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1
Scholes, Chris, Paul V. McGraw, and Neil W. Roach. "Learning to silence saccadic suppression." Proceedings of the National Academy of Sciences 118, no. 6 (February 1, 2021): e2012937118. http://dx.doi.org/10.1073/pnas.2012937118.
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Perceptual stability is facilitated by a decrease in visual sensitivity during rapid eye movements, called saccadic suppression. While a large body of evidence demonstrates that saccadic programming is plastic, little is known about whether the perceptual consequences of saccades can be modified. Here, we demonstrate that saccadic suppression is attenuated during learning on a standard visual detection-in-noise task, to the point that it is effectively silenced. Across a period of 7 days, 44 participants were trained to detect brief, low-contrast stimuli embedded within dynamic noise, while eye position was tracked. Although instructed to fixate, participants regularly made small fixational saccades. Data were accumulated over a large number of trials, allowing us to assess changes in performance as a function of the temporal proximity of stimuli and saccades. This analysis revealed that improvements in sensitivity over the training period were accompanied by a systematic change in the impact of saccades on performance—robust saccadic suppression on day 1 declined gradually over subsequent days until its magnitude became indistinguishable from zero. This silencing of suppression was not explained by learning-related changes in saccade characteristics and generalized to an untrained retinal location and stimulus orientation. Suppression was restored when learned stimulus timing was perturbed, consistent with the operation of a mechanism that temporarily reduces or eliminates saccadic suppression, but only when it is behaviorally advantageous to do so. Our results indicate that learning can circumvent saccadic suppression to improve performance, without compromising its functional benefits in other viewing contexts.
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Irwin, David E., and Laura A. Carlson-Radvansky. "Cognitive Suppression During Saccadic Eye Movements." Psychological Science 7, no. 2 (March 1996): 83–88. http://dx.doi.org/10.1111/j.1467-9280.1996.tb00334.x.
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Saccadic eye movements are made at least 100,000 times each day It is well known that sensitivity to visual input is suppressed during saccades, we examined whether cognitive activity (specifically, mental rotation) is suppressed as well If cognitive processing occurs during saccades, a prime viewed in one fixation should exert a larger influence on a target viewed in a second fixation when a long rather than a short saccade separates their viewing No such effect was found, even though the time difference between long and short saccades was effective in a no-saccade control These results indicate that at least some cognitive operations are suppressed during saccades
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Crowder, Nathan A., Nicholas S. C. Price, Michael J. Mustari, and Michael R. Ibbotson. "Direction and Contrast Tuning of Macaque MSTd Neurons During Saccades." Journal of Neurophysiology 101, no. 6 (June 2009): 3100–3107. http://dx.doi.org/10.1152/jn.91254.2008.
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Saccades are rapid eye movements that change the direction of gaze, although the full-field image motion associated with these movements is rarely perceived. The attenuation of visual perception during saccades is referred to as saccadic suppression. The mechanisms that produce saccadic suppression are not well understood. We recorded from neurons in the dorsal medial superior temporal area (MSTd) of alert macaque monkeys and compared the neural responses produced by the retinal slip associated with saccades (active motion) to responses evoked by identical motion presented during fixation (passive motion). We provide evidence for a neural correlate of saccadic suppression and expand on two contentious results from previous studies. First, we confirm the finding that some neurons in MSTd reverse their preferred direction during saccades. We quantify this effect by calculating changes in direction tuning index for a large cell population. Second, it has been noted that neural activity associated with saccades can arrive in the parietal cortex ≤30 ms earlier than activity produced by similar visual stimulation during fixation. This led to the question of whether the saccade-related responses were visual in origin or were motor signals arising from saccade-planning areas of the brain. By comparing the responses to saccades made over textured backgrounds of different contrasts, we provide strong evidence that saccade-related responses were visual in origin. Refinements of the possible models of saccadic suppression are discussed.
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Burman, Douglas D., and Charles J. Bruce. "Suppression of Task-Related Saccades by Electrical Stimulation in the Primate's Frontal Eye Field." Journal of Neurophysiology 77, no. 5 (May 1, 1997): 2252–67. http://dx.doi.org/10.1152/jn.1997.77.5.2252.
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Burman, Douglas D. and Charles J. Bruce. Suppression of task-related saccades by electrical stimulation in the primate's frontal eye field. J. Neurophysiol. 77: 2252–2267, 1997. Patients with frontal lobe damage have difficulty suppressing reflexive saccades to salient visual stimuli, indicating that frontal lobe neocortex helps to suppress saccades as well as to produce them. In the present study, a role for the frontal eye field (FEF) in suppressing saccades was demonstrated in macaque monkeys by application of intracortical microstimulation during the performance of a visually guided saccade task, a memory prosaccade task, and a memory antisaccade task. A train of low-intensity (20–50 μA) electrical pulses was applied simultaneously with the disappearance of a central fixation target, which was always the cue to initiate a saccade. Trials with and without stimulation were compared, and significantly longer saccade latencies on stimulation trials were considered evidence of suppression. Low-intensity stimulation suppressed task-related saccades at 30 of 77 sites tested. In many cases saccades were suppressed throughout the microstimulation period (usually 450 ms) and then executed shortly after the train ended. Memory-guided saccades were most dramatically suppressed and were often rendered hypometric, whereas visually guided saccades were less severely suppressed by stimulation. At 18 FEF sites, the suppression of saccades was the only observable effect of electrical stimulation. Contraversive saccades were usually more strongly suppressed than ipsiversive ones, and cells recorded at such purely suppressive sites commonly had either foveal receptive fields or postsaccadic responses. At 12 other FEF sites at which saccadic eye movements were elicited at low thresholds, task-related saccades whose vectors differed from that of the electrically elicited saccade were suppressed by electrical stimulation. Such suppression at saccade sites was observed even with currents below the threshold for eliciting saccades. Pure suppression sites tended to be located near or in the fundus, deeper in the anterior bank of the arcuate than elicited saccade sites. Stimulation in the prefrontal association cortex anterior to FEF did not suppress saccades, nor did stimulation in premotor cortex posterior to FEF. These findings indicate that the primate FEF can help orchestrate saccadic eye movements by suppressing inappropriate saccade vectors as well as by selecting, specifying, and triggering appropriate saccades. We hypothesize that saccades could be suppressed both through local FEF interactions and through FEF projections to subcortical regions involved in maintaining fixation.
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Krock, Rebecca M., and Tirin Moore. "Visual sensitivity of frontal eye field neurons during the preparation of saccadic eye movements." Journal of Neurophysiology 116, no. 6 (December 1, 2016): 2882–91. http://dx.doi.org/10.1152/jn.01140.2015.
