Key Words
asymmetry - cVEMP - motion sickness - refixation saccades - VOR gains
INTRODUCTION
Motion sickness is an autonomic phenomenon resulting in discomforts due to the conflict
among the balancing systems (vestibular, somatosensory, and visual systems) where
there is a mismatch signal between static physical conditions of the susceptible individual
exposed to a dynamic environment ([Reason, 1978]; [Owen et al,1998]; [Yates and Miller, 1998]; [Tal et al, 2006]). Different varieties of motion sickness may include traveling sickness ([Turner and Griffin, 1999]; [Turner et al, 2000]), space sickness ([Bacal et al, 2003]; [Paule et al, 2004]; [Heer and Paloski, 2006]), seasickness ([Tal et al, 2007]; [Golding and Gresty, 2015]), and sickness induced in tilting and nontilting trains ([Bromberger, 1996]; [Persson, 2008]), featuring nausea, emesis, vomiting, paleness, cold sweats, headache, drowsiness,
malaise, poor forward visibility, distress, and affected psychomotor functioning.
However, the strength of these symptoms may vary across individuals, depending on
the exposure of type of stimuli, their intensity, and individualistic motion sickness
susceptibility variance ([Buyuklu et al, 2009]).
Even though there are many published studies and theories on motion sickness, none
have been able to describe the complete physiological basis of it. Most familiar of
all, sensory rearrangement theory by [Reason (1978)] has tried describing the incongruity of sensory, somatosensory, and vestibular systems
for maintaining balance, resulting in features such as vomiting and nausea, as the
brain assumes the discordance created due to intoxication, resulting in vomiting to
flush out the problem ([Treisman, 1977]). Similarly, the subjective vertical conflict theory ([Bos and Bles, 1998]) has attempted to explain motion sickness as the by-product of otolith asymmetry
or canal-otolith conflict ([Yates et al, 1998]; [Tal et al, 2006]) due to the variation in otoconial masses across two labyrinths ([Scherer et al, 2001]; [Helling et al, 2003]). Likewise, the postulates by Guedry and [Benson (1978)] on intersensory conflict between vestibular and proprioceptive systems, visual and
vestibular systems, or intrasensory conflict of functional otoliths and semicircular
canals ([Yates et al,1998]; [Dai et al, 2007]) do not explain motion sickness generated in some conditions, such as passive low-frequency
vertical acceleration ([Yates et al, 1998]), which emphasizes the fact that there is presence of motion sickness even when
visual and vestibular systems deliver the same information to the central nervous
system (CNS).
All the mentioned studies are in agreement with the notion that there is an involvement
of the vestibular system in individuals with motion sickness. Therefore, the conflicts
among the motion-sensing peripheral vestibular structures of the inner ear are to
be assessed well in understanding the phenomenon of motion sickness. Earlier studies
were done to measure canals’ functionality via electronystagmography in individuals
with motion sickness where the incidence of faster slow-phase velocity has been suggestive
of a hyperactive vestibular system ([Lidvall, 1962]), which is the converse of the study by [Mallinson and Longridge (2002)]. Also the study by [Buyuklu et al (2009)] reported no significant difference for canal paresis between individuals with motion
sickness and without motion sickness, concluding the caloric test to be an insensitive
tool in detecting individuals with motion sickness. Also, cervical vestibular-evoked
myogenic potentials (cVEMPs) have been reported with affected amplitude and thresholds
of cVEMP response in individuals with seasickness in comparison to normal individuals
([Tal et al, 2006]). However, other studies have come across with no significant statistical difference
between the two groups ([Tal et al, 2006]; [Buyuklu et al, 2009]). Also the presence of a higher interaural asymmetry ratio in the motion-sickness
population was reported in a few studies ([Singh et al, 2014]), but other studies assert the converse ([Buyuklu et al, 2009]; [Fowler et al, 2014]). Furthermore, a recent study on ocular VEMP revealed the presence of higher interaural
asymmetry ratio and no difference across latency and amplitude in the motion-sickness
population ([Xie et al, 2012]).
