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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4382_Библиотеки_им_академика_М_И_Перельмана
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248 Rotational Vestibular Assessment
FIGURE 7–33. Corrected 240°/sec step test response data. Initial 10 seconds of data have been expanded to
illustrate the peak slow phase eye velocity selection.
step velocity (240°/second in this case). As with
all other rotational analysis measures, reduced
VOR gain can significantly decrease the spectral
purity from which most analyses are derived,
particularly when the gain falls below 0.15. Furthermore, there are no established normative data
regarding VOR step gain. Baloh and Honrubia
report lower limits for normal high velocity step
gain to be approximately 0.27, whereas others
report lower VOR gain limits of 0.40 (Shepard et
al., 2016). Because of such a wide discrepancy of
normative limits, it is highly recommended that
site-specific step gain values be established if such
values are to be used for clinical interpretation.
Although high velocity gain is not traditionally
a response parameter that has received a great
deal of clinical attention, Shepard and colleagues
(2016) have reported a possible clinical value for
comparing high velocity step gain against low
velocity step gain to infer compensated versus
uncompensated vestibular status. They suggest
that a directionally similar abnormal gain asymmetry for both low velocity step stimuli and high
velocity stimuli suggest an uncompensated vestibular status with hypofunction assigned to the
weaker labyrinthine response. Conversely, they
suggest that when VOR symmetry for low velocity stimuli is within normal limits, and a significant VOR asymmetry persists for high velocity
step stimuli, that a centrally compensated vestibular status is likely, with hypofunction assigned according to the high velocity asymmetry.
7. Velocity Step Testing 249
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They summarize by indicating that the low velocity data assist in assigning compensation, whereas
the high velocity data assist in segregating asymmetries. However, it is important to realize that
establishing VOR gain normative reference ranges
is absolutely vital when applying this interpretive
strategy, as even slight changes in test protocols
can change VOR gain data.
High Velocity Step Response:
Peak Slow-Phase Eye Velocity Symmetry
Use of high velocity step data is analyzed to assist
in the identification of labyrinthine asymmetry.
Similar to caloric analysis, peak slow-phase nystagmus velocities from the right and left labyrinthine responses are compared and a symmetry
ratio is calculated. However, unlike the caloric
analysis where warm (excitation) and cool (inhibition) responses are totaled for each ear and
compared, right and left labyrinthine responses
are determined from the two step stimuli conditions that incite excitation. Specifically, an excitatory right labyrinthine response is elicited from
per-rotational acceleration to the right and postrotational deceleration from the left. Conversely,
an excitatory left labyrinthine response is elicited from per-rotational acceleration to the left
and post-rotational deceleration from the right.
A response symmetry ratio is then calculated
much like how the Jongkees formula is applied
during caloric irrigations.
Right Response − Left Response
Right Response + Left Response
× 100
Specifically, the equation for high velocity step
testing is written as such:
(per rotation right + post rotation left) − (per rotation left + rotation right)
(per rotation right + post rotation left) + (per rotation left + rotation right)
× 100
Once the symmetry ratio is determined, labyrinthine asymmetry (or labyrinthine hypofunction) can be determined. Although an asymmetry
ratio as high as 30% has been reported to be significant for unilateral dysfunction (Shepard et al.,
2016), an asymmetry greater than 20% (similar to
a caloric asymmetry) is generally agreed upon as
significant for unilateral dysfunction (Baloh & Honrubia, 2001). As always, it may be useful to establish site-specific normative cutoff limits for the
identification of unilateral asymmetry as site-specific test protocols, specifically the intensity of the
high velocity stimulus, can often vary from one
clinic to another. Figure
of a normal high velocity step test. Figure
7–34 shows an example
7–35
shows an example of a high velocity step test demonstrating a significant asymmetry. The difference
in peak slow phase eye velocity is clear in this
example and can easily be visualized by comparing the positive slow-phase peak VOR responses
(left acceleration and right deceleration) against
the negative slow-phase peak VOR responses
(right acceleration and left deceleration).
