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DNB Otorhinolaryngology — Model Answers

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Question 1

(a) Labelled Diagram: Branches Arising from the Intratemporal Part of the Facial Nerve [5 marks]

Facial nerve enters Internal Auditory Meatus (IAM)
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GENICULATE GANGLION (first genu, at junction of labyrinthine & tympanic segments)
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        ├──► Greater Superficial Petrosal Nerve (GSPN)
        |        → Carries preganglionic parasympathetic fibers to pterygopalatine ganglion
        |        → Supplies lacrimal gland, nasal & palatal glands
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        ├──► (External Petrosal Nerve — small, inconsistent)
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TYMPANIC (HORIZONTAL) SEGMENT
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        ▼ (Second genu — at posterior wall of tympanic cavity)
MASTOID (VERTICAL) SEGMENT
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        ├──► Nerve to Stapedius (from upper mastoid segment)
        |        → Innervates stapedius muscle
        |        → Dysfunction → Hyperacusis
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        ├──► Chorda Tympani (2–3 mm above stylomastoid foramen)
        |        → Crosses middle ear between malleus & incus
        |        → Carries taste fibers (anterior 2/3 tongue) via lingual nerve
        |        → Carries preganglionic parasympathetic fibers to submandibular & sublingual glands
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STYLOMASTOID FORAMEN (exits temporal bone → extratemporal course)

• GSPN arises at the geniculate ganglion (most proximal branch)
• Nerve to stapedius arises in the mastoid segment
• Chorda tympani arises just above the stylomastoid foramen in the mastoid segment
• Lesion above GSPN: loss of lacrimation, taste, salivation + hyperacusis + facial palsy
• Lesion between GSPN and nerve to stapedius: loss of taste, salivation + hyperacusis + facial palsy
• Lesion between nerve to stapedius and chorda tympani: loss of taste + salivation + facial palsy
• Lesion below chorda tympani: pure lower motor neuron facial palsy only

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(b) Electrodiagnostic Tests and Their Significance in Assessing Prognosis in Facial Palsy [5 marks]

1. Nerve Excitability Test (NET) / Minimal Excitability Test

• Compares minimum current (mA) required to produce minimal visible twitch on the affected vs normal side.
• A difference of >3.5 mA indicates degeneration.
• Simple, bedside test; subjective; less precise.
• Significance: If difference >3.5 mA → poor prognosis.

2. Maximal Stimulation Test (MST) — Hilger

• Maximum stimulus applied; response graded as equal, slightly reduced, markedly reduced, or absent.
• Absent response = severe degeneration → poor prognosis.
• More sensitive than NET.

3. Electroneurography (ENoG / ENOG) — Most Important Test

• Evoked electromyography; compares amplitude of compound muscle action potential (CMAP) on affected vs normal side.
• Expressed as percentage of degeneration.
• Done from 3rd day onward (before this, wallerian degeneration incomplete).
• >90% degeneration within 14 days of onset → indication for surgical decompression.
• Significance: Gold standard for prognosis; guides surgical decision-making.

4. Electromyography (EMG)

• Detects electrical activity of facial muscles at rest and during voluntary movement.
• Fibrillation potentials at rest → active denervation.
• Polyphasic reinnervation potentials → beginning of recovery (can be detected even before clinical recovery).
• Most useful after 3 weeks when ENOG is less informative.
• Significance: Detects early recovery; prognostic value in late presentation.

5. Antidromic / Trans-cranial Magnetic Stimulation

• Stimulates the proximal nerve transcranially; less commonly used.

Clinical Pearl: ENoG is the most objective and clinically significant test. If ENoG shows >90% degeneration within the first 2 weeks, surgical decompression of the facial nerve should be considered.

