Archives of Ophthalmology

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150012001

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.

Freeman, William R.;Azen, Stanley P.;Kim, Jung W.;El-Haig, Wael;Mishell, Daniel R.;Bailey, Ian

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150013002pmid: 9006420

Abstract Objective: To prospectively assess the risks and benefits of vitrectomy surgery for eyes with stage 3 or 4 macular holes. Design: A multicentered, controlled, randomized clinical trial. Setting: Community- and university-based ophthalmology clinics. Patients: One hundred twenty patients (129 eyes) with stage 3 or 4 macular holes. Interventions: Standardized macular hole surgery vs observation alone. Main Outcome Measures: Four measures of bestcorrected visual function, standardized photographic evaluation of the extent of hole closure, evaluation of lens opacification, and determination of adverse events. Outcomes were determined at 6 months after randomization. Results: Compared with observation alone, a significant benefit due to surgery was found in the rate of hole closure (4% vs 69%, P<.001). After adjusting for baseline visual acuity, hole duration, and maximum hole diameter, a significant benefit due to surgery was found in visual acuity for the Bailey-Lovie Word Reading (P=.02) and the Potential Acuity Meter (P<.01) tests; a marginally significant benefit due to surgery was found in visual acuity for the Early Treatment Diabetic Retinopathy Study chart (P=.05) Although the proportion of eyes achieving a change in visual acuity of 2 or more lines on the Early Treatment Diabetic Retinopathy Study chart was significantly greater for the surgery group vs the observed group (11 [19%] of 59 eyes vs 3[5%] of 58 eyes, adjusted P=.05), 20(34%) of 59 eyes randomized to surgery had a loss in visual acuity of 1 or more lines. Compared with the observation group, eyes randomized to surgery had higher nuclear sclerosis scores (2.4 vs 1.3, P<.001). Fourteen adverse events were noted in the surgery group; none were noted in the observed group. Conclusions: Some visual benefit of vitrectomy surgery for macular holes exists, despite a notable incidence of adverse events. The large variability in visual acuity outcome in the surgical group may be because of complications or progressive cataract. A study of the longterm outcome after macular hole surgery is needed. References 1. Guyer DR. Green WR, de Bustros S, Fine SL. Histopathologic features of idiopathic macular holes and cysts . Ophthalmology . 1990;97:1045-1051.Crossref 2. Schocket SS, Lakhanpal V, Xiaoping M, Kelman S, Billings E. Laser treatment of macular holes . Ophthalmology . 1988;95:574-582.Crossref 3. Gass JDM. Idiopathic senile macular hole . Arch Ophthalmol . 1988;106:629-639.Crossref 4. Johnson RN, Gass JDM. Idiopathic macular holes: observations, stages of formation, and implications for surgical intervention . Ophthalmology . 1988;95:917-924.Crossref 5. Smiddy WE. Michels RG, Glaser BM, de Bustros S. Vitrectomy for impending idiopathic macular holes . Am J Ophthalmol . 1988;105:371-376.Crossref 6. de Bustros S, the Vitrectomy for Prevention of Macular Hole Study Group. Vitrectomy for prevention of macular holes: results of a randomized multicenter clinical trial . Ophthalmology . 1994;101:1055-1059.Crossref 7. Gass JDM, Joondeph BC. Observations concerning patients with suspected impending macular holes . Am J Ophthalmol . 1990;109:638-646. 8. Bartsch D-U, Intaglietta M, Bille JF, Dreher AW, Gharib M, Freeman WR. Confocal laser tomographic analysis of the retina in eyes with macular hole formation and other macular diseases . Am J Ophthalmol . 1989;108:277-287. 9. Shahidi M, Ogura Y, Blair NP, Rusin MM, Zeimer R. Retinal thickness analysis for quantitative assessment of diabetic macular edema . Arch Ophthalmol . 1991;109:1115-1119.Crossref 10. Kishi S, Shimizu K. Posterior precortical vitreous pocket . Arch Ophthalmol . 1990;108:979-982.Crossref 11. Kelly NE, Wendel RT. Vitreous surgery for idiopathic macular holes: results of a pilot study . Arch Ophthalmol . 1991;109:654-659.Crossref 12. Wendel RT, Patel AC, Kelly NE, Salzano TC, Wells JW. Novack GD. Vitreous surgery for macular holes . Ophthalmology . 1992;100:1671-1676.Crossref 13. Glaser BM, Michels RG, Kuppermann BD, Sjaarda RN, Pena RA. Transforming growth factor β2 for the treatment of full thickness macular holes . Ophthalmology . 1992;99:1162-1173.Crossref 14. le D, Glaser BM, Thompson JT, Sjaarda RN, Gordon LW. Retreatment of fullthickness macular holes persisting after prior vitrectomy . Ophthalmology . 1993;100:1787-1793.Crossref 15. Smiddy WE, Glaser BM, Thompson JT, et al. Transforming growth factor-β2 significantly enhances the ability to flatten the rim of subretinal fluid surrounding macular holes . Retina . 1993;13:296-301.Crossref 16. Glaser BM, Michels RG, Kupperman BD, Sjaarda RN, Pena RA. Transforming growth factor-β2 for the treatment of full-thickness macular holes . Ophthalmology . 1992;99:1162-1172.Crossref 17. Celtrix shares plunge . San Francisco Chronicle . (November 1) , 1995:D-1. 18. Freeman WR. Vitrectomy surgery for full thickness macular holes . Am J Ophthalmol . 1993;116:233-235. 19. Ferris FL III, Kassoff A, Bresnick GH, Bailey I. New visual acuity charts for clinical research . Am J Ophthalmol . 1982;94:91-96. 20. Bailey IL, Bullimore MA. Raasch TW, Taylor HR. Clinical grading and the effect of scaling . Invest Ophthalmol Vis Sci . 1991;32:422-432. 21. Eliott DB, Bullimore MA, Bailey IL. Improving the reliability of the Pelli-Robson Contrast Sensitivity Test . Clin Vis Sci . 1991;6:471-475. 22. Bailey IL, Lovie JE. The design and use of a new near-vision chart . Am J Optom Physiol Opt . 1980;57:378-387.Crossref 23. Afifi AA, Azen SP. Statistical Analysis: A Computer Oriented Approach . 2nd ed. Orlando, Fla: Academic Press Inc; 1979. 24. Kitchin JE, Bailey IL. Task complexity and visual acuity in senile macular degeneration . Aust J Ophthalmol . 1981;63:235-242. 25. Tetz MR, Klein U, Volcker HE. Measurement of potential visual acuity in 343 patients with cataracts: a prospective clinical study . Ger J Ophthalmol . 1992;1:403-408. 26. Bradley A, Thibos L, Still D. Visual acuity measured with clinical Maxwellianview systems: effects of beam entry location . Optom Vis Sci . 1990;67:8101-8107.Crossref 27. Barrett BT, Davison PA, Eustace PE. Effects of posterior segment disorders on oscillatory displacement thresholds, and on acuities as measured using the potential acuity meter and laser interferometer . Ophthalmic Physiol Opt . 1994;14:132-138.Crossref

Wall, Michael;Jennisch, Charles S.;Munden, Paul M.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150028003pmid: 9006421

