Adaptation of voluntary saccades, but not of reactive saccades, transfers to hand pointing movements

Studying the transfer of visuomotor adaptation from a given effector (e.g., the eye) to another (e.g., the hand) allows us to question whether sensorimotor processes influenced by adaptation are common to both effector control systems and thus to address the level where adaptation takes place. Previous studies have shown only very weak transfer of the amplitude adaptation of reactive saccades--i.e., produced automatically in response to the sudden appearance of visual targets--to hand pointing movements. Here we compared the amplitude of hand pointing movements recorded before and after adaptation of either reactive or voluntary saccades, produced either in a saccade sequence task or in a single saccade task. No transfer to hand pointing movements was found after adaptation of reactive saccades. In contrast, a substantial transfer to the hand was obtained following adaptation of voluntary saccades produced in sequence. Large amounts of transfer between the two saccade types were also found. These results demonstrate that the visuomotor processes influenced by saccadic adaptation depend on the type of saccades and that, in the case of voluntary saccades, they are shared by hand pointing movements. Implications for the neurophysiological substrates of the adaptation of reactive and voluntary saccades are discussed.     

On the short-term adaptation of eye saccades and its transfer to head movements

During a sequence of eye saccades toward a target that is systematically displaced during initiation of the saccade, the oculomotor system adjusts saccadic amplitude and direction in less than 100 trials to directly reach the second target position. The goal of the present work was to test whether and under which conditions these short-term, adaptive modifications in eye movements are transferred from horizontal eye saccades to horizontal head-pointing movements. In the first series of experiments subjects had to execute head yaw rotations to an extent defined by verbal command (assessed movements). These head movements were not part of visually elicited gaze shifts. They were recorded before and after a period of saccadic adaptation. Saccades were adapted to reduced amplitudes by using target displacements from 30 to 20° and from 40 to 30°. After 40–50 trials per target displacement, the amount of eye saccade adaptation was 79% (30–20°) and 97% (40–30°) of the displacement amplitude. In the second series of experiments, visually triggered head movements to briefly illuminated targets (100 ms) were measured before and after adaptation. The data obtained from both series did not reveal a functionally significant transfer of saccadic adaptation to head movements. The amount of possible transfer given as a percentage of the amount of achieved adaptation was: assessed head movements, 40°, 1.9%, 20°, -8.6%; visually triggered movements, 40°, 5.1%, 20°, 10.0%. No values significantly deviated from zero.     

Mislocalization of stationary and flashed bars after saccadic inward and outward adaptation of reactive saccades

Recent studies have shown that saccadic inward adaptation (i.e., the shortening of saccade amplitude) and saccadic outward adaptation (i.e., the lengthening of saccade amplitude) rely on partially different neuronal mechanisms. There is increasing evidence that these differences are based on differences at the target registration or planning stages since outward but not inward adaptation transfers to hand-pointing and perceptual localization of flashed targets. Furthermore, the transfer of reactive saccade adaptation to long-duration overlap and scanning saccades is stronger after saccadic outward adaptation than that after saccadic inward adaptation, suggesting that modulated target registration stages during outward adaptation are increasingly used in the execution of saccades when the saccade target is visually available for a longer time. The difference in target presentation duration between reactive and scanning saccades is also linked to a difference in perceptual localization of different targets. Flashed targets are mislocalized after inward adaptation of reactive and scanning saccades but targets that are presented for a longer time (stationary targets) are mislocalized stronger after scanning than after reactive saccades. This link between perceptual localization and adaptation specificity suggests that mislocalization of stationary bars should be higher after outward than that after inward adaptation of reactive saccades. In the present study we test this prediction. We show that the relative amount of mislocalization of stationary versus flashed bars is higher after outward than that after inward adaptation of reactive saccades. Furthermore, during fixation stationary and flashed bars were mislocalized after outward but not after inward adaptation. Thus, our results give further evidence for different adaptation mechanisms between inward and outward adaptation and harmonize some recent research.     

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.     

