Introduction
Balance is maintained through the interaction of 3 systems, the vestibular, visual,
and proprioceptive systems. All of the afferent information from these systems is
sent to the cerebellum, which harmonically coordinates, plans, and executes the automatic
responses of the body that maintain static and dynamic balance. All of this information
must be consistent and symmetrical because any conflicting data can generate dizziness
or imbalance[1 ].
Dizziness is a feeling of disturbance of body balance that can be triggered by any
change in the responses originating from the vestibular or central system. It can
be classified as rotational or non-rotational. Rotational dizziness, or vertigo, originates
fundamentally as an intensified response of the vestibular system[2 ].
Benign Paroxysmal Positional Vertigo (BPPV) is a fairly common vestibular disorder
characterized by brief but intense episodes of rotational vertigo triggered by rapid
movement of the head. The diagnosis of BPPV is primarily clinical and can be corroborated
by the use of the Dix-Hallpike maneuver and otoneurological examination[3 ]
[4 ]
[5 ].
In patients with BPPV, the Dix-Hallpike maneuver is expected to produce nystagmus
in response to rapid movements. This response occurs within a few seconds and exhibits
a latency period, a limited duration, and fatigue (i.e., a diminished response) upon
repetition of the causative maneuver. This positional nystagmus in patients with BPPV
can be explained by the anatomy and physiology of the vestibular system. The endolymph
contains freely moving particles, and the movement of detached statoconia (or calculations)
that occurs in conjunction with movement of the head generates an abnormal acceleration
of the endolymph, causing abnormal deflection of the cupula[3 ]
[6 ].
Patients often describe the BPPV episodes as brief but intense periods of rotational
vertigo triggered by rapid head movements. The triggering events most often reported
are standing, lying down and turning over in bed, and looking up and down. Gait abnormalities,
dizziness, and other types of disability are often reported between crises[7 ].
The quality of life of these patients is seriously impaired, as BPPV causes physical,
functional (everyday activities), and emotional problems that are directly linked
to psychological issues; these often progress to depression[8 ].
Digital vectoelectronystagmography (VENG) is an examination that can assess the integrity
of the vestibular pathways. The description of the exam can be divided into 2 phases:
first, oculomotor testing, which primarily assesses the different patterns of ocular
movements, and then evaluation through direct stimulation of the semicircular canals,
rotational chair testing (PRPD), and caloric testing[1 ]
[9 ].
Patients with BPPV patients may present with findings related to each affected channel
and its corresponding effects on the results of caloric testing. The findings range
from normal reflexes to hyperreflexia or hyporeflexia contralateral or ipsilateral
to the side affected by BPPV[4 ]
[10 ]
[11 ].
Another tool that can be used to evaluate the neural pathways of the vestibular system
is Vestibular Evoked Myogenic Potential (VEMP) testing. This is a painless test that
is rapid and easy to perform. The VEMP is a reflex triggered by a high-pitched sound
in the ipsilateral ear; the response can be captured by surface electrodes. The latency,
reliability, and distance between the peak (p13) and valley (n23) of the wave are
used to assess whether the vestibular system is normal or altered. VEMP testing is
complementary to VENG and provides valuable information that can help to solidify
the diagnosis[12 ]
[13 ].
VEMP testing is a relatively new examination that is an important supplement to digital
vectoelectronystagmography in otoneurologic diagnosis. The phonoaudiologist's role
is to study the scope of this examination in order to enrich his or her clinical practice
and to support and promote study of this area.
While BPPV is a fairly common peripheral otoneurological disorder, little is known
of the VEMP findings in patients with this disease. Researching and describing these
findings is very important both to increase the knowledge in the field and to open
new therapeutic horizons. VENG quantitatively assesses the operation and interaction
of the vestibulo-ocular reflex as well as the operation of the semicircular canals,
as pairs or individually, while VEMP provides data regarding the vestibulospinal reflex[2 ]
[6 ] and the function of the otolithic organs, which are very important in the detection
of linear acceleration. Together, these 2 methods complement the patient's reports
and the clinical examination and provide the health professional with precious data
on the mechanism of body balance beyond the limits of the vestibular labyrinth[14 ]
[15 ]. The object of this project was to relate the findings of VEMP testing and VENG
in patients with BPPV.
