EAR

10 marks

Here’s a complete set of 350-word answers for each of the ENT questions you listed. I’ve
structured them in a concise, exam-appropriate manner.

1. Intracranial and intratemporal complications of CSOM; Lateral sinus thrombophlebitis

Chronic suppurative otitis media (CSOM) can lead to serious complications if untreated.
Intratemporal complications include: mastoiditis, subperiosteal abscess, facial nerve palsy,
labyrinthitis, petrositis, and sigmoid sinus thrombosis. Intracranial complications include
meningitis, brain abscess, lateral sinus thrombophlebitis, epidural abscess, subdural
empyema, and otitic hydrocephalus.

Lateral sinus thrombophlebitis is a septic thrombosis of the sigmoid/lateral sinus, commonly

due to cholesteatomatous CSOM. Infection spreads from mastoid air cells to the sinus via eroded
bony walls or septic emissary veins. Clinically, patients present with high fever, headache,
vomiting, papilledema, and signs of raised intracranial pressure. On examination, there may be
mastoid tenderness, postauricular swelling, and sometimes a tender neck along the jugular
vein.

Investigations include CT/MRI with contrast, showing filling defects in the sinus, and MR
venography confirming thrombus. Blood cultures may reveal causative organisms like
Staphylococcus aureus, Streptococcus species, Pseudomonas, or anaerobes.

Management involves aggressive intravenous antibiotics (e.g., third-generation cephalosporin

± metronidazole) for 4–6 weeks. Surgical intervention includes mastoidectomy to eradicate the
primary infection and, if required, internal jugular vein ligation in cases of septicemia or
persistent thrombus. Anticoagulation is controversial but may be used selectively. Prognosis is
good with early recognition; delay can lead to fatal complications such as brain abscess or
generalized sepsis.
⸻

2. Structures in the medial wall of the middle ear

The medial wall of the middle ear (labyrinthine wall) separates the tympanic cavity from the
inner ear. Key structures include:
1. Promontory – rounded bulge formed by basal turn of cochlea.
2. Oval window (fenestra vestibuli) – transmits stapes footplate vibrations to
vestibule; sealed by annular ligament.
3. Round window (fenestra cochleae) – covered by secondary tympanic
membrane, allows pressure release from perilymph.
4. Promontory nerves – tympanic plexus of autonomic fibers; branch of
glossopharyngeal nerve.
5. Facial canal – prominence of facial nerve in medial wall.
6. Eustachian tube orifice – anterior inferior part, connecting to nasopharynx.

Blood supply: mainly from tympanic branches of maxillary and ascending pharyngeal arteries.

Diagram:

Roof
----
Lateral wall | Middle ear cavity | Medial wall
|| || ||
Facial prominence Promontory Oval window
Round window
Tympanic plexus
Fenestration of Eustachian tube

Functionally, these structures are essential for sound transmission, pressure equalization, and
neural innervation of the middle ear.

3. Functions of the Eustachian tube and clinical tests

The Eustachian tube connects the middle ear to the nasopharynx. Functions:
1. Ventilation – equalizes air pressure across the tympanic membrane.
2. Protection – prevents nasopharyngeal secretions and pathogens from
entering the middle ear.
3. Clearance – drains middle ear secretions into nasopharynx.

Clinical tests:
• Valsalva maneuver – patient blows with nostrils closed; movement of
tympanic membrane indicates patency.
• Toynbee test – swallowing with nose pinched; movement of drum is
observed.
• Impedance audiometry (tympanometry) – measures compliance changes in
tympanic membrane.
• Otoscopic examination – retraction or fluid suggests dysfunction.

4. Routes of spread of infection in chronic otitis media and otogenic brain abscess

In CSOM, infection may spread directly, hematogenously, or via venous channels:

• Direct: erosion through tegmen tympani → temporal lobe abscess, posterior
fossa involvement.
• Venous: septic thrombophlebitis of sigmoid sinus → brain abscess.
• Perineural/CSF: via cochlear aqueduct or internal auditory canal.

