PubMed · 1602924
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L I Terr. 1992. Cochlear nucleus stimulation.. https://doi.org/10.1288/00005537-199206000-00023
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A 15-month-old female infant with nystagmus, gait disturbance, diminished reflexes, ophthalmoplegia, and facial paresis was diagnosed as having Fisher syndrome. Magnetic resonance imaging revealed a transient, high-signal-intensity lesion on the left side of the cerebellum on T2-weighted images. The ataxia of Fisher syndrome is not compatible with polyneuritis, but can be explained by a cerebellar lesion, as seen in this case.
What happens when the goal is changed before the movement is executed? Both the double-step and colliding saccade paradigms address this issue as they introduce a discrepancy between the retinal images of targets in space and the commands generated by the oculomotor system necessary to attain those targets. To maintain spatial accuracy under such conditions, transformations must update "retinal error' as eye position changes, and must also accommodate neural transmission delays in the system so that retinal and eye position information are temporally aligned. Different hypotheses have been suggested to account for these phenomena, based on observations of dissociable cortical and subcortical compensatory mechanisms. We now demonstrate how a single compensatory mechanism can be invoked to explain both double-step and colliding saccade paradigm results, based on the use of a damped signal of change in position that is used in both cases to update retinal error and, thereby, account for intervening movements. We conclude that the collision effect is not an artifact, but instead reveals a compensatory mechanism for saccades whose targets appear near the onset of a preceding saccade.
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