The Sensitivity of Vestibular Evoked Myogenic Potentials in the diagnosis of Semicircular Canal Dehiscence

The Sensitivity of Vestibular Evoked Myogenic Potentials in the diagnosis of Semicircular Canal Dehiscence.

Abstract

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Background: Semicircular Canal Dehiscence (SCD) syndrome is a rare disorder involving the inner ear.  A dehiscence is an absence of an area of bone, and in this case of SCD it occurs in the superior semicircular canals (SCC) creating a mobile third window in the system.

Stimulus evoked electromyography changes can be recorded from various muscles.  Two types of vestibular evoked myogenic potentials (VEMP) are recordable.  The first is the cervical VEMP, which is recorded from the sternocleidomastoid muscle on the neck.  The other is the ocular VEMP, which is usually recorded below the eye.  Both cVEMP and oVEMP have been previously been used clinically in the diagnosis of SCD.

Objective: To establish if there is sensitivity between cVEMP and oVEMP in the diagnosis of SCD.

Method: A literature search using the keywords “semicircular canal dehiscence” and “vestibular evoked myogenic potentials” was performed using SCOPUS and ScienceDirect databases.  These results were narrowed to include studies of adults with SCD, testing oVEMP and cVEMP for the period of January 2012 to December 2016.

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Results: Of the 61 results, 4 were considered relevant, two of the studies researched both oVEMP and cVEMP, while the others researched oVEMP and cVEMP independently.  The analysis of the research focused on the tone used, the electrode montage and the amplitude measured.

Conclusion:In the diagnosis of SCD, oVEMP tested using a modified electrode placement using a bone vibration at the Fz position develops a large amplitude that is significant in patients with a SCD.

Table of Contents

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List of Tables and Figures………………………………………………………………1

Abbreviations……………………………………………………………. 2

1. Introduction…………………………………………………………….. 3
   1. Symptoms of SCD……………………………………5
   2. Types of VEMP………………………………………6
2. Objectives……………………………………………..…………………9
3. Method………………………………………………………………………………………..10

3.1 Inclusion/Exclusion Criteria……………………………10

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3.2 Search Strategy……………………………………………..10

3.3 Assessment of Study………………………………………11

3.4 Data Analysis………………………………………………..11

4. Results…………………………………………………………………………………………13

4.1  oVEMP Results………………………………………………………..13

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4.1.0 oVEMP Protocol……………………………………………13

4.1.1 oVEMP Stimulus and Recording Parameters…….14

4.1.2 oVemp Response Parameters…………………………..15

4.2 cVEMP Results………………………………………………………..17

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4.2.0 cVEMP Protocol……………………………………………17

4.2.1 cVEMP Stimulus and Recording Parameters…….18

4.2.2 cVemp Response Parameters…………………………..19

5. Discussion……………………………………………………………………………………20

5.1 Electrode Montage……………………………………….. 20

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5.2 Tone…………………………………………………………….24

5.3 Amplitude and Latency………………………………….26

6. Conclusion………………………………………………………………28
7. References……………………………………………………………….29
8. Appendix 1………………………………………………………………33

Appendix 2………………………………………………………………34

Appendix 3………………………………………………………………35

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Appendix 4………………………………………………………………41

Appendix 5………………………………………………………………49

Appendix 6…………………………………………………………………………………..55

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List of Tables and Figures

Figure 1 – CT Image of SSCD

Figure 2 – VCR Pathway

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Figure 3 – cVEMP Response

Figure 4 – oVEMP Response

Table 1 – Study Summary

Figure 5 – oVEMP amplitude

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Figure 6 – cVEMP threshold

Abbreviations

SCD– Semicircular Canal Dehiscence

SCC – Semicircular Canals

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VEMP – Vestibular Evoked Myogenic Potentials

oVEMP – ocular Vestibular Evoked Myogenic Potentials

cVEMP – cervical Vestibular Evoked Myogenic Potentials

CT – Computed Tomography

EMG – Electromyography

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VCR – Vestibulo Colic Reflex

N – Negative Peak

P – Positive Peak

ms – Milliseconds

TB – Tone Burst

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BC – Bone Conduction

BCV – Bone Conduction Vibrations

Fz – Frontal zero

Cz – Central zero

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ACS – Air Conducted Sound

dB – Decibel

SPL – Sound Pressure Level

µV – microVolts

pSP – peak-equivalent sound pressure level

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nHL – normal Hearing Level

1. Introduction

Semicircular Canal Dehiscence (SCD) syndrome is a rare disorder involving the inner ear that was first described by Lloyd Minor in 1998 (Minor et al., 1998).

