775

Eye Movement Recordings: Practical Applications

in Neurology
John-Ross Rizzo, MD, MSCI1 Mahya Beheshti, MD2 Weiwei Dai, PhD3 Janet C. Rucker, MD4

1 Department of Physical Medicine and Rehabilitation, Department of Address for correspondence Janet C. Rucker, MD, Departments of
Neurology, Department of Biomedical Engineering, Department of Neurology and Ophthalmology, New York University School of
Mechanical and Aerospace Engineering, New York University School Medicine, 222 E. 41st St, 14th Floor, New York, NY 10016
of Medicine and New York University Tandon School of Engineering, (e-mail: janet.rucker@nyulangone.org).
New York
2 Department of Physical Medicine and Rehabilitation, New York
University School of Medicine, New York, New York
3 Department of Electrical and Computer Engineering, New York
University Tandon School of Engineering, Brooklyn, New York
4 Departments of Neurology and Ophthalmology, New York

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University School of Medicine, New York, New York

Semin Neurol 2019;39:775–784.

Abstract Accurate detection and interpretation of eye movement abnormalities often guides
differential diagnosis, discussions on prognosis and disease mechanisms, and directed
treatment of disabling visual symptoms and signs. A comprehensive clinical eye
movement examination is high yield from a diagnostic standpoint; however, skillful
Keywords recording and quantification of eye movements can increase detection of subclinical
► saccades deficits, confirm clinical suspicions, guide therapeutics, and generate expansive
► ocular flutter research opportunities. This review encompasses an overview of the clinical eye
► nystagmus movement examination, provides examples of practical diagnostic contributions
► video-oculography from quantitative recordings of eye movements, and comments on recording equip-
► eye movements ment and related challenges.

Accurate detection and interpretation of eye movement
abnormalities in clinical neurology often guides differential
diagnosis, contributes to discussions of prognosis and dis-
ease mechanisms, and allows for directed treatment of
disabling visual symptoms and signs such as diplopia and
oscillopsia (i.e., a subjective sense of visual motion). Al-
though performance of a comprehensive clinical eye move-
ment examination is high yield from a diagnostic
standpoint, quantitative eye movement recordings provide
a powerful complement. Technology leveraged within the
electrophysiologic domain increases the sensitivity to de-
tect many clinical disorders. Neurology has embraced many
diagnostic tools as ‘gold standards’ to supplement the
clinical examination, such as automated visual field peri-
metry, which is more sensitive than confrontation visual
fields,1 and electromyography for confirmation of a clinical
impression of peripheral neuropathy or myopathy. Similar-
ly, recording and quantifying eye movements increases the
detection sensitivity of subclinical deficits and confirms
suspected clinical impressions to increase diagnostic
accuracy.2
A vast scientific research literature exists for the pur-
pose of documenting subclinical eye movement abnormal-
ities in various diseases and applying eye movements as a
research tool for the assessment of cognitive processing.
While many of these findings might be considered by the
practicing neurologist to be applicable mainly to research
and lacking in practical clinical applications, we aim in this
review to highlight examples of the immediate practical
utility of eye movement recording and quantification. To do
so, we intentionally keep terminology as simple as possi-
ble; in-depth and comprehensive reviews of ocular motor
anatomy, and normal and abnormal ocular motor physiol-
ogy may be found elsewhere.2 We begin by reviewing a

Issue Theme Neuro-Ophthalmology; Copyright © 2019 by Thieme Medical DOI https://doi.org/