Intracranial complications: brain abscess, meningitis, lateral sinus thrombosis, epidural/

subdural empyema, otitic hydrocephalus.

Otogenic brain abscess usually arises in temporal lobe or cerebellum. Clinical features:
headache, vomiting, fever, focal neurological deficits, papilledema. CT/MRI shows ring-
enhancing lesion.

Management:
• Medical: IV antibiotics (cephalosporin + metronidazole).
• Surgical: abscess aspiration via burr hole or craniotomy.
 • Eradicate primary source: mastoidectomy or tympanomastoid surgery.

5. Acute suppurative otitis media in a 10-year-old

Probable diagnosis: Acute otitis media with mastoiditis.

Investigations: CBC, CRP, blood cultures, tympanic membrane examination, CT temporal bone if
complications suspected.

Medical management: High-dose IV antibiotics (amoxicillin-clavulanate, ceftriaxone),

analgesics, antipyretics, nasal decongestants.

Surgical options:
• Myringotomy with grommet – drainage of pus, relieves pressure.
• Mastoidectomy if mastoid involvement persists.

Myringotomy procedure: under general anesthesia, small incision in anterior-inferior quadrant of

tympanic membrane, pus aspirated, grommet placed to allow drainage and ventilation.

6. Chronic otitis media with hearing loss in 30-year-old male

Type of deafness: Conductive (Rinne negative, Weber lateralizes to affected ear).

Probable diagnosis: Chronic otitis media – mucosal type with possible ossicular erosion.

Causative organisms: Pseudomonas aeruginosa, Proteus, Staphylococcus aureus.

Investigations: Pure tone audiometry, tympanometry, high-resolution CT temporal bone, ear

swab culture.

Surgical procedure: Tympanoplasty (Type III or IV) – repair of tympanic membrane and
ossicular chain reconstruction (autologous incus or prosthesis). Postoperative care includes
antibiotic ear drops and hearing evaluation.

7. Secretory otitis media

Etiology: Eustachian tube dysfunction due to URTI, allergy, cleft palate, or adenoids.

Clinical features: Conductive hearing loss, aural fullness, mild tinnitus, retracted tympanic
membrane, air-fluid level or bubbles.

Treatment:
• Medical: nasal decongestants, steroids, antihistamines, treatment of URTI/
allergy.
• Surgical: myringotomy with grommet insertion, adenoidectomy if persistent.

8. Chronic otitis media types and cholesteatoma

Types:
1. Mucosal type: safe, perforation of pars tensa, non-foul smelling discharge.
2. Atticoantral type: unsafe, cholesteatoma, attic perforation, recurrent foul
discharge.

Cholesteatoma: abnormal keratinizing squamous epithelium in middle ear/mastoid.

Formation theories:
• Invagination (retraction pocket),
• Epithelial migration,
• Metaplasia,
• Basal cell proliferation.

9. Episodic vertigo with hearing loss

Most probable diagnosis: Meniere’s disease.

Causes of vertigo: Endolymphatic hydrops, labyrinthitis, vestibular neuritis, BPPV, central

lesions.

Treatment:
• Medical: salt restriction, diuretics, betahistine, vestibular suppressants.
• Surgical: endolymphatic sac decompression, labyrinthectomy if refractory.

10. Foul-smelling discharge with mastoid swelling

Diagnosis: Chronic suppurative otitis media with acute mastoiditis.

Investigation: CBC, pus culture, high-resolution CT temporal bone.

Treatment: IV antibiotics, modified radical mastoidectomy, post-op dressing.

Complications: Facial nerve injury, hearing loss, labyrinthitis, recurrence, intracranial spread.

11. Otosclerosis

Etiology: Genetic, hormonal (female predominance), viral (measles).

Pathogenesis: Abnormal bone remodeling at stapes footplate → fixation.

