What triggers catch-up saccades during visual tracking?

When tracking moving visual stimuli, primates orient their visual axis by combining two kinds of eye movements, smooth pursuit and saccades, that have very different dynamics. Yet, the mechanisms that govern the decision to switch from one type of eye movement to the other are still poorly understood, even though they could bring a significant contribution to the understanding of how the CNS combines different kinds of control strategies to achieve a common motor and sensory goal. In this study, we investigated the oculomotor responses to a large range of different combinations of position error and velocity error during visual tracking of moving stimuli in humans. We found that the oculomotor system uses a prediction of the time at which the eye trajectory will cross the target, defined as the "eye crossing time" (T(XE)). The eye crossing time, which depends on both position error and velocity error, is the criterion used to switch between smooth and saccadic pursuit, i.e., to trigger catch-up saccades. On average, for T(XE) between 40 and 180 ms, no saccade is triggered and target tracking remains purely smooth. Conversely, when T(XE) becomes smaller than 40 ms or larger than 180 ms, a saccade is triggered after a short latency (around 125 ms).     

Shortening and prolongation of saccade latencies following microsaccades

When the eyes fixate at a point in a visual scene, small saccades rapidly shift the image on the retina. The effect of these microsaccades on the latency of subsequent large-scale saccades may be twofold. First, microsaccades are associated with an enhancement of visual perception. Their occurrence during saccade target perception could, thus, decrease saccade latencies. Second, microsaccades are likely to indicate activity in fixation-related oculomotor neurons. These represent competitors to saccade-related cells in the interplay of gaze holding and shifting. Consequently, an increase in saccade latencies would be expected after microsaccades. Here, we present evidence for both aspects of microsaccadic impact on saccade latency. In a delayed response task, participants made saccades to visible or memorized targets. First, microsaccade occurrence up to 50 ms before target disappearance correlated with 18 ms (or 8%) faster saccades to memorized targets. Second, if microsaccades occurred shortly (i.e., <150 ms) before a saccade was required, mean saccadic reaction time in visual and memory trials was increased by about 40 ms (or 16%). Hence, microsaccades can have opposite consequences for saccade latencies, pointing at a differential role of these fixational eye movements in the preparation of saccade motor programs.     

Transcranial magnetic stimulation of the posterior parietal cortex delays the latency of both isolated and combined vergence-saccade movements in humans

To explore the 3D visual environment most frequently we make combined saccade-vergence eye movements. We studied the effect of transcranial magnetic stimulation (TMS) of the right posterior parietal cortex (rPPC) on such combined eye movements versus isolated saccade and vergence. In the main experiment, TMS was applied on the rPPC 80, 90 or 100 ms after target onset. In a control experiment, TMS was applied over the primary motor cortex at 90 ms after the target presentation. TMS trials were compared with no-TMS trials. TMS of the motor cortex had no effect at all on eye movements. TMS of the rPPC had no effect on the accuracy of eye movements, but it caused a latency increase: the increase was similar for the two components of the combined saccade-vergence movements, and it did not alter the naturally existing tight relationship of latency between the two components. Furthermore, the amount of latency prolongation was similar to that of isolated vergence, and of saccades in either direction (ipsilateral or contralateral relative to the stimulated site). Latency prolongation was time-specific but in a different way for different types of eye movements: for combined and convergence eye movements, the critical time window was -130 ms or more prior to the onset of eye movement, while for saccades and divergence TMS was disruptive later, -110 ms or more prior to the onset of eye movements. The latency increase is attributed to the interference by the TMS with the fixation disengagement process, for which the rPPC is believed to be instrumental. These results suggest that fixation disengagement occurs earlier for convergence and combined eye movements than for saccades and divergence.     

