Control Of Saccadic Eye Movements Research Articles

Control of saccadic eye movements and combined eye/head gaze shifts by the medio-posterior cerebellum

The cerebellar areas involved in the control of saccades have recently been identified in the medio-posterior cerebellum (MPC). Unit activity recordings, experimental lesions and electrical microstimulation of this region in cats and monkeys have provided a considerable amount of data and allowed the development of new computational models. In this paper, we review these data and concepts about cerebellar function, discuss their importance and limitations and suggest future directions for research. The anatomical data indicate that the MPC has more than one site of action in the visuo-oculomotor system. In contrast, most models emphasize the role of cerebellar connections with immediate pre-oculomotor circuits in the reticular formation, and only one recent model also incorporates the ascending projections of the MPC to the superior colliculus. A major challenge for future studies, in continuation with this initial attempt, is to determine whether the various cerebellar output pathways correspond to distinct contributions to the control of saccadic eye movements. Also, a series of recent studies in the cat have indicated a more general role of the MPC in the control of orienting movements in space, calling for an increasing effort to the study of the MPC in the production of head-unrestrained saccadic gaze shifts.

Cortical control of ocular saccades in humans: a model for motricity

Our knowledge of the cortical control of saccadic eye movements (saccades) in humans has recently progressed mainly thanks to lesion and transcranial magnetic stimulation (TMS) studies, but also to functional imaging. It is now well-known that the frontal eye field is involved in the triggering of intentional saccades, the parietal eye field in that of reflexive saccades, the supplementary eye field (SEF) in the initiation of motor programs comprising saccades, the pre-SEF in learning of these programs, and the dorsolateral prefrontal cortex (DLPFC) in saccade inhibition, prediction and spatial working memory. Saccades may also be used as a convenient model of motricity to study general cognitive processes preparing movements, such as attention, spatial memory and motivation. Visuo-spatial attention appears to be controlled by a bilateral parieto-frontal network comprising different parts of the posterior parietal cortex and the frontal areas involved in saccade control, suggesting that visual attentional shifts and saccades are closely linked. Recently, our understanding of the cortical control of spatial memory has noticeably progressed by using the simple visuo-oculomotor model represented by the memory-guided saccade paradigm, in which a single saccade is made to the remembered position of a unique visual item presented a while before. TMS studies have determined that, after a brief stage of spatial integration in the posterior parietal cortex (inferior to 300 ms), short-term spatial memory (i.e. up to 15-20 s) is controlled by the DLPFC. Behavioral and lesion studies have shown that medium-term spatial memory (between 15-20 s and a few minutes) is specifically controlled by the parahippocampal cortex, before long-term memorization (i.e. after a few minutes) in the hippocampal formation. Lastly, it has been shown that the posterior part of the anterior cingulate cortex, called the cingulate eye field, is involved in motivation and the preparation of all intentional saccades, but not in reflexive saccades. These different but complementary study methods used in humans have thus contributed to a better understanding of both eye movement physiology and general cognitive processes preparing motricity as whole.

Visuo-motor deficits induced by fastigial nucleus inactivation.

The contribution of the cerebellar vermal lobules Vic/VII and of the caudal part of the fastigial nucleus (cFN) to the control of saccadic eye movements has been established by converging neurophysiological approaches. The precise delineation of these saccade-related territories in the medio-posterior cerebellum (MPC) has stimulated the development of detailed investigations of its output nucleus, the cFN. In the present paper, we review recent studies that describe the deficits of the saccadic displacement of the line of sight (gaze) induced by a reversible cFN inactivation under different experimental situations (head restrained, head-unrestrained or body-unrestrained). These data first indicate that the MPC does not solely influence the generation of saccadic eye movements but also the accompanying head movements during saccadic shifts of gaze in the head-unrestrained animal. They also support, in agreement with anatomical data, a distributed influence of the MPC on several levels of the sensory-motor system for orienting gaze, rather than a limited control of the immediate pre-motor structures.

The role of the oculomotor vermis in the control of saccadic eye movements.

The oculomotor vermis is a part of the posterior cerebellum, characterized by a low threshold (<10 micro A) for evoked saccades. It comprises vermal lobuli VIc and VIIA. Many Purkinje cells in this area show eye position or saccade-related responses or combinations of the two and usually lack responses to the presentation of visual targets, guiding the oculomotor behavior. The saccade-related responses are directionally selective and show preferences for saccade amplitude or duration, which differ widely between cells. However, at the population level, these saccade-related Purkinje cells give a very precise account of the timing of the saccadic eye movement and, specifically, of the time it ends. This population signal might therefore contribute to determining the end of the saccadic eye movement. Furthermore, by changing the duration of the population response, the amplitude of the saccade could be changed. In other words, saccadic adaptation could be a consequence of changing a representation of time in the cerebellum.

