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Goffart L (2009) Saccadic Eye Movements. In: Squire LR (ed.) Encyclopedia of
Neuroscience, volume 8, pp. 437-444. Oxford: Academic Press.
Author's personal copy
Saccadic Eye Movements 437
Saccadic Eye Movements
L Goffart, CNRS, Marseille, France
ã 2009 Elsevier Ltd. All rights reserved.
The sudden appearance of an object in the visual field
triggers an orienting shift of the line of sight (gaze)
toward its location. This movement is an extremely
rapid, steplike rotation of the two eyes – the saccade –
which can sometimes be accompanied by a head
movement. By positioning the object’s image on
the retinal region of highest acuity – the fovea – the
saccade permits a more refined visual analysis of the
object. But saccades are not exclusively aimed at
objects that suddenly appear; scanning saccades are
also generated when we explore the environment.
In this case, saccade goals must be extracted from
the visual scene based on their saliency or relevance
for subsequent actions (e.g., grasping an object, heading toward a location, avoiding an obstacle, or
reading the next word in a sentence).
Studying the neural control of saccades is a choice
research theme for investigating how the central nervous system controls goal directed action, not only
because the saccade is an essential movement used by
vertebrates to spatially organize their sensory experience but also because it is a relatively simple model of
the transformations that must be applied to sensory
signals in order to generate motor commands for reaching a goal. This research is facilitated by the fact that eye
movements can nowadays be recorded with very good
spatial and temporal resolutions. Figure 1 illustrates the
trajectory and the time course of a saccade aimed at
a small target appearing in the peripheral visual field.
The trajectory is shown by plotting the vertical versus
the horizontal angular deviation (also commonly called
position) of the eye (Figure 1(a)). The time course
shows that, after a latency (reaction time) of approximately 150 ms, the change in eye orientation is
extremely rapid (velocity profiles in Figure 1(c)) and
ends with the maintenance of the eye in a new orientation (Figure 1(b)). It also shows that a secondary correction saccade sometimes follows the primary saccade.
This apparently very simple movement is the result
of complex muscular and neural activities with a functional organization that is now fairly well understood.
In this article instead of describing the path leading
from the target-evoked retinal activity to the changes
in muscle tension that rotate the eyes, we take the
reverse path. Starting from the muscle contractions,
we proceed upstream and present the neural mechanisms involved in generating the commands for saccadic
eye movements.
Extraocular Muscles and Rotation of
the Eyes
Saccades are elicited by the cooperative action of six
muscles attached to the eyeball. These muscles are
called extraocular muscles, to distinguish them from
those located inside the eyeball which influence the
diameter of the pupil or the lens curvature. Two pairs
of muscles are involved during horizontal rotations of
the eyes (i.e., rotations around a vertical axis through
the eyeball): the lateral rectus (LR) and medial rectus
(MR) muscles. Orienting the right eye toward the
right is accomplished by the contraction of the LR
and the relaxation of the MR (Figure 2(a)) while in
the left eye the MR is contracted and the LR relaxed.
Conversely, shifting the gaze toward the left is produced by MR contraction and LR relaxation in the
right eye (Figure 2(b)) concomitantly with LR contraction and MR relaxation in the left eye. The muscles that contract are called the agonist muscles; those
that relax are called the antagonist muscles.
The muscle contraction generates a torque which is
delivered to the eyeball through tendinous attachments. Figure 2(b) shows the tension developed by
the LR and MR muscles during a horizontal saccade.
The agonist muscle tension waveform first shows
a rapid rise in tension, which is followed by a quasiexponential decay until a steady-state tension is
reached that maintains the eye deviated in the orbit.
For the antagonist muscle, the tension waveform
shows a symmetrical pattern, with a sudden drop in
tension followed by an exponential increase until the
steady-state tension is also reached. These muscle
tension recordings reveal that, after every saccade,
the orientation of the eye is settled well before the
agonist and antagonist muscle forces reach their final
equilibrium. They also illustrate the three components of the innervation signal supplied to the extraocular muscles: a pulse, a slide, and a step component.