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Primate vision is continuously disrupted by saccadic eye movements, and yet this disruption goes unperceived. One mechanism thought to reduce perception of this self-generated movement is saccadic suppression, a global loss of visual sensitivity just before, during, and after saccadic eye movements. The frontal eye field (FEF) is a candidate source of neural correlates of saccadic suppression previously observed in visual cortex, because it contributes to the generation of visually guided saccades and modulates visual cortical responses. However, whether the FEF exhibits a perisaccadic reduction in visual sensitivity that could be transmitted to visual cortex is unknown. To determine whether the FEF exhibits a signature of saccadic suppression, we recorded the visual responses of FEF neurons to brief, full-field visual probe stimuli presented during fixation and before onset of saccades directed away from the receptive field in rhesus macaques ( Macaca mulatta). We measured visual sensitivity during both epochs and found that it declines before saccade onset. Visual sensitivity was significantly reduced in visual but not visuomotor neurons. This reduced sensitivity was also present in visual neurons with no movement-related modulation during visually guided saccades and thus occurred independently from movement-related activity. Across the population of visual neurons, sensitivity began declining ∼80 ms before saccade onset. We also observed a similar presaccadic reduction in sensitivity to isoluminant, chromatic stimuli. Our results demonstrate that the signaling of visual information by FEF neurons is reduced during saccade preparation, and thus these neurons exhibit a signature of saccadic suppression.
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Chen, Jing, Matteo Valsecchi, and Karl R. Gegenfurtner. "Saccadic suppression measured by steady-state visual evoked potentials." Journal of Neurophysiology 122, no. 1 (July 1, 2019): 251–58. http://dx.doi.org/10.1152/jn.00712.2018.
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Visual sensitivity is severely impaired during the execution of saccadic eye movements. This phenomenon has been extensively characterized in human psychophysics and nonhuman primate single-neuron studies, but a physiological characterization in humans is less established. Here, we used a method based on steady-state visually evoked potential (SSVEP), an oscillatory brain response to periodic visual stimulation, to examine how saccades affect visual sensitivity. Observers made horizontal saccades back and forth, while horizontal black-and-white gratings flickered at 5–30 Hz in the background. We analyzed EEG epochs with a length of 0.3 s either centered at saccade onset (saccade epochs) or centered at fixations half a second before the saccade (fixation epochs). Compared with fixation epochs, saccade epochs showed a broadband power increase, which most likely resulted from saccade-related EEG activity. The execution of saccades, however, led to an average reduction of 57% in the SSVEP amplitude at the stimulation frequency. This result provides additional evidence for an active saccadic suppression in the early visual cortex in humans. Compared with previous functional MRI and EEG studies, an advantage of this approach lies in its capability to trace the temporal dynamics of neural activity throughout the time course of a saccade. In contrast to previous electrophysiological studies in nonhuman primates, we did not find any evidence for postsaccadic enhancement, even though simulation results show that our method would have been able to detect it. We conclude that SSVEP is a useful technique to investigate the neural correlates of visual perception during saccadic eye movements in humans. NEW & NOTEWORTHY We make fast ballistic saccadic eye movements a few times every second. At the time of saccades, visual sensitivity is severely impaired. The present study uses steady-state visually evoked potentials to reveal a neural correlate of the fine temporal dynamics of these modulations at the time of saccades in humans. We observed a strong reduction (57%) of visually driven neural activity associated with saccades but did not find any evidence for postsaccadic enhancement.
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Born, Sabine. "Saccadic Suppression of Displacement Does Not Reflect a Saccade-Specific Bias to Assume Stability." Vision 3, no. 4 (September 24, 2019): 49. http://dx.doi.org/10.3390/vision3040049.
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Across saccades, small displacements of a visual target are harder to detect and their directions more difficult to discriminate than during steady fixation. Prominent theories of this effect, known as saccadic suppression of displacement, propose that it is due to a bias to assume object stability across saccades. Recent studies comparing the saccadic effect to masking effects suggest that suppression of displacement is not saccade-specific. Further evidence for this account is presented from two experiments where participants judged the size of displacements on a continuous scale in saccade and mask conditions, with and without blanking. Saccades and masks both reduced the proportion of correctly perceived displacements and increased the proportion of missed displacements. Blanking improved performance in both conditions by reducing the proportion of missed displacements. Thus, if suppression of displacement reflects a bias for stability, it is not a saccade-specific bias, but a more general stability assumption revealed under conditions of impoverished vision. Specifically, I discuss the potentially decisive role of motion or other transient signals for displacement perception. Without transients or motion, the quality of relative position signals is poor, and saccadic and mask-induced suppression of displacement reflects performance when the decision has to be made on these signals alone. Blanking may improve those position signals by providing a transient onset or a longer time to encode the pre-saccadic target position.
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Findlay, J. M., R. Walker, V. Brown, I. Gilchrist, and M. Clarke. "Saccade Programming in Strabismic Suppression." Perception 25, no. 1_suppl (August 1996): 47. http://dx.doi.org/10.1068/v96l0303.
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Individuals with strabismus frequently show a suppression phenomenon in which part of the visual input in one eye is apparently ignored when both eyes are seeing, although the eye may have normal vision when used monocularly. This is often described as an adaptive response to avoid diplopia. We have examined two patients with microstrabismus (angle of squint less than 5 deg) who show strong suppression but with only mild amblyopia. We studied saccade generation in the two eyes using a red — green anaglyph display which allowed us to present stimuli independently to each eye. When single targets were presented in the suppressing eye, saccadic responses usually occurred. However the latencies of these saccades were increased with respect to those elicited from the normal eye (by about 70 ms for one subject and 270 ms for the other). The amplitudes of the saccades were less consistent than those of the normal eye, and saccades were sometimes made in the opposite direction to the target. We also investigated the remote distractor effect. This effect is found consistently in normal subjects and consists of an increase in the latency of a target-elicited saccade when a distractor is simultaneously presented elsewhere in the visual field. When distractors were presented in the suppressing eye, they had no effect on the latency of saccades to a simultaneous target in the other eye. We conclude that visual stimulation in a suppressing eye has no rapid access to the saccadic system.
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Izawa, Yoshiko, Hisao Suzuki, and Yoshikazu Shinoda. "Suppression of Visually and Memory-Guided Saccades Induced by Electrical Stimulation of the Monkey Frontal Eye Field. I. Suppression of Ipsilateral Saccades." Journal of Neurophysiology 92, no. 4 (October 2004): 2248–60. http://dx.doi.org/10.1152/jn.01021.2003.
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When a saccade occurs to an interesting object, visual fixation holds its image on the fovea and suppresses saccades to other objects. Electrical stimulation of the frontal eye field (FEF) has been reported to elicit saccades, and recently also to suppress saccades. This study was performed to characterize properties of the suppression of visually guided (Vsacs) and memory-guided saccades (Msacs) induced by electrical stimulation of the FEF in trained monkeys. For any given stimulation site, we determined the threshold for electrically evoked saccades (Esacs) at ≤50 μA and then examined suppressive effects of stimulation at the same site on Vsacs and Msacs. FEF stimulation suppressed the initiation of both Vsacs and Msacs during and about 50 ms after stimulation at stimulus intensities lower than those for eliciting Esacs, but did not affect the vector of these saccades. Suppression occurred for ipsiversive but not contraversive saccades, and more strongly for saccades with larger amplitudes and those with initial eye positions shifted more in the saccadic direction. The most effective stimulation timing for suppression was about 50 ms before saccade onset, which suggests that suppression occurred in the efferent pathway for generating Vsacs at the premotor rather than the motoneuronal level, most probably in the superior colliculus and/or the paramedian pontine reticular formation. Suppression sites of ipsilateral saccades were distributed over the classical FEF where saccade-related movement neurons were observed. The results suggest that the FEF may play roles in not only generating contraversive saccades but also maintaining visual fixation by suppressing ipsiversive saccades.
