The superior colliculus (SC) provides signals for the generation of
saccades via a direct pathway to the brain stem burst generator (BG). In
addition, it sends saccade-related activity to the BG indirectly through the
cerebellum via a relay in the nucleus reticularis tegmenti pontis (NRTP).
Lesions of the oculomotor vermis, lobules VIc and VII, and inactivation of the
caudal fastigial nucleus, the cerebellar output nucleus to which it projects,
produce saccade dysmetria but have little effect on saccade peak velocity and
duration. We expected similar deficits from inactivation of the NRTP. Instead,
injections as small as 80 nl into the NRTP first slowed ipsiversive saccades and
then gradually reduced their amplitudes. Postinjection saccades had slower peak
velocities and longer durations than preinjection saccades with similar
amplitudes. Contraversive saccades retained their normal kinematics. When the
gains of ipsiversive saccades to 10° target steps had fallen to
their lowest values (0.28 ± 0.19; mean ± SD;
n = 10 experiments), the gains of contraversive
saccades to 10° target steps had decreased very little (0.82
± 0.11). Eventually, ipsiversive saccades did not exceed
5°, even to 20° target steps. Moreover, these small
remaining saccades apparently were made with considerable difficulty because
their latencies increased substantially. When ipsiversive saccade gain was at
its lowest, the gain and kinematics of vertical saccades to 10°
target steps exhibited inconsistent changes. We argue that our injections did
not compromise the direct SC pathway. Therefore these data suggest that the
cerebellar saccade pathway does not simply modulate BG activity but is required
for horizontal saccades to occur at all.
Studying saccades can illuminate the more complex decision-making processes required for everyday movements. The double-step task, in which a target jumps to two successive locations before the subject has time to react, has proven a powerful research tool to investigate the brain’s ability to program sequential responses. We asked how patients with a range of cerebellar disorders responded to the double-step task, specifically, whether the initial saccadic response made to a target is affected by the appearance of a second target jump. We also sought to determine whether cerebellar patients were able to make corrective saccades towards the remembered second target location, if it were turned off soon after presentation. We tested saccades to randomly interleaved single- and double-step target jumps to eight locations on a circle. Patient’s initial responses to double-step stimuli showed 50% more error than saccades to single target jumps, and often, they failed to make a saccade to the first target jump. The presence of a second target jump had similar, but smaller effects in control subjects (error increased by 18%). During memory-guided double-step trials, both patients and controls made corrective saccades in darkness to the remembered location of the second jump. We conclude that in cerebellar patients, the second target jump interferes with programming of the saccade to the first target jump of a double-step stimulus; this defect highlights patients’ impaired ability to respond appropriately to sudden, conflicting changes in their environment. Conversely, since cerebellar patients can make corrective memory-guided saccades in darkness, they retain the ability to remember spatial locations, possibly due to non-retinal neural signals (corollary discharge) from cerebral hemispheric areas concerned with spatial localization.
Saccades; double-step; dysmetria; cerebellum, fastigial nucleus; efference copy
Two patients with well defined lesions of midline cerebellar structures including the fastigial nuclei on both sides presented with saccadic hypermetria but well preserved smooth pursuit eye movements. This is a remarkable finding as the oculomotor vermis (lobules VI, VII) and the fastigial nucleus are known to play a part in the control of smooth pursuit eye movements and unilateral fastigial lesions lead to a smooth pursuit deficit to the contralateral side (besides saccadic dysmetria). The results are discussed with regard to related deficits seen in patients with Wallenberg's syndrome and after lesions of the pontine reticular formation.
Saccade-generating burst neurons (BN) are inhibited by omnipause neurons (OPN), except during saccades. OPN activity pauses before saccade onset and resumes at the saccade end. Microstimulation of OPN stops saccades in mid-flight, which shows that OPN can end saccades. However, OPN pause duration does not correlate well with saccade duration, and saccades are normometric after OPN lesions. We tested whether OPN were responsible for stopping saccades both in late-onset Tay–Sachs, which causes premature saccadic termination, and in individuals with cerebellar hypermetria. We studied gaze shifts between two targets at different distances aligned on one eye, which consist of a disjunctive saccade followed by vergence. High-frequency conjugate oscillations during the vergence movements that followed saccades were present in all subjects studied, indicating OPN silence. Thus, mechanisms other than OPN discharge (e.g., cerebellar caudal fastigial nucleus–promoting inhibitory BN discharge) must contribute to saccade termination.
