Early Saccades Research Articles

Concurrent oculomotor hyperactivity and deficient anti-saccade performance in obsessive-compulsive disorder

Existing studies mainly focused on the inhibition of the task-interfering response to understand the inhibitory deficits of obsessive-compulsive disorder (OCD). However, recent studies suggested that inhibitory function is broadly involved in response preparation and implementation. It is yet unknown if the inhibition dysfunction in OCD extends beyond the task-interfering response to the general inhibitory function. Here we address this issue based on the multidimensional eye-movement measurements, which can better capture the inhibitory deficits than manual responses. Thirty-one OCD patients and 32 healthy controls (HCs) completed the anti-saccade task where multidimensional eye-movement features were developed. Confirmatory factor analysis (CFA) suggested two components of inhibitory function that negatively correlated with each other: one component of oculomotor hyperactivity in generating oculomotor output which is characterized with early premature saccades, early cross rates and saccade number; the other component of task-specific oculomotor efficiency which is characterized with task accuracy, saccade latency, correction rate, and amplitude gain. Importantly, OCD showed both stronger oculomotor hyperactivity and deficient oculomotor efficiency than HCs, and the machine-learning-based classifications showed that the features of oculomotor hyperactivity had higher prediction accuracy than the features of oculomotor efficiency in distinguishing OCD from HCs. Our results suggested that OCD has concurrent deficits in oculomotor hyperactivity and oculomotor efficiency, which may originate from a common inhibitory dysfunction.

Symptoms in unilateral vestibular hypofunction are associated with number of catch-up saccades and retinal error: results from the population-based KORA FF4 study

ObjectiveThe presence and intensity of symptoms vary in patients with unilateral vestibular hypofunction. We aimed to determine which saccadic and vestibulo-ocular reflex parameters best predict the presence of symptoms in unilateral vestibular hypofunction in order to better understand vestibular compensation and its implications for rehabilitation therapy.MethodsVideo head impulse test data were analyzed from a subpopulation of 23 symptomatic and 10 currently symptom-free participants with unilateral vestibular hypofunction, embedded in the KORA (Cooperative Health Research in the Region of Augsburg) FF4 study, the second follow-up of the KORA S4 population-based health survey (2,279 participants).ResultsA higher number of catch-up saccades, a higher percentage of covert saccades, and a larger retinal error at 200 ms after the onset of the head impulse were associated with relevant symptoms in participants with unilateral vestibular hypofunction (p = 0.028, p = 0.046, and p = 0.038, respectively). After stepwise selection, the number of catch-up saccades and retinal error at 200 ms remained in the final logistic regression model, which was significantly better than a null model (p = 0.014). Age, gender, saccade amplitude, saccade latency, and VOR gain were not predictive of the presence of symptoms.ConclusionThe accuracy of saccadic compensation seems to be crucial for the presence of symptoms in unilateral vestibular hypofunction, highlighting the role of specific gaze stabilization exercises in rehabilitation. Early saccades, mainly triggered by the vestibular system, do not seem to compensate accurately enough, resulting in a relevant retinal error and the need for more as well as more accurate catch-up saccades, probably triggered by the visual system.

Corrective saccades in acute vestibular neuritis: studying the role of prediction with automated passively induced head impulses.

