Clinical Characteristics of Unilateral Meniere's Disease Patients without Endolymphatic Hydrops as Revealed by Magnetic Resonance Imaging

Abstract

Background: : This study investigated the heterogeneity of unilateral Meniere's disease (MD) by comparing the clinical characteristics and laboratory results between patients with and without endolymphatic hydrops (EH), analyze the correlation between the severity of hydrops and clinical manifestations, auditory, and vestibular function impairment.

Materials and methods:: In this retrospective study, 95 patients diagnosed with unilateral MD underwent 3D-FLAIR MRI scanning 24 hours after intratympanic gadolinium injection. Vestibular hydrops was graded on MRI using a 4-grade scale. Pure-tone audiometry, air-conducted sound and galvanic vestibular stimulation for cervical and ocular vestibular evoked myogenic potentials (ACS-cVEMP, GVS-cVEMP, ACS-oVEMP, GVS-oVEMP), caloric testing, and video head impulse test (vHIT) were performed, and their correlations with EH were analyzed.

Results: : Significant differences were found between the non-hydrops and hydrops groups in mean pure-tone average (PTA) and ACS-cVEMP response rate (p = 0.020, p = 0.023, respectively). The severity of vestibular hydrops correlated with disease duration (p = 0.001), PTA (p = 0.001), ACS-cVEMP response rate (p = 0.022), and vHIT gain of the posterior semicircular canal (p = 0.037).

Conclusion: : This study confirms the important diagnostic value of MRI-visualized EH in MD. It also identifies MD patients without detectable hydrops, suggesting the necessity of a comprehensive diagnostic approach integrating symptoms, functional tests, and imaging characteristics.

Graphical abstract

Keywords

Meniere's disease / endolymphatic hydrops / magnetic resonance imaging / vestibular evoked myogenic potentials / video head impulse test

1 Introduction

Meniere's disease (MD) is an idiopathic inner ear disorder characterized by recurrent episodes of vertigo, fluctuating hearing loss, tinnitus, and aural fullness. Current clinical diagnosis of MD primarily relies on history and necessary audiovestibular function tests. By combining different vestibular assessments, clinicians can evaluate saccular, utricular, and semicircular canal functions using cervical vestibular evoked myogenic potentials (cVEMP), ocular vestibular evoked myogenic potentials (oVEMP), caloric testing, and the video head impulse test (vHIT), respectively.

Endolymphatic hydrops (EH), the key pathological hallmark of MD, was historically confirmable only postmortem through temporal bone histopathology, severely limiting its clinical application for diagnosis and dynamic monitoring. However, in 2007, Nakashima et al.^[1] first visualized EH in living MD patients using MRI following intratympanic gadolinium injection, enabling morphological assessment. Subsequently, Nakashima further proposed grading criteria for EH^[2], providing a basis for quantification. Bernaerts et al.^[3] later simplified this grading method for easier clinical adoption.

MD has long been considered a typical vestibular dysfunction caused by EH. However, growing clinical evidence suggests that some patients exhibit classic MD symptoms—episodic vertigo, fluctuating hearing loss, tinnitus, and aural fullness—without clear radiological signs of EH. This phenomenon indicates that MD likely encompasses different subtypes, with some possibly driven by retro-labyrinthine pathway damage (e.g., vestibular nerve or central conduction abnormalities) or immune-mediated inflammatory mechanisms^[4]. This pathogenic diversity underscores the need for more refined imaging and biomarker studies to delineate MD subtypes, which is crucial for developing optimized and personalized treatment strategies.

This study compares the clinical characteristics (e.g., age, disease duration, hearing loss severity) and laboratory findings between unilateral MD patients with and without EH, aiming to reveal potential heterogeneity and explore the existence of distinct clinical subtypes. Furthermore, by grading EH severity on MRI, we analyzed differences in clinical manifestations and laboratory indicators among different hydrops severity groups to investigate correlations between hydrops degree and clinical features as well as audiovestibular function impairment.