The pulse and the slide quickly rotate the eyes and
stop them abruptly against the viscosity of the muscles and orbital tissues, respectively. The step generates the force required to hold the eyes deviated in the
orbit, overcoming the elastic forces that tend to drag
the eyes toward their resting position.
Vertical movements of the eyes (rotations about a
horizontal axis through the eyeball) are slightly more
complex than horizontal ones because they are the
result of a synergy between four other extraocular
muscles. The joint contraction of the superior rectus
(SR) and inferior oblique (IO) muscles of both eyes,
combined with the relaxation of the inferior rectus
(IR) and superior oblique (SO) muscles, rotates the
Encyclopedia of Neuroscience (2009), vol. 8, pp. 437-444
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438 Saccadic Eye Movements
H
Vertical position (°)
24
V
4⬚
Correction
saccade
50 ms
16
Primary
saccade
b
8
Target
8
−4
16
−4
24
100⬚ s−1
Horizontal
position (°)
a
50 ms
H
V
c
Figure 1 Oblique saccade: (a) spatial trajectory; (b) time course of eye position; (c) time course of eye velocity. The oblique saccade is
initiated from a fixation stimulus located straight ahead (intersection between the axes in (a)) and aimed at peripheral target located 16 to
the right and 8 upward (green diamond). Positive values of horizontal (H) and vertical (V) positions correspond to rightward and upward
eye deviations in the orbit.
SR
SO
LR
MR
IR
a
IO
Rightward saccade
Leftward saccade
MR
V
H
b
50 ms
LR
10% Fmax
Figure 2 (a) Extraocular muscles of the right eye; (b) changes in LR and MR muscles tensions during a 16 horizontal saccade. Forces
(black traces) are given as percentage of the maximum force (Fmax). Upward deflection corresponds to muscle contraction; downward
deflection corresponds to muscle relaxation. H, horizontal position; IO, inferior oblique; IR, inferior rectus; LR, lateral rectus; MR, medial
rectus; SO, superior oblique; SR, superior rectus; V, vertical position. (b) Reproduced from Miller JM and Robins D (1992) Extraocular
muscle forces in alert monkey. Vision Research 32: 1099–1113, with permission from Elsevier and the authors.
eyes upward. The bilateral contraction of the IR and
SO, combined with the relaxation of SR and IO,
rotates them downward. To date, there is no recording of the forces developed by these muscles during
vertical or oblique saccades. Oblique saccades are
generated by tensions simultaneously developed by
the muscles rotating the eye horizontally and those
rotating the eye vertically.
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Saccadic Eye Movements 439
The Saccade Generators
The force generated by extraocular muscles is driven
by the activity of motor neurons (MNs) located in
cranial nerve nuclei III (oculomotor), IV (trochlear),
and VI (abducens). The schema in Figure 3 shows the
current view of the network of motor and premotor
neurons which are involved in generating a rightward
horizontal saccade (leftward saccades involve a similar neuronal network but located in contralateral
territories of the reticular formation). The recruitment of MNs driving the agonist muscles is ensured
by a population of excitatory burst neurons (EBNs)
located in the ipsilateral pontine reticular formation (path p1). These EBNs drive the activity of abducens MNs innervating the LR of the ipsilateral eye. For
contracting the MR in the contralateral eye, the EBN
command is relayed to MNs in the oculomotor
nucleus by internuclear neurons (INs), also located in
the abducens nucleus. In parallel, EBNs activate a
population of inhibitory burst neurons (IBNs) located
in the ipsilateral medullary reticular formation and
which inhibit the activity of EBNs and MNs in the
contralateral side (path p2). The burst of ipsilateral
IBNs thereby participates in the inhibition of MNs
innervating the antagonist muscles (the LR of the left
eye and MR of the right eye). In this way, the antagonist muscles relax while the agonist muscles contract.