Abstract Objective: To determine whether patients with ocular hypertension (OHT) have elevated motion perimetry thresholds. Design: Motion perimetry uses a customized computer graphics program to detect the ability to identify a coherent shift in position of 50% of dots in a defined circular area against a background of fixed dots. Motion size threshold is defined as the smallest circular area in which dot motion is detected. Subjects respond by touching the area of the computer monitor with a light pen where motion stimuli are perceived. Reaction times (milliseconds) to stimuli and localization error (number of pixels from target center) are also obtained for each trial. Setting: University hospital ophthalmology clinic. Patients or Other Participants: Twenty-seven patients with OHT and 27 age-matched normal subjects. One eye was tested in each subject. Main Outcome Measures: Random dot motion stimuli size thresholds and total deviation probability plot data, reaction times, and spatial localization errors. Results: The patients with OHT had more abnormal test points in the total deviation probability plot analysis compared with the controls (P<.001,×2). The abnormal test points were concentrated in the superior and inferior nasal regions. Six subjects had nerve fiber bundlelike defects to motion stimuli. Six subjects (5 overlapping with the probability plot analysis) had abnormal glaucoma hemifield test results. The patients with OHT also had significantly greater localization errors. Conclusion: Motion threshold perimetry may be a more sensitive method to detect visual field abnormalities in OHT than conventional automated perimetry. References 1. Johnson CA, Adams AJ, Casson EJ, Brandt JD. Blue-on-yellow perimetry can predict the development of glaucomatous visual field loss . Arch Ophthalmol . 1993;111:645-650.Crossref 2. Hart WM Jr, Gordon MO. Color perimetry of glaucomatous visual field defects . Ophthalmology . 1984;91:338-346.Crossref 3. Phelps CD. Acuity perimetry and glaucoma . Trans Am Ophthalmol Soc . 1984;82:753-791. 4. Drum B, Breton M, Massof R, et al. Pattern discrimination perimetry: a new concept in visual field testing . Doc Ophthalmol Proc Ser . 1987;49:433-440. 5. Wanger P, Persson HE. Pattern-reversal electroretinograms and high-pass resolution perimetry in suspected or early glaucoma . Ophthalmology . 1987;94:1098-1103.Crossref 6. Kardon RH, Kirkali PA, Thompson HS. Automated pupil perimetry; pupil field mapping in patients and normal subjects . Ophthalmology . 1991;98:485-495.Crossref 7. Quigley HA, Dunkelberger GR, Green WR. Retinal ganglion cell atrophy correlated with automated perimetry in human eyes with glaucoma . Am J Ophthalmol . 1989;107:453-464. 8. Tuulonen A, Lehtola J, Airaksinen JP. Nerve fiber layer defects with normal visual fields: do normal optic disc and normal visual field indicate absence of glaucomatous abnormality? Ophthalmology . 1993;100:587-598.Crossref 9. Quigley HA, Dunkelberger GR, Green WR. Chronic human glaucoma causing selectively greater loss of large optic nerve fibers . Ophthalmology . 1988;95:357-363.Crossref 10. Glovinsky Y, Quigley HA, Dunkelberger GR. Retinal ganglion cell loss is sizedependent in experimental glaucoma . Invest Ophthalmol Vis Sci . 1991;32:484-491. 11. Chaturvedi N, Hedley-Whyte ET, Dreyer EB. Lateral geniculate nucleus in glaucoma . Am J Ophthalmol . 1993;116:182-188. 12. Schiller PH, Logothetis NK, Charles ER. Functions of the colour-opponent and broad-band channels of the visual system . Nature . 1990;343:68-70.Crossref 13. Nakayama K, Silverman GH. Serial and parallel processing of visual feature conjunctions . Nature . 1986;320:264-265.Crossref 14. Treisman A, Souther J. Search Asymmetry: a diagnostic for preattentive processing of separable features . J Exp Psychol Gen . 1985;114:285-310.Crossref 15. Corbetta M, Miezin FM, Dobmeyer S, Shulman GL, Petersen SE. Selective and divided attention during visual discriminations of shape, color, and speed: functional anatomy by positron emission tomography . J Neurosci . 1991;11:2383-2402. 16. Rumelhart DE, McClelland JL, and the PDP research group. Parallel Distributed Processing: Explorations in the Microstructure of Cognition Foundations . Boston, Mass: The MIT Press; 1986;1:472. 17. Wall M, Ketoff KM. Random dot motion perimetry in glaucoma patients and normal subjects . Am J Ophthalmol . 1996;120:587-596. 18. Wall M, Montgomery EB. Using motion perimetry to detect visual field defects in patients with idiopathic intracranial hypertension: a comparison with conventional automated perimetry . Neurology . 1995;45:1167-1175.Crossref 19. Nawrot M, Steinman SB. Real-time color-frame animation for visual psychophysics on the Macintosh computer . Behav Res Methods Instr Comput . 1994;24:439-452. 20. Fredericksen RE, Verstraten FA, van de Grind WA. Spatial summation and its interaction with the temporal integration mechanism in human motion perception . Vision Res . 1994;34:3171-3188.Crossref 21. Chauhan BC, House PH. Intratest variability in conventional and high-pass resolution perimetry . Ophthalmology . 1991;98:79-83.Crossref 22. Wall M, Lefante J, Conway M. Variability of high-pass resolution perimetry in normals and patients with idiopathic intracranial hypertension . Invest Ophthalmol Vis Sci . 1991;32:3091-3095. 23. van de Grind WA, Koenderink JJ, van Doom AJ, Milders MV, Voerman H. Inhomogeneity and anisotropies for motion detection in the monocular visual field of human observers . Vision Res . 1993;33:1089-1107.Crossref 24. House P, Schulzer M, Drance S, Douglas G. Characteristics of the normal central visual field measured with resolution perimetry . Graefes Arch Clin Exp Ophthalmol . 1991;229:8-12.Crossref 25. Wirtschafter JD, Becker WL, Howe JB, Younge BR. Glaucoma visual field analysis by computed profile of nerve fiber function in optic disc sectors . Ophthalmology . 1982;89:255-267.Crossref 26. Wall M, Conway MD, House PH, Allely R. Evaluation of sensitivity and specificity of spatial resolution and Humphrey automated perimetry in pseudotumor cerebri patients and normal subjects . Invest Ophthalmol Vis Sci . 1991;32:3306-3312. 27. Katz J, Sommer A, Gaasterland DE, Anderson DR. Comparison of analytic algorithms for detecting glaucomatous visual field loss . Arch Ophthalmol . 1991;109:1684-1689.Crossref 28. Asman P, Heijl A. Glaucoma hemifield test: automated visual field evaluation . Arch Ophthalmol . 1992;110:812-819.Crossref 29. Asman P, Heijl A. Evaluation of methods for automated hemifield analysis in perimetry . Arch Ophthalmol . 1992;110:820-826.Crossref 30. Silverman SE, Trick GL, Hart WM Jr. Motion perception is abnormal in primary open-angle glaucoma and ocular hypertension . Invest Ophthalmol Vis Sci . 1990;31:722-729. 31. Bullimore MA, Wood JM, Swenson K. Motion perception in glaucoma . Invest Ophthalmol Vis Sci . 1993;34:3526-3533. 32. Trick GL, Steinman SB, Amyot M. Motion perception deficits in glaucomatous optic neuropathy . Vision Res . 1995;35:2225-2233.Crossref 33. Johnson CA. Selective versus nonselective losses in glaucoma . J Glaucoma . 1994;3( (suppl) ):32-44. 34. Johnson CA, Marshall D, Eng KM. Displacement threshold perimetry in glaucoma using a Macintosh computer system and a 21-inch monitor . In: Mills RP, Wall M, eds. Perimetry Update 1994/1995 . Amsterdam, the Netherlands: Kugler Publications; 1995:103-110. 35. Ruben S, Fitzke F. Correlation of peripheral displacement thresholds and optic disc parameters in ocular hypertension . Br J Ophthalmol . 1994;78:291-294.Crossref 36. Sample PA, Taylor JDN, Martinez G, Lusky M, Weinreb RN. Short-wavelength color visual fields in glaucoma suspects at risk . Am J Ophthalmol . 1993;115:225-233. 37. Mateeff S, Gourevich A. Brief stimuli localization in visual periphery . Acta Physiol Pharmacol Bulg . 1984;10:64-71. 38. Aitsebaomo AP, Bedell HE. Psychophysical and saccadic information about direction for briefly presented visual targets . Vision Res . 1992;32:1729-1737.Crossref 39. Bartz AE. Eye-movement latency, duration, and response time as a function of angular displacement . J Exp Psychol . 1962;64:318-324.Crossref 40. Brito CF. Age-related Changes in the Detection and Classification of Motion in the Periphery of the Visual Field. Iowa City: University of Iowa; 1994. Thesis.

Soparkar, Charles N. S.;Wilhelmus, Kirk R.;Koch, Douglas D.;Wallace, Gary W.;Jones, Dan B.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150036004pmid: 9006422

