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and Colebatch (2013) and Smith, McCaslin, Jacob­son, and Burkard (2019). In the study by Lim et al. (2013), stimuli were delivered by both air and bone conduction. For the study by Smith et al. (2019), stim­uli were delivered by air conduction only. The stimu­lus in both studies was a 500 Hz tone burst. Lim et al. examined the effects of increasing stimulus duration from 2 to 10 ms. Smith et al. (2019) presented subjects with stimulus durations of 2 to 25 ms. In both inves­tigations, increasing the stimulus duration beyond 2 ms produced a reduction of oVEMP amplitude. Thus,
figure 16–23. The effect of stimulus intensity on the oVEMP amplitude.
Murnane, O. D., Akin, F. W., Kelly, K. J., and Byrd, S. (2011). Effects
From of stimulus and recording parameters on the air conduction ocular vestibular-evoked myogenic potential. Journal of the American Acad- emy of Audiology, 22, 469–480. Used with permission.
there was no benefit to increasing stimulus duration beyond 2 ms.
Stimulus Monaural/Binaural
Wang, Jaw, and Young (2009) reported their experience recording oVEMPs in response to monaural and binau­ral 500 Hz tone burst stimulation (i.e., 95 dB nHL). The authors reported no significant differences in response threshold, latencies, or amplitudes when data obtained from the two modes of stimulation were compared.
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figure 16–24. The effect of stimulus rate on oVEMP amplitude from the right and left eye. negative is up in this figure. From Chang, C. Young, Y. H. (2010). Effects of repetition rate of bone-conducted vibration on ocular and cervical vestibular-evoked myogenic potentials. Clinical Neurophysiology, 121, 2121–2127.
Used with permission.
M., Cheng, P. W., Wang, S. J., and
The investigators suggested that binaural stimula­tion produced significant time savings over monaural stimulation.
Despite the oVEMP being represented intermit­tently ipsilateral to the stimulus ear, Kim and Ban (2012) examined what effect, if any, binaural stimu­lation would have on the oVEMP. The investigators presented 500 Hz tone burst stimuli monaurally and binaurally on three occasions. The investigators mea­sured peak latency of N1, amplitude of N1–P1, and the interaural differences for these data points. The authors reported no significant differences in the peak­to-peak amplitude and amplitude asymmetry ratios when monaural and binaural data were compared. The interclass correlation coefficients ranged from 0.68 to
0.98. The latency of N1 was significantly later for the binaural presentation compared with monaural stimu­lation. This latency delay occurred possibly because the response to binaural stimulation represented the admix­ture of ipsilateral and contralateral waveforms. Also, the ipsilaterally recorded oVEMP occurred later than the contralaterally recorded oVEMP. Accordingly, the prod­uct of bilateral stimulation would be expected to be a distortion of the waveform recorded in response to mon­aural stimulation. The greatest effect was the reduction
in test time that occurred for binaural stimulation. The oVEMP air-conducted and bone-conducted stimulus protocols are presented in Tables 16–7 and 16–8.
tab le 16 –7. oVEMP Air-Conducted Stimulus Protocol
Frequency 500 Hz
Level 95 dB nHL
Gating Blackman
Rate 5.1/s
table 16–8. oVEMP Bone-Conducted Stimulus Protocol
Frequency 500 Hz
Level 150 dB peak FL (31.6 N peak)
(Papathanasiou et al., 2014)
Gating 6 ms duration (2 ms rise/fall)
Rate 5 Hz
Location of stimulator
Mastoid or Glabella
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Recording Variables
Electrode Placement
Electrodes are silver/silver chloride disposable elec­trodes. The locations of the recording electrodes are shown in Figures 16–25 and 16–26.
The skin should be degreased with rubbing alco­hol at the left and right infraorbital midlines (i.e., the electrodes should be placed as close to the middle bot­tom of the lower eyelid as possible). These electrodes serve as active (or non-inverting) inputs to channels 1 (left eye) and 2 (right eye) of the differential amplifier. The reference (or inverting) input for channels 1 and 2
Figure 16–25. A model prepared for a two-channel oVEMP recording using the active electrode (infraorbital 1 cm) referenced to the infra­orbital 3 cm electrode.
