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204 BALANCE FUNCTION ASSESSMENT AND MANAGEMENT
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table 10–4. Normative Data
Age 20–49 Years
0.2 0.3 0.4 0.5 0.61 0.71
Gain L 0.82
0.42–1.22
Gain R 0.85
0.45–1.25
Phase −0.36
6.36–5.64
Age 50–69 Years
0.2 0.3 0.4 0.5 0.61 0.71
Gain L 0.86
0.56–1.16
Gain R 0.83
0.53–1.13
Phase −0.4
6.40
Age 70–79 Years
0.2 0.3 0.4 0.5 0.61 0.71
Gain L 0.90
0.68–1.12
Gain R 0.87
0.59–1.15
0.84
0.64–1.04
0.84
0.58–1.1
−0.13
4.13–3.87
0.82
0.60–1.04
0.84
0.56–1.12
−0.79
4.79–3.21
0.82
0.60–1.04
0.85
0.65–1.05
0.82
0.62–1.02
0.87
0.67–1.07
−0.25
4.25–3.75
0.82
0.58–1.06
0.80
0.56–1.04
−0.89
4.89–3.11
0.75
0.45–1.05
0.8
0.6–1.00
0.83
0.63–1.03
0.82
0.62–1.02
−1.85
7.85–4.15
0.78
0.50–1.06
0.76
0.40–1.12
−2.38
8.38–3.62
0.7
0.34–1.06
0.7
0.4–1.00
0.72
0.32–1.12
0.78
0.52–1.04
−2.36
8.36–3.64
0.69
0.39–0.99
0.73
0.43–1.03
−5.06
13.06–2.9
0.63
0.27–0.99
0.68
0.46–0.9
0.71
0.37–0.95
0.73
0.39–0.97
−4.72
12.72–3.2
0.61
0.27–0.95
0.66
0.32–1.00
−7.89
17.89–2.1
0.48
0.08–0.88
0.5
0.24–0.76
Phase 0.13
3.87–4.13
Age 80–89 Years
0.2 0.3 0.4 0.5 0.61 0.71
Gain L 0.77
0.49–1.05
Gain R 0.83
0.57–1.09
Phase −0.49
4.29–3.32
−0.01
3.81–3.79
0.81
0.61–1.01
0.8
0.5–1.1
−2.64
−12–6.8
−1.4
−6.8–4.0
0.76
0.54–0.97
0.71
0.39–1.03
−2.3
−6.3–1.7
the actual gain is manufacturer specific. As noted in the
leftmost plots in the second and third panels of Figure
10–11, the stippled region represents the age-related
low range of normal (two standard deviations below
the mean) for persons 49 years old.
Asymmetry, shown in the middle plot of panels
2 and 3 in Figure 10–11, is simply the percentage dif-
−2.32
−10.3–5.7
0.7
0.54–0.96
0.61
0.31–0.91
−4.07
−14.1–5.9
−4.2
−11.4–3.0
0.61
0.27–0.95
0.63
0.29–0.97
−7.8
−15.8–0.2
−3.7
−12.7–5.3
0.6
0.38–0.82
0.6
0.23–0.87
−8.9
−20.9–3.1
ference for velocity gain for the right or left eye moving rightward and leftward. This provides a means to
indicate asymmetric performance in smooth pursuit
tracking for rightward versus leftward eye movements.
Phase angle, the third parameter, provides a measure of how much the eye is lagging or leading the
target. In general, given the instructions to follow or
10. EYE MOVEMENT RECORDING AND OCULAR MOTILITY TESTING 205
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figure 10–11. Smooth pursuit analysis shown is from a 49-year-old female being evaluated for possible vestibular
neuritis event.
of the three frequencies tested; 0.2, 0.4, and 0.6 Hz.
peak excursion of the target at 15° subtended arc.
gain, asymmetry in velocity gain in percentage, and phase angle between the target movement and the eye
movement in degrees each as a function of frequency of the target, as seen from left to right (refer to the text for
an explanation of the parameters).