Ocular gaze is anchored to the target of an ongoing pointing movement

It is well known that, typically, saccadic eye movements precede goal-directed hand movements to a visual target stimulus. Also pointing in general is more accurate when the pointing target is gazed at. In this study, it is hypothesized that saccades are not only preceding pointing but that gaze also is stabilized during pointing in humans. Subjects, whose eye and pointing movements were recorded, had to make a hand movement and a saccade to a first target. At arm movement peak velocity, when the eyes are usually already fixating the first target, a new target appeared, and subjects had to make a saccade toward it (dynamical trial type). In the statical trial type, a new target was offered when pointing was just completed. In a control experiment, a sequence of two saccades had to be made, with two different interstimulus intervals (ISI), comparable with the ISIs found in the first experiment for dynamic and static trial types. In a third experiment, ocular fixation position and pointing target were dissociated, subjects pointed at not fixated targets. The results showed that latencies of saccades toward the second target were on average 155 ms longer in the dynamic trial types, compared with the static trial types. Saccades evoked during pointing appeared to be delayed with approximately the remaining deceleration time of the pointing movement, resulting in "normal" residual saccadic reaction times (RTs), measured from pointing movement offset to saccade movement onset. In the control experiment, the latency of the second saccade was on average only 29 ms larger when the two targets appeared with a short ISI compared with trials with long ISIs. Therefore the saccadic refractory period cannot be responsible for the substantially bigger delays that were found in the first experiment. The observed saccadic delay during pointing is modulated by the distance between ocular fixation position and pointing target. The largest delays were found when the targets coincided, the smallest delays when they were dissociated. In sum, our results provide evidence for an active saccadic inhibition process, presumably to keep steady ocular fixation at a pointing target and its surroundings. Possible neurophysiological substrates that might underlie the reported phenomena are discussed.     

Early- and late-responding cells to saccadic eye movements in the cortical area V6A of macaque monkey

The cortical area V6A, located in the dorsal part of the anterior bank of the parieto-occipital sulcus, contains retino- and craniocentric visual neurones together with neurones sensitive to gaze direction and/or saccadic eye movements, somatosensory stimulation and arm movements. The aim of this work was to study the dynamic characteristics of V6A saccade-related activity. Extracellular recordings were carried out in six macaque monkeys performing a visually guided saccade task with the head restrained. The task was performed in the dark, in both the dark and light, and sometimes in the light only. The discharge of certain neurones during saccades is due to their responsiveness to visual stimuli. We used a statistical method to distinguish responses due to visual stimulation from those responsible for saccadic control. Out of 597 V6A neurones tested, 66 (11%) showed responses correlated with saccades; 26 of 66 responded also to visual stimulation and 31 of 66 did not; the remaining 9 were not visually tested. We calculated the response latency to saccade onset and its inter-trial variance in 24 of 66 neurones. Saccade neurones could respond before, during or after the saccade. Neurones responding before saccade-onset or during saccades had much higher latency variance than neurones responding after saccades. The early-responding cells had a mean latency (±SD) of –64±62 ms, while the late-responding cells a mean latency of +89±20 ms. The responses to saccadic eye movements were directionally sensitive and varied with the amplitude of the saccade. Responses of late-responding cells disappeared in complete darkness. We suggest that the activity of early-responding cells represents the intended saccadic eye movement or the shift of attention towards another part of the visual space, whereas that of late-responding cells is a visual response due to retinal stimulation during saccades. Electronic Publication     

The ability to execute saccades on the basis of efference copy: impairments in double-step saccade performance in children with developmental co-ordination disorder

The double-step saccade task (DSST) was used to test the hypothesis that children with developmental co-ordination disorder (DCD) who experience deficits in motor imagery have difficulty processing the visual spatial consequences of intended movements using efference copy signals. In order to ensure that the second saccade in the DSST was executed in the absence of visual cues and had to be programmed on the basis of extra-retinal information (efference copy), we analysed only those double-step ensembles where latency plus duration of first saccades was greater than 240 ms (total presentation time of the targets). No significant differences between DCD and control children were evident on measures of latency of first saccades, intersaccadic interval and first saccade error. As predicted, children with DCD who have impaired motor imagery demonstrated specific deficits on the DSST where efference copy had been used to program the saccade sequence. More specifically, these children were less accurate in terms of final eye position on second saccades. Our results raise the possibility that abnormalities in the processing of efference copy signals could underlie motor clumsiness in the majority of children with DCD. Furthermore, the origin of this deficit in efference copy probably exists at the level of the parietal lobe.     

