Saccadic instabilities in albinism without nystagmus

Albinism effects a surprising manipulation of the visual pathway in which some of the normally uncrossed axons of the temporal retina instead cross at the chiasm. An expected consequence of this misrouting is that subjects with albinism will have difficulty in specifying the targets of saccades. Usually albinos have nystagmus so the stability of their saccadic eye movements is not readily accessible, but some albinos do not have nystagmus. In these subjects it was found that they had frequent saccadic intrusions, the sizes of which were correlated with velocities of steady drifts in fixations (r = 0.802, P < 0.05). An explanation for the correlation between the amplitudes of the intrusions and the velocities of the drifts is that it is due to a common failure in the development of a saccadic system which is responsible for converting a given retinal displacement into a matching eye movement, with the extent of the failure reflecting the severity of the misrouting.     

Disconnection of parietal and occipital access to the saccadic oculomotor system

Summary The experiment explored the networks through which signals arising from visual areas of cortex control saccadic eye movements. Electrical stimulation of the inferior parietal and the occipital cortex (here termed the posterior eye fields) normally evokes saccadic eye movements. We replicated previous reports that these evoked eye movements ceased after large tectal ablations. This initial finding suggested that the posterior eye fields depended on a single route of access to the saccade generator, one descending through the superior colliculus (SC). On closer examination, the critical lesion appeared to be one which removed the SC and cut efferents from the frontal eye field (FEE) coursing nearby. Subsequently we confirmed that eye movements evoked from the posterior eye fields ceased after cooling the SC, or cutting its efferents- but only when one of these procedures was combined with FEF ablation. Thus, visual signals from the occipital and inferior parietal cortex have more than one, but perhaps only two routes of access to the oculomotor system. One passes through the superior colliculus, the other through the frontal eye field. Ancillary experiments revealed that inferior parietal and FEF ablations, alone or combined, do not disrupt saccades evoked from the occipital lobe. Striate and prestriate areas can therefore use their own direct input to the SC or to the basal ganglia to drive saccadic eye movements.Abbreviations for Nuclei C interstitial, of Cajal - CL central lateral - CM centromedianum - D Darkschewitsch - HL lateral habenula - IC inferior colliculus - LD lateral dorsal - LP lateral posterior nucl - MD medial dorsal - MG medial geniculate - MR midbrain reticular formation - NPA nuc. of the pretectal area - NPC nuc. of the posterior commissure - PC posterior commissure - PF parafascicular - PI inferior pulvinar - PL lateral pulvinar - PM medial pulvinar - PO oral pulvinar - R red - SG suprageniculate - SL sublentiform - SN substantia nigra - VPL ventral posterolateral - VPM ventral posteromedial - ZI zona incerta - III oculomotor - IV trochlear Supported by grants NIH EY02941 and EY04005, NSF BNS8603915     

Expression of a re-centering bias in saccade regulation by superior colliculus neurons

In previous studies of saccadic eye movement reaction time, the manipulation of initial eye position revealed a behavioral bias that facilitates the initiation of movements towards the central orbital position. An interesting hypothesis for this re-centering bias suggests that it reflects a visuo-motor optimizing strategy, rather than peripheral muscular constraints. Given that the range of positions that the eyes can take in the orbits delimits the extent of visual exploration by head-fixed subjects, keeping the eyes centered in the orbits may indeed permit flexible orienting responses to engaging stimuli. To investigate the influence of initial eye position on central processes such as saccade selection and initiation, we examined the activity of saccade-related neurons in the primate superior colliculus (SC). Using a simple reaction time paradigm wherein an initially fixated visual stimulus varying in position was extinguished 200 ms before the presentation of a saccadic target, we studied the relationship between initial eye position and neuronal activation in advance of saccade initiation. We found that the magnitude of the early activity of SC neurons, especially during the immediate pre-target period that followed the fixation stimulus disappearance, was correlated with changes in initial eye position. For the great majority of neurons, the pre-target activity increased with changes in initial eye position in the direction opposite to their movement fields, and it was also strongly correlated with the concomitant reduction in reaction time of centripetal saccades directed within their movement fields. Taking into account the correlation with saccadic reaction time, the relationship between neuronal activity and initial eye position remained significant. These results suggest that eye-position-dependent changes in the excitability of SC neurons could represent the neural substrate underlying a re-centering bias in saccade regulation. More generally, the low frequency SC pre-target activity could use eccentric eye position signals to regulate both when and which saccades are produced by promoting the emergence of a high frequency burst of activity that can act as a saccadic command. However, only saccades initiated within ~200 ms of target presentation were associated with SC pre-target activity. This eye-dependent pre-target activation mechanism therefore appears to be restricted to the initiation of saccades with relatively short reaction times, which specifically require the integrity of the SC. Electronic Publication     

