Stimulation of the caudate nucleus induces contraversive saccadic eye movements as well as head turning in the cat.

The effects of stimulation of the caudate nucleus were investigated in alert cats, with special reference to the induction of eye and head movements. Stimulation of caudal portions of the caudate nucleus on one side with trains of current pulses induced gaze shifts towards the contralateral side. When the head of the animal was restrained, the majority of evoked eye movements were single conjugate saccades. The amplitude and direction of the evoked saccade varied depending on the initial eye position. The amplitude of the horizontal component tended to be larger for saccades initiated from more ipsilateral positions, and became gradually smaller as the initial eye position shifted to the contralateral side. If the eye was far into the contralateral positions, no saccades were induced. Furthermore, the saccades tended to have a downward component when the eye was initially focused upward, and an upward component when the eye was focused downward. When the head was made free to move, the same stimulation induced a sequence of contraversive staircase gaze shifts composed of coordinated eye and head movements. The eye movements in the orbit resembled nystagmus, consisting of contraversive saccades followed by reverse compensatory movements. The head turning, though smooth and continuous, was also suggested to consist of a series of movements coupled with saccadic eye movements. This study indicates a potential role of the caudate nucleus in the control of orienting reflexes.     

Microstimulation of the frontal eye field and its effects on covert spatial attention

Many studies have established that the strength of visual perception and the strength of visual representations within visual cortex vary according to the focus of covert spatial attention. While it is clear that attention can modulate visual signals, the source of this modulation remains unknown. We have examined the possibility that saccade related mechanisms provide a source of spatial attention by studying the effects of electrical microstimulation of the frontal eye fields (FEF) on spatial attention. Monkeys performed a task in which they had to detect luminance changes of a peripheral target while ignoring a flashing distracter. The target luminance change could be preceded by stimulation of the FEF at current levels below that which evoked saccadic eye movements. We found that when the target change was preceded by stimulation of FEF, the monkey could detect smaller changes in target luminance. The increased sensitivity to the target change only occurred when the target was placed in the part of the visual field represented by neurons at the stimulation site. The magnitude of improvement depended on the temporal asynchrony of the stimulation onset and the target event. No significant effect of stimulation was observed when long intervals (>300 ms) between stimulation and the target event were used, and the magnitude of the increased sensitivity decreased systematically with increasing asynchrony. At the shortest asynchrony, FEF stimulation temporally overlapped the target event and the magnitude of the improvement was comparable to that of removing the distracter from the task. These results demonstrate that transient, but potent improvements in the deployment of covert spatial attention can be obtained by microstimulation of FEF sites from which saccadic eye movements are also evoked.     

Involvement of Purkinje cells in evoking saccadic eye movements by microstimulation of the posterior cerebellar vermis of monkeys

Neural mechanisms for evoking saccadic eye movements by microstimulation of the posterior vermis were investigated in monkeys trained to fixate a visual target. The low-threshold region from which saccadic eye movements could be evoked with currents less than 10 microA was confined to lobule VII in two monkeys and it included a posterior part of lobule VI (lobule VIc) in another monkey. The region from which saccade-related neural activity was recordable coincided with the low-threshold region. This region corresponded to the vermal lobules from which eye position and saccade-related Purkinje cells were recorded. Kainic acid (kainate) injected in the white matter of lobule VII resulted in severe losses of Purkinje cells within a radius of 1-2 mm of the injection site. The lesion tended to be larger toward the peripheral cerebellar cortices, which were connected to the injection site by natural courses of the afferent and efferent fibers. After the kainate administration, the distribution of saccade-related neural activity did not differ significantly from that of the preoperative mapping, in spite of the severe losses of cortical neurons. Burst discharges of mossy fibers were recordable in the white matter near the injection site, indicating that afferent fibers were relatively unaffected by kainate. After kainate administration, the saccadic eye movements could no longer be evoked by microstimulation applied to the posterior vermis. The stimulus sites from which saccades could be evoked after kainate administration were always associated with the presence of intact Purkinje cells. In such cases, the minimum current necessary to evoke saccades depended on the percentages of intact Purkinje cells spared. In the folia with normal Purkinje cell layers, the amplitude and direction of evoked saccades and the thresholds for evoking such eye movements were almost comparable to the preoperative data. Saccadic eye movements in response to microstimulation of the posterior vermis were caused by orthodromic impulses conveyed through the axons of the Purkinje cells. Insofar as the saccades elicited from lobule VII with currents less than 10 microA are concerned, antidromic activation of the afferent fibers is not the neural mechanisms subserving the oculomotor responses.     