Tay–Sachs disease; saccades; omnipause neurons; fastigial nucleus; Müller paradigm
An intact cerebellum is a prerequisite for optimal ocular motor performance. The cerebellum fine-tunes each of the subtypes of eye movements so they work together to bring and maintain images of objects of interest on the fovea. Here we review the major aspects of the contribution of the cerebellum to ocular motor control. The approach will be based on structural–functional correlation, combining the effects of lesions and the results from physiologic studies, with the emphasis on the cerebellar regions known to be most closely related to ocular motor function: (1) the flocculus/paraflocculus for high-frequency (brief) vestibular responses, sustained pursuit eye movements, and gaze holding, (2) the nodulus/ventral uvula for low-frequency (sustained) vestibular responses, and (3) the dorsal oculomotor vermis and its target in the posterior portion of the fastigial nucleus (the fastigial oculomotor region) for saccades and pursuit initiation.
saccade; vestibular; pursuit; flocculus; paraflocculus; nodulus; vermis; fastigial
OBJECTIVE--To determine the roles of the putamen and pallidum in ocular motor control. METHODS--Eye movements were recorded electro-oculographically in nine patients with bilateral focal lesions affecting the lentiform nucleus, and in 12 age matched control subjects. Reflexive visually guided saccades (gap task), antisaccades, memorised sequences of saccades, memory guided saccades (with visual input only, and with both visual and vestibular inputs), and predictive saccades (with and without gap) were studied. RESULTS--Latency and accuracy of visually guided saccades were normal. The percentage of errors in the antisaccade task and latency of correct antisaccades did not differ significantly from the results of controls. The percentage of errors in saccade sequences was significantly increased. Accuracy of the two types of memory guided saccades was impaired bilaterally. The percentage of predictive saccades was significantly decreased when a gap existed, but unchanged without a gap, compared with controls. Therefore, saccades made immediately in response to an external target (reflexive visually guided saccades and antisaccades) were performed without difficulty, whereas those requiring an internal representation of such a target (such as memory guided saccades, predictive saccades, and saccade sequences) were performed with significant disturbances. CONCLUSIONS--The lentiform nucleus influences the cortical areas involved in the control of saccades when the experimental paradigm requires the use of an internal representation of the target for correct planning and execution of the ensuing saccade.
We investigated how saccade target selection by humans and macaque monkeys reacts to unexpected changes of the image. This was explored using double step and search step tasks in which a target, presented alone or as a singleton in a visual search array, steps to a different location on infrequent, random trials. We report that human and macaque monkey performance are qualitatively indistinguishable. Performance is stochastic with the probability of producing a compensated saccade to the final target location decreasing with the delay of the step. Compensated saccades to the final target location are produced with latencies relative to the step that are comparable to or less than the average latency of saccades on trials with no target step. Noncompensated errors to the initial target location are produced with latencies less than the average latency of saccades on trials with no target step. Noncompensated saccades to the initial target location are followed by corrective saccades to the final target location following an intersaccade interval that decreases with the interval between the target step and the initiation of the noncompensated saccade. We show that this pattern of results cannot be accounted for by a race between two stochastically independent processes producing the saccade to the initial target location and another process producing the saccade to the final target location. However, performance can be accounted for by a race between three stochastically independent processes – a GO process producing the saccade to the initial target location, a STOP process interrupting that GO process, and another GO process producing the saccade to the final target location. Furthermore, if the STOP process and second GO process start at the same time, then the model can account for the incidence and latency of mid-flight corrections and rapid corrective saccades. This model provides a computational account of saccade production when the image changes unexpectedly.
saccade; race model; latency; double step; search step; decision making
The objective was to describe in multiple sclerosis, a
cerebellar eye movement syndrome that resulted from an acute episode of
inflammatory demyelination. Contrapulsion is an ocular motor disturbance characterised by a triad of (1) hypermetric saccadic eye
movements in a direction opposite from a precisely localised lesion
within a specific white matter pathway, the uncinate fasciculus, at the
level of the superior cerebellar peduncle (SCP); (2) hypometric saccades towards the side of the lesion; (3) oblique saccades directed
away from the side of the lesion on attempted vertical saccades.
