Latency Of Saccadic Eye Movements Research Articles

Motion Extrapolation for Eye Movements Predicts Perceived Motion-Induced Position Shifts.

Transmission delays in the nervous system pose challenges for the accurate localization of moving objects as the brain must rely on outdated information to determine their position in space. Acting effectively in the present requires that the brain compensates not only for the time lost in the transmission and processing of sensory information, but also for the expected time that will be spent preparing and executing motor programs. Failure to account for these delays will result in the mislocalization and mistargeting of moving objects. In the visuomotor system, where sensory and motor processes are tightly coupled, this predicts that the perceived position of an object should be related to the latency of saccadic eye movements aimed at it. Here we use the flash-grab effect, a mislocalization of briefly flashed stimuli in the direction of a reversing moving background, to induce shifts of perceived visual position in human observers (male and female). We find a linear relationship between saccade latency and perceived position shift, challenging the classic dissociation between "vision for action" and "vision for perception" for tasks of this kind and showing that oculomotor position representations are either shared with or tightly coupled to perceptual position representations. Altogether, we show that the visual system uses both the spatial and temporal characteristics of an upcoming saccade to localize visual objects for both action and perception.SIGNIFICANCE STATEMENT Accurately localizing moving objects is a computational challenge for the brain due to the inevitable delays that result from neural transmission. To solve this, the brain might implement motion extrapolation, predicting where an object ought to be at the present moment. Here, we use the flash-grab effect to induce perceptual position shifts and show that the latency of imminent saccades predicts the perceived position of the objects they target. This counterintuitive finding is important because it not only shows that motion extrapolation mechanisms indeed work to reduce the behavioral impact of neural transmission delays in the human brain, but also that these mechanisms are closely matched in the perceptual and oculomotor systems.

Rewards modulate saccade latency but not exogenous spatial attention.

The eye movement system is sensitive to reward. However, whilst the eye movement system is extremely flexible, the extent to which changes to oculomotor behavior induced by reward paradigms persist beyond the training period or transfer to other oculomotor tasks is unclear. To address these issues we examined the effects of presenting feedback that represented small monetary rewards to spatial locations on the latency of saccadic eye movements, the time-course of learning and extinction of the effects of rewarding saccades on exogenous spatial attention and oculomotor inhibition of return. Reward feedback produced a relative facilitation of saccadic latency in a stimulus driven saccade task which persisted for three blocks of extinction trials. However, this hemifield-specific effect failed to transfer to peripheral cueing tasks. We conclude that rewarding specific spatial locations is unlikely to induce long-term, systemic changes to the human oculomotor or attention systems.

Implicit and explicit timing in oculomotor control.

The passage of time can be estimated either explicitly, e.g. before leaving home in the morning, or implicitly, e.g. when catching a flying ball. In the present study, the latency of saccadic eye movements was used to evaluate differences between implicit and explicit timing. Humans were required to make a saccade between a central and a peripheral position on a computer screen. The delay between the extinction of a central target and the appearance of an eccentric target was the independent variable that could take one out of four different values (400, 900, 1400 or 1900 ms). In target trials, the delay period lasted for one of the four durations randomly. At the end of the delay, a saccade was initiated by the appearance of an eccentric target. Cue&target trials were similar to target trials but the duration of the delay was visually cued. In probe trials, the duration of the upcoming delay was cued, but there was no eccentric target and subjects had to internally generate a saccade at the estimated end of the delay. In target and cue&target trials, the mean and variance of latency distributions decreased as delay duration increased. In cue&target trials latencies were shorter. In probe trials, the variance increased with increasing delay duration and scalar variability was observed. The major differences in saccadic latency distributions were observed between visually-guided (target and cue&target trials) and internally-generated saccades (probe trials). In target and cue&target trials the timing of the response was implicit. In probe trials, the timing of the response was internally-generated and explicitly based on the duration of the visual cue. Scalar timing was observed only during probe trials. This study supports the hypothesis that there is no ubiquitous timing system in the brain but independent timing processes active depending on task demands.

