Brain Advance Access originally published online on November 21, 2006
Brain 2007 130(1):10-35; doi:10.1093/brain/awl309
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Review Article |
What clinical disorders tell us about the neural control of saccadic eye movements
1 University of Pavia Pavia, Italy 2 Case Western Reserve University, Cleveland OH 3 Johns Hopkins University Baltimore, MD, USA 4 National Eye Institute Bethesda, MD, USA
Correspondence to: Lance M. Optican, PhD, Laboratory of Sensorimotor Research, NEI, NIH, DHHS, Building 49, Room 2A50, Bethesda, MD 20892-4435, USA E-mail: LanceOptican{at}nih.gov
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.
Key Words: cerebellum; macrosaccadic oscillations; opsoclonus; saccadic palsy; superior colliculus
Abbreviations: cFN, caudal FN; cMRF, central mesencephalic reticular formation; EBN, excitatory PBN; FN, fastigial nucleus; FNN, FN neuron; IBN, inhibitory PBN; IN, internuclear neuron; INC, interstitial nucleus of Cajal; LLBN, long-lead burst neuron; LR, lateral rectus muscle; MedRF, medullary reticular formation; MN, motor neuron; MR, medial rectus; MVN, medial vestibular nucleus; NMDA, n-methyl D-aspartate; NPH, nucleus prepositus hypoglossi; NRTP, nucleus reticularis tegmenti pontis; OPN, omnipause neuron; PBN, premotor burst neuron; PG, pulse generator; PMT, paramedian tract; PPRF, paramedian pontine reticular formation; riMLF, rostral interstitial nucleus of the medial longitudinal fasciculus; RIP, raphe interpositus nucleus; SC, superior colliculus; SCBN, SC burst neurons; SCBUN, SC build-up neurons; SO, superior oblique; SR, superior rectus; T-channel, T-type Ca2+ channel; VIn, sixth nerve
Received July 17, 2006. Revised October 5, 2006. Accepted October 6, 2006.
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