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A. Chern and L. Lustig
Table 3.1
ENG electronystagmography, VNG videonystagmography
Components of bedside vestibular examination and subtests of standard VNG/ENG
VNG/ENG
subtests Description of the test
Smooth pursuit
tracking
Optokinetic
nystagmus
Spontaneous
nystagmus
Saccade testing Observe the velocity, accuracy, and latency of rapid eye movements from
Gaze-evoked
nystagmus
Static positional
nystagmus
Dix–Hallpike
maneuver
Bithermal caloric
testing
Clinical tests of vestibular loss
Head thrust sign Looking for a catch-up saccade with quick head turns toward the side of
Head shaking
nystagmus
Vibration-induced
nystagmus
Subjective visual
vertical
Dynamic visual
acuity
Eye movement tracking of a moving target
Eye movement response to an optokinetic stimulus
Observe for xation stability and spontaneous nystagmus, if any
one target to another
Observe for nystagmus and gaze holding during eccentric gaze
Observe for nystagmus during or after head position testing
Observe for nystagmus after rapid head positioning from the sitting or head
hanging right or left position
Warm and cool irrigation applied to each ear for comparison of vestibular
responses
unilateral vestibular loss
Observe for nystagmus away from the side of unilateral vestibular loss after
head shaking
Observe for nystagmus away from the side of unilateral vestibular loss
when mastoid vibration is applied
Patient directs bar or line to what he or she perceives to be straight vertical;
in acute otolith dysfunction, the bar or line deviates to the side of unilateral
vestibular (otolith) loss
Look for three-line decrease in visual acuity during rapid head turning
indicative of bilateral peripheral vestibular loss
frontal lobe, basal ganglia, superior colliculus, cerebellum, and brainstem. Saccades
can be elicited by the appearance of a novel target subject’s visual eld (reexive
saccade) or by the intention of the subject (volitional saccade).
Test Administration andParameters
To test saccadic eye movement, the patient is asked to follow a randomly moving
LED target with as much accuracy as possible. The ashes occur sequentially in two
positions: at the center of the array and then 15–20° to the right and left from the
center. The interval between ashes is usually a few seconds, and the test is then
repeated vertically.
Saccades are tested for accuracy, velocity, and latency. Latency (the difference
in time between the presentation of a new target and the initiation of eye movement)
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is normal between 150 and 250ms in random patterns and shorter than 75ms when
the pattern is predictable. Abnormalities include prolonged latency, shortened
latency, and differences in latency between the right and left eyes; these are seen in
neurodegenerative diseases.
Peak velocity is the maximum velocity that the eyes reach during a saccadic
movement. There is no upper limit to normal, as velocities have been measured as
high as 700°/s, but they generally range from 283 to 581°/s for 20° of amplitude in
normal subjects. Velocities slower than 400°/s for large-amplitude saccades and
slower than 200°/s for small-amplitude saccades are considered abnormal. Abnormal
saccadic velocities include fast saccades, slow saccades, or differences in velocity
between the right and left eye. Fast saccades can be observed in calibration errors
and eye muscle restrictions. Sedative drug use is the most common cause of abnormally slow saccades. Other causes include drowsiness, cerebellar disorders, basal
ganglia disorders, and brainstem lesions. Velocity asymmetry between the left and
right eye is seen in intranuclear ophthalmoplegia, eye muscle restrictions, ocular
muscle palsies, and palsies of cranial nerves III, IV, and VI.
Accuracy is established by comparing the eye position relative to a target position. A saccadic eye movement that goes farther than the target position is considered a hypermetric saccade (or overshoot dysmetria). This is considered abnormal
if it is greater than 115–120% of the target value. A saccadic movement that is
shorter than the target position is referred to as a hypometric saccade (or undershoot
dysmetria). This is considered abnormal if it is less than 75–80% of the target value.
Undershooting by 10% of the amplitude of the saccade may be seen in healthy individuals, while hypermetric saccades are rarely observed in normal individuals.
Inaccurate saccades suggest a pathologic condition of the cerebellum, brainstem, or
basal ganglia.
See Figs.3.1 and 3.2 for examples of saccade testing.
Smooth Pursuit Tests (Sinusoidal Tracking)
In contrast to saccades, smooth pursuit describes much slower tracking movements
designed to keep a moving stimulus xated on the fovea. The neural pathways
involved are distributed in the cortical and subcortical areas of the brain, as well as
the fovea.
Test Administration andParameters
To assess smooth pursuit, the LED moves back and forth between points on a light
bar at a constant frequency, usually between 0.2 and 0.8Hz/s, and a velocity between
20°/s and 40°/s in a sinusoidal pattern. Smooth pursuit performance declines with
higher velocities and increasing age. The primary parameters of pursuit testing
include gain, phase, and trace morphology.