Even though these vestibular test batteries were performed previously on individuals
with motion sickness, lacunae still persist. The well-known caloric test gives us
an overview of vestibular functioning, but it lags with assessment of only two lateral
semicircular canals in the frequency range of ∼0.002–0.004 Hz, which is beyond the
daily exposure ([Perez and Rama-Lopez, 2003]). Hence the other two planes of semicircular canals—that is, the right anterior
left posterior (RALP) and left anterior right posterior (LARP)—still remain unexamined.
This urgent requirement of the objective tests in examining dynamic functions of all
six semicircular canals has been possible with the recent advancement of the noninvasive
instrument known as the video head impulse test (vHIT) ([Halmagyi and Curthoys, 1988]), based on the principle of the head impulse test ([Baloh et al, 1977]; [Böhmer et al, 1985]).
The vHIT is a software-based test with lightweight goggles, consisting of a gyroscope
to measure the refixation saccades and vestibulo-ocular reflex (VOR) gain function
([MacDougall et al, 2009]). Also it is found to have good sensitivity and specificity across both the healthy
and the pathological vestibular population. The presence of refixation saccades as
an indicator of compensatory mechanism was observed in individuals with vestibular
migraine ([McGarvie et al, 2015]), benign paroxysmal positional vertigo ([Blödow et al, 2014]), vestibular neuritis ([Bartolomeo et al, 2014]), and also in the case of Ménière’s disease ([McCaslin et al, 2014]).
There is a dearth of studies in the assessment of all six semicircular canals in individuals
with motion sickness. Also no other reports are present in the literature regarding
examination of all six semicircular canals and the sacculocollic reflex pathway in
the same set of motion-sickness population. Therefore, there is a need to understand
the functioning of these organs of the vestibular system in individuals with motion
sickness. Hence, the aim of the present study is to evaluate the functioning of the
sacculocollic reflex pathway and all six semicircular canals in individuals susceptible
to motion sickness and compare with normal individuals, checking for any difference
in vestibular functioning in the motion-sickness group.
METHOD
Participants
A total of 60 participants in the age range of 17–25 yr, with a mean age of 22 yr,
were included in the study and divided into two groups. Group I had 30 participants
with motion sickness, and group II consisted of 30 participants without motion sickness.
The Motion Sickness Susceptibility Questionnaire–Short form was administered to classify
the participants into groups with or without motion sickness. The questionnaire is
designed to find out susceptibility to motion sickness and the most effective motion
(transport/swings/amusement rides) resulting in sickness. It has two parts: part A
for any experience of motion sickness during childhood and part B for a period lasting
>10 yr. It has a 4-point rating scale, ranging from 0 (never felt sick) to 3 (frequently
felt sick). A cutoff score of 3.0 was used as the indication criterion for presence
of motion sickness. Similar criteria have been adapted in other studies ([Simmons et al, 2010]; [Singh et al, 2014]). All the participants were informed initially about the study in detail, and a
written consent form was obtained from all the participants.
Instrumentation
A calibrated GSI-61 audiometer (GSI VIASYS Healthcare, Madison, WI) with TDH-39 headphones
(Telephonics, Farmingdale, NY) encased in an MX-41/AR supra-aural cushion was used
for estimation of air-conduction pure-tone thresholds. Bone-conduction threshold was
estimated using a RadioEar B-71 bone vibrator (Radioear, KIMMETRICS, Smithsburg, MD).
Middle ear status was evaluated by using a calibrated Grason-Stadler Tympstar middle
ear analyzer. cVEMP was recorded using the intelligent hearing system version 4.3.02
(Intelligent Hearing System, Miami, FL) with ER-3A insert earphone (Etymotic Research,
Inc., Elk Grove Village, IL). vHITs were carried out with prototype ICS Impulse video
goggles (GN Otometrics, Taastrup, Denmark), with a camera speed of 250 frames/s, recording
motion of the right eye. All the measurements were carried out in an acoustically
treated double-room situation.
