Journal articles on the topic 'Saccadic eye movements'

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1

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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2

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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Havermann, Katharina, Eckart Zimmermann, and Markus Lappe. "Eye position effects in saccadic adaptation." Journal of Neurophysiology 106, no. 5 (November 2011): 2536–45. http://dx.doi.org/10.1152/jn.00023.2011.

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Saccades are used by the visual system to explore visual space with the high accuracy of the fovea. The visual error after the saccade is used to adapt the control of subsequent eye movements of the same amplitude and direction in order to keep saccades accurate. Saccadic adaptation is thus specific to saccade amplitude and direction. In the present study we show that saccadic adaptation is also specific to the initial position of the eye in the orbit. This is useful, because saccades are normally accompanied by head movements and the control of combined head and eye movements depends on eye position. Many parts of the saccadic system contain eye position information. Using the intrasaccadic target step paradigm, we adaptively reduced the amplitude of reactive saccades to a suddenly appearing target at a selective position of the eyes in the orbitae and tested the resulting amplitude changes for the same saccade vector at other starting positions. For central adaptation positions the saccade amplitude reduction transferred completely to eccentric starting positions. However, for adaptation at eccentric starting positions, there was a reduced transfer to saccades from central starting positions or from eccentric starting positions in the opposite hemifield. Thus eye position information modifies the transfer of saccadic amplitude changes in the adaptation of reactive saccades. A gain field mechanism may explain the eye position dependence found.
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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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5

Maxwell, J. S., and W. M. King. "Dynamics and efficacy of saccade-facilitated vergence eye movements in monkeys." Journal of Neurophysiology 68, no. 4 (October 1, 1992): 1248–60. http://dx.doi.org/10.1152/jn.1992.68.4.1248.

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1. Four macaque monkeys were trained to fixate visual targets. Eye movements were recorded binocularly using the search coil technique. Saccades, vergence movements, and combinations of the two were elicited by training the monkeys to alternate the gaze between real visual targets that differed in viewing distance and eccentricity with respect to the monkeys' heads. 2. When they shifted the gaze between targets that were at different viewing distances, the monkeys made vergence eye movements. For targets placed along the midsagittal plane, the monkeys often made binocularly symmetric vergence movements. The peak speed of symmetric divergence movements increased linearly with vergence amplitude by 5.7 deg/s per degree of vergence. The peak speed of symmetric convergence movements increased linearly with vergence amplitude by 7.9 deg/s per degree of vergence. 3. For gaze shifts between targets placed eccentrically with respect to the midsagittal plane and at different viewing distances, the monkeys made saccades in combination with vergence eye movements. When a saccade occurred during a vergence movement, peak vergence eye speed increased abruptly and reached a peak that was proportional to the speed of the saccade. For four monkeys, peak divergence speed ranged from 242 to 315 deg/s and peak convergence speed ranged from 257 to 340 deg/s for 16-deg vergence and 20-deg saccadic eye movements. 4. For gaze shifts between far targets at the same viewing distance but different eccentricities, saccadic eye movements were transiently disjunctive even though there was no vergence requirement. Initially, the eyes diverged and then converged to restore fixation to the correct depth plane. Divergence was followed by convergence regardless of the direction of the saccade. 5. The presence of transient saccade-related disjunctive eye movements suggested that the abrupt increase in peak vergence speed during combined saccadic and vergence eye movements was produced by the linear addition of a vergence eye movement and the saccade-related transients. Consistent with this hypothesis, the rate of change in peak vergence speed during various-sized saccades between far targets (no vergence required) was similar to the rate of change in peak vergence speed during combined saccadic and vergence movements. However, the peak vergence speeds during the combined movements were higher than predicted by the linear addition hypothesis, suggesting the presence of an additional mechanism. 6. The saccade-related increase in peak vergence speed during combined saccades and vergences led to a significant decrease in the amount of time required to complete vergence movements.(ABSTRACT TRUNCATED AT 400 WORDS)
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6

Van Horn, Marion R., and Kathleen E. Cullen. "Dynamic Coding of Vertical Facilitated Vergence by Premotor Saccadic Burst Neurons." Journal of Neurophysiology 100, no. 4 (October 2008): 1967–82. http://dx.doi.org/10.1152/jn.90580.2008.

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To redirect our gaze in three-dimensional space we frequently combine saccades and vergence. These eye movements, known as disconjugate saccades, are characterized by eyes rotating by different amounts, with markedly different dynamics, and occur whenever gaze is shifted between near and far objects. How the brain ensures the precise control of binocular positioning remains controversial. It has been proposed that the traditionally assumed “conjugate” saccadic premotor pathway does not encode conjugate commands but rather encodes monocular commands for the right or left eye during saccades. Here, we directly test this proposal by recording from the premotor neurons of the horizontal saccade generator during a dissociation task that required a vergence but no horizontal conjugate saccadic command. Specifically, saccadic burst neurons (SBNs) in the paramedian pontine reticular formation were recorded while rhesus monkeys made vertical saccades made between near and far targets. During this task, we first show that peak vergence velocities were enhanced to saccade-like speeds (e.g., >150 vs. <100°/s during saccade-free movements for comparable changes in vergence angle). We then quantified the discharge dynamics of SBNs during these movements and found that the majority of the neurons preferentially encode the velocity of the ipsilateral eye. Notably, a given neuron typically encoded the movement of the same eye during horizontal saccades that were made in depth. Taken together, our findings demonstrate that the brain stem saccadic burst generator encodes integrated conjugate and vergence commands, thus providing strong evidence for the proposal that the classic saccadic premotor pathway controls gaze in three-dimensional space.
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7

Goossens, H. H. L. M., and A. J. Van Opstal. "Blink-Perturbed Saccades in Monkey. I. Behavioral Analysis." Journal of Neurophysiology 83, no. 6 (June 1, 2000): 3411–29. http://dx.doi.org/10.1152/jn.2000.83.6.3411.

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Saccadic eye movements are thought to be influenced by blinking through premotor interactions, but it is still unclear how. The present paper describes the properties of blink-associated eye movements and quantifies the effect of reflex blinks on the latencies, metrics, and kinematics of saccades in the monkey. In particular, it is examined to what extent the saccadic system accounts for blink-related perturbations of the saccade trajectory. Trigeminal reflex blinks were elicited near the onset of visually evoked saccades by means of air puffs directed on the eye. Reflex blinks were also evoked during a straight-ahead fixation task. Eye and eyelid movements were measured with the magnetic-induction technique. The data show that saccade latencies were reduced substantially when reflex blinks were evoked prior to the impending visual saccades as if these saccades were triggered by the blink. The evoked blinks also caused profound spatial-temporal perturbations of the saccades. Deflections of the saccade trajectory, usually upward, extended up to ∼15°. Saccade peak velocities were reduced, and a two- to threefold increase in saccade duration was typically observed. In general, these perturbations were largely compensated in saccade mid-flight, despite the absence of visual feedback, yielding near-normal endpoint accuracies. Further analysis revealed that blink-perturbed saccades could not be described as a linear superposition of a pure blink-associated eye movement and an unperturbed saccade. When evoked during straight-ahead fixation, blinks were accompanied by initially upward and slightly abducting eye rotations of ∼2–15°. Back and forth wiggles of the eye were frequently seen; but in many cases the return movement was incomplete. Rather than drifting back to its starting position, the eye then maintained its eccentric orbital position until a downward corrective saccade toward the fixation spot followed. Blink-associated eye movements were quite rapid, albeit slower than saccades, and the velocity-amplitude-duration characteristics of the initial excursions as well as the return movements were approximately linear. These data strongly support the idea that blinks interfere with the saccade premotor circuit, presumably upstream from the neural eye-position integrator. They also indicated that a neural mechanism, rather than passive elastic restoring forces within the oculomotor plant, underlies the compensatory behavior. The tight latency coupling between saccades and blinks is consistent with an inhibition of omnipause neurons by the blink system, suggesting that the observed changes in saccade kinematics arise elsewhere in the saccadic premotor system.
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8

Lueck, C. J., S. Tanyeri, T. J. Crawford, L. Henderson, and C. Kennard. "Saccadic Eye Movements in Parkinson's Disease: I. Delayed Saccades." Quarterly Journal of Experimental Psychology Section A 45, no. 2 (August 1992): 193–210. http://dx.doi.org/10.1080/14640749208401324.

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The saccadic eye movements of nine patients with Parkinson's disease were compared to those of nine age-matched controls in two paradigms generating volitional saccades. In both paradigms, subjects had to make delayed saccades to peripheral LED targets: a peripheral target appeared 700 msec before a buzzer sounded, the buzzer being the signal to make a saccade to the target. In the first paradigm (“centre-off”), the fixation target was extinguished simultaneously with buzzer onset. In the second (“centre-remain”) it was not extinguished until 1000 msec later. The results showed that for outward saccades in both paradigms, there was no difference between Parkinsonian patients and controls, but saccadic latencies were significantly shorter in the “centre-remain” paradigm. The initial outward saccades were indistinguishable from the normal, reflex saccades of the same subjects. However, saccades returning to the centre (a type of remembered target saccade) were hypometric and showed multistepping. Both effects were more pronounced in patients with Parkinson's disease. The significance of these findings in terms of current hypotheses about the nature of the Parkinsonian saccadic deficit is discussed.
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9

Blohm, Gunnar, Marcus Missal, and Philippe Lefèvre. "Interaction Between Smooth Anticipation and Saccades During Ocular Orientation in Darkness." Journal of Neurophysiology 89, no. 3 (March 1, 2003): 1423–33. http://dx.doi.org/10.1152/jn.00675.2002.