Methods
This was a retrospective, descriptive study performed by collecting and analyzing
the results of vestibular exams and Evoked Myogenic Potential tests performed in the
Otoneurology Division of Universidade Federal of São Paulo and Hospital Paulista.
The inclusion criteria used in this study were a diagnosis of BPPV by an otolaryngologist,
age between 18 and 60 years, and the availability of the results of both VEMP testing
and VENG.
The diagnosis of BPPV was made through examination by an otolaryngologist and monitoring,
at the Otoneurology Clinic, of patients who complained of vertigo generated by the
rapid movement of the head. The diagnosis considered the responses to tests such as
the position and positioning maneuvers and the latency and fatigability of the nystagmus.
This project included patients with posterior semicircular canal BPPV regardless of
the physiological cause.
The examinations collected and analyzed were Digital Vectoelectronystagmography (VENG)
and Evoked Myogenic Potential (VEMP) tests conducted between 2009 and 2011.
The VENG included normal vestibular exams, vestibular dysfunction with deficient unilateral
or bilateral modification, and hyperreflexia.
The exclusion criteria included positive central vestibular exam findings (presence
of signs and symptoms), age less than 18 years, exams performed before January 2009
or for which the results were incomplete (i.e., without a final diagnosis), absence
of either VENG or VEMP results in the same patient, the presence of another vestibular
disease, diseases of the external and middle ear that could interfere with the results
of VEMP testing, use of medication that could affect the vestibular system and/or
muscle tone, neuromuscular disorders, hearing impairment (unless deemed compatible
with age, i.e., presbycusis), and history of vestibular rehabilitation. Patients who
had not undergone only 1 of the tests (oculomotor phase of VENG: NEOA (spontaneous
nystagmus with the eyes open), NEOF (spontaneous nystagmus with the eyes closed),
NSE (semi-spontaneous nystagmus), RP (tracking movements), OPTO (optokinetic nystagmus),
vestibular phase of VENG: PRPD or PC; VEMP testing: analysis of latencies or wave
reproducibility) within each examination were included in the study. However, patients
who failed to perform 2 or more of the tests listed above were excluded from the sample.
VENG was performed using registration equipment with VECWIN Software and an NGR –
05 air otocalorimeter with temperatures of 42°C and 18°C and the capacity to be chilled
to 10°C if necessary, both from Neurograff Eletromedicina, Ltda. The tests that were
included were: study of positional nystagmus using the Dix and Hallpike maneuver,
calibration, spontaneous and semi-spontaneous nystagmus, saccades, pendular tracking,
optokinetic nystagmus, rotational chair testing (PRPD), and caloric testing.
Are standards and recommendations are reported to all patients subject to search for
greater uniformity of data: before the exam, the patient was instructed to suspend
the use of medicine for the treatment of dizziness, tranquilizers, and muscle relaxants
for 72 hours prior to the examination (vital medicine such as that for the treatment
of heart disease or blood pressure control was not suspended) and to avoid food or
other substances that stimulate the vestibular system (i.e., substances high in caffeine
or stimulants, such as chocolate, cigarettes, soft drinks, alcoholic beverages, or
tea) for 24 hours prior to the examination. For the day of the exam, the patients
were also instructed to bring their most current audiometry results, to bring someone
to accompany them, if possible, to fast for at least 3 hours before the exam, and
not to wear makeup or contact lenses.
The reference values for the VENG testing used in this research were those of Costa
and other authors[6 ]
[9 ]
[16 ]
[17 ]; these and the reference values for VEMP are shown in the frame(below);[Chart 1 ].
