Clinical examinations and eye movement recordings of 91 consecutive patients with DBN were analyzed to describe the characteristics of DBN and to localize the lesions producing this abnormality. Horizontal and vertical eye movement recordings were made with EOG and/or magnetic search coil. The most frequent causes were infarction, cerebellar and spinocerebellar degeneration syndromes, MS and developmental anomalies affecting the pons and cerebellum. Toxicity from anticonvulsant drugs probably caused nystagmus in a few patients. Clinical examinations, excluding electronic eye movement recordings, were used to localize lesions. Localizations included the cerebellum in 88% of the patients. However, localizations to structures outside of the cerebellum were made in several patients. The effects of DBN of gaze position, convergence, blockage of fixation, and positioning of the head and body were observed. Almost all patients had DBN in some position of gaze while sitting and fixating a distant target. A few patients demonstrated DBN only with convergence, in the dark, or with positioning of the head and body. Horizontal gaze increased DBN in most patients. The nystagmus slow components usually had constant-velocity or increasing-velocity waveforms. The effects of vertical gaze on DBN were variable. In general, statistically significant differences in the frequencies of these effects among the various causes and localizations of lesions were not found. Horizontal eye movements were electronically recorded in DBN patients, in a group of normal subjects, and in a group of patients with isolated cerebellar atrophy who did not have DBN. The pattern of abnormal horizontal eye movements characteristic of damage to the midline structures of the cerebellum (impaired pursuit, impaired OKN, and inability to suppress VOR) was found in almost all DBN patients (99%), including patients with lesions localized to structures outside the cerebellum by clinical examination. DBN is usually produced by lesions in the cerebellum that also damage pathways that control horizontal tracking and visual-vestibulo-ocular interactions.