Skip to main content
NCBI home page
Journal of the American Academy of Audiology logoLink to Journal of the American Academy of Audiology
. 2026 May 1;37(3):265–271. doi: 10.3766/jaaa.250018

The Degree of Audiovestibular Loss Is Not Related to Current Vertigo Attacks in Refractory Unilateral Ménière’s Disease

Mitesh Patel *,✉
PMCID: PMC13327962  PMID: 42403960

Abstract

Background:

Unilateral Ménière’s disease (MD) is characterized by severe episodic attacks of rotational vertigo and audiovestibular signs that include fluctuating sensorineural hearing loss, aural fullness, tinnitus, and vestibular loss.

Purpose:

To investigate the relationship between the degree of audiovestibular loss, symptoms, and the number of vertigo attacks during the previous 6 months and 1 month of patients with MD.

Study Sample:

Sixty patients with active MD refractory to oral treatment.

Data Collection and Analysis:

Hearing (pure-tone audiometry and speech discrimination) and vestibular (caloric test, vestibular evoked myogenic potential [VEMP]) tests were performed. Symptoms were scored using the following validated questionnaires: Vertigo Symptom Scale-short form, Dizziness Handicap Inventory, Tinnitus Handicap Inventory, Aural Fullness Scale, and Functional Level Scale. Linear regression, a factor analysis, and a correlation analysis were conducted.

Results:

Patients experienced a mean number of 16 attacks (range, 2–65) during the previous 6 months and five attacks (range, 0–30) during the previous 1 month. Hearing and vestibular functions were reduced in the affected ear. Linear regression, the factor analysis, and the correlation analysis showed no association between the degree of audiovestibular loss and the number of vertigo attacks during the previous 6 months or 1 month or symptoms of disease activity. An exploratory analysis showed evidence of some associations between the degree of hearing loss, caloric paresis, and VEMP asymmetry, indicating a consistent pattern of loss across the cochlear semi-circular canals and saccules.

Conclusion:

Although audiovestibular tests help establish diagnoses, they cannot determine current disease activity of unilateral refractory MD.

Clinical Relevance Statement:

It may be prudent to assume that patients with MD and high remaining vestibular function in the affected ear would experience more frequent episodes of vertigo and intense dizziness and experience more troublesome symptoms. Conversely, it may be prudent to assume that patients with MD with low remaining vestibular function in the affected ear would experience fewer episodes of vertigo; however, as shown by these results, this does not seem to be the case. No obvious audiovestibular markers suggest that intratympanic therapy for vertigo treatment should be delayed.

Keywords: hearing, Ménière’s disease, vestibular, vertigo

INTRODUCTION

Ménière’s disease (MD) is characterized by episodic vertigo, sensorineural hearing loss, aural fullness, tinnitus, and vestibular loss (AAOH-N, 1995). A failure of one or more of the many inner ear homoeostatic systems that regulate endolymph and perilymph, afferent and efferent nerve signaling, and blood flow may lead to MD, although the mechanisms are unclear (Yang et al., 2023). Treatment of MD is palliative and comprises a combination of dietary adjustments, medication to improve blood flow, or semi-invasive intratympanic injections (Lopez-Escamez & Perez-Carpena, 2024). Although the type of treatment is influenced by the current level of disease activity, specifically the frequency of vertigo attacks, whether any audiovestibular test reflects the level of disease activity is unclear. Establishing indicators of current disease activity is particularly important because patients can experience total remission of several years and ablative treatment is associated with the risk of hearing destruction and iatrogenic vertigo; therefore, clinicians must exercise caution before using this treatment.

Vertigo attacks in MD are thought to be attributable to endolymph draining into the cochlear and vestibular apparatus causing rupture, distortion, or collapse of the membranous labyrinth (Strupp & Brandt, 2009). This damage is believed to lead to the production of endolymphatic hydrops (Strupp & Brandt, 2013) and alterations in the mechanical and electrical properties in the inner ear (Frejo & Lopez-Escamez, 2023), which could explain reduced hearing and vestibular functions. Moreover, the typical vertigo attack is ushered in by an increased sense of aural fullness, deafness, or tinnitus in the affected ear (Pyykkö et al., 2013), thus indicating a link between audiovestibular signs and current disease activity.

