We experienced four cases of vertical gaze palsy induced by midbrain lesions. Lesions commonly covered the rostral midbrain, including the rostral interstitial nucleus, dorsomedial to the red nucleus. Two of the four cases resulted from vascular insult, in which a single, unpaired perforator is supposed to innervate the rostral midbrain and medial thalamus bilaterally. One case showed vertical gaze palsy accompanied by bilateral ptosis. The findings agree with recent experimental evidence that a neural substrate in eyelid control lies in the supraoculomotor area immediately dorsal to the oculomotor nucleus. The remaining two cases, a brain hemorrhage and an inflammatory tumor, showed unilateral lesions of the rostral midbrain. In these cases, vertical gazes were not abolished, but were limited in an incomplete way. This may be explained by partial damages of the descending fibers, some of which decussate through the posterior commissure before it reaches the oculomotor nucleus. Thus, clinical signs and symptoms were clarified based on anatomical and physiological points of view.