Intraocular Lens Power Prediction in Patients Who Undergo Cataract Surgery Following Previous Radial KeratotomyLyle, W. Andrew;Jin, George J. C.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150459001pmid: 9109752
Abstract Background: Previous experience has shown that there is no technical difficulty in performing cataract surgery on patients who have previously undergone radial keratotomy. However, some researchers have reported inaccuracy in intraocular lens (IOL) power selection. Objectives: To assess the visual and refractive outcomes of our patients and to compare different formulas and variables to improve accuracy in power determination. Main Outcome Measures: Ten eyes subjected to phacoemulsification with in-the-bag posterior chamber lens implantation 79 months (range, 36-118 months) after radial keratotomy were evaluated in this study. The IOL power was retrospectively calculated for each eye using the Binkhorst, SRK II, and Holladay formulas with the current keratometry reading, the refractive-derived keratometric value (K), the current refractive-derived K, and the adjusted K. The final refractive result was used as a criterion to judge the accuracy and predictability for each approach. Results: Three eyes underwent an IOL exchange after initial surgery. Among the 7 eyes that did not undergo an IOL exchange, a hyperopic shift that regressed approximately 3 months after surgery occurred in the early post-operative period. At the final examination, 5 of the 7 eyes had a hyperopic error, with 2 eyes showing more than 1.00 diopter (D). Overall, in an average of 27 months (range, 9-80 months) of follow-up, an uncorrected visual acuity of 20/40 or better was obtained in 6 (60%) of the eyes. All 10 eyes had a 20/25 or better postoperative best-corrected visual acuity. The mean (±SD) spherical equivalent refraction was changed from −0.78±3.49 D preoperatively to 0.45±1.31 D postoperatively. We found that the Binkhorst and Holladay formulas are more accurate than the SRK II formula. With the use of an adjusted K (ie, the current average K minus 1.0 D) in combination with the Binkhorst and Holladay formulas, most of the eyes would achieve a refraction of −2.00 to +0.50 D. Conclusions: A corneal flattening effect caused by cataract surgery tends to occur in eyes that have undergone previous radial keratotomy. The use of an average between the Binkhorst and Holladay formulas, aiming for −0.75 D with an adjusted K, seems to be a more accurate and predictable method for IOL power calculation. This approach could reduce the chance of postoperative hyperopia. References 1. Waring GO, Lynn MJ, McDonnell PJ, and the PERK Study Group. Results of the Prospective Evaluation of Radial Keratotomy (PERK) study 10 years after surgery . Arch Ophthalmol . 1994;112:1298-1308.Crossref 2. Koch DD, Liu JF, Hyde LL, Rock RL, Emery JM. Refractive complications of cataract surgery after radial keratotomy . Am J Ophthalmol . 1989;108:676-682. 3. Markovits AS. Extracapsular cataract extraction with posterior chamber intraocular lens implantation in a postradial keratotomy patient . Arch Ophthalmol . 1986;104:329-331.Crossref 4. Holladay JT. Consultations in refractive surgery . Refract Corneal Surg . 1989;5:203. 5. Binder PS, Charlton KH. Surgical procedures performed after refractive surgery . Refract Corneal Surg . 1992;8:61-74. 6. Hotter KJ. Intraocular lens power calculation for eyes after refractive surgery . J Refract Surg . 1995;11:490-493. 7. Celikkol L, Paulopoulos G, Weinstein B, Celikkol G, Feldman ST. Calculation of intraocular lens power after radial keratotomy with computerized videokeratography . Am J Ophthalmol . 1995;120:739-750. 8. Lyle WA, Jin GJC. Phacoemulsification with intraocular lens implantation in high myopia . Cataract Refract Surg . 1996;22:238-242.Crossref 9. Binder PS, Nayak SK, Deg JK, Zavala EY, Sugar J. An ultrastructural and histochemical study of long-term wound healing after radial keratotomy . Am J Ophthalmol . 1987;103:432-440.
Use of Routine Antibiotic Sensitivity Testing for the Management of Corneal UlcersKowal, Vera O.;Levey, Stephanie B.;Laibson, Peter R.;Rapuano, Christopher J.;Cohen, Elisabeth J.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150464002pmid: 9109753
Abstract Objective: To prospectively evaluate the clinical importance of antibiotic sensitivities for the management of corneal ulcers. Methods: Thirty-two consecutive patients referred to the Cornea Service at Wills Eye Hospital, Philadelphia, Pa, between October 1,1993, and May 31,1994, with a culture-positive corneal ulcer were studied prospectively. Broad-spectrum empirical antibiotic therapy with intensive topical fortified antibiotics was initiated after smear and culture results were obtained. The therapy was modified based on clinical appearance, stain results, or organism identification. Clinicians were masked to the sensitivity results. Results: Fifteen patients healed after receiving the initial empirical antibiotic therapy (group 1). The antibiotic regimens of 6 patients were modified after the stain and/or culture results were available, although the clinical appearance suggested continued improvement while taking the initial regimen (group 2). Eleven patients had ulcers that either failed to improve or worsened after receiving the initial empirical therapy (group 3). Seven of these patients ultimately improved with a change in therapy; treatment failed in 4 patients. Nine patients (5 for whom antibiotic therapy succeeded and 4 for whom it failed) should have been adequately treated by the initial antibiotic therapy, according to sensitivity results. In the remaining 2 patients, in vitro sensitivity testing did not include the antibiotics used for the initial treatment. In all cases, the organisms were sensitive to the empirically altered regimen of antibiotics. Conclusions: These preliminary results suggest that routine antibiotic susceptibility tests do not provide clinically useful information for the management of corneal ulcers. The identification of the organisms based on the results of smears and cultures was sufficient for the selection and modification of topical antibiotic therapy. References 1. Ogawa GSH, Hyndiuk RA. Bacterial keratitis and conjunctivitis . In: Smolin G, Thoft RA, eds. The Cornea . 3rd ed. Boston, Mass: Little Brown & Co Inc; 1994: chap 5. 2. Baum JL. Initial therapy of suspected microbial corneal ulcers, I: broad antibiotic therapy based on prevalence of organisms . Surv Ophthalmol . 1979;24:97-105.Crossref 3. Jones DB. Initial therapy of suspected microbial corneal ulcers, II: specific antibiotic therapy based on corneal smears . Surv Ophthalmol . 1979;24:105-116.Crossref 4. Jones DB. Early diagnosis and therapy of bacterial corneal ulcers . Int Ophthalmol Clin . 1973;13:1-29.Crossref 5. McDonnell PJ, Nobe J, Gauderman WJ, et al. Community care of corneal ulcers . Am J Ophthalmol . 1992;114:531-538. 6. McLeod SD, Kolahdouz-Isfahani A, Rosamian K, et al. The role of smears, cultures, and antibiotic sensitivity testing in the management of suspected infectious keratitis . Ophthalmology . 1996;103:23-28.Crossref 7. Poggio EC, Glynn RJ, Schein OD, et al. The incidence of ulcerative keratitis among users of daily-wear and extended-wear soft contact lenses . N Engl J Med . 1989;321;779-783.Crossref 8. Ormerod LD, Heseltine PNR, Alfonso E, et al. Gentamicin-resistant pseudomonal infection: rationale for a redefinition of ophthalmic microbial sensitivities . Cornea . 1989;8:195-199.Crossref 9. McDonnell PJ. Empirical or culture-guided therapy for microbial keratitis? Arch Ophthalmol . 1996;114:84-87.Crossref 10. Leibowitz HM. Clinical evaluation of ciprofloxacin 0.3% ophthalmic solution for treatment of bacterial keratitis . Am J Ophthalmol . 1991;112( (suppl) ):34-47. 11. Gelender J, Rettich C. Gentamicin-resistant Pseudomonas aeruginosa corneal ulcers . Cornea . 1984;3:21-26.Crossref 12. Allen HF. Current status of prevention, diagnosis, and management of bacterial corneal ulcers . Ann Ophthalmol . 1971;3:235-246. 13. Coster DJ, Badenoch PR. Host, microbial, and pharmacological factors affecting the outcome of suppurative keratitis . Br J Ophthalmol . 1987;71:96-101.Crossref 14. Musch DC, Sugar A, Meyer RF. Demographic and predisposing factors in corneal ulceration . Arch Ophthalmol . 1983;101:1545-1548.Crossref 15. Jones DB. Emerging antibiotic resistance: real and relative . Arch Ophthalmol . 1996;114:91-92.Crossref
Syphilitic Uveitis in Human Immunodeficiency Virus—Infected PatientsShalaby, Ismail A.;Dunn, James P.;Semba, Richard D.;Jabs, Douglas A.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150471003pmid: 9109754
Abstract Objective: To document the incidence and clinical features of syphilitic uveitis in patients coinfected with human immunodeficiency virus (HIV). Design: Retrospective chart review. Setting: Single tertiary uveitis referral center. Patients: The charts of HIV-infected patients with uveitis and a reactive fluorescent treponemal antibody absorption test seen between November 1983 and June 1995 were reviewed. Results: Syphilis was the most common bacterial cause of uveitis in this group. Thirteen patients (0.6% of the 2085 HIV-positive patients seen in the clinic during the study period) were dually infected. Twelve patients were male. Six patients (46%) had previously been treated for syphilis, 4 with intramuscular penicillin G benzathine only. Four patients (31%) had isolated anterior uveitis, 3 patients (23%) had anterior and intermediate uveitis, and 5 patients (38%) had panuveitis. One patient (8%) presented with optic nerve and retinal atrophy. Eight patients were treated with intravenous penicillin, 3 with intravenous and intramuscular penicillin, and 1 with intravenous ceftriaxone sodium. Of the 12 patients for whom follow-up examinations were available after treatment, ocular inflammation decreased in 11 (92%) and visual acuity improved in 8 (67%). Rapid plasma reagin titers decreased a median of 64-fold compared with pretreatment levels, and all patients with reactive cerebrospinal fluid who underwent pretreatment and posttreatment lumbar punctures normalized following therapy with intravenous antibiotics. Conclusions: Syphilis is an uncommon cause of uveitis in HIV-infected patients. Anterior uveitis is the most common ocular manifestation, but panuveitis is more common than isolated anterior uveitis. Intravenous penicillin is effective therapy. References 1. Rolfs RT, Nakashima AK. Epidemiology of primary and secondary syphilis in the United States, 1981 through 1989 . JAMA . 1990;264:1432-1437.Crossref 2. Centers For Disease Control. Primary and secondary syphilis—United States, 1981-1990 . MMWR Morb Mortal Wkly Rep . 1991;40:314-323. 3. Tramont EC. Treponema pallidum (syphilis) . In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and Bennett's Principles and Practice of Infectious Diseases . 4th ed. New York, NY: Churchill Livingstone; 1995;2:2117-2133. 4. Johns DR, Tierney M, Felsenstein D. Alteration in the natural history of neurosyphilis by concurrent infection with the human immunodeficiency virus . N Engl J Med . 1987;316:1569-1572.Crossref 5. Musher DM, Hamill RJ, Baughn RE. Effect of human immunodeficiency virus (HIV) infection on the course of syphilis and on the response to treatment . Ann Intern Med . 1990;113:872-881.Crossref 6. Horowitz HW, Valsamis MP, Wicher V, et al. Cerebral syphilitic gumma confirmed by the polymerase chain reaction in a man with human immunodeficiency virus infection . N Engl J Med . 1984;331:1488-1491.Crossref 7. Berry CD, Hooton TM, Collier AC, Lukehart SA. Neurological relapse after benzathine penicillin therapy for secondary syphilis in a patient with HIV infection . N Engl J Med . 1987;316:1587-1589.Crossref 8. Gordon SM, Eaton ME, George R, et al. The response of symptomatic neurosyphilis to high-dose intravenous penicillin G in patients with human immunodeficiency virus infection . N Engl J Med . 1994;331:1469-1473.Crossref 9. Becerra LI, Kziazek SM, Savino PJ, et al. Syphilitic uveitis in human immunodeficiency virus—infected and non-infected patients . Ophthalmology . 1989;96:1727-1730.Crossref 10. McLeish WM, Pulido JS, Holland S, et al. The ocular manifestations of syphilis in the human immunodeficiency virus type 1—infected host . Ophthalmology . 1990;97:196-203.Crossref 11. Levy JH, Liss RA, Maguire AM. Neurosyphilis and ocular syphilis in patients with concurrent human immunodeficiency virus infection . Retina . 1989;9:175-180.Crossref 12. Ross WH, Hugo FSS. Acquired syphilitic uveitis . Arch Pharmacol . 1980;98:496-498. 13. Kleiner RC, Najarian L, Levenson J, Kaplan HJ. AIDS complicated by syphilis can mimic uveitis and Crohn's disease . Arch Ophthalmol . 1987;105:1486-1487.Crossref 14. Richards BW, Hessburg TJ, Nussbaum JN. Recurrent syphilitic uveitis . N Engl J Med . 1989;320:62. 15. Tamesis RR, Foster CS. Ocular syphilis . Ophthalmology . 1990;97:1281-1287.Crossref 16. Pillai S, DiPaolo F. Bilateral panuveitis, sebopsoriasis, and secondary syphilis in a patient with acquired immunodeficiency syndrome . Am J Ophthalmol . 1992;114:773-775. 17. Passo MS, Rosenbaum JT. Ocular syphilis in patients with human immunodeficiency virus infection . Am J Ophthalmol . 1988;106:1-6. 18. Joyce PW, Haye KR, Ellis ME. Syphilitic retinitis in a homosexual man with concurrent HIV infection: case report . Genitourin Med . 1989;65:244-247. 