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Fig. 3.1 Normal saccades and tracking seen in both eyes
A. Chern and L. Lustig
Fig. 3.2 Delayed latencies with leftward gaze deviation and reduced rightward and leftward
velocity
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Gain is the peak-to-target velocity ratio. For a stimulus of 0.5Hz with a sweeping amplitude of 40°, a gain greater than 0.8 is considered normal. Saccade movements are eliminated from the calculation of gain. A low gain is suggestive of a CNS
disorder.
Phase is the difference in time between eye movement and target movement.
Under optimal conditions, healthy subjects can track a target with a phase of 0°. The
level of attention and drugs affecting the CNS can destroy pursuit performance.
A morphological assessment of the tracings is also performed. A morphologic
abnormality is referred to as a staircase of saccades, where the trace demonstrates
a step-like eye movement when the target is being followed. Pursuit traces can be
impaired symmetrically or asymmetrically—the asymmetrically impaired pursuit is
more indicative of a CNS lesion than symmetrically impaired pursuit. Peripheral
vestibular lesions may also impair smooth pursuit contralateral to the pathological
side when the patient’s eyes are moving against the slow phase of spontaneous nystagmus. See Figs.3.3 and 3.4 comparing normal smooth pursuit and abnormal saccadic pursuit.
Optokinetic Tracking
When actively experiencing vertigo, a patient relies on vestibular system stimulation and OKN to facilitate steady focus on objects as they move in a circular pattern
around him or her. As the patient’s vestibular system fatigues with stimulation, the
optokinetic system is solely responsible for the stabilization of the visual eld. ENG
tests the optokinetic tracking of targets by passing a light rapidly in front of a patient
Fig. 3.3 Normal smooth pursuit
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Fig. 3.4 Abnormal saccadic pursuit; central vestibular abnormality seen in a patient with cerebellar degeneration
A. Chern and L. Lustig
from one direction, then the other. Asymmetries are noted and are signs of CNS
dysfunction. Various tests have been done that have shown high rates of falsepositive results with this test. Patients with optokinetic abnormalities in VNG/ENG
may not need further neurological workup.
OKN is an involuntary oculomotor response to a moving target lling at least
90° of the visual eld. An optokinetic stimulus is presented using a 360°-turning
cloth drum with black and white stripes. The normal response to an optokinetic
stimulator is a smooth eye movement that follows the stimulus direction, both
clockwise and counterclockwise. OKN is produced by the cortical and brainstem
structures that produce pursuit and aims to stabilize the visual eld on the retina.
Optokinetic after-nystagmus is a form of nystagmus produced by the brainstem
after a 10-s, constant velocity optokinetic stimulus and lasts approximately 30s.
OKN abnormalities are seen in deep parietal-lobe lesions and may be used to identify subtle ocular motor abnormalities (e.g., incomplete internuclear ophthalmoplegia). See Figs.3.5 and 3.6 for normal and symmetric optokinetic tracking compared
to abnormal tracking.
Gaze Test
A gaze test is conducted by recording eye movements while the subject xes his or
her vision on the center of a target. The patient then xes his or her gaze 30–40° to
the right, left, above, and below the center of the eld. The patient’s gaze and gaze
recording are sustained for a minimum of 30s. Patients with gaze nystagmus cannot
maintain stable conjugate eye deviation away from the primary position; thus, their
vision is refocused back to the center by resetting corrective saccades. Gaze testing
may uncover peripheral or CNS lesions that are either vestibular or nonvestibular in
etiology, as well as congenital or spontaneous nystagmus.
During and after unilateral vestibular dysfunction, vestibular spontaneous nystagmus is seen and beats away from the pathologic side. Typically, it manifests as
horizontal nystagmus in an ENG recording, but it is actually both horizontal and
torsional in nature. The intensity of vestibular spontaneous nystagmus increases
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Fig. 3.5 Normal and symmetric optokinetic tracking. Right and left 20°/s
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when the gaze is oriented toward the direction of the nystagmus. See Fig.3.7 for an
example of spontaneous nystagmus.
Peripheral gaze-evoked nystagmus is typically unidirectional on a horizontal
plane—both horizontal and torsional. When the gaze is directed toward the nystagmus direction, its intensity increases; gaze-evoked nystagmus of CNS origin may
change direction with the patient’s gaze. Vertical gaze nystagmus is always indicative of a CNS pathology.
Gaze nystagmus is categorized as symmetric, asymmetric, rebound, or disassociated. In symmetric gaze nystagmus, the eyes move with equal amplitude in both
directions. Ingestion of drugs affecting the CNS, such as multiple sclerosis, myasthenia gravis, and cerebellar atrophy, may cause symmetric gaze nystagmus.