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A saccade triggered during sustained smooth pursuit is programmed using retinal information about the relative position and velocity of the target with respect to the eye. Thus the smooth pursuit and saccadic systems are coordinated by using common retinal inputs. Yet, in the absence of retinal information about the relative motion of the eye with respect to the target, the question arises whether the smooth and saccadic systems are still able to be coordinated possibly by using extraretinal information to account for the saccadic and smooth eye movements. To address this question, we flashed a target during smooth anticipatory eye movements in darkness, and the subjects were asked to orient their visual axis to the remembered location of the flash. We observed multiple orientation saccades (typically 2–3) toward the memorized location of the flash. The first orienting saccade was programmed using only the position error at the moment of the flash, and the smooth eye movement was ignored. However, subsequent saccades executed in darkness compensated gradually for the smooth eye displacement (mean compensation ≅ 70%). This behavior revealed a 400-ms delay in the time course of orientation for the compensation of the ongoing smooth eye displacement. We conclude that extraretinal information about the smooth motor command is available to the saccadic system in the absence of visual input. There is a 400-ms delay for smooth movement integration, saccade programming and execution.
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10

King, W. M., S. G. Lisberger, and A. F. Fuchs. "Oblique saccadic eye movements of primates." Journal of Neurophysiology 56, no. 3 (September 1, 1986): 769–84. http://dx.doi.org/10.1152/jn.1986.56.3.769.

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The objective of these experiments was to determine whether the trajectories of the horizontal and vertical components of oblique saccades in primates were coupled. Human and monkey eye movements were recorded during a visual tracking task that jumped a small visible target spot to different locations on a tangent screen. For oblique saccades larger than ca. 3 deg, there was coupling between the horizontal and vertical components so that the duration of the smaller component was longer ("stretched") than would have been expected from its amplitude-duration relationship. The duration of a stretched component of an oblique saccade was linearly related to the vector amplitude of the eye movement but not to the amplitude of the stretched component. Stretched components of oblique saccades had lower peak and average velocities than would have occurred with pure horizontal or vertical saccades of the same size. Decreased component velocity was not caused by low-velocity eye movement components inserted at the beginning or end of the saccade, but was a function of the saccade's direction and component amplitude. For any saccade, there was a linear relationship between peak and average component velocity. We compared the discharge of monkey abducens neurons with the characteristics of the on-direction horizontal components of oblique saccades. The burst duration of an abducens neuron was lengthened when the horizontal component of an oblique saccade was stretched. Intraburst firing frequency was also decreased in correspondence with a decrease in horizontal component velocity. For an oblique saccade, the duration of the neuron's burst was correlated with the duration of the horizontal component and with the vector amplitude of the saccade, but was not correlated with the amplitude of the horizontal component itself. The duration of the smaller component of an oblique saccade was proportional but not always equal to the duration of the larger component. Usually, the smaller component began later and ended earlier than the larger component. These results show that the horizontal and vertical components of oblique saccades are coupled centrally so that the velocity of the smaller component is decreased and its duration is increased. For oblique saccades, larger than ca. 3 deg, amplitude-duration and amplitude-velocity relationships based on pure horizontal or vertical saccade data are not applicable. These findings are discussed in relation to three recently proposed models of coupled saccadic burst generators.
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11

Hogendoorn, Hinze. "Voluntary Saccadic Eye Movements Ride the Attentional Rhythm." Journal of Cognitive Neuroscience 28, no. 10 (October 2016): 1625–35. http://dx.doi.org/10.1162/jocn_a_00986.

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Visual perception seems continuous, but recent evidence suggests that the underlying perceptual mechanisms are in fact periodic—particularly visual attention. Because visual attention is closely linked to the preparation of saccadic eye movements, the question arises how periodic attentional processes interact with the preparation and execution of voluntary saccades. In two experiments, human observers made voluntary saccades between two placeholders, monitoring each one for the presentation of a threshold-level target. Detection performance was evaluated as a function of latency with respect to saccade landing. The time course of detection performance revealed oscillations at around 4 Hz both before the saccade at the saccade origin and after the saccade at the saccade destination. Furthermore, oscillations before and after the saccade were in phase, meaning that the saccade did not disrupt or reset the ongoing attentional rhythm. Instead, it seems that voluntary saccades are executed as part of an ongoing attentional rhythm, with the eyes in flight during the troughs of the attentional wave. This finding for the first time demonstrates that periodic attentional mechanisms affect not only perception but also overt motor behavior.
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Soetedjo, Robijanto, Chris R. S. Kaneko, and Albert F. Fuchs. "Evidence That the Superior Colliculus Participates in the Feedback Control of Saccadic Eye Movements." Journal of Neurophysiology 87, no. 2 (February 1, 2002): 679–95. http://dx.doi.org/10.1152/jn.00886.2000.

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There is general agreement that saccades are guided to their targets by means of a motor error signal, which is produced by a local feedback circuit that calculates the difference between desired saccadic amplitude and an internal copy of actual saccadic amplitude. Although the superior colliculus (SC) is thought to provide the desired saccadic amplitude signal, it is unclear whether the SC resides in the feedback loop. To test this possibility, we injected muscimol into the brain stem region containing omnipause neurons (OPNs) to slow saccades and then determined whether the firing of neurons at different sites in the SC was altered. In 14 experiments, we produced saccadic slowing while simultaneously recording the activity of a single SC neuron. Eleven of the 14 neurons were saccade-related burst neurons (SRBNs), which discharged their most vigorous burst for saccades with an optimal amplitude and direction (optimal vector). The optimal directions for the 11 SRBNs ranged from nearly horizontal to nearly vertical, with optimal amplitudes between 4 and 17°. Although muscimol injections into the OPN region produced little change in the optimal vector, they did increase mean saccade duration by 25 to 192.8% and decrease mean saccade peak velocity by 20.5 to 69.8%. For optimal vector saccades, both the acceleration and deceleration phases increased in duration. However, during 10 of 14 experiments, the duration of deceleration increased as fast as or faster than that of acceleration as saccade duration increased, indicating that most of the increase in duration occurred during the deceleration phase. SRBNs in the SC changed their burst duration and firing rate concomitantly with changes in saccadic duration and velocity, respectively. All SRBNs showed a robust increase in burst duration as saccadic duration increased. Five of 11 SRBNs also exhibited a decrease in burst peak firing rate as saccadic velocity decreased. On average across the neurons, the number of spikes in the burst was constant. There was no consistent change in the discharge of the three SC neurons that did not exhibit bursts with saccades. Our data show that the SC receives feedback from downstream saccade-related neurons about the ongoing saccades. However, the changes in SC firing produced in our study do not suggest that the feedback is involved with producing motor error. Instead, the feedback seems to be involved with regulating the duration of the discharge of SRBNs so that the desired saccadic amplitude signal remains present throughout the saccade.
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McSorley, Eugene, Iain D. Gilchrist, and Rachel McCloy. "The role of fixation disengagement in the parallel programming of sequences of saccades." Experimental Brain Research 237, no. 11 (September 17, 2019): 3033–45. http://dx.doi.org/10.1007/s00221-019-05641-9.

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Abstract One of the core mechanisms involved in the control of saccade responses to selected target stimuli is the disengagement from the current fixation location, so that the next saccade can be executed. To carry out everyday visual tasks, we make multiple eye movements that can be programmed in parallel. However, the role of disengagement in the parallel programming of saccades has not been examined. It is well established that the need for disengagement slows down saccadic response time. This may be important in allowing the system to program accurate eye movements and have a role to play in the control of multiple eye movements but as yet this remains untested. Here, we report two experiments that seek to examine whether fixation disengagement reduces saccade latencies when the task completion demands multiple saccade responses. A saccade contingent paradigm was employed and participants were asked to execute saccadic eye movements to a series of seven targets while manipulating when these targets were shown. This both promotes fixation disengagement and controls the extent that parallel programming can occur. We found that trial duration decreased as more targets were made available prior to fixation: this was a result both of a reduction in the number of saccades being executed and in their saccade latencies. This supports the view that even when fixation disengagement is not required, parallel programming of multiple sequential saccadic eye movements is still present. By comparison with previous published data, we demonstrate a substantial speeded of response times in these condition (“a gap effect”) and that parallel programming is attenuated in these conditions.
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Vikesdal, Gro Horgen, Helle Kristine Falkenberg, Mark Mon-Williams, Patricia Riddell, and Trine Langaas. "Normal saccades but decreased fixation stability in a population of children with dyslexia." Scandinavian Journal of Optometry and Visual Science 14, no. 2 (December 31, 2021): 1–7. http://dx.doi.org/10.5384/sjovs.v14i2.137.

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Developmental dyslexia affects around 5-15% of the population and has a heterogeneous aetiology. Optometric disorders are more prevalent in dyslexic populations but the relationship be- tween eye movement control and dyslexia is not well established. In this study, we investigated whether children with dyslexia show saccadic or fixation deficits and whether these deficits are related to deficits in visual acuity and/or accommodation. Thirty-four children with and without dyslexia were recruited for the project. All participants had an optometric examination and performed a saccade and fixation experiment. We used two eye movement paradigms: the step and the gap task. Eye movements were recorded by an infrared eye-tracker and saccade and fixation parameters were analysed separately. Saccadic latencies, premature saccades, and directional errors were similar between children with dyslexia and typically developing children. In contrast, fixations were significantly less stable in the dyslexic group. Neither saccades nor fixations were associated with deficits in accommodation or visual acuity. Children with dyslexia showed no difficulties in saccadic performance, but their fixation stability was reduced compared to the control group. The reduced fixation stability can be explained by general deficits in the cognitive processes that underpin eye movement control, that have also been found in other neuro-developmental disorders.
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Blohm, Gunnar, Marcus Missal, and Philippe Lefèvre. "Processing of Retinal and Extraretinal Signals for Memory-Guided Saccades During Smooth Pursuit." Journal of Neurophysiology 93, no. 3 (March 2005): 1510–22. http://dx.doi.org/10.1152/jn.00543.2004.