Stimulus intensity modifies saccadic reaction time and visual response latency in the superior colliculus

Performance in a reaction time task can be strongly influenced by the physical properties of the stimuli used (e.g., position and intensity). The reduction in reaction time observed with higher-intensity visual stimuli has been suggested to arise from reduced processing time along the visual pathway. If this hypothesis is correct, activity should be registered in neurons sooner for higher-intensity stimuli. We evaluated this hypothesis by measuring the onset of neural activity in the intermediate layers of the superior colliculus while monkeys generated saccades to high or low-intensity visual stimuli. When stimulus intensity was high, the response onset latency was significantly reduced compared to low-intensity stimuli. As a result, the minimum time for visually triggered saccades was reduced, accounting for the shorter saccadic reaction times (SRTs) observed following high-intensity stimuli. Our results establish a link between changes in neural activity related to stimulus intensity and changes to SRTs, which supports the hypothesis that shorter SRTs with higher-intensity stimuli are due to reduced processing time.     

Collicular involvement in a saccadic colour discrimination task

Summary We have recorded the neural activity of single superior colliculus (SC) neurons in monkeys engaged in a saccadic target/nontarget discrimination task based on a colour cue. Since correct execution of this task probably depends on cortical signal processing, our experiments are of interest for getting a better insight in the problem of how cortical and subcortical signals, relevant for the visual guidance of saccades, are combined. The experiments were designed to distinguish between two extreme possibilities: 1) The crucial cortical signal affects the saccadic system at or above the level of the SC movement-related cells (serial hypothesis); 2) The colour-based target information bypasses the motor colliculus and affects the saccadic system at a level more downstream (bypass hypothesis). Under conditions where the saccadic system had to select a green target stimulus and to ignore the red nontarget spot, the saccade-related activity in SC visuomotor neurons remained as tightly coupled to the metrics of the saccade as it was in a simple spot-detection task. Since the saccade-related activity of these cells appeared to be based on colour information, we conclude that our data corroborate the serial hypothesis. The initial activity after stimulus onset appeared to be colour nonopponent in all neurons. In some cells the neural activity was quantitatively slightly different for the green target and the red nontarget. Since these minor differences were colour rather than motor response dependent, they were probably not part of the target-selection process. These data suggest the possibility that the decision as to which saccade should be made was largely imposed upon the SC visuomotor cells by an external source. We discuss various possibilities for the origin of the putative intervening signal which orders a saccade by causing a burst in the appropriate SC visuomotor neurons.     

Differential effects of target probability on saccade latencies in gap and warning tasks

Saccade latencies are significantly reduced by extinguishing a foveal fixation stimulus before the appearance of a saccade target. It has been shown recently that this fixation offset effect (FOE) can be modulated by varying target probability. Cortico-collicular top-down effects have been assumed to mediate this strategic FOE modulation. Here, we have investigated strategic FOE modulation in 14 healthy human subjects performing gap and warning tasks. In the former task, the central fixation point was extinguished 200 ms before target onset. In the latter task, the central fixation point changed its colour 200 ms before target onset, but remained illuminated until the target appeared. Target probability was varied block-wise between 25 and 75%. In both tasks, mean latencies decreased with increasing target probability. However, in contrast with what can be expected from preceding studies, we found no differential modulation of mean latencies by target probability between tasks. Instead, we observed differential probability-dependent changes in latency distributions. In the gap task, discrete changes of saccade latencies were found, with a probability-dependent change in frequency of express and regular latencies. By contrast, in the warning task a shift of the entire latency distribution towards longer latencies with low target probability was found. We conclude that strategic modulation of saccade latencies by target probability may be mediated by two distinct neural mechanisms. Selection of either mechanism seems to depend critically on activation of the fixation system.     

