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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4433_Библиотеки_им_академика_М_И_Перельмана
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figure 13–23. Fast phase components of the vestibular nystagmus are deleted and the degree for each slow
phase component of the vestibular nystagmus is plotted below on the eye velocity plot (arrows to the lower graph)
for each one-half cycle of rotation.
figure 13–24. Plot of chair velocity and corresponding vestibular slow phase velocity data. Arrows identify the peak
target velocity of the chair rotation in relationship to the peak vestibular slow phase component of the eye velocity
data. Data shows a strong temporal relationship between peak eye data and peak chair data. As dictated by the
vestibular ocular reflex, the slow phase velocity data will always be in the opposing direction of chair rotation thus
forming a mirror eye velocity sinusoid in relation to the chair velocity.
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algorithms are applied to the data in order to characterize the vestibular response with respect to its response
gain, phase, and symmetry.
Sinusoidal Harmonic Acceleration
Analysis Parameters
Analysis of the VOR in response to sinusoidal chair
rotations produces three salient response parameters:
gain, phase, and symmetry (Brey et al., 2008b; Shepard
& Telian, 1996; Figure 13–25). Comparison of the peak
ocular response to that of peak chair rotational velocity
can be easily determined. This ratio of peak eye velocity to peak chair velocity is known as the sensitivity, or
gain, of the vestibular system, and through a series of
rotations (accelerations), the gain of the vestibular system can be effectively determined across a wide range
of frequencies during SHA testing.
In addition, as the chair begins to accelerate in one
direction and the eyes begin to slowly deviate in the
opposite direction due to the vestibular response, the
timing relationship between the exact moment chair
rotation begins and the exact moment the eyes begin to
move in the opposite direction can also be determined.
This timing relationship is known as the phase of the
VOR response, and describes the temporal movement
of the eyes in relation to the movement of the chair (see
Figure 13–25).
Finally, the degree of peak eye response can be
compared from rotations in the clockwise (CW) direction with those from the counterclockwise (CCW)
direction. The ratio between these two peak responses
is known as the symmetry of the VOR. Therefore, three
primary measures are specifically analyzed during
rotational testing: VOR gain, phase, and symmetry (see
Figure 13–25).
VOR Response Gain
Gain defines the relationship between peak eye velocity and peak chair velocity (Brey et al., 2008b; Shepard
& Telian, 1996). It is simply the sensitivity, or responsiveness, of the vestibular system to a particular stimulus (or rotational frequency). A perfect compensation of
eye movement to that of chair rotation would produce
a VOR response that is truly equal (and opposite) with
respect to chair movement. That is, the relationship
between peak eye and peak chair velocity would be
exactly the same, which is expressed as the ratio 1:1, or
simply a gain of 1.0. A perfect response is often referred
to as response unity. VOR response gain is calculated for
each stimulus rotational frequency performed during
SHA testing.
Because the exact acceleration and velocity stimulus being delivered to the vestibular system is known,
simple calculations of the slow-phase eye velocity in
relation to chair acceleration can be precisely determined. If the VOR were truly an equal and opposite
response to head acceleration, then the degree of ocular reflex (slow-phase velocity slope calculation) would
exhibit a relative increase or decrease in relation to an
increase or decrease in chair rotational frequency. That
is, as the frequency of chair rotation is increased, so
too is the response velocity of the peak eye response.
Although this is generally the case, we know that for
Figure 13–25. Single cycle of chair rotation illustrating how the various analysis parameters of SHA testing (gain,
phase, and symmetry) are determined.
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the frequencies assessed during rotational testing (0.01
to 0.64 Hz) the response of the VOR is always opposite
the direction of head (chair) rotation; however, it is
seldom, if ever, truly equal to the intensity of the chair
rotation. This concept is especially true for the slower
rotational frequencies below 0.08 Hz and, to a lesser
extent, truer for the mid-to-high rotational frequencies
above 0.04 Hz. This is not surprising as the frequency
stimuli used during SHA testing remain below the
vestibular system’s optimum operating range of 1 to
5 Hz. Most physiologic systems fail to exhibit sufficient
responses for stimuli that do not adequately stimulate
their ideal operating range (visual acuity in darkness is
one such example). In fact, many physiologic systems
have adapted to work synergistically to overcome their
deficiencies. For example, the deficiency of the vestibular response for frequencies below 1 Hz is most often
augmented by the visual system, whereby the gain of
the VOR is brought close to unity with extreme effi-
ciency. If one could adequately and reliably assess the
vestibular system using rotational stimuli between 1
to 5 Hz, the data would show that the degree of VOR
response would not only continue to be opposite (this
is always the case) but would also be truly equal (or
nearly equal) to the degree of stimuli input. That is,
response unity would be present within our functional
operating range of 1 to 5 Hz.