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It is an essential feature for the visual system to keep track of self-motion to maintain space constancy. Therefore the saccadic system uses extraretinal information about previous saccades to update the internal representation of memorized targets, an ability that has been identified in behavioral and electrophysiological studies. However, a smooth eye movement induced in the latency period of a memory-guided saccade yielded contradictory results. Indeed some studies described spatially accurate saccades, whereas others reported retinal coding of saccades. Today, it is still unclear how the saccadic system keeps track of smooth eye movements in the absence of vision. Here, we developed an original two-dimensional behavioral paradigm to further investigate how smooth eye displacements could be compensated to ensure space constancy. Human subjects were required to pursue a moving target and to orient their eyes toward the memorized position of a briefly presented second target (flash) once it appeared. The analysis of the first orientation saccade revealed a bimodal latency distribution related to two different saccade programming strategies. Short-latency (<175 ms) saccades were coded using the only available retinal information, i.e., position error. In addition to position error, longer-latency (>175 ms) saccades used extraretinal information about the smooth eye displacement during the latency period to program spatially more accurate saccades. Sensory parameters at the moment of the flash (retinal position error and eye velocity) influenced the choice between both strategies. We hypothesize that this tradeoff between speed and accuracy of the saccadic response reveals the presence of two coupled neural pathways for saccadic programming. A fast striatal-collicular pathway might only use retinal information about the flash location to program the first saccade. The slower pathway could involve the posterior parietal cortex to update the internal representation of the flash once extraretinal smooth eye displacement information becomes available to the system.
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Aizawa, Hiroshi, and Robert H. Wurtz. "Reversible Inactivation of Monkey Superior Colliculus. I. Curvature of Saccadic Trajectory." Journal of Neurophysiology 79, no. 4 (April 1, 1998): 2082–96. http://dx.doi.org/10.1152/jn.1998.79.4.2082.

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Aizawa, Hiroshi and Robert H. Wurtz. Reversible inactivation of monkey superior colliculus. I. Curvature of saccadic trajectory. J. Neurophysiol. 79: 2082–2096, 1998. The neurons in the intermediate layers of the monkey superior colliculus (SC) that discharge before saccadic eye movements can be divided into at least two types, burst and buildup neurons, and the differences in their characteristics are compatible with different functional contributions of the two cell types. It has been suggested that a spread of activity across the population of the buildup neurons during saccade generation may contribute to the control of saccadic eye movements. The influence of any such spread should be on both the horizontal and vertical components of the saccade because the map of the movement fields on the SC is a two-dimensional one; it should affect the trajectory of saccade. The present experiments used muscimol injections to inactivate areas within the SC to determine the functional contribution of such a spread of activity on the trajectory of the saccades. The analysis concentrated on saccades made to areas of the visual field that should be affected primarily by alteration of buildup neuron activity. Muscimol injections produced saccades with altered trajectories; they became consistently curved after the injection, and successive saccades to the same targets had similar curvatures. The curved saccades showed changes in their direction and speed at the very beginning of the saccade, and for those saccades that reached the target, the direction of the saccade was altered near the end to compensate for the initially incorrect direction. Postinjection saccades had lower peak speeds, longer durations, and longer latencies for initiation. The changes in saccadic trajectories resulting from muscimol injections, along with the previous observations on changes in speed of saccades with such injections, indicate that the SC is involved in influencing the eye position during the saccade as well as at the end of the saccade. The changes in trajectory when injections were made more rostral in the SC than the most active burst neurons also are consistent with a contribution of the buildup neurons to the control of the eye trajectory. The results do not, however, support the hypothesis that the buildup neurons in the SC act as a spatial integrator.
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Neggers, S. F. W., and H. Bekkering. "Ocular Gaze is Anchored to the Target of an Ongoing Pointing Movement." Journal of Neurophysiology 83, no. 2 (February 1, 2000): 639–51. http://dx.doi.org/10.1152/jn.2000.83.2.639.

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It is well known that, typically, saccadic eye movements precede goal-directed hand movements to a visual target stimulus. Also pointing in general is more accurate when the pointing target is gazed at. In this study, it is hypothesized that saccades are not only preceding pointing but that gaze also is stabilized during pointing in humans. Subjects, whose eye and pointing movements were recorded, had to make a hand movement and a saccade to a first target. At arm movement peak velocity, when the eyes are usually already fixating the first target, a new target appeared, and subjects had to make a saccade toward it ( dynamical trial type). In the statical trial type, a new target was offered when pointing was just completed. In a control experiment, a sequence of two saccades had to be made, with two different interstimulus intervals (ISI), comparable with the ISIs found in the first experiment for dynamic and static trial types. In a third experiment, ocular fixation position and pointing target were dissociated, subjects pointed at not fixated targets. The results showed that latencies of saccades toward the second target were on average 155 ms longer in the dynamic trial types, compared with the static trial types. Saccades evoked during pointing appeared to be delayed with approximately the remaining deceleration time of the pointing movement, resulting in “normal” residual saccadic reaction times (RTs), measured from pointing movement offset to saccade movement onset. In the control experiment, the latency of the second saccade was on average only 29 ms larger when the two targets appeared with a short ISI compared with trials with long ISIs. Therefore the saccadic refractory period cannot be responsible for the substantially bigger delays that were found in the first experiment. The observed saccadic delay during pointing is modulated by the distance between ocular fixation position and pointing target. The largest delays were found when the targets coincided, the smallest delays when they were dissociated. In sum, our results provide evidence for an active saccadic inhibition process, presumably to keep steady ocular fixation at a pointing target and its surroundings. Possible neurophysiological substrates that might underlie the reported phenomena are discussed.
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18

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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19

Goossens, H. H. L. M., and A. J. Van Opstal. "Local Feedback Signals Are Not Distorted By Prior Eye Movements: Evidence From Visually Evoked Double Saccades." Journal of Neurophysiology 78, no. 1 (July 1, 1997): 533–38. http://dx.doi.org/10.1152/jn.1997.78.1.533.

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Goossens, H.H.L.M. and A. J. Van Opstal. Local feedback signals are not distorted by prior eye movements: evidence from visually evoked double saccades. J. Neurophysiol. 78: 533–538, 1997. Recent experiments have shown that the amplitude and direction of saccades evoked by microstimulation of the monkey superior colliculus depend systematically on the amplitude and direction of preceding visually guided saccades as well as on the postsaccade stimulation interval. The data are consistent with the hypothesis that an eye displacement integrator in the local feedback loop of the saccadic burst generator is gradually reset with a time constant of ∼45 ms. If this is true, similar effects should occur during naturally evoked saccade sequences, causing systematic interval-dependent errors. To test this prediction in humans, saccades toward visual single- and double-step stimuli were elicited, and the properties of the second saccades were investigated as a function of the intersaccadic interval (ISI). In 15–20% of the saccadic responses, ISIs fell well below 100 ms. The errors of the second saccades were not systematically affected by the preceding primary saccade, irrespective of the ISI. Only a slight increase in the endpoint variability of second saccades was observed for the shortest ISIs. These results are at odds with the hypothesis that the putative eye displacement integrator has a reset time constant >10 ms. Instead, it is concluded that the signals involved in the internal feedback control of the saccadic burst generator reflect eye position and/or eye displacement accurately, irrespective of preceding eye movements.
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20

Bruce, C. J., M. E. Goldberg, M. C. Bushnell, and G. B. Stanton. "Primate frontal eye fields. II. Physiological and anatomical correlates of electrically evoked eye movements." Journal of Neurophysiology 54, no. 3 (September 1, 1985): 714–34. http://dx.doi.org/10.1152/jn.1985.54.3.714.

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We studied single neurons in the frontal eye fields of awake macaque monkeys and compared their activity with the saccadic eye movements elicited by microstimulation at the sites of these neurons. Saccades could be elicited from electrical stimulation in the cortical gray matter of the frontal eye fields with currents as small as 10 microA. Low thresholds for eliciting saccades were found at the sites of cells with presaccadic activity. Presaccadic neurons classified as visuomovement or movement were most associated with low (less than 50 microA) thresholds. High thresholds (greater than 100 microA) or no elicited saccades were associated with other classes of frontal eye field neurons, including neurons responding only after saccades and presaccadic neurons, classified as purely visual. Throughout the frontal eye fields, the optimal saccade for eliciting presaccadic neural activity at a given recording site predicted both the direction and amplitude of the saccades that were evoked by microstimulation at that site. In contrast, the movement fields of postsaccadic cells were usually different from the saccades evoked by stimulation at the sites of such cells. We defined the low-threshold frontal eye fields as cortex yielding saccades with stimulation currents less than or equal to 50 microA. It lies along the posterior portion of the arcuate sulcus and is largely contained in the anterior bank of that sulcus. It is smaller than Brodmann's area 8 but corresponds with the union of Walker's cytoarchitectonic areas 8A and 45. Saccade amplitude was topographically organized across the frontal eye fields. Amplitudes of elicited saccades ranged from less than 1 degree to greater than 30 degrees. Smaller saccades were evoked from the ventrolateral portion, and larger saccades were evoked from the dorsomedial portion. Within the arcuate sulcus, evoked saccades were usually larger near the lip and smaller near the fundus. Saccade direction had no global organization across the frontal eye fields; however, saccade direction changed in systematic progressions with small advances of the microelectrode, and all contralateral saccadic directions were often represented in a single electrode penetration down the bank of the arcuate sulcus. Furthermore, the direction of change in these progressions periodically reversed, allowing particular saccade directions to be multiply represented in nearby regions of cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
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21

Lee, Tsz Lok, Michael K. Yeung, Sophia L. Sze, and Agnes S. Chan. "Computerized Eye-Tracking Training Improves the Saccadic Eye Movements of Children with Attention-Deficit/Hyperactivity Disorder." Brain Sciences 10, no. 12 (December 21, 2020): 1016. http://dx.doi.org/10.3390/brainsci10121016.