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Herdman, Anthony T., and Jennifer D. Ryan. "Spatio-temporal Brain Dynamics Underlying Saccade Execution, Suppression, and Error-related Feedback." Journal of Cognitive Neuroscience 19, no. 3 (March 2007): 420–32. http://dx.doi.org/10.1162/jocn.2007.19.3.420.
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Human and nonhuman animal research has outlined the neural regions that support saccadic eye movements. The aim of the current work was to outline the sequence by which distinct neural regions come on-line to support goal-directed saccade execution and error-related feedback. To achieve this, we obtained behavioral responses via eye movement recordings and neural responses via magnetoencephalography (MEG), concurrently, while participants performed an antisaccade task. Neural responses were examined with respect to the onset of the saccadic eye movements. Frontal eye field and visual cortex activity distinguished subsequently successful goal-directed saccades from (correct and erroneous) reflexive saccades prior to the deployment of the eye movement. Activity in the same neural regions following the saccadic movement distinguished correct from incorrect saccadic responses. Error-related activity in the frontal eye fields preceded that from visual regions, suggesting a potential feedback network that may drive corrective eye movements. This work provides the first empirical demonstration of simultaneous remote eyetracking and MEG recording. The coupling of behavioral and neuroimaging technologies, used here to characterize dynamic brain networks underlying saccade execution and error-related feedback, demonstrates a novel within-paradigm converging evidence approach by which to outline the neural underpinnings of cognition.
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Intoy, Janis, Naghmeh Mostofi, and Michele Rucci. "Fast and nonuniform dynamics of perisaccadic vision in the central fovea." Proceedings of the National Academy of Sciences 118, no. 37 (September 8, 2021): e2101259118. http://dx.doi.org/10.1073/pnas.2101259118.
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Humans use rapid eye movements (saccades) to inspect stimuli with the foveola, the region of the retina where receptors are most densely packed. It is well established that visual sensitivity is generally attenuated during these movements, a phenomenon known as saccadic suppression. This effect is commonly studied with large, often peripheral, stimuli presented during instructed saccades. However, little is known about how saccades modulate the foveola and how the resulting dynamics unfold during natural visual exploration. Here we measured the foveal dynamics of saccadic suppression in a naturalistic high-acuity task, a task designed after primates’ social grooming, which—like most explorations of fine patterns—primarily elicits minute saccades (microsaccades). Leveraging on recent advances in gaze-contingent display control, we were able to systematically map the perisaccadic time course of sensitivity across the foveola. We show that contrast sensitivity is not uniform across this region and that both the extent and dynamics of saccadic suppression vary within the foveola. Suppression is stronger and faster in the most central portion, where sensitivity is generally higher and selectively rebounds at the onset of a new fixation. These results shed light on the modulations experienced by foveal vision during the saccade-fixation cycle and explain some of the benefits of microsaccades.
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Chen, Chih-Yang, and Ziad M. Hafed. "A neural locus for spatial-frequency specific saccadic suppression in visual-motor neurons of the primate superior colliculus." Journal of Neurophysiology 117, no. 4 (April 1, 2017): 1657–73. http://dx.doi.org/10.1152/jn.00911.2016.
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Saccades cause rapid retinal-image shifts that go perceptually unnoticed several times per second. The mechanisms for saccadic suppression have been controversial, in part because of sparse understanding of neural substrates. In this study we uncovered an unexpectedly specific neural locus for spatial frequency-specific saccadic suppression in the superior colliculus (SC). We first developed a sensitive behavioral measure of suppression in two macaque monkeys, demonstrating selectivity to low spatial frequencies similar to that observed in earlier behavioral studies. We then investigated visual responses in either purely visual SC neurons or anatomically deeper visual motor neurons, which are also involved in saccade generation commands. Surprisingly, visual motor neurons showed the strongest visual suppression, and the suppression was dependent on spatial frequency, as in behavior. Most importantly, suppression selectivity for spatial frequency in visual motor neurons was highly predictive of behavioral suppression effects in each individual animal, with our recorded population explaining up to ~74% of behavioral variance even on completely different experimental sessions. Visual SC neurons had mild suppression, which was unselective for spatial frequency and thus only explained up to ~48% of behavioral variance. In terms of spatial frequency-specific saccadic suppression, our results run contrary to predictions that may be associated with a hypothesized SC saccadic suppression mechanism, in which a motor command in the visual motor and motor neurons is first relayed to the more superficial purely visual neurons, to suppress them and to then potentially be fed back to cortex. Instead, an extraretinal modulatory signal mediating spatial-frequency-specific suppression may already be established in visual motor neurons. NEW & NOTEWORTHY Saccades, which repeatedly realign the line of sight, introduce spurious signals in retinal images that normally go unnoticed. In part, this happens because of perisaccadic suppression of visual sensitivity, which is known to depend on spatial frequency. We discovered that a specific subtype of superior colliculus (SC) neurons demonstrates spatial-frequency-dependent suppression. Curiously, it is the neurons that help mediate the saccadic command itself that exhibit such suppression, and not the purely visual ones.
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Santer, Roger D., Richard Stafford, and F. Claire Rind. "Retinally-generated saccadic suppression of a locust looming-detector neuron: investigations using a robot locust." Journal of The Royal Society Interface 1, no. 1 (November 22, 2004): 61–77. http://dx.doi.org/10.1098/rsif.2004.0007.
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A fundamental task performed by many visual systems is to distinguish apparent motion caused by eye movements from real motion occurring within the environment. During saccadic eye movements, this task is achieved by inhibitory signals of central and retinal origin that suppress the output of motion-detecting neurons. To investigate the retinally-generated component of this suppression, we used a computational model of a locust looming-detecting pathway that experiences saccadic suppression. This model received input from the camera of a mobile robot that performed simple saccade-like movements, allowing the model's response to simplified real stimuli to be tested. Retinally-generated saccadic suppression resulted from two inhibitory mechanisms within the looming-detector's input architecture. One mechanism fed inhibition forward through the network, inhibiting the looming-detector's initial response to movement. The second spread inhibition laterally within the network, suppressing the looming-detector's maintained response to movement. These mechanisms prevent a loomingdetector model response to whole-field visual stimuli. In the locust, this mechanism of saccadic suppression may operate in addition to centrally-generated suppression. Because lateral inhibition is a common feature of early visual processing in many organisms, we discuss whether the mechanism of retinally-generated saccadic suppression found in the locust looming-detector model may also operate in these species.
