Vestibular Aqueduct Grading: an Early Predictor of Progression from Low-Frequency Sensorineural Hearing Loss to Ménière’s Disease

Vestibular Aqueduct Grading: an Early Predictor of Progression from Low-Frequency Sensorineural Hearing Loss to Ménière’s Disease | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Vestibular Aqueduct Grading: an Early Predictor of Progression from Low-Frequency Sensorineural Hearing Loss to Ménière’s Disease Linglan Gu, Qianru Wu, Rujian Hong, Yongzhen Wu, Wuqing Wang, and 1 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7224413/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Objective This study investigated vestibular aqueduct (VA) morphology in acute low-frequency sensorineural hearing loss (ALHL) and Ménière’s disease (MD), assessing its association with endolymphatic hydrops (EH) and potential as a predictor for ALHL progression to MD. Methods A retrospective analysis of 135 patients (ALHL = 67, MD = 44, controls = 24) conducted between March 2019 and July 2024 utilized MRI-T2 for VA grading (Grade 0: continuous; Grade 1: discontinuous; Grade 2: non-visible) and 3D real inversion recovery (IR) sequences for EH detection. Results The cohort comprised 135 patients (66 males, 69 females; mean age 45.00 ± 13.79 years), stratified into ALHL (n = 67; 32 without EH, 35 with EH), MD (n = 44), and control (n = 24) groups. Mean age increased progressively from ALHL without EH to ALHL with EH and MD groups (P < 0.0001). VA grading differed significantly between the MD and control groups (P < 0.0001) and between ALHL and control groups (P < 0.05). ALHL without EH showed no VA differences compared to controls. ALHL with EH exhibited VA patterns resembling MD (P = 0.985) and bilateral VA asymmetry (affected vs. unaffected ears, P < 0.05). Grade 2 VA conferred a 5.1-fold increased risk of EH (P = 0.008). During follow-up, 10.45% of ALHL patients progressed to MD, exclusively within the EH subgroup (20% of this subgroup), with 85.7% of progressions occurring in Grade 2 VA patients. Conclusion MRI-T2 thin-slice SPACE sequences can reliably assess VA grading, revealing parallels between ALHL with EH and MD. Elevated VA grades, particularly grade 2, in patients with ALHL serve as predictive indicators for disease progression, with the VA grading system demonstrating clinical value for risk stratification and early MD diagnosis. Vestibular Aqueduct Acute Low-Frequency Sensorineural Hearing Loss Ménière’s Disease Endolymphatic Hydrops Magnetic Resonance Imaging Figures Figure 1 Figure 2 Figure 3 Figure 4 Introduction Acute Low-Frequency Sensorineural Hearing Loss (ALHL) is an idiopathic sudden-onset auditory condition, primarily characterized by symptoms such as aural fullness, low-frequency sensorineural hearing loss, tinnitus, and hyperacusis. The incidence of ALHL is approximately 40–60 per 100,000, with a higher prevalence among young adults[ 1 ]. Although ALHL exhibits higher spontaneous recovery rates than other forms of sudden sensorineural hearing loss, its 15.2% recurrence rate significantly exceeds that of comparable disorders[ 2 ]. The diagnostic criteria for Ménière's disease (MD), a debilitating otological condition, share diagnostic overlap with ALHL, as transient ALHL recovery on serial audiograms supports the diagnosis of MD[ 3 ]. Approximately 10–30% of patients with ALHL progress to MD within three years, and this proportion increases with longer follow-up periods[ 4 ]. While endolymphatic hydrops (EH) constitutes the pathological hallmark of MD, its exact role in disease mechanisms remains unclear. Importantly, EH is also frequently observed in ALHL, with emerging evidence suggesting its association with MD progression[ 5 ]. Shimono et al. reported that EH in ALHL patients involves both cochlear and vestibular compartments, similar to EH in MD[ 6 ]. Therefore, understanding the mechanism of ALHL with EH and identifying factors that might drive EH progression remains crucial. The endolymphatic duct (ED) leads to the blind-ending endolymphatic sac (ES) through the vestibular aqueduct (VA), a bony channel running from the medial wall of the vestibule to the posterior surface of the petrous bone. Histological studies have demonstrated hypoplasia of the VA, atrophy of the ES, and ED luminal narrowing in MD patients[ 7 , 8 ]. Congenital hypoplasia of the VA and calcium ion augmentation in hydropic ears may exacerbate VA calcification and stenosis, potentially disrupting endolymphatic flow and contributing to inner ear dysfunction[ 9 ]. Histopathologically, the VA and ES were detected to be shorter in MD patients compared to healthy individuals[ 7 ]. Numerous scholars have reported that morphological abnormalities of the VA on imaging are significantly associated with EH[ 10 – 12 ]. Morphological abnormalities of the VA are significantly associated with the clinical diagnosis of MD with a sensitivity of 90%, and can also be detected in asymptomatic ears[ 10 ]. Based on these observations, we hypothesize that VA morphological abnormalities may serve as early predictors in the development and progression of ALHL to MD. The goal of this retrospective study was to evaluate the clinical characteristics and VA morphology assessed by MRI in ALHL patients with and without EH, as well as in MD patients. We aimed to gain a deeper understanding of the relationship between VA and EH, as well as the disease correlation between ALHL and MD. Materials and Methods 2.1 Participants This single-center retrospective study was conducted at a tertiary referral hospital. This study was conducted in accordance with the Declaration of Helsinki and was approved by the local institutional Ethics Committee (permit number 2022054), and the requirement for informed consent was waived due to the retrospective analysis of anonymized clinical data. A total of 135 patients were enrolled between March 2019 and July 2024, stratified into three groups: the ALHL group, the MD group and the control group. Analyses focused on affected ears in the ALHL and MD groups, and healthy ears in the control group. All participants underwent standardized diagnostic evaluations, including a thorough history inquiry, otoscopy, audiometry, and imaging examination, conducted by otologists at the Department of Otology and Skull Base Surgery of the Eye, Ear, Nose and Throat Hospital, Fudan University. Unilateral definite MD was diagnosed according to the 2015 diagnostic criteria established by the Bárány Society[ 3 ]. The inclusion criteria for ALHL were as follows: (1) unilateral unfluctuating sensorineural hearing loss with sudden onset that occurs within 72 h or less; (2) low-tone hearing loss, i.e., the sum of hearing levels at 0.125, 0.25 and 0.5 kHz is 70 dB or greater and the sum of hearing levels at 2, 4 and 8 kHz is 60 dB or less; (3) without vertigo; (4) no identifiable cause. The exclusion criteria for ALHL were as follows: (1) middle or inner ear infections (otitis media, mastoiditis, labyrinthitis, etc.); (2) bilateral hearing loss; (3) having received previous ear surgery or intratympanic injections; (4) neurological diseases; (5) head trauma; (6) immunological diseases. Patients in the control group were suffering unilateral ES tumor, unilateral acoustic neuroma, or unilateral vestibular or cochlear occupation, without EH in healthy ears. 2.2 Radiological evaluations All imaging examinations were carried out on a 3T MRI scanner (Magnetom Verio, Siemens Healthineers, Erlangen, Germany) with an 8-channel ear-surface phased-array coil, 4 hours after undergoing intravenous injection with the double dose (0.4 mL/kg) of gadolinium (ProHance, Bracco Imaging Italia SRL, Milano, Italy). The T2 SPACE and three-dimensional real inversion recovery (3D-real IR) sequences were applied in all patients. The parameters for the T2 SPACE sequence were as follows: slice thickness 0.6 mm, repetition time 1000 ms, echo time 132 ms, flip angle 120◦, matrix size 384 × 384, field of view 200 mm × 200 mm, scan time 2 min 44 s. The parameters for the 3D-real IR sequence were as follows: slice thickness 0.6 mm, repetition time 6000 ms, echo time 181 ms, flip angle 180◦, matrix size 768 × 768, field of view 160 mm × 160 mm, scan time 15 min 20 s. All images were independently reviewed by an experienced neuroradiologist and a senior otolaryngologist blinded to clinical diagnoses. Inter-reader agreement for VA grading was evaluated using Cohen's kappa coefficient, with values > 0.80 indicating very good agreement. 