Figure 16–26. A model prepared for a two-channel oVEMP using the electrode montage described by Sandhu et al (2013). Active elec­trodes are placed on the belly of inferior oblique muscle and refer­enced to the electrode at the inner canthus position.
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is a single electrode placed on the chin (i.e., common reference in our protocol) that is “jumpered” into the reference electrode inputs for channels 1 and 2 (see Figure 16–25). Alternately, the reference can be two electrodes placed 2 to 3 cm inferior to each of the near infraorbital electrodes. This is the protocol followed by most clinicians. The ground electrode is placed at FPz or Fz for the sake of convenience but could be placed anywhere on the body (Colebatch, 2013). Closely spaced bipolar electrodes are very sensitive to signals occurring between the two electrodes and relatively insensitive to other signals generated on the face/ body. However, we found (Piker et al., 2011) that the near infraorbital reference electrodes were recording, on average, 30% of the oVEMP amplitude recorded by the active electrode, creating a problem called reference contamination.
When reference contamination occurs, the oVEMP recorded by the reference electrode is subtracted in the differential amplifier from the oVEMP recorded by the active electrode. The net effect is an “artificial” reduc­tion or phase cancellation of part or all of the oVEMP recorded by the active electrode. In our experience very little of the oVEMP is volume conducted to the chin. The advantage of the referential technique (i.e., as opposed to the bipolar recording method) is the enhancement of the N1–P1 amplitude. The single disadvantage of this technique is the potential for EMG generated at the chin to be “injected” into the signal-averaged responses recorded from the infraorbital electrodes.
An interesting recent report by Sandhu, George, and Rea (2013) was a reexamination of the effects of the location of the active electrode. The investigators placed the reference electrode at its normal location (i.e., below the contralateral eye at midline) but placed a series of five active electrodes infraorbitally and equi­distant from the inner canthus to the outer canthus. The ground electrode was placed on the sternum (see Fig­ure 16–26). The investigators reported that the largest oVEMP was recorded from the electrode just lateral to the infraorbital midline electrode when it was ref­erenced to the electrode placed at the inner canthus. The investigators reasoned that that electrode montage optimized the recording of the oVEMP, since the active electrode was placed over the belly of the inferior oblique muscle (i.e., where the maximum response is recorded) and the reference was placed over its tendon at the inner canthus, which is electrically neutral (i.e., theoretically none of the evoked potential is recorded from that location). It has been our experience that the inner canthus reference site provides superior oVEMP amplitudes regardless of age. Over the past five years our recommendation for a reference electrode location
has evolved from the chin (as a common reference to the two channels) to the inner canthi.
Lastly it should be mentioned that it is possible to record the oVEMP without a reference electrode (i.e., a monopolar or “reference free” recording). A monopolar reference is useful when placement of a reference elec­trode would be expected to inject reference contamina­tion into the recording.
Amplification
The oVEMP is one to two orders of magnitude smaller than the cVEMP and therefore requires 10 to 100 times more amplification to bring the signal within range of the signal averager. This means that ampli­fication values of 50,000× to 100,000× are necessary to increase the magnitude of the raw EMG signal to be within the range of the signal averaging computer so that the oVEMP can be extracted. Since this is a much smaller response than the cVEMP and because this is not entirely a stimulus-synchronized attenuation of evoked EMG from the inferior oblique (IO) muscle, it is necessary to reject EMG artifacts. This means artifact rejection must be enabled to record the oVEMP.
Filtering
The subject of optimal bandpass filtering has been addressed in the recent literature. Wang, Jaw, and Young (2013) recorded the oVEMP to acoustical stimuli using high-pass filter settings of 1, 10, and 100 Hz and low-pass filter settings of 500, 1000, and 2000 Hz. The investigators reported that the bandpass yielding the best amplitude oVEMP without affecting its latency was 1 to 1000 Hz.
