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Departments of Ophthalmology (Dr. Barton) and Neurology (Dr. Rizzo), University of Iowa Hospitals and Clinics, Iowa City, IA was supported by NIH PO NS 19632.
We tested motion perception in 15 eyes of 13 patients with optic neuropathy. Eleven of the eyes had optic neuritis. The motion perception paradigm tested subjects' ability to discriminate the direction of a global coherent motion signal amid varying levels of background noise. The results showed defective motion processing in eight of the 15 eyes. This defect was not due to low visibility (poor spatial resolution), since 11 of the 15 eyes had Snellen acuities of 20/20 or better. Neither was impaired motion perception due to decreased luminance sensitivity, since attenuating the display signal by 2.1 log units (0.6 units more than the worst relative afferent pupillary defect in any patient) in five normal eyes had no effect. Motion perception and critical flicker fusion were independent of each other. Given proposals that both depend exclusively on the same M, or transient, channel, we had not predicted this double dissociation between flicker and motion perception.
Address correspondence and reprint requests to Dr. Jason J.S. Barton, Department of Neurology, Toronto Western Hospital, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8.
Presented in part at the annual meeting of the North American Neuro-ophthalmologic Society, Park City, UT, February 1991.
Received April 1, 1993. Accepted for publication in final form July 28, 1993.
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