Explicit eye movements failed to facilitate the precision of subsequent attentional localization

This study investigated the usefulness of explicit spatial coordinates from eye movements for the precision of covert shifts of attention within dense arrays of items. Observers shifted their attention covertly from one item to the next in response to a series of beeps and reported the color of the disc on which the series ended, providing an estimate of the accuracy of the “attentional walk”. We compared performance in this task when only covert shifts of attention were done to performance when observers first executed an explicit eye movement to the starting point of the attentional walk before beginning the covert attentional walk. The hypothesis was that the eye movement would activate explicit coordinates of the starting point of the attentional walk within brain systems that are involved in controlling both shifts of attention and eye movements. This in turn would provide an anchor for the attentional walk, thereby improving performance. The evidence did not support this hypothesis. Performance was no better with an explicit eye movement prior to the attentional walk than without one. This suggests that covert orienting—shifting attention—and overt orienting—shifting the eyes—access the same coordinate system and therefore activating new coordinates interferes with the old ones, no matter what the system of orienting is.     

Interaction between smooth anticipation and saccades during ocular orientation in darkness

A saccade triggered during sustained smooth pursuit is programmed using retinal information about the relative position and velocity of the target with respect to the eye. Thus the smooth pursuit and saccadic systems are coordinated by using common retinal inputs. Yet, in the absence of retinal information about the relative motion of the eye with respect to the target, the question arises whether the smooth and saccadic systems are still able to be coordinated possibly by using extraretinal information to account for the saccadic and smooth eye movements. To address this question, we flashed a target during smooth anticipatory eye movements in darkness, and the subjects were asked to orient their visual axis to the remembered location of the flash. We observed multiple orientation saccades (typically 2-3) toward the memorized location of the flash. The first orienting saccade was programmed using only the position error at the moment of the flash, and the smooth eye movement was ignored. However, subsequent saccades executed in darkness compensated gradually for the smooth eye displacement (mean compensation congruent with 70%). This behavior revealed a 400-ms delay in the time course of orientation for the compensation of the ongoing smooth eye displacement. We conclude that extraretinal information about the smooth motor command is available to the saccadic system in the absence of visual input. There is a 400-ms delay for smooth movement integration, saccade programming and execution.     

Effect of reversible inactivation of macaque lateral intraparietal area on visual and memory saccades

Previous studies from our laboratory identified a parietal eye field in the primate lateral intraparietal sulcus, the lateral intraparietal area (area LIP). Here we further explore the role of area LIP in processing saccadic eye movements by observing the effects of reversible inactivation of this area. One to 2 microl of muscimol (8 mg/ml) were injected at locations where saccade-related activities were recorded for each lesion experiment. After the muscimol injection we observed in two macaque monkeys consistent effects on both the metrics and dynamics of saccadic eye movements at many injection sites. These effects usually took place within 10-30 min and disappeared after 5-6 h in most cases and certainly when tested the next day. After muscimol injection memory saccades directed toward the contralesional and upper space became hypometric, and in one monkey those to the ipsilesional space were slightly but significantly hypermetric. In some cases, the scatter of the end points of memory saccades was also increased. On the other hand, the metrics of visual saccades remained relatively intact. Latency for both visual and memory saccades toward the contralesional space was increased and in many cases displayed a higher variance after muscimol lesion. At many injection sites we also observed an increase of latency for visual and memory saccades toward the upper space. The peak velocities for memory saccades toward the contralesional space were decreased after muscimol injection. The peak velocities of visual saccades were not significantly different from those of the controls. The duration of saccadic eye movements either to the ipsilesional or contralesional space remained relatively the same for both visual and memory saccades. Overall these results demonstrated that we were able to selectively inactivate area LIP and observe effects on saccadic eye movements. Together with our previous recording studies these results futher support the view that area LIP plays a direct role in processing incoming sensory information to program saccadic eye movements. The results are consistent with our unit recording data and microstimulation studies, which suggest that area LIP represents contralateral space and also has a bias for the upper visual field.     

