Effects of Voluntary Blinks on Saccades, Vergence Eye Movements, and Saccade-Vergence Interactions in Humans

2002 ◽  
Vol 88 (3) ◽  
pp. 1220-1233 ◽  
Author(s):  
H. Rambold ◽  
A. Sprenger ◽  
C. Helmchen
Keyword(s):  
Eye Movements ◽  
Peak Velocity ◽  
Saccade Onset ◽  
Vertical Saccades ◽  
Acceleration And Deceleration ◽  
Tightly Coupled ◽  
Measured Effect ◽  
Straight Ahead ◽  
Omnipause Neurons ◽  
Saccade Duration

Blinks are known to change the kinematic properties of horizontal saccades, probably by influencing the saccadic premotor circuit. The neuronal basis of this effect could be explained by changes in the activity of omnipause neurons in the nucleus raphe interpositus or in the saccade-related burst neurons of the superior colliculus. Omnipause neurons cease discharge during both saccades and vergence movements. Because eyelid blinks can influence both sets of neurons, we hypothesized that blinks would influence the kinematic parameters of saccades in all directions, vergence, and saccade-vergence interactions. To test this hypothesis, we investigated binocular eye and lid movements in five normal healthy subjects with the magnetic search coil technique. The subjects performed conjugate horizontal and vertical saccades from gaze straight ahead to targets at 20° up, down, right, or left while either attempting not to blink or voluntarily blinking. While following the same blink instruction, subjects made horizontal vergence eye movements of 7° and combined saccade-vergence movements with a version amplitude of 20°. The movements were performed back and forth from two targets simultaneously presented nearby (38 cm) and more distant (145 cm). Small vertical saccades accompanied most vergence movements. These results show that blinks change the kinematics (saccade duration, peak velocity, peak acceleration, peak deceleration) of not only horizontal but also of vertical saccades, of horizontal vergence eye movements, and of combined saccade-vergence eye movements. Peak velocity, acceleration, and deceleration of eye movements were decreased on the average by 30%, and their duration increased by 43% on the average when they were accompanied by blinks. The blink effect was time dependent with respect to saccade and vergence onset: the greatest effect occurred 100 ms prior to saccade onset, whereas there was no effect when the blink started after saccade onset. The effects of blinks on saccades and vergence, which are tightly coupled to latency, support the hypothesis that blinks cause profound spatiotemporal perturbations of the eye movements by interfering with the normal saccade/vergence premotor circuits. However, the measured effect may to a certain degree but not exclusively be explained by mechanical interference.

Properties of Horizontal Saccades Accompanied by Blinks

1998 ◽  
Vol 79 (6) ◽  
pp. 2895-2902 ◽  
Author(s):  
Klaus G. Rottach ◽  
Vallabh E. Das ◽  
Walter Wohlgemuth ◽  
Ari Z. Zivotofsky ◽  
R. John Leigh
Keyword(s):  
Eye Movements ◽  
Peak Velocity ◽  
Dynamic Properties ◽  
Human Subjects ◽  
Saccadic Eye Movements ◽  
Stationary Target ◽  
Normal Human ◽  
The Right ◽  
Straight Ahead ◽  
Omnipause Neurons

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.

Saccade–Vergence Interactions in Macaques. I. Test of the Omnipause Multiply Model

2005 ◽  
Vol 94 (4) ◽  
pp. 2295-2311 ◽  
Author(s):  
C. Busettini ◽  
L. E. Mays
Keyword(s):  
Eye Movements ◽  
Main Sequence ◽  
Peak Velocity ◽  
Alternative Models ◽  
Omnipause Neurons ◽  
Velocity Enhancement

