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Show IOllrnll! of C/illicll! Nt'lIro-0l'hthll!ltIl>!ogv 7(4): 250--253, 1987. Literature Abstracts Unilateral Blurred Vision and Dilated Retinal Veins. Gittinger JW Jr. With comments by NR Miller, JL Keltner, and RM Burde. Surv Ophthalmol 1987;31:270-6 (Jan-Feb). [Reprints not available.] A 39-year-old woman with a protracted period of left optic disc edema, venule distension, and perimacular hemorrhage but good visual function is discussed. Her disease is considered venous statis retinopathy, papillophlebitis, optic disc vasculitis, "big blind spot syndrome," etc. by the three discussants and all recommend limited warkup for clotting or blood abnormalities and then expectant follow-up. Corticosteroids may be used in recalcitrant cases. Be sure to add this article to your file of "unilateral disc edema" as the discussion is exhaustive and you will not be able to locate the article again based on "key words" as the editors have coded this as "inflammatory central vein occlusion" and "ischemic" and "nonischemic central vein occlusion" (one wonders whether the key-ward-coders read the article!). LYIl A. Sedwick, M,D. The Syndrome of Paradoxical Worsening of Dural-Cavernous Sinus Arteriovenous Malformations. Sergott RC, Grossman RI, Savino PJ, Bosley TM, Schatz NJ. Ophthalmology 1987;94:205-12 (March), [Reprint requests to Dr. R. C. Sergott, Neuro-Ophthalmology Service, Wills Eye Hospital, 9th and Walnut Streets, Philadelphia, PA 19107,] Three patients with dural-cavernous sinus arteriovenous maHormations are discussed all of whom had sudden clinical worsening followed approximately 3 weeks later by resolution of signs and symptoms. All three were found by magnetic resonance scanning and/or arteriography to have a thrombosed superior ophthalmic vein and the authors postulate that clinical deterioration occurred because of insufficient collateral circulation and that improvement occurred coincident with the development of such collaterals. They suggest that 250 © 1987 Raven Press, Ltd., New York all patients with presumed dural cavernous fi~tulae and clinical deterioration undergo magnetic resonance scanning and, if this shows superior ophthalmic vein thrombosis, be followed with?ut intervention for the expected spontaneous Improvement. A very nice paper, easily read, which is succinct and whose message is eminently practical. Lyn A. Sedwick, M,D, Gaze-Evoked Amaurosis. Orcutt JC, Tucker WM, Mills RP, Smith CH. Ophthalmology 1987;94:213-8 (March). [Reprint requests to Dr. Je Orcutt, Department of Ophthalmology, RJ-lO, University of Washington, Seattle, WA 98195,] Six patients are discussed, three with presumed optic nerve sheath meningioma and three with presumed orbital cavernous hemangioma, all of whom reported reproducible unilateral decreased vision in eccentric positions of gaze, Two computerized tomographic scans show the change in position of the optic nerve in relation to the tumor in the gaze area in question and the authors postulate transient optic nerve ischemia as the etiology of the decreased vision. Follow-up ranged from 0 to 9 years with a mean of ~3 years and only one patient lost significant vision in the eye with gazeprovoked amaurosis leading the authors to conclude that this symptom is not predictive of poor clinical outcome. . LYIl A. Sedwick, M.D, Saccadic Eye Movements in Myasthenia Gravis. Yee RD, Whitcup SM, Williams 1M, Balah RW, Honrubia V. Ophthalmology 1987;94:219-25 (March). [Reprint requests to Dr, R. D. Yee, Jules Stein Eye Institute, 800 Westwood Plaza, Los Angeles, CA 90024,] Peak velocity of horizontal saccades was measured using electrooculography or infrared scleral |