19. Gass JDM, Braunstein RA, Chenoweth RG. Acute syphilitic posterior placoid chorioretinitis . Ophthalmology . 1990;97:1288-1297.Crossref 20. Zaidman GW. Neurosyphilis and retrobulbar neuritis in a patient with AIDS . Ann Ophthalmol . 1986;18:260-261. 21. Carter JB, Hamill RJ, Matoba AY. Bilateral syphilitic optic neuritis in a patient with a positive test for HIV . Arch Ophthalmol . 1987;105:1485-1486.Crossref 22. Zambrano W, Perez GM, Smith JL. Acute syphilitic blindness in AIDS . J Clin Neuro Ophthalmol . 1987;7:1-5.Crossref 23. Toshniwal P. Optic perineuritis and secondary syphilis . J Clin Neuro Ophthalmol . 1987;7:6-10. 24. Winward KE, Hamed LM, Glaser JS. The spectrum of optic nerve disease in human immunodeficiency virus infection . Am J Ophthalmol . 1989;107:373-380. 25. Smith JL, Byrne SF, Cambron CR. Syphiloma/gumma of the optic nerve and human immunodeficiency virus seropositivity . J Clin Neuro Ophthalmol . 1990;10:175-184. 26. Centers for Disease Control and Prevention. 1993 Revised classification system for HIV infection and expanded surveillance case definition for AIDS among adolescents and adults . MMWR Morb Mortal Wkly Rep . 1992;41( (RR-17) ):1-13. 27. Schechter M, Harrison LH, Nalsey NA, et al. Coinfection with human T-cell lymphotropic virus type 1 and HIV in Brazil . JAMA . 1994;271:353-357.Crossref 28. Schlaegel TF, Kao SF. A review (1970-1980) of 28 presumptive cases of syphilitic uveitis . Am J Ophthalmol . 1982;93:412-414. 29. Henderly DE, Gentsler AJ, Smith RE, Rao NA. Changing patterns of uveitis . Am J Ophthalmol . 1987;103:131-136. 30. Jabs DA. Ocular manifestations of HIV infection . Trans Am Ophthalmol Soc . 1995;93:623-683. 31. Musher DM. Syphilis, neurosyphilis, penicillin, and AIDS . J Infect Dis . 1991;163:1201-1206.Crossref 32. Spoor TC, Ramocki JM, Nesi FA, Sorcher M. Ocular syphilis 1986: prevalence of FTA-ABS reactivity and cerebrospinal fluid findings . J Clin Neuro Ophthalmol . 1987;7:191-195. 33. Margo CE, Hamed LM. Ocular syphilis . Surv Ophthalmol . 1992;37:203-220.Crossref 34. Marshall DW, Brey RL, Cahill WT, et al. Spectrum of cerebrospinal fluid findings in various stages of human immunodeficiency virus infection . Arch Neurol . 1988;45:954-958.Crossref 35. Centers for Disease Control. Recommendations for diagnosing and treating syphilis in HIV-infected patients . MMWR Morb Mortal Wkly Rep . 1989;37:1-2. 36. Spoor TC, Wynn P, Hartel WC, Bryan CS. Ocular syphilis: acute and chronic . J Clin Neuro Ophthalmol . 1983;3:197-203. 37. Tramont EC. Syphilis in the AIDS era . N Engl J Med . 1987;316:1600-1601.Crossref 38. Peterman TA, Zaidi AA, Lieb S, Wroten JE. Incubating syphilis in patients treated for gonorrhea: a comparison of treatment regimens . J Infect Dis . 1994;170:689-692.Crossref 39. Hook III EW, Baker-Zander S, Moskovitz BL, et al. Ceftriaxone therapy for asymptomatic neurosyphilis . Sex Transm Dis . 1986;13:185-188.Crossref 40. Mendelsohn AD, Jampol LM. Syphilitic retinitis: a cause of necrotizing retinitis . Retina . 1984;4:221-224.Crossref 41. Stoumbos VD, Klein MC. Syphilitic retinitis in a patient with acquired immunodeficiency syndrome—related complex . Am J Ophthalmol . 1987;103:103-104. 42. Felman YM. Lumbar puncture in asymptomatic neurosyphilis . Arch Intern Med . 1985;145:422-423.Crossref 43. Hicks CB, Benson PM, Lupton GP, Tramont EC. Seronegative secondary syphilis in a patient with the human immunodeficiency virus (HIV) with Kaposi sarcoma: a diagnostic dilemma . Ann Intern Med . 1987;107:492-494.Crossref 44. Haas JS, Bolan G, Larsen SA, et al. Sensitivity of treponemal tests for detecting prior treated syphilis during human immunodeficiency virus infection . J Infect Dis . 1990;162:862-866.Crossref 45. Johnson PDR, Graves SR, Stewart L, et al. Specific syphilis serological tests may become negative in HIV infection . AIDS . 1991;5:419-423.Crossref
Comparison of Transillumination and Histologic Slide Measurements of Choroidal MelanomaUmlas, James;Diener-West, Marie;Robinson, Nancy L.;Green, W. Richard;Grossniklaus, Hans E.;Albert, Daniel M.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150476004pmid: 9109755
Abstract Objective: To compare transillumination and histologic slide measurements of choroidal melanomas in 479 eyes randomized to enucleation in the Collaborative Ocular Melanoma Study. Design: Transillumination defects were measured during gross examination of enucleated eyes. Tumor basal diameter and height were measured on histologic slides and each tumor was assigned to 1 of 8 distinct shape categories. Comparison of the transillumination and histologic slide measurements revealed 3 categories of difference: underestimation (transillumination measurement more than 4 mm smaller than the histologic slide measurement), overestimation (transillumination measurement more than 4 mm larger than the histologic slide measurement), and agreement within 4 mm. Results: There was good correlation between transillumination and histologic slide estimates of largest basal diameter, particularly when the basal diameter was 16 mm or less. Measurement discrepancies were related to the shape of the tumors but not to the presence of subretinal fluid or fixation. Conclusion: Agreement was high between measurements of transillumination defect and histologic sections. References 1. Char DH, Phillips TL. The potential for adjuvant radiotherapy in choroidal melanoma . Arch Ophthalmol . 1982;100:247-248.Crossref 2. Robertson DM, Earle J, Anderson JA. Preliminary observations regarding the use of I-125 in the management of choroidal melanoma . Trans Ophthalmol Soc U K . 1983;103:155-160. 3. Cruess AF, Augsburger JJ, Shields JA, et al. Visual results following cobalt plaque radiotherapy for posterior uveal melanomas . Ophthalmology . 1984;91:131-136.Crossref 4. Cruess AF, Augsburger JJ, Shields JA, et al. Regression of posterior uveal melanoma following cobalt-60 plaque radiotherapy . Ophthalmology . 1984;91:1716-1719.Crossref 5. Goodman DH, Char DH, Crawford JB, et al. Uveal melanoma necrosis after helium ion therapy . Am J Ophthalmol . 1986;101:643-645. 6. Augsburger JJ, Gamel JW, Sardi V, et al. Enucleation vs cobalt plaque radiotherapy for malignant melanomas of the choroid and ciliary body . Arch Ophthalmol . 1986;104:655-661.Crossref 7. Gragoudas ES, Seddon JM, Egan KM, et al. Long term results of proton beam irradiated uveal melanomas . Ophthalmology . 1987;94:349-353.Crossref 8. Earle J, Kline RW, Robertson DM. Selection of iodine 125 for the Collaborative Ocular Melanoma Study . Arch Ophthalmol . 1987;105:763-764.Crossref 9. Char DH, Castro JR, Quivey JM, et al. Uveal melanoma radiation: 125-I brachytherapy versus helium ion radiation . Ophthalmology . 1989;96:1708-1715.Crossref 10. Lean EK, Cohen DM, Liggett PE, et al. Episcleral radioactive plaque therapy: initial clinical experience with 56 patients . Am J Clin Oncol . 1990;13:185-190.Crossref 11. Mameghan H, Karolis C, Fisher R, et al. Iodine-125 irradiation of choroidal melanoma: clinical experience from the Prince of Wales and Sydney Eye Hospitals . Australas Radiol . 1992;36:249-251.Crossref 12. Fontanesi J, Meyer D, Xu S, Tai D. Treatment of choroidal melanoma with I-125 plaque . Int J Radiat Oncol . 1993;26:619-623.Crossref 13. Robertson DM, Earle J, Kline RW. Brachytherapy for choroidal melanoma . In: Ryan SJ, ed. Retina . 2nd ed. St Louis, Mo: CV Mosby Co; 1994:772-784. 14. Collaborative Ocular Melanoma Study Group. Design and methods of a clinical trial for a rare condition: the Collaborative Ocular Melanoma Study: COM Report No. 3 . Control Clin Trials . 1993;14:362-391.Crossref 15. Collaborative Ocular Melanoma Study Group. COMS Manual of Procedures . Springfield, Va: National Technical Information Service; January 1995. Publication PB95-179693. 16. Polivogianis L, Seddon JM, Glynn R, et al. Comparison of transillumination and histologic slide measurements of tumor diameter in uveal melanoma . Ophthalmology . 1988;95:1576-1582.Crossref 17. Folberg R, Gamel JW, Greenberg RA, Donoso LA, Naids RM. Comparison of direct and microslide pathology measurements of uveal melanomas . Invest Ophthalmol Vis Sci . 1985;86:1788-1791. 18. Hopwood D. Fixation and fixatives . In: Bancroft JD, Stevens A, eds. Theory and Practice of Histological Techniques . 2nd ed. New York, NY: Churchill Livingstone; 1982:20-40. 19. Robertson DM, Fuller DG, Anderson RE. A technique for accurate placement of episcleral iodine-125 plaques . Am J Ophthalmol . 1987;103:63-65. 20. Olsen KR, Curtin VT. Enucleation and plaque treatment . In: Albert DM, Jakobiec FA, eds. Principles and Practice of Ophthalmology . Philadelphia, Pa: WB Saunders Co; 1994:3217-3232.
The Expanding Clinical Spectrum of Idiopathic Polypoidal Choroidal VasculopathyYannuzzi, Lawrence A.;Ciardella, Antonio;Spaide, Richard F.;Rabb, Maurice;Freund, K. Bailey;Orlock, Dennis A.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150480005pmid: 9109756
Abstract Objective: To expand the clinical spectrum of idiopathic polypoidal choroidal vasculopathy based on historical cases and newly recognized observations. Methods: A review of the previously reported 45 cases was carried out. An additional 20 cases were retrospectively reviewed to examine the clinical nature and course of idiopathic polypoidal choroidal vasculopathy. Results: New observations on the clinical spectrum of idiopathic polypoidal choroidal vasculopathy were noted for demographic features, the nature and course of the vascular lesion, the possible association with intraocular inflammation, and the indocyanine green angiographic characteristics. Conclusions: Idiopathic polypoidal choroidal vasculopathy seems to be a distinct clinical entity that has a predilection for individuals of pigmented races. The disorder should be differentiated from typical choroidal neovascularization and other known choroidal degenerative, inflammatory, and ischemic disorders because of differences in clinical course and treatment. References 1. Yannuzzi LA. Idiopathic polypoidal choroidal vasculopathy. Presented at the Macula Society Meeting; February 5, 1982; Miami, Fla. 2. Kleiner RC, Brucker AJ, Johnston RL. Posterior uveal bleeding syndrome . Ophthalmology . 1984;91( (suppl 9) ):110. Abstract.Crossref 3. Kleiner RC, Brucker AJ, Johnston RL. The posterior uveal bleeding syndrome . Retina . 1990;10:9-7.Crossref 4. Stern RM, Zakov N, Zegarra H, et al. Multiple recurrent serous sanguineous retinal pigment epithelial detachments in black women . Am J Ophthalmol . 1985;100:560-569. 5. Perkovich BT, Zakov ZN, Berlin LA, Weidenthal D, Avins LR. An update on multiple recurrent serosanguineous retinal pigment epithelial detachments in black women . Retina . 1990;10:18-26.Crossref 6. Yannuzzi LA, Sorenson J, Spaide RF, Lipson B. Idiopathic polypoidal choroidal vasculopathy . Retina . 1990;10:1-8.Crossref 7. Spaide RF, Yannuzzi LA, Slakter JS, Sorenson JA, Orlock DA. Indocyanine green videoangiography of idiopathic choroidal vasculopathy . Retina . 1995;15:100-110.Crossref 8. Ross RD, Gitter KA, Cohen G, Shomaker KS. Idiopathic polypoidal choroidal vasculopathy associated with retinal arterial macroaneurysm and hypertensive retinopathy . Retina . 1996;16:105-111.Crossref 9. Yannuzzi LA, Slakter JS, Sorenson JA, et al. Digital indocyanine green videoangiography and choroidal neovascularization . Retina . 1992;12:191-223.Crossref 10. Ferris FL III. Senile macular degeneration: review of epidemiologic features . Am J Epidemiol . 1983;118:213-221. 11. Capone A Jr, Wallace RT, Meredith TA. Symptomatic choroidal neovascularization in blacks . Arch Ophthalmol . 1994;112:1091-1097.Crossref 12. MacCumber MW, Dastgheib K, Bressler NM, et al. Clinicopathological correlation of the multiple recurrent serosanguineous retinal pigment epithelial detachments syndrome . Retina . 1995;15:100-110.Crossref 13. Trimble SN, Schatz H, Schneider GB. Spontaneous decalcification of a choroidal osteoma . Ophthalmology . 1988;95:631-635.Crossref 14. Kinkaid J, Schatz H. Bilateral retinal arteritis with multiple aneurysmal dilations . Retina . 1983;3:171-175.Crossref 15. Chang T, Aylward W, Davis JL, et al. Idiopathic retinal vasculitis, aneurysms, and neuro-retinitis . Ophthalmology . 1995;102:1089-1097.Crossref 16. Yannuzzi L, Slakter JS, Kaufman SR, Gupta K. Laser treatment of diffuse retinal pigment epitheliopathy . Eur J Ophthalmol . 1992;2:103-114. 17. Green WR, McDonnel PJ, Yeo JH. Pathological features of senile macular degeneration . Ophthalmology . 1985;92:615-627.Crossref 18. Gass JDM. Stereoscopic Atlas of Macular Diseases . St Louis, Mo; CV Mosby Co; 1987. 19. Hyman LG, Lilienfeld AM, Ferris FL III. Senile macular degeneration: a case control study . Am J Epidemiol . 1983;118:213-221. 20. Arnold JJ, Sarks SH, Killingworth MC, Sarks JP. Reticular pseudodrusen . Retina . 1995;15:183-191.Crossref 21. Guyer DR, Yannuzzi LA, Ladas I, Slakter JS, Sorenson JA, Orlock DA. Indocyaninegreen guided laser photocoagulation of focal spots at the edge of plaques of choroidal neovascularization . Arch Ophthalmol . 1996;114:693-697.Crossref 22. Chang TS, Freund KB, de la Cruz Z, Yannuzzi LA, Green WR. Clinicopathological correlation of choroidal neovascularization demonstrated by indocyanine green angiography in a patient with retention of good vision for almost four years . Retina . 1994;14:114-124.Crossref 23. Green WR. Retina . In: Spencer WH, ed. Ophthalmic Pathology Volume 2 . Philadelphia, Pa: WB Saunders Co; 1985:647-651.