Horizontal vergence eye movements are movements in opposite directions used to change fixation between far and near targets. The occurrence of a saccade during vergence causes vergence velocity to be transiently enhanced. The goal of this study was to test in the monkey the previously described Multiply Model (Zee et al. 1992) that holds that, in humans, the speeding of vergence during a saccade may be the result of the disinhibition of a subgroup of vergence-related neurons by the saccadic omnipause neurons (OPNs). In agreement with the Multiply Model: 1) the onset of the enhancement was closely related to saccadic onset, and thus linked to the onset of the OPN pause; 2) the magnitude of the vergence velocity enhancement was strongly dependent on saccade–vergence timing. Contrary to the Multiply Model: 1) the peak of the vergence velocity enhancement was dependent on saccadic peak velocity; 2) the dependency on saccadic peak velocity was not the indirect result of a dependency on saccadic duration and therefore on the duration of the OPN pause; 3) the decline of the vergence enhancement, identified by the time of the peak of the enhancement velocity, occurred too early to be linked to the end of the OPN pause; 4) vergence enhancement had a saccadic-like peak-velocity/size main sequence. Overall, the evidence is incompatible with the OPN Multiply hypothesis of vergence enhancement. Alternative models are described in an accompanying paper.

Differences in intersaccadic adaptation transfer between inward and outward adaptation

2011 ◽  
Vol 106 (3) ◽  
pp. 1399-1410 ◽  
Author(s):  
Fabian Schnier ◽  
Markus Lappe
Keyword(s):  
Peak Velocity ◽  
The Other ◽  
Saccade Target ◽  
Control Mechanisms ◽  
Saccadic Adaptation ◽  
Saccade Onset ◽  
Independent Parameters ◽  
Saccade Duration ◽  
Velocity Decrease

Saccadic adaptation is a mechanism to increase or decrease the amplitude gain of subsequent saccades, if a saccade is not on target. Recent research has shown that the mechanism of gain increasing, or outward adaptation, and the mechanism of gain decreasing, or inward adaptation, rely on partly different processes. We investigate how outward and inward adaptation of reactive saccades transfer to other types of saccades, namely scanning, overlap, memory-guided, and gap saccades. Previous research has shown that inward adaptation of reactive saccades transfers only partially to these other saccade types, suggesting differences in the control mechanisms between these saccade categories. We show that outward adaptation transfers stronger to scanning and overlap saccades than inward adaptation, and that the strength of transfer depends on the duration for which the saccade target is visible before saccade onset. Furthermore, we show that this transfer is mainly driven by an increase in saccade duration, which is apparent for all saccade categories. Inward adaptation, in contrast, is accompanied by a decrease in duration and in peak velocity, but only the peak velocity decrease transfers from reactive saccades to other saccade categories, i.e., saccadic duration remains constant or even increases for test saccades of the other categories. Our results, therefore, show that duration and peak velocity are independent parameters of saccadic adaptation and that they are differently involved in the transfer of adaptation between saccade categories. Furthermore, our results add evidence that inward and outward adaptation are different processes.

Saccades From Torsional Offset Positions Back to Listing's Plane

2000 ◽  
Vol 83 (6) ◽  
pp. 3241-3253 ◽  
Author(s):  
Choongkil Lee ◽  
David S. Zee ◽  
Dominik Straumann
Keyword(s):  
Eye Movements ◽  
Three Dimensional ◽  
Normal Subjects ◽  
Medial Longitudinal Fasciculus ◽  
Rapid Eye Movements ◽  
Listing's Plane ◽  
Vertical Saccades ◽  
Horizontal Saccade ◽  
Saccade Duration ◽  
Listing’S Plane

Rapid eye movements include saccades and quick phases of nystagmus and may have components around all three axes of ocular rotation: horizontal, vertical, and torsional. In this study, we recorded horizontal, vertical, and torsional eye movements in normal subjects with their heads upright and stationary. We asked how the eyes are brought back to Listing's plane after they are displaced from it. We found that torsional offsets, induced with a rotating optokinetic disk oriented perpendicular to the subject's straight ahead, were corrected during both horizontal and vertical voluntary saccades. Thus three-dimensional errors are synchronously reduced during saccades. The speed of the torsional correction was much faster than could be accounted for by passive mechanical forces. During vertical saccades, the peak torsional velocity decreased and the time of peak torsional velocity was delayed, as the amplitude of vertical saccades increased. In contrast, there was no consistent reduction of torsional velocity or change in time of peak torsional velocity with an increase in the amplitude of horizontal saccades. These findings suggest that 1) the correction of stimulus-induced torsion is neurally commanded and 2) there is cross-coupling between the torsional and vertical but not between the torsional and horizontal saccade generating systems. This latter dichotomy may reflect the fact that vertical and torsional rapid eye movements are generated by common premotor circuits located in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). When horizontal or vertical saccade duration was relatively short, the torsional offset was not completely corrected during the primary saccade, indicating that although the saccade itself is three-dimensional, saccade duration is determined by the error in the horizontal or the vertical, but not by the error in the torsional component.

