Commentary on "Assessment of the Eustachian tube: a review"

Aldè, Mirko; Cantarella, Giovanna

doi:10.1007/s00405-023-08241-0

Cited by 1 publication

(1 citation statement)

References 5 publications

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“…Therefore, the typical clinical picture consistent with a TMWM includes vestibular symptoms such as sound/pressure-induced nystagmus (also known as Tullio phenomenon and Hennebert's sign, respectively) and chronic imbalance, and auditory manifestations such as autophony, aural fullness, bone-conducted (BC) sound hyperacusis, hearing loss (HL) and pulsatile tinnitus [1][2][3][4][5][6][7][8]. Even though aural fullness and autophony can also be found in both patulous Eustachian tube and SCD, patients with a patulous Eustachian tube generally have autophony for their own breath sounds, while patients with SCD usually do not [9]. Besides SCD, other conditions resulting in a TMWM have been described over the years, including an enlarged vestibular aqueduct, X-linked gusher disorder and cochlear dehiscence either involving the internal carotid artery or the facial nerve (FN) [3,5,6,[10][11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

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

Castellucci,

Dumas,

Abuzaid

et al. 2024

Audiology Research

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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.

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