Natural History and Clinical Management of Central Retinal Vein Occlusion1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150488006pmid: 9109757
Abstract Objective: To provide clinical management guidelines for eyes with central retinal vein occlusion. Design: Prospective cohort study with randomized clinical trials of specific subgroups of patients. Three-year follow-up every 4 months. Setting: Nine ophthalmology practices. Patients: Seven hundred twenty-five patients with central vein occlusion. Main Outcome Measures: Iris neovascularization (INV), neovascular glaucoma, and visual acuity. Results: Visual acuity outcome was largely dependent on initial acuity. Sixty-five percent of patients with initially good visual acuity (20/40 or better) maintained visual acuity in the same range at the end of the study. Patients with intermediate initial acuity (20/50-20/200) showed a variable outcome: 19% improved to better than 20/50, 44% stayed in the intermediate group, and 37% had final visual acuity worse than 20/200. Patients who had poor visual acuity at the first visit (<20/200) had an 80% chance of having a visual acuity less than 20/200 at final visit, whether perfused or nonperfused initially. In the first 4 months of follow-up, 81 (15%) of the 547 eyes with perfusion converted to ischemia. During the next 32 months of follow-up, an additional 19% of eyes were found to have converted to ischemia for a total of 34% after 3 years. The development of nonperfusion or ischemia was most rapid in the first 4 months and progressed continuously throughout the entire duration of follow-up. Iris neovascularization of at least 2-clock hours, and/or angle neovascularization (ANV) developed in 117 (16%) of the 714 eyes. Sixty-one of the 117 eyes that had INV/ANV were initially categorized as nonperfused or indeterminate; 56 of the 117 eyes were initially categorized as perfused. When INV/ANV occurred, it was treated promptly with panretinal photocoagulation. The strongest predictors of INV/ANV were visual acuity (P<.001) and the amount of nonperfusion seen by fluorescein angiogram (P<.001). For eyes initially categorized as nonperfused or indeterminate, 35% (61/176) developed INV/ANV, compared with 10% (56/538) for eyes initially categorized as perfused. Other risk factors were venous tortuosity (P=.02), extensive retinal hemorrhage (P=.07), and duration less than 1 month (P=.08). Neovascular glaucoma that was unsuccessfully managed with medical treatment developed in only 10 eyes. No eye was enucleated. Conclusions: Visual acuity at baseline is a strong predictor of visual acuity at 3 years for eyes with good vision and eyes with poor vision, but a poor predictor for intermediate acuities. Visual acuity is also a strong predictor for the development of INV/ANV, as is nonperfusion. During the course of follow-up, one third of the eyes with perfusion converted to eyes with ischemia. Clinical management guidelines, developed from these and previously reported Central Vein Occlusion Study data, are presented. References 1. Central Vein Occlusion Study Group. Central Vein Occlusion Study of photocoagulation therapy: manual of operations . Online J Curr Clin Trials . 1993. 2. Central Vein Occlusion Study Group. Central Vein Occlusion Study of photocoagulation therapy: design and baseline . Online J Curr Clin Trials . 1993. 3. The Central Vein Occlusion Study Group. Baseline and early natural history report: the Central Vein Occlusion Study . Arch Ophthalmol . 1993;111:1087-1095.Crossref 4. The Central Vein Occlusion Study Group. A randomized clinical trial of early panretinal photocoagulation for ischemic central vein occlusion: the Central Vein Occlusion Study Group N report . Ophthalmology . 1995;102:1434-1444.Crossref 5. The Central Vein Occlusion Study Group. Evaluation of grid pattern photocoagulation for macular edema in central vein occlusion: the Central Vein Occlusion Study Group M report . Ophthalmology . 1995;102:1425-1433.Crossref
Orbital Color Doppler Imaging in Carotid Occlusive DiseaseMawn, Louise A.;Hedges, Thomas R.;Rand, William;Heggerick, Paula A.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150494007pmid: 9109758
Abstract Objective: To define orbital circulation abnormalities identified by color Doppler imaging in patients with severe carotid occlusive disease. Patients: Twenty-four patients referred to a hospital-based neuro-ophthalmology service with hemodynamically significant carotid occlusive disease (>75% stenosis) were prospectively studied. Eight had signs of ocular ischemic syndrome; 12 of the 24 patients underwent endarterectomy. Main Outcome Measures: Peak systolic velocity of the central retinal, posterior ciliary, and ophthalmic artery and pulsatility indexes as determined by color Doppler imaging. Methods: Color Doppler imaging was performed using a 7.5-MHz probe. Both eyes were studied in all patients and carotid duplex imaging was obtained. Results: All patients with hemodynamically significant carotid occlusive disease had lower mean peak systolic velocities in the central retinal, posterior ciliary, and ophthalmic arteries and higher pulsatility indexes compared with normal control patients. Endarterectomy improved peak systolic velocities. Reversal of ophthalmic flow direction as a separate variable was unassociated with altered mean central retinal or posterior ciliary artery flow velocities. Patients with ocular ischemic syndrome may have similar orbital color Doppler imaging findings compared with patients with severe carotid occlusive disease without overt manifestations of chronic ocular ischemia. Conclusion: Orbital circulation is highly adaptable even when faced with severe compromise in proximal blood flow. References 1. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade stenosis . N Engl J Med . 1991;325:445-453.Crossref 2. Haynes RB, Taylor DW, Sackett DL, Thorpe K, Ferguson GG, Barnett HJ. Prevention of functional impairment by endarterectomy for symptomatic high-grade carotid stenosis . JAMA . 1994;271:1256-1259.Crossref 3. Mayberg MR, Wilson SE, Yatsu F, et al. Carotid endarterectomy and prevention of cerebral ischemia in symptomatic carotid stenosis . JAMA . 1991;266:3289-3294.Crossref 4. Ho AC, Lieb WE, Flaharty PM, et al. Color Doppler imaging of the ocular ischemic syndrome . Ophthalmology . 1992;99:1453-1462.Crossref 5. Hu H-H, Sheng W-Y, Yen M-Y, Lai S-T, Teng M-H. Color Doppler imaging of orbital arteries for detection of carotid occlusive disease . Stroke . 1993;24:1196-1203.Crossref 6. Kerty E, Eide N, Horven I. Ocular hemodynamic changes in patients with high-grade carotid occlusive disease and development of chronic ocular ischaemia, II: clinical findings . Acta Ophthalmol Scand . 1995;73:72-76.Crossref 7. Kerty E, Horven I. Ocular hemodynamic changes in patients with high-grade carotid occlusive disease and development of chronic ocular, I: Doppler and dynamic tonometry findings . Acta Ophthalmol Scand . 1995;73:66-71.Crossref 8. Ward JB, Hedges TR III, Heggerick PA. Reversible abnormalities in the ophthalmic arteries detected by color Doppler imaging . Ophthalmology . 1995;102:1606-1610.Crossref 9. Greenfield DS, Heggerick PA, Hedges TR III. Color Doppler imaging of normal orbital vasculature . Ophthalmology . 1995;102:1598-1605.Crossref
Nitric Oxide Synthase in the Human Glaucomatous Optic Nerve HeadNeufeld, Arthur H.;Hernandez, M. Rosario;Gonzalez, Miriam
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150499009pmid: 9109759
Abstract Objectives: To investigate the hypothesis that nitric oxide contributes to neurotoxicity in the optic nerve heads of patients with primary open-angle glaucoma, we have determined the presence of the 3 isoforms of nitric oxide synthase (NOS) in the tissue. Methods: Histological sections of optic nerve heads from normal subjects and patients with glaucoma who have moderate to advanced nerve damage were studied by immunohistochemistry. Polyclonal antibodies to NOS-1, NOS-2, and NOS-3 were localized with immunoperoxidase staining. Results: In normal eyes, NOS-1 is sparsely present in astrocytes throughout the optic nerve head. In glaucomatous optic nerve heads, almost every astrocyte is positive for NOS-1. Nitric oxide synthase—1 immunoreactivity is abundantly present throughout the prelaminar region and the lamina cribrosa and is localized inside the diminished nerve fiber bundles. Nitric oxide synthase—2 is present in a few cells in the disorganized lamina cribrosa of the glaucomatous eye and is not present at all in normal tissue. Nitric oxide synthase—3 is present in normal eyes in the vascular endothelia of small blood vessels of the prelaminar region. In glaucomatous tissue, NOS-3 is present in astrocytes and in the vascular endothelia of large and small vessels. Conclusions: The 3 isoforms of NOS are present in apparently increased amounts in the optic nerve head of patients with primary open-angle glaucoma. The increased presence of NOS-1 and the induction of NOS-2 in astrocytes of the lamina cribrosa suggest that the glaucomatous optic nerve head is exposed to excessive levels of nitric oxide, which may be neurodestructive, locally, to the axons of the retinal ganglion cells. Conversely, the increased presence of NOS-3 in vascular endothelia may be neuroprotective by causing vasodilation and increased blood flow in the tissue. References 1. Moncada S, Higgs A. The l-arginine—nitric oxide pathway . N Engl J Med . 1993;329:2002-2012.Crossref 2. Bredt DS, Snyder SH. Nitric oxide, a physiological messenger molecule . Ann Rev Biochem . 1994;63:175-195.Crossref 3. Dawson TM, Dawson VL. Nitric oxide: actions and pathological roles . Neuroscientist . 1994;1:9-20. 4. Bredt DS, Hwang PM, Glatt CE, et al. Cloned and expressed nitric oxide synthase structurally resembles cytochrome P-450 reductase . Nature . 1991;351:714-718.Crossref 5. Dawson TM, Snyder SH. Gases as biological messengers: nitric oxide and carbon monoxide in the brain . J Neurosci . 1994;14:5147-5159. 6. Koistinado J, Sagar SM. NADPH-diaphorase—reactive neurones in the retina . Prog Retina Eye Res . 1995;15:69-87.Crossref 7. Nathan C, Xie Q-W. Regulation of biosynthesis of nitric oxide . J Biol Chem . 1994;19:13725-13728. 8. Lamas S, Marsden PA, Li GK, Tempst P, Michel T. Endothelial nitric oxide synthase: molecular cloning and characterization of a distinct constitutive enzyme isoform . Proc Natl Acad Sci U S A . 1992;89:6348-6352.Crossref 9. Moncada S. The l-arginine:nitric oxide pathway . Acta Physiol Scand . 1992;145:201-227.Crossref 10. Lyons CR, Orloff GJ, Cunningham JM. Molecular cloning and functional expression of an inducible nitric oxide synthase from murine macrophage cell line . J Biol Chem . 1992;267:6370-6374. 11. Dawson VL, Dawson TM, London ED, Bredt DS, Snyder SH. Nitric oxide mediates glutamate neurotoxicity in primary cortical cultures . Proc Natl Acad Sci U S A . 1991;88:6368-6371.Crossref 12. Dawson VL, Dawson TM, Bartley DA, Uhl GR, Snyder SH. Mechanisms of nitric oxide—mediated neurotoxicity in primary brain cultures . J Neurosci . 1993;13:2651-2661. 13. Dawson VL, Kizushi VM, Huang PL, Snyder SH, Dawson TM. Resistance to neurotoxicity in cortical cultures from neuronal nitric oxide synthase—deficient mice . J Neurosci . 1996;16:2479-2487. 14. Malinski T, Bailey F, Zhang ZG, Chopp M. Nitric oxide measured by a porphyrinic microsensor in rat brain after middle cerebral artery occlusion . J Cereb Blood Flow Metab . 1993;13:355-358.Crossref 15. Santiago M, Nachado A, Cano J. Effect of I-arginine/nitric oxide pathway on MPP(+)-induced cell injury in the striatum of rats . Br J Pharmacol . 1994;111:837-842.Crossref 16. Resink AM, Brahmbhatt HP, Cordell B, Dawson VL, Dawson TM. Nitric oxide mediates a component of amyloid neurotoxicity in cortical cultures . Soc Neurosci Abstr . 1995;21:1010. 17. Bo L, Dawson TM, Wesselingh S, et al. Induction of nitric oxide synthase in demyelinating regions of multiple sclerosis brains . Ann Neurol . 1994;36:778-786.Crossref 18. Huang Z, Huang PL, Panahian N, et al. Effects of cerebral ischemia in mice deficient in neuronal nitric oxide synthase . Science . 1994;265:1883-1885.Crossref 19. Bignami A, Eng LF, Dahl D, Uyeda CT. Localization of the glial fibrillary acidic protein in astrocytes by immunofluorescence . Brain Res . 1972;43:429-435.Crossref 20. Quigley HA, Hohman RM, Addicks EM, Massof RW, Green WR. Morphologic changes in the lamina cribrosa correlated with neural loss in open angle glaucoma . Am J Ophthalmol . 1983;95:673-691. 21. Hernandez MR, Andrzejewska WM, Neufeld AH. Changes in the extracellular matrix of the human optic nerve head in primary open angle glaucoma . Am J Ophthalmol . 1990;109:180-189. 22. Kugler P, Drenckhahn D. Astrocytes and Bergmann glia as an important site of nitric oxide synthase I . Glia . 1996;16:165-173.Crossref 23. Stuehr DJ, Marletta MA. Induction of nitrite/nitrate synthesis in murine macrophages by BCG infection, lymphokines or interferon-γ . J Immunol . 1987;139:518-525. 24. Chao CC, Hu S, Sheng WS, et al. Cytokine-stimulated astrocytes damage human neurons via a nitric oxide mechanism . Glia . 1996;16:276-284.Crossref 25. Hunot S, Boissiere F, Faucheux B, et al. Nitric oxide synthase and neuronal vulnerability in Parkinson's disease . Neurosci . 1996;72:355-363.Crossref 26. Hunot S, Boissiere F, Faucheux B, et al. Nitric oxide synthase and neuronal vulnerability in Parkinson's disease . Neurosci . 1996;72:355-363.Crossref 27. Tripathi BJ, Li T, Li J, Chalam KV, Tripathi RC. Upregulated expression of γ-interferon and transforming growth factor-β1 in the optic nerve head of glaucomatous eyes . Invest Ophthalmol Vis Sci . 1996;37:S411. 28. Buerk DG, Riva CE, Cranstoun SD. Nitric oxide has a vasodilatory role in cat optic nerve head during flicker stimuli . Microvasc Res . 1996;52:13-26.Crossref 29. Arnet UA, McMillan A, Dinerman JL, Ballermann B, Lowenstein CJ. Regulation of endothelial nitric-oxide synthase during hypoxia . J Biol Chem . 1996;271:15 069-15 073.Crossref 30. Huang Z, Huang PL, Ma J, et al. Enlarged infarcts in endothelial nitric oxide synthase mice are attenuated by nitro-L-arginine . J Cereb Blood Flow Metab . 1996;16:981-987.Crossref 31. Murphy S, Simmons ML, Agullo L, et al. Synthesis of nitric oxide in CNS glial cells . Trends Neurosci . 1993;16:323-328.Crossref 32. Garthwaite J, Boulton CL. Nitric oxide signaling in the central nervous system . Ann Rev Physiol . 1995;57:683-706.Crossref 33. Stamler JS. Redox signaling: nitrosylation and related target interactions of nitric oxide . Cell . 1994;78:931-936.Crossref 34. Lipton SA, Choi Y-B, Pan Z-H, et al. A redox-based mechanism for the neuroprotective and neurodestructive effects of nitric oxide and related nitrosocompounds . Nature . 1993;364:626-632.Crossref 35. Minckler DS, McLean IW, Tso MOM. Distribution of axonal and glial elements in the rhesus optic nerve head studied by electron microscopy . Am J Ophthalmol . 1976;82:179-186. 36. Hollander H, Makarov F, Stefani FH, Stone J. Evidence of constriction of optic nerve axons at the lamina cribrosa in the normotensive eye in humans and other mammals . Ophthalmic Res . 1995;27:296-309.Crossref
Controlling the Capsular Shape in Lens RefillingNishi, Okihiro;Nishi, Kayo;Mano, Chizuko;Ichihara, Masuji;Honda, Tomoaki
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150509010pmid: 9109760
Abstract Objectives: To investigate control of the capsular shape by determining the ability of the lens capsule to mold injected silicone and to evaluate the relationship among the volume of silicone injected, refraction, and the amplitude of accommodation. Methods: After endocapsular phacoemulsification following an upper, minicircular capsulorhexis, the lens capsule of a pig eye was refilled with a silicone mixture that polymerizes in vitro in 2 hours. The minicircular capsulorhexis opening was sealed by a small silicone plug to prevent leakage. The anterior capsule curvature and refraction of the lens were measured by a Scheimpflug camera and lensometer, respectively, with and without zonular tension. Zonular tension was created using a ciliary ring sutured to the ciliary bodies and expanded. Results: The mean (±SD) anterior curvature of the lenses without zonular tension was 6.50±0.07 mm after 17 hours and 6.54±0.04 mm after 42 hours; with zonular tension it was 7.01±0.11 mm and 7.23±0.24 mm, respectively. The curvature became flatter when zonular tension was applied or steeper when zonular tension was abolished momentarily during measurements after 17 hours, but after 42 hours the curvature was unaffected by the application or removal of zonular pressure. The mean (±SD) amplitude of accommodation (the difference between refraction without zonular tension and that with it) was 3.2±0.5 diopters (D), 6.1±1.8 D, 4.8±0.8 D, and 2.8±1.3 D, when the lens was refilled with a silicone volume corresponding to 45%, 55%, 75%, and 95%, respectively, of the mean normal lens volume. Conclusions: The lens capsule possesses some ability to mold the injected silicone during its polymerization. When the eye is atropinized, the lens capsule may conform to its nonaccommodated state. Accommodation could be obtained by various degrees of refilling. Moderate refilling yields a greater amplitude of accommodation than does more complete refilling. Using a silicone plug to seal the capsular opening facilitates lens refilling with excellent reproducibility and seems to be useful in research. References 1. Parel J-M, Gelender H, Treffers WF, Norton EWD. Phaco-ersatz . Graefes Arch Clin Exp Ophthalmol . 1986;224:165-173.Crossref 2. Gindi JJ, Wan WL, Schanzlin DJ. Endocapsular cataract surgery . I Cataract . 1985;2:6-10. 3. Haefliger E, Parel J-M, Fantes F, et al. Accommodation of an endocapsular silicone lens (Phaco-Ersatz) in the nonhuman primate . Ophthalmology . 1987;94:471-477.Crossref 4. Nishi O. Refilling the lens of the rabbit eye after endocapsular cataract surgery . Folia Ophthalmol (Japan) . 1987;38:1615-1618. 5. Nishi O, Hara T, Hara T, Sakka Y, Hayashi F, Yamada Y. Refilling the lens with an inflatable endocapsular balloon . Graefes Arch Clin Exp Ophthalmol . 1992;230:47-55.Crossref 6. Nishi O, Nakai Y, Yamada Y, Mizumoto Y. Amplitudes of accommodation of primate lenses refilled with two types of inflatable endocapsular balloons . Arch Ophthalmol . 1993;111:1677-1684.Crossref 7. Hettlich HJ, Lucke K, Asiyo-Vogel MN, Schulte M, Vogel A. Lens refilling and endocapsular polymerization of an injectable intraocular lens: in vitro and in vivo study of potential risks and benefits . J Cataract Refract Surg . 1994;20:115-123.Crossref 8. Fisher RF. The significance of the shape of the lens and capsular energy changes in accommodation . J Physiol (Lond) . 1969;201:21-47.