Procedure
Case history was initially taken from all the participants, and the Motion Sickness
Susceptibility Questionnaire–Short was administered to place the participants into
one of the two groups (either with motion sickness or without). Informed consent was
taken from all the participants before the testing procedure. Pure-tone thresholds
were obtained for all the participants using modified version of the Hughson and Westlake
procedure ([Carhart and Jerger, 1959]) at octave frequencies between 250 and 8000 Hz for air conduction and between 250
and 4000 Hz for bone conduction. Immittance audiometry was carried out in both ears
using a probe tone frequency of 226 Hz. Later ipsilateral and contralateral acoustic
reflex threshold was measured for 500, 1000, 2000, and 4000 Hz stimuli.
Recording of cVEMP
The cVEMP was recorded for both groups of participants, who were seated in an upright
position in a reclining chair. Surface electrodes were placed as follows: active electrode
to the upper third of the ipsilateral sternocleidomastoid muscle, reference electrode
to the ipsilateral sternoclavicular joint, and the ground electrode to the midline
of the forehead after scrubbing the skin surface with an abrasive gel to obtain both
absolute and interelectrode impedance of 5 and 2 kΩ, respectively. Electromyogenic
potential was monitored through the electromyography monitoring device to ensure an
equal amount of muscle contraction from all the participants. Intelligent hearing
system electromyography monitoring device averaged the cVEMP response only when the
sufficient amount of muscle contraction was achieved. The 500 Hz short-tone bursts
with 2-0-2 cycle were used as stimulus. A total of 200 stimuli were presented at 95
dB nHL (equivalent to 125 dB SPL) at a repetition rate of 5.1 Hz. The responses were
band-pass filtered between 30 and 1500 Hz. Analysis time was kept at 70 msec with
a prestimulus baseline recording of 10 msec.
Video Head Impulse Test
Using the Otosuite vestibular software (GN Otometrics, Taastrup, Denmark), vHIT was
administered in a well-lit room. A Frenzel glass with a clean attached face cushion
was tightened appropriately to avoid slippage, such that the camera could track participants’
pupil movement. Calibration was performed by the participant, keeping his or her head
still and viewing a laser light alternately on each side of a target placed 1 m ahead.
This was followed by a simple slow head sinusoid with the participant watching the
target, thereby allowing a calibration check by ensuring that head and eye velocities
were overlaid. Once calibrated, participants were instructed to fix their gaze at
a target point, which was kept according to the height of the participant, even when
head thrust was given. The head thrust of 40 times was given by the examiner for each
of the planes (pitch, roll, and yaw planes) at an angle of 10–20° in randomized order.
For LARP and RALP positions, that is, during the vertical canal testing, the head
was rotated 30° toward the right or left, whereas gaze was directed and the head impulse
was applied in the plane of canals. The VOR gain for all six semicircular canals was
measured with the help of a high-speed digital infrared camera attached to the instrument.
Data Analysis
For cVEMP, the absolute latencies, peak to peak amplitude ratio, and asymmetry ratio
were measured for both groups. Interaural asymmetry ratio was measured with the formula
−[{(AI − AS)/(AI + AS)} × 100], where higher amplitude is AI and lower amplitude is
AS between two ears of an individual ([Li et al, 1999]).
Furthermore, based on the Hex plot, the vHIT response was analyzed, where the VOR
gain of all the six semicircular canals were calculated. The refixation saccades (if
any) at the time of head thrust (i.e., covert saccade) and after the head thrust (i.e.,
overt saccade) were also measured. In the present study, we have measured VOR gain,
VOR gain asymmetry value, and measurement of refixation saccades in individuals with
and without motion sickness. To the best of our knowledge, this is the first study
that has analyzed the VOR gain asymmetry values in vHIT.
RESULTS
The latency and amplitude of cVEMP and VOR gain, VOR gain asymmetry, and refixation
saccades were calculated for all the participants in both groups.
Cervical Vestibular Myogenic Potentials
cVEMP responses were present for all the participants in both groups. The cVEMP grand
averaged waveform of both groups is shown in [Figure 1].
