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seventies with a diagnosed cervical cranial junction
abnormality (discussed further in the site-of-lesion section). Video 10–14 also shows this type of nystagmus
superimposed on a patient’s gaze-evoked nystagmus
on gazes left and right. The patient in Video 10–14 also
illustrates disrupted pursuit tracking. As fixation is
removed in the patient in Video 10–14, it is noted that
no change in gaze-evoked nystagmus intensity is seen,
another characteristic of gaze-evoked nystagmus of
central origin (see Table 10–6). However, an exacerbation in his vertical nystagmus with the headshake test
is seen (see Tables 10–5 and 10–6).
Is pure vertical down- or up-beating nystagmus
to be considered of peripheral or central origin? In
answering this question, it is useful to consider the specific eye movements that are provoked in a normal subject when each of the semicircular canals is stimulated
individually. The movements considered below are the
compensatory eye movement (slow component of nystagmus) and the VOR, when the canal in question is
stimulated, not the beat or fast component. The direction of the nystagmus is referenced to the left/right of
the subject’s (or patient’s) head frame of reference for
all forms of eye movement — horizontal, vertical, and
torsional. For torsional, the superior pole of the eye is
used as the point of reference to describe the movement
of the eye (see further description in Chapter 3):
n Horizontal (lateral) canals right and left —
VOR response would be to the left and right,
respectively.
n Anterior (superior) canals right and left —
VOR response would be up for both with a
torsional movement to the left for the right
canal and to the right for the left canal.
n Inferior (posterior) canals right and left —
VOR response would be down for both, with
a torsional movement to the left for the right
canal and to the right for the left canal.
Using the above descriptions of the VOR responses
for each of the canals, the only way to produce a downbeating nystagmus from the periphery would be with
simultaneous stimulation of both anterior canals. The
VOR response would be pure up, with the torsional
components canceling, and the beat would be down.
To have this happen via a pathological insult would
require that both anterior canals have simultaneous
irritative lesions or have simultaneous paretic lesions
of both posterior and horizontal canals. Currently,
there is only one condition that has been reported that
is a peripheral disorder known to produce at least transient pure down-beating nystagmus: bilateral superior
canal dehiscence (Deutschlander, Strupp, Jahn, Quiring, & Brandt, 2004). Otherwise, the likelihood of a
peripheral disorder capable of causing pure vertical
up- or down-beating nystagmus is so remote that pure
vertical nystagmus should be considered of central origin until proven otherwise. This same rationale may
be applied with the use of the specific individual canal
eye signatures to pure torsional (note that occasionally
posterior canal BPPV can appear with primary gaze
as pure torsional to the observer when visual fixation
is not removed but will have the vertical component
introduced with change in the direction of gaze away
from primary) and pure up-beating nystagmus (Leigh
& Zee, 2006).
Rebound Nystagmus. Another aspect of gaze-evoked
nystagmus of central origin is a feature referred to as
rebound nystagmus (Gordon, Hain, Zee, & Fetter,
1986). In this situation nystagmus is produced beating in the last direction the eye moved as the eye is
returned to primary position from eccentric gaze. The
Bárány Society has developed an International Classification for Vestibular Disorders (ICVD) in which definitions of nystagmus are given. For rebound nystagmus
the definition is: “Nystagmus appearing transiently
upon return to the straight-ahead gaze position after
sustained eccentric gaze, with the fast phases beating
away from the original direction of eccentric gaze”
(Eggers et al., in press). Even for a normal individual,
if the eccentric gaze is held for an extended period, one
or two beats of nystagmus may be visualized. What is
being tested for is a burst of nystagmus lasting several
seconds, with the fast component in the last direction of
movement of the eye (Hood, 1981). For example, if persistent gaze-evoked right-beating nystagmus is noted
on right gaze then on return to center a leftward eye
movement, a brief event of left-beating nystagmus is
seen that does not persist. Figure 10–16 illustrates this
for the diagnosis of multiple sclerosis in the patient.
The rebound nystagmus can be seen on return from
both right and left gaze.
