Les oscillopsies sont une anomalie de la perception visuelle, caractérisée par la perception de déplacements d’un environnement visuel stable. Elles sont dues aux glissements sur la rétine de l’image ...de panorama visuel. Il en existe deux grandes catégories selon le contexte dans lequel elles surviennent. Dans une première catégorie, les oscillopsies ne surviennent que lors de mouvements de la tête. Elles sont alors secondaires à une anomalie du réflexe vestibulo-oculaire (RVO) ou de la transmission de ce réflexe vers les globes oculaires. Lors des mouvements de la tête, le RVO assure normalement l’immobilité des globes par rapport à l’environnement en déclenchant une rotation des globes d’amplitude égale mais de direction contraire. Une anomalie de ce réflexe (ou de sa transmission) entraînera donc une compensation oculomotrice imparfaite des mouvements de la tête, donc un glissement de l’image de l’environnement sur la rétine lors des mouvements de la tête. Dans une seconde catégorie, les oscillopsies surviennent même lorsque la tête reste immobile. Elles sont alors dues à la présence de mouvements oculaires anormaux tels que certains nystagmus acquis (pendulaires et à ressort) ou certaines intrusions saccadiques (flutter-opsoclonus). Elles peuvent aussi être monoculaires, liées le plus souvent à la présence de myokimies du IV ou, plus rarement, d’un nystagmus pendulaire monoculaire. Elles sont alors dues aux glissements sur la rétine de l’image de l’objet observé du fait des déplacements intempestifs des globes oculaires. Il existe enfin des oscillopsies d’origine centrale, pouvant survenir par exemple lors de crises comitiales occipitales. Une question primordiale devant un patient se plaignant d’oscillopsies est donc de savoir si celles-ci ne surviennent que lors des mouvements de la tête, ou même lorsque la tête reste immobile.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Prefrontal dysfunction in neuropsychiatric disorders such as schizophrenia has been shown to impair inhibition of reflexive saccadic eye movements; however, it is unclear whether reflexive saccade ...inhibition can be attributed to a distinct subregion of the human prefrontal cortex.
We tested 15 patients with acute unilateral ischemic lesions of the prefrontal cortex and 20 control subjects with an antisaccade task. Lesions were reconstructed using Talairach coordinates, and possible candidate regions for reflexive saccade inhibition were identified.
Significantly increased antisaccade error rates were observed in patients with lesions affecting a region in mid-dorsolateral prefrontal cortex or the white matter between this region and the anterior portions of the internal capsule. Antisaccade error rates of patients with lesions outside this region were normal. These findings were largely independent of lesion volume, postlesion delay, and subject age.
Our findings suggest that inhibition of reflexive saccades depends on a circumscribed subregion of the human dorsolateral prefrontal cortex. This region closely corresponds to Brodmann area 46 as defined by recent cytoarchitectonic studies. Increased antisaccade error rates in patients with prefrontal pathology may be explained by dysfunction of this region.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Highlights • Latency of saccades lengthens with age, for targets presented left, up and down. • The error rate of antisaccades may reach up to 80% by the seventh decade of life. • Subjects of all age ...groups correct over 99% of the errors made on antisaccade task. • Skewness of horizontal saccades is stable throughout the lifespan. • The gain of horizontal and vertical smooth pursuit is not affected by senescence.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
A combination of oculometric measurements, invasive electrophysiological recordings and microstimulation have proven instrumental to study the role of the Frontal Eye Field (FEF) in saccadic ...activity. We hereby gauged the ability of a non-invasive neurostimulation technology, Transcranial Magnetic Stimulation (TMS), to causally interfere with frontal activity in two macaque rhesus monkeys trained to perform a saccadic antisaccade task. We show that online single pulse TMS significantly modulated antisaccade latencies. Such effects proved dependent on TMS site (effects on FEF but not on an actively stimulated control site), TMS modality (present under active but not sham TMS on the FEF area), TMS intensity (intensities of at least 40% of the TMS machine maximal output required), TMS timing (more robust for pulses delivered at 150 ms than at 100 post target onset) and visual hemifield (relative latency decreases mainly for ipsilateral AS). Our results demonstrate the feasibility of using TMS to causally modulate antisaccade-associated computations in the non-human primate brain and support the use of this approach in monkeys to study brain function and its non-invasive neuromodulation for exploratory and therapeutic purposes.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
The oculomotor role of the basal ganglia has been supported by extensive evidence, although their role in scanning eye movements is poorly understood. Nineteen Parkinsońs disease patients, which ...underwent implantation of deep brain stimulation electrodes, were investigated with simultaneous intraoperative microelectrode recordings and single channel electrooculography in a scanning eye movement task by viewing a series of colored pictures selected from the International Affective Picture System. Four patients additionally underwent a visually guided saccade task. Microelectrode recordings were analyzed selectively from the subthalamic nucleus, substantia nigra pars reticulata and from the globus pallidus by the WaveClus program which allowed for detection and sorting of individual neurons. The relationship between neuronal firing rate and eye movements was studied by crosscorrelation analysis. Out of 183 neurons that were detected, 130 were found in the subthalamic nucleus, 30 in the substantia nigra and 23 in the globus pallidus. Twenty percent of the neurons in each of these structures showed eye movement-related activity. Neurons related to scanning eye movements were mostly unrelated to the visually guided saccades. We conclude that a relatively large number of basal ganglia neurons are involved in eye motion control. Surprisingly, neurons related to scanning eye movements differed from neurons activated during saccades suggesting functional specialization and segregation of both systems for eye movement control.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Patients with ephedrone parkinsonism (EP) show a complex, rapidly progressive, irreversible, and levodopa non-responsive parkinsonian and dystonic syndrome due to manganese intoxication. Eye ...movements may help to differentiate parkinsonian syndromes providing insights into which brain networks are affected in the underlying disease, but they have never been systematically studied in EP. Horizontal and vertical eye movements were recorded in 28 EP and compared to 21 Parkinson's disease (PD) patients, and 27 age- and gender-matched healthy subjects using standardized oculomotor tasks with infrared videooculography. EP patients showed slow and hypometric horizontal saccades, an increased occurrence of square wave jerks, long latencies of vertical antisaccades, a high error rate in the horizontal antisaccade task, and made more errors than controls when pro- and antisaccades were mixed. Based on oculomotor performance, a direct differentiation between EP and PD was possible only by the velocity of horizontal saccades. All remaining metrics were similar between both patient groups. EP patients present extensive oculomotor disturbances probably due to manganese-induced damage to the basal ganglia, reflecting their role in oculomotor system.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
