Superior semicircular canal dehiscence (SSCD) is a defect of the middle cranial fossa
floor (MCFF) in which an anomalous opening is present between the vestibular system
and the intracranial space. This rare defect correlates with a syndrome consisting
of auditory and vestibular symptoms in some patients.1 Improvement in clinical outcomes has been shown in symptomatic patients after SSCD
repair through a middle cranial fossa approach.2 However, this defect's etiology remains unknown. Some associations have been shown
between SSCD and bone thinning or dehiscence of nearby structures in the MCFF.3 However, this finding has not been examined in a large SSCD surgical series. In this
study, we investigated the prevalence of bone thinning or dehiscence in key areas
of the MCFF in SSCD patients compared with normal patients. Computed tomography (CT)
was used to measure bone thickness and qualitatively assess osseous quality of key
areas of the MCFF. We retrospectively reviewed routine preoperative temporal bone
CTs of SSCD patients undergoing repair between March 2011 and June 2017, along with
CTs of non-SSCD patients' non-affected ear status post temporal bone fracture. Bone
thickness and/or dehiscence and quality of bone overlying both the geniculate ganglion
(GG) and over the midpoint of the internal auditory canal (IAC) were measured. Additionally,
extent of bony covering of the tegmen tympani was recorded. 100 patients undergoing
118 surgeries were identified, for a total of 200 ears. Twelve ears were excluded
due to lack of preoperative CT or history of prior SSCD repair at an outside facility.
101 CTs of normal patients with temporal bone fractures were identified, for a total
of 101 ears. Twenty-six ears were excluded due to lack of equivalent imaging. Preliminary
univariate analyses reveal SSCD diagnosis to be associated with higher rates of GG
dehiscence compared with non-SSCD diagnosis (42.6 vs. 24.0%; Χ
2 (1) = 7.89, p = 0.00496). For patients without GG dehiscence, the study found that individuals
with SSCD had statistically significantly thinner bone overlying the GG (0.22 ± 0.12
cm) compared with normal patients (0.28 ± 0.18 cm), t(164) = 2.462, p = 0.015. Further statistical analyses of measurements of other surrounding structures
are forthcoming. This study demonstrates increased incidence of bone thinning or dehiscence
of the MCFF in SSCD patients when compared with normal patients, suggesting that the
etiology of SSCD may also affect surrounding structures. Furthermore, this underscores
the importance of considering skull base defects that may predispose patients to facial
nerve damage during SSCD repair surgery.