Centrifugal Saccades Research Articles

Quantifying eye dominance strength – New insights into the neurophysiological bases of saccadic asymmetries

The saccadic system presents asymmetries. Notably, saccadic peak velocity is higher in temporal than in nasal saccades, and in centripetal than in centrifugal saccades. It has already been shown that eye dominance strength relates to naso-temporal asymmetry, but its links with centripetal-centrifugal asymmetry has never been tested. The current study tested both naso-temporal and centripetal-centrifugal asymmetries simultaneously to provide a finer and continuous measure of eye dominance strength. We asked 63 participants to make centripetal and centrifugal saccades from five different locations. Analysis of saccadic peak velocity shows that eye dominance strength modulates every saccadic asymmetry tested. For the first time, we propose a graduated measure of eye dominance strength on a continuum model. The model ranges from weak to very strong eye dominance. Weak eye dominance corresponds to increased saccadic asymmetries whereas strong eye dominance corresponds to no asymmetries. Furthermore, our results provide new insights into the neurophysiological origins of saccadic asymmetries. Modulation of both naso-temporal and centripetal-centrifugal asymmetries by eye dominance strength supports the involvement of V1 in these saccadic asymmetries.

Saccadic and Postsaccadic Disconjugacy in Zebrafish Larvae Suggests Independent Eye Movement Control.

Spontaneous eye movements of zebrafish larvae in the dark consist of centrifugal saccades that move the eyes from a central to an eccentric position and postsaccadic centripetal drifts. In a previous study, we showed that the fitted single-exponential time constants of the postsaccadic drifts are longer in the temporal-to-nasal (T->N) direction than in the nasal-to-temporal (N->T) direction. In the present study, we further report that saccadic peak velocities are higher and saccadic amplitudes are larger in the N->T direction than in the T->N direction. We investigated the underlying mechanism of this ocular disconjugacy in the dark with a top-down approach. A mathematic ocular motor model, including an eye plant, a set of burst neurons and a velocity-to-position neural integrator (VPNI), was built to simulate the typical larval eye movements in the dark. The modeling parameters, such as VPNI time constants, neural impulse signals generated by the burst neurons and time constants of the eye plant, were iteratively adjusted to fit the average saccadic eye movement. These simulations suggest that four pools of burst neurons and four pools of VPNIs are needed to explain the disconjugate eye movements in our results. A premotor mechanism controls the synchronous timing of binocular saccades, but the pools of burst and integrator neurons in zebrafish larvae seem to be different (and maybe separate) for both eyes and horizontal directions, which leads to the observed ocular disconjugacies during saccades and postsaccadic drifts in the dark.

Electrophysiological recordings in humans reveal reduced location-specific attentional-shift activity prior to recentering saccades

Being able to effectively explore the visual world is of fundamental importance, and it has been suggested that the straight-ahead gaze position within the egocentric reference frame ("primary position") might play a special role in this context. In the present study we employed human electroencephalography (EEG) to examine neural activity related to the spatial guidance of saccadic eye movements. Moreover, we sought to investigate whether such activity would be modulated by the spatial relation of saccade direction to the primary gaze position (recentering saccades). Participants executed endogenously cued saccades between five equidistant locations along the horizontal meridian. This design allowed for the comparison of isoamplitude saccades from the same starting position that were oriented either toward the primary position (centripetal) or further away from it (centrifugal). By back-averaging time-locked to the saccade onset on each trial, we identified a parietally distributed, negative-polarity EEG deflection contralateral to the direction of the upcoming saccade. Importantly, this contralateral presaccadic negativity, which appeared to reflect the location-specific attentional guidance of the eye movement, was attenuated for recentering saccades relative to isoamplitude centrifugal saccades. This differential electrophysiological signature was paralleled by faster saccadic reaction times and was substantially more apparent when time-locking the data to the onset of the saccade rather than to the onset of the cue, suggesting a tight temporal association with saccade initiation. The diminished level of this presaccadic component for recentering saccades may reflect the preferential coding of the straight-ahead gaze position, in which both the eye-centered and head-centered reference frames are perfectly aligned and from which the visual world can be effectively explored.