Sites of Lesion. When gaze-evoked nystagmus is
direction fixed in character, follows Alexander’s law,
and is enhanced with fixation removed, it is considered
of peripheral origin most likely beating away from the
involved side. However, this is not always the case. The
nystagmus will certainly beat toward the more active
neural side, but that could be an irritative labyrinthine lesion, as seen in Ménière’s disease (Bance, Mai,
Tomlinson, & Rutka, 1991; McClure & Lycett, 1983).
Therefore, the presence of gaze-evoked nystagmus of
peripheral origin has two possible lesion sites, labyrin-
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thine hypofunction on the side away from the beat or
an irritative lesion on the side ipsilateral to the beat.
It will require further information from the patient’s
history and presenting symptoms together with other
tests and presenting signs to resolve the periphery
involved.
When the gaze-evoked nystagmus is of central origin by its characteristics, the possible lesion sites will
depend on whether the gaze-evoked nystagmus is in
a horizontal or vertical direction. The primary neurologic substrate responsible for maintaining binocular
horizontal gaze to the left or the right involves the
nucleus prepositus hypoglossi (NPH) and the medial
vestibular nucleus (MVN) (Leigh & Zee, 2006; McConville, Tomlinson, King, Paige, & Na, 1994; Sylvestre,
Choi, & Cullen, 2003). These structures would be ipsilateral to the direction of gaze and therefore one can
have gaze-evoked nystagmus during only left or right
gaze, suggesting a unilateral lesion in this region of the
brainstem. While these are the primary central structures in horizontal eccentric gaze, one must realize that
areas of the vestibulocerebellum (flocculus and paraflocculus) participate to enhance the neural integration
process in the brainstem needed for maintaining horizontal eccentric gaze (Zee, Yamazaki, Butler, & Gücer,
1981). The ability to move the eye in a saccade movement from primary to a left or right position requires a
different region of the brainstem (burst neurons of the
PPRF) (Van Gisbergen, Robinson, & Geilen, 1981).
Vertical gaze-evoked nystagmus during up or
down gaze suggests a different site of lesion. The primary region for neural integration during gaze holding
up or down is engendered by the interstitial nucleus of
Cajal of the midbrain (Fukushima, Kaneko, & Fuchs,
1992). However, this is not the only structure in the
midbrain that contributes to gaze holding, and lesions
in the cerebellum and brainstem can affect vertical
gaze holding (Leigh & Zee, 2006). The vertical gazeevoked nystagmus is most often seen in association
with horizontal gaze-evoked nystagmus with cerebellar flocculus/paraflocculus lesions secondary to the
loss of influence of the cerebellum on the horizontal
and vertical neural integrators (see full discussion of
these pathways in Chapter 3).
As discussed above, pure vertical or torsional nystagmus in primary position is to be considered of central
origin until proven otherwise. For up and down beats,
the most likely lesion sites are in the midline from the
low posterior fossa at the level of the pontomedullary
junction to the pontomesencephalic junction (Brandt
& Dieterich, 2000). For down-beat nystagmus, one of
the common causes would be craniocervical junction
pathology. This can be of a mechanical compression
form, as in Arnold–Chiari malformation, or from other
pathologies affecting the low posterior fossa, but most
commonly the vestibulocerebellum (Walker & Zee,
2005; Zee et al., 1981). In contrast, up-beating nystagmus is more likely to originate from the lower brainstem and medullary regions (Pierrot-Deseilligny &
Milea, 2005). The patient illustrated in Video 10–13 had
a mechanical compression of the midline pontomedullary region by the dens process secondary to a congenitally foreshortened C1 and severe progressive kyphotic
condition. It is important to realize that lesions in the
low posterior fossa that may produce pure down-beat
nystagmus may not disrupt other ocular motor functions such as horizontal saccades or pursuit, yet may
cause disruption in vertical especially downward pursuit from the down-beat nystagmus in paraflocculus
lesions. Therefore, on an ENG/VNG when pure vertical nystagmus is noted with or without fixation in a
persistent manner, such as during positional testing,
lesions of the low posterior fossa need to be ruled out.