Flexibility of saccade adaptation in the monkey: different gain states for saccades in the same direction

Saccadic accuracy, measured as the ratio of the size of a saccade to the size of the target step that elicits it, i.e., saccade gain, can be altered by jumping the target surreptitiously during the targeting saccade. The gain change produced by this paradigm does not generalize or transfer to saccades of all sizes. Instead, the amount of transfer decreases the more the tested saccade differs in amplitude and direction from that adapted. Here, we tested the limits of this saccade-size specificity by attempting to impose quite different gain states on saccades in the same direction. We altered the saccadic gain by intrasaccadic target jumps of 30% of the initial target step, either forward to produce a gain increase or backward to produce a gain decrease. Three different conditions were studied: (1) saccades to target steps of 20 degrees or 7 degrees were adapted in individual sessions with backward and forward jumps, respectively; (2) saccades to target steps of 20 degrees caused backward target jumps during the same session in which saccades to 7 degrees target steps caused forward steps; (3) the target jumps accompanying 20 and 7 degrees saccades were the same as in (2), but in addition, there were intermediate-sized saccades to 13.5 degrees target steps with no intrasaccadic target jumps. Saccadic gain adaptation was quite flexible. In condition 2, we could simultaneously increase the gain of saccades to 7 degrees target steps while decreasing the gain of saccades to 20 degrees steps in the same direction. Intermediate horizontal saccades to 13.5 degrees target steps experienced gain reductions (average: 6.9%), which were not the sum of gain changes expected from separate 20 degrees gain decreases and 7 degrees gain increases alone, as predicted from condition 1. If adaptation at 20 degrees and 7 degrees occurred while an animal also tracked a non-adapting 13.5 degrees target step (paradigm 3), the gain reduction of saccades to the 13.5 degrees step was reduced considerably (3.4%). Thus, the mechanism that adapts saccade size can support a robust gain increase for saccades of one size while simultaneously supporting a robust gain decrease for saccades only 13 degrees larger. Furthermore, the presence during adaptation of a non-adapted target step with a size intermediate to the two adapting steps reestablishes a nearly normal gain within only 6.5 degrees of a robust gain increase and decrease. These data indicate that saccadic gain adaptation can set very different gain states for saccades with rather similar vectors.     

Eye position effects in saccadic adaptation

Saccades are used by the visual system to explore visual space with the high accuracy of the fovea. The visual error after the saccade is used to adapt the control of subsequent eye movements of the same amplitude and direction in order to keep saccades accurate. Saccadic adaptation is thus specific to saccade amplitude and direction. In the present study we show that saccadic adaptation is also specific to the initial position of the eye in the orbit. This is useful, because saccades are normally accompanied by head movements and the control of combined head and eye movements depends on eye position. Many parts of the saccadic system contain eye position information. Using the intrasaccadic target step paradigm, we adaptively reduced the amplitude of reactive saccades to a suddenly appearing target at a selective position of the eyes in the orbitae and tested the resulting amplitude changes for the same saccade vector at other starting positions. For central adaptation positions the saccade amplitude reduction transferred completely to eccentric starting positions. However, for adaptation at eccentric starting positions, there was a reduced transfer to saccades from central starting positions or from eccentric starting positions in the opposite hemifield. Thus eye position information modifies the transfer of saccadic amplitude changes in the adaptation of reactive saccades. A gain field mechanism may explain the eye position dependence found.     

Segment interdependency and gaze anchoring during manual two-segment sequences

This study examined two-segment pointing movements with various accuracy constraints to test whether there is segment interdependency in saccadic eye movements that accompany manual actions. The other purpose was to examine how planning of movement accuracy and amplitude for the second pointing influences the timing of gaze shift to the second target at the transition between two segments. Participants performed a rapid two-segment pointing task, in which the first segment had two target sizes, and the second segment had two target sizes and two movement distances. The results showed that duration and peak velocity of the initial pointing were influenced by altered kinematic characteristics of the second pointing due to task manipulations of the second segment, revealing segment interdependency in hand movements. In contrast, saccade duration and velocity did not show such segment interdependency. Thus, unlike hand movements, saccades are planned and organized independently for each segment during sequential manual actions. In terms of the timing of gaze shift to the second target, this was delayed when the initial pointing was made to the smaller first target, indicating that gaze anchoring to the initial target is used to verify the pointing termination. Importantly, the gaze shift was delayed when the second pointing was made to the smaller or farther second target. This suggests that visual information of the hand position at the initial target is important for the planning of movement distance and accuracy of the next pointing. Furthermore, timings of gaze shift and pointing initiation to the second target were highly correlated. Thus, at the transition between two segments, gazes and hand movements are highly coupled in time, which allows the sensorimotor system to process visual and proprioceptive information for the verification of pointing termination and planning of the next pointing.     