Because the diagnosis of MD can be difficult to differentiate from other conditions such as vestibular migraine, clinical audiovestibular tests form an important part of its assessment. In unilateral MD, the bithermal caloric test is pathologically asymmetrical in 65 to 73 percent of cases (Taylor et al., 2011), and cervical vestibular evoked myogenic potentials (VEMPs) are reduced unilaterally in approximately 30 to 50 percent of cases (Huang et al., 2011; Kim et al., 2013). New research has suggested that a pathological cervical VEMP can distinguish definite MD from probable MD (Gündoğdu et al., 2025). Interestingly, some authors have found that the degree of audiovestibular loss is associated with the distribution of hydrops (Gürkov et al., 2012; Seo et al., 2013). However, previous studies have also indicated no change in audiovestibular function immediately before or after a vertigo attack. McNeill et al. (2009) reported no significant change in the hearing threshold of five out of six patients with MD before or after a vertigo attack. Similarly, Proctor (2000) found that soon after an acute vertigo attack, only one of eight patients with MD exhibited a decreased ipsilesional caloric response, but three exhibited an increased response.

This study aimed to investigate whether the degree of audiovestibular loss is associated with the number of vertigo attacks in active MD. With time, attacks tend to be briefer, less violent, and less frequent; this appears to be linked to reduced vestibular function as the disease “burns out” (Pyykkö et al., 2024). The disease also appears to have an increased prevalence in female patients (Thompson-Harvey et al., 2023). Therefore, whether patient history (age, disease duration, side of disease, and sex) affects the frequency of vertigo attacks was also investigated. The final aim was to investigate the relationship between the degree of audiovestibular loss and clinical scales of aural fullness, tinnitus, vertigo, dizziness, and functional level.

METHODS

Subjects

Sixty participants were recruited by and tested at a single center. Inclusion criteria were age 18 to 70 years of age, definite unilateral MD defined according to the American Academy (AAOH-N, 1995), experienced at least two episodes of rotational vertigo that lasted at least 20 min during the previous 6 months, and no response to standard medical treatment (i.e., betahistine, diuretics, dietary restrictions). Disease duration was considered the time elapsed since the onset of the first definitive episode of vertigo or first auditory symptom (fluctuating hearing loss, tinnitus, or aural fullness). Exclusion criteria were other active neuro-otological disorders (e.g., vestibular migraine), central disorders, active middle ear disease, and pregnancy. Three patients had grommets in situ, did not undergo the caloric test, and had preserved tympanic reflexes. Two different patients underwent previous endolymphatic sac surgery. No patients had received intratympanic therapies (e.g., gentamicin or corticosteroids) or other ablative procedures. However, all had received instructions to perform Cawthorne-Cooksey head exercises to facilitate vestibular compensation and reduce dizziness between attacks. All patients provided written informed consent before enrollment, and the study was performed in accordance with the Declaration of Helsinki 1964 and its later amendments. The study was approved by the London-Fulham Research Ethics Committee, Imperial College Joint Research Compliance Office (CRO1135), and it was sufficiently powered (60 participants; a sample size of 47 was required for an alpha [two-tailed] = 0.05 and expected correlation coefficient r = 0.4).

Procedure

Audiometry

Pure-tone audiometry tests contralesional and ipsilesional air conduction thresholds at 0.25, 0.5, 1, 2, 3, 4, 6, and 8 kHz and bone conduction thresholds at 0.5, 1, 2, and 4 kHz. In the analysis, the mean ipsilesional pure-tone low-frequency thresholds across 0.5, 1, 2, and 3 kHz were measured in line with the recommendations (AAOH-N, 1995). Bone conduction was performed as necessary.