In contrast to the pure vertical nystagmus of central origin, which is more likely from a midline lesion,
pure torsional in primary gaze and torsional with a
horizontal component as a form of gaze-evoked nystagmus of central origin are more likely to result from
a lesion that lateralizes to the right or left in the pontomedullary/medullary area ipsilesional or above the
pons contralesional (Brandt & Dieterich, 2000). With
two-dimensional ENG/VNG, pure torsional nystagmus will not be recognized and a combined torsion
and horizontal nystagmus (Video 10–15) will appear
as a diagonal nystagmus. On VNG the same printout
traces will result as with ENG, yet during testing the
examiner will be able to observe the actual eye movements and comment on such in the report. An example
of the pure torsion in primary gaze (right torsional
nystagmus) changing to a mixed right torsional nystagmus with right horizontal nystagmus on gaze right
is seen in Video 10–15. This female, in her forties, suffered a posterior inferior cerebellar artery (PICA) ischemic stroke on the right, resulting in a dorsolateral
medullary infarct producing the nystagmus noted in
the video. In this situation the nystagmus, both the torsion and the horizontal components, beat toward the
lesion side; however, this is not an irritative-style lesion
as referred to with a peripheral labyrinthine insult but
a possible complex combination of increased inhibition in the vestibular nucleus ipsilateral and decreased
excitation of the contralateral brainstem reticular formation (Solomon, Galetta, & Liu 1995). The final point
illustrated in the video is that of ocular-lateral pulsion
(Waespe & Wichmann, 1990). As shown when the fixation point in primary gaze is eliminated by having the
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patient close his or her eyes, the eyes deviate consistently toward the lesion side, to the right. This can be
seen on an ENG/VNG if recording is ongoing when
fixation is removed. This is shown in Figure 10–17 for
a 65-year-old male also suffering from a PICA distribution stroke event on the left.
It is also possible to have combinations of gazeevoked nystagmus of both peripheral and central origin. Videos 10–16A and 10–16B demonstrate a patient
with Bruns nystagmus (Bruns, 1908) in addition to a
persistent down beat during direct video examination.
Bruns nystagmus is commonly a manifestation of a cerebellar-pontine angle mass lesion or may be seen even
after resection of a mass in this region from damage
by the tumor to the labyrinth and the brainstem/cerebellum ipsilateral to the tumor. On gaze contralateral
to the tumor, a gaze-evoked nystagmus is seen that is
usually smaller in amplitude and higher in frequency
than the gaze-evoked nystagmus on ipsilateral gaze.
The gaze-evoked nystagmus to the contralateral side is
likely a result of an uncompensated peripheral vestibular hypofunction from the compressive effects of the
mass lesion. The gaze-evoked nystagmus on ipsilateral
gaze results from gaze-holding abnormalities from the
CNS damage (Leigh & Zee, 2006).
When fixation is removed, one can see the contralateral gaze nystagmus enhance, whereas the ipsilateral
gaze-evoked nystagmus remains unchanged, features
expected for gaze nystagmus of peripheral and central
origin (see Tables 10–5 and 10–6). The patient in Videos
10–16A and 10–16B had a Chiari malformation with surgical repair at age 15, resulting in the persistent downbeating nystagmus. At age 47, a vestibular schwannoma
was diagnosed on her left side. She underwent a tumor
resection procedure via a retrosigmoid approach with
preservation of VIIIth nerve function, as evidenced by
preserved hearing. In Video 10–16A, fixation is present
and she demonstrates a persistent down beat with a
large-amplitude, left-beating gaze-evoked nystagmus
on gaze left and small-amplitude, weak right-beating
nystagmus on gaze right. In Video 10–16B, fixation
has been removed and no change is seen in the downbeating or left-beating nystagmus, but the right-beating
nystagmus is significantly enhanced.
figure 10–17. The ENG horizontal and vertical eye movement tracing for a 65-year-old
male with a left-sided dorsolateral medullary distribution stroke. The top panel shows the
horizontal eye movements with the bottom panel demonstrating the vertical eye movement. As indicated by the arrow, the patient went from a lighted condition to a dark condition and had an immediate deviation of the eyes to the left returning to the center when
fixation was restored. His ocular lateral pulsion was noted during routine ocular motor
testing when changing from fixation present during gaze testing to fixation removed by
eye closure. From Practical Management of the Balance Disorder Patient by Shepard, N.