Four-week test-retest stability of individual differences in the saccadic CNV, two saccadic task parameters, and selected neuropsychological tests

The aim of the present study was the comparative assessment of the 4-week test-retest stabilities of the saccadic CNV (sCNV) and saccadic reaction times (SRT) during the execution of pro- and antisaccades, as well as the stability of RT during execution of two neuropsychological tests of alertness and S-R incompatibility. Prosaccades were elicited under the 200-ms gap and overlap conditions, antisaccades under the overlap condition (64 trials each). The EEG was recorded from 25 channels with a DC amplifier (MES, Munich). Data of 20 healthy participants were statistically analyzed. We found high test-retest correlations for all SRT (.76 < or = r(tt) < or = .88) and neuropsychological (.62 < or = r(tt) < or = .88) measures. For the sCNV, coefficients ranging between .58 (pro/gap) and .77 (anti/overlap) were obtained. Whereas SRT were significantly faster during the second than during the first session, group means for the saccadic CNV were stable across the sessions. Our results suggest high 4-week stability of individual differences in SRT, and moderate to good stabilities of saccadic CNV amplitudes. Our results recommend these "traitlike" measures to be used in individual differences research.     

Contextual abnormalities of saccadic inhibition in children with attention deficit hyperactivity disorder

Abnormalities of executive function are observed consistently in children with attention-deficit hyperactivity disorder (ADHD), and it is hypothesised that these arise because of disruption to a behavioural inhibition system. Executive and inhibitory functions were compared between unmedicated and medicated children with ADHD (combined type), age-matched healthy children and healthy adults. Executive functions were measured using a test of spatial working memory shown previously to be sensitive to ADHD and to stimulant medication. Inhibitory functions were measured using an ocular motor paradigm that required individuals to use task context to control the release of fixation. Context was set according to the probability that a target would appear at either of the two locations. In one block, targets appeared on 80% of trials. In the other block, targets appeared on 20% of trials. The ability to control the release of fixation was inferred from the fixation offset effect (FOE), or the difference in saccade latency when the current fixation is offset 200 ms prior to the onset of the saccade target (gap condition), compared with when there is no offset (overlap condition). Although the healthy children made more errors on the spatial working memory task than the healthy adults, there was no difference between the two groups in their ability to control fixation using context. Both showed a larger FOE when target probability was low. As expected, the unmedicated ADHD group made more errors on the spatial working memory test than the healthy children, although spatial working memory performance was normal in the medicated ADHD group. However, both the unmedicated and medicated ADHD groups were unable to modulate the FOE according to context, and this was due to their inability to voluntarily inhibit saccades when there was a low target probability. These data suggest that the context-based modulation of fixation release is not controlled by the same systems that control executive function. Furthermore, deficits in executive function and inhibitory control appear independent in children with ADHD.     

Minimal synaptic delay in the saccadic output pathway of the superior colliculus studied in awake monkey

The synaptic organization of the saccade-related neuronal circuit between the superior colliculus (SC) and the brainstem saccade generator was examined in an awake monkey using a saccadic, midflight electrical-stimulation method. When microstimulation (50–100 A, single pulse) was applied to the SC during a saccade, a small, conjugate contraversive eye movement was evoked with latencies much shorter than those obtained by conventional stimulation. Our results may be explained by the tonic inhibition of premotor burst neurons (BNs) by omnipause neurons that ceases during saccades to allow BNs to burst. Thus, during saccades, signals originating from the SC can be transmitted to motoneurons and seen in the saccade trajectory. Based on this hypothesis, we estimated the number of synapses intervening between the SC and motoneurons by applying midflight stimulation to the SC, the BN area, and the abducens nucleus. Eye position signals were electronically differentiated to produce eye velocity to aid in detecting small changes. The mean latencies of the stimulus-evoked eye movements were: 7.9±1.0 ms (SD; ipsilateral eye) and 7.8±0.9 ms (SD; contralateral eye) for SC stimulation; 4.8±0.5 ms (SD; ipsilateral eye) and 5.1±0.7 ms (SD; contralateral eye) for BN stimulation; and 3.6±0.4 ms (SD; ipsilateral eye) and 5.2±0.8 ms (SD; contralateral eye) for abducens nucleus stimulation. The time difference between SC- and BN-evoked eye movements (about 3 ms) was consistent with a disynaptic connection from the SC to the premotor BNs.     