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776 Eye Movement Recording in Clinical Neurology Rizzo et al.
comprehensive bedside eye movement examination and
then review how eye tracking can be used to record normal
eye movements. We then turn our attention to examples of
how quantitative eye movement recordings may impact
diagnosis and treatment. We conclude with a brief section
on types of available eye movement recording equipment
and related challenges.
Normal Eye Movements
The Clinical Exam
Few aspects of the neurological examination allow for as
precise localization as does the clinical eye movement
examination, which can allow localization of a lesion to
a single neuronal nucleus, tract, or nerve. In the presence
of abnormal eye movements, external ocular features (i.e.,
ptosis, proptosis, lid edema, lid retraction, and lid fatiga-
bility) have tremendous localization value. Notation of
any abnormal head position, such as resting position tilts
or turns, or head thrusting to elicit eye movements,
should be made prior to and during the eye movement
examination.
The first step in the eye movement exam is evaluation of
ductions (the range of motion of each eye independently)
and versions (the range of both eyes together) in the nine
cardinal positions of gaze (i.e., central fixation, right, up-
right, up, up-left, left, down-left, down, down-right). The
second step involves assessment of ocular alignment, noting
any eso-, exo-, or hyper-deviations of an eye and how any
misalignment changes in different gaze and head tilt posi-
tions. Review of techniques for examining ocular alignment
may be found elsewhere.3
The eyes should be examined together and independent-
ly (by covering each eye in turn) during fixation of distant
and near targets for any abnormal spontaneous eye move-
ments, such as saccadic intrusions or nystagmus. Abnormal
spontaneous eye movements should also be noted in the
nine cardinal positions of gaze and in the supine and supine
head-hanging positions. If abnormal movements are pres-
ent in central fixation, the behavior of those movements in
the different gaze and postural positions should be docu-
mented. The next component of the eye movement exami-
nation is assessment of the functional classes of eye
movements: saccades, smooth pursuit, optokinetic nystag-
mus, vestibulo-ocular reflexes, and vergence which consists
of both convergence and divergence. All types, with excep-
tion of vergence, should be tested in horizontal and vertical
planes. Features of saccades important to note during
examination include latency (reaction time), speed, accura-
cy (and any corrective movements if inaccurate), trajectory,
and conjugacy. Corrective saccades during smooth pursuit
should be noted. Generation of both slow and quick phases
should occur during optokinetic testing with a red/white
striped tape or optokinetic drum. Methods of clinical ex-
amination of the functional classes of eye movements in the
horizontal plane are shown in ►Video 1. If abnormal
spontaneous eye movements are observed in examination,
the remainder of the eye movement examination should be
Seminars in Neurology Vol. 39 No. 6/2019
carefully conducted to ascertain additional behavioral
abnormalities.
Video 1
Clinical examination of functional classes of eye
movements in the horizontal plane, including
saccades, smooth pursuit, optokinetic nystagmus,
vestibulo-ocular reflexes, and vergence. Online
content including video sequences viewable at:
https://www.thieme-connect.com/products/
ejournals/html/10.1055/s-0039-1698742.
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Eye Movement Recordings
Eye movement recording and quantification can increase the
yield of detection of subtle eye movement abnormalities that
may be directly pertinent to establishing a clinical diagnosis.
In addition, eye tracking permits robust characterization of
the ocular motor phenotype of a disease process. To consider
abnormalities of eye movements on recorded eye position
and velocity traces, two essential ingredients are required:
familiarity with a suitable eye tracking device and with the
normal appearance and characteristics of recorded eye
movements. All functional classes of eye movements can
be recorded. The examples that follow will predominantly
concern fixation and saccades.
Saccades are rapid eye movements by which gaze is shifted