T., and Telian, S. A. Copyright © 1996.
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Saccade Intrusions and Oscillations. During the
execution of gaze testing, especially with primary gaze
evaluation, another group of abnormal eye movements
may be observed that are collectively referred to as saccadic intrusions and oscillations (Leigh & Zee, 2006).
These are seen with fixation present and when seen
are suggestive of cerebellar and/or brainstem involvement. Characteristics of each of these eye movements
are described below in the section on “Infantile Nystagmus.” Associated video examples are provided for
the eye movements described. It is important to realize that during the execution of an ENG/VNG, the
larger-amplitude movements in this grouping may
well obscure other spontaneous or positional nystagmus. However, the recognition of these movements as
something other than “random eye noise” is critical in
the evaluation of the patient’s condition. None of the
saccadic intrusions or oscillations is a result of peripheral system involvement, although square-wave jerks
and voluntary flutter are both seen in normal subjects.
Therefore, when identified, the implication is involvement in the brainstem and/or cerebellar region. The
reader desiring a more in-depth discussion of each of
these, including pathogenesis and treatments for the
conditions, is referred to Leigh and Zee (2006) and Eggers et al. (in press).
Square-Wave Jerks. These are the 0.5- to 5-degree
subtended arc movements in a direction away from
the point of fixation, with intersaccade intervals up to
200 ms. These movements occur in normal individuals
at frequencies less than 20 to 30 per minute, becoming more frequent with age (Herishanu & Sharpe,
1981). They represent likely cerebellar or upper motor
neuron pathology when the frequency exceeds this
range (Leigh & Zee, 2006). Video 10–17 shows the
eye movements of a 68-year-old male diagnosed with
a form of spinocerebellar atrophy. He had a 12-year
history of slow progressive imbalance and upper
limb coordination difficulties. The eye movements are
repeated saccades first taking his gaze away from the
target, and then he volitionally returned to the target.
No gaze-evoked nystagmus is seen on lateral gaze
right or left. He demonstrates saccadic disrupted
smooth pursuit. Fixation is then removed, and the
square-wave jerks continue. He shows no nystagmus following headshake test but continues with his
square-wave jerks. Figure 10–18 shows horizontal
and vertical eye movement tracings for a male in his
thirties (unusually young for this disorder) with multiple system atrophy, another form of spinocerebellar
atrophy. Figure 10–18 illustrates his frequent squarewave jerks.
figure 10–18. Recording of square-wave jerks from a male in his thirties with multiple
system atrophy. The top panel is a sample of his horizontal eye trace recorded using
electrooculography techniques. Note the presence of repeated square-wave jerks. The
bottom panel shows the tracing of his vertical eye movements. These recordings were
made during gaze stability testing. Each trace represents 14 s of recording.
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Macro Square-Wave Jerks. These are the 5- to
15-degree subtended arc movements in a direction
away from the point of fixation, with intersaccade
intervals of up to 150 ms that are typically shorter than
that of square-wave jerks. They represent pathology of
brainstem and/or cerebellum (Leigh & Zee, 2006). Figure 10–19 illustrates macro square-wave jerks recorded
during a VNG while testing smooth pursuit. This was
from a 20-year-old female with significant cerebellar
damage from a closed head injury and traumatic brain
injury. Even though her eyes were in constant motion
from the macro square-wave jerks, a complete VNG
was able to detect right-beating positional nystagmus
and a full set of caloric irrigations showing no peripheral asymmetry (see Video 10–18).
Macro Saccadic Oscillations. These are eyes
moving in both directions laterally around a fixation
point with intersaccade intervals of 150 to 200 ms. The
finding is suggestive of cerebellar involvement (Selhorst, Stark, Ochs, & Hoyt, 1976). The Bárány Society
ICVD defines macro saccadic oscillations as “oscillations around a fixation point due to saccadic hypermetria, typically consisting of runs of (usually horizontal)
saccades that build up and then decrease in amplitude,
with intersaccadic intervals of about 200 msec” (Eggers
et al., in press) (see Video 10–19 for example).
