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The rostral mesencephalon may influence ocular motility in the vertical, horizontal, and torsional trajectories through intricate supranuclear, internuclear, and infranuclear neural networks. Strategic unilateral midbrain lesions may result in contralateral horizontal gaze palsy with saccadic failure due to combined interruption of supranuclear corticofugal fibers from the frontal eye field and colliculofugal fibers from the superior colliculus. In this article, we report a patient who sustained combined vertical and horizontal gaze deficits after a single infarct involving the mesodiencephalic junction. The neural substrate for each deficit is briefly discussed in light of clinical findings. This case presented a triad of three distinct syndromes of horizontal gaze paresis, vertical one-and-a-half syndrome, and pseudoabducens palsy due to damage of nuclear and supranuclear projections within the rostral mesencephalon. This combination was due to a single embolic infarct in the territory of the posterior thalamosubthalamic artery (artery of Percheron) that arises at the basilar bifurcation. Coexistence of these phenomena exemplified how rostral midbrain lesions may affect ocular motility in the vertical, horizontal, and torsional planes, along with disruption of normal vergence control.

Vertical One-and-a-Half Syndrome with Pseudoabducens Palsy and Midbrain Horizontal Gaze Paresis