A dehiscence is an absence of an area of bone, and in this case of SCD it occurs in the superior semicircular canals (SCC) creating a mobile third window in the system. This third mobile window is likely to create a path of lower impedance for the transmission of pressure and acoustic energy to the vestibule, making the vestibular system more sensitive to sound and pressure changes (Chilvers & Davies 2015).

In a normal functioning ear sound travels along the external ear, into the middle ear moving the stapes, and this sound pressure enters via the oval window to dissipate the fluid, not through the normal pathway to the cochlea but through the labyrinith (Ward et al., 2017).

The aetiology of SCD is highly contentious, there are many theories as to why these dehiscence’s occur, it is unclear whether it is congenital (Takahashi et al., 2012), acquired (Parlea et al., 2012) or a two hit phenomenon (Minor et al., 2000).

One theory is that there is a “first event” where some patients who are born with a thin or absent bone overlying the superior semi-circular canal and that a “second event” such as a head trauma or a valsalva manoeuvre (when a person forcefully expires against a closed glottis) that causes the onset of the signs and symptoms of SCD.

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Another theory to explain SCD is that dural pulsations (caused by pressure changes in the vascular system of the brain) over the arcuate eminence (a prominence on the anterior surface of the petrous portion of the temporal bone indicating the position of the superior semi-circular canal) result in progressive loss of bone.

Theories that support progressive bone loss of the SCC are supported by observations that the prevalence of SCD increases among older adults (Nadgir et al., 2011).

Figure 1. CT Image of SSCD.Computed tomography scan through the right mastoid cavity and middle cranial fossa. Superior semicircular canal indicated with asterisk. Dehiscence between the superior semicircular canal and the middle cranial fossa indicated with arrow. (Jacqueline et al., 2009)

Overall, the lack of agreement regarding the aetiology of SCD suggests that the syndrome is multifactorial.

1.1 Symptoms of SCD

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Patients with SCD syndrome can present with a range of auditory and/or vestibular signs and symptoms that are associated with a bony defect of one or both superior semi-circular canals.  The audiological symptoms are due to the presence of the mobile third window, which results in air conducted sounds losing energy and so an increased threshold is need to hear these sounds.  However in bone conducted sounds, the opposite is true, the low impedance caused by the dehiscence allows sound to travel through the perilymph in the inner ear via the labyrinth resulting in bone conduction sound being heard better than normal.  These results can be distinguished in an audiological appointment where PTA is performed (Ward, et al., 2017).  Vestibular signs and symptoms include vertigo and oscillopsia (movement of objects in the visual field) in response to sound (Tullio phenomenon) and/or pressure (Hennebert sign) and chronic disequilibrium, while auditory complaints include autophony (perception of one’s own body sounds at unusually high levels e.g. eyes moving), bone-conductive hyperacusis (sensitivity to low frequency sounds e.g. heartbeat) and pulsatile tinnitus(Minor et al., 1998).

The diagnosis of SCD syndrome can sometimes be difficult due to the variety of signs and symptoms that are not necessarily unique to SCD, thus “mimicking” other diseases (Merchant et al., 2007).  The audio-vestibular examination for patients with SCD requires a detailed medical history, physical examination, audiometric testing, vestibular evoked myogenic potential (VEMP) testing and imaging by using high resolution computed tomography (CT).

1.2 Types of VEMP

VEMP recording comprise of short latency surface electromyography potentials (EMG – which is a measurement of the electrical activity in muscles as a by-product of contraction) (Colebatch & Halmagyi., 1992).  They may be recorded from over the sternocleidomastoid (SCM) muscles of the neck – termed cervical VEMP or cVEMP (Colebatch et al., 1994),or through the inferior oblique muscles below the eyes during upward gaze – termed ocular VEMP or oVEMP (Rosengren et al., 2005).

cVEMP assess vestibular function through the vestibulocollic reflex (VCR), the VCR arc is often less often studies in literature compared to the well studied VOR (Vestibular Ocular Reflex).  Research presumes the pathway of the VCR is evoked by both of the otholitic organs, their corresponding vestibular nerve fibers, the vestibular nuceli, the vestibule – spinal tract, accessory nucleus, the accessory cranial nerve and then the SCM muscle (Rosengren, Welgampola & Colebatch., 2010).  The VCR is thought to allow for the stability of the head in space as it acts directly on the neck muscles (Mudduwa, Kara, Whelan and Banderjee 2010).

