Torsional nystagmus was recorded in 3 patients with the lateral medullary syndrome. Magnetic search coil oculography demonstrated slow phases of nystagmus of increasing, decreasing, and constant velocity. Neural integration of torsional eye velocity commands to position commands is impaired by lateral medullary infarction. Torsional pulsion of saccades, consisting of torsional fast eye movements induced during saccades downward or away from the side of infarction, was recorded in 2 patients. All patients had skew deviation with hypotropia on the side of brainstem damage. The torsional nystagmus beat away from the side of infarction in each patient, but in one it alternated direction as the eyes drifted about a neutral position of torsion. We attribute the torsional nystagmus to an imbalance of central projections from the anterior and posterior semicircular canals and the otolith receptors that mediate ocular counterroll.