The brainstem control of saccadic eye movements.

The modern era of oculomotor research began with the advent of the chronic single-unit recording method in the late 1960s. Research carried out in the intervening years has made it possible to provide a detailed description of the saccadic command signals that are generated by motor neurons and the formation of these signals in premotor brainstem regions. These findings have been assimilated in control-systems models that simulate important behavioural features of saccades. Despite these great advances, key issues, such as the nature of the feedback signal and the location of the comparator, are unresolved and some of the factors that have impeded progress can be identified.

A turn-key transportable eye-tracking instrument for clinical assessment.

This paper describes a combined instrument (eye tracker and target generator, both head mounted, with integrated data analysis) that tests parameters of saccadic eye movement and fixation control to give insight into the status of functional brain systems. Using three minilasers, the target generato rprojects three visual stimuli, a fixation point and two lateral stimuli, with programmable timing. The controller allows the selection of overlap, 200-msec gap, or remembered saccade trials. Size, maximal velocity, and reaction time are determined for each primary saccade. The number of prosaccades and antisaccades are counted. More saccades--for example, the occurrence and latency of corrective saccades--may be evaluated off line by an interactive PC analysis program. The eye position data can be transferred to a PC. Off-line analysis compares each observed variable relative to an age-matched control group (300 healthy control subjects 7-70 years of age, tested in the overlap condition with prosaccade instructions and in the gap condition with antisaccades). The diagnostic results can be used to elaborate an individual optomotor training program.

Effects of cortical lesions on saccadic: eye movements in humans.

Our knowledge of the cortical control of saccadic eye movements (saccades) in humans has recently progressed mainly because of lesion and transcranial magnetic stimulation (TMS) studies, but also because of functional imaging. It is now well known that the frontal eye field is involved in the control of intentional saccades, the parietal eye field in that of reflexive saccades, the supplementary eye field (SEF) in the initiation of motor programs comprising saccades, the pre-SEF in the learning of these programs, and the dorsolateral prefrontal cortex (DLPFC) in saccade inhibition, prediction and spatial working memory. Saccades may also be used as a convenient model of motricity to study general cognitive processes such as motivation and spatial memory. Thus, it has been shown that the posterior part of the anterior cingulate cortex, called the cingulate eye field, is involved in motivation and the preparation of all intentional saccades, but not in reflexive saccades. Recently, our understanding of the cortical control of spatial memory has noticeably progressed by using the simple visuo-oculomotor model represented by the memory-guide saccade paradigm, in which a single saccade is made to the remembered position of a unique visual item presented a while before. Transcranial magnetic stimulation studies have determined that after a brief stage of spatial integration in the posterior parietal cortex (inferior to 300 ms), short-term spatial memory (i.e., up to 15-20 seconds) is controlled by the DLPFC. Behavioral and lesion studies have shown that medium-term spatial memory (between 15 and 20 seconds and a few minutes) is specifically controlled by the parahippocampal cortex, before long-term memorization (i.e., after a few minutes) in the hippocampal formation. These different but complementary study methods used in humans have thus contributed to a better understanding of both eye movement physiology and general cognitive processes preparing motricity as whole.

Evidence that the superior colliculus participates in the feedback control of saccadic eye movements.