Primate frontal eye fields. II. Physiological and anatomical correlates of electrically evoked eye movements

We studied single neurons in the frontal eye fields of awake macaque monkeys and compared their activity with the saccadic eye movements elicited by microstimulation at the sites of these neurons. Saccades could be elicited from electrical stimulation in the cortical gray matter of the frontal eye fields with currents as small as 10 microA. Low thresholds for eliciting saccades were found at the sites of cells with presaccadic activity. Presaccadic neurons classified as visuomovement or movement were most associated with low (less than 50 microA) thresholds. High thresholds (greater than 100 microA) or no elicited saccades were associated with other classes of frontal eye field neurons, including neurons responding only after saccades and presaccadic neurons, classified as purely visual. Throughout the frontal eye fields, the optimal saccade for eliciting presaccadic neural activity at a given recording site predicted both the direction and amplitude of the saccades that were evoked by microstimulation at that site. In contrast, the movement fields of postsaccadic cells were usually different from the saccades evoked by stimulation at the sites of such cells. We defined the low-threshold frontal eye fields as cortex yielding saccades with stimulation currents less than or equal to 50 microA. It lies along the posterior portion of the arcuate sulcus and is largely contained in the anterior bank of that sulcus. It is smaller than Brodmann's area 8 but corresponds with the union of Walker's cytoarchitectonic areas 8A and 45. Saccade amplitude was topographically organized across the frontal eye fields. Amplitudes of elicited saccades ranged from less than 1 degree to greater than 30 degrees. Smaller saccades were evoked from the ventrolateral portion, and larger saccades were evoked from the dorsomedial portion. Within the arcuate sulcus, evoked saccades were usually larger near the lip and smaller near the fundus. Saccade direction had no global organization across the frontal eye fields; however, saccade direction changed in systematic progressions with small advances of the microelectrode, and all contralateral saccadic directions were often represented in a single electrode penetration down the bank of the arcuate sulcus. Furthermore, the direction of change in these progressions periodically reversed, allowing particular saccade directions to be multiply represented in nearby regions of cortex.(ABSTRACT TRUNCATED AT 400 WORDS)     

The contribution of the human PPC to the orienting of visuospatial attention during smooth pursuit

Smooth pursuit eye movements function to stabilize the retinal image of small moving targets. In order for those targets to be foveated, however, they must first be “captured” by an attentional mechanism which then interacts with the oculomotor system. Cortical sites involved with producing smooth pursuit overlap with areas known to be involved in directing visuospatial attention, particularly the posterior parietal cortex (PPC). The goal of the current study was to characterize the contributions made by the left and right posterior parietal cortices (lPPC and rPPC) to the interaction between visuospatial attention and the generation of smooth pursuit eye movements. Transcranial magnetic stimulation (TMS) was used to temporarily disrupt each area at different times around target motion onset in a pursuit task that explicitly manipulated the covert orienting of attention. TMS over the lPPC, rPPC and a control site (the vertex) evoked a similar pattern of results, in that the earlier TMS delivery times caused a reduced pursuit latency compared to baseline measures, while TMS immediately prior to target motion onset resulted in latencies slower than baseline. In addition, however, TMS over the lPPC and rPPC (but not the vertex) preferentially influenced the generation of contralateral pursuit, with the lPPC doing so in a relatively time-independent manner, and the rPPC doing so in a time-dependent manner. This pattern of results implies that both the left and right PPC are directly involved in the interaction between attention and smooth pursuit preparation.     