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Question 2

(a) Clinical Features of a Patient with Cerebellar Abscess [5 marks]

Symptoms:

1. Headache — occipital, severe, throbbing (due to raised ICP and local expansion)
2. Vomiting — projectile, not related to food (cerebellar/ICP-related)
3. Fever — may be low-grade (otogenic source may be quiescent)
4. Vertigo and dizziness — due to involvement of vestibular connections
5. Gait disturbance / ataxia — difficulty walking in a straight line, broad-based gait
6. Tinnitus and hearing loss — from the underlying ear disease (CSOM)

Signs (Cerebellar Signs — DANISH):

1. Dysdiadochokinesia — inability to perform rapid alternating movements
2. Ataxia — positive Romberg's (but falls to the side of lesion), wide-based gait
3. Nystagmus — horizontal, coarse; fast component toward the side of the lesion
4. Intention tremor — tremor worsens as the finger approaches the target (finger–nose test)
5. Slurred speech (Dysarthria)
6. Hypotonia — ipsilateral reduced muscle tone

Signs of Raised ICP:

• Papilloedema on fundoscopy
• Bradycardia, hypertension (Cushing's triad)
• Neck stiffness (if rupture or tonsillar herniation)
• Deteriorating consciousness

Localising Signs (ipsilateral to lesion):

• Ipsilateral past-pointing (finger–nose test)
• Ipsilateral dysdiadochokinesia
• Patient falls toward the side of the abscess

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(b) Management of Otogenic Cerebellar Abscess [5 marks]

Initial Stabilisation:

1. IV antibiotics immediately — broad spectrum (ceftriaxone + metronidazole + vancomycin)
2. Mannitol 20% (1 g/kg IV) to reduce cerebral oedema and ICP
3. Corticosteroids (dexamethasone) to reduce oedema
4. Phenytoin — if seizures present
5. Neurosurgical consultation immediately

Diagnostic Workup:

• CT scan of brain (with contrast) — gold standard; shows ring-enhancing lesion with central hypodensity in the posterior fossa
• CT mastoid — shows underlying CSOM/cholesteatoma
• MRI brain — better delineates cerebellar abscess and surrounding oedema
• Lumbar puncture is contraindicated (risk of tonsillar herniation)

Surgical Management (Two-Stage vs Simultaneous Approach):

• Burr hole aspiration — preferred (less morbidity); CT-guided stereotactic aspiration
• Craniotomy and excision — if aspiration fails, multiloculated or recurrent abscess
• Ommaya reservoir insertion for repeated drainage if needed

• Modified Radical Mastoidectomy (MRM) or Canal Wall Down tympanomastoidectomy to remove cholesteatoma and chronically infected mucosa
• This is done after the abscess is controlled (2–3 weeks later)
• In selected stable cases: simultaneous ear surgery + drainage (controversial)

• Must cross blood-brain barrier
• Duration: minimum 6–8 weeks IV, then oral
• Guided by pus culture and sensitivity

• Mortality 30–40% if untreated; with modern management 10–15%
• Worse prognosis: deep coma on admission, ruptured abscess, delayed diagnosis

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Question 3

(a) How to Clinically Examine for Spontaneous Nystagmus in an OPD Setting [2 marks]

1. Visual inspection: Observe the patient's eyes in primary gaze without any instruction.
2. Gaze testing (Frenzel's glasses preferred): Ask patient to look:
   • Straight ahead (primary position)
   • 30° to the right
   • 30° to the left
   • Upward
   • Downward
   • Note: Gaze >30° beyond center can produce end-gaze physiological nystagmus — must be avoided.
3. Remove visual fixation using Frenzel's goggles (+20 dioptre lenses) — these blur vision and eliminate fixation suppression, thereby unmasking peripheral vestibular nystagmus.
4. Note: direction, plane (horizontal, vertical, torsional), and whether it increases/decreases with gaze direction.
5. Alexander's Law: In peripheral nystagmus, intensity increases when gaze is in the direction of the fast phase.

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(b) Differentiation Between Central and Peripheral Nystagmus [5 marks]

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(c) Grades of Nystagmus [3 marks]

• Nystagmus present only when looking in the direction of the fast phase (i.e., only in the direction the eye is beating).

• Nystagmus present in primary/neutral gaze (eyes looking straight ahead) AND when looking in the direction of the fast phase.

• Nystagmus present even when looking in the direction of the slow phase (i.e., in all directions of gaze, including opposite to the fast phase).

Significance: Higher grades indicate more severe vestibular pathology. Grade III peripheral nystagmus may suggest an acute complete unilateral vestibular lesion (e.g., vestibular neuritis). Central lesions may show grade III without corresponding severe vertigo.