Adaptation of eye and hand movements to target displacements of different size

Previous work has documented that the direction of eye and hand movements can be adaptively modified using the double-step paradigm. Here we report that both motor systems adapt not only to small direction steps (5° gaze angle) but also to large ones (28° gaze angle). However, the magnitude of adaptation did not increase with step size, and the relative magnitude of adaptation therefore decreased from 67% with small steps to 15% with large steps. This decreasing efficiency of adaptation may reflect the participation of directionally selective neural circuits in double-step adaptation.     

Vestibuloocular reflex inhibition and gaze saccade control characteristics during eye-head orientation in humans

1. In natural conditions, gaze (i.e., eye + head) orientation is a complex behavior involving simultaneously the eye and head motor systems. Thus one of the key problems of gaze control is whether or not the vestibuloocular reflex (VOR) elicited by head rotation and saccadic eye movement linearly add. 2. Kinematics of human gaze saccades within the oculomotor range (OMR) were quantified under different conditions of head motion. Saccades were visually triggered while the head was fixed or passively moving at a constant velocity (200 deg/s) either in the same direction as, or opposite to, the saccade. Active eye-head coordination was also studied in a session in which subjects were trained to actively rotate their head at a nearly constant velocity during the saccade and, in another session, during natural gaze responses. 3. When the head was passively rotated toward the visual target, both maximum and mean gaze velocities increased with respect to control responses with the head fixed; these effects increased with gaze saccade amplitude. In addition, saccade duration was reduced so that corresponding gaze accuracy, although poorer than for control responses, was not dramatically affected by head motion. 4. The same effects on gaze velocity were present during active head motion when a constant head velocity was maintained throughout saccade duration, and gaze saccades were as accurate as with the head fixed. 5. During natural gaze responses, an increased gaze velocity and a decreased saccade duration with respect to control responses became significant only for gaze displacement larger than 30 degrees, due to the negligible contribution of head motion for smaller responses. 6. When the head was passively rotated in the opposite direction to target step, gaze saccades were slower than those obtained with the head fixed; but their average accuracy was still maintained. 7. These results confirm a VOR inhibition during saccadic eye movements within the OMR. This inhibition, present in all 16 subjects studied, ranged from 40 to 96% (for a 40 degree target step) between subjects and increased almost linearly with target step amplitude. Furthermore, the systematic difference between instantaneous VOR gain estimated at the time of maximum gaze velocity and mean VOR gain estimated over the whole saccadic duration indicates a decay of VOR inhibition during the ongoing saccade. 8. A simplified model is proposed with a varying VOR inhibition during the saccade. It suggests that VOR inhibition is not directly controlled by the saccadic pulse generator.(ABSTRACT TRUNCATED AT 400 WORDS)     

Predictive remapping of visual features precedes saccadic eye movements

The frequent occurrence of saccadic eye movements raises the question of how information is combined across separate glances into a stable, continuous percept. Here I show that visual form processing is altered at both the current fixation position and the location of the saccadic target before the saccade. When human observers prepared to follow a displacement of the stimulus with the eyes, visual form adaptation was transferred from current fixation to the future gaze position. This transfer of adaptation also influenced the perception of test stimuli shown at an intermediate position between fixation and saccadic target. Additionally, I found a presaccadic transfer of adaptation when observers prepared to move their eyes toward a stationary adapting stimulus in peripheral vision. The remapping of visual processing, demonstrated here with form adaptation, may help to explain our impression of a smooth transition, with no temporal delay, of visual perception across glances.     

Gaze anchoring to a pointing target is present during the entire pointing movement and is driven by a non-visual signal

A well-coordinated pattern of eye and hand movements can be observed during goal-directed arm movements. Typically, a saccadic eye movement precedes the arm movement, and its occurrence is temporally correlated with the start of the arm movement. Furthermore, the coupling of gaze and aiming movements is also observable after pointing initiation. It has recently been observed that saccades cannot be directed to new target stimuli, away from a pointing target stimulus. Saccades directed to targets presented during the final phase of a pointing movement were delayed until after pointing movement offset ("gaze anchoring"). The present study investigated whether ocular gaze is anchored to a pointing target during the entire pointing movement. In experiment 1, new targets were presented at various times during the duration of a pointing movement, triggered by the kinematics arm moment itself (movement onset, peak acceleration/velocity/deceleration, and offset). Subjects had to make a saccade to the new target as fast as possible while maintaining the pointing movement to the initial target. Saccadic latencies were increased by an amount of time that approximately equaled the remaining pointing time after saccadic target presentation, with the majority of saccades executed after pointing movement offset. The nature of the signal driving gaze stabilization during pointing was investigated in experiment 2. In previous experiments where ocular gaze was anchored to a pointing target, subjects could always see their moving arm, thus it was unknown whether a visual image of the moving arm, an afferent (proprioceptive) signal or an efferent (motor control related) signal produced gaze anchoring. In experiment 2 subjects had to point with or without vision of the moving arm to test whether a visual signal is used to anchor gaze to a pointing target. Results indicate that gaze anchoring was also observed without vision of the moving arm. The findings support the existence of a mechanism enforcing ocular gaze anchoring during the entire duration of a pointing movement. Moreover, such a mechanism uses an internally generated, or proprioceptive, nonvisual signal. Possible neural substrates underlying these processes are discussed, as well as the role of selective attention.     