The origin of the oVEMP is also controversial with no consensus among researchers.  Some research consider the utricle to be responsible for the response (Manzari et al., 2010), this is the most widely accepted hypothesis, however other research has named the saccule as the organ responsible,(Murofushi & Curthoys, 1997), others suggest both may be responsible (Curthoys & Vulovic.,2011).

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Research does agree that the response is mediated by the superior vestibular nerve.  In studies in which patients have a superior vestibular neuritis, the response for oVEMP is absent, and the response for cVEMP is present.  In patients with inferior vestibular neuritis, results show oVEMP present and cVEMP absent (Shin et al., 2012).  These results however do not help in the argument of which otolithic organ is affected.  All of the afferent fibres of the utricle pass through the superior vestibular nerve, whereas the saccule fibres have a pathway that runs through both the superior and inferior vestibular nerve.  Therefore it is summarised that the superior vestibular nerve innervates the utricle, part of the saccule and the lateral SCC.  The inferior vestibular nerve innervates the posterior semicircular canal and most of the saccule.

The cVEMP is composed of two sets of waveforms.   The labelling system used when measuring myogenic potentials was established by Yoshie and Okudaira (1969).  The first potential has a positive peak (p) with an average latency of 13 milliseconds (ms), followed by a negative peak (n) with an average latency of 23 ms, making it known as p13–n23 complex.

Figure 3 illustrates the p13 – n23 complex response waveform in an adult with a normal functioning vestibular system

The oVEMP is also composed of two sets of positive and negative waveforms. The first potential has a negative peak (n) with an average latency of 10 ms, followed by a positive peak (p) with an average latency of 15 ms, making it known as n10–p15 complex.

Figure4 illustrates the n10 – p15 oVEMP complex response waveform in an adult with a normal functioning vestibular system

If is not absolutely certain whether the threshold or the amplitude of the oVEMP or cVEMP to air conducted  or bone conducted sound, or low or high frequency stimulation along these pathways has the greatest sensitivity and specificity for the diagnosis of semicircular canal dehiscence (Manzari et al., 2012, Zuniga et al., 2013).

2. Objectives

The primary research question of this study is to establish if there is sensitivity between cVEMP and oVEMP in the diagnosis of SCD. Do the differences between oVEMP and cVEMP, change the diagnosis of SCD?

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3. Methods

3.1 Inclusion/Exclusion criteria for studies

This review considered the following research methods for inclusion; systematic reviews and non-randomised case control trials.  To be included for appraisal, the publications must meet the following inclusion criteria:

a)articles published from January 2012 to December 2016;

b) articles available in English;

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c) articles available in full;

d) articles where participants were male or female,

e) only articles were the SCM was used to measure cVEMP,

f) articles that used either oVEMP or cVEMP individually or together to investigate SCD.

Papers were excluded from the review if the patient group, intervention or outcome measures were not relevant to the clinical question.  The following exclusion criteria were also adopted: duplicates, notes, dissertations, letters, conference papers and editorials. Paediatric articles were excluded and animal studies were excluded.

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3.2 Search strategy

The scientific database SCOPUS and Science Direct, were used to enable a multi-pronged strategy, as they cover multiple health related databases and they have full Med Line and PubMed coverage. The strategies searched can be seen in Appendix 1.

The 61 papers identified from the search were examined for their relevance to the clinical question posed and the inclusion/exclusion criteria.  If ambiguous measures were reported these papers were also excluded.

3.3 Assessment of study

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Selected studies were also measured for their evidences and appropriateness to the clinical question.  The following criteria appraisal areas were assessed:

1. The population studied (A sufficient risk factor group to control group population),
2. Presence of a healthy control group,
3. Methodology (The procedure of physically measuring the VEMP),
4. Measurement methods similar in all studies,
5. Confounding factors accounted for,
6. Suitable data analysis,
7. Precise values of results,
8. Plausibility of results,
9. Results in comparisons to other available evidences.

3.4 Data analysis

The analysis of the material found was performed at this stage.  First the duplicate references in the databases consulted were eliminated.  Second, by virtue of reading the abstracts, articles that did not meet the established objectives were excluded. (Appendix 2. Process of selecting evidence).

Table 1 -Study Summary