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 Table of Contents  
ORIGINAL ARTICLE
Year : 2020  |  Volume : 26  |  Issue : 4  |  Page : 247-253

Is cervical vestibular evoked myogenic potentials an effective tool for the evaluation of saccular function in patients suffering from peripheral vertigo? An analytical study


Department of ENT, Armed Forces Medical College, Pune, 1Department of ENT, INHS Asvini, Mumbai, Maharashtra, India

Date of Submission14-May-2020
Date of Acceptance30-Jul-2020
Date of Web Publication23-Apr-2021

Correspondence Address:
Dr. Renu Rajguru
Department of ENT, INHS Asvini, Mumbai - 400 005, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/indianjotol.INDIANJOTOL_90_20

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  Abstract 


Introduction: Vertigo, a multisensory symptom, is one of the most common presentations to otolaryngology clinic and may occur in a multitude of ENT-related diseases, thus making a correct diagnosis challenging. In the last few decades, there has been a paradigm shift in the diagnostics of vertigo due to the availability of better objective modalities that allow assessment of different components of the complex vestibular labyrinth with relative ease. With the advent of vestibular evoked myogenic potentials (VEMP) since the last few decades, it is possible to test otolith organs in isolation and objectively. Aim: The aim of this study is to study the effectiveness of cervical VEMP (cVEMP) in the evaluation of saccular function in patients suffering from peripheral vertigo. Study Design: Analytical cross-sectional study. Setting: Tertiary care hospital. Materials and Methods: The study was conducted over a period of 2 years, from December 2016 to October 2018 at the ENT department of a tertiary care hospital. A sample size of 40 patients of peripheral vertigo and 40 age-matched healthy controls was selected. Air conduction cVEMP was performed in cases of posterior canal benign paroxysmal positional vertigo (pBPPV), vestibular neuritis (VN), superior semicircular canal dehiscence syndrome (SCD), and Meniere's disease (MD) and their values were compared with contralateral healthy ears and controls. Results: cVEMP parameters in VN, SCD, and MD were found to be abnormal, and the difference from normal was statistically significant. However, in the case of pBPPV patients, they did not show any difference from the normal. Conclusion: cVEMP is found to be a useful screening tool for conditions such as VN, SCD, and MD.

Keywords: Saccular dysfunction, vestibular evoked myogenic potentials, vestibular neuritis, superior semicircular canal dehiscence syndrome, menieres's disease, posterior canal benign paroxysmal positional vertigo


How to cite this article:
Tripathi S, Rajguru R, Gupta AK, Patil B. Is cervical vestibular evoked myogenic potentials an effective tool for the evaluation of saccular function in patients suffering from peripheral vertigo? An analytical study. Indian J Otol 2020;26:247-53

How to cite this URL:
Tripathi S, Rajguru R, Gupta AK, Patil B. Is cervical vestibular evoked myogenic potentials an effective tool for the evaluation of saccular function in patients suffering from peripheral vertigo? An analytical study. Indian J Otol [serial online] 2020 [cited 2021 Jun 22];26:247-53. Available from: https://www.indianjotol.org/text.asp?2020/26/4/247/314353




  Introduction Top


Vertigo, a multisensory symptom, is one of the most common presentations to otolaryngology clinic. Vertigo has a considerable impact on social and working life. Despite a lifetime prevalence of about 30% and an annual incidence that increases with age, diagnosing the cause of vertigo remains a considerable challenge as the pathology may involve many sensory organs.[1]

Vertigo may occur as main or accompanying symptoms in a multitude of ENT related diseases involving the inner ear. The impairment of quality of life caused due to episodic or chronic vertigo can be substantial and can cause anxiety, depression, reduced physical activity, and possible inability to work. Fall from giddiness in the elderly adds to existing morbidity.[2]

In the last few decades, there has been a paradigm shift in the diagnostics of vertigo due to the availability of better objective modalities which allow the assessment of different components of the complex vestibular labyrinth with relative ease. This leads to precise localisation of the vestibular disorder more rapidly, reliably, and effectively.