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Krekelberg, Bart. "Saccadic suppression." Current Biology 20, no. 5 (March 2010): R228—R229. http://dx.doi.org/10.1016/j.cub.2009.12.018.
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Munoz, Douglas P., Irene T. Armstrong, Karen A. Hampton, and Kimberly D. Moore. "Altered Control of Visual Fixation and Saccadic Eye Movements in Attention-Deficit Hyperactivity Disorder." Journal of Neurophysiology 90, no. 1 (July 2003): 503–14. http://dx.doi.org/10.1152/jn.00192.2003.
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Attention-deficit hyperactivity disorder (ADHD) is characterized by the overt symptoms of impulsiveness, hyperactivity, and inattention. A frontostriatal pathophysiology has been hypothesized to produce these symptoms and lead to reduced ability to inhibit unnecessary or inappropriate behavioral responses. Oculomotor tasks can be designed to probe the ability of subjects to generate or inhibit reflexive and voluntary responses. Because regions of the frontal cortex and basal ganglia have been identified in the control of voluntary responses and saccadic suppression, we hypothesized that children and adults diagnosed with ADHD may have specific difficulties in oculomotor tasks requiring the suppression of reflexive or unwanted saccadic eye movements. To test this hypothesis, we measured eye movement performance in pro- and anti-saccade tasks of 114 ADHD and 180 control participants ranging in age from 6 to 59 yr. In the pro-saccade task, participants were instructed to look from a central fixation point toward an eccentric visual target. In the anti-saccade task, stimulus presentation was identical, but participants were instructed to suppress the saccade to the stimulus and instead look from the central fixation point to the side opposite the target. The state of fixation was manipulated by presenting the target either when the central fixation point was illuminated (overlap condition) or at some time after it disappeared (gap condition). In the pro-saccade task, ADHD participants had longer reaction times, greater intra-subject variance, and their saccades had reduced peak velocities and increased durations. In the anti-saccade task, ADHD participants had greater difficulty suppressing reflexive pro-saccades toward the eccentric target, increased reaction times for correct anti-saccades, and greater intra-subject variance. In a third task requiring prolonged fixation, ADHD participants generated more intrusive saccades during periods when they were required to maintain steady fixation. The results suggest that ADHD participants have reduced ability to suppress unwanted saccades and control their fixation behavior voluntarily, a finding that is consistent with a fronto-striatal pathophysiology. The findings are discussed in the context of recent neurophysiological data from nonhuman primates that have identified important control signals for saccade suppression that emanate from frontostriatal circuits.
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Izawa, Yoshiko, Hisao Suzuki, and Yoshikazu Shinoda. "Suppression of Visually and Memory-Guided Saccades Induced by Electrical Stimulation of the Monkey Frontal Eye Field. II. Suppression of Bilateral Saccades." Journal of Neurophysiology 92, no. 4 (October 2004): 2261–73. http://dx.doi.org/10.1152/jn.00085.2004.
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To understand the neural mechanism of fixation, we investigated effects of electrical stimulation of the frontal eye field (FEF) and its vicinity on visually guided (Vsacs) and memory-guided saccades (Msacs) in trained monkeys and found that there were two types of suppression induced by the electrical stimulation: suppression of ipsilateral saccades and suppression of bilateral saccades. In this report, we characterized the properties of the suppression of bilateral Vsacs and Msacs. Stimulation of the bilateral suppression sites suppressed the initiation of both Vsacs and Msacs in all directions during and ∼50 ms after stimulation but did not affect the vector of these saccades. The suppression was stronger for ipsiversive larger saccades and contraversive smaller saccades, and saccades with initial eye positions shifted more in the saccadic direction. The most effective stimulation timing for the suppression of ipsilateral and contralateral Vsacs was ∼40–50 ms before saccade onset, indicating that the suppression occurred most likely in the superior colliculus and/or the paramedian pontine reticular formation. Suppression sites of bilateral saccades were located in the prearcuate gyrus facing the inferior arcuate sulcus where stimulation induced suppression at ≤40 μA but usually did not evoke any saccades at 80 μA and were different from those of ipsilateral saccades where stimulation evoked saccades at ≤50 μA. The bilateral suppression sites contained fixation neurons. The results suggest that fixation neurons in the bilateral suppression area of the FEF may play roles in maintaining fixation by suppressing saccades in all directions.
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Lueck, C. J., T. J. Crawford, L. Henderson, J. A. M. Van Gisbergen, J. Duysens, and C. Kennard. "Saccadic Eye Movements in Parkinson's Disease: II. Remembered Saccades— towards a Unified Hypothesis?" Quarterly Journal of Experimental Psychology Section A 45, no. 2 (August 1992): 211–33. http://dx.doi.org/10.1080/14640749208401325.
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Ten patients with mild to moderate Parkinson's disease were compared with ten age-matched normal controls in a series of saccadic paradigms in order to test various hypotheses relating to the origin of the Parkinsonian saccadic defect. The paradigms comprised a reflex saccade paradigm, a standard remembered saccade paradigm, a remembered saccade paradigm with delayed centre-offset, and a remembered saccade paradigm with a second target flash immediately prior to saccade execution. Finally, subjects executed both reflex and remembered saccades in a standard remembered paradigm (the “two-saccade” paradigm). As has been reported previously, Parkinsonian subjects demonstrated hypometria on all remembered saccade paradigms, particularly the “two-saccade” paradigm. There was, however, no significant difference between the first three remembered saccade paradigms. These studies serve to refute a simple attentional capture hypothesis, and a hypothesis that suggests that the abnormality of remembered saccades is due to concurrent reflex saccade suppression. On the basis of the results, further hypotheses are advanced in an attempt to explain all published work on Parkinsonian saccades.
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Agaoglu, Mehmet N., and Susana T. L. Chung. "Interaction between stimulus contrast and pre-saccadic crowding." Royal Society Open Science 4, no. 2 (February 2017): 160559. http://dx.doi.org/10.1098/rsos.160559.
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Objects that are briefly flashed around the time of saccades are mislocalized. Previously, robust interactions between saccadic perceptual distortions and stimulus contrast have been reported. It is also known that crowding depends on the contrast of the target and flankers. Here, we investigated how stimulus contrast and crowding interact with pre-saccadic perception. We asked observers to report the orientation of a tilted Gabor presented in the periphery, with or without four flanking vertically oriented Gabors. Observers performed the task either following a saccade or while maintaining fixation. Contrasts of the target and flankers were independently set to either high or low, with equal probability. In both the fixation and saccade conditions, the flanked conditions resulted in worse discrimination performance—the crowding effect. In the unflanked saccade trials, performance significantly decreased with target-to-saccade onset for low-contrast targets but not for high-contrast targets. In the presence of flankers, impending saccades reduced performance only for low-contrast, but not for high-contrast flankers. Interestingly, average performance in the fixation and saccade conditions was mostly similar in all contrast conditions. Moreover, the magnitude of crowding was influenced by saccades only when the target had high contrast and the flankers had low contrasts. Overall, our results are consistent with modulation of perisaccadic spatial localization by contrast and saccadic suppression, but at odds with a recent report of pre-saccadic release of crowding.