Infrared oculography was used to demonstrate the
characteristic features of contrapulsion in two patients with multiple sclerosis.
Brain MRI showed lesions within the region of the uncinate
fasciculus and superior cerebellar peduncle in both patients. Eye
movement recordings showed saccadic hypermetria away from the side of
the lesion and saccadic hypometria towards the side of the lesion. The
hypometria decomposed into a series of stepwise movements as the eye
approached the target. Oblique saccades directed away from the side of
the lesion were seen on attempted vertical saccades.
In conclusion, ocular contrapulsion can be seen in patients
with multiple sclerosis and results from a lesion in the region of the
SCP, involving the uncinate fasciculus.
Slow saccades are often found in degenerative ataxia. Experimental studies have shown that horizontal saccades are generated in the paramedian pontine reticular formation and that lesions in this area produce slow saccades. Based on these findings, saccade slowing should be a frequent feature of olivopontocerebellar atrophy, a type of cerebellar degeneration with prominent involvement of the pons. To test this hypothesis, saccade velocity was measured in 31 patients with autosomal dominant cerebellar ataxia (ADCA) and 17 patients with idiopathic cerebellar ataxia (IDCA). Saccade velocity was reduced in most patients with ADCA whereas it was normal in IDCA although olivopontocerebellar atrophy occurred in both groups. Saccade velocities correlated with pontine size in ADCA but not in IDCA. The data disprove the hypothesis that saccadic slowing is a clinical hallmark of olivopontocerebellar atrophy. Instead, only patients with ADCA and morphological features of olivopontocerebellar atrophy have slow saccades.
Motor impairments have been found to be a significant clinical feature associated with autism and Asperger’s disorder (AD) in addition to core symptoms of communication and social cognition deficits. Motor deficits in high-functioning autism (HFA) and AD may differentiate these disorders, particularly with respect to the role of the cerebellum in motor functioning. Current neuroimaging and behavioral evidence suggests greater disruption of the cerebellum in HFA than AD. Investigations of ocular motor functioning have previously been used in clinical populations to assess the integrity of the cerebellar networks, through examination of saccade accuracy and the integrity of saccade dynamics. Previous investigations of visually guided saccades in HFA and AD have only assessed basic saccade metrics, such as latency, amplitude, and gain, as well as peak velocity. We used a simple visually guided saccade paradigm to further characterize the profile of visually guided saccade metrics and dynamics in HFA and AD. It was found that children with HFA, but not AD, were more inaccurate across both small (5°) and large (10°) target amplitudes, and final eye position was hypometric at 10°. These findings suggest greater functional disturbance of the cerebellum in HFA than AD, and suggest fundamental difficulties with visual error monitoring in HFA.
autism; Asperger’s disorder; saccades; eye movements; Verbal Comprehension Index
The cerebellum may monitor motor commands and through internal feedback corrects for anticipated errors. Saccades provide a test of this idea because these movements are completed too quickly for sensory feedback to be useful. Earlier we reported that motor commands that accelerate the eyes toward a constant amplitude target showed variability. Here, we demonstrate that this variability is not random noise, but is due to the cognitive state of the subject. Healthy people showed within saccade compensation for this variability with commands that arrived later in the same saccade. However, in people with cerebellar damage, the same variability resulted in dysmetria. This ability to correct for variability in the motor commands that initiated a saccade was a predictor of each subject’s ability to learn from endpoint errors. In a paradigm in which a target on the horizontal meridian jumped vertically during the saccade (resulting in an endpoint error), the adaptive response exhibited two timescales: a fast timescale that learned quickly from endpoint error but had poor retention, and a slow timescale that learned slowly but had strong retention. With cortical cerebellar damage, the fast timescale of adaptation was effectively absent, but the slow timescale was less impaired. Therefore the cerebellum corrects for variability in the motor commands that initiate saccades within the same movement via an adaptive response that not only exhibits strong sensitivity to previous endpoint errors, but also rapid forgetting.
