Saccades induced electrically from the dorsomedial frontal cortex: evidence for a head-centered representation

The amplitude and direction of saccadic eye movements evoked electrically from the dorsomedial frontal cortex (DMFC) of monkeys vary with starting eye position. This observation has been used to argue that the DMFC codes saccadic eye movements in head-centered coordinates. Whether the amplitude and direction of the evoked saccades are also affected by changes in head position has never been demonstrated. Such a result would argue against a head-centered representation, and instead would suggest a representation anchored to another body part. Tests were conducted on rhesus monkeys to determine whether changing the position of the head with respect to the trunk or changing the position of the head with respect to the gravitational axis alters saccadic parameters. The amplitude and direction of saccadic eye movements remained invariant to such manipulations. These findings confirm the claim that the DMFC encodes saccadic eye movements in head-centered coordinates.     

Eye-head coordination in labyrinthine-defective humans

Eye-head coordination during saccadic gaze shifts normally relies on vestibular information. A vestibulo-saccadic reflex (VSR) is thought to reduce the eye-in-head saccade to account for current head movement, and the vestibulo-ocular reflex (VOR) stabilizes postsaccadic gaze while the head movement is still going on. Acute bilateral loss of vestibular function is known to cause overshoot of gaze saccades and postsaccadic instability. We asked how patients suffering from chronic vestibular loss adapt to this situation. Eye and head movements were recorded from six patients and six normal control subjects. Subjects tracked a random sequence of horizontal target steps, with their heads (1) fixed in primary position, (2) free to move, or (3) preadjusted to different head-to-target offsets (to provoke head movements of different amplitudes). Patients made later and smaller head movements than normals and accepted correspondingly larger eye eccentricities. Targeting accuracy, in terms of the mean of the signed gaze error, was better in patients than in normals. However, unlike in normals, the errors of patients exhibited a large scatter and included many overshoots. These overshoots cannot be attributed to the loss of VSR because they also occurred when the head was not moving and were diminished when large head movements were provoked. Patients' postsaccadic stability was, on average, almost as good as that of normals, but the individual responses again showed a large scatter. Also, there were many cases of inappropriate postsaccadic slow eye movements, e.g., in the absence of concurrent head movements, and correction saccades, e.g., although gaze was already on target. Performance in patients was affected only marginally when large head movements were provoked. Except for the larger lag of the head upon the eye, the temporal coupling of eye and head movements in patients was similar to that in normals. Our findings show that patients with chronic vestibular loss regain the ability to make functionally appropriate gaze saccades. We assume, in line with previous work, three main compensatory mechanisms: a head movement efference copy, an active cervico-ocular reflex (COR), and a preprogrammed backsliding of the eyes. However, the large trial-to-trial variability of targeting accuracy and postsaccadic stability indicates that the saccadic gaze system of patients does not regain the high precision that is observed in normals and which appears to require a vestibular head-in-space signal. Moreover, this variability also permeates their gaze performance in the absence of head movements.     

Nucleotide sequences and functional characterization of two tobacco UAG suppressor tRNA(Gln) isoacceptors and their genes

The hypothesis was tested that peak velocity of saccadic eye movements in visual motor tasks varies with variables related to energy regulation. The hypothesis is based on the cognitive-energetical performance model of Sanders. An experimental paradigm was developed in which saccadic peak velocity of task-relevant eye movements is measured while a choice reaction task is carried out. Confounding factors of saccadic amplitude and movement direction were controlled. The task was designed in such a way that in each trial subjects performed a target saccade towards an imperative stimulus and a return saccade after the manual response back to the centre of the screen. For both types of saccades the experimental variables were foreperiod duration (short versus long), knowledge of results (with versus without), postsaccadic demand (low versus high) and time on task (five 30-min intervals). In two experiments, there are main and interaction effects of the task variables on peak saccadic velocity. Return saccades are slower than target saccades, but not in the case of high postsaccadic demand. Knowledge of results increases peak saccadic velocity, but more so for return than for target saccades. Time on task leads to a decrease in peak saccadic velocity, which is much stronger for return than for target saccades; furthermore this effect is more pronounced after short than after long foreperiods. Peak saccadic velocity is changed within seconds. The results support the hypothesis. Peak saccadic velocity of task related eye movements reflects energy regulation during task performance. The paradigm will be developed as a diagnostic tool in workload measurement.     