Perception of images moving at saccadic velocities during saccades and during fixation

Summary During saccadic eye movements, images of external objects move rapidly across the retina. Small, unpredictable displacements imposed upon a target moving at saccadic velocity were detected with equal accuracy when (1) the retinal image velocity was caused by an eye movement, or (2) when the same velocity was produced during fixation (simulated saccadic conditions). The results provide no evidence of a specific non-visual suppression of vision during saccades, nor of any other compensatory modification of afferent visual inflow which might contribute to our sense of directional stability during saccades.     

Coordination of the eyes and head during visual orienting

Changing the direction of the line of sight is essential for the visual exploration of our environment. When the head does not move, re-orientation of the visual axis is accomplished with high velocity, conjugate movements of the eyes known as saccades. Our understanding of the neural mechanisms that control saccadic eye movements has advanced rapidly as specific hypotheses have been developed, evaluated and sometimes rejected on the basis of new observations. Constraints on new hypotheses and new tests of existing models have often arisen from the careful assessment of behavioral observations. The definition of the set of features (or rules) of saccadic eye movements was critical in the development of hypotheses of their neural control. When the head is free to move, changes in the direction of the line of sight can involve simultaneous saccadic eye movements and movements of the head. When the head moves in conjunction with the eyes to accomplish these shifts in gaze direction, the rules that helped define head-restrained saccadic eye movements are altered. For example, the slope relationship between duration and amplitude for saccadic eye movements is reversed (the slope is negative) during gaze shifts of similar amplitude initiated with the eyes in different orbital positions. Modifications to the hypotheses developed in head-restrained subjects may be needed to account for these new observations. This review briefly recounts features of head-restrained saccadic eye movements, and then describes some of the characteristics of coordinated eye–head movements that have led to development of new hypotheses describing the mechanisms of gaze shift control.     

Reversible inactivation of macaque frontal eye field

 The macaque frontal eye field (FEF) is involved in the generation of saccadic eye movements and fixations. To better understand the role of the FEF, we reversibly inactivated a portion of it while a monkey made saccades and fixations in response to visual stimuli. Lidocaine was infused into a FEF and neural inactivation was monitored with a nearby microelectrode. We used two saccadic tasks. In the delay task, a target was presented and then extinguished, but the monkey was not allowed to make a saccade to its location until a cue to move was given. In the step task, the monkey was allowed to look at a target as soon as it appeared. During FEF inactivation, monkeys were severely impaired at making saccades to locations of extinguished contralateral targets in the delay task. They were similarly impaired at making saccades to locations of contralateral targets in the step task if the target was flashed for ≤100 ms, such that it was gone before the saccade was initiated. Deficits included increases in saccadic latency, increases in saccadic error, and increases in the frequency of trials in which a saccade was not made. We varied the initial fixation location and found that the impairment specifically affected contraversive saccades rather than affecting all saccades made into head-centered contralateral space. Monkeys were impaired only slightly at making saccades to contralateral targets in the step task if the target duration was 1000 ms, such that the target was present during the saccade: latency increased, but increases in saccadic error were mild and increases in the frequency of trials in which a saccade was not made were insignificant. During FEF inactivation there usually was a direct correlation between the latency and the error of saccades made in response to contralateral targets. In the delay task, FEF inactivation increased the frequency of making premature saccades to ipsilateral targets. FEF inactivation had inconsistent and mild effects on saccadic peak velocity. FEF inactivation caused impairments in the ability to fixate lights steadily in contralateral space. FEF inactivation always caused an ipsiversive deviation of the eyes in darkness. In summary, our results suggest that the FEF plays major roles in (1) generating contraversive saccades to locations of extinguished or flashed targets, (2) maintaining contralateral fixations, and (3) suppressing inappropriate ipsiversive saccades. Received: 2 February 1996 / Accepted: 26 February 1997     