Clinical features: Slowly progressive conductive hearing loss, tinnitus, stapedial reflex absent.

Management:
• Medical: sodium fluoride, bisphosphonates (early disease).
• Surgical: stapedotomy/stapedectomy with prosthesis insertion.
⸻

12. Temporal bone fractures

Etiology: Blunt head trauma, RTAs, falls.

Classification:
• Longitudinal – conductive hearing loss, hemotympanum, facial nerve intact.
• Transverse – sensorineural hearing loss, facial palsy.

Clinical features: Hemotympanum, CSF otorrhea/rhinorrhea, vertigo, facial palsy.

Management:
• Conservative for uncomplicated cases.
• Surgical repair for facial nerve injury, perilymph fistula, or persistent CSF
leak.
• Audiological follow-up essential.

5 marks

Perfect
We’ll do it in parts so it’s easier to read and study.
Each part will have 3–4 topics, written in exam-style (≈250 words each) with clear headings —
just like in answer sheets.

Here’s Part 1 (Topics 1–4):

1. Otoacoustic Emissions

Definition:
Otoacoustic emissions (OAEs) are low-intensity sounds generated by the outer hair cells of the
cochlea in response to auditory stimulation. They indicate normal cochlear function.
Types:
1. Spontaneous OAEs – occur without external stimulus.
2. Transient Evoked OAEs (TEOAE) – elicited by click stimuli.
3. Distortion Product OAEs (DPOAE) – produced by two pure tones.

Principle:
Outer hair cells amplify sound vibrations; their motion generates backward-traveling sound
waves recorded in the ear canal.

Clinical Uses:
• Neonatal hearing screening.
• Differentiates cochlear from retrocochlear lesions.
• Ototoxicity monitoring.

Procedure:
A probe with a speaker and microphone is inserted into the ear canal to record the emissions.

Interpretation:
Presence of OAE = normal cochlear function;
Absence = cochlear pathology or middle ear obstruction.

Advantages:
Objective, quick, non-invasive.

2. Furuncle of the Ear (Furunculosis)

Definition:
Localized infection of a hair follicle in the outer cartilaginous part of the external auditory canal
caused by Staphylococcus aureus.

Etiology:
Minor trauma (scratching, ear cleaning), unhygienic habits, diabetes.

Clinical Features:
 • Severe throbbing ear pain.
• Tenderness on movement of pinna or jaw.
• Red, localized swelling in canal.
• Conductive hearing loss if canal blocked.
• Regional lymphadenitis.

Treatment:
1. Analgesics and anti-inflammatory drugs.
2. Systemic antibiotics (Cloxacillin, Amoxicillin).
3. Warm compress.
4. Incision and drainage if abscess forms.
5. Avoid manipulation of ear.

Complications:
Cellulitis, perichondritis, or abscess spread.

3. Auditory Pathway

Receptors: Hair cells in the organ of Corti.

Pathway Steps:
1. Cochlear nerve (spiral ganglion).
2. Cochlear nuclei (ventral & dorsal) in medulla.
3. Superior olivary complex (pons) – first site of binaural hearing.
4. Lateral lemniscus → inferior colliculus (midbrain).
5. Medial geniculate body (thalamus).
6. Auditory cortex (Brodmann areas 41, 42).

Features:
• Bilateral representation above cochlear nuclei.
• Lesions above nuclei cause partial rather than complete hearing loss.

Clinical Importance:
Helps localize site of lesion in sensorineural deafness and auditory processing disorders.
⸻

4. Course of Facial Nerve in Middle Ear and Its Branches

Segments in Middle Ear:

1. Labyrinthine segment – from internal acoustic meatus to geniculate
ganglion.
2. Tympanic (horizontal) segment – runs above oval window.
3. Mastoid (vertical) segment – descends behind pyramid to stylomastoid
foramen.