The vestibular system has been broadly subdivided into otolith organs (saccule and utricle) and the three semi-circular canals. The clinical tests for vestibular function such as the Dix-Hallpike test, caloric test, head impulse test, supine roll test, subjective visual vertical, VNG, rotational tests, etc., mainly assess the semicircular canals.

However, it is possible to test otolith organs objectively by using vestibular evoked myogenic potentials (VEMP). It was found that high intensity sound stimulus, apart from stimulating cochlea, also activates vestibule, and generates electromyographic reflexes in many muscles including sternocleidomastoid (SCM) and extraocular muscles. These reflexes are called VEMP and can be easily recorded with surface electrodes placed on SCM (cervical VEMP or cVEMP) which records sacculo-collic reflex, or on the extra ocular muscles (ocular VEMP or oVEMP) which records utrculo-collic reflex.[3]

This study utilizes cVEMP as a tool for recording the inhibitory signals of sacculo-collic reflex being generated from ipsilateral SCM in response to direct acoustic stimulation of saccule due to its close proximity to oval window which itself is stimulated by sound. The reflex pathway is through inferior vestibular nerve (IVN) and the central nervous system, subsequently generating inhibitory electrical responses which are picked up by electrodes placed on ipsilateral SCM.[4] This recording is aimed to evaluate possible role of cVEMP in the evaluation of saccular function in the diagnosis of peripheral vestibular causes of vertigo by analyzing cVEMP parameters in patients with peripheral vertigo and comparing them with healthy side in same patient and also comparing them with normal individuals. We wanted to know whether the cVEMP parameters (threshold, latency of P13 and N23 peak and the amplitude) are affected in patients of vertigo due to abnormal saccular function.


  Materials and Methods Top


We conducted an analytical cross-sectional study over a period of 2 years, from December 2016 to October 2018 at ENT department of a tertiary care academic medical hospital.

A sample size of 40 patients of peripheral vertigo and 40 age-matched healthy controls was selected for this study. The sample size was calculated based on the data record of patient load in the ENT outpatient department. Patients included in the study were cases of posterior canal benign paroxysmal positional vertigo (pBPPV), Superior semicircular canal dehiscence syndrome (SCD), Meniere's disease (MD) and vestibular neuritis (VN), both males and females in the age group of 18–60 years who had consented for the study. Patients with known history/diagnosis of neurological and muscular disorders or nonvestibular causes of vertigo, such as hypoglycemia, adrenal failure, pheochromocytoma, vasovagal syncope, orthostatic hypotension, embolic disease, cardiac dysrhythmias, medications affecting vestibular system, and muscle tone or any conductive hearing loss were excluded from the study. Furthermore, normal healthy individuals with absent biphasic waves were not considered for this study.

Controls considered for the study to generate normative data for cVEMP parameters were age matched healthy individuals free from any disease.

The latency of P13 and N23 peak were measured, where P13 is the first positive peak in the cVEMP waveform and N23 Peak is the first negative peak in the cVEMP waveform, both measured in terms of millisecond. Amplitude is the difference between the P13 and N23 peaks, measured in terms of microvolts.

Institutional ethics committee clearance was obtained vide letter no. IEC/Nov/2016 dt 16 Nov 2016.

Methodology

A thorough clinical examination was performed after taking detailed history and informed written consent, followed by neuro-otologic examination of all patients with complains of vertigo. Audiometry, tympanometry, Dix-Hallpike test, supine roll test, caloric test, and radiological investigations like HRCT Temporal Bone and MRI brain were done as indicated. Bilateral air conduction cVEMP was done for all cases.

Clinical diagnosis of pBPPV was made by clinical history of positional vertigo and a positive Dix-Hallpike test in the presence of normal hearing and normal tympanic membrane.[5]

SCD patients were diagnosed by clinical history of vestibular symptoms induced by intense sound stimuli or pressure changes, autophony, hyperacusis, pulsatile tinnitus, and HRCT temporal bone (<0.0625 mm) showing dehiscence in the plane of superior semi-circular canal on reformatted images.[6]

Acute unilateral VN was diagnosed by history of sudden-onset vertigo in the absence of hearing loss with nausea/vomiting, gait instability, spontaneous nystagmus on clinical examination and a normal tympanic membrane, while persisting for a day or more.[7]

MD was diagnosed in patients with a history of episodic vertigo, fluctuating hearing loss, tinnitus, aural pressure, and a progressive loss of audiovestibular functions.[8] Two or more definitive spontaneous episodes of vertigo lasting for 20 min to 12 h with audiometrically documented low-to-medium-frequency sensorineural hearing loss in the affected ear on at least one occasion before, during, or after one of the episodes of vertigo along with fluctuating aural symptoms (hearing, tinnitus, or fullness) in the affected ear was taken as a clinical diagnosis of MD.