Saccadic eye movements to visual and auditory targets

 Recent neurophysiological studies of the saccadic ocular motor system have lent support to the hypothesis that this system uses a motor error signal in retinotopic coordinates to direct saccades to both visual and auditory targets. With visual targets, the coordinates of the sensory and motor error signals will be identical unless the eyes move between the time of target presentation and the time of saccade onset. However, targets from other modalities must undergo different sensory-motor transformations to access the same motor error map. Because auditory targets are initially localized in head-centered coordinates, analyzing the metrics of saccades from different starting positions allows a determination of whether the coordinates of the motor signals are those of the sensory system. We studied six human subjects who made saccades to visual or auditory targets from a central fixation point or from one at 10° to the right or left of the midline of the head. Although the latencies of saccades to visual targets increased as stimulus eccentricity increased, the latencies of saccades to auditory targets decreased as stimulus eccentricity increased. The longest auditory latencies were for the smallest values of motor error (the difference between target position and fixation eye position) or desired saccade size, regardless of the position of the auditory target relative to the head or the amplitude of the executed saccade. Similarly, differences in initial eye position did not affect the accuracy of saccades of the same desired size. When saccadic error was plotted as a function of motor error, the curves obtained at the different fixation positions overlapped completely. Thus, saccadic programs in the central nervous system compensated for eye position regardless of the modality of the saccade target, supporting the hypothesis that the saccadic ocular motor system uses motor error signals to direct saccades to auditory targets. Received: 8 September 1995 / Accepted: 22 November 1996     

Processing of retinal and extraretinal signals for memory-guided saccades during smooth pursuit

It is an essential feature for the visual system to keep track of self-motion to maintain space constancy. Therefore the saccadic system uses extraretinal information about previous saccades to update the internal representation of memorized targets, an ability that has been identified in behavioral and electrophysiological studies. However, a smooth eye movement induced in the latency period of a memory-guided saccade yielded contradictory results. Indeed some studies described spatially accurate saccades, whereas others reported retinal coding of saccades. Today, it is still unclear how the saccadic system keeps track of smooth eye movements in the absence of vision. Here, we developed an original two-dimensional behavioral paradigm to further investigate how smooth eye displacements could be compensated to ensure space constancy. Human subjects were required to pursue a moving target and to orient their eyes toward the memorized position of a briefly presented second target (flash) once it appeared. The analysis of the first orientation saccade revealed a bimodal latency distribution related to two different saccade programming strategies. Short-latency (<175 ms) saccades were coded using the only available retinal information, i.e., position error. In addition to position error, longer-latency (>175 ms) saccades used extraretinal information about the smooth eye displacement during the latency period to program spatially more accurate saccades. Sensory parameters at the moment of the flash (retinal position error and eye velocity) influenced the choice between both strategies. We hypothesize that this tradeoff between speed and accuracy of the saccadic response reveals the presence of two coupled neural pathways for saccadic programming. A fast striatal-collicular pathway might only use retinal information about the flash location to program the first saccade. The slower pathway could involve the posterior parietal cortex to update the internal representation of the flash once extraretinal smooth eye displacement information becomes available to the system.     

Correlates of motor planning and postsaccadic fixation in the macaque monkey lateral geniculate nucleus

