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Diagnostic Value of Prolonged Latencies in the Vestibular Evoked Myogenic Potential
Toshihisa Murofushi, MD;
Ken Shimizu, MD;
Hideki Takegoshi, MD;
Po-Wen Cheng, MD
Arch Otolaryngol Head Neck Surg. 2001;127:1069-1072.
ABSTRACT
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Background As a parameter for the evaluation of the vestibular evoked myogenic
potential (VEMP), amplitude has been used clinically. However, the significance
of latency has not been considered.
Objective To clarify the diagnostic value of latencies of the VEMP.
Design We reviewed records of the VEMP of patients with various diseases and
compared them with records of healthy volunteers.
Setting Data were collected from patients in an outpatient clinic of a tertiary
care center and healthy volunteers.
Subjects Clinical records of 134 patients (61 men and 73 women, aged 20-75 years)
were reviewed. Diagnoses were Meniere disease in 43 patients, acoustic neuroma
in 62 patients, vestibular neuritis in 23 patients, and multiple sclerosis
in 6 patients. Also, 18 healthy volunteers (13 men and 5 women, aged 25-38
years) were enrolled.
Intervention Diagnostic.
Main Outcome Measures Click-evoked myogenic potentials were recorded with surface electrodes
over each sternocleidomastoid muscle. Latencies and amplitudes of responses
were measured.
Results Vestibular evoked myogenic potentials were absent or decreased in 51%
of patients with Meniere disease (n = 22), 39% with vestibular neuritis (n
= 9), 77% with acoustic neuroma (n = 48), and 25% with multiple sclerosis
(3 of 12 sides of 6 patients). Concerning latency, patients with Meniere disease
or vestibular neuritis hardly showed any latency prolongation. Four patients
with acoustic neuroma showed prolonged p13; all had large tumors. All patients
with multiple sclerosis showed prolonged p13.
Conclusion Prolonged latencies of the VEMP suggest lesions in the retrolabyrinthine,
especially in the vestibulospinal tract.
INTRODUCTION
CLICK-EVOKED myogenic potentials on the sternocleidomastoid muscle have
been used as a clinical test of the vestibulospinal reflex. This response
is known as the vestibular evoked myogenic potential (VEMP).1-3
Although we have mainly used the amplitude of the first positive-negative
response (p13-n23) for the evaluation of VEMP, we have not used the peak latency
(p13 and/or n23). Recently, Shimizu et al4
reported that latencies of p13 and n23 were prolonged in 3 patients with multiple
sclerosis (MS) who are included in this study and that latencies could be
a useful parameter for the evaluation of lesions in the vestibulospinal tract.
We speculated whether the prolongation of the latencies was pathognomonic
for MS or lesions in the vestibulospinal tract. However, there are no reports
concerning latency in other diseases. To clarify the diagnostic value of VEMP
latencies, we reviewed VEMP recordings from patients with Meniere disease
(MD), vestibular neuritis (VN), acoustic neuroma (AN), and MS and compared
their results with those of healthy subjects.
SUBJECTS AND METHODS
SUBJECTS
Clinical records of 134 patients (61 men and 73 women, aged 20-75 years)
were reviewed. Diagnoses were MD in 43 patients, AN in 62 patients, VN in
23 patients, and MS in 6 patients. Both MD and VN were diagnosed according
to standard neurotologic criteria.2, 5-6
Diagnoses of AN were confirmed by neurosurgery. In other words, AN in this
article represents vestibular schwannoma. The diagnosis of MS was made by
standard neurological criteria.7 In patients
11, 12, 13, and 14, T2-weighted magnetic resonance imaging showed high-intensity
lesions in the pontine tegmentum involving the vestibular nuclei and vestibulospinal
tract bilaterally (Figure 1). In
patients 15 and 16, T2-weighted magnetic resonance imaging did not show high-intensity
lesions in these areas. Except for patients with MS, patients had unilateral
diseases. Also, 18 healthy volunteers (13 men and 5 women, aged 25-38 years)
underwent VEMP testing.
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Figure 1. Parameters of the latency measured.
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METHODS
The methods for recording VEMPs are described elsewhere.2-3
Briefly, surface electromyographic activity was recorded in the supine patient
from symmetrical sites over the upper half of each sternocleidomastoid muscle,
with a reference electrode on the lateral end of the upper sternum. During
recording, the patients were instructed to rotate their heads to the opposite
side to the stimulated ear as much as possible to activate the sternocleidomastoid
muscle. Electromyographic activities were monitored on a display during the
recording to maintain muscle activities at a constant level in each patient.