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Abnormal saccadic eye movements, such as longer anti-saccade latency and lower pro-saccade accuracy, are common in children with attention-deficit/hyperactivity disorder (ADHD). The present study aimed to investigate the effectiveness of computerized eye-tracking training on improving saccadic eye movements in children with ADHD. Eighteen children with ADHD (mean age = 8.8 years, 10 males) were recruited and assigned to either the experimental (n = 9) or control group (n = 9). The experimental group underwent an accumulated 240 min of eye-tracking training within two weeks, whereas the control group engaged in web game playing for the same amount of time. Saccadic performances were assessed using the anti- and pro-saccade tasks before and after training. Compared to the baseline, only the children who underwent the eye-tracking training showed significant improvements in saccade latency and accuracy in the anti- and pro-saccade tasks, respectively. In contrast, the control group exhibited no significant changes. These preliminary findings support the use of eye-tracking training as a safe non-pharmacological intervention for improving the saccadic eye movements of children with ADHD.
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22

Li, Chiang-Shan Ray, Pietro Mazzoni, and Richard A. Andersen. "Effect of Reversible Inactivation of Macaque Lateral Intraparietal Area on Visual and Memory Saccades." Journal of Neurophysiology 81, no. 4 (April 1, 1999): 1827–38. http://dx.doi.org/10.1152/jn.1999.81.4.1827.

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Effect of reversible inactivation of macaque lateral intraparietal area on visual and memory saccades. Previous studies from our laboratory identified a parietal eye field in the primate lateral intraparietal sulcus, the lateral intraparietal area (area LIP). Here we further explore the role of area LIP in processing saccadic eye movements by observing the effects of reversible inactivation of this area. One to 2 μl of muscimol (8 mg/ml) were injected at locations where saccade-related activities were recorded for each lesion experiment. After the muscimol injection we observed in two macaque monkeys consistent effects on both the metrics and dynamics of saccadic eye movements at many injection sites. These effects usually took place within 10–30 min and disappeared after 5–6 h in most cases and certainly when tested the next day. After muscimol injection memory saccades directed toward the contralesional and upper space became hypometric, and in one monkey those to the ipsilesional space were slightly but significantly hypermetric. In some cases, the scatter of the end points of memory saccades was also increased. On the other hand, the metrics of visual saccades remained relatively intact. Latency for both visual and memory saccades toward the contralesional space was increased and in many cases displayed a higher variance after muscimol lesion. At many injection sites we also observed an increase of latency for visual and memory saccades toward the upper space. The peak velocities for memory saccades toward the contralesional space were decreased after muscimol injection. The peak velocities of visual saccades were not significantly different from those of the controls. The duration of saccadic eye movements either to the ipsilesional or contralesional space remained relatively the same for both visual and memory saccades. Overall these results demonstrated that we were able to selectively inactivate area LIP and observe effects on saccadic eye movements. Together with our previous recording studies these results futher support the view that area LIP plays a direct role in processing incoming sensory information to program saccadic eye movements. The results are consistent with our unit recording data and microstimulation studies, which suggest that area LIP represents contralateral space and also has a bias for the upper visual field.
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23

Lisi, Matteo, Joshua A. Solomon, and Michael J. Morgan. "Gain control of saccadic eye movements is probabilistic." Proceedings of the National Academy of Sciences 116, no. 32 (July 23, 2019): 16137–42. http://dx.doi.org/10.1073/pnas.1901963116.

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Saccades are rapid eye movements that orient the visual axis toward objects of interest to allow their processing by the central, high-acuity retina. Our ability to collect visual information efficiently relies on saccadic accuracy, which is limited by a combination of uncertainty in the location of the target and motor noise. It has been observed that saccades have a systematic tendency to fall short of their intended targets, and it has been suggested that this bias originates from a cost function that overly penalizes hypermetric errors. Here, we tested this hypothesis by systematically manipulating the positional uncertainty of saccadic targets. We found that increasing uncertainty produced not only a larger spread of the saccadic endpoints but also more hypometric errors and a systematic bias toward the average of target locations in a given block, revealing that prior knowledge was integrated into saccadic planning. Moreover, by examining how variability and bias covaried across conditions, we estimated the asymmetry of the cost function and found that it was related to individual differences in the additional time needed to program secondary saccades for correcting hypermetric errors, relative to hypometric ones. Taken together, these findings reveal that the saccadic system uses a probabilistic-Bayesian control strategy to compensate for uncertainty in a statistically principled way and to minimize the expected cost of saccadic errors.
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Reuther, Josephine, Ramakrishna Chakravarthi, and Amelia R. Hunt. "The eye that binds: Feature integration is not disrupted by saccadic eye movements." Attention, Perception, & Psychophysics 82, no. 2 (December 5, 2019): 533–49. http://dx.doi.org/10.3758/s13414-019-01873-7.

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AbstractFeature integration theory proposes that visual features, such as shape and color, can only be combined into a unified object when spatial attention is directed to their location in retinotopic maps. Eye movements cause dramatic changes on our retinae, and are associated with obligatory shifts in spatial attention. In two experiments, we measured the prevalence of conjunction errors (that is, reporting an object as having an attribute that belonged to another object), for brief stimulus presentation before, during, and after a saccade. Planning and executing a saccade did not itself disrupt feature integration. Motion did disrupt feature integration, leading to an increase in conjunction errors. However, retinal motion of an equal extent but caused by saccadic eye movements is spared this disruption, and showed similar rates of conjunction errors as a condition with static stimuli presented to a static eye. The results suggest that extra-retinal signals are able to compensate for the motion caused by saccadic eye movements, thereby preserving the integrity of objects across saccades and preventing their features from mixing or mis-binding.
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25

Noda, H., and T. Fujikado. "Involvement of Purkinje cells in evoking saccadic eye movements by microstimulation of the posterior cerebellar vermis of monkeys." Journal of Neurophysiology 57, no. 5 (May 1, 1987): 1247–61. http://dx.doi.org/10.1152/jn.1987.57.5.1247.

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Neural mechanisms for evoking saccadic eye movements by microstimulation of the posterior vermis were investigated in monkeys trained to fixate a visual target. The low-threshold region from which saccadic eye movements could be evoked with currents less than 10 microA was confined to lobule VII in two monkeys and it included a posterior part of lobule VI (lobule VIc) in another monkey. The region from which saccade-related neural activity was recordable coincided with the low-threshold region. This region corresponded to the vermal lobules from which eye position and saccade-related Purkinje cells were recorded. Kainic acid (kainate) injected in the white matter of lobule VII resulted in severe losses of Purkinje cells within a radius of 1-2 mm of the injection site. The lesion tended to be larger toward the peripheral cerebellar cortices, which were connected to the injection site by natural courses of the afferent and efferent fibers. After the kainate administration, the distribution of saccade-related neural activity did not differ significantly from that of the preoperative mapping, in spite of the severe losses of cortical neurons. Burst discharges of mossy fibers were recordable in the white matter near the injection site, indicating that afferent fibers were relatively unaffected by kainate. After kainate administration, the saccadic eye movements could no longer be evoked by microstimulation applied to the posterior vermis. The stimulus sites from which saccades could be evoked after kainate administration were always associated with the presence of intact Purkinje cells. In such cases, the minimum current necessary to evoke saccades depended on the percentages of intact Purkinje cells spared. In the folia with normal Purkinje cell layers, the amplitude and direction of evoked saccades and the thresholds for evoking such eye movements were almost comparable to the preoperative data. Saccadic eye movements in response to microstimulation of the posterior vermis were caused by orthodromic impulses conveyed through the axons of the Purkinje cells. Insofar as the saccades elicited from lobule VII with currents less than 10 microA are concerned, antidromic activation of the afferent fibers is not the neural mechanisms subserving the oculomotor responses.
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26

Zivotofsky, A. Z., K. G. Rottach, L. Averbuch-Heller, A. A. Kori, C. W. Thomas, L. F. Dell'Osso, and R. J. Leigh. "Saccades to remembered targets: the effects of smooth pursuit and illusory stimulus motion." Journal of Neurophysiology 76, no. 6 (December 1, 1996): 3617–32. http://dx.doi.org/10.1152/jn.1996.76.6.3617.

