What stops a saccade?

Optican, Lance M.; Pretegiani, Elena

doi:10.1098/rstb.2016.0194

Cited by 31 publications

(36 citation statements)

References 64 publications

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“…It requires the active suppression of an automated saccade plan, and the generation of a voluntary saccade to an abstract location. The saccadic suppression described here may be different than stopping ongoing movements as discussed elsewhere in the issue [86][87][88], but involve very similar neural circuitry. Additionally, we posit that the two types of saccade suppression we discussed are also different from the need to cancel a voluntarily planned saccade, which is better studied using the countermanding and stop-signal tasks that are also reviewed elsewhere in this issue [85,[89][90][91].…”

Section: Resultsmentioning

confidence: 82%

Mechanisms of saccade suppression revealed in the anti-saccade task

Coe¹,

Munoz²

2017

Phil. Trans. R. Soc. B

130

122

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The anti-saccade task has emerged as an important tool for investigating the complex nature of voluntary behaviour. In this task, participants are instructed to suppress the natural response to look at a peripheral visual stimulus and look in the opposite direction instead. Analysis of saccadic reaction times (SRT: the time from stimulus appearance to the first saccade) and the frequency of direction errors (i.e. looking toward the stimulus) provide insight into saccade suppression mechanisms in the brain. Some direction errors are reflexive responses with very short SRTs (express latency saccades), while other direction errors are driven by automated responses and have longer SRTs. These different types of errors reveal that the anti-saccade task requires different forms of suppression, and neurophysiological experiments in macaques have revealed several potential mechanisms. At the start of an anti-saccade trial, pre-emptive top-down inhibition of saccade generating neurons in the frontal eye fields and superior colliculus must be present before the stimulus appears to prevent express latency direction errors. After the stimulus appears, voluntary anti-saccade commands must compete with, and override, automated visually initiated saccade commands to prevent longer latency direction errors. The frequencies of these types of direction errors, as well as SRTs, change throughout the lifespan and reveal time courses for development, maturation, and ageing. Additionally, patients diagnosed with a variety of neurological and/or psychiatric disorders affecting the frontal lobes and/or basal ganglia produce markedly different SRT distributions and types of direction errors, which highlight specific deficits in saccade suppression and inhibitory control. The anti-saccade task therefore provides valuable insight into the neural mechanisms of saccade suppression and is a valuable tool in a clinical setting.This article is part of the themed issue 'Movement suppression: brain mechanisms for stopping and stillness'.

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Section: Resultsmentioning

confidence: 82%

Mechanisms of saccade suppression revealed in the anti-saccade task

Coe¹,

Munoz²

2017

Phil. Trans. R. Soc. B

130

122

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“…Optican (2009) indeed proposed that these saccades are driven by a combination of commands issued by neurons in the dSC and the cFN. According to this "dual drive" hypothesis, the locus of dSC activity would encode the location where the target initially appeared whereas the cFN component would encode the complementary command related to the target motion after the collicular "snapshot" (see also Optican and Pretegiani 2017). However, a recent study showed that the population of active neurons in the dSC cannot be reduced to a discrete signal encoding the location where the target initially appeared.…”

Section: Discussionmentioning

confidence: 99%

“…More specifically, according to this "dual drive" hypothesis (Optican 2009), interceptive saccades would be driven by a combination of commands issued by neurons in the deep superior colliculus (dSC) and caudal fastigial nucleus (cFN). The locus of dSC activity would encode the location where the target appeared initially, whereas the cFN component would encode the command related to the target motion after the collicular "snapshot" (see also Optican and Pretegiani 2017). This hypothesis rested upon the observation that the "center" of the movement field of dSC neurons (i.e., the amplitude and direction of saccades associated with the most vigorous burst) shifts to larger amplitudes during saccades made toward a target moving away from the central visual field (Keller et al 1996).…”

Section: Introductionmentioning

confidence: 99%

The caudal fastigial nucleus and the steering of saccades toward a moving visual target