Speech Discrimination

Speech discrimination was assessed using suprathreshold word recognition testing. Arthur Boothroyd’s isophonemic word lists (AB wordlists, Guymark, Southampton) comprising sets of 10 words were played for the ipsilesional ear at the low-frequency pure-tone thresholds of 0.5, 1 and 2 kHz + 30 dB with masking sound in the contralesional ear when necessary. The formula for the level of masking was as follows: low-frequency pure-tone threshold in the ipsilesional ear − the bone conduction mean threshold (0.5, 1, and 2 kHz) in the contralesional ear – 40 dB. Step increments and decrements of 10 dB for speech loudness and masking were used to attain the maximum speech discrimination score.

Caloric Test

Bithermal (30 and 44°C) water caloric tests were conducted, thus providing the percentage of caloric paresis from slow-phase velocity eye movements (Jongkees formula: 100 × [(Left Cold + Left Warm) − (Right Cold + Right Warm)/(Left Cold + Left Warm + Right Cold + Right Warm)]).

Cervical Vestibular Evoked Myogenic Potential

A custom system delivered air-conducted sound monaurally via audiological headphones and recorded ipsilateral sternocleidomastoid electromyographic activity. Sound was delivered as 500-Hz tone bursts at 110 dB (normal hearing level) of positive polarity. Electromyographic signals were averaged over 200 sweeps and rectified. Electrical resistance across electrodes was <5 KΩ. The electrode montage comprised the right and left sternocleidomastoid muscle bellies, right and left ipsilateral midclavical bones (reference), and sternum (ground). Patients were supine on an examination bed, with the upper torso elevated, backrest at 30°, and lower body flat. Then, they were asked to elevate the head from the support and turn the head either to the left (right ear test) or to the right (left ear test) to increase tonic neck muscle activity. A biofeedback device regulated contractile strength (approximately 30 µV). The VEMP amplitudes were the differences in µV between the first distinctive peak in waveform (p13) and the first trough (n23) for the ipsilesional and contralesional sides. The percentage amplitude asymmetry was used in analyses (asymmetry ratio: 100 × [(Left – Right)/(Left + Right)].

Frequency of Vertigo Attacks and Questionnaires

According to the American Academy guidelines (AAOH-N, 1995) patients were asked: “How many attacks of rotational vertigo lasting longer than 20 min have you had in the past 6 months?” and “How many attacks of rotational vertigo lasting longer than 20 min have you had in the last month?” Symptom questionnaires were the Vertigo Symptom Scale-short form (VSS) (Yardley et al., 2012), Dizziness Handicap Inventory (DHI) (Jacobson & Newman, 1990), Tinnitus Handicap Inventory (THI) (Newman et al., 1998), Aural Fullness Scale (AFS), and Functional Level Scale (FLS) (AAOH-N, 1995). Age, disease duration, side of disease, and sex were possible predictive cofactors.

Statistical Analysis

Linear regression, factor analyses, and Pearson’s correlation were used to explore predictor variables for the number of vertigo attacks and clinical scales (VSS, DHI, THI, AFS, and FLS questionnaires). Negative values were used when the direction of asymmetry was contralesional. In the factor analysis, any loadings <0.4 were treated as nonsignificant. With a Bonferroni correction, p < 0.005 was deemed significant. For transparency, p < 0.05 is reported in the text.

RESULTS

The 60 study patients (28 female patients, 25 with right-sided disease) had a mean age of 51.6 years (standard deviation [SD], ±11.3 years; range, 20–70 years) and mean disease duration of 3.9 years (SD, ±4.5 years; range, 6 months–22 years). Patients reported means of 16 vertigo attacks (SD, ±14; range, 2–65) during the previous 6 months and five vertigo attacks (SD, ±6; range, 0–30) during the previous 1 month. As expected, a positive association was observed between the number of vertigo attacks during the previous 6 months and that during the previous 1 month (Spearman’s rank correlation = 0.71; p < 0.001).

