目的：确定在平板CT上发现的上管裂开（SCD）是否会增加耳胶囊中其他缺陷的风险。
方法：回顾性队列研究。
方法：三级护理中心。
方法：一百只耳朵（50只患有SCD，50只没有SCD的对照组）。
方法：平板CT成像。
方法：（1）SCD耳朵中其他开裂的患病率，(2)控制装置的开裂，和(3)其他报告的裂开位置的耳囊厚度(耳蜗-颈动脉，外侧半规管[SCC]和乳突，面神经外侧SCC，前庭水管,后SCC-颈静脉球，后SCC-后颅窝）。在应用Bonferroni校正进行多重比较后，组间比较在p<0.007时被认为是显著的。
结果：不包括SCD，SCD组（n=2/50，4％）和对照组（n=2/50，4％，p>0.007)。在SCD组中，耳蜗和颈动脉之间有一个裂开,后SCC和后颅窝之间有一个裂开.对照组有一个扩大的前庭水管和一个在面神经和外侧SCC之间的裂开。作为一个群体,SCD耳朵的前庭水管较宽（0.68±0.20vs0.51±0.30mm，p<0.007），后SCC和后窝之间的骨骼较薄（3.12±1.43vs4.34±1.67mm，p<0.007)。SCD耳中面神经与外侧SCC之间的骨较厚（0.77±0.23vs0.55±0.27mm，p<0.007)，耳蜗颈动脉没有差异，外侧SCC和乳突（p>0.007）。
结论：SCD不会增加同一耳胶囊中第二次开裂的可能性。与对照组相比，SCD患者的先天性耳囊骨可能更薄，特别是在后SCC附近，前庭导水管可能会扩大。
OBJECTIVE: Determine if superior canal dehiscence (SCD) found on flat-panel CT increases the risk for other defects in the otic capsule.
METHODS: Retrospective cohort
study.
METHODS: Tertiary care center.
METHODS: One hundred ears (50 with SCD and 50 matched controls without SCD).
METHODS: Flat-panel CT imaging.
METHODS: (1) Prevalence of other dehiscences in SCD ears, (2) dehiscences in controls, and (3) otic capsule thickness in other reported dehiscence locations (cochlea-carotid, lateral semicircular canal [SCC] and mastoid, facial nerve-lateral SCC, vestibular aqueduct, posterior SCC-jugular bulb, posterior SCC-posterior fossa). Between-group comparisons were considered significant at p < 0.007 after applying the Bonferroni correction for multiple comparisons.
RESULTS: Not including the SCD, there was a mean of 0.04 additional dehiscences in the SCD group (n = 2/50, 4%) and 0.04 non-SCD dehiscences in the controls (n = 2/50, 4%, p > 0.007). In the SCD group, there was one dehiscence between the cochlea and carotid artery and one between the posterior SCC and posterior fossa. The control group had one enlarged vestibular aqueduct and one dehiscence between the facial nerve and lateral SCC. As a group, SCD ears had wider vestibular aqueducts (0.68 ± 0.20 vs 0.51 ± 0.30 mm, p < 0.007) and thinner bone between the posterior SCC and posterior fossa (3.12 ± 1.43 vs 4.34 ± 1.67 mm, p < 0.007). The bone between the facial nerve and lateral SCC was thicker in SCD ears (0.77 ± 0.23 vs 0.55 ± 0.27 mm, p < 0.007) and no different for cochlea-carotid, and lateral SCC and mastoid (p > 0.007).
CONCLUSIONS: SCD does not increase the likelihood of a second dehiscence in the same otic capsule. SCD patients may have congenitally thinner otic capsule bones compared to controls, particularly near the posterior SCC, where the vestibular aqueduct may be enlarged.
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