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Knowledge of cognitive and neural architecture and processes that control eye movements has advanced enough to allow precise and quantitative analysis of hitherto unsolved phenomena. In this review, we revisit from a neuropsychological viewpoint Hering vs. Helmholtz' hypotheses on binocular coordination. Specifically, we reexamine the behavior and the neural bases of saccade-vergence movement, to move the gaze in both direction and depth under natural conditions. From the psychophysical viewpoint, neo-Heringian and neo-Helmholtzian authors have accumulated arguments favoring distinct conjugate (for saccades) and disconjugate (for vergence) systems, as well as advocating for monocularly programmed eye movements. From the neurophysiological viewpoint, which reports brain cell recordings during the execution of a given task, neo-Heringian and neo-Helmholtzian physiologists have also provided arguments in favor of both hypotheses at the level of the brainstem premotor circuitry. Bridging the two, we propose that Hering and Helmholtz were both right. The emphasis placed by the latter on adaptive processes throughout life cycle is compatible with the importance of neurobiological constraints pointed out by the former. In the meanwhile, the study of saccade-vergence eye movements recalls how much the psychophysical definition of the task determines the interpretation that is made from neurophysiological data., (Copyright © 2014 Elsevier Masson SAS. All rights reserved.)

Introduction: Attention-Deficit and Hyperactivity Disorder (ADHD) affects 3 to 5% of school-aged children. Diagnosis is based on criteria defined by the Diagnostic and Statistical Manual of Mental Disorders fourth edition (DSM-IV), and there is no specific marker for the disease. Eye movements may be altered in ADHD. The goal of this study was to identify difficulties in oculomotor tasks in children with ADHD., Patients and Methods: Subjects were children with untreated ADHD (n=7) and age- and gender-matched healthy controls (n=7). Two different tasks (prosaccades and pursuit) were used to examine functions necessary for the planning and execution of eye movements. Student's t-test was used for the statistical analysis., Results: Prosaccades were able to be recorded in five children with ADHD and in all control subjects. In two patients, no saccades could be recorded due to their hyperactivity. There were significant differences (P<0.01) in prosaccade latency, children with ADHD showing significantly longer latency on the prosaccade task than controls (299±91 ms versus 197±14 ms). Pursuit performance was saccadic with a gain of 0.4 versus 0.6 and was not significantly altered in the ADHD group with respect to controls., Conclusion: Oculomotor measurements can be a simple, non-invasive test, easily performed in children with ADHD. Longer latency on the prosaccade task is observed in ADHD children., (Copyright © 2012 Elsevier Masson SAS. All rights reserved.)

Introduction: Voluntary or reactive saccades predominate in rapid eye movements. Their goal is to preserve an active and optimal visual perception of the environment. Saccades cannot be guided once launched. Oculomotor plasticity, or saccadic adaptation, is still partially unknown, in particular the role played by the basal ganglia. New neuro-ophthalmological rehabilitation techniques require understanding the neurophysiological basis and demonstrating the neuronal structures involved in this plasticity., Objectives: This study assessed the reactive saccade adaptation in patients with idiopathic Parkinson disease, as a model of basal ganglia dysfunction. We predicted that saccadic adaptation would be preserved in this pathology., Patients and Methods: Five patients with mild idiopathic hemi-Parkinson disease were included, as well as four age-matched controls. Reactive saccade adaptation was studied using the double-step target paradigm, in patients with OFF-Dopa treatment and in controls., Results: Group analysis demonstrated that patients had a lower level of adaptation than the controls (p<0.05). Individually, two patients did not adapt for bilateral saccades and one for ipsilateral (compared to Parkinson motor clinical syndrome) saccades. Two additional patients adapted on both sides but with a deficit in contralateral saccades when compared to the control group., Discussion: These preliminary results suggest basal ganglia involvement in reactive saccadic adaptation, which remains to be clarified., (Copyright © 2011 Elsevier Masson SAS. All rights reserved.)