Programming saccadic eye movements.

This article addresses questions about the preparatory processes that immediately precede saccadic eye movements. Saccade latencies were measured in a task in which subjects were provided partial advance information about the spatial location of a target fixation. In one experiment, subjects were faster in initiating saccades when they knew either the direction or amplitude of the required movement in advance compared to a condition with equal uncertainty about the number of potential saccade targets but without knowledge of the parameters required to execute the movement. These results suggest that the direction and amplitude for an upcoming saccade were calculated separately, and not in a fixed serial order. In another experiment, subjects appear to have programmed the saccades more holistically—with computations of direction and amplitude parameters occurring simultaneously. The implications of these results for models of eye movement preparation are discussed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A modification of eye-head coordination by CNS disease

When a subject, seated and facing ahead, was asked to look toward one side, the result was a combined movement of the eyes and head. Normal subjects began the eye movement just before the onset of head movement; 4 neurologic patients who showed abnormalities in eye movements (saccades that tended to be smaller in amplitude and lower in velocity than those of the control subjects) regularly began eye movement after the onset of head movement. Thus the initiation of the head rotation was not as much retarded in these patients as that of eye movement. Amplitudes of the movements were reduced in the patients, but this change too was less for the head than for the eyes. Because the amplitude and velocity of the head movement were less affected in the patient group, the relative contribution of the head to the total gaze shift was increased. It appears as if, when the oculomotor system is affected, the head can assume a leading role in the initiation and execution of gaze shifts.     

Saccade amplitude influences pointing movement kinematics

The amplitude of open-loop pointing movements to step displacements in target position is influenced by the amplitude of simultaneously produced saccadic eye movements. The time course over which this occurs was addressed in the present study. Analysis of the pointing kinematics showed that saccade amplitude had its effect only during the initial acceleration of the hand. Moreover, the magnitude of the initial acceleration was correlated with the difference in the onset times of the eye and hand movements: the closer in time the saccadic and pointing responses were initiated the larger the initial hand acceleration. Taken together, these results demonstrate that saccades influence the kinematics of simultaneously produced limb movements but only over a limited time frame.     

Infant attention and the development of smooth pursuit tracking.

The effect of attention on smooth pursuit and saccadic tracking was studied in infants at 8, 14, 20, and 26 weeks of age. A small rectangle was presented moving in a sinusoidal pattern in either the horizontal or vertical direction. Attention level was distinguished with a recording of heart rate. There was an increase across age in overall tracking, the gain of the smooth pursuit eye movements, and an increase in the amplitude of compensatory saccades at faster tracking speeds. One age change was an increase in the preservation of smooth pursuit tracking ability as stimulus speed increased. A second change was the increasing tendency during attentive tracking to shift from smooth pursuit to saccadic tracking when the stimulus speed increased to the highest velocities. This study shows that the development of smooth pursuit and targeted saccadic eye movements is closely related to the development of sustained attention in this age range. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Contribution of the rostral fastigial nucleus to the control of orienting gaze shifts in the head-unrestrained cat

