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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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A
B
FIGURE 7–16. Example illustrating the effect of noise on the calculation
of the time decay slow phase eye velocity plot. A. Shows a significant elevation in the slow phase velocity best-fit line secondary to the extraneous
noise occurring in the mid-to-late portion of the step interval. This causes a
consequential prolongation of the time decay constant, which is calculated
at 31.35 seconds. B. Shows the corrected data with the extraneous noise
deleted from the analysis. The slow phase velocity best-fit line now nicely
approximates the data with a corrected time decay of 8.43 seconds. As a
result of “cleaning” the data, the time decay constant now falls within the
abnormal range. (In this example, the peak slow phase velocity did not
have to be adjusted.)
228
FIGURE 7–17. A. Uncorrected
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60°/sec step response to leftward
acceleration. B. Slow phase eye
velocity data cleaned (noise
deleted) during primary nystagmus
portion from 122 through 160
seconds. Peak slow phase eye
velocity adjusted from 40.44°/sec to
37.60°/sec. Extraneous occurring
noise is elevating the best-fit line
above the actual slow phase data
plots. C. Corrected slow phase
eye velocity data (cleaned for the
remaining step portion), bringing
the best-fit line into better match to
the slow phase velocity plots, thus
reducing the decay time constant
from 28.70 seconds to 18.34
seconds.
A
B
C
229
FIGURE 7–18. Identical
response data from a rightward
(clockwise) 60°/second step
acceleration. A. Illustrates the
best-fit line and resultant time
decay constant when the response
considers the entire portion of
the 60-second constant velocity
interval (less a few slow phase
data; points that were determined
to be noise and have been
deleted). B. Illustrates the same
data, however, only the data from
the first 30 seconds are included
in the analysis as the data from
30 to 60 seconds is judged to be
A
noise. This effectively reduces the
analysis period to 30 seconds and
brings the best-fit line closer to the
actual slow phase data plot within
this time frame. Consequently, the
time decay constant is reduced
from 12.27 seconds (normal) to
8.09 seconds (abnormal), which
is in agreement with concomitant
vestibular data identifying a
peripheral vestibulopathy. This
example illustrates the importance
of confining data analysis only
to data that is relevant, and how
noise (highlighted boxed areas)
can inappropriately be accepted
as actual response data, which
can contribute to an incorrect
interpretation.
B
230
A
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B
FIGURE 7–19. Example illustrating an inappropriate data analysis for a
60°/second step test where the peak slow phase eye velocity data point
is inaccurately identified (A) — the algorithm will generally “look” for the
strongest measured velocity during or post acceleration and assign it as
the peak response. Consequently, the time decay is deleteriously impacted
(shortened to 5.59 seconds). Correction of this error is thankfully quite
straightforward as deleting the extraneous data point(s) will cause the analysis algorithm to identify the correct peak response (or the correct data
point can manually be selected) and the time decay constant will recalculate accordingly. Following the correct identification of the peak slow phase
velocity response (as shown in B), the time decay constant increased from
5.59 seconds (abnormal) to 16.66 seconds (normal).
231
232 Rotational Vestibular Assessment
Because the peak nystagmus on a low-gain response is inherently small, the time constant often
appears incredibly long (often times it fails to calculate a time constant (infinity) as the 63% decay
point cannot be identified within the 60 second step
interval). For example, in a case where the peak
nystagmus is 4°/second, the time constant of the
response would not occur until nearly 1.48°/
second, which may be difficult to identify within
the 60-second poststimulus interval (due to
background noise contributing to to a poor signal to noise ratio). Likewise, the poststimulus response may have produced only a few beats of
nystagmus from which effective decay cannot be
A
measured. Figure 7–20 illustrates two examples of
such cases.
A third critical error not yet discussed is the
possible “blunting” of the peak eye velocity step
response due to inattentiveness or suppression at
the critical moment the peak response is expected
to occur immediately post acceleration. Because
the period of acceleration stimulus is so brief (0.3
seconds for a 60°/sec velocity target stimulus),
the initial peak response could be missed or suppressed if the patient is not attentive to the test
procedures or is inattentive to the mental tasking procedures, respectively. The “blunted” or
significantly reduced peak eye response would,
FIGURE 7–20. Two frequent
60°step results that often occur
as a result of an absence or nearabsence of VOR. A. 60° step
response to rightward acceleration.
A near absence of a peak slowphase velocity response, or in
this case, a slight underlying
spontaneous is identified. This
often creates a scenario which
produces a best fit analysis of the
slow-phase data that fails to reach
the criteria for a 63% time decay,
thus producing an infinite time
decay response. In such a case,
the time decay response should be
disregarded as the response to the
step stimuli is essentially absent.
B. 60° step response to leftward
acceleration showing a near
absence of a peak slow-phase
velocity response that produces
only a few beats of nystagmus
post acceleration. In such a
scenario, a meaningful time decay
cannot be determined. In such
cases, identifying a precise time
decay value is deferred in favor
of reporting an absence, to nearabsence of VOR response (note
the gain of 8%).