Impaired volitional saccade control: first evidence for a new candidate endophenotype in obsessive–compulsive disorder

Recent research suggests that patients with obsessive-compulsive disorder (OCD) have deficits in the volitional control of saccades. Specific evidence comes from increased latencies of saccadic eye movements when they were volitionally executed but not when they were visually guided. The present study sought to test whether this deviance represents a cognitive endophenotype. To this end, first-degree relatives of OCD patients as genetic risk carriers were compared with OCD patients and healthy controls without a family history of OCD. Furthermore, as volitional response generation comprises selection and initiation of the required response, the study also sought to specify the cognitive mechanisms underlying impaired volitional response generation. Twenty-two unaffected first-degree relatives of OCD patients, 22 unmedicated OCD patients, and 22 healthy comparison subjects performed two types of volitional saccade tasks measuring response selection or only response initiation, respectively. Visually guided saccades were used as a control condition. Our results showed that unaffected first-degree relatives and OCD patients were significantly slowed compared to healthy comparison subjects in volitional response selection. Patients and relatives did not differ from each other. There was no group difference in the visually guided control condition. Taken together, the study provides first evidence that dysfunctional volitional response selection is a candidate endophenotype for OCD.

Manipulations of the relationship between response alternatives and exogenous saccade latencies

The relationship between the latencies of saccadic eye movements and the number of response alternatives is complex. Previously, we have found a decrease in exogenous saccade latencies with an increase in the number of response alternatives (i.e., an anti-Hick's effect). In the present study, we examined the effect of bottom up and top down influences on the effect. In Experiment 1, we found that the anti-Hick's effect is dependent upon the number, as opposed to the configuration, of response alternatives, suggesting that the effect is not a purely bottom up phenomenon. In Experiment 2, we examined whether top down processes, such as expectancy, influence the magnitude and/or direction of the relationship between response alternatives and reaction time. We found that interleaving, as opposed to blocking, the number of alternatives negated the anti-Hick's effect. Taken together, these results suggest that the anti-Hick's effect arises not only from stimulus-based perceptual signals but also from higher-order control signals.

Effect of nicotine on saccadic eye movement latencies in non‐smokers

Recently, saccadic eye movement tasks have been used to assess the effects of nicotine on higher cognitive processes, including inhibitory control. Saccadic task switching methods suggest that there is prolonged inhibition of the saccadic eye movement system following antisaccade trials. The objective of this research was to examine effects of nicotine on inhibition using saccadic task switching paradigms. Nicotine and placebo lozenges were administered on separate days to 40 non-smokers who performed prosaccade and antisaccade tasks. In addition, participants performed a series of trials in which prosaccade and antisaccade tasks were switched. Eye movement latencies were recorded. Participants responded significantly faster for the nicotine condition than for the placebo condition. A switch benefit was observed for only placebo antisaccade trials, in that latencies of repetition trials were significantly longer than those of switch trials. In addition, an analysis of the repetition trials showed an interaction between saccade type and sequence position for the placebo condition, but not the nicotine condition. Inhibition persists after antisaccade trials in a switching paradigm, but that the duration of this inhibition is reduced by nicotine.

Effects of structured backgrounds on the latency of saccadic eye movements

Effects of structured backgrounds on the latency of saccadic eye movements

The eccentricity effect for auditory saccadic reaction times is independent of target frequency

Although much is understood about the stimulus properties affecting the latency of saccadic eye movements to visual targets, relatively little is known about the properties affecting saccades to auditory targets. This study examined the effect of three primary acoustic features—frequency, intensity, and spatial location—on auditory saccade characteristics in humans, and compared them to visual saccades. Saccade targets were presented from an azimuthal array of speakers and LEDs spanning ±36°. There was an ‘eccentricity effect’ for auditory saccades such that latencies decreased by up to 70 ms with eccentricity. This was observed for all frequencies and intensities tested. There was a smaller effect in the opposite direction effect for visual saccades. Auditory saccades had similar latencies to visual saccades (within 5 ms) for near midline locations, but were up to 90 ms faster at eccentric locations (±36°). Overall, saccadic latencies were shortest for wideband noise and narrowband noises with center frequencies falling within the human speech range. Examination of saccade accuracy showed decreasing accuracy with increasing eccentricity, and a negative correlation between accuracy and latency for auditory stimuli.

Conditions that alter saccadic eye movement latencies and affect target choice to visual stimuli and to electrical stimulation of area V1 in the monkey

In this study, we examined procedures that alter saccadic latencies and target selection to visual stimuli and electrical stimulation of area V1 in the monkey. It has been shown that saccadic eye movement latencies to singly presented visual targets form a bimodal distribution when the fixation spot is turned off a number of milliseconds prior to the appearance of the target (the gap period); the first mode has been termed express saccades and the second regular saccades. When the termination of the fixation spot is coincident with the appearance of the target (0 ms gap), express saccades are rarely generated. We show here that a bimodal distribution of saccadic latencies can also be obtained when an array of visual stimuli is presented prior to the appearance of the visual target, provided the elements of the array overlap spatially with the visual target. The overall latency of the saccadic eye movements elicited by electrical stimulation of area V1 is significantly shortened both when a gap is introduced between the termination of the fixation spot and the stimulation and when an array is presented. However, under these conditions, the distribution of saccadic latencies is unimodal. When two visual targets are presented after the fixation spot, introducing a gap has no effect on which target is chosen. By contrast, when electrical stimulation is paired with a visual target, introducing a gap greatly increases the frequency with which the electrical stimulation site is chosen.