Branches:
• Greater petrosal nerve: parasympathetic to lacrimal gland.
• Nerve to stapedius: motor to stapedius muscle.
• Chorda tympani: taste (anterior 2/3 tongue), secretomotor to submandibular
& sublingual glands.

Clinical Relevance:
Injury can occur during chronic otitis media, surgery, or fractures, leading to facial paralysis.

Great
Here’s Part 2 (Topics 5–8) — written in exam-style MBBS notes format (≈250 words each):

5. Benign Paroxysmal Positional Vertigo (BPPV) – Presentation and Treatment

Definition:
BPPV is a peripheral vestibular disorder characterized by brief episodes of vertigo triggered by
changes in head position. It is caused by dislodged otoliths (canaliths) from the utricle entering
a semicircular canal (commonly posterior).

Etiology:
 • Idiopathic (most common)
• Post head injury or vestibular neuronitis
• Degeneration of otolithic membrane

Clinical Features:
• Sudden, brief vertigo (seconds) precipitated by head movements (looking
up, rolling in bed).
• No tinnitus or hearing loss.
• Nystagmus: rotatory, fatigable, and transient.

Diagnosis:
• Dix–Hallpike maneuver: reproduces vertigo and characteristic nystagmus.
• Normal neurological examination.

Treatment:
1. Canalith repositioning maneuvers – Epley’s or Semont’s maneuver to move
otoliths back to utricle.
2. Vestibular sedatives – short-term (Cinnarizine, Betahistine).
3. Reassurance – self-limiting; recurrences are common.

Prognosis:
Excellent; symptoms resolve with maneuvers in most patients.

6. Auditory Neural Pathway

Definition:
The auditory neural pathway transmits impulses from the cochlea to the auditory cortex for
sound perception.

Course:
1. Receptor: Inner hair cells in organ of Corti.
2. First-order neuron: Bipolar cells of the spiral ganglion (cochlear nerve).
3. Second-order: Cochlear nuclei in medulla.
4. Third-order: Neurons in superior olivary complex (pons) – site for sound
 localization.
5. Fourth-order: Lateral lemniscus fibers ascend to inferior colliculus
(midbrain).
6. Fifth-order: From medial geniculate body (thalamus) to auditory cortex
(temporal lobe – areas 41, 42).

Features:
• Bilateral representation ensures partial hearing loss in unilateral lesions.
• Important for localization, intensity, and interpretation of sound.

Clinical Correlation:
Lesions in brainstem or temporal lobe can cause auditory agnosia, tinnitus, or central hearing
loss.

7. Otosclerosis

Definition:
Otosclerosis (otospongiosis) is a primary bone dysplasia of the otic capsule that causes
progressive conductive hearing loss due to stapes fixation at the oval window.

Etiology:
• Genetic (autosomal dominant with incomplete penetrance).
• Hormonal influence (common in females, pregnancy worsens).
• Viral infections (measles virus).

Pathology:
Normal dense bone replaced by spongy vascular bone around oval window (fissula ante
fenestram). Eventually, it ossifies, fixing stapes footplate.

Clinical Features:
• Slowly progressive conductive deafness, bilateral, starting in young adults.
• Paracusis Willisii – better hearing in noisy surroundings.
• Tinnitus common; no vertigo.
Diagnosis:
• Pure tone audiometry: Conductive hearing loss with Carhart’s notch at 2
kHz.
• Tympanometry: Type As (stiff) curve.
• Schwartze’s sign: Reddish hue over promontory.

Treatment:
1. Hearing aid – for mild cases.
2. Surgery: Stapedectomy or stapedotomy with prosthesis.
3. Sodium fluoride therapy – may slow progression.

8. Etiology of Sensorineural Hearing Loss (SNHL)

Definition:
SNHL results from pathology of the inner ear (cochlea) or auditory nerve.

Etiological Classification:

1. Congenital Causes:
• Genetic (autosomal recessive syndromic or non-syndromic).
• Maternal infections: Rubella, CMV, Toxoplasmosis.
• Ototoxic drugs during pregnancy.
• Perinatal hypoxia or hyperbilirubinemia.

