Thickness of the Bony Otic Capsule: Etiopathogenetic Perspectives on Superior Canal Dehiscence Syndrome

Abstract

The etiology of superior canal dehiscence (SCD) is controversial. An embryological perspective suggests that SCD may occur through the failure of postnatal bone formation over the superior semicircular canal (SC), whereas an acquired theory suggests that trauma or pressure from the overlying temporal lobe could break or gradually thin the SC. We infer the etiology of SCD by comparing the thickness of the bony otic capsule of the unaffected side of SCD patients with that of non-SCD participants. Twelve SCD patients (13 SCD ears and 11 normal ears) and 34 age-matched controls (68 ears) were included. The control group was subdivided into an aerated group (49 ears) and a nonaerated group (19 ears), as defined by the presence of air cells above the SC. A high-resolution temporal bone CT was performed in all participants. The thicknesses of the SC, horizontal canal (HC) and posterior canal (PC) of the unaffected ears of SCD patients were compared with those of the controls. The SC of the unaffected side in the SCD group (n = 11, 0.41 ± 0.23 mm) was significantly thinner than the one in the control group (n = 68, 0.64 ± 0.21 mm, p = 0.002). The HC and PC were also thinner in the SCD group (n = 24, 0.58 ± 0.11 and 1.39 ± 0.31 mm, respectively) than in the controls (0.70 ± 0.08 and 1.61 ± 0.32 mm; p < 0.0001 and p = 0.005, respectively). The SC, HC and PC thicknesses were also compared between the aerated and nonaerated ears within the control group. The SC was significantly thicker in the aerated group (0.73 ± 0.14 mm) than in the nonaerated group (0.60 ± 0.23 mm; p = 0.046); however, no significant difference was observed for the HC and PC thickness (aerated group, n = 49, 0.72 ± 0.07 and 1.67 ± 0.34 mm; nonaerated group, n = 19, 0.70 ± 0.09 and 1.59 ± 0.34 mm; p = 0.350 and p = 0.428, respectively). The bony otic capsule was significantly thinner in the SCD patients than in the controls. However, even within unaffected individuals, SCs lacking overlying air cells were also thinner than those with overlying air cells. These results suggest that both embryological and acquired factors affect the occurrence of SCD.

Anatomical Characteristics of Facial Nerve and Cochlea Interaction

“…We examined whether CD and SSCD coexist, suggesting a general thinning of the OC as a causative factor. According to Park et al [2015] the bony OC is significantly thinner in SSCD patients than in controls. We found that the CFD was reduced in SSCD but not in SSCC "blue line".…”

Superior Canal Dehiscence Syndrome: Lessons from the First 20 Years

“…However, many patients do not report an inciting event. It may therefore be some combination of congenital and acquired pathology (112). Identifying the etiology is important for purposes of treatment, for if the etiology can be identified, research toward medical management may become feasible.…”

Evidence of Osteoclastic Activity in the Human Temporal Bone

“…Since Minor et al [1998] initially reported SSCD syndrome in 1998, the etiology of SSCD has been debated [Minor et al, 1998;Takahashi et al, 2012;Chilvers and McKay-Davies, 2015;Park et al, 2015;Schutt et al, 2015]. Congenital, acquired, or both factors have been reported to be involved in the pathogenesis of SSCD [Nadgir et al, 2011;Takahashi et al, 2012;Yu et al, 2012;Park et al, 2015;Schutt et al, 2015;Sugihara et al, 2016]. Takahashi et al [2012] proposed a congenital factor based on macroscopic observation and CT scans of adult and fetal cadavers.…”

“…Nadgir et al [2011] demonstrated an increased radiologic prevalence of SSCD among older age groups in 608 CT examinations of the temporal bone and suggested that SSCD is more commonly due to an acquired rather than a congenital condition. Moreover, Park et al [2015] suggested that both congenital/developmental thinning of the bony otic capsule and an acquired factor such as increased intracranial pressure are involved in the formation of SSCD. The presence of microcavitations at the middle fossa floor and superior semicircular canal in the 3 patients with SSCD suggests that osteoclastic activity may play a role in the formation of SSCD and supports, or at least does not preclude, previous reports proposing an acquired factor as causative of SSCD [Nagdir et al, 2011;Yu et al, 2012;Schutt et al, 2015].…”

“…Microcavitations were also seen in 3 cases with SSCD. The etiology of this syndrome and whether it is congenital or acquired are unknown [Minor et al, 1998;Takahashi et al, 2012;Chilvers and McKayDavies, 2015;Park et al, 2015;Schutt et al, 2015].…”