2.2.1 Evaluation of the VA The T2 SPACE sequence was used to evaluate the VA and exclude middle ear or neurological disorders. The VA was defined as a linear bony duct extending from the vestibule to the posterior temporal bone surface. A three-stage grading system was applied (Fig. 1 ): Grade 0: Continuous VA throughout its course. Grade 1: Discontinuous VA with partial visibility. Grade 2: Complete non-visualization of VA. 2.2.2 Evaluation of EH An enlarged endolymphatic space was considered as having a large negative signal dilating to the contrast-enhanced signal of the perilymphatic space on 3D-real IR sequences. For vestibular hydrops quantification, the endolymphatic space ratio was calculated by dividing the endolymphatic area by the total vestibular fluid space (endolymph + perilymph), with a threshold ratio of 1/3 used to differentiate non-hydropic (≤ 1/3) from hydropic (> 1/3) status. In the cochlea, patients with no hydrops showed no displacement of Reissner’s membrane. Based on these imaging criteria, the ALHL cohort was stratified into two subgroups: ALHL with EH and ALHL without EH. 2.3 Follow-up of patients in ALHL group All patients in the ALHL group were followed up until December 31, 2024. Progression to Ménière’s disease (MD) was defined as the occurrence of two or more spontaneous vertigo episodes, each lasting between 20 minutes and 12 hours, during the follow-up period. 2.4 Statistical analysis The statistical data were analyzed using SPSS Statistics (Version 20.0, SPSS, Inc., Chicago, IL). Categorical variables were compared using the Chi-square test or Fisher’s exact test, while continuous variables were analyzed using the two-sample t-test, analysis of variance (ANOVA), or Mann–Whitney U test, as appropriate. Statistical significance was set at p ≤ 0.05, and continuous data were presented as mean ± standard deviation (SD). Additionally, diagnostic performance metrics, including sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV), were calculated for MRI findings in the MD group compared to controls. Figures were generated using GraphPad Prism (Version 10.1.2, GraphPad Software, San Diego, CA). Results 3.1 Patient Characteristics A total of 135 patients (66 males, 69 females) were enrolled and stratified into three groups: ALHL group (n = 67; 32 without EH and 35 with EH), MD group (n = 44), and control group (n = 24). No significant differences were observed in gender distribution or laterality between groups (P > 0.05), whereas age differed significantly among the four groups (P < 0.0001). Post hoc analysis revealed significant age differences between the ALHL without EH subgroup, ALHL with EH subgroup, and MD group (P 0.05). Within the ALHL group, patients were further classified based on episode frequency into single-episode and recurrent-episode (≥ 2) subgroups. Although no significant association was observed between episode frequency and EH (P = 0.07), patients with recurrent episodes demonstrated a notably higher risk of developing EH in the affected ear (odds ratio [OR] = 3.556, 95% confidence interval [CI]: 0.852–14.836) (Table 1). Table 1 Characteristics of Patients in Different Groups ALHL without EH Group ALHL with EH Group MD group Control group P value (n = 32) (n = 35) (n = 44) (n = 24) Age, mean ± SD, yr 36.13 ± 1.94 41.60 ± 1.76 53.73 ± 1.79 45.79 ± 3.22 0.00 **** Sex,n(%) 0.40 Male 17(53.1%) 14(40.0%) 25(56.8%) 10(41.7%) Female 15(46.9%) 21(60.0%) 19(21.8%) 14(58.3%) Side,n(%) 0.82 Left 15(46.9%) 16(17.0%) 23(52.3%) Right 17(53.1%) 19(54.3%) 21(47.7%) Episode frequency 0.07 Single 8(25.0%) 3(8.6%) Recurrent 24(75.0%) 32(91.4%) ****p < 0.0001, ALHL Acute Low-frequency Sensorineural Hearing Loss, EH Endolymphatic Hydrops, MD Ménière’s Disease 3.2 VA Grading Analysis 3.2.1 VA Grading Criteria and MD Group Findings Characteristic VA morphologies on T2-weighted SPACE sequences, categorized using a three-stage grading system, and their corresponding EH status are demonstrated in Fig. 1. In the MD group, the VA grade distribution on the affected side differed significantly from that of controls (P < 0.0001): grade 0 in 6 cases, grade 1 in 13 cases, and grade 2 in 25 cases (Table 2). While the number of abnormal vestibular aqueducts (VA ≥ 1) showed no difference between affected and unaffected sides (P > 0.05), comparative analysis using the three-stage grading system revealed significant inter-side differences (P = 0.0332). Table 2 Vestibular Aqueduct (VA) Grading Comparison between Ménière’s Disease (MD) Group and Control Group MD group Control group Chi 2 (P-value) Se(%)/Sp(%) PPV(%)/NPV(%) VA = 0(%) 6(13.64) 14(58.33) 14.94(P = 0.0001) 86.36/41.67 73.08/62.5 VA ≥ 1(%) 38(86.37) 10(41.67) 14.94(P = 0.0001) 86.36/58.33 79.17/70 VA = 2(%) 25(56.82) 1(4.17) 18.23(P < 0.0001) 56.82/95.83 96.15/54.76 Se Sensitivity, Sp Specificity, PPV Positive Predictive Value, NPV Negative Predictive Value 3.2.2 VA Grading in ALHL Group The ALHL group exhibited significantly different VA grade distribution on the affected side compared to controls (P = 0.0014), primarily driven by increased grade 2 cases. Subgroup analysis showed no significant difference between the ALHL without EH subgroup and controls (P = 0.075), whereas the ALHL with EH subgroup differed markedly (P < 0.0001). Specifically, the EH subgroup demonstrated significantly more grade 2 VA cases in both grade 1 vs. 2 (P = 0.001) and grade 0 vs. 2 comparisons (P < 0.0001). 3.2.3 Comparative Analysis Among Clinical Groups Significant differences in VA grading emerged among ALHL without EH, ALHL with EH, and MD groups (P = 0.002). Pairwise comparisons revealed differences between the ALHL with EH and MD groups (P = 0.002), particularly in grade 0 vs. 2 comparisons. The ALHL with EH group displayed VA distribution patterns comparable to the MD group (P = 0.985) (Fig. 2). 3.2.4 Bilateral Comparison and Group Distribution While no significant interaural differences were observed in the ALHL without EH subgroup, both the ALHL with EH and MD groups demonstrated significant bilateral VA grade discrepancies (Fig. 3a, 3b). A progressive trend emerged across groups, characterized by decreasing grade 0 proportions and increasing grade ≥ 1 proportions from controls to MD (Fig. 4). 3.3 VA Grading and EH Analysis of the ALHL group revealed a significant association between VA grading and EH presence (P = 0.008, Table 3). Notably, patients with grade 2 VA had a 5.107-fold increased risk of EH development compared to those with grade 0 VA (95% CI: 1.501–17.375). Table 3 Distribution of Endolymphatic Hydrops (EH) Across Different Vestibular Aqueduct (VA) Grades VA Grade With EH n(%) Without EH n(%) P Value 0 7(20.0) 13(40.6) 0.008 ** 1 6(17.1) 11(34.4) 2 22(62.9) 8(25.0) Total 35(100) 32(100) **p < 0.01 3.4 Follow-up of ALHL Patients During the follow-up period (mean duration, 31.63 ± 17.64 months; range, 4–81 months), seven patients (10.45%) progressed to definite MD. All progression cases originated from the EH subgroup, representing 20% of this cohort, with a mean progression interval of 13.00 ± 9.09 months (range: 2–27 months). Among these patients, VA grade distribution was grade 2:grade 1:grade 0 = 6:1:0, with non-visible VA (grade 2) accounting for 85.7% of cases. Discussion This study elucidates the association between VA morphology and EH in patients with ALHL and MD. Three principal findings emerged from our investigation: (1) ALHL patients with EH exhibited VA grading patterns closely resembling those of MD patients, suggesting shared anatomical substrates; (2) VA grade 2 (non-visualization) was strongly associated with elevated hydrops risk, highlighting its role as a potential biomarker; and (3) VA invisibility emerged as a predictor for ALHL progression to MD. These results enhance our understanding of the link between anatomical changes and disease progression in inner ear disorders. Anatomical abnormalities are increasingly recognized as key factors in impaired endolymphatic drainage[ 13 ], with multiple studies confirming the relationship between VA morphological changes and the pathogenesis of MD[ 14 – 16 ]. Our findings regarding VA non-visualization rates confirm previous MD studies[ 11 , 17 , 18 ]. Notably, while MD patients showed significant VA morphological differences compared to controls (P 0.05), aligning with Attyé's cohort findings[ 10 ]. Given the larger cohort in our study, we utilized the three-stage grading system (grades 0, 1, and 2) for comparison instead of grouping grades ≥ 1 as abnormal VA, enabling a more detailed analysis and enhancing the identification of potential associations between VA morphological changes and MD. Although FLAIR sequences are widely utilized for VA evaluation due to their superior fluid suppression, our findings indicate that 0.6-mm thin-slice MRI-T2 sequences achieve comparable accuracy to FLAIR in VA visibility assessment, while offering lower technical demands, enhanced operational simplicity, and greater practical advantages in resource-limited clinical settings. Extending morphological assessments of the VA to ALHL—a condition sharing EH features with MD[ 6 , 19 ]—revealed critical pathophysiological