saccade adaptation; forward model; SCA-6; fatigue; saccade repetition; saccade kinematics; repetition attenuation
The cerebellar vermis (lobules VI-VII) has been implicated in both postmortem and neuroimaging studies of autism spectrum disorders (ASD). This region maintains the consistent accuracy of saccadic eye movements and plays an especially important role in correcting systematic errors in saccade amplitudes such as those induced by adaptation paradigms. Saccade adaptation paradigms have not yet been used to study ASD. Fifty-six individuals with ASD and 53 age-matched healthy controls performed an intrasaccadic target displacement task known to elicit saccadic adaptation reflected in an amplitude reduction. The rate of amplitude reduction and the variability of saccade amplitude across 180 adaptation trials were examined. Individuals with ASD adapted slower than healthy controls, and demonstrated more variability of their saccade amplitudes across trials prior to, during and after adaptation. Thirty percent of individuals with ASD did not significantly adapt, whereas only 6% of healthy controls failed to adapt. Adaptation rate and amplitude variability impairments were related to performance on a traditional neuropsychological test of manual motor control. The profile of impaired adaptation and reduced consistency of saccade accuracy indicates reduced neural plasticity within learning circuits of the oculomotor vermis that impedes the fine-tuning of motor behavior in ASD. These data provide functional evidence of abnormality in the cerebellar vermis that converges with previous reports of cellular and gross anatomic dysmorphology of this brain region in ASD.
Saccade accuracy is maintained by adaptive mechanisms that continually modify saccade amplitude to reduce dysmetria. Previous studies suggest that adaptation occurs upstream of the caudal fastigial nucleus (CFN), the output of the oculomotor cerebellar vermis but downstream from the superior colliculus (SC). The nucleus reticularis tegmenti pontis (NRTP) is a major source of afferents to both the oculomotor vermis and the CFN and in turn receives direct input from the SC. Here we examine the activity of NRTP neurons in four rhesus monkeys during behaviorally induced changes in saccade amplitude to assess whether their discharge might reveal adaptation mechanisms that mediate changes in saccade amplitude. During amplitude decrease adaptation (average, 22%), the gradual reduction of saccade amplitude was accompanied by an increase in the number of spikes in the burst of 19/34 neurons (56%) and no change for 15 neurons (44%). For the neurons that increased their discharge, the additional spikes were added at the beginning of the saccadic burst and adaptation also delayed the peak-firing rate in some neurons. Moreover, after amplitude reduction, the movement fields changed shape in all 15 open field neurons tested. Our data show that saccadic amplitude reduction affects the number of spikes in the burst of more than half of NRTP neurons tested, primarily by increasing burst duration not frequency. Therefore adaptive changes in saccade amplitude are reflected already at a major input to the oculomotor cerebellum.
Saccadic eye movements are often grouped in pre-programmed sequences. The mechanism underlying the generation of each saccade in a sequence is currently poorly understood. Broadly speaking, two alternative schemes are possible: first, after each saccade the retinotopic location of the next target could be estimated, and an appropriate saccade could be generated. We call this the goal updating hypothesis. Alternatively, multiple motor plans could be pre-computed, and they could then be updated after each movement. We call this the motor updating hypothesis. We used McLaughlin’s intra-saccadic step paradigm to artificially create a condition under which these two hypotheses make discriminable predictions. We found that in human subjects, when sequences of two saccades are planned, the motor updating hypothesis predicts the landing position of the second saccade in two-saccade sequences much better than the goal updating hypothesis. This finding suggests that the human saccadic system is capable of executing sequences of saccades to multiple targets by planning multiple motor commands, which are then updated by serial subtraction of ongoing motor output.
eye movements; memory; plasticity
In the classic double-step paradigm, subjects are required to make a
saccade to a visual target that is briefly presented at one location and then
shifted to a new location before the subject has responded. The saccades in this
situation are “reflexive” in that they are made in
response to the appearance of the target itself. In the present experiments we
adapted the double-step paradigm to study “voluntary”
saccades. For this, several identical targets were always visible and subjects
were given a cue to indicate that they should make a saccade to one of them.