Burkard and colleagues (2013, personal communi­cation) also have examined systematically the effect of filter bandpass on oVEMP amplitude. They observed that the critical frequencies that must be available for signal averaging are ~20 Hz for the high-pass fil­ter and 200 Hz for the low-pass filter. The spectra of the oVEMP show little energy in the response beyond
Hz (Burkard 2013, personal communication).
140
Subject Factors
Gaze Effects
Although it has been reported that the oVEMP can be recorded with the patient’s eyes at center gaze (Huang, Yang, & Young, 2012) and in patients with closed eyes (i.e., although the waveforms looked quite different
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from the conventional oVEMP; Huang et al., 2012), the oVEMP is best recorded with the patient gazing upward ~20 degrees or more (Govender, Rosengren, & Colebatch, 2009; Hsu, Wang, & Young, 2009). Moving the eye from center gaze to upward gaze is believed to position the contralateral inferior oblique muscle closer to the active (non-inverting) infraorbital elec­trode. This observation about gaze position effects on the oVEMP was also supported by the results of Mur­nane et al. (2011), who reported that maximal ampli­tude of the oVEMP was recorded with subjects gazing at 30 degrees vertically (i.e., the study examined the effects of gaze angles from 5–30 degrees; Figure 16–27).
It is significant that Rosengren, Colebatch, Strau­mann, and Weber (2013), who systematically exam­ined gaze effects, reported that the increase in oVEMP
amplitude with upward gaze could not be explained entirely by the reduction in the distance of the contra­lateral infraorbital recording electrode to the IO mus­cle. Instead, it was the investigator’s contention that upward gaze increased the tonic activity in the IO mus­cle, and much as occurs with the SCM, the onset of the tone burst results in a stimulus-initiated reduction in that tonic activity. If this is in fact true, what is not clear is why the oVEMP is a negative-positive waveform instead of a positive-negative waveform. The oVEMP recording protocol is shown in Table 16–9.
Age Effects
A number of processes occur as we age that have an effect on the normal function of the peripheral and
figure 16–27. The effect of gaze angle on oVEMP amplitude. From Murnane, O.D., Akin, F. W., Kelly, K. J., and Byrd, S. (2011). Effects of stimu­lus and recording parameters on the air conduction ocular vestibu­lar-evoked myogenic potential. Journal of the American Academy of Audiology, 22, 469–480. Used with permission.
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table 16–9. oVEMP Recording Protocol
Inverting electrode (reference) 3 cm infraorbital or chin (conventional
reference electrode placement is immediately below the infraorbital midline electrode)
Noninverting electrode (active) Infraorbital midline
Ground (Earth) Forehead (i.e., Fz)
Electrode impedances ≤10,000 ohms, with interelectrode
impedance differences ≤
Channels Two (ipsilateral and contralateral
infraorbital midline responses)
Amplification (gain)
Artifact rejection Enabled
Filter bandpass 1–10 Hz to 500–1000 Hz
Epoch 100 ms (with a 20-ms prestimulus period)
Number of accepted samples 150
Number of completed averages 2
× 30,000 to 50,000
2000 ohms
central vestibular systems. These age-related changes are addressed in detail elsewhere in this text (Chap­ter 25); however, we address a few of the age-related changes here.
There have been documented age-related effects at the hair cell level as well as at the level of the afferent neurons (Ishiyama, 2009). The loss of both hair cells and first-order afferents has been documented in the cris­tae, the utricle, and the saccule. A decrease in hair cell density occurs after age 50 years. The greatest effects may be observed in the saccules and the cristae, with less age-related damage occurring for the utricle. That is, when young and older individuals were compared, hair cell density was reduced by 40% at the cristae, 24% at the saccule, and 21% at the utricle (Rosenhall, 1973). More specifically the fetal cristae contain ~7,800 hair cells and this is reduced to 4,700 for adults between the ages of 71 and 95 years (i.e., a reduction of 38% on average). A reduction of 30% in hair cell density in the senescent mouse produces a reduction of VOR gain at
0.8 Hz. That gain reduction produces “retinal smear” during movements of the head or head and body. In the human, VOR gain shows significant reductions beyond age 70 years.