2 Methods

2.1 Subjects

This study was approved by the Ethics Committee of Xinhua Hospital, Shanghai Jiao Tong University School of Medicine（No.XHEC-C-2024-135-1). Written informed consent was obtained from all participants. We retrospectively analyzed clinical data from 95 patients diagnosed with unilateral MD at the Department of Otolaryngology-Head and Neck Surgery, Xinhua Hospital, between January 2020 and April 2024. Diagnosis was based on the 2015 Barany Society consensus criteria^[5].

Inclusion criteria: (1) Unilateral MD patients with complaints such as tinnitus, aural fullness; (2) Availability of MRI scans, audiovestibular function tests, and detailed medical records from our hospital.

Exclusion criteria: (1) History of chronic otitis media or other middle/inner ear diseases; (2) Recurrent vertigo in the absence of fluctuating hearing loss; (3) History of migraine; (4) Use of vasodilators or diuretics within two weeks prior; (5) Contraindications to MRI (claustrophobia, pregnancy, gadolinium allergy).

2.2 Intratympanic gadolinium injection and MRI examination

The procedure followed our previous study^[6]. Gadolinium contrast agent (Omniscan, Xudonghaipu Pharmaceutical Co. Ltd, Shanghai, China) was diluted 8-fold with saline (v/v, 1:7). Under otoscopic guidance, an experienced otolaryngologist injected approximately 0.4-0.6 ml of diluted gadolinium into the tympanic cavity. The patient remained supine for 60 minutes to facilitate permeation into the inner ear.

MRI was performed 24 hours post-injection using a 3.0T scanner (UMR 770, United Imaging, Shanghai, China) with a 24-channel head coil, followed by 3D-FLAIR imaging. 3D-FLAIR parameters: Repetition time (TR) = 6500 ms, echo time (TE) = 286.1 ms, inversion time (TI) = 1950 ms, flip angle = 67°, slice thickness = 0.6 mm, echo train length = 160, field of view (FOV) = 200 mm × 200 mm, matrix size = 256 × 256, voxel size = 0.78 mm × 0.78 mm × 1.1 mm. Scan time: 6 min 11 s. 3D-T2-SPAIR sequence parameters: voxel size=0.65 × 0.52 × 0.76 mm, scan time = 4 min 30 s, TR = 1300 ms, TE = 254.7 ms, flip angle = 110°, slice thickness = 0.4 mm, FOV = 200 mm × 200 mm, matrix size = 384 × 384.

2.3 Image analysis

Images were independently assessed by an experienced radiologist and an otolaryngologist blinded to clinical data. In cases of disagreement among radiologist and otolaryngologist regarding imaging grading for the same patient, a consensus shall be reached through joint consultation between otolaryngologist and radiologist, and the images shall be re‑evaluated until a uniform grading result is obtained. Vestibular EH was graded using the visual assessment method proposed by Bernaerts et al.^[3] into four grades: Grade 0 (Normal): Saccule and utricle normal in size and shape; Grade 1: Saccule equal to or larger than utricle, without fusion; Grade 2: Fusion of saccule and utricle, with peripheral rim enhancement of the perilymphatic space still visible; Grade 3: Marked enlargement and fusion of saccule and utricle, with no visible perilymphatic signal. Representative images are shown in Figure 1.

2.4 Audiovestibular Function Tests

2.4.1 Audiometric evaluation

All MD patients underwent air- and bone-conduction pure-tone audiometry across frequencies (250–8000 Hz). The pure-tone average (PTA) was calculated from thresholds at 0.5, 1, and 2 kHz, following the 2017 Chinese Guideline for Diagnosis and Treatment of Meniere's Disease^[7]. Hearing stage was determined based on the worst PTA during interictal periods within the last 6 months: Stage I: PTA ≤ 25 dB HL; Stage II: PTA 26–40 dB HL; Stage III: PTA 41–70 dB HL; Stage IV: PTA > 70 dB HL.