Preservation of the Inner Retina in Retinitis Pigmentosa: A Morphometric AnalysisSantos, Arturo;Humayun, Mark S.;de Juan, Eugene;Greenburg, Robert J.;Marsh, Marta J.;Klock, Ingrid B.;Milam, Ann H.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150513011pmid: 9109761
Abstract Objective: To determine the extent of preservation in the inner retina in retinitis pigmentosa (RP). Methods: We analyzed sectioned maculae of 21 postmortem eyes with RP and 19 age-matched, normal, postmortem eyes. Eyes were divided into 2 groups: severe and moderate RP. Cell nuclei were counted in the outer nuclear, inner nuclear, and ganglion cell layers within thirty 100-μm intervals from the foveola to 1500-μm eccentricity. Results: Statistically significant (P≤.05) loss of both the outer nuclear and ganglion cell layers was present in the groups with moderate and severe RP when compared with the control groups. However, even in the group with severe RP, 30% of the ganglion cells were histologically intact. Similarly, 78% and 88% of the inner nuclear layer cells were preserved in the groups with severe and moderate RP, respectively. Different inheritance modes showed no statistically significant differences in any of the retinal layers. Conclusions: Despite a statistically significant (P≤.05) loss of cells found in all retinal layers, a large percentage of the inner retinal neurons remained histologically intact. Current experimental therapies, such as photoreceptor transplantation and implantation of a visual prosthesis, are based on the premise that some inner retinal neurons are preserved after death of photoreceptors in RP. Our observations support this assumption. References 1. Marmor MF, Aguirre G, Arden G, et al. Retinitis pigmentosa: a symposium on terminology and methods of examination . Ophthalmology . 1983;90:126131.Crossref 2. Newsome DA. Retinitis pigmentosa, Usher's syndrome, and other pigmentary retinopathies . In: Newsome DA, ed. Retinal Dystrophies and Degenerations . New York, NY: Raven Press; 1988:161-194. 3. Bird AC, Heckenlively JR. X-linked recessive retinitis pigmentosa . In: Heckenlively JR, ed. Retinitis Pigmentosa . Philadelphia, Pa: JB Lippincott; 1988:163. 4. Pagon RA. Retinitis pigmentosa . Surv Ophthalmol . 1988;33:137-177.Crossref 5. Del Cerro M, Gash DM, Rao GN, Notter MF, Wiegand SJ, Gupta M. Intraocular retinal transplants . Invest Ophthalmol Vis Sci . 1985;26:1182-1185. 6. Gouras P, Du J, Kjeldbye H, Kwun R, Lopez R, Zack DJ. Transplanted photoreceptors identified in dystrophic mouse retina by a transgenic reporter gene . Invest Ophthalmol Vis Sci . 1991;32:3167-3174. 7. Blair JR, Gaur V, Laedke TW, et al. In oculo transplantation studies involving the neural retina and its pigment epithelium . Prog Retinal Res . 1991;10:69-88.Crossref 8. Silverman MS, Hughes SE, Valentino TL, Liu Y. Photoreceptor transplantation: anatomic, electrophysiologic and behavioral evidence for the functional reconstruction of retinas lacking photoreceptors . Exp Neurol . 1992;115:87-94.Crossref 9. Humayun MS, de Juan E Jr, Dagnelie G, Greenberg RJ, Propst RH, Phillips DH. Visual perception elicited by electrical stimulation of retina in blind humans . Arch Ophthalmol . 1996;114:40-46.Crossref 10. Stone JL, Barlow WE, Humayun MS, de Juan E Jr, Milam H. Morphometric analysis of macular photoreceptors and ganglion cells in retinas with retinitis pigmentosa . Arch Ophthalmol . 1992;110:1634-1639.Crossref 11. Graftein B, Murray M, Ingoglia NA. Protein synthesis and axonal transport in retinal ganglion cells of mice lacking visual receptors . Brain Res . 1972;44:3748. 12. Portera-Cailliau C, Sung CH, Nathans J, Adler R. Apoptotic photoreceptor cell death in mouse models of retinitis pigmentosa . Proc Natl Acad Sci U S A . 1994;91:974-978.Crossref 13. Eisenfeld AJ, LaVail MM, LaVail JH. Assessment of possible transneuronal changes in the retina of rats with inherited retinal dystrophy: cell size, number, synapses, and axonal transport by retinal ganglion cells . J Comp Neurol . 1984;223:22-34.Crossref 14. Marshall J, Heckenlively JR. Pathologic findings and putative mechanisms in retinitis pigmentosa . In: Heckenlively JR, ed. Retinitis Pigmentosa . Philadelphia, Pa: JB Lippincott; 1988:37-67. 15. Gartner S, Henkind P. Pathology of retinitis pigmentosa . Ophthalmology . 1982;89:1425-1432.Crossref 16. Panda-Jonas S, Jonas JB, Jakobczyk-Zmija M. Retinal photoreceptor density decreases with age . Ophthalmology . 1995;102:1853-1859.Crossref 17. Curcio CA, Millican CL, Allen KA, Kalina RE. Aging of the human photoreceptor mosaic: evidence for selective vulnerability of rods in central retina . Invest Ophthalmol Vis Sci . 1993;34:3278-3296. 18. Gao H, Hollyfield JC. Aging of the human retina: differential loss of neurons and retinal pigment epithelial cells . Invest Ophthalmol Vis Sci . 1992;33:1-17. 19. Milam AH, Li Z-Y. Retinal pathology in retinitis pigmentosa. considerations for therapy . In: Anderson RE, ed. Degenerative Diseases of the Retina . New York, NY: Plenum Publishing Corp: 1995:275-284. 20. Lewis GP, Matsumoto B, Fisher SK. Changes in the organization and expression of cytoskeletal proteins during retinal degeneration induced by retinal detachment . Invest Ophthalmol Vis Sci . 1995;36:2404-2416. 21. Fisher SK, Erickson PA, Lewis GP, Anderson DH. Intraretinal proliferation induced by retinal detachment . Invest Ophthalmol Vis Sci . 1991;32:1739-1748. 22. Fisher SK, Anderson DH. Cellular effects of detachment on the neural retina and the retinal pigment epithelium . In: Ryan SJ, ed. Retina . St Louis, Mo: Mosby-Year Book Inc; 1994:2035-2061. 23. Li Z-Y, Possin DE, Milam AH. Histopathology of bone spicule pigmentation in retinitis pigmentosa . Ophthalmology . 1995;102:805-816.Crossref
Norrie Disease in a Family With a Manifesting Female CarrierSims, Katherine B.;Irvine, Alexander R.;Good, William V.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150519012pmid: 9109762
Abstract Objectives: To show that Norrie disease can occur in a girl and to describe her ophthalmologic and genetic features. Methods: Amplification of DNA polymerase chain reaction and sequencing of asymmetric polymerase chain reaction for exon 3 were performed on the blood specimen obtained from a girl born with bilateral retinal detachments. Patient: A female child with bilateral retinal detachment who had 2 uncles in whom Norrie disease had already been diagnosed. Results: The child had a mutation in the third exon (T776→A; Ile 123→Asn) identical to the mutation found in her uncles. Conclusions: Norrie disease can occur in girls. The most likely explanation is nonrandom or unfavorable X inactivation, although timing of development of the peripheral retina and its blood supply could render it vulnerable to effects of the mutant allele at a critical developmental phase. References 1. Norrie G. Causes of blindness in children . Acta Ophthalmol . 1927;5:357-386.Crossref 2. Warburg M. Norrie's disease: a congenital progressive oculo-acousticscerebral degeneration . Acta Ophthalmol . 1966;89( (suppl) ):1-47. 3. Parving A, Warurg M. Audiological findings in Norrie's disease . Audiology . 1977;16:124-131.Crossref 4. Gal A, Bleecker-Wagemakers L, Wienker TF, Warburg M, Ropers HH. Localization of the gene for Norrie disease by linkage to DXS7locus . Cytogenet Cell Genet . 1985;40:633. 5. Sims KB, de la Chapelle A, Nono R, et al. Monoamide oxidase deficiency in males with an X chromosome deletion . Neuron . 1989;2:1069-1076.Crossref 6. Sims KB, Lebo RV, Benson G, et al. The Norrie disease maps to a 150-kb region on chromosome Xp11 . Hum Mol Genet . 1992;1:83-89.Crossref 7. Chen Z-Y, Hendriks RW, Jobling MA, et al. Isolation and characterization of a candidate gene for Norrie disease . Nat Genet . 1992;1:204-208.Crossref 8. Berger W, Meindl A, van de Pol TJ, et al. Isolation of a candidate gene for Norrie disease by positional cloning . Nat Genet . 1992;1:199-203.Crossref 9. Meindl A, Berger W, Meitinger T, et al. Norrie disease is caused by mutations in an extracellular protein resembling C-terminal globular domain of mucins . Nat Genet . 1992;1:199-203.Crossref 10. Schuback DE, Chen Z-Y, Craig IW, Breakefield XO, Sims KB. Mutations in the Norrie disease gene . Hum Mutat . 1995;5:285-292.Crossref 11. Fuchs S, Xu SY, Caballero M, et al. A missense point mutation (Leu/13 Ang) of the Norrie disease gene in a large Cuban kindred with Norrie disease . Hum Mol Genet . 1994;3:655-656.Crossref 12. Chen Z-Y, Battinelli EM, Fielder A, et al. A mutation in the Norrie disease gene (NDP) associated with X-linked familial exudative vitroretinopathy . Nat Genet . 1993;5:180-183.Crossref 13. Johnson K, Mintz-Hittner H, Perry YM, Ferrell RE. X-linked familial exudative vitreoretinopathy caused by an arginine to leucine substitution in exon 3 of the Norrie gene . Am J Hum Genet . 1994;55( (suppl) ):A224. Abstract 1309. 14. Chen Z-Y, Battinelli EM, Woodruff G, Young I, Breakefield XO, Craig IW. Characterization of a mutation within the NDP gene in a family with a manifesting female carrier . Hum Mol Genet . 1993;2:1727-1729.Crossref 15. Woodruff G, Newbury-Ecob R, Plaha DS, Young ID. Manifesting heterozygosity in Norrie's disease . Br J Ophthalmol . 1993;77:813-814.Crossref 16. Ohba N, Yamashita T. Primary vitreoretinal dysplasia resembling Norrie's disease in a female: association with X autosome chromosomal translocation . Br J Ophthalmol . 1986;70:64-71.Crossref 17. Lindenbaum RH, Clarke G, Patel C, Moncrieff M, Hughes JT. Muscular dystrophy in an Xi: 1 translocation female suggests that Duchenne locus is on X chromosome short arm . J Med Genet . 1979;16:389-392.Crossref 18. Migeon BR, Moser HW, Moser AB, Axelman J, Sillence D, Norum RA. Adenoleukodystrophy: evidence of X linkage, inactivation, and selection favoring the mutant allele in heterozygous cells . Proc Natl Acad Sci U S A . 1981;78:5066-5070.Crossref 19. Conley ME. Molecular approaches to analysis of X-linked immunodeficiencies . Annu Rev Immunol . 1992;10:215-238.Crossref 20. Goodman G, Ripps H, Siegel IM. Sex-linked ocular disorders: trait expressivity in males and carrier females . Arch Ophthalmol . 1965;73:387-398.Crossref
Immunologic Mechanisms of Uveitis: New Targets for ImmunomodulationWhitcup, Scott M.;Nussenblatt, Robert B.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150522013pmid: 9109763