The top panel shows the left eye raw movement and the right raw eye trace, superimposed for each
The testing was done using a video-recording system with the
The second and third panels provide the analysis for velocity
The second panel is for the left eye whereas the third is for the right.
track the target, it is expected that the eyes will be in
phase with the target or be minimally lagging behind.
Patients who consistently lead the target do so with
saccadic movements and usually do not understand
the task requested of them.
Sinusoidal Target
This represents the most commonly used method for
testing smooth pursuit tracking abilities. The target is
presented via a light bar or projection system moving
with a sinusoidal trajectory (see Video 10–3). The peak
excursion of the target would be fixed between 15 and
20 degrees of subtended arc movement to either side
of center. The excursion is maintained the same and
the frequency of the target is varied between 0.2 and
0.6 Hz, thereby increasing the difficulty of the task. It
is suggested that subtle abnormalities may be detected
by increasing the task difficulty to evaluate the smooth
pursuit system across its full physiologic range. However, in doing such and given the age effect on smooth
pursuit, it is critical to have age-sensitive normative
data to prevent false-positive identifications of pathology that actually represent degraded performance secondary to age alone. It is this paradigm that typically
uses some version of the three major analysis parameters in interpretation.
Fixed-Velocity Pursuit
For some patients the sinusoidal movements of a target
produces nausea, which results in poor performance
or inability to complete the task. An alternative is the
fixed-velocity smooth pursuit task. In this paradigm
the target can be presented moving left to right (or the
reverse) at a speed of 20 to 40 deg/s. Each target traverses the light bar or is within the video projection
field and a new target is presented at the same speed
and in the same direction. After several samples, the
direction is reversed at the same speed. The alternative
to constant direction is to use a triangular waveform to
produce the stimulus target movement. In this case the
target moves left to right and then reverses back right
to left. Be aware that, as the target makes a sudden stop
and sudden change in direction, smooth pursuit performance will be less than perfect, as the smooth pursuit
system does not handle abrupt changes without introducing a saccadic eye movement to track the target.
To increase the sensitivity of the test to more subtle
abnormalities, the speed is increased up to 40 deg/s.
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Speeds up to 70 deg/s are possible but the smooth
pursuit tracking system’s performance is significantly
poorer at these high speeds (Meyer, Lasker, & Robinson, 1985). As in the sinusoidal task, age-sensitive
normative data for each of the speeds tested should be
available for testing. The analysis in this situation is significantly simpler, as it is just the eye velocity divided
by the target velocity that produces the gain value.
Interpretations of Smooth Pursuit Tracking
The principal parameters for interpreting smooth pursuit tracking are paradigm specific. The most widely
used protocol is the predictable sinusoidal or fixedvelocity target movement. For this type of paradigm,
the velocity gain and phase of the eye movement with
regard to the target are used for the sinusoidal target,
with velocity gain as the main factor when using fixedvelocity stimuli. As with other ocular motor tasks,
these parameters are highly susceptible to the state
of the subject, but unlike gaze stability and saccades,
smooth pursuit tracking is the task most sensitive to
age. Data demonstrating the effects of age on various
aspects of smooth pursuit are available in the literature
(Paige, 1994; Spooner, Sakala, & Baloh, 1980; Zackon &
Sharpe, 1987).
The neurologic substrate (for a complete description, see the discussion in Chapter 3 of this volume)
for the generation and sustaining of accurate smooth
pursuit tracking starts with retinal stimulation and
involves multiple areas of the cortex with projections
through the pontine area of the brainstem to the cerebellum and onto the nuclei of the extraocular muscles.
These pathways are suggested from both primate and
human studies (Berman et al., 1999; Leigh & Zee, 2006).
The complexity of the multiple pathways and the various contributions of the individual components make
specific site-of-lesion identification within the pathways difficult at best, even when multiple protocols
are used to investigate patient performance.
No specific differentiation in lesion site has been
determined when comparing reduced velocity gain
for sustained target presentation at fixed velocity versus changing velocity stimuli of the sinusoidal target.