Perisaccadic Gamma Modulation in Parkinson Disease Patients and Healthy Subjects

We quantified the anterior-posterior distribution of the gamma modulation index (GMI), an index of perisaccadic phasic modulation of the gamma (35-45 Hz) range electroencephalogram (EEG), in healthy human subjects and Parkinson disease (PD) patients. The EEG was recorded over the frontal, parietal, temporal and occipital sites in 11 idiopathic PD patients (age 50-70 years, four females), 4 age matched healthy volunteers (1 female) and 17 young healthy controls (age 21-30 years, four females) Eye movements were recorded with EOG and ISCAN camera. Subjects executed saccades to a mark at right and back to fixation point and vice versa. The saccades directed away from center/fixation (centrifugal CF) were analyzed. Two minutes of EEG were obtained from each subject for the two possible saccade types (centrifugal rightwards and leftwards at 15 degrees). Each perisaccadic EEG segment was analyzed using continuous wavelet transform for quantifying the power and time course of gamma EEG ranges for each saccade type. A three way ANOVA was used for statistical analysis. Perisaccadic GMI (peak intrasaccadic power divided by mean power) in healthy subjects was higher over the contralateral hemisphere to the saccade direction, for both centrifugal saccades at anterior, posterior and occipital recording sites. Contrary to the healthy subject GMI remained near one in PD, i.e., there was no evidence of intrasaccadic gamma power increase in PD patients.

High-Field fMRI Reveals Brain Activation Patterns Underlying Saccade Execution in the Human Superior Colliculus

BackgroundThe superior colliculus (SC) has been shown to play a crucial role in the initiation and coordination of eye- and head-movements. The knowledge about the function of this structure is mainly based on single-unit recordings in animals with relatively few neuroimaging studies investigating eye-movement related brain activity in humans.Methodology/Principal FindingsThe present study employed high-field (7 Tesla) functional magnetic resonance imaging (fMRI) to investigate SC responses during endogenously cued saccades in humans. In response to centrally presented instructional cues, subjects either performed saccades away from (centrifugal) or towards (centripetal) the center of straight gaze or maintained fixation at the center position. Compared to central fixation, the execution of saccades elicited hemodynamic activity within a network of cortical and subcortical areas that included the SC, lateral geniculate nucleus (LGN), occipital cortex, striatum, and the pulvinar.Conclusions/SignificanceActivity in the SC was enhanced contralateral to the direction of the saccade (i.e., greater activity in the right as compared to left SC during leftward saccades and vice versa) during both centrifugal and centripetal saccades, thereby demonstrating that the contralateral predominance for saccade execution that has been shown to exist in animals is also present in the human SC. In addition, centrifugal saccades elicited greater activity in the SC than did centripetal saccades, while also being accompanied by an enhanced deactivation within the prefrontal default-mode network. This pattern of brain activity might reflect the reduced processing effort required to move the eyes toward as compared to away from the center of straight gaze, a position that might serve as a spatial baseline in which the retinotopic and craniotopic reference frames are aligned.

The Saccadic Re-Centering Bias is Associated with Activity Changes in the Human Superior Colliculus

Being able to effectively explore our visual world is of fundamental importance, and it has been suggested that the straight-ahead gaze (primary position) might play a special role in this context. We employed fMRI in humans to investigate how neural activity might be modulated for saccades relative to this putative default position. Using an endogenous cueing paradigm, saccade direction and orbital starting position were systematically manipulated, resulting in saccades toward primary position (centripetal) and away from primary position (centrifugal) that were matched in amplitude, directional predictability, as well as orbital starting position. In accord with earlier research, we found that fMRI activity in the superior colliculus (SC), as well as in the frontal eye fields and the intraparietal sulcus, was enhanced contralateral to saccade direction across all saccade conditions. Furthermore, the SC exhibited a relative activity decrease during re-centering relative to centrifugal saccades, a pattern that was paralleled by faster saccadic reaction times. In contrast, activity within the cortical eye fields was not significantly modulated during re-centering saccades as compared to other saccade types, suggesting that the re-centering bias is predominantly implemented at a subcortical rather than cortical processing stage. Such a modulation might reflect a special coding bias facilitating the return of gaze to a default position in the gaze space in which retinotopic and egocentric reference frames are aligned and from which the visual world can be effectively explored.

