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EN4.{12-14,16-20} | Hearing Vestibular and Neuro Otology — Practice Quiz
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A 45-year-old woman has a 2-year history of recurrent episodes of severe rotatory vertigo lasting 20–30 minutes, fluctuating low-frequency sensorineural hearing loss, tinnitus and a feeling of fullness in the left ear. The most likely diagnosis is:
Correct. The triad of episodic rotatory vertigo, fluctuating low-frequency sensorineural hearing loss, and tinnitus with aural fullness is classic Meniere's disease — caused by endolymphatic hydrops. The low-frequency component and the episodic nature are key distinguishing features.
Meniere's disease = episodic vertigo + fluctuating low-frequency SNHL + tinnitus ± aural fullness (endolymphatic hydrops). BPPV causes brief positional vertigo with no hearing loss. Vestibular neuritis causes a single prolonged episode of vertigo with no hearing change. Acoustic neuroma causes unilateral progressive SNHL without episodic vertigo.
BPPV (A) causes brief positional vertigo (seconds–minutes) triggered by head movement; there is no hearing loss. Vestibular neuritis (C) causes a single prolonged episode of vertigo without hearing change. Acoustic neuroma (D) causes slowly progressive unilateral SNHL without episodic vertigo. Only Meniere's combines all four features: episodic vertigo + fluctuating SNHL + tinnitus + aural fullness.
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On performing a Rinne test in a patient with right conductive hearing loss, the tuning fork (512 Hz) placed on the right mastoid is heard louder and longer than when held beside the right ear. This result is described as:
Correct. Rinne NEGATIVE means bone conduction is better than air conduction (BC > AC). This indicates a conductive hearing loss — the middle ear mechanism (tympanic membrane, ossicular chain) is not transmitting sound efficiently, so bypassing it via bone conduction yields a louder percept.
Rinne NEGATIVE = BC > AC = conductive hearing loss. Rinne POSITIVE = AC > BC = normal OR sensorineural loss. These definitions are fixed — never invert them. A Rinne-negative result indicates that the middle ear mechanism is impaired so that direct bone conduction bypasses the conductive pathway.
A Rinne POSITIVE result is when air conduction is better than bone conduction (AC > BC) — this is normal or occurs in sensorineural loss. When BC > AC (as in this question), the result is Rinne NEGATIVE, indicating conductive loss. There is no formal 'Rinne equivocal' category in standard clinical use.
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In Weber's test, a 512 Hz tuning fork is placed on the vertex of a patient with unilateral right sensorineural hearing loss. Where will the patient localise the sound?
Correct. In unilateral sensorineural hearing loss, Weber lateralises to the BETTER (unaffected) ear — the left ear in this case. The impaired cochlea on the right cannot perceive the vibration as well, so the normal cochlea on the left dominates. This is opposite to conductive loss, where Weber lateralises to the affected ear.
Weber lateralises TO the affected ear in conductive loss (better BC on that side). Weber lateralises AWAY from the affected ear — i.e. to the better ear — in sensorineural loss. The cochlea on the SNHL side is less sensitive, so the vibration is perceived more strongly in the normal cochlea on the opposite side.
Weber lateralises to the affected ear in CONDUCTIVE loss — the opposite of SNHL. In sensorineural loss, the cochlea on the affected side is less sensitive, so Weber lateralises to the better (unaffected) ear. Equal bilaterally suggests symmetric hearing or is normal.
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A 28-year-old man develops sudden severe vertigo with nausea and vomiting. He cannot stand without support. The vertigo is constant (not triggered by head position) and has persisted for 48 hours. He reports no hearing loss, no tinnitus and no ear symptoms. The most likely diagnosis is:
Correct. Vestibular neuritis presents as a single acute episode of severe, prolonged vertigo without auditory symptoms (no hearing loss, no tinnitus). It lasts days and is not triggered by head position. The absence of hearing loss distinguishes it from Meniere's disease and labyrinthitis.
Vestibular neuritis = acute single episode of severe prolonged vertigo (days), no hearing loss, no tinnitus. It is caused by viral inflammation of the vestibular nerve. BPPV = brief positional vertigo (seconds). Meniere's = episodic vertigo + SNHL + tinnitus + aural fullness. Otosclerosis = progressive conductive hearing loss, no vertigo.