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1. Measurements were made in four normal human subjects of the accuracy of saccades to remembered locations of targets that were flashed on a 20 x 30 deg random dot display that was either stationary or moving horizontally and sinusoidally at +/-9 deg at 0.3 Hz. During the interval between the target flash and the memory-guided saccade, the “memory period” (1.4 s), subjects either fixated a stationary spot or pursued a spot moving vertically sinusoidally at +/-9 deg at 0.3 Hz. 2. When saccades were made toward the location of targets previously flashed on a stationary background as subjects fixated the stationary spot, median saccadic error was 0.93 deg horizontally and 1.1 deg vertically. These errors were greater than for saccades to visible targets, which had median values of 0.59 deg horizontally and 0.60 deg vertically. 3. When targets were flashed as subjects smoothly pursued a spot that moved vertically across the stationary background, median saccadic error was 1.1 deg horizontally and 1.2 deg vertically, thus being of similar accuracy to when targets were flashed during fixation. In addition, the vertical component of the memory-guided saccade was much more closely correlated with the “spatial error” than with the “retinal error” this indicated that, when programming the saccade, the brain had taken into account eye movements that occurred during the memory period. 4. When saccades were made to targets flashed during attempted fixation of a stationary spot on a horizontally moving background, a condition that produces a weak Duncker-type illusion of horizontal movement of the primary target, median saccadic error increased horizontally to 3.2 deg but was 1.1 deg vertically. 5. When targets were flashed as subjects smoothly pursued a spot that moved vertically on the horizontally moving background, a condition that induces a strong illusion of diagonal target motion, median saccadic error was 4.0 deg horizontally and 1.5 deg vertically; thus the horizontal error was greater than under any other experimental condition. 6. In most trials, the initial saccade to the remembered target was followed by additional saccades while the subject was still in darkness. These secondary saccades, which were executed in the absence of visual feedback, brought the eye closer to the target location. During paradigms involving horizontal background movement, these corrections were more prominent horizontally than vertically. 7. Further measurements were made in two subjects to determine whether inaccuracy of memory-guided saccades, in the horizontal plane, was due to mislocalization at the time that the target flashed, misrepresentation of the trajectory of the pursuit eye movement during the memory period, or both. 8. The magnitude of the saccadic error, both with and without corrections made in darkness, was mislocalized by approximately 30% of the displacement of the background at the time that the target flashed. The magnitude of the saccadic error also was influenced by net movement of the background during the memory period, corresponding to approximately 25% of net background movement for the initial saccade and approximately 13% for the final eye position achieved in darkness. 9. We formulated simple linear models to test specific hypotheses about which combinations of signals best describe the observed saccadic amplitudes. We tested the possibilities that the brain made an accurate memory of target location and a reliable representation of the eye movement during the memory period, or that one or both of these was corrupted by the illusory visual stimulus. Our data were best accounted for by a model in which both the working memory of target location and the internal representation of the horizontal eye movements were corrupted by the illusory visual stimulus. We conclude that extraretinal signals played only a minor role, in comparison with visual estimates of the direction of gaze, in planning eye movements to remembered targ
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Bourrelly, Clara, Julie Quinet, and Laurent Goffart. "Pursuit disorder and saccade dysmetria after caudal fastigial inactivation in the monkey." Journal of Neurophysiology 120, no. 4 (October 1, 2018): 1640–54. http://dx.doi.org/10.1152/jn.00278.2018.

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The caudal fastigial nuclei (cFN) are the output nuclei by which the medio-posterior cerebellum influences the production of saccadic and pursuit eye movements. We investigated the consequences of unilateral inactivation on the pursuit eye movement made immediately after an interceptive saccade toward a centrifugal target. We describe here the effects when the target moved along the horizontal meridian with a 10 or 20°/s speed. After muscimol injection, the monkeys were unable to track the present location of the moving target. During contralesional tracking, the velocity of postsaccadic pursuit was reduced. This slowing was associated with a hypometria of interceptive saccades such that gaze direction always lagged behind the moving target. No correlation was found between the sizes of saccade undershoot and the decreases in pursuit speed. During ipsilesional tracking, the effects on postsaccadic pursuit were variable across the injection sessions, whereas the interceptive saccades were consistently hypermetric. Here also, the ipsilesional pursuit disorder was not correlated with the saccade hypermetria either. The lack of correlation between the sizes of saccade dysmetria and changes of postsaccadic pursuit speed suggests that cFN activity exerts independent influences on the neural processes generating the saccadic and slow eye movements. It also suggests that the cFN is one locus where the synergy between the two motor categories develops in the context of tracking a moving visual target. We explain how the different fastigial output channels can account for these oculomotor tracking disorders. NEW & NOTEWORTHY Inactivation of the caudal fastigial nucleus impairs the ability to track a moving target. The accuracy of interceptive saccades and the velocity of postsaccadic pursuit movements are both altered, but these changes are not correlated. This absence of correlation is not compatible with an impaired common command feeding the circuits producing saccadic and pursuit eye movements. However, it suggests an involvement of caudal fastigial nuclei in their synergy to accurately track a moving target.
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28

Schmidt, M. "Neurons in the cat pretectum that project to the dorsal lateral geniculate nucleus are activated during saccades." Journal of Neurophysiology 76, no. 5 (November 1, 1996): 2907–18. http://dx.doi.org/10.1152/jn.1996.76.5.2907.

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1. Neurons in the pretectal nuclear complex that project to the ipsilateral dorsal lateral geniculate nucleus (LGNd) were identified by antidromic activation after electrical LGNd stimulation in awake cats, and their response properties were characterized to retinal image shifts elicited either by external visual stimulus movements or during spontaneous saccadic eye movements on a stationary visual stimulus, and to saccades in darkness. Eye position was monitored with the use of a scleral search coil and care was taken to assure stability of the eyes during presentation of moving visual stimuli. 2. Of a total sample of 134 cells recorded, 27 neurons were antidromically activated by electrical LGNd stimulation. In addition, responses from neurons that were not activated from the LGNd were also analyzed, including 19 “retinal slip” cells, which selectively respond to slow horizontal stimulus movements, and 21 “jerk” cells, which are specifically activated by rapid stimulus shifts. All recorded neurons were located in the nucleus of the optic tract and in the posterior pretectal nucleus. 3. In the light, neurons identified as projecting to the LGNd responded maximally to saccadic eye movements and to externally generated sudden shifts of large visual stimuli. Slow stimulus drifts did not activate these neurons. Response latencies were shorter and peak activities were increased during saccades compared with pure visual stimulation. No systematic correlation between response latency, response duration, or the number of spikes in the response and saccade direction, saccade amplitude, or saccade duration was found. Saccades and rapid stimulus shifts in the light also activated jerk cells but not retinal slip cells. 4. All 27 antidromically activated neurons also responded to spontaneous saccadic eye movements in complete darkness. Responses to saccades in the dark, however, had longer response latencies and lower peak activities than responses to saccades in light. As in the light, response parameters in darkness seemed not to code specific saccade parameters. Cells that were not activated from LGNd were found to be unresponsive to saccades in the dark. 5. According to their specific activation by saccades in darkness, LGNd-projecting pretectal neurons are termed “saccade neurons” to distinguish them from other pretectal cell populations, in particular from jerk neurons, which show similar response properties in light. 6. The saccade-related activation of pretectal saccade neurons may be used to modulate visual responses of LGNd relay cells following saccadic eye movements. Because the pretectogeniculate projection in cat most likely is GABAergic and terminates on inhibitory LGNd interneurons, its activation may lead to a saccade-locked disinhibition of relay cells. This input could counter the strong inhibition induced in the LGNd after shifts of gaze direction and lead to a resetting of LGNd cell activity.
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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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30

Petit, L., V. P. Clark, J. Ingeholm, and J. V. Haxby. "Dissociation of Saccade-Related and Pursuit-Related Activation in Human Frontal Eye Fields as Revealed by fMRI." Journal of Neurophysiology 77, no. 6 (June 1, 1997): 3386–90. http://dx.doi.org/10.1152/jn.1997.77.6.3386.

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Petit, L., V. P. Clark, J. Ingeholm, and J. V. Haxby. Dissociation of saccade-related and pursuit-related activation in human frontal eye fields as revealed by fMRI. J. Neurophysiol. 77: 3386–3390, 1997. The location of the human frontal eye fields (FEFs) underlying horizontal visually guided saccadic and pursuit eye movements was investigated with the use of functional magnetic resonance imaging in five healthy humans. Execution of both saccadic and pursuit eye movements induced bilateral FEF activation located medially at the junction of the precentral sulcus and the superior frontal sulcus and extending laterally to the precentral gyrus. These findings extend previous functional imaging studies by providing the first functional imaging evidence of a specific activation in the FEF during smooth pursuit eye movements in healthy humans. FEF activation during smooth pursuit performance was smaller than during saccades. This finding, which may reflect the presence of a smaller pursuit-related region area in human FEF than the saccade-related region, is consistent with their relative size observed in the monkey. The mean location of the pursuit-related FEF was more inferior and lateral than the location of the saccade-related FEF. These results provide the first evidence that there are different subregions in the human FEF that are involved in the execution of two different types of eye movements, namely saccadic and pursuit eye movements. Moreover, this study provides additional evidence that the human FEF is located in Brodmann's area 6, unlike the monkey FEF which is located in the posterior part of Brodmann's area 8.
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Van Horn, Marion R., Pierre A. Sylvestre, and Kathleen E. Cullen. "The Brain Stem Saccadic Burst Generator Encodes Gaze in Three-Dimensional Space." Journal of Neurophysiology 99, no. 5 (May 2008): 2602–16. http://dx.doi.org/10.1152/jn.01379.2007.