Abstract Objective: To describe patterns of conjunctivitis caused by ophthalmic decongestants. Design: Case series. Setting: Outpatient eye clinic. Patients: We selected patients with conjunctival inflammation who were using nonprescription decongestant eyedrops, who had no other cause for conjunctivitis, and whose conditions improved after discontinuing the incriminated preparations. Main Outcome Measures: Clinical characteristics of conjunctival inflammation and time to resolution of symptoms and signs after discontinuing the use of eyedrops. Results: Seventy patients (137 eyes) were identified. Preparations containing the vasoconstrictors naphazoline, tetrahydrozoline, or phenylephrine were associated with 3 clinical patterns of conjunctivitis: conjunctival hyperemia (50 cases), follicular conjunctivitis (17 cases), and eczematoid blepharoconjunctivitis (3 cases). Decongestants were used daily for a median of 3 years (range, 8 hours to 20 years) prior to presentation. The median time to resolution of symptoms and signs was 4 weeks (range, 1-24 weeks), and patients remained asymptomatic for a median follow-up of 6 months (range, 0-12 years). Conclusion: Nonprescription decongestant eyedrops can produce acute and chronic forms of conjunctivitis by pharmacological, toxic, and allergic mechanisms. Once recognized, conjunctival inflammation often takes several weeks to resolve. References 1. Abelson MB, Allansmith MR, Friedlaender MH. Effects of topically applied ocular decongestant and antihistamine . Am J Ophthalmol . 1980;90:254-257. 2. Abelson MB. Paradis A, George MA, Smith SM. Maguire L, Burns R. Effects of Vasocon-A in the Allergen challenge model of acute allergic conjunctivitis . Arch Ophthalmol . 1990;108:520-524.Crossref 3. Abelson MB, Yamamoto GK, Allansmith MR. Effects of ocular decongestants . Arch Ophthalmol . 1980;98:856-858.Crossref 4. Friedlaender MH. Current concepts in ocular allergy . Ann Allergy . 1991;67:5-10. 5. Gordon DM. Ocular decongestants . Am J Ophthalmol . 1959;48:395-396. 6. Hurwitz P. Local antihistamine agents in ophthalmology . Ill Med J . 1950;98:113-116. 7. Hurwitz P, Thompson JM. Uses of naphazoline (privine) in ophthalmology . Arch Ophthalmol . 1950;43:712-717.Crossref 8. Miller J, Wolf EH. Antazoline phosphate and naphazoline hydrochloride, singly and in combination for the treatment of allergic conjunctivitis: a controlled, double blind clinical trial . Ann Allergy . 1975;35:81-86. 9. Nemeth L. Antihistamines in ophthalmology . Br J Ophthalmol . 1949;33:665-669.Crossref 10. Salem H. Dunn BJ. Loux JJ. Conjunctival temperature: a measure of ocular decongestant and anti-inflammatory activity . Ann Ophthalmol . 1975;7:819-824. 11. Smith JP, Lanier BQ, Tremblay N, Ward RL, deFaller JM. Treatment of allergic conjunctivitis with ocular decongestants . Curr Eye Res . 1982;2:141-147.Crossref 12. Mertins PS. Excessive self-medication with naphazoline hydrochloride (privine hydrochloride) . JAMA . 1947;134:1175.Crossref 13. Caputo AR, Schnitzer RE. Systemic response to mydriatic eye drops in neonates: mydriatics in neonates . J Pediatr Ophthalmol Strabismus . 1979;15:109-122. 14. Fraunfelder FT, Scafidi AF. Possible adverse effects from topical ocular 10% phenylephrine . Am J Ophthalmol . 1978;85:447-453. 15. Meyer SM, Fraunfelder FT. Phenylephrine hydrochloride . Ophthalmology . 1980;87:1177-1179.Crossref 16. Lansche RK. Systemic reactions to topical epinephrine and phenylephrine . Am J Ophthalmol . 1966;61:95-98. 17. Mindlin RL. Accidental poisoning from tetrahydrozoline eyedrops . N Engl J Med . 1966;275:112. 18. Rogers GW. Safe use of eye drops . N Engl J Med . 1966;275:447. 19. Heath P. Neosynephrine hydrochloride: some uses and effects in ophthalmology . Arch Ophthalmol . 1936;16:839-846.Crossref 20. Rosales T, Isenberg S, Leake R, Everett S. Systemic effects of mydriatics in low-weight infants . J Pediatr Ophthalmol Strabismus . 1981;18:42-44. 21. Hanna C, Brainard J. Allergic dermatoconjunctivitis caused by phenylephrine . Am J Ophthalmol . 1983;95:703-704. 22. Mathias CGT. Maibach HI, Irvine A, Adler W. Allergic contact dermatitis to echothiophate iodide and phenylephrine . Arch Ophthalmol . 1979;97:286-287.Crossref 23. Epstein DL, Boger WP III, Grant WM. Phenylephrine provocative testing in the pigmentary dispersion syndrome . Am J Ophthalmol . 1978;85:43-50. 24. Rumelt MB. Blindness from misuse of over-the-counter eye medications . Ann Ophthalmol . 1988;20:26-30. 25. Weiss DI, Shaffer RN. Mydriatic effects of one-eighth percent phenylephrine: a potential cause of angle-closure glaucoma . Arch Ophthalmol . 1962;68:41-43. 26. Komi T, Maeda I, Uno Y, Otsuka H. Inhibitory effect of sodium chondroitin sulfate on epithelial keratitis induced by naphazoline . Nippon Geka Gakkai Zasshi . 1964;68:154-158. 27. Lisch K. Conjunctival alterations by sympathomimetic drugs . Klin Monatsbl Augenheilkd . 1978;173:404-406. 28. Saraux H, Offret H, de Rancourt de Mimerand E. Pseudo-pemiphigus oculaire induit par les collyres: a prpos de 3 observations . Bull Soc Ophthalmol Fr . 1980;80:41-45. 29. Herman DC, Bartley GB. Corneal opacities secondary to topical naphazoline and antazoline (Albalon-A) . Am J Ophthalmol . 1987;103:110-111. 30. Aronson SB, Yamamoto EA. Ocular hypersensitivity to epinephrine . Invest Ophthalmol . 1966;5:75-80. 31. Hill K. What's the angle on mydriasis? Arch Ophthalmol . 1968;79:804.Crossref 32. Lee PF. The influence of epinephrine and phenylephrine on intraocular pressure . Arch Ophthalmol . 1958;60:863-867.Crossref 33. Cohen SC. Antistene eyedrops . Am J Ophthalmol . 1952;35:1704-1705. 34. Wilson FM. Adverse external ocular effects of topical ophthalmic medications . Surv Ophthalmol . 1979;24:57-88.Crossref 35. Isenberg SJ, Green BF. Effect of phenylephrine hydrochloride on conjunctival Po2 . Arch Ophthalmol . 1984;102:1185-1186.Crossref 36. Kully BM. The use and abuse of nasal vasoconstrictor medications . JAMA . 1945;127:307-310.Crossref 37. Feinberg SM, Friedlaender SJ. Nasal congestion from frequent use of privine hydrochloride . JAMA . 1945;128:1095-1096.Crossref 38. Fennenbaum JI. Allergic rhinitis . Paterson R, ed. Allergic Diseases: Diagnosis and Management . 2nd ed. Philadelphia, Pa: JB Lippincott; 1980:87. 39. Schiller IW. Deleterious effects of privine hydrochloride . N Engl J Med . 1945;232:333-335. 40. Sternberg L. The abuse of vasoconstrictors in hay fever and vasomotor rhinitis . N Y State J Med . 1944;44:1573-1574. 41. Shaffer RN. Autonomic ocular drugs . Invest Ophthalmol . 1964;3:498-499. 42. Abelson MB, Butrus SI, Weston JH, Rosner B. Tolerance and absence of rebound vasodilation following topical ocular decongestant usage . Ophthalmology . 1984;91:1364-1367.Crossref 43. Grossmann EE, Lehman RH. Ophthalmic use of tyzine: a clinical study of this new vasoconstrictor . Am J Ophthalmol . 1956;42:121-123. 44. Menger HC. New ophthalmic decongestant, tetrahydrozoline hydrochloride: clinical use in 1,156 patients with conjunctival irritation . JAMA . 1959;170:178-179.Crossref 45. Stokes JJ. Clinical evaluation of tetrahydrozoline ophthalmic solution . J Med Assoc Ga . 1958;47:540-541. 46. Mamelok AE. Allergic conjunctivitis . Cutis . 1976;17:244-248. 47. Spector SL, Raizman MB. Conjunctivitis medicamentosa . J Allergy Clin Immunol . 1994;94:134-136.Crossref 48. Liesegang TJ. Bulbar conjunctival follicles associated with dipivefrin therapy . Ophthalmology . 1985;92:228-233.Crossref 49. Fisher AA, Pascher F, Kanof NB. Allergic contact dermatitis due to ingredients of vehicles: a 'vehicle tray' for patch testing . Arch Dermatol . 1971;104:286-290.Crossref 50. Fisher AA, Stillman MA. Allergic contact sensitivity to benzalkonium chloride: cutaneous, ophthalmic, and general medical implications . Arch Dermatol . 1972;106:169-171.Crossref 51. Gasset AR, Ishii Y, Kaufman HE. Cytotoxicity of ophthalmic preservatives . Am J Ophthalmol . 1974;78:98-105. 52. Lemp MA, Zimmerman LE. Toxic endothelial degeneration in ocular surface disease treated with topical medications containing benzalkonium chloride . Am J Ophthalmol . 1988;105:670-673. 53. Sussman JD, Friedman M. Irritation of rabbit eye caused by contact-lens wetting solutons . Am J Ophthalmol . 1969;68:703-706. 54. Theodore FH, Schlossman A. Ocular Allergy . Baltimore, Md: Williams & Wilkins; 1958:64-77. 55. Raymond JZ, Gross PR. EDTA: preservative dermatitis . Arch Dermatol . 1969;100:436-440.Crossref 56. IMS America Ltd staff. Ophthalmic decongestants, in US pharmaceutical market: drug store and hospital purchases. Presented at the Plymouth Meeting of IMS America Ltd; January 1990-June 1991; Plymouth, Pa.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150040005

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.

Lucas-Glass, Tina C.;Baratz, Keith H.;Nelson, Leif R.;Hodge, David O.;Bourne, William M.;Nelson,