The equipment used for performing air conduction cVEMP testing was Epic Plus, manufactured by labat international. The patient was made to sit on a chair with head turned to contralateral side from the ear being tested. The electrodes were positioned as positive or active electrode on the middle one-third of ipsilateral SCM muscle to be tested, reference or inactive electrode on sternal head of SCM muscle and ground electrode on forehead [Figure 1]. The stimulus was presented by insert ear phone with foam ear tips, to the test ear in form of tone bursts which were given at 500 Hz as 200 stimuli of 0.2 ms each at an intensity of 105 dB nHL and at 50 dB nHL. The potentials were recorded with standard disposable, self-adhesive surface electrodes. The electrode impedance was kept within optimum level by using conduction gel in all cases.[9]
Figure 1: Position of electrodes

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The results were obtained from the software in form of a graph, with amplitude measured as microvolt and recorded on Y-axis and the latency measured as milli-second and recorded on X-axis. The waves in this pattern of electrodes were recorded as positive deflection downward. The P13 wave was recognized as first positive peak, i.e., downward deflection, recorded at 13 ms and N23 wave was recognized as the first negative peak recorded at 23 ms for each ear separately [Figure 2].[9] The summation potentials recorded were analyzed. Three consecutive summation potential recordings were done to confirm the presence of cVEMP.
Figure 2: Cervical vestibular evoked myogenic potentials waveform as obtained from software

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Statistical analysis

A descriptive statistical analysis was performed, calculating the mean and the standard deviation (SD). The data were tabulated in excel sheet and statistical analysis was done using IBM SPSS version 24. The result of cVEMP were analyzed for latency and amplitude of P13 and N23 waves in patients with vertigo and compared with controls for same parameters (amplitude and latency of P13 and N23 waves). The amplitude and latency of P13 and N23 waves were also analysed for any significant change between the diseased and nondiseased ear in vertigo patients. The distribution of data was tested by Shapiro–Wilk test for parametric distribution. Unpaired t-test was used. Value of P < 0.05 was considered statistically significant.


  Results Top


In this study, 25 pBPPV, two SCD, three MD, and ten VN patients participated. Out of a total of 40 patients 19 (47.5%) were male patients and 21 (52.5%) patients were female. The disease specific distribution in male patients was: eight (42.10%) pBPPV, two (10.52%) SCD, two (10.52%) MD and seven (36.84%) VN patients. The disease-specific distribution in female patients was: 17 (80.95%) pBPPV, one (4.76%) MD, and three (14.28%) VN patients.

Analysis of cervical vestibular evoked myogenic potentials parameters in various conditions is as follows

Healthy controls (80 ears)

At 105 dB nHL the mean latency of P13 peak in normal individuals (80 ears) was found to be 12.92 ms with SD of 1.82. The N23 peak had mean latency of 21.91 ms, with SD of 1.50. The mean amplitude was 153.70 micro volts with SD of 8.65 [Table 1]. No recordings were obtained at 50 dB nHL.
Table 1: Comparison of P13, N23 peak and amplitude between the affected ear and ear of normal individuals at 105 dB nHL

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Affected ears in posterior canal benign paroxysmal positional vertigo patients (25 ears)

At 105 dB nHL, the P13 peak in the affected ears (25 ears) was found to have mean latency of 13.30 ms with SD of 1.78. The N23 peak had mean latency of 22.68 ms, SD of 1.85. The mean amplitude was 155.03 micro volts with SD of 11.44 [Table 1].

No recordings were obtained at 50 dB nHL in all affected ears.