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When we look between objects located at different depths the horizontal movement of each eye is different from that of the other, yet temporally synchronized. Traditionally, a vergence-specific neuronal subsystem, independent from other oculomotor subsystems, has been thought to generate all eye movements in depth. However, recent studies have challenged this view by unmasking interactions between vergence and saccadic eye movements during disconjugate saccades. Here, we combined experimental and modeling approaches to address whether the premotor command to generate disconjugate saccades originates exclusively in “vergence centers.” We found that the brain stem burst generator, which is commonly assumed to drive only the conjugate component of eye movements, carries substantial vergence-related information during disconjugate saccades. Notably, facilitated vergence velocities during disconjugate saccades were synchronized with the burst onset of excitatory and inhibitory brain stem saccadic burst neurons (SBNs). Furthermore, the time-varying discharge properties of the majority of SBNs (>70%) preferentially encoded the dynamics of an individual eye during disconjugate saccades. When these experimental results were implemented into a computer-based simulation, to further evaluate the contribution of the saccadic burst generator in generating disconjugate saccades, we found that it carries all the vergence drive that is necessary to shape the activity of the abducens motoneurons to which it projects. Taken together, our results provide evidence that the premotor commands from the brain stem saccadic circuitry, to the target motoneurons, are sufficient to ensure the accurate control shifts of gaze in three dimensions.
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32

Reuter, Eva-Maria, Welber Marinovic, Timothy N. Welsh, and Timothy J. Carroll. "Increased preparation time reduces, but does not abolish, action history bias of saccadic eye movements." Journal of Neurophysiology 121, no. 4 (April 1, 2019): 1478–90. http://dx.doi.org/10.1152/jn.00512.2018.

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The characteristics of movements are strongly history-dependent. Marinovic et al. (Marinovic W, Poh E, de Rugy A, Carroll TJ. eLife 6: e26713, 2017) showed that past experience influences the execution of limb movements through a combination of temporally stable processes that are strictly use dependent and dynamically evolving and context-dependent processes that reflect prediction of future actions. Here we tested the basis of history-dependent biases for multiple spatiotemporal features of saccadic eye movements under two preparation time conditions (long and short). Twenty people performed saccades to visual targets. To prompt context-specific expectations of most likely target locations, 1 of 12 potential target locations was specified on ~85% of the trials and each remaining target was presented on ~1% trials. In long preparation trials participants were shown the location of the next target 1 s before its presentation onset, whereas in short preparation trials each target was first specified as the cue to move. Saccade reaction times and direction were biased by recent saccade history but according to distinct spatial tuning profiles. Biases were purely expectation related for saccadic reaction times, which increased linearly as the distance from the repeated target location increased when preparation time was short but were similar to all targets when preparation time was long. By contrast, the directions of saccades were biased toward the repeated target in both preparation time conditions, although to a lesser extent when the target location was precued (long preparation). The results suggest that saccade history affects saccade dynamics via both use- and expectation-dependent mechanisms and that movement history has dissociable effects on reaction time and saccadic direction. NEW & NOTEWORTHY The characteristics of our movements are influenced not only by concurrent sensory inputs but also by how we have moved in the past. For limb movements, history effects involve both use-dependent processes due strictly to movement repetition and processes that reflect prediction of future actions. Here we show that saccade history also affects saccade dynamics via use- and expectation-dependent mechanisms but that movement history has dissociable effects on saccade reaction time and direction.
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33

Tomlinson, R. D. "Combined eye-head gaze shifts in the primate. III. Contributions to the accuracy of gaze saccades." Journal of Neurophysiology 64, no. 6 (December 1, 1990): 1873–91. http://dx.doi.org/10.1152/jn.1990.64.6.1873.

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1. The behavior of the combined eye-head gaze saccade mechanism was investigated in the rhesus monkey under both normal circumstances and in the presence of perturbations delivered to the head by a torque motor. Animals were trained to follow a target light that stepped at regular intervals through an angle of 68 degrees (+/- 34 degrees with respect to the midsagittal plane). Thus all primary saccades were center crossing. On randomly occurring trials the torque motor was pulsed so as to perturb the trajectory of the head, thus allowing us to assess both the functional state of the vestibuloocular reflex (VOR) and the effects of such perturbations on gaze saccade accuracy (gaze is defined as the sum of eye-in-head plus head-in-space, and a gaze saccade as a combined eye-head saccadic gaze shift). 2. Gaze shifts can be divided into two discrete sections: the portion during which the gaze angle is changing (the saccadic portion), and the portion during which the gaze is stationary but the head continues to move (the terminal head-movement portion). For the system to accurately acquire eccentric targets, at least two criteria must be met: 1) the saccadic portion must be accurate, and 2) the compensatory eye movement that occurs during the terminal head-movement portion must be equal and opposite to the head movement, thereby maintaining gaze stability. Perturbations delivered during the terminal head-movement portion of the gaze shift indicated that VOR was functioning normally, and thus we concluded that the compensatory eye movements that accompany head movements were vestibular in origin. 3. As reported previously, during the saccadic portion of large-amplitude gaze saccades, the VOR ceases to function. In spite of this observation, the accuracy of the gaze saccade is not affected by perturbations delivered to the head. Gaze accuracy is maintained both by changing the duration of the saccadic portion and by altering the head trajectory. 4. Because rhesus monkeys often make very rapid head movements (1,200 degrees/s), we wished to discover the velocity range over which the monkey VOR might be expected to operate. Accordingly, in a second series of experiments, VOR function was assessed during passive whole-body rotations with the head fixed. By the use of spring-assisted manual rotations, peak velocities up to 850 degrees/s were achieved. When VOR gain was measured during such rotations, it was found to be equal to 0.9 up to the maximum velocities used.(ABSTRACT TRUNCATED AT 400 WORDS)
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34

Sobotka, Stanislaw, Anna Nowicka, and James L. Ringo. "Activity Linked to Externally Cued Saccades in Single Units Recorded From Hippocampal, Parahippocampal, and Inferotemporal Areas of Macaques." Journal of Neurophysiology 78, no. 4 (October 1, 1997): 2156–63. http://dx.doi.org/10.1152/jn.1997.78.4.2156.

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Sobotka, Stanislaw, Anna Nowicka, and James L. Ringo. Activity linked to externally cued saccades in single units recorded from hippocampal, parahippocampal, and inferotemporal areas of macaques. J. Neurophysiol. 78: 2156–2163, 1997. We studied whether target-directed, externally commanded saccadic eye movements (saccades) induced activity in single units in inferotemporal cortex, the hippocampal formation, and parahippocampal gyrus. The monkeys first were required to fix their gaze on a small cross presented to the left or right of center on the monitor screen. The cross was extinguished, and a random 600–1,000 ms thereafter, a small dot was presented for 200 ms. The dot was located either 10° above, below, right, or left of the position on which the fixation cross had been. The monkey made a saccadic eye movement to this dot (in darkness). The neuronal activity around this goal-directed saccade was analyzed. In addition, control conditions were imposed systematically in which similar dots were presented, but the monkey's task was to withhold the saccade. We recorded 290 units from two monkeys. From this group, 134 met two criteria, they did not show visual response in control trials and they had spike rates >2 Hz. These were analyzed further; 53% (71/134) showed modulation related to the target directed saccade, and 29% (39/134) showed saccadic modulation during spontaneous eye movements. These two groups were correlated only weakly. Of the units with significant saccadic modulation, 17% (12/71) showed significant directional selectivity, and 13% (9/71) showed significant position selectivity ( P < 0.01). At a lower criterion ( P < 0.05), almost one-half (33/71) showed one or the other spatial selectivity. Primates use saccades to acquire visual information. The appearance of strong saccadic modulation in brain structures previously characterized as mnemonic suggests the possibility that the mnemonic circuitry uses an extraretinal signal linked to saccades to control visual memory processes, e.g., synchronizing mnemonic processes to the pulsatile visual data inflow.
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35

Waitzman, D. M., V. L. Silakov, and B. Cohen. "Central mesencephalic reticular formation (cMRF) neurons discharging before and during eye movements." Journal of Neurophysiology 75, no. 4 (April 1, 1996): 1546–72. http://dx.doi.org/10.1152/jn.1996.75.4.1546.

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1. One hundred twenty neurons were recorded in the central mesencephalic reticular formation (cMRF) of four rhesus monkeys, trained to make visually guided and targeted saccadic eye movements. Eye movements were recorded with the head fixed, using electrooculography (EOG) or subconjunctival scleral search coils. Seventy-six percent (92/120) of cells discharged before and during contraversive visually guided or targeted rapid eye movements, and 76% of these (70/92) responded during contraversive spontaneous saccades in the dark. cMRF neurons had large contraversive movement fields and either a high (> 10 spikes/s) or low background level of spontaneous activity in the dark. The optimal movement vectors (i.e., saccades with greatest response) were predominantly horizontal, although many had a vertical component. Cells with optimal movement vectors within +/- 25 degrees of pure vertical were more rostral in the MRF and were excluded from the analysis. 2. A subgroup of cMRF neurons (31 of 92) that discharged before and during visually guided saccades were examined for visual sensitivity. Slightly less than one-half of these cells (42%, 13/31) were visuomotor units, i.e., they responded to visual targets in the absence of eye movement. The other 58% (n = 18) did not discharge during the visual probe trial; they were movement-related cells. 3. Microstimulation (threshold 40-60 microA at 333 Hz) at the sites of many of these cMRF neurons produced contraversive saccadic eye movements at short latency (< 40 ms). The amplitude and direction of the elicited saccades were similar to the optimal movement vector determined from single-unit recording. This suggested that cMRF cells recorded at the same locus of electrical microstimulation participated in the network responsible for the production and control of rapid eye movements. 4. The 92 saccade-related neurons were divided into two groups on the basis of their background discharge rate. Firing rates for both low background (28%, n = 26) and high background (72%, n = 66) cells increased approximately 30 ms before contraversive saccades and reached a peak discharge just before saccade onset. The low background neurons had either no activity or generated a few spikes just before the end of ipsiversive saccades. The steady rate of discharge (> 10 spikes/s) of high background neurons was inhibited from approximately 20 ms before ipsiversive saccades until just before saccade end. 5. Cells were also subdivided on the basis of how their discharge rates fell at the end of saccades. Clipped cells (38%, n = 35) had activity that fell sharply with saccade offset. Partially clipped cells (62%, n = 57) had persistent firing in the 100 ms following the saccade that was > 20% higher than the firing during the 100 ms before the saccade. 6. Latencies between the 90% point on the rising edge of the peak discharge and the start of the saccade were < or = 5.3 ms for eye movement-related cells in two monkeys. Longer latencies (11-19 ms) were found when measured between the 10% point on the rising edge of the peak discharge and saccade onset. These latencies were equal to or shorter than those obtained for eye movement-related burst neurons in the intermediate and deep layers of the superior colliculus analyzed similarly. Delays between the peak discharge and peak eye velocity were 13.6-15.1 ms for the same group of cMRF eye movement-related cells. These were significantly shorter than the delays measured for eye movement neurons in the superior colliculus (SC) of one of the monkeys. These findings suggest that the buildup discharge of cMRF neurons occurs early enough before saccades to contribute to saccade triggering. The peak discharge, however, occurs with or after the burst in the SC, suggesting that this portion of the discharge serves a function other than saccade triggering. 7. The number of spikes in bursts associated with eye movement was correlated with saccade parameters.
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36