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150042006pmid: 9006423

Abstract Objective: To evaluate the corneal endothelial morphometric measures of the contralateral, clinically uninvolved eye of patients with the iridocorneal endothelial (ICE) syndrome. Design: A retrospective review of the specular microscopic photographs of the contralateral corneal endothelium of all patients with ICE syndrome seen at Mayo Clinic, Rochester, Minn. Setting: Ophthalmology department, Mayo Clinic. Participants: Twenty-eight patients with unilateral ICE syndrome who had bilateral endothelial photographs (ICE group) and 28 normal, age-matched control subjects (control group). Main Outcome Measures: Percentage of hexagonal cells, coefficient of variation of cell area, and endothelial cell density. Methods: For each patient and control, 100 endothelial cells were digitized from projected endothelial photomicrographs of the central corneas in the uninvolved eyes. Results: A statistically significant decrease was noted in the mean percentage of hexagonal cells (ICE, 62%; control, 69%; P=.002), and an increase was noted in the mean coefficient of variation of cell area (ICE, 0.28; control, 0.25; P=.02) in the patients with ICE syndrome compared with normal, age-matched controls. The mean endothelial cell density did not differ significantly between the 2 groups (ICE, 2588; control, 2759; P=.10). Conclusion: Our data suggest that the clinically uninvolved, contralateral eyes in patients with ICE syndrome have subclinical endothelial abnormalities as evidenced by a relatively low percentage of hexagonal cells and a relatively high coefficient of variation of cell area. References 1. Shields MB. Progressive essential iris atrophy, Chandler's syndrome, and the iris nevus (Cogan-Reese) syndrome: a spectrum of disease . Surv Ophthalmol . 1979;24:3-20.Crossref 2. Cogan DG, Reese AB. A syndrome of iris nodules, ectopic Descemet's membrane, and unilateral glaucoma . Doc Ophthalmol . 1969;26:424-433.Crossref 3. Henderson JW, Benedict WL. Essential progressive atrophy of the iris . Am J Ophthalmol . 1940;23:644-650. 4. Scheie HG, Yanoff M. Iris nevus (Cogan-Reese) syndrome . Arch Ophthalmol . 1975;93:963-970.Crossref 5. Chandler PA. Atrophy of the stroma of the iris . Am J Ophthalmol . 1956;41:607-615. 6. Wood DJ. Melanosis of the iris and new formation of a hyaline membrane on its surface . Br J Ophthalmol . 1928;12:140-146.Crossref 7. Wilson MC, Shields MB. A comparison of the clinical variations of the iridocorneal endothelial syndrome . Arch Ophthalmol . 1989;107:1465-1468.Crossref 8. Bourne WM. Partial corneal involvement in the iridocorneal endothelial syndrome . Am J Ophthalmol . 1982;94:774-781.Crossref 9. Hirst LW, Quigley HA, Stark WJ. Specular microscopy of iridocorneal endothelial syndrome . Am J Ophthalmol . 1980;89:11-21. 10. Ullern M, Massin M, Pozzo J, Boureau C. Apport de la microscopie speculaire dans le diagnostic du syndrome endothelial irido-corneen . J Fr Ophthalmol . 1985;8:721-728. 11. Campbell DG, Shields MB, Smith TR. The corneal endothelium and the spectrum of essential iris atrophy . Am J Ophthalmol . 1978;86:317-324. 12. Eagle RC, Font RL, Yanoff M, Fine BS. Proliferative endotheliopathy with iris abnormalities . Arch Ophthalmol . 1979;97:2104-2111.Crossref 13. Eagle RC, Font RL, Yanoff M, Fine BS. The iris naevus (Cogan-Reese) syndrome: light and electron microscopic observations . Br J Ophthalmol . 1980;64:446-452.Crossref 14. Bahn CF, Falls HF, Varley GA, Meyer RF, Edelhauser HF. Classification of corneal endothelial disorders based on neural crest origin . Ophthalmology . 1984;91:558-563.Crossref 15. Eagle RC, Shields JA. Iridocorneal endothelial syndrome with contralateral guttate endothelial dystrophy . Ophthalmology . 1987;94:862-870.Crossref 16. Alvarado JA, Murphy CG, Maglio M, Hetherington J. Pathogenesis of Chandler's syndrome, essential iris atrophy and the Cogan-Reese syndrome . Invest Ophthalmol Vis Sci . 1986;27:853-882. 17. Tsai CS, Ritch R, Straus SE, Perry HD, Hsieh FY. Antibodies to Epstein-Barr virus in iridocorneal endothelial syndrome . Arch Ophthalmol . 1990;108:1572-1576.Crossref 18. Alvarado JA, Underwood JL, Green WR, et al. Detection of herpes simplex viral DNA in the iridocorneal endothelial syndrome . Arch Ophthalmol . 1994;112:1601-1609.Crossref 19. Fine M, Barkan H. Essential progressive iris atrophy . Am J Ophthalmol . 1937;20:277-280. 20. Gedda L, Berard-Magistretti DS. Atrofia ereditaria progressiva dell' iride . Acta Genet Med . 1959;8:39-64. 21. Blum JV, Allen JH, Holland MG. Familial bilateral essential iris atrophy (group 2) . Trans Am Acad Ophthalmol Otolaryngol . 1962;66:493-500. 22. Gassett AR, Worthen DM. Keratoconus and Chandler's syndrome . Ann Ophthalmol . 1974;6:819-820. 23. Cross HE, Maumenee AE. Progressive spontaneous dissolution of the iris . Surv Ophthalmol . 1973;18:186-199. 24. Kaiser-Kupfer M, Kuwabara T, Kupfer C. Progressive bilateral essential iris atrophy . Am J Ophthalmol . 1977;83:340-346. 25. Shields MB, Campbell DG, Simmons RJ. The essential iris atrophies . Am J Ophthalmol . 1978;85:749-759. 26. Kupfer C, Kaiser-Kupfer Ml, Datiles M, McCain L. The contralateral eye in the iridocorneal endothelial (ICE) syndrome . Ophthalmology . 1983;90:1343-1350.Crossref 27. Frangoulis MA, Sherrard ES, Kerr Muir MG, Buckley RJ. Clinical features of iridocorneal endothelial syndrome . Trans Ophthalmol Soc U K . 1985;104:775-781. 28. Blair SD, Seabrooks D, Shields WJ, Pillai S, Cavanagh HD. Bilateral progressive essential iris atrophy and keratoconus with coincident features of posterior polymorphous dystrophy: a case report and proposed pathogenesis . Cornea . 1992;11:255-261.Crossref 29. Hemady RK, Patel A, Blum S, Nirankari VS. Bilateral iridocorneal endothelial syndrome: case report and review of the literature . Cornea . 1994;13:368-372.Crossref 30. Laing RA, Sandstrom MM, Berrespi AR, Leibowitz HM. Changes in the corneal endothelium as a function of age . Exp Eye Res . 1976;22:587-594.Crossref 31. Carlson KH, Bourne WM, McLaren JW, Brubaker RF. Variations in human corneal endothelial cell morphology and permeability to fluorescein with age . Exp Eye Res . 1988;47:27-51.Crossref 32. Bland JM, Altman DG. Matching . BMJ . 1994;309:1128.Crossref 33. Kupfer C, Kaiser-Kupfer Ml. Observations on the developmental anomalies of the anterior chamber angle with reference to the pathogenesis of congenital glaucomas . Am J Ophthalmol . 1979;88:424-426. 34. Knudson AG. Genetics of human cancer . Ann Rev Genet . 1986;20:231-251.Crossref 35. Knudson AG. Retinoblastoma: a prototypic hereditary neoplasm . Semin Oncol . 1978;5:57-60. 36. Waring GO, Bourne WM, Edelhauser HF, Kenyon KR. The corneal endothelium . Ophthalmology . 1982;89:531-590.Crossref 37. Polack FM, Bourne WM, Forstot SL, Yamaguchi T. Scanning electron microscopy of posterior polymorphous corneal dystrophy . Am J Ophthalmol . 1980;89:574-584. 38. Henriquez AS, Kenyon KR, Dohlman CH, et al. Morphologic characteristics of posterior polymorphous dystrophy: a study of nine corneas and review of the literature . Surv Ophthalmol . 1984;29:139-147.Crossref 39. Waring GO. Posterior collagenous layer of the cornea . Arch Ophthalmol . 1982;100:122-134.Crossref 40. Johnson BL, Browns I. Posterior polymorphous dystrophy: a light and EM study . Br J Ophthalmol . 1978;62:89-96.Crossref 41. Rodrigues MM, Stulting RD, Waring GO. Clinical, electron microscopic and immunohistochemical study of the corneal endothelium and Descemet's membrane in the iridocorneal endothelial syndrome . Am J Ophthalmol . 1986;101:16-27.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150046007

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 titled "Changes in Descemet Membrane and Endothelium After Corneal Epithelial Abrasion Alone and With Photorefractive Keratectomy in Rabbits," published in the September Archives (1996;114:1105-1108), Figure 4 was faultily cropped during processing for publication. Figure 4 is reprinted correctly here. The journal regrets the error.

Maus, Todd L.;Larsson, Lill-Inger;McLaren, Jay W.;Brubaker, Richard F.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150047008pmid: 9006424