Interpreting the High Velocity Step Test
Like many physiological stimuli, the more robust
the velocity step stimuli, the greater the ability to
segregate asymmetries, and, subsequently, potential pathology. When compared to the low velocity step stimuli of 60° per second, an increase in
the peak chair velocity over 200°/second can often
expose a peripheral vestibular asymmetry that
would otherwise be masked by less robust velocities (Paige, 1989). This was previously alluded
to, insomuch that higher target velocity stimuli
are more effective in driving the periphery into
saturation on the lesion side when compared to
the 60°/second step stimuli (Baloh & Honrubia,
1990; Brey et al., 2008a). This is further elaborated
by Tusa, Grant, Buettner, Herdman, and Zee
(1996) insomuch that “high-velocity step rotations toward the intact ear generate higher gain
values than when rotating toward the ear with a
unilateral lesion because the lagging ear in unable
to drive the firing rate below zero” (p. 294). The
sensitivity of this measure, however, is dependent
on the severity of the vestibular lesion. In general,
Baloh, Sills and Honrubia (1979) found that asymmetries were more commonly associated with
patients exhibiting more severe unilateral lesions,
even when higher velocity step frequencies were
administered. They reported an 87% sensitivity
for 240° step testing when caloric responses were
250 Rotational Vestibular Assessment
FIGURE 7–34. Normal 240°/second velocity step test (after correcting/deleting for noise). Asym-
metry calculation is shown.
absent, but only a 67% sensitivity when caloric responses were reduced (but not absent). Therefore,
despite increasing the target step stimuli above
200°/second, the greater the unilateral damage, the
greater the likelihood of an observed physiologic
high velocity step asymmetry. That being said, it
is likely true that if an abnormal high velocity step
asymmetry exists, that a significant labyrinthine
asymmetry is almost always present, regardless of
the frequency being tested. However, when a high
velocity asymmetry is within normal limits, a borderline to marginal asymmetry may still actually
be present, especially for lower frequency stimuli
(i.e., caloric stimuli). The reason for this is likely
secondary to the preferential loss of labyrinthine
function for lower frequency stimuli, similar to
Right Excitation
166.87 + 201.87 = 368.74
368.74 – 321.85
368.74 + 321.85
=
Left Excitation
166.95 + 154.90 = 321.85
46.89
690.59
= 0.0679 (6.79%)
a preferential loss of SHA gain for the lower frequencies when vestibular pathology is present.
Before finishing our discussion on the significance of identifying labyrinthine asymmetries
using 240° step testing, it is important to also highlight the usefulness of 240° step data for identifying residual bilateral labyrinthine hypofunction.
We have determined that the intensity of the high
velocity 240° step stimulus is essentially the strongest (or at least one of the most robust) stimuli
that we clinically present to the vestibular system.
That being said, it is conceivable that, if a 240° step
stimuli failed to provoke a labyrinthine response,
then the plausibility that the vestibular system
was severely (if not entirely) damaged is greater
than if caloric, SHA, or 60° step stimuli were
7. Velocity Step Testing 251
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Right Excitation
99.82 + 83.10 = 182.92
182.92 – 369.21
182.92 + 369.92
=
Left Excitation
178.58 + 190.63 = 369.21
-186.29
552.13
= -0.3374 (-33.74%)
FIGURE 7–35. Abnormal 240°/second velocity step test (after correcting/deleting for noise). Asymmetry
calculation is shown. The VOR gain is greater than 20%. Labyrinthine hypo-function is assigned to the weaker
excitation conditions (right ear).
used alone. Therefore, the complete lack of VOR
response to a 240° step stimulus provides strong
evidence to suggest profound labyrinthine hypofunction. However, if a minimal response were obtained, does this provide evidence to suggest a minimal degree of labyrinthine reactivity is present?