Some neurons in the IBN area also burst during contralateral saccades. If these neurons also inhibit
contralateral MNs, the motor command sent to the
MNs innervating the agonist muscles must be viewed
as the combination of two inputs: an excitatory input
from ipsilateral EBNs (path p1) and an inhibitory
input from the contralateral IBNs (path p3).
The activity of EBNs and IBNs located in the left
and right pontomedullary reticular formations is silenced between every saccade (e.g., when the eyes fixate)
through the activity of another class of inhibitory neurons called omnipause neurons (OPNs), which are
located in the nuclei raphe interpositus. These OPNs
display a sustained activity which is interrupted every
time a saccade is generated, irrespective of the amplitude and direction. Released from this sustained inhibition, EBNs and IBNs drive the MNs, which results in
a saccadic eye movement.
During upward and downward saccades, different
neuronal populations are involved. They are located
in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), and their organization has
not yet been completely elucidated. One major difference between the neural control of horizontal and
vertical saccades is that the former are mostly driven
by a unilateral excitatory input (from the ipsilateral
pontine reticular region), whereas the latter are
driven by a bilateral excitatory input from the left
and right riMLF. The direction of oblique saccades
is determined by the activation ratios between a unilateral horizontal saccade generator (left or right) and
a bilateral vertical saccade generator (up or down).
In normal healthy subjects, the examination of
Contraction
of agonist muscles
LR
Relaxation
of antagonist muscles
MR
MN
MN
MN
MN
IN
IN
IBN
p3
EBN
p2
IBN
EBN
p1
Figure 3 Neuronal organization involved during a rightward saccade. Arrows indicate excitatory connections; connecting lines ended
by a circle indicate inhibitory connections. The connecting lines have different colors for clarity. EBN, excitatory burst neuron; IBN,
inhibitory burst neuron; IN, interneuron; LR, lateral rectus; MN, motor neuron; MR, medial rectus; p1, path 1; p2, path 2; p3, path 3.
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440 Saccadic Eye Movements
oblique saccades shows that both the horizontal and
vertical rotations are initiated simultaneously, not
sequentially (see Figure 1). Moreover, some observations show that the horizontal and vertical components are coupled – when the velocity of one
component is reduced, the other component is also
slowed down, thereby reducing the delay between the
completion of horizontal and vertical components.
Despite this component-stretching mechanism, the
horizontal and vertical components may end at
slightly different times. The analysis of saccades generated by neurology patients is very instructive in this
matter. For example, in patients suffering from
Niemann–Pick type C disease, the horizontal component precedes the vertical component, resulting in the
completion of the vertical component well after the
end of the horizontal component.
In Figure 3, the same network is involved for a horizontal saccade aimed at an object located 4 or 16 to
the right. Additional mechanisms must be added to
this network to generate saccades of different amplitudes and durations. In the next section, we describe
what is known about how the central nervous system
controls the amplitude and duration of saccades.
reactive saccades and voluntary saccades, as well as for
the fast phases of optokinetic and rotatory nystagmi.
However, these duration–amplitude and peak
velocity–amplitude relationships show considerable
variability between subjects and even within the
same subject. They are sensitive to alertness, motivation, and several other parameters such as saccade
direction, initial deviation of the eyes in the orbit,
and the testing conditions (i.e., whether the saccade
is memory-guided or immediate). Saccade velocity also
depends on the sensory nature of the target. Saccades
toward somatosensory and auditory targets are much
slower than saccades of comparable amplitude and
direction aimed at visual targets. Saccades to moving
targets are also slower than saccades of matched
amplitude toward stationary targets and are characterized by a lower peak velocity and a prolonged deceleration phase. In some cases, a second peak eye velocity
appears during the deceleration phase, presumably
reflecting the late influence of a mechanism that compensates for the target displacement occurring before
saccade end. Similar late reacceleration peaks are
observed in saccades that accompany head movements
during very large gaze shifts.