overlaps. The ALHL with EH group and MD group demonstrated similar characteristics, with both showing statistical differences in MRI-VA grading between affected and unaffected sides, while the without EH group showed no such difference. Moreover, VA abnormalities were significantly more prevalent in both the ALHL with EH group and MD group compared to the without EH and control groups, suggesting shared pathophysiological mechanisms. Importantly, the increased EH risk associated with VA grade 2 (95% CI:1.501–17.375) implies that abnormal VA morphology in ALHL patients may predispose to EH development. These findings provide particular significance for early disease stratification and progression risk assessment in ALHL patients. Previous epidemiological studies have documented the proportion of ALHL progressing to MD[ 4 , 19 , 20 ]. However, the specific progression rate among ALHL patients with EH had not been previously documented. In our study, the overall progression rate to MD was 10.45%, aligning with published data. Significantly, we found that 20% of patients in the with EH subgroup progressed to definite MD, while no progression occurred in the without EH subgroup, supporting EH as a crucial pathological marker for MD development[ 5 ]. Patients with recurrent ALHL are more likely to develop EH, which is consistent with the clinical characteristics of fluctuating low-frequency hearing loss observed in MD. Furthermore, considering the progressive increase in average age across the ALHL without EH, ALHL with EH, and MD groups, we propose that ALHL patients with EH may represent an early stage of MD. However, EH alone cannot definitively predict progression from ALHL to MD[ 21 ]. Given that ALHL onset and outcomes are influenced by multifactorial mechanisms, further multi-dimensional validation is necessary. It is important to note that EH does not exclusively indicate MD[ 22 – 24 ]. Conversely, EH is not universally observed in all patients with Ménière's disease[ 25 ]. EH in MD is a dynamic process that can longitudinally evolve over the natural disease course[ 26 , 27 ]. Critically, VA morphological abnormalities exhibit specificity in ALHL populations: ALHL patients with VA anomalies are more prone to EH development or MD progression. The predominance of VA grade 2 (non-visualization) among MD progressors underscores VA invisibility as a potential pathological basis for ALHL-to-MD transition. MD is characterized by EH as its core pathological hallmark, though EH alone cannot fully account for all clinical manifestations, such as progressive hearing loss or the fluctuating frequency of vertigo attacks[ 28 ]. The underlying pathophysiology involves multifactorial mechanisms, including anatomical variations, autoimmune dysfunction, viral infections, genetic predisposition, ionic imbalances, vascular irregularities, and allergic responses and others[ 29 ]. Clinically, MD is diagnosed primarily through medical history and symptom assessment, yet its heterogeneity in presentation—such as variable hearing loss severity and vestibular symptom patterns—complicates phenotyping and subtyping[ 30 ]. To address this, classification systems have been proposed: phenotypic subtypes (based on dominant symptoms: cochlear, vestibular, or mixed) and endotypic subtypes (based on pathological mechanisms: ES-hypoplasia or ES-degeneration), with distinct therapeutic responses observed across subtypes[ 31 ]. In early disease stages, vertigo episodes are often frequent but tend to diminish over time[ 28 ]. Our study revealed that all analyzed cases originated from the EH subgroup (20% of the cohort), with disease progression spanning 2 to 27 months. Notably, patients with anatomical abnormalities, such as VA anomalies, may experience delayed onset of vertigo and prolonged disease courses. This suggests that anatomical factors, including VA morphology, could serve as predictive markers for ALHL progression or refine MD classification, offering potential clinical utility in risk stratification and personalized management. Study Limitations Several limitations should be acknowledged when interpreting our findings. Unlike CT’s direct visualization of bony structures, MRI indirectly assesses VA morphology through fluid or vascular signals within the aqueduct[ 13 ]. Additionally, while MRI-T2 can identify morphological abnormalities, it lacks the resolution to distinguish between the two recently described histopathological subtypes of MD: hypoplasia and degeneration of the ES[ 32 ]. Furthermore, the presence of ALHL patients without detectable EH but with non-visible VA raises unanswered questions about whether these individuals represent a preclinical MD state and how extended follow-up durations may reveal progressive EH development and MD conversion. Future studies should prioritize CT-based evaluation of VA angular trajectories[ 33 ] to clarify pathological subtypes and the ALHL-to-MD transition mechanism. Longitudinal cohorts with extended timelines are imperative to validate potential progression rates. Conclusion Thin-slice MRI-T2 SPACE sequence enables reliable VA grading and reveals similar patterns between ALHL with EH and MD patient cohorts. This non-invasive assessment method shows significant promise for evaluating disease progression risk and facilitating early MD diagnosis. Importantly, the strong correlation between VA non-visualization and EH development highlights its potential applications in patient stratification and personalized therapeutic strategies. Abbreviations vestibular aqueduct (VA), acute low-frequency sensorineural hearing loss (ALHL), Ménière’s disease (MD), endolymphatic hydrops (EH), inversion recovery (IR), endolymphatic duct (ED), endolymphatic sac (ES) Declarations Human Ethics and Consent to Participate declarations This study was conducted in accordance with the Declaration of Helsinki. Ethical approval was obtained from the Institutional Review Board of a tertiary hospital in Shanghai, China (approval number: 2022054). The requirement for informed consent was waived due to the retrospective nature of the study involving anonymized clinical data. Declaration of conflicting interest The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. Funding information Health Research Project of the Health Commission of Pudong New Area, Shanghai, China National Clinical Research Center for Otolaryngologic Diseases, Beijing, China Youth Program of National Natural Science Foundation of China References Kawashima K SHOM (2006) Epidemiological study of acute low-tone sensorineural hearing loss in Kanagawa and Iwate prefectures. Audiol Jpn 49:373-380. Roh KJ, Lee EJ, Park AY, Choi BI, Son EJ (2015) Long-Term Outcomes of Acute Low-Tone Hearing Loss. 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Neuroimage Clinical 30:102656. https://10.1016/j.nicl.2021.102656 Seo T, Okano Y, Aomi M, Yamada Z, Kasugai S, Nakamura M et al (2022) Endolymphatic hydrops presumption tests for patients with vestibular migraine. Acta Otolaryngol 142(5):406-409. https://10.1080/00016489.2022.2080251 Attyé A, Eliezer M, Galloux A, Pietras J, Tropres I, Schmerber S et al (2017) Endolymphatic hydrops imaging: Differential diagnosis in patients with Meniere disease symptoms. Diagn Interv Imaging 98(10):699-706. https://10.1016/j.diii.2017.06.002 Li J, Wang L, Hu N, Li L, Song G, Xu H et al (2023) Longitudinal variation of endolymphatic hydrops in patients with Ménière's disease. Ann Transl Med 11(2):44. https://10.21037/atm-22-6313 Nakashima T, Pyykko I, Arroll MA, Casselbrant ML, Foster CA, Manzoor NF et al (2016) Meniere's disease. Nat Rev Dis Primers 2:16028. https://10.1038/nrdp.2016.28 Iwasaki S, Shojaku H, Murofushi T, Seo T, Kitahara T, Origasa H et al (2021) Diagnostic and therapeutic strategies for Meniere's disease of the Japan Society for Equilibrium Research. Auris, Nasus, Larynx 48(1):15-22. https://10.1016/j.anl.2020.10.009 Merchant SN, Adams JC, Nadol JJ (2005) Pathophysiology of Meniere's syndrome: are symptoms caused by endolymphatic hydrops? Otol Neurotol 26(1):74-81. https://10.1097/00129492-200501000-00013 Phillips JS, Murdin L, Rea P, Sutton L (2018) Clinical Subtyping of Ménière’s Disease. Otolaryngol Head Neck Surg 159(3):407-409. https://10.1177/0194599818773077 Zhang S, Guo Z, Tian E, Liu D, Wang J, Kong W (2022) Meniere disease subtyping: the direction of diagnosis and treatment in the future. Expert Rev Neurother 22(2):115-127. https://10.1080/14737175.2022.2030221 Eckhard AH, Zhu M, O'Malley JT, Williams GH, Loffing J, Rauch SD et al (2019) Inner ear pathologies impair sodium-regulated ion transport in Meniere's disease. Acta Neuropathol 137(2):343-357. https://10.1007/s00401-018-1927-7 Bachinger D, Luu NN, Kempfle JS, Barber S, Zurrer D, Lee DJ et al (2019) Vestibular Aqueduct Morphology Correlates With Endolymphatic