Figure 1 cVEMP grand average waveform of individuals respectively with and without motion
sickness. (A) and (B) are the respective right and left ear cVEMP response of an individual
with motion sickness. (C) and (D) are the respective right and left ear cVEMP response
of an individual without motion sickness.
SPSS version 23 (IBM Corporation, New York, NY) was used to analyze the data. Descriptive
statistics was done to calculate the mean and standard deviation (SD) for latency
of P1 and N1 peak and amplitude of P1N1 complex for right and left ears separately
in both groups. The mean and SDs for the latency, amplitude, and asymmetry ratio of
cVEMP for both groups are given in [Table 1], [Table 2], and [Table 3], respectively.
Table 1
Mean and SD of P1 and N1 Peak Latencies for Both Groups Bilaterally
|
Right Ear
|
Left Ear
|
|
P1
|
N1
|
P1
|
N1
|
|
Group
|
Mean (msec)
|
SD
|
Mean (msec)
|
SD
|
Mean (msec)
|
SD
|
Mean (msec)
|
SD
|
|
Individuals with motion sickness
|
1 3.59
|
1.22
|
20.55
|
1.79
|
13.78
|
1.32
|
20.97
|
1.53
|
|
Individuals without motion sickness
|
1 3.25
|
0.96
|
20.77
|
1.39
|
13.06
|
1.02
|
20.79
|
1.34
|
Table 2
Mean and SD of P1N1 Amplitude for Both Groups Bilaterally
|
P1N1 Amplitude
|
|
Right Ear
|
Left Ear
|
|
Group
|
Mean (μV)
|
SD
|
Mean (μV)
|
SD
|
|
Individuals with motion sickness
|
70.33
|
39.22
|
62.83
|
30.98
|
|
Individuals without motion sickness
|
80.17
|
27.88
|
76.95
|
29.42
|
Table 3
Mean and SD of Asymmetry Ratio for Both Groups
|
Asymmetry Ratio
|
|
Group
|
Mean
|
SD
|
|
Individuals with motion sickness
|
34.56
|
11.91
|
|
Individuals without motion sickness
|
17.60
|
13.21
|
From [Table 1], it is evident that there is prolonged mean P1 and N1 latencies for both ears in
individuals with motion sickness, except for N1 latency in right ear. The same can
be seen in [Figure 2].
Figure 2 Bar graph represents mean and SD of latency of cVEMP for both groups.
It can be observed from [Table 2] that the mean amplitude of P1NI complex for both ears is higher in individuals without
motion sickness than in the individuals with motion sickness. Similarly, in [Figure 3], a bar graph shows the amplitude values of cVEMP for both groups.
Figure 3 The graph represents mean and SD of amplitude of P1N1 complex of cVEMP for both groups.
It can be observed from [Table 3] that the mean asymmetry ratio is higher in individuals with motion sickness than
in individuals without motion sickness. The bar graph showing the amplitude asymmetry
ratio values of cVEMP for both groups is shown in [Figure 4].
Figure 4 The graph represents mean and SD of asymmetry ratio of cVEMP for both groups.
The Shapiro–Wilk test was done to check the normality of the data, and it revealed
a normal distribution of the data (p > 0.05), and hence a parametric independent samples t test was done to check the significant difference in mean latency, amplitude, and
asymmetry ratio of cVEMP between the two groups. An independent sample t test between the two groups showed no significant difference for the P1 latency [t
(58) = 1.21, p = 0.23], N1 latency [t
(58) = 0.54, p = 0.59], and P1N1 amplitude complex [t
(58) = 1.120, p = 0.27] for the right ear. Also for the left ear, no significant difference for P1
latency [t
(58) = 2.96, p = 0.22], N1 latency [t
(58) = 0.47, p = 0.64], and P1N1 amplitude complex [t
(58) = 1.81, p = 0.75] was observed. However, the t test revealed significant higher asymmetry ratio in individuals with motion sickness
as compared to individuals without motion sickness [t
(58) = 5.22, p = 0.00].
Analysis of VOR Gain Function
Descriptive statistics was used to calculate the mean and SD of VOR gain values, and
asymmetry was calculated for all three planes of all six semicircular canals in both
groups. The vHIT responses recorded from one of the participants from each group are
given in [Figures 5] and [6].