The implication of the caudal part of the fastigial nucleus (cFN) in the control of saccadic shifts of the visual axis is now well established. In contrast a possible involvement of the rostral part of the fastigial nuceus (rFN) remains unknown. In the current study we investigated in the head-unrestrained cat the contribution of the rFN to the control of visually triggered saccadic gaze shifts by measuring the deficits after unilateral muscimol injection in the rFN. A typical gaze dysmetria was observed: gaze saccades directed toward the inactivated side were hypermetric, whereas those with an opposite direction were hypometric. For both movement directions, gaze dysmetria was proportional to target retinal eccentricity and could be described as a modified gain in the translation of visual signals into eye and head motor commands. Correction saccades were triggered when the target remained visible and reduced the gaze fixation error to 2.7 +/- 1.3 degrees (mean +/- SD) on average. The hypermetria of ipsiversive gaze shifts resulted predominantly from a hypermetric response of the eyes, whereas the hypometria of contraversive gaze shifts resulted from hypometric responses of both eye and head. However, even in this latter case, the eye saccade was more affected than the motion of the head. As a consequence, for both directions of gaze shift the relative contributions of the eye and head to the overall gaze displacement were altered by muscimol injection. This was revealed by a decreased contribution of the head for ipsiversive gaze shifts and an increased head contribution for contraversive movements. These modifications were associated with slight changes in the delay between eye and head movement onsets. Inactivation of the rFN also affected the initiation of eye and head movements. Indeed, the latency of ipsiversive gaze and head movements decreased to 88 and 92% of normal, respectively, whereas the latency of contraversive ones increased to 149 and 145%. The deficits induced by rFN inactivation were then compared with those obtained after muscimol injection in the cFN of the same animals. Several deficits differed according to the site of injection within the fastigial nucleus (tonic orbital eye rotation, hypermetria of ipsiversive gaze shifts and fixation offset, relationship between dysmetria and latency of contraversive gaze shifts, postural deficit). In conclusion, the present study demonstrates that the rFN is involved in the initiation and the control of combined eye-head gaze shifts. In addition our findings support a functional distinction between the rFN and cFN for the control of orienting gaze shifts. This distinction is discussed with respect to the segregated fastigiofugal projections arising from the rFN and cFN.     

Task dependent variations of ocular lateropulsion in Wallenberg''s syndrome

The eye movements of a patient with a left lateral medullary infarct (Wallenberg's syndrome) were recorded using the scleral search coil in magnetic field technique. When asked to look at spontaneously appearing targets, saccades to the left were generally accurate but those to the right reached the target by multiple step refixation saccades. Large amplitude rightward saccades were possible between two continuously visible targets or when making voluntary saccades in the dark. Vertical saccades, up or down, between spontaneously appearing targets were always associated with a leftward eye movement (lateropulsion). Voluntary vertical saccades between continuously visible targets showed that upward movements had left lateropulsion but downward movements were normal. Vertical voluntary saccades in the dark were oblique, upward saccades showing left lateropulsion and downward saccades rightward deviation. The aberrant horizontal components of normal oblique saccades. Possibly impaired assessment of verticality with incorrect eye position information produced by the infarct accounts for the lateropulsion in saccades in Wallenberg's syndrome.     

Role of the oculomotor vermis in generating pursuit and saccades: effects of microstimulation

We studied the eye movements evoked by applying small amounts of current (2-50 microA) within the oculomotor vermis of two monkeys. We first compared the eye movements evoked by microstimulation applied either during maintained pursuit or during fixation. Smooth, pursuitlike changes in eye velocity caused by the microstimulation were directed toward the ipsilateral side and occurred at short latencies (10-20 ms). The amplitudes of these pursuitlike changes were larger during visually guided pursuit toward the contralateral side than during either fixation or visually guided pursuit toward the ipsilateral side. At these same sites, microstimulation also often produced abrupt, saccadelike changes in eye velocity. In contrast to the smooth changes in eye velocity, these saccadelike effects were more prevalent during fixation and during pursuit toward the ipsilateral side. The amplitude and type of evoked eye movements could also be manipulated at single sites by changing the frequency of microstimulation. Increasing the frequency of microstimulation produced increases in the amplitude of pursuitlike changes, but only up to a certain point. Beyond this point, the value of which depended on the site and whether the monkey was fixating or pursuing, further increases in stimulation frequency produced saccadelike changes of increasing amplitude. To quantify these effects, we introduced a novel method for classifying eye movements as pursuitlike or saccadelike. The results of this analysis showed that the eye movements evoked by microstimulation exhibit a distinct transition point between pursuit and saccadelike effects and that the amplitude of eye movement that corresponds to this transition point depends on the eye movement behavior of the monkey. These results are consistent with accumulating evidence that the oculomotor vermis and its associated deep cerebellar nucleus, the caudal fastigial, are involved in the control of both pursuit and saccadic eye movements. We suggest that the oculomotor vermis might accomplish this role by altering the amplitude of a motor error signal that is common to both saccades and pursuit.     

