Neural mechanisms of gaze, vertical and rotatory nystagmus are reviewed. For all eye movements, eye velocity is an oculomotor parameter. Eye velocity signals are transformed by a neural integrator in the brain stem to obtain the eye position signal. A lesion of neural integrator leads to gaze-evoked nystagmus. Vertical nystagmus arises from a lesional or functional tone imbalance, which is due to disruption of the central vestibulo-ocular reflex pathway in the pitch plane. Downbeat nystagmus is caused by lesions between the vestibular nuclei or flocculus. Upbeat nystagmus is caused by lesions in the brachium conjunctivum, the ventral tegmental pathway and the prepositus hypoglossal nucleus. Rotatory nystagmus involves an epicodic ocular tilt reaction, which is a clinical sign of an imbalance of the central vestibulo-ocular reflex in the roll plane. Unilateral infarction of the brain stem leads to rotatory nystagmus.
