|Year : 2022 | Volume
| Issue : 1 | Page : 26-31
A study of vestibular evoked myogenic potential and clinical features in benign paroxysmal positional vertigo: An institutional experience
Poonam Kumar Saidha, Dali Chandran, Natashya Sima, Ophelia D'souza
Department of ENT and Head and Neck Surgery, St. John's Medical College and Hospital, Bengaluru, Karnataka, India
|Date of Submission||25-Jan-2021|
|Date of Decision||01-Mar-2021|
|Date of Acceptance||13-Mar-2021|
|Date of Web Publication||25-Apr-2022|
Dr. Poonam Kumar Saidha
St. John's Medical College and Hospital, Bengaluru, Karnataka
Source of Support: None, Conflict of Interest: None
Background: Benign paroxysmal positional vertigo (BPPV) is the most common vestibular disorder in adults caused by degeneration of the otolithic organs in most cases but may also be a consequence of head injury, labyrinthitis, and ischemia in the distribution of the anterior vestibular artery or prolonged bed rest. The aim of the study is to find the correlation of alterations in vestibular evoked myogenic potential (VEMP) recordings in BPPV patients, with other associated symptoms. Materials and Methods: The study was conducted in 29 BPPV patients over a 3-year period. All patients were investigated with pure-tone audiometry, bithermal caloric test with Electronystagmography (ENG) recording, and VEMP recording. Clinical tests included Romberg, Sharpened Romberg, and Dix–Hallpike tests. Associated parameters were recorded, and any association with abnormal VEMP was evaluated. Results: VEMP was abnormal in three patients. There was no association of abnormal p or n latency with BPPV. No significant relationship with any clinical parameter was observed. Conclusions: BPPV is associated with the occurrence of abnormal VEMP recordings, possibly due to degeneration of the saccular macula, but a reproducible association is not demonstrable in a significant way.
Keywords: Benign paroxysmal positional vertigo, Electronystagmography (ENG), vestibular evoked myogenic potentials
|How to cite this article:|
Saidha PK, Chandran D, Sima N, D'souza O. A study of vestibular evoked myogenic potential and clinical features in benign paroxysmal positional vertigo: An institutional experience. Indian J Otol 2022;28:26-31
|How to cite this URL:|
Saidha PK, Chandran D, Sima N, D'souza O. A study of vestibular evoked myogenic potential and clinical features in benign paroxysmal positional vertigo: An institutional experience. Indian J Otol [serial online] 2022 [cited 2022 May 20];28:26-31. Available from: https://www.indianjotol.org/text.asp?2022/28/1/26/343756
| Introduction|| |
Benign paroxysmal positional vertigo (BPPV) is the most common vestibular disorder in adults, with a lifetime prevalence of 2.4%.
The probable cause is a degeneration of the otolithic organs (utricle and saccule) in most cases but may also be a consequence of head injury, labyrinthitis, and ischemia in the distribution of the anterior vestibular artery or prolonged bed rest.
The pathophysiology of the disease was proposed by Shuknecht in 1969, which claimed that otoconia, with a specific gravity greater than that of the endolymph, detaches from a degenerating utricular macula and settles on the cupula of the posterior semicircular canal, rendering it gravity sensitive.
The posterior semicircular canal is most frequently affected. The inferior vestibular nerve synapses with the posterior semicircular canal and the saccule.
The clinical utility of vestibular evoked myogenic potential (VEMP) is still ill defined despite the availability of the study of otolithic function selectively in both its saccular (cervical VEMPs [cVEMPs]) and utricular (ocular VEMPs [oVEMPs]) parts.
The aim of the study is to find the frequency of possible alterations in VEMP recordings in BPPV patients, and if there is a pattern of abnormal clinical findings present with alterations in VEMP recordings.