Accuracy of visually and memory-guided antisaccades in man

Primary saccades to remembered targets are generally not precise, but rather undershoot target position. The major source of this saccadic undershoot may be (a) a memory-related process or (b) a poor spatial resolution in those processes which transfer the retinotopic target information into an intermediate memory-linked representation of space. The aim of this study was to investigate whether distortions of eye positions in the antisaccade task, which are characterized by inherent co-ordinate transformation processes, may completely account for the spatial inaccuracies of memory-guided antisaccades. The results show that the spatial inaccuracy of primary and secondary eye movements in the visually guided antisaccade task was comparable to that in the memory-guided antisaccade task. In both conditions, the direction error component was less dysmetric than the amplitude error component. Secondary eye movements were significantly corrective. This increase of eye position accuracy was achieved by reducing the amplitude error only. It is concluded from this study that at least some of the distortion of memory-guided saccades is due to inaccuracies in the sensorimotor co-ordinate transformations.     

Eye tracking dysfunction in schizophrenia: Characterization of component eye movement abnormalities, diagnostic specificity, and the role of attention.

To characterize oculomotor components and diagnostic specificity of eye tracking abnormalities in schizophrenia, we examined a large consecutively admitted series of psychotic patients and matched controls. The most common abnormality in schizophrenic patients was low gain (slow) pursuit eye movements (47% of cases). Pursuit and saccadic eye movement abnormalities were no more severe in schizophrenic Ss than in those with affective psychoses, except that high rates of catch-up saccades were unique to schizophrenic Ss (17% of cases). These findings indicate that impaired pursuit eye movements are a major cause of eye tracking impairments in schizophrenia, that tracking dysfunctions commonly occur in affective psychoses, and that markedly high rates of catch-up saccades during eye tracking may be specific to schizophrenia. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Detection of cortical activities on eye movement using functional magnetic resonance imaging

Cortical activity during eye movement was examined with functional magnetic resonance imaging. Horizontal saccadic eye movements and smooth pursuit eye movements were elicited in normal subjects. Activity in the frontal eye field was found during both saccadic and smooth pursuit eye movements at the posterior margin of the middle frontal gyrus and in parts of the precentral sulcus and precentral gyrus bordering the middle frontal gyrus (Brodmann's areas 8, 6, and 9). In addition, activity in the parietal eye field was found in the deep, upper margin of the angular gyrus and of the supramarginal gyrus (Brodmann's areas 39 and 40) during saccadic eye movement. Activity of V5 was found at the intersection of the ascending limb of the inferior temporal sulcus and the lateral occipital sulcus during smooth pursuit eye movement. Our results suggest that functional magnetic resonance imaging is useful for detecting cortical activity during eye movement.     

Decrease in saccadic performance after many visually guided saccadic eye movements in monkeys

PURPOSE: To investigate the influence of repeated saccades and of background illumination on the metrics and dynamics of visually guided targeting saccades. METHODS: Eye movements were measured by magnetic search coil technique in seven trained monkeys (Macaca mulatta) while they performed many visually guided saccades in the dark or in dim background light. RESULTS: After 2000 to 7000 saccades in the dark, peak eye velocity on the average decreased by 20%, saccadic gain decreased slightly by 4.5%, and saccadic latency increased by 15%. All parameters also showed increased variability. In contrast, when testing was done in dim light, there was little to no change in average saccadic metrics and latency. CONCLUSIONS: The changes in saccadic metrics and dynamics in the dark do not reflect a change of the ocular plant but may reflect a change in the cortical or cerebellar influences on the brain stem burst generator linked to the monkeys attentional state. Background light mostly prevents this change.     

