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.
A 73-year-old woman referred to our center for a follow-up evaluation of right-sided canal wall down (CWD) mastoidectomy due to a COM with cholesteatoma. The surgical procedure was conducted two years earlier without simultaneous functional stage. She experienced symptoms consistent with right-sided cochleo-vestibular loss following surgery. Pressure-induced unsteadiness and dizziness represented her prominent residual vestibular symptoms. Otoscopy highlighted dry right EAC and well-preserved postoperative conditions. Her audiogram showed right-sided mixed HL with widened air-bone gap at lower frequencies and contralateral age-related sensorineural HL (). Although spontaneous nystagmus could not be observed with video-Frenzel goggles, mastoid vibrations elicited left-beating nystagmus. Horizontal nystagmus directed toward the affected side was evoked applying positive pressure on her right EAC, reversing on removal of the pressure. Conversely, no nystagmus could be noticed with Valsalva maneuvers. Even though she denied positional vertigo, left-beating nystagmus could be observed on supine positioning and slightly persistent geotropic direction-changing nystagmus was elicited after head rolls, with stronger amplitude on right-sided positioning (). vHIT measurements were taken on the same day, showing VOR-gain reduction for all SCs of the right side and mildly impaired function for left PSC (). High-resolution CT scan detected postoperative LF involving right HSC without inflammatory recurrences (). Although we proposed revision surgery for LF closure and hearing restoration, she refused additional procedures as audio-vestibular symptoms did not prevent her from leading a normal life.