Sac Pathologies in Meniere's Disease-A Correlative Histology and Computed Tomography Study. Otol Neurotol 40(5):e548-e555. https://10.1097/MAO.0000000000002198 Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-7224413","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":498178305,"identity":"d9655149-e773-4901-8ef7-5c8f65983a9c","order_by":0,"name":"Linglan Gu","email":"","orcid":"","institution":"Eye \u0026 ENT Hospital, Fudan University","correspondingAuthor":false,"prefix":"","firstName":"Linglan","middleName":"","lastName":"Gu","suffix":""},{"id":498178306,"identity":"4550cad2-7c81-445e-9e53-35e089fa615a","order_by":1,"name":"Qianru Wu","email":"","orcid":"","institution":"Eye \u0026 ENT Hospital, Fudan University","correspondingAuthor":false,"prefix":"","firstName":"Qianru","middleName":"","lastName":"Wu","suffix":""},{"id":498178307,"identity":"8fcb18bd-106b-4076-818f-e4c2b699442d","order_by":2,"name":"Rujian Hong","email":"","orcid":"","institution":"Eye \u0026 ENT Hospital, Fudan University","correspondingAuthor":false,"prefix":"","firstName":"Rujian","middleName":"","lastName":"Hong","suffix":""},{"id":498178308,"identity":"ab2d426c-f466-48d2-9b30-ed1b0a6d57bc","order_by":3,"name":"Yongzhen Wu","email":"","orcid":"","institution":"Eye \u0026 ENT Hospital, Fudan University","correspondingAuthor":false,"prefix":"","firstName":"Yongzhen","middleName":"","lastName":"Wu","suffix":""},{"id":498178309,"identity":"1c9b901b-61b3-4a49-a261-7ea808f233ad","order_by":4,"name":"Wuqing Wang","email":"","orcid":"","institution":"Eye \u0026 ENT Hospital, Fudan University","correspondingAuthor":false,"prefix":"","firstName":"Wuqing","middleName":"","lastName":"Wang","suffix":""},{"id":498178310,"identity":"c013b75e-bd15-4d00-a8e2-b8173c6cfaaf","order_by":5,"name":"Yibo Zhang","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA3klEQVRIiWNgGAWjYDACZh4GBsYGKOeDgY0dSVoYG2cUpCUTYQ2SlmaeD4fgNuIEBsd5Dz78ucMuT9699/hjG4MDzAzsh49uwKvlMF+ygeSZ5GLDM+cSm3MM7vAx8KSl3cCvhcdMwrCNOXHjjBxDoJZnzAwSPGaEtSS21SdunP/GsNnC4DBjA1FaDrYdTpwvwWPYzECMFkmgXwwb244nbuDJMZzZY5CWzEbIL3znzwJDrK06cX77GYMPP/7Y2PGzHz6GV4vCAZgLYQw2fMpBQL4BnTEKRsEoGAWjAB0AAGr5Tmtqr1/UAAAAAElFTkSuQmCC","orcid":"","institution":"Eye \u0026 ENT Hospital, Fudan University","correspondingAuthor":true,"prefix":"","firstName":"Yibo","middleName":"","lastName":"Zhang","suffix":""}],"badges":[],"createdAt":"2025-07-27 06:23:12","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-7224413/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-7224413/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":89066998,"identity":"251fb297-1920-4a38-8717-c0f41597a617","added_by":"auto","created_at":"2025-08-14 10:43:03","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":1055557,"visible":true,"origin":"","legend":"\u003cp\u003eVestibular Aqueduct (VA) Grading Illustration\u003c/p\u003e\n\u003cp\u003eA:MRI-Ga, B:MRI-T2, C:Schematic illustration; 1:VA=0 2:VA=1 3:VA=2\u003c/p\u003e\n\u003cp\u003eillustrates the imaging findings and corresponding schematic representations of the same patient under different VA conditions. Column A1-B1-C1 depict MRI-Ga, MRI-T2, and schematic images for VA grade 0; Column A2-B2-C2 show MRI-Ga, MRI-T2, and schematic images for VA grade 1; and Column A3-B3-C3 demonstrate MRI-Ga, MRI-T2, and schematic images for VA grade 2. The thick arrows indicate endolymphatic hydrops, while the thin arrows indicate VA.\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-7224413/v1/c4c4223126113ad3cb9450d2.png"},{"id":89066924,"identity":"82fd44e4-d617-498a-86c2-a2fc6d802bee","added_by":"auto","created_at":"2025-08-14 10:42:59","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":223381,"visible":true,"origin":"","legend":"\u003cp\u003eComparison of Vestibular Aqueduct Grading Among Acute Low-frequency Sensorineural Hearing Loss (ALHL) without Endolymphatic Hydrops (EH) Group, ALHL With EH Group, and Ménière’s Disease (MD) Group on the Affected Side\u003c/p\u003e\n\u003cp\u003e*p \u0026lt; 0.05, ns p \u0026gt; 0.05\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-7224413/v1/0ef17719da6851b0af02a2ff.png"},{"id":89066765,"identity":"2e980310-94ab-4920-81d2-f5f62a6586f4","added_by":"auto","created_at":"2025-08-14 10:42:51","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":363099,"visible":true,"origin":"","legend":"\u003cp\u003e(a,b) Comparison of Vestibular Aqueduct (VA) Grading Between Affected and Unaffected Ears\u003c/p\u003e\n\u003cp\u003e(a) Table displaying the absolute counts of VA grades in affected vs. unaffected ears stratified by group. (b) Within-group comparisons of VA grading differences between affected and unaffected ears.\u003c/p\u003e\n\u003cp\u003eGrade 0 indicates continuous VA, grade 1 represents discontinuous VA, and grade 2 denotes non-visualization of VA.\u003c/p\u003e\n\u003cp\u003e*p \u0026lt; 0.05, ns p \u0026gt; 0.05, ALHL Acute Low-frequency Sensorineural Hearing Loss, EH Endolymphatic Hydrops, MD Ménière’s Disease\u003c/p\u003e","description":"","filename":"3.png","url":"https://assets-eu.researchsquare.com/files/rs-7224413/v1/a5219e2015361d6a194358f9.png"},{"id":89066481,"identity":"18e23756-df1f-43d1-a91d-afc55b868b55","added_by":"auto","created_at":"2025-08-14 10:42:42","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":725056,"visible":true,"origin":"","legend":"\u003cp\u003eDistribution of Vestibular Aqueduct (VA) Grades in Affected and Unaffected Sides Across Groups\u003c/p\u003e\n\u003cp\u003eGroups: Control Group, Acute Low-frequency Sensorineural Hearing Loss (ALHL) without Endolymphatic Hydrops (EH) Group, ALHL With EH Group, and Ménière’s Disease (MD) Group\u003c/p\u003e\n\u003cp\u003eGrade 0 indicates continuous VA, grade 1 represents discontinuous VA, and grade 2 denotes non-visualization of VA.\u003c/p\u003e","description":"","filename":"4.png","url":"https://assets-eu.researchsquare.com/files/rs-7224413/v1/90ec464eada4840bb7d4ec86.png"},{"id":90706262,"identity":"18500334-7105-46f0-bf02-a105408d9e57","added_by":"auto","created_at":"2025-09-06 04:16:48","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":3805911,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-7224413/v1/77c9388d-9650-445a-89a8-50ccf7c1ef1b.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Vestibular Aqueduct Grading: an Early Predictor of Progression from Low-Frequency Sensorineural Hearing Loss to Ménière’s Disease","fulltext":[{"header":"Introduction","content":"\u003cp\u003eAcute Low-Frequency Sensorineural Hearing Loss (ALHL) is an idiopathic sudden-onset auditory condition, primarily characterized by symptoms such as aural fullness, low-frequency sensorineural hearing loss, tinnitus, and hyperacusis. The incidence of ALHL is approximately 40\u0026ndash;60 per 100,000, with a higher prevalence among young adults[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Although ALHL exhibits higher spontaneous recovery rates than other forms of sudden sensorineural hearing loss, its 15.2% recurrence rate significantly exceeds that of comparable disorders[\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. The diagnostic criteria for M\u0026eacute;ni\u0026egrave;re's disease (MD), a debilitating otological condition, share diagnostic overlap with ALHL, as transient ALHL recovery on serial audiograms supports the diagnosis of MD[\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. Approximately 10\u0026ndash;30% of patients with ALHL progress to MD within three years, and this proportion increases with longer follow-up periods[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. While endolymphatic hydrops (EH) constitutes the pathological hallmark of MD, its exact role in disease mechanisms remains unclear. Importantly, EH is also frequently observed in ALHL, with emerging evidence suggesting its association with MD progression[\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. Shimono et al. reported that EH in ALHL patients involves both cochlear and vestibular compartments, similar to EH in MD[\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. Therefore, understanding the mechanism of ALHL with EH and identifying factors that might drive EH progression remains crucial.