Introduction: Superior oblique myokymia (SOM/MOS) is an under-recognised and probably under-diagnosed disorder. We describe the clinical signs of this condition among three patients. Next, from review of the literature, we suggest an algorithm for diagnosis and treatment., Observation: Retrospective study of three patients aged 40 to 55 presenting with brief, intermittent monocular episodes of oscillopsia., Discussion: The acute symptomatology of superior oblique myokymia follows a recognizable pattern: it always presents with brief, intermittent monocular vertical oscillopsia and/or vertical diplopia with torsion. The clinical signs are related to a neurogenic hyperexcitability of the superior oblique muscle. Treatment may be medical (carbamazepine, gabapentin, beta-blocker) or surgical. Recent publications report that superior oblique myokymia may result from vascular compression of the trochlear nerve (fourth cranial nerve), which controls the action of the superior oblique muscle, placing this condition in the category of vasculonervous conflicts., Conclusion: Superior oblique myokymia is a relatively poorly known disorder, despite classic pathognomonic symptoms. It is a benign condition, which can nonetheless become incapacitating. It occasionally portends an intracranial pathologic process, which must then be addressed with specific treatment., (Copyright © 2011 Elsevier Masson SAS. All rights reserved.)

Introduction: Oculomotor deficiencies in multiple sclerosis (MS) are frequently characterized by internuclear ophthalmpoplegia or isolated abduction or adduction palsies. Complete unilateral conjugate gaze paralysis and the "one and a half" syndrome are rare. Complete bilateral horizontal gaze paralysis has been exceptionally reported., Observation: Here, we describe an unusual oculomotor paralysis as a suspected first event of MS. A 24-year-old woman with an uneventful medical history presented for sudden onset of binocular diplopia. On examination, abduction and adduction saccades were impossible, whereas vertical eye saccades and convergence were normal. Oculocephalic reflex failed to improve horizontal eye movement. No nystagmus and no other sign of brainstem dysfunction were observed. Visual acuity was 4/10 in the right eye and 6/10 in the left eye. A sign of Marcus Gunn was noted in the right eye. Blood samples and cerebrospinal fluid were normal, no oligoclonal bands were detected. Visual evoked potentials were significantly impaired in both eyes and argued for bilateral optic neuritis. Brain MRI scans showed white matter T2-hypersignal abnormalities, which fulfill Barkhof criteria for MS. A small symmetric lesion was noted in the posterior part of the medial pontine tegmentum. As a first episode of MS was suspected, treatment with methylprednisolone 1000 mg/d for 3 days was started, and was followed by complete recovery of eye movements and visual acuity after 3 weeks., Discussion: To our knowledge, only two cases of complete horizontal bilateral ophthalmoplegia have been reported in the literature. Both were associated with peripheral facial nerve palsy as a first event in MS. In our case report, we describe for the first time a complete bilateral horizontal ophthalmoplegia with no other brainstem dysfunction. By analogy with the "one and a half" syndrome, such complete horizontal gaze paralysis could be named a "one and one" syndrome and seems to be specifically related to a first event of MS., (Copyright © 2010 Elsevier Masson SAS. All rights reserved.)

We studied, in healthy elderly subjects (aged from 63 to 83 years) and adults (aged from 20 to 32 years), ocular saccades in two conditions: one the one hand, the gap condition, where the central target disappears; then follows a period of 200 ms during which the fixation and attention were disengaged; finally, a visual target appears in the periphery. On the other hand, the overlap condition, in which the peripheral target appears when the central target is still present, the subject should voluntarily disengage his attention and fixation to orient them toward the peripheral target. These paradigms stimulate automatic versus controlled triggering of saccades. The average saccade latency (measured by video-oculography) was longer in the elderly, and irrespectively of the condition. However, the elderly as the young subjects produced shorter latencies in the gap condition than in the overlap condition. Moreover, in the gap condition, we observed the emergence of a considerable number of reflex saccades with very short latency (between 80 and 120 ms, minimal conduction time) called "express saccades". The occurrence rate of such saccades was similar in the young and the elderly subjects. These results suggest the existence of separate circuits, one non-being sensitive to age (express saccades), the other suffering the effects of aging (controlled saccades). In another ongoing study, this methodology has been applied to patients with Lewy body dementia. The preliminary results from three patients showed an abnormal slowness of latencies, even in the gap condition expected to promote automatic and reflex saccades. Furthermore, we observed a total absence of saccades with express latency. These promising results suggest a deficit even for automatic and express saccades in these patients.