VEMP measures electrophysiological field potentials that are recorded from sternocleidomastoid muscle (SCM) which contracts in response to transient intense acoustic stimulus. It is a measure of the level of saccular stimulation. Usually, VEMP is recorded over the ipsilateral SCM which is tonically contracted by the patient. Variations in latencies and recordings as well as asymmetry between right and left can be used to provide diagnostic information about vestibular function centered on response of the saccule. VEMPs are now recorded using symmetric sites over the SCMs. The response consists of an initial positivity or inhibition (p13) followed by a negativity or excitation (n23). Later, components (n34 and p44) have a lower stimulus threshold and are nonvestibular (probably cochlear) in origin. The short-onset latency of the VEMP (about 8 msonds) indicates that it is likely to be mediated by an oligosynaptic pathway, possibly disynaptic, consisting of primary vestibular afferents projecting to the vestibular nuclear complex and thence via the medial vestibulospinal tract to the accessory nucleus.
| Materials and Methods|| |
The study was carried out in a tertiary care medical college and hospital from March 2017 to December 2019. The study population consisted of 29 patients.
The patients were diagnosed with BPPV at the start of the investigation.
Informed consent was obtained from all individual participants included in the study.
Diagnosis was established with observation of geotropic upbeating nystagmus triggered by supine position with the head overextended toward one side, the Dix–Hallpike maneuver. A thorough medical history was obtained, including note of the time of the first occurrence, number of vertiginous episodes in the past, and number of Epley and Semont maneuvers needed.
Patients with diagnosed vestibular neuronitis or any other known vestibular problems or conductive hearing loss (CHL) were excluded.
In all patients, Romberg's test, Sharpened Romberg's test, and Dix–Hallpike's tests were performed.
All patients underwent pure-tone audiometry (PTA), bithermal caloric test with Electronystagmography (ENG) recording, and finally, cVEMP recording.
Procedure for vestibular evoked myogenic potential
VEMP was done in our institution using eclipse platform.
One electrode is placed on the forehead (ground electrode), two electrodes placed on either side of the mastoid, and two electrodes called vertex electrodes placed on both SCMs.
When stimulus begins, the patient is asked to raise their head to contract SCM muscle.
Turning the head slightly to the opposite side helps to increase the muscle tonus.
This position is held during the whole VEMP recording.
Optimum results are obtained when the patient is trained to maintain the contraction of SCM during stimulation.
The VEMP response is demonstrated by reproducible wave deflections with latencies around 13–23 ms.
VEMP morphologies and exact latencies are stimulus dependent and patient dependent. The VEMP result is evaluated by 2–4 reproducible waveforms with deflection at approximately 13 and 23 ms.
The first positive peak is called P1 or P13 and negative peak N1 or N23.
From each composite average, P1 and N1 peak latencies and P1-N1 amplitude are measured. Amplitude and latency asymmetries between right and left sides are compared using the following asymmetry ratio calculation.
The ratio is calculated using stimulus intensities >90 db to ensure a suprathreshold stimulus. Data entry was done for all the parameters tested.
Descriptive statistics were reported using numbers and percentages for the categorical variable, and Fisher's exact test was done to test the association between the normal and abnormal VEMPs with demographical, clinical, and laboratory variables.
The analysis was done using the statistical software STATA/IC 12.1 (Stata Corp LP, Texas, USA), and P < 0.05 was considered statistically significant.
Our study included 29 patients. The mean age group was 50 years. The youngest patient was 32 years and the oldest 68 years. Males and females were found to be almost equal in number with a slight female preponderance [Chart 1].
Duration/severity of vertigo
Sixteen had dizziness lasting 5–10 s, five patients had giddiness lasting up to 2 min, and six patients also reported lightheadedness lasting up to 10 min. Two patients had giddiness which lasted over 1 h.
Severity of giddiness
Patients were asked to subjectively grade the degree of severity of giddiness as follows:
- Mild : Giddiness with no limitation of physical activity
- Moderate : Giddiness with moderate restriction of physical activity
- Severe : Giddiness needing rest.
Fourteen patients had mild giddiness, 3 had moderate giddiness, and 12 had severe giddiness [Chart 2].
Relief of giddiness was attained spontaneously without any intervention in 8 cases, by bed rest in 15 patients. Six patients required vestibular sedatives [Chart 3].
Incidence/type of tinnitus
Fifteen patients also reported tinnitus, continuous in eight, and intermittently in seven. In 14 patients, there was no history of tinnitus [Chart 4].
Vestibular evoked myogenic potential
VEMP was normal in 26 (89.6%) patients. Three cases had abnormal VEMP findings with asymmetry in the latencies of the first positive deflection on the waveforms (P1) and the first negative deflection (N1) [Chart 5].