When the demands for visual stabilization during head rotations overwhelm the ability of the vestibuloocular reflex (VOR) to produce compensatory eye movements, the brain produces corrective saccades that bring gaze toward the fixation target, even without visual cues (covert saccades). What triggers covert saccades and what might be the role of prediction in their generation are unknown. We studied 14 subjects with acute vestibular neuritis. To minimize variability of the stimulus, head impulses were imposed with a motorized torque generator with the subject on a bite bar. Predictable and unpredictable (timing, amplitude, direction) stimuli were compared. Distributions of covert corrective saccade latencies were analyzed with a "LATER" (linear approach to threshold with ergodic rate) approach. On the affected side, VOR gain was higher (0.47 ± 0.28 vs. 0.39 ± 0.22, P ≪ 0.001) with predictable than unpredictable head impulses, and gaze error at the end of the head movement was less (5.4 ± 3.3° vs. 6.9 ± 3.3°, P ≪ 0.001). Analyzing trials with covert saccades, gaze error at saccade end was significantly less with predictable than unpredictable head impulses (4.2 ± 2.8° vs. 5.5 ± 3.2°, P ≪ 0.001). Furthermore, covert corrective saccades occurred earlier with predictable than unpredictable head impulses (140 ± 37 vs. 153 ± 37 ms, P ≪ 0.001). Using a LATER analysis with reciprobit plots, we were able to divide covert corrective saccades into two classes, early and late, with a break point in the range of 88-98 ms. We hypothesized two rise-to-threshold decision mechanisms for triggering early and late covert corrective saccades, with the first being most engaged when stimuli are predictable.NEW & NOTEWORTHY We successfully used a LATER (linear approach to threshold with ergodic rate) analysis of the latencies of corrective saccades in patients with acute vestibular neuritis. We found two types of covert saccades: early (<90 ms) and late (>90 ms) covert saccades. Predictability led to an increase in VOR gain and a decrease in saccade latency.

Attention deficit and hyperactivity disorder disrupts selective mechanisms of action

ObjectivePeople with attention deficit and hyperactivity disorder (ADHD) present attentional and emotional deficits and show paradoxical qualities such as hyperfocus. Previous studies have reported errors, slowness, and reaction time (RT) variability using eye movements. This study aimed to explore the underlying mechanisms of ADHD further. MethodsThirty French children and teenagers, 15 with ADHD and 15 neurotypical (NT), underwent a saccadic eye movement task. We conducted conventional analysis (movement duration, precision, velocity, RT) and Bayesian analysis. ResultsSaccade duration and velocity failed to differentiate the two groups, whereas amplitude was higher in ADHD than in NT participants. Saccade RT and variability were higher in ADHD than in NT participants. In the Bayesian analysis, ADHD altered the main distribution of saccades and of early saccades but did not influence the express saccade triggering. ConclusionsADHD disrupts two mechanisms of action: it reduces the gain of the decision signal, thus explaining slowness and variability; it quickens the decision process of early responses at the origin of short-latency but controlled movements. SignificanceThese premises and their interconnections explain previous observations and support the striatal-frontal wiring of ADHD, thus explaining ADHD complexity in its negative and positive manifestations.

Speed-accuracy tradeoffs influence the main sequence of saccadic eye movements

Several studies have proposed that an optimal speed-accuracy tradeoff underlies the stereotyped relationship between amplitude, duration and peak velocity of saccades (main sequence). To test this theory, we asked 8 participants to make saccades to Gaussian-blurred spots and manipulated the task’s accuracy constraints by varying target size (1, 3, and 5°). The largest targets indeed yielded more endpoint scatter (and lower gains) than the smallest targets, although this effect subsided with target eccentricity. The main sequence depended on several interacting factors: saccade latency, saccade gain and target size. Early saccades, which were faster than amplitude-matched late saccades, followed the target-size dependency one would expect from a speed-accuracy tradeoff process. They had higher peak velocities and shorter durations for larger targets than for smaller targets. For late saccades, however, the opposite was found. Deviations from the main sequence also covaried with saccade gain, in line with the idea that motor noise underlies part of the endpoint variability. Thus, our data provide partial evidence that the saccadic system weighs the detrimental effects of motor noise on saccade accuracy against movement duration and speed, but other factors also modulate the kinematics. We discuss the possible involvement of parallel saccade pathways to account for our findings.

Influence of predictability on saccade timing in a head impulse VOR suppression task.