Audiovestibular Findings

Reduced ipsilesional hearing and vestibular function were observed (mean ± SD): ipsilesional hearing threshold, 50.6 ± 17.8 dB; speech discrimination, 69 ± 25 percent (contralesional side, 100 percent); caloric paresis, 40 ± 22 percent; and VEMP asymmetry, 31.3 ± 27.6 percent.

Audiovestibular Function Versus Vertigo Attacks

Linear regression was performed. The dependent variables were the number of vertigo attacks during the previous 6 months and 1 month. The predictor variables were ipsilesional pure-tone hearing threshold (dB), ipsilesional speech discrimination (%), caloric paresis (%), and VEMP asymmetry (%). However, no variables were entered into the regression for the number of vertigo attacks during the previous 6 months (6.4 percent variance; adjusted R2) or 1 month (8.1 percent variance). A factor analysis was conducted to explore potential groupings among predictor variables related to the vertigo attack frequency. Sampling adequacy was confirmed (Kaiser-Meyer-Olkin measure = 0.46; Bartlett’s test of sphericity, χ2 = 449; p < 0.001), indicating that the data were suitable for the factor analysis. Using principal components extraction with varimax rotation, no clear factor structure emerged because all variable loadings were <0.4. Consequently, no factors were retained, suggesting that the predictor variables did not form distinct clusters associated with the number of vertigo attacks. Finally, two-tailed Spearman’s correlations showed no correlations confirming the findings of regression. An example of this nonassociation is shown in Figure 1, which shows the hearing function in relation to the number of vertigo attacks.

Figure 1.

Figure 1.

Open in a new tab

Mean pure-tone hearing thresholds at 0.5, 1, 2, and 3 kHz (line graph) are shown in relation to the number of vertigo attacks reported over the preceding 6 months (black bars) and 1 month (gray bars) across all 60 participants. No significant association was observed between the degree of hearing loss and attack frequency over either time interval. As illustrated, participants who experienced a higher number of attacks during the preceding 6 months generally reported more frequent attacks during the preceding month.

Patient History Versus Vertigo Attacks

The same analyses were repeated, but they included age, disease duration, side, and sex data in the regression, factor analyses, and correlation analyses to examine the contribution of patient history to the number of vertigo attacks. No association between age, disease duration, side, and sex and the number of vertigo attacks were observed with linear regression, factor analysis (all loadings <0.4), or two-tailed Spearman’s correlations. However, a trend association between decreased vertigo attacks during the previous 6 months and disease duration (Spearman’s rank correlation = −0.242; p = 0.058) in the correlational analysis was observed.

Symptom Questionnaires

Audiovestibular function was not correlated with any of the symptom questionnaires. The following scores (mean ± SD) were produced: VSS, 22 ± 12; DHI, 54 ± 20; THI, 44 ± 26; AFS, 5.7 ± 3.1; and FLS, 3.6 ± 0.8. The VSS score was associated with the number of vertigo attacks during the previous 6 months and was above the Bonferroni cutoff for significance (Spearman’s rank correlation = 0.35; p = 0.010), and it was significantly associated with vertigo attacks during the previous 1 month (Spearman’s rank correlation = 0.43; p = 0.004). A higher FLS score was associated with a higher number of vertigo attacks during the previous 1 month and was above the Bonferroni cutoff for significance (Spearman’s rank correlation = 0.38, p = 0.018). No other questionnaire scores showed significant correlations with the number of vertigo attacks during the previous 6 months or 1 month.

Significant associations between symptom scores were observed (Table 1). The factor analysis also confirmed a high degree of overlap in symptom questionnaire data (i.e., all questionnaires grouped together).

Table 1.

Spearman’s Rank Correlation between the Vertigo Symptom Scale, Dizziness Handicap Inventory, Tinnitus Handicap Inventory, Functional Level Scale, and Aural Fullness Scale

Correlation coefficient VSS DHI THI FLS AFS
VSS 0.51*** 0.40** 0.36**
DHI 0.38** 0.52***
THI
FLS 0.31**
AFS
Open in a new tab

Significance is shown as follows: ***p < 0.001, **p < 0.005. Italics indicate p < 0.01, which is above the Bonferroni cutoff level. All other nonsignificant correlations are suppressed for clarity.