between visual targets. On clinical examination, they are most
often tested by having the individual make rapid eye move-
ments between two constantly present stationary targets on
verbal command (►Video 1). In the eye movement recording
laboratory, they are most often tested by having the individual
make rapid eye movements between a central fixation target
(typically a circle of small diameter on a computer screen) and
a suddenly appearing peripheral target, the appearance of
which is simultaneously accompanied by disappearance of the
central fixation target. The location of the peripherally appear-
ing target can be manipulated to test saccades of specific sizes
(i.e., 5, 10, and 15 degrees) and in different directions (i.e.,
horizontal, vertical, and oblique). The saccades assessed by the
paradigm above are called visually-guided saccades. It is worth
noting that the timing of offset of the central fixation target
and onset of the peripheral saccade target can also be manip-
ulated in the laboratory to assess additional types of saccades,
deficits of which may assist with localization. For example, the
individual may be asked to make a memory-guided saccade to
the location of the previously flashed peripheral saccade
target; specific deficits in this paradigm may localize to frontal
saccade centers. To focus attention on the most clinically
practical information, the remainder of the discussion will
pertain to visually-guided saccades.
In terms of saccadic analysis, conventionally assessed met-
rics include latency, speed, accuracy, trajectory, and conjugacy.
While these may be subjectively qualified at the bedside, these
parameters may be precisely quantified in the laboratory and
 Eye Movement Recording in Clinical Neurology
compared with normative values, thereby increasing the sen-
sitivity of detection of subtle variations from normal eye
movement behavior. To minimize the disruption of vision
during eye movement, saccades are fast (up to 900 deg/s)
and brief (less than 100 msec). Normal saccades occur in a
single smooth motion with a single-peaked velocity waveform
(►Fig. 1A), and adhere to relationships between saccade
amplitude and peak velocity and between saccade amplitude
and duration. These relationships are referred to as the ‘main
sequence’ of saccades4,5 (►Fig. 1B). The larger the amplitude of
the saccade, the faster its speed and the longer its duration (for
saccades up to 15 degrees). For saccades larger than 15 degrees,
speed saturates and peak velocities and durations are similar.
Practical Clinical Applications of Eye
Movement Recordings
Enhanced diagnostic accuracy of subclinical or subtle clin-
ical defects (“Eye movements appear normal on exam” or
“I think I see something but am not sure”)
Slow Saccades
The presence of slow saccades may signify either peripheral
ocular motor pathway (i.e., extraocular muscle or cranial nerve)
pathology or dysfunction of specific populations of brainstem
neurons known as excitatory burst neurons which serve as the
final supranuclear premotor command center for saccade initi-
ation.6 Two populations of excitatory burst neurons exist: those
in the paramedian pontine reticular formation (PPRF) in the
caudal pons7 for horizontal saccades, and those in the rostral
interstitial medial longitudinal fasciculus (RIMLF) in the rostral
midbrain8 for vertical and torsional saccades. Peripheral ocular
motor pathway pathology is usually evident on clinical exami-
nation. Thyroid eye disease with extraocular muscle involve-
ment is often obvious by its clinical appearance, as
ophthalmoplegia is typically accompanied by orbital signs of
proptosis, lid edema, and lid retraction; a third, fourth, or sixth
nerve palsy is also usually evident by its patterns of ophthal-
moplegia and ocular misalignment on clinical examination (and
in the case of the third nerve, by the presence of ptosis and
possibly a dilated pupil). Although saccades with these disorders
are typically slow,9,10 detection of saccadic slowing is not usually
critical to establishing the proper diagnosis. In contrast, detec-
tion of saccadic slowing in the presence of multifocal central
neurological dysfunction is key to establishing a diagnosis.
A common example of brainstem supranuclear saccadic
slowing contributing to a diagnosis is in the setting of atypical
parkinsonism in older patients, where identification of vertical
