Acquired nystagmus causes excessive motion of images on the retina, which often reduces visual acuity and produces oscillopsia (illusory motion of the seen world). The pathogenesis of several forms of acquired nystagmus is now better understood and can be related to abnormalities of mechanisms that normally hold gaze steady. Basic research on the pharmacology of the neural pathways responsible for gaze holding has demonstrated an important role for gamma aminobutyric acid and led to new drug treatments for acquired nystagmus and its visual consequences.