Lesions could involve large cerebral infarcts, basal
ganglia regions, pontine projection pathways to the
cerebellum, and various areas of the cerebellum (Leigh
& Zee, 2006). The principal region of the cerebellum
involved in the production of smooth pursuit eye
movements is that of the paraflocculus of the vestibulocerebellum (Rambold, Churchland, Selig, Jasmin, &
Lisberger, 2002). The dorsal vermis of the cerebellum is
involved in the initial movement of pursuit during the
onset of the task (open-loop period) but does not seem
to participate in the steady-state aspects of the performance seen with fixed-velocity or sinusoidal (increasing acceleration) protocols (Takagi, Zee, & Tamargo,
2000). Therefore, although there are numerous other
neurologic substrate contributions to various aspects
of the performance of pursuit contingent on the specific
task, the vestibulocerebellum is a common final pathway that is always involved in the production of the
eye movements. Even though it is a significant oversimplification, an interpretive suggestion is that persistent abnormalities of pursuit using sustained target
tasks may relate to lesions in the vestibulocerebellum
(especially with coexisting gaze-evoked nystagmus) or
the immediate projection pathways from the pontine
nuclei of the brainstem. One must always be cognizant of the other pathway possibilities that could be
involved in pursuit disruptions.
The use of the phase parameter for sinusoidal
target tasking is a measure of the temporal arrangement between target and eye movements. In general,
at younger ages the phase angle should be close to zero
for properly performed smooth pursuit. As we age or
as the task becomes more difficult, by increasing the
frequency of target movement the phase lag becomes
more apparent. A leading phase is not usually taken
as an indication of pathologic activity but rather as
anticipatory behavior on the part of the patient. The
leading could be anxiety regarding the testing situation
or simply a lack of understanding the task. Most often
this is corrected with reinstruction of the patient and
repeating of the task. It is typical that reduction in gain
will be seen with abnormal phase lag. However, when
the phase lag is outside the normal range with velocity gain normal and reinstruction and repeated testing
does not remove the abnormality, possible central system involvement should be considered but it would be
less likely to involve the dorsolateral pontine nuclei or
the vestibulocerebellum (Leigh & Zee, 2006).
Pursuit disruptions can be bidirectional or unidirectional. When asymmetric gain is encountered,
lesion sites can again range from the cortex to the pontine nuclei and vestibulocerebellum. In most cases, the
pursuit abnormality is toward the lesion side due to a
double decussation between the cortex and ocular motor
nuclei. The magnitude of the gain disruption is usually
greater for lesions in the lower system pathways versus lesion in the cortex (Leigh & Zee, 2006). Video 10–4
and Figure 10–12 demonstrate asymmetrical pursuit
in a 20-year-old male with indications of cortex and
10. EYE MOVEMENT RECORDING AND OCULAR MOTILITY TESTING 207
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figure 10–12. The top panel shows the target and the recorded eye movements for the right eye from a
20-year-old male following a severe closed head injury accident.
analysis for the eye movements shown in the top panel and
the average performance over several cycles of the target movement with the small black dots the velocity
gain for an individual cycle. All are shown as a function of frequency of target movement for a fixed target
excursion of 20 degrees to each side of center.
See the text for discussion of the asymmetry.
right.
Note the significant asymmetry in performance for left versus
subcortical involvement resulting from a closed head
injury accident. The eye movements demonstrate classic saccadic disruptions to the attempt to move the eyes
in a smooth manner when tracking the light bar target.
This is referred to as “cog wheeling” pursuit. Note that
the performance of the pursuit worsens for leftward
movements yet improves for rightward movements
as the frequency of the target increases. The analysis
of his eye movement shown in Figure 10–12 brings up
the question as to whether pursuit is interpreted as
abnormal when performance at the lower frequencies
is abnormal, yet as the difficulty of the task increases
the performance returns to the normal region as shown
Video 10–4. In the analysis the larger gray dots are
frequencies yet normal performance at the more rapid
movements? It would take comparisons of fixed-velocity paradigms and the accelerating target paradigm (as
used in this example) to suggest that situation (Leigh &
Zee, 2006). However, in most situations, if the sinusoidal pursuit returns to a normal range as the frequency
of the target for a fixed excursion is increased, the study
is taken as normal, especially when the performance is
symmetrical. Video 10–6 demonstrates pursuit abnormality that is strictly unidirectional with no abnormal
performance to the right as a contrast with the example
in Video 10–4. The quantitative analysis for this video
is shown in Figure 10–13.
for eye movement to the right in Figure 10–12. Could
it be possible to have lesions in areas other than the
cerebellum that may cause abnormalities at the lower
head injury and diagnosed traumatic brain injury.