Effects of Reversible Inactivation of the Primate Mesencephalic Reticular Formation. II. Hypometric Vertical Saccades

2000 ◽  
Vol 83 (4) ◽  
pp. 2285-2299 ◽  
Author(s):  
David M. Waitzman ◽  
Valentine L. Silakov ◽  
Stacy DePalma-Bowles ◽  
Amanda S. Ayers
Keyword(s):  
Reticular Formation ◽  
Main Sequence ◽  
Mesencephalic Reticular Formation ◽  
Medial Longitudinal Fasciculus ◽  
Saccade Amplitude ◽  
Burst Neurons ◽  
Vertical Saccades ◽  
Vertical Saccade ◽  
Omnipause Neurons ◽  
Saccade Duration

Electrical microstimulation and single-unit recording have suggested that a group of long-lead burst neurons (LLBNs) in the mesencephalic reticular formation (MRF) just lateral to the interstitial nucleus of Cajal (INC) (the peri-INC MRF, piMRF) may play a role in the generation of vertical rapid eye movements. Inactivation of this region with muscimol (a GABAA agonist) rapidly produced vertical saccade hypometria (6 injections). In three of six injections, there was a marked reduction in the velocity of vertical saccades out of proportion to saccade amplitude (i.e., saccades fell below the main sequence). This was associated with a moderate increase in saccade duration. Inadvertent inactivation of the INC could not account for these observations because vertical, postsaccadic drift was not observed. Similarly, pure downward saccade hypometria, the hallmark of rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) inactivation, was always preceded by loss of upward saccades in our experiments. We also found a downward and ipsiversive displacement of initial eye position and evidence of a contraversive head tilt following piMRF injections. Saccade latency was shorter after two of six injections. Simulation of a local feedback model provided three possible explanations for vertical saccade hypometria: 1) a shift in the input to the model to request smaller saccades, 2) a reduction of LLBN input to the vertical saccade medium lead burst neurons (MLBNs), or 3) an increase in the gain of the feedback pathway. However, when the second hypothesis was coupled to a shortened duration of the saccade trigger (i.e., the discharge of the omnipause neurons), the physiological observations of piMRF inactivation could be replicated. This suggested that muscimol had targeted structures that provided both long-lead burst activity to the MLBNs in the riMLF and were critical for reactivation of the omnipause neurons. Evidence of markedly reduced vertical saccade amplitude, curved saccade trajectories, increased saccade duration, and saccades that fall below the amplitude/velocity main sequence in these monkeys closely parallels the oculomotor findings of patients with progressive supranuclear palsy (PSP).

Evidence That the Superior Colliculus Participates in the Feedback Control of Saccadic Eye Movements

2002 ◽  
Vol 87 (2) ◽  
pp. 679-695 ◽  
Author(s):  
Robijanto Soetedjo ◽  
Chris R. S. Kaneko ◽  
Albert F. Fuchs
Keyword(s):  
Superior Colliculus ◽  
Firing Rate ◽  
Saccadic Eye Movements ◽  
Burst Duration ◽  
Saccadic Amplitude ◽  
Optimal Vector ◽  
Deceleration Phase ◽  
Acceleration And Deceleration ◽  
Motor Error ◽  
Saccade Duration

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.

