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May 1973

The Lesions Producing Paralysis of Downward But Not Upward Gaze

Author Affiliations

New York
From the departments of neurology (Drs. Jacobs and Bender) and pathology (Dr. Anderson), Mount Sinai School of Medicine, New York. Dr. Jacobs is now with the Dent Neurologic Institute, Millard Fillmore Hospital, Buffalo, NY.

Arch Neurol. 1973;28(5):319-323. doi:10.1001/archneur.1973.00490230055007

We here present the second clinicopathologic study of a patient with paralysis of downward, but not upward gaze. The findings confirm that bilateral lesions medial and dorsal to the red nuclei cause the syndrome. Since bilateral lesions of the pretectum-posterior commissure have reliably produced paralysis of upward gaze it is likely that components for upward movement are concentrated in this region. This study indicates that components for down-ward movement pass (bilaterally) more ventro-caudally than those for upward gaze. Anatomic structures situated medialdorsal to the red nuclei (eg, fasciculus retroflexus) seem to be particularly important substrates mediating downward movement of the eyes. It is possible, but unlikely, that bilateral small lesions of the rostral Edinger-Westphal nuclei may contribute to the syndrome.

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