Abstract Objective: To compare the efficacy of topical 2% dorzolamide hydrochloride (Trusopt) as a suppressor of aqueous humor flow in the human eye with the efficacy of systemically administered acetazolamide (Diamox). Design: A randomized, double-masked, placebo-controlled study of 40 human subjects in 2 academic centers. The effect of dorzolamide on aqueous humor flow was compared with that of acetazolamide as measured by the rate of clearance of topically applied fluorescein. Results: Acetazolamide reduced aqueous flow from 3.18±0.70 (mean±SD) to 2.23±0.48 μL per minute, a reduction of 30% (P<.001), and dorzolamide reduced the flow to 2.65±0.64 μL per minute, a reduction of 17% (P<.001). The difference between the effect of acetazolamine and dorzolamide was significant (P<.001). When acetazolamide is added to dorzolamide, the aqueous flow was reduced further to 2.21±0.47 μL per minute, an additional reduction of 16% (P<.001). When dorzolamide was added to acetazolamide, no additional reduction was observed (P=.73). Similar effects were observed for intraocular pressure. Acetazolamide reduced pressure from 12.5±2.2 (mean±SD) to 10.1±2.2 mm Hg, a decrease of 19% (P<.001) and dorzolamide reduced it to 10.8±2.1 mm Hg, or a decrease of 13% (P<.001). The greater effect of acetazolamide than dorzolamide was significant (P=.03). Conclusions: For reasons that are not known, the topically applied carbonic anhydrase inhibitor 2% dorzolamide hydrochloride is not as effective as systemically administered acetazolamide. Clinicians who prescribe dorzolamide should expect less of an ocular hypotensive effect than that experienced from systemically administered acetazolamide. References 1. Roblin RO, Clapp JW. The preparation of heterocyclic sulfonamides . J Am Chem Soc . 1950;72:4890-4892.Crossref 2. Miller WH, Dessert AM, Roblin RO Jr. Hererocyclic sulfonamide as carbonic anhydrase inhibitors . J Am Chem Soc . 1950;72:4893-4896.Crossref 3. Grant WM, Trotter RR. Diamox (acetazolamide) in treatment of glaucoma . Arch Ophthalmol . 1954;51:735-739.Crossref 4. Becker B. Decrease in intraocular pressure in man by a carbonic anhydrase inhibitor, Diamox: a preliminary report . Am J Ophthalmol . 1954;37:13-15. 5. Breinin GM, Gortz H. Carbonic anhydrase inhibitor acetazolamide (Diamox): a new approach to the therapy of glaucoma . Arch Ophthalmol . 1954;52:333-348.Crossref 6. Maren TH, Haywood JR, Chapman SK, Zimmerman TZ. The pharmacology of methazolamide in relation to the treatment of glaucoma . Invest Ophthalmol . 1977;16:730-742. 7. Wistrand PJ, Garg LCL. Evidence of a high-activity C type of carbonic anhydrase in human ciliary processes . Invest Ophthalmol Vis Sci . 1979;18:802-806. 8. Wistrand PJ, Schenholm M, Lonnerholm G. Carbonic anhydrase isoenzymes CA I and CA II in human eye . Invest Ophthalmol Vis Sci . 1986;27:419-428. 9. Maren TH, Jankowska L, Sanyal G, Edelhauser HF. The transcorneal permeability of sulfonamide carbonic anhydrase inhibitors and their effect on aqueous humor secretion . Exp Eye Res . 1983;36:457-480.Crossref 10. Stein A, Pinke R, Krupin T, et al. The effect of topically administered carbonic anhydrase inhibitors on aqueous humor dynamics in rabbits . Am J Ophthalmol . 1983;95:222-228.Crossref 11. Lewis RA, Schoenwald RD, Eller MG, Barfknecht CF, Phelps CD. Ethoxzolamide analogue gel . Arch Ophthalmol . 1984;102:1821-1824.Crossref 12. Schoenwald RD, Eller MG, Dixson JA, Barfknecht CF. Topical carbonic anhydrase inhibitors . J Med Chem . 1984;27:810-812.Crossref 13. Kalina PH, Shetlar DJ, Lewis RA, Kullerstrand U, Brubaker RF. 6-Amino-2-benzothiazole-sulfonamide: the effect of a topical carbonic anhydrase inhibitor on aqueous humor formation in the normal human eye . Ophthalmology . 1988;95:772-777.Crossref 14. Sugrue MF, Mallorga P, Schwam H, Baldwin JJ, Ponticello GS. A comparison of L-671,152 and MK-927, two topically effective ocular hypotensive carbonic anhydrase inhibitors, in experimental animals . Curr Eye Res . 1990;9:607-615.Crossref 15. Sugrue MF, Gautheron P, Schmitt C, et al. On the pharmacology of L-645,151: a topically effective ocular hypotensive carbonic anhydrase inhibitor . J Pharmacol Exp Ther . 1985;232:534-540. 16. Ponticello GS, Freedman MB, Habecker CN, et al. Thienothiopyran-2-sulfonamides: a novel class of water-soluble carbonic anhydrase inhibitors . J Med Chem . 1987;30:591-597.Crossref 17. Bron AM, Lippa EA, Hofmann HM, etal. MK-927: a topically effective carbonic anhydrase inhibitor in patients . Arch Ophthalmol . 1989;107:1143-1146.Crossref 18. Pfeiffer N, Hennekes R, Lippa EA, Grehn F, Garus H, Brunner-Ferber FL. A single dose of the topical carbonic anhydrase inhibitor MK-927 decreases IOP in patients . Br J Ophthalmol . 1990;74:405-408.Crossref 19. Matuszewski BK, Constanzer ML. Indirect chiral separation and analyses in human biological fluids of the stereoisomers of a thienothiopyran-2-sulfonamide (Trusopt), a novel carbonic anhydrase inhibitor with two chiral centers in the molecule . Chirality . 1992;4:515-519.Crossref 20. Kitazawa Y, Azuma I, Iwata K, et al. Dorzolamide, a topical carbonic anhydrase inhibitor: a two-week dose-response study in patients with glaucoma or ocular hypertension . J Glaucoma . 1994;3:275-279.Crossref 21. Lippa EA, Carlson L-E, Ehinger B, et al. Dose response and duration of action of dorzolamide, a topical carbonic anhydrase inhibitor . Arch Ophthalmol . 1992;110:495-499.Crossref 22. Lippa EA, Schuman JS, Higginbotham EJ, et al. MK-507 versus sezolamide: comparative efficacy of two topically active carbonic anhydrase inhibitors . Ophthalmology . 1991;98:308-313.Crossref 23. Gunning FP, Greve EL, Bron AM, et al. Two topical carbonic anhydrase inhibitors sezolamide and dorzolamide in Gelrite vehicle: a multiple-dose efficacy study . Graefes Arch Clin Exp Ophthalmol . 1993;231:384-388.Crossref 24. Wilkerson M, Cyrlin M, Lippa EA, et al. Four-week safety and efficacy study of dorzolamide, a novel, active topical carbonic anhydrase inhibitor . Arch Ophthalmol . 1993;111:1343-1350.Crossref 25. Yamazaki Y, Miyamoto S, Sawa M. Effect of MK-507 on aqueous humor dynamics in normal human eyes . Jpn J Ophthalmol . 1994;38:92-96. 26. The MK-507 Clinical Study Group. Long-term glaucoma treatment with MK-507, dorzolamide, a topical carbonic anhydrase inhibitor . J Glaucoma . 1995;4:6-10. 27. Strahlman E, Tipping R, Vogel R, the International Dorzolamide Study Group. A double-masked, randomized 1-year study comparing dorzolamide (Trusopt), timolol, and betaxolol . Arch Ophthalmol . 1995;113:1009-1016.Crossref 28. Wang R-F, Serle JB, Podos SM, Sugrue MF. MK-507 (L-671,152), a topically active carbonic anhydrase inhibitor, reduces aqueous humor production in monkeys . Arch Ophthalmol . 1991;109:1297-1299.Crossref 29. Johnson S, Coakes RL, Brubaker RF. A simple photogrammetric method of measuring anterior chamber volume . Am J Ophthalmol . 1978;85:469-474. 30. Brubaker RF. Clinical evaluation of the circulation of aqueous humor . In: Tasman W, Jaeger EA, eds. Duane's Clinical Ophthalmology . Philadelphia, Pa: JB Lippincott; 1990;3(chap 46):1-11. 31. Brubaker RF. Flow of aqueous humor in humans . Invest Ophthalmol Vis Sci . 1991;32:3145-3166. 32. Dixon WJ, Massey JF Jr. Introduction to Statistical Analysis . New York, NY: McGraw-Hill Book Co; 1969:516. 33. Dailey RA, Brubaker RF, Bourne WM. The effects of timolol maleate and acetazolamide on the rate of aqueous formation in normal human subjects . Am J Ophthalmol . 1982;93:232-237. 34. Topper JE, Brubaker RF. Effects of timolol, epinephrine, and acetazolamide on aqueous flow during sleep . Invest Ophthalmol Vis Sci . 1985;26:1315-1319. 35. McCannel CA, Heinrich SR, Brubaker RF. Acetazolamide but not timolol lowers aqueous humor flow in sleeping humans . Graefes Arch Clin Exp Ophthalmol . 1992;230:518-520.Crossref 36. Gharagozloo NZ, Relf SJ, Brubaker RF. Aqueous flow is reduced by the alpha-adrenergic agonist, apraclonidine hydrochloride (ALO 2145) . Ophthalmology . 1988;95:1217-1220.Crossref 37. Reiss GR, Brubaker RF. The mechanism of betaxolol, a new ocular hypotensive agent . Ophthalmology . 1983;90:1369-1372.Crossref 38. Lee DA, Topper JE, Brubaker RF. Effect of clonidine on aqueous humor flow in normal human eyes . Exp Eye Res . 1984;38:239-246.Crossref 39. Gaul GR, Will NJ, Brubaker RF. Comparison of a noncardioselective β-adrenoceptor blocker and a cardioselective blocker in reducing aqueous flow in humans . Arch Ophthalmol . 1989;107:1308-1311.Crossref 40. Yablonski ME, Zimmerman TJ, Waltman SR, Becker B. A fluorophotometric study of the effect of topical timolol on aqueous humor dynamics . Exp Eye Res . 1978;27:135-142.Crossref 41. Coakes RL, Brubaker RF. The mechanism of timolol in lowering intraocular pressure: in the normal eye . Arch Ophthalmol . 1978;96:2045-2048.Crossref 42. Larsson L-I, Rettig ES, Brubaker RF. Aqueous flow in open-angle glaucoma . Arch Ophthalmol . 1995;113:283-286.Crossref 43. Larsson L-I, Rettig ES, Sheridan PT, Brubaker RF. Aqueous humor dynamics in low-tension glaucoma . Am J Ophthalmol . 1993;116:590-593. 44. Gharagozloo NZ, Baker RH, Brubaker RF. Aqueous dynamics in exfoliation syndrome . Am J Ophthalmol . 1992;114:473-478. 45. Brown JD, Brubaker RF. A study of the relation between intraocular pressure and aqueous humor flow in the pigment dispersion syndrome . Ophthalmology . 1989;96:1468-1470.Crossref