2. Acquired Causes:
• Infectious: Meningitis, mumps, measles.
• Trauma: Acoustic or barotrauma.
• Ototoxic Drugs: Aminoglycosides, loop diuretics, cisplatin.
• Noise-induced hearing loss: Long-term loud sound exposure.
• Age-related (Presbycusis): Degeneration of hair cells.
• Autoimmune inner ear disease.
• Tumors: Acoustic neuroma.

Clinical Features:
Bilateral, symmetrical hearing loss, tinnitus, difficulty understanding speech, no improvement
with increased volume.

Management:
• Remove causative agent.
• Hearing aids or cochlear implant (for profound loss).
• Avoid ototoxic drugs and excessive noise exposure.

Perfect
Here’s Part 3 (Topics 9–12) — each written in exam-style MBBS format (≈250 words each)
with key headings for easy memorization and writing practice.

9. Anterior Wall of the Middle Ear

Anatomy:
The anterior wall of the middle ear is the carotid wall, separating the tympanic cavity from the
internal carotid artery.

Features (From above to below):

1. Openings for the auditory (Eustachian) tube – connects middle ear to
nasopharynx; maintains air pressure.
2. Semicanal for tensor tympani muscle – lies above the tube; both separated
by a thin bony septum.
3. Carotid canal – anteriorly related to the carotid artery, often thin or partially
dehiscent.
4. Processus cochleariformis – a small projection that changes direction of the
tensor tympani tendon laterally to attach to the malleus handle.

Clinical Importance:
• Carotid canal dehiscence can lead to vascular injury during ear surgery.
• Eustachian tube dysfunction may cause otitis media with effusion.
• The anterior wall provides access for ventilation tube placement and middle
 ear surgeries.

Summary:
Boundaries –
• Superior: Tegmen tympani
• Inferior: Floor of tympanic cavity
• Anterior: Carotid canal
• Posterior: Tympanic cavity proper

10. Theories of Cholesteatoma Formation

Definition:
A cholesteatoma is a keratinizing squamous epithelium-lined sac in the middle ear or mastoid
that can cause bone erosion.

Theories:
1. Invagination (Retraction Pocket) Theory – Most accepted
• Due to Eustachian tube dysfunction, pars flaccida retracts forming a
pocket that collects keratin debris → forms cholesteatoma.
2. Invasion Theory
• Squamous epithelium from external canal migrates into middle ear
through perforation.
3. Metaplasia Theory
• Chronic infection causes transformation of middle ear mucosa into
squamous epithelium.
4. Basal Cell Hyperplasia Theory
• Basal layer of epithelium proliferates forming keratinizing cyst.
5. Congenital Theory
• Due to embryonic epithelial rests in middle ear.

Clinical Significance:
Understanding pathogenesis guides treatment — surgery aims to remove sac and restore
ventilation.
⸻

11. Dix–Hallpike Maneuver (Diagnostic Maneuver for BPPV)

Purpose:
To diagnose posterior semicircular canal BPPV, the most common type.

Procedure:
1. Patient sits upright with legs extended.
2. Head turned 45° to one side.
3. Patient quickly laid back so head hangs 20° below the table.
4. Examiner observes eyes for nystagmus and asks for vertigo sensation.
5. Repeat on opposite side.

Positive Test:
• Vertigo with torsional, upbeating nystagmus appearing after latency (2–5
sec).
• Lasts <30 sec and fatigues on repetition.

Interpretation:
• Positive when maneuver reproduces symptoms → diagnostic of posterior
canal BPPV on side tested.

Mechanism:
Dislodged otoliths move in endolymph stimulating cupula abnormally, causing vertigo.

Differential Diagnosis:
Central vertigo (no latency, non-fatigable nystagmus).

Clinical Note:
Often followed by Epley’s maneuver for treatment.

