Saccades (horizontal and vertical) and dissociated nystagmus were quantitatively assessed in four patients with internuclear ophthalmoplegia. Two patients had bilateral medial longitudinal fasciculus (MLF) lesions associated with multiple sclerosis and two had unilateral lesions associated with brain stem vascular disease. Adducting saccades made on the side of an MLF lesion were slowed in each patient (P less than .01). At the same time, abducting saccades in the contralateral eye had normal velocity, but consistently overshot the target. After the overshoot, the eye returned to the target with an exponentially decaying course. With large angular deviations (usually more than 15 degrees), the abducting eye developed nystagmus characterized by slow components that moved toward the midposition with an initially high velocity followed by a segment of slower velocity. The adducting eye had either no nystagmus or a low-amplitude nystagmus characterized by a rounded junction between the fast and slow component. The saccade abnormalities and waveform of the dissociated nystagmus can be explained by a pulse-step mismatch at the agonist motoneurons.