There is significant controversy regarding the ability of the primate visual system to construct stable percepts from a never-ending stream of brief fixations and rapid saccadic eye movements. In this study, we examined the timing and occurrence of perisaccadic modulation of LGN single-unit activity in awake-behaving macaque monkeys while they made spontaneous saccades in the dark and made visually guided saccades to discrete stimuli located outside the receptive field. Our hypothesis was that the activity of LGN cells is modulated by efference copies of motor plans to produce saccadic eye movements and that this modulation depends neither on the presence of feedforward visual information nor on a corollary discharge of signals directing saccadic eye movements. On average, 25% of LGN cells demonstrated significant perisaccadic modulation. This modulation consisted of a moderate suppression of activity that began more than 100 ms prior to the initiation of a saccadic eye movement and continued beyond the termination of the saccadic eye movement. This suppression was followed by a large enhancement of activity after the eyes arrived at the next fixation. Although members of all three LGN relay cell classes (magnocellular, parvocellular, and koniocellular) demonstrated significant saccade-related suppression and enhancement of activity, more cells demonstrated postsaccadic enhancement (25%) than perisaccadic suppression (17%). In no case did the timing of the modulation coincide directly with saccade duration. The degree of modulation observed did not vary with LGN cell class, LGN receptive field center location, center sign (ON-center or OFF-center), or saccade latency or velocity. The time course of modulation did, however, vary with saccade size such that suppression was longer for longer saccades. The fact that activity from a percentage of LGN cells from all cell classes was modulated in relationship to saccadic eye movements in the absence of direct visual stimulation suggests that this modulation is a general phenomenon not tied to specific types of visual stimuli. Similarly, because the onset of the modulation preceded eye movements by more than 100 ms, it is likely that this modulation reflects higher order motor-planning rather than a corollary of mechanisms in direct control of eye movements themselves. Finally, the fact that the largest modulation is a postsaccadic enhancement of activity may suggest that perisaccadic modulations are designed more for the facilitation of visual information processing once the eyes land at a new location than for filtering unwanted visual stimuli.     

Blink-perturbed saccades in monkey. I. Behavioral analysis

Saccadic eye movements are thought to be influenced by blinking through premotor interactions, but it is still unclear how. The present paper describes the properties of blink-associated eye movements and quantifies the effect of reflex blinks on the latencies, metrics, and kinematics of saccades in the monkey. In particular, it is examined to what extent the saccadic system accounts for blink-related perturbations of the saccade trajectory. Trigeminal reflex blinks were elicited near the onset of visually evoked saccades by means of air puffs directed on the eye. Reflex blinks were also evoked during a straight-ahead fixation task. Eye and eyelid movements were measured with the magnetic-induction technique. The data show that saccade latencies were reduced substantially when reflex blinks were evoked prior to the impending visual saccades as if these saccades were triggered by the blink. The evoked blinks also caused profound spatial-temporal perturbations of the saccades. Deflections of the saccade trajectory, usually upward, extended up to approximately 15 degrees. Saccade peak velocities were reduced, and a two- to threefold increase in saccade duration was typically observed. In general, these perturbations were largely compensated in saccade mid-flight, despite the absence of visual feedback, yielding near-normal endpoint accuracies. Further analysis revealed that blink-perturbed saccades could not be described as a linear superposition of a pure blink-associated eye movement and an unperturbed saccade. When evoked during straight-ahead fixation, blinks were accompanied by initially upward and slightly abducting eye rotations of approximately 2-15 degrees. Back and forth wiggles of the eye were frequently seen; but in many cases the return movement was incomplete. Rather than drifting back to its starting position, the eye then maintained its eccentric orbital position until a downward corrective saccade toward the fixation spot followed. Blink-associated eye movements were quite rapid, albeit slower than saccades, and the velocity-amplitude-duration characteristics of the initial excursions as well as the return movements were approximately linear. These data strongly support the idea that blinks interfere with the saccade premotor circuit, presumably upstream from the neural eye-position integrator. They also indicated that a neural mechanism, rather than passive elastic restoring forces within the oculomotor plant, underlies the compensatory behavior. The tight latency coupling between saccades and blinks is consistent with an inhibition of omnipause neurons by the blink system, suggesting that the observed changes in saccade kinematics arise elsewhere in the saccadic premotor system.     

