellar signs occur late. temporal bone where it is not usually present.
• Unilateral deafness is the earliest symptom of 14. (b) Retrocochlear deafness (Ref. Cummings, 6th ed.,
Acoustic neuroma. 2751)
7. (d) 8th (Ref. Scott Brown, 8th ed., Vol 2 page 1371) • Acoustic neuroma arising in the internal acoustic
8. (a) 5th (Ref. Scott Brown, 8th ed., Vol 2 page 1371) meatus compresses the cochlear nerve and therefore
Of the mentioned choices, 5th cranial nerve is the the patient presents most commonly with unilateral
best answer, please see the text. retrocochlear hearing loss usually slowly progressive.
9. (d) Loss of corneal sensation (Ref. Scott Brown, 8th 15. (d) Acute episode of vertigo (Ref. Cummings, 6th ed.,
ed., Vol 2 page 1371) 2750)
• Involvement of 3rd cranial nerve causing diplopia • Though the most common site of origin of acoustic
and ptosis is not described in Acoustic neuroma. neuroma is from the Schwann cells of the inferior
• Motor involvement of facial and thereby inability to vestibular nerve, compression and destruction of the
close eye occurs uncommonly and that too very late vestibular nerve usually does not cause severe
in Acoustic neuroma. disturbance of equilibrium and acute episode of
• Papilloedema because of increased intracranial vertigo. This is because it is a very slow growing
pressure occurs in the terminal stage of Acoustic tumour and compensation occurs by the CNS.
neuroma. However mild disequilibrium can be present.
10. (a) Absent corneal reflex (Ref. Cummings, 6th ed., • Acoustic neuroma arising in the internal acoustic
2750) meatus compresses the cochlear nerve and therefore
• Involvement of 3rd and 4th cranial nerve causing the patient presents most commonly with unilateral
pupillary dilatation and medial rectus and superior retrocochlear hearing loss.
oblique palsy is not described in Acoustic neuroma. • The involvement of 5th nerve is manifested as a loss
11. (d) Bitemporal hemianopia (Ref. Cummings, 6th ed., of corneal reflex and this is the ‘earliest ocular sign’
2750) of acoustic neuroma. This is also the ‘most common
Ear
sign’ seen in these patients.
• Bitemporal hemianopia is loss of right and left
temporal side of visual fields. It is due to lesions of • Because of the growth of Acoustic neuroma in the
optic chiasm which is not seen in acoustic neuroma. CP angle there is cerebellar compression leading to
ataxia, dysmetria, dyssynergia, dysdiadochokinesia
12. (c) Acoustic neuroma (Ref. Cummings, 6th ed., 2750)
and nystagmus.
• Otitis media presents with ear discharge and
Section I

conductive hearing loss. 16. (a) Ptosis (Ref. Cummings, 6th ed., 2750)
• Glioma is a type of tumour that starts in the brain or • 3rd nerve involvement leading to ptosis does not
spine from glial cells. The three main types of glioma occur in Acoustic neuroma.
include: ependymoma, astrocytoma and oligodendro- • Facial numbness and loss of corneal reflex is due to
glioma The first symptoms of a glioma are likely to the involvement of Vth nerve.
be caused by increased intracranial pressure within • Nystagmus due to cerebellar involvement occurs late
the skull (headache, nausea, vomiting, seizures, and in the course of Acoustic neuroma.
 182 ENT for Entrance Exams

17. (d) Normal corneal reflex (Ref. Cummings, 6th ed., • The most common site of origin of acoustic neuroma
2750) is from the Schwann cells of the inferior vestibular
• The involvement of 5th nerve is manifested as a loss nerve followed by superior vestibular nerve.
of corneal reflex and this is the ‘earliest ocular sign’ • Acoustic neuroma is the most common benign
of acoustic neuroma. This is also the ‘most common tumour of the CP angle.
sign’ seen in these patients. • When the tumour invades CP angle its upper pole
18. (a) 5th (Ref. Scott Brown, 8th ed., Vol 2 page 1370) compresses trigeminal nerve which is situated at the
• In corneal reflex the sensory afferent part of the reflex upper pole of CP angle.
arc is trigeminal and motor efferent part is facial • 9th, 10th and 11th cranial nerves present at the base
nerve. of CP angle are compressed by the lower pole of
• The involvement of 5th nerve, at the upper pole in Acoustic neuroma.
CP angle by acoustic neuroma is manifested as a loss 20. (b) MRI scan (Ref. Cummings, 6th ed., 2751)
of corneal reflex. • The gold standard investigation for the diagnosis of
• Facial nerve being mainly a motor nerve therefore is acoustic neuroma is gadolinium enhanced MRI.
resistant to compression. The motor fibres of Facial Even very small asymptomatic lesions can be
nerve take a very long time to get affected hence observed by MRI.
facial weakness is seen quiet late in acoustic 21. (b) Gadolinium enhanced MRI (Ref. Cummings, 6th
neuroma. So loss of corneal reflex in acoustic ed., 2751)
neuroma, initially and largely, is due to involvement 22. (d) Surgical excision (Ref. Shambaugh, 6th ed., 651)
of the sensory efferent element of the reflex arc, i.e. 23. (d) Brain stem implant (Ref. Shambaugh, 6th ed., 688)
5th nerve. Technically involvement of motor aspect • Since it is a retrocochlear pathology hearing aid and
of facial nerve occurring late in the course of Acoustic cochlear implant will not help. Rehabilitation of
neuroma will also contribute to loss of corneal reflex hearing is by auditory brainstem implant (ABI),
but better signs for looking facial nerve involvement, which is placed in the lateral recess of 4th ventricle
i.e. the signs eliciting facial muscle movements will where it directly stimulates the cochlear nuclei.
now be there. 24. (a) Acoustic neuroma (Ref. Shambaugh, 6th ed., 647)
• Corneal reflex is done primarily to check 5th nerve 25. (a), (c), (d), (e) (Ref. Shambaugh, 6th ed., 644)
involvement. This reflex should be elicited carefully 26. (c) Acoustic schwannoma (Ref. Cummings, 6th ed.,
avoiding injury to the cornea. See Chapter on facial 2751)
nerve for further details of corneal reflex. 27. (c) Acoustic neuroma (Ref. Shambaugh, 6th ed., 647)
19. (b) Arises from vestibular nerve (Ref. Shambaugh, 28. (c) Antoni A or B cells (Ref. Scott Brown, 8th ed., Vol
6th ed., 645) 2 page 1232)
Ear
Section I
 190 ENT for Entrance Exams