Szlyk, Janet P.;Fishman, Gerald A.;Alexander, Kenneth R.;Revelins, Beatrise I.;Derlacki, Deborah J.;Anderson, Robert J.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150055009pmid: 9006425

Abstract Objectives: To assess the level of perceived difficulty experienced by patients with retinitis pigmentosa (RP) in the performance of everyday activities and to determine the correlation between patients' self-reported difficulty and clinical measures of visual function. Methods: One hundred sixty-seven patients with typical RP and Usher syndrome type 2, with a wide range of disease severity, rated their difficulty in the performance of 33 activities. We obtained data on visual acuity and visual field area for all patients, and electroretinogram (ERG) recordings on a subgroup of 49 of these patients. Results from the questionnaire were analyzed with factor analysis, and patients' self-reports were compared with their clinical data using correlational analyses and multiple regression. Results: The patients' questionnaire responses clustered into 6 factors: activities involving central vision, miscellaneous activities (no discernible common factor), activities related to mobility, driving, negotiating steps, and eating meals. Of the clinical tests, visual acuity was most strongly related to the patients' ratings of their difficulty in performance. Visual field area also was related to patients' self-assessments but not as strongly as visual acuity. Because visual field area and the ERG measures were correlated, adding ERG information did not improve predictability. Conclusions: In patients with RP, perceived difficulty in performing common tasks was most strongly related to level of visual acuity and visual fields. Although certain ERG amplitude measures did show positive correlations with some self-reported activities, overall, the ERG amplitude measures showed the least relationship with patients' self-reports. Our results provide insight into RP patients' perceived difficulties in performing everyday activities and the clinical measures of visual function that most highly correlate with these difficulties. References 1. Massof RW, Dagnelie G, Benzschawel T, Palmer RW, Finkelstein D. First order dynamics of visual field loss in retinitis pigmentosa . Clin Vis Sci . 1990;5:1-26. 2. Massof RW, Finkelstein D. Two forms of autosomal dominant primary retinitis pigmentosa . Doc Ophthalmol . 1981;51:289-346.Crossref 3. Fishman GA. Retinitis pigmentosa: genetic percentages . Arch Ophthalmol . 1978;96:822-826.Crossref 4. Szlyk JP, Alexander KR, Severing K, Fishman GA. Assessment of driving performance in patients with retinitis pigmentosa . Arch Ophthalmol . 1992;110:1709-1713.Crossref 5. Berson EL, Rosner B, Sandberg MA, et al. A randomized trial of vitamin A and vitamin E supplementation for retinitis pigmentosa . Arch Ophthalmol . 1993;111:761-772.Crossref 6. Fishman GA, Farber MD. Derlacki DJ. X-linked retinitis pigmentosa: profile of clinical findings . Arch Ophthalmol . 1988;106:369-375.Crossref 7. Perlman JT. Retinitis pigmentosa: an improved clinical approach. In: Documenta Ophthalmologica Proceedings of the 14th ISCERG Symposium; May 10-14, 1976; Louisville, Ky. 8. Massof RW, Finkelstein D, Starr SJ, Kenyon KR, Fleischman JA, Maumenee IH. Bilateral symmetry of vision disorders in typical retinitis pigmentosa . Br J Ophthalmol . 1979;63:90-96.Crossref 9. Mangione CM, Phillips RS, Seddon JM, et al. Development of the Activities of Daily Vision Scale: a measure of visual functional status . Med Care . 1992;30:1111-1126.Crossref 10. Szlyk JP, Arditi A, Coffey-Bucci P, Laderman D. Self-report in functional assessment of low vision . J Vis Impairment Blindness . 1990;84:61-66. 11. International Standardization Committee. Standard for Clinical Electroretinography . Arch Ophthalmol . 1989;107:816-819.Crossref

Lyons, Jennifer L.;Rosenbaum, James T.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150063010pmid: 9006426

Abstract Background: Inflammatory bowel disease (IBD) and spondyloarthropathy (SA) such as Reiter syndrome may be characterized by diarrhea, arthritis, stomatitis, and uveitis. Objective: To determine if the characteristics of the eye disease could help distinguish these 2 diagnoses. Design: Seventeen patients with uveitis and IBD referred to a university clinic were compared retrospectively with 89 patients with uveitis and SA referred to the same clinic. Results: Twelve (80%) of the 15 patients with evaluable IBD had Crohn disease. In marked contrast to patients with SA, patients with IBD were usually female (82%). Whereas uveitis with SA was predominantly anterior, unilateral, sudden in onset, and limited in duration, patients with IBD frequently had uveitis that was bilateral, posterior, insidious in onset, and/or chronic in duration. Results for 89% of the patients with SA who underwent HLA-B27 typing were positive, compared with only 46% of such patients with IBD. Episcleritis, scleritis, and glaucoma were more common among patients with IBD. Arthritis did not easily distinguish the 2 groups, as 13 (76%) of the patients with IBD had a history of joint disease. In 10 (59%) of the patients with IBD, the diagnosis of uveitis preceded that of IBD. Conclusion: The hallmarks of uveitis can often distinguish SA and IBD. References 1. Mielants H, Erick M, Veys RJ, Cuvelier C, De Vos M. Repeat ileocolonoscopy in reactive arthritis . J Rheumatol . 1987;14:456-458. 2. Simenon G, Van Gossum A, Adler M, Rickaert F, Appelboom T. Macroscopic and microscopic gut lesions in seronegative spondyloarthritis . J Rheumatol . 1990;17:1491-1494. 3. Hopkins DJ, Horan E, Burton IL, et al. Ocular disorders in a series of 332 patients with Crohn's disease . Br J Ophthalmol . 1974;58:732-737.Crossref 4. Billson FA, De Dombal FT, Watkinson G, Goligher JC. Ocular complications of ulcerative colitis . Gut . 1967;8:102-106.Crossref 5. Knox DL, Schachat AP, Mustonen E. Primary, secondary, and coincidental ocular complications of Crohn's disease . Ophthalmology . 1984;91:163-173.Crossref 6. Rosenbaum JT. Characterization of uveitis associated with spondyloarthritis . J Rheumatol . 1989;16:792-796. 7. Ellis PP, Gentry JH. Ocular complications of ulcerative colitis . Am J Ophthalmol . 1964;58:779-785. 8. Salmon JF, Wright JP, Murray ADN. Ocular inflammation in Crohn's disease . Ophthalmology . 1991;98:480-484.Crossref 9. Ernst B, Lowder C, Meisler M, Gutman F. Posterior segment manifestations of inflammatory bowel disease . Ophthalmology . 1991;98:1272-1280.Crossref 10. Soukiasian SH, Foster CS, Raizman MB. Treatment strategies for scleritis and uveitis associated with inflammatory bowel disease . Am J Ophthalmol . 1994;118:601-611. 11. Rothova A, Buntenhuis HJ, Christiaans BJ, et al. Acute anterior uveitis (AAU) and HLA-B27 . Br J Rheumatol . 1983;22:144-145.Crossref 12. Rothova A, Van Veenendaal WG, Linssen A, Glasius E, Kijlstra A, de Jong PTVM. Clinical features of acute anterior uveitis . Am J Ophthalmol . 1987;103:137-145. 13. Mallas EG, Mackintosh P, Asquith P, Cook WT. Histocompatibility antigens in inflammatory bowel disease . Gut . 1976;17:906-910.Crossref 14. Mielants H, Veys EM. HLA-B27 related arthritis and bowel inflammation, I: sulfasalazine (Salazopyrin) in HLA-B27 related reactive arthritis . J Rheumatol . 1985;12:287-293. 15. Mielants H, Veys EM, Verbaclan H, De Vos M, Cuvelier C. HLA-B27 positive idiopathic acute anterior uveitis: a unique manifestation of subclinical gut inflammation . J Rheumatol . 1990;17:841-842. 16. Banares AA, Jover JA, Fernandez-Gutierrez B, et al. Bowel inflammation in anterior uveitis and spondyloarthropathy . J Rheumatol . 1995;22:1112-1117. 17. Ruby AJ, Jampol LM. Crohn's disease and retinal vascular disease . Am J Ophthalmol . 1990;110:349-353. 18. Duker JS, Brown GC, Brooks L. Retinal vasculitis in Crohn's disease . Am J Ophthalmol . 1987;102:664-668. 19. Joung RSK, Hodes BL, Cruse RP. Orbital pseudotumor and Crohn's disease . J Pediatr . 1981;99:250-252.Crossref

Brodsky, Michael C.;Conte, Felix A.;Taylor, David;Hoyt, Creig S.;Mrak, Robert E.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150068011pmid: 9006427