Gain adaptation of eye and head movement components of simian gaze shifts

Gain adaptation of eye and head movement components of simian gaze shifts. J. Neurophysiol. 78: 2817-2821, 1997. To investigate the site of gaze adaptation in primates, we reduced the gain of large head-restrained gaze shifts made to 50 degrees target steps by jumping the target 40% backwards during a targeting saccade and then tested gain transfer to the eye- and head-movement components of head-unrestrained gaze shifts. After several hundred backstep trials, saccadic gain decreased by at least 10% in 8 of 13 experiments, which were then selected for further study. The minimum saccadic gain decrease in these eight experiments was 12.8% (mean = 18.4%). Head-unrestrained gaze shifts to ordinary 50 degrees target steps experienced a gain reduction of at least 9.3% (mean = 14.9%), a mean gain transfer of 81%. Both the eye and head components of the gaze shift also decreased. However, average head movement gain decreased much more (22.1%) than eye movement gain (9.2%). Also, peak head velocity generally decreased significantly (20%), but peak eye velocity either increased or remained constant (average increase of 5.6%). However, the adapted peak eye and head velocities were appropriate for the adapted, smaller gaze amplitudes. Similar dissociations in eye and head metrics occurred when head-unrestrained gaze shifts were adapted directly (n = 2). These results indicated that head-restrained saccadic gain adaptation did not produce adaptation of eye movement alone. Nor did it produce a proportional gain change in both eye and head movement. Rather, normal eye and head amplitude and velocity relations for a given gaze amplitude were preserved. Such a result could be explained most easily if head-restrained adaptation were realized before the eye and head commands had been individualized. Therefore, gaze adaptation is most likely to occur upstream of the creation of separate eye and head movement commands.     

Anticipatory saccades during smooth pursuit eye movements and familial transmission of schizophrenia

BACKGROUND: Smooth pursuit eye movement (SPEM) abnormalities are a putative marker of genetic risk for schizophrenia. Accurate SPEM performance requires the subject to activate neural systems responsible for smooth pursuit tracking, while simultaneously suppressing activity of neurons responsible for saccadic movements that would move the eye ahead of the target. This study examined whether specific aspects of SPEM dysfunction cosegregate with genetic risk in parents of schizophrenic probands. METHODS: Eighteen probands and their parents had SPEM recorded. Parents with an ancestral history of schizophrenia were hypothesized to be more likely than their spouses without such a history to carry a genetic risk for schizophrenia. RESULTS: Ten families had a single parent with a positive ancestral history for schizophrenia. The frequency of anticipatory saccades, which were mostly small, and the fraction of total eye movement that they represented were the only measures that differentiated the more likely genetic carrier parents in these families from their spouses and age-matched normals. CONCLUSIONS: Failure to suppress saccadic anticipation of target motion during smooth pursuit appears an aspect of SPEM dysfunction related to presumed genetic risk for schizophrenia.     

When is it best to hear a verb? The effects of the timing and focus of verb models on children''s learning of verbs