To help illustrate this point, consider Figure 7–36,
which depicts the VOR 240° step response from
an individual with significant bilateral peripheral
labyrinthine areflexia. The data not shown in this
example were the absence of any detectable VOR
to standard caloric stimuli, SHA stimuli, and 60°
step stimuli. Therefore, the only data that provides
some salient evidence to refute complete labyrinthine areflexia were the 240° step stimuli. This,
however, does not speak to the functional “usability” or rehabilitation of such labyrinthine re-
activity; only that minimal residual response exists.
vestibular disease. In this example, an appropriately beating VOR response is clearly identified in
response to each step stimuli. These data suggest
Late “Reversal” Nystagmus During
High Velocity Step Testing
that, if given an appropriate amount of stimuli,
this patient’s labyrinth (or at least the horizontal
semicircular canals) retain some residual function
and provide some evidence to refute complete
At times, the presence of a reversing nystagmus
may occur toward the end of a high velocity stim-
ulus period, either per or post acceleration. In fact,
252 Rotational Vestibular Assessment
FIGURE 7–36. The VOR and slow phase eye velocity plots for rightward and leftward, acceleration and decel-
eration stimuli during a 240° step test. Despite the incredibly weak VOR response, these data confirm very limited
labyrinthine activity (VOR response is appropriately beating to all stimuli conditions) that would otherwise have
gone undetected by traditional caloric or even SHA stimuli.
it is actually quite common for a burst of opposite
beating nystagmus to occur following complete
decay of the nystagmus response. Figure 7–37
shows a nystagmus reversal in a healthy individual following a 240° rightward step stimuli. Reversal of nystagmus is generally more prominent
following acceleration than deceleration stimuli.
Furthermore, reversal of nystagmus most often
occur when cupulae are subjected to constant
acceleration of a moderate-to-high velocity, such
as step stimuli greater than 100°/second (Baloh
& Honrubia, 2011; Baloh et al., 1979). Although
nearly all nystagmus during rotational testing
can effectively be explained by the pendulum model
and cupular mechanics, the primary explanation
for this reversal is known as the adaptation phenom-
enon (Baloh et al., 2011).
To explain the adaptation phenomenon, we
must first summarize the fundamental principles
of the pendulum model of cupular mechanics we
have previously discussed. The pendulum model
states two fundamental properties of cupular
dynamics. First, the degree of cupular deflection
is in direct relationship to the degree of the accel-
7. Velocity Step Testing 253
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FIGURE 7–37. Example illustrating a robust “reversal nystagmus” follow-
ing a 240°/second step test on a healthy individual.
eration stimulus. Second, the time it takes the
cupulae to reach maximum deviation is directly
proportional to the viscosity of the endolymph
and inversely proportional to the elasticity properties of the cupulae (Baloh et al., 2011). What is
implied, however, but not directly stated, is that
the pendulum model is constrained to explaining cupular dynamics and fails to take into consideration the regular and irregular afferent firing
properties of the vestibular nerve. Following sustained accelerations, a substantial portion of afferent nerve fibers exhibit adaptation properties that
are not explained by the pendulum model. When
exposed to a sustained velocity of approximately
100°/second, or greater, these adaptation neurons experience a biphasic response that demonstrate a secondary prolonged decrease in firing
rate that return to baseline at a much slower rate
than the monotonic phasic excitatory neurons. It
is this slower return of biphasic neurons that is
most likely responsible for the emergence of the
reversal nystagmus observed during high velocity step testing. Although the exact origins of this
response is not know (anatomic versus synaptic), this adaptation phenomenon is a more pronounced behavior from irregular neurons than
regular neurons (Baloh et al., 2011). Recall, that
properties of irregular afferent nerve fibers also
respond best to stimuli with more robust onset
characteristics such as those experienced during
(high velocity) step testing, whereas regular afferent nerve fibers respond best to more sustained
angular stimuli such as those experienced during SHA testing. Clinically speaking, however,
the absence of a reversal nystagmus in an otherwise healthy and intact vestibular system has
not received any prognostic attention and should
not be interpreted as abnormal until identified
as such.