Covert attention regulates saccadic reaction time by routing between different visual-oculomotor pathways

Covert attention modulates saccadic performance, e.g., the abrupt onset of a task-irrelevant visual stimulus grabs attention as measured by a decrease in saccadic reaction time (SRT). The attentional advantage bestowed by the task-irrelevant stimulus is short-lived: SRT is actually longer ~200 ms after the onset of a stimulus than it is when no stimulus appears, known as inhibition of return. The mechanism by which attention modulates saccadic reaction is not well-understood. Here, we propose two possible mechanisms: by selective routing of the visuomotor signal through different pathways (routing hypothesis) or by general modulation of the speed of visuomotor transformation (shifting hypothesis). To test them, we designed a cue gap paradigm in which a 100-ms gap was introduced between the fixation point disappearance and the target appearance to the conventional cued visual reaction time paradigm. The cue manipulated the location of covert attention, and the gap interval resulted in a bimodal distribution of SRT, with an early mode (express saccade) and a late mode (regular saccade). The routing hypothesis predicts changes in the proportion of express saccades vs. regular saccades, whereas the shifting hypothesis predicts a shift of SRT distribution. The addition of the cue had no effect on mean reaction time of express and regular saccades, but it changed the relative proportion of two modes. These results demonstrate that the covert attention modification of the mean SRT is largely attributed to selective routing between visuomotor pathways rather than general modulation of the speed of visuomotor transformation.     

Neuron-specific contribution of the superior colliculus to overt and covert shifts of attention

The analysis of a peripheral visual location can be improved in two ways: either by orienting one's gaze (usually by making a foveating saccade) or by 'covertly' shifting one's attention to the peripheral location without making an eye movement. The premotor theory of attention holds that saccades and spatial shifts of attention share a common functional module with a distinct neuronal basis. Using single-unit recording from the brains of trained rhesus monkeys, we investigated whether the superior colliculus, the major subcortical center for the control of saccades, is part of this shared network for attention and saccades. Here we show that a distinct type of neuron in the intermediate layer of the superior colliculus, the visuomotor neuron, which is known to be centrally involved in the preparation of saccades, is also active during covert shifts of attention.     

Effect of a local ibotenic acid lesion in the visual association area on the prelunate gyrus (area V4) on saccadic reaction times in trained rhesus monkeys

Summary Two rhesus monkeys were trained to make saccadic eye movements from a central fixation point towards a peripheral target. Saccadic reaction times (SRTs) were measured in the gap paradigm (200 ms pause between offset of fixation point and onset of peripheral target). Target position for extensive training (SRTs of 150 to 250 saccades were collected per day) was four degrees eccentric in the lower quadrant of the visual field contralateral to the intended lesion site in area V4. For control the monkeys were also trained for target positions either in the lower quadrant ipsilateral to the intended lesion site or in the upper visual half field. After several weeks of training a bimodal distribution of saccadic reaction times, one peak at 85 ms (express saccades) and the other around 160 ms (regular saccades) was obtained for each target position. Local injection of ibotenic acid into the 4 deg representation of area V4 resulted in a unimodal distribution of saccadic reaction times (over 90% express saccades) towards the corresponding target position, leaving the distribution of reaction times for the control position unchanged. Recovery began after 5 days and was complete 8 to 10 days after the injection. From these results we conclude that V4 is involved in the generation of the longer latency peak in the distribution of saccadic reaction times by delaying the initiation of visually guided saccades.     