Video 10–7 demonstrates abnormal pursuit that is
The bottom panel gives the quantitative
The patient is a 33-year-old male with a closed
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Figure 10–13. Quantitative analysis for the eye movements shown in Video 10–6 from a 33-year-old male with
diagnosed traumatic brain injury.
in the analysis panel.
asymmetric pursuit performance in Figure 10–12, suggesting possible abnormalities in both directions of different magnitudes.
Note that this analysis shows strictly unidirectional pursuit disruption compared to the
See the legend for Figure 10–12 for an explanation of the symbols shown
bidirectional and symmetric. This is from the 46-year-old
female with diffuse brainstem and cerebellar involvement secondary to alcohol abuse. The quantitative analysis for her eye movements is given in Figure 10–14.
There can be interactions between saccade performance and that of smooth pursuit that can give the
appearance of unidirectional pursuit abnormalities
that is a false positive. This is illustrated in Videos 10–8
and 10–9. These videos show random saccade performance (see Video 10–8) followed by smooth pursuit
performance (see Video 10–9) in a 52-year-old female
with multiple sclerosis. As can be seen in Video 10–8,
the patient is displaying bilateral INO with significant
slowing of each eye on adduction. Therefore, when
viewing her performance for smooth pursuit, it would
appear that as each eye adducts with the pursuit task,
the eye is moving smoothly while the abducting eye
has a saccadic appearance. The smooth movements of
each eye on the pursuit task for adduction are a result
of the effects of the INO causing saccades to not be produced, as is seen when abducting movement is made.
It is the combination of the INO and the central system lesion to the pursuit neuro-substrate that gives the
appearance of unidirectional pursuit abnormality.
tral brainstem/cerebellar lesions, whereas abnormalities in gaze stability can occur from either a central or
peripheral vestibular system lesion. Criteria for differentiating between central and peripheral lesions are
discussed below.
Technical Considerations
Filter settings and sampling rates would be the same
as that for smooth pursuit tracking, and usually individual eye recordings would not be necessary. However, if one eye is observed with a visual occluding
camera while the other has vision, a form of nystagmus known as latent nystagmus (jerk nystagmus that
has its fast component away from the occluded eye)
can result from an ocular misalignment, specifically
that of congenital strabismus, most likely esotropia,
(Dell’Osso, Ellenberger, Abel, & Flynn, 1983) and may
not be representative of either a peripheral or a central
lesion. Because of this, when using a video system with
a single visual occluding camera, it is always best to
check gaze stability with both eyes viewing the target
prior to the formal recording of gaze stability.
Parameters for Analysis
Gaze Stability Testing
This evaluates a patient’s ability to maintain gaze on a
target in primary position or eccentric positions (right,
left, up, or down) in a steady manner without the production of eye movements, principally jerk nystagmus,
or presence of saccadic intrusions. The sole purpose of
saccade and pursuit testing is the identification of cen-
In the majority of abnormal gaze stability, the type of
eye movement is that of jerk nystagmus. If the nystagmus is persistent in primary gaze, it is referred to as
fixation present spontaneous, designating the direction
of the beat, and one can give the average slow component velocity. When jerk nystagmus is noted in any
of the eccentric positions, it is referred to as fixation
present gaze-evoked nystagmus, again designating the
figure 10–14. Quantitative analysis for the eye movements from the 46-year-old female shown in Video 10–7.
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Shown are the sample recordings for both the right eye in the upper panel and the left eye in the lower panel.
