We studied electro-oculographic and videotape recordings of eye movements in six patients with Wallenberg's syndrome. With fixation, all patients had a spontaneous rotatory nystagmus with the fast phase directed toward the intact side. With loss of fixation, the patients' eyes deviated tonically toward the side of the lesion. Voluntary and involuntary saccades had larger amplitude when directed toward the side of the lesion than away from it. The spontaneous nystagmus predictably interacted with all slow eye movements, producing asymmetric smooth-pursuit, optokinetic, and vestibular responses. In addition, smooth-pursuit and optokinetic responses were decreased significantly in both directions compared to normal subjects. Fixation suppression of vestibular nystagmus also was impaired in both directions. We concluded that two different types of oculomotor bias were present in these patients--a velocity bias and a position bias. The former resulted from damage to the caudal lateral vestibular nuclei, and the latter from interruption of cerebellopontine pathways.