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.
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 ().