The quantitative analysis for each eye is shown below the eye tracings. See text for further information and
Figure 10–12 legend for explanation of the symbols on the figure.
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direction of the fast component. A specific nomenclature is used when nystagmus is horizontal and direction fixed. Designation as to fixation present or fixation
removed is made along with an indication as to the
direction of the nystagmus beat. Next, it is indicated
whether the nystagmus was present when gazing only
in the direction of the fast component (first degree), in
the direction of the fast component and in primary (second degree), or in the direction of the beat, primary,
and while gazing away from the beat of the nystagmus
(third degree). Last, it is indicated whether the nystagmus followed Alexander’s law (see Chapter 3 for a full
explanation) — if it follows Alexander’s law, the nystagmus will increase in its briskness (slow component
velocity) as the gaze is directed further in the direction
of the fast component of the nystagmus). For example,
the phrase “third degree, left-beating gaze evoked nystagmus with fixation present following Alexander’s
law” implies a left-beating nystagmus that is present
with fixation when the individual is looking at a target to the right, primary, and left, and the nystagmus
increases in intensity as the gaze is shifted toward
the direction of the fast component, to the left. In all
other situations, when nystagmus changes direction or
another nonjerk nystagmus eye movement is noted, a
verbal description of those movements is required.
Although these are descriptive techniques instead
of quantitative analysis as used for saccades and
smooth pursuit, they are adequate for the analysis of
gaze-stability testing, as the primary focus is the presence or absence of abnormal eye movements. This is
especially true when one encounters saccadic intrusions,
although some minor analysis of the eye movement
recording may be needed to distinguish between certain
forms of saccadic intrusions (see discussion below).
Protocol
Gaze stability testing is usually performed first with
fixation present using a target in the primary position.
The target is then moved 25 to 30 degrees (this would
be considered the minimum subtended arc movement
to elicit gaze-evoked nystagmus) to the right, left,
up, or down. If the subtended arc movement exceeds
degrees laterally or up, the possibility of physi-
30
ologic endpoint nystagmus is increased. However,
physiologic endpoint nystagmus is not persistent when
fixation is present, decaying to stable eye movement
typically within seconds (Leigh & Zee, 2006). Between
each of the eccentric gaze positions, it is important to
return to the primary position to observe for rebound
nystagmus (a jerk nystagmus that beats in the direction
of the last movement of the eyes). Each of the positions
(primary, eccentric, and primary for rebound) should
be held for at least 10 s to observe for nystagmus. Avoid
prolonged eccentric gaze (>1 min) as that can produce
a rebound nystagmus in normal subjects (Leigh & Zee,
2006). In all positions, other than testing for rebound,
the nystagmus, if seen, should be persistent; rebound
nystagmus will decay. Following gaze stability with
fixation present, it is repeated with fixation removed,
asking the patient to gaze straight ahead, then to the
right, left, up, and down, each time returning to center
between each of the eccentric positions. It is not necessary to try and control the position of the eccentric eye
locations laterally or up or down. Some patients will
move the eyes to the extreme in the lateral directions,
and this may produce physiologic endpoint nystagmus
that without a visual target can be persistent. This is
recognized by the following features: (1) the nystagmus is symmetric looking to the right or left; (2) it is
of typically low slow component velocity (<5 deg/s);
and (3) there was no persistent nystagmus in the visual
fixation present condition. If these characteristics are
noted, then the nystagmus may be written off as physiologic endpoint and ignored in the interpretation.
