Objective: Computed tomography (CT) images of the temporal bone of large vestibular aqueduct syndrome (LVAS) patients were used to establish 3D numerical models based on the structure of the inner ear, which are, in turn, used to construct inner ear fluid-solid coupling models. The physiological features and pathophysiology of LVAS were analyzed from a biomechanical perspective using finite element analysis. Methods: CT images of the temporal bone were collected from five children attending the Second Hospital of Dalian Medical University in 2022. The CT images were used to build 3D models of the inner ear containing the vestibular aqueduct (VA) by Mimics and Geomagic software, and round window membrane models and fluid-solid coupling models were built by ANSYS software to perform fluid-solid coupling analysis. Results: By applying different pressure loads, the deformation of the round window membranes occurred, and their trend was basically the same as that of the load. The deformation and stress of the round window membranes increased with the increase in load. Under the same load, the deformation and stress of the round window membranes increased with the expansion of the midpoint width of the VA. Conclusion: CT images of the temporal bone used clinically could establish a complete 3D numerical model of the inner ear containing VA. Fluctuations in cerebrospinal fluid pressure could affect inner ear pressure, and VA had a limiting effect on the pressure from cerebrospinal fluid. The larger the VA, the smaller the limiting effect on the pressure.

UNASSIGNED: Anatomical variations of the inner ear may contribute to the development of Ménière\'s disease (MD), which is a complex inner ear disorder histopathologically characterized by idiopathic endolymphatic hydrops (ELH). Abnormalities of the vestibular aqueduct (VA) and the jugular bulb (JB) have been suggested as predisposing factors. Yet, few studies have investigated the correlation between JB abnormalities and VA variations as well as its clinical relevance in these patients. In this retrospective study, we investigated the differences in the incidence of radiological abnormalities of the VA and JB in patients with definite MD.
UNASSIGNED: Anatomical variations of JB and VA were evaluated based on high-resolution CT (HRCT) in a series of 103 patients with MD (93 unilateral cases and 10 bilateral cases). JB-related indices included JB anteroposterior and mediolateral diameter, JB height, JB type regarding to Manjila classification system, and incidences of JB diverticulum (JBD), JB related inner ear dehiscence (JBID), and inner ear adjacent JB (IAJB). VA-related indices included CT-VA visibility, CT-VA morphology (funnel, tubular, filiform, hollow, and obliterated-shaped type), and peri-VA pneumatization. Radiological indices were compared between MD ears and control ears.
UNASSIGNED: Radiological JB abnormalities were comparable between MD ears and control ears. As for VA-related indices, the CT-VA visibility was lower in MD ears than in control ears (p = 0.004). The distribution of CT-VA morphology was significantly different between MD and control ears (p = 0.013), with a higher proportion of obliterated-shaped type in MD ears (22.1%) than in control ears (6.6%).
UNASSIGNED: Compared with JB abnormalities, the anatomical variations of VA are more likely to be an anatomically predisposing factor for MD.

Improved radiological examinations with newly developed 3D models may increase understanding of Meniere\'s disease (MD). The morphology and course of the vestibular aqueduct (VA) in the temporal bone might be related to the severity of MD. The presented study explored, if the VA of MD and non-MD patients can be grouped relative to its angle to the semicircular canals (SCC) and length using a 3D model. Scans of temporal bone specimens (TBS) were performed using micro-CT and micro flat panel volume computed tomography (mfpVCT). Furthermore, scans were carried out in patients and TBS by computed tomography (CT). The angle between the VA and the three SCC, as well as the length of the VA were measured. From these data, a 3D model was constructed to develop the vestibular aqueduct score (VAS). Using different imaging modalities it was demonstrated that angle measurements of the VA are reliable and can be effectively used for detailed diagnostic investigation. To test the clinical relevance, the VAS was applied on MD and on non-MD patients. Length and angle values from MD patients differed from non-MD patients. In MD patients, significantly higher numbers of VAs could be assigned to a distinct group of the VAS. In addition, it was tested, whether the outcome of a treatment option for MD can be correlated to the VAS.

BACKGROUND: Although, the diagnostic criteria for enlarged vestibular aqueduct syndrome (EVAS) were determined by years. On the shoulders of predecessors, we still detected some new discoveries about EVAS by using 3D-real IR MRI.
OBJECTIVE: To analyze the signal intensity of membranous and osseous labyrinths of vestibular aqueduct (VA) and endolymphatic sac (ES) in EVAS using three-dimensional real inversion recovery (3D-Real-IR) magnetic resonance imaging (MRI) after intratympanic injection of gadolinium.
METHODS: The study is a prospective trial, diagnosed EVAS patients (n = 10) and none- patients (n = 10) were included. 3D-real-IR MRIs were performed to assess the endolymphatic hydrops (EH) and differentiated the endolymphatic and perilymphatic signal intensities of VA and ES.
RESULTS: Compared to control group, EVAS group had VA osseous labyrinths middle diameter >1.5 mm different from membranous labyrinths. The cochlear EH was correlated with Mondini malformation and irrelation with the level of hearing loss (HL).
CONCLUSIONS: Interspace of osseous labyrinths of VA and ES are much larger than their membranous labyrinths, which is not consistance with previous research. And cochlear Mondini malformation may cause endolymphatic fluid malabsorption, inducing cochlear EH. Osteal ampliative of VA and ES and cochlear EH, which are morphogenetic anomalies, may not the direct cause of HL in EVAS.