High intraindividual performance variability is one of the most robust findings to emerge in cognitive-experimental research of attention deficit hyperactivity disorder (ADHD). Evidences from studies ...incorporating structural or functional human brain mapping methods indicate that this increased intraindividual variability is not simply a sequel of general brain dysfunction, but is likely related to the functioning of neural circuits that engage the prefrontal cortex, particularly the dorsolateral areas (dlPFC). In order to examine further the anatomical and pharmacological substrate responsible for this high intraindividual variability disorder, we injected GABA(A) antagonist (bicuculline) or GABA(A) agonist (muscimol) in the dlPFC of monkeys performing a reflexive oculomotor task. Here we show that, whereas GABA(A) agonist injection induced no or minimal impairments, injection of GABA(A) antagonist dramatically increased the intraindividual variability of saccade response time and of saccade spatial accuracy (amplitude and direction). Overall, this study demonstrates that the balance between excitatory/inhibitory activities in the dlPFC is fragile but crucial, since local micro-injection of GABA(A) antagonist can induce marked behavioural effects. It also reveals that higher cognitive areas such as the dlPFC are markedly capable to influence the productions and metrics of reflexive movements. Altogether, this study provides promising perspectives for the development of new therapeutic strategies for the treatment of diseases in which high intravariability disorders are a prominent feature.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
In the anti‐saccade paradigm, subjects are instructed not to make a reflexive saccade to an appearing lateral target but to make an intentional saccade to the opposite side instead. The inhibition of ...reflexive saccade triggering is under the control of the dorsolateral prefrontal cortex (DLPFC). The critical time interval at which this inhibition takes place during the paradigm, however, is not exactly known. In the present study, we used single‐pulse transcranial magnetic stimulation (TMS) to interfere with DLPFC function in 15 healthy subjects. TMS was applied over the right DLPFC either 100 ms before the onset of the visual target (i.e. −100 ms), at target onset (i.e. 0 ms) or 100 ms after target onset (i.e. +100 ms). Stimulation 100 ms before target onset significantly increased the percentage of anti‐saccade errors to both sides, while stimulation at, or after, target onset had no significant effect. All three stimulation conditions had no significant influence on saccade latency of correct or erroneous anti‐saccades. These findings show that the critical time interval at which the DLPFC controls the suppression of a reflexive saccade in the anti‐saccade paradigm is before target onset. In addition, the results suggest the view that the triggering of correct anti‐saccades is not under direct control of the DLPFC.
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BFBNIB, DOBA, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, SIK, UILJ, UKNU, UL, UM, UPUK
Administration of subanesthetic doses of ketamine, a noncompetitive N-methyl-D-aspartate receptor antagonist, induces a spectrum of behavioral disorders that are commonly observed in patients with ...schizophrenia. Although it has been demonstrated that poor antisaccade performance is a core dysfunction in schizophrenia, the ability of ketamine to induce an increased distractibility has not been demonstrated. The present study aimed to determine whether ketamine administration would reproduce the same antisaccade deficit as that observed in schizophrenic subjects.
We studied the effect of acute ketamine or saline administration on the performance of two monkeys trained on a reflexive visually guided saccade task and an antisaccade task.
The main result is that ketamine administration induced a markedly increased antisaccade error rate and increased antisaccade latency, similar to that seen in schizophrenic subjects. Other impairments consisted of increased reflexive saccade latency and the presence of a gaze-evoked nystagmus.
This study supports the validity of ketamine as a pharmacological model of schizophrenia. Based on the known pharmacological effects of ketamine, further studies should allow the investigation of the pharmacological basis of distractibility.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
10.
Cortical control of saccades Pierrot-Deseilligny, C; Rivaud, S; Gaymard, B ...
Annals of neurology,
19/May , Volume:
37, Issue:
5
Journal Article
Peer reviewed
A scheme for the cortical control of saccadic eye movements is proposed based partly on defects revealed by specific test paradigms in humans with discrete lesions. Three different cortical areas are ...capable of triggering saccades. The frontal eye field disengages fixation, and triggers intentional saccades to visible targets, to remembered target locations, or to the location where it is predicted that the target will reappear (i.e., saccades concerned with intentional exploration of the visual environment). The parietal eye field triggers saccades made reflexively on the sudden appearance of visual targets (i.e., saccades concerned with reflexive exploration of the visual environment). The supplementary eye field is important for triggering sequences of saccades and in controlling saccades made during head or body movement (i.e., saccades concerned with complex motor programming). Three other areas contribute to the preparation of certain types of saccades. The prefrontal cortex (area 46 of Brodmann) plays a crucial role for planning saccades to remembered target locations. The inferior parietal lobule is involved in the visuospatial integration used for calculating saccade amplitude. The hippocampus appears to control the temporal working memory required for memorization of the chronological order of sequences of saccades.
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