Figure 5 vHIT results in three different planes of an individual with motion sickness. The
head and eye velocities throughout different head impulses to the right or left side
are shown. The gain values and refixation saccades are also shown.
Figure 6 vHIT results in three different planes of an individual without motion sickness.
The head and eye velocities throughout different head impulses to the right or left
side are shown. Gain values are also shown.
Mean and SDs of VOR gain in all three planes in both directions are given in [Table 4] and [Table 5], respectively. Likewise, the refixation saccades in individuals with motion sickness
are represented in [Table 6].
Table 4
Mean and SD of VOR Gain Values for Both Groups
|
Individuals with Motion Sickness
|
Individuals without Motion Sickness
|
|
Planes
|
Mean
|
SD
|
Mean
|
SD
|
|
LL
|
0.98
|
0.15
|
0.97
|
0.11
|
|
RL
|
1.02
|
0.17
|
1.02
|
0.12
|
|
LA
|
0.84
|
0.29
|
0.91
|
0.17
|
|
RP
|
0.84
|
0.29
|
0.91
|
0.14
|
|
LP
|
0.79
|
0.19
|
0.87
|
0.10
|
|
RA
|
0.83
|
0.22
|
0.96
|
0.17
|
Table 5
Mean and SD of Asymmetry of Three Planes of VOR for Both Groups
|
Planes
|
Individuals with Motion Sickness
|
Individuals without Motion Sickness
|
|
Mean
|
SD
|
Mean
|
SD
|
|
Lateral
|
10.73
|
8.75
|
7.00
|
5.15
|
|
LARP
|
15.30
|
9.31
|
7.80
|
5.68
|
|
RALP
|
21.20
|
13.36
|
10.73
|
4.52
|
Table 6
Refixation Saccades at All Six Semicircular Canals Present in Individuals with Motion
Sickness
|
Semicircular Canals
|
Covert Saccade
|
Overt Saccade
|
Covert + Overt
|
None
|
|
LL
|
8
|
4
|
10
|
7
|
|
RL
|
4
|
5
|
16
|
3
|
|
LA
|
11
|
1
|
8
|
9
|
|
RA
|
12
|
1
|
5
|
11
|
|
LP
|
6
|
2
|
8
|
12
|
|
RP
|
4
|
4
|
8
|
15
|
From [Table 4], it is evident that there is lower VOR gain in individuals with motion sickness
in all six semicircular canals in comparison to normal individuals, except in the
left lateral (LL). The mean and SDs of VOR gain values are also represented in [Figure 7].
Figure 7 The graph represents mean and SD of VOR gain values for all six semicircular canals
in both groups.
[Table 5] reveals higher asymmetry value for all three planes of semicircular canals in individuals
with motion sickness than in individuals without motion sickness. The bar graphs showing
mean as well as SD for asymmetry of three planes of semicircular canals are given
in [Figure 8].
Figure 8 The graph represents mean and SD of asymmetry for all three planes of semicircular
canals for both groups.
A Shapiro–Wilk test revealed normal distribution (p > 0.05) of the VOR gain data. Therefore, a parametric independent sample t test performed
between two groups for both ears revealed no significant difference in right lateral
(RL) [t
(58) = 2.38, p = 0.02], LL [t
(58) = 2.38, p = 0.02], right posterior (RP) [t
(58) = 2.38, p = 0.02], and left anterior (LA) [t
(58) = 2.38, p = 0.02], except in the right anterior (RA) and left posterior (LP), with significant
difference of [t
(58) = 2.38, p = 0.02] and [t
(58) = 2.02, p = 0.05], respectively. Also, the significant difference in asymmetry of lateral [t
(58) = 2.01, p = 0.05], LARP [t
(58) = 3.77, p = 0.00], and RALP [t
(58) = 4.06, p = 0.00] planes were observed, where there were significantly higher asymmetry values
in individuals with motion sickness than in individuals without motion sickness.