Short-latency ocular following responses of monkey. II. Dependence on a prior saccadic eye movement

The ocular following responses elicited by brief unexpected movements of the visual scene were studied in eight rhesus monkeys. Test patterns were random dots except in one experiment when sine-wave gratings were used. Test stimuli were velocity steps of 100-ms duration applied after spontaneous saccades. Two response measures were used: the initial peak in the eye velocity profile (ei), and the average final eye velocity over the period of 110-140 ms measured from stimulus onset (ef). Responses were best when the test ramps began soon after saccades and attenuated progressively as the postsaccadic delay interval was increased: postsaccadic enhancement of ocular following. The decline in ei was roughly exponential: average time constant, 60 ms; average asymptote, 22%. Later measures (ef) were generally less affected. We suggest that this transient enhancement aids the visual suppression of postsaccadic ocular drifts (glissades) and the tracking of moving images newly acquired with a saccade. The magnitude of the postsaccadic enhancement was dependent on the amount of retinal stimulation during the antecedent saccade; when this stimulation was compromised, as when a vertical saccade was made while viewing a grating pattern with vertically oriented stripes, subsequent enhancement of ocular following was much reduced. Further, saccade-like conditioning movements of the visual scene resulted in an enhancement of the ocular following, elicited by subsequent test ramps, that was similar in magnitude and time course to that in the wake of real saccades. We conclude that the postsaccadic enhancement of ocular following is largely due to the visual stimulation produced by the saccade sweeping the scene across the retina. Data obtained with the visual field partitioned into central and peripheral regions (center 20-60 degrees diam) and with gaze centered suggested that the short-latency ocular following system and the enhancement mechanism that modulates it both receive their major inputs from the central 40 degrees of the retina. Further, when this central region was partitioned, enhancement was obtained only when the conditioning and test stimuli were presented to the same region of retina. Visual enhancement showed only weak interocular transfer: the conditioning and test stimuli had to be seen by the same eye to produce appreciable enhancement. These data suggest that the enhancement involves local spatial interactions at an "early" point in the visual pathway before the inputs from the two eyes have converged. When the conditioning and test stimuli impinged on different regions of the retina, brief powerful suppression of ocular following was obtained.(ABSTRACT TRUNCATED AT 400 WORDS)     

Eye position and target amplitude effects on human visual saccadic latencies

Gaze shifts vary in the extent of eye and head contribution; a large amplitude and/or an eccentric ocular orbital starting position alter the participation of head movement in the shift. The interval between eye onset and head onset determines compensatory counterrolling before and after the shift and the extent of vestibular ocular reflex reduction during the shift. The latency of eye saccades in the head-fixed condition was measured with respect to target amplitude and orbital position in order to establish base-line operations of these two variables as they apply to the headfree condition. Eye movements were measured during single-step saccades in nine young adult humans. The target step, hereafter called a jump, started from three possible fixation lights; e.g., rightward saccades started from the midline (0°) or from -20 or -40° left of the midline, with a maximum amplitude of 80°. The latency of saccades starting from the primary position increased with jump amplitude (amplitude-latency relation). When the eye started eccentrically, the latency was decreased (orbital position-latency relation), with the largest jump amplitudes most affected. These changes can be related to active eye-head coordination. Thus, with a leftward maximal orbital eccentricity, compensatory eye rotation would be impossible with a rightward head movement; however, incorporating the orbital position-latency relation, the forward ocular saccade is expedited by 90 ms. Conversely, with a primary starting position, the ocular component of an 80° gaze saccade could be slowed 125 ms by incorporating the amplitude-latency relation, thus facilitating a head contribution to the gaze shift. The orbital position and amplitude-latency relations were prominent in those subjects with habitually large head contributions to the gaze shift and minimal in individuals with typically small head contributions.     

