LACK OF OPTOKINETIC NYSTAGMUS AND VISUAL-MOTION PERCEPTION IN ACQUIRED CORTICAL BLINDNESS

An 81-year-old man with persistent cortical blindness caused by bilate ral temporo-occipital infarctions was followed for six months. He had no light or visual motion perception. Optokinetic stimulation did not elicit any optokinetic nystagmus (OKN), slow eye deviation responses, or circular vection, but the vestibulo-ocular reflex (VOR) was intact. Previously reported human cases of acquired cortical blindness with s ufficient follow-up have shown similar features or otherwise either pa rtial recovery of vision, OKN or slow eye deviation responses, or reco very of (subcortical?) OKN even without the recovery of vision and/or visual movement discrimination. It has been demonstrated that patients with acquired blindness due to anterior visual pathway dysfunction sh ow the ability to generate smooth pursuit eye movements or to suppress the VOR by 'tracking' or 'fixating' their outstretched hand. Our pati ent was unable to do so. Preservation of subcortical OKN after ablatio n of the visual cortex is well-known in animal experiments (afoveate s pecies, cat, and monkey). In monkeys, recovery of visual functions aft er cortical lesions seems to be be more rapid and more complete than i n humans. This might be because monkeys can reorganize subcortical or extrastriate visual processing more successfully than humans and they are less reliant on cortical visual functions. For subcortical OKN in man, areas homologous to the MST and/or MT areas in the monkey are imp ortant, while for cortical OKN residual vision also seems necessary.