Activity of Mesencephalic Vertical Burst Neurons During Saccades and Smooth Pursuit

2000 ◽  
Vol 83 (4) ◽  
pp. 2080-2092 ◽  
Author(s):  
M. Missal ◽  
S. de Brouwer ◽  
P. Lefèvre ◽  
E. Olivier
Keyword(s):  
Vertical Velocity ◽  
Smooth Pursuit ◽  
Medial Longitudinal Fasciculus ◽  
Eye Position ◽  
Interstitial Nucleus Of Cajal ◽  
Burst Neurons ◽  
Preferred Direction ◽  
Saccade Onset ◽  
Vertical Saccades ◽  
Eye Velocity

The activity of vertical burst neurons (BNs) was recorded in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF-BNs) and in the interstitial nucleus of Cajal (NIC-BNs) in head-restrained cats while performing saccades or smooth pursuit. BNs emitted a high-frequency burst of action potentials before and during vertical saccades. On average, these bursts led saccade onset by 14 ± 4 ms (mean ± SD, n = 23), and this value was in the range of latencies (∼5–15 ms) of medium-lead burst neurons (MLBNs). All NIC-BNs ( n = 15) had a downward preferred direction, whereas riMLF-BNs showed either a downward ( n = 3) or an upward ( n = 5) preferred direction. We found significant correlations between saccade and burst parameters in all BNs: vertical amplitude was correlated with the number of spikes, maximum vertical velocity with maximum of the spike density, and saccade duration with burst duration. A correlation was also found between instantaneous vertical velocity and neuronal activity during saccades. During fixation, all riMLF-BNs and ∼50% of NIC-BNs (7/15) were silent. Among NIC-BNs active during fixation (8/15), only two cells had an activity correlated with the eye position in the orbit. During smooth pursuit, most riMLF-BNs were silent (7/8), but all NIC-BNs showed an activity that was significantly correlated with the eye velocity. This activity was unaltered during temporary disappearance of the visual target, demonstrating that it was not visual in origin. For a given neuron, its on-direction during smooth pursuit and saccades remained identical. The activity of NIC-BNs during both saccades and smooth pursuit can be described by a nonlinear exponential function using the velocity of the eye as independent variable. We suggest that riMLF-BNs, which were not active during smooth pursuit, are vertical MLBNs responsible for the generation of vertical saccades. Because NIC-BNs discharged during both saccades and pursuit, they cannot be regarded as MLBNs as usually defined. NIC-BNs could, however, be the site of convergence of both the saccadic and smooth pursuit signals at the premotoneuronal level. Alternatively, NIC-BNs could participate in the integration of eye velocity to eye position signals and represent input neurons to a common integrator.

scholarly journals The role of action intentionality and effector in the subjective expansion of temporal duration after saccadic eye movements

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
David Melcher ◽  
Devpriya Kumar ◽  
Narayanan Srinivasan
Keyword(s):  
Eye Movements ◽  
Visual Processing ◽  
Saccadic Eye Movements ◽  
Intentional Binding ◽  
Opposite Pattern ◽  
Motor Action ◽  
Saccade Onset ◽  
Backward Shift ◽  
The Moment

Abstract Visual perception is based on periods of stable fixation separated by saccadic eye movements. Although naive perception seems stable (in space) and continuous (in time), laboratory studies have demonstrated that events presented around the time of saccades are misperceived spatially and temporally. Saccadic chronostasis, the “stopped clock illusion”, represents one such temporal distortion in which the movement of the clock hand after the saccade is perceived as lasting longer than usual. Multiple explanations for chronostasis have been proposed including action-backdating, temporal binding of the action towards the moment of its effect (“intentional binding”) and post-saccadic temporal dilation. The current study aimed to resolve this debate by using different types of action (keypress vs saccade) and varying the intentionality of the action. We measured both perceived onset of the motor action and perceived onset of an auditory tone presented at different delays after the keypress/saccade. The results showed intentional binding for the keypress action, with perceived motor onset shifted forwards in time and the time of the tone shifted backwards. Saccades resulted in the opposite pattern, showing temporal expansion rather than compression, especially with cued saccades. The temporal illusion was modulated by intentionality of the movement. Our findings suggest that saccadic chronostasis is not solely dependent on a backward shift in perceived saccade onset, but instead reflects a temporal dilation. This percept of an effectively “longer” period at the beginning of a new fixation may reflect the pattern of suppressed, and then enhanced, visual processing around the time of saccades.