The electromyographic signal from the stimulated side was amplified and bandpass
filtered (20-2000 Hz). Rarefaction clicks (0.1 millisecond [ms], 95-dB normal
hearing level) were presented through a headphone (type DR-531, Elega Acous.
Co Ltd, Tokyo, Japan). The stimulation rate was 5 Hz, and the analysis time
was 50 ms. The responses to 100 stimuli were averaged twice.
We analyzed the amplitude of the first positive-negative peak, p13-n23
ipsilateral to the stimulated ear and the latencies of p13 and n23.8 The average of 2 runs was taken for the amplitudes
and latencies.
For the evaluation of the amplitude, the percentage of VEMP asymmetry
(VA) was calculated as 100[(Au - Aa)/(Aa + Au)], where Au is the p13-n23
amplitude on the unaffected side and Aa is the p13-n23 amplitude on the affected
side. In healthy volunteers, the percentage of VA was evaluated as 100[|Ar -
Al|/(Ar + Al)], where Ar is the p13-n23 amplitude on the right and Al is the
p13-n23 amplitude on the left and |Ar - Al| is the absolute value of
(Ar - Al).3
As parameters of the latency, we measured the peak latencies of p13
and n23. p13 is the first positive peak of VEMPs, and n23 is the first negative
peak following p13.8 We defined the latency
as the time from the onset of the stimulus to the peak (Figure 2).
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Figure 2. A T2-weighted magnetic resonance
image of patient 14 (a 50-year-old man with multiple sclerosis) showing high-intensity
lesions in the pontine tegmentum involving the vestibular nuclei and vestibulospinal
tract bilaterally.
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RESULTS
HEALTHY VOLUNTEERS
Clear responses were obtained on both sides from all healthy subjects.
The mean ± SD latencies of p13 and n23 were 11.8 ± 0.86 and
20.8 ± 2.2 ms, respectively. When we defined the mean latencies +2
SDs as the upper limits of the normal ranges, the upper limits were 13.5 ms(p13)
and 25.2 ms (n23). When the latency of p13 or n23 was longer than the mean
latency +2 SDs of healthy volunteers, we regarded the latency as prolonged.
Because the mean ± SD of the percentage of VA was 12.5% ±
8.7%, the upper limit was 30.0%. When the percentage of VA was greater than
the mean +2 SDs of healthy volunteers, we regarded the amplitude of the smaller
side as decreased.
PATIENTS
Meniere Disease
Fifteen of the 43 patients showed absence of p13-n23 on the affected
side, 7 showed decreased responses, and 21 showed normal responses. In other
words, 22 (51%) of 43 showed abnormal amplitudes on the affected side (Figure 3). Concerning latencies, only 1 patient
showed prolongation of p13 (14.0 ms) (Figure
4). None of the patients with MD showed prolongation of n23.
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Figure 3. Amplitudes of p13-n23 on the affected
side. Responses were absent or decreased in 22 (51%) of the 43 patients with
Meniere disease (MD), 9 (39%) of the 23 patients with vestibular neuritis
(VN), and 48 (77%) of the 62 patients with acoustic neuroma (AN).
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Figure 4. Latencies of p13 patients with
Meniere disease (MD) or vestibular neuritis (VN) hardly showed any prolonged
p13. Among patients with acoustic neuroma (AN), 4 patients showed prolonged
p13. All had large tumors. All patients with multiple sclerosis (MS) showed
prolongation of p13 if they showed any response. No. represents the number
of patients in the MD, VN, and AN groups and the number of sides in the MS
group.
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Vestibular Neuritis
Nine (39%) of the 23 patients showed absence of p13-n23 on the affected
side, and 14 showed normal responses (Figure
3). Concerning latencies, only 1 of the 14 patients showed prolonged
p13 (13.7 ms) (Figure 4). None of
the patients with VN showed prolongation of n23.
Acoustic Neuroma (Vestibular Schwannoma)
Thirty-nine of the 62 patients showed absence of responses on the affected
side, 9 showed decreased responses, and 14 showed normal responses. In other
words, 48 patients (77%) showed abnormal amplitudes (Figure 3). Concerning latencies, 4 (17%) of the 23 patients with
responses showed prolongation of p13 (Figure
4). Three of the 4 patients also showed prolongation of n23 (Table 1, Figure 5).
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Table 1. Patients With Acoustic Neuroma and Prolonged p13 and/or n23*
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Figure 5. Vestibular evoked myogenic potentials
of patient 3 (a 43-year-old man with right-sided acoustic neuroma). Latencies
of p13 and n23 on the right were prolonged significantly.
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We classified patients into 2 groups according to their tumor sizes.