Relationship between directed visual attention and saccadic reaction times

Summary Saslow (1967) and Fischer and Ramsperger (1984) found that saccadic reaction time (SRT) depends on the interval between the fixation point offset and the target onset. Using a continuously visible fixation point, we asked whether a similar function would be obtained if subjects attended to a peripherally viewed point extinguished at variable intervals before or after the target onset. The interval was varied between -500ms (i.e., attention stimulus offset after saccade target onset = overlap trials) and 500ms (i.e., attention stimulus offset before saccade target onset = gap trials). The results show a constant mean SRT of about 240 ms for overlap trials, and a U-shaped function with a minimum of 140 ms, at a gap duration of 200 ms, for gap trials. These findings suggest that saccadic latencies do not depend on the cessation of fixation per se, but rather on the disengagement of attention from any location in the visual field. The time required for subjects to disengage their attention is approximately 100 ms. This disengaged state of attention — during which short latency (express) saccades can be made — can be sustained only for a gap duration of 300 ms. At longer gap durations mean SRTs increase again.     

Effects of reappearance of fixated and attended stimuli upon saccadic reaction time

Summary The effects of visual attention and fixation upon the distribution of saccadic latencies: express (E-), fast regular (FR-), and slow regular (SR-) saccades were investigated. Extinguishing a fixation or an attention point 200–300 ms before target onset increases the incidence of E-saccades while concurrently decreasing the proportion of SR-saccades. Since this extinction forces a disengaging of attention, these changes in relative proportions of saccades reflect the elimination of one of the steps involved in programming saccades. It is shown that a previously attended stimulus has a favored status relative to other stimuli in the visual field. If, after being turned off, the previously attended fixation point or a peripheral attention stimulus is turned on near the time of the target's appearance, the occurrence of the E-saccades is greatly reduced. However, the appearance of any other stimulus in the visual field at or near the time of the target onset does not inhibit E-saccades. Contrary to the conclusions reached by Posner and Cohen (1984), a stimulus presented at the formerly attended location can attract attention more efficiently than a stimulus presented at another, new location.     

A study of neuronal circuitry mediating the saccadic suppression in the rabbit

Summary Stimulation of the deep layers of the superior colliculus (SC) evoked an IPSP in the relay cells of the lateral geniculate nucleus (LGN). The latency of the JPSP ranged from 3.3 to 4.7 ms with an average of 3.87±0.56 ms (S.D.). The IPSP from SC stimulation was proposed to be mediated by the recurrent inhibitory circuit to LGN, since the recurrent inhibitory interneurones in the thalamic reticular nucleus (R) responded to the same stimulation with a latency of 2.14±0.43 ms, which was 1.73 ms shorter than the latency of the IPSP in LGN relay cells. This was in good agreement with our previous observation that the recurrent interneurones always fired about 1.8 ms prior to the onset of the recurrent IPSP in LGN (Lo and Xie 1987b). The recurrent inhibitory interneurones could also be excited by stimulation of the central lateral nucleus (CL) with a very short latency (0.57±0.15 ms), suggesting a monosynaptic connection between the central lateral nucleus and the reticular recurrent interneurones. This suggestion was supported by the fact that CL neurones, which projected to the striate cortex (Cx), were antidromically excited by stimulation of the caudal part of R where the recurrent inhibitory interneurones were situated. CL neurone's response to stimulation of the deep layers of SC (SC-CL response) has a latency of 1.68±0.56 ms, which was comparable with the difference between the latency of SC-R response and that of CL-R response, just as expected from the notion that the saccadic suppression is mediated by a circuit of SC (deep layers) -CL-R-LGN.     

Recovery of saccadic dysmetria following localized lesions in monkey superior colliculus

Damage to the monkey superior colliculus (SC) produces deficits in the generation of saccadic eye movements. Recovery of the accuracy of saccades is rapid, but saccadic latency and peak velocity recover slowly or not at all. In the present experiments we revisited the issue of recovery of function following localized lesions of the SC using three methodological advances: implantation of wire recording electrodes into the SC for the duration of the experiment to ensure that we were recording from the same site on the SC map on successive days; quantification of changes in saccadic accuracy, latency, and velocity using a standard grid of target points in the visual field contralateral to the SC lesion; measurement of movement field size to quantitatively determine any changes following the lesion. We confirmed a decrease in saccadic accuracy following electrolytic lesions of the SC, and we found that this dysmetria recovered within about 4 days. Saccadic latency increased for saccades to the lesion area and this deficit persisted. Peak saccadic velocity decreased immediately after the lesion and decreased further during the 10 days to 2 weeks of the experiment. We found no indication of an expansion of the movement fields of neurons adjacent to the lesion area. This lack of reorganization suggests that movement field changes within the SC cannot mediate the recovery in accuracy of the saccade. The persistence of the latency and velocity deficits despite the recovery of amplitude deficits indicates that saccadic latency and peak velocity are dependent upon the SC whereas saccadic amplitude is not.     