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 anti-orienting phenomenon revisited: effects of gaze cues on antisaccade performance

When the eye gaze of a face is congruent with the direction of an upcoming target, saccadic eye movements of the observer towards that target are generated more quickly, in comparison with eye gaze incongruent with the direction of the target. This work examined the conflict in an antisaccade task, when eye gaze points towards the target, but the saccadic eye movement should be triggered in the opposite direction. In a gaze cueing paradigm, a central face provided an attentional gaze cue towards the target or away from the target. Participants (N = 38) generated pro- and antisaccades to peripheral targets that were congruent or incongruent with the previous gaze cue. Paradoxically, facilitatory effects of a gaze cue towards the target were observed for both the pro- and antisaccade tasks. The results are consistent with the idea that eye gaze cues are processed in the task set that is compatible with the saccade programme. Thus, in an antisaccade paradigm, participants may anti-orient with respect to the gaze cue, resulting in faster saccades on trials when the gaze cue is towards the target. The results resemble a previous observation by Fischer and Weber (Exp Brain Res 109:507–512, 1996) using low-level peripheral cues. The current study extends this finding to include central socially communicative cues.     

Visual signals contribute to the coding of gaze direction

Accurate information about gaze direction is required to direct the hand towards visual objects in the environment. In the present experiments, we tested whether retinal inputs affect the accuracy with which healthy subjects indicate their gaze direction with the unseen index finger after voluntary saccadic eye movements. In experiment 1, subjects produced a series of back and forth saccades (about eight) of self-selected magnitudes before positioning the eyes in a self-chosen direction to the right. The saccades were produced while facing one of four possible visual scenes: (1) complete darkness, (2) a scene composed of a single light-emitting diode (LED) located at 18 degrees to the right, (3) a visually enriched scene made up of three LEDs located at 0 degrees, 18 degrees and 36 degrees to the right, or (4) a normally illuminated scene where the lights in the experimental room were turned on. Subjects were then asked to indicate their gaze direction with their unseen index finger. In the conditions where the visual scenes were composed of LEDs, subjects were instructed to foveate or not foveate one of the LEDs with their last saccade. It was therefore possible to compare subjects' accuracy when pointing in the direction of their gaze in conditions with and without foveal stimulation. The results showed that the accuracy of the pointing movements decreased when subjects produced their saccades in a dark environment or in the presence of a single LED compared to when the saccades were generated in richer visual environments. Visual stimulation of the fovea did not increase subjects' accuracy when pointing in the direction of their gaze compared to conditions where there was only stimulation of the peripheral retina. Experiment 2 tested how the retinal signals could contribute to the coding of eye position after saccadic eye movements. More specifically, we tested whether the shift in the retinal image of the environment during the saccades provided information about the reached position of the eyes. Subjects produced their series of saccades while facing a visual environment made up of three LEDs. In some trials, the whole visual scene was displaced either 4.5 degrees to the left or 3 degrees to the right during the primary saccade. These displacements created mismatches between the shift of the retinal image of the environment and the extent of gaze deviation. The displacements of the visual scene were not perceived by the subjects because they occurred near the peak velocity of the saccade (saccadic suppression phenomenon). Pointing accuracy was not affected by the unperceived shifts of the visual scene. The results of these experiments suggest that the arm motor system receives more precise information about gaze direction when there is retinal stimulation than when there is none. They also suggest that the most relevant factor in defining gaze direction is not the retinal locus of the visual stimulation (that is peripheral or foveal) but rather the amount of visual information. Finally, the results suggest an enhanced egocentric encoding of gaze direction by the retinal inputs and do not support a retinotopic model for encoding gaze direction.     