Interpretation of Gaze-Stability Testing
Of the four routine ocular motor tests, this is the only
one in which lesions of either the peripheral or central vestibular and ocular motor systems can produce
abnormalities. Therefore, it is best to lay out distinguishing and contrasting features that will allow for
this peripheral versus CNS differentiation. Therefore,
we start with spontaneous nystagmus that is typically
seen in primary (straight-ahead gaze) that is direction
fixed. In other than during acute onset (within the first
72 hr) of symptoms, this nystagmus is seen only with
fixation removed. This nystagmus then continues with
the fast component in the same direction with gaze in
eccentric directions. Because this nystagmus is seen
without provocation of eccentric gaze, it is referred to
as spontaneous nystagmus. The principal abnormality
noted in gaze stability testing would be the development of nystagmus or another repetitive eye movement
in place of steady fixation. When it is jerk nystagmus
and seen only on eccentric gaze, the abnormality is
referred to as gaze-evoked nystagmus. The general
characterizations of spontaneous and gaze-evoked
nystagmus of peripheral origin are given in Table 10–5;
characterizations associated with gaze-evoked nystagmus of central origin are given in Table 10–6 (Leigh
& Zee, 2006). Although all of the characteristics listed
can be observed, the dominant ones for determining
that the gaze-evoked nystagmus is of peripheral origin
table 10–5. Characteristics of Gaze-Evoked Nystagmus of Peripheral Origin
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• Acute lesion — in a peripheral lesion nystagmus is usually only visible with fixation
present when the lesion is acute in nature.
Direction-fixed — nystagmus with fixation present or absent should be direction
•
fixed in nature with the patient sitting, head in primary position. (
direction may vary when testing positional and be of peripheral origin.)
have both horizontal and vertical components but must have a horizontal
component to be considered of peripheral origin
nystagmus is taken as central until proven otherwise (see text for explanation).
Alexander’s law — the horizontal nystagmus should follow Alexander’s law; that
•
is, the nystagmus increases in its intensity as the patient gazes further in the
direction of the fast component of the nystagmus (this applies to horizontal
nystagmus component only).
•
Enhanced with fixation removed — this is the primary determiner of the periphery
being the source of the nystagmus. When fixation is removed nystagmus is
brought forth when absent with fixation or nystagmus intensity increases if it was
seen with fixation present.
Nystagmus enhanced with head-shake test — if ongoing direction fixed
•
nystagmus of peripheral origin is present, it can usually be enhanced with
head-shake testing
• Linear slow component — on the tracing of the nystagmus the slow component is
a linear trace (straight line).
— that is, pure vertical
Nystagmus
May
table 10–6. Characteristics of Gaze-Evoked Nystagmus of Central Origin
• Acute or chronic — when nystagmus is seen with fixation it can be from an acute
or chronic (beyond 12 weeks) lesion.
onset without any significant diminution in intensity with time.
• Direction-fixed or changing — although the nystagmus could be direction fixed in
nature such as pure up or down beat it is likely to be direction changing based
on the direction of gaze; that is, right beat with right gaze, left beat with left gaze,
and so on.
With rebound nystagmus the direction of the beat is always in the last direction
that the eye moved. Also, pure vertical or pure torsional nystagmus even though
direction fixed is taken as indicative of central involvement until proven otherwise.
• Rarely in primary — it is rare to have horizontal nystagmus persist in the primary
(straight ahead) gaze position (can be there for a brief interval when rebound
is present and returning from eccentric gaze). Pure vertical or pure torsional
nystagmus can persist in the primary gaze position with central involvement.
• Enhanced with fixation present — typically, nystagmus is increased in its intensity
with fixation present and no change or a reduction in the nystagmus is seen
when fixation is removed.
•
Vertical nystagmus post-head-shake test — it would be unusual to see horizontal
nystagmus enhanced with horizontal head shake when the nystagmus is of
central origin only. It is possible that following either a horizontal or vertical headshake test the nystagmus produced is that of pure vertical when a central lesion
is the source of the nystagmus.
This also applies to a form of nystagmus called “rebound” nystagmus.
The nystagmus persists following the lesion
• Decreasing speed of slow component — the horizontal nystagmus trace many
times will show a slow component that is nonlinear implying a slowing in the
speed of the eye as it moves from an eccentric horizontal position toward the
primary gaze position.
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are the enhancement in the nystagmus in the same
direction with fixation removed, direction-fixed nature
obeying Alexander’s law, and post-headshake testing (although this can be seen in cerebellar lesions, it
is rare, and sensitivity/specificity for identification of
peripheral lesion is 30%–35%/90%–95%; see Chapter 9
text for a complete discussion). For gaze-evoked nystagmus of central origin, the dominant characteristic is
that of direction-changing, pure vertical, or pure torsional nystagmus.