A literature review of the important findings discovered over the past three decades on ocular movements during reading is presented herein. This fairly recent function in human evolution is a sophisticated sensorimotor and cognitive activity that brings very complex neurological and motor mechanisms into play. However, knowledge in this field is limited, even though reading problems are very common in children. We collected all the references in PubMed dating from 1969 to 2009 using the following "binocular coordination", "eye movements", "reading", and "dyslexia". When reading, the visual axes move in a very particular way, notably with regard to the parallelism of the ocular axes when saccades are triggered to reach the words to be read and during fixations, which enable decoding. In fact, when reading, the visual axes are often disassociated, even going as far as to intersect in a considerable number of cases. There are relatively few studies that have examined binocular coordination during reading. We are beginning to understand how the ocular axes move during horizontal saccades. Three-dimensional studies could be the next step to providing more precise data., (Copyright (c) 2010 Elsevier Masson SAS. All rights reserved.)

Multiple sclerosis is the most common disabling neurological disease in young people. Many neuro-ophthalmological manifestations can occur during the course of the illness, and optic neuritis is both the most frequent and the best known. However, some ocular motility disorders can also occur, but since there may be no symptoms, they often remain underdiagnosed. These eye movement disorders are mostly related to brain-stem and cerebellum lesions. They can be acute, indicating a spatial dissemination of the demyelinating disease, and consequently may indicate the need for systemic treatment of multiple sclerosis. More often, they evolve slowly, progressing with the multiple sclerosis. In this case, they could provide a clue to the prognosis of the disease. In this survey, we discuss the two major symptoms of ocular motor disorders likely to occur during multiple sclerosis: oscillopsia and diplopia.

Oscillopsia is an illusion of an unstable visual world. It is associated with poor visual acuity and is a disabling and stressful symptom reported by numerous patients with neurological disorders. The goal of this paper is to review the physiology of the systems subserving stable vision, the various pathophysiological mechanisms of oscillopsia and the different treatments available. Visual stability is conditioned by two factors. First, images of the seen world projected onto the retina have to be stable, a sine qua non condition for foveal discriminative function. Vestibulo-ocular and optokinetic reflexes act to stabilize the retinal images during head displacements; ocular fixation tends to limit the occurrence of micro ocular movements during gazing; a specific system also acts to maintain the eyes stable during eccentric gaze. Second, although we voluntary move our gaze (body, head and eye displacements), the visual world is normally perceived as stable, a phenomenon known as space constancy. Indeed, complex cognitive processes compensate for the two sensory consequences of gaze displacement, namely an oppositely-directed retinal drift and a change in the relationship between retinal and spatial (or subject-centered) coordinates of the visual scene. In patients, oscillopsia most often results from abnormal eye movements which cause excessive motion of images on the retina, such as nystagmus or saccadic intrusions or from an impaired vestibulo-ocular reflex. Understanding the exact mechanisms of impaired eye stability may lead to the different treatment options that have been documented in recent years. Oscillopsia could also result from an impairment of spatial constancy mechanisms that in normal condition compensate for gaze displacements, but clinical data in this case are scarce. However, we suggest that some visuo-perceptive deficits consecutive to temporo-parietal lesions resemble oscillopsia and could result from a deficit in elaborating spatial constancy.