Ocular Flutter. These are bursts (typically 2 to 5 s
in length) of eye movement in horizontal or horizontal
and vertical dimensions. The eyes are taken away from
the point of fixation without intersaccade intervals.
When the flutter occurs in both horizontal and vertical directions simultaneously, it is referred to as opsoclonus. Although ocular flutter and opsoclonus can
originate from either brainstem or cerebellar lesions,
one must consider the possibility of paraneoplastic
cerebellar degeneration when opsoclonus is noted
(Bataller et al., 2003). Video 10–20 was obtained during
a direct bedside examination of a 71-year-old female
with a subsequent diagnosis of paraneoplastic cerebellar degeneration secondary to breast cancer. The video
illustrates ocular flutter with opsoclonus (also see the
discussion of ocular flutter in Chapter 3 of this text).
Voluntary Flutter. This is a form of flutter behav-
ior in which the eyes are disconjugate in their movement by converging and diverging. The movements
are unable to be sustained longer than 20 to 30 s. The
movements can be provoked by voluntarily performing a near target convergence or by convergence of the
eyes with no target fixation. A person can gain control
over the movement and use it for “entertaining” others,
hence the name “party nystagmus.” It is not representative of a pathological process (Hotson, 1984). It occurs
as a combination of convergence, likely for initiation,
with small repeated saccades (Yee, Spiegel, Yamada,
Abel, & Zee, 1994). It is distinguished from pathologic
ocular flutter in that as the eyes are converging, the
pupils will contract, whereas in pathologic flutter the
eyes move in the same direction together and there is
no pupillary contraction (Eggers et al., in press).
Infantile Nystagmus (Congenital Nystagmus).
Another form of nystagmus noted during gaze testing as well as during casual observation of a patient
is that of infantile nystagmus syndrome. The older
term, “congenital nystagmus,” is being dropped from
the literature because the nystagmus usually develops
within the first 8 to 12 weeks and is not present at birth.
Appearance is that of a horizontal beating nystagmus
in an eye reference frame as opposed to head reference,
typically mixed with pendular nystagmus. Infantile
nystagmus may be accentuated by visual attention
or arousal and suppressed by convergence, inattention, eye closure, or sleep. The amplitude, frequency,
and waveform can vary with eye position, typically
increasing on lateral gaze (right-beating in right gaze,
figure 10–19. An attempt at smooth pursuit testing during a VNG on a 20-year-old female with significant cerebellar damage from a head injury. The horizontal eye tracing illustrates macro square-wave jerks. The top trace in the
figure shows the trajectory of the sinusoidal target. The bottom trace is the horizontal eye movement recorded from
the right eye.
10. EYE MOVEMENT RECORDING AND OCULAR MOTILITY TESTING 219
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left-beating in left gaze) but diminishing in intensity in
a null zone, leading individuals to adopt a head position that minimizes the oscillations. Infantile nystagmus may occur in the setting of other visual sensory
disorders or with a normal visual system. Therefore,
this nystagmus can appear as a direction-changing,
gazed-evoked nystagmus with nystagmus present in
the primary eye position (mild forms may have primary position nystagmus absent). Although it may not
change significantly, with fixation removed the usual
presentation would be to note that the nystagmus
reduces in frequency of the beat, regularity, and slow
component velocity (SCV). If not recognized as infantile
nystagmus, this finding could easily be confused as an
indication of CNS pathology. In the majority of patients,
the infantile nystagmus has little or nothing to do with
the reason why the patient has sought evaluation for
dizziness. In that sense it becomes a “noise” interference that must be dealt with during the ENG/VNG
evaluation. There are specific characteristics that distinguish ongoing, fixation-present nystagmus as infantile:
1. A history of the ongoing eye movements since as
early as the patient can remember. The patient may
be able to relate incidences of being teased by other
children because of the ongoing eye movement
activity (Hertle, Maldanado, Maybodi, & Yang,
2002). However, forms of this type of nystagmus
may develop later in life (Gresty, Bronstein, Page,
& Rudge, 1991).
2. Nystagmus is usually horizontal even during up or
down gaze in an eye reference plane.
