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Brain Advance Access published online on November 21, 2006
Brain, doi:10.1093/brain/awl309
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Published by Oxford University Press on behalf of the Guarantors of Brain, 2006. The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org.
Received July 17, 2006
Revised October 5, 2006
Accepted October 6, 2006

Review

What clinical disorders tell us about the neural control of saccadic eye movements

Stefano Ramat 1, R. John Leigh 2, David S. Zee 3, and Lance M. Optican 4 *

1 University of Pavia, Pavia, Italy
2 Case Western Reserve University, Cleveland, OH, USA
3 Johns Hopkins University, Baltimore, MD, USA
4 National Eye Institute, Bethesda, MD, USA

* To whom correspondence should be addressed.
Lance M. Optican, E-mail: LanceOptican{at}nih.gov


  Abstract

Saccades are rapid eye movements that redirect the fovea from one object to another. A great deal has been learned about the anatomy and physiology of saccades, making them an ideal system for studying the neural control of movement. Basic research on normal eye movements has greatly increased our understanding of saccadic performance, anatomy and physiology, and led to a large number of control system models. These models simulate normal saccades well, but are challenged by clinical disorders because they often do not incorporate the specific anatomical and physiological substrates needed to model clinically important abnormalities. Historically, studies of saccadic abnormalities in patients have played a critical role in understanding the neural control of saccades because they provide information that complements basic research and thus restricts hypotheses to those that are biologically plausible. This review presents four examples of clinical disorders (slow saccades, interrupted saccades, high-frequency saccadic oscillations and macrosaccadic oscillations) that have provided insights into the neurobiology of saccades, have driven the development of new models, and have suggested an explanation or treatment for these disorders. We raise general questions for both scientists and clinicians that will assist in their efforts to understand the neural control of movement, improve diagnostic criteria and develop new treatments.

Keywords: cerebellum; macrosaccadic oscillations; opsoclonus; saccadic palsy; superior colliculus.
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