The Neural Control of Visually Guided Eye Movements

1998 ◽  
pp. 13-60
2019 ◽  
Vol 5 (1) ◽  
pp. 247-268 ◽  
Author(s):  
Peter Thier ◽  
Akshay Markanday

The cerebellar cortex is a crystal-like structure consisting of an almost endless repetition of a canonical microcircuit that applies the same computational principle to different inputs. The output of this transformation is broadcasted to extracerebellar structures by way of the deep cerebellar nuclei. Visually guided eye movements are accommodated by different parts of the cerebellum. This review primarily discusses the role of the oculomotor part of the vermal cerebellum [the oculomotor vermis (OMV)] in the control of visually guided saccades and smooth-pursuit eye movements. Both types of eye movements require the mapping of retinal information onto motor vectors, a transformation that is optimized by the OMV, considering information on past performance. Unlike the role of the OMV in the guidance of eye movements, the contribution of the adjoining vermal cortex to visual motion perception is nonmotor and involves a cerebellar influence on information processing in the cerebral cortex.


1999 ◽  
Vol 22 (1) ◽  
pp. 241-259 ◽  
Author(s):  
Jeffrey D. Schall ◽  
Kirk G. Thompson

2009 ◽  
Vol 101 (6) ◽  
pp. 2889-2897 ◽  
Author(s):  
Andre Kaminiarz ◽  
Kerstin Königs ◽  
Frank Bremmer

Different types of fast eye movements, including saccades and fast phases of optokinetic nystagmus (OKN) and optokinetic afternystagmus (OKAN), are coded by only partially overlapping neural networks. This is a likely cause for the differences that have been reported for the dynamic parameters of fast eye movements. The dependence of two of these parameters—peak velocity and duration—on saccadic amplitude has been termed “main sequence.” The main sequence of OKAN fast phases has not yet been analyzed. These eye movements are unique in that they are generated by purely subcortical control mechanisms and that they occur in complete darkness. In this study, we recorded fast phases of OKAN and OKN as well as visually guided and spontaneous saccades under identical background conditions because background characteristics have been reported to influence the main sequence of saccades. Our data clearly show that fast phases of OKAN and OKN differ with respect to their main sequence. OKAN fast phases were characterized by their lower peak velocities and longer durations compared with those of OKN fast phases. Furthermore we found that the main sequence of spontaneous saccades depends heavily on background characteristics, with saccades in darkness being slower and lasting longer. On the contrary, the main sequence of visually guided saccades depended on background characteristics only very slightly. This implies that the existence of a visual saccade target largely cancels out the effect of background luminance. Our data underline the critical role of environmental conditions (light vs. darkness), behavioral tasks (e.g., spontaneous vs. visually guided), and the underlying neural networks for the exact spatiotemporal characteristics of fast eye movements.


Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
John-Ross Rizzo ◽  
Todd Hudson ◽  
Briana Kowal ◽  
Michal Wiseman ◽  
Preeti Raghavan

Introduction: Visual abnormalities and manual motor control have been studied extensively after stroke, but an understanding of oculomotor control post-stroke has not. Recent studies have revealed that in visually guided reaches arm movements are planned during eye movement execution, which may contribute to increased task complexity. In fact, in healthy controls during visually guided reaches, the onset of eye movement is delayed, its velocity reduced, and endpoint errors are larger relative to isolated eye movements. Our objective in this experiment was to examine the temporal properties of eye movement execution for stroke patients with no diagnosed visual impairment. The goal is to improve understanding of oculomotor control in stroke relative to normal function, and ultimately further understand its coordination with manual motor control during joint eye and hand movements. We hypothesized that stroke patients would show abnormal initiation or onset latency for saccades made in an eye movement task, as compared to healthy controls. Methods: We measured the kinematics of eye movements during point-to-point saccades; there was an initial static, fixation point and the stimulus was a flashed target on a computer monitor. We used a video-based eye tracker for objective recording of the eye at a sampling frequency of 2000 Hz (SR Research, Eyelink). 10 stroke subjects, over 4 months from injury and with no diagnosed visual impairment, and 10 healthy controls completed 432 saccades in a serial fashion. Results: Stroke patients had significantly faster onset latencies as compared to healthy controls during saccades (99.5ms vs. 245.2ms, p=0.00058). Conclusion: A better understanding of the variations in oculomotor control post-stroke, which may go unnoticed during clinical assessment, may improve understanding of how eye control synchronizes with arm or manual motor control. This knowledge could assist in tailoring rehabilitative strategies to amplify motor recovery. For next steps, we will perform objective eye and hand recordings during visually guided reaches post-stroke to better understand the harmonization or lack thereof after neurologic insult.


2001 ◽  
Vol 86 (4) ◽  
pp. 1546-1554 ◽  
Author(s):  
S. Glasauer ◽  
M. Dieterich ◽  
Th. Brandt

To find an explanation of the mechanisms of central positional nystagmus in neurological patients with posterior fossa lesions, we developed a three-dimensional (3-D) mathematical model to simulate head position-dependent changes in eye position control relative to gravity. This required a model implementation of saccadic burst generation, of the neural velocity to eye position integrator, which includes the experimentally demonstrated leakage in the torsional component, and of otolith-dependent neural control of Listing's plane. The validity of the model was first tested by simulating saccadic eye movements in different head positions. Then the model was used to simulate central positional nystagmus in off-vertical head positions. The model simulated lesions of assumed otolith inputs to the burst generator or the neural integrator, both of which resulted in different types of torsional-vertical nystagmus that only occurred during head tilt in roll plane. The model data qualitatively fit clinical observations of central positional nystagmus. Quantitative comparison with patient data were not possible, since no 3-D analyses of eye movements in various head positions have been reported in the literature on patients with positional nystagmus. The present model, prompted by an open clinical question, proposes a new hypothesis about the generation of pathological nystagmus and about neural control of Listing's plane.


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