Chart 1.
VENG Proofs[9 ]
Latency
Precision
Speed
Gain
Average VACL
PDN
Fixed Saccades
71 a 243 ms
89 a 111 ms
105 a 152 ms
———
———
———
Saccades Randomized
110 a 187 ms
81 a 125 ms
61 a 152 ms
———
———
———
Tracking Movements – 0,10Hz
———
———
———
0,6 a 1,2
———
———
Tracking Movements – 0,20Hz
———
———
———
0,8 a 1,3
———
———
Tracking Movements – 0,40Hz
———
———
———
0,8 a 1,3
———
———
Optokinetic Nystagmus
———
———
———
0,6 a 1,2
7 a 15°/s
0 a 13%
PRPD - Previous Channels
———
———
———
———
7 a 30°/s
0 a 25%
PRPD – S uperior Channels
———
———
———
———
7 a 30°/s
0 a 26%
PRPD –Posterior Channels
———
———
———
———
7 a 30°/s
0 a 27%
Caloric Testing - Hot
———
———
———
———
2 a 24°/s
———
Caloric Testing - Cold
———
———
———
———
2 a 24°/s
———
Caloric Testing - Ice
According to JongKees's Index Symmetry ( up to 30%)
VEMP Proofs[6 ]
Lp13
Ln23
p13-n23
IA (%)
Left Ear
12,04 a 17 ms
19,07 a 26,06 ms
58,09 a 524,03µV
−33,37 a 34,53
Right Ear
12,04 a 17,62 ms
19,09 a 27,93 ms
69,13 a 542,04µV
The second part of the exam consisted of VEMP testing conducted with Navigator
® equipment from Bio-logic Systems Corporation and AEP software version 6.2.0 in a soundproof environment. The sound stimuli were
presented through insert earphones.
The skin where the electrodes were to be placed was cleaned with gauze and pulp scrub,
and self-adhesive surface electrodes were placed on the skin with a hypoallergenic
conductive gel; these measures ensured impedance equal to or less than 5 kilohms (KΩ)
for each electrode with a difference smaller than 2 KΩ among them. The electrodes
were positioned on the upper third of the sternocleidomastoid muscle ipsilateral to
the side of sound stimulation (positive polarity), on the upper portion of the sternum
(negative polarity), and on the upper third of the sternocleidomastoid muscle contralateral
to the sound stimulation (ground electrode). During the presentation of the sound
stimulus, the patient was asked to perform a 30° flexion of the head to the trunk
to maintain the sternocleidomastoid muscles in a contracted state during registration,
thus obtaining muscle activation between the sides. The response parameters were the
absolute latencies of p13 and n23 in ms, and values greater than the mean plus 2 standard
deviations (2SD) were interpreted as altered responses.
The tracings obtained from the first biphasic potential consisting of p13 and n23
corresponded to the reflex evoked by sound stimulation of the saccular macula.
The data were organized using a Microsoft Excel 2010 spreadsheet. SPSS (Statistical
Product and Service Solution) version 16.0 and Minitab 15 were used for statistical
analysis. The data were collected at the institution using spreadsheets. After the
data were examined, statistical analysis was performed to ensure the validity of the
results. The analysis of variance (ANOVA), Confidence Interval for Mean Calculator,
and Equality of Two Proportions tests were performed. The P-value for each comparison
was also determined and used with a significance level of 0.05 (5%). All confidence
intervals used throughout the study represent 95% statistical confidence.
Results and Discussion
Application of the inclusion and exclusion criteria yielded 35 patients, 26 women
and 9 men. The results of 34 examinations were better for women than for men, in agreement
with the findings of previous studies[11 ]
[16 ]
[17 ]
[18 ]
[19 ]
[20 ].The average age of the patients was 53 years, with a range of 51 to 60 years. The
age distribution was quite similar to those in several previous studies of patients
with BPPV, in which increasing age was cited as a predisposing factor for BPPV; one
of the most plausible explanations for this is that age-related hormonal changes,
especially in women in this age group, cause a massive loss of calcium, making the
statocones less dense and more mobile[11 ]
[16 ]
[21 ] ([Table 1 ]).