Predictive remapping of attention across eye movements

Many cells in retinotopic brain areas increase their activity when saccades (rapid eye movements) are about to bring stimuli into their receptive fields. Although previous work has attempted to look at the functional correlates of such predictive remapping, no study has explicitly tested for better attentional performance at the future retinal locations of attended targets. We found that, briefly before the eyes start moving, attention drawn to the targets of upcoming saccades also shifted to those retinal locations that the targets would cover once the eyes had moved, facilitating future movements. This suggests that presaccadic visual attention shifts serve to both improve presaccadic perceptual processing at the target locations and speed subsequent eye movements to their new postsaccadic locations. Predictive remapping of attention provides a sparse, efficient mechanism for keeping track of relevant parts of the scene when frequent rapid eye movements provoke retinal smear and temporal masking.     

The gap effect and express saccades in the auditory modality

Latencies of eye movements to peripheral targets are reduced when there is a short delay (typically 200 ms) between the offset of a central visual fixation point and the target onset. This has been termed the gap effect. In addition, some subjects, usually with practice, exhibit a separate population of very short latency saccades, called express saccades. Both these phenomena have been attributed to disengagement of visual attention when the fixation point is extinguished. A competing theory of the gap effect attributes it to disengagement of oculomotor fixation during the temporal gap. It is known that auditory targets are effective in eliciting saccadic eye movements, and also that covert attention operates in the auditory modality. If the gap effect and express saccades are due to disengagement of spatial attention, both should persist in the auditory modality. However, fixation of gaze is largely under visual control. If the gap effect results from disengagement of fixation, then at least a reduced effect should be seen in the auditory modality. Human subjects performed the gap task and a control task in the dark, using auditory fixation points and saccadic targets, on five successive days. Despite this practice, express saccades were not observed. There was a reliable gap effect, but the reduction in saccadic latency was only 17 ms, compared with 32 ms for the same subjects in the visual modality. This suggests that about half the gap effect is due to disengagement of visual fixation. The remainder was not due to non-specific warning effects and could be attributed to offset of the auditory fixation stimulus. Received: 1 March 1996 / Accepted: 11 July 1997     

Combined deficits of saccades and visuo-spatial orientation after cortical lesions

Functionally, saccadic eye movements are closely linked to visuo-spatial orientation. Anatomically, the network of cortical areas controlling saccades also seems to be involved in spatial attention and orientation. Consequently, lesions should cause deficits in both categories. We investigated this in 34 patients with focal unilateral lesions of the posterior parietal cortex (PPC), the frontal eye fields (FEF), the supplementary motor area (SMA), or the dorsolateral prefrontal cortex (PFC). Saccadic eye movements were recorded using infrared reflection oculography. Visual hemineglect or other visuo-spatial disorders were investigated by a series of standardized paper-pencil tests. Further, the internal spatial coordinates (subjective visual vertical and subjective straight ahead) were assessed psychophysically. Depending on the site of the lesion, different patterns of deficits were identified: lesions of the PPC impaired reflexive exploration of visual space in terms of delayed and hypometric visually triggered saccades into the contralesional hemifield, related to the severity of visual hemineglect. Further, PPC lesions specifically affected basic functions of the perceptual analysis of space, such as the internal spatial coordinates and spatial constancy across saccades. The latter was tested by applying visual double-step stimuli, where saccade-related extraretinal information had to be taken into account for achieving spatial accuracy. Frontal lesions left these functions intact. FEF lesions, however, impaired systematic intentional exploration of space, thus causing an exploratory-motor type of visual hemineglect. Prefrontal (PFC) lesions impaired the working memory for saccade-related spatial information, and SMA lesions affected temporal properties such as the timing of saccadic sequences, but did not cause specific visuo-spatial deficits. In conclusion, patients with frontal or parietal cortical lesions often exhibit combined saccadic and visuo-spatial disorders, most of which are topically specific.     