Also, the refixation saccades were measured in both groups. Refixation saccades were
present in individuals with motion sickness and were absent in individuals without
motion sickness. [Table 6] represents the presence of refixation saccades in different planes in individuals
with motion sickness.
DISCUSSION
The present study revealed no significant difference for cVEMP latencies (P1 and N1)
in individuals with motion sickness from that of individuals without motion sickness.
The results of the present study are in coherence with earlier studies ([Tal et al, 2006]; [Fowler et al, 2014]; [Singh et al, 2014]). The results suggest that the neural portion of the sacculocollic pathway is not
affected in individuals with motion sickness. It has been reported that affected latencies
of cVEMP peaks are the key signs of neural pathologies rather than the labyrinthine
pathology ([Ochi and Ohashi, 2003]; [Lee et al, 2008]). Therefore, the latency parameter is not a sensitive tool in detecting sacculocollic
pathway pathology in individuals with motion sickness.
Similarly, the present study also revealed no significant difference in P1N1 complex
amplitudes between the two groups. These findings are consistent with earlier studies
([Tal et al, 2007]; [Buyuklu et al, 2009]; [Singh et al, 2014]). However, a few of the earlier studies ([Tal et al, 2006]; [Fowler et al, 2014]) are in incongruity with these findings, where it was reported to have affected
amplitude in individuals with motion sickness more than that of individuals without
motion sickness. This could be due to the smaller sample size taken in the previous
studies. However, the present study includes a comparatively larger sample (N = 30).
Although the mean amplitude value was smaller in individuals with motion sickness
in the present study, a significant difference was not observed between the two groups.
This could be because of a larger SD obtained for the amplitude parameters.
However, significantly higher cVEMP asymmetry ratio was observed in individuals with
motion sickness than in those without motion sickness. Higher asymmetry ratio of cVEMP
amplitude is an indication of pathology in sacculocollic pathway in various vestibular
pathologies ([Baier et al, 2009]; [Taylor et al, 2011]; [Taylor et al, 2012]). Thus, it can be interpreted that individuals with motion sickness may have pathology
of the sacculocollic pathway. This finding is in coherence with the studies reported
previously ([Helling et al, 2003]; [Singh et al, 2014]). However, a few studies ([Tal et al, 2007]; [Buyuklu et al, 2009]; [Fowler et al, 2014]) show inconsistency with it.
According to [Bles (1998)], the condition of motion sickness occurred due to the vertical acceleration information
achieved, which is in variance with the previous subjective experience of vertical
orientation. This incongruence in postural vertical orientation could be due to the
difference in otoconial masses of two saccules, thus giving rise to asymmetry. Dysrhythmic
discharge due to asymmetry would be balanced and normalized by central compensatory
mechanism under normal terrestrial situation in almost all individuals, as it’s not
large enough to generate an incongruent signal to the cortical areas. However, under
the influence of unusual motion patterns, it generates larger asymmetric differences
between the otoliths with rarer central compensatory mechanism in individuals with
motion sickness. This leads two otoliths to supply an unequal amount of neural impulses
to cortical balance areas, therefore generating confusion even when whole body is
undergoing the same acceleration ([von Baumgarten et al, 1977]).
Hence, this phenomenon may end up with symptoms such as dizziness, headache, cold
sweats, nausea, and ultimately vomiting as the CNS assumes the occurrence of discordance
due to intoxication ([Treisman, 1977]). A similar result was observed in an animal study where fish with difference in
otoconial mass between two labyrinths showed uncoordinated swimming behavior compared
to fish with active compensatory mechanism under the Coriolis force environment ([Helling et al, 2003]). Hence the asymmetry ratio can be taken as one of the parameters of cVEMP in detecting
the motion-sickness population in the vestibular test battery.