Control of eye movement reflexes

We investigated the effect of strategic suppression of reflexive eye movements on external control over fixation using a fixation offset paradigm. A visual signal at fixation facilitates the fixation reflex and inhibits eye movements. Certain preparatory states render the fixation reflex less reactive to visual stimulation at fixation, as evidenced by a reduction in the fixation offset effect (FOE). For example, past studies have suggested that the reduced FOE during anti-saccade tasks results from the requirement to inhibit reflexive eye movements. We tested whether suppressing reflexive saccades reduces external control over ocular fixation using a go-nogo saccade paradigm. During each trial, one of two targets appeared in the periphery. Participants were instructed to saccade to one target (go), but when the other target appeared they either had to maintain fixation (nogo) or move their eyes in the direction opposite the target (anti). When nogo trials were admixed with target-directed saccades a large FOE was observed compared to when target-directed saccades occurred alone (experiment 1); however, when anti-saccades were mixed with target-directed saccades, a small FOE was observed for both types of eye movements (experiment 2). We conclude that suppressing reflexive eye movements does not reduce external control over fixation. Further research is necessary to elucidate which other component of preparing to make an anti-saccade diminishes the FOE.     

A startle speeds up the execution of externally guided saccades

The control of eye movements depends in part on subcortical motor centres. Gaze is often directed towards salient visual stimuli of our environment with no conscious voluntary commands. To further understand to what extent preprogrammed eye movements can be triggered subcortically, we carried out a study in normal volunteers to examine the effects of a startling auditory stimulus (SAS) on externally guided saccades. A peripheral visual cue was presented in the horizontal plane at a site distant 15° from the fixation point, and subjects were instructed to make a saccade to it. SAS was presented together with the peripheral visual cue in 20% of trials. To force rapid visual fixation at the end of the saccade, targets were loaded with a second cue, a small arrow pointing towards the right or the left (or a neutral sign), not distinguishable with peripheral vision. Subjects were requested to perform a flexion/extension wrist movement, according to the direction of the arrow (or not to move if the second cue was the neutral sign). SAS presented together with the visual target caused a significant shortening of the latency of saccadic movements. The wrist movements performed as a response to the second cue had similar reaction times regardless of whether the trial contained a SAS or not. Our results show that voluntary saccades to peripheral targets are speeded up by activation of the startle circuit, and that this effect does not cause a significant disturbance in the execution of simple in-target cues. These results suggest that subcortical structures play a main role in preparation of externally guided saccades.     

Visual-ocular motor activity in the macaque pregeniculate complex

The anatomical connections of the pregeniculate complex (PrGC) with components of the visual-ocular motor system suggested its contribution to ocular motor behavior. Subsequent studies reported saccade-related activity in the primate PrGC. To determine its contribution, we characterized pregeniculate units (n = 128) in alert macaques during ocular motor tasks and visual stimulation. We found that 36/109 saccade-related units exhibited postsaccadic bursts or pauses in tonic discharge for saccades of any amplitude or direction. In contrast to previous results, 46/109 responses preceded or coincided with the saccade, while 47/109 responses were directionally tuned. Pregeniculate units were modulated not only in association with saccades (109/128) but also with smooth eye movements and visual motion (20/128) or eye position (23/128). Multiple ocular motor signals were recorded from 19% of the units, indicating signal convergence on individual neurons. Visual responses were demonstrated in 51% of PrGC units: visual field illumination modulated the resting discharge of 33 units; the responses of 37 saccade-related units and all 23 position-dependent units were modulated by visual stimulation. Early saccadic activity in the PrGC suggests that it contributes more to gaze than postsaccadic modulation of visual or ocular motor activity. The patterns of saccadic responses and the modulation of PrGC activity in association with a variety of visual-ocular motor behaviors suggest its potential role as a relay between the parietal cortex and elements of the brain stem ocular motor pathways, such as the superior colliculus and pretectal nucleus of the optic tract.     

Neuronal activity related to visually guided saccadic eye movements in the supplementary motor area of rhesus monkeys.