Contralateral healthy ears in posterior canal benign paroxysmal positional vertigo patients (25 ears)

At 105 dB, the mean latency of P13 peak 13.25 ms with SD of 1.80. The N23 peak had mean latency of 22.83 ms, with SD of 2.32. The mean amplitude was 152.10 microvolts with SD of 11.46. No recordings were obtained at 50 dB nHL [Table 2].
Table 2: Comparison of P13, N23 peak and amplitude between the affected ear and contralateral healthy ear at 105 dB nHL

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Affected ears in Meniere's disease patients (03 ears)

At 105 dB nHL and 50 dB nHL VEMP amplitude responses were absent in all three patients [Table 1].

Contralateral healthy ears in Meniere's disease patients (03 ears)

At 105 dB nHL the mean latency of P13 peak 13.02 ms with SD of 1.82. The N23 peak had mean latency of 21.91 ms, with SD of 1.50. The mean amplitude was 153.70 micro volts with SD of 8.65. No recordings were obtained at 50 dB nHL [Table 2].

Affected ears in vestibular neuritis patients (10 ears)

On presenting sound of intensity 105 dB nHL, normal parameters were observed in seven patients. In these patients the mean latency of P13 peak was found to be 12.98 ms with SD of 1.82. The N23 peak had mean latency of 22.01 ms, with SD of 1.50. The mean amplitude was 154.05 micro volts with SD of 8.65. In the other three patients cVEMP parameters were abnormal. The P13 peak had latency of 6.2 ms with SD of 0.72, N23 peak had mean latency of 10.4 ms with SD of 0.529 and the mean amplitude was 115 micro volts with SD of 5 [Table 1].

On presenting sound of intensity 50 dB nHL, VEMP responses were absent in all patients.

Contralateral healthy ears in vestibular neuritis patients (10 ears)

At 105 dB nHL the mean latency of P13 peak 13.24 ms with SD of 2.82. The N23 peak had mean latency of 25.04 ms, with SD of 1.15. The mean amplitude was 153.06 micro volts with SD of 12.01. No recordings were obtained at 50 dB nHL [Table 2].

Affected ears in patients with SCD (two ears)

At 105 dB nHL, the P13 peak in the affected ears (two ears) was found to have mean latency of 5.78 ms with SD of 0.28. The N23 peak had mean latency of 10.9 ms with SD of 0.14. The mean amplitude was 242.5 micro volts with SD of 3.53 [Table 1].

At 50 dB nHL, the mean latency of P13 peak was found to be 13.5 ms with SD of 1.82. The N23 peak had mean latency of 22.91 ms with SD of 1.50. The mean amplitude was 152.90 micro volts with SD of 8.65 [Table 3] and [Figure 3].
Table 3: Comparison of P13, N23 peak and amplitude between the affected ear of SCD and ear of normal individuals at 105 dB nHL

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Figure 3: Cervical vestibular evoked myogenic potentials with recordable P13 and N23 waves obtained in a patient with left SCD at 50 dB

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Contralateral healthy ears in patients with SCD

The cVEMP parameters were similar to those of healthy controls. At 105 dB nHL the mean latency of P13 peak 13.98 ms with SD of 1.82. The N23 peak had mean latency of 17 ms with SD of 0.70. The mean amplitude was 158.70 micro volts with SD of 8.65. No recordings were obtained at 50 dB nHL [Table 2].

To summarise the results of our study,

  1. The cVEMP parameters recorded in affected ear and contralateral healthy ear of patients with pBPPV did not show any significant variation from the normal range of parameters. On reducing the threshold from 105 dB nHL to 50 dB nHL, no VEMP response was obtained in either affected or contralateral healthy ears
  2. The cVEMP parameters recorded in affected ear of patients with MD was absent in all three patients. Normal values were obtained in contralateral healthy ears. The responses were absent at 50 dB nHL in both affected and contralateral healthy ears
  3. The cVEMP parameters recorded in affected ear of VN patients with superior vestibular nerve involvement did not show any significant variation from the normal range but those with IVN involvement showed abnormality in terms of reduced amplitude, though the latencies were normal in all patients in both ears. Normal values were obtained in contralateral healthy ears of all ten patients. The responses were absent at 50 dB nHL in both affected and contralateral healthy ears in all ten patients
  4. The cVEMP parameters recorded in affected ear of patients with SCD showed high amplitude at 105 dB nHL. When tested with sound intensity of 50 dB nHL cVEMP responses were still obtained, though statistically nonsignificant, suggesting low threshold. Normal values were obtained in contralateral healthy ears at 105 dB nHL, but the responses were absent at 50 dB nHL.