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Question 4

(a) Define Otosclerosis [1 mark]

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(b) Clinical Features and Audiological Evaluation [3 marks]

• Age: Usually 2nd–4th decade; onset around puberty
• Sex: Female > Male (2:1); pregnancy may accelerate progression
• Heredity: Autosomal dominant, variable penetrance (~25–40% penetrance)
• Bilateral in 70–80% (may be asymmetric)
• Slowly progressive conductive hearing loss — insidious onset
• Paracusis Willisii: Patient hears better in noisy environments (because others raise their voice; the noise does not interfere because it is not transmitted efficiently via the ossicular chain)
• Tinnitus: Low-frequency, pulsatile
• Flamingo pink blush (Schwartze sign): Reddish/pink blush seen through the tympanic membrane, representing vascular active otospongiosis over the cochlear promontory
• Tympanic membrane: Normal
• Absence of stapedial reflex

1. Pure Tone Audiogram (PTA):
   • Conductive hearing loss
   • Carhart's notch: Characteristic dip at 2000 Hz on bone conduction (mechanical artefact, not true sensorineural loss; disappears after stapedectomy)
   • Air-bone gap present (>40 dB in moderate disease)
2. Tympanometry: Type AS (shallow, reduced compliance) — "stiffness-dominated" curve
3. Acoustic reflex: Absent (due to stapes fixation)
4. Speech audiometry: Good speech discrimination score (SDT normal)
5. HRCT temporal bone: To assess footplate thickness, cochlear involvement

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(c) Fenestration of Stapes Footplate and Advantages of LASER [2 marks]

• A small window (0.6–0.8 mm) is created in the stapes footplate using:
  • A perforator (hand drill/microdrill) — traditional
  • CO₂ LASER or KTP (532 nm) LASER — modern

1. Bloodless, precise fenestration — no mechanical trauma to perilymph or membranous labyrinth
2. No contact with footplate → reduces risk of plunging footplate (subluxation into the vestibule)
3. Controlled perforation size → consistent window diameter
4. Reduced heat trauma (pulsed mode) vs traditional drill
5. Better in obliterative otosclerosis — can vaporise dense bone without force
6. Shorter operative time once skilled
7. Reduces post-operative floating footplate risk
8. Preferred in revision stapedectomy — avoids trauma to already-fragile footplate

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(d) Complications of Stapedectomy [4 marks]

1. Perilymph gusher — excessive CSF/perilymph flow; associated with X-linked stapes gusher (DFNX2, POU3F4 mutation); must pack and avoid suctioning
2. Plunging/depressed footplate — stapes footplate driven into vestibule; leads to SNHL/vertigo
3. Floating footplate — footplate becomes mobile but intact, difficult to remove
4. Injury to facial nerve — especially if dehiscent
5. Rupture of membranous labyrinth → severe SNHL
6. Chorda tympani injury → dysgeusia, metallic taste

1. Sensorineural hearing loss (SNHL) — most dreaded complication
2. Dead ear (total SNHL) — 1–2%
3. Vertigo — common initially; should resolve; persistent → perilymph fistula
4. Tinnitus — usually improves; may worsen
5. Perilymph fistula — through piston prosthesis interface

1. Prosthesis dislocation/extrusion
2. Reparative granuloma — around prosthesis; presents as fluctuating SNHL + vertigo, 1–6 weeks post-op
3. Re-fixation of stapes — due to recurrent otosclerosis
4. Tympanic membrane perforation
5. Cholesteatoma formation (if skin tags implanted)
6. SNHL due to progressive cochlear otosclerosis (despite successful surgery)

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Question 5

(a) Impedance Audiometry Curves and Their Clinical Significance [5 marks]

Type A — Normal

• Peak compliance occurs at atmospheric pressure (0 daPa)
• Peak height: 0.3–1.6 ml (cubic centimetres)
• Clinical significance: Normal middle ear; no middle ear pathology

• Peak at 0 daPa but reduced compliance (<0.3 ml)
• Clinical significance: Otosclerosis, tympanosclerosis, healed perforations, ossicular fixation

• Peak at 0 daPa but increased compliance (>1.6 ml)
• Clinical significance: Ossicular discontinuity, flaccid tympanic membrane, monomeric TM

Type B — Flat / Dome-shaped

• No identifiable peak throughout pressure sweep
• Flat curve
• Clinical significance: Otitis media with effusion (glue ear), middle ear fluid, TM perforation (with large ear canal volume), wax impaction
• Ear canal volume (ECV): Normal in OME; large if TM is perforated

Type C — Negative Peak

• Peak compliance occurs at negative pressure (–100 daPa or more negative)
• Clinical significance: Eustachian tube dysfunction (ETD), early OME, retracted TympTM

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(b) Stenger's Principle [2 marks]

"When two tones of the same frequency are presented simultaneously to both ears, only the louder tone is perceived; the tone in the other ear is completely suppressed."