There are age effects specific to the utricle and saccule. Many of the changes affect the otolith crystals. The density of the calcium carbonate crystals is reduced and the normal regeneration of the crystals is impaired with age. This results in reduced otoconial volume, fractured otoconia (i.e., producing debris in the canal
and an increasing the likelihood of benign paroxysmal positional vertigo), and even the generation of “giant” otoconia. In parallel with structural changes affecting the end organ, there can be impaired perfusion of the end organ. Over and above these changes there has been reported a 25% reduction in neurons at Scarpa’s ganglion, and a 37% loss of afferents when comparing younger adults with older adults.
Hsu et al. (2009) evaluated age-related differences in oVEMP latency and amplitude. Subjects were adults (24–33 years of age, N = 15) and children (3–13 years of age, N = 15). The stimulus was a tone burst presented at 105 dB nHL. The authors did not report age-related dif­ferences in N1 latency, P1 latency, or the N1–P1 interval or the peak-to-peak amplitude of the oVEMP.
Chang et al. (2012) evaluated the effect of age on oVEMPs recorded in response to bone-conducted vibra­tion and galvanic stimulation. Since the galvanic stimu­lus bypasses the end organ and stimulates the afferent nerve fibers directly, an abnormal or absent bone­conducted oVEMP with a normal galvanic oVEMP would suggest an end organ impairment, whereas a unilaterally delayed galvanic oVEMP would suggest an impairment in neural conduction. The investiga­tors reported significant N1 latency delays for a group of subjects older than 60 years compared with groups younger than 60 years. There were nonsignificant dif­ferences in the prevalence of the galvanic oVEMP sug­gesting that age differences observed in the prevalence of bone-conducted oVEMPs reflected age changes
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in the peripheral vestibular system. The effect of age and stimulus type on the prevalence of the oVEMP is shown in Table 16–10.
The study of age effects on the oVEMP is com­plicated by the differing stimuli used by investigators to evoke the response (e.g., electrical/galvanic, bone conduction, skull tap, acoustical click, acoustical tone burst) and the methods used to obtain the data (e.g., threshold versus suprathreshold stimulation for evalu­ation of effects of stimulus frequency).
Tseng, Chou, and Young (2010) examined 70 sub­jects with an age range of 24 to 76 years. They placed the subjects into six groups representing six age decades. The stimuli were delivered by bone conduction stimu­lation. All subjects from ages 20 to 59 years generated oVEMPs. Conversely 55% of those subjects aged 60 to 69 years and 40% 70 years and older failed to generate an oVEMP. With age treated as a continuous variable, both N1 latency (r = 0.54) and N1–P1 amplitude (r =
−0.37) showed age effects. The investigators reported a positive correlation between N1 latency and age and a significant negative correlation between age and N1– P1 amplitude.
Nguyen, Welgampola, and Carey (2010) evaluated 53 subjects between the ages of 20 and 70 years. Stimuli were acoustical clicks and 500 Hz bursts, skull taps (i.e., delivered with a specially modified tendon hammer), and skull vibration (i.e., delivered with a Bruel & Kjaer Mini-shaker). The interclass correlation coefficients between subject age and oVEMP for tone burst stimuli ranged from 0.81 (N10 amplitude) to 0.79 (N10–P15 peak-to-peak amplitude) to 0.50 (for the amplitude asymmetry of the N10–P15 peak-to-peak amplitude). Unlike the report by Tseng, when age and oVEMP amplitudes were plotted as continuous variables there was no significant relationship. This finding was also at odds with the findings of Iwasaki et al. (2007), who reported a linear decrease in oVEMP amplitude with
table 16–10. Prevalence of the oVEMP in Response to Galvanic and Bone-Conducted Stimuli
Galvanic oVEMP
Age Group
20 to 29 years 100 100
30 to 39 years 100 100
40 to 49 years 100 100
50 to 59 years 100 86
60 to 69 years 84 63
% Prevalence
BC oVEMP
% Prevalence
age when the stimuli were skull taps and skull vibra­tion (i.e., mini-shaker).
