I recorded smooth pursuit and saccadic eye movements in six patients with unilateral cerebral infarction. By comparing responses within the hemiranges of eye position to the right and left of the orbital midline and in rightward and leftward directions, I quantified craniotopic and directional ocular motor deficits. Two patients had ipsiversive gaze deviation and severe craniotopic defects in which they could not generate smooth pursuit or saccadic eye movement into the contralateral orbital hemirange. Three patients without gaze deviation generated worse smooth pursuit in the contralateral hemirange than in the ipsilateral hemirange, but each had symmetric saccades according to eye position. All patients with craniotopic pursuit defects also had directional smooth tracking asymmetries in which eye velocities were lower for targets moving ipsilaterally than for targets moving contralaterally. Craniotopic and directional defects were associated with damage in the frontal eye field region. Orbital position is taken into account by cerebral circuits that govern smooth pursuit and saccades.