Recent neurophysiological studies of the saccadic ocular motor system have lent support to the hypothesis that this system uses a motor error signal in retinotopic coordinates to direct saccades to both visual and auditory targets. With visual targets, the coordinates of the sensory and motor error signals will be identical unless the eyes move between the time of target presentation and the time of saccade onset. However, targets from other modalities must undergo different sensory-motor transformations to access the same motor error map. Because auditory targets are initially localized in head-centered coordinates, analyzing the metrics of saccades from different starting positions allows a determination of whether the coordinates of the motor signals are those of the sensory system. We studied six human subjects who made saccades to visual or auditory targets from a central fixation point or from one at 10 degrees to the right or left of the midline of the head. Although the latencies of saccades to visual targets increased as stimulus eccentricity increased, the latencies of saccades to auditory targets decreased as stimulus eccentricity increased. The longest auditory latencies were for the smallest values of motor error (the difference between target position and fixation eye position) or desired saccade size, regardless of the position of the auditory target relative to the head or the amplitude of the executed saccade. Similarly, differences in initial eye position did not affect the accuracy of saccades of the same desired size. When saccadic error was plotted as a function of motor error, the curves obtained at the different fixation positions overlapped completely. Thus, saccadic programs in the central nervous system compensated for eye position regardless of the modality of the saccade target, supporting the hypothesis that the saccadic ocular motor system uses motor error signals to direct saccades to auditory targets.     

Memory-guided saccadic eye movements: effects of cerebellar disease

We compared the accuracy of oblique, memory-guided saccades if the eye is stationary or moves horizontally during the memory period. We studied 11 patients with cerebellar disease and 11 age-matched control subjects. Normal subjects showed similar accuracy of saccades for both conditions. In contrast, all patients showed greater errors if the eye moved horizontally during the memory period; however, errors of both vertical and horizontal components of memory-guided saccades were similar. Thus, inaccuracy of memory-guided saccades could not be simply attributed to failure to internally monitor change in horizontal gaze during the memory period. Instead, we propose that the greater saccadic errors which occurred when gaze changed during the memory period reflected a disruption of predictive mechanisms governing eye movements.     

Ocular motor abnormalities in Huntington's disease

We review here the eye movements in patients with Huntington's disease (HD), concentrating upon saccades as they show the most prominent abnormalities. Inability to suppress reflexive glances to suddenly appearing novel visual stimuli and delayed initiation of voluntary saccades, including predictive saccades, are early and consistent findings. These two abnormalities can be interpreted in the context of a model, based upon the idea that the frontal lobes and basal ganglia contribute more to the control of voluntary than to reflexive types of saccades. Most patients eventually also show slow saccades but they are most prominent when the disease is early-onset. Slowing of saccades may reflect involvement of both the higher-level cerebral centers that trigger saccades and the areas in the brain stem that produce premotor saccade commands. The study of eye movements in HD has led to a fruitful interaction between basic science and clinical investigation, and has served as a paradigm for examining higher-level defects in saccadic eye movement control in patients with various degenerative, neurological diseases or with focal cerebral hemispheral lesions.     

Gaze-related activity of putative inhibitory burst neurons in the head-free cat

1. Previous studies in the cat have demonstrated that output neurons of the superior collicular as well as brain stem omnipause neurons have discharges that are best correlated, not with the trajectory of the eye in the head but, with the trajectory of the visual axis in space (gaze = eye-in-head + head-in-space) during rapid orienting coordinated eye and head movements. In this study, we describe the gaze-related activity of cat premotor "inhibitory burst neurons" (IBNs) identified on the basis of their position relative to the abducens nucleus. 2. The firing behavior of IBNs was studied during 1) saccades made with the head stationary, 2) active orienting combined eye-head gaze shifts, and 3) passive movements of the head on the body. IBN discharges were well correlated with the duration and amplitude of saccades made when the head was stationary. In both head-free paradigms, the behavior of cat IBNs differed from that of previously described primate "saccade bursters". The duration of their burst was better correlated with gaze than saccade duration, and the total number of spikes in a burst was well correlated with gaze amplitude and generally poorly correlated with saccade amplitude. The behavior of cat IBNs also differed from that of previously described primate "gaze bursters". The slope of the relationship between the total number of spikes and gaze amplitude observed during head-free gaze shifts was significantly lower than that observed during head-fixed saccades. 3. These studies suggest that cat IBNs do not fit into the categories of gaze-bursters or saccade-bursters that have been described in primate studies.(ABSTRACT TRUNCATED AT 250 WORDS)