Abstract The uvea consists of the choroid, ciliary body, and iris, and inflammation of the uveal tract is termed uveitis. Nevertheless, uveitis is commonly used to more generally describe intraocular inflammation involving not only the uvea, but also the retina, vitreous, and sclera. Fifty years ago, infectious organisms such as syphilis and tuberculosis were thought to be the cause of most forms of uveitis.1 Since that time, many causes of uveitis have been described as infectious and noninfectious. Scientists have shown that the immune response plays a critical role in the development of infectious and noninfectious forms of the disease. With a more detailed understanding of the immune mechanisms leading to the development of uveitis, we are now able to develop new therapeutic approaches based on targeting various components of the immune response. References 1. Guyton JS, Woods AC. Etiology of uveitis: a clinical study of 562 cases . Arch Ophthalmol . 1941;26:983-1018.Crossref 2. Percopo CM, Hooks JJ, Shinohara T, Caspi R, Detrick B. Cytokine-mediated activation of a neuronal retinal resident cell provokes antigen presentation . J Immunol . 1990;145:4101-4107. 3. Elschnig A. Studien zur sympathischen Ophthalmitis: Die antigene Wirkung des Augenpigmentes . Graefes Arch Clin Exp Ophthalmol . 1910;76:509-546.Crossref 4. Wacker WB, Donoso LA, Kalsow CM, et al. Experimental allergic uveitis: isolation, characterization, and localization of a soluble uveitopathogenic antigen from bovine retina . J Immunol . 1977;119:1949-1958. 5. Nussenblatt RB, Whitcup S, Palestine AG. Uveitis: Fundamentals and Clinical Practice . 2nd ed. St Louis, Mo: Mosby-Year Book Inc; 1996. 6. Hirose S, Kuwabara T, Nussenblatt RB, Wiggert B, Redmond TM, Gery I. Uveitis induced in primates by interphotoreceptor retinoid-binding protein . Arch Ophthalmol . 1986;104:1698-1702.Crossref 7. Schalken JJ, van Jugt AH, Winkens HG, et al. Experimental autoimmune uveoretinitis in rats induced by rod visual pigment: rhodopsin is more pathogenic than opsin . Graefes Arch Clin Exp Ophthalmol . 1988;226:255-261.Crossref 8. Gery I, Chanaud NP III, Anglade E. Recoverin is highly uveitogenic in Lewis rats . Invest Ophthalmol Vis Sci . 1994;35:3342-3345. 9. Chan CC, Mochizuki M, Nussenblatt RB, et al. T-lymphocyte subsets in experimental autoimmune uveitis . Clin Immunol Immunopathol . 1985;35:103-110.Crossref 10. Chan CC, Mochizuki M, Palestine AG, et al. Kinetics of T-lymphocyte subsets in the eyes of Lewis rats with experimental autoimmune uveitis . Cell Immunol . 1985;96:430-434.Crossref 11. Mochizuki M, Kuwabara T, Chan CC, et al. An association between susceptibility to experimental autoimmune uveitis and choroidal mast cell numbers . J Immunol . 1984;133:1699-1701. 12. Lubin JR, Albert DM, Weinstein M. Sixty-five years of sympathetic ophthalmia: a clinicopathologic review of 105 cases . Ophthalmology . 1980;87:109-121. 121.Crossref 13. Chan CC, Ben Ezra D, Hsu SM, Palestine AG, Nussenblatt RB. Granulomas in sympathetic ophthalmia and sarcoidosis: immunohistochemical study . Arch Ophthalmol . 1985;103:198-202.Crossref 14. Chan CC, Nussenblatt RB, Fujikawa LS, et al. Sympathetic ophthalmia: immunopathological findings . Ophthalmology . 1986;93:690-695.Crossref 15. Nussenblatt RB, Kuwabara T, de Monasterio FM, Wacker WB. S-antigen uveitis in primates: a new model for human disease . Arch Ophthalmol . 1981;99:1090-1092.Crossref 16. Marak GE Jr. Recent advances in sympathetic ophthalmia . Surv Ophthalmol . 1979;24:141-156.Crossref 17. Cross SI, Halden NF, Lenardo MJ, Leonard WJ. Functionally distinct NF-Kappa B binding sites in the immunoglobulin kappa and IL-2 receptor alpha chain genes . Science . 1989;244:466-469.Crossref 18. Granelli-Piperno A, Nolan P, Inaba K, Steinman RM. The effect of immunosuppressive agents on the induction of nuclear factors that bind to sites on the interleukin 2 promoter . J Exp Med . 1990;172:1869-1872.Crossref 19. Nussenblatt RB, Rodrigues MM, Wacker WB, et al. Cyclosporin A: inhibition of experimental autoimmune uveitis in Lewis rats . J Clin Invest . 1981;67:1228-1231.Crossref 20. Nussenblatt RB, Palestine AG, Rook AH, et al. Cyclosporine therapy in the treatment of intraocular inflammatory disease resistant to systemic corticosteroids or cytotoxic agents . Am J Ophthalmol . 1983;96:275-282. 21. Masuda K, Nakajima A, Urayama A, Nakae K, Kogure M, Inaba G. Double-masked trial of cyclosporin versus colchicine and long-term open study of cyclosporin in Behçet's disease . Lancet . 1989;1:1093-1096.Crossref 22. Whitcup SM, Salvo EC Jr, Nussenblatt RB. Combined cyclosporine and corticosteroid therapy for sight-threatening uveitis in Behçet's disease . Am J Ophthalmol . 1994;118:39-45. 23. Wells HG. Studies on the chemistry of anaphylaxis, III: experiments with isolated proteins, especially those of the hen's egg . J Infect Dis . 1911;8:147-171.Crossref 24. Whitacre CC, Gienapp IE, Orosz CG, Bitar D. Oral tolerization in experimental autoimmune encephalomyelitis, III: evidence for clonal anergy . J Immunol . 1991;147:2155-2163. 25. Thompson HSG, Staines NA. Gastric administration of type II collagen delays the onset and severity of collagen-induced arthritis in rats . Clin Exp Immunol . 1986;64:581-586. 26. Al-Sabbagh A, Miller A, Santos LMB, Weiner HL. Antigen-driven tissuespecific suppression following oral tolerance: orally administered myelin basic protein suppresses proteolipid induced experimental autoimmune encephalomyelitis in the SJL mouse . Eur J Immunol . 1994;24:2104-2109.Crossref 27. Bergerot J, Fabien N, Maguer V, Thivolet C. Oral administration of human insulin to NOD mice generates CD4+ T-cells that suppress adoptive transfer of diabetes . J Autoimmun . 1994;7:655-663.Crossref 28. Okumura S, Mclntosh K, Drachman DB. Oral administration of acetylcholine receptor: effects on experimental myasthenia gravis . Ann Neurol . 1994;36:704-713.Crossref 29. Nussenblatt RB, Caspi RR, Mahdi R, et al. Inhibition of S-antigen induced experimental autoimmune uveoretinitis by oral induction of tolerance with S-antigen . J Immunol . 1990;144:1689-1695. 30. Rizzo LV, Miller-Rivero NE, Chan CC, Wiggert B, Nussenblatt RB, Caspi RR. Interleukin-2 treatment potentiates induction of oral tolerance in a murine model of autoimmunity . J Clin Invest . 1994;157:439-447. 31. Gregerson DS, Obritsch WF, Donoso LA. Oral tolerance in experimental autoimmune uveoretinitis: distinct mechanisms of resistance are induced by low dose versus high dose feeding protocols . J Immunol . 1993;151:5751-5761. 32. Dick AD, Cheng YF, Liversidge J, Forrester JV. Intranasal administration of retina antigens suppresses retinal antigen-induced experimental autoimmune uveoretinitis . Immunology . 1994;82:625-631. 33. Weiner HL, Friedman A, Miller A, et al. Oral tolerance: immunologic mechanisms and treatment of animal and human organ-specific autoimmune diseases by oral administration of autoantigens . Ann Rev Immunol . 1994;12:809-837.Crossref 34. Nussenblatt RB, Whitcup SM, de Smet MD, et al. Intraocular inflammatory disease (uveitis) and the use of oral tolerance: a status report . Ann N Y Acad Sci . 1996;778:325-337.Crossref 35. Nussenblatt RB, Gery I, Weiner H, et al. Treatment of uveitis by oral administration of retinal antigens: results of a phase I/II randomized masked trial. Am J Ophthalmol. In press. 36. Weiner HL, Mackin GA, Matsui J, et al. Double-blind pilot trial of oral tolerization with myelin antigens in multiple sclerosis . Science . 1993;259:1321-1324.Crossref 37. Trentham DE, Dynesius-Trentham RA, Orav EJ, et al. Effects of oral administration of type II collagen on rheumatoid arthritis . Science . 1993;261:1727-1730.Crossref 38. Barnett ML, Combitchi D, Trentham DE. A pilot trial of oral type II collagen in the treatment of juvenile rheumatoid arthritis . Arthritis Rheum . 1996;39:623-628.Crossref 39. Mulligan MS, Varani J, Dame MK, et al. Role of endothelial-leukocyte adhesion molecule 1 (ELAM-1) in neutrophil-mediated lung injury in rats . J Clin Invest . 1991;88:1396-1406.Crossref 40. Spinger TA. Traffic signals for lymphocyte recirculation and leukocyte emigration: the multistep paradigm . Cell . 1994;76:301-314.Crossref 41. Whitcup SM, Chan CC, Li Q, Nussenblatt RB. Expression of cell adhesion molecules in posterior uveitis . Arch Ophthalmol . 1992;110:662-666.Crossref 42. Whitcup SM, Wakefield D, Li Q, Nussenblatt RB, Chan CC. Endothelial leukocyte adhesion molecule-1 in endotoxin-induced uveitis . Invest Ophthalmol Vis Sci . 1992;33:2626-2630. 43. Whitcup SM, Nussenblatt RB, Price FW Jr, Chan CC. Expression of cell adhesion molecules in corneal graft failure . Cornea . 1993;12:475-480.Crossref 44. Whitcup SM, DeBarge LR, Caspi RR, Harning R, Nussenblatt RB, Chan CC. Monoclonal antibodies against ICAM-1 (CD54) and LFA-1 (CD11a/CD18) inhibit experimental autoimmune uveitis . Clin Immunol Immunopathol . 1993;67:143-150.Crossref 45. Whitcup SM. Cell Adhesion molecules in endotoxin-induced uveitis . Reg Immunol . 1994;6:58-63. 46. Whitcup SM, DeBarge LR, Rosen H, Nussenblatt RB, Chan CC. Monoclonal antibody against CD11b/CD18 inhibits endotoxin-induced uveitis . Invest Ophthalmol Vis Sci . 1993;34:673-681. 47. Uchio E, Kijima M, Tanaka S, Ohno S. Suppression of experimental uveitis with monoclonal antibodies to ICAM-1 and LFA-1 . Invest Ophthalmol Vis Sci . 1994;35:2626-2631. 48. Fukushima A, Vistica BP, Caspi RR, et al. Lymphocyte stimulation and expression of cell adhesion molecules are critical for adoptive transfer of cellular immunity and disease . Invest Ophthalmol Vis Sci . 1996;37( (suppl) ):S540. Abstract. 49. Haug CE, Colvin RB, Delmonico FL, et al. A phase I trial of immunosuppression with anti-ICAM-1 (CD54) mAb in renal allograft recipients . Transplantation . 1993;55:766-773.Crossref
Error in the Results Section of the Abstract1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150527014
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract In the clinical sciences article titled "Chemotherapy With Focal Therapy Can Cure Intraocular Retinoblastoma Without Radiotherapy," published in the November 1996 Archives (1996;114:1321-1328), the median follow-up in the first sentence of the "Results" section of the abstract was published incorrectly. The sentence is reprinted correctly here. Results: At the median follow-up of 2⅔ years (range, 1/10-4¾ years), the results of treatment were excellent.
A Bicenquinquagenary Worth Noting: Daviel's Introduction of the Modern Cataract OperationLetocha, Charles E.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150528015pmid: 9109764
Abstract Patient: NA. Date: 7 April, 1751. Surgeon: Jacques Daviel. Procedure: Cataract extraction, left eye. Anesthesia: None. Findings: This 59-year-old woman has had decreasing vision in both eyes for more than 15 years. She can no longer read or sew. Examination reveals count fingers visual acuity in the right eye, hand motions vision in the left eye. Bilateral mature cataracts, with thickened anterior capsules, are present in both eyes. The pupils react briskly and she has good 2-point discrimination. Procedure: The patient was seated on a low stool before the surgeon. The right eye was covered with a cotton patch. The assistant steadied the patient's chin with his right hand and retracted the left upper eyelid with 2 fingers of his left hand. The surgeon retracted the lower eyelid with his left hand. The anterior chamber was entered at the 6-o'clock position with a keratome. The wound was enlarged slightly to the left and right with the same keratome. The corneoscleral section was completed with curved corneoscleral scissors between the 2- and 10-o'clock positions. The cornea was elevated with a blunt curved spatula. The thickened anterior capsule was excised in a circular manner with scissors and removed with a forceps. The spatula was then used to free the nucleus from the surrounding capsule and cortex. It was used to break the nucleus into pieces and extract these from the eye. A small iris prolapse was reposited with the same instrument. The edges of the wound were carefully apposed. The wound was cleaned with a cotton-tipped applicator that had been dipped in collyrium. The eyelids were closed with a plaster, cotton pledgets were applied, and a light bandage, exerting no pressure, was applied. The patient tolerated the procedure well and left the surgical suite in good condition. Postoperative diagnosis: Same. Time of surgery: 9 minutes. References 1. Based on: Wood CA, ed. Shastid TH, trans. Jacques Daviel. In: American Encyclopedia and Dictionary of Ophthalmology . Chicago, III: Cleveland Press; 1914;5:3751-3777. 2. Daviel J. Sur une nouvelle methode de guérir la cataracte par l'extraction du crystallin . Mémoires de I'Académie Royale de Chirurgie . 1753;2:337-352. 3. Albert DM. The History of Ophthalmology. Cambridge , Mass: Blackwell Publishers; 1996:28. 4. Columbo R. De Re Anatomica . Venice, Italy: Nicolai Beuilacquae; 1559;15. 5. Wood CA, ed. Shastid TH, trans. History of Ophthalmology . In: American Encyclopedia and Dictionary of Ophthalmology . Chicago, III: Cleveland Press; 1914;11:8754-8759. 6. von Graefe FWEA. Nachtragliche Bemerkungen tiber diemordificirte Linearextraction . v Graefes Arch Ophthalmol . 1866;1:150-223.Crossref 7. Intraocular Lens Implantation: The Early Years [videotape] . Fairfax, Va: American Society of Cataract and Refractive Surgery; 1989.