  Discussion Top


We studied cVEMP parameters in cases of pBPPV, MD, VN, and SCD and compared them with age matched healthy controls and also contralateral healthy ear in case of vertigo patients. We have analysed our results in various disorders studied in the following sections.

Our study has shown that the cVEMP parameters could be recorded in all participants at 105 dB nHL except in affected ears of three patients with MD (157 ears), but could not be recorded in any participant at 50 dB nHL except in effected ears of two cases of SCD.

We studied cVEMP parameters in 25 cases of pBPPV. The pathophysiology of BPPV can be explained by the concept of a degenerative process that effects macula of the utricle causing detachment of otoliths into the ampulla of posterior semicircular canal owing to its anatomical proximity.[10] As it is the utricle which is primarily involved and not saccule, hence it is possible that the cVEMP parameters may be normal.

In our study, the cVEMP parameters in pBPPV patients did not show any statistical difference when compared between affected ear and contralateral healthy ear and also with normal individuals. The plausible explanation can be, first, that it is the utricular otoconia which causes the symptoms. Second, due to small sample size none of the patients whom we considered for study had saccular involvement.

Our results are similar to the studies done by Korres and Gkoritsa and Lira-Batista et al.[11],[12] The study done by Korres and Gkoritsa, showed that though there were abnormalities in VEMP parameters, there was no statistical difference in the latencies, amplitudes and thresholds between affected and unaffected ears.[11],[12] In fact the VEMP abnormalities were present in almost equal percentages in both the groups. Another study done by Lira-Batista et al. showed normal morphology of VEMP waveforms in all BPPV patients.[12]

However, our study was not in agreement with the study done by Godha et al. in which VEMP showed a positive correlation with Dix–Hallpike test and with Lee et al. where VEMP abnormalities were detected in a significant proportion of patients.[13],[14]

The diagnosis of acute VN requires objective findings indicating complete or partial unilateral loss of vestibular function. Caloric test and head impulse test assess only lateral semicircular canal. Patients who present with similar symptoms but normal caloric test may erroneously be diagnosed as central vertigo patients. In our study, out of the ten VN patients, cVEMP was bilaterally normal in seven patients indicating that they had superior VN, but in three patients cVEMP was abnormal in the effected ears in terms of reduced amplitude indicating inferior VN (IVN) in these patients. Similar study has been published by Halmagayi et al. for diagnosis of IVN.[15] Also the latencies were normal in all patients in both ears, similar to the study done by Murofushi et al. wherein they found prolonged latencies only in retrolabyrinthine lesions.[16] Similar results are obtained by Nola et al. in their study. in which superior VN patients showed normal amplitude and latency on both sides, but IVN patients showed abnormal parameters which changed to normal once the acute attack was over.[17] This study suggested use of VEMP as a screening test for VN. Monstad et al. reported similar findings in their case series.[18]

We had included three patients of MD in our study. The most supported pathophysiological mechanism in MD is endolymphatic hydrops, characterised by excessive endolymphatic accumulation in the cochlea and vestibule.[19] Cochlea and the saccule are most commonly affected structures, followed by utricle and semicircular canals.[20] Hence, cVEMP parameters, if abnormal, support the diagnosis of MD in case of diagnostic dilemma. In our study, cVEMP in the effected ear was absent in all three patients, whereas normal values were obtained in contralateral healthy ear of these patients. These abnormalities are attributed to the saccular dysfunction resulting from saccular hydrops. Our findings are similar to the study done by Zuniga et al. and Salviz et al. wherein they found reduced peak to peak amplitudes as compared with controls.[21],[22] A study by Angeli and Goncalves also found absent or reduced cVEMP response in 74% of patients with active MD and 50% of patients with stable MD.[23]

