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Saccade dynamics in peripheral vs central sixth nerve palsies

From the Department of Ophthalmology and Vision Sciences (A.M.F.W., K.M., J.A.S.) and Division of Neurology (A.M.F.W., J.A.S.), University Health Network, University of Toronto, Ontario, Canada.

Address correspondence and reprint requests to Dr. Agnes Wong, Elm Wing S102D, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8; e-mail: agnes.wong{at}utoronto.ca

Objective: To investigate differences between peripheral idiopathic and central sixth nerve palsies from brainstem damage by comparing peak velocities and durations of horizontal saccades.

Methods: Fourteen patients with unilateral incomplete sixth nerve palsies caused by idiopathic, presumed ischemic, peripheral damage, 5 with incomplete central (fascicular) palsy caused by brainstem lesions, and 10 controls were studied. Palsies under 1 month in duration were designated as acute and those of longer duration were chronic. Among peripheral palsies, five were acute, nine were chronic. Among central palsies, two were acute, three were chronic. Subjects made ± 10 deg horizontal saccades while wearing search coils. Serial recordings were made in seven patients with acute palsy (five peripheral, two central).

Results: Centrifugal abducting saccadic velocities in the paretic eye were subnormal in both central and peripheral acute palsies, as anticipated from lateral rectus weakness. In chronic central palsies, abducting velocities in the paretic eye remained reduced. However, in chronic peripheral palsies, velocities became normal in the tested range of excursion, within 2 months of onset, despite persisting abduction deficit.

Conclusions: Saccade peak velocities are reduced and their durations are prolonged in the field of action of acutely palsied peripheral and central nerves. Speeds remain reduced in chronic central (fascicular) palsies, consistent with limited regeneration within the brain. Saccade speeds are repaired in chronic peripheral palsies, probably by remyelination and axonal regeneration, and perhaps also by central monocular adaptation of innervation selectively to the paretic eye, in order to drive both eyes rapidly and simultaneously into the paretic field of motion.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the May 9 issue to find the title link for this article.

Supported by the New Investigator Award (MSH 55058) (A.M.F.W.) and grants MT 5404, ME 5509 (J.A.S.), and MOP 57853 (A.M.F.W. and J.A.S.) from the Canadian Institutes of Health Research (CIHR), and the University Health Network Ophthalmology (A.M.F.W.) and Neurology (J.A.S.) Practice Plans.

Disclosure: The authors report no conflicts of interest.

Presented in part at the 29th Annual North American Neuro-ophthalmology Society (NANOS) Meeting; Salt Lake City, UT; February 9–13, 2003.

Received September 28, 2005. Accepted in final form January 23, 2006.

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