Analysis of the step response of the saccadic feedback: system behavior

We used prolonged stimulation of the monkey superior colliculus to elicit staircase eye movements. By changing the parameters of the stimulating current we were able to obtain movements with different dynamics. An increase in the current frequency resulted in the shortening of the intersaccadic interval and a decrease of the amplitudes in the staircase. In cases of high stimulation, after an initial saccade of fixed metrics, the eyes moved in an apparently smooth fashion. The movement was conjugate and in the same direction as the first saccade. By analyzing the velocity trace we found that the movement consisted of a chain of small saccades, each of which started before the previous one ended. We conducted a quantitative analysis of the staircase movements including the cases of apparently smooth movement of the eyes. We conclude that all of the movements elicited by prolonged SC stimulation were generated by the saccadic feedback circuitry. The dynamic profiles of the elicited movements changed continuously with the stimulating current parameters. On one end of the continuum we observed the classically described staircase movements with individual movements separated in time. On the other end of the continuum we saw the apparent smooth movement as the limit case produced by high stimulation of the SC.     

Control of recurrent inhibition of the lateral geniculate nucleus by afferents from the superior colliculus of the rabbit: a possible mechanism of saccadic suppression

Summary Stimulation of the ipsilateral superior colliculus elicited a short burst of discharges of the recurrent inhibitory interneurones in the geniculocortical pathway of the rabbit. The most effective stimulating sites for this excitation were located in the deep layers rather than the superficial layers of the superior colliculus. The short latency of the response (2.3±0.6 ms) implied an oligo-synaptic excitatory pathway from the deep layers of the superior colliculus to the recurrent interneurones located in the caudal reticular nucleus of the thalamus. Following the excitation of the inter-neurone, there was a prolonged inhibition which started 10–30 ms and ended 150 ms after the collicular stimulation. The maximal inhibition occurred 50–70 ms after the stimulation. The effects of collicular stimulation on the recurrent inhibitory interneurones may be concerned with the inhibition of the visual pathway during saccades and with the disinhibition of facilitation during fixation of a new visual target.     

Saccadic eye movements following kainic acid lesions of the pulvinar in monkeys

Summary Behavioral and anatomical experiments have suggested that the pulvinar might play a role in the generation of saccadic eye movements to visual targets. To test this idea, we trained monkeys to make visually-guided saccades by requiring them to detect the dimming of a small target. We used three different saccade paradigms. On single-step trials, saccades were made from a central fixation point (FP) to a target at 12, 24 or 36° to the left or right. On overlap trials, the FP remained lit during presentation of a target at 12 or 24°. On double-step trials, the target stepped first to 24°, and then back to 12° on the same side. Animals were trained to criterion, received kainic acid lesions of the pulvinar, and were retested on all three tasks. The lesions were very large, destroying almost all of the visually responsive pulvinar. They also encroached on the lateral geniculate nucleus, thereby producing small foveal scotomas, and this resulted in some behavioral changes, including difficulty in maintaining fixation on the target and in detecting its dimming. Results on the saccade tests suggest that the pulvinar is not crucial for initiation of saccadic eye movements. Saccade latency and amplitude were unimpaired on both single-step and overlap trials. Saccadic performance was also normal on double-step trials. In a second experiment, we measured the average length of fixations during spontaneous viewing of a complex visual scene. Fixation lengths did not differ from those of unoperated control monkeys. We suggest that the neglect, increased saccadic latencies, and prolonged fixations attributed to pulvinar damage in previous studies were probably the result instead of inadvertent damage to tectal afferents. The present results, together with single unit data, point to a role for the pulvinar not in the generation of saccades, but rather in the integration of saccadic eye movements with visual processing.     