3. The nystagmus can be slowed with convergence
and during gaze just lateral to primary called the
null point. By handing patients something to read
and watching how they position the material, one
observes that they will likely move the material in
closer than expected and to the right or left from
primary gaze by a turn of their head. In this position they take advantage of both the quieting of the
nystagmus with convergence and the null point.
4. Trace recordings will many times show the slow
component of the nystagmus to be one of increasing velocity. This presentation is just the opposite
of the decreasing velocity noted in gaze-evoked
nystagmus of central origin (see Table 10–6). Figure 10–20 illustrates in a schematized form the nystagmus seen in gaze-evoked nystagmus of central
and peripheral origin. Compare that with the nystagmus tracings from ENG testing from a patient
with infantile nystagmus shown in Figure 10–21.
The trace in Figure 10–21 illustrates the increasing
figure 10–20. Schematized examples of right-beating jerk nystagmus of central origin in the top trace and of peripheral origin in
the bottom trace. Note that in the top trace the slow component
of the nystagmus shows a decreasing velocity. In the bottom trace
the slow component has a constant (linear) velocity. From Practical
Management of the Balance Disorder Patient by Shepard, N. T.,
and Telian, S. A. Copyright © 1996.
220 BALANCE FUNCTION ASSESSMENT AND MANAGEMENT
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Figure 10–21. A. Recording from a patient with infantile nystagmus. Note that the slow component
of the nystagmus demonstrates an increasing velocity curve for the right-beating nystagmus.
sample was taken during E
same patient.
increasing velocity behavior for the slow component of the superimposed right beat. From Practical
Management of the Balance Disorder Patient by Shepard, N. T., and Telian, S. A. Copyright © 1996.
The right-beating nystagmus is superimposed on the pursuit tracking but also shows the
NG saccade testing. B. Trace recorded during smooth pursuit testing in the
This
velocity of the slow component drift of the eyes to
the left.
The above descriptions are the more common
presentation of infantile nystagmus. It can, however,
take other forms and be associated with other ocular
system abnormalities. One example of a variation is
shown in Video 10–5, recorded during VNG evaluation of a 16-year-old female with migraine-related dizziness. The nystagmus seen in the video is effectively
direction-changing, gaze-evoked nystagmus on lateral
gaze. On investigation by neurology and magnetic
resonance imaging (MRI), it was determined that this
was a mild form of congenital nystagmus secondary
to ocular misalignment for which she had been treated
years prior. For a complete description of the variants
and associated abnormalities and a discussion of the
pathogenesis of congenital nystagmus, the reader is
referred to Leigh and Zee (2006).
Optokinetic Nystagmus
Technical Considerations
The production of true optokinetic nystagmus (OKN)
involves a combination of the neurologic substrate
involved with smooth pursuit tracking together with
areas that respond to moving visual stimuli in a full
field format but do not respond to head movement of
the optokinetic areas (Leigh & Zee, 2006). Furthermore,
when viewing a stimulus in full field (≥90% of the visual
field filled with the repeated moving targets), the initiation of the nystagmus is dominantly a result of smooth
pursuit tracking with the OKN component added as
the stimulus is continued, requiring seconds to fully
develop. The response then continues as a combination
of both smooth pursuit tracking and optokinetics with
smooth pursuit dominant. Therefore, to evaluate OKN
function in isolation from smooth pursuit, one must
take advantage of a perseveration of nystagmus caused
by stimulation of the optokinetic system when the person is suddenly put into the dark after a minimum of
30 s of stimulation (called optokinetic after nystagmus
[OKAN]). As soon as the target has been extinguished
for 1 s, the smooth pursuit system no longer has any
influence and the OKAN is a direct result of the activity
of the optokinetic system reflected through the area of
the brainstem referred to as the velocity storage system (Tijssen, Straathof, Hain, & Zee, 1989). To produce
the OKN stimulation through retinal stimulation and
signals transmitted via the accessory optic track, the
stimulus needs to fill a minimum of 90% of the visual
field and be capable of producing a circularvection
effect (the illusion of circular motion when not moving) (Leigh & Zee, 2006). Note that since OKAN is not
routinely used in the clinic, it will not be discussed further in this chapter and the interested reader is referred
elsewhere (Leigh & Zee, 2006).