2.4.2 Vestibular evoked myogenic potentials (VEMP)

VEMP testing used a Biologic Navigator PRO system.

cVEMP: Recording electrodes placed at the midpoint of the sternocleidomastoid muscles, reference at the sternoclavicular joint, ground on the nasion. Impedance <5 kΩ.

Air-conducted sound (ACS) consisted of 500 Hz tone bursts delivered via headphones at 95 dB nHL, with 1-ms rise/fall time, 2-ms plateau, 5 Hz stimulation rate, and 50 repetitions. galvanic vestibular stimulation (GVS) was applied with the cathode on the mastoid and the anode at the midpoint of the frontal hairline. The initial intensity was 5.0 mA at 5 Hz, and was reduced stepwise by 1.0 mA until no stable and reproducible waveforms were elicited. EMG responses were recorded using an amplifier with a bandpass filter of 20–2000 Hz and a 50-ms analysis window, averaged over 50 epochs. Patients lifted their head 30° from supine to tense muscles. A reproducible P13-N23 complex defined a response. Latencies of P13 (first positive peak) and N23 (first negative peak), and P13-N23 amplitude were recorded.

oVEMP: Parameters as above. Recording electrode placed 1 cm below the contralateral lower eyelid center, reference on the chin, ground on nasion. Patients gazed upward 25°–30° to maintain inferior oblique muscle tension, minimizing blinking.

2.4.3 Caloric testing

Caloric testing was performed using videonystagmography (VNG, Chartr 200, GN Otometrics, Denmark). Patients lay supine with head elevated 30° to align horizontal canals vertically. Air irrigation at 24 °C (cool) and 50 °C (warm) was applied to the external auditory canal. Induced nystagmus was recorded via electronystagmography in darkness. Canal paresis (CP%) was calculated using Jongkees' formula; CP% > 25% indicated significant unilateral weakness.

2.4.4 Video head impulse test (vHIT)

vHIT was conducted using an Interacoustics EyeSeeCam system (Denmark). Patients focused on a fixed target while an examiner delivered at least 20 rapid, unpredictable head impulses in each direction (amplitude 10°–20°, duration 150–200 ms, peak velocity > 150°/s). Vestibulo-ocular reflex (VOR) gain was automatically calculated as the ratio of eye velocity to head velocity at 60 ms. A VOR gain of the semicircular canal < 0.8 at 60 ms, with or without corrective saccades, was defined as abnormal.

2.5 Statistical analysis

Data were analyzed using SPSS v.27. Continuous data are presented as mean ± standard deviation. Non-normally distributed data were compared using Wilcoxon rank-sum test. Categorical variables were compared using Chi-square test. The Kruskal‑Wallis test was used to compare differences in hearing and vestibular function test results among different groups stratified by the severity of MRI‑detected endolymphatic hydrops. p < 0.05 was considered statistically significant.

3 Results

3.1 Demographic data

The study included 95 unilateral MD patients (41 male, 54 female), with 52 left-sided and 43 right-sided cases. Age ranged from 26 to 78 years (mean 60.04 ± 8.93). Mean disease duration was 5.27 ± 5.20 years. Mean PTA was 65.28 ± 16.03 dB HL. According to hearing stage: 0 (0%) Stage I, 7 (7.37%) Stage II, 54 (56.84%) Stage III, and 34 (35.79%) Stage IV patients. Baseline characteristics are summarized in Table 1.