• Used when unilateral (or asymmetric) hearing loss is suspected to be non-organic (functional/malingered).
• A tone at 10 dB above the admitted threshold in the "good" ear and simultaneously 10 dB below the admitted threshold of the "bad" ear is presented.
• Positive Stenger's test (ABNORMAL): Patient fails to respond — because the louder tone in the supposedly "bad" ear suppresses the tone in the good ear (patient can't admit hearing only in the "bad" ear without revealing the malingering). Suggests non-organic hearing loss.
• Negative Stenger's test (NORMAL): Patient responds — the admitted thresholds are genuine.

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(c) Clinical and Audiological Tests to Establish Malingering [3 marks]

Clinical Tests:

1. Watch tick test / Whisper test: Inconsistent responses — does not correlate with audiogram
2. "Stethoscope test": Patient denies hearing conversational speech through a stethoscope applied to mastoid — not physiologically possible
3. Delayed Speech Feedback (Lee's test): Speaking into a microphone with a 0.2-second delay — malingerers show disrupted speech even at thresholds they "cannot hear"

Audiological Tests:

1. Stenger's Test (see above)
2. Pure tone audiometry inconsistency: Threshold variability >10 dB on repeated testing; inconsistent shadow curve (shadow hearing should appear at 40–60 dB better than the good ear — if not seen, suspect malingering)
3. Speech audiometry: Speech reception threshold (SRT) should match PTA average within 10 dB — discrepancy suggests non-organic loss
4. Auditory Brainstem Response (ABR / BERA): Objective test; cannot be faked; shows true hearing thresholds independent of patient cooperation
5. Otoacoustic Emissions (OAE): Present cochlear function even if patient claims to not hear — unmasked by OAE
6. Acoustic Reflex Testing: Reflex present at normal levels despite claimed hearing loss
7. LOMBART test: Raising one's voice in background noise — malingerer raises voice appropriately in noise they "cannot hear"

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Question 6

(a) Differentiate Between Case Control and Cohort Study [4 marks]

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(b) Odds Ratio and Relative Risk [4 marks]

Odds Ratio (OR):

• Used in case-control studies
• Odds = probability of event / probability of non-event
• OR = (odds of exposure in cases) / (odds of exposure in controls)
• Using 2×2 table (a, b, c, d):

                Disease (+)   Disease (-)
Exposed (+)        a              b
Unexposed (-)      c              d

OR = (a/c) / (b/d) = ad/bc

• OR = 1: No association
• OR > 1: Positive association (exposure is risk factor)
• OR < 1: Negative association (exposure is protective)
• Approximates RR when disease is rare ("rare disease assumption")

Relative Risk (RR) / Risk Ratio:

• Used in cohort studies and RCTs
• RR = Incidence in exposed / Incidence in unexposed

RR = [a/(a+b)] / [c/(c+d)]

• RR = 1: No association
• RR > 1: Increased risk (positive association)
• RR < 1: Decreased risk (protective effect)
• Attributable Risk = Incidence (exposed) − Incidence (unexposed) = a/(a+b) − c/(c+d)

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(c) Impact Factor and Its Relevance [2 marks]

IF (Year X) = Citations in year X to articles published in (X–1) + (X–2)
              ÷ Total articles published in that journal in (X–1) + (X–2)

1. Journal prestige: High IF = higher quality, more widely read journal (e.g., NEJM IF ~100; Lancet ~60; Indian specialty journals ~1–3)
2. Research credibility: Publishing in high-IF journals implies rigorous peer review
3. Academic promotion and funding: Researchers assessed by publications in high-IF journals
4. Literature quality assessment: Helps identify authoritative sources