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Berman, Rebecca A., James Cavanaugh, Kerry McAlonan, and Robert H. Wurtz. "A circuit for saccadic suppression in the primate brain." Journal of Neurophysiology 117, no. 4 (April 1, 2017): 1720–35. http://dx.doi.org/10.1152/jn.00679.2016.
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Saccades should cause us to see a blur as the eyes sweep across a visual scene. Specific brain mechanisms prevent this by producing suppression during saccades. Neuronal correlates of such suppression were first established in the visual superficial layers of the superior colliculus (SC) and subsequently have been observed in cortical visual areas, including the middle temporal visual area (MT). In this study, we investigated suppression in a recently identified circuit linking visual SC (SCs) to MT through the inferior pulvinar (PI). We examined responses to visual stimuli presented just before saccades to reveal a neuronal correlate of suppression driven by a copy of the saccade command, referred to as a corollary discharge. We found that visual responses were similarly suppressed in SCs, PI, and MT. Within each region, suppression of visual responses occurred with saccades into both visual hemifields, but only in the contralateral hemifield did this suppression consistently begin before the saccade (~100 ms). The consistency of the signal along the circuit led us to hypothesize that the suppression in MT was influenced by input from the SC. We tested this hypothesis in one monkey by inactivating neurons within the SC and found evidence that suppression in MT depends on corollary discharge signals from motor SC (SCi). Combining these results with recent findings in rodents, we propose a complete circuit originating with corollary discharge signals in SCi that produces suppression in visual SCs, PI, and ultimately, MT cortex. NEW & NOTEWORTHY A fundamental puzzle in visual neuroscience is that we frequently make rapid eye movements (saccades) but seldom perceive the visual blur accompanying each movement. We investigated neuronal correlates of this saccadic suppression by recording from and perturbing a recently identified circuit from brainstem to cortex. We found suppression at each stage, with evidence that it was driven by an internally generated signal. We conclude that this circuit contributes to neuronal suppression of visual signals during eye movements.
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Hamker, Fred H., Marc Zirnsak, Arnold Ziesche, and Markus Lappe. "Computational models of spatial updating in peri-saccadic perception." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1564 (February 27, 2011): 554–71. http://dx.doi.org/10.1098/rstb.2010.0229.
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Perceptual phenomena that occur around the time of a saccade, such as peri-saccadic mislocalization or saccadic suppression of displacement, have often been linked to mechanisms of spatial stability. These phenomena are usually regarded as errors in processes of trans-saccadic spatial transformations and they provide important tools to study these processes. However, a true understanding of the underlying brain processes that participate in the preparation for a saccade and in the transfer of information across it requires a closer, more quantitative approach that links different perceptual phenomena with each other and with the functional requirements of ensuring spatial stability. We review a number of computational models of peri-saccadic spatial perception that provide steps in that direction. Although most models are concerned with only specific phenomena, some generalization and interconnection between them can be obtained from a comparison. Our analysis shows how different perceptual effects can coherently be brought together and linked back to neuronal mechanisms on the way to explaining vision across saccades.
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Seirafi, Mehrdad, Peter De Weerd, and Beatrice de Gelder. "Suppression of Face Perception during Saccadic Eye Movements." Journal of Ophthalmology 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/384510.
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Lack of awareness of a stimulus briefly presented during saccadic eye movement is known as saccadic omission. Studying the reduced visibility of visual stimuli around the time of saccade—known as saccadic suppression—is a key step to investigate saccadic omission. To date, almost all studies have been focused on the reduced visibility of simple stimuli such as flashes and bars. The extension of the results from simple stimuli to more complex objects has been neglected. In two experimental tasks, we measured the subjective and objective awareness of a briefly presented face stimuli during saccadic eye movement. In the first task, we measured the subjective awareness of the visual stimuli and showed that in most of the trials there is no conscious awareness of the faces. In the second task, we measured objective sensitivity in a two-alternative forced choice (2AFC) face detection task, which demonstrated chance-level performance. Here, we provide the first evidence of complete suppression of complex visual stimuli during the saccadic eye movement.
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Gremmler, Svenja, and Markus Lappe. "Saccadic Suppression during Voluntary vs Reactive Saccades." Journal of Vision 17, no. 10 (August 31, 2017): 1162. http://dx.doi.org/10.1167/17.10.1162.
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Gremmler, Svenja, and Markus Lappe. "Saccadic suppression during voluntary versus reactive saccades." Journal of Vision 17, no. 8 (July 13, 2017): 8. http://dx.doi.org/10.1167/17.8.8.
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Souto, David, Karl Gegenfurtner, and Alexander Schütz. "Saccade adaptation and saccadic suppression of displacement." Journal of Vision 15, no. 12 (September 1, 2015): 209. http://dx.doi.org/10.1167/15.12.209.
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Wenzel, Rüdiger, Petra Wobst, Hauke H. Heekeren, Kenneth K. Kwong, Stephan A. Brandt, Matthias Kohl, Hellmuth Obrig, Ulrich Dirnagl, and Arno Villringer. "Saccadic Suppression Induces Focal Hypooxygenation in the Occipital Cortex." Journal of Cerebral Blood Flow & Metabolism 20, no. 7 (July 2000): 1103–10. http://dx.doi.org/10.1097/00004647-200007000-00010.
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This study investigated how a decrease in neuronal activity affects cerebral blood oxygenation employing a paradigm of acoustically triggered saccades in complete darkness. Known from behavioral evidence as saccadic suppression, electrophysiologically it has been shown in monkeys that during saccades an attenuation of activity occurs in visual cortex neurons ( Duffy and Burchfiel, 1975 ). In study A, using blood oxygen level-dependent (BOLD) contrast functional magnetic resonance imaging (fMRI), the authors observed signal intensity decreases bilaterally at the occipital pole during the performance of saccades at 2 Hz. In study B.1, the authors directly measured changes in deoxyhemoglobin [deoxy-Hb] and oxyhemoglobin [oxy-Hb] concentration in the occipital cortex with near-infrared spectroscopy (NIRS). Whereas a rise in [deoxy-Hb] during the performance of saccades occurred, there was a drop in [oxy-Hb]. In a second NIRS study (B.2), subjects performed saccades at different rates (1.6, 2.0, and 2.3 Hz). Here the authors found the increase in deoxy-Hb and the decrease of oxy-Hb to be dependent on the frequency of the saccades. In summary, the authors observed a focal hypooxygenation in the human visual cortex dependent on the saccade-frequency in an acoustically triggered saccades paradigm. This could be interpreted as evidence that corresponding to the focal hyperoxygenation observed in functional brain activation, caused by an excessive increase in cerebral blood flow (CBF) over the increase in CMRO2 during decreased neuronal activity CBF, is more reduced than oxygen delivery.