Aims of the Study: To assess to which extent performing saccadic eye movements modifies the postural strategies aimed at maintaining balance., Materials and Methods: Twelve healthy adults were tested on a force platform in several conditions including one in which they were required to stare a visual target and four in which small and larger saccadic eyes movements were performed vertically and horizontally. The displacements of the centre of pressure (CP) were then processed through frequency analysis and modelled as fractional Brownian motion (fBm). Through the latter, one may objectively assess from which distance and after which delay corrective process are initiated. In addition, the degree with which the CP movement is successively controlled is determined., Results: A decrease of the magnitudes of the CP trajectories is observed during saccades, especially along the anteroposterior axis. The fBm modelling emphasises the setting of a particular postural strategy whose main effect consists in more delayed corrective processes associated with a better capacity to control the corrective CP displacements., Conclusion: This particular strategy could be linked to the difficulty for the subjects to detect pertinent visual information in this very axis and/or an increased cognitive constraint due to the saccades. On the whole, these data underline the necessity, when performing postural protocols, to ask the patients to stare a visual target in order to limit their eye movements.

Eye movements are an integral part of visual function. They are particularly well developed in frontal-eyed predator species. The abducens nuclei ensure lateral ocular motor synergy, while the oculomotor nuclei control vertical eye movements and convergence. The two main types of conjugate eye movement--saccades (image switching) and slow movements (image stabilization)--are controlled by specific brainstem premotor structures (respectively reticular and vestibular). Upstream of the brainstem, the cortical and subcortical pathways involved in eye movements are gradually being elucidated. Saccades are being used as a motor model to study the different cognitive processes, such as spatial memory, prediction and decision, involved in general movement preparation. The classical approaches based on lesion analysis, combined with transcranial magnetic stimulation and functional cerebral imaging, are contributing to our understanding of how the brain functions. Eye movements can be used for bedside diagnostic purposes, but also for sophisticated laboratory studies designed to explore the universe of cognition.

Advances in our knowledge on eye movements over the last 25 years are reviewed, focusing on the author's experience. First, the advantages of binocular frontal vision, which is a common characteristic of all predator mammals, are compared to those of lateral vision, characterizing their preys. Binocular frontal vision implies a perfect parallelism of both eyes, which is ensured in the pons by means of the abducens nucleus, controlling abduction as well as adduction. The pathological example of the "one-and-a-half" syndrome, in which the abducens nucleus and the adjacent medial longitudinal fasciculus are simultaneously impaired, is described. The main brainstem syndromes involving vertical eye movements are also reviewed: in particular, the third nerve nucleus syndrome, in which both ipsilateral third nerve paralysis and contralateral superior rectus paralysis (with hypotropia) result from a unilateral third nerve nucleus lesion. A case of upbeat nystagmus (in the primary position of gaze) due to a small upper pontine lesion, probably affecting the ventral tegmental tract (VTT) is also reported. This is an opportunity to emphasize that, although a number of cases of upbeat nystagmus due to focal brainstem lesions affecting the upward vestibular pathway (UVP)--either at the upper pontine (VTT) or caudal medullary level--exist in the literature, no convincing cases with downbeat nystagmus (in the primary position of gaze) due to a focal brainstem lesion have been reported. Downbeat nystagmus could result from a UVP hyperactivity (secondary to a floccular lesion) and the notion that this pathway is physiologically predominant compared to the downward pathway, maybe due to gravity, is developed. A new hypothesis about the role of the caudal medulla in UVP is also proposed. Next, the cortical control of saccadic eye movements is reviewed, with a reminder that reflexive saccades are mainly triggered by the parietal eye field whereas intentional saccades depend upon the frontal eye field. The inhibition of reflexive saccades is mainly controlled by the dorsolateral frontal cortex (DLPFC), i.e. area 46 of Brodmann. A few examples of the use of saccades as a research tool and model in cognitive neurosciences are given. The use of memory-guided saccades allowed us to study spatial memory and led us to propose a relatively original conception of the cortical control of spatial memory in which the DLPFC, the parahippocampal cortex and the hippocampal formation could be involved successively according to specific periods of time. An experiment using functional magnetic resonance imaging in a paradigm studying decision is described, again with the involvement of the DLPFC in the decisional process. Lastly, the usefulness of eye movements in clinical neuro-ophthalmology at the bedside as well as in neurophysiological or even neuropsychological research in the laboratory is emphasized.