Common Inhibitory Mechanism for Saccades and Smooth-Pursuit Eye Movements

2002 ◽  
Vol 88 (4) ◽  
pp. 1880-1892 ◽  
Author(s):  
M. Missal ◽  
E. L. Keller
Keyword(s):  
Eye Movements ◽  
Smooth Pursuit ◽  
Statistical Significance ◽  
Smooth Pursuit Eye Movements ◽  
Inhibitory Mechanism ◽  
Inhibitory System ◽  
Electrical Microstimulation ◽  
Pursuit Eye Movements ◽  
Premotor Neurons ◽  
Omnipause Neurons

The premotor pathways subserving saccades and smooth-pursuit eye movements are usually thought to be different. Indeed, saccade and smooth-pursuit eye movements have different dynamics and functions. In particular, a group of midline cells in the pons called omnipause neurons (OPNs) are considered to be part of the saccadic system only. It has been established that OPNs keep premotor neurons for saccades under constant inhibition during fixation periods. Saccades occur only when the activity of OPNs has completely stopped or paused. Accordingly, electrical stimulation in the region of OPNs inhibits premotor neurons and interrupts saccades. The premotor relay for smooth pursuit is thought to be organized differently and omnipause neurons are not supposed to be involved in smooth-pursuit eye movements. To investigate this supposition, OPNs were recorded during saccades and during smooth pursuit in the monkey ( Macaca mulatta). Unexpectedly, we found that neuronal activity of OPNs decreased during smooth pursuit. The resulting activity reduction reached statistical significance in ∼50% of OPNs recorded during pursuit of a target moving at 40°/s. On average, activity was reduced by 34% but never completely stopped or paused. The onset of activity reduction coincided with the onset of smooth pursuit. The duration of activity reduction was correlated with pursuit duration and its intensity was correlated with eye velocity. Activity reduction was observed even in the absence of catch-up saccades that frequently occur during pursuit. Electrical microstimulation in the OPNs' area induced a strong deceleration of the eye during smooth pursuit. These results suggest that OPNs form an inhibitory mechanism that could control the time course of smooth pursuit. This inhibitory mechanism is part of the fixation system and is probably needed to avoid reflexive eye movements toward targets that are not purposefully selected. This study shows that saccades and smooth pursuit, although they are different kinds of eye movements, are controlled by the same inhibitory system.

Visual Fatigue and Saccadic Eye Movement Parameters

1983 ◽  
Vol 27 (8) ◽  
pp. 728-732 ◽  
Author(s):  
Ted Megaw ◽  
Tayyar Sen
Keyword(s):  
Eye Movements ◽  
Eye Movement ◽  
Peak Velocity ◽  
Cognitive Task ◽  
Saccadic Eye Movements ◽  
Tracking Task ◽  
Frequency Of Occurrence ◽  
Saccadic Eye Movement ◽  
Visual Fatigue ◽  
Movement Parameters

It has been suggested by Bahill and Stark (1975) that visual fatigue can be identified by changes in some of the saccadic eye movement parameters. These include increases in the frequency of occurrence of glissades and overlapping saccades and reductions in the peak velocity and duration of saccades. In their study, fatigue was induced by the same step tracking task that was used to evaluate the changes in saccadic parameters. However, there is evidence that subjects experience extreme feelings of fatigue while performing such a task and that somehow the task is unnatural. The present study was designed to assess whether there are any differences in the various saccadic parameters obtained while subjects perform a step tracking task and a cognitive task involving the comparison of number strings. Both tasks were presented on a VDU screen. The second objective was to establish whether there are any changes in the parameters for either task as a result of prolonged performance. The results showed no major differences in the saccadic eye movements between the two tasks and no consistent changes resulting from prolonged performance.

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