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Question 7

(a) Composition of Endolymph and Perilymph [2 marks]

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(b) Etiological Factors for Primary Endolymphatic Hydrops [3 marks]

1. Defective endolymphatic sac (ES) absorption: ES is responsible for endolymph absorption; any obstruction/dysfunction → hydrops. This is the most widely accepted mechanism.
2. Immune-mediated mechanisms: Autoimmune labyrinthitis — antibodies against inner ear antigens; associated with systemic autoimmune diseases (e.g., Hashimoto's thyroiditis, rheumatoid arthritis, Cogan's syndrome)
3. Viral/infectious: Reactivation of latent viral infections (HSV-1 reportedly found in vestibular ganglion); prior viral labyrinthitis
4. Genetic factors: Family history in ~10–20% cases; possible genetic predisposition to abnormal fluid regulation
5. Allergy/Atopy: High prevalence of allergy in Meniere's patients; allergic response in endolymphatic sac
6. Anatomical factors: Narrow endolymphatic duct, hypoplastic endolymphatic sac (seen on MRI)
7. Vascular: Microangiopathy of stria vascularis → altered fluid secretion
8. Hormonal: Antidiuretic hormone (ADH) dysregulation → excess fluid retention in labyrinth

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(c) Surgical Modalities for Managing Meniere's Disease [5 marks]

A. Destructive Procedures (ablate labyrinthine function):

• Gentamicin injected into the middle ear → absorbed through round window → selectively destroys type I vestibular hair cells
• Most commonly used ablative procedure today
• Advantage: Minimally invasive, OPD procedure, hearing preserved (selective vestibulotoxicity)
• Vertigo control: ~85–90%
• Risk: SNHL in 10–30%

• Complete removal of labyrinthine contents (membranous labyrinth)
• Performed via transmastoid approach
• Indicated: Non-serviceable hearing + refractory vertigo
• Complete vertigo control (~95%) but total ipsilateral hearing loss

• Sectioning of vestibular nerve (superior + inferior divisions) via middle cranial fossa, retrolabyrinthine, or retrosigmoid approach
• Preserves hearing while ablating vestibular input
• Vertigo control: ~90–95%
• Risk: CSF leak, facial nerve injury, hearing loss; requires craniotomy

B. Conservative / Non-Destructive Procedures:

• Endolymphatic sac decompression: Removal of bone over the sac in the posterior fossa dura
• Endolymphatic sac shunt: Insertion of T-tube into sac lumen for drainage to mastoid/subarachnoid space
• Reduces hydrops without destroying hearing/balance
• Vertigo control: ~60–70% (less reliable; similar to sham procedure in some trials)
• Advantage: Preserves hearing and vestibular function; safest option

• Non-surgical: intermittent low-pressure pulses via ventilation tube in TM → transmitted to perilymph → reduces hydrops
• Modest evidence; some patients benefit

• First-line: Intratympanic gentamicin (if hearing serviceable) or labyrinthectomy (if hearing lost)
• In young patients with serviceable hearing: Endolymphatic sac surgery or vestibular neurectomy

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Question 8

(a) Acoustic Reflex Pathway with Schematic Diagram [4 marks]

STIMULUS (loud sound)
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Cochlear Hair Cells
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Cochlear (Auditory) Nerve (CN VIII)
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Cochlear Nucleus (Ventral — both sides, via trapezoid body)
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        ├──► IPSILATERAL Superior Olivary Complex
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        |     Ipsilateral Facial Motor Nucleus (CN VII)
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        |     Ipsilateral Stapedius muscle (IPSILATERAL REFLEX)
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        └──► CONTRALATERAL Superior Olivary Complex (via trapezoid body)
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             Contralateral Facial Motor Nucleus (CN VII)
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             Contralateral Stapedius muscle (CONTRALATERAL/CONSENSUAL REFLEX)

• Both ipsilateral and contralateral reflexes are elicited by unilateral stimulation (bilateral reflex — like consensual pupillary reflex)
• The reflex arc crosses the brainstem at the superior olivary complex level
• Efferent limb: CN VII (facial nerve) → stapedius muscle
• Afferent limb: CN VIII (auditory nerve) → cochlear nucleus
• Threshold: 70–90 dB HL in normal ears

