An 83-year-old female presented with long-lasting left ear discharge, hearing loss (HL), and recent onset of headache. Her history was consistent with bilateral chronic otitis media (COM) and diabetes mellitus, whereas she denied oscillopsia, pressure-induced vertigo, or other vestibular symptoms. On otoscopy, her left EAC was obliterated by polypoid soft tissue. Pure tone audiometry detected ipsilateral profound HL and right-sided mixed HL (). Vestibular examination with video-Frenzel goggles showed neither spontaneous nor positional nystagmus. Nevertheless, left tragal compression evoked strong left-beating horizontal nystagmus that reversed on release of the positive pressure on EAC (). Neither glottic nor nasal Valsalva maneuver resulted in detectable nystagmus or vertigo. An ICS Impulse device (Otometrics, Natus Medical Inc, Denmark) was used to measure VOR-gain values for all six SCs on the same day. Gains were considered normal if >0.8 for horizontal SCs and >0.7 for vertical canals (). vHIT highlighted left global canal deficit and slight right-sided posterior SC (PSC) hypofunction (). Bedside oculomotor testing excluded signs of impaired function of central vestibular pathways. Temporal bones CT scan showed soft tissue occupying the left EAC, mastoid, and tympanic cavities with bony erosion involving ossicular chain, HSC, fallopian canal, tympanic medial wall, and tegmen tympani (). Magnetic resonance imaging (MRI) of the brain showed contrast enhanced tissue invading the intracranial compartment through superior and posteromedial walls of the temporal bone (). Histologic examination of the polypoid tissue within the left EAC was consistent with squamous cell carcinoma. Diagnosis of T4-stage disease according to the modified Pittsburgh staging system () was made, and the patient was addressed to palliative radiation therapy.
Patient 2. A 22-year-old man suffered sudden vestibular damage in the context of his cholesteatomatous chronic otitis media. The fistula test (performed as above) was negative and the bedside head impulse test was positive. With the vHIT we were able to record a very low gain for head impulses towards the affected side with covert and overt refixation saccades as a response to the vestibular deficit and because of the spontaneous nystagmus beating towards the normal ear as well as anticompensatory quick eye movements for head movements towards the nonaffected side ().