Sparks, D. L., L. E. Mays, and J. D. Porter. "Eye movements induced by pontine stimulation: interaction with visually triggered saccades." Journal of Neurophysiology 58, no. 2 (August 1, 1987): 300–318. http://dx.doi.org/10.1152/jn.1987.58.2.300.

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1. Rhesus monkeys were trained to look to brief visual targets presented in an otherwise darkened room. On some trials, after the visual target was extinguished but before a saccade to it could be initiated, the eyes were driven to another orbital position by microstimulation of the paramedian pontine reticular formation. If, as current models of the saccadic system suggest, a copy of the motor command is used as a feedback signal of eye position, failure to compensate for stimulation-induced movements would indicate that stimulation occurred at a site beyond the point from which the eye position signal was derived. 2. Animals compensated for perturbations of eye position induced by stimulation of most pontine sites by making saccades that directed gaze to the position of the visual target. With stimulation at other pontine sites, compensatory saccades did not occur. 3. Pontine stimulation sometimes triggered, prematurely, impending visually directed saccades. The direction and amplitude of the premature movement depended upon the location of the briefly presented visual target. The amplitude of the premature movement was also a function of the interval between the stimulation train and the impending saccade. These data suggest that input signals for the horizontal and vertical pulse/step generators develop gradually during the presaccadic interval. Saccade trigger signals need to be delayed until the formation of these signals is completed. 4. The implications of these findings for models of the saccadic system are discussed. Robinson's local feedback model of the saccadic system can explain compensation for pontine stimulation-induced changes in eye position but cannot easily account for the failure to compensate for perturbations in eye position produced by stimulation at other sites. Modified versions of Robinson's model, which assume that the input signal to the pulse/step generator is the desired displacement of the eye, can account for both compensation and the failure to compensate since two separate neural integrators are employed. However, these models ignore kinematic arguments that commands to the extraocular muscles must specify the absolute position of the eye in the orbit rather than a relative movement from a previous position.
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37

Prime, Steven L., Michael Vesia, and J. Douglas Crawford. "Cortical mechanisms for trans-saccadic memory and integration of multiple object features." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1564 (February 27, 2011): 540–53. http://dx.doi.org/10.1098/rstb.2010.0184.

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Constructing an internal representation of the world from successive visual fixations, i.e. separated by saccadic eye movements, is known as trans-saccadic perception. Research on trans-saccadic perception (TSP) has been traditionally aimed at resolving the problems of memory capacity and visual integration across saccades. In this paper, we review this literature on TSP with a focus on research showing that egocentric measures of the saccadic eye movement can be used to integrate simple object features across saccades, and that the memory capacity for items retained across saccades, like visual working memory, is restricted to about three to four items. We also review recent transcranial magnetic stimulation experiments which suggest that the right parietal eye field and frontal eye fields play a key functional role in spatial updating of objects in TSP. We conclude by speculating on possible cortical mechanisms for governing egocentric spatial updating of multiple objects in TSP.
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38

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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39

Hepp, K., A. J. Van Opstal, D. Straumann, B. J. Hess, and V. Henn. "Monkey superior colliculus represents rapid eye movements in a two-dimensional motor map." Journal of Neurophysiology 69, no. 3 (March 1, 1993): 965–79. http://dx.doi.org/10.1152/jn.1993.69.3.965.

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1. Although the eye has three rotational degrees of freedom, eye positions, during fixations, saccades, and smooth pursuit, with the head stationary and upright, are constrained to a plane by ListingR's law. We investigated whether Listing's law for rapid eye movements is implemented at the level of the deeper layers of the superior colliculus (SC). 2. In three alert rhesus monkeys we tested whether the saccadic motor map of the SC is two dimensional, representing oculocentric target vectors (the vector or V-model), or three dimensional, representing the coordinates of the rotation of the eye from initial to final position (the quaternion or Q-model). 3. Monkeys made spontaneous saccadic eye movements both in the light and in the dark. They were also rotated about various axes to evoke quick phases of vestibular nystagmus, which have three degrees of freedom. Eye positions were measured in three dimensions with the magnetic search coil technique. 4. While the monkey made spontaneous eye movements, we electrically stimulated the deeper layers of the SC and elicited saccades from a wide range of initial positions. According to the Q-model, the torsional component of eye position after stimulation should be uniquely related to saccade onset position. However, stimulation at 110 sites induced no eye torsion, in line with the prediction of the V-model. 5. Activity of saccade-related burst neurons in the deeper layers of the SC was analyzed during rapid eye movements in three dimensions. No systematic eye-position dependence of the movement fields, as predicted by the Q-model, could be detected for these cells. Instead, the data fitted closely the predictions made by the V-model. 6. In two monkeys, both SC were reversibly inactivated by symmetrical bilateral injections of muscimol. The frequency of spontaneous saccades in the light decreased dramatically. Although the remaining spontaneous saccades were slow, Listing's law was still obeyed, both during fixations and saccadic gaze shifts. In the dark, vestibularly elicited fast phases of nystagmus could still be generated in three dimensions. Although the fastest quick phases of horizontal and vertical nystagmus were slower by about a factor of 1.5, those of torsional quick phases were unaffected. 7. On the basis of the electrical stimulation data and the properties revealed by the movement field analysis, we conclude that the collicular motor map is two dimensional. The reversible inactivation results suggest that the SC is not the site where three-dimensional fast phases of vestibular nystagmus are generated.(ABSTRACT TRUNCATED AT 400 WORDS)
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40

Rottach, Klaus G., Vallabh E. Das, Walter Wohlgemuth, Ari Z. Zivotofsky, and R. John Leigh. "Properties of Horizontal Saccades Accompanied by Blinks." Journal of Neurophysiology 79, no. 6 (June 1, 1998): 2895–902. http://dx.doi.org/10.1152/jn.1998.79.6.2895.

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Rottach, Klaus G., Vallabh E. Das, Walter Wohlgemuth, Ari Z. Zivotofsky, and R. John Leigh. Properties of horizontal saccades accompanied by blinks. J. Neurophysiol. 79: 2895–2902, 1998. Using the magnetic search coil technique to record eye and lid movements, we investigated the effect of voluntary blinks on horizontal saccades in five normal human subjects. The main goal of the study was to determine whether changes in the dynamics of saccades with blinks could be accounted for by a superposition of the eye movements induced by blinks as subjects fixated a stationary target and saccadic movements made without a blink. First, subjects made voluntary blinks as they fixed on stationary targets located straight ahead or 20° to the right or left. They then made saccades between two continuously visible targets 20 or 40° apart, while either attempting not to blink, or voluntarily blinking, with each saccade. During fixation of a target located straight ahead, blinks induced brief downward and nasalward deflections of eye position. When subjects looked at targets located at right or left 20°, similar initial movements were made by four of the subjects, but the amplitude of the adducted eye was reduced by 65% and was followed by a larger temporalward movement. Blinks caused substantial changes in the dynamic properties of saccades. For 20° saccades made with blinks, peak velocity and peak acceleration were decreased by ∼20% in all subjects compared with saccades made without blinks. Blinks caused the duration of 20° saccades to increase, on average, by 36%. On the other hand, blinks had only small effects on the gain of saccades. Blinks had little influence on the relative velocities of centrifugal versus centripetal saccades, and abducting versus adducting saccades. Three of five subjects showed a significantly increased incidence of dynamic overshoot in saccades accompanied by blinks, especially for 20° movements. Taken with other evidence, this finding suggests that saccadic omnipause neurons are inhibited by blinks, which have longer duration than the saccades that company them. In conclusion, the changes in dynamic properties of saccades brought about by blinks cannot be accounted for simply by a summation of gaze perturbations produced by blinks during fixation and saccadic eye movements made without blinks. Our findings, especially the appearance of dynamic overshoots, suggest that blinks affect the central programming of saccades. These effects of blinks need to be taken into account during studies of the dynamic properties of saccades.
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41

Van der Stigchel, Stefan. "The Search for Oculomotor Inhibition." Experimental Psychology 57, no. 6 (January 1, 2010): 429–35. http://dx.doi.org/10.1027/1618-3169/a000053.

