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Show 70 L1nRATURE ABSTRACTS In this series of 14 patients with congenital oculomotor nerve palsy, 10 had associated neurological disorders. Details of these cases are well presented and compared to the other reported cases. LYIl A. Sedwick, M. D. Late Recovery of Function After Oculomotor Nerve Palsy. Golnik KC, Miller NR. Am / Oplrtlwlmol 1991; 111: 566- 70 ( May). [ Reprint requests to Dr. N. R. Miller, Johns Hopkins Hospital, Wilmer Eye Institute, 600 N. Wolfe Street, Maumenee Bldg., Rm. B- 109, Baltimore, MD 21205.) Three patients with differing etiologies for oculomotor nerve palsy ( orbital trauma, orbital hemorrhage, pituitary apoplexy) had late improvement in ocular motility, i. e. 2 or 3+ years post insult. All had month to years of stability before this improvement occurred. Perhaps the common recommendation for eye muscle surgery after 6 months to a year of stable measurement should be reconsidered. LYIl A. Sedwick, M. D. Cilioretinal Artery Occlusion in Young Adults with Central Retinal Vein Occlusion. Schatz H, Fong ACO, McDonald HR, Johnson RN, Joffe L, Wilkinson CP, de Laey JI, Yannuzzi LA, Wendel RT, Joondeph BC, Angioletti LV, Meredith TA. Ophthalmology 1991; 98: 594-- 601 ( May). [ Reprint requests to Dr. H. Schatz, 1 Daniel Burnham Court, Suite 210, San Francisco, CA 94109.) The authors report 10 patients, aged 23- 44 years, with a picture of central retinal vein occlusion and cilioretinal artery occlusion. In most, good visual function was eventually recovered. The authors discuss the etiology of these " mild" cilioretinal artery occlusions and Dr. Orth comments on the paper and other relevant literature in his discussion following it. LYIl A. Sedwick, M. D. The Clinical Characteristics of Pedigrees of Leber's Hereditary Optic Neuropathy With the 11778 Mutation. Newman NI, Lott MT, Wallace DC. Am / Ophtlwlmol 1991; 111: 750- 62 Oune). [ Reprint requests to Dr. N. J. Newman, Neuro- Ophthalmology Unit, Emory Eye Center, 1327 Clifton Road, N. E., Atlanta, GA 30322.) Leber's Hereditary Optic Neuropathy and KearnsSayre Syndrome: Mitochondrial DNA Mutations. Phillips CI, Gosden CM. Surv Ophthalmol 1991; 35: 463- 72 ( May- June) [ Reprint requests to Prof. C. Gosden, MRC Human Genetics Unit, Western General Hospital, Edinburgh EH4 2XU, Scotland, U. K.) The first article, a " mega- article" of twelve pages, describes 49 cases of Leber's optic neuropathy with a mitochondrial DNA mutation at position 11778 ( testing with Sfa N1 restriction endonuclease was positive in all; most cases were " confirmed" by testing with Mae 3 restriction enzyme). About half of the cases had no identifiable relative in the maternal line with symptoms of Leber's, but about half did. The clinical characteristics of their cases are presented in detailed fashion and compared to other reported groups of patients with Leber's. The second article is an overview of mitochondrial DNA ocular disease, specifically leber's and Kearns- Sayre, in terms of specifics of the genetics involved. Interestingly- and important to remember with restriction enzymes Sfa N1 and Mae 3 ( which are discussed in fascinating basic- science detail)- only about 509C of cases and families of clinical Leber's will have positive endonuclease testing, presumably because a different subunit of mitochondrial DNA also coding for a different but also crucial part of the respiratory enzyme NADH can produce Leber's. LYIl A. Sedwick, M. D. Orbital and Eyelid Involvement With ErdheimChester Disease: A Report of Two Cases. Shields JA, Karcioglu ZA, Shields Cl, Eagle RC, Wong S. Arch OphtlzalmoI1991; 109: 850-- 4 Oune). [ Reprint requests to Dr. J. Shields, Ocular Oncology Service, Wills Eye Hospital, Ninth and Walnut Streets, Philadelphia, PA 19107.] Two patients with this unusual disease are described in whom there were prominent orbital finding~ prop~ osis, lid retraction, and/ or ophthalmoplegIa. ThIS IdIOpathic condition causes infiltra- |