The Spatiotemporal Transformation
The Control of Saccade Execution
The Duration and Velocity of Saccades
In almost all studies, the duration of a saccade is
defined as the time elapsed from when the eye velocity
exceeds a certain threshold (e.g., 15 s 1) to when it
returns below it. The duration of saccades increases
linearly with saccade amplitude, ranging from 1 to
50 at a rate of approximately 2–3 ms deg 1 in humans
(1–2 ms deg 1 in monkeys). For saccades less than
approximately 30 , the velocity profile is bell-shaped
(see Figure 1(c)), with a rapid rise to a peak value
(acceleration phase) followed by a symmetrical decline
in velocity (deceleration phase). For larger saccades,
the velocity profile becomes skewed, with the duration
of deceleration phase being longer than the acceleration phase. The peak velocity increases linearly with
saccade amplitude until a value of approximately 15 ,
beyond which the increase in velocity begins to saturate to a maximum value as large as 700 s 1 (900 s 1
in monkeys). These relationships between the amplitude and the duration or peak velocity of saccades are
called the main sequences. Because their graphical
shapes are relatively similar across healthy subjects,
the main sequences have become a tool for studying
the oculomotor deficits in brain-lesioned patients.
Some authors have also suggested that common physiological systems are responsible for the generation of
On the motor output side, the duration and velocity
of saccades are defined by the temporal properties of
MN activity. For saccades initiated from the straight
ahead position in the orbit, different saccade amplitudes do not involve different groups of MNs; all
MNs are recruited. Saccades of increasing amplitude
are caused by increases in the duration of MN activity,
the instantaneous firing rate dictating instantaneous
saccade velocity (rate code). On the other side, at the
sensory level, the code is topographic; targets at different locations in the visual field activate different zones
in the retina. A topographical organization is found
in several regions in the brain, including the intermediate and deep layers of the superior colliculi, the neurons
of which are located two to three synapses from the
motor nuclei. From a macroscopic point of view, the
two deep superior colliculi (dSC) form a motor map,
which appears to be in agreement with the retinal map,
with the anterior (rostral) regions of both colliculi
representing the foveal and perifoveal visual fields,
posterior (caudal) regions representing the peripheral
visual field, medial regions representing the upper visual field, and the lateral regions representing the
lower visual field. In the dSC, neurons discharge a
burst of action potentials prior to every contralateral
saccade within their movement field (i.e., the range of
saccade amplitude and direction that is preceded by
a burst). Neurons in the rostral region discharge
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Saccadic Eye Movements 441
maximally prior to small contralateral saccades,
whereas neurons in more caudal regions burst before
saccades of larger amplitude. Neurons located in the
medial border burst prior to upward oblique saccades,
and those located on the lateral border burst before
downward oblique saccades. Interestingly, the electrical
microstimulation of a particular site in the dSC evokes a
saccade with amplitude and direction corresponding to
those for which the stimulated neurons would maximally discharge. Thus, the amplitude and direction of
impending saccades are almost fully determined by
the location of active neurons in the dSC, although
exceptions exist for some particular saccades.
One fundamental problem is to understand how the
locus of collicular activity is converted into the MN
firing rate. This transformation was initially considered to be performed by a putative spatiotemporal
translator (STT) located in the cerebellum. This STT
was viewed as a look-up table mechanism which associated a specific temporal pattern of motor activity
with each locus of collicular activity. But, this explanation was not satisfactory because saccades generated
toward the same target and from the same starting
position can be slower in velocity (longer in duration),
yet still have the same amplitude. A solution to this
problem was proposed by David A Robinson in 1975 –
the duration of saccades is determined by a negative
feedback loop. According to this hypothesis, the saccade generators are driven by a motor error signal
which results from the comparison between a reference signal, specifying the goal or desired state (e.g.,
desired eye orientation or desired change in eye orientation), and a feedback signal estimating the current
state (current eye orientation or actual change in eye
orientation). As long as there is a mismatch between
these two internal signals, the motor error drives
the saccade generators until the estimated current
state matches the desired one. In this framework, the
motor error is a dynamic command that changes as the
direction of gaze is approaching that of the target.