Gaze stabilization performance has been shown to be influenced differently when the head is either passively or actively moved in normal healthy participants. However, for a visual fixation suppression task, it remains unknown if the pattern of coordinated head and eye movement is influenced differently by passive or active head movements. We used a suppression head impulse paradigm (SHIMP), where the subject's goal was to maintain gaze stabilized on a visual target that moved with the head during rapid impulsive head movements, to evaluate gaze fixation performance in three conditions: (1) passive-unpredictable where the examiner applied impulsive head yaw rotations with random timing and direction, (2) passive-predictable where the direction of head rotation was announced and then the examiner repeatedly applied impulses in the same direction, and (3) active where the test subject self-generated their head movements. Thirteen young healthy adults performed all three conditions to assess the percentage of early saccades that initiated the gaze shift toward the final visual target position and the latency of first saccades. Early saccades were defined as those occurring within the duration of the head impulse. Results showed that active head impulses generated the greatest percentage of early saccades, followed by predictable and unpredictable. Among the two passive conditions, predictability shortened the first saccade onset latencies. Active condition onset latencies were shorter than in either of the passive conditions, showing a consistent head-leads-eye pattern defining a specific behavioral pattern that could vary across patient groups leading to insights into central neural mechanisms that control eye-head coordination.

Gaze control during reaching is flexibly modulated to optimize task outcome

When reaching for an object with the hand, the gaze is usually directed at the target. In a laboratory setting, fixation is strongly maintained at the reach target until the reaching is completed, a phenomenon known as "gaze anchoring." While conventional accounts of such tight eye-hand coordination have often emphasized the internal synergetic linkage between both motor systems, more recent optimal control theories regard motor coordination as the adaptive solution to task requirements. We here investigated to what degree gaze control during reaching is modulated by task demands. We adopted a gaze-anchoring paradigm in which participants had to reach for a target location. During the reach, they additionally had to make a saccadic eye movement to a salient visual cue presented at locations other than the target. We manipulated the task demands by independently changing reward contingencies for saccade reaction time (RT) and reaching accuracy. On average, both saccade RTs and reach error varied systematically with reward condition, with reach accuracy improving when the saccade was delayed. The distribution of the saccade RTs showed two types of eye movements: fast saccades with short RTs, and voluntary saccade with longer RTs. Increased reward for high reach accuracy reduced the probability of fast saccades but left their latency unchanged. The results suggest that gaze anchoring acts through a suppression of fast saccades, a mechanism that can be adaptively adjusted to the current task demands.NEW & NOTEWORTHY During visually guided reaching, our eyes usually fixate the target and saccades elsewhere are delayed ("gaze anchoring"). We here show that the degree of gaze anchoring is flexibly modulated by the reward contingencies of saccade latency and reach accuracy. Reach error became larger when saccades occurred earlier. These results suggest that early saccades are costly for reaching and the brain modulates inhibitory online coordination from the hand to the eye system depending on task requirements.

Fast saccades towards faces are robust to orientation inversion and contrast negation

Eye movement studies show that humans can make very fast saccades towards faces in natural scenes, but the visual mechanisms behind this process remain unclear. Here we investigate whether fast saccades towards faces rely on mechanisms that are sensitive to the orientation or contrast of the face image. We present participants pairs of images each containing a face and a car in the left and right visual field or the reverse, and we ask them to saccade to faces or cars as targets in different blocks. We assign participants to one of three image conditions: normal images, orientation-inverted images, or contrast-negated images. We report three main results that hold regardless of image conditions. First, reliable saccades towards faces are fast – they can occur at 120–130 ms. Second, fast saccades towards faces are selective – they are more accurate and faster by about 60–70 ms than saccades towards cars. Third, saccades towards faces are reflexive – early saccades in the interval of 120–160 ms tend to go to faces, even when cars are the target. These findings suggest that the speed, selectivity, and reflexivity of saccades towards faces do not depend on the orientation or contrast of the face image. Our results accord with studies suggesting that fast saccades towards faces are mainly driven by low-level image properties, such as amplitude spectrum and spatial frequency.