Based on the above discussion, the size of the target used in testing for OKN must basically fill the visual
field with its movements. Therefore, light bars are not
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tapping into the optokinetic system even though they
can produce a nystagmus that looks like OKN but is
created primarily by the smooth pursuit system. Light
bar stimuli do not produce OKAN, which would be
the indicator of optokinetic system stimulation and the
means by which it can be directly evaluated. The projection systems have a better opportunity to produce
true optokinetic system stimulation even though for a
standard ENG/VNG system this is projected onto a flat
surface. The most efficient manner to provide for optokinetic system stimulation is to have the subject seated
within a full-field stimulus configuration. An example
of such is provided in a rotary chair environment with
a projection light system in the ceiling, as shown in
Figure 10–22. Other arrangements may consist of a
patterned cloth enclosure that surrounds the patient,
and the entire cloth system is placed into motion. Even
with all of the appropriate arrangements of a full-field
stimulus and the production of the sensation of circularvection, the OKN response is still dominated by the
smooth pursuit system, and hence the same normative
data are used for analysis of sinusoidal OKN as are
used for smooth pursuit.
Filter settings and sampling rates would be as set
for gaze-stability testing. The nystagmus would have
parametric features of slow component and fast component velocity similar to those of other jerk nystagmus.
When testing for OKN, the instructions given the
patient are critical, as the form of the nystagmus can
be easily altered. If the patient is to capture and follow a single target out of the optokinetic visual presentation (e.g., stripes, checkerboard, random dots),
the nystagmus will have a large excursion for the slow
component, giving a coarse appearance to the jerk nystagmus; this is referred to as “look” nystagmus. If the
instructions are to have the patient stare or gaze in the
center of the target display and try to count the targets
as they go by, this results in a low-amplitude slow component nystagmus called “stare” nystagmus. “Look”
nystagmus emphasizes the smooth pursuit compo-
figure 10–22. An immersive optokinetic stimulation system as a component of a rotational chair system. From
Practical Management of the Balance Disorder Patient
Shepard, N. T., and Telian, S. A. Copyright © 1996.
by
nent, whereas “stare” nystagmus increases the optokinetic component in a full-field presentation but the
OKN component is still less than the smooth pursuit
Parameters for Analysis
portion. Patients can inadvertently eliminate the OKN
response by “staring through” the target to an imagined stationary target on the other side of the display.
If this type of full-field stimulus in daily routine causes
the patient symptoms, he/she may have adopted this
“looking through” strategy as a means for controlling the unwanted sensations. Therefore, shaping the
character of the nystagmus is important, along with an
appropriately sized visual presentation if stimulation
of the optokinetic system is to be achieved.
The analysis for OKN is performed by calculating the
velocity gain of the eye movement response. This is
defined as the peak eye velocity divided by the target
velocity. The velocity gain is used for either the fixed
velocity or sinusoidal protocols. The gain is calculated
for target movement to the right and to the left. These
gains are expected to be symmetric (within a 25% difference range) with a minimum 0.5 for the fixed velocity target protocol with speeds up to 60 deg/s.
222 BAlAnCE FunCtion AssEssmEnt And mAnAgEmEnt
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For the sinusoidal target profile, velocity gain is
the dominant outcome parameter. In this protocol the
velocity gain is expected to fall within the ranges given
for smooth pursuit tracking at the same frequency (see
Table 10–4). This results from the domination of the
neurologic substrate responsible for smooth pursuit in
the production of OKN. Additionally, phase angle can
be calculated for the sinusoidal protocol with results
expected to be within the range given for smooth pursuit. Again, in this protocol the outcome parameters are
given for target movement to both the right and the left.