saccade slowing with or without ophthalmoplegia11 strongly
suggests a diagnosis of progressive supranuclear palsy (PSP).12
A pearl to apply to the clinical examination of saccades is that
normal saccades should be so fast that it is not possible for the
observer to follow the entire trajectory of the movement. In
other words, the eye is seen at starting point A and ending point
B, but the trajectory of the saccade is barely noticeable.
Definitively pathologic saccade slowing can be seen on clinical
examination through the entire course of the movement
(►Video 2, Clip 1). Severely, and even moderately, slowed
Rizzo et al. 777
saccades should be detectable on clinical examination by a
skilled examiner; mild saccadic slowing, however, is very
difficult to detect with certainty on clinical examination
(►Video 2, Clip 2). In this setting, quantification of saccadic
velocity with confirmation of saccade slowing (►Fig. 2) is
critical to establishing an early diagnosis of PSP,13 which is ever
more important, given the burgeoning clinical treatment trials
involving an anti-tau antibody.14 Such treatments will likely be
more effective if applied as early in the disease course as
possible.
Video 2
Examples of pathological eye movements.
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Clip 1
Slow horizontal saccades in an individual with
spinocerebellar atrophy type 2. In addition to the
slowing, note the abnormal trajectory, especially
evident in saccades from left to right. There is a
downward movement accompanying the slow
horizontal saccade. This so called ‘round-the-house’
type of trajectory abnormality may be seen when
saccades are slower in one plane than another (in this
case slow horizontally and normal vertically).
Clip 2
Saccades in the vertical plane (down and back to
midposition and up and back to midposition) in a 49-
year-old man with subtle cognitive impairment and a
slow shuffling gait. The vertical eye movement range is
full and it is difficult to determine with 100% certainty
whether the saccades are slow and suggestive of a
diagnosis of progressive supranuclear palsy (PSP). Eye
movement recordings obtained at the same time as the
video are included in Fig. 2, which confirms slowing of
saccades that is much more severe than suggested by
the clinical examination. PSP was confirmed by
autopsy a few years after these initial recordings.
Clip 3
Smooth pursuit testing in a patient with a mild left
internuclear ophthalmoplegia (INO). In right gaze, a mild
adduction defect of the left eye is seen, along with very
subtle abducting nystagmus in the right eye. Eye
movement range is full to the left, although trace left-
beating gaze-evoked nystagmus is observed. This may be
physiologically normal gaze-evoked nystagmus in left
gaze.
Clip 4
Saccade testing in the individual in Video clip 3 allows
visualization of the slowing of adducting saccades in
the left eye that typically accompanies an INO.
Clip 5
Nearly continuous square wave jerks in an individual
with PSP.
Clip 6
Burst of ocular flutter in an individual with
parainfectious brainstem encephalitis.
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Fig. 1 (A) Recording of a normal 10-degree rightward horizontal saccade, showing the position of the eye during the saccade in the top trace and
the velocity of the eye during the saccade in the bottom trace. By convention, an upward deflection in the position trace represents an eye
movement to the right in a horizontal position trace or an eye movement upward in a vertical position trace. The light gray vertical line on the
position trace just after 0.2 seconds indicates the start of the saccade. The duration of time between the rightward jump of the target (blue
hatched line) and the start of the saccade is the saccade latency or reaction time. In the velocity trace, note the single peak velocity for a normal
saccade of this amplitude. (B) Relationships between saccade amplitude and peak saccade velocity for horizontal saccades in normal healthy
individuals. The 5th and 95th percentile prediction intervals are shown by the light gray hatched lines. These relationships are referred to as the
‘main sequence’. The data are fit with exponential equation peak velocity ¼ Vmax X (1-e- A/C), where Vmax is the asymptotic peak velocity, A is the
amplitude, and C is a constant defining the exponential rise.