Meniere's (A) requires the triad: episodic vertigo + SNHL + tinnitus ± aural fullness — absent here. BPPV (B) causes brief vertigo (seconds) triggered by specific head positions, not constant prolonged vertigo. Otosclerosis (D) causes progressive conductive hearing loss with no vertigo.
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A 35-year-old man presents with gradual progressive unilateral left sensorineural hearing loss, tinnitus in the left ear, and occasional unsteadiness. MRI of the internal auditory canal reveals a 2.5 cm enhancing mass at the cerebellopontine angle. The most likely diagnosis is:
Correct. Acoustic neuroma (vestibular schwannoma) is the commonest CPA tumour, arising from the vestibular nerve Schwann cells in the IAC. It causes slowly progressive unilateral SNHL, tinnitus and mild disequilibrium. MRI shows a gadolinium-enhancing lesion in the IAC/CPA angle.
Acoustic neuroma (vestibular schwannoma) is the commonest tumour of the cerebellopontine angle (80–85% of CPA tumours). It arises from Schwann cells of the superior/inferior vestibular nerve within the IAC. Classic presentation: unilateral SNHL + tinnitus + unsteadiness. MRI with gadolinium is the investigation of choice — shows an enhancing IAC/CPA mass.
Glomus jugulare (A) arises from the jugular bulb, presents with pulsatile tinnitus and lower cranial nerve palsies. Meningioma (C) is the second commonest CPA tumour but does not arise in the IAC and hearing loss is less prominent. Cholesteatoma (D) is a middle ear lesion causing conductive (not sensorineural) hearing loss and cannot cause a CPA mass.
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A 42-year-old woman presents with progressive conductive hearing loss in the right ear without any history of ear discharge, pain or trauma. Otoscopy reveals a normal-looking tympanic membrane with a pinkish hue visible through it (Schwartze sign). Audiometry shows a Carhart notch at 2000 Hz. The most likely diagnosis is:
Correct. Otosclerosis presents with progressive conductive hearing loss, a normal tympanic membrane, and the Schwartze sign (pink/red blush = active otospongiosis). The Carhart notch at 2000 Hz on pure-tone audiometry is a characteristic finding. Stapes fixation is the mechanism. Stapedectomy or hearing aid is the treatment.
Otosclerosis = abnormal spongy bone formation fixing the stapes footplate → progressive conductive hearing loss with a normal-looking TM. Schwartze sign (flamingo pink hue through TM) = active otospongiosis with increased vascularity. Carhart notch at 2000 Hz is the characteristic audiometric dip in otosclerosis (not true SNHL — a mechanical artefact). Definitive treatment is stapedectomy/stapedotomy.
CSOM (A) presents with ear discharge and a perforated tympanic membrane. Otitis media with effusion (C) ('glue ear') shows a dull, retracted amber TM; it is common in children and lacks the Schwartze sign or Carhart notch. Glomus tympanicum (D) is a vascular tumour causing pulsatile tinnitus and a reddish pulsatile mass behind the TM.
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A 6-year-old boy is referred because his parents are concerned he does not respond to speech and has had delayed language development. Otoacoustic emissions (OAEs) are absent bilaterally and auditory brainstem response (ABR) shows absent waves at all intensities. The most useful next investigation for establishing the aetiology of his profound hearing loss is:
Correct. GJB2 (connexin 26) mutations account for up to 50% of cases of autosomal recessive non-syndromic SNHL in children. Genetic testing is the highest-yield single investigation for aetiology in bilateral profound paediatric SNHL after ABR and OAEs have confirmed the diagnosis.
GJB2 mutations (encoding connexin 26) are the commonest cause of autosomal recessive non-syndromic congenital SNHL worldwide. Genetic testing is the highest-yield investigation for aetiology in a child with bilateral profound SNHL once conductive causes are excluded. ABR and OAEs confirm SNHL; aetiology requires genetic + imaging workup. CT temporal bone and MRI are also part of the workup but genetic testing establishes the most common aetiology.