VOR Gain Interpretation. Figure 13–26 depicts the
raw nystagmus response of the VOR during a rotational stimulus. The slow-phase responses are plotted
against the rotational stimulus for 0.16 Hz. The figure
depicts right-beating nystagmus in response to rightward rotation and left-beating nystagmus in response
to leftward rotation. It can clearly be seen that the VOR
nystagmus response (i.e., the slope of the nystagmus)
crescendos and decrescendos in relation to chair acceleration and deceleration. A healthy VOR nystagmus
figure 13–26. Complete data for 0.16 Hz rotation. Top graph shows raw nystagmus tracing.
Middle graph shows a plot of the slow phase component of the vestibular data in relation to
chair velocity. Bottom graph shows averaged slow phase data in relation to chair velocity. Peak
eye velocity data is determined and VOR gain for rightward and leftward rotation is calculated.
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response will, therefore, have a peak response that is
often associated with, or occurs near, the peak response
of chair rotation.
The gain of the VOR is determined by comparing
the peak eye response to peak chair response. The peak
velocity of chair rotation is always held constant, most
often at 50° or 60°/sec (depending on the predetermined stimulus parameters of the rotational paradigm
or chair setup). The peak VOR response, however,
will often vary with respect to the frequency of chair
rotation and physiology of the vestibular system. For
lower frequencies of rotation, like that in Figure 13–27,
the peak VOR response crescendos to approximately
30°/sec in response to a 0.02 Hz rotational stimulus, whereas the peak VOR response crescendos to a
much more robust peak response at 35° to 38°/sec
in re-sponse to a 0.32 Hz rotational stimulus (Figure
13–28). Identifying the “peak” slow-phase velocity
during rightward and leftward rotation is critical as it
is this response parameter that is compared against
the peak chair velocity response of 60°/sec when determining the gain of the system. Simply put, the VOR
gain of the system is the ratio between the peak slowphase eye velocity compared with (or divided by) the
peak chair velocity (which is always 60°/sec or 50°/
sec). The gain of the VOR is determined for both rightward and leftward rotations, as well as combined for
an averaged VOR response gain for each frequency of
rotation.
Other than classifying patient VOR gain response
as falling within normal limits, patient results are often
categorized with respect to either abnormally high or
figure 13–27. Complete data for 0.02 Hz rotation. Top graph shows raw nystagmus tracing.
Middle graph shows a plot of the slow phase component of the vestibular data in relation to
chair velocity. Bottom graph shows averaged slow phase data in relation to chair velocity. Peak
eye velocity data is determined and VOR gain for rightward and leftward rotation is calculated.
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figure 13–28. Complete data for 0.32 Hz rotation. Top graph shows raw nystagmus tracing.
Middle graph shows a plot of the slow phase component of the vestibular data in relation to
chair velocity. Bottom graph shows averaged slow phase data in relation to chair velocity. Peak
eye velocity data is determined and VOR gain for rightward and leftward rotation is calculated.
low VOR gain. Abnormally low gain is certainly the
more common of the clinical findings. When impacting all test frequencies, its interpretation is generally
restricted to a bilateral reduction of vestibular reactivity. Although this is often associated with a bilateral
peripheral pathology, a central pathology can also less
frequently cause a bilateral reduction in VOR gain
(Shepard & Telian, 1996; Wall, 1990). Therefore the
site-of-lesion value for reduced rotational VOR gain
is bilateral peripheral unless purely central indicators
are suggested (Shepard & Telian, 1996). In addition,
abnormally low VOR gain is often frequency dependent. Incomplete damage to the vestibular periphery
causes VOR gain effects that often occur first in the low
frequencies. This is juxtaposed to audiometric hearing
loss, where loss often occurs first in the high frequencies. As vestibular pathology progresses, a loss of midto-high frequency vestibular reactivity ensues. This
also helps to explain why caloric irrigations (comparable to a rotational frequency of 0.003 Hz) are so often
reduced or absent with even slight peripheral vestibular damage. Moreover, this also sheds some light as to
why rotational testing can be critical to the evaluation
of a dizzy patient. Because VOR is frequency dependent, verifying intact or even reduced but viable VOR
gain for the higher frequencies is imperative when
determining the potential for vestibular rehabilitation.
