The cortex is in overall control of ‘voluntary’ eye movement

Pouget, Pierre

doi:10.1038/eye.2014.284

Cited by 42 publications

(19 citation statements)

References 43 publications

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“…The parietal eye field (PEF) of the posterior parietal cortex projects to the FEF and the superior colliculus. In turn, PEF also receives input from the FEF [12].…”

Section: Introductionmentioning

confidence: 99%

Slow saccades in cerebellar disease

2019

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Eye movements are frequently considered diagnostic markers indicating involvement of the cerebellum. Impaired amplitude of saccades (saccade dysmetria), impaired gaze holding function (horizontal or downbeat nystagmus), and interrupted (choppy) pursuit are typically considered hallmarks of cerebellar disorders. While saccade dysmetria is a frequently considered abnormality, the velocity of saccades are rarely considered part of the constellation of cerebellar involvement. Reduced saccade velocity, frequently called “slow saccades” are typically seen in a classic disorder of the midbrain called progressive supranuclear palsy. It is also traditionally diagnostic of spinocerebellar ataxia type 2. In addition to its common causes, the slowness of vertical saccades is not rare in cerebellar disorders. Frequently this phenomenology is seen in multisystem involvement that substantially involves the cerebellum. In this review we will first discuss the physiological basis and the biological need for high saccade velocities. In subsequent sections we will discuss disorders of cerebellum that are known to cause slowing of saccades. We will then discuss possible pathology and novel therapeutic strategies.

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“…The parietal eye field (PEF) of the posterior parietal cortex projects to the FEF and the superior colliculus. In turn, PEF also receives input from the FEF [12].…”

Section: Introductionmentioning

confidence: 99%

Slow saccades in cerebellar disease

2019

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“…Those approaches have provided causal evidence about the role of the FEF, with direct bearing on ocular motor and attentional function (18,19). More recently, the causal involvement of FEF in attentional orienting has been demonstrated (20,21) as well as its ability to modulate different aspects of visual perception (22,23) while indirect control and monitoring processes have been assigned to SEF functions (24,25). In order to examine the possible distant role of neuromodulation caused by FUS applied to a cortical brain region, we decided to target a cortical circuit controlling voluntary eye movement.…”

Section: Introductionmentioning

confidence: 99%

Transcranial ultrasonic stimulation modulates single-neuron discharge in macaques performing an antisaccade task

et al. 2017

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Our study demonstrates that the neuromodulatory effects of non-invasive focused ultrasound can be assessed in real time in awake behaving monkeys by recording discharge activity from a brain region reciprocally connected with the stimulated region. The study opens the door for further parametric studies for fine-tuning the ultrasonic parameters. The ultrasonic effect could indeed be quantified based on the direct measurement of the intensity of the modulation induced on a single neuron in a freely performing animal. The technique should be readily reproducible in other primate laboratories studying brain function, both for exploratory and therapeutic purposes and to facilitate the development of future clinical TUS devices.

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“…Accordingly, the posterior focus of the power increase might reflect a neural source in the visual cortex, or in posterior areas controlling eye movements (e.g. posterior temporoparietal areas or cerebellum [69]). It would be interesting to assess these possibilities through high-density EEG, which allows a more precise estimation of EEG activity's neural sources.…”

Section: Discussionmentioning

confidence: 99%

The spectral fingerprint of sleep problems in post-traumatic stress disorder

Talamini

2019

Sleep Medicine

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Study Objectives: Sleep problems are a core feature of post-traumatic stress disorder (PTSD). The aim of this study was to find a robust objective measure for the sleep disturbance in patients having PTSD. Methods:The current study assessed EEG power across a wide frequency range and multiple scalp locations, in matched trauma-exposed individuals with and without PTSD, during rapid eye movement (REM) and non-REM (NREM) sleep. In addition, a full polysomnographical evaluation was performed, including sleep staging and assessment of respiratory function, limb movements, and heart rate. The occurrence of sleep disorders was also assessed. Results:In patients having PTSD, NREM sleep shows a substantial loss of slow oscillation power and increased higher frequency activity compared with controls.The change is most pronounced over right-frontal sensors and correlates with insomnia. PTSD REM sleep shows a large power shift in the opposite direction, with increased slow oscillation power over occipital areas, which is strongly related to nightmare activity and to a lesser extent with insomnia. These pronounced spectral changes occur in the context of severe subjective sleep problems, increased occurrence of various sleep disorders and modest changes in sleep macrostructure.Conclusions: This is the first study to show pronounced changes in EEG spectral topologies during both NREM and REM sleep in PTSD. Importantly, the observed power changes reflect the hallmarks of PTSD sleep problems: insomnia and nightmares and may thus be specific for PTSD. A spectral index derived from these data distinguishes patients from controls with high effect size, bearing promise as a candidate biomarker.

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The cortex is in overall control of ‘voluntary’ eye movement

Cited by 42 publications

References 43 publications

Slow saccades in cerebellar disease

Slow saccades in cerebellar disease

Transcranial ultrasonic stimulation modulates single-neuron discharge in macaques performing an antisaccade task

The spectral fingerprint of sleep problems in post-traumatic stress disorder

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