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When a saccadic target is presented simultaneously with a distractor, the distractor has to be inhibited in order to successfully perform an eye movement to the target. Insufficient inhibition results in an erroneous eye movement to the distractor. This study investigated whether the influence of a distractor on eye movements is mediated by working memory. A working memory task was added to a saccadic paradigm in which an irrelevant element had to be inhibited. Results show that participants made more erroneous saccades to the distractor when working memory was occupied. This suggests that working memory is involved in the oculomotor inhibition of saccadic distractors.
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42

Oliva, Giulia A., Maria P. Bucci, and Roberto Fioravanti. "Impairment of Saccadic Eye Movements by Scopolamine Treatment." Perceptual and Motor Skills 76, no. 1 (February 1993): 159–67. http://dx.doi.org/10.2466/pms.1993.76.1.159.

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The effects of Scopolamine on the dynamics of saccadic eye movements, stimulated over a random time interval, have been investigated in humans. A 0.5-mg dose of the drug (intramuscular injection) had various influences on the basic saccadic parameters. For all subjects duration increased and peak velocity decreased, while for 50% of the subjects saccades became hypometric and latency increased. Standard deviations increased consistently too. Moreover, the Scopolamine treatment affected postsaccadic fixation; at the end of many saccades, the eye drifted considerably, but stability was recovered after a few seconds.
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43

Asscheman, Susanne J., Katharine N. Thakkar, and Sebastiaan F. W. Neggers. "Changes in Effective Connectivity of the Superior Parietal Lobe during Inhibition and Redirection of Eye Movements." Journal of Experimental Neuroscience 9s1 (January 2015): JEN.S32736. http://dx.doi.org/10.4137/jen.s32736.

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Executive control is the ability to flexibly control behavior and is frequently studied with saccadic eye movements. Contrary to frontal oculomotor areas, the role of the superior parietal lobe (SPL) in the executive control of saccades remains unknown. To explore the role of SPL networks in saccade control, we performed a saccadic search-step task while acquiring functional magnetic resonance imaging data for 41 participants. Psychophysiological interaction analyses assessed task-related differences in the effective connectivity of SPL with other brain regions during the inhibition and redirection of saccades. Results indicate an increased coupling of SPL with frontal, posterior, and striatal oculomotor areas for redirected saccades versus visually guided saccades. Saccade inhibition versus unsuccessful inhibition revealed an increased coupling of SPL with dorsolateral prefrontal cortex and anterior cingulate cortex. We discuss how these findings relate to ongoing debates about the implementation of executive control and conclude that early attentional control and rapid updating of saccade goals are important signals for executive control.
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44

Economides, John R., Daniel L. Adams, and Jonathan C. Horton. "Normal correspondence of tectal maps for saccadic eye movements in strabismus." Journal of Neurophysiology 116, no. 6 (December 1, 2016): 2541–49. http://dx.doi.org/10.1152/jn.00553.2016.

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The superior colliculus is a major brain stem structure for the production of saccadic eye movements. Electrical stimulation at any given point in the motor map generates saccades of defined amplitude and direction. It is unknown how this saccade map is affected by strabismus. Three macaques were raised with exotropia, an outwards ocular deviation, by detaching the medial rectus tendon in each eye at age 1 mo. The animals were able to make saccades to targets with either eye and appeared to alternate fixation freely. To probe the organization of the superior colliculus, microstimulation was applied at multiple sites, with the animals either free-viewing or fixating a target. On average, microstimulation drove nearly conjugate saccades, similar in both amplitude and direction but separated by the ocular deviation. Two monkeys showed a pattern deviation, characterized by a systematic change in the relative position of the two eyes with certain changes in gaze angle. These animals' saccades were slightly different for the right eye and left eye in their amplitude or direction. The differences were consistent with the animals' underlying pattern deviation, measured during static fixation and smooth pursuit. The tectal map for saccade generation appears to be normal in strabismus, but saccades may be affected by changes in the strabismic deviation that occur with different gaze angles.
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45

Van Donkelaar, Paul, Ji-Hang Lee, and Anthony S. Drew. "Transcranial Magnetic Stimulation Disrupts Eye-Hand Interactions in the Posterior Parietal Cortex." Journal of Neurophysiology 84, no. 3 (September 1, 2000): 1677–80. http://dx.doi.org/10.1152/jn.2000.84.3.1677.

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Recent neurophysiological studies have started to shed some light on the cortical areas that contribute to eye-hand coordination. In the present study we investigated the role of the posterior parietal cortex (PPC) in this process in normal, healthy subjects. This was accomplished by delivering single pulses of transcranial magnetic stimulation (TMS) over the PPC to transiently disrupt the putative contribution of this area to the processing of information related to eye-hand coordination. Subjects made open-loop pointing movements accompanied by saccades of the same required amplitude or by saccades that were substantially larger. Without TMS the hand movement amplitude was influenced by the amplitude of the corresponding saccade; hand movements accompanied by larger saccades were larger than those accompanied by smaller saccades. When TMS was applied over the left PPC just prior to the onset of the saccade, a marked reduction in the saccadic influence on manual motor output was observed. TMS delivered at earlier or later periods during the response had no effect. Taken together, these data suggest that the PPC integrates signals related to saccade amplitude with limb movement information just prior to the onset of the saccade.
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46

Abrams, Richard A., and John Jonides. "Programming saccadic eye movements." Journal of Experimental Psychology: Human Perception and Performance 14, no. 3 (1988): 428–43. http://dx.doi.org/10.1037/0096-1523.14.3.428.

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47

Walker, John. "Human saccadic eye movements." Scholarpedia 7, no. 7 (2012): 5095. http://dx.doi.org/10.4249/scholarpedia.5095.

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48

Handel, Ari, and Paul W. Glimcher. "Contextual Modulation of Substantia Nigra Pars Reticulata Neurons." Journal of Neurophysiology 83, no. 5 (May 1, 2000): 3042–48. http://dx.doi.org/10.1152/jn.2000.83.5.3042.

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Neurons in the substantia nigra pars reticulata (SNr) are known to encode saccadic eye movements within some, but not all, behavioral contexts. However, the precise contextual factors that effect the modulations of nigral activity are still uncertain. To further examine the effect of behavioral context on the SNr, we recorded the activity of 72 neurons while monkeys made saccades during a delayed saccade task and during periods of free viewing. We quantified and compared the movement fields of each neuron for saccades made under three different conditions: 1) spontaneous saccades, which shifted gaze during periods of free viewing when no stimuli were presented and no reinforcements were delivered; 2) fixational saccades, which brought gaze into alignment with a fixation target at the start of a delayed saccade trial, were necessary for trial completion, but were not directly followed by reinforcement; and 3) terminal saccades, which brought gaze into alignment with a visual target at the end of a delayed saccade trial and were directly followed by reinforcement. For three of the four SNr neuron classes, saccade-related modulations were only present before terminal saccades. For the fourth class, discrete pausers, saccade-related modulations were substantially larger for terminal saccades than for fixational saccades, and modulations were absent for spontaneous saccades. These results and other recent work on the basal ganglia suggest that some saccade-related signals in the SNr may be influenced by the reinforcement associated with a particular saccadic eye movement.
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49

Petit, Laurent, and James V. Haxby. "Functional Anatomy of Pursuit Eye Movements in Humans as Revealed by fMRI." Journal of Neurophysiology 82, no. 1 (July 1, 1999): 463–71. http://dx.doi.org/10.1152/jn.1999.82.1.463.

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We have investigated the functional anatomy of pursuit eye movements in humans with functional magnetic imaging. The performance of pursuit eye movements induced activations in the cortical eye fields also activated during the execution of visually guided saccadic eye movements, namely in the precentral cortex [frontal eye field (FEF)], the medial superior frontal cortex (supplementary eye field), the intraparietal cortex (parietal eye field), and the precuneus, and at the junction of occipital and temporal cortex (MT/MST) cortex. Pursuit-related areas could be distinguished from saccade-related areas both in terms of spatial extent and location. Pursuit-related areas were smaller than their saccade-related counterparts, three of eight significantly so. The pursuit-related FEF was usually inferior to saccade-related FEF. Other pursuit-related areas were consistently posterior to their saccade-related counterparts. The current findings provide the first functional imaging evidence for a distinction between two parallel cortical systems that subserve pursuit and saccadic eye movements in humans.
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50

Kurylo, Daniel D., Ram L. Pandey Vimal, and Peter H. Hartline. "Effects of Multiple Stimuli on Ocular Orientation by Cats." Journal of Cognitive Neuroscience 4, no. 2 (April 1992): 165–74. http://dx.doi.org/10.1162/jocn.1992.4.2.165.

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We investigated the characteristics of saccades made by cats in response to single and double stimuli. Stimuli were either visual, auditory, or bimodal. We initially trained cats to look toward the location of briefly presented single visual or single auditory targets that were extinguished before the initiation of eye movements. Following training, we monitored eye movements during and after the presentation of double targets, either two visual, two auditory, or bimodal, that were at disparate spatial locations. Cats made saccadic eye movements to positions that ranged between the location of the two targets. If the eye position at the start of a saccade was near the mid point of the targets, cats were less likely to initiate a saccade, and saccadic latencies were longer, compared to when starting eye position was at a distance from this location. These behavioral results are consistent with the hypothesis that the neural representations of briefly presented targets are combined and treated as a unitary, low resolution stimulus from which an orienting motor program is derived. The similarity of responses to double visual, double auditory, and bimodal stimuli suggests that a common sensorimotor mechanism applies within and between these sensory modalities.
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