Idiosyncratic variations in eye–head coupling observed in the laboratory also manifest during spontaneous behavior in a natural setting

The tendency to generate head movements during saccades varies from person to person. Head movement tendencies can be measured as subjects fixate sequences of illuminated targets, but the extent to which such measures reflect eye-head coupling during more natural behaviors is unknown. We quantified head movement tendencies in 20 normal subjects in a conventional laboratory experiment and in an outdoor setting in which the subjects directed their gaze spontaneously. In the laboratory, head movement tendencies during centrifugal saccades could be described by the eye-only range (EOR), customary ocular motor range (COMR), and the customary head orientation range (CHOR). An analogous EOR, COMR, and CHOR could be extracted from the centrifugal saccades executed in the outdoor setting. An additional six measures were introduced to describe the preferred ranges of eyes-in-head and head-on-torso manifest throughout the outdoor recording, i.e., not limited to the orientations following centrifugal saccades. These 12 measured variables could be distilled by factor analysis to one indoor and six outdoor factors. The factors reflect separable tendencies related to preferred ranges of visual search, head eccentricity, and eye eccentricity. Multiple correlations were found between the indoor and outdoor factors. The results demonstrate that there are multiple types of head movement tendencies, but some of these influence behavior across rather different experimental settings and tasks. Thus behavior in the two settings likely relies on common neural mechanisms, and the laboratory assays of head movement tendencies succeed in probing the mechanisms underlying eye-head coupling during more natural behaviors.

Saccadic Eye Movements Minimize the Consequences of Motor Noise

The durations and trajectories of our saccadic eye movements are remarkably stereotyped. We have no voluntary control over these properties but they are determined by the movement amplitude and, to a smaller extent, also by the movement direction and initial eye orientation. Here we show that the stereotyped durations and trajectories are optimal for minimizing the variability in saccade endpoints that is caused by motor noise. The optimal duration can be understood from the nature of the motor noise, which is a combination of signal-dependent noise favoring long durations, and constant noise, which prefers short durations. The different durations of horizontal vs. vertical and of centripetal vs. centrifugal saccades, and the somewhat surprising properties of saccades in oblique directions are also accurately predicted by the principle of minimizing movement variability. The simple and sensible principle of minimizing the consequences of motor noise thus explains the full stereotypy of saccadic eye movements. This suggests that saccades are so stereotyped because that is the best strategy to minimize movement errors for an open-loop motor system.

Discharge properties of saccade-related neurons in the primate fastigial oculomotor region.

To clarify the mechanisms by which the cerebellar fastigial oculomotor region (FOR) contributes to the control of saccadic eye movements, we recorded saccade-related FOR units in alert monkeys that made horizontal saccades between neighboring points of a three-by-three grid of target positions (16 degrees amplitude). As in previous studies, FOR units exhibited saccade-related bursts that occurred earlier for contralateral than for ipsilateral saccades. In addition, many FOR units reflected variations in the kinematic profiles of the saccades by exhibiting bursts with earlier onset and shorter peak latencies and higher peak discharge rates for fast as compared with slow saccades of the same amplitude. Moreover, reflecting systematic differences in saccade velocity rather than an influence of eye position itself, FOR bursts showed subtle but recurrent and, at the population level, statistically significant differences between centripetal and centrifugal saccades that closely paralleled the eye position dependency of saccadic dysmetria seen after FOR lesions. We conclude that the FOR output signal is not, as previously proposed, specifically related to the temporal properties of the saccade, but also contains information about saccade velocity. Moreover, the FOR output signal appears to change systematically depending on the actual kinematic properties of the saccade, in a way that would help to maintain saccadic accuracy.

Saccade-related neurons in the primate fastigial nucleus: what do they encode?