Saccades are very rapid eye movements allowing us to explore the visual world. Although most of the time unconscious, the programming of each saccade implies a complex decision which depends upon both the perceptual context and the intentions of the subject. The cerebral cortex is critically involved in deciding where, when and in which sequence we move the eyes. Using sophisticated experimental designs, such as the learning of sequences of saccades, has revealed that besides a core fronto-parietal circuit, prefrontal, cingulate, and mediotemporal regions seem critically involved in higher level oculomotor control. Understanding precisely the cortical networks associated to different components of ocular movements can certainly be very useful to characterize, test, and eventually detect various kinds of neurological pathology.

Exploration of ocular motricity can be helpful for diagnosis in certain parkinsonian syndromes. Oculomotricity is perturbed in Parkinson's disease (PD) and in multiple system atrophy (MSA). The minimal anomalies, sometimes observed in these conditions, both clinically and on oculomotor recordings, cannot contribute significantly to diagnosis. In corticobasal degeneration (CBD), infraclinical oculomotor anomalies can be identified on oculomotor recordings and are relatively specific to atypical parkinsonian syndrome: particularly long latency of ocular saccades related to posterior parietal involvement. The most significant contribution is observed for progressive supanuclear palsy (PSP) where the oculomotor anomalies are evident at clinical examination and are even the cardinal signs of the condition: particularly paralysis of vertical ocular saccades (downbeat and upbeat) or downbeat saccades, ocular pursuit also being perturbed but not reflex movements (preservation of oculocephalic reflexes). This dissociation between palsy of saccade and pursuit movements and preservation of oculocephalic reflexes is the sign of the supranuclear origin of the oculomotor disorder in PSP. In early stage PSP before clinical expression, requiring oculomotor recordings to be recognized, it is relatively specific in the context of degenerative parkinsonian degeneration. PSP also involves other less specific anomalies such as a perturbation of the antisaccade movements (related to a frontal syndrome), anomalous ocular pursuit (becoming saccadic) and presence of square wave. A rigorous clinical examination of oculomotor function at a more advanced stage of PSP, or oculomotor recordings at an early stage of PSP or CBD, can thus contribute significantly to the diagnosis of both conditions.