Which Visual Pathways Cause Fixation-Related Inhibition?

Visual stimuli can both inhibit and activate motor mechanisms. In one well-known example, the latency of saccadic eye movements is prolonged in the presence of a fixation stimulus, relative to the case in which the fixation stimulus disappears before the target appears. This automatic sensory-motor effect, known as the gap effect or fixation-offset effect, has been associated with inhibitory connections within the superior colliculus (SC). Visual information is provided to the SC and other oculomotor areas, such as the frontal eye fields (FEF), mainly by the magnocellular geniculostriate pathway, and also by the retinotectal pathway. We tested whether signals in these pathways are necessary to create fixation-related inhibition, by using stimuli invisible to them. We found that such stimuli, visible only to short-wave-sensitive cones (S cones), do produce fixation-related inhibition (including when warning effects were equated). We also demonstrate that this fixation-related inhibition cannot be explained by residual activation of luminance pathways and must be caused by a route separate from that of luminance fixation signals. Thus there are at least two routes that cause fixation-related inhibition, and direct sensory input to the SC or FEF by the magnocellular or retinotectal pathways is not required. We discuss the implications that there may be both cortical and collicular mechanisms.

Effects of diazepam on the latency of saccades for luminance and binocular disparity defined stimuli

Saccadic latency is composed of separate sensory and motor processing delays. Therefore, any alteration in the sensory processing should effect the saccadic latency. Because the highest density of benzodiazepine (Bz) binding sites is located in cerebral cortex, sensory processing of stimuli in this cortical area is expected to be substantially effected by administration of Bzs. It is well known that sensory processing of binocular disparity occurs in the cerebral cortical areas and therefore the latency of saccades to stimuli defined by binocular disparity should be substantially affected by Bz intake. In this study, we tested this prediction by comparing the latency of saccadic eye movements for binocular disparity defined stimuli (stereo stimuli) with those for luminance contrast defined stimuli (luminance stimuli), after diazepam or placebo. Eye movements were mainly recorded by use of the magnetic search coil technique, and the study was performed in a randomized, double-blind way. Although diazepam prolonged the latency of saccades for stereo and luminance stimuli, the percentage increases in saccadic latency for the stereo stimuli were significantly larger than those for the luminance stimuli. Saccadic peak velocity, and saccadic amplitude, also significantly decreased after diazepam under conditions of stereo and luminance stimuli. However, there was no significant difference for either saccadic peak velocity or amplitude between the two types of target. The results suggest that the latency of saccades to binocular disparity defined random-dot stimuli could more sensitively reflect the pharmacodynamic effects of Bzs on the cerebral cortex.

No evidence for prolonged latency of saccadic eye movements due to intermittent light of a CRT computer screen

Despite previous studies it remains unclear, whether saccadic eye movements across computer screens may be adversely affected by the intermittency of light of cathode ray tubes (CRT). We measured the latency of simple saccades to peripheral targets presented on a CRT-screen, operated at refresh rates of 50, 100 and 150 Hz, compared with a special fluorescent lamp display (FLD). Our results suggest that the intermittent light of CRT screens does not prolong the latency of saccades not even relative to a control condition of unmodulated steady light at the FLD. Further, there was no evidence for any individual effect in possibly susceptible subjects, e.g. at high critical flicker frequencies (CFF).

Effects of informative peripheral cues on eye movements: Revisiting William James’ “derived attention”

Two experiments examined effects of peripheral information on the latency of saccadic eye movements. In Experiment 1, simple target stimuli were presented to the left or right visual field. Prior to each target, a pair of cue letters was presented for 40msec bilaterally. The relative location of the letters (W-S or S-W) was related to target location, but participants were not informed of this contingency. After a brief practice period, saccadic latencies were faster for targets at the likely location, as indicated by the letter pair. This derived peripheral cueing effect was related to participants' awareness of the relation between cue type and target location. Experiments 2A and 2B employed monocular viewing in order to compare performance across the nasal and temporal visual fields. The effect observed in Experiment 1 was confined to the nasal visual field. In a reflexive orienting condition, the effect of a unilateral letter cue was larger in the temporal visual field. It is concluded that the neurocognitive processes responsible for derived peripheral cueing are distinct from those involved in either reflexive or voluntary orienting.