The cerebellar fastigial oculomotor region (FOR) and the overlying oculomotor vermis (OV) are involved in the control of saccadic eye movements, but nature and function of their saccade-related neuronal signals are not fully understood. There is controversy in at least two major aspects: first, lesion studies in OV/FOR reported eye-position-dependent dysmetria-with FOR lesions, centripetal saccades became more hypermetric than centrifugal saccades-suggesting that the cerebellum may compensate for orbital mechanics. However, single-unit studies failed to reveal corresponding eye-position dependencies in FOR saccade-related discharge patterns. Second, some single-unit studies reported precise correlation between burst and saccade duration in the FOR. However, others stated that FOR bursts were only weakly related to saccade properties. In an attempt to resolve these discrepancies, we recorded single FOR units in monkeys that made horizontal saccades (16 degrees ) from different starting positions. Sampling saccades of one fixed amplitude and application of an objective, computer-based burst-detection-routine allowed us to correlate burst parameters (onset latency, peak latency, peak amplitude, number of spikes, duration) and kinematic properties of individual saccades. FOR bursts were found to start and peak earlier and exhibit higher peak burst amplitudes for faster than for slower saccades of the same amplitude. While these correlations between FOR bursts and saccade properties were statistically significant for a minority of approximately 20-25% of individual units, the same effects were also predominant in the remainder of the neuronal sample and statistically significant on the population level. Neuronal activity was not significantly modulated by eye position itself. However, reflecting differences in saccade velocities but not an actual influence of eye position per se, FOR bursts for centripetal and centrifugal saccades exhibited subtle but systematic differences, which closely paralleled, and hence probably explain, the eye-position dependency of deficits observed after FOR inactivation. Our findings indicate that FOR signals reflect much of the kinematic properties of the saccade. Moreover, they are consistent with the idea that the FOR output is purposefully modified according to these kinematic properties to maintain saccadic accuracy.

Eye-head coordination and the variation of eye-movement accuracy with orbital eccentricity.

Different humans vary widely in the tendency to move the head during saccadic shifts in gaze. The reasons for this variation are unknown. Because combined eye-head movements are associated with a recentering of the eyes in the orbits, humans who are "head movers" tend to maintain the eyes within a narrower range than do non-head movers. We explored the possibility that variations in the ability to control eye movements at eccentric positions lead to variations in customary ocular motor range and, by extension, explain the variations in head-movement tendencies. We studied ten normal adults. In each, we measured the full-scale ocular motor range and customary ocular motor range (the eccentricity range within which the eye was found at the conclusion of eye- or eye-head saccades). We also determined the eye-only range, the orbital range within which the probability of a head movement accompanying a gaze shift was low. Customary, eye-only, and full-scale ranges spanned (mean +/-SD) 41.1+/-16.9 degrees, 30.2+/-18.8 degrees, and 92.8+/- 9.1 degrees, respectively. We then assessed variations in kinematics of several ocular motor behaviors as functions of eye eccentricity. The stable fixation range, defined by the range over which drift velocities were below 1 degree/s, spanned 81.1+/-11.2 degrees in the light and 69.5+/-21.5 degrees in the dark. The range over which the gains of the vestibulo-ocular reflex in the light and smooth pursuit approached their values at zero eccentricity spanned 66.3+/-7.1 degrees and 69.0+/-10.0 degrees, respectively. Small centrifugal saccades (5-10 degrees) tended to become either slowed or hypometric with increasing eccentricity. Sensitive to both slowing and hypometria, the ratio of peak gaze velocity to target shift amplitude was flat over a range spanning 65.7+/-14.9 degrees. Finally, the ranges over which the initial saccade placed the fovea upon the target averaged 35.5+/-10.7 degrees for eye-only saccades and 36.6+/-15.0 degrees for eye-head saccades. With the exception of the range of stable fixation in the light, the kinematic ranges were either unrelated or inconsistently related to full-scale range, indicating that the deterioration of eye movements with increasing ocular eccentricity is not a simple consequence of the eyes encountering the limits of their excursion. None of the kinematic ranges correlated positively with customary or eye-only range. Thus, while head movements may be orchestrated so as to maintain the eyes within a desired range, that range (and thus head movement tendencies) is not predicated upon the range of ocular eccentricity over which eye movements are accurately controlled.

Amplitude of human head movements associated with horizontal saccades.

