Lack of optokinetic nystagmus and visual motion perception in acquired cortical blindness

Abstract

An 81-year-old man with persistent cortical blindness caused by bilateral 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 sufficient follow-up have shown similar features or otherwise either partial recovery of vision, OKN or slow eye deviation responses, or recovery 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 show the ability to generate smooth pursuit eye movements or to suppress the VOR by ‘tracking’ or ‘fixating’ their outstretched hand. Our patient was unable to do so. Preservation of subcortical OKN after ablation of the visual cortex is well-known in animal experiments (afoveate species, cat, and monkey). In monkeys, recovery of visual functions after cortical lesions seems to be be more rapid and more complete than in 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 important, while for cortical OKN residual vision also seems necessary.

Key Words:

• Posterior cerebral artery
• subcortical optokinetic nystagmus
• fixation suppression
• brain infarction