Asymmetric gaze nystagmus suggests a cerebellar or brainstem lesion. Rebound
nystagmus starts in lateral positions and reverses its direction to the primary posi-
tion, even with no evidence of initial nystagmus in the primary position. It is also
strongly indicative of cerebellar or brainstem lesions. Disassociated (disconjugate)
nystagmus is the difference in eye movements during gaze testing, usually resulting
from medial longitudinal fasciculus lesions. See Figs.3.8 and 3.9 for examples of
normal and abnormal gaze testing.
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Fig. 3.6 Abnormal optokinetic tracking (40°/s), poor morphology. No visible or repeatable
nystagmus
A. Chern and L. Lustig
Fig. 3.7 Left beating spontaneous nystagmus (1–2°/s)
Fixation Suppression Testing
Spontaneous nystagmus is established by placing the patient with vision denied
(i.e., eyes closed) in a completely darkened room without visual or positional stimuli. If spontaneous nystagmus is found, slow-phase velocity is recorded. The patient
is then asked to xate on the center of a visual target (i.e., the central gaze). The
xation-suppression index is then calculated by determining the ratio of the slowphase velocity with xation to the slow-phase velocity without xation. This index
should be <50%. Nystagmus from a peripheral cause should decay by over 50%
ab
cd
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e
f
Fig. 3.8 Normal center, gaze right, gaze left. In each of these six panels, horizontal eye position is
plotted as a function of time. The patient is instructed to stare at a dot straight ahead (a, center gaze
with vision), 30° to the right (c, with vision), and 30° to the left (e, with vision) while eye movement is recorded through the use of infrared goggles. The same conditions are then recorded with
vision denied (b, d, f, respectively). No gaze nystagmus is noted in any condition
with xation. Of note, xation suppression is more accurately measured after caloric
irrigation, when nystagmus is much stronger. See Fig.3.10 for an example of xation suppression testing.
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Fig. 3.9 Abnormal gaze
testing. Up-beating
nystagmus in gaze testing
(vision denied). Vestibular
dysfunction likely central
in origin (i.e., brainstem or
cerebellar lesion)
A. Chern and L. Lustig
Fig. 3.10 Fixation suppression, measured 120s after the onset of caloric irrigation
Positioning Tests
Positioning and positional testing are also part of the oculomotor test battery.
Positioning testing (as discussed earlier) is conducted to establish the effect of head
movement from one position to another on the vestibular system. Positioning testing
is used to determine the presence of BBPV. Examples are the Dix–Hallpike
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maneuver and the roll test. These bedside tests can also be conducted using VNG or
Frenzel goggles. BBPV is most commonly the result of otoliths in the posterior
canal. Stimulation using the Dix–Hallpike maneuver commonly causes torsional
nystagmus, which is difcult to measure. Moreover, patients may fatigue the
response, and patients with true BBPV may test negative on the initial visit. It is
therefore important in both VNG/ENG testing and clinical testing that patients with
a strong history of BBPV be tested on multiple occasions using the Dix–Hallpike
maneuver.
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Positional Tests
Positional testing examines the effect of varying stationary head positions (and not
head movements) on the vestibular system, enabling the physician to determine if a
patient’s nystagmus is generated as a result of the orientation of the patient’s head
to gravity. When there is an inner ear vestibular insult, compensation occurs through
constant stimulation. It is natural that the subject will become compensated in the
position that he or she most frequently uses, namely the upright position. When
placed in different positions, dizziness and nystagmus may occur due to incomplete
compensation in that particular position. In patients with dizziness and no nystagmus provoked by different positions, nonvestibular etiologies are considered. When
performing positional tests, it is important to eliminate the inuence of neck exion,
which may cause vascular insufciency that can provoke symptoms suggestive of
peripheral vestibular disorders.
Test Administration andParameters
With positional tests, the patient’s head is brought slowly into the following positions: (1) turned right and then left while sitting, (2) turned right and then left in
supine position, (3) turned right and then left in decubitus position, and (4) hung
straight down. Each position is maintained for at least 20s. During this test, the
patient is asked to wear Frenzel goggles; alternatively, the test may be performed
while the patient’s eyes are closed. Positional nystagmus can be described as intermittent or persistent, while the direction may be xed or changing.
Positional nystagmus may be observed in patients with both peripheral and CNS
lesions; thus it is not a localizing nding. However, some features can help distinguish positional nystagmus from a peripheral lesion from positional nystagmus due
to a central lesion. First, xation suppresses positional nystagmus caused by a
peripheral lesion. Second, nystagmus that changes directionality may be indicative
of a central lesion. The examiner should be careful about contamination by spontaneous nystagmus with positional changes. Persistent nystagmus should be observed
for at least 2 min—this is particularly important with periodic alternating
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