Seminars in Neurology Vol. 39 No. 6/2019

 Eye Movement Recording in Clinical Neurology
Fig. 2 Amplitude versus peak velocity main sequence relationships for
vertical saccades in an individual with progressive supranuclear palsy (PSP),
showing severe saccadic slowing (see ►Video 2, Clip 2 for an eye
movement video obtained simultaneous to the eye movement recordings).
Red circles represent right eye vertical saccades and pink squares represent
left eye vertical saccades. Saccades in normal healthy individuals are
represented by small black dots, which are accompanied by hatched lines
representing the 5th and 95th percentile prediction intervals. Horizontal
saccades (not shown) were at the lower limit of normal and not as severely
affected, in keeping with the typical pattern of vertical worse than
horizontal saccade slowing in PSP.
Clip 7
Burst of horizontal saccadic oscillations that clinically
appeared most suggestive of ocular flutter. However,
corresponding eye movement traces, as seen in ►Fig. 5,
confirmed them to be square wave oscillations with an
intersaccadic interval rather than ocular flutter. Online
content including video sequences viewable at: https://
www.thieme-connect.com/products/ejournals/html/
10.1055/s-0039-1698742.
While PSP is a prototypical example of saccadic slowing,
it is important to keep in mind that saccadic slowing is a
pathological finding with a broad differential diagnosis that
varies depending on whether saccades are slowed more in
the vertical plane (due to RIMLF involvement), horizontal
plane (due to PPRF involvement), or both. This differential
includes degenerative, inflammatory, neoplastic and para-
neoplastic, ischemic, metabolic, and hereditary condi-
tions.15 Given the breadth of diagnoses with saccadic
slowing as a diagnostic clinical feature, the potential diag-
nostic value of quantification of eye movements should be
considered in any individual with an unexplained multifo-
cal neurological progressive disease.
Internuclear Ophthalmoplegia
Three clinical features related to horizontal eye movements
define the presence of internuclear ophthalmoplegia (INO):
impaired range of adduction in an eye ipsilateral to the
affected medial longitudinal fasciculus (MLF), slowing of
adducting saccades in the eye ipsilateral to the affected
Rizzo et al. 779
MLF, and compensatory abducting nystagmus in the oppo-
site eye. Saccade testing in the presence of an INO often more
clearly demonstrates the severity of the adduction defect and
abducting nystagmus, as compared with smooth pursuit
testing. Saccade testing also allows for clinical detection of
the accompanying adduction slowing (►Video 2, Clips 3 and
4), which may be the only clinical sign indicating that an INO
is present in some individuals.16,17 Akin to the above discus-
sion on generalized saccadic slowing, mild isolated adduc-
tion slowing indicative of the presence of an INO is very
difficult to detect on clinical examination, leading to poor
recognition of mild INO on clinical examination.16 In a study
evaluating the ability of examiners to detect INO on videos,
mild INO was missed in 71% of cases.16 Adducting slowing
can be readily detected on quantitative recordings by mea-
surement of the velocities of abducting versus adducting
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saccades (►Fig. 3), especially when the abducting/adducting
velocity ratio lies outside predictions for normal individua-
ls.18 Caution is indicated to avoid overdiagnosis of INO with
this method, however, as normal adducting saccades are
slightly slower than abducting saccades in healthy individu-
als with normal eye movements.19
Clarification of eye movement pathology (“I see the eyes
moving abnormally but am not certain what it represents”)
Saccadic Intrusions
Saccadic intrusions are a group of abnormal spontaneous eye
movements that consist of saccades that intrude upon fixation
and are divided into two broad categories: those with and
those without an intersaccadic interval. Saccadic intrusions
with an intersaccadic interval include square wave jerks, while
those without include ocular flutter, a horizontal-only oscilla-
tion, and opsoclonus, a multivectorial oscillation. These eye
movements have been defined and categorized by specific
features of quantitative eye movement recordings, including
the amplitude and trajectory of the movements, whether the
eyes cross the midline of fixation during the saccadic intrusion,
whether there is a brief pause called an intersaccadic interval
in between the saccades, and the duration of the intersaccadic
interval if present. Application of these features to differentiate
square wave jerks from ocular flutter (►Fig. 4), both of which
occur in the horizontal plane, is as follows: square wave jerks
(►Video 2, Clip 5) consist of a small amplitude (0.5–5 degrees)
saccade away from central fixation, followed by a brief inter-
saccadic interval (200 msec), with a subsequent saccade
returning the eye to midline without crossing the midline;
in contrast, ocular flutter (►Video 2, Clip 6) consists of back-to-
back small amplitude (typically 1–5 degrees) saccades that
oscillate about the midline of fixation without an intersaccadic
interval between the saccades. These two eye movements can
often be differentiated on clinical examination by the experi-
enced examiner; however, 100% accuracy is unlikely, especial-
ly with the entity of square wave oscillations comprising bursts
of back-to-back square wave jerks (►Fig. 5) (►Video 2, Clip 7).
Another example of the importance of quantitative eye move-
ment recordings in clinical practice is the possibility of micro-
ocular flutter and micro-opsoclonus, which are too small to be
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Fig. 3 Recording of 35-degree rightward and leftward horizontal saccades in the left eye of an individual with a left internuclear
ophthalmoplegia (INO), showing the position of the eye during saccades in the top trace and the velocity of the eye during the saccades in the
bottom trace. By convention, an upward deflection in the position trace represents an eye movement to the right in a horizontal position trace or
an eye movement upward in a vertical position trace. The pink hatched line represented the visual target jumps. Note the difference in the shape
of the position traces of the first rightward adducting saccade and the second leftward abducting saccade, corresponding on the velocity traces
to severe slowing of the adducting saccade and normal peak velocity of the abducting saccade.