B
7. Velocity Step Testing 233
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therefore, underestimate the accurate peak slow
phase velocity response and would subsequently
produce an inaccurate time decay constant. An
example of this is illustrated in Figure 7–21. This
type of error may be difficult to detect or realize
as the clinician may have no way of knowing if
the true response could have been stronger. This
is most often problematic when the tasking procedures are inappropriate or insufficient. It is clear
that the best way to avert such error is often to
task throughout the entire four-plus minutes of the
test, with a task that is both appropriate as well as
sufficiently difficult.
Finally, because the peak response is fundamentally the strongest part of the nystagmus
response, it may be subverted by blinks and spurious data points that obscure and often inflates
the correct identification of the “true” peak VOR
response. Every effort should be made by the clinician to obtain as clean data as possible throughout the entire test.
Certainly, analyzing step results take great
care and scrutiny. The response analysis algo-
rithms are only as good as the program (or analysis filters) permit them to be. Each response must
carefully be examined and the programming
filters adjusted accordingly to ensure accurate
and reliable results. Each rotational device and
associated software will have its unique aspects
of analysis that will often require a keen eye
and experienced clinical judgment to determine
the validity of the results. Take for example Figure
7–22. This example illustrates an extreme case
of intrusive noise within the response recording.
Upon careful examination (panel C) it is evident
that a slow-phase eye velocity response exists and,
moreover, there appears to have a vague collection of slow-phase velocity data points that seem
to approximate a decaying nystagmus (panel A).
The clinical challenge, however, is determining
how to validate these data to ensure a reliable
result and interpretation. Retesting this was likely
not an option, as this origin of this noise was secondary to poor eye tracking due to significant blink
artifact and mascara (although EOG recordings
could be performed). Figure 7–23 depicts a more
FIGURE 7–21. Example of a “blunted” VOR peak response during a 60°
rightward acceleration step stimulus, due to either inappropriate tasking
or inadequate tasking. The VOR slow phase eye velocity peak response
should occur during or immediately post completion of the acceleration (or
deceleration) stimulus. In this example, the peak response occurs at approximately 11 seconds, which is approximately 10 seconds post completion of
the rightward acceleration stimulus. It is likely the peak response may have
exceeded the −28.38°/sec if the appropriate tasking was conducted. As a
result, these data should be interpreted with significant caution.
A
B
FIGURE 7–22. Example
illustrating a 60° step test marked
by an extreme degree of ocular
noise. A. Represents the entire
step response for all four-response
intervals. B. Represents a
magnified view of only the right step
acceleration interval. C. Represents
only the initial 6.5 seconds of the
rightward acceleration interval.
A gross decay of the response can
be “visualized” for each interval (A),
however, the extraneous noise must
be isolated if the slow phase velocity
best-fit line is to be determined.
This noise was due to eye tracking
“scatter” related to mascara as
well as significant blink artifact.
Response nystagmus can clearly be
seen within the noise (C).
C
234
7. Velocity Step Testing 235
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A
B
FIGURE 7–23. Example illustrating the effect of noise on the determina-
tion of the peak slow-phase eye velocity and the calculation of the time
decay slow phase eye velocity plot in response to a leftward acceleration
during a 60°-step test. A. Shows an incorrect peak slow phase velocity of
53.05°/sec and an erroneous prolongation of the time decay constant to
23.68 seconds. B. Shows the correct peak slow phase eye velocity immediately post leftward acceleration of 38.79°/sec and the correct time decay
constant of 12.72 seconds after the raw data have been cleaned and all
appropriate noise has been deleted.
common example of noise impacting a 60° step
response. This example of leftward acceleration
depicts an uncorrected 60° step velocity response
versus the same data that have been “cleaned.”
The peak slow phase eye velocity point has been
correctly identified and the extraneous noise has
been appropriately deleted from the analysis. In
the corrected response panel (B), the slow phase
236 Rotational Vestibular Assessment
eye velocity best-fit line intersects nicely with the
slow phase eye velocity data. Finally, the corresponding time constants are shown for each step.
What Is a Normal Time Decay Constant?
We have already discussed that the persistence
of the VOR response beyond that of cupular
mechanics has been attributed to the velocity
storage mechanism (Curthoys & Halmagyi, 1996;
Highstein, 1996). The fundamental question, however, is how much longer is the velocity storage
mechanism expected to propagate the response
beyond the 4 to 7 seconds provided by the viscoelastic properties of the cupulae? The velocity
storage mechanism extends the peripheral cupular time decay response to an average of 14 to 16
seconds (Goulson, McPherson, & Shepard, 2016).