There is general agreement that saccades are guided to their targets by means of a motor error signal, which is produced by a local feedback circuit that calculates the difference between desired saccadic amplitude and an internal copy of actual saccadic amplitude. Although the superior colliculus (SC) is thought to provide the desired saccadic amplitude signal, it is unclear whether the SC resides in the feedback loop. To test this possibility, we injected muscimol into the brain stem region containing omnipause neurons (OPNs) to slow saccades and then determined whether the firing of neurons at different sites in the SC was altered. In 14 experiments, we produced saccadic slowing while simultaneously recording the activity of a single SC neuron. Eleven of the 14 neurons were saccade-related burst neurons (SRBNs), which discharged their most vigorous burst for saccades with an optimal amplitude and direction (optimal vector). The optimal directions for the 11 SRBNs ranged from nearly horizontal to nearly vertical, with optimal amplitudes between 4 and 17 degrees. Although muscimol injections into the OPN region produced little change in the optimal vector, they did increase mean saccade duration by 25 to 192.8% and decrease mean saccade peak velocity by 20.5 to 69.8%. For optimal vector saccades, both the acceleration and deceleration phases increased in duration. However, during 10 of 14 experiments, the duration of deceleration increased as fast as or faster than that of acceleration as saccade duration increased, indicating that most of the increase in duration occurred during the deceleration phase. SRBNs in the SC changed their burst duration and firing rate concomitantly with changes in saccadic duration and velocity, respectively. All SRBNs showed a robust increase in burst duration as saccadic duration increased. Five of 11 SRBNs also exhibited a decrease in burst peak firing rate as saccadic velocity decreased. On average across the neurons, the number of spikes in the burst was constant. There was no consistent change in the discharge of the three SC neurons that did not exhibit bursts with saccades. Our data show that the SC receives feedback from downstream saccade-related neurons about the ongoing saccades. However, the changes in SC firing produced in our study do not suggest that the feedback is involved with producing motor error. Instead, the feedback seems to be involved with regulating the duration of the discharge of SRBNs so that the desired saccadic amplitude signal remains present throughout the saccade.

Cognition and the inhibitory control of saccades in schizophrenia and Parkinson's disease

Historically, various lines of evidence have converged on the view that the brain expends much of its neural resources on inhibiting its own activity in a critical step towards the cognitive control of behaviour. The loss of inhibitory control is widely reported in neurological and psychiatric disorders; however, the consequences of reduced inhibition in terms of wider cognitive effects on cognitive control operations such as planning, abstract thought, working memory and the ability to appreciate the perspective of others ('theory of mind') has been widely overlooked. The antisaccade paradigm examines the conflict between a prepotent stimulus that produces a powerful urge to fixate the target, and the overriding goal to 'look' in the opposite direction. In this chapter we illustrate how this paradigm is increasingly used to explore the relationship of inhibitory control and cognition in Parkinson's disease, schizophrenia and healthy participants. Evidence is presented that is consistent with the theory of cognitive inhibition as a distinct process that can be dissociated from working memory. We conclude that the inhibitory control of saccadic eye movement should be studied in the wider context of cognitive operations.

Commentary: Saccadic eye movements: overview of neural circuitry

Recent neuroanatomical, neurophysiological, clinical, and brain imaging studies have generated a wealth of data describing the neural control of saccadic eye movements and visual fixation. These studies have identified many of the cortical and subcortical structures involved in controlling the behavior. Critical nodes in the network include regions of the parietal and frontal cortices, basal ganglia, thalamus, superior colliculus, cerebellum, and brainstem reticular formation. Specific functions are likely not localized to only one brain area, but rather, they may be distributed across multiple areas. This commentary is used to review briefly the neural circuitry controlling saccadic eye movements and visual fixation.

Eye movements during reading: a theory of saccade initiation times

As people read continuous text, on occasional single eye fixations the text was replaced by one of six alternate stimulus patterns. Frequency distributions of the durations of these fixations were used to test predictions from four types of theories of saccadic eye movement control. Contrary to current cognitive theories, cognitive influences appeared to delay saccades rather than trigger them. Two saccade disruption times were identified, suggesting the existence of three distributions of saccades, labeled early, normal and late. The Competition–inhibition theory, an enhanced version of Findlay and Walker's (1999) theory, is proposed to account for eye movement control during reading.

Evidence for subcortical involvement in the visual control of human reaching.

To test whether the most rapid visually evoked reach adjustments are cortically organized in humans, we have measured their latency in a healthy subject with complete agenesis of the corpus callosum. This condition precludes direct communication between left and right cerebral cortices and so, in this subject, a purely cortical visuomotor process would be expected to produce longer-latency responses to a target that appears in the visual hemifield contralateral to the responding limb (crossed) compared with the ipsilateral hemifield (uncrossed). As predicted, when performing simple reaction time tasks that involved lifting a finger or an arm in response to a visual stimulus presented to either hemifield, this acallosal subject showed a significant crossed-uncrossed latency difference (mean 35.8 ms) that was not present in control subjects (group mean 2.2 ms). In contrast, when she reached for a target that unexpectedly jumped into either visual hemifield, the latencies of mid-flight adjustment were the same (approximately 120 ms) irrespective of either the target jump direction or which hand was used. This was not due to an early movement of the eyes bringing the target back on to the fovea since this subject's finger always deviated towards the new target position in advance of her eyes. Neither could it be explained by the use of ipsilateral corticospinal projections since transcranial magnetic stimulation over the motor cortex failed to evoke ipsilateral responses in arm or hand muscles. These results suggest that, even in humans, subcortical structures are involved in the fastest adjustments of the reaching arm made in response to fresh visual information. An additional finding in this subject was that, when reaching, the eye saccadic latency was greater by 36 ms on average when the target jumped right compared with left, irrespective of which hand was being used. This is the same value as the mean interhemispheric transfer time obtained in the simple reaction time tasks and may indicate right-hemispheric dominance for saccadic eye movement control.

