Saccadic palsy after cardiac surgery: characteristics and pathogenesis
Article first published online: 14 AUG 2007
Copyright © 2007 American Neurological Association
Annals of Neurology
Volume 63, Issue 3, pages 355–365, March 2008
How to Cite
Solomon, D., Ramat, S., Tomsak, R. L., Reich, S. G., Shin, R. K., Zee, D. S. and Leigh, R. J. (2008), Saccadic palsy after cardiac surgery: characteristics and pathogenesis. Ann Neurol., 63: 355–365. doi: 10.1002/ana.21201
- Issue published online: 26 MAR 2008
- Article first published online: 14 AUG 2007
- Manuscript Accepted: 29 JUN 2007
- Manuscript Revised: 23 JUN 2007
- Manuscript Received: 2 MAY 2007
- NIH. Grant Numbers: EY06717, EY01849
- Department of Veterans Affairs
- Evenor Armington Fund
To characterize the syndrome of saccadic palsy that may follow cardiac surgery, and to interpret the findings using current concepts of the neurobiology of fast eye movements.
Using the magnetic search coil technique, we measured eye, eyelid, and head movements of 10 patients who developed selective palsy of saccades after cardiac surgery.
Patients showed varying degrees of slowing and hypometria of saccades in the vertical plane or both horizontal and vertical planes, with complete loss of all saccades in one patient. Quick phases of nystagmus were also affected, but smooth pursuit, vergence, and the vestibuloocular reflex were usually spared. The smallest saccades were less slowed than larger saccades. Affected patients were visually disabled by loss of ability to voluntarily shift their direction of gaze. Blinks and head thrusts modestly improved the range and speed of voluntary movement. The syndrome usually followed aortic valve replacement. Common accompanying features included dysarthria, labile emotions, and unsteady gait. The saccadic palsy either improved during the early part of the course or remained static.
Selective loss of all forms of saccades, with sparing of other eye movements, indicates malfunction of the brainstem machinery that generates saccades. A current model of brainstem circuits could account for both hypometria and slowing. This syndrome and the visual disability it causes often go unrecognized unless saccades are systematically tested at the bedside. Ann Neurol 2007