Neural Mechanisms of Overt Attention Shifts to Emotional Faces

Emotional faces draw attention and eye-movements towards them. However, the neural mechanisms of attention have mainly been investigated during fixation, which is uncommon in everyday life where people move their eyes to shift attention to faces. Therefore, the current study combined eye-tracking and Electroencephalography (EEG) to measure neural mechanisms of overt attention shifts to faces with happy, neutral and angry expressions, allowing participants to move their eyes freely towards the stimuli. Saccade latencies towards peripheral faces did not differ depending on expression and early neural response (P1) amplitudes and latencies were unaffected. However, the later occurring Early Posterior Negativity (EPN) was significantly larger for emotional than for neutral faces. This response appears after saccades towards the faces. Therefore, emotion modulations only occurred after an overt shift of gaze towards the stimulus had already been completed. Visual saliency rather than emotional content may therefore drive early saccades, while later top-down processes reflect emotion processing.

Saccadic inhibition in a guided saccade task.

The eye movement system reacts very systematically to visual transients that are presented during the planning phase of a saccade. About 50 to 70 ms after the onset of a transient, the number of saccades that are started decreases, a phenomenon that has been termed saccadic inhibition. Saccades started just before this time window are hypometric compared to regular saccades, presumably because the presentation of the transient stops them in mid-flight. Recent research investigating the properties of repeated saccades to fixed locations found that these early saccades were additionally faster than expected from the main sequence relation, suggesting that a saccadic dead time during which saccades can no longer be modified does not exist. The present study investigated the properties of saccades to random locations in a guided saccade task. As expected, early saccades starting just before the saccadic inhibition dip in frequency were hypometric. Their velocity profiles implied that these saccades were actively stopped after reaching peak velocity. However, the peak velocities of these saccades did not generally deviate from the main sequence relation. The question whether an active stop of early saccades is incompatible with the idea of a saccadic dead time is open to debate.

Vestibulo-ocular reflex gain values in the suppression head impulse test of healthy subjects.

To assess whether there are differences in vestibulo-ocular reflex (VOR) gain for suppression head impulse (SHIMP) and head impulse (HIMP) video head impulse test paradigms, and if so, what are their causes. Prospective multicenter observational double-blind nonrandomized clinical study was performed by collecting 80 healthy subjects from four reference hospitals. SHIMP data was postprocessed to eliminate impulses in which early SHIMP saccades were detected. Differences between HIMP and SHIMP VOR gain values were statistically evaluated. Head impulse maximum velocity, gender, age, direction of impulse, and hospital center were considered as possible influential factors. A small significant statistical difference between HIMP and SHIMP VOR gain values was found on repeated measures analysis of variance (-0.05 ± 0.006, P < 0.001). Optimized linear model showed a significant influence of age variable on the observed differences for HIMP and SHIMP gain values and did not find influence between gain values differences and maximum head impulse velocity. Both HIMP and SHIMP VOR gain values were significant lower (-0.09, P < 0.001) when the impulses were performed to the left side. We had observed a difference in SHIMP and HIMP gain values not adequately explained by known gain modification factors. The persistence of this slight but significant difference indicates that there are more factors causing lower SHIMP VOR gain values. This difference must to be considered in further studies as well as in the clinical SHIMP testing protocols. We hypothesized that VOR phasic response inhibition could be the underlying cause of this difference. 2b. Laryngoscope, 128:2383-2389, 2018.

The Role of Predictability in Saccadic Eye Responses in the Suppression Head Impulse Test of Horizontal Semicircular Canal Function.