There is no need for an explicit STT; the duration of
saccades is simply determined by the time taken to
zero-out the motor error command. To date, the negative feedback loop has been the only hypothesis proposed for the spatiotemporal transformation problem.
More recently, neuromimetic modeling taught us that
the neuronal solutions to the computations involved in
saccade generation (e.g., spatiotemporal transformation and component stretching) may not be explicitly
performed by separate groups of neurons that neurophysiologists ought to identify. Instead, these computations are implemented implicitly, emerging from the
activities of populations of neurons that are massively
interconnected and distributed over several neural
territories.
The Feedback Control of Saccades
One of the strengths of the negative feedback control is
that it endows the oculomotor system with a high level
of flexibility for the execution of saccades. If for some
reason – pathological (e.g., spinocerebellar degeneration), experimental (functional perturbation by brief
electrical microstimulation or by systemic/local injection of pharmacological agents), or natural (drop in
vigilance or blink) – the saccade is executed with a
velocity which is much slower than normal, its accuracy should be preserved as long as the feedback signal
conveys information about the change in velocity.
The feedback signal can originate from several
sources. The intrasaccadic visual signals (optic flow
and/or target-elicited retinal trace) could participate
in estimating the direction of the ongoing saccade.
In patients affected by spinocerebellar degeneration,
saccades are so dramatically slowed that saccades can
even be redirected in flight toward a new target presented during the saccade. But in normal healthy
subjects, most saccades are too short in duration for
visual signals to influence their ongoing trajectory.
Inflow signals originating from sensory receptors
located in the orbital tissues or from extraocular muscle proprioception could also be involved in the feedback. But their elimination by sectioning of
the ophthalmic branch of the trigeminal nerve does
not affect the accuracy and velocity of saccades, nor
does it affect the ability to compensate for unexpected
changes in eye position prior to saccades toward
flashed targets. The estimation of the ongoing oculomotor state could also be based on copies of commands sent to the MNs (efference copy). These
outflow signals could originate from collaterals of
the burst neurons that immediately drive the MNs.
Interestingly, partial pharmacological inactivation of
the region involved in the generation of the horizontal
component of saccades barely affects the accuracy
of the horizontal component of saccades, despite a
dramatic reduction in velocity. This result, which
demonstrates the feedback control of saccade accuracy also suggests that the number of active neurons
influences the velocity of saccades.
The hypothesis of saccade accuracy being controlled
by a negative feedback loop also predicts that a defect
in estimating the current state should lead to dysmetric
saccades. For example, an underestimation of the displacement performed by the eyes from saccade onset is
expected to lead to hypermetric saccades (saccades
larger in amplitude than required) because the motor
error is canceled later than normally (i.e., until the time
when the defective estimated displacement matches
the desired displacement). Conversely, an overestimation of the actual displacement is expected to lead to
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442 Saccadic Eye Movements
hypometric saccades (i.e., saccades that are smaller
in amplitude than required). From this perspective,
an optimal control of saccade accuracy requires a
calibration of feedback signals such that they accurately represent the actual oculomotor output. A calibration is also required because the neural encoding
of feedback signals is not necessarily commensurable
with the signals encoding the desired state. Interestingly, one of the major structures involved in the visuomotor calibration of saccades, the medial-posterior
cerebellum (composed of the vermal lobules VIc–VII
and caudal fastigial nuclei), receives visual motionrelated signals from pontine nuclei, proprioceptive signals from extraocular muscles, and eye position/
displacement information from the nucleus prepositus
hypoglossi/medial vestibular nucleus complex. In
return, the output nuclei of the medial-posterior cerebellum, the caudal fastigial nuclei, send distributed
projections to the territories housing the premotor
neurons of the saccade generators. When the normal
function of fastigial oculomotor region (FOR) is
impaired, saccades become severely dysmetric.