This is similar to verifying usable hearing for the low
to mid frequencies when determining the potential success for hearing aid outcomes.
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Abnormally high VOR gain is a less common
occurrence. The interpretation of this finding is similar to abnormally high caloric responses and is usually
associated with a central site of lesion that localizes to
the cerebellum (Shepard & Telian, 1996). This finding
is certainly uncommon, just as hypercaloric responses
are uncommon. Less information is also known about
hyperactive VOR gain during SHA testing than hypoactive VOR gain. Hyperactive VOR gain has most often
been reported in central pathologies, most often implicating the cerebellum (Baloh, Sills, & Honrubia, 1979;
Hirsch, 1986; Shepard & Telian, 1996). Migraine and
traumatic brain injury (TBI) have been implicated in
producing high VOR gain results (Brey et al., 2008b).
Both of these pathologies have abnormal processes that
have strongly implicated the central nervous system.
There is one more final comment to consider
regarding VOR gain. Although not discussed yet,
VOR phase and VOR symmetry are both calculated
from VOR gain, and thus, when there is an absence
of VOR response for either one or all SHA frequencies
(i.e., zero gain), phase and symmetry values cannot be
determined for any frequency where gain is absent.
Moreover, when the VOR gain is minimal, phase and
symmetry should be interpreted with caution. Anytime
VOR gain values are low, there is a higher probability
that physiologic noise (e.g., blink artifact, ocular wandering, ocular vertical drift) has significantly reduced
the VOR response. Therefore, VOR gain between 0.10
and 0.15 has been suggested as the lowest acceptable
cut-off value when reliably calculating VOR phase and
symmetry (Shepard & Telian, 1996). However, when
VOR gain values are near or below 0.15, it is highly
recommended that the raw data be scrutinized to
determine its signal-to-noise ratio in order to decide if
the quality of the recording is “clean” enough to warrant calculation of phase and symmetry. Although it
is good practice to always review the raw nystagmus
response, it is even more imperative when analyzing
reduced signal-to-noise conditions that are common to
low frequencies (given the inherent low gain naturally
present at these frequencies) as well as during conditions of overall poor VOR gain where the response
is small.
VOR Phase
In its simplest definition, phase refers to the timing
relationship between chair movement and eye movement (Shepard & Telian, 1996). It can be thought of as
the degree to which eye movement lags behind the
applied stimulus, which in this case is head accelera-
tion. By definition, the VOR dictates that an equal and
opposite compensatory eye movement must occur
in response to head movement. The exact time in
which the eye begins to move in the opposite direction (in relation to chair movement) is known as phase.
Phase is the least intuitive of the three (measures) but
has the greatest clinical significance in its ability to
document peripheral system dysfunction (Shepard &
Telian, 1996).
VOR Phase Interpretation. Fully understanding VOR
phase and its related abnormalities is the least straightforward of all the SHA parameters. At its heart, VOR
phase is a reflection of the central processing of the
labyrinthine afferent input from the horizontal semicircular by the neural integrator in order to augment
an insufficient afferent drive into a sufficient VOR eye
velocity response when confronted with impuissant
acceleration stimuli. It is, in short, a centrally mediated increase of a weak afferent drive in order to more
efficiently drive the VOR during slow rotational (head)
movements (<0.04 Hz). The lack of understanding of
VOR phase and its intimate relationship to VOR gain,
as well as acute and chronic pathology (to say nothing
of central compensation), is likely the primary driver of
many clinicians’ dismissal of reporting its significance.
Not being withheld, the “plotting” of VOR phase during rotational assessment is, indeed, confusing and
often misunderstood. Its “appearance” of eye movement preceding chair (head) movement is undoubtedly perplexing; however, the leading of eye movement
to that of head movement is more of a by-product of
how the data are plotted rather than the eyes actually
leading head movement. Unfortunately, a comprehensive discussion regarding the significance of VOR
phase and its relationship to vestibular physiology
and pathology is outside of the scope of this chapter.
However, the reader is encouraged to review multiple
sources for a better understanding of the comprehensive nature of VOR phase (Goldberg et al., 2012; Wall,
1990; Zalewski, 2018).