Pure-tone audiometry (A) requires behavioural cooperation and is not reliable at age 6 when there is profound loss — ABR has already established this. Tympanometry (C) assesses middle ear function; in SNHL with absent OAEs/ABR it will be normal and does not establish aetiology. CT temporal bone alone (D) can show structural causes (Mondini dysplasia, LVAS) but GJB2 mutation (the commonest cause) is invisible on CT.
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A 55-year-old patient presents with right-sided facial weakness involving the forehead, inability to close the right eye, and loss of taste over the anterior two-thirds of the right tongue. There is no parotid swelling. The site of facial nerve lesion is:
Correct. Loss of taste over the anterior two-thirds of the tongue (chorda tympani function) with an LMN complete facial palsy localises the lesion to ABOVE the origin of the chorda tympani within the temporal bone — at or proximal to the geniculate ganglion level (e.g. Bell's palsy, Ramsay Hunt syndrome). The forehead weakness confirms LMN (not UMN) involvement.
Chorda tympani (taste anterior 2/3 tongue) leaves the facial nerve within the petrous temporal bone. Loss of taste with LMN facial palsy localises the lesion to a site ABOVE (proximal to) the origin of the chorda tympani — within the temporal bone (e.g. Bell's palsy, Ramsay Hunt). If taste is preserved, the lesion is distal to chorda tympani origin. UMN palsy spares the forehead (bilateral cortical representation of frontalis).
A parotid/extratemporal lesion (A) would spare the chorda tympani (which has already branched off inside the temporal bone) — so taste would be intact. A lesion below the chorda tympani origin (C) also spares taste. UMN lesion (D) spares the forehead due to bilateral cortical representation of the frontalis muscle.
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The MOST effective treatment for a young patient with Dix-Hallpike positive posterior semicircular canal BPPV is:
Correct. Epley's canalith repositioning manoeuvre is the treatment of choice for posterior canal BPPV. It moves displaced otoconia (canalolithiasis) through the posterior SCC and out via the common crus into the utricle. A single manoeuvre is curative in >80% of patients.
Epley's canalith repositioning manoeuvre is the definitive first-line treatment for posterior canal BPPV — it moves displaced otoconia out of the posterior SCC back to the utricle. Success rate >80%. Betahistine is used for Meniere's disease (not BPPV). Intratympanic gentamicin (chemical labyrinthectomy) and endolymphatic sac surgery are reserved for refractory Meniere's disease.
Betahistine (A) reduces endolymphatic pressure and is used for Meniere's disease — not BPPV. Intratympanic gentamicin (C) ablates vestibular function (chemical labyrinthectomy) and is reserved for refractory Meniere's. Endolymphatic sac decompression (D) is a surgical option for refractory Meniere's disease.
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A 60-year-old man with long-standing tinnitus in the right ear undergoes a hearing assessment. The audiogram shows a bilateral symmetrical high-frequency sensorineural hearing loss with the classic 4 kHz notch. The most likely aetiology is:
Correct. The 4 kHz notch is pathognomonic of noise-induced hearing loss. Acoustic trauma selectively damages outer hair cells at the base of the cochlea (which respond to ~4 kHz) before affecting adjacent frequencies. The bilateral symmetrical pattern is typical of occupational noise exposure. Presbycusis causes a gradual downsloping SNHL without the discrete 4 kHz notch.
Noise-induced hearing loss (NIHL) characteristically shows a bilateral symmetrical SNHL with a 4 kHz (4000 Hz) notch on audiometry — the inner hair cells at the basal turn of the cochlea (tuned to high frequencies) are maximally vulnerable to acoustic trauma. Presbycusis shows a gradual downsloping SNHL at all high frequencies without a discrete notch. Otosclerosis = conductive loss. Meniere's = fluctuating low-frequency SNHL.
Presbycusis (A) causes a gradual symmetrical high-frequency SNHL — a smooth downslope across all high frequencies without a discrete 4 kHz notch. Otosclerosis (C) causes progressive CONDUCTIVE hearing loss, not SNHL. Meniere's (D) causes fluctuating LOW-frequency SNHL (250–1000 Hz), not high-frequency.
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