This cue was then changed to indicate another of the targets before the subject
had responded: double-cue (DC) paradigm. The saccadic eye movements in our DC
paradigm had many features in common with those in the double-step paradigm and
we show that apparent differences can be attributed to the spatio-temporal
arrangements of the cues/ targets rather than to any intrinsic differences in
the programming of these two kinds of eye movements. For example, a feature of
our DC paradigm that is not seen in the usual double-step paradigm is that the
second cue could cause transient delays of the initial saccade, and these delays
still occurred when the second cue was reflexive—provided that it was
at the fovea (as in our DC paradigm) and not in the periphery (as in the usual
double-step paradigm). Thus, the critical factor for the delay was the retinal
(foveal) location of the second cue/target—not whether it was
cognitive or reflexive—and we argue that the second cue/target is
here acting as a distractor. We conclude that the DC paradigm can be used to
study the programming of voluntary saccades in the same way that the double-step
paradigm can be used to study reflexive saccades.
Saccadic eye movements; Double-step paradigm; Cognitive cues
In this study, we have used the double-step paradigm to test saccadic gain adaptation during monocular viewing in one normal monkey, two monkeys with exotropia, and one monkey with esotropia. In this paradigm, the target for the saccade is displaced during the saccade, resulting in a consistent visual error. Studies in normal humans and monkeys have shown that the brain responds to this consistent visual error by gradually changing saccade gain. Using this technique, we were able to elicit adaptation in both the viewing eye and the nonviewing eye in the normal monkey and in monkeys with strabismus. The rate of adaptation was not significantly different in the viewing and nonviewing eyes in the normal and strabismic monkeys. The magnitude of adaptation as calculated by a percentage change in gain was also not significantly different in the viewing and the nonviewing eyes in the normal and strabismic monkeys. Our data show that animals with strabismus retain the ability to elicit a conjugate adaptation of saccades using this mechanism. We also suggest that the double-step paradigm elicits a conjugate adaptation of saccades whether the animal is viewing monocularly (our studies) or binocularly (data published in literature).
Saccades under four specific test conditions (visually guided, visually remembered, vestibular remembered, and cervical remembered) were studied in a 38 year old man with ocular dysmetria due to an angioma of the dorsal cerebellar vermis. The aim of the study was to investigate if the saccadic disorder was specific to certain subsets of saccades elicited by different sensory modalities. The experiments showed that initial saccades were equally hypermetric in all four conditions and that final eye position was normal in all memory guided saccade tests. Eye movements differed after the initial saccade, however. Whereas corrective saccades were seen in most visually guided and visually remembered experiments, postsaccadic centripetal drifts were documented in non-visual (vestibular and cervical) remembered saccades. These results indicate that the cerebellar vermis modulates the amplitude of the initial saccade (pulse size of saccadic innervation) independently of the saccadic task. The finding that post-saccadic drift never occurred when saccades were programmed using visual positional information suggests that the dorsal vermis may participate in the process of pulse step integration of saccades elicited by memorised vestibulo-cervical information.
Three signals are used to visually localize targets and stimulate saccades: (1) retinal-location signals for intended saccade amplitude, (2) sensory-motor transform (SMT) of retinal signals to extra-ocular muscle innervation, (3) estimates of eye position from extra-retinal signals. We investigated effects of adapting saccade amplitude to a double-step change in target location on perceived direction. In a flashed-pointing task, subjects pointed an unseen hand at a briefly displayed eccentric target without making a saccade. In a sustained-pointing task, subjects made a horizontal saccade to a double-step target. One second after the second step, they pointed an unseen hand at the final target position. After saccade-shortening adaptation, there was little change in hand-pointing azimuth toward the flashed target suggesting that most saccade adaptation was caused by changes in SMT. After saccade-lengthening adaptation, there were small changes in hand-pointing azimuth to flashed targets, indicating that 1/3 of saccade adaptation was caused by changes in estimated retinal location signals and 2/3 by changes in SMT. The sustained hand-pointing task indicated that estimates of eye position adapted inversely with changes of SMT. Changes in perceived direction resulting from saccade adaptation are mainly influenced by extra-retinal factors with a small retinal component in the lengthening condition.