Table 1.
Sex distribution of the total sample (N = 35).
Sex
N
%
P-value
Female
26
74.3%
< 0.001
Male
09
25.7%
Audiological evaluation showed a statistically significant relationship between normal
unilateral hearing and contralateral sensorineural loss (PASNC), as shown in [Table 2 ]. This relationship (normal hearing + PASNC) is not frequently described in studies
of patients with BPPV. Most research reports no changes in hearing in patients with
BPPV; however, this finding may be suggestive owing to the association of BPPV with
Ménière's disease, which produces frequent changes in hearing thresholds due to endolymphatic
hidropisia[15 ].
Table 2.
Frequency distribution of the hearing assessment results (%).
Hearing Assessment
N
%
P-value
Normal Hearing in Both Ears
17
48.6%
0.684
Speech Recognition Threshold Preserved—Decreased at High Frequencies
15
42.9%
0.631
Normal Hearing—Left Ear
3
8.6%
< 0.001
Sensorineural Hearing Loss in Both Ears, Mild
3
8.6%
< 0.001
Normal Hearing—Right Ear
2
5.7%
< 0.001
Sensorineural Hearing Loss—Left Ear, Mild
1
2.9%
< 0.001
The data for the qualitative variables of VENG were analyzed by Equality of Two Proportions,
with the following results [Table 3 ].
Table 3.
Distribution of the results of the oculomotor tests: calibration, spontaneous nystagmus
with the eyes open, and spontaneous nystagmus with the eyes closed.
Calibration
N
%
P-value
NEOA
N
%
P-value
NEOF
N
%
P-value
Regular
35
100
< 0.001
Absent
35
100
< 0.001
Absent
34
97.1
< 0.001
Irregular
0
0
Present
0
0
Between 2 and 4°/s
1
2.9
Legend: NEOA: spontaneous nystagmus with the eyes open; NEOF: spontaneous nystagmus with
the eyes closed
Although the proportions of normal and abnormal findings were significantly different
(p < 0.001), nothing was found that relates to the results of the oculomotor tests
in patients with BPPV. No irregular calibration or NEOA should be expected, as their
presence may suggest central vestibular disease[1 ].
[Table 4 ] shows a pattern similar to that of [Table 3 ]: there was no NSE or asymmetry in the optokinetic nystagmus, both of which responses
are considered pathognomonic for central vestibular alteration and therefore incompatible
with the inclusion criteria of this study[1 ]. Analysis of the pendular tracking results showed a significantly (p > 0.001) greater
proportion of Type I relative to Type I/II or Type II. For all tests, statistically
significant differences were found between the proportions of normal and abnormal
findings. The percentage findings are shown in detail below in [Graph 1 ].
Table 4.
Distribution of the results of the oculomotor tests: semi-spontaneous nystagmus, optokinetic
nystagmus, and tracking movements.
NSE
N
%
P-value
Type I
TypeI/II
TypeII
OPTO
N
%
P-value
Absent
35
100
< 0.001
Type I/II
< 0.001
−
−
Symmetrical
35
100
< 0.001
Present
0
0
Type II
< 0.001
0.690
−
Asymmetrical
0
00
Unrealized
< 0.001
0.393
0.643
Legend: NSE: semi-spontaneous nystagmus; Type I, I/II, and II: tracking movements; OPTO:
optokinetic nystagmus
Graph 1. Frequency distribution of the tracking test results in (%).
It is noteworthy the present study attempted to classify the RP according to its morphology
(type I, I/II, II, or III), whereas previous studies have used quantitative variables,
i.e., gain values; however, all studies obtained the same result: RP type I[9 ]
[20 ]
[22 ]. Yet another study reported that age influenced the velocity of the slow phase of
nystagmus (VACL) of the PR, thereby decreasing the gain values.
