Posterior Semicircular Canal Dehiscence with Vestibulo-Ocular Reflex Reduction for the Affected Canal at the Video-Head Impulse Test: Considerations to Pathomechanisms

• Published in: Audiology research Vol. 14; no. 2; pp. 317 - 333
• Main Authors: Castellucci, Andrea, Dumas, Georges, Abuzaid, Sawsan M, Armato, Enrico, Martellucci, Salvatore, Malara, Pasquale, Alfarghal, Mohamad, Ruberto, Rosanna Rita, Brizzi, Pasquale, Ghidini, Angelo, Comacchio, Francesco, Schmerber, Sébastien
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 24.03.2024; MDPI
• Subjects: Audiometry; conductive hearing loss; horizontal canal dehiscence; Life Sciences; Patients; posterior canal dehiscence; Sound; third mobile window; Tinnitus; Vertigo; vestibular evoked myogenic potentials; video-head impulse test; conductive hearing loss; Meniere’s disease; video-head impulse test; posterior canal dehiscence; third mobile window; vestibular evoked myogenic potentials; horizontal canal dehiscence; Meniere's disease
• ISSN: 2039-4330; 2039-4349; 2039-4349
• DOI: 10.3390/audiolres14020028

Posterior semicircular canal dehiscence (PSCD) has been demonstrated to result in a third mobile window mechanism (TMWM) in the inner ear similar to superior semicircular canal dehiscence (SSCD). Typical clinical and instrumental features of TMWM, including low-frequency conductive hearing loss (CHL), autophony, pulsatile tinnitus, sound/pressure-induced vertigo and enhanced vestibular-evoked myogenic potentials, have been widely described in cases with PSCD. Nevertheless, video-head impulse test (vHIT) results have been poorly investigated. Here, we present six patients with PSCD presenting with a clinical scenario consistent with a TMWM and an impaired vestibulo-ocular reflex (VOR) for the affected canal on vHIT. In two cases, an additional dehiscence between the facial nerve and the horizontal semicircular canal (HSC) was detected, leading to a concurrent VOR impairment for the HSC. While in SSCD, a VOR gain reduction could be ascribed to a spontaneous "auto-plugging" process due to a dural prolapse into the canal, the same pathomechanism is difficult to conceive in PSCD due to a different anatomical position, making a dural herniation less likely. Alternative putative pathomechanisms are discussed, including an endolymphatic flow dissipation during head impulses as already hypothesized in SSCD. The association of symptoms/signs consistent with TMWM and a reduced VOR gain for the posterior canal might address the diagnosis toward PSCD.