Antisaccade eye movement abnormalities in Tourette syndrome: evidence for cortico-striatal network dysfunction?

Saccadic eye movements are rapid eye movements which act to redirect the eyes from one object of interest to another. Accurately and objectively measurable, their underlying neuroanatomical mechanisms have been extensively studied. The antisaccade task allows the study of the frontocortico-striatal network involved in the voluntary control of saccadic eye movements. In this task, the subject is instructed to inhibit a reflex eye movement towards a peripheral target light and, instead, to generate a movement in the equal and opposite direction. An error occurs when the subject fails to suppress reflexive saccades towards the target. Significantly high error rates and increased latencies in the antisaccade task have been reported in disorders associated with dysfunction of the frontocortico-striatal network. Increased saccadic eye movement latencies and error rates have been reported in Tourette syndrome patients (n = 4) who were receiving antipsychotic medication. To investigate this further, we tested the antisaccade task on six male Tourette syndrome patients. The results were compared with 18 age- and sex-matched mentally and physically healthy, medication/alcohol-free controls. Antisaccade latencies were (mean +/- SD; ms) 751.2+/-186.7 for the Tourette syndrome group and 417+/-75.3 for controls, and error rates were 59+/-14.3 for the Tourette syndrome group and 11.9+/-6.4 for controls, respectively. These significant results may further support dysfunction of the frontocortico-striatal network in Tourette syndrome.

Saccades require focal attention and are facilitated by a short-term memory system

We performed two sets of experiments in which observers were instructed to make saccades to an odd colored target embedded in an array of distractors. First, we found that when the colors of the target and distractors switched unpredictably from trial to trial (the mixed condition), saccadic latencies decreased with increasing numbers of distractors. In contrast, saccadic latencies were independent of the number of distractors when the color of the target and distractors remained the same on each trial (the blocked condition). This pattern of results mirrors visual search tasks in which focal rather than distributed attention is required (Bravo, M.J., Nakayama, K. (1992). The role of attention in different visual search tasks. Perception and Psychophysics, 51, 465–472.). Second, we found that saccades to an odd target were made more quickly and accurately when the target was the same color as on previous trials than when it changed color. This priming of the target color accumulates across five to seven trials over a period of approximately 30 s. A similar priming effect has been previously shown for the deployment of focal attention (Maljkovic, V., Nakayama, K. (1994). Priming of popout: III. Role of features. Memory and Cognition, 22(6), 657–672.). Thus, we show a close congruence between the pattern of saccadic eye movement latencies and the deployment of focal attention. This supports the view that (1) the execution of saccades requires focal as opposed to distributed attention and that (2) this focal attention is guided by a short term memory system which facilitates the rapid refixation of gaze to recently foveated targets.

Spatial attention and latencies of saccadic eye movements

Recent theories of visual attention, such as the oculomotor readiness theory of Klein (1980) (Does oculomotor readiness mediate cognitive control of the visual attention. In: R. Nickerson, Attention and performance, Hillsdale: Erlbaum), the premotor theory of Rizzolati (1983) (Mechanisms of selective attention in mammals. In: J.P. Ewart, R.R. Capranica, D.J. Ingle, Advances in vertebrate Neuroethology (pp. 261–297). New York: Plenum) and the sequential attention theory of Henderson (1992) (Visual attention and eye movement control during reading and scene perception. In K. Rayner, Eye movements and visual cognition (260–283). New York: Springer-Verlag), propose a link between shifts in spatial attention and the generation of saccadic eye movements. In this paper we show that a winner-take-all model of spatial attention, combined with a simple model for the link between attention and eye movements, can account for the variation in saccadic latency observed in many oculomotor phenomena. These phenomena include the gap effect (Saslow M.G. (1967). Effects of components of displacement-step stimuli upon latency for saccadic eye movement. Journal of the Optical Society of America, 57, 1024–1029), the effect of target jumps on saccadic latency (Becker W. & Jurgens R. (1979). An analysis of the saccadic system by means of double step stimuli. Vision Research, 19, 967–983), the increase of saccadic latency as target eccentricity drops (Kalesnykas R.P. & Hallett P.E. (1994). Retinal eccentricity and the latency of eye saccades. Vision Research, 34, 517–531), and the modulation of saccadic accuracy using target predictability and saccadic latency (Coëffé C. & O’Regan J.K. (1987). Reducing the influence of non-target stimuli on saccade accuracy: predictability and latency effects. Vision Research, 27 (2), 227–240).