12. Fractures of Temporal Bone – Longitudinal vs Transverse

Feature Longitudinal Fracture Transverse Fracture
Incidence Common (80%) Less common (20%)
Direction Parallel to long axis of petrous bone Perpendicular to long axis
Cause Lateral blow to skull Frontal or occipital blow
Middle Ear Involved, may rupture TM Usually spared
Ossicular Chain Commonly disrupted → Conductive HL Intact or rarely affected
Facial Nerve Injury Delayed, due to edema Immediate, due to nerve transection
Hearing Loss Conductive Sensorineural
Vertigo Mild Severe due to labyrinthine injury
CSF Otorrhea Common Less common

Diagnosis: CT temporal bone.

Treatment: Conservative; surgical exploration for facial palsy or persistent CSF leak.

Excellent
Here’s Part 4 (Topics 13–15) — written in exam-style MBBS notes, each around 250 words,
concise yet complete for exam writing and viva preparation.

13. Causes of Conductive Hearing Loss

Definition:
Conductive hearing loss (CHL) occurs when sound transmission is impaired from the external
ear to the oval window of the inner ear.

Etiological Classification:

A. External Ear Causes:

1. Congenital: Atresia or stenosis of external auditory canal, microtia.
2. Acquired:
• Wax impaction
• Foreign body
• Otitis externa, furunculosis
 • Exostosis, osteoma
• Trauma (TM perforation)

B. Middle Ear Causes:

1. Tympanic Membrane:
• Chronic perforation
• Tympanosclerosis
2. Ossicular Chain:
• Discontinuity (trauma)
• Fixation (otosclerosis)
• Congenital malformation
3. Eustachian Tube Dysfunction:
• Adenoid hypertrophy, nasopharyngeal mass
• Barotrauma
4. Middle Ear Effusion:
• Otitis media with effusion, chronic suppurative otitis media (CSOM)
5. Tumors: Glomus tympanicum

Clinical Features:
• Reduced hearing, often improving with loud sounds
• Normal bone conduction (Rinne negative)
• Air-bone gap on audiogram

Management:
• Treat reversible causes (wax removal, infection control).
• Hearing aids or tympanoplasty/stapedectomy for structural lesions.

14. Anatomy of Posterior Wall of Middle Ear (with Diagram Description)

Boundaries:
Posterior (mastoid) wall separates middle ear cavity from mastoid antrum.

Features (from above downward):

1. Aditus ad antrum:
 • Opening leading into the mastoid antrum.
• Communicates middle ear with mastoid air cells.
2. Pyramidal eminence:
• Contains the stapedius muscle, whose tendon emerges to attach to the
stapes.
3. Fossa incudis:
• Small depression lodging the short process of the incus.
4. Facial canal (vertical segment):
• Descends behind the pyramid containing facial nerve.
5. Chorda tympani nerve:
• Runs between malleus and incus before exiting via petrotympanic
fissure.
6. Posterior tympanic recess (sinus tympani):
• Deep recess important surgically as it may harbor residual disease
(cholesteatoma).

Clinical Importance:
• Landmark in mastoidectomy and tympanoplasty.
• Infection may spread to mastoid through aditus.

(Diagram should label: Aditus, Pyramid, Facial canal, Fossa incudis, Chorda tympani, Sinus
tympani.)

15. Meniere’s Disease – Description and Management

Definition:
Meniere’s disease is an idiopathic disorder of the inner ear characterized by recurrent vertigo,
fluctuating hearing loss, tinnitus, and aural fullness, due to endolymphatic hydrops (excess
endolymph).

Etiology:
• Idiopathic (primary endolymphatic hydrops)
• Secondary causes: trauma, infection, allergy, autoimmune disease
Pathophysiology:
Increased endolymph volume causes rupture of Reissner’s membrane → mixing of endolymph
and perilymph → sudden vestibular dysfunction.