Romberg and Sharpened Romberg tests
Romberg's test was negative in more than 90% (27) of cases and positive in 2 cases, while Sharpened Romberg's test was normal in 23 cases and abnormal in 6 patients. Almost all of those positive patients had presented during an acute event [Chart 6].
Dix–Hallpike's diagnostic test for vertigo was positive in 26 (89.6%) patients, and the remaining three (10.3%) had no nystagmus on Dix–Hallpike testing but subjective giddiness during the test [Chart 7].
Sixteen (55.1%) patients had normal PTA, seven (24.1%) showed mild sensorineural hearing loss, and six (20.6%) had mild CHL on PTA [Chart 8].
ENG was normal in 23 (79.3%) patients; one patient did not cooperate, and in five cases, there was abnormal response with gaze nystagmus testing (2), positional test (1), and optokinetic testing (2) [Chart 9].
The summary of clinical findings is given in [Table 1].
Research Project titled “Study of VEMP and Clinical Features in BPPV” has been approved by Institutional Ethical Committee (IEC), SJMC- IEC/1/203/2015 dated 17 Sep 2015.
| Discussion|| |
In our study, the mean latencies at p13 and n23 for the 26 patients were 12.0 ± 1.1 and 20.6 ± 2.0 ms, respectively, which fell in the normal range as given in literature.
In the remaining three patients, the mean latencies at p13 were 13 ms, 15 ms, and 16 ms and latencies at n23 were 26 ms, 21 ms, and 28 ms which showed increased latencies of p1 and n1.
Correlation of vestibular evoked myogenic potential with symptomatology
In our study, we found that two patients having abnormal VEMP findings did not have tinnitus as a symptom [Table 2].
Duration of benign paroxysmal positional vertigo
Three (out of 16) patients who had giddiness lasting only a few seconds had abnormal VEMP findings, while patients who reported giddiness for a few minutes or hours had normal cVEMP [Table 3].
|Table 3: Duration of benign paroxysmal positional vertigo and vestibular evoked myogenic potential|
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Correlation of vestibular evoked myogenic potential with clinical tests
All the three patients in our study who had abnormal VEMP had negative Romberg's and Sharpened Romberg's tests. Two (out of five) patients who had abnormal ENG also had abnormal p1 latency; However, no significant relationship could be shown between the abnormal VEMP and abnormal ENG in any patient [Table 4].
Correlation of vestibular evoked myogenic potential with electronystagmographic
In two cases, an abnormal VEMP was found in relation to abnormal ENG finding but not statistically significant [Table 5].
|Table 5: Vestibular evoked myogenic potential and electronystagmographic|
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In the study by Toshihisa Murofushi et al., the mean ± SD latencies of p13 and n23 were 11.8 ± 0.86 and 20.8 ± 2.2 ms, respectively.
In the study by Akkuzu et al., the mean latencies at p13 and n23 in the 17 controls were 13.7 ± 1.0 and 22.1 ± 1.9 ms, respectively.
These are similar to our observations as described earlier.
The present study showed no significantly increased abnormal VEMP recordings in the BPPV patients.
However, review of literature shows the conflicting reports of diagnostic or prognostic value of VEMP in BPPV.
Akkuzu et al. found a significantly higher frequency of abnormal VEMP in BPPV patients compared with their control group. They proposed that BPPV patients with abnormal recordings are those with a history of more resistant positional vertigo, leading them to suppose that chronicity of the disease may imply saccular degeneration in addition to the expected utricular degeneration.
Murofushi et al. in 2001 studied the diagnostic value of abnormal latencies in VEMPs in BPPV patients and found to have no correlation.
In another study, Korres et al. concluded that the P1 latency and N1 latency did not present any statistical difference between control ears and affected ears of the BPPV population even though the percentage of abnormal VEMP in the BPPV population was statistically higher than in the control ears (P < 0.005). Similarly, no significant relationship could be shown between the occurrence of canal paresis and abnormal VEMP, and no relationship was found between the side (right or left ear) where BPPV appeared clinically and the side where abnormal VEMP was registered.
A systematic review of literature by Scarpa et al., on the other hand, recently concluded that VEMPs may represent a useful aid in improving the diagnostic accuracy for Ménière's disease, vestibular neuritis, and BPPV.