\u003c/p\u003e\u003cp\u003eThe endolymphatic duct (ED) leads to the blind-ending endolymphatic sac (ES) through the vestibular aqueduct (VA), a bony channel running from the medial wall of the vestibule to the posterior surface of the petrous bone. Histological studies have demonstrated hypoplasia of the VA, atrophy of the ES, and ED luminal narrowing in MD patients[\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. Congenital hypoplasia of the VA and calcium ion augmentation in hydropic ears may exacerbate VA calcification and stenosis, potentially disrupting endolymphatic flow and contributing to inner ear dysfunction[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. Histopathologically, the VA and ES were detected to be shorter in MD patients compared to healthy individuals[\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. Numerous scholars have reported that morphological abnormalities of the VA on imaging are significantly associated with EH[\u003cspan additionalcitationids=\"CR11\" citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. Morphological abnormalities of the VA are significantly associated with the clinical diagnosis of MD with a sensitivity of 90%, and can also be detected in asymptomatic ears[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. Based on these observations, we hypothesize that VA morphological abnormalities may serve as early predictors in the development and progression of ALHL to MD. The goal of this retrospective study was to evaluate the clinical characteristics and VA morphology assessed by MRI in ALHL patients with and without EH, as well as in MD patients. We aimed to gain a deeper understanding of the relationship between VA and EH, as well as the disease correlation between ALHL and MD.\u003c/p\u003e"},{"header":"Materials and Methods","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e\u003ch2\u003e2.1 Participants\u003c/h2\u003e\u003cp\u003eThis single-center retrospective study was conducted at a tertiary referral hospital. This study was conducted in accordance with the Declaration of Helsinki and was approved by the local institutional Ethics Committee (permit number 2022054), and the requirement for informed consent was waived due to the retrospective analysis of anonymized clinical data.\u003c/p\u003e\u003cp\u003eA total of 135 patients were enrolled between March 2019 and July 2024, stratified into three groups: the ALHL group, the MD group and the control group. Analyses focused on affected ears in the ALHL and MD groups, and healthy ears in the control group. All participants underwent standardized diagnostic evaluations, including a thorough history inquiry, otoscopy, audiometry, and imaging examination, conducted by otologists at the Department of Otology and Skull Base Surgery of the Eye, Ear, Nose and Throat Hospital, Fudan University.\u003c/p\u003e\u003cp\u003eUnilateral definite MD was diagnosed according to the 2015 diagnostic criteria established by the B\u0026aacute;r\u0026aacute;ny Society[\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. The inclusion criteria for ALHL were as follows: (1) unilateral unfluctuating sensorineural hearing loss with sudden onset that occurs within 72 h or less; (2) low-tone hearing loss, i.e., the sum of hearing levels at 0.125, 0.25 and 0.5 kHz is 70 dB or greater and the sum of hearing levels at 2, 4 and 8 kHz is 60 dB or less; (3) without vertigo; (4) no identifiable cause. The exclusion criteria for ALHL were as follows: (1) middle or inner ear infections (otitis media, mastoiditis, labyrinthitis, etc.); (2) bilateral hearing loss; (3) having received previous ear surgery or intratympanic injections; (4) neurological diseases; (5) head trauma; (6) immunological diseases. Patients in the control group were suffering unilateral ES tumor, unilateral acoustic neuroma, or unilateral vestibular or cochlear occupation, without EH in healthy ears.\u003c/p\u003e\u003c/div\u003e\u003cdiv id=\"Sec4\" class=\"Section2\"\u003e\u003ch2\u003e2.2 Radiological evaluations\u003c/h2\u003e\u003cp\u003eAll imaging examinations were carried out on a 3T MRI scanner (Magnetom Verio, Siemens Healthineers, Erlangen, Germany) with an 8-channel ear-surface phased-array coil, 4 hours after undergoing intravenous injection with the double dose (0.4 mL/kg) of gadolinium (ProHance, Bracco Imaging Italia SRL, Milano, Italy). The T2 SPACE and three-dimensional real inversion recovery (3D-real IR) sequences were applied in all patients. The parameters for the T2 SPACE sequence were as follows: slice thickness 0.6 mm, repetition time 1000 ms, echo time 132 ms, flip angle 120◦, matrix size 384 \u0026times; 384, field of view 200 mm \u0026times; 200 mm, scan time 2 min 44 s. The parameters for the 3D-real IR sequence were as follows: slice thickness 0.6 mm, repetition time 6000 ms, echo time 181 ms, flip angle 180◦, matrix size 768 \u0026times; 768, field of view 160 mm \u0026times; 160 mm, scan time 15 min 20 s. All images were independently reviewed by an experienced neuroradiologist and a senior otolaryngologist blinded to clinical diagnoses. Inter-reader agreement for VA grading was evaluated using Cohen's kappa coefficient, with values\u0026thinsp;\u0026gt;\u0026thinsp;0.80 indicating very good agreement.\u003c/p\u003e\u003cdiv id=\"Sec5\" class=\"Section3\"\u003e\u003ch2\u003e2.2.1 Evaluation of the VA\u003c/h2\u003e\u003cp\u003eThe T2 SPACE sequence was used to evaluate the VA and exclude middle ear or neurological disorders. The VA was defined as a linear bony duct extending from the vestibule to the posterior temporal bone surface. A three-stage grading system was applied (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e1\u003c/span\u003e):\u003c/p\u003e\u003cp\u003eGrade 0: Continuous VA throughout its course.\u003c/p\u003e\u003cp\u003eGrade 1: Discontinuous VA with partial visibility.\u003c/p\u003e\u003cp\u003eGrade 2: Complete non-visualization of VA.\u003c/p\u003e\u003c/div\u003e\u003cdiv id=\"Sec6\" class=\"Section3\"\u003e\u003ch2\u003e2.2.2 Evaluation of EH\u003c/h2\u003e\u003cp\u003eAn enlarged endolymphatic space was considered as having a large negative signal dilating to the contrast-enhanced signal of the perilymphatic space on 3D-real IR sequences. For vestibular hydrops quantification, the endolymphatic space ratio was calculated by dividing the endolymphatic area by the total vestibular fluid space (endolymph\u0026thinsp;+\u0026thinsp;perilymph), with a threshold ratio of 1/3 used to differentiate non-hydropic (\u0026le;\u0026thinsp;1/3) from hydropic (\u0026gt;\u0026thinsp;1/3) status. In the cochlea, patients with no hydrops showed no displacement of Reissner\u0026rsquo;s membrane. Based on these imaging criteria, the ALHL cohort was stratified into two subgroups: ALHL with EH and ALHL without EH.\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv id=\"Sec7\" class=\"Section2\"\u003e\u003ch2\u003e2.3 Follow-up of patients in ALHL group\u003c/h2\u003e\u003cp\u003eAll patients in the ALHL group were followed up until December 31, 2024. Progression to M\u0026eacute;ni\u0026egrave;re\u0026rsquo;s disease (MD) was defined as the occurrence of two or more spontaneous vertigo episodes, each lasting between 20 minutes and 12 hours, during the follow-up period.\u003c/p\u003e\u003c/div\u003e\u003cdiv id=\"Sec8\" class=\"Section2\"\u003e\u003ch2\u003e2.4 Statistical analysis\u003c/h2\u003e\u003cp\u003eThe statistical data were analyzed using SPSS Statistics (Version 20.0, SPSS, Inc., Chicago, IL). Categorical variables were compared using the Chi-square test or Fisher\u0026rsquo;s exact test, while continuous variables were analyzed using the two-sample t-test, analysis of variance (ANOVA), or Mann\u0026ndash;Whitney U test, as appropriate. Statistical significance was set at p\u0026thinsp;\u0026le;\u0026thinsp;0.05, and continuous data were presented as mean\u0026thinsp;\u0026plusmn;\u0026thinsp;standard deviation (SD). Additionally, diagnostic performance metrics, including sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV), were calculated for MRI findings in the MD group compared to controls. Figures were generated using GraphPad Prism (Version 10.1.2, GraphPad Software, San Diego, CA).\u003c/p\u003e\u003c/div\u003e"},{"header":"Results","content":"\u003cdiv id=\"Sec10\"\u003e\n \u003ch2\u003e3.1 Patient Characteristics\u003c/h2\u003e\n \u003cp\u003eA total of 135 patients (66 males, 69 females) were enrolled and stratified into three groups: ALHL group (n = 67; 32 without EH and 35 with EH), MD group (n = 44), and control group (n = 24). No significant differences were observed in gender distribution or laterality between groups (P \u0026gt; 0.05), whereas age differed significantly among the four groups (P \u0026lt; 0.0001). Post hoc analysis revealed significant age differences between the ALHL without EH subgroup, ALHL with EH subgroup, and MD group (P \u0026lt; 0.0001), but not between the control group and other groups (P \u0026gt; 0.05).\u003c/p\u003e\n \u003cp\u003eWithin the ALHL group, patients were further classified based on episode frequency into single-episode and recurrent-episode (≥ 2) subgroups. Although no significant association was observed between episode frequency and EH (P = 0.07), patients with recurrent episodes demonstrated a notably higher risk of developing EH in the affected ear (odds ratio [OR] = 3.556, 95% confidence interval [CI]: 0.852–14.836) (Table\u0026nbsp;1).