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MacAskill, Michael R., Richard D. Jones, and Tim J. Anderson. "Saccadic Suppression of Displacement: Effects of Illumination and Background Manipulation." Perception 32, no. 4 (April 2003): 463–74. http://dx.doi.org/10.1068/p3474.
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In contrast to other functions which are suppressed during saccades, saccadic suppression of displacement (SSD—a decrease in sensitivity to visual displacements during saccades) has often been considered to be due to efferent processes rather than to visual masking. The aim of this study was to explicitly assess the importance of visual conditions in SSD. In two experiments, a small computer-generated target made random horizontal jumps. An infrared eye tracker was used to detect the saccade toward the new position, triggering a smaller centripetal displacement of the target. Subjects reported awareness of these intrasaccadic displacements by pressing a key. In the first experiment, the task was performed in both a well-lit environment and in darkness. In the second experiment these conditions were replicated and additional factors such as the contrast of the background and the effect of moving the target spot alone or the target plus the entire background were investigated. Unlike other forms of saccadic suppression, SSD was stronger in the dark, although subjects also had a greater bias to report detections in that condition. Other background manipulations had no effect. The effect of ambient lighting on SSD is small and subtle. Effects of other background manipulations may be overridden by the focusing of attention on a small moving target.
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Crewther, David P., Daniel Crewther, Stephanie Bevan, Melvyn A. Goodale, and Sheila G. Crewther. "Greater magnocellular saccadic suppression in high versus low autistic tendency suggests a causal path to local perceptual style." Royal Society Open Science 2, no. 12 (December 2015): 150226. http://dx.doi.org/10.1098/rsos.150226.
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Saccadic suppression—the reduction of visual sensitivity during rapid eye movements—has previously been proposed to reflect a specific suppression of the magnocellular visual system, with the initial neural site of that suppression at or prior to afferent visual information reaching striate cortex. Dysfunction in the magnocellular visual pathway has also been associated with perceptual and physiological anomalies in individuals with autism spectrum disorder or high autistic tendency, leading us to question whether saccadic suppression is altered in the broader autism phenotype. Here we show that individuals with high autistic tendency show greater saccadic suppression of low versus high spatial frequency gratings while those with low autistic tendency do not. In addition, those with high but not low autism spectrum quotient (AQ) demonstrated pre-cortical (35–45 ms) evoked potential differences (saccade versus fixation) to a large, low contrast, pseudo-randomly flashing bar. Both AQ groups showed similar differential visual evoked potential effects in later epochs (80–160 ms) at high contrast. Thus, the magnocellular theory of saccadic suppression appears untenable as a general description for the typically developing population. Our results also suggest that the bias towards local perceptual style reported in autism may be due to selective suppression of low spatial frequency information accompanying every saccadic eye movement.
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Bruno, Aurelio, Simona Maria Brambati, Daniela Perani, and Maria Concetta Morrone. "Development of Saccadic Suppression in Children." Journal of Neurophysiology 96, no. 3 (September 2006): 1011–17. http://dx.doi.org/10.1152/jn.01179.2005.
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We measured saccadic suppression in adolescent children and young adults using spatially curtailed low spatial frequency stimuli. For both groups, sensitivity for color-modulated stimuli was unchanged during saccades. Sensitivity for luminance-modulated stimuli was greatly reduced during saccades in both groups but far more for adolescents than for young adults. Adults' suppression was on average a factor of about 3, whereas that for the adolescent group was closer to a factor of 10. The specificity of the suppression to luminance-modulated stimuli excludes generic explanations such as task difficulty and attention. We suggest that the enhanced suppression in adolescents results from the immaturity of the ocular-motor system at that age.
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Munoz, D. P., and R. H. Wurtz. "Role of the rostral superior colliculus in active visual fixation and execution of express saccades." Journal of Neurophysiology 67, no. 4 (April 1, 1992): 1000–1002. http://dx.doi.org/10.1152/jn.1992.67.4.1000.
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1. In the rostral pole of the monkey superior colliculus (SC) a subset of neurons (fixation cells) discharge tonically when a monkey actively fixates a target spot and pause during the execution of saccadic eye movements. 2. To test whether these fixation cells are necessary for the control of visual fixation and saccade suppression, we artificially inhibited them with a local injection of muscimol, an agonist of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). After injection of muscimol into the rostral pole of one SC, the monkey was less able to suppress the initiation of saccades. Many unwanted visually guided saccades were initiated less than 100 ms after onset of a peripheral visual stimulus and therefore fell into the range of express saccades. 3. We propose that fixation cells in the rostral SC form part of a fixation system that facilitates active visual fixation and suppresses the initiation of unwanted saccadic eye movements. Express saccades can only occur when activity in this fixation system is reduced.
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Sendhilnathan, Naveen, Debaleena Basu, and Aditya Murthy. "Simultaneous analysis of the LFP and spiking activity reveals essential components of a visuomotor transformation in the frontal eye field." Proceedings of the National Academy of Sciences 114, no. 24 (June 1, 2017): 6370–75. http://dx.doi.org/10.1073/pnas.1703809114.
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The frontal eye field (FEF) is a key brain region to study visuomotor transformations because the primary input to FEF is visual in nature, whereas its output reflects the planning of behaviorally relevant saccadic eye movements. In this study, we used a memory-guided saccade task to temporally dissociate the visual epoch from the saccadic epoch through a delay epoch, and used the local field potential (LFP) along with simultaneously recorded spike data to study the visuomotor transformation process. We showed that visual latency of the LFP preceded spiking activity in the visual epoch, whereas spiking activity preceded LFP activity in the saccade epoch. We also found a spatially tuned elevation in gamma band activity (30–70 Hz), but not in the corresponding spiking activity, only during the delay epoch, whose activity predicted saccade reaction times and the cells’ saccade tuning. In contrast, beta band activity (13–30 Hz) showed a nonspatially selective suppression during the saccade epoch. Taken together, these results suggest that motor plans leading to saccades may be generated internally within the FEF from local activity represented by gamma activity.
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Klingenhoefer, S., and F. Bremmer. "Saccadic suppression of displacement in face of saccade adaptation." Vision Research 51, no. 8 (April 2011): 881–89. http://dx.doi.org/10.1016/j.visres.2010.12.006.
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FISCHER, W. H., M. SCHMIDT, and K. P. HOFFMANN. "Saccade-induced activity of dorsal lateral geniculate nucleus X- and Y-cells during pharmacological inactivation of the cat pretectum." Visual Neuroscience 15, no. 2 (February 1998): 197–210. http://dx.doi.org/10.1017/s0952523898151106.
