Abstract
A relatively simple model of the fast eye movement (saccadic) system has been developed and simulated on an analog computer. The model is capable of producing normal saccadic eye movements and has several provisions which permit the simulation of clinical signs of gaze-evoked nystagmus. According to the model, gaze-evoked nystagmus may result from various abnormalities in the neuronal pool responsible for integration of the pulse of high frequency fiing which initiates each saccade. Simulation of these inferred neuronal deficits produced subtle differences in saccadic behavior as well as gaze-evoked nystagmus. These differences occurred both in the nystagmus-free range of gaze angles and after the nystagmus appeared. The subtlety of the deficits and the sparsity of studies of gaze-evoked nystagmus using modem oculographic recording techniques, probably explains why such saccadic behavior has not been previously noted. If one, or more than one, of these simulated mechanisms is, in fact, an accurate model of the actual physiological deficit, future studies of such patients should reveal the corresponding abnormal saccadic behavior.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