AFS = Aural Fullness Scale; DHI = Dizziness Handicap Inventory; FLS = Fullness Level Scale; THI = Tinnitus Handicap Inventory; VSS = Vertigo Symptom Scale.

Audiovestibular Loss Progression

A further exploratory correlation analysis was performed to examine whether audiovestibular functions followed a consistent pattern of loss across the labyrinth in patients with active MD. Patients with greater ipsilesional hearing loss had a larger caloric paresis that was above the Bonferroni cutoff for significance (Spearman’s rank correlation = 0.320; p = 0.012) (Figure 2A) but a significant association with poorer speech discrimination (Spearman’s rank correlation = −0.60; p < 0.001) (Figure 2B).

Figure 2.

Figure 2.

Open in a new tab

Significant correlations between audiovestibular functions. (A) Larger ipsilesional hearing loss was associated with larger caloric paresis. (B) Larger ipsilesional hearing loss was associated with poorer speech discrimination.

DISCUSSION

As expected, patients with MD had reduced ipsilesional audiological function and weaker ipsilesional vestibular responses. However, the degree of audiovestibular loss was not associated with the number of vertigo attacks during the previous 6 months or 1 month according to linear regression, factor analyses, or correlational analyses. Patient history, including sex, age, disease duration, and disease side, did not influence the outcomes of linear regression or factor analyses and was not correlated with the number of vertigo attacks. An analogous finding by McNeill et al. (2009) showed that hearing thresholds and daily hearing fluctuations were not associated with the occurrence of vertigo attacks or their frequency over an 8-week investigational period in definite MD. Consistent with this view, 20 percent of patients with MD experience hearing loss at least 5 years before vertigo attacks (Pyykkö et al., 2024); during that time, significant hearing loss may have developed. Magnetic resonance imaging performed immediately after a vertigo attack showed no obvious collapse of the labyrinthine membrane (Nakashima et al., 2016; Nakada et al., 2021), thus creating doubt regarding the suspected cause of audiovestibular loss during vertigo attacks in MD. In contrast, a recent study showed that cervical VEMP and ocular VEMP through galvanic responses are associated with the frequency of vertigo attacks (Wu et al., 2020). This new method of eliciting VEMPs may reveal findings that available routine clinical techniques do not.

In addition to vertigo attacks, disease activity in MD is signaled by ongoing vertiginous, dizziness, tinnitus, and aural fullness symptoms. Audiovestibular loss was not associated with clinical scales of vertigo, dizziness, tinnitus aural fullness symptoms, or the level of disability (i.e., functional level), indicating discrepancy between vestibular peripheral and vestibular perceptual investigations. However, understanding the patient perspective is particularly relevant to the management of vestibular disorders. In fact, dizziness estimates are associated with anxiety and depression in MD (Yeo et al., 2025). The significant co-relationships between subjective symptoms (Table 1) may indicate difficulty disentangling symptoms; therefore, each symptom may be difficult to clearly distinguish. As a result, when one symptom perceivably improves, the patient’s overall wellbeing is improved; however, when one symptom worsens, the patient may feel substantially affected.

In an exploratory correlation analysis, some evidence suggested a consistent loss of function across the horizontal semi-circular canal (caloric asymmetry), cochlea (ipsilesional pure-tone average, speech discrimination), and saccule (VEMP amplitude asymmetry). Accordingly, a relationship between audiovestibular function and endolymphatic hydrops distribution has been found (Gürkov et al., 2011; Hu et al., 2023; Leng et al., 2023), but not between hydrops distribution and the number of vertigo attacks, tinnitus, aural fullness, or Functional Level Scale scores (Fiorino et al., 2011), corroborating the current findings.