3.2 Non-hydrops vs. hydrops Groups in MD

Among 95 patients, 11 (11.58%) showed no significant vestibular or cochlear hydrops (Figure 2), while 84 (88.42%) exhibited varying degrees of vestibular hydrops. Patients were divided into Non-hydrops (n = 11) and Hydrops (n = 84) groups. Statistical analysis compared age, disease duration, mean PTA, response rates for ACS-cVEMP, ACS-oVEMP, GVS-cVEMP, GVS-oVEMP, caloric test abnormality rate, vHIT abnormality rate, and vHIT gains for the three semicircular canals. Two non-hydrops patients and 18 hydrops patients lacked GVS-VEMP data; one hydrops patient lacked caloric test data. Significant differences were found between groups for mean PTA and ACS-cVEMP response rate (p = 0.02, p = 0.023). No significant differences were found for gender, age, disease duration, ACS-oVEMP, GVS-cVEMP, GVS-oVEMP response rates, caloric test abnormality, vHIT abnormality rate, or vHIT gains (p = 0.817, p = 0.193, p = 0.231, p = 0.986, p = 0.678, p = 1.000, p = 0.496, p = 0.089, p = 0.084, p = 0.375, p = 0.352, respectively). See Table 2.

3.3 Grading of hydrops and associated characteristics

Based on vestibular hydrops grading: Grade 0: 11 (11.58%), Grade I: 10 (10.53%), Grade II: 36 (37.89%), Grade III: 38 (40.00%). Patients were divided into four groups accordingly. Vestibular hydrops severity correlated significantly with disease duration (p = 0.001), mean PTA (p = 0.001), ACS-cVEMP response rate (p = 0.022), and vHIT gain of the posterior canal (p = 0.037). No significant correlation was found with age, ACS-oVEMP, GVS-cVEMP, GVS-oVEMP response rates, caloric test abnormality, vHIT abnormality rate, or vHIT gains of lateral and anterior canals (p = 0.452, p = 0.888, p = 0.734, p = 0.827, p = 0.319, p = 0.154, p = 0.273, p = 0.640). See Table 3.

PTA, pure-tone average (0.5, 1, 2 kHz); ACS-cVEMP, air-conducted sound cervical VEMP; ACS-oVEMP, air-conducted sound ocular VEMP; (+), response present; (−), response absent. vHIT, video head impulse test; ^*, p < 0.05.

3.4 Representative case

A 49-year-old female presented with recurrent vertigo and left hearing loss for 3 years. She experienced sudden left hearing loss with persistent high-frequency tinnitus and aural fullness, followed by rotatory vertigo lasting 6-7 hours, accompanied by nausea and vomiting. She had two episodes within a month. Initial outpatient diagnosis was left MD, treated with betahistine and citicoline, with lifestyle/dietary modifications. Vertigo improved, but tinnitus and fullness persisted. Two years later, vertigo recurred (3 episodes/month), unresponsive to medication. PTA was 70 dB HL in the left ear. MRI with intratympanic gadolinium showed no hydrops. She subsequently underwent three semicircular canal occlusion surgery, resulting in successful vertigo control. See Figure 3 for MRI, audiometric, and vestibular test results.

4 Discussion

MD is associated with recurrent episodic vertigo, tinnitus, aural fullness, and fluctuating hearing loss, and is considered an inner ear disorder with multiple contributing factors, classically featuring EH or endolymphatic space dilation. However, our data suggest the existence of a special MD type—one without detectable EH. Patients in this exhibit classic MD symptoms and meet diagnostic criteria, yet show no hydrops in the vestibule or cochlea on gadolinium-enhanced MRI.

Temporal bone histopathology remains the gold standard for EH detection, first identified in MD by Yamakawa^[8] and Hallpike & Cairns^[9]. However, some histopathological studies report MD cases without EH. For instance, Fraysee et al.^[10] found 7% of clinically diagnosed MD ears lacked EH; Foster et al.^[13] observed at least 2 out of 165 MD temporal bones without definite EH. These findings support the possible existence of a non-hydrops MD, providing important anatomical-pathological evidence.

While histopathology is the EH diagnostic gold standard, its requirement for postmortem tissue limits clinical utility. Therefore, gadolinium-enhanced inner ear MRI is used for in vivo EH assessment. Similar to histopathology, some clinically definite MD patients show no EH on MRI. Clinical studies report EH detection rates of 81%–94% in MD patients^[15-^23], consistent with our finding (88.42%).