Unlabelled: Several studies have confirmed the existence of genetic factors in schizophrenia. However, the genotype predisposing for the disease is not known yet. Nevertheless, those genetic factors in the families of schizophrenic patients urge us to search for genetic vulnerability markers of schizophrenia. Ocular pursuit disorders, in particular, could be one of those vulnerability markers. Eye movements have been often tested in schizophrenia. Most of the schizophrenic patients have eye-tracking disorders and their biological relatives demonstrate an increased prevalence of eye-tracking impairments. The aim of the study was to research if smooth pursuit eye movements could be a vulnerability marker of schizophrenia. In order to have an indication about this hypothesis, impairments of smooth pursuit eye movements were researched in both schizophrenics and their parents., Methods: Fifteen DSM IV schizophrenic patients stabilized at the time of the inclusion and not treated with lithium, benzodiazepines, barbiturates, or chloral hydrate; 19 parents without history of schizophrenic spectrum disorders (SADSLA and IPDE), and 2 groups of healthy subjects matched in age and sex with probands and with the parents, were included in the study. Parents only were included (fathers or mothers) in order to have an homogeneous population for the genetic risk and age. The eye-tracking paradigm used was a smooth pursuit task. The stimulus was a sinusoidal wave form moving on a horizontal line, with a frequency of 0.4 Hz and an amplitude of 30 degrees. Different parameters were measured: gain (ratio between the eye velocity and the target velocity) and saccades frequencies (catch-up saccades, back-up saccades, anticipatory saccades and square-wave-jerks). For each parameter, analysis of covariance (ANCOVA) with age as covariable was carried out. For the results reaching the significance of 0.05, the Bonferroni correction was applied (level of significance 0.016). The effect size of the parameter was calculated ((the mean of the subjects minus the mean of the matched controls) divided by standard deviation of the two groups). According to Cohen, 0.20 indicates a small effect size, 0.50 indicates a medium effect size and 0.80 indicates a large effect size., Results: Comparison between patients and matched controls: the means of global gain, of gain for the movements to the left and of gain for the movements to the right did not differ significantly between patients and their matched controls. The size effects are 0.31 for the global gain, 0.20 for the movements to the left and 0.41 for the movements to the right. The frequencies of total saccades, catch-up saccades, back-up saccades, anticipatory saccades and square-wave-jerks did not differ significantly between patients and their controls. The size effects for those parameters were 0.09, 0.03, 0.00, 0.39 and 0.63 respectively. Comparison between parents and matched controls: the means of global gain, of gain for the movements to the left and of gain for the movements to the right did not differ significantly between the two groups. The size effects for those parameters were 0.00, 0.05 and 0.17 respectively. The frequency of total saccades did not differ significantly between the groups whereas the size effect was 0.63. The frequency of catch-up saccades was significantly more important in parents than in controls (p = 0.006) and the size effect was 0.80. The other saccadic parameters did not differ significantly between groups, their size effects were 0.24 for the back-up saccades, 0.21 for the anticipatory saccades and 0.00 for the square-wave-jerks. Whereas the gain of the patients had a tendency to be lower than the gain of their controls, no significant difference was observed between patients and their controls. Only a size effect of 0.63 for the frequency of square-wave-jerks was obtained. This large effect size suggests that the difference between patients and controls might be significant in a larger sample. The catch-up saccades frequency between parents and controls was significant. The differences between our study and the previous studies could be due to several factors. The paradigms used were different between the studies and our sample was small (only 15 patients and 19 relatives). Moreover, some patients in the previous studies were treated by lithium, drug well known to modify ocular pursuit and, finally the relatives in the other studies were 10 years older than ours and age is known to alter ocular pursuit. Since an impairment of the smooth pursuit was observed in the relatives of schizophrenic patients but not in the probands, this study does not support the hypothesis that eye-tracking disorders could be considered as a marker of vulnerability of schizophrenia.

Eye movement anomalies are more frequent in schizophrenic patients than in healthy subjects. This study deals with visually guided saccadic eye movements in seventeen schizophrenic patients [ten untreated (neuroleptic-naive or free), seven treated patients] and their correlations between symptoms presented by patients and oculomotor performances. There was no significant difference between the patients and the control group in visually guided saccades tasks. However, negative correlations between oculomotor performance and positive or disorganisation symptomatology were found. Thus, although no major oculomotor dysfunction in response to external stimulus was seen in schizophrenic patients, some symptoms were linked to oculomotor performance impairment. Thus psychiatric symptoms might share some common cerebral circuits which those involved in oculomotor tasks.

What are the distinctive criteria for the diagnosis of multiple system atrophy? The combination of motor, dysautonomic, neuropsychological and eyes movements may help to distinguish, at a early stage, multiple system atrophy from other neurodegenerative diseases such as Parkinson's disease, progressive supranuclear palsy or corticobasal degeneration. Thus, these criteria are suitable both for clinical care and drug trials.

Normal binocular function is defined as the bifoveal connection of the central and peripheral structures of the visual system. Binocular function in strabismus is defined as connections, more or less strong and more or less labile, of the fovea of the fixating eye with the "pseudo-fovea" of the deviating eye including all central and peripheral structures, and this connection represents, in fact, a progress of adaptation of all parameters to the new conditions of vision.

