Step 2 CK · Ophthalmology & ENT

Hearing Loss & Vertigo

Name: Hearing Loss & Vertigo
Creator: Veli Bakalov, MD

Tuning forks and nystagmus localize the lesion

Ophthalmology & ENT·Ear & Vestibular Disorders·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Weber lateralizes to the BAD ear in conductive loss and to the GOOD ear in sensorineural loss; conductive loss makes Rinne bone greater than air in the affected ear.
Otosclerosis: autosomal dominant stapes fixation causing progressive conductive loss in a young adult (Schwartze sign); hearing aid or stapedectomy.
Presbycusis = bilateral symmetric high-frequency SNHL with trouble hearing in noise; noise-induced loss notches at 4000 Hz; ototoxins are aminoglycosides, cisplatin, loop diuretics, and high-dose salicylates.
Sudden unilateral SNHL (hours to 3 days) is an otologic emergency: confirm it is sensorineural, offer high-dose oral steroids within 2 weeks (intratympanic if systemic steroids are contraindicated, or as salvage for incomplete recovery; no antivirals or routine CT), and get an MRI to exclude vestibular schwannoma.
Vestibular schwannoma: progressive unilateral SNHL, tinnitus, imbalance, and a reduced corneal reflex (CN V) from a cerebellopontine angle mass; gadolinium MRI; bilateral = NF2.
BPPV: vertigo under 1 minute with head movement, no hearing loss, fatigable upbeat-torsional nystagmus on Dix-Hallpike (posterior canal otoconia); treat with the Epley maneuver.
Meniere disease (endolymphatic hydrops): vertigo lasting 20 minutes to hours + fluctuating low-frequency SNHL + tinnitus + aural fullness; low-salt diet and diuretics, intratympanic gentamicin if refractory.
Vestibular neuritis = days of continuous vertigo after a viral illness with unidirectional nystagmus and normal hearing; labyrinthitis adds hearing loss.
Central vertigo: vertical or direction-changing nystagmus not suppressed by fixation, with neuro signs; on HINTS, a NORMAL head impulse, direction-changing nystagmus, or skew deviation means stroke.

Localizing hearing loss: Weber and Rinne

Two questions frame the problem. Hearing loss is either conductive (outer or middle ear) or sensorineural (cochlea or CN VIII), and a 512-Hz tuning fork sorts them at the bedside. Vertigo is either peripheral (labyrinth or CN VIII, usually benign) or central (brainstem or cerebellum, dangerous), sorted by the nystagmus pattern and the HINTS exam.

Tuning fork tests

Test	Conductive loss	Sensorineural loss
Weber (fork on forehead)	Lateralizes TO the bad ear	Lateralizes to the GOOD ear
Rinne (air vs bone)	Bone greater than air in the affected ear (negative Rinne)	Air greater than bone (normal, positive Rinne)
Classic causes	Cerumen, otitis media or effusion, perforation, cholesteatoma, otosclerosis	Presbycusis, noise, ototoxins, Meniere, acoustic neuroma

Formal audiometry confirms the pattern: an air-bone gap means conductive loss.

In a left sensorineural loss, Weber lateralizes to the right (good) ear and Rinne stays normal on both sides. Symmetric loss leaves Weber midline.

Causes of hearing loss

Conductive. Cerumen impaction, otitis media or effusion, tympanic membrane perforation, cholesteatoma (a keratin-filled retraction pocket with foul otorrhea that erodes the ossicles), and otosclerosis.

Otosclerosis. Autosomal dominant fixation of the stapes footplate causes progressive conductive loss in a young adult, often with a family history, sometimes with a reddish blush over the promontory behind the drum (Schwartze sign). Treat with a hearing aid or stapedectomy.

Presbycusis. Age-related, bilateral, symmetric sensorineural loss that takes the high frequencies first, from loss of hair cells at the cochlear base. The typical complaint is trouble following speech in noisy rooms. Management is amplification with hearing aids.