Infant Cortical Development and the Prospective Control of Saccadic Eye Movements

Babies, like everyone else in this world, need to learn how to coordinate their actions with events that are not under their direct control. Response latency is an obstacle in this process, and the primary goal of sensorimotor development is to overcome it through the application of foresight (Piaget, 1937/1954). Visual exploration is where the infant first seriously confronts the problem of response latency. The infant moves his or her eye to inspect something in the periphery, only to find that when his or her eye has rotated to its final position, the object of interest may no longer be there. To solve this problem, he or she must learn to make good guesses about the future and be ready to act when, or even before, the future arrives. In other words, the baby will need to organize his or her behavior in a prospective manner. Rather than simply reacting to what happens to him or her, the baby needs to start thinking ahead. Eventually, the baby will be guided by plans, goals, anticipatory schemata, expectations, and memories of the future. By developing prospective sensorimotor control, not only will the baby become the master of his or her domain, he or she will be building a foundation INFANCY, 2(2), 197–211 Copyright © 2001, Lawrence Erlbaum Associates, Inc.

Dyslexia and the centre-of-gravity effect.

When human observers are presented with a double target display, a saccadic eye movement is triggered to an intermediate position close to the 'centre-of-gravity' of the configuration. This study examined the saccadic eye movements of dyslexic and normal readers in response to displays of single and double targets. Eye movement analyses revealed no differences in the spatial position of saccadic eye movements of dyslexic and normal readers in response to single targets presented at 5 degrees or 10 degrees. However, when presented with two targets simultaneously at 5 degrees AND 10 degrees, in contrast to normal readers who generated saccades to an intermediate position between the two targets (towards the 'centre-of gravity'), dyslexics generated saccades that landed close to the near target eccentricity. These findings suggest that dyslexia is associated with a deficit in the processing of global spatial information for the control of saccadic eye movements.

Kortikale Lokalisation von Sakkaden und langsamen Augenfolgebewegungen mittels funktioneller Bildgebung

In recent years, modern neuroimaging has provided a more precise anatomical localisation and functional characterisation of cortical areas for the control of saccadic and smooth-pursuit eye movements. For both functions, a largely overlapping network of fronto-parietal and cerebellar areas could be delineated which was equally well or even more activated by covert shifts of the attentional focus without the performance of eye movements. Imaging of ocular motor subfunctions by applying specific experimental paradigms in active and control conditions has yielded new insights into the functional specialisation of these areas. The frontal, the parietal, and the supplementary eye fields (FEF, PEF, SEF) are the key structures for the initiation of voluntary and reflexive saccades, and of covert attentional shifts. Saccade-specific functions could be demonstrated only for the FEF and SEF (saccadic sequences). The dorsolateral prefrontal cortex (spatial working memory) and the anterior cingulate cortex (self-paced saccades) are also involved. Key areas for smooth pursuit are the FEF and the V5 complex in the parieto-temporo-occipital junction, but the SEF, the intraparietal sulcus and extrastriate visual areas are also involved. It is controversial whether saccades and smooth-pursuit movements activate different compartments of these areas. In the cerebellum, both functions activate the posterior vermis, whereas additional activation of the paravermal and lateral hemispheres rather reflects the cognitive processes involved, such as directed visuo-spatial attention.

The effects of antipsychotic medication on saccadic eye movement abnormalities in Huntington's disease

1. 1. The study was a prospective open trial done to determine the effect of antipsychotic medication on saccadic eye movements in patients with Huntington's disease (HD). The authors tested 16 outpatients with HD, 8 of whom were drug free and 8 of whom were on antipsychotic medication. We also tested 24 healthy control subjects. 2. 2. The antisaccade task was used to investigate the voluntary control of saccadic eye movements. Antisaccade latencies and error rates were used as outcome measures. Both HD patient groups showed significantly more antisaccade abnormalities than controls and the rate of abnormalities was very similar between the drug-free and medicated patient groups. 3. 3. The results suggest that these abnormalities are related to underlying neuropathology rather than effects of medication. Either specific dysfunction of the dorsolateral prefrontal cortex or of the subcortical circuit connecting this cortical area to the superior colliculus via the striatum are likely to be responsible for the generation of such antisaccade eye movement abnormalities.