In the present study, the recent advanced noninvasive instrument, vHIT, was used for
the first time in analyzing the functioning of semicircular canals of the individuals
with motion sickness. VOR gain analysis of three planes of semicircular canals revealed
significant difference, with lower VOR values in RA and LP semicircular canals. Similar
results of reduced VOR gain were explained earlier in various peripheral vestibular
disorders ([Weber et al, 2008]; [Macdougall et al, 2013]; [MacDougall et al, 2016]). Most of these studies that have reported reduced gain in vestibular pathologies
have explained the VOR gain values only in the lateral planes and not in the RALP
and LARP planes. In the present study, the significant difference in VOR gain values
could be observed only in the RALP plane between the two groups. The VOR gain values
have been reported to be less reliable compared to the presence of saccades ([Korsager et al, 2016]). Thus, [Korsager et al (2016)] have reported that for diagnosis of vestibular pathologies, clinicians shall depend
on the presence of saccades followed by the VOR gain values in vHIT recording.
The study revealed significantly higher asymmetry of VOR gain values in three orthogonal
planes, that is, RALP, LARLP, and lateral, for individuals with motion sickness than
for those without. This explains the intrasensory conflict of semicircular canals
([Yates and Miller, 1998]; [Dai et al, 2007]) in individuals with motion sickness. This conflict gives rise to the variance in
neural input from different planes to the cortical balance areas, where a dilemmatic
situation is generated in understanding the precise postural orientation of the body
even when whole body is getting the same acceleration ([von Baumgarten et al, 1977]). Hence, the CNS intake this discordance as intoxication, resulting in vomiting
to flush out the toxins ([Treisman, 1977]). Although the VOR gain values did not show any significant difference between two
groups except for the RALP plane, the asymmetry in VOR gain values did show significant
difference between the two groups, suggesting asymmetry values could be a better parameter
than the absolute VOR gain values. None of the published studies have reported the
asymmetry ratio of VOR gain values in any of the vestibular pathologies. This is the
first study in which the significant difference in VOR gain values of vHIT in individuals
with motion sickness has been reported. However, before VOR gain asymmetry values
could be taken as important parameters to detect the semicircular canal pathology,
the sensitivity of VOR gain asymmetry values needed to be verified with various other
vestibular disorders.
The present study also explains the existence of refixation saccades in 100% of the
individuals with motion sickness compared to that of their counterparts. The presence
of refixation saccades is in agreement with various studies reported earlier with
vestibular-related pathologies ([MacDougall et al, 2009]; [Macdougall et al, 2013]; [Jiménez and Fernández, 2016]; [Redondo-Martínez et al, 2016]). Refixation saccades occur when the variation is present between the stimulated
sides of the coplanar canals and that of the nonstimulated side, therefore making
the VOR generate compensatory eye movement to maintain gaze stability even during
head rotation ([Bronstein and Gresty, 1991]). These corrective saccades are suggestive of impaired semicircular canals, such
that the gaze stability with movement of the eye in equal velocity and opposite direction
to that of the head rotation is unable to be retained ([Weber et al, 2008]). Therefore, the presence of refixation saccade can be a good indicator in assessing
individuals with motion sickness.
CONCLUSIONS
The present study focused on understanding the physiology of saccule and semicircular
canals via cVEMP and vHIT, respectively, in a group of individuals with motion sickness.
Among the several parameters of cVEMP evaluated, only asymmetry ratio could distinguish
the individuals with motion sickness from those without motion sickness. The individuals
with motion sickness had higher asymmetry ratio than those without motion sickness;
however, no variations were present in latency and peak-to-peak amplitude of cVEMP
in between the groups. Also the VOR gain measured in all six semicircular canals revealed
the presence of significantly lower gain values in RA and LP semicircular canals in
individuals with motion sickness. Furthermore, the present study revealed significantly
higher asymmetry differences in three orthogonal planes of semicircular canals across
the two groups. Thus, higher asymmetry ratio in cVEMP and vHIT and also refixation
saccades can suggest some degree of vestibular anomalies in individuals with motion
sickness.
Abbreviations
CNS:
central nervous system
cVEMP:
cervical vestibular-evoked myogenic potential
LA:
left anterior
LARP:
left anterior right posterior
LL:
left lateral
LP:
left posterior
RA:
right anterior
RALP:
right anterior left posterior
RL:
right lateral
RP:
right posterior
vHIT:
video head impulse test
VOR:
vestibulo-ocular reflex