However, the consensus for a normal time decay
reference range (±2SD from the mean) across
studies is between 10 to 30 seconds (Baloh &
Honrubia, 2001; Brey et al., 2008b; Shepard et al.,
2016). Therefore, time decay constants that are
below 10 seconds are usually considered abnormal. Figure 7–24 depicts an abnormal 60° step
velocity response. This example illustrates the
sharp decline of the nystagmus response down to
5 to 7 seconds, which is no more than the time
decay provided by simple cupular mechanics
alone. That being said, the answer to the question
of how much longer is the velocity storage mechanism expected to propagate the response beyond
the 4 to 7 seconds provided by the viscoelastic
properties of the cupulae, is approximately 3 seconds. Both peripheral and central pathologies can
negate this 3-second propagation and shorten the
time constant below 10 seconds. Conversely, the
prolongation of time constants greater than 30 seconds is less understood and largely agreed upon
to be secondary to central pathologies.
TC
TC
TC
TC
FIGURE 7–24. Abnormal (corrected) 60°/
sec velocity step test results. Abnormally
shortened decay time constants are identified for each stimulus interval. Notice the
sharp decline of each decaying nystagmus
in the slow phase eye velocity plots. TC =
One Time Constant.
7. Velocity Step Testing 237
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Relationship Between Velocity Storage
and the
We have discussed how the propagation of the
VOR response beyond the 4 to 7 seconds provided
by the viscoelastic properties of the cupulae is secondary to an intact velocity storage mechanism.
We also know that one of the primary disadvantages of the vestibular system is its ability to integrate sustained rotational accelerations. Cupular
mechanics, as well as the sharp onset and offset of
the vestibular afferents, are ideally situated to detect
transitory accelerations such as brief head turns encountered during daily life activities. The sustained afferent drive that accompanies sustained accelerations, causes a temporary “unrelenting” influx
of afferent input to the central vestibular nuclei
that far exceeds the required amount needed to
drive the VOR. As a result, the solution is to simply “store” the afferent vestibular drive centrally
and dispense it over time, hence the propagation
and prolongation of the VOR response beyond
cupular mechanics and the afferent drive.
input is mediated by the velocity storage mechanism and the neural integrator. This process actually helps to explain the reason for the significant
reduction in the time decay constant below 10
seconds following either a peripheral or central
vestibular lesion. A reduction in the peripheral
response secondary to a peripheral vestibulopathy (e.g., vestibular schwannoma) would certainly
reduce the amount of afferent input and subsequent recruitment of velocity storage. Similarly,
a central pathology could affect the velocity storage mechanism’s ability to effectively store the
“unrelenting” afferent input and inappropriately
“release” the stored neural response as quickly as
it is received. This would also serve to reduce the
decay time constant to that of cupular mechanics alone (<10 seconds). Therefore, both a peripheral and central pathology has the potential to
reduce the time decay constant below the lower
10-second limit.
cause a significant prolongation of the decay time
constant. In such cases, a central pathology can
inadvertently cause the velocity storage mechanism to get “hung up” on itself and create a pro-
Time Decay Constant
The “storing” of this “unrelenting” afferent
Conversely, a central pathology could also
longation in the neural integrator’s “feedback
loop.” As a result, the “release” of neural response
is appreciably extended, and perpetuation of the
VOR is significantly longer than the upper limits of the normal velocity storage propagated
response (>30 seconds). Although this is uncommon, such prolongations in the VOR decay time
constant have been suggested to be secondary to
central pathology (Brey et al., 2008b).
These concepts are further illustrated in
Figure 7–25. Let us first consider how a normal velocity storage mechanism manages step
stimuli. By conceptualizing the afferent neural
input as “incoming water” into a central neural
“storage bucket,” the bucket quickly fills up in
response to the “unrelenting” step stimuli, as the
outflow needed to drive the VOR is significantly
less than the high neural input being supplied
by the prolonged acceleration step stimuli. This
is not the case with SHA testing, as the degree of
acceleration is either constantly changing, is sig-
2
nificantly less than 200°/sec
are too brief
— which is also the reason that brief
, and/or the stimuli
head movements during daily life activities do
not follow this model. During a peripheral lesion,
the afferent neural drive (incoming water) to the
central storage neural integrator (“bucket”) is
significantly reduced and more closely matches
the outflow required to move the ocular motor
system, hence no central storage is needed, and
a significant reduction in time decay constant
is documented to be no longer than cupular
mechanics alone (Figure 7–25B). Finally, during a
central lesion, either the outflow of incoming neural activity is not “maintained” and the increased
afferent drive during a step stimuli is released as
quickly as it comes in (which can often produce
a subsequent high, “uncontrolled” VOR gain), or
the neural outflow is released too slowly and the
VOR is subsequently extended beyond the normal
storage time (i.e., time constants greater than 30
seconds) (Figure 7–25C).
Relationship Between VOR Phase
and the Time Decay Constant
If you recall our discussion regarding VOR phase
during SHA testing, the fundamental component
that is responsible for the observed low frequency
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