Bourrelly

Quinet

Goffart

2018

Journal of Neurophysiology

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The caudal fastigial nuclei (cFN) are the output nuclei by which the medio-posterior cerebellum influences the production of visual saccades. We investigated in two head-restrained monkeys their contribution to the generation of interceptive saccades toward a target moving centrifugally by analyzing the consequences of a unilateral inactivation (10 injection sessions). We describe here the effects on saccades made toward a centrifugal target that moved along the horizontal meridian with a constant (10, 20, or 40°/s), increasing (from 0 to 40°/s over 600 ms), or decreasing (from 40 to 0°/s over 600 ms) speed. After muscimol injection, the monkeys were unable to foveate the current location of the moving target. The horizontal amplitude of interceptive saccades was reduced during contralesional target motions and hypermetric during ipsilesional ones. For both contralesional and ipsilesional saccades, the magnitude of dysmetria increased with target speed. However, the use of accelerating and decelerating targets revealed that the dependence of dysmetria upon target velocity was not due to the current velocity but to the required amplitude of saccade. We discuss these results in the framework of two hypotheses, the so-called "dual drive" and "bilateral" hypotheses. NEW & NOTEWORTHY Unilateral inactivation of the caudal fastigial nucleus impairs the accuracy of saccades toward a moving target. Like saccades toward a static target, interceptive saccades are hypometric when directed toward the contralesional side and hypermetric when they are ipsilesional. The dysmetria depends on target velocity, but the use of accelerating or decelerating targets reveals that velocity is not the crucial parameter. We extend the bilateral fastigial control of saccades and fixation to the production of interceptive saccades.

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“…It must instead be ballistic, with some kind of internal mechanism determining the moment at which to stop moving; one possibility is to use internal feedback, based on the output of a real-time dynamic model of the movement in progress [44,45]. These possibilities are discussed in this issue by Optican [15]. Impairment of such a mechanism will tend to give rise to dysmetria, for instance the overshoot characteristic of cerebellar dysfunction [46].…”

Section: (B) Short-term Specific (I) Determination Of Movement Durationmentioning

confidence: 99%

“…On a much shorter timescale, the same problem arises whenever we attempt a precise movement when feedback is only available after a delay. A good example, discussed by Optican and Pretegiana in this issue [15], is the control of saccades; the movement is so fast, and visual feedback so slow, that we cannot simply stop moving the eye when we see that the visual target has been achieved, for this will result in gross overshoot. The oculomotor system has to construct an internal model of the mechanics of the eye, operating in real time, that halts the eye at the correct moment [16,17].…”

Section: Introduction: the Elephant In The Roommentioning

confidence: 99%

Not moving: the fundamental but neglected motor function

Noorani¹,

Carpenter²

2017

Phil. Trans. R. Soc. B

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One contribution of 17 to a theme issue 'Movement suppression: brain mechanisms for stopping and stillness'. The function of the motor system in preventing rather than initiating movement is often overlooked. Not only are its highest levels predominantly, and tonically, inhibitory, but in general behaviour it is often intermittent, characterized by relatively short periods of activity separated by longer periods of stillness: for most of the time we are not moving, but stationary. Furthermore, these periods of immobility are not a matter of inhibition and relaxation, but require us to expend almost as much energy as when we move, and they make just as many demands on the central nervous system in controlling their performance. The mechanisms that stop movement and maintain immobility have been a greatly neglected area of the study of the brain. This paper introduces the topics to be examined in this special issue of Philosophical Transactions, discussing the various types of stopping and stillness, the problems that they impose on the motor system, the kinds of neural mechanism that underlie them and how they can go wrong.This article is part of the themed issue 'Movement suppression: brain mechanisms for stopping and stillness'.

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What stops a saccade?

Abstract: One contribution of 17 to a theme issue 'Movement suppression: brain mechanisms for stopping and stillness'.

Cited by 31 publications

References 64 publications

Mechanisms of saccade suppression revealed in the anti-saccade task

Mechanisms of saccade suppression revealed in the anti-saccade task

The caudal fastigial nucleus and the steering of saccades toward a moving visual target

Not moving: the fundamental but neglected motor function

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