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Department of Neurology, University of Iowa College of Medicine, Iowa City, IA (Drs. Rizzo, Nawrot, and Damasio)
Department of Psychology, Vanderbilt University, Nashville, TN. (Dr. Blake)
We surveyed a broad range of visual functions in a man who complained of abnormal color experience and inability to recognize faces following bilateral damage in the visual cortex. A lesion in his right visual cortex caused complete left visual field loss. A lesion in his left visual cortex, located entirely below the calcarine fissure, affected the vision in his remaining hemifield, the right one. Psychophysical testing showed severely defective color vision and pattern processing, but relatively normal luminance contrast detection thresholds. The finding of normal spatial contrast sensitivity and static stereopsis did not resemble a parvocellular defect of the type described in the monkey. The abilities to detect global coherent motion among noise, structure from motion and dynamic stereopsis, and to pursue moving targets showed normal motion processing at several levels. Together with normal flicker perception, these results excluded magnocellular or MT-like defects. Altogether, the findings mimic area V4 dysfunction.
Address correspondence and reprint requests to Dr. Matthew Rizzo, Department of Neurology, The University of Iowa Hospitals and Clinics, Iowa City, IA 52242.
Supported by NINDS PO NS 19632 (Drs. Rizzo and Damasio) and by NIH EY 07760 (Dr. Blake).
Received September 9, 1991. Accepted for publication in final form November 11, 1991.
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