\u003c/p\u003e\n \u003cdiv\u003e\n \u003ctable id=\"Tab1\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv\u003eTable 1\u003c/div\u003e\n \u003cdiv\u003e\n \u003cp\u003eCharacteristics of Patients in Different Groups\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\" rowspan=\"2\"\u003e\u0026nbsp;\u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eALHL without EH Group\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eALHL with EH Group\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eMD group\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eControl group\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\u0026nbsp;\u003c/th\u003e\n \u003cth align=\"left\" rowspan=\"2\"\u003e\n \u003cp\u003eP value\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e(n = 32)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e(n = 35)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e(n = 44)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e(n = 24)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\u0026nbsp;\u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAge,\u003c/p\u003e\n \u003cp\u003emean ± SD, yr\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e36.13 ± 1.94\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e41.60 ± 1.76\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e53.73 ± 1.79\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e45.79 ± 3.22\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.00\u003csup\u003e****\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eSex,n(%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.40\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMale\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e17(53.1%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e14(40.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e25(56.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e10(41.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eFemale\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e15(46.9%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e21(60.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e19(21.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e14(58.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eSide,n(%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.82\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eLeft\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e15(46.9%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e16(17.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e23(52.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eRight\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e17(53.1%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e19(54.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e21(47.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eEpisode frequency\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.07\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eSingle\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e8(25.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3(8.6%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eRecurrent\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e24(75.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e32(91.4%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n \u003c/div\u003e\n \u003cp\u003e****p \u0026lt; 0.0001, ALHL Acute Low-frequency Sensorineural Hearing Loss, EH Endolymphatic Hydrops, MD Ménière’s Disease\u003c/p\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec11\"\u003e\n \u003ch2\u003e3.2 VA Grading Analysis\u003c/h2\u003e\n \u003cdiv id=\"Sec12\"\u003e\n \u003ch2\u003e3.2.1 VA Grading Criteria and MD Group Findings\u003c/h2\u003e\n \u003cp\u003eCharacteristic VA morphologies on T2-weighted SPACE sequences, categorized using a three-stage grading system, and their corresponding EH status are demonstrated in Fig.\u0026nbsp;1. In the MD group, the VA grade distribution on the affected side differed significantly from that of controls (P \u0026lt; 0.0001): grade 0 in 6 cases, grade 1 in 13 cases, and grade 2 in 25 cases (Table\u0026nbsp;2). While the number of abnormal vestibular aqueducts (VA ≥ 1) showed no difference between affected and unaffected sides (P \u0026gt; 0.05), comparative analysis using the three-stage grading system revealed significant inter-side differences (P = 0.0332).\u003c/p\u003e\n \u003cdiv\u003e\n \u003ctable id=\"Tab2\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv\u003eTable 2\u003c/div\u003e\n \u003cdiv\u003e\n \u003cp\u003eVestibular Aqueduct (VA) Grading Comparison between Ménière’s Disease (MD) Group and Control Group\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\u0026nbsp;\u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eMD\u003c/p\u003e\n \u003cp\u003egroup\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eControl group\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eChi\u003csup\u003e2\u003c/sup\u003e (P-value)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eSe(%)/Sp(%)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ePPV(%)/NPV(%)\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eVA = 0(%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e6(13.64)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e14(58.33)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e14.94(P = 0.0001)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e86.36/41.67\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e73.08/62.5\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eVA ≥ 1(%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e38(86.37)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e10(41.67)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e14.94(P = 0.0001)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e86.36/58.33\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e79.17/70\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eVA = 2(%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e25(56.82)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1(4.17)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e18.23(P \u0026lt; 0.0001)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e56.82/95.83\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e96.15/54.76\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n \u003c/div\u003e\n \u003cp\u003eSe Sensitivity, Sp Specificity, PPV Positive Predictive Value, NPV Negative Predictive Value\u0026nbsp;\u003c/p\u003e\n \u003c/div\u003e\n \u003cdiv id=\"Sec13\"\u003e\n \u003ch2\u003e3.2.2 VA Grading in ALHL Group\u003c/h2\u003e\n \u003cp\u003eThe ALHL group exhibited significantly different VA grade distribution on the affected side compared to controls (P = 0.0014), primarily driven by increased grade 2 cases. Subgroup analysis showed no significant difference between the ALHL without EH subgroup and controls (P = 0.075), whereas the ALHL with EH subgroup differed markedly (P \u0026lt; 0.0001). Specifically, the EH subgroup demonstrated significantly more grade 2 VA cases in both grade 1 vs. 2 (P = 0.001) and grade 0 vs. 2 comparisons (P \u0026lt; 0.0001).\u003c/p\u003e\n \u003c/div\u003e\n \u003cdiv id=\"Sec14\"\u003e\n \u003ch2\u003e3.2.3 Comparative Analysis Among Clinical Groups\u003c/h2\u003e\n \u003cp\u003eSignificant differences in VA grading emerged among ALHL without EH, ALHL with EH, and MD groups (P = 0.002). Pairwise comparisons revealed differences between the ALHL with EH and MD groups (P = 0.002), particularly in grade 0 vs. 2 comparisons. The ALHL with EH group displayed VA distribution patterns comparable to the MD group (P = 0.985) (Fig.\u0026nbsp;2).\u003c/p\u003e\n \u003c/div\u003e\n \u003cdiv id=\"Sec15\"\u003e\n \u003ch2\u003e3.2.4 Bilateral Comparison and Group Distribution\u003c/h2\u003e\n \u003cp\u003eWhile no significant interaural differences were observed in the ALHL without EH subgroup, both the ALHL with EH and MD groups demonstrated significant bilateral VA grade discrepancies (Fig.\u0026nbsp;3a, 3b). A progressive trend emerged across groups, characterized by decreasing grade 0 proportions and increasing grade ≥ 1 proportions from controls to MD (Fig.\u0026nbsp;4).\u003c/p\u003e\n \u003c/div\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec16\"\u003e\n \u003ch2\u003e3.3 VA Grading and EH\u003c/h2\u003e\n \u003cp\u003eAnalysis of the ALHL group revealed a significant association between VA grading and EH presence (P = 0.008, Table\u0026nbsp;3). Notably, patients with grade 2 VA had a 5.107-fold increased risk of EH development compared to those with grade 0 VA (95% CI: 1.501–17.375).