Human saccades may or may not be associated with head movements. To date, little attention has been devoted to the mechanisms determining head movement recruitment and scaling. Normal human subjects made horizontal, centrifugal saccades along an encircling array of light-emitting diodes. Measurements of gaze, head, and eye-in-head angle were made at the conclusion of the head movement (or at the end of the eye movement in eye-only saccades). We found that head movement amplitude (deltaH) related in a simple fashion to the eye eccentricity that would have resulted if the gaze shift had been performed without a head movement. Plots of deltaH vs this predicted eye eccentricity (E(PRED)) had a central flat region in which gaze shifts were unaccompanied by head movements (the eye-only range) and two flanking lobes in which deltaH was a linear function of E(PRED) (the eye-head ranges). DeltaH correlated with EPRED better than with gaze shift amplitude, as would be expected if head movements were controlled so as to keep eye eccentricity within a particular range. Head movement tendencies were quantified by the width of the eye-only range, the slope of the eye-head range, and the width of the region within which the eye was likely to be found at the conclusion of the completed gaze-shifting behavior (the customary ocular motor range). The measures ranged widely in these normal subjects: 35.8+/-31.9 degrees for the eye-only range (mean+/-SD), 0.77+/-0.16 for the slope of the eye-head range, and 44.0+/-23.8 degrees for the customary ocular motor range. Yet for a given subject, the measurements were reproducible across experimental sessions, with the customary ocular motor range being the most consistent measure of the three. The form of the deltaH vs E(PRED) plots suggests that the neural circuitry underlying eye-head coordination carries out two distinct functions--gating the head movement and scaling the head movement. The reason for the large intersubject variability of head movement tendencies is unknown. It does not parallel intersubject differences in full-scale eye (in orbit) range or full-scale neck range.

Disconjugate adaptation of saccades: contribution of binocular and monocular mechanisms

We studied the effects of prism–induced disparity on static and intrasaccadic alignment in six normal human subjects. A ten diopter base–out prism, calling for convergence, was placed in front of the central field of the right eye, so that at the center the eye viewed through the prism; at left and right, outside the prism. During 15 min of training, subjects made repetitive saccades solely in the right field of vision (C-R-C sequence). This paradigm required relative divergence for centrifugal (C-R) saccades and relative convergence for centripetal (R-C) saccades, as well as increase of the amplitude for all saccades made by the right eye. We found that during training, all subjects incorporated the necessary change in alignment into the saccades. After training the resultant intrasaccadic disconjugacy persisted when tested during monocular viewing, indicating that motor learning had occurred. Subjects demonstrated increased divergence for C-R and increased convergence for R-C saccades, in accordance with the change acquired during adaptation to the prism. In addition, five subjects developed increased divergence for C-L saccades, for which they did not train. Smaller and less consistent divergence was also observed for L-C saccades. Changes in intrasaccadic alignment were accompanied by changes in the relative velocities of the two eyes’ saccades and slowing of the peak velocities in both eyes during training. Static alignment showed a general tendency toward convergence that did not parallel the changes in the intrasaccadic alignment, suggesting that saccade adaptation is system–specific. The pattern of transfer of the intrasaccadic disconjugacy to saccades in the untrained field and the changes in the relative speeds of the two eyes cannot be explained by monocular adjustment of the saccades. Our results indicate that both a binocular mechanism—saccade–vergence interaction—and monocular adaptation contribute to disconjugate adaptation of saccades.

Effects of lesions of the oculomotor vermis on eye movements in primate: saccades.

We studied the effects on saccades of ablation of the dorsal cerebellar vermis (lesions centered on lobules VI and VII) in three monkeys in which the deep cerebellar nuclei were spared. One animal, with a symmetrical lesion, showed bilateral hypometric horizontal saccades. Two animals, with asymmetrical lesions, showed hypometric ipsilateral saccades, and saccades to vertically positioned targets were misdirected, usually deviating away from the side to which horizontal saccades were hypometric. Postlesion, all animals showed an increase (2- to 5-fold) in trial-to-trial variability of saccade amplitude. They also showed a change in the ratio of the amplitudes of centripetal to centrifugal saccades (orbital-position effect); usually centrifugal saccades became smaller. In the two animals with asymmetrical lesions, for saccades in the hypometric direction, latencies were markedly increased (up to approximately 500 ms). There was also an absence of express and anticipatory saccades in the hypometric direction. When overall saccade latency was increased, centrifugal saccades became relatively more delayed than centripetal saccades. The dynamic characteristics of saccades were affected to some extent in all monkeys with changes in peak velocity, eye acceleration, and especially eye deceleration. There was relatively little effect of orbital position on saccade dynamics, however, with the exception of one animal that showed an orbital position effect for eye acceleration. In a double-step adaptation paradigm, animals showed an impaired ability to adaptively adjust saccade amplitude, though increased amplitude variability postlesion may have played a role in this deficit. During a single training session, however, the latency to corrective saccades-which had been increased postlesion-gradually decreased and so enabled the animal to reach the final position of the target more quickly. Overall, both in the early postlesion period and during recovery, changes in saccade amplitude and latency tended to vary together but not with changes in saccade dynamics or adaptive capability, both of which behaved relatively independently. These findings suggest that the cerebellum can adjust saccade amplitude and saccade dynamics independently. Our results implicate the cerebellar vermis directly in every aspect of the on-line control of saccades: initiation (latency), accuracy (amplitude and direction), and dynamics (velocity and acceleration) and also in the acquisition of adaptive ocular motor behavior.