detected by the clinical examination but can have important
implications.20 More than one type of saccadic intrusion can
also occur in the same individual. The only way to definitively
clarify the eye movement disorder present in certain cases is
with quantitative eye movement recordings.
It is critical to correctly identify the eye movement
abnormality, as these different types of saccadic intrusions
have substantially different etiologies and prognoses, some
more ominous than others. If more than one type of saccadic
intrusion is present in eye movement recordings in a given
individual, diagnostic evaluation should be guided by the
most worrisome oscillation present. Thus, eye movement
recordings should definitely be considered for any individual
with oscillopsia unaccompanied by oscillations apparent on
clinical examination.
Square wave jerks can be a completely normal physiologic
finding, especially with advancing age. Nonetheless, square
wave jerks in young individuals or nearly continuous square
wave jerks at any age warrant evaluation for underlying
neurological disease. Excess square wave jerks are often asso-
ciated with PSP21,22 (►Video 2, Clip 6), Parkinson’s disease, and
Friedreich’s ataxia.23 Bursts of back-to-back square wave jerks,
called square wave oscillations, may occur with cerebellar
disease24–26 and may be difficult to distinguish clinically from
ocular flutter (►Fig. 5) (►Video 2, Clip 7). In contrast to square
wave jerks and square wave oscillations, ocular flutter is most
often caused by either parainfectious brainstem encephalitis
or a paraneoplastic syndrome.
Nystagmus
Jerk nystagmus, whether acquired or congenital, comprises a
slow drift of the eye from a desired position (the so-called
slow phase of the nystagmus), followed by a corrective fast
movement back toward the desired position (the fast, or
quick, phase of the nystagmus). Slow phases may be of linear,
decreasing, or increasing velocity.

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Fig. 4 (A) Horizontal eye position trace showing square wave jerks. Note the pairs of saccades that remove and return the eye to central fixation
after a brief intersaccadic interval. (B) Horizontal eye position trace showing bursts of ocular flutter in left gaze. Note the back-to-back saccades
that oscillate about the midline target position (pink hatched line) with no intersaccadic interval.

Fig. 5 Square wave oscillations in a 53-year-old woman with a history of lymphoma. Note the presence of brief intersaccadic intervals between
consecutive saccades that remove and return the eye to central fixation. Coregistered body PET/CT scan and paraneoplastic panel were normal.
Prognosis of this type of eye movement remains unclear.

Infantile nystagmus syndrome, previously called congen- position in which the nystagmus is minimized). Eye move-
ital nystagmus, is characterized by horizontal oscillations ment recording traces reveal other features that are charac-
that are identical in all gaze directions, unaccompanied by teristic, including foveation periods (brief moments when
oscillopsia, and accompanied by a null position (a gaze the nystagmus stops and the eye is still and, thus, can