In the suppression head impulse paradigm (SHIMP) vHIT protocol, the participant is instructed to follow with his gaze a mobile target generated by a laser placed on the participant's head. Recent studies have reported that the refixation saccade latencies are in relation with the time evolution of the vestibular dysfunction in both (standard and SHIMP) procedures. We hypothesized that some central mechanisms like head impulse prediction could be one of the causes for the differences in the saccadic eye responses. A prospective cohort non-randomized study was designed. For the SHIMP protocol, recorded with the ICS Impulse ver. 4.0® (Otometrics A/S, Taastrup, Denmark) vHIT device, three different algorithms were performed: "predictable," "less predictable," and "unpredictable" depending on the target's predictability. A mathematical method was developed to analyze the SHIMP responses. The method was implemented as an additional tool to the MATLAB open source script for the extended analysis of the vHIT responses named HITCal. In cohort 1, 52 participants were included in "predictable" SHIMP protocol. In cohort 2, 60 patients were included for the "less predictable" and 35 patients for the "unpredictable" SHIMP protocol. The participants made more early saccades when instructed to perform the "predictable" paradigm compared with the "less predictable" paradigm (p < 0.001). The less predictable protocol did not reveal any significant difference when compared with the unpredictable protocol (p = 0.189). For the latency of the first saccade, there was statistical difference between the "unpredictable" and "predictable" protocols (p < 0.001) and between the "less predictable" and "predictable" protocols (p < 0.001). Finally, we did not find any relationship between the horizontal vestibulo-ocular reflex (hVOR) gain and the latency of the saccades. We developed a specific method to analyze and detect early SHIMP saccades. Our findings offer evidence regarding the influence of predictability on the latency of the SHIMP saccadic responses, suggesting that early saccades are probably caused by a conditioned response of the participant. The lack of relationship between the hVOR gain and the latency of the saccades suggests that the predictive behavior that caused the early eye saccades are independent of the vestibular function.

Causal Role of Noradrenaline in the Timing of Internally Generated Saccades in Monkeys

We recently found that when monkeys performed an oculomotor version of the time production task, the trial-by-trial latency of self-timed saccades was negatively correlated with pupil diameter just before the delay period (Suzuki et al., 2016). Since pupil diameter has been shown to correlate with neuronal activity in the locus coeruleus, the level of noradrenaline (NA) in the brain might regulate the subjective passage of time. To examine this, we orally administered a selective noradrenaline reuptake inhibitor (reboxetine, 0.4–0.8 mg) when animals made a self-initiated memory-guided saccade >1 s following the appearance of a brief visual cue. We found that reboxetine delayed self-timed saccades, while the latency of visually triggered saccades remained unchanged. Because the changes in proportions and latencies of early impulsive saccades were comparable between conditions with and without drug administration, alteration of self-timing might not result from reduced impulsivity. We also assessed other behavioral parameters (saccade accuracy, velocity, and latency variance), but failed to find any drug effect except for the accuracy of visually triggered saccades in the high-dose condition, indicating that reboxetine specifically altered self-timing under our experimental conditions. Our results suggest that NA-related internal states may causally regulate temporal information processing in the brain.

Eye Control Deficits Coupled to Hand Control Deficits: Eye-Hand Incoordination in Chronic Cerebral Injury.

It is widely accepted that cerebral pathology can impair ocular motor and manual motor control. This is true in indolent and chronic processes, such as neurodegeneration and in acute processes such as stroke or those secondary to neurotrauma. More recently, it has been suggested that disruptions in these control systems are useful markers for prognostication and longitudinal monitoring. The utility of examining the relationship or the coupling between these systems has yet to be determined. We measured eye and hand-movement control in chronic, middle cerebral artery stroke, relative to healthy controls, in saccade-to-reach paradigms to assess eye–hand coordination. Primary saccades were initiated significantly earlier by stroke participants relative to control participants. However, despite these extremely early initial saccades to the target, reaches were nevertheless initiated at approximately the same time as those of control participants. Control participants minimized the time period between primary saccade onset and reach initiation, demonstrating temporal coupling between eye and hand. In about 90% of all trials, control participants produced no secondary, or corrective, saccades, instead maintaining fixation in the terminal position of the primary saccade until the end of the reach. In contrast, participants with stroke increased the time period between primary saccade onset and reach initiation. During this temporal decoupling, multiple saccades were produced in about 50% of the trials with stroke participants making between one and five additional saccades. Reaches made by participants with stroke were both longer in duration and less accurate. In addition to these increases in spatial reach errors, there were significant increases in saccade endpoint errors. Overall, the magnitude of the endpoint errors for reaches and saccades were correlated across participants. These findings suggest that in individuals with otherwise intact visual function, the spatial and temporal relationships between the eye and hand are disrupted poststroke, and may need to be specifically targeted during neurorehabilitation. Eye–hand coupling may be a useful biomarker in individuals with cerebral pathology in the setting of neurovascular, neurotraumatic, and neurodegenerative pathology.