Rosengren et al. (2011) examined age effects on the oVEMP in response to forehead taps, lateral (mas­toid) vibration, and both air- and bone-conducted tone bursts. Subjects were 61 normal individuals aged 18 to 80 years. The oVEMPs evoked with taps and vibration did not demonstrate age effects. The authors reported a moderate correlation between oVEMP amplitude and age for acoustical clicks and bone-conducted tone bursts. The authors reported elevated oVEMP thresh­olds by 6 dB on average when oVEMP threshold inten­sities were compared with cVEMP threshold intensities for 500 Hz tone burst stimuli. Response prevalence was 93% for stimuli of an intensity of 110 dB L
. Ocular
Aeq
VEMPs demonstrated latencies that were significantly longer with age for air-conducted clicks and 500 Hz tone bursts.
Piker et al. (2011) examined the effects of age on N1 and P1 latency, N1–P1 peak-to-peak amplitude, N1 interaural latency difference, and interaural N1– P1 amplitude asymmetry. Subjects were young individu­als (mean age 12.5 years), middle-aged adults (mean age 34 years), and old adults (mean age 63 years). The authors reported significant decreases in N1–P1 peak­to-peak amplitude when young subjects and middle­age subjects were compared with older subjects. With age treated as a continuous variable, the correlation coefficient for oVEMP peak-to-peak amplitude was negative and statistically significant (r2 = .14, p < .001). Further, there were significant age differences in N1 threshold intensity (see below).
Age Effects of oVEMP Threshold. Increased age
results in elevated oVEMP thresholds. When treated as a continuous variable, oVEMP threshold correlated positively with subject age (r2 = .11, p = .002). In fact, there was a 3.4 dB difference in N1 thresholds when data from young adults and old adults were compared (i.e., threshold occurred at higher intensities for old adult subjects) (Piker et al., 2011).
Age Effects of oVEMP Tuning. The effects of age on
the “tuning” of the oVEMP was addressed by Piker and colleagues (2013). Stimuli consisted of acoustical tone bursts of frequencies 125, 250, 500, 1000, 1500, and 2000 Hz that were presented at 127 dB pSPL. All stimuli were presented in a pseudo-randomized man­ner for each run so that the effects of fatigue might be distributed evenly across all stimuli. Subjects ranged in age from 22 to 78 years (N = 39, mean age 46 years, ±15.7 years). Subjects were placed into three age groups consisting of young, middle, and older adults. The
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investigators reported that best frequency occurred for 500 and 750 Hz tone bursts (i.e., stimulus yielding the greatest amplitude oVEMP), although there were no significant differences in oVEMP amplitudes across age groups for each frequency. Whereas the best fre­quency to evoke the oVEMP for young adult subjects was 750 Hz, the best frequency increased to 1000 Hz stimulus for older adult subjects. Armed with this information, the authors cautioned that clinicians might choose different evoking stimuli depending on the age of their patients (e.g., 500 Hz tone bursts for younger adults and 1000 Hz for older adults if they failed to generate an oVEMP in response to the 500 Hz stimulus).
It is our practice to first record the oVEMP in response to 95 dB nHL, 500 Hz tone bursts delivered monaurally. Responses are replicated at least one time so that reproducibility of the data can be assessed. Where the response exists we then use a bracketing technique to estimate oVEMP threshold separately for the left and right ears.