eye movements; saccade; adaptation; extra-retinal; retinal; arm-hand movements; visuomotor control
Adaptation of saccadic eye movements provides an excellent motor learning model to study theories of neuronal plasticity. When primates make saccades to a jumping target, a backward step of the target during the saccade can make it appear to overshoot. If this deception continues for many trials, saccades gradually decrease in amplitude to go directly to the back-stepped target location. We used this adaptation paradigm to evaluate the Marr-Albus hypothesis that such motor learning occurs at the Purkinje (P-) cell of the cerebellum. We recorded the activity of identified P-cells in the oculomotor vermis, lobules VIc and VII. After determining the on and off error directions of a P-cell’s complex spike activity, we determined whether its saccade-related simple spike (SS) activity changed during saccade adaptation in those two directions. Before adaptation, 57 of 61 P-cells exhibited a clear burst, pause or a combination of both for saccades in one or both directions. Sixty-two percent of all cells, including 2 of the 4 initially unresponsive ones, behaved differently for saccades whose size changed because of adaptation than for saccades of similar sizes gathered before adaptation. In at least 42% of these, the changes were appropriate to decrease saccade amplitude based on our current knowledge of cerebellum and brain stem saccade circuitry. Changes in activity during adaptation were not compensating for the potential fatigue associated with performing many saccades. Therefore, many P-cells in the oculomotor vermis exhibit changes in SS activity specific to adapted saccades and therefore appropriate to induce adaptation.
Saccade; Adaptation; Motor Learning; Purkinje Cell; Primate; plasticity; Cerebellum; Motor Control; Oculomotor
The ability to adapt a variety of motor acts to compensate for persistent natural or artificially induced errors in movement accuracy requires the cerebellum. For adaptation of the rapid shifts in the direction of gaze called saccades, the oculomotor vermis (OMV) of the cerebellum must be intact. We disrupted the neural circuitry of the OMV by manipulating gamma aminobutyric acid (GABA), the transmitter used by many neurons in the vermis. We injected either muscimol, an agonist of GABA, to inactivate the OMV or bicuculline, an antagonist, to block GABA inhibition. Our previous study showed that muscimol injections cause ipsiversive saccades to fall short of their targets, whereas bicuculline injections cause most ipsiversive saccades to overshoot. Once these dysmetrias had stabilized, we tested the monkey’s ability to adapt saccade size to intra-saccadic target steps that produced a consistent saccade under-shoot (amplitude increase adaptation required) or overshoot (amplitude decrease adaptation required). Injections of muscimol abolished the amplitude increase adaptation of ipsiversive saccades, but had either no effect, or occasionally facilitated, amplitude decrease adaptation. In contrast, injections of bicuculline impaired amplitude decrease adaptation and usually facilitated amplitude increase adaptation. Neither drug produced consistent effects on the adaptation of contraversive saccades. Taken together, these data suggest that OMV activity is necessary for amplitude increase adaptation, whereas amplitude decrease adaptation may involve the inhibitory circuits within the OMV.
monkey; cerebellum; saccade adaptation; oculomotor vermis; muscimol; bicuculline; GABA
In a typical short-term saccadic adaptation protocol, the target moves intra-saccadically either toward (gain-down) or away (gain-up) from initial fixation, causing the saccade to complete with an endpoint error. A central question is how the motor system adapts in response to this error: are the motor commands changed to bring the eyes to a different goal, akin to a remapping of the target, or is adaptation focused on the processes that monitor the ongoing motor commands and correct them midflight, akin to changes that act via internal feedback? Here, we found that in the gain-down paradigm, the brain learned to produce a smaller amplitude saccade by altering the saccade's trajectory. The adapted saccades had reduced peak velocities, reduced accelerations, shallower decelerations, and increased durations compared to a control saccade of equal amplitude. These changes were consistent with a change in an internal feedback that acted as a forward model. On the other hand, in the gain-up paradigm the brain learned to produce a larger amplitude saccade with trajectories that were identical to those of control saccades of equal amplitude. Therefore, whereas the gain-down paradigm appeared to induce adaptation via an internal feedback that controlled saccades midflight, gain-up induced adaptation primarily via target remapping. Our simulations explained that for each condition, the specific adaptation produced a saccade that brought the eyes to the target with the smallest motor costs.