This paper presents a summary of results which concern the neuronal mechanisms underlying the control of gaze. The development of techniques of recording from alert animals and combining functional analysis of neuronal activity with intracellular marking by horse-radish peroxidase has allowed a study of the neuronal mechanisms underlying the vestibulo-ocular reflex and the generation of saccades. The results of these analysis show that there is a close interaction at the level of the brainstem between this two elements of the oculomotor repertoire. This interaction involves both the action of premotor burst neurons involved in the generation of the saccade but also ponto-bulbar reticulo-spinal neurons belonging to the tecto-reticulo-spinal system and involved in the coordination between eye and head movements. This interactions has a very important consequence in the field of recuperation from vestibular lesions. It has been suggested that after vestibular lesions, in addition to local plasticity at the level of the vestibular nuclei it has been suggested that recuperation of function can be due to a functional creation of pseudo-vestibular reflexes by a sequence of blended saccades induced by the saccadic generator mechanisms and with the contribution of the reticulo-spinal system. These interactions have been studied in humans. We have also shown that after prism adaptation the non functional vestibulo-ocular reflex could be replaced by saccades confirming our previous studies in animals. In order to try to approach the neuronal mechanisms underlying these cortical influences we have been able to delineate by position emission tomography techniques the areas of the brain contributing to the generation of voluntary or remembered saccades (parietal cortex, frontal eye fields, supplementary motor eye field, cingulate gyrus, etc.). We have also shown that in patients with lesions of these areas the major deficit in the execution of saccades derived from vestibular information about body motion was the prefrontal cortex and SMA.

Among saccades triggered by the cerebral cortex, visually guided saccades are the best known and their cortical control is reviewed here. Only two immediately supra-reticular structures are able to trigger saccades (whatever their type): the frontal eye fields (FEF) and the superior colliculus (SC). These structures control two parallel excitatory pathways, which can replace each other in the event of lesion. Experimental findings have suggested that the colliculo-reticular pathway would, in the normal state, play the main role in the triggering of reflexive visually guided saccades. Furthermore experimental and clinical data suggest that the SC would receive an excitatory afference from the posterior part of the intraparietal sulcus, which could be involved in the triggering of these saccades. The parietal lobe could influence the SC by increasing the pre-excitation due to the onset of the visual target. There are also inhibitory pathways which prevent saccades, in particular during fixation. Two groups of tonic neurons inhibit the excitatory pathways. These are the omnipause neurons and the neurons of the substantia nigra (pars reticulata), which project upon the premotor reticular formations and the SC respectively. The pathways projecting upon these 2 types of neurons are multiple and still little known. Nevertheless, some arguments suggest that the frontal lobe partly controls inhibition. These arguments are based on a somewhat disinhibited triggering of reflexive visually guided saccades in focal or degenerative (progressive supranuclear palsy) frontal lesions. The prefrontal cortex could be involved in inhibition control, and it could act functionally above the FEF.

Neuronal mechanisms of production of ocular saccadic movements are discussed, together with stabilizing movements of vestibular origin, and descriptions given of several neuronal elements constituting the tecto-reticulo-spinal system, the generator of horizontal saccadic movements in the brain stem, the vestibulo-ocular pathway, etc... Analysis of these pathways and of the signals travelling through them suggests that the overall apparatus is not constituted of isolated reflex modules but acts as a true functional unit for cooperation between orientation and stabilization mechanisms. In addition, coordination of synergies between eye and head movements appear to be based on the activity of clearly identifiable neurons. This neuronal implementation of the concept of synergy is completed further by a remarkable functional flexibility. The latter allows substitution by the brain, for example, fo saccades instead of vestibular reflex movements when the latter are deficient because of lesions or disturbances in the coherence of sensory information. The principal conclusion reached is that cognitive factors, which imply representations of body movements in space activated as a function of the subject's goals, must be considered when ocular movement, and gaze control is described.

The function of the oculomotor system is to assure gaze movements. Its equilibrium is essential to allows the stability of gaze, especially fixation. Therefore, an opto-static system is necessary to complete the kinetic organisation of eye movements. A disorder in this opto-static system produces abnormal eye movements. Their appearance depends on the location nd on the nature of the lesion in the opto-static system.