When a negative waveform is plotted as a down­ward deflection, the normal oVEMP appears as a “W.” with the first negative peak occurring at ~11 ms. The variables we quantify include: N1 latency, P1 latency, N1–P1 peak-to-peak amplitude, interaural N1 latency differences, and interaural differences in N1–P1 ampli­tude (in percent). The most common abnormality encountered is either a unilaterally or bilaterally absent oVEMP, or a unilaterally abnormal reduction in oVEMP amplitude. Rarely does a latency prolongation occur. When a latency prolongation occurs, it usually occurs bilaterally and signifies an impairment in central trans-
mission occurring either in the afferent or efferent limbs of the reflex arc. Table 16–11 shows normative data for the oVEMP gathered in our laboratory.
cVEMP AND oVEMP TEST RESULTS
IN
SELECT DISEASES
Superior Semicircular Canal Dehiscence Syndrome (SSCDS)
The approach to the identification of SSCDS with the oVEMP has gone in two directions. The underlying assumption for each approach is that the dehiscence results in an abnormal “augmentation” of the normal response to either air-conducted or bone-conducted stimuli. For example, normals do not generate oVEMPs in response to 4000 Hz tone bursts. However, Manzari, Burgess, McGarview, and Curthoys (2013) observed that patients with SSCDS clearly generated oVEMPs in response to either an air- or bone-conducted 4000 Hz tone burst. None of their normal controls generated oVEMPs to the same stimulus. In this way the investi­gators suggested that they had created a one-trial pro­tocol for the identification of SSCDS.
In a slightly different implementation, Zuniga, Janky, Nguyen, Welgampola, and Carey (2013) recorded both oVEMPs and cVEMPs in response to air-conducted and bone-conducted clicks and 500 Hz tone bursts. They recorded responses from patients placed in different age groups. The authors reported that the absolute peak-to-peak amplitude of N1–P1
Ta ble 16–11. Comparison of Characteristic Parameters of oVEMP Among the Three Age Groups
Age Group (yr)
1 (<18) 20 12.1 (1.1) 17.1 (1.3) 5.2 (1.1) 1.2 (.9) 5.3 (2.8) 14 (10) 90.7 (3.7)
2 (18–49) 58 12.5 (.88) 17.6 (1.1) 5.0 (.84) .61 (.59) 5.1 (3.1) 13 (10) 92.8 (2.9)
3 (≥ 50) 22 12.7 (1.3) 17.2 (2.3) 4.0 (2.3) 1.4 (1.1) 1.5* (1.4) 16 (12) 94.1* (1.9)
Total 100 12.4 (1.0) 17.4 (1.3) 5.0 (1.3) .85 (.81) 4.4 (3.1) 14 (10) 92.5 (3.2)
p value 0.116 0.346 0.077 0.019 <0.001 0.755 0.007
Note. p value = one-way analysis of variance test. Data are expressed as mean (sd). *p < .05, Bonferroni-adjusted t-test.
Source: Data from Piker, E. G., Jacobson, G. P., McCaslin, D. L., and Hood, L. J. (2011). Normal characteristics of the ocular vestibular evoked myogenic potential. Journal of the American Academy of Audiology, 22, 222–230.
N
(ears)
N1
Latency,
ms
P1
Latency,
ms
N1–P1
Latency,
ms
Interaural
N1
Latency
Difference,
ms
N1–P1
Amplitude,
µV
Interaural
Amplitude
Asymmetry
Ratio, %
Threshold,
dB nHL
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discriminated well between patients with (sensitiv­ity) and without (specificity) SSCDS. In fact, using their absolute amplitude criterion, both sensitivity and specificity values exceeded 90%. For example, the investigators reported that using an upper limit of 17.1 µV yielded sensitivity and specificity of 100% and 98%, respectively This absolute N1 amplitude upper limit varied by age (Tables 16–12 and 16–13 from Zuniga et al., 2013).
It would appear that there now exist two methods that have been offered by investigators for the identi­fication of SSCDS that do not rely on the tedious activ­ity of oVEMP threshold estimation. The authors of this
table 16–12. oVEMP Sensitivity and Specificity for the Diagnosis of Superior Canal Dehiscence Syndrome
Cutoff Value Sensitivity (%) Specificity (%)
Tone-burst oVEMP Peak-to-peak
amplitudes
Tone-burst oVEMP N1 amplitudes >7.5
Click oVEMP Peak-to-peak
amplitudes
Click o
VEMP N1 amplitudes >2.5
>11.7 >17.1 >20.3
chapter suggest that the examiner might create two­stage criteria for the identification of SSCDS patients: (1) “Does there exist an oVEMP in response to a 4000 Hz, air-conducted tone burst stimulus?” and (2) “Does the amplitude of the oVEMP in response to a 500 Hz, 95 dB nHL, air-conducted tone burst stimulus equal or exceed 17.1 µV?” If the answer to either or both of these questions is “yes,” the likelihood is high that the patient has a dehiscent or even a “near dehiscent” (Ward et al.,
2013) superior semicircular canal. It is important to note that the 17.1 µV criterion applies only to data col­lected with the same reference electrode site that was reported by Zuniga et al. (2013).
