Several studies have demonstrated the importance of the pretectal Nucleus of the Optic Tract (NOT) and the Dorsal Terminal Nucleus of the accessory optic system (DTN) for the generation of horizontal optokinetic nystagmus (OKN). Although single unit data from trained rhesus monkey NOT/DTN cells are available it is still unclear if there is a link between the pursuit and the optokinetic system at this level of motion analysis. In order to address the question whether the NOT/DTN is important for the optokinetic as well as the pursuit system an electrolytic lesion was placed where NOT/DTN activity was recorded previously. The monkey was tested on optokinetic and pursuit paradigms. Immediately following the lesion the monkey performed a spontaneous nystagmus with slow phases directed away from the lesioned side. This spontaneous nystagmus persisted even during optokinetic stimulation in the opposite direction. During the first week postlesion the spontaneous nystagmus disappeared and the monkey regained the ability to perform optokinetic nystagmus toward the lesioned side. The gain of the mean slow phase eye velocity was, however, largely reduced for this stimulus direction. The onset of OKN following the onset of optokinetic stimulation was not affected by the lesion. During smooth pursuit the mean eye velocity was more reduced for pursuit towards the lesioned side. The resulting position error was compensated by an increase in the number of catch-up saccades. In addition to the confirmation of the well-known directional deficits of the optokinetic system caused by a lesion of the pretectum, a directional deficit in the pursuit system was demonstrated.