Evaluation of utricular and saccular functions using both cVEMP and oVEMP by Xu et al. showed that more patients with BPPV showed abnormal responses in c/oVEMPs as compared to the control group (P < 0.05).
Another study by Semmanaselvan et al. has found that individuals with posterior canal BPPV may have otoconia dislodgment or macular degeneration of utricle, saccule, both utricle and saccule unilaterally, or bilaterally and that VEMP may be useful in evaluating degeneration of both otolith organs associated with BPPV.
In a recent Indian study by Godha et al., VEMP showed a positive correlation with Dix–Hallpike test in the diagnosis of vertigo of postural origin, and the authors recommended that it can be used as a diagnostic tool for BPPV since VEMP was found to have high specificity.
A meta-analysis of literature on BPPV/VEMP from PubMed and Scopus by Oya et al. reported that the differences of latencies between BPPV patients and control patients were too small to use VEMPs as a prognostic predictor.
Similar to our study, abnormal ENG findings in BPPV patients have also been studied earlier and no statistical association was reported.
| Conclusions|| |
VEMP is not a standardized tool for diagnosing BPPV as no statistically significant relation with BPPV is seen consistently.
Similarly, our study did not find an association of VEMP with any clinical feature in the spectrum of BPPV.
More research is probably needed to establish the role of VEMP in BPPV.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Bhattacharyya N, Baugh RF, Orvidas L, Barrs D, Bronston LJ, Cass S, et al
. Clinical practice guideline: Benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg 2008;139:S47-81.
Yazıcı A, İnanç Y. Evaluation of BPPV with vertebral artery values. Neuropsychiatr Dis Treat 2018;14:1975-9.
Pearce JM. Benign paroxysmal vertigo, and Bárány's caloric reactions. Eur Neurol 2007;57:246-8.
Akkuzu G, Akkuzu B, Ozluoglu LN. Vestibular evoked myogenic potentials in benign paroxysmal positional vertigo and Meniere's disease. Eur Arch Otorhinolaryngol 2006;263:510-7.
Welgampola MS, Colebatch JG. Characteristics and clinical applications of vestibular-evoked myogenic potentials. Neurology 2005;64:1682-8.
Lin MY, Timmer FC, Oriel BS, Zhou G, Guinan JJ, Kujawa SG, et al
. Vestibular evoked myogenic potentials (VEMP) can detect asymptomatic saccular hydrops. Laryngoscope 2006;116:987-92.
Murofushi T, Halmagyi GM, Yavor RA, Colebatch JG. Absent vestibular evoked myogenic potentials in vestibular neurolabyrinthitis. An indicator of inferior vestibular nerve involvement? Arch Otolaryngol Head Neck Surg 1996;122:845-8.
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.
Korres S, Gkoritsa E, Giannakakou-Razelou D, Yiotakis I, Riga M, Nikolpoulos TP. Vestibular evoked myogenic potentials in patients with BPPV. Med Sci Monit 2011;17:CR42-47.
Scarpa A, Gioacchini FM, Cassandro E, Tulli M, Ralli M, Re M, et al
. Clinical application of cVEMPs and oVEMPs in patients affected by Ménière's disease, vestibular neuritis and benign paroxysmal positional vertigo: A systematic review. Acta Otorhinolaryngol Ital 2019;39:298-307.
Xu H, Liang FY, Chen L, Song XC, Tong MC, Thong JF, et al
. Evaluation of the utricular and saccular function using oVEMPs and cVEMPs in BPPV patients. J Otolaryngol Head Neck Surg 2016;45:12.
Semmanaselvan K, Vignesh SS, Muthukumar R, Jaya V. Vestibular evoked myogenic potentials after epleys manoeuvre among individuals with benign paroxysmal positional vertigo. Indian J Otolaryngol Head Neck Surg 2019;71:195-200.
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.
Oya R, Imai T, Takenaka Y, Sato T, Oshima K, Ohta Y, et al
. Clinical significance of cervical and ocular vestibular evoked myogenic potentials in benign paroxysmal positional vertigo: A meta-analysis. Eur Arch Otorhinolaryngol 2019;276:3257-65.
Korres SG, Balatsouras DG, Ferekidis E. Electronystagmographic findings in benign paroxysmal positional vertigo. Ann Otol Rhinol Laryngol 2004;113:313-8.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]