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The influence of neurons projecting from the pretectal nuclear complex to the ipsilateral dorsal lateral geniculate nucleus (LGNd) was investigated in awake cats. Responses from relay cells in the A-laminae of the LGNd were extracellularly recorded and analyzed during saccadic eye movements and visual stimulation in association with reversible inactivation of the ipsilateral pretectum with the GABA agonist, muscimol. Pretectal inactivation (PTI) resulted in spontaneous nystagmic eye movements in the dark with slow phases directed away from the injected side. In the control situation, all Y-cells and about two thirds of X-cells were excited during saccades or saccade-like visual stimulation but one third of X-cells were inhibited. During PTI all recorded X-cells were inhibited, either during saccades or saccade-like visual stimulation. The PTI-associated inhibition was stronger than in inhibited X-cells in control experiments only during saccades but not during stimulation with a moving pattern while the eyes were stationary. In Y-cells a reduction in the response peak width at half-height was seen during PTI, again only during saccades but not during stimulation with a moving pattern. These results indicate that during saccades the pretecto-geniculate pathway has a stronger influence on X LGNd relay cells than on Y-cells. The findings are discussed in terms of saccadic suppression and postsaccadic facilitation.
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Benedetto, Alessandro, and Paola Binda. "Dissociable saccadic suppression of pupillary and perceptual responses to light." Journal of Neurophysiology 115, no. 3 (March 1, 2016): 1243–51. http://dx.doi.org/10.1152/jn.00964.2015.
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We measured pupillary constrictions in response to full-screen flashes of variable luminance, occurring either at the onset of a saccadic eye movement or well before/after it. A large fraction of perisaccadic flashes were undetectable to the subjects, consistent with saccadic suppression of visual sensitivity. Likewise, pupillary responses to perisaccadic flashes were strongly suppressed. However, the two phenomena appear to be dissociable. Across subjects and luminance levels of the flash stimulus, there were cases in which conscious perception of the flash was completely depleted yet the pupillary response was clearly present, as well as cases in which the opposite occurred. On one hand, the fact that pupillary light responses are subject to saccadic suppression reinforces evidence that this is not a simple reflex but depends on the integration of retinal illumination with complex “extraretinal” cues. On the other hand, the relative independence of pupillary and perceptual responses suggests that suppression acts separately on these systems—consistent with the idea of multiple visual pathways that are differentially affected by saccades.
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Tabak, S., J. B. Smeets, and H. Collewijn. "Modulation of the human vestibuloocular reflex during saccades: probing by high-frequency oscillation and torque pulses of the head." Journal of Neurophysiology 76, no. 5 (November 1, 1996): 3249–63. http://dx.doi.org/10.1152/jn.1996.76.5.3249.
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1. We probed the gain and phase of the vestibuloocular reflex (VOR) during the execution of voluntary gaze saccades, with continuous oscillation or acceleration pulses, applied through a torque helmet. 2. Small-amplitude (< 1 degree), high-frequency (10-14 Hz) head oscillations in the horizontal or vertical plane were superimposed on ongoing horizontal gaze saccades (40-100 degrees). Torque pulses to the head (“with” or “against” gaze) were superimposed on 40 degrees horizontal saccades. Eye and head movements were precisely measured with sensor coils in magnetic fields. 3. Techniques were developed to separate the oscillatory (horizontal or vertical) component from the gaze shift and obtain VOR gain and phase with Fourier techniques from the relation between eye-in-head and head oscillations. These involved either subtraction of exactly matching saccades with and without oscillation (drawback: low yield) or time shifting of successive trials to synchronize the oscillations (drawback: slight time blurring of saccades). 4. The results of these matching and synchronization methods were essentially identical and consistent. Presaccadic gain values of the horizontal VOR (typically about unity) were reduced by, on average, approximately 20 and 50% during horizontal saccades of 40 and 100 degrees, respectively. These percentages may be truncated because of methodological limitations, but even after taking these into account (on the basis of simulation experiments with 2 different, theoretical profiles of suppression) our results do not support a complete saccadic VOR suppression for any substantial fraction of saccadic duration. Qualitatively similar changes were found when the vertical VOR was probed during 100 degrees horizontal saccades. 5. Concomitantly with the reductions in gain, VOR phase was advanced by approximately 20 degrees during the saccade. 6. In the wake of gaze saccades, VOR gain was consistently elevated (to approximately 1.0) above the presaccadic level (approximately 0.9). We submit that this mechanism ensures stable fixation of the newly acquired target at a time when the head is still moving substantially. 7. Although the responses to head torque pulses showed idiosyncratic asymmetries, analysis of the differences in eye and head movements for pulses with and against consistently showed a sharp fall of VOR gain at saccadic onset, following an approximately exponential course with a time constant of approximately 50 ms. This decay may be assumed to reflect VOR gain for a period of approximately 50 ms, after which secondary gaze control mechanisms become dominant. 8. The time course of the gain decay and phase shift of the VOR suggest that suppression of the “integrative (position) loop” of the VOR circuit was more complete than suppression of the direct, “velocity” pathway.
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Penney, Trevor B., Xiaoqin Cheng, Yan Ling Leow, Audrey Wei Ying Bay, Esther Wu, Sophie K. Herbst, and Shih Cheng Yen. "Saccades and Subjective Time in Seconds Range Duration Reproduction." Timing & Time Perception 4, no. 2 (June 10, 2016): 187–206. http://dx.doi.org/10.1163/22134468-00002066.
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A transient suppression of visual perception during saccades ensures perceptual stability. In two experiments, we examined whether saccades affect time perception of visual and auditory stimuli in the seconds range. Specifically, participants completed a duration reproduction task in which they memorized the duration of a 6 s timing signal during the training phase and later reproduced that duration during the test phase. Four experimental conditions differed in saccade requirements and the presence or absence of a secondary discrimination task during the test phase. For both visual and auditory timing signals, participants reproduced longer durations when the secondary discrimination task required saccades to be made (i.e., overt attention shift) during reproduction as compared to when the discrimination task merely required fixation at screen center. Moreover, greater total saccade duration in a trial resulted in greater time distortion. However, in the visual modality, requiring participants to covertly shift attention (i.e., no saccade) to complete the discrimination task increased reproduced duration as much as making a saccade, whereas in the auditory modality making a saccade increased reproduced duration more than making a covert attention shift. In addition, we examined microsaccades in the conditions that did not require full saccades for both the visual and auditory experiments. Greater total microsaccade duration in a trial resulted in greater time distortion in both modalities. Taken together, the experiments suggest that saccades and microsaccades affect seconds range visual and auditory interval timing via attention and saccadic suppression mechanisms.
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Optican, L. M., and F. A. Miles. "Visually induced adaptive changes in primate saccadic oculomotor control signals." Journal of Neurophysiology 54, no. 4 (October 1, 1985): 940–58. http://dx.doi.org/10.1152/jn.1985.54.4.940.