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782 Eye Movement Recording in Clinical Neurology Rizzo et al.
Fig. 6 Eye movement recording trace from a young woman with paraneoplastic cerebellar degeneration and downbeat nystagmus. The traces
show a single-slow phase and a single-quick phase of the nystagmus. The red line indicates the eye position and shows a slow drift of the eye
upward, followed by a quick corrective downward movement, and recurrent upward drift beginning the next slow phase of the nystagmus. The
blue line indicates the eye velocity and shows increasing velocity during the slow phase of the nystagmus.
visualize a still image) and slow phases of the nystagmus
with increasing velocity. Linear and decreasing velocity
waveforms are common with acquired forms of nystagmus,
whereas increasing velocity waveforms are characteristic of,
but not pathognomonic for, congenital nystagmus. In instan-
ces in which there is uncertainty as to whether nystagmus in
an individual is acquired or congenital, quantitative record-
ings may assist in differentiation. It is important to note,
however, that a few cases of acquired nystagmus with
increasing velocity slow phase waveforms have been
reported (►Fig. 6),27–29 although foveation periods would
be highly atypical in acquired nystagmus.
Eye movement recordings are also critical to evaluate
possible therapeutic options for treating nystagmus. While
most forms of nystagmus are recognizable on clinical exami-
nation (i.e., acquired pendular nystagmus, periodic alternating
nystagmus, downbeat nystagmus, etc.), best evidence-based
treatment approaches with immediate practical implications
arise from careful clinical trials that assess the effect of a
medication on the objectively determined amplitude and
frequency of nystagmus. Subjective improvement in vision
and reduction of oscillopsia are key outcomes in these trials,
but quantitative characterization of the nystagmus enables
one to carefully assess therapeutic modulation posttreatment
and probe the underlying pathophysiology.
Eye Movement Recording Equipment and Its
Challenges
Several methods are available for recording and quantifying
eye movements, including but not limited to the scleral search
coil (historically considered the gold standard), electro-ocu-
lography, photo-oculography, and video-oculography. Scleral
search coil is the most precise, allowing for calibration without
participant cooperation, recordings with high temporal and
spatial resolution, and data integrity without concern for
typical confounders such as blinking and lid closure.30 With
this system, a doughnut-shaped contact lens containing the
search coil is placed on the eye, and a wire connected to the coil
exits the medial portion of the palpebral fissure. As the eye
moves, current is induced in the coils and detected by a
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magnetic field.31 Major disadvantages of the scleral search
coil include the semi-invasive nature with risk of corneal
trauma, prohibitive cost, and a high technical barrier.
Despite the precision afforded by scleral search coil, video-
based eye tracking systems are in much more widespread use
currently, due to ease of accessibility, noninvasiveness, and low
relative cost. Many noninvasive eye trackers have emerged,
which are based on photography and/or active illumination
models that track both corneal light reflection and the pupil.
Table-mounted (remote) and head-mounted (forehead- or
eyeglass-based) devices are available. These devices record
the gaze angle of the eye by tracking the location of the pupil
center and/or the location of the corneal light reflection
emitted from an active infrared light source; these spatial
features are tracked and processed through each collected
video frame, and ultimately converted to the eye’s x- and y-
coordinates relative to the display monitor used for the
assessment. From a technical standpoint, two-dimensional
eye position is captured in real time and often with high
spatial resolution. Both scleral search coil and video-based
devices are capable of recording torsional eye movements,
although additional technical and analysis methodology is
often required. Noninvasive eye tracking systems are largely
limited by their sampling rate. A minimum of 200 Hz (frames/
second) is recommended for accurate assessment of saccade
peak velocity, with precision comparable to scleral search coil
methodology.32,33 Lower frame rates lead to underestimation
of peak velocity and incorrect conclusions.34 A comparative
analysis of the technical specifications for different eye track-
ing devices was recently published.35 A list of tracking devices,
along with information comparing performance and the ex-
tent of data loss between trackers, can be found online at wiki.
cogain.org, as published by a European Network of Excellence
on Communication on Gaze Interaction (COGAIN).
Many challenges arise with eye tracking, including video-
oculography. Video-oculography requires spatial calibration,
which is dependent on the participant maintaining gaze in
different positions on demand. Nystagmus and other ocular
oscillations pose problems, as does the presence of ophthal-
moplegia or cognitive dysfunction. Calibration is also chal-
lenging with head-mounted devices, as movement of the
 Eye Movement Recording in Clinical Neurology
headset can change the inferred head position and affect the
precision of recorded eye movements. In addition, establish-
ing a sound methodology to analyze raw data output from an
eye tracking device can be challenging, as no uniform set of
instructions is applied across laboratories. Recorded data are
contaminated by noise, and thus filtering is required to
smooth the data and calculate the velocity. Unavoidably,
there is a trade-off between noise suppression and signal
preservation in the selection of a filter.36 This is especially
problematic in the measurement of slow saccades, where the
use of automated algorithms often results in missed or
misidentified saccades.37,38
Conclusions
Eye movement recording and quantification is a valuable tool
for enhancing the detection and confirmation of pathological
eye movements essential to establishing a proper diagnosis.
Noninvasive and relatively low-cost video-oculographic
devices are in widespread use for this purpose. Familiarity
with the eye recording traces that are most diagnostically
helpful, such as saccadic slowing, saccadic intrusions, and
nystagmus patterns will enhance the neurologist’s clinical
acumen and contribute to diagnostic accuracy and therapeu-
tic efficacy.
Conflict of Interest
None.
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