Response latencies and event-related potentials during the gap paradigm using saccadic responses in human subjects

An experiment was conducted in naive human subjects to measure the time benefits of the latencies of saccadic eye movements to peripheral targets when the offset of a central fixation point precedes the switching on of the peripheral target by 200 ms. Naive subjects produced a shift advancement of the eye movement latencies to the targets with respect to when there is no such temporal gap. Simultaneously, the event-related potentials produced by visual stimuli and saccadic eye movements were recorded. The switching on of the central fixation point induced a negative component that could be considered a contingent negative variation. Subsequently, in the control non-gap condition visual evoked potentials and P300 appear. The temporal gap paradigm induced offset visual-evoked potentials and a frontal negativity; it also induced a higher P300 than the non-gap condition. The saccadic ERPs also showed a frontal negativity preceding the saccade during the gap condition. The results suggest that fast regular saccades during the gap paradigm occur by a priming of premotor and motor frontal circuits indexed by the recorded negativity during the gap paradigm.

Saccade latency toward auditory targets depends on the relative position of the sound source with respect to the eyes

The latency of saccadic eye movements evoked by the presentation of auditory and visual targets was studied while starting eye position was either 0 or 20 deg right, or 20 deg left. The results show that for any starting position the latency of visually elicited saccades increases with target eccentricity with respect to the eyes. For auditory elicited saccades and for any starting position the latency decreases with target eccentricity with respect to the eyes. Therefore auditory latency depends on a retinotopic motor error, as in the case of visual target presentation.

Effects of Diazepam and Buspirone on Reaction Time of Saccadic Eye Movements

Effects of the anxiolytic drugs diazepam and buspirone were studied on the reaction time of saccadic eye movements. The study was performed with 8 healthy volunteers in a double-blind, placebo-controlled way. The purpose was to investigate the putative drug effects on the first step of an attention shifting task: the disengagement of attention. Saccadic reaction time was measured in two conditions: the 'gap' and the 'overlap' condition. In the first condition a delay is present between the offset of a fixation spot and the onset of a target, while in the second condition the offset of the spot is overlapped by the onset of the target. Clear differences in saccadic reaction time in the expected direction were found between the two conditions, with longer reaction times of saccadic eye movements in the overlap condition. The nonsedative anxiolytic buspirone in a dose of 5 mg had no significant effects on saccadic reaction times, while clear effects of diazepam in a dose of 5 mg were established. Diazepam slowed down saccadic reaction times, reduced the number of fast saccades and facilitated the number of slow saccades. However, the effects induced by this drug were identical for the two conditions. The latter result implies that the disengagement of attention is not selectively disrupted by diazepam. Perhaps, the action of diazepam is expressed in other attention factors, such as in shifting attention or in the reengagement of attention. A slowing down of these processes by the vigilance-lowering properties of diazepam might be the cause of the prolonged latencies. The increased latencies of saccadic eye movements induced by a low dose of diazepam may have practical implications.

The effects of visual scene composition on the latency of saccadic eye movements of the rhesus monkey

This study examined how variations in the visual scene affect the generation of bimodal saccadic latency distributions, the first mode of which is called the population of “express saccades”. The surface media used to make stimuli visible and the composition of the background were varied to determine the conditions under which express saccades can be generated in rhesus monkeys. The results show that express saccades to singly presented targets can readily be elicited when the stimuli are made visible by virtue of either luminance contrast, color contrast or motion cues. Express saccades are rarely obtained when stimuli are made visible by virtue of only stereoscopic depth or texture cues. Express saccades can, however, be elicited using random-dot stereograms or textures when luminance or chrominance information is added to the target. When single target stimuli are presented simultaneously with a set of non-target stimuli, express saccades are for the most part prevented unless either the non-target stimuli are near threshold or their numerosity is very high, in which case they form a texture-like array. However, when the non-target stimuli are continuously present in the display, express saccades reemerge. These findings suggest that express saccades are not unique to experimental situations in which only a single stimulus appears on an otherwise homogeneous surface; they can readily be generated as long as the target stimulus is made visible by virtue of luminance, chrominance, motion or a combination of more than one surface medium and as long as the target does not appear concurrently with a salient group of other non-target stimuli.