Clinical Features:
• Recurrent spontaneous vertigo (20 min – 12 hrs)
• Fluctuating sensorineural hearing loss (low frequency initially)
• Tinnitus (roaring type)
• Aural fullness before attacks
• Nausea, vomiting during episodes

Diagnosis:
• Pure tone audiometry: Low-frequency SNHL.
• Electrocochleography: Increased SP/AP ratio.
• MRI to rule out acoustic neuroma.

Treatment:
1. Medical:
• Salt restriction, diuretics (acetazolamide)
• Vestibular suppressants (betahistine, cinnarizine)
2. Surgical:
• Endolymphatic sac decompression, vestibular nerve section, or
labyrinthectomy (for intractable cases).

Perfect
Here’s the final section — Part 5 (Topics 16–18) written in exam-style MBBS format (~250
words each).

16. Impedance Audiometry

Definition:
Impedance audiometry is an objective test that evaluates the function of the middle ear by
measuring its compliance (mobility) in response to varying air pressures and sound stimuli.

Components:
1. Tympanometry – measures tympanic membrane compliance.
2. Acoustic reflex testing – evaluates stapedius muscle contraction.

Principle:
Sound reflected from the tympanic membrane varies with the pressure in the ear canal. A probe
alters air pressure and emits sound; the amount reflected indicates middle ear impedance.

Tympanogram Types:
• Type A: Normal middle ear function.
• Type As: Stiff system (otosclerosis).
• Type Ad: Hypermobile (ossicular discontinuity).
• Type B: Flat (fluid or perforation).
• Type C: Negative pressure (Eustachian tube dysfunction).

Acoustic Reflex:
• Involuntary contraction of the stapedius muscle in response to loud sound;
absent in facial nerve palsy and middle ear pathology.

Clinical Uses:
• Diagnose otitis media with effusion, otosclerosis, ossicular discontinuity.
• Evaluate Eustachian tube function.
• Detect facial nerve integrity.

Advantages:
Objective, quick, and reproducible.

17. Superior Semicircular Canal Dehiscence Syndrome (SSCDS)

Definition:
SSCDS is a rare vestibular disorder caused by a bony defect (“dehiscence”) in the roof of the
superior semicircular canal, creating an abnormal “third window” in the inner ear.
Etiology:
• Congenital bone thinning or post-traumatic erosion.
• Chronic elevated intracranial pressure may contribute.

Pathophysiology:
The dehiscence allows transmission of pressure/sound energy abnormally into the canal →
vertigo or oscillopsia with sound or pressure changes.

Clinical Features:
• Sound-induced vertigo (Tullio phenomenon).
• Pressure-induced vertigo (e.g., with sneezing, coughing).
• Conductive hearing loss with normal tympanic membrane.
• Autophony (hearing one’s own voice or eyeball movement loudly).
• Imbalance and disequilibrium.

Diagnosis:
• CT temporal bone: shows dehiscence.
• Vestibular evoked myogenic potentials (VEMP): enhanced response.
• Audiometry: pseudo-conductive hearing loss.

Treatment:
• Avoid triggers (noise, pressure).
• Surgical repair: resurfacing or plugging of the superior canal via middle
cranial fossa approach.

18. Summary – Integration of ENT Concepts

• External Ear Disorders: Furunculosis, wax impaction cause conductive loss.
• Middle Ear Disorders: Otosclerosis, chronic otitis media, and cholesteatoma
lead to progressive hearing loss and may affect the facial nerve.
• Inner Ear Disorders: SNHL due to noise, drugs, infections, or Meniere’s
disease affects hair cells or auditory nerve.
• Vestibular Disorders: BPPV and SSCDS cause positional or sound-induced
vertigo.
 • Diagnostic Tools:
• OAE: tests cochlear (outer hair cell) function.
• Impedance audiometry: evaluates middle ear mechanics.
• Dix-Hallpike: identifies BPPV.
• Management Principle: Identify level of lesion → treat medically or surgically
→ provide rehabilitation (hearing aids, cochlear implants).