The wide disease duration among patients (6 months–22 years) introduces an element of heterogeneity because MD evolves considerably over time. Patients with earlier stages of disease may exhibit more active, fluctuating symptoms, whereas those with later stages of disease may experience fewer attacks but more persistent auditory dysfunction. Consequently, the inclusion of participants across a broad disease spectrum may have diluted potential associations or obscured stage-specific patterns. Notably, patients with the delayed subtype of MD may have been included in this study, which may have introduced further heterogeneity into the cohort. However, because disease duration was defined as the time elapsed since the onset of the first definitive episode of vertigo or the first auditory symptom, this approach likely captures the clinical course of both typical and delayed subtypes. Nevertheless, the inclusion of delayed-onset cases could influence interpretations. Furthermore, the results may be influenced by current disease activity. Participants with active MD who experienced vertigo during the preceding 6 months, which is defined by the AAOH-N (1995) as currently symptomatic, were recruited. The results of asymptomatic individuals or those assessed later after an acute episode of vertigo may be somewhat different.

A limitation of this study was the absence of video Head Impulse Testing. Although the video Head Impulse Test gain is often normal in MD, the inclusion of the video Head Impulse Test gain and asymmetry would have provided a more complete picture of vestibular function across frequency domains.

In the clinic, it may be prudent to assume that a patient with MD with high remaining vestibular function in the affected ear would experience more frequent episodes of vertigo and intense dizziness and have more troublesome symptoms. Conversely, it may be prudent to assume that a patient with MD with lower remaining vestibular function in the affected ear would experience fewer episodes of vertigo; however, as shown by the current results, this does not seem to be the case. No obvious audiovestibular markers suggest that intratympanic therapy for vertigo treatment should be delayed.

CONCLUSION

The results suggest that although audiovestibular tests help to establish diagnosis, they are less useful for determining current disease activity. No obvious audiovestibular markers suggest that intratympanic therapy for vertigo treatment should be delayed.

Acknowledgments

I thank Dr. Qadeer Arshad, Dr. Kiran Agarwal, and Professor Adolfo Bronstein.

Abbreviations

AFS

Aural Fullness Scale

DHI

Dizziness Handicap Inventory

MD

Ménière’s disease

FLS

Functional Level Scale

SD

standard deviation

THI

Tinnitus Handicap Inventory

VEMP

vestibular evoked myogenic potential

VSS

Vertigo Symptom Scale

Footnotes

Any mention of a product, service, or procedure in the Journal of the American Academy of Audiology does not constitute an endorsement of the product, service, or procedure by the American Academy of Audiology.