100 100
97
100 >9.3 >9.9
>9.9 100 100
>6.6
100
93
100
94
88 98
100
94 100 100
68 100
Source: Data from Zuniga, M. G., Janky, K. L., Nguyen, K. D., Welgampola, M. S., and Carey, J. P. (2013). Ocular versus cervical VEMPs in the diagnosis of superior semicircular canal dehiscence syndrome. Otology and Neurotology, 34, 121–126.
table 16–13. Ocular Vestibular Evoked Myogenic Potential Sensitivity and Specificity for Patients with Superior Canal Dehiscence
Cutoff Value (µv)
(Peak-to-Peak-
Age Decade
30s 17.5 100 100
40s 22
50s 16.6
60s 14.8 100 100
Source: Data from Zuniga, M. G., Janky, K. L., Nguyen, K. D., Welgampola, M. S., and Carey, J. P. (2013). Ocular versus cervical VEMPs in the diagnosis of superior semicir­cular canal dehiscence syndrome. Otology and Neurotology, 34, 121–126.
Amplitude) Sensitivity (%) Specificity (%)
.0 100 100
21.3
100
90
94
100
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Vestibular Neuritis
Shin et al. (2012) examined 30 patients with superior vestibular neuritis (SVN), 3 patients with inferior ves­tibular neuritis (IVN), and 8 patients with both branches impaired, then compared them with data obtained from 60 normal controls. The investigators reported absent oVEMPs and caloric responses and normal cVEMPs for patients with SVN. They reported normal caloric responses and oVEMPs and absent cVEMPs in patients with IVN, and absent cVEMPS and oVEMPs and caloric responses for patients with both vestibular nerve branches affected.
SUMMARY: CAVEATS
REGARDING VEMP TESTING
It would be misleading to end this chapter without stat­ing briefly a few caveats about pathologies affecting the oVEMPs and cVEMPs (adapted from Curthoys, Man­zari, Smulders, & Burgess, 2009). Abnormal oVEMP and cVEMP certainly can occur in the presence of sig­nificant impairments affecting either or both the sac­cules, utricles, and superior and/or inferior vestibular nerves. However, absent VEMPs can occur when there is a conductive hearing impairment that reduces the sound intensity reaching the vestibular end organs. So it is essential to obtain a recent audiogram and immit­tance test before acoustical stimuli are used to evoke a VEMP. When a conductive impairment significantly reduces the intensity of the acoustical stimulus, the examiner must use an alternative method to translate the otoliths (e.g., mechanical stimulation, vibratory stimulation). Additionally, significant neuromuscu­lar disease (e.g., myasthenia gravis) can produce an abnormal VEMP even when the vestibular end organs are intact. Diseases of the central nervous system (e.g., multiple sclerosis) can also produce abnormal VEMP tests where the end organs are normally functioning. Last, and certainly not least, there are a myriad of technical mistakes that young and seasoned clinicians can make that can reduce or eliminate the likelihood of recording a VEMP. These errors include: incorrect placement of electrodes, over- or under-amplification of the bioelectrical activity, incorrect routing of the stimulus (i.e., sending the stimulus to the right ear for a left ear VEMP test), and testing an ear that is occluded with cerumen. This is only the beginning of a long list of possible technical errors. Given these assumptions it is best to approach each patient as “normal until proven otherwise.”
REFERENCES
Agrawal, Y., Bremova, T., Kremmyda, O., & Strupp, M.
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