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Saccades are the rapid eye movements used to change visual fixation. Normal saccades end abruptly with very little postsaccadic ocular drift, but acute ocular motor deficits can cause the eyes to drift appreciably after a saccade. Previous studies in both patients and monkeys with peripheral ocular motor deficits have demonstrated that the brain can suppress such postsaccadic drifts. Ocular drift might be suppressed in response to visual and/or proprioceptive feedback of position and/or velocity errors. This study attempts to characterize the adaptive mechanism for suppression of postsaccadic drift. The responses of seven rhesus monkeys were studied to postsaccadic retinal slip induced by horizontal exponential movements of a full-field stimulus. After several hours of saccade-related retinal image slip, the eye movements of the monkeys developed a zero-latency, compensatory postsaccadic ocular drift. This ocular drift was still evident in the dark, although smaller (typically 15% of the amplitude of the antecedent saccade, up to a maximum drift of 8 degrees). Retinal slip alone, without a net displacement of the image, was sufficient to elicit these adaptive changes, and compensation for leftward and rightward saccades was independent. It took several days to complete adaptation, but recovery (in the light) was much quicker. The decay of this adaptation in darkness was very slow; after 3 days the ocular drift was reduced by less than 50%. The time constants of single exponential curve fits to adaptation time courses of data from five animals were 35 h for acquisition, 4 h for recovery, and at least 40 h for decay in darkness. Descriptions of the central innervation for a saccade are usually simplified to only two components: a pulse and a step. It has been hypothesized that suppression of pathological postsaccadic drift is achieved by adjusting the ratio of the pulse to the step of innervation (19, 26). However, we show that the time constant of the ocular drift is influenced by the time constant of the adapting stimulus, which cannot be explained by the simple pulse-step model of saccadic innervation. A more realistic representation of the saccadic innervation has three components: a pulse, an exponential slide, and a step. Normal saccades were accurately simulated by a fourth-order, linear model of the ocular motor plant driven by such a pulse-slide-step combination. Saccades made after prolonged exposure to optically induced retinal image slip could also be simulated by properly adjusting the slide and step components.(ABSTRACT TRUNCATED AT 400 WORDS)
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Thilo, Kai V., Loredana Santoro, Vincent Walsh, and Colin Blakemore. "The site of saccadic suppression." Nature Neuroscience 7, no. 1 (December 21, 2003): 13–14. http://dx.doi.org/10.1038/nn1171.
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Wexler, M., and T. Collins. "Orthogonal steps relieve saccadic suppression." Journal of Vision 14, no. 2 (February 17, 2014): 13. http://dx.doi.org/10.1167/14.2.13.
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Thiele, A. "Neural Mechanisms of Saccadic Suppression." Science 295, no. 5564 (March 29, 2002): 2460–62. http://dx.doi.org/10.1126/science.1068788.
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Greenhouse, Daniel S., and Theodore E. Cohn. "Saccadic suppression and stimulus uncertainty." Journal of the Optical Society of America A 8, no. 3 (March 1, 1991): 587. http://dx.doi.org/10.1364/josaa.8.000587.
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Bremmer, F., M. Kubischik, K. P. Hoffmann, and B. Krekelberg. "Neural Dynamics of Saccadic Suppression." Journal of Neuroscience 29, no. 40 (October 7, 2009): 12374–83. http://dx.doi.org/10.1523/jneurosci.2908-09.2009.
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Braun, Doris, Alexander C. Schütz, Jutta Billino, and Karl R. Gegenfurtner. "Age effects on saccadic suppression." Journal of Vision 19, no. 10 (September 6, 2019): 146a. http://dx.doi.org/10.1167/19.10.146a.
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Diamond, Mark R., John Ross, and M. C. Morrone. "Extraretinal Control of Saccadic Suppression." Journal of Neuroscience 20, no. 9 (May 1, 2000): 3449–55. http://dx.doi.org/10.1523/jneurosci.20-09-03449.2000.
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Chahine, G., and B. Krekelberg. "Cortical contributions to saccadic suppression." Journal of Vision 8, no. 6 (April 8, 2010): 930. http://dx.doi.org/10.1167/8.6.930.
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Chahine, George, and Bart Krekelberg. "Cortical Contributions to Saccadic Suppression." PLoS ONE 4, no. 9 (September 4, 2009): e6900. http://dx.doi.org/10.1371/journal.pone.0006900.
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Irwin, D. E., and L. E. Thomas. "Cognitive saccadic suppression: number comparison is suppressed during leftward saccades." Journal of Vision 5, no. 8 (September 1, 2005): 104. http://dx.doi.org/10.1167/5.8.104.
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Coe, Brian C., and Douglas P. Munoz. "Mechanisms of saccade suppression revealed in the anti-saccade task." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1718 (February 27, 2017): 20160192. http://dx.doi.org/10.1098/rstb.2016.0192.
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The anti-saccade task has emerged as an important tool for investigating the complex nature of voluntary behaviour. In this task, participants are instructed to suppress the natural response to look at a peripheral visual stimulus and look in the opposite direction instead. Analysis of saccadic reaction times (SRT: the time from stimulus appearance to the first saccade) and the frequency of direction errors (i.e. looking toward the stimulus) provide insight into saccade suppression mechanisms in the brain. Some direction errors are reflexive responses with very short SRTs (express latency saccades), while other direction errors are driven by automated responses and have longer SRTs. These different types of errors reveal that the anti-saccade task requires different forms of suppression, and neurophysiological experiments in macaques have revealed several potential mechanisms. At the start of an anti-saccade trial, pre-emptive top-down inhibition of saccade generating neurons in the frontal eye fields and superior colliculus must be present before the stimulus appears to prevent express latency direction errors. After the stimulus appears, voluntary anti-saccade commands must compete with, and override, automated visually initiated saccade commands to prevent longer latency direction errors. The frequencies of these types of direction errors, as well as SRTs, change throughout the lifespan and reveal time courses for development, maturation, and ageing. Additionally, patients diagnosed with a variety of neurological and/or psychiatric disorders affecting the frontal lobes and/or basal ganglia produce markedly different SRT distributions and types of direction errors, which highlight specific deficits in saccade suppression and inhibitory control. The anti-saccade task therefore provides valuable insight into the neural mechanisms of saccade suppression and is a valuable tool in a clinical setting. This article is part of the themed issue ‘Movement suppression: brain mechanisms for stopping and stillness’.
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Burr, David C., Michael J. Morgan, and M. Concetta Morrone. "Saccadic suppression precedes visual motion analysis." Current Biology 9, no. 20 (October 1999): 1207–9. http://dx.doi.org/10.1016/s0960-9822(00)80028-7.
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Knoll, J., J. Beyer, and F. Bremmer. "Spatio-temporal topography of saccadic suppression." Journal of Vision 8, no. 6 (April 8, 2010): 927. http://dx.doi.org/10.1167/8.6.927.
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Allison, Robert Scott, Jens Schumacher, Shabnam Sadr, and Rainer Herpers. "Apparent motion during saccadic suppression periods." Experimental Brain Research 202, no. 1 (December 19, 2009): 155–69. http://dx.doi.org/10.1007/s00221-009-2120-y.
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