Striatal dopamine modulates timing of self-initiated saccades

The ability to adjust movement timing is essential in daily life. Explorations of the underlying neural mechanisms have reported a gradual increase or decrease in neuronal activity prior to self-timed movements within the cortico-basal ganglia loop. Previous studies in both humans and animals have shown that endogenous dopamine (DA) plays a modulatory role in self-timing. However, the specific site of dopaminergic regulation remains elusive because the systemic application of DA-related substances can directly alter both cortical and subcortical neuronal activities. To investigate the role of striatal DA in self-timing, we locally injected DA receptor agonists or antagonists into the striatum of two female monkeys (Macaca fuscata) while they performed two versions of the memory-guided saccade (MS) task. In the conventional, triggered MS task, animals made a saccade to the location of a previously flashed visual cue in response to the fixation point offset. In the self-timed MS task, monkeys were rewarded for making a self-initiated saccade within a predetermined time interval following the cue. Infusion of a small amount of a D1 or D2 antagonist led to early saccades in the self-timed, but not the triggered MS tasks, while infusion of DA agonists produced no consistent effect. We also found that local administration of nicotinic but not muscarinic acetylcholine receptor agonists and antagonists altered the timing of self-initiated saccades. Our data suggest that the timing of self-initiated movements may be regulated by the balance of signals in the direct and indirect basal ganglia pathways, as well as that between both hemispheres of the brain.

Beyond the point of no return: effects of visual distractors on saccade amplitude and velocity.

Visual transients, such as a bright flash, reduce the proportion of saccades executed, ∼60-125 ms after flash onset, a phenomenon known as saccadic inhibition (SI). Across three experiments, we apply a similar time-course analysis to the amplitudes and velocities of saccades. Alongside the expected reduction of saccade frequency in the key time period, we report two perturbations of the "main sequence": one before and one after the period of SI. First, saccades launched between 30 and 70 ms, following the flash, were hypometric, with peak speed exceeding that expected for a saccade of similar amplitude. This finding was in contrast to the common idea that saccades have passed a "point of no return," ∼60 ms before launching, escaping interference from distractors. The early hypometric saccades observed were not a consequence of spatial averaging between target and distractor locations, as they were found not only following a localized central flash (experiment 1) but also following a spatially generalized flash (experiment 2). Second, across experiments, saccades launched at 110 ms postflash, toward the end of SI, had normal amplitude but a peak speed higher than expected for that amplitude, suggesting increased collicular excitation at the time of launching. Overall, the results show that saccades that escape inhibition following a visual transient are not necessarily unaffected but instead, can reveal interference in spatial and kinematic measures.

Visual anticipation biases conscious decision making but not bottom-up visual processing.

Prediction plays a key role in control of attention but it is not clear which aspects of prediction are most prominent in conscious experience. An evolving view on the brain is that it can be seen as a prediction machine that optimizes its ability to predict states of the world and the self through the top-down propagation of predictions and the bottom-up presentation of prediction errors. There are competing views though on whether prediction or prediction errors dominate the formation of conscious experience. Yet, the dynamic effects of prediction on perception, decision making and consciousness have been difficult to assess and to model. We propose a novel mathematical framework and a psychophysical paradigm that allows us to assess both the hierarchical structuring of perceptual consciousness, its content and the impact of predictions and/or errors on conscious experience, attention and decision-making. Using a displacement detection task combined with reverse correlation, we reveal signatures of the usage of prediction at three different levels of perceptual processing: bottom-up fast saccades, top-down driven slow saccades and consciousnes decisions. Our results suggest that the brain employs multiple parallel mechanism at different levels of perceptual processing in order to shape effective sensory consciousness within a predicted perceptual scene. We further observe that bottom-up sensory and top-down predictive processes can be dissociated through cognitive load. We propose a probabilistic data association model from dynamical systems theory to model the predictive multi-scale bias in perceptual processing that we observe and its role in the formation of conscious experience. We propose that these results support the hypothesis that consciousness provides a time-delayed description of a task that is used to prospectively optimize real time control structures, rather than being engaged in the real-time control of behavior itself.

