Otology and Neurotology: Hearing Loss, Vertigo, and the Facial Nerve
Build your otology reasoning around three frameworks: (1) conductive vs. sensorineural hearing loss on tuning forks and audiometry; (2) the site-of-lesion approach to vertigo (peripheral vs. central); and (3) temporal bone anatomy as it relates to complications and the facial nerve.
For hearing loss, know Weber and Rinne cold: Weber lateralizes to the conductive-loss ear (or better cochlea); Rinne is negative (bone > air) in conductive loss. Recognize sudden sensorineural hearing loss (SSNHL) as an emergency-prompt high-dose corticosteroids (oral or intratympanic) and MRI to exclude retrocochlear pathology such as vestibular schwannoma. Differentiate otosclerosis (young adult, progressive conductive loss, normal tympanic membrane) from chronic otitis media with effusion and cholesteatoma (epitympanic retraction, scutum erosion, foul discharge).
For vertigo, use HINTS in acute vestibular syndrome: normal head impulse, direction-changing nystagmus, and skew deviation suggest central pathology. BPPV is diagnosed by the Dix-Hallpike maneuver and treated with canalith repositioning; vestibular neuritis follows a viral prodrome with a positive head impulse; Ménière disease features episodic vertigo, fluctuating hearing loss, tinnitus, and aural fullness.
Traps: missing a central cause by anchoring on "peripheral"; treating SSNHL as "watch and wait"; and forgetting that facial nerve decompression decisions depend on whether paralysis is complete and whether function is preserved.
Rule of thumb: "Sudden SNHL is a stroke of the inner ear-treat now, image soon."
Worked example: A 48-year-old with acute vertigo, vomiting, and horizontal nystagmus has a positive head impulse test and no skew deviation. This pattern favors a peripheral cause (vestibular neuritis); supportive care and vestibular rehabilitation are appropriate, with imaging if any atypical feature emerges.