Thus, the ability of cVEMP to detect saccular dysfunction could potentially be used to identify patients whose symptoms are suggestive, but not diagnostic for MD, as well as to track saccular function over time. Unilateral MD patients can be can be followed up over time to determine the value of cVEMP metrics obtained from the non-symptomatic ear in predicting which patients will develop MD in this ear.[24]

We included two patients of SCD in our study. Dehiscence of bone over Superior semicircular canal creates a third mobile window in the labyrinth with a low resistance pathway for transmission of low frequency sound energy through the labyrinth, thus lowering the threshold required for generation of potentials and also high amplitude. It renders the membranous labyrinth unusually susceptible to sound and pressure changes. Though SCD is typically confirmed using HRCT Temporal bone, but it may over estimate the size of the dehiscence or can falsely detect dehiscence in patients with very thin bony covering, resulting in erroneous diagnosis of SCD. VEMP can be used to detect whether it is the dehiscence which is causing pathological pressure transmission in the vestibular labyrinth and hence uniquely suited for identification of SCD.

In our study, both SCD patients showed reduced threshold and high amplitude in the effected ears, and normal parameters in contralateral healthy ears. We confirmed our diagnosis by doing HRCT temporal bone for these patients and found dehiscence of superior semicircular canal [Figure 4]. Similar findings were seen in studies done by Streubel et al.[25] Also, Zhou et al. in their study of 65 patients, obtained abnormally low VEMP thresholds and found VEMP to be highly sensitive and specific for SCD, possibly better than CT.[26] Welgampola et al. in their study of 12 SCD cases found VEMP thresholds to be pathologically lowered in all, which normalised after corrective surgery.[27]
Figure 4: HRCT temporal bone of the same patient confirming the diagnosis of left SCD

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Conclusion

cVEMP is an objective test for saccule and the IVN. It has the advantage of being noninvasive, has better acceptability and is comfortable for patients as it does not induce vertigo. The potentials are stable and repeatable, can be documented and reproduced objectively. It is recommended that the cVEMP parameters testing for threshold and amplitude be used for routine screening in cases of SCD, MD, and IVN.

Consent

Written informed consent was obtained from all individual participants included in the study.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Strupp M. Challenges in neuro-otology. Front Neurol 2010;1:121.  Back to cited text no. 1
    
2.
Bronstein AM. Evaluation of balance. In: Gleeson M, editor. Scott-Brown's Otorhinolaryngology, Head and Neck Surgery. 7th ed.. Hodder Arnold; 2008. p. 3706-47.  Back to cited text no. 2
    
3.
Rauch SD. Vestibular evoked myogenic potentials. Curr Opinion Otolaryngol Head Neck Surg 2006;14:299-304.  Back to cited text no. 3
    
4.
Cal R, Bahmad F Jr. Vestibular evoked myogenic potentials: An overview. Braz J Otorhinolaryngol 2009;75:456-62.  Back to cited text no. 4
    
5.
Strupp M, Brandt T. Peripheral vestibular disorders. Curr Opin Neurol 2013;26:81-9.  Back to cited text no. 5
    
6.
Diaz MP, Lesser JC, Alarcón AV. Superior semicircular canal dehiscence syndrome – Diagnosis and surgical management. Int Arch Otorhinolaryngol 2017;21:195-8.  Back to cited text no. 6
    
7.
Hegemann SC, Wenzel A. Diagnosis and treatment of vestibular neuritis/neuronitis or peripheral vestibulopathy (PVP)? Open questions and possible answers. Otol Neurotol 2017;38:626-31.  Back to cited text no. 7
    
8.
Gürkov R, Pyykö I, Zou J, Kentala E. What is Menière's disease? A contemporary re-evaluation of endolymphatic hydrops. J Neurol 2016;263:71-81.  Back to cited text no. 8
    
9.
Felipe L, Kingma H, Gonçalves DU. Vestibular evoked myogenic potential. Int Arch Otorhinolaryngol 2012;16:103-7.  Back to cited text no. 9
    
10.
Parnes LS, McClure JA. Free-floating endolymph particles: A new operative finding during posterior semicircular canal occlusion. Laryngoscope 1992;102:988-92.  Back to cited text no. 10
    
11.
Korres S, Gkoritsa E. Vestibular evoked myogenic potential in BPPV. Med Sci Monit 2011;17:CR42-7.  Back to cited text no. 11
    