The OPTO results also exhibited statistical significance, as the result was symmetrical
in all cases. This result, like those of the other tests, may indicate the absence
of pathognomonic signs of central vestibular disorders; it was also similar to the
findings of previous studies[1 ]
[9 ]
[20 ]
[22 ].
Although most studies using VENG in patients with BPPV have prioritized only the vestibular
testing (PRPD and caloric testing)[24 ]
[25 ]
26 , those in which the oculomotor tests were also examined showed results quite similar
to those of the present study, with findings within the normal reference ranges in
most cases.
The PRPD was performed in 34 patients, of whom 91.4% (N = 32), a statistically significant
(p < 0.001) preponderance, showed symmetry between both the anterior and superior
side channels, as shown in [Table 5 ]. This finding is also similar to those of previous studies[22 ]. However, another study found no statistical significance in this regard[23 ] ([Table 5 ]).
Table 5.
Distribution of the vestibular test results: PRPD according to symmetry.
PRPD*
N
%
Asymmetryin Previous
Channels
P-value
Asymmetry In Previous Channels
2
5.7
Unrealized
0.555
<0.001
Unrealized
1
2.9
Symmetrical
<0.001
Symmetrical
32
91.4
Legend: PRPD*: decreasing pendular rotatory test.
Caloric testing showed normal reflexes in most (n = 20; 60%) cases, similar to the
findings of some previous studies[4 ]
[25 ]. However, most of the studies converge on normoreflexia as the overall result of
the test. This result can be explained by the fact that BPPV is a mechanical condition
caused by displacement of the otoconia, which directly influences the operation of
the lateral semicircular canals (the region evaluated by caloric testing)[23 ]. In this study, normoreflexia was more prevalent than hyperreflexia in the left
ear (LE) or hyperreflexia in the cold in both ears ([Table 6 ] e [7 ]).
Table 6.
Distribution of the results of the vestibular tests in terms of the absolute values
of the caloric test.
Caloric Test
N
%
Bilateral Normoreflexia
21
60.0
Hyperreflexia in the Cold, Left Ear
2
5.7
Hyperreflexia in the Cold, Both Ears
12
34.3
Table 7.
Distribution of the results of the vestibular tests in terms of the statistical significance
of the laterality of hyperreflexia in the caloric test.
Bilateral Normoreflexia
Hyperreflexia in the Cold, Left Ear
Hyperreflexia in the Cold, Left Ear
< 0.001
Hyperreflexia in the Cold, Both Ears
0.031
0.003
Analysis of the etiology of BPPV showed statistical significance. Although the idiopathic
form was the most prevalent, it was the etiology for which there was no statistical
significance (see [Table 8 ]). This is in contrast to the findings of other studies that reported associations
of idiopathic hidropisia[6 ]
[13 ], trauma, and impact[16 ] with otological problems.
Table 8.
Distribution of the VEMP results according to etiology
Etiology
N
%
P-value
Idiopathic
18
51.4%
—
Otological Disease
4
11.4%
< 0.001
Impact
4
11.4%
< 0.001
Migraine
3
8.6%
< 0.001
Hydrops
3
8.6%
< 0.001
Other
2
5.7%
< 0.001
Neuritis
1
2.9%
< 0.001
Examination of the side of onset showed that the left ear was more often affected
than the right, while right onset was more prevalent in turn than bilateral onset.
Although this difference was not statistically significant and there is no plausible
pathophysiological explanation, this result was similar to those of other studies,
with a recurrence rate in this study of approximately 69%27–29, 30 .
The physiological cause of BPPV was more often ductolithiasis than cupulolithiasis.
The percentages of these findings were very similar to those in several previous studies16.The
rarity with which cupulolithiasis is associated with BPPV can be explained by the
firm adhesion of the statocones to the cupulae, whereas in ductolithiasis these same
particles float freely through the endolymph of the semicircular canals, facilitating
the treatment (i.e., decreasing the number of repositioning maneuvers required)[19 ] ([Table 9 ]).