The Adaptive Control of Saccade Accuracy
Saccade accuracy is also maintained by adaptive
mechanisms that assess the error at the end of each
saccade and modify the visuomotor transformation
to reduce the error of the following saccade. These
adaptive mechanisms have been studied in human
patients and in monkeys with weakened muscles in
one eye. When the subject monocularly views a visual
target, saccades are accurate if the normal eye is
used but are too small in amplitude when the weakened eye is the viewing eye. If the normal eye is
patched and the subject is forced to use the weakened
eye to look at visual targets, the amplitude of saccades
gradually increases until they are nearly accurate. The
fact that the amplitude changes are observed in both
the weakened eye and the normal patched eye (which
now makes hypermetric saccades) indicates that the
adaptive changes affect a command that is issued for
conjugate movements of both eyes. This flexibility of
the oculomotor system to adjust saccade accuracy has
also been studied in experiments in which the target is
displaced to a new location during the ongoing saccade. Initially, saccades land near the initial target
location, but gradually they land closer to the new
one. Despite the plethora of studies characterizing the
adaptive properties of the saccadic system, very few
studies have tried to decipher the underlying neural
mechanisms.
A mismatch between saccade amplitude and target
eccentricity seems to also characterize saccades
generated by newborns. When orienting toward a
peripheral target, infants as young as 1–2 months
of age frequently execute a series of consecutive saccades of approximately equal size, whether accompanied by the head or not. Although hypometric, the
amplitude of saccades increases with the eccentricity
of the target.
The Specification of the Desired State
Saccades are not exclusively aimed at visual targets.
They can also be generated in the dark, toward
sounds, and to stimuli applied to the skin surface.
Localizing such stimuli is a much more complicated
task. In the case of a somatosensory stimulus, estimating its location requires the knowledge of the stimulated body region (e.g., the index fingertip of the right
hand) and of the posture of the limb on which the
stimulus is applied. For auditory stimuli, they are
localized on the basis of the interaural differences in
intensity and timing of acoustic signals. The dSC
seems to be the interface through which these different sensory signals have access to the saccadic motor
system. Several saccade-related cells in the dSC are
active prior to saccades to visual, somatosensory, or
auditory stimuli, suggesting that the converging sensory signals are translated into oculocentric coordinates by the level of the dSC. But the differences in
velocity observed among these different groups of
saccades suggest that an error signal specifying the
desired displacement is not the sole output signal that
the dSC sends to the saccade generators. These differences could be due to different levels of firing rate in
the population of active neurons or to different population sizes. It is indeed worth mentioning that regular visual saccades also have a reduced velocity and
increased duration (accuracy relatively spared) during pharmacological inactivation either of small portions within the dSC or the source of one of its major
cortical afferents, the frontal eye fields.
The locus of active neurons in the dSC is not sufficient for determining the amplitude and direction of
impending saccades. Some studies show a mismatch
between the amplitude and direction of saccades that
are actually executed and those represented by the
topography of active neurons in the dSC. Indeed, for
the same target location, the amplitude and direction
are very different between saccades to a permanent
target and saccades to a memorized target location.
The latter systematically end above the target location. Yet the same population of collicular neurons is
involved in both saccade types, suggesting that the
change in saccade accuracy is due to different neural
activities below the level of the dSC. The same dissociation holds when we compare saccades toward stationary versus moving targets. The latter do not land
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Saccadic Eye Movements 443
on the location where the target was initially
detected. Some mechanism tries to compensate for
the target displacement that occurred during the
period preceding the end of the catch-up saccade.