12.
Lira-Batista MM, Dorigueto RS, Gananca CF. VEMP and digital vectoelectronystagmography's study in patients with benign paroxysmal positional vertigo. Int Arch Otorhinolaryngol 2013;17:147-56.  Back to cited text no. 12
    
13.
Godha S, Upadhyay Mundra A, Mundra RK, Bhalot L, Singh A. VEMP: An objective test for diagnosing the cases of BPPV. Indian J Otolaryngol Head Neck Surg 2020;72:251-6.  Back to cited text no. 13
    
14.
Lee JD, Park MK, Lee BD, Lee TK, Sung KB, Park JY. Abnormality of cervical vestibular – Evoked myogenic potentials and ocular vestibular – Evoked myogenic potentials in patients with recurrent benign paroxysmal positional vertigo. Acta Otolaryngol 2013;133:150-3.  Back to cited text no. 14
    
15.
Halmagayi GM, Aw ST, Arlberg MK, Curthoys IS, Todd MJ. Inferior vestibular neuritis. Ann NY Acad Sci 2002;956:306-13.  Back to cited text no. 15
    
16.
Murofushi T, Shimizu K, Takegoshi H, Cheng PW. Diagnostic value of prolonged latencies in the vestibular evoked myogenic potential. Arch Otolaryngol Head Neck Surg 2001;127:1069-72.  Back to cited text no. 16
    
17.
Nola G, Guastini L, Crippa B, Deiana M, Mora R, Ralli G. Vestibular evoked myogenic potential in vestibular neuritis. Eur Arch Otorhinolaryngol 2011;268:1671-7.  Back to cited text no. 17
    
18.
Monstad P, Okstad S. Mygland A. Inferior vestibular neuritis: 3 cases with clinical features of acute vestibular neuritis, normal calorics but indication of saccular failure. BMC Neurol 2006;6:45.  Back to cited text no. 18
    
19.
Lopez-Escamez JA, Carey J, Chung WH, Goebel JA, Magnusson M, Mandala M, et al. Diagnostic criteria for Meniere's disease. J Vestib Res 2015;25:1-7.  Back to cited text no. 19
    
20.
Okuno T, Sando I. Localisation, frequency, and severity of endolymphatic hydrops and the pathology of the labyrinthine membrane in Meniere's Disease. Ann Otol Rhin Laryngol 1987;96:438-45.  Back to cited text no. 20
    
21.
Zuniga MG, Janky KL, Schubert MC, Carey JP. Can vestibular-evoked myogenic potentials help differentiate Ménière disease from vestibular migraine? Otolaryngol Head Neck Surg 2012;146:788-96.  Back to cited text no. 21
    
22.
Salviz M, Yuce T, Acar H, Taylan I, Yuceant GA, Karatas A. Diagnostic value of vestibular evoked myogenic potentials in Meniere disease and vestibular migraine. J Vestib Res 2016;25:261-6.  Back to cited text no. 22
    
23.
Angeli SI, Goncalves S. Cervical VEMP tuning changes by Meniere's disease stages. Laryngoscope Investig Otolaryngol 2019;4:543-9.  Back to cited text no. 23
    
24.
van Tilburg MJ, Herrmann BS, Guinan JJ Jr., Rauch SD. Serial cVEMP testing is sensitive to disease progression in Ménière patients. Otol Neurotol 2016;37:1614-9.  Back to cited text no. 24
    
25.
Streubel SO, Cremer PD, Carey JP, Weg N, Minor LB. Vestibular evoked myogenic potentials in the diagnosis of superior semicircular canal dehiscence syndrome. Acta Otolaryngol Suppl 2001;545:41-9.  Back to cited text no. 25
    
26.
Zhou G, Gopen Q, Poe DS. Clinical and diagnostic characterisation of canal dehiscence syndrome: A great otologic mimicker. Oto Neurotol 2007;28:920-6.  Back to cited text no. 26
    
27.
Welgampola MS, Myrie OA, Minor LB, Carey JP. Vestibular-evoked myogenic potential thresholds normalize on plugging superior canal dehiscence. Neurology 2008;70:464-72.  Back to cited text no. 27
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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