Table 9.
Frequency distribution of the physiological causes of BPPV.
Physiological Cause
N
%
P-value
Cupulolithiasis
2
5.7%
< 0.001
Ductolithiasis
33
94.3%
Analysis of the semicircular canal most often involved showed a massive and statistically
significant (p < 0.001) predominance of the posterior canal ([Table 10 ]). Some studies with similar findings explain this result in terms of the anatomical
position of this canal close to the saccular macula, where the otoconia originate[4 ]
[10 ]
[11 ]
[14 ]
[15 ]
[16 ]
[25 ].
Table 10.
Frequency distribution of the affected semicircular canal in patients with BPPV.
Canal
N
%
P-value
Multiple
1
2.9%
< 0.001
Posterior
34
97.1%
BPPV recurred in a majority of patients (n = 20, 57.1%), as shown in [Table 11 ]. These results are very similar to those of more recent studies[6 ]
[12 ]
[13 ]. The present study found a statistically significant association between recurrence
and persistence, suggesting that if a patient experiences several episodes of BPPV,
it is likely that the condition will become refractory to the positioning maneuver.
Some authors propose that age influences recurrence, as aging usually leads to a decrease
in neural activity combined with a decrease in the effectiveness of central inhibitory
control, which implies more excessive reactions, as well as to progressive loss of
calcium from the body, leading to less-dense statoconia requiring a greater number
of maneuvers[21 ] ([Table 11 ]).
Table 11.
Frequency distribution of the patterns of BPPV occurrence over time in (%) and the
correlation between them.
Mode
N
%
Self-limiting
Persistent
Self-limiting
12
34.3%
Persistent
0.009
Persistent
3
8.6%
Recurrent
0.055*
<0.001
Recurrent
20
57.1%
(*) trend towards significance.
The VEMP waveforms were similar in all patients, with normal morphology but abnormalities
in some of the quantitative parameters. Although the values for the right ear (Lp13od
and Ln23od) were below the reference range adopted for this research[6 ], the corresponding values between the peaks and the asymmetry index (AI) were within
normal limits[12 ]
[13 ]. Other studies have described such findings as prolonged latency and reduced amplitude
in patients with BPPV[13 ]; these were generally associated with concomitant impairments[12 ]
28 . Another factor that influenced the research on this topic is the positive correlation
between inter-peak amplitude and age30 ; in other words, as the individual with BPPV ages, the latency period of the reflex
increases. However, the results of all studies agree that an altered VEMP is expected
in patients with BPPV even when the results of caloric testing are normal[12 ]
[13 ]
27–29 , and the low inter-peak latency in the patients' right ears in the present study
corroborates this consensus.
The effect of the positioning maneuver was almost statistically significant and would
likely have been significant in a study with a larger sample size; in other words,
it is safe to say that the effects of the positioning maneuver on the VEMP results
for the left ear tend to reflect the morphology and latencies of normal waves ([Table 12 ]). However, analysis of the VEMP results with respect to the audiological profile
yielded no relevant statistically significant findings, as shown in [Table 13 ].
Table 12.
Effect of the positioning maneuver on the VEMP findings.