Limitations to 240° Step Testing
There are a couple of critical limitations to the high
velocity step test. First, it is absolutely critical that
appropriate mental tasking and sharpened mental
alertness occur during administration of all step
stimuli, and especially during high velocity step
testing. Although this is true of all measures that
assess the VOR, such mental tasking during step
testing is essential, particularly during the initial
burst of acceleration and deceleration to ensure
equivalent and maximum peak responses are
produced and recorded. Because the high velocity step test is primarily concerned with only
four discrete beats of nystagmus, it is imperative
that the signal to noise ratio during these precise
(and extremely brief) periods of data collection
be extremely high. Keep in mind that the peak
slow-phase eye velocity responses should occur
immediately post the acceleration and deceleration stimulus periods. It is not uncommon for
patients to experience significant vertigo and even
a “jolt of suspense” or “surprise” immediately following such high velocity stimuli. Consequently,
their physiological “knee jerk” (or more precisely
“ocular jerk”) response may be to close their eyes,
tense their ocular muscles, or even roll their eyes
up into the orbits. Figure 7–38 depicts an example of a patient for whom reliable data was not
obtained during the critical recording period secondary to increased ocular tension. All of these
physiological responses will contribute to lower
peak eye velocities and subsequently create a
254 Rotational Vestibular Assessment
FIGURE 7–38. Example illustrating the difficulty with obtaining the single
peak slow phase eye velocity response during a 240°/sec step test due
to ocular tightening. This example shows the absence of any eye velocity
data in response to decelerating from a leftward 240°/sec step velocity.
As a result of an abrupt onset of vertigo often experienced secondary to
the abrupt deceleration from the chair rotation, the peak slow phase eye
velocity was missed for the first 6 seconds following deceleration (from 110
seconds to 116 seconds). Subsequently, the slow phase peak eye velocity
response of −107.24°/sec is considered inaccurate and the test must be
either repeated or negated. This example again highlights the importance
of capturing “clean” data at the critical periods of acceleration and deceleration — as the entire four-minute test must be repeated due to the single
loss of one slow phase eye velocity data point.
diminished response. When you’re only collecting
a single beat of nystagmus, a significant (although
transient) decrease in signal to noise ratio during
this critical “first second” time period immediately post the acceleration or deceleration stimulus, will often cause peak responses to be missed,
or recorded a few seconds after the acceleration
or deceleration period (only after the “knee jerk”
ocular reflex has abated and the patient re-opens
their eyes). By this time, the peak response may
have declined by a significant percentage. Unfortunately, there is not a great deal of flexibility in
the administration protocols during step testing
that would allow a clinician the tractability to stop
the test in order to quickly repeat a single step
acceleration or deceleration period (i.e., portions of
a step test cannot be repeated; the entire test must
be repeated). Figure 7–39 depicts an example of a
patient who experienced a difficult time keeping
their eyes open during and immediately after the
onset of the acceleration and deceleration stimulus. In this example, the test was performed a second time with a significant degree of cajoling by
the clinician to maintain eye opening throughout
the entire test, and particularly during the critical
recording periods. As can be seen in the example,
an increase in peak slow phase eye velocity by
157% would potentially have been missed if the
test had not been performed another time. Such
a difference can create significant problems with
your data analysis, particularly when a single data
point constitutes 25% of your entire data! In light
of this, it is critical for the clinician to know precisely when the step of acceleration and/or deceleration is going to occur so as to appropriately
prepare and task the patient just prior to, during,
A
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B
FIGURE 7–39. Example illustrating the occasional difficulty with obtain-
ing the peak slow phase eye velocity response during a 240°/sec step
test. A. Shows the absence of any eye velocity data immediately following
a rightward 240°/sec step acceleration due to eye closure. As a result,
the peak slow phase eye velocity was subsequently identified as −76.24°/
sec at 5 seconds. The 240° step test was repeated while the patient was
encouraged to keep their eyes open. These data are shown in B. Despite
the patient’s eyes being closed for a brief period of time between 1 and
3 seconds, the slow phase peak eye velocity response was nevertheless
cleanly obtained within the first second of the test. The peak slow phase
velocity response was −195.91°/sec (an increase in the slow phase peak
velocity response from the previous test by 157%). This example clearly
illustrates the importance of data collection during the critical time period
during and immediately post acceleration (or deceleration).
255
256 Rotational Vestibular Assessment
and a few seconds post the onset of each stimulus.
Of course, another foolproof method to combat
missing these discrete time periods is to task the
entire 4-plus minutes of testing. This is generally
good clinical practice.