TMS pulses on the frontal eye fields break coupling between visuospatial attention and eye movements

While preparing a saccadic eye movement, visual processing of the saccade goal is prioritized. Here, we provide evidence that the frontal eye fields (FEFs) are responsible for this coupling between eye movements and shifts of visuospatial attention. Functional magnetic resonance imaging (fMRI)-guided transcranial magnetic stimulation (TMS) was applied to the FEFs 30 ms before a discrimination target was presented at or next to the target of a saccade in preparation. Results showed that the well-known enhancement of discrimination performance on locations to which eye movements are being prepared was diminished by TMS contralateral to eye movement direction. Based on the present and other reports, we propose that saccade preparatory processes in the FEF affect selective visual processing within the visual cortex through feedback projections, in that way coupling saccade preparation and visuospatial attention.     

Expression of a re-centering bias in saccade regulation by superior colliculus neurons

In previous studies of saccadic eye movement reaction time, the manipulation of initial eye position revealed a behavioral bias that facilitates the initiation of movements towards the central orbital position. An interesting hypothesis for this re-centering bias suggests that it reflects a visuo-motor optimizing strategy, rather than peripheral muscular constraints. Given that the range of positions that the eyes can take in the orbits delimits the extent of visual exploration by head-fixed subjects, keeping the eyes centered in the orbits may indeed permit flexible orienting responses to engaging stimuli. To investigate the influence of initial eye position on central processes such as saccade selection and initiation, we examined the activity of saccade-related neurons in the primate superior colliculus (SC). Using a simple reaction time paradigm wherein an initially fixated visual stimulus varying in position was extinguished 200 ms before the presentation of a saccadic target, we studied the relationship between initial eye position and neuronal activation in advance of saccade initiation. We found that the magnitude of the early activity of SC neurons, especially during the immediate pre-target period that followed the fixation stimulus disappearance, was correlated with changes in initial eye position. For the great majority of neurons, the pre-target activity increased with changes in initial eye position in the direction opposite to their movement fields, and it was also strongly correlated with the concomitant reduction in reaction time of centripetal saccades directed within their movement fields. Taking into account the correlation with saccadic reaction time, the relationship between neuronal activity and initial eye position remained significant. These results suggest that eye-position-dependent changes in the excitability of SC neurons could represent the neural substrate underlying a re-centering bias in saccade regulation. More generally, the low frequency SC pre-target activity could use eccentric eye position signals to regulate both when and which saccades are produced by promoting the emergence of a high frequency burst of activity that can act as a saccadic command. However, only saccades initiated within ~200 ms of target presentation were associated with SC pre-target activity. This eye-dependent pre-target activation mechanism therefore appears to be restricted to the initiation of saccades with relatively short reaction times, which specifically require the integrity of the SC. Electronic Publication     

Effects of stimulus-induced saccades on manual response times in healthy elderly and in patients with right-parietal lesions

Response delays of hemi-neglect patients to invalidly cued left targets in Posner's visual cueing task have been interpreted as reflecting disorders of covert attention, although shifts of overt attention have so far not been systematically measured in patients performing this task. Therefore, we measured saccades (i.e., fast goal-directed eye movements) induced by cues and targets in this task in ten patients with lesions of the right posterior parietal cortex and in age-matched healthy subjects. Participants were not aware that their saccades were studied. Of greatest interest was whether the presence or absence of saccades would modify the patients' response delay with invalidly cued left targets. In both groups, saccades occurred in many trials, key-press responses were slower in saccade trials than in no-saccade trials, and the delay by invalid cues was larger in saccade trials. The patients' responses were in particular delayed if preceded by saccades to the left. Their delay to invalidly cued left targets almost doubled (144 ms vs 76 ms) when only saccade trials were analyzed compared to when only no-saccade trials were analyzed. Thus, overt shifts (saccades) have a similar but larger effect on manual responses than covert shifts of attention. In particular, overt shifts make a considerable contribution to the patients' pathological delay of responses to invalidly cued left targets.