Possible mechanisms of disorders in saccadic eye movements in parkinsonian patients

Electrooculogram recording was used to examine the centrifugal horizontal saccades through an angle of 40° in patients with Parkinson's disease and healthy subjects. The patients demonstrated prolongation of latency and duration, as well as appearance of multiple saccades. The mean values of latency in the right and left saccades were significantly longer in patients than in normal subjects. Although the saccade duration in patients did not differ significantly from that in normal subjects, this parameter tended to increase in value and dispersion. The courses of the vision-controlled saccade disturbances in parkinsonian patients are discussed and hypothesis is forwarded on the disorder mechanisms with particular attention to GABAergic system.

Abnormalities of ocular motility in myotonic dystrophy.

Are the oculomotor disturbances in myotonic dystrophy (MD), i.e. reduced smooth pursuit (SP) gain and reduced saccadic peak velocity (PV), of muscular or central origin? To answer this question the following two approaches were used. (i) The performance of SP was compared with the patient's ability to suppress the vestibulo-ocular reflex (VOR) visually (VOR suppression; VOR-S). In the latter task the SP system is involved, but the eyes hardly move within the orbits. A parallel impairment of SP and VOR-S would indicate a central dysfunction. (ii) Peak saccadic velocity was compared between two saccades performed to and fro in rapid succession. The intention was to measure any myotonic effect which might build up after the first saccade and slow down the second saccade. We studied 15 MD patients and 15 age-matched controls. Stimuli for slow eye responses consisted of sinusoidal horizontal rotations of the SP target and/or the vestibular rotation chair at frequencies between 0.1 and 0.8 Hz. Saccades were analysed in terms of PV. accuracy, duration and latency, comparing centripetal versus centrifugal saccades at short and long intersaccadic intervals (ISI; 400 ms and 900 ms, respectively). The SP gain was reduced in patients compared with the controls, the effect being most pronounced (32% less) at the highest stimulus frequency. Whereas VOR was normal in the patients, VOR-S was clearly impaired (50% worse at 0.8 Hz). Despite normal saccadic accuracy, peak saccadic velocity was significantly lower in the patient group (23% less for saccades of 12 degrees amplitude), similarly for centrifugal and centripetal saccades; all these differences were independent of the ISI. Latency was normal with centrifugal saccades, but was considerably increased with centripetal saccades at short ISI (67% longer compared with controls). The observation of a parallel degradation of SP and VOR-S in the patients is interpreted in terms of a central deficit in the SP pathways. Thus, it appears that slow eye movements were not impaired by muscle dystrophy and myotonia to a considerable degree in our patients. The increase in saccadic latency for centripetal saccades at the short ISI also reflects a central deficit. However, the observed slowing of saccades might have a myopathic or neural origin; a distinction was not possible at present. A myotonic origin of the saccade slowing seems unlikely, because the effect was independent of the presaccadic activation of the relaxing (antagonistic) eye muscle.

Immediate saccade amplitude disconjugacy induced by unequal images

We tested the ability of normal subjects to make changes in the conjugacy of their saccades. Subjects dichoptically viewed a grid the size of which was 10% larger in one eye. The grids were centred onto a flat screen at 57 cm or 1 m from the subject. Horizontal saccades immediately became larger in the eye viewing the larger grid. For some subjects this disconjugacy persisted even under subsequent monocular viewing. Such persistent changes occurred mainly in the field where the required disconjugacy was divergent for centrifugal saccades, convergent for centripetal saccades. Vertical saccades also developed compensatory disconjugacy; its amplitude was smaller but less variable. To explain these results we propose a fast associative learning mechanism that pairs peripheral disparity with saccades and is capable of producing saccade disconjugacy even in the absence of disparity. For horizontal saccades a secondary conditioning of monocular depth cues by the disparity would also be involved.

Effects of edrophonium on saccadic velocity in normal subjects and myasthenic and nonmyasthenic ocular palsies.