Twenty-nine patients had small tumors, which protruded from the porus of the
internal auditory meatus less than 2 cm. Among the 29 patients, 16 showed
absent VEMP, 4 showed decreased VEMP, and 9 showed normal VEMP. None of them
showed prolongation of the latency of p13 or n23. Thirty-three patients had
large tumors, which protruded from the porus of the internal auditory meatus
equal to or more than 2 cm. Among the 33 patients, 23 showed absent VEMP,
5 showed decreased VEMP, and 5 showed normal amplitudes of VEMP. All 4 patients
who showed prolongation of p13 had large tumors (Table 1). Prolongation of p13 latency was significantly greater
in the group of large tumors than the group of small tumors (Fisher exact
test, P<.05).
Multiple Sclerosis
Among 12 sides of the 6 patients with MS, 3 sides showed absence of
responses. All of the other sides (9 sides) showed prolongation of p13, and
4 showed prolongation of n23 (Table 2, Figure 4).
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Table 2. Latencies of Patients With Multiple Sclerosis*
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STATISTICAL ANALYSES
The mean latencies and SDs of p13 and n23 are summarized in Table 3. Concerning latencies of p13 and
n23, significant differences were found among 5 groups (control, MD, VN, AN,
and MS) (P<.001, 1-way analysis of variance).
Significant differences of p13 latencies were found between the MS group and
each of the other 4 groups (P<.001, Scheffé
test). Significant differences of n23 latencies were also found between the
MS group and each of the other 4 groups (P<.001
for control, P<.001 for MD, P = .006 for VN, and P = .02 for AN, Scheffé
test).
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Table 3. Mean Latencies of p13 and n23
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COMMENT
For clinical evaluation of VEMP, amplitude has been mainly used.1-3 In patients with the
Tullio phenomenon, the threshold has also been used for evaluation.9-10 The latency is a useful parameter
in other types of evoked potentials such as auditory brainstem responses.
However, latency was seldom used for the evaluation of VEMP, although Shimizu
et al4 reported that 3 patients with MS showed
prolongation of p13 latency. It was not yet clear if prolonged VEMP latencies
are pathognomonic for MS.
In this study, we reviewed the results of VEMPs in patients with MD,
VN, AN, and MS. Meniere disease is a representative disease of labyrinthine
lesions, and VN is a representative disease of the vestibular nerve. Acoustic
neuroma is a disease in which the vestibular nerve and brainstem can be involved,
whereas MS is a representative disease of the central nervous system.
In this study, patients who had MD hardly showed any prolongation of
VEMP latency, whereas many patients showed decreased amplitudes or absent
responses. It is unlikely that prolonged VEMP latencies are a sign of inner
ear lesions. Patients with VN did not show latency prolongation either. To
explain this, we can consider 2 possibilities. First, some patients may have
complete damage in the inferior vestibular nerve, resulting in absence of
the VEMP, whereas in other patients the inferior vestibular nerve could be
spared as reported by Murofushi et al2 and
Fetter and Dichgans.11 In other words, patients
with VN may have complete damage or no damage to the inferior vestibular nerve.
Second, damage only to the vestibular nerve may be insufficient for VEMP latency
prolongation beyond the normal range. In fact, all patients with AN who showed
latency prolongation had large tumors that compressed the brainstem. The most
marked findings were obtained in patients with MS. All subjects showed latency
prolongation if they showed any responses. These results suggest that brainstem
lesions, especially those in the vestibulospinal tract, are required for the
prolongation of p13.
From the practical viewpoint, p13 showed prolongation of the latency
more frequently than n23. As we showed, the SD of n23 was greater than that
of p13, resulting in a wider normal range of n23 than p13. Therefore, p13
is a better parameter for evaluation of the latency of VEMP.
In conclusion, prolonged VEMP latencies, especially prolonged p13, would
strongly suggest lesions in the vestibulospinal tract, although they are not
pathognomonic for MS.
AUTHOR INFORMATION
Accepted for publication March 20, 2001.
This study was supported by a research grant from the Intractable Diseases
Fund (Vestibular Disorders) of the Ministry of Health and Welfare, Tokyo,
Japan.
Corresponding author and reprints: Toshihisa Murofushi, MD, Department
of Otolaryngology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo,
Tokyo 113-8655, Japan (e-mail: toshi-tky{at}umin.ac.jp).
From the Department of Otolaryngology, Faculty of Medicine, University
of Tokyo, Tokyo, Japan (Drs Murofushi, Shimizu, Takegoshi, and Cheng); and
Department of Otolaryngology, Far Eastern Memorial Hospital, Taipei, Taiwan
(Dr Cheng).
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