Do We Understand the Effects of 'Managed Care' in Ophthalmology?: A Review and AnalysisAsch, Steve;Goldzweig, Caroline L.;Lee, Paul
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150533016pmid: 9109765
Abstract Little has been published that directly assesses the effect of structures for providing managed care or the effects of capitated, prepaid financing on the cost and quality of eye care services. Managed care organizations use fewer ophthalmologists and may provide more screening for diabetic retinopathy. Studies of nonophthalmologic care show lower patient satisfaction with care, and mixed effects on cost, quality of care, and access to care, but are difficult to generalize to eye care. We reviewed the published peer-reviewed literature about this topic. Notable gaps exist in the knowledge of critical elements of the influence of managed care on providing eye care and on patient outcomes. Existing measures of quality, cost, satisfaction, and access could easily be adapted for use in evaluating the influence of managed care and guiding health care policy. References 1. Manning WG, Leibowitz A, Goldberg G, et al. A controlled trial of the effect of a prepaid group practice on use of services . N Engl J Med . 1984;310:1505-1510.Crossref 2. Greenfield S, Nelson EC, Zubkoff M, et al. Variations in resource utilization among medical specialties and systems of care: results from the Medical Outcomes Study . JAMA . 1992;267:1624-1630.Crossref 3. Stern RS, Juhn PI, Gertler PJ, Epstein AM. A comparison of length of stay and costs for health maintenance organizations and fee-for-service patients . Arch Intern Med . 1989;149:1185-1188.Crossref 4. Bradbury RC, Golec JH, Stearns FE. Comparing hospital length of stay in independent practice association HMOs and traditional insurance programs . Inquiry . 1991;28:87-93. 5. The Effects of Managed Care and Managed Competition . Washington, DC: Congressional Budget Office; 1995. 6. McCall N, Wrightson CW, Paringer L, et al. Managed medicaid cost savings: the Arizona experience . Health Aff . (Spring) 1994:235-245. 7. Brown RS. Does Managed Care Work for Medicare? An Evaluation of the Medicare Risk Program for HMOs . Princeton, NJ: Mathematica Policy Research Inc; 1993. 8. Enthoven AC. Why managed care has failed to contain health costs . Health Aff . (Fall) 1993:27-43. 9. Schwartz WB, Mendelson DN. Why managed care cannot contain hospital costs—without rationing . Health Aff . (Summer) 1992:99-107. 10. Luff HS. Trends in medical care costs: do HMOs lower the rate of growth . Med Care . 1980;18:1-16. 11. Newhouse JP, Schwartz WB, Williams AP, et al. Are fee-for-service costs increasing faster than HMO costs? Med Care . 1985;23:960-966.Crossref 12. Page L. Employers look to managed care to rein in benefit costs . Am Med News . (February 19) , 1996:5. 13. Miller RH, Luft HS. Managed care plan performance since 1980: a literature analysis . JAMA . 1994;271:1512-1519.Crossref 14. Physician Payment Review Commission. Annual Report to Congress . Washington, DC: Physician Payment Review Commission; 1995. 15. Javitt JC. Early glimpses of capitated eye care . Arch Opthalmol . 1994;112:887.Crossref 16. Dillon EC, Sergott RC, Savino PJ, et al. Diagnostic management by gatekeepers is not cost effective for neuro-ophthalmology . Ophthalmology . 1994;101:1627-1630.Crossref 17. Mitka M. Doctor pay shrinks for first time in '94 . Am Med News . (January 22/29) , 1996:1. 18. Soroka M. Vision care benefits and optometric services in HMOs . J Am Optom Assoc . 1989;60:832-835. 19. Retchin SM, Preston J. Effects of cost containment on the care of elderly diabetics . Arch Intern Med . 1991;151:2244-2248.Crossref 20. Bass EB, Steinberg EP, Luthra R, et al. Variation in ophthalmic testing prior to cataract surgery: results of a national survey of optometrists . Arch Ophthalmol . 1995;113:27-31.Crossref 21. Steinberg EP, Bass EB, Luthra R, et al. Variation in ophthalmic testing before cataract surgery: results of a national survey of ophthalmologists . Arch Ophthalmol . 1994;112:896-902.Crossref 22. Awh CC, Cupples HP, Javitt JC. Improved detection and referral of patients with diabetic retinopathy by primary care physicians: effectivness of education . Arch Intern Med . 1991;151:1405-1408.Crossref 23. Abrams LS, Scott IU, Spaeth GL, el al. Agreement among optometrists, ophthalmologists, and residents in evaluating the optic disc for glaucoma . Ophthalmology . 1994;101:1662-1667.Crossref 24. Lee PP, Jackson CJ, Relies DA. Estimating Eye Care Provider Supply and Workforce Requirements . Santa Monica, Calif: RAND; 1995. 25. Mangione CM, Lee PP, Hays RD. Measurement of visual functioning and healthrelated quality of life in eye disease and cataract surgery . In: Spilker B, ed. Quality of Life and Pharmacoeconomics in Clinical Trials . 2nd ed. New York, NY: Raven Press; 1996. 26. Ware JE Jr, Brook RH, Rogers WH, et al. Comparison of health outcomes at a health maintenance organisation with those of fee-for-service care . Lancet . 1986;1:1017-1022.Crossref 27. Rubin HR, Gandek B, Rogers WH, Kosinski M, McHorney CA, Ware JE Jr. Patients' ratings of outpatient visits in different practice settings: results from the medical outcomes study . JAMA . 1993;270:835-840.Crossref 28. Rogers WH, Wells KB, Meredith LS, Rogers W, Greenfield S, Ware JE Jr. Outcomes for adult outpatients with depression under prepaid or fee-for-service financing . Arch Gen Psychiatry . 1993;50:517-525.Crossref 29. Wells KB, Hays RD, Burnam MA, et al. Detection of depressive disorder for patients receiving prepaid or fee-for-service care: results from the Medical Outcomes Study . JAMA . 1989;262:3298-3302.Crossref 30. Greenfield S, Rogers W, Mangotich M, Carney MF, Tarlov AR. Outcomes of patients with hypertension and non-insulin dependent diabetes mellitus treated by different systems and specialties: results from the Medical Outcomes Study . JAMA . 1995;274:1436-1444.Crossref 31. Safran DG, Tarlov AR, Rogers WH. Primary care performance in fee-for-service and prepaid health care systems: results from the Medical Outcomes Study . JAMA . 1994;271:1579-1586.Crossref 32. Lee-Feldstein A, Anton-Culver H, Feldstein PJ. Treatment differences and other prognostic factors related to breast cancer survival: delivery systems and medical outcomes . JAMA . 1994;271:1163-1168.Crossref 33. Preston JA, Retchin SM. The management of geriatric hypertension in health maintenance organizations . J Am Geriatr Soc . 1991;39:683-690. 34. Retchin SM, Brown B. The quality of ambulatory care in Medicare health maintenance organizations . Am J Public Health . 1990;80:411-415.Crossref 35. Lichtenstein R, Thomas JW, Watkins B, et al. HMO marketing and selection bias: are TEFRA HMOs skimming? Med Care . 1992;30:329-346.Crossref 36. Allen HM Jr, Darling H, McNeill DN, Bastien F. The employee health care value survey: round one . Health Aff . 1994;13:25-41.Crossref 37. Andersen R, Aday LA. Access to medical care in the US: realized and potential . Med Care . 1978;7:533-546.Crossref 38. Mulhausen R, McGee J. Physician need: an alternative projection from a study of large, prepaid group practices . JAMA . 1989;261:1930-1934.Crossref 39. Weiner JP. Forecasting the effects of health reform on US physician workforce requirement: evidence from HMO staffing patterns . JAMA . 1994;272:222-230.Crossref 40. L Page. Specialties try to slim down . American Medical News . 1995. 41. Sommer A. Health (care) reform, managed care, and ophthalmology . Arch Ophthalmol . 1994;112:1417-1418.Crossref 42. Billi JE, Wise CG, Bills EA, et al. Potential effects of managed care on specialty practice at a university medical center . N Engl J Med . 1995;333:979-983.Crossref 43. Shapiro MF, Ware JE Jr, Sherbourne CD. Effects of cost sharing on seeking care for serious and minor symptoms: results of a randomized controlled trial . Ann Intern Med . 1986;104:246-251.Crossref 44. Tielsch JM, Steinberg EP, Cassard SD, et al. Preoperative functional expectations and postoperative outcomes among patients undergoing first eye cataract surgery . Arch Ophthalmol . 1995;113:1312-1318.Crossref 45. Davies AR, Ware JE Jr, Brook RH, Peterson JR, Newhouse JP. Consumer acceptance of prepaid and fee-for-service medical care: results from a randomized controlled trial . Health Serv Res . 1986;21:429-452. 46. Davis K, Collins KS, Schoen C, Morris C. Choice matters: enrollees' views of their health plans . Health Aft 1995;14:99-112. 47. Murray JP. A follow-up comparison of patient satisfaction among prepaid and fee-for-service patients . J Earn Pract . 1988;26:576-581. 48. Wilson IB, Cleary PD. Linking clinical variables with health-related quality of life: a conceptual model of patient outcomes . JAMA . 1995;273:59-65.Crossref
Epidemiologic Study of Time and Space Clustering of 4 Cases of Choroidal Malignant MelanomaGanley, James P.;Fontenot, Kerwin
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150539017pmid: 9109766
Abstract Objective: To identify common risk factors that might be associated with a cluster of 4 cases of choroidal malignant melanoma that occurred in a manufacturing plant between 1982 and 1985. Design: Survey of choroidal malignant melanoma cases in Caddo and Bossier parishes during the same time frame. Methods: We identified 4 additional individuals with choroidal malignant melanoma first diagnosed during the study period. Characteristics of the workplace were examined and a questionnaire was administered to all subjects to ascertain exposures to putative carcinogens and to putative risk factors for intraocular malignant melanoma. Observed and expected incidence rates were calculated. Results: The overall incidence of intraocular malignant melanoma for the 2 parishes during the 4-year period was 0.56 cases per 100 000 population per year, similar to the expected rates for this population. The incidence rate for the manufacturing plant employees was 16.5 cases per 100 000 per year. The mean age at diagnosis for workers at the plant was 38.7 years compared with 69.2 years for nonplant employees. Conclusions: The close occurrence of manufacturing plant cases in time and space and the younger age of the people are consistent with a cluster of intraocular melanoma cases. No specific risk factors were found in the workplace environment to impute a causal association. References 1. Ganley JP, Comstock GW. Benign nevi and malignant melanomas of the choroid . Am J Ophthalmol . 1973;76:19-25. 2. Scotto J, Fraumeni JF, Lee JAH. Melanomas of the eye and other noncutaneous sites: epidemiologic aspects . J Natl Cancer Inst . 1976;56:489-491. 3. Wilkes SR, Robertson DM, Kurland LT, Campbell, RJ. Incidence of uveal malignant melanoma in the resident population of Rochester and Olmstead County, Minnesota . Am J Ophthalmol . 1979;87:639-641. 4. Tucker MA, Shields JA, Hartge P, Augsburger J, Hoover RN, Fraumeni JF. Sunlight exposure as a risk factor for intraocular malignant melanoma . N Engl J Med . 1985;313:789-792.Crossref 5. Egan KM, Seddon JM, Glynn RJ, Gragoudas ES, Albert DM. Epidemiologic aspects of uveal melanoma . Surv Ophthalmol . 1988;32:239-251.Crossref 6. Jensen OA. Malignant melanoma of the uvea in Denmark, 1943-1952 . Acta Ophthalmol Scand Suppl . 1963;75:1-220.Crossref 7. Yanoff M, Zimmerman LE. Histogenesis of malignant melanomas of the uvea, II: relationship of uveal nevi to malignant melanomas . Cancer . 1967;20:493-507.Crossref 8. Arnesen K, Nornes M. Malignant melanoma of the choroid as related to coexistent benign nevus . Acta Ophthalmol Scand . 1975;53:139-152.Crossref 9. Albert DM, Puliafito CA. Choroidal melanoma: possible exposure to industrial toxins . N Engl J Med . 1977;296:634-635. 10. Albert DM, Puliafito CA, Fulton AB, et al. Increased incidence of choroidal malignant melanomas occurring in a single population of chemical workers . Am J Ophthalmol . 1980;89:323-337. 11. Louria DB, Coumbis RJ, Lavenhar MA, et al. An apparent small cluster of choroidal melanoma cases . Am J Ophthalmol . 1982;94:172-180. 12. Keeney AH, Waddell WJ, Perraut TC. Carcinogenesis and nicotine in malignant melanoma of the choroid . Trans Am Ophthalmol Soc . 1982;80:131-142. 13. Snedecor GW, Cochran WG. Statistical Methods . 6th ed. Ames: The Iowa State University Press; 1967. 14. Rothman KJ. Clustering of disease . Am J Public Health . 1987;77:13-15.Crossref 15. Schulte PA, Ehrenberg RL, Singal M. Investigation of occupational cancer clusters: theory and practice . Am J Public Health . 1987;77:52-56.Crossref 16. Strickland D, Lee JAH. Melanomas of eye: stability of rates . Am J Epidemiol . 1981;113:700-702. 17. Cole P. Cancer and occupation: status and needs of epidemiologic research . Cancer . 1977;39:1788-1791.Crossref 18. Huff JE, McConnell EE, Haseman JK, et al. Carcinogenesis studies: results of 398 experiments on 104 chemicals from the US National Toxicology Program . Ann N Y Acad Sci . 1988;534:1-30.Crossref 19. Maltoni C, Lefemine G, Cotti G, Perino G. Long-term carcinogenicity bioassays on trichlorethylene administered by inhalation to Sprague-Dawley rats and Swiss and B6C3FI mice . Ann N Y Acad Sci . 1988;534:316-342.Crossref 20. Cantelli-Forti G, Bronzetti G. Mutagenesis and carcinogenesis of halogenated ethylenes . Ann N Y Acad Sci . 1988;534:679-693.Crossref 21. Patz A, Wulff LB, Rogers SW. Experimental production of ocular tumors . Am J Ophthalmol . 1959;48:98-117. 22. Benson WR. Intraocular tumor after ethionine and N-2-fluorenylacetamide . Arch Pathol . 1962;73:404-406. 23. Seddon JM, Maclaughlin DT, Albert DM, Gragoudes ES, Ference M. Uveal melanoma presenting during pregnancy and the investigation of estrogen receptors in melanomas . Br J Ophthalmol . 1982;66:695-704.Crossref 24. Swerdlow AJ. Epidemiology of eye cancer in adults in England and Wales, 1962-1977 . Am J Epidemiol . 1983;118:294-300. 25. Gallagher RP, Elwood JR, Rootman J, et al. Risk factors for ocular melanoma: Western Canada Melanoma Study . J Natl Cancer Inst . 1985;74:775-778.
Can We Avoid an Epidemic of Refractive 'Surprises' After Cataract Surgery?McDonnell, Peter J.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150544018pmid: 9109767
Abstract A FEW YEARS AGO, it was common for speakers at continuing medical education meetings to ask for a show of hands in response to the following questions: "How many of you perform refractive surgery?" (Approximately 10% of the hands go up.) "How many of you perform cataract extraction and intraocular lens implantation?" (Almost all hands are raised.) "Well in fact," says the speaker, "all of you who perform cataract surgery are actually performing the most common refractive surgical procedure." See also pages 457 This exercise, meant to drive home the important refractive implications of cataract surgery, would be as valid today, because optimistic projections of millions of people with myopia electing to undergo laser photorefractive keratectomy (PRK) have yet to be realized. More and more, our patients take the "miracle" of modern small-incision cataract extraction and intraocular lens (IOL) implantation for granted. "The surgery is very simple, isn't it?" they References 1. Koch DD, Liu JF, Hyde LL, Rock RL, Emery JM. Refractive complications on cataract surgery after radial keratotomy . Am J Ophthalmol . 1989;108:676-682. 2. Hoffer KJ. Intraocular lens power calculation for eyes after refractive surgery . J Refract Surg . 1995;11:490-493. 3. McDonnell PJ, Smith RE. Intraocular lens power selection in triple procedure surgery: discussion . In: Cavanagh D, ed. Transactions of the World Congress on the Cornea III . New York, NY: Raven Press; 1988:333-334. 4. Lyle WA, Jin GJC. Intraocular lens power prediction in patients who undergo cataract surgery after having undergone radial keratotomy . Arch Ophthalmol . 1997;115:457-461.Crossref 5. Celikkol L, Paulopoulos G, Weinstein B, Celikkol G, Feldman ST. Calculation of intraocular lens power after radial keratotomy with computerized videokeratography . Am J Ophthalmol . 1995;120:730-750. 6. Waring GO, Lynn MJ, McDonnell PJ, and the PERK Study Group. Results of the Prospective Evaluation of Radial Keratotomy (PERK) study 10 years after surgery . Arch Ophthalmol . 1994;112:1298-1308.Crossref
The Emergence of Women in OphthalmologyRoss, Robin D.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150546019pmid: 9109768
Abstract This YEAR marks the 125th anniversary of women practicing ophthalmology in the United States. The thousands of pages of recorded ophthalmic history feature dedications to the "great men of ophthalmology"—Albercht Von Graefe, Theodor Leber, Ernst Fuchs, and David G. Cogan—but ignore the contributions of "great women." Women did play visionary roles in ocular pathology, physiologic optics, research, and international ophthalmology, although they were not always recognized with the same enthusiasm in the literature. In the scientific gallery of genderless first initials and masculine noms de plume, the unveiling of women pictured side by side with their male colleagues is long overdue. In Washington, DC, Isabel Hayes Chapin Barrows inserted her calling card into the Daily Morning Chronicle in 1871,1 becoming the first "lady oculist" in the United States. She established a list of firsts during her career: first woman admitted to the University of Vienna in Austria to References 1. Daily Morning Chronicle . Washington, DC; May 29, 1871:1. 2. Bonner TN. Rendezvous in Zürich . J Hist Med Allied Sci . 1989;44:7-27.Crossref 3. Koelbing HM, Morgel C. Johann Friedrich Horner. Zürich, Switzerland: Verlag Hans Rohr; 1986:105-106. 4. Wood CA. American Encyclopedia and Dictionary of Ophthalmology . Chicago,III: Cleveland Press; 1913;2:896-898. 5. Hirschberg J; Blodi FC, trans. The History of Ophthalmology . Bonn, West Germany: JP Wayenborgh Verlag; 1985-1991;10:148-150. 6. Snyder C. Massachusetts Eye and Ear Infirmary: Studies on Its History . Boston: Massachusetts Eye and Ear Infirmary; 1984;136. 7. David Glendenning Cogan: A Link With Our Past, an Oral History Conducted in 1989 by Sally Smith Hughes. Berkeley: Regional Oral History Office, University of California, Berkeley, in cooperation with the Foundation of the American Academy of Ophthalmology, San Francisco, Calif. Ophthalmology History Series. 8. Kronfeld PC. Georgiana Dvorak-Theobold . Trans Am Ophthalmol Soc . 1971;60:20-23. 9. Duke-Elder WS. System of Ophthalmology . St Louis, Mo: CV Mosby Co; 1961;9:411-413. 10. Newell FW. Bertha A. Klien. Am J Ophthalmol . 1978;87:431-432. 11. Gorin G. History of Ophthalmology . Wilmington, Del: Publish or Perish Press Inc; 1982:406. 12. Cuendet JF. Noëlle Chomé-Bercioux . Doc Ophthalmol . 1992;81:75-77.Crossref 13. Bell J. In: Pearson K, ed. The Treasury of Human Inheritance . Cambridge, England: Cambridge University Press; 1922-1958. 14. Loewenfeld I. The Pupil: Anatomy, Physiology, and Clinical Applications . Ames: Iowa State University Press; Detroit, Mich; Wayne State University Press; 1993. 15. Ragge NK, Falk RE, Cohen WE, et al. Images of Lisch nodules across the spectrum . Eye . 1993;7:95-101.Crossref 16. Fujino T. Contributions of our seniors—Dr. Inoue and Dr. Sakurai [translated personal communication, November 19,1993] . Neuro-ophthlamol Jpn . 1993;10( (1) ):6-7. 17. Sakurai T. Multiple neurofibroma patient showing multiple flecks on the anterior surface of the iris . Acta Soc Ophthalmol Jpn . 1935;39:87-93. 18. Campbell CJ. Dr. Gertrude Rand. Am J Ophthalmol . 1970;70:653. 19. Maumenee IH. Louise L. Sloan. Am J Ophthalmol . 1982;93:796-797. 20. Potter D. Ida Mann—her wartime career, 1939-1949 . Aust N Z J Ophthalmol . 1989;17:95-101.Crossref 21. Kinoshita JH. On the presentation of the Proctor Medal of the Association for Research in Ophthalmology to Antoinette Pirie . Invest Ophthalmol Vis Sci . 1968;7:625-627. 22. Dische Z. Ruth van Heyningen . Exp Eye Res . 1980;31:xi-xiii.Crossref 23. Collins ET. The History and Traditions of the Moorfields Eye Hospital: One Hundred Years of Ophthalmic Discovery and Development . London, England: Lewis; 1929.