REFERENCES

  1. AAOH-N. (1995). Committee on hearing and equilibrium guidelines for the diagnosis and evaluation of therapy in Meniere’s disease. Otolaryngology-Head and Neck Surgery, 113(3), 181–185. 10.1016/S0194-5998(95)70102-8. [DOI] [PubMed] [Google Scholar]
  2. Fiorino, F., Pizzini, F. B., Beltramello, A., & Barbieri, F. (2011). MRI performed after intratympanic gadolinium administration in patients with Ménière’s disease: correlation with symptoms and signs. European Archives of Oto-Rhino-Laryngology, 268(2), 181–187. 10.1007/s00405-010-1353-5. [DOI] [PubMed] [Google Scholar]
  3. Frejo, L., & Lopez-Escamez, J. A. (2023). Recent advances in understanding molecular bases of Ménière’s disease. Faculty Reviews, 12, 11. 10.12703/r/12-11. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Gündoğdu, O., Yeral, C., Tunç, A. A., Mutlu, B. Ö., Yaman, H., & Yılmaz, O. (2025). Vestibular function in probable vs. definite Menière's disease: A cross-sectional retrospective analysis. The Journal of Laryngology and Otology, 139(7), 572–576. 10.1017/s0022215125000349. [DOI] [PubMed] [Google Scholar]
  5. Gürkov, R., Flatz, W., Louza, J., Strupp, M., Ertl-Wagner, B., & Krause, E. (2012). Herniation of the membranous labyrinth into the horizontal semicircular canal is correlated with impaired caloric response in Ménière’s disease. Otology and Neurotology, 33(8), 1375–1379. 10.1097/MAO.0b013e318268d087. [DOI] [PubMed] [Google Scholar]
  6. Gürkov, R., Flatz, W., Louza, J., Strupp, M., & Krause, E. (2011). In vivo visualization of endolyphatic hydrops in patients with Meniere’s disease: correlation with audiovestibular function. European Archives of Oto-Rhino-Laryngology, 268(12), 1743–1748. 10.1007/s00405-011-1573-3. [DOI] [PubMed] [Google Scholar]
  7. Hu, Y., Zhang, Y., Zhao, X., & Li, J. (2023). Endolymphatic hydrops imaging and correlation with clinical characteristics, audiovestibular function and mental impairment in patients with Meniere’s disease. European Archives of Oto-Rhino-Laryngology, 280(9), 4027–4036. 10.1007/s00405-023-07899-w. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Huang, C. H., Wang, S. J., & Young, Y. H. (2011). Localization and prevalence of hydrops formation in Meniere’s disease using a test battery. Audiology and Neurotology, 16(1), 41–48. 10.1159/000312199. [DOI] [PubMed] [Google Scholar]
  9. Jacobson, G. P., & Newman, C. W. (1990). The development of the dizziness handicap inventory. Archives of Otolaryngology - Head and Neck Surgery, 116(4), 424–427. 10.1001/archotol.1990.01870040046011. [DOI] [PubMed] [Google Scholar]
  10. Kim, M. B., Choi, J., Park, G. Y., Cho, Y. S., Hong, S. H., & Chung, W. H. (2013). Clinical value of vestibular evoked myogenic potential in assessing the stage and predicting the hearing results in ménière's disease. Clinical and Experimental Otorhinolaryngology, 6(2), 57–62. 10.3342/ceo.2013.6.2.57. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Leng, Y., Fan, W., Liu, Y., Xia, K., Zhou, R., … Liu, B. (2023). Comparison between audio-vestibular findings and contrast-enhanced MRI of inner ear in patients with unilateral Ménière’s disease. Frontiers in Neuroscience, 17, 1128942. 10.3389/fnins.2023.1128942. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Lopez-Escamez, J. A., & Perez-Carpena, P. (2024). Update on the pathophysiology, diagnosis and management of ménière's disease. Current Opinion in Otolaryngology & Head & Neck Surgery, 32(5), 306–312. 10.1097/MOO.0000000000001002. [DOI] [PubMed] [Google Scholar]
  13. McNeill, C., Cohen, M. A., & Gibson, W. P. (2009). Changes in audiometric thresholds before, during and after attacks of vertigo associated with Meniere’s syndrome. Acta Oto-Laryngologica, 129(12), 1404–1407. 10.3109/00016480902751672. [DOI] [PubMed] [Google Scholar]