Chemical lesions of middle temporal (MT) cortical
area or of its pontine target, the dorsolateral pontine nucleus (DLPN), two structures known to be
involved in the processing of visual motion, impair
the accuracy of saccades to moving targets without
altering that of saccades to stationary targets.
Because the DLPN is one of the major sources of
motion-related visual signals to the cerebellum,
the compensatory mechanism probably involves
cerebellar oculomotor regions. Thus, the specification of the saccade goal presumably involves
input from the dSC and the cerebellar oculomotor
nuclei. Interestingly, for saccades to memorized targets and to moving targets, relationships exist
between the accuracy and latency of saccades
which may untangle the dynamics of the saccade
goal specification.
A dependence of saccade endpoints on the latency
has also been documented in studies testing saccades
aimed at two stimuli that are simultaneously presented at close locations in the visual field. Under
these conditions, the saccade endpoints are scattered
along an axis joining the two target locations, characterizing an averaging process. This averaging
depends on the relative properties of visual targets
(size and energy) – the saccade landing position will
be closer to the larger or the brighter target. Moreover, it mostly occurs for short latency saccades and
not when the latency exceeds 300 ms. The time window of the averaging process can be delimited by
presenting the two targets in a successive manner;
short-latency saccades end at the location of the first
target, whereas long-latency saccades end at the second target location. The amplitude transition function defines the averaging window that accounts for
endpoints that proportionately change with saccade
latency.
The Control of Saccade Initiation
Saccades are planned on the basis of information
gathered during the time interval that precedes saccade onset. This reaction time is far longer than would
be expected by adding the synaptic delays and nerve
conduction times between the excitation of sensors
and the contraction of extraocular muscles. It reflects
the time taken to extract relevant signals from sensors;
to make decisions about whether, and how, to respond
to the stimulus; and to transmit a goal to the saccadic
system. In response to the incoming information about
a stimulus, a decision signal is supposed to rise from an
initial level until it reaches a threshold level, at which
point the saccade is initiated. A rate of rise that varies
randomly between trials would explain the wide distribution of saccade latencies.
Several factors influence the latency of saccades.
On the retinal side, latency depends, for instance, on
the eccentricity of the target, on its energy, and on its
contrast relative to the background. Saccade latency
also depends on the presence and location of distractors and cues, as well as on more cognitive factors
such as the probability of the target location, the
amount of reward associated with the target, and
the target valence.
Under certain experimental conditions, the distribution of saccade latencies is bimodal. The first mode,
which can peak as low as 90 ms, designates the express
saccades, whereas the second mode corresponds to
regular saccades. The observation of express saccades is facilitated when a temporal gap separates
the fixation target offset and second target appearance. Express saccades are suppressed when the deep
superior colliculus is lesioned.
Conclusion
Saccadic eye movements are an important component
of the animal’s behavior for exploring and spatially
organizing its sensory environment. They provide a
useful tool for understanding how the central nervous
system relates the sensorium with the motor repertoire. The neurophysiological approach’s aim is to
reveal the underlying neuronal organization. It helps
us understand why and how the two eyes move
together and at the same time and why and how it
is possible to look in any direction and orient our gaze
exactly to the location where a visual object has
appeared. Further empirical research is required to
determine the extent to which these basic neural
mechanisms participate in the construction of spatial cognition and whether a similar organization
underlies the control of other types of goal-directed
movements.
See also: Basal Ganglia and Oculomotor Control;
Cerebellum and Oculomotor Control; Cortical Control of
Eye Movements; Eye and Head Movements; Eye
Movement Disorders; Frontal Eye Fields; Oculomotor
Control: Anatomical Pathways; Saccade–Pursuit
Interactions; Saccades and Visual Search; Superior
Colliculus; Supplementary Eye Fields; Target Selection
for Pursuit and Saccades.
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444 Saccadic Eye Movements
Further Reading
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