VEMP/Positioning
Maneuver
Mean
Median
Standard Deviation
Min
Max
N
IC
P-value
Lp13 (oe)
Absent
11.73
136
5.11
0.0
16.1
20
2.24
0.059*
Present
14.31
14.2
1.34
11.9
17.4
16
0.66
Lp13 (od)
Absent
11.18
13.4
5.85
0.0
17.1
20
2.56
0.499
Present
12.44
13.7
5.04
0.0
18.2
16
2.47
Ln23 (oe)
Absent
19.58
21.8
8.81
0.0
30.6
20
3.86
0.109
Present
23.37
22.9
2.93
19.5
29.0
16
1.44
Ln23 (od)
Absent
18.10
21.7
9.45
0.0
26.2
20
4.14
0.555
Present
19.87
22.5
7.96
0.0
26.3
16
3.90
p13n23 (oe)
Absent
153.2
151.5
112.2
0.0
361.8
20
49.2
0.226
Present
208.6
155.7
157.1
19.5
615.0
16
77.0
p13n23 (od)
Absent
152.2
129.6
134.2
0.0
527.6
20
58.8
0.478
Present
183.6
166.7
125.3
0.0
468.3
16
61.4
ILp13
Absent
0.56
0.0
5.53
−13.5
14.2
20
2.42
0.462
Present
1.90
0.1
4.89
−1.1
15.5
15
2.48
ILn23
Absent
1.47
0.0
10.13
−24.9
26.8
20
4.44
0.482
Present
3.69
0.5
7.49
−1.6
23.7
15
3.79
IA
Absent
3.14
−1.2
49.59
−100.0
100.0
18
22.91
0.436
Present
15.70
9.7
39.96
−32.4
100.0
15
20.22
Legend: Min: minimum; Max: maximum; IC: confidence interval; VEMP: Vestibular Evoked
Myogenic Potential
OD: right ear; OE: left ear
Lp13: Latency of the first positive deflection of the vestibular evoked myogenic potentials
Ln23: Latency of the first negative deflection of the vestibular evoked myogenic potentials
p13n23: Amplitude between the first positive deflection and the first negative deflection
of the vestibular evoked myogenic potentials
IA: Index of the asymmetry amplitudes
ILp13: Index of the first positive deflection of the vestibular evoked myogenic potentials
ILn23: Index of the first negative deflection of the vestibular evoked myogenic potentials
Table 13.
Associations between the audiological profile results and binaural VEMP findings.
VEMP/Hearing
Assessment
Mean
Median
Standard Deviation
Min
Max
N
IC
P-value
Lp13 (oe)
Normal
13.25
13.7
3.64
0.0
17.4
17
1.73
0.526
Decreased at High Frequencies
12.26
14.0
5.06
0.0
15.9
15
2.56
Lp13 (od)
Normal
12.37
13.7
4.89
0.0
18.2
17
2.32
0.339
Decreased at High Frequencies
10.40
13.5
6.56
0.0
16.3
15
3.32
Ln23 (oe)
Normal
21.93
21.7
6.52
0.0
30.6
17
3.10
0.421
Decreased at High Frequencies
19.80
22.8
8.20
0.0
26.2
15
4.15
Ln23 (od)
Normal
19.64
21.1
7.68
0.0
26.3
17
3.65
0.360
Decreased at High Frequencies
16.65
21.9
10.44
0.0
24.9
15
5.28
p13n23 (oe)
Normal
186.6
155.2
129.3
0.0
482.5
17
61.5
0.540
Decreased at High Frequencies
155.6
135.1
154.1
0.0
615.0
15
78.0
p13n23 (od)
Normal
184.1
187.6
120.0
0.0
468.3
17
57.0
0.405
Decreased at High Frequencies
143.2
120.7
153.4
0.0
527.6
15
77.6
ILp13
Normal
0.88
0.3
3.53
−1.7
14.2
17
1.68
0.622
Decreased at High Frequencies
1.89
0.0
7.39
−13.5
15.5
14
3.87
ILn23
Normal
2.29
0.5
6.52
−1.6
26.8
17
3.10
0.769
Decreased at High Frequencies
3.33
0.0
12.51
−24.9
24.9
14
6.55
IA
Normal
0.77
−1.2
37.50
−52.7
100.0
16
18.38
0.349
Decreased at High Frequencies
17.79
6.8
58.28
−100.0
100.0
13
31.68
Analysis of the caloric testing results with respect to the VEMP findings demonstrated
that normoreflexia is associated with a normal inter-peak amplitude in the left ear.
