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Craniotopic defects of smooth pursuit and saccadic eye movement

From the Department of Neurology, UCLA School of Medicine and Olive View-UCLA Medical Center, Sylmar, CA.
Supported by NIH/NEI Grant EY-10225, Olive View-UCLA Education and Research Institute Grant 545, and UCLA Academic Senate Grant 4588.
Presented in part at the annual meeting of the Clinical Eye Movement Society, Toronto, ON, Canada, October 1992.
Received October 18, 1994. Accepted in final form May 4, 1995.
Address correspondence and reprint requests to Dr. Mark J. Morrow, Department of Neurology, Olive View-UCLA Medical Center, Sylmar, CA 91342.

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.

NEUROLOGY 1996;46: 514-521

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