  14. Nakada, T., Teranishi, M., Sugiura, S., Uchida, Y., Naganawa, S., & Sone, M. (2021). Imaging of endolymphatic hydrops on a vertigo attack of Meniere’s disease. Nagoya Journal of Medical Science, 83(1), 209–216. 10.18999/nagjms.83.1.209. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Nakashima, T., Pyykkö, I., Arroll, M. A., Casselbrant, M. L., Foster, C. A., … Young, Y. H. (2016). Meniere's disease. Nature Reviews Disease Primers, 2, 16028. 10.1038/nrdp.2016.28. [DOI] [PubMed] [Google Scholar]
  16. Newman, C. W., Sandridge, S. A., & Jacobson, G. P. (1998). Psychometric adequacy of the tinnitus handicap inventory (THI) for evaluating treatment outcome. Journal of the American Academy of Audiology, 9(2), 153–160. [PubMed] [Google Scholar]
  17. Proctor, L. R. 2000. Results of serial vestibular testing in unilateral Ménière's disease. The American Journal of Otology, 21(4), 552–558. [PubMed] [Google Scholar]
  18. Pyykkö, I., Nakashima, T., Yoshida, T., Zou, J., & Naganawa, S. (2013). Meniere's disease: a reappraisal supported by a variable latency of symptoms and the MRI visualisation of endolymphatic hydrops. BMJ Open, 3(2), e001555. 10.1136/bmjopen-2012-001555. [DOI] [PMC free article] [PubMed] [Google Scholar]
  19. Pyykkö, I., Zou, J., & Vetkas, N. (2024). Changes in symptom pattern in Meniere’s disease by duration: the need for comprehensive management. Frontiers in Neurology, 15, 1496384. 10.3389/fneur.2024.1496384. [DOI] [PMC free article] [PubMed] [Google Scholar]
  20. Seo, Y. J., Kim, J., Choi, J. Y., & Lee, W. S. (2013). Visualization of endolymphatic hydrops and correlation with audio-vestibular functional testing in patients with definite Meniere’s disease. Auris Nasus Larynx, 40(2), 167–172. 10.1016/j.anl.2012.07.009. [DOI] [PubMed] [Google Scholar]
  21. Strupp, M., & Brandt, T. (2009). Current treatment of vestibular, ocular motor disorders and nystagmus. Therapeutic Advances in Neurological Disorders, 2(4), 223–239. 10.1177/1756285609103120. [DOI] [PMC free article] [PubMed] [Google Scholar]
  22. Strupp, M., & Brandt, T. (2013). Peripheral vestibular disorders. Current Opinion in Neurology, 26(1), 81–89. 10.1097/WCO.0b013e32835c5fd4. [DOI] [PubMed] [Google Scholar]
  23. Taylor, R. L., Wijewardene, A. A., Gibson, W. P., Black, D. A., Halmagyi, G. M., & Welgampola, M. S. (2011). The vestibular evoked-potential profile of Ménière's disease. Clinical Neurophysiology, 122(6), 1256–1263. 10.1016/j.clinph.2010.11.009. [DOI] [PubMed] [Google Scholar]
  24. Thompson-Harvey, A., Friedland, D. R., Adams, J. A., Tong, L., Osinski, K., & Luo, J. (2023). The demographics of menière's disease: Selection bias or differential susceptibility? Otology & Neurotology, 44(2), e95–e102. 10.1097/MAO.0000000000003780. [DOI] [PMC free article] [PubMed] [Google Scholar]
  25. Wu, P. H., Chang, C. M., Lo, W. C., Wang, C. T., Wen, M. H., … Cheng, P. W. (2020). Prediction of unilateral Meniere’s disease attack using inner ear test battery. Ear & Hearing, 41(3), 615–621. 10.1097/AUD.0000000000000785. [DOI] [PubMed] [Google Scholar]
  26. Yang, C. H., Yang, M. Y., Hwang, C. F., & Lien, K. H. (2023). Functional and molecular markers for hearing loss and vertigo attacks in Meniere’s disease. International Journal of Molecular Sciences, 24(3), 2504. 10.3390/ijms24032504. [DOI] [PMC free article] [PubMed] [Google Scholar]
  27. Yardley, L., Barker, F., Muller, I., Turner, D., Kirby, S., … Little, P. (2012). Clinical and cost effectiveness of booklet based vestibular rehabilitation for chronic dizziness in primary care: single blind, parallel group, pragmatic, randomised controlled trial. BMJ, 344, e2237. 10.1136/bmj.e2237. [DOI] [PMC free article] [PubMed] [Google Scholar]
  28. Yeo, B. S. Y., Toh, E. M. S., Lim, N. E., Lee, R. S., Ho, R. C. M., … Ngo, R. Y. S. (2025). Association of Menière's disease with depression and anxiety: a systematic review and meta-analysis. European Archives of Oto-Rhino-Laryngology, 282(8), 3869–3881. 10.1007/s00405-025-09297-w. [DOI] [PubMed] [Google Scholar]

Articles from Journal of the American Academy of Audiology are provided here courtesy of American Academy of Audiology

RESOURCES