Studies have reported that age is a confounding factor, as the response and the chance
of hyperreflexia both increase with increasing age[23 ], but normoreflexia was present in the absolute majority of cases in this sample
despite the changes in the VEMP findings[12 ] described in [Table 14 ]. In other disorders, such as kinetosis, bithermal stimulation is expected to produce
bilateral hyperreflexia. However, there are few publications in the field of otoneurology
on the relationships among BPPV, VENG, and VEMP.
Table 14.
Correlation between the caloric test (PC) and VEMP results.
VEMP/Caloric
Testing
Mean
Median
Standard Deviation
Min
Max
N
IC
P-value
Lp13 (oe)
Normoreflexia
12.83
13.7
4.42
0.0
17.4
21
1.89
0.990
Hyperreflexia
12.85
14.0
3.82
0.0
15.5
14
2.00
Lp13 (od)
Normoreflexia
11.54
13.6
5.92
0.0
18.2
21
2.53
0.869
Hyperreflexia
11.86
13.6
5.09
0.0
16.3
14
2.67
Ln23 (oe)
Normoreflexia
21.35
22.7
7.51
0.0
30.6
21
3.21
0.757
Hyperreflexia
20.58
22.1
6.42
0.0
29.0
14
3.36
Ln23 (od)
Normoreflexia
18.42
22.0
9.34
0.0
26.3
21
4.00
0.812
Hyperreflexia
19.16
21.7
8.25
0.0
25.0
14
4.32
p13n23 (oe)
Normoreflexia
211.3
172.3
154.8
0.0
615.0
21
66.2
0.082*
Hyperreflexia
129.2
131.2
87.9
0.0
297.4
14
46.0
p13n23 (od)
Normoreflexia
169.0
160.5
131.7
0.0
468.3
21
56.3
0.944
Hyperreflexia
165.8
132.2
134.8
0.0
527.6
14
70.6
ILp13
Normoreflexia
1.29
0.0
4.31
−2.3
14.2
21
1.84
0.860
Hyperreflexia
0.95
0.1
6.82
−13.5
15.5
13
3.71
ILn23
Normoreflexia
2.93
0.5
7.76
−2.1
26.8
21
3.32
0.661
Hyperreflexia
1.48
−0.3
11.38
−24.9
23.7
13
6.19
IA
Normoreflexia
12.94
6.8
38.07
−41.1
100.0
19
17.12
0.527
Hyperreflexia
2.25
−11.7
56.57
−100.0
100.0
13
30.75
This study may help to clarify the relationship between VENG and VEMP results in patients
with BPPV. The hearing threshold results indicate that patients with Benign Paroxysmal
Positional Vertigo tend to have normal hearing and mild sensorineural hearing loss
simultaneously; however, this phenomenon does not significantly affect the results
of Vestibular Evoked Myogenic Potential testing.
All of the results of oculomotor testing were normal, and this finding was statistically
significant. Furthermore, vestibular testing showed normal results and normal function
of all of the semicircular canals. Caloric testing tended to show an influence of
the inter-peak p13n23 in the left ear.
Based on this research, one would expect patients with BPPV to have normal results
for both the oculomotor and vestibular components of VENG despite the correlation
between mild contralateral and unilateral sensorineural hearing loss. However, at
least 1 abnormal VEMP finding (increased latency in cases in which the positioning
maneuver produces positional nystagmus) is expected in these cases.
Conclusion
The results of this research indicate that patients with BPPV are predominantly female,
with an average age of 52.7 years, and have ductolithiasis as the physiological cause.
We can conclude that although there are average differences between the values of
some Digital Vectoelectronystagmography variables with respect to the results of Vestibular
Evoked Myogenic Potential testing, these effects are not significant. Therefore, we
conclude that there were no associations between the results of audiologic evaluation,
symmetry, positioning maneuver, or caloric testing and the quantitative results of
Vestibular Evoked Myogenic Potential testing.