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(b) Acoustic Reflex Decay Test — Principle and Application [3 marks]

• A continuous tone at 10 dB above the acoustic reflex threshold (ART) is presented for 10 seconds
• The amplitude of stapedius muscle contraction is monitored over time
• In normal individuals and cochlear lesions, the reflex is maintained (no decay)
• In retrocochlear lesions (e.g., acoustic neuroma/vestibular schwannoma), the nerve cannot sustain firing at high rates → the reflex decays (adapts) rapidly

• Abnormal (positive decay): Reflex amplitude drops to <50% of initial amplitude within the 10-second period
• Normal (negative decay): Reflex sustained ≥50% amplitude for 10 seconds
• Tested at 500 Hz and 1000 Hz (decay more likely at higher frequencies)

• Positive (abnormal) decay at 500 & 1000 Hz: Strongly suggests retrocochlear pathology (acoustic neuroma, CN VIII tumour, demyelinating disease)
• Used as a screening test before ABR and MRI
• Sensitivity ~70–90% for acoustic neuroma

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(c) Diagnostic Applications of Acoustic Reflex [3 marks]

1. Diagnosing Otosclerosis: Absent reflex due to stapes fixation (Type As tympanogram + absent reflex is pathognomonic)
2. Site of lesion in hearing loss:
   • Cochlear lesion: Reflex present at lower sensation levels (recruitment — reflex within 60 dB SL)
   • Retrocochlear: Elevated or absent reflex; positive decay test → suggests acoustic neuroma
   • Conductive: Absent reflex due to middle ear pathology
3. Facial nerve testing: Localisation of facial nerve lesion using reflex
   • Lesion above the nerve to stapedius → Absent reflex
   • Lesion below nerve to stapedius → Reflex present
4. Predicting hearing level in non-cooperative patients: Reflex threshold predicts hearing levels (reflex typically at 70–90 dB HL); useful in children, malingerers
5. Auditory neuropathy (ANSD): Absent acoustic reflex despite present OAEs → diagnostic hallmark
6. Diagnosis of VIIth nerve lesions: Assessing stapedius innervation integrity
7. Post-stapedectomy assessment: Confirms successful mobilization when reflex returns

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Question 9

(a) Limitations and Fallacies of Pure Tone Audiometry [6 marks]

Limitations:

• Entirely dependent on patient cooperation and voluntary response
• Cannot be used in: infants, uncooperative patients, those with cognitive/intellectual disability
• Subject to malingering and functional hearing loss

• Standard PTA tests 250–8000 Hz only
• Does not test extended high frequencies (9000–20000 Hz) — early ototoxicity begins here
• Does not test low frequencies accurately in noisy test environments

• Bone conduction vibrator may produce harmonics and vibrotactile sensations at low frequencies, leading to false-positive (better) responses
• Interoctave masking problems with narrow-band noise

• Clinical threshold has ±5–10 dB variability — normal test-retest variability
• A single frequency can have responses varying due to fatigue, attention

• When bilateral asymmetric hearing loss exists, adequate masking of the non-test ear is difficult
• Over-masking (masking noise crosses to test ear) can give falsely elevated thresholds
• Undermasking gives falsely improved thresholds (cross-hearing)

• PTA average (500, 1000, 2000 Hz) only approximates speech intelligibility
• No information on suprathreshold function (discrimination, recruitment, distortion)
• A patient with high-frequency loss may have normal PTA average but poor speech in noise

• A mechanical artefact in otosclerosis causing a dip in bone conduction at 2000 Hz
• Not a true SNHL — disappears after stapedectomy
• Can mislead into diagnosing mixed hearing loss when it is purely conductive

• Cannot differentiate cochlear vs retrocochlear pathology (needs ABR, OAE, speech audiometry)

• In unilateral profound deafness, sound may cross transcranially and be heard in the good ear
• This "shadow response" gives falsely better thresholds in the dead ear unless masked

• ANSI/ISO standard uses average threshold of young adults — may not represent individual norms
• Patients with normal aging patterns may show "loss" that is actually physiological

• Requires sound-treated booth — ambient noise in OPD can raise apparent thresholds
• Noise floor limitations affect low-frequency testing

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(b) Pathways of Bone Conduction [4 marks]