Fixation and saccade control in an express-saccade maker

In express-saccade makers a large incidence of express saccades (latencies around 100 ms) is paralleled by a reduced ability to suppress saccade generation when required. Such a behavior occurs frequently in dyslexies. We studied the latencies and the metrical properties of saccades in the very rare case of an adult, nondyslexic express-saccade maker (male, age 29 years). The subject produced 65–95% express saccades in the gap (fixation point removed 200 ms before target onset) as well as in the overlap (fixation point not removed) paradigm, which qualified the subject as the most clear case of an express-saccade maker found so far. The number of express saccades increased rather than decreased when fixation foreperiod, gap duration, and target location were randomized from trial to trial as compared to when they remained constant. In the memory-guided saccade and in the antisaccade paradigms in which immediate saccade execution to a visual target had to be suppressed, the subject often reacted to the target with express saccades in an involuntary way. The amplitudes of express saccades were — in some conditions — found to progressively decrease with increasing latency, giving rise to amplitude transition functions. The present findings disprove the notion that express saccades are generated based on the prediction of the time and location of target appearance and support the notion that they are the result of an optomotor reflex. It is argued that the operation of the reflex is gated by a separate fixation system. Express-saccade makers are described as subjects with a dysfunction of the fixation system. Recent neurophysiological findings suggest that the subject studied in the present study has a selective dysfunction of the fixation system at the level of the superior colliculus.     

Saccadic adaptation in lateral medullary and cerebellar infarction

To determine the adaptive capability of saccadic eye movements, and its association with enduring saccadic dysmetria in cerebellar and lateral medullary infarction (LMI), we investigated saccadic accuracy and adaptation in 15 patients with cerebellar or lateral medullary infarction, compared with those of 7 patients with diffuse cerebellar atrophy and 11 normal subjects. Saccade adaptation was elicited by a 37.5% backward target step during the primary saccade in both horizontal directions. Horizontal preadaptive saccadic gains were decreased in patients with cerebellar infarction, and contralesionally in patients with LMI. In contrast, adaptive saccadic gain change was reduced in patients with diffuse cerebellar atrophy and cerebellar infarction. Saccadic hypometria and reduced saccadic adaptability were dissociated in the majority of the patients with cerebellar infarctions; seven of the eight patients with cerebellar infarction showed saccadic hypometria and only three of them showed reduced saccadic adaptation, uni- or bilaterally in two with bilateral infarctions and ipsilesionally in one with unilateral infarction. The most commonly affected structure on MRI was the cerebellar hemisphere in the patients either with saccadic hypometria or with reduced saccadic adaptation. All patients with unilateral LMI exhibited normal saccadic gain adaptation in both directions, including those patients with enduring saccadic ipsipulsion. Our results suggest that the cerebellar hemispheres as well as the dorsal vermis and fastigial nucleus may be involved in the control of saccadic accuracy and adaptation. Reduced saccadic adaptation and persisting dysmetria are not tightly linked to each other in the cerebellar or lateral medullary lesions.     

Superior colliculus neurons provide the saccadic motor error signal

Summary Studies of the intermediate layers of the superior colliculus have suggested that it provides a desired change in eye position signal (E) for the generation of saccadic eye movements. Recent evidence, however, has shown that some neurons in these layers may be related to the velocity of saccades. We present single cell recordings from the intermediate layers of monkey superior colliculus that are consistent with the hypothesis that many superior colliculus neurons provide instead a motor error signal, e_m. Our hypothesis about the function of these cells places them inside the local feedback loop controlling the waveform of the saccade.Supported by Individual NRSA F32-EY05950 from the National Eye Institute     

The ability to produce express saccades as a function of gap interval among schizophrenia patients

The ability to produce express sacccades is associated with adequate functioning of saccadic burst cells in the superior colliculus. Saccadic burst cells appear to be under the inhibitory control of both the collicular and the dorsolateral frontal fixation systems. Twenty schizophrenia patients and 20 nonpsychiatric subjects were presented a saccade task that included five different gap intervals (0, 100, 200, 300, and 400 ms) between fixation point offset and peripheral target onset (at ±4°). All subjects generated the highest frequency of express saccades in trials with a gap interval of 200 ms. Schizophrenia patients had an increased frequency of express saccades across gap intervals, especially for targets presented in the right visual field. The groups did not differ in the percentages of anticipatory saccades or saccadic amplitudes. These results suggest that schizophrenia patients' saccadic burst cells in the superior colliculus are functioning adequately, but may be consistent with dys-function of dorsolateral frontal cortex and/or its interconnecting subcortical circuitry.