\u003c/p\u003e\n \u003cdiv\u003e\n \u003ctable id=\"Tab3\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv\u003eTable 3\u003c/div\u003e\n \u003cdiv\u003e\n \u003cp\u003eDistribution of Endolymphatic Hydrops (EH) Across Different Vestibular Aqueduct (VA) Grades\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eVA Grade\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eWith EH n(%)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eWithout EH n(%)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eP Value\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7(20.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13(40.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\" rowspan=\"4\"\u003e\n \u003cp\u003e0.008\u003csup\u003e**\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6(17.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e11(34.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e22(62.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e8(25.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTotal\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e35(100)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e32(100)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n \u003c/div\u003e\n \u003cp\u003e**p \u0026lt; 0.01\u003c/p\u003e\n\u003c/div\u003e\n\u003cdiv id=\"Sec17\"\u003e\n \u003ch2\u003e3.4 Follow-up of ALHL Patients\u003c/h2\u003e\n \u003cp\u003eDuring the follow-up period (mean duration, 31.63 ± 17.64 months; range, 4–81 months), seven patients (10.45%) progressed to definite MD. All progression cases originated from the EH subgroup, representing 20% of this cohort, with a mean progression interval of 13.00 ± 9.09 months (range: 2–27 months). Among these patients, VA grade distribution was grade 2:grade 1:grade 0 = 6:1:0, with non-visible VA (grade 2) accounting for 85.7% of cases.\u003c/p\u003e\n\u003c/div\u003e"},{"header":"Discussion","content":"\u003cp\u003eThis study elucidates the association between VA morphology and EH in patients with ALHL and MD. Three principal findings emerged from our investigation: (1) ALHL patients with EH exhibited VA grading patterns closely resembling those of MD patients, suggesting shared anatomical substrates; (2) VA grade 2 (non-visualization) was strongly associated with elevated hydrops risk, highlighting its role as a potential biomarker; and (3) VA invisibility emerged as a predictor for ALHL progression to MD. These results enhance our understanding of the link between anatomical changes and disease progression in inner ear disorders.\u003c/p\u003e\u003cp\u003eAnatomical abnormalities are increasingly recognized as key factors in impaired endolymphatic drainage[\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e], with multiple studies confirming the relationship between VA morphological changes and the pathogenesis of MD[\u003cspan additionalcitationids=\"CR15\" citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]. Our findings regarding VA non-visualization rates confirm previous MD studies[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e, \u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e]. Notably, while MD patients showed significant VA morphological differences compared to controls (P\u0026thinsp;\u0026lt;\u0026thinsp;0.0001), the bilateral prevalence of abnormal VA (\u0026ge;\u0026thinsp;grade 1) remained comparable between affected and unaffected ears (P\u0026thinsp;\u0026gt;\u0026thinsp;0.05), aligning with Atty\u0026eacute;'s cohort findings[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. Given the larger cohort in our study, we utilized the three-stage grading system (grades 0, 1, and 2) for comparison instead of grouping grades\u0026thinsp;\u0026ge;\u0026thinsp;1 as abnormal VA, enabling a more detailed analysis and enhancing the identification of potential associations between VA morphological changes and MD. Although FLAIR sequences are widely utilized for VA evaluation due to their superior fluid suppression, our findings indicate that 0.6-mm thin-slice MRI-T2 sequences achieve comparable accuracy to FLAIR in VA visibility assessment, while offering lower technical demands, enhanced operational simplicity, and greater practical advantages in resource-limited clinical settings.\u003c/p\u003e\u003cp\u003eExtending morphological assessments of the VA to ALHL\u0026mdash;a condition sharing EH features with MD[\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]\u0026mdash;revealed critical pathophysiological overlaps. The ALHL with EH group and MD group demonstrated similar characteristics, with both showing statistical differences in MRI-VA grading between affected and unaffected sides, while the without EH group showed no such difference. Moreover, VA abnormalities were significantly more prevalent in both the ALHL with EH group and MD group compared to the without EH and control groups, suggesting shared pathophysiological mechanisms. Importantly, the increased EH risk associated with VA grade 2 (95% CI:1.501\u0026ndash;17.375) implies that abnormal VA morphology in ALHL patients may predispose to EH development. These findings provide particular significance for early disease stratification and progression risk assessment in ALHL patients.\u003c/p\u003e\u003cp\u003ePrevious epidemiological studies have documented the proportion of ALHL progressing to MD[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e, \u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]. However, the specific progression rate among ALHL patients with EH had not been previously documented. In our study, the overall progression rate to MD was 10.45%, aligning with published data. Significantly, we found that 20% of patients in the with EH subgroup progressed to definite MD, while no progression occurred in the without EH subgroup, supporting EH as a crucial pathological marker for MD development[\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. Patients with recurrent ALHL are more likely to develop EH, which is consistent with the clinical characteristics of fluctuating low-frequency hearing loss observed in MD. Furthermore, considering the progressive increase in average age across the ALHL without EH, ALHL with EH, and MD groups, we propose that ALHL patients with EH may represent an early stage of MD. However, EH alone cannot definitively predict progression from ALHL to MD[\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e]. Given that ALHL onset and outcomes are influenced by multifactorial mechanisms, further multi-dimensional validation is necessary. It is important to note that EH does not exclusively indicate MD[\u003cspan additionalcitationids=\"CR23\" citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e]. Conversely, EH is not universally observed in all patients with M\u0026eacute;ni\u0026egrave;re's disease[\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e]. EH in MD is a dynamic process that can longitudinally evolve over the natural disease course[\u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e, \u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e]. Critically, VA morphological abnormalities exhibit specificity in ALHL populations: ALHL patients with VA anomalies are more prone to EH development or MD progression. The predominance of VA grade 2 (non-visualization) among MD progressors underscores VA invisibility as a potential pathological basis for ALHL-to-MD transition.\u003c/p\u003e\u003cp\u003eMD is characterized by EH as its core pathological hallmark, though EH alone cannot fully account for all clinical manifestations, such as progressive hearing loss or the fluctuating frequency of vertigo attacks[\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e]. The underlying pathophysiology involves multifactorial mechanisms, including anatomical variations, autoimmune dysfunction, viral infections, genetic predisposition, ionic imbalances, vascular irregularities, and allergic responses and others[\u003cspan citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e]. Clinically, MD is diagnosed primarily through medical history and symptom assessment, yet its heterogeneity in presentation\u0026mdash;such as variable hearing loss severity and vestibular symptom patterns\u0026mdash;complicates phenotyping and subtyping[\u003cspan citationid=\"CR30\" class=\"CitationRef\"\u003e30\u003c/span\u003e]. To address this, classification systems have been proposed: phenotypic subtypes (based on dominant symptoms: cochlear, vestibular, or mixed) and endotypic subtypes (based on pathological mechanisms: ES-hypoplasia or ES-degeneration), with distinct therapeutic responses observed across subtypes[\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e]. In early disease stages, vertigo episodes are often frequent but tend to diminish over time[\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e]. Our study revealed that all analyzed cases originated from the EH subgroup (20% of the cohort), with disease progression spanning 2 to 27 months. Notably, patients with anatomical abnormalities, such as VA anomalies, may experience delayed onset of vertigo and prolonged disease courses. This suggests that anatomical factors, including VA morphology, could serve as predictive markers for ALHL progression or refine MD classification, offering potential clinical utility in risk stratification and personalized management.