Conjunctival Neurilemoma: Report of 3 CasesCharles, Norman C.;Fox, Donald M.;Avendaño, José A.;Marroquín, Lelia S.;Appleman, Warren
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150549020pmid: 9109769
Abstract Neurilemoma (schwannoma) of the conjunctiva is a rare ocular tumor. We report 3 cases of benign conjunctival neurilemoma occurring in women without other ocular or systemic disease. Two of these tumors arose from the bulbar conjunctiva and 1 from the tarsal conjunctiva. Immunoperoxidase staining for S-100 protein was positive in each case. References 1. Tumours of the Russell DS, Rubinstein LJ, eds. Tumours of the cranial, spinal and peripheral nerve sheaths . In: Pathology of Tumours of the Nervous System . 5th ed. Baltimore, Md; Williams & Wilkins; 1989:533-589. 2. Kennedy RE. An evaluation of 820 orbital cases . Trans Am Ophthalmol Soc . 1984;82:134-157. 3. Fan JT, Campbell RJ, Robertson DM. A survey of intraocular schwannoma with a case report . Can J Ophthalmol . 1995;30:37-41. 4. McLean IW, Burnier MN, Zimmerman LE, Jakobiec FA. Tumors of the Eye and Ocular Adnexa . In: Atlas of Tumor Pathology . Washington, DC: Armed Forces Institute of Pathology; 1994;3(pt 12). 5. Shields JA, Guibor P. Neurilemoma of the eyelid resembling a recurrent chalazion . Arch Ophthalmol . 1984;102:1650.Crossref 6. Rennie IG, Parsons MA, Benson MT. Neurilemoma of the caruncle: a clinicopathological report . Br J Ophthalmol . 1991;75:749-751.Crossref 7. Szabó G, Cseh E. Sklera-Neurinom in der Nähe des Limbus . Ophthalmologica . 1943;106:14-26.Crossref 8. Vincent NJ, Cleasby GW. Schwannoma of the bulbar conjunctiva . Arch Ophthalmol . 1968;80:641-642.Crossref 9. Grossniklaus HE, Green WR, Luckenbach M, Chan CC. Conjunctival lesions in adults: a clinical and histopathologic review . Cornea . 1987;6:78-116.Crossref 10. Quintana M, Lee WR. Intrascleral schwannoma . Ophthalmologica . 1976;173:64-69.Crossref 11. Graham CM, McCartney ACE, Buckley RJ. Intrascleral neurilemmoma . Br J Ophthalmol . 1989;73:378-381.Crossref 12. Masson P. Experimental and spontaneous schwannomas (peripheral gliomas) . Am J Pathol . 1932;8:367-416. 13. Luse SA. Electron microscopic studies of brain tumors . Neurology . 1960;10:881-905.Crossref 14. Dabezies OM, Penner R. Neurofibroma or neurilemmoma of the bulbar conjunctiva . Arch Ophthalmol . 1961;66:73-75.Crossref 15. Jakobiec FA, Font RL, Zimmerman LE. Malignant peripheral nerve sheath tumors of the orbit: a clinicopathologic study of eight cases . Trans Am Ophthalmol Soc . 1985;83:332-366. 16. Lyons CJ, McNab AA, Garner A, Wright JE. Orbital malignant peripheral nerve sheath tumors . Br J Ophthalmol . 1989;73:731-738.Crossref
Stevens-Johnson Syndrome Induced by Methazolamide TreatmentShirato, Shiraoki;Kagaya, Fumie;Suzuki, Yasuyuki;Joukou, Satoru
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150552021pmid: 9109770
Abstract Four cases of Stevens-Johnson syndrome considered to be induced by methazolamide were reported. In all of the cases, the first signs of Stevens-Johnson syndrome (ie, swelling of the skin and mucous membranes or slight fever) appeared about 2 weeks after the patient started taking methazolamide (75 or 100 mg/d). After the appearance of erythema, the skin and mucous membrane lesions progressed rapidly and spread over the entire body, even after the patient ended methazolamide treatment and started treatment with prednisolone. During prednisolone treatment, the skin and mucous lesions became bullous, ruptured spontaneously, and dried with crust or erosion. HLA typing was positive for HLA-B59 in 3 of 4 cases. Methazolamide should be prescribed with caution in patients of Japanese or Korean descent. References 1. Derick RJ. Carbonic anhydrase inhibitors . In: Mauger TF, Craig EL, eds. Hevener's Ocular Pharmacology . 6th ed. St Louis, Mo: CV Mosby Co; 1994:chap 4. 2. Stevens AM, Johnson FC. A new eruptive fever associated with stomatitis and ophthalmia . AJDC . 1922;24:526-533. 3. Breathnach SM. Drug reactions . In: Champion RH, Bruton JL, Ebling FJG, eds. Textbook of Dermatology . 5th ed. London, England: Blackwell Scientific Publications; 1992:chap 74. 4. Aminlari A. Falling scalp hairs: a side effect of the carbonic anhydrase inhibitor, acetazolamide . Glaucoma . 1984;6:41-42. 5. Weiss IS. Hirsutism after chronic administration of acetazolamide . Am J Ophthalmol . 1974;78:327-328. 6. Gandham SB, Spaeth GL, Leonardo MD, Costa VP. Methazolamide-induced skin eruptions . Arch Ophthalmol . 1993;111:370-372.Crossref 7. Sud RN, Grewal SS. Stevens Johnson syndrome due to Diamox . Indian J Ophthalmol . 1981;29:101-103. 8. Nayak AJ, Rao PNS. Erythema multiforme secondary to acetazolamide (Diamox) . Indian J Ophthalmol . 1981;29:105-106. 9. Tanaka M. Methazolamide induced toxic epidermal necrolysis . Rinsho Derma . 1989;43:327-330. 10. Totsuka S. Early treatment with topical corticosteroid in Stevens-Johnson syndrome . Rinsho Ganka . 1991;45:1001-1005. 11. Nishioka K, Murata M, Ihara Y, et al. A case of toxic epidermal necrolysis due to methazolamide . Rinsho Derma . 1994;36:1201-1204. 12. Yamasaki Y, Kobayashi T, Inazumi T. A case of toxic epidermal necrolysis due to methazolamide . Rinsho Derma .1994;36:1206-1207. 13. Uchida M, Morikawa M. A case of Stevens-Johnson syndrome due to methazolamide . Rinsho Derma . 1994;36:1208-1209. 14. Flach AJ, Smith RE, Fraunfelder FT. Stevens-Johnson syndrome associated with methazolamide treatment reported in two Japanese-American women . Ophthalmology . 1995;102; 1677-1680.Crossref 15. Champion RH. Disorders of blood vessels . In: Champion RH, Bruton JL, Ebling FJG, eds. Textbook of Dermatology . 5th ed. London, England: Blackwell Scientific Publications; 1992: chap 41. 16. Yetiv JZ, Bianchine JR, Owen JA. Etiologic factors of the Stevens-Johnson syndrome . South Med J . 1980;73:599-602.Crossref 17. Carrol OM, Bryan PA, Robinson RJ. Stevens-Johnson syndrome associated with long-acting sulfonamides . JAMA . 1966;195:691-693.Crossref 18. Huff JC, Weston WL, Tonnesen MG. Erythema multiforme: critical review of characteristics, diagnostic criteria and causes . J Am Acad Dermatol . 1983;8:763-775.Crossref 19. Genvert GI, Cohen EJ, Donnenfeld ED, Blecher MH. Erythema multiforme after use of topical sulfacetamide . Am J Ophthalmol . 1985;99:465-468. 20. Imanishi T, Akaza T, Kimura A, Tokunaga K, Gojobori T. Allele and haplotype frequencies for HLA and complement loci in various ethnic groups . In: Tshuji K, Aizawa M, Sasazuki T, eds. HLA 1991 . New York, NY: Oxford University Press Inc; 1991:1065-1220. 21. Roujeau JC, Huynh TN, Bracq C, Guillaume JC, Revuz J, Touraine R. Genetic susceptibility to toxic epidermal necrolysis . Arch Dermatol . 1987;123:1171-1173.Crossref
A Case of Visual Acuity Loss Following Laser Photocoagulation for Macular DrusenHyver, Scott W.;Schatz, Howard;McDonald, H. Richard;Johnson, Robert N.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150556022pmid: 9109771
Abstract Multiple reports have documented the disappearance of soft drusen in age-related macular degeneration after laser photocoagulation.1-3 We describe a patient with a deposit of a granular subfoveal material who suffered visual acuity loss following this treatment. To our knowledge, this is the first such complication reported for this form of therapy. Report of a Case. A 70-year-old Asian woman with bilateral pseudophakia who had a history of diabetes was initially seen with visual acuities of 20/125 OD and 20/25 OS. The right eye showed a largepigment epithelial tear with serous detachment of the macula caused by a large choroidal neovascular membrane. The left eye demonstrated many large, soft macular drusen with central confluence and mild subfoveal pigment clumping (Figure 1). Fluorescein angiography confirmed these findings.As part of a pilot study investigating the role of light laser treatment in stimulating drusen resorption and its safety, light laser burns were References 1. Wetzig PC. Treatment of drusen-related aging macular degeneration by photocoagulation . Trans Am Ophthal Soc . 1988;6:276-290. 2. Sigelman J. Foveal drusen resorption one year after perifoveal laser photocoagulation . Ophthalmology . 1991;98:1379-1383.Crossref 3. Figueroa MS, Regueras A, Bertrand J. Laser photocoagulation to treat macular soft drusen in agerelated macular degeneration . Retina . 1994;14:391-396.Crossref
Vitrectomy for Caterpillar Seta-Induced EndophthalmitisShibui, Hirobumi;Kawashima, Hidetoshi;Kamata, Keiko;Sasaki, Hiroshi;Inoda, Shigeru;Shimizu, Hiroyuki
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150557023pmid: 9109772
Abstract Insect hairs are a well-known cause of dermal irritation and sometimes can be an occupational hazard for planters.1 These hairs can migrate into the eye and occasionally elicit ocular manifestations, ie, ophthalmia nodosa. This ocular injury is sometimes caused by tarantula hairs.2 It is rare, though, for these hairs to induce such an endophthalmitis that vitrectomy is required to eliminate the inflammation.3 We report 2 cases of endophthalmitis caused by caterpillar setae. Surgical removal of the setae during vitrectomy was imperative to terminate the inflammation in the first case. Report of Cases. Case 1. On September 3, 1993, a 45-year-old man visited our clinic complaining of irritation in the left eye since he had spent some time gardening. Slitlamp examination revealed that several caterpillar setae were embedded in the cornea (Figure 1, left), subconjunctival space, and ocular angle. Endophthalmitis with hypopyon soon developed (Figure 1, right). Removal References 1. Steele C, Lucas DR, Ridgway AEA. Endophthalmitis due to caterpillar setae: surgical removal and electron microscopic appearances of the setae . Br J Ophthalmol . 1984;68:284-288.Crossref 2. Rutzen AR, Weiss JS, Kachadoorian H. Tarantula hair ophthalmia nodosa . Am J Ophthalmol . 1993;116:381-382. 3. D' Hermies F, Parent De Curzon H, Mathieu L, Furia M, Campinchi R. Les chorioretinopathies par migration de poils de chenille . J Fr Ophtalmol . 1985;8:471-478.