16. (c) Auditory nerve (Ref. Scott Brown, 8th ed., Vol 2
ANSWERS AND EXPLANATIONS
page 93)
1. (a) William F House (Ref. Scott Brown, 8th ed., Vol 2 17. (a) 1 year (Ref. Cummings, 6th ed., 2434)
page 93) 18. (c) Sound energy to electrical impulses (Ref.
2. (b) Cochlear implant (Ref. Cummings, 6th ed., 2432) Cummings, 6th ed., 2429)
3. (c) Auditory nerve (Ref. Cummings, 6th ed., 2434) 19. (a) Congenital canal atresia (Ref. Cummings, 6th ed.,
• Cochlear implant is done when the defect lies in the 2425)
Organ of Corti.
20. (d) Auditory nerve (Ref. Scott Brown, 8th ed., Vol 2
4. (d) MRI has no role in preoperative assessment (Ref. page 93)
Shambaugh, 6th ed., 589; 608)
21. (c) BAHA (Ref. Cummings 6th ed., 2423, Scott Brown
• MRI is contraindicated postoperatively and not pre
8th ed., Vol 2 page 1152)
operatively, please see the text.
22. (d) BAHA (Ref. Scott Brown, 8th ed., Vol 2 page
5. (b) Round window (Ref. Scott Brown, 8th ed., Vol 2
1150)
page 99)
6. (c) Electrode array (Ref. Scott Brown, 8th ed., Vol 2 23. (b) Round window (Ref. Scott Brown, 8th ed., Vol 2
page 99) page 99)
7. (b) Scala tympani (Ref. Scott Brown, 8th ed., Vol 2 page 24. (a) Facial recess (Ref. Scott Brown, 8th ed., Vol 2 page
94) 1162)
8. (a) Cochlear implant (Ref. Cummings, 6th ed., 2434) 25. (c) A 7-year-old child with bilateral microtia, canal
• Stapedectomy is done for otosclerosis. atresia and congenital hearing loss (Ref. Cummings,
6th ed., 2425)
• Fenestration operation used to be done previously for
otosclerosis, though stapedotomy is done these days. • A 50-year-old male with bilateral profound hearing
loss can be managed by cochlear implant
• Stapes fixation is no surgery
• A 6-year-old child with bilateral SOM is managed
9. (a) Not contraindicated in cochlear malformation
medically and if chronic then by myringotomy and
(Ref. Cummings, 6th ed., 2434)
grommet
10. (d) Tinnitus enhancement in patients with tinnitus • In a 25 year old with bilateral acoustic neuroma
prior to implantation. (Ref. Scott Brown, 8th ed., Vol planned for surgery rehabilitation of hearing is done
2 page 1158) with auditory brainstem implant (ABI)
11. (d) Brain stem implant (Ref. Cummings, 6th ed., 2474) 26. (a) Cochlear implant (Ref. Cummings, 6th ed., 2442)
12. (d) Mondini deformity (Ref. Cummings, 6th ed., 2474) 27. (c) 24 (Ref. Scott Brown, 8th ed., Vol 2 page 94)
• In Mondini deformity the defect is in the cochlea 28. (c) Lateral recess of 4th ventricle (Ref. Scott Brown,
which can be corrected by a cochlear implant. 8th ed., Vol 2 page 1180)
13. (d) Atresia of external ear (Ref. Scott Brown, 8th ed., 29. (a) 6 months (Ref. Scott Brown, 8th ed., Vol 2 page 86)
Vol 2 page 1150) • Cochlear implant is done at 1 year but prior to that
14. (b) 5–7 years of age (Ref. Cummings, 6th ed., 3000) hearing aid or BAHA soft band is given as early as
15. (a) Receiver stimulator (Ref. Cummings, 6th ed., 2437) possible.
Ear
Section I