We measured saccadic peak velocities in 8 patients with myasthenia gravis, 9 patients with proven nonmyasthenic ocular palsies, and 3 controls. Patients followed a target moving to and from primary position at 1-second intervals for 8 minutes. We measured the amplitudes and velocities of centrifugal saccades at the start of the task, after 3 minutes of the task (fatigue) and 1 minute after receiving IV edrophonium. The effects of fatigue, though prominent in some myasthenic patients, did not distinguish between the groups. However, edrophonium increased saccadic peak velocities in myasthenic patients but decreased them in both controls and nonmyasthenic patients. Analysis of saccades by amplitude bins showed that these changes in peak velocity reflected shifts in the velocity-amplitude relationship.

Saccadic burst neurons in the fastigial nucleus are not involved in compensating for orbital nonlinearities

1. To test whether the cerebellum is involved in compensating for orbital nonlinearities, we recorded discharges of saccadic burst neurons in the fastigial oculomotor region (FOR) during both centrifugal and centripetal saccades in two trained macaque monkeys. 2. We also investigated the metrics of centrifugal and centripetal saccades with the same amplitude while output signals from the fastigial nucleus were blocked by muscimol, an agonist of inhibitory neurotransmitter gamma-aminobutyric acid (GABA), injected into the FOR. 3. We studied discharges of 32 fastigial neurons that were inhibited by microstimulation of the oculomotor vermis. These neurons exhibited unique burst responses during contralaterally and ipsilaterally directed saccades, as shown in our previous report. The discharge pattern, the peak burst frequency, the burst lead time, and the burst duration were consistent, regardless of initial eye position. 4. The muscimol injection produced hypermetric saccades toward the injection side and hypometric saccades to the opposite side, regardless of whether saccade was centripetally or centrifugally directed. 5. These findings suggest that the FOR is not involved in the compensation of saccade metrics for orbital nonlinearities.

Role of the caudal fastigial nucleus in saccade generation. II. Effects of muscimol inactivation.

1. We studied the effect of temporarily inhibiting neurons in the caudal fastigial nucleus in two rhesus macaques trained to make saccades to jumping targets. We placed injections of the gamma-aminobutyric acid (GABA) agonist muscimol unilaterally or bilaterally at sites in the caudal fastigial nucleus where we had recorded saccade-related neurons a few minutes earlier. 2. Unilateral injections (n = 9) made horizontal saccades to the injected side hypermetric and those to the other side hypometric (mean gain of 1.37 and 0.61, respectively, for 10 degrees target steps, and 1.26 and 0.81 for 20 degrees target steps; normal saccade gain was 0.96). Saccades to vertical targets showed a small but significant hypermetria and curved strongly toward the side of the injection. The trajectories and end points of all targeted saccades were more variable than normal. 3. After unilateral injections, centripetal saccades were slightly larger than centrifugal saccades (mean gains for ipsilateral saccades were 1.42 and 1.31, respectively, for 10 degrees target steps, and 1.37 and 1.15 for 20 degrees target steps). 4. Unilateral injections increased the average acceleration of ipsilateral saccades and decreased the acceleration of contralateral saccades. Injections decreased both the acceleration and deceleration of vertical saccades. 5. After dysmetric saccades, monkeys acquired the target with an abnormally high number of hypometric corrective saccades. Injection increased the average number of corrective saccades from 0.6 to 2.1 after 10 degrees horizontal target steps and from 0.8 to 2.1 after 20 degrees steps. The size of each successive corrective saccade in a series decreased, and the latency from the previous corrective saccade increased. 6. Bilateral injections (n = 2) of muscimol, in which we injected first into the left caudal fastigial nucleus and then, within 30 min, into the right, made all saccades hypermetric (mean gain for 10 degrees right, left, up, and down saccades was 1.18, 1.49, 1.43, and 1.10, respectively). Paradoxically, bilateral injection decreased both saccade acceleration and deceleration. Saccade trajectories and end points were more variable than normal. 7. To account for the effects of our injections, we propose that the activity of caudal fastigial neurons on one side normally helps to decelerate ipsilateral saccades and helps to accelerate contralateral saccades by influencing the feedback loop of the saccade burst generator in the brain stem. Without caudal fastigial activity the brain stem burst generator produces hypermetric, variable saccades. We therefore also propose that the influence of caudal fastigial neurons on the burst generator makes saccades more consistent and accurate.(ABSTRACT TRUNCATED AT 400 WORDS)