It is generally accepted that two different mechanisms underly the generation of optokinetic nystagmus (OKN); an initial rapid rise which is related to the transcortical-cerebellar route and is thought to reflect the participation of the smooth pursuit mechanism and a slower rise of slow-phase OKN velocity that resembles OKN found in nonfoveal animals. Therefore, the pursuit eye movements and the rapid rise OKN velocity would be expected to be impaired in patients with retinal lesions. In the present experiment, both the rapid rise OKN and the smooth pursuit were investigated in patients with retinal lesions with or without hemianopsia. In four subjects who had retinal lesions in and around the fovea, with or without hemianopsia, the rapid rise OKN decreased in response to high velocity OKN stimulation and the gain of pursuit decreased to the upper limits of abnormal values. In a patient who has both foveal lesions and hemianopsia, the gain of the rapid rise was preserved more when the target was moved toward the fovea than when it was away from the fovea. It is concluded that the central retina is very important weight in eliciting the rapid rise and also pursuit eye movements supported by the peripheral retina.