1. Osseotympanic / Radiational Bone Conduction:

• Vibration of the skull → vibration of the external auditory canal walls → acts as a sound source → produces sound waves in the ear canal → stimulates the tympanic membrane and ossicular chain → reaches cochlea
• Important at low frequencies
• Blocking the ear canal with a plug enhances this component (occlusion effect)

2. Inertial Bone Conduction (Middle Ear Inertia):

• Skull vibrates → ossicular chain lags behind (due to inertia) → relative movement between skull and ossicular chain → stapes footplate moves relative to oval window → cochlear stimulation
• Important at low frequencies (250–1000 Hz)
• Affected by ossicular fixation (e.g., otosclerosis — Carhart's notch at 2000 Hz)

3. Compressional / Distortional Bone Conduction:

• Direct compression of the skull and cochlear capsule → alternating compression and expansion of the cochlea itself → differential movement of cochlear windows (oval vs round) → fluid movement in scala → hair cell stimulation
• Important at high frequencies (>1000 Hz)
• Most important mechanism of bone conduction

4. Fluid Conduction (Sensorineural Component):

• Vibration → direct stimulation of cochlear fluids via bone
• CSF pathway — sound transmitted through CSF from skull

5. Central Bone Conduction (Transcranial Stimulation):

• With strong vibration, sound energy crosses the skull and stimulates the contralateral cochlea — this is the basis of "cross-hearing" and why BC audiometry always requires masking of the non-test ear (contralateral masking with narrow-band noise)

• Bone conduction thresholds represent cochlear reserve (sensorineural sensitivity)
• Air-bone gap = conductive component of hearing loss
• Occlusion effect: plugging ear raises BC threshold at 250–500 Hz due to enhanced osseotympanic component

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Question 10

(a) Define Otitic Barotrauma [1 mark]

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(b) Differences Between Inner Ear Barotrauma and Inner Ear Decompression Illness [4 marks]

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(c) Management of Barotrauma-Induced Perilymphatic Fistula [5 marks]

Diagnosis:

• Clinical: Sudden SNHL + tinnitus + vertigo after barotrauma or Valsalva
• Positive fistula test (Hennebert's sign): Pneumatoscopy → + and − pressure changes cause nystagmus
• CT temporal bone: May show gas in cochlea (pneumolabyrinth)
• HRCT: May show fluid level in middle ear; rarely shows fistula directly
• Definitive diagnosis: Only on surgical exploration (presence of perilymph pooling in middle ear on Valsalva)

Conservative Management (First-line, 4–6 weeks):

1. Strict bed rest — head elevation 30–45° (reduces intracranial pressure and perilymph leak)
2. Avoid all pressure-raising activities:
   • No nose blowing, sneezing with mouth open
   • No straining (stool softeners if needed)
   • No heavy lifting, bending, coughing
   • No diving or flying
3. Analgesics and anti-nausea medications (prochlorperazine, promethazine) for vertigo
4. Betahistine for vestibular symptoms
5. Corticosteroids (controversial): Some use to reduce cochlear inflammation (prednisolone 1 mg/kg/day, 10–14 days)
6. Avoid anticoagulants — promote clot formation for spontaneous sealing

Surgical Management (if conservative fails after 4–6 weeks):

1. Patient under GA; tympanotomy flap elevated
2. Middle ear explored: round window niche and oval window annular ligament examined
3. Valsalva maneuver by anaesthetist → perilymph leaks from fistula site (confirms diagnosis)
4. Fistula sealed with:
   • Fat graft (most common — from lobule of ear)
   • Perichondrium from tragus
   • Connective tissue graft
5. Packing maintained; post-op bed rest mandatory
6. Avoid pressure for minimum 4–6 weeks post-operatively

• Hearing improvement expected in 50–60% of cases
• Vertigo resolves in ~80%
• SNHL may be permanent if fistula was longstanding

• Best outcomes when treated early (within weeks)
• Delayed treatment → permanent SNHL

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• Draw the facial nerve diagram for Q1 — examiners love labelled diagrams
• Memorize the Jerger tympanogram table for Q5
• For Q9, group the limitations into: subjective / frequency / masking / clinical utility categories
• Q6 is the only non-clinical question — the 2×2 table formulas are high-yield