Development of voluntary control of saccadic eye movements

To investigate the development of the voluntary control of saccadic eye movement, we examined eye movements in 99 normal children (4-13 years of age). Subjects were asked to fixate a central light for 3-5 s. A target was then presented, either to its right or left. In visually guided saccades, the mean latencies of the child group were longer than those of the adults, and decreased with age until the age of 12 where they reached adult levels. On the other hand, their peak saccadic velocities were not different from those of the adults. In the antisaccade task, they showed a higher rate of directional errors, indicating an inability to suppress reflexive saccades to the target. Mean latencies of correct antisaccades were significantly longer in the children than in the adults. Error rates and antisaccadic latency tended to decrease with age. We also examined the effects of an auditory warning signal during the fixation period and compared the results with those without. The warning stimulus was less effective in children than in adults in both tasks. Similar peak saccadic velocities between children and adults suggest the earlier development of the saccadic burst generator in the brainstem. In contrast, the delayed development of latency of saccades and antisaccades and the error rates of antisaccades suggest delayed maturation of the cerebral cortex, particularly the frontal association areas that are involved in both eye movement control and attentional processes.

Introduction to Biomedical Engineering

Over the past 50 years, as the discipline of biomedical engineering has evolved, is has come to include aspects of many different branches of engineering. This new book, intended to serve as an introduction to the field, brings together those aspects of the subject which have contributed most. The text divides naturally into two parts, the first dealing with physiological systems and modelling, the second with various health care technologies. Early chapters on anatomy and physiology contain more detail than is customary in engineering texts, with the chapter on bioelectric phenomena providing a particularly good account of the biophysics of excitable membranes. Chapters then deal in turn with sensors, instrumentation and signal processing. A chapter on modelling uses as an example the control of saccadic eye movement. The latter half of the book begins with a chapter on biomaterials. Chapters follow on two relatively new aspects of bioengineering, namely tissue engineering and biotechnology. Chapters then deal in turn with the engineering principals behind the commonly encountered imaging modalities, covering images produced by ionizing radiation, ultrasound and magnetic resonance phenomena. The text is written primarily for engineering students, and as such assumes a fairly high level of mathematical ability. As well as providing information on the fundamental principles underlying design, chapters also include some historical perspective on the developments described. Edited by three well-known teachers in the field of biomedical education, the book contains contributions from some 20 individual authors, all based in the USA. Course organizers will find the book particularly useful as numerous examples and exercises are included to help students consolidate their new-found knowledge. The text is adequately supported by line drawings, and each chapter is followed by a list of suggestions for further reading. Overall, the authors have succeeded in their task and are to be congratulated on the production of what is sure to become a popular textbook.

Antisaccade eye movement abnormalities in Tourette syndrome: evidence for cortico-striatal network dysfunction?

Saccadic eye movements are rapid eye movements which act to redirect the eyes from one object of interest to another. Accurately and objectively measurable, their underlying neuroanatomical mechanisms have been extensively studied. The antisaccade task allows the study of the frontocortico-striatal network involved in the voluntary control of saccadic eye movements. In this task, the subject is instructed to inhibit a reflex eye movement towards a peripheral target light and, instead, to generate a movement in the equal and opposite direction. An error occurs when the subject fails to suppress reflexive saccades towards the target. Significantly high error rates and increased latencies in the antisaccade task have been reported in disorders associated with dysfunction of the frontocortico-striatal network. Increased saccadic eye movement latencies and error rates have been reported in Tourette syndrome patients (n = 4) who were receiving antipsychotic medication. To investigate this further, we tested the antisaccade task on six male Tourette syndrome patients. The results were compared with 18 age- and sex-matched mentally and physically healthy, medication/alcohol-free controls. Antisaccade latencies were (mean +/- SD; ms) 751.2+/-186.7 for the Tourette syndrome group and 417+/-75.3 for controls, and error rates were 59+/-14.3 for the Tourette syndrome group and 11.9+/-6.4 for controls, respectively. These significant results may further support dysfunction of the frontocortico-striatal network in Tourette syndrome.

Inhibitory inefficiency and failures of intention activation: Age-related decline in the control of saccadic eye movements.

Inhibitory inefficiency and failures of intention activation: Age-related decline in the control of saccadic eye movements.