Abstract Objectives: To report our experience with sudden death in children with septo-optic dysplasia and to identify specific risk factors and suggest preventive measures to minimize mortality. Methods: Clinical data from 5 children with septooptic dysplasia who died suddenly and unexpectedly were evaluated retrospectively. Results: All children had corticotropin deficiency, all had thermoregulatory disturbances, and 4 children had diabetes insipidus. In at least 4 children, clinical deterioration was caused by fever and dehydration from a presumed viral illness, which appeared to precipitate adrenal crisis. Conclusions: Children with septo-optic dysplasia and hypocortisolism are at risk for sudden death during febrile illness. Thermoregulatory disturbances and dehydration from diabetes insipidus may potentiate clinical deterioration. Prevention of sudden death in septo-optic dysplasia requires early recognition and treatment of these major risk factors. References 1. de Morsier G. Etudes sur les dysraphies crânio-encéphaliques, III: agénésie du septum lucidum avec malformation du tractus optique: la dysplasie septooptique . Schweiz Arch Neurol Neurochir Psychiatr . 1956;77:267-292. 2. Hoyt WF, Kaplan SL, Grumbach MM, et al. Septo-optic dysplasia and pituitary dwarfism . Lancet . 1970;2:893-894.Crossref 3. Brodsky MC. Glasier CM. Optic nerve hypoplasia: clinical significance of associated central nervous system abnormalities on magnetic resonance imaging . Arch Ophthalmol . 1993;111:66-74.Crossref 4. Lemire RJ, Loeser JD, Leech RW, Alvord EC Jr. Normal and Abnormal Development of the Human Nervous System . New York, NY: Harper & Row Publishers Inc; 1975. 5. Huseman CA, Kelch RP, Hopwood NJ, et al. Sexual precocity in association with septo-optic dysplasia and hypothalamic hypopituitarism . J Pediatr . 1978;92:748-753.Crossref 6. Zaias B, Becker D. Septo-optic dysplasia: developmental or acquired abnormality? a case report . Trans Am Neurol Assoc . 1978;103:273-277. 7. Benoit Gonin JJ, David M, Feit JP, et al. La dysplasie septo-optique avec déficit en hormone antidiurétique et insufficance surrénale central . Nouv Presse Med . 1978;7:3327-3331. 8. Greenfield PS, Wilcox LM, Weiter JJ, Adelman L. Hypoplasia of the optic nerve in association with porencephaly . J Pediatr Ophthalmol Strabismus . 1980;17:75-80. 9. Donat JGF: Septo-optic dysplasia in an infant of a diabetic mother . Arch Neurol . 1981;38:590-591.Crossref 10. Michaud J, Mizrahi EM, Urich H. Agenesis of the vermis with fusion of the cerebellar hemispheres, septo-optic dysplasia and associated anomalies . Acta Neuropathol . 1982;56:161-166.Crossref 11. Kobori JA, Herrick MK, Urich H. Arrhinencephaly: the spectrum of associated malformations . Brain . 1987;110:237-260.Crossref 12. Patel H, Tze WJ, Crichton JU, et al. Optic nerve hypoplasia with hypopituitarism . AJDC . 1975;129:175-180. 13. Roessmann U, Velasco ME, Small EJ, Hori A. Neuropathology of 'septo-optic dysplasia' (de Morsier syndrome) with immunohistochemical studies of the hypothalamus and pituitary gland . J Neuropathol Exp Neurol . 1987;46:597-608.Crossref 14. Costello JM, Gluckman PD. Neonatal hypopituitarism: a neurological perspective . Dev Med Child Neurol . 1988;30:190-199.Crossref 15. Coulter CL, Leech RW, Schaefer GB, et al. Midline cerebral dysgenesis, dysfunction of the hypothalamic-pituitary axis, and fetal alcohol effects . Arch Neurol . 1993;50:771-775.Crossref 16. Werbel SS, Ober KP. Acute adrenal insufficiency . Endocrinol Metabol Clin North Am . 1993;22:303-328. 17. Cross KW, Hey DL, Kennaird DL, et al. Lack of temperature control in infants with abnormalities of the central nervous system . Arch Dis Child . 1971;46:437-446.Crossref 18. Karch SB, Urich H. Occipital encephalocele: a morphological study . J Neurol Sci . 1972;15:89-112.Crossref 19. Kyllerman M, Bager B, Bensch B, et al. Dyskinetic cerebral palsy, I: clinical categories, associated neurological abnormalities, and incidences . Acta Paediatr Scand . 1982;71:543-550.Crossref 20. Cooper PE. Disorders of the hypothalamus and pituitary gland . In: Joynt RJ, ed. Clinical Neurology . Philadelphia, Pa: JB Lippincott, 1991;3:1-116. 21. Shapiro WR, Williams GH, Plum F. Spontaneous recurrent hypothermia accompanying agenesis of the corpus callosum . Brain . 1969;92:423-436.Crossref 22. Guihard J, Velot-Lerou A, Poitrat C, et al. Hypothermie spontanée récidvante avec agénésie du corps calleux: syndrome de Shapiro (nouvelle observation) . Ann Pediatr . 1971;18:645-656. 23. Noël P, Hubert JP, Ectors M, et al. Agenesis of the corpus callosum associated with relapsing hypothermia: a clinico-pathological report . Brain . 1973;96:359-368.Crossref 24. Kaufman LM, Miller MT, MaFee MR. Magnetic resonance imaging of pituitary stalk hypoplasia: a discrete midline anomaly associated with endocrine abnormalities in septo-optic dysplasia . Arch Ophthalmol . 1989;107:1485-1489.Crossref 25. Kucharczyk W, Lenkinski R, Kucharczyk J, Henkelman RM. The effect of phospholipid vesicles on the NMR relaxation of water: an explanation for the MR appearance of the neurohypophysis? AJNR Am J Neuroradiol . 1990;11:693-700. 26. Kelly WM, Kucharczyk W, Kucharczyk J, et al. Posterior pituitary ectopia: an MR feature of pituitary dwarfism . Am J Neuroradiol . 1988;9:453-460. 27. Ultmann MC, Siegel SF, Hirsch WL, et al. Pituitary stalk and ectopic hyperintense T1 signal on magnetic resonance imaging: implications for anterior pituitary hormone dysfunction . AJDC . 1993;147:647-652. 28. Taback SP, Dean HJ, and Members of the Canadian Growth Hormone Advisory Comittee. Mortality in Canadian children with growth hormone (GH) deficiency receiving GH therapy 1967-1992 . J Clin Endocrinol Metab . 1996;81:1693-1696. 29. Hintz RL. Eternal vigilance: mortality in children with growth hormone deficiency . J Clin Endocrinol Metab . 1996;81:1691-1693. 30. Sherlock DA, McNicol LR. Anaesthesia and septo-optic dysplasia: implications of missed diagnosis in the peri-operative period . Anaesthesia . 1987;42:1302-1305.Crossref

Groessl, Sarah A.;Sires, Bryan S.;Lemke, Bradley N.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150073012pmid: 9006428

Abstract Objective: To measure any sex size differences in the bony nasolacrimal drainage systems in a normal, agematched population. Methods: A retrospective study of axial cut maxillofacial computed tomographic scans was conducted. Three levels of the bony nasolacrimal duct (NLD) system on the right and left sides were measured along the anteroposterior diameter. The data were analyzed using 2-tail t test, analysis of variance, and linear regression methods. Results: Scans from 71 adult patients (36 men and 35 women) were reviewed. Women were found to have a smaller bony diameter at the level of the lower fossa (P=.01) and the middle NLD (P=.06) compared with those of men. The adult inferior bony fossa increased in size with age in both men and women, while the middle NLD increased in size in men only. No significant size difference was found between the right and left side at any level. Conclusions: Size differences are found in measurements of bony nasolacrimal excretory systems in men vs women. Women have significantly smaller dimensions in the lower nasolacrimal fossa and the middle NLD. The anteroposterior dimension of the bony nasolacrimal canal at the fossa level enlarged in both sexes, with age coinciding with osteoporotic changes throughout the body. These quantitative anatomical observations provide a contributory factor to explain the increased prevalence of primary acquired NLD obstruction in women. References 1. Bartley GB. Acquired lacrimal drainage obstruction: an etiologic classification system, case reports and a review of the literature, I . Ophthal Plast Reconstr Surg . 1992;4:237-242.Crossref 2. Linberg JV, McCormick SA. Primary acquired nasolacrimal duct obstruction: a clinicopathologic report and biopsy technique . Ophthalmology . 1986;93:1055-1062.Crossref 3. Traquair HM. Chronic dacryocystitis: its causation and treatment . Arch Ophthalmol . 1941;26:165-180.Crossref 4. Roussos J, Bouza A. Essai d'explication par des factures hormonaux de la grande frequence d'apparition de la dacryocystite chronique chez les femmes plutot que chez les hommes . Bull Mem Soc Fr Opthalmol . 1973:96-99. 5. Zolli CL, Shannon GM. Dacryocystorhinostomy: a review of 119 cases . Ophthal Surg . 1982;13:905-910. 6. Tarbet KJ, Custer PL. External dacryocystorhinostomy: surgical success, patient satisfaction, and economic cost . Ophthalmology . 1995;102:1065-1070.Crossref 7. Mauriello JA, Palydowycz S, DeLuca. Clinicopathologic study of lacrimal sac and nasal mucosa in 44 patients with complete acquired nasolacrimal duct obstruction . Ophthal Plast Reconstr Surg . 1992;8:13-21.Crossref 8. Farkas LG. Anthropometry of the Head and Face . 2nd ed. New York, NY: Raven Press Ltd; 1994:255, 272-275. 9. Hyde KJ, Berger ST. Epidemic keratoconjunctivitis and lacrimal excretory system obstruction . Ophthalmology . 1988;95:1447-1449.Crossref 10. Wyngaarden JB, Smith LH, Bennett JC, ed. Cecil's Textbook of Medicine . 19th ed. Philadelphia, Pa: WB Saunders Co; 1992:1508, 1522, 1544, 1547. 11. Duke-Elder S. Textbook of Ophthalmology . London, England: Henry Kimpton; 1952;5:5302. 12. Meller J. Diseases of the lacrimal apparatus . Trans Ophthalmol Soc U K . 1929;49:233-311.