1. The purpose of this study was to describe the response properties of neurons in the supplementary motor area (SMA), including the supplementary eye fields (SEF) of three rhesus monkeys (Macaca mulatta) performing visually guided eye and forelimb movements. Seven hundred thirty single units were recorded in the dorsomedial agranular cortex while monkeys performed a go/no-go visual tracking task. The unit activity associated with rewarded, task-related movements was compared with that associated with unrewarded, spontaneous movements executed in the intertrial interval or when the task was not running. A number of neuronal response types were identified. 2. Sensory cells were characterized by their response to the visual and/or auditory target stimuli combined with no discharge associated with eye or forelimb movements. New information was provided about the receptive fields of the visual cells; they varied in size and, although many included the ipsilateral hemifield, they tended to emphasize the contralateral. A significant proportion of the visually responsive cells had receptive fields restricted to within 8 degrees of the fovea. The response latency was relatively long (greater than 90 ms) and variable. 3. Preparatory set cells were activated from the appearance of the target until the presentation of the go/no-go cue. This subpopulation ceased firing 50-100 ms before the movement was initiated. These cells tended to respond best in relation to contralateral movements. The response latency was similar to that of the sensory cells, although some of these units began to discharge in anticipation of predictable target presentations. These neurons were not active before unrewarded, spontaneous saccades. 4. Sensory-movement cells comprised the largest population of neurons identified in SMA. They were active from the appearance of the target until after the execution of the saccade. These neurons tended to respond preferentially in association with contraversive saccades. The latency of response to the target was significantly longer than that of the sensory cells. There was a large amount of variability in the time to reach the peak level of activation, and this population of units generally became inactivated shortly after the saccade was initiated. Although there were counterexamples, most sensory-movement cells responded equally in association with visually and auditory guided movements. In addition, these neurons were not active in relation to self-generated eye movements made during the intertrial intervals. 5. Pause-rebound cells were identified by their suppression at the appearance of the target and subsequent discharge associated with the saccade. These units tended to respond preferentially to contralateral targets.(ABSTRACT TRUNCATED AT 400 WORDS)     

Retinal image motion alone does not control disconjugate postsaccadic eye drift

1. In these experiments, postsaccadic ocular drift was induced by postsaccadic motion of the visual scene. In the most important case, the scene was moved in one eye but not the other. Six human subjects viewed the interior of a full-field hemisphere filled with a random-dot pattern. During training, eye movements were recorded by the electrooculogram. A computer detected the end of every saccade and immediately moved the pattern horizontally in the same or, in different experiments, in the opposite direction as the saccade. The pattern motion was exponential with an amplitude of 25% of the size of the antecedent saccade and a time constant of 50 ms. Before and after 3-4 h of such training, movements of both eyes were measured simultaneously by the eye coil-magnetic field method while subjects looked between stationary targets for calibration, explored the visual pattern with saccades, or made saccades in the dark to measure the effects of adaptation on postsaccadic ocular drift. The amplitude of this drift was expressed as a percentage of the size of the antecedent saccade. 2. In monocular experiments, subjects viewed the random-dot pattern with one eye. The other eye was patched. With two subjects, the pattern drifted backward in the direction opposite to the saccade; with the third, it drifted onward. The induced ocular drift was exponential, always in the direction to reduce retinal image motion, had zero latency, and persisted in the dark. After training, drift in the dark changed by 6.7% in agreement with our prior study with binocular vision, which produced a change of 6.0%. 3. In a dichoptic arrangement, one eye regarded the moveable random-dot pattern; the other, through mirrors, saw a different random-dot pattern (with similar spacing, contrast, and distance) that was stationary. These visual patterns were not fuseable and did not evoke subjective diplopia. In this case, the induced change in postsaccadic drift in the same three subjects was only 4.8%. In all cases the changes in postsaccadic drift were conjugate--they obeyed Hering's law. 4. Normal human saccades are characterized by essentially no postsaccadic drift in the abducting eye and a pronounced onward drift (approximately 4%) in the adducting eye. After training, this abduction-adduction asymmetry was preserved in the light and dark with monocular or dichoptic viewing, indicating again that all adaptive changes were conjugate. 5. When the subjects viewed the adapting stimulus after training, the zero-latency, postsaccadic drift always increased from levels in the dark.(ABSTRACT TRUNCATED AT 400 WORDS)     