\u003c/p\u003e\u003cp\u003eStudy Limitations\u003c/p\u003e\u003cp\u003eSeveral limitations should be acknowledged when interpreting our findings. Unlike CT\u0026rsquo;s direct visualization of bony structures, MRI indirectly assesses VA morphology through fluid or vascular signals within the aqueduct[\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]. Additionally, while MRI-T2 can identify morphological abnormalities, it lacks the resolution to distinguish between the two recently described histopathological subtypes of MD: hypoplasia and degeneration of the ES[\u003cspan citationid=\"CR32\" class=\"CitationRef\"\u003e32\u003c/span\u003e]. Furthermore, the presence of ALHL patients without detectable EH but with non-visible VA raises unanswered questions about whether these individuals represent a preclinical MD state and how extended follow-up durations may reveal progressive EH development and MD conversion. Future studies should prioritize CT-based evaluation of VA angular trajectories[\u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e] to clarify pathological subtypes and the ALHL-to-MD transition mechanism. Longitudinal cohorts with extended timelines are imperative to validate potential progression rates.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThin-slice MRI-T2 SPACE sequence enables reliable VA grading and reveals similar patterns between ALHL with EH and MD patient cohorts. This non-invasive assessment method shows significant promise for evaluating disease progression risk and facilitating early MD diagnosis. Importantly, the strong correlation between VA non-visualization and EH development highlights its potential applications in patient stratification and personalized therapeutic strategies.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003evestibular aqueduct (VA), acute low-frequency sensorineural hearing loss (ALHL), M\u0026eacute;ni\u0026egrave;re\u0026rsquo;s disease (MD), endolymphatic hydrops (EH), inversion recovery (IR), endolymphatic duct (ED), endolymphatic sac (ES)\u003c/p\u003e\n"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eHuman Ethics and Consent to Participate declarations\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study was conducted in accordance with the Declaration of Helsinki. Ethical approval was obtained from\u0026nbsp;the Institutional Review Board of a tertiary hospital in Shanghai, China (approval number: 2022054). The requirement for informed consent was waived due to the retrospective nature of the study involving anonymized clinical data.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eDeclaration of conflicting interest\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding information\u003c/strong\u003e\u003c/p\u003e\n\u003col start=\"1\" type=\"1\"\u003e\n \u003cli\u003eHealth Research Project of the Health Commission of Pudong New Area, Shanghai, China\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eNational Clinical Research Center for Otolaryngologic Diseases, Beijing, China\u003c/li\u003e\n \u003cli\u003eYouth Program of National Natural Science Foundation of China\u003c/li\u003e\n\u003c/ol\u003e\n"},{"header":"References ","content":"\u003col\u003e\n\u003cli\u003eKawashima K SHOM (2006) Epidemiological study of acute low-tone sensorineural hearing loss in Kanagawa and Iwate prefectures. 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Nat Rev Dis Primers 2:16028. https://10.1038/nrdp.2016.28\u003c/li\u003e\n\u003cli\u003eIwasaki S, Shojaku H, Murofushi T, Seo T, Kitahara T, Origasa H et al (2021) Diagnostic and therapeutic strategies for Meniere\u0026apos;s disease of the Japan Society for Equilibrium Research. Auris, Nasus, Larynx 48(1):15-22. https://10.1016/j.anl.2020.10.009\u003c/li\u003e\n\u003cli\u003eMerchant SN, Adams JC, Nadol JJ (2005) Pathophysiology of Meniere\u0026apos;s syndrome: are symptoms caused by endolymphatic hydrops? Otol Neurotol 26(1):74-81. https://10.1097/00129492-200501000-00013\u003c/li\u003e\n\u003cli\u003ePhillips JS, Murdin L, Rea P, Sutton L (2018) Clinical Subtyping of M\u0026eacute;ni\u0026egrave;re\u0026rsquo;s Disease. Otolaryngol Head Neck Surg 159(3):407-409. https://10.1177/0194599818773077\u003c/li\u003e\n\u003cli\u003eZhang S, Guo Z, Tian E, Liu D, Wang J, Kong W (2022) Meniere disease subtyping: the direction of diagnosis and treatment in the future. Expert Rev Neurother 22(2):115-127. https://10.1080/14737175.2022.2030221\u003c/li\u003e\n\u003cli\u003eEckhard AH, Zhu M, O\u0026apos;Malley JT, Williams GH, Loffing J, Rauch SD et al (2019) Inner ear pathologies impair sodium-regulated ion transport in Meniere\u0026apos;s disease. Acta Neuropathol 137(2):343-357. https://10.1007/s00401-018-1927-7\u003c/li\u003e\n\u003cli\u003eBachinger D, Luu NN, Kempfle JS, Barber S, Zurrer D, Lee DJ et al (2019) Vestibular Aqueduct Morphology Correlates With Endolymphatic Sac Pathologies in Meniere\u0026apos;s Disease-A Correlative Histology and Computed Tomography Study. Otol Neurotol 40(5):e548-e555. https://10.1097/MAO.0000000000002198\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Vestibular Aqueduct, Acute Low-Frequency Sensorineural Hearing Loss, Ménière’s Disease, Endolymphatic Hydrops, Magnetic Resonance Imaging","lastPublishedDoi":"10.21203/rs.3.rs-7224413/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7224413/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eObjective\u003c/h2\u003e\u003cp\u003eThis study investigated vestibular aqueduct (VA) morphology in acute low-frequency sensorineural hearing loss (ALHL) and M\u0026eacute;ni\u0026egrave;re\u0026rsquo;s disease (MD), assessing its association with endolymphatic hydrops (EH) and potential as a predictor for ALHL progression to MD.\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e\u003cp\u003eA retrospective analysis of 135 patients (ALHL\u0026thinsp;=\u0026thinsp;67, MD\u0026thinsp;=\u0026thinsp;44, controls\u0026thinsp;=\u0026thinsp;24) conducted between March 2019 and July 2024 utilized MRI-T2 for VA grading (Grade 0: continuous; Grade 1: discontinuous; Grade 2: non-visible) and 3D real inversion recovery (IR) sequences for EH detection.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e\u003cp\u003eThe cohort comprised 135 patients (66 males, 69 females; mean age 45.00\u0026thinsp;\u0026plusmn;\u0026thinsp;13.79 years), stratified into ALHL (n\u0026thinsp;=\u0026thinsp;67; 32 without EH, 35 with EH), MD (n\u0026thinsp;=\u0026thinsp;44), and control (n\u0026thinsp;=\u0026thinsp;24) groups. Mean age increased progressively from ALHL without EH to ALHL with EH and MD groups (P\u0026thinsp;\u0026lt;\u0026thinsp;0.0001). VA grading differed significantly between the MD and control groups (P\u0026thinsp;\u0026lt;\u0026thinsp;0.0001) and between ALHL and control groups (P\u0026thinsp;\u0026lt;\u0026thinsp;0.05). ALHL without EH showed no VA differences compared to controls. ALHL with EH exhibited VA patterns resembling MD (P\u0026thinsp;=\u0026thinsp;0.985) and bilateral VA asymmetry (affected vs. unaffected ears, P\u0026thinsp;\u0026lt;\u0026thinsp;0.05). Grade 2 VA conferred a 5.1-fold increased risk of EH (P\u0026thinsp;=\u0026thinsp;0.008). During follow-up, 10.45% of ALHL patients progressed to MD, exclusively within the EH subgroup (20% of this subgroup), with 85.7% of progressions occurring in Grade 2 VA patients.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e\u003cp\u003eMRI-T2 thin-slice SPACE sequences can reliably assess VA grading, revealing parallels between ALHL with EH and MD. Elevated VA grades, particularly grade 2, in patients with ALHL serve as predictive indicators for disease progression, with the VA grading system demonstrating clinical value for risk stratification and early MD diagnosis.\u003c/p\u003e","manuscriptTitle":"Vestibular Aqueduct Grading: an Early Predictor of Progression from Low-Frequency Sensorineural Hearing Loss to Ménière’s Disease","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-08-14 10:03:50","doi":"10.21203/rs.3.rs-7224413/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"d1e29529-b574-4987-96cc-b6ad1653c16d","owner":[],"postedDate":"August 14th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2025-09-06T04:08:40+00:00","versionOfRecord":[],"versionCreatedAt":"2025-08-14 10:03:50","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-7224413","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-7224413","identity":"rs-7224413","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}