| OCR Text |
Show Journal of Clillical Nellro-ophthalmology 7(3):178-179, 1987. Literature Abstracts Optic Nerve Sheath Decompression. Hupp SL, Glaser JS, Frazier-Byrne S. Arch Ophthalmol 1987;105:386-9 (Mar). [Reprint requests to Dr. S. L. Hupp, P.O. Box 81327, Mobile, AL 36689.] This is a review of 17 patients who underwent optic nerve sheath decompression at Bascom Palmer between 1969 and 1984. Unfortunately, the most interesting data which concerns pre- and postoperative visual function are presented on two different pages of the article which needlessly confuses one's ability to quickly assess the success or failure of the procedure. For example, in the five patients with presumed or known optic nerve sheath meningioma, four were worse either immediately postoperatively or at the end of follow-up (not specified how long in most cases) and only one improved postoperatively. Curiously, only two patients had decompression for chronic disk edema secondary to pseudotumor cerebri. Other preoperative diagnoses included, for example, basilar artery aneurysm, optic nerve trauma, and central retinal vein occlusion. Only nine of the 17 eyes had improved visual function postoperatively and not always was this sustained in follow-up. The non-optic-nerve-sheath-decompression surgeon will be astonished at, and probably skeptical of, the breadth of conditions causing disk edema deemed appropriate for surgical decompression in this series. Other published review series of optic nerve sheath decompression include mostly patients with pseudotumor cerebri, either idiopathic or secondary to vascular anomalies, as these authors discuss. Lyn A. Sedwick, M.D. Cancer-Associated Retinopathy. Thirkill CE, Roth AM, Keltner JL. Arch Ophthalmol 1987;105:372-5 (Mar). [Reprint requests to Dr. C. E. Thirkill, Department of Ophthalmology, University of California, 1603 Alhambra Blvd., Sacramento, CA 95816.] Four patients are discussed who had visual loss and known or subsequently diagnosed cancer. All '0,~ lp\,(']s (If immunoglobulin to- 178 1[1 1987 Raven Press, Ltd., New York ward retina as evaluated by ELISA and electrophoresis. What is perhaps most inter~sting about these patients is the development of vIsual loss ~p to 8 months before the diagnosis of cancer and Its steroid-responsiveness in some cases. Characteri~tically, electroretinograms are ~at. Those J?hY~Icians who have patients who rmght have thIS dISorder should consider sending serum to Dr. Thirkill. Lyn A. Sedwick, M.D. Leber's Congenital Amaurosis. Schroeder R, Mets MB, Maumenee IH. Arch OphthalmoI1987;105:3569 (Mar). [Reprint requests to Dr. M. B. Mets, Department of Ophthalmology, Eye Research Laboratories, 939 E. 57th St., Chicago, IL 60637.] Congenital Stationary Night Blindness Presenting as Leber's Congenital Amaurosis. Weleber RG, Tongue AC. Arch Ophthalmol 1987;105:360-5 (Mar). [Reprint requests to Dr. R. G. Weleber, Department of Ophthalmology, Oregon Health Sciences University, 3181 S.W. Sam Jackson Park Rd., Portland, OR 97201.] The first article is a succinct review of 43 cases of Leber's congenital amaurosis. The data are easily grasped and comment section contrasts Leber's to other causes of congenital blindness with special note made of treatable, metabolic disorders. A previously unreported fundus pattern was observed in two patients ("nummular" pigmentary pattern) and color photos are included. The second article describes two siblings who in early infancy appeared blind and were eventually found to have congenital stationary night blindness. The eldest sibling had an extinguished electroretinogram at 4 and 7 months and a third electroretinogram at age 1 year with findings consistent with congenital stationary night blindness. Subsequently, paradoxical pupils were noted, and at age 4.3 years Snellen acuity was binocular 20/50- at distance. The authors note that these siblings had profound visual impairment that improved during infancy. Lyn A. Sedwick, M.D. |