Gap effects on saccade and vergence latency

To explore visual space, we make saccades, vergence, and, most frequently, combined saccade–vergence eye movements. The initiation of saccades is well studied, while that of vergence is less explored. Saccade latency is influenced by the fixation task: when the target appears simultaneously with the offset of the fixation point, latencies tend to be regular, whereas the introduction of a gap period before target onset causes the emergence of express latencies (80- to 120-ms). This study examines in ten normal adults whether the gap paradigm has a similar effect on the latency of vergence and combined eye movements. The second goal is to identify contextual factors that favor the emergence of short latencies, by comparing a condition in which gap and simultaneous trials were performed in separate blocks (pure blocks) with a condition in which the two types of trials were interleaved randomly (mixed blocks). The results are: (1) the gap paradigm reduced similarly (by approximately –30 ms) the mean latency of saccades, convergence, divergence, and both the saccadic and vergence components of combined eye movements; (2) the gap paradigm was responsible for the emergence of 80– to 120-ms latencies for saccades and divergence (pure or combined), but rarely for convergence; (3) inspection of the latency distributions showed that such short latencies formed a clearly distinct population, different from anticipatory responses or regular latencies, for saccades (pure or combined) but not for pure vergence; importantly, distinct express latencies were found also for the convergence and divergence components of combined eye movements; (4) no difference was found for the group of subjects between pure and mixed blocks, but the latter yielded shorter latencies for some subjects, suggesting an idiosyncratic phenomenon. We suggest that distinct express latencies are specific to saccades and could correspond to a specific mode of saccade initiation. Interestingly, the express mode of triggering can be transferred to the vergence component in the ecological condition in which saccade is combined with vergence.     

Latency of saccades during smooth-pursuit eye movement in man Directional asymmetries

To examine the effects of smooth-pursuit eye movements on the initiation of saccades, their latency was measured when subjects initially fixated or pursued a target. In half of the block of trials, the fixation or pursuit target was extinguished 200 ms before the saccade target was illuminated (gap trials). Reduction of the mean saccade latency in the gap trials (the “gap effect”) was evident even when the subjects were pursuing a moving target, consistent with previous observations. The effect of pursuit direction on saccade latency was also examined. Saccades in the same direction as the preceding pursuit (forward saccades) had shorter latencies than those in the opposite direction (backward saccades). This asymmetry was observed in both the gap and nongap trials. Although the forward-backward asymmetry was much smaller than the “gap effect”, it was statistically significant in six of eight cases. These results suggest that the preparation of saccades is affected by smooth-pursuit eye movements. Received: 2 June 1997 / Accepted: 6 November 1997     

Interactions between visually and electrically elicited saccades before and after superior colliculus and frontal eye field ablations in the rhesus monkey

Recent work has shown that humans and monkeys utilize both retinal error and eye position signals to compute the direction and amplitude of saccadic eye movements (Hallett and Lightstone 1976a, b; Mays and Sparks 1980b). The aim of this study was to examine the role the frontal eye fields (FEF) and the superior colliculi (SC) play in this computation. Rhesus monkeys were trained to acquire small, briefly flashed spots of light with saccadic eye movements. During the latency period between target extinction and saccade initiation, their eyes were displaced, in total darkness, by electrical stimulation of either the FEF, the SC or the abducens nucleus area. Under such conditions animals compensated for the electrically induced ocular displacement and correctly reached the visual target area, suggesting that both a retinal error and eye position error signal were computed. The amplitude and direction of the electrically induced saccades depended not only on the site stimulated but also on the amplitude and direction of the eye movement initiated by the animal to acquire the target. When the eye movements initiated by the animal coincided with the saccades initiated by electrical stimulation, the resultant saccade was the weighted average of the two, where one weighing factor was the intensity of the electrical stimulus. Animals did not acquire targets correctly when their eyes were displaced, prior to their intended eye movements, by stimulating in the abducens nucleus area. After bilateral ablation of either the FEF or the SC monkeys were still able to acquire visual targets when their eyes were displaced, prior to saccade initiation, by electrical stimulation of the remaining intact structure. These results suggest that neither the FEF nor the SC is uniquely responsible for the combined computation of the retinal error and the eye position error signals.