Self-mutilating Intraocular Injection of Metallic MercuryAuer, Carlos;Ducrey, Nicolas;Uffer, Sylvie;Othenin-Girard, Philippe;Herbort, Carl P.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150558024pmid: 9109773
Abstract We report a case of fulminant bilateral intraocular endophthalmitis and necrosis due to self-mutilating intraocular injection of metallic mercury. Report of a Case. A 27-year-old woman was seen with a 2-day history of bilateral photophobia and rapidly progressive painless loss of vision. Her clinical history revealed no particular physical illness, occasional intravenous heroin use in the past, and a negative human immunodeficiency virus (HIV) test result 3 months earlier. Under psychiatric care for longer than 5 years, the patient's treatment consisted of clozapine, 100 mg, 3 times daily, but her diagnosis was not available at entry. Visual acuity was 20/800 OD and light perception in the left eye. Results of a clinical examination revealed bilateral subconjunctival hemorrhages and massive bilateral nongranulomatous panuveitis including fibrinous anterior uveitis with hypopyon and vitritis (Figure 1). Fundus, only partially visible in the right eye, showed peripheral acute retinal necrosis. Ocular pressures were normal. Bilateral References 1. Field HL, Waldvogel S. Severe ocular selfinjury . Gen Hosp Psychiatry . 1995;17:224-227.Crossref 2. Yang HK, Brown GC, Magargal LE. Selfinflicted ocular mutilation . Am J Ophthalmol . 1981;91:658-663. 3. Rosenberg PN, Krohel GB, Webb RM, Helper RS. Ocular Munchausen's syndrome . Ophthalmology . 1986;93:1120-1123.Crossref 4. Hannigen BG. Self-administration of metallic mercury by intravenous injection . BMJ . 1978;2:933.Crossref 5. Kipling MD. Mercury and the eye . Ann Occup Hyg . 1965;8:81-83.Crossref
Acquired Trichomegaly Associated With Acquired Immunodeficiency SyndromeGraham, Debra A.;Sires, Bryan S.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150559025pmid: 9109774
Abstract Trichomegaly (hypertrichosis of the eyelashes) is associated with congenital syndromes, numerous medications, and systemic disease including immunodeficient states. Trichomegaly associated with acquired immunodeficiency syndrome (AIDS) has been reported in the recent nonophthalmologic literature.1-3 We report a case documented during an ophthalmologic examination. Report of a Case. A 24-year-old, black, bisexual man's condition was diagnosed as being positive for the human immunodeficiency virus (HIV) in 1990. Treatment with zidovudine was started in August 1993 but was stopped after 1 week because it caused the patient to vomit. The patient continued receiving zalcitabine from August 1993 until November 1995, when this treatment was discontinued because of peripheral neuropathy. Treatment with zidovudine was restarted at a 100-mg dose. Bactrim was the only other medicine being taken. His CD4+ lymphocyte count was 0 for 1 year prior to presentation. An HIV-1 titer in November 1995 revealed that HIV-1 RNA copies were greater than References 1. Kaplan MH, Sadick NS, Talmor M. Acquired trichomegaly of the eyelashes: a cutaneous marker of acquired immunodeficiency syndrome . J Am Acad Dermatol . 1991;25:801-804.Crossref 2. Baccard M, Morel P. Excessive growth of eyelashes in patients with acquired immunodeficiency syndrome . Cutis . 1994;53:83-84. 3. Klutman NE, Hinthorn DR. Excessive growth of eyelashes in a patient with AIDS being treated with zidovudine . N Engl J Med . 1991;324:1896. 4. Berglund EF, Burton GV, Mills GM, Nichols GM. Hypertrichosis of the eyelashes associated with Interferon-α therapy for chronic granulocytic leukemia . South Med J . 1990;83:363.Crossref
Figure Errors1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150561026
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract In the article entitled "Acquired Immunodeficiency Syndrome-Associated Herpes Simplex Virus Retinitis," published in the July Archives (1996;114:834-840), there were errors in the published numbering of Figures 2, 3, and 4. Figure 2 and the accompanying legend on page 837 should have been Figure 4, and Figures 3 and 4 on page 838 should have been Figures 2 and 3, respectively. Also, the legends for the latter 2 figures were switched. The correct Figures 2 and 3 and the appropriate legends are shown below. The journal regrets the errors.
Surgical Removal of a Subretinal Proliferating Cysticercus of Taeniaeformis crassicepsChuck, Roy S.;Olk, R. Joseph;Weil, Gary J.;Akduman, Levent;Benenson, Igor L.;Smith, Morton E.;Kaplan, Henry J.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150564028pmid: 9109776
References 1. Gevorkian G, Manoutcharian K, Larralde C, et al. Immunodominant synthetic peptides of Taenia crassiceps in murine and human cysticercosis . Immunol Lett . 1996;49:185-189.Crossref 2. Shea M, Maberley AL, Walters J, Freeman RS, Fallis AM. Intraocular Taenia crassiceps (Cestoda) . Trans Am Acad Ophthalmol Otol . 1973;77:OP778-783. 3. Arocker-Mettinger E, Huber-Spitzy V, Auer H, Grabner G, Stur M. Taenia crassiceps in the anterior chamber of the human eye: a case report . Klin Monatsbl Augenheilkd . 1992;201:34-37.Crossref 4. Klinker H, Tintelnot K, Joeres R, et al. Taenia crassiceps infection in AIDS . Dtsch Med Wochenschrift . 1992;117:133-138.Crossref 5. Santos R, Chavarria M, Aguirre AE. Failure of medical treatment in two cases of intraocular cysticercosis . Am J Ophthalmol . 1984;97:249-250.
Postoperative Management of Cataract Surgery Patients-ReplyBass, Eric B.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150566030
Abstract In reply Our survey was not designed to determine whether the postoperative care of cataract surgery patients is better or worse when delivered by optometrists rather than ophthalmologists. We asked ophthalmologists and optometrists about the number of dilated fundus examinations, slit-lamp examinations, tonometry tests, and refractions that they performed for their cataract surgery patients because the guidelines promulgated by the American Academy of Ophthalmology and the Agency for Health Care Policy and Research specify the number of times that each of these tests should be performed.1 These guidelines do not indicate the percentage of visits in which the tests should be performed. Because differences in the frequency of test use between ophthalmologists and optometrists may be partly explained by the fact that an ophthalmologist generally performs the first postoperative visit, the observed differences in test use between ophthalmologists and optometrists should not be the basis for making conclusions about References 1. Cataract Management Guideline Panel. Cataract in Adults: Management of Functional Impairment. Clinical Practice Guideline, Number 4 . Rockville, Md: US Dept of Health and Human Services, Public Health Service; 1993. Agency for Health Care Policy and Research publication 93-0542.
Use of Quality-of-Life Instruments in Randomized Clinical TrialsSommer, Alfred
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150566031pmid: 9109778
Abstract I read with interest the insightful editorial by Carl Kupfer, MD, in the July 1996 issue of the Archives1 stressing the importance of obtaining "cost outcomes along with the clinical and quality-of-life outcomes" as integral components of randomized clinical trials. Recent studies more than justify Dr Kupfer's focus on the need for identifying clinical outcomes that actually affect the everyday functioning of individuals we seek to help. It was interesting to note that the National Eye Institute, Bethesda, Md, is developing "a vision function assessment-quality-of-life instrument to be used in all RCTs." At least 2 types of quality-of-life measures have generally been employed. One measures an individual's sense of well-being, such as the instrument indicating that patients with myopia who are undergoing refractive surgery are more concerned with improved vision than with ridding themselves of glasses.2 The second measures changes in an individual's perceived ability to function, like References 1. Kupfer C. General principles for AIDS research . Arch Ophthalmol . 1996;114:862.Crossref 2. Powers MK, Meyerowitz BE, Arrowsmith PN, Marks RG. Psychosocial findings in radial keratotomy patients two years after surgery . Ophthalmology . 1984;91:1193-1198.Crossref 3. Steinberg EP, Tielsch JM, Schein OD, et al. National study of cataract surgery outcomes: variation in 4-month postoperative outcomes as reflected in multiple outcome measures . Ophthalmology . 1994;101:1131-1141.Crossref 4. Wu AW, Coleson LC, Holbrook J, Jabs DA, for The Studies of Ocular Complication of AIDS Research Group. Measuring visual function and quality of life in patients with cytomegalovirus retinitis . Arch Ophthalmol . 1996;114; 841-847.Crossref
Postoperative Management of Cataract Surgery PatientsArtman, Molly
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150566029pmid: 9109777
Abstract I would like to remark about an article by Bass et al1 that appeared in the September 1996 issue of the Archives. The manner in which the data were presented will certainly skew the reader toward concluding that ophthalmologic care for postoperative patients is superior to that of optometric care. First, the authors discovered that 88% of responding ophthalmologists reported 4 or more postoperative visits. However, most optometrists (78%) claimed that they saw patients only 3 or more times after surgery (probably because 97% of the doctors of medicine claimed to perform the first postoperative examination). Realizing this difference, it was pointless for the authors to then question the doctors of medicine and the doctors of optometry on the total number of slit-lamp, tonometry, and dilated fundus examinations if the doctors of medicine have just admitted seeing these patients more times overall. A more intelligent presentation of the data References 1. Bass EB, Sharkey PD, Luthra R, et al. Postoperative management of cataract surgery patients by ophthalmologists and optometrists . Arch Ophthalmol . 1996;114:1121-1127.Crossref
Use of Quality-of-Life Instruments in Randomized Clinical Trials-ReplyKupfer, Carl
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150566032
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract In reply Dr Sommer correctly notes the 2 quality-of-life domains that must be addressed in such an instrument. The National Eye Institute-Visual Functioning Questionnaire (NEI-VFQ) does address both of the quality-of-life domains identified by Dr Sommer. With respect to customizing the instrument for a particular condition, this is not only expensive but fortunately unnecessary. In developing the NEI-VFQ, 25 focus groups were held in 5 sites around the country with patient impairment due to age-related cataract, glaucoma, diabetic retinopathy, age-related macular degeneration, and cytomegalovirus retinitis. Despite differences in the disease entity, the effect of these different causes of visual impairment on daily visual functioning and the quality of life was quite similar. Therefore, the NEI-VFQ was considered to be relevant to most visually impaired adults regardless of the underlying cause of the chronic visual problem. If it were necessary to customize the instrument, as for example to assess various forms
Uveitis and Systemic Lupus Erythematosus-ReplyFoster, C. Stephen
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150567034
Abstract In reply Dr Howe assumes that we are "apparently making the common mistake of referring to lupus retinopathy as a retinal vasculitis." On the contrary, we described in our epidemiological series of 1237 patients with uveitis only those patients with lupus who had true inflammatory disease (ie, uveitis or retinal vasculitis). Dr Howe wonders if the 19 patients we studied who were "lupus suspects" (ie, who failed by one diagnostic parameter "score" to completely fulfill the criteria for having definite lupus) are legitimate for inclusion in the report, and she further wonders if these patients were removed from the epidemiological figures, would that affect our claim that SLE can truly be a cause of uveitis. A similar question could be asked of anyone reporting on observations in a population of patients with sarcoidosis or with Behcet disease.Many such reports do not require biopsy proof of the diagnosis but routinely References 1. No Sal A, Schleissler LA, Mishkin FS, Lieberman J. Angiotensin converting enzyme in non-invasive evaluation of sarcoidosis . Ann Intern Med . 1979;90:328.Crossref 2. Behcet's Disease Research Committee of Japan. Behcet's disease: guide to diagnosis of Behcet's disease . Jpn J Ophthalmol . 1974;18:291. 3. Neves RA, Rodriquez A, Power WJ, et al. The value of combined serum angiotensin converting enzyme and gallium scan in the diagnosis of ocular sarcoidosis . In: Advances in Ocular Immunology . Amsterdam, the Netherlands: Elsevier Science BV; 1994:353. 4. Opremcak EM. Uveitis: A Clinical Manual for Ocular Inflammation . New York, NY: Springer-Verlag NY Inc; 1995:217. 5. Aronson AJ, Ordoñez NG, Diddie KR, Ernest JT. Immune-complex deposition in the eye in systemic lupus erythematosus . Arch Intern Med . 1979;139:1312-1313.Crossref 6. Saunders MD. Retinal vasculitis: a review . J R Soc Med . 1979;72:908.
Uveitis and Systemic Lupus ErythematosusHowe, Lucy
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150567033pmid: 9109779
Abstract The article by Rodriguez and coworkers1 on uveitis referral patterns to a tertiary ophthalmic center reports systemic lupus erythematosus (SLE) as a common cause of anterior uveitis, posterior uveitis, and retinal vasculitis (3.3%, 7.9%, and 15.3%, respectively). The authors state that SLE (along with various other systemic conditions) is an "important and well-known cause of retinal vasculitis," but this is not the case. The authors are apparently making the common mistake of referring to lupus retinopathy as a retinal vasculitis. Indeed the article2 that they cite as a reference for the above statement reiterates this point: clinically, inflammation of the anterior chamber or vitreous is not a feature of lupus retinopathy, even in severe disease,2,3 while pathologically, in keeping with the cerebral vasculopathy,4 there is microocclusion rather than vasculitis.5 However, inflammatory infiltration of the choroid has been reported,5 and it has been postulated that References 1. Rodriguez A, Calonge M, Pedroza-Seres M, et al. Referral patterns of uveitis in a tertiary eye care center . Arch Ophthalmol . 1996;114:593-599.Crossref 2. Sanders MD, Graham EM. Retinal vasculitis . Postgrad Med J . 1988;64:488-496.Crossref 3. Gold DH, Morris DA, Henkind P. Ocular findings in systemic lupus erythematosus . Br J Ophthalmol . 1972;56:800-804.Crossref 4. Johnson RT, Richardson EP. The neurological manifestations of systemic lupus erythematosus: a clinical-pathological study of 24 cases and review of the literature . Medicine (Baltimore) . 1968;47:337-369.Crossref 5. Graham EM, Spalton DJ, Barnard RO, Garner A, Ross Russell RW. Cerebral and retinal vascular changes in systemic lupus erythematosus . Ophthalmology . 1985;92:444-448.Crossref
Simplified Technique for Eyelid Margin RepairDevoto, Martin H.;Kersten, Robert C.;Teske, Scott A.;Kulwin, Dwight R.
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150568035pmid: 9109780
Abstract The repair of the eyelid margin is a commonly used technique in cases of traumatic lacerations or for reconstructions after full-thickness excision. The classic technique and its minor variations rely on the use of three 6-0 silk sutures to approximate the cut ends of the eyelid margin.1 However, this produces a bulky knot, and sutures have to be removed, with the associated risk of wound dehiscence. Despite being a common procedure, there is a paucity of published articles in the literature. We have been pleased with a technique of eyelid margin repair, using a single vertical mattress 7-0 polyglactin 910 suture to align the margin. The use of absorbable sutures avoids the need for removal and gives better cosmesis than the classic 6-0 silk 3-suture technique. Our technique relies on a single 7-0 polyglactin 910 suture to exactly align the meibomian gland orifices as a vertical mattress suture (Figure References 1. Collin JRO. A Manual of Systematic Eyelid Surgery . Edinburgh, Scotland: Churchill Livingstone Inc; 1989;5:79-80. 2. Kersten RC. Lid laceration repair . In: Phelps CD, ed. Manual of Common Ophthalmic Surgical Procedures . New York, NY: Churchill Livingstone Inc; 1985;20:123-126.
Visual DevelopmentTychsen, Lawrence
1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150572037
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract Few books come along in visual science that can be considered ground breaking. This is one. Nigel Daw is a world-class neurophysiologist at Yale University, New Haven, Conn, whose expertise is in visual plasticity. For years he organized the neurosciences course for medical students at Washington University in St Louis, Mo, while at the same time running a busy animal research laboratory. I know firsthand the accolades he received from students for his lectures and discussions. He has distilled that knowledge into this single-authored, easy-to-read, well-organized text. In 228 pages, the book conveys cogently the fascination we should all share for questions in visual development. Daw devotes the first third of the book to development of normal human and animal vision. The remaining two thirds covers the sciences of amblyopia and strabismus. The book's greatest strength is the ease with which it can be read by any clinician or student.
PRODUCTS & SERVICES1997 Archives of Ophthalmology
doi: 10.1001/archopht.1997.01100150576039
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract THERAPEUTIC. Neoptx Inc. introduces an easy-to-use, affordable solution for workers who need to wear protective eye gear but who also need help seeing things up close—MagnOptx, (formerly MagnaVue), the peel-and-stick, magnified reading lenses for safety glasses. MagnOptx lenses are completely reusable and removable, easy-to-apply and can be customized to fit any style or size of protective eye gear. They are available in nine diopter powers, ranging from +1.00 to +3.00 in.25 diopter steps. MagnOptx can be mail ordered for $30. A sample of the lenses and product photos are available upon request by calling (206) 441-3077. For more information, contact NEOPTX, 2205 152nd Ave NE, Redmond, WA 98052, Tel: 800-344-2020, Web: www.neoptx.com DIAGNOSTIC INSTRUMENT. Gulden Ophthalmics has introduced the SAFE, the Stereopsis And Fusion Evaluator. The SAFE is designed to detect and quantify relative afferent defects, determine fusion status, and measure stereopsis. This quick screening device is easy to use,