A 46-year-old man with a history of left ear discharge presented with newly onset HL and vertigo. His medical history was otherwise silent besides head trauma (car accident) that occurred seven months prior to the admission with residual positional vertigo. He denied oscillopsia, pressure-induced vertigo, or other vestibular symptoms. The otoscopy revealed a left thickened tympanic membrane with EAC discharge. Audiometric testing showed down-sloping sensorineural HL on the right and left-sided mixed HL with predominant conductive loss for low frequencies (). Right-beating spontaneous nystagmus enhanced by mastoid vibrations consistent with left acute vestibular loss could be observed on video-Frenzel examination. Nystagmus reduced in backward head bending, while increased with downbeat components in forward head tilts. Left Dix-Hallpike maneuver elicited paroxysmal up-beating nystagmus with left torsional components consistent with benign paroxysmal positional vertigo (BPPV) involving left-sided PSC, so he received Epley's repositioning procedures (). At the following examination 2 days later, positioning tests were uneventful, whereas right-beating spontaneous nystagmus enhanced by head shakings could be still detectable. Left tragal compression induced right-torsional nystagmus, followed by stronger opposite eye movements on release of the pressure (), whereas both nasal and glottic Valsalva maneuvers were uneventful. The patient underwent vHIT measurements on the same day, showing left global hypofunction and slightly reduced VOR-gain for the right PSC (). Temporal bones CT scan revealed soft tissue consistent with cholesteatoma obliterating the right-sided tympano-mastoid cavity and eroding ossicular chain, all SCs, sigmoid sinus bony wall, and tegmen tympani (). Angio-MRI of the brain ruled out venous thrombosis and meningeal involvement (). He received CWD mastoidectomy that evidenced bony erosions of each SC and permitted achievement of cholesteatoma removal. A thin matrix layer was left upon each bony defect, whereas tegmen dehiscence was repaired with bone-pate. Additional procedures for hearing restoration and LF obliteration were postponed at a later stage. Postoperative care included bed rest, intravenous broad-spectrum antibiotics, and corticosteroids tapering for additional two weeks. The patient's conditions progressively recovered and hearing threshold remained unchanged at 30 days. Spontaneous nystagmus was progressively reduced whereas vHIT findings and PIN aligning in the same axis persisted over time.\nWritten informed consent was obtained from each patient for the publication of this case report, including all data and images.
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.