Saccade adaptation; saccade kinematics; forward models; optimal control; computational neuroscience; Sensorimotor
There is strong evidence that the brain can use an internally generated copy of motor commands, a corollary discharge, to guide rapid sequential saccades. Much of this evidence comes from the double-step paradigm: after two briefly flashed visual targets have disappeared, the subject makes two sequential saccades to the targets. Recent studies on the monkey revealed that amplitude variations of the first saccade led to compensation by the second saccade, mediated by a corollary discharge. Here, we investigated whether such saccade-by-saccade compensation occurs in humans, and we made three new observations. First, we replicated previous findings from the monkey: following first saccade amplitude variations, the direction of the second saccade compensated for the error. Second, the change in direction of the second saccade followed variations in vertical as well as horizontal first saccades although the compensation following horizontal saccades was significantly more accurate. Third, by examining oblique saccades, we are able to show that first saccade variations are compensated by adjustment in saccade amplitude in addition to direction. Together, our results demonstrate that it is likely that a corollary discharge in humans can be used to adjust both saccade direction and amplitude following variations in individual saccades.
Corollary Discharge; Saccadic Eye Movement; Movement Vector
The recruitment of extra-vestibular mechanisms to assist a deficient angular vestibulo-ocular reflex (aVOR) during ipsilesional head rotations is well established and includes saccades of reduced latency that occur in the direction of the lesioned aVOR, termed compensatory saccades (CS). Less well known is the functional relevance of these unique saccades. Here we report a 42 y.o. male diagnosed with right unilateral vestibular hypofunction due to vestibular neuronitis who underwent a vestibular rehabilitation program including gaze stabilization exercises. After three weeks, he had a significant improvement in his ability to see clearly during head rotation. Our data show a reduction in the recruitment and magnitude of CS as well as improved peripheral aVOR gain (eye velocity/head velocity) and retinal eye velocity. Our data suggest an inverse, dynamic relationship between the recruitment of CS and the gain of the aVOR.
Vestibular neuronitis; rehabilitation; vestibulo-ocular reflex; saccades
Methods: A visually guided saccade task was performed by 46 high-functioning individuals with autism with and without delayed language acquisition, and 104 age and IQ matched healthy individuals.
Results: Individuals with autism had increased variability in saccade accuracy, and only those without delayed language development showed a mild saccadic hypometria. Neither autistic group showed a disturbance in peak saccade velocity or latency.
Conclusions: The observed saccadic abnormalities suggest a functional disturbance in the cerebellar vermis or its output through the fastigial nuclei, consistent with reported cerebellar histopathology in autism. The pattern of mild hypometria and variable saccade accuracy is consistent with chronic rather than acute effects of cerebellar vermis lesions reported in clinical and non-human primate studies, as might be expected in a neurodevelopmental disorder. The different patterns of oculomotor deficits in individuals with autism with and without delayed language development suggest that pathophysiology at the level of the cerebellum may differ depending on an individual's history of language development.
A stimulus that is flashed around the time of a saccade tends to be mislocalized in the direction of the saccade target. Our question is whether the mislocalization is related to the position of the saccade target within the image or to the gaze position at the end of the saccade. We separated the two with a visual illusion that influences the perceived distance to the target of the saccade and thus saccade endpoint without affecting the perceived position of the saccade target within the image. We asked participants to make horizontal saccades from the left to the right end of the shaft of a Müller-Lyer figure. Around the time of the saccade, we flashed a bar at one of five possible positions and asked participants to indicate its location by touching the screen. As expected, participants made shorter saccades along the fins-in (<–>) configuration than along the fins-out (>–<) configuration of the figure. The illusion also influenced the mislocalization pattern during saccades, with flashes presented with the fins-out configuration being perceived beyond flashes presented with the fins-in configuration. The difference between the patterns of mislocalization for bars flashed during the saccade for the two configurations corresponded quantitatively with a prediction based on compression towards the saccade endpoint considering the magnitude of the effect of the illusion on saccade amplitude. We conclude that mislocalization is related to the eye position at the end of the saccade, rather than to the position of the saccade target within the image.