When primates maintain their gaze directed toward a visual target (visual fixation), their eyes display a combination of miniature fast and slow movements. An involvement of the cerebellum in visual fixation is indicated by the severe gaze instabilities observed in patients suffering from cerebellar lesions. Recent studies in non-human primates have identified a cerebellar structure, the fastigial oculomotor region (FOR), as a major cerebellar output nucleus with projections toward oculomotor regions in the brain stem. Unilateral inactivation of the FOR leads to dysmetric visually guided saccades and to an offset in gaze direction when the animal fixates a visual target. However, the nature of this fixation offset is not fully understood. In the present work, we analyze the inactivation-induced effects on fixation. A novel technique is adopted to describe the generation of saccades when a target is being fixated (fixational saccades). We show that the offset is the result of a combination of impaired saccade accuracy and an altered encoding of the foveal target position. Because they are independent, we propose that these two impairments are mediated by the different projections of the FOR to the brain stem, in particular to the deep superior colliculus and the pontomedullary reticular formation. Our study demonstrates that the oculomotor cerebellum, through the activity in the FOR, regulates both the amplitude of fixational saccades and the position toward which the eyes must be directed, suggesting an involvement in the acquisition of visual information from the fovea.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1152/jn.00771.2009 | DOI Listing |
Front Neurol
September 2022
Department of Neurology, University Hospitals Schleswig-Holstein, Campus Lübeck, Lübeck, Germany.
Background: "Central dizziness" due to acute bilateral midline cerebellar disease sparing the posterior vermis has specific oculomotor signs. The oculomotor region of the cerebellar fastigial nucleus (FOR) crucially controls the accuracy of horizontal visually-guided saccades and smooth pursuit eye movements. Bilateral FOR lesions elicit bilateral saccade hypermetria with preserved pursuit.
View Article and Find Full Text PDFJ Neuroophthalmol
June 2022
Department of Neurology (JN, GB, FW, XZ, and JK), University of Illinois College of Medicine Peoria, Illinois Neurologic Institute, OSF St. Francis Medical Center, Peoria, Illinois; Department of Neurology (JK and FW), Illinois Neurologic Institute OSF St. Francis Medical Center, Peoria, Illinois; and Department of Internal Medicine (SB), University of Illinois College of Medicine Peoria, OSF St. Francis Medical Center, Peoria, Illinois.
Background: The opsoclonus-myoclonus-ataxia syndrome (OMAS) represents a pathophysiology and diagnostic challenge. Although the diverse etiologies likely share a common mechanism to generate ocular, trunk, and limb movements, the underlying cause may be a paraneoplastic syndrome, as the first sign of cancer, or may be a postinfectious complication, and thus, the outcome depends on identifying the trigger mechanism. A recent hypothesis suggests increased GABAA receptor sensitivity in the olivary-oculomotor vermis-fastigial nucleus-premotor saccade burst neuron circuit in the brainstem.
View Article and Find Full Text PDFVis Neurosci
May 2021
Department of Neurobiology and Anatomical Sciences, University of Mississippi Medical Center, Jackson, Mississippi.
Since most gaze shifts are to targets that lie at a different distance from the viewer than the current target, gaze changes commonly require a change in the angle between the eyes. As part of this response, lens curvature must also be adjusted with respect to target distance by the ciliary muscle. It has been suggested that projections by the cerebellar fastigial and posterior interposed nuclei to the supraoculomotor area (SOA), which lies immediately dorsal to the oculomotor nucleus and contains near response neurons, support this behavior.
View Article and Find Full Text PDFJ Neurophysiol
June 2021
Aix Marseille Université, CNRS, Institut de Neurosciences de la Timone, Marseille, France.
The caudal fastigial nuclei (cFN) are the output nuclei by which the medio-posterior cerebellum influences the production of saccades toward a visual target. On the basis of the organization of their efferences to the premotor burst neurons and the bilateral control of saccades, the hypothesis was proposed that the same unbalanced activity accounts for the dysmetria of all saccades during cFN unilateral inactivation, regardless of whether the saccade is horizontal, oblique, or vertical. We further tested this hypothesis by studying, in two head-restrained macaques, the effects of unilaterally inactivating the caudal fastigial nucleus on saccades toward a target moving vertically with a constant, increasing or decreasing speed.
View Article and Find Full Text PDFNeurology
March 2021
Department of Neurology (I.M.), Medical University of Vienna, Vienna, Austria; Division of Neuroradiology and Musculoskeletal Radiology (G.K.), Department of Biomedical Imaging and Image-guided Therapy, Medical University of Vienna, Vienna, Austria; and Department of Neurology (G.W.), Medical University of Vienna, Vienna, Austria.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!