Electrical stimulation of rhesus monkey nucleus reticularis gigantocellularis

Saccade kinematics are altered by ongoing head movements. The hypothesis that a head movement command signal, proportional to head velocity, transiently reduces the gain of the saccadic burst generator (Freedman 2001, Biol Cybern 84:453-462) can account for this observation. Using electrical stimulation of the rhesus monkey nucleus reticularis gigantocellularis (NRG) to alter the head contribution to ongoing gaze shifts, two critical predictions of this gaze control hypothesis were tested. First, this hypothesis predicts that activation of the head command pathway will cause a transient reduction in the gain of the saccadic burst generator. This should alter saccade kinematics by initially reducing velocity without altering saccade amplitude. Second, because this hypothesis does not assume that gaze amplitude is controlled via feedback, the added head contribution (produced by NRG stimulation on the side ipsilateral to the direction of an ongoing gaze shift) should lead to hypermetric gaze shifts. At every stimulation site tested, saccade kinematics were systematically altered in a way that was consistent with transient reduction of the gain of the saccadic burst generator. In addition, gaze shifts produced during NRG stimulation were hypermetric compared with control movements. For example, when targets were briefly flashed 30 degrees from an initial fixation location, gaze shifts during NRG stimulation were on average 140% larger than control movements. These data are consistent with the predictions of the tested hypothesis, and may be problematic for gaze control models that rely on feedback control of gaze amplitude, as well as for models that do not posit an interaction between head commands and the saccade burst generator.     

Vastus lateralis surface and single motor unit electromyography during shortening,lengthening and isometric contractions corrected for mode‐dependent differences in force‐generating capacity

Aim: Knee extensor neuromuscular activity, rectified surface electromyography (rsEMG) and single motor unit EMG was investigated during isometric (60° knee angle), shortening and lengthening contractions (50–70°, 10° s^?1) corrected for force–velocity‐related differences in force‐generating capacity. However, during dynamic contractions additional factors such as shortening‐induced force losses and lengthening‐induced force gains may also affect force capacity and thereby neuromuscular activity. Therefore, even after correction for force–velocity‐related differences in force capacity we expected neuromuscular activity to be higher and lower during shortening and lengthening, respectively, compared to isometric contractions. Methods: rsEMG of the three superficial muscle heads was obtained in a first session [10 and 50% maximal voluntary contraction (MVC)] and additionally EMG of (46) vastus lateralis motor units was recorded during a second session (4–76% MVC). Using superimposed electrical stimulation, force‐generating capacity for shortening and lengthening contractions was found to be 0.96 and 1.16 times isometric (Iso) force capacity respectively. Therefore, neuromuscular activity during submaximal shortening and lengthening was compared with isometric contractions of respectively 1.04Iso (=1/0.96) and 0.86Iso (=1/1.16). rsEMG and discharge rates were normalized to isometric values. Results: rsEMG behaviour was similar (P > 0.05) during both sessions. Shortening rsEMG (1.30 ± 0.11) and discharge rate (1.22 ± 0.13) were higher (P < 0.05) than 1.04Iso values (1.05 ± 0.05 and 1.03 ± 0.04 respectively), but lengthening rsEMG (1.05 ± 0.12) and discharge rate (0.90 ± 0.08) were not lower (P > 0.05) than 0.86Iso values (0.76 ± 0.04 and 0.91 ± 0.07 respectively). Conclusion: When force–velocity‐related differences in force capacity were taken into account, neuromuscular activity was not lower during lengthening but was still higher during shortening compared with isometric contractions.     

Functional adaptation of reactive saccades in humans: a PET study

It is known that the saccadic system shows adaptive changes when the command sent to the extraocular muscles is inappropriate. Despite an abundance of supportive psychophysical investigations, the neurophysiological substrate of this process is still debated. The present study addresses this issue using H2(15)O positron emission tomography (PET). We contrasted three conditions in which healthy human subjects were required to perform saccadic eye movements toward peripheral visual targets. Two conditions involved a modification of the target location during the course of the initial saccade, when there is suppression of visual perception. In the RAND condition, intra-saccadic target displacement was random from trial-to-trial, precluding any systematic modification of the primary saccade amplitude. In the ADAPT condition, intra-saccadic target displacement was uniform, causing adaptive modification of the primary saccade amplitude. In the third condition (stationary, STAT), the target remained at the same location during the entire trial. Difference images reflecting regional cerebral-blood-flow changes attributable to the process of saccadic adaptation (ADAPT minus RAND; ADAPT minus STAT) showed a selective activation in the oculomotor cerebellar vermis (OCV; lobules VI and VII). This finding is consistent with neurophysiological studies in monkeys. Additional analyses indicated that the cerebellar activation was not related to kinematic factors, and that the absence of significant activation within the frontal eye fields (FEF) or the superior colliculus (SC) did not represent a false negative inference. Besides the contribution of the OCV to saccadic adaptation, we also observed, in the RAND condition, that the saccade amplitude was significantly larger when the previous trial involved a forward jump than when the previous trial involved a backward jump. This observation indicates that saccade accuracy is constantly monitored on a trial-to-trial basis. Behavioral measurements and PET observations (RAND minus STAT) suggest that this single-trial control of saccade amplitude may be functionally distinct from the process of saccadic adaptation.     