Nevertheless, the application of VOR phase during
rotational assessment can have a profound impact on
our understanding of vestibular pathology. In general,
VOR phase has both contributions of peripheral input
as well as central input. In short, central vestibular
processing (velocity storage) requires both a sufficient
amount of peripheral drive to manage as well as an
intact (healthy) neural integrator to process the incoming afferent input. Thus, a decrease in peripheral input
from end-organ pathology, as well as an abnormal central processing from a defective neural integrator, can
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independently produce VOR phase abnormalities; and
concomitant pathologies impact both the peripheral
labyrinthine end organs and the neural integrator.
Without a doubt, abnormal VOR phase lead in
the presence of normal VOR gain is the most common
rotational abnormality. This pattern strongly suggests
effective compensation for a previous peripheral vestibulopathy, and is consistent with a normal rebalancing of central VOR gain with a concomitant (requisite)
permanent sacrificing of velocity storage (Zalewski,
2018). This pattern is likely secondary to peripheral labyrinthine pathology, and other corroborating evidence
during a comprehensive assessment should provide
sufficient evidence for this interpretation. However, in
a case where normal peripheral vestibular function is
suspected and VOR phase abnormalities exist, a central
pathology needs to be considered and ruled out. Interpretation of isolated VOR phase abnormalities should
be made with caution as reflecting pathology confined
to either the peripheral or the central system. However,
interpretation of VOR phase should always be made
in conjunction with supplemental vestibular findings
during your comprehensive assessment. For a more
comprehensive discussion of VOR abnormalities, the
reader is encouraged to review Zalewski (2018).
VOR Symmetry
VOR symmetry refers to the equality of the VOR
gain when stimulated during rightward (CW) rotations versus leftward (CCW) rotations. The compensatory VOR response occurs following both CW and
CCW rotations, but in opposite directions. That is, the
left-beating vestibular slow phase in response to CW
(rightward) rotations produces a VOR gain that can be
compared with the right-beating vestibular slow-phase
gain from CCW rotations. The relationship between the
generated VOR gain from CW and CCW rotations represents the symmetry of the vestibular system.
testing is, in fact, analogous to directional preponderance measured during caloric irrigations. However, it
is important to realize that directional preponderance
calculated from caloric irrigations is determined from
the slow-phase velocity component of the nystagmus,
but named in accordance with the fast phase (i.e., rightbeating or left-beating directional preponderance).
Rotational asymmetries, on the other hand, are calculated and named in accordance with the slow-phase
velocity component. Therefore, a right caloric directional preponderance (i.e., left slow-phase velocity component) is analogous to a left rotational asymmetry (i.e.,
left slow-phase velocity component) and vice versa.
Most often, however, the presence of an asymmetry (similar to that of an observed directional preponderance during caloric irrigations) will be the result of
a spontaneous nystagmus. The presence of a spontaneous nystagmus will generally force such an asymmetry until central compensation occurs and tonic neural
symmetry is once again restored. In time central compensation effectively resolves both the static (spontaneous nystagmus) as well as the dynamic (rotational)
asymmetry. It is important to note, however, that such
conditional asymmetry will only exist during a unilateral peripheral weakness. Everything discussed at this
point regarding asymmetry and the direction of the
slow-phase velocity component will be reversed in the
presence of an irritative lesion such as Ménière’s disease. Thus, a rotational asymmetry can be secondary
to either peripheral system, and care should be given to
ensure the underlying etiology and laterality of the vestibulopathy. In light of this, a comprehensive vestibular assessment is essential to elucidate a more complete
peripheral vestibular phenotype for such patients. In
addition, corroborating evidence suggesting incomplete
compensated VOR gain, low frequency VOR phase leads
and even a caloric asymmetry should also be apparent
during this acute (and semi post-acute) stage.
VOR Symmetry Interpretation. Because both laby-
rinths are actively providing an excitatory and inhibitory response during head rotations, laterality should
not always be inferred from the symmetry measure.
