title: Saccadic dysmetria in a patient with a right frontoparietal lesion. The importance of corollary discharge for accurate spatial behaviour.
abstract: Double-step experiments have demonstrated that retinotopic coding is inadequate to explain the spatial performance of the saccadic system. In such experiments a subject is asked to make two successive saccades to fixate two sequentially flashed targets each of which disappears before the first saccade. Despite the dissonance thus created between the retinal location of the second target and the saccade necessary to acquire it, normal humans and monkeys perform the task perfectly well. Single unit recording in monkeys indicates that neurons in the superior colliculus, frontal eye fields and in parietal cortex generate a spatially accurate signal during the performance of double-step saccades, which is thought to be obtained by combining a retinotopic signal with a signal corollary to the previous saccadic eye movement. We studied saccadic eye movements in a patient with a right fronto-parietal lesion using single- and double-step tasks. Single saccades into the left (contralesional) hemifield had longer latency and were hypometric relative to those into the right (ipsilesional) hemifield. Varying the initial orbital position had no effect on the latency and accuracy of saccades to left and right retinal stimuli. When the patient was asked to do a double-step task with targets flashed first into the right field and then into the left field, she performed well. When she was asked to do the same task with a target flashed first into the left field and then into the right field she made the first saccade correctly but never acquired the second target, even though this required her to make a saccade in the normal direction to a stimulus that appeared in the normal field. Such a deficit therefore cannot be one of retinotopic or spatial coding, nor can it be one of generating a certain direction of saccade. We suggest that the deficit is a failure of corollary discharge, the inability to register the amplitude and direction of a saccade into the contralesional field, and use that information to update the representation of the location of the next saccade target.
authors.affiliation: Laboratory of Sensorimotor Research, National Eye Institute, NIH, Bethesda, Maryland.
authors.forename: J R
authors.initials: JR
authors.lastname: Duhamel
authors.forename: M E
authors.initials: ME
authors.lastname: Goldberg
authors.forename: E J
authors.initials: EJ
authors.lastname: Fitzgibbon
authors.forename: A
authors.initials: A
authors.lastname: Sirigu
authors.forename: J
authors.initials: J
authors.lastname: Grafman
mesh_terms: D000368:Aged; D001927:Brain Diseases / Q000503:physiopathology*; D005260:Female; D005625:Frontal Lobe / Q000503:physiopathology*; D006801:Humans; D010296:Parietal Lobe / Q000503:physiopathology*; D010775:Photic Stimulation; D011930:Reaction Time; D012160:Retina / Q000503:physiopathology; D012438:Saccades; D013037:Spatial Behavior; D014794:Visual Fields; D014796:Visual Perception