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Ocular NeuromyotoniaA Clinical Description of Six Patients
W. Thomas Shults, MD;
William F. Hoyt, MD;
Myles Behrens, MD;
James MacLean, MD;
Robert F. Saul, MD;
James J. Corbett, MD
Arch Ophthalmol. 1986;104(7):1028-1034.
Abstract
We report the cases of six patients with ocular neuromyotonia, a disorder believed to result from episodic involuntary discharge of ocular motor nerves producing sustained and inappropriate contraction of their respective ocular muscles. Transient disturbances of ocular motility and diplopia result. Four patients had involvement of ocular muscles supplied by the third cranial nerve: one had presumed involvement of the superior oblique muscle, and one the lateral rectus muscle, suggesting abnormal discharge in the fourth and and cranial nerves, respectively. Four of six patients received prior radiation therapy for pituitary tumors, implying a possible pathogenic link. Three patients improved after treatment with membrane-stabilizing medication, suggesting that unstable membranes of injured ocular motor axons may generate spontaneous impulses, which produce involuntary sustained and inappropriate ocular muscle contraction.
Author Affiliations
From the Oregon Lions Sight and Hearing Institute, Good Samaritan Hospital, Portland (Dr Shults); the Departments of Ophthalmology, Neurology, and Neurosurgery, University of California, San Francisco (Dr Hoyt); the Edward S. Harkness Eye Institute, New York (Dr Behrens); the Department of Neurology, Mason Clinic, Seattle (Dr MacLean); the Department of Neuro ophthalmology, Geisinger Medical Center, Danville, Pa (Dr Saul); and the Department of Neurology, University of Iowa, Iowa City (Dr Corbett).
Footnotes
Accepted for publication Jan 22, 1986.
Reprint requests to Oregon Lions Sight and Hearing Institute, Neurological Sciences Center, Good Samaritan Hospital, 1040 NW 22nd, Portland, OR 97210 (Dr Shults).
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