VOR asymmetry, therefore, does not directly reflect
a state of weakened laterality in the system. Rather,
it reflects a physiologic preponderance within the ves-
tibular system (Shepard & Telian, 1996). A vestibular
preponderance merely indicates that the system has a
preferential bias toward a particular direction of rotation (movement) or production of slow-phase VOR
response. The measure of VOR symmetry during SHA
Sinusoidal Harmonic
Acceleration Interpretation
Normal Sinusoidal Harmonic
Acceleration Response
Although VOR gain in the absence of any visual stimuli is not perfectly compensatory as is VOR phase for
frequencies below 1.0 Hz, responses can be compared
against normative reference ranges for determination
of vestibular function in association with the rotational
stimulus frequency range delivered. It should be noted
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here that site-specific normative reference ranges, using
site-specific protocols, should be obtained when assisting in the diagnosis and identification of labyrinthine
pathology. Normative reference ranges for SHA testing
obtained from the National Institutes of Health vestibular lab are presented in Figure 13–29 and Table 13–4.
Figure 13–30 illustrates VOR response parameters from
a patient during a normal rotational examination.
Unilateral Peripheral Impairments
Unilateral peripheral labyrinthine disorders can generate a varied pattern of SHA results depending on the
severity and acute nature of the impairment. In cases
where a lesioned end organ is only mildly impaired, the
results of rotational testing may be completely normal
due to central compensation. In instances where there
is more severe dysfunction in one of the labyrinths, the
most commonly observed abnormality is increased
phase in lower frequencies. Results can, therefore, vary
depending on the severity and acute nature of the unilateral peripheral vestibulopathy.
When assessing patients who have incurred an
acute peripheral vestibulopathy, there are a number
of characteristic findings that can be expected. Figure 13–31 illustrates such an example. First, VOR gain is
figure 13–29. Normal reference range for VOR gain, phase, and symmetry showing mean and two standard deviations for octave frequencies from 0.01 to 2.0 Hz.
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table 13–4. Means and 2 Standard Deviations for Sinusoidal Acceleration Testing for
VOR Gain, VOR Phase, VOR Symmetry, and Spectral Purity from 0.01 to 2.0 Hz*
Response
Parameter
VOR Gain 0.3951 0.15468 0.458 0.18274 0.3951 0.15468
VOR Phase 39.47 12.69 21.94 10.82 39.47 12.69
VOR Symmetry 4.238 16.348 3.457 17.442 4.238 16.348
Spectral Purity 92.82 6.394 93.87 7.896 92.82 6.394
Response
Parameter
VOR Gain 0.508 0.2856 0.5108 0.2816 0.5376 0.302
VOR Phase 2.714 13.128 0.6483 13.428 0.2806 11.67
VOR Symmetry 3.777 16.868 −4.227 19.072 5.345 16.276
Spectral Purity 95.72 6.96 95.47 6.846 97.32 3.7
Response
Parameter
0.01 Hz 0.02 Hz 0.04 Hz
Mean 2SD Mean 2SD Mean 2SD
0.08 Hz 0.16 Hz 0.32 Hz
Mean 2SD Mean 2SD Mean 2SD
0.64 Hz 1.28 Hz 2.0 Hz
Mean 2SD Mean 2SD Mean 2SD
VOR Gain 0.6018 0.2708 0.7925 0.216 0.7594 0.4214
VOR Phase 3.942 9.624 9.681 11.752 1.745 28.76
VOR Symmetry 2.883 14.538 0.5278 8.422 −2.675 48.52
Spectral Purity 98.46 3.672 99.12 1.1518 96.52 7.316
Note. *Means and standard deviations based on a sample size of 50 healthy volunteers aged
18–61 years.
often reduced and phase prolonged immediately after
the event. Secondly, findings often reveal a significant
asymmetry that is biased in the direction of the spontaneous nystagmus. Symmetry is calculated using the
slow-phase eye velocities and indicates a bias in VOR
responses during rotation. A right asymmetry corresponds to left-beating nystagmus and left asymmetry
corresponds to right-beating nystagmus. A significant
asymmetry is a non-localizing finding that can be
indicative of central or peripheral dysfunction. Asymmetry measures can be isolated as well as found in the
presence of phase and gain abnormalities. Significant
asymmetries are commonly found in patients with
acute or uncompensated unilateral vestibular dysfunction. In rare cases, significant asymmetry may indicate
the presence of a lesion in the central pathways.
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figure 13–30. Normal SHA results for VOR gain (A), VOR phase (B), and VOR symmetry (C) from 0.01 through 2.0
Hz. Abnormal response regions are indicated by the gray regions for each results graph.
figure 13–31. Common SHA results for an acute unilateral labyrinthine hypofunction. Results for VOR gain (A), VOR
phase (B), and VOR symmetry (C) from 0.01 through 0.32 Hz. Abnormal response regions are indicated by the gray
regions for each results graph.
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