Video 10–10 demonstrates these features for a
peripheral lesion. The patient is a 77-year-old female
with the diagnosis of vestibular neuronitis. She has a
documented severe right peripheral hypofunction via
head thrust direct examination and caloric irrigation
testing during her laboratory evaluation. Her smooth
pursuit tracking and saccade testing are all within normal limits. In the video, she is seen with just a hint of
first-degree (seen only when gazing in the direction of
the fast component), left-beating, gaze-evoked nystagmus with fixation present. When fixation is removed,
she develops second-degree (seen when gazing in the
direction of the fast component and in center gaze),
left-beating gaze-evoked nystagmus. Both with and
without fixation, her nystagmus follows Alexander’s
law. Alexander’s law, simply stated, indicates that nystagmus will increase in its slow component velocity as
gaze is directed farther in the direction of the fast component of nystagmus, a result of an uncompensated
peripheral asymmetry (Kasai & Zee, 1978). Finally,
the headshake test is given, and her post-headshake
nystagmus is a third-degree (seen when gazing in the
direction of the fast component, center gaze, and when
gaze is directed away from the fast component), leftbeating, gaze-evoked nystagmus again following Alexander’s law.
In contrast, Videos 10–11A and 10–11B shows rightbeating nystagmus on gaze right (Video 10–11A) and
left-beating on gaze left (Video 10–11B). These are eye
movements recorded during the patient’s VNG testing. She was a 46-year-old female with diffuse cerebellar and brainstem involvement secondary to prior
long-term alcohol abuse. In this case, when fixation is
removed (not shown in the video), gaze-holding abnormalities continue, but there is no enhancement of the
nystagmus.
Gaze-evoked nystagmus can be produced for
gazes right and left, as shown in Videos 10–10 and
10–11, as well as up and down. Video 10–12 demonstrates abnormal gaze holding on up gaze for the same
patient in Video 10–11A and 10–11B. Figure 10–15
shows tracings from a VNG of a 54-year-old male with
multiple sclerosis. In the figure, no nystagmus is noted
in primary (center) gaze; however, on up gaze a persistent up-beating nystagmus is seen and no nystagmus on down gaze. This patient also has gaze-holding
deficits when gazing to the right and left, as shown in
Figure 10–16.
figure 10–15. Gaze recordings of a male 54-year-old patient with multiple sclerosis. Each of the panels present the
horizontal (upper half ) and the vertical (lower half ) video eye movement recordings. The panel on the left is gaze
in primary position. The panel in the center shows results from gaze up with the panel on the right representative of
results for gaze down. In the center panel the horizontal trace (upper half ) shows several eye blinks indicated by
the large asymmetric sharp downward excursions of the trace. No persistent horizontal nystagmus is noted. In the
lower half of the center panel a vertical up-beat nystagmus is noted. No horizontal or vertical nystagmus is seen
for primary or down gaze tracings.
10. EYE MOVEMENT RECORDING AND OCULAR MOTILITY TESTING 213
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figure 10–16. Gaze recordings of a 54-year-old male patient with multiple sclerosis. The top two panels give the
horizontal and vertical eye movement traces during gaze right, right-beating nystagmus (panel on top left ), and
the resulting nystagmus on return to center gaze, left-beating nystagmus (panel on top right ). In each panel the
top trace is the horizontal eye movement and the bottom trace is the vertical movement. The two bottom panels
give the same information for gaze left, left-beating nystagmus (bottom left ), and the nystagmus on returning to
center gaze from gaze left, right-beating nystagmus (bottom right ).
Prior to discussions of special forms of primary or
eccentric gaze stability abnormalities, consider the situation of pure vertical nystagmus noted in primary gaze
which is persistent with fixation present and removed.
Video 10–13 illustrates this type of nystagmus in the
form of pure down-beating nystagmus in primary gaze
that is exacerbated on lateral gaze but is persistent in
nature. The case from Video 10–13 is a female in her
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