This article was originally published in the Encyclopedia of Neuroscience published by Elsevier, and the attached copy is provided by Elsevier for the author's benefit and for the benefit of the author's institution, for noncommercial research and educational use including without limitation use in instruction at your institution, sending it to specific colleagues who you know, and providing a copy to your institution’s administrator. All other uses, reproduction and distribution, including without limitation commercial reprints, selling or licensing copies or access, or posting on open internet sites, your personal or institution’s website or repository, are prohibited. For exceptions, permission may be sought for such use through Elsevier's permissions site at: http://www.elsevier.com/locate/permissionusematerial 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 Author's personal copy 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. Encyclopedia of Neuroscience (2009), vol. 8, pp. 437-444 Author's personal copy 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. Encyclopedia of Neuroscience (2009), vol. 8, pp. 437-444 Author's personal copy 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 Encyclopedia of Neuroscience (2009), vol. 8, pp. 437-444 Author's personal copy 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 Encyclopedia of Neuroscience (2009), vol. 8, pp. 437-444 Author's personal copy 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 Encyclopedia of Neuroscience (2009), vol. 8, pp. 437-444 Author's personal copy 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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