Visuomotor mental rotation of saccade direction

This investigation studied the latencies of saccadic eye movements that were directed away from a target by a variable angular distance, which was given by instruction. Such a movement presumably requires an intentional, visuomotor mental rotation of the saccade vector, resulting in prolonged reaction times. From a study on the control of directed hand movements, it has been hypothesized that all visuomotor and visual mental rotation tasks share a common processing stage. We tested this hypothesis with a saccade task in which subjects shifted their gaze either towards (0°, pro-saccade), or 30, 60, 90, 120, 150, or 180° (anti-saccade) away from a randomly cued position on an imaginary clock face. With four different cueing conditions, latencies increased monotonically with required gaze shift from 0–150°, thus exhibiting a mental rotation latency pattern. However, we also found anti-saccades faster than 150° gaze shift and slower rotation speeds with peripheral cues than with central cues. Together with the overall shallower latency increase compared with previous findings with mental rotation tasks, these results cast doubt on the notion of a common, central processing mechanism for the different types of tasks. Received: 11 August 1998 / Accepted: 9 February 1999     

The Duncker illusion and eye-hand coordination

A moving background alters the perceived direction of target motion (the Duncker illusion). To test whether this illusion also affects pointing movements to remembered/extrapolated target locations, we constructed a display in which a target moved in a straight line and disappeared behind a band of moving random dots. Subjects were required to touch the spot where the target would emerge from the occlusion. The four directions of random-dot motion induced pointing errors that were predictable from the Duncker illusion. Because it has been previously established that saccadic direction is influenced by this illusion, gaze was subsequently recorded in a second series of experiments while subjects performed the pointing task and a similar task with eye-tracking only. In the pointing task, subjects typically saccaded to the lower border of the occlusion zone as soon as the target disappeared and then tried to maintain fixation at that spot. However, it was particularly obvious in the eye-tracking-only condition that horizontally moving random dots generally evoked an appreciable ocular following response, altering the gaze direction. Hand-pointing errors were related to the saccadic gaze error but were more highly correlated with final gaze errors (resulting from the initial saccade and the subsequent ocular following response). The results suggest a model of limb control in which gaze position can provide the target signal for limb movement.     

The characteristics and neuronal substrate of saccadic eye movement plasticity

Saccadic eye movements are shifts in the direction of gaze that rapidly and accurately aim the fovea at targets of interest. Saccades are so brief that visual feedback cannot guide them to their targets. Therefore, the saccadic motor command must be accurately specified in advance of the movement and continually modified to compensate for growth, injury, and aging, which otherwise would produce dysmetric saccades. When a persistent dysmetria occurs in subjects with muscle weakness or neural damage or is induced in normal primates by the surreptitious jumping of a target forward or backward as a saccade is made to acquire the target, saccadic amplitude changes to reduce the dysmetria. Adaptation of saccadic amplitude or direction occurs gradually and is retained in the dark, thus representing true motor plasticity. Saccadic adaptation is more rapid in humans than in monkeys, usually is incomplete in both species, and is slower and less robust for amplitude increases than decreases. Adaptation appears to be motor rather than sensory. In humans, adaptation of saccades that would seem to require more sensory-motor processing does not transfer to saccades that seem to require less, suggesting the existence of distributed adaptation loci. In monkeys, however, transfer from more simple to more complex saccades is robust, suggesting a common adaptation site. Neurophysiological data from both species indicate that the oculomotor cerebellum is crucial for saccadic adaptation. This review shows that the precise, voluntary behaviors known as saccadic eye movements provide an alternative to simple reflexes for the study of the neuronal basis of motor learning.