A second critical limitation to high velocity
step testing is the physiological contamination
of the peak slow phase eye velocity response.
Because of the intense step velocity stimulus, the
slow phase eye response data (and subjective
response) can often be similarly intense. This may
cause spurious physiological noise in the individual slow phase components of the nystagmus,
such as noisy beats due to tracking inadequacies
or, worse, unwanted physiologic noise (such as
blink artifact) that can often be misinterpreted
as actual data. The problem with these spurious
data points is that the beat detection algorithms
employed in many software programs often identify and may include these aberrant data points
within your analysis (i.e., the algorithms cannot
distinguish between noise and real nystagmus
data). Moreover, these data points can often be
significantly greater in their velocity than the
actual surrounding “true” data points. Unfortunately, unless the clinician recognizes this error,
and either deletes the spurious “noise” or adjusts
the peak velocity response to the “correct” data
point, the symmetry calculation will erroneously
include a possibly inflated peak slow phase velocity response, and inaccurately reflect the true labyrinthine symmetry. Figure 7–40 illustrates such an
example of blink artifact inappropriately identified as the peak slow phase eye velocity response.
This example constitutes a single data point that,
if taken to be true, would have elevated the peak
slow phase response by 335%. Therefore, it is vital
that the response data be carefully scrutinized.
Fortunately, the analysis is fairly simple, as you
only need to confine your data analysis to four
discrete “true” beats of nystagmus that should
occur within the first 1 to 2 seconds after completion of the acceleration or deceleration stimulus.
Figure 7–41 is another example of both an incorrect identification of the peak velocity response
as well as the corrected response. Although this
example is less extreme, it is just as common and
just as easy to identify. Finally, similar to the low
velocity step test, contraindicated medications
that could deleteriously suppress or stimulate the
CNS, as well as significantly alter the VOR gain,
should be avoided unless otherwise instructed by
the patient’s administering physician.
ALTERNATIVE STIMULUS
VELOCITIES AND VELOCITY
STEP PROTOCOLS
Certainly a variety of target velocities can be
selected when performing low and high velocity
step testing; however, there is no clear knee-point
as to what constitutes “low” versus “high” velocity step stimuli. Although a 60°/second velocity is
almost universally chosen for performing the low
velocity step test, from which the VOR time decay
constant is calculated, the choice of high velocity step stimuli is less “unanimous.” One could
argue that the velocity at which reversal nystagmus occurs may be sufficient evidence to suggest
that the knee-point exists at approximately 100°/
second. Regardless of what velocity is designated
for the low versus the high velocity step target
stimuli, it is critical that site-specific normative
values for VOR gain and/or time decay constants
be obtained given slight variations in protocol
administration. Remember though, the higher the
velocity stimuli, the better the chance of segregating and identifying unilateral pathology.
Velocity Storage
“Cancellation” Protocol
For patients who have a suspected uncompensated vestibular pathology, it is often useful to
determine the functional integrity of the velocity storage mechanism, or the lack thereof. As we
have already discussed, the velocity storage mechanism is uniquely responsible for both the initiation and maintenance of central compensation, as
well as the preservation of the VOR beyond that of
simple cupular mechanics. We have already discussed various outcome measures that infer velocity storage function, specifically the VOR decay
time constant during 60° step testing. However,
there is an additional outcome measure that can
provide insight into velocity storage function.
The velocity storage “cancellation” protocol (also
A
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B
FIGURE 7–40. Example illustrating the effects of noise offsetting peak
detection during a 240°/sec rightward step acceleration. A. Shows an
inappropriate selection of the −111.72°/sec peak response just prior to 9
seconds. The raw tracing clearly shows this response to be noise (likely
a blink response). B. Shows the correct selection of the -25.66°/sec peak
response during the rightward step acceleration just prior to 1 second.
Proper inspection of the data has significantly changed the interpretation
of this response from a robust peak VOR response (47% gain) to a significantly weak VOR response (11% gain) — all due to a single introduction of
blink artifact misinterpreted by the response algorithm as actual data.
257
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