Optokinetic Testing Interpretation
The technical aspects to evaluate the optokinetic system are significant. Even if all of the technical points
are achieved, abnormalities of OKN regarding asymmetric velocity gain in the absence of abnormalities of
smooth pursuit tracking are likely related to unilateral
peripheral hypofunction, resulting in a bias of the nystagmus beating away from the hypofunction or as a
result of abnormalities in the visual pathways including the eye (Baloh, Yee, & Honrubia, 1982; Valmaggia,
Proudlock, & Gottlob, 2003). In general, if asymmetrical
performance for OKN gains is to be reflective of central
vestibular system lesions of the cerebellum/brainstem
regions, it would be expected that abnormalities would
be noted for the more specific tests for these regions:
smooth pursuit tracking and saccade testing. The principal reason for the lack of sensitivity to CNS lesions
with OKN is that the production of OKN is dependent
on two overlapping systems sharing a neurologic substrate: the optokinetic system and the smooth pursuit
system. This has been shown in a variety of primate
and human studies summarized by Leigh and Zee
(2006) and in recent work with functional MRI studies in human subjects (Bense et al., 2006; Konen, Kleiser, Seitz, & Bremmer, 2005). As would therefore be
expected, the gain for OKN does decline with age in a
manner parallel to that of smooth pursuit at least up to
ages under 75 years with some suggested stabilization
after age 75 (Kerber, Ishiyama, & Baloh, 2006; Valmaggia et al., 2004).
Because of this overlap between pursuit and OKN,
a common manner for analysis is the comparison of the
velocity gains from OKN to smooth pursuit for a given
patient in order to suggest whether OKN performance
is abnormal yet possibly explainable based on abnormalities in pursuit if present.
To investigate lesions affecting the optokinetic system activity of the velocity storage system in the vestibular nuclei in the pons, OKAN must be used together
with OKN. Hypothetically, abnormalities of gain asym-
metry may not be seen with OKN, yet asymmetries in
initial slow component velocity (initial gain), the time
constant of decay, or the slow cumulative eye velocity
of the OKAN may be noted, implicating the region of
the velocity storage integrator (Leigh & Zee, 2006). The
reader is, however, reminded as to the significant variability and difficulty in reliably acquiring the OKAN
response. Because of the technical issues and the lack of
sensitivity and specificity in lesion detection, this combination is not considered currently to be part of a routine ocular motor investigation and beyond the scope
of this chapter. For a full discussion of these issues, the
interested reader is referred to the literature (Hain &
Zee, 1991; Hain et al., 1994; Leigh & Zee, 2006).
In routine clinical ocular motor testing, the evaluation of OKN is the least useful of the tests we have
discussed. Yet it can be brought into play in specific situations precisely because of its relationship to smooth
pursuit. The first is in the evaluation of smooth pursuit
testing in children. Smooth pursuit gains are lower and
the phase lag larger in children (8 to 19 years of age)
than in adults or children reaching adult values for horizontal movement of the eyes between 12 and 15 years
of age (Salman, Sharpe, Lillakas, Dennis, & Steinbach,
2006). Yet to test smooth pursuit in an infant, although
obtainable, is not an easy task. Studies concentrating
on children in the first year of life have shown, as in
the adults, that pursuit and optokinetic systems work
together to produce OKN and that the evaluation of
pursuit may be approximated with evaluation of OKN
velocity gains (Rosander & von Hofsten, 2002; Valmaggia et al., 2004; Von Hofsten & Rosander, 1996, 1997)
(see Chapter 18 for further discussion). The second use
of OKN can be in the adult with severely disrupted
pursuit performance. In situations of this type OKN
would also be expected to be significantly abnormal.
Thus, OKN testing may serve as a cross-check for the
pursuit findings. In patients who cannot complete a
smooth pursuit task secondary to complaints of symptom generation with sinusoidal movements, OKN
velocity gain with fixed velocity movement and a small
target (like that of a light bar) may serve to approximate pursuit performance.
summary
The foregoing discussion provides general guidelines
for interpretation of the routine ocular motor studies
used in the evaluation of the dizzy and balance disorder patient population. Although the principal utility
of these studies is to investigate the possible involve-
10. EyE movEmEnt rECording And oCulAr motility tEsting 223
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ment of the central vestibular and ocular motor control
regions of the CNS, other uses for investigation of eye
movement disorders not related to dizziness are well
documented and are discussed by Leigh and Zee (2006)
for the interested reader. Additionally, the area of eye
movement abnormalities using the above investigational tools for characterization of psychiatric disease
not related to dizziness has recently been described
in the literature. A summary article is available that
synthesizes this area of work (Trillenberg, Lencer, &
Heide, 2004).
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