Early saccades in amyotrophic lateral sclerosis

Our objective was to correlate saccadic abnormalities, including early saccades, in patients with amyotrophic lateral sclerosis (ALS) with measures of motor and functional impairment. A portable saccadometer was used to record saccades in ALS patients and control subjects. The linear approach to threshold with ergodic rate model was used to characterize saccades, including sub-populations of early saccades. Patients with established cognitive impairment or frontotemporal dementia were excluded. Limb-onset (Limb ALS) and bulbar-onset (Bulbar ALS) patient groups were compared and saccadic abnormalities were correlated with measures of motor and functional impairment. In total, 48 participants were included in the study; 24 patients with ALS (15 males, 9 females; mean age 57.0 +/− 13.9 years; mean symptom duration 22.4 +/− 16.3 months, of whom 62.5% had Limb ALS) and 24 age-matched controls. Early saccades were increased in both Limb ALS and Bulbar ALS patients, but other saccadic parameters were normal in ALS. Saccadic abnormalities did not correlate with motor or functional impairment. In conclusion, ALS patients show increased early saccades, but exhibit no significant differences across ALS phenotypes.

Alteration of the timing of self‐initiated but not reactive saccades by electrical stimulation in the supplementary eye field

Although we can generate movements whenever we feel like doing so, the way in which neuronal signals regulate the timing of self-initiated movements remains elusive. There is evidence that the dorsomedial frontal cortex, including the supplementary eye field (SEF), is involved in the self-triggering of movements. Because the gradual evolution of cortical activity over the dorsomedial frontal cortex is known to reflect the temporal prediction of an upcoming event, we postulated that the timing of self-initiated movements is regulated by the time course of neuronal activity in the SEF. To test the causal role, we applied electrical microstimulation to the SEF when monkeys prepared for memory-guided saccades. Stimulation delayed the initiation of saccades when animals were required to make saccades 1200 ± 300 ms following the cue (self-timed task), but not when they generated memory-guided saccades in response to the offset of the fixation point (conventional task). As well as the increment in median saccade latencies, stimulation at ∼24% of sites also increased the occurrence of early erroneous saccades. Saccades facilitated by stimulation were always directed toward the cue, even when the cue was located away from the movement field. In contrast, stimulation to the frontal eye fields during saccade preparation exerted no effects in either task. These results suggest that the preparatory signals in the SEF may play a causal role in regulating the timing rather than the direction of self-initiated saccades.

Visual sampling during walking in people with Parkinson’s disease and the influence of environment and dual-task

Visuospatial dysfunction may play a crucial role in gait disturbance in Parkinson’s disease (PD), in particular how visual exploration of the environment is integrated into gait control. In this study, we tested the hypothesis that people with PD would visually sample their environment less frequently than controls when walking under different levels of environmental complexity and dual-task. We also explored associations between saccadic outcomes and clinical measures. Visual sampling (saccadic frequency) and gait were measured concurrently for 21 people with PD and 12 age-matched controls during a series of walking tasks using electrooculography (EOG) synchronised with 3D motion analysis (VICON). Participants walked under four environmental conditions during single and dual-task. Saccade frequency and task duration were measured. PD participants took longer to complete all tasks than controls (p =.004). Environment and dual-task impacted on saccadic frequency especially for PD. For both groups, saccadic frequency increased when approaching a turn compared with straight walking. Prior to turning, PD made less frequent early preparatory saccades than controls (p =.012). Under dual-task conditions, people with PD made less frequent saccades than controls when walking straight ahead (p =.040) and in preparation for a turn (p =.032). Increased saccadic frequency was related to poorer attention, cognition and spatial memory in controls and people with PD for single-task conditions but not dual-task conditions. Impaired visual sampling may contribute to the gait disorder in PD, especially when navigating through complex environments and when distracted.