Noise and ototoxins. Noise-induced loss classically notches at 4000 Hz. Ototoxic drugs are aminoglycosides, cisplatin, loop diuretics, and high-dose salicylates; salicylate and loop-diuretic effects are often reversible, whereas aminoglycoside and cisplatin damage tends to be permanent, and aminoglycosides plus loop diuretics compound the risk.

Sudden hearing loss and vestibular schwannoma

Sudden sensorineural hearing loss is rapid unilateral SNHL developing over hours to 3 days, an otologic emergency.

Confirm it is sensorineuralWeber lateralizes to the good ear, and the canal is clear (rule out cerumen); confirm with audiometry.
Steroids promptlyOffer high-dose oral corticosteroids within 2 weeks (shared decision); intratympanic if systemic steroids are contraindicated or as salvage for incomplete recovery. Antivirals and routine CT are not recommended.
MRIGadolinium MRI of the internal auditory canals to exclude a vestibular schwannoma.

Sudden SNHL

Vestibular schwannoma (acoustic neuroma). A CN VIII tumor at the cerebellopontine angle causing progressive unilateral sensorineural loss, tinnitus, and imbalance. As it grows it compresses CN V (a reduced corneal reflex) and CN VII. Diagnose with gadolinium MRI; options are observation, surgery, or stereotactic radiosurgery.

Any asymmetric or unilateral SNHL needs an MRI. Bilateral vestibular schwannomas mean neurofibromatosis type 2.

Peripheral vertigo syndromes

Timing and hearing sort the peripheral causes. Ask how long each episode lasts, what triggers it, and whether hearing is affected.

Peripheral vertigo by duration

Disorder	Duration and trigger	Hearing	Key test and treatment
BPPV	Under 1 minute; head-position change (rolling in bed, looking up)	Normal	Dix-Hallpike provokes fatigable upbeat-torsional nystagmus; Epley maneuver
Meniere disease	Episodes of 20 minutes to hours	Fluctuating low-frequency SNHL, tinnitus, aural fullness	Low-salt diet and diuretics; avoid caffeine and alcohol; intratympanic gentamicin if refractory
Vestibular neuritis	Continuous for days, after a viral illness	Normal	Unidirectional horizontal nystagmus; short-term suppressants, steroids may help
Labyrinthitis	Continuous for days	Hearing loss	Same as neuritis, plus hearing assessment

BPPV is the most common cause of peripheral vertigo: displaced otoconia in the posterior semicircular canal. The Epley canalith-repositioning maneuver returns them to the utricle and resolves most cases, so intratympanic gentamicin, steroids, and long-term meclizine have no role.

Meniere disease results from endolymphatic hydrops; the full tetrad is episodic vertigo, fluctuating low-frequency sensorineural loss, tinnitus, and aural fullness.

Vestibular suppressants such as meclizine are for a few days at most; prolonged use delays central compensation. Vestibular rehabilitation helps recovery after neuritis.

Central versus peripheral vertigo and HINTS

Peripheral versus central vertigo

Feature	Peripheral	Central (brainstem or cerebellum)
Nystagmus	Horizontal or rotatory; unidirectional; fatigable	Vertical or direction-changing
Visual fixation	Suppresses the nystagmus	Does not suppress it
Nausea	Severe	Variable; imbalance often dominates
Neuro exam	Normal	Diplopia, dysarthria, ataxia suggest stroke

HINTS. In acute, continuous vertigo with ongoing nystagmus, the three-step HINTS exam outperforms early MRI, which can miss a small posterior circulation stroke in the first day or two.

Head ImpulseA corrective saccade (abnormal) = peripheral; a normal impulse = central.
NystagmusUnidirectional = peripheral; direction-changing = central.
Test of SkewVertical skew deviation on cover testing = central.

HINTS for acute vertigo

A NORMAL head-impulse test in an acutely vertiginous patient is worrisome for stroke. Any central feature (normal impulse, direction-changing nystagmus, or skew) means a posterior circulation stroke until proven otherwise.