The etiology of MD remains incompletely understood. Although labyrinthine hydrops is closely related to MD pathophysiology, our study identifies definite MD patients (per 2015 AAO-HNS criteria) without radiologically detectable EH. This observation has dual implications: first, MD pathogenesis may involve non-hydrops pathological factors yet to be identified; second, evidence supports the involvement of inflammatory responses, immune dysregulation, and other multifactorial mechanisms that may independently or synergistically trigger characteristic MD symptoms^[4, ^14].

Although EH is traditionally viewed as a core pathological feature of MD, and previous studies suggest EH severity increases with disease progression^[24], the association between EH status and clinical features remains debated. Regarding disease duration, Yang et al.^[25] found no significant link between duration and vestibular/cochlear EH, while Gurkov et al.^[26], Guo et al.^[27], Wu et al.^[28], and Fiorino et al.^[29] reported positive correlations. Our study also found vestibular EH severity correlated with duration (p = 0.001), while non-hydrops MD patients did not show this association. Regarding hearing, multiple studies indicate hearing thresholds correlate positively with cochlear/vestibular EH grade^[25, ²⁶, ³⁰-^33], particularly low and mid-frequency PTA^[28], with low-frequency hearing impairment indirectly reflecting EH severity^[34]. Our findings align: hydrops patients had higher mean PTA, and greater hydrops severity associated with longer duration and worse hearing. Regarding vestibular function, tests like VEMP, vHIT, and caloric testing show EH group patients had lower ACS-cVEMP response rates, higher caloric and vHIT abnormality rates, and EH degree correlated positively with vHIT abnormality. Gurkov et al.^[26] found vestibular EH negatively correlated with VEMP amplitude ratio, and Guo et al.^[27] observed decreasing oVEMP response rates with worsening EH. Non-hydrops MD patients showed significantly lower vestibular test abnormality rates compared to the EH group, except for Kahn et al.^[32] who found no association. Our study found lower ACS-cVEMP response rates in the hydrops group, a positive correlation between hydrops severity and vHIT abnormality rate, but no clear correlation with VEMP response rates. The difference in the detection rate between groups may be confounded by factors such as hearing level and disease duration. Distinct differences in clinical characteristics exist between MD patients with and without EH, suggesting EH status may be key for distinguishing MD subtypes.

Although EH is widely regarded as central to MD, its absence on MRI in some patients suggests diverse etiology. This indicates EH is not the sole diagnostic criterion. Diagnosis should integrate patient history, clinical symptoms, and cochleovestibular function assessment to avoid missing this special subgroup. Recent advances in EH imaging, such as 3D-MIP (maximum intensity projection) hydrops models enabling 3D volumetric analysis and potential direct hydrops volume calculation, promise enhanced precision in inner ear assessment and may represent a milestone in MRI diagnosis of EH^[33, ^36].

5 Conclusion

This study confirms the significant diagnostic role of MRI-visualized EH in MD while identifying a patient subgroup without radiological evidence of hydrops. This finding suggests MD may encompass subtypes with pathogenesis independent of EH. Clinically, while emphasizing the value of MRI for hydrops assessment, physicians must not overlook patients with typical symptoms but negative imaging. We recommend establishing a comprehensive diagnostic framework integrating clinical symptoms, vestibular function tests, and imaging characteristics to improve diagnostic accuracy.

6 Limitations

The cohort of this study mainly consisted of patients with MD at stages Ⅲ–Ⅳ, which may to a certain extent limit the extrapolation of the study results to the early-stage patient population. Future studies will include more patients with early-stage MD to further improve the relevant conclusions. The unbalanced sample size between groups in this study may reduce the statistical test power and increase the risk of Type Ⅱ error. Future studies should optimize the sample design to improve the reliability of the results. This study detected multiple auditory and vestibular function indicators, and multiple between-group comparisons may increase the risk of Type Ⅰ error. No multiple comparison correction was performed in this study, so the interpretation of the results should be more cautious. Future studies may consider correction to improve reliability.

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