Johnson, Thomas E.;Tabbara, Khalid F.;Weatherhead, Robert G.;Kersten, Robert C.;Rice, Charles;Nasr, Amin M.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150077013pmid: 9006429

Abstract Objective: To evaluate the origin and biological behavior of secondary orbital squamous cell (SCC) and mucoepidermoid carcinoma. Methods: A retrospective review of 30 consecutive patients with SCC and mucoepidermoid carcinoma of the orbit seen over a period of 8 years at a large ophthalmic hospital in Saudi Arabia. Results: A total of 51 secondary orbital tumors were seen in the 8-year period from 1983 through 1991; 30 (60%) of the 51 cases were SCC. There were 16 male and 14 female patients, with an age range of 38 to 80 years and a mean age of 65 years. In 28 (93%) of the 30 patients, the tumor originated in the conjunctiva. Orbital involvement by conjunctival SCC was the most common cause of secondary orbital tumors encountered in patients older than 19 years. Four patients had concomitant paranasal sinus involvement, 4 patients exhibited intraocular invasion, and 2 others were found to have intracranial extension of the SCC. Six (20%) of the 28 patients developed regional lymph node metastases during the course of their illness. All patients were treated by orbital exenteration, with or without radiation therapy. Seven (23%) of the 28 patients died of their disease. Conclusions: Orbital SCC is an aggressive and lifethreatening condition. Most cases result from secondary extension of conjunctival SCC, a common disease in Saudi Arabia. Several factors contribute to the aggressiveness of conjunctival SCC in this geographic location, including continual exposure to UV rays, chronic irritation, and genetic factors. Delay in presentation for treatment, inadequate initial resection of conjunctival lesions, and the aggressive mucoepidermoid carcinoma variant of SCC are also factors contributing to orbital invasion. References 1. Henderson JW. Orbital Tumors . 3rd ed. New York, NY: Raven Press: 1994:343-360. 2. Rootman J, Robertson WD. Tumors . In: Rootman J, ed. Diseases of the Orbit . Philadelphia, Pa: JB Lippincott Co; 1988:121-123, 427, 440-441. 3. Tabbara KF, Kersten R, Daouk N, Blodi FC. Metastatic squamous cell carcinoma of the conjunctiva . Ophthalmology . 1988;95:318-321.Crossref 4. Zimmerman LE. Squamous cell carcinoma and related lesions of the bulbar conjunctiva . In: Boniuk M, ed. Ocular and Adnexal Tumors: New and Controversial Aspects . St Louis, Mo: CV Mosby Co; 1964:49-74. 5. Zimmerman LE. The cancerous, precancerous and pseudocancerous lesions of the cornea and conjunctiva . In: Rycroft PV, ed. Corneoplastic Surgery: Proceedings of the Second International Corneoplastic Conference . New York, NY: Pergamon Press; 1969:547-555. 6. Pizzarello LD, Jacobiec FA. Bowen's disease of the conjunctiva: a misnomer . In: Jacobiec FA, ed. Ocular and Adnexal Tumors . Birmingham, Ala: Aesculapius Publishing Co; 1978:553-571. 7. Iliff WJ, Marback R, Green WR. Invasive squamous cell carcinoma of the conjunctiva . Arch Ophthalmol . 1975;93:119-122.Crossref 8. Malik MO, El Sheikh EH. Tumors of the eye and adnexa in the Sudan . Cancer . 1979;44:293-303.Crossref 9. Clear AS, Chirambo MC, Hutt MS. Solar keratosis, pterygium, and squamous cell carcinoma of the conjunctiva in Malawi . Br J Ophthalmol . 1979;63:102-109.Crossref 10. Blodi FC. Squamous cell carcinoma of the conjunctiva . Doc Ophthalmol . 1973;34:93-108.Crossref 11. Shields JA. Bakewell B, Augsburger JJ, Flanagan JC. Classification and incidence of space-occupying lesions of the orbit: a survey of 645 biopsies . Arch Ophthalmol . 1984;102:1606-1611.Crossref 12. Bullock JD, Augsburger J. Squamous cell carcinoma of the orbit . Ann Ophthalmol . 1980;2:255-258. 13. Grutzmacher RD, Fraunfelder FT. Corneal and bulbar conjunctival tumors . In: Abbott RL, ed. Surgical Intervention in Corneal and External Diseases . Orlando, Fla: Grune & Stratton; 1987:119-139. 14. McDonnell JM, McDonnell PJ, Mounts P, Wu T-C, Green WR. Demonstration of papillomavirus capsid antigen in human conjunctival neoplasia . Arch Ophthalmol . 1986;104:1801-1805.Crossref 15. Donn WL. Climate and Ice Ages: Meteorology . 4th ed. New York, NY: McGraw-Hill Book Co; 1975:429. 16. Cooper JS, Pajak TF, Rubin PR. et al. Second malignancies in patients who have head and neck cancer: incidence, effect on survival and implications based on the RTOG experience . Int J Radiation Oncology Biol Phys . 1989;17:449-456.Crossref 17. de Vries N, Drexhage HA, de Waal LP, de Lange G, Snow GB. Human leukocyte antigens and immunoglobulin allotypes in head and neck cancer patients with and without multiple primary tumors . Cancer . 1987;60:957-961.Crossref 18. Nicholson DH, Herschler J. Intraocular extension of squamous cell carcinoma of the conjunctiva . Arch Ophthalmol . 1977;95:843-846.Crossref 19. Thackray AC, Lucas RB. Tumors of the major salivary glands . Atlas of Tumor Pathology . Washington, DC: Armed Forces Institute of Pathology; 1974;2:69-80. 20. Brownstein S. Mucoepidermoid carcinoma of the conjunctiva with intraocular invasion . Ophthalmology . 1981;88:1226-1230.Crossref 21. Rao NA, Font RL. Mucoepidermoid carcinoma of the conjunctiva . Cancer . 1976;38:1699-1709.Crossref 22. Searl SS, Krigstein HJ, Albert DM, Grove AS. Invasive squamous cell carcinoma with intraocular mucoepidermoid features: conjunctival carcinoma with intraocular invasion and diphasic morphology . Arch Ophthalmol . 1982;100:109-111.Crossref 23. Gamel JW, Eiferman RA, Guibor P. Mucoepidermoid carcinoma of the conjunctiva . Arch Ophthalmol . 1984;102:730-731.Crossref 24. Shields JA. Secondary orbital tumors . In: Shields JA, ed. Diagnosis and Management of Orbital Tumors . Philadelphia, Pa: WB Saunders Co; 1989:350-352. 25. Fraunfelder FT, Wingfield D. Management of intraepithelial conjunctival tumors and squamous cell carcinoma . Am J Ophthalmol . 1983;95:359-363. 26. Buus DR. Tse DT, Folberg R. Microscopically controlled excision of conjunctival squamous cell carcinoma . Am J Ophthalmol . 1994;117:97-102. 27. Reese AB. Epithelial tumors of the lid, conjunctiva, corneal and lacrimal sac . In: Reese AB, ed. Tumors of the Eye . 3rd ed. Hagerstown, Md: Harper & Row; 1976:55.

Kim, Eung K.;Cristol, Stephen M.;Geroski, Dayle H.;McCarey, Bernard E.;Edelhauser, Henry F.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150083014pmid: 9006430

Abstract Objective: To characterize the mechanism by which air bubbles damage the corneal endothelium during phacoemulsification. Materials and Methods: A series of experiments was conducted to expose the corneal endothelium of New Zealand white rabbit and human eyes that were obtained from an eye bank to air under different conditions. Phacoemulsification at different power settings and irrigation with and without the introduction of air into the anterior chamber were performed. Corneal endothelial perfusion experiments were conducted with air bubbles that were introduced into the perfusion chamber for 2 seconds to 1 hour. Air was also injected into the anterior chambers of anesthetized rabbits for 2 minutes to 3 hours. Corneas were stained with nitrobenzoxadiazole-phallacidin and examined with fluorescence microscopy. Selected corneas were also examined with scanning and transmission electron microscopy. Results: Intracameral air bubbles during phacoemulsification, irrigation, and perfusion studies resulted in a severe injury to the corneal endothelium in as little as 20 seconds. Intracameral air bubbles in a living rabbit resulted in a slower injury that was morphologically different from the more rapid injury. Conclusions: Air bubbles in intraocular fluids with a high surface tension can cause a ring-shaped pattern of damage to the corneal endothelium. The mechanism that caused this pattern of damage appears to be a surface tension phenomenon. References 1. Van Horn DL, Edelhauser HF, Aaberg TM, Pederson HJ. In vivo effects of air and sulfur hexafluoride gas on rabbit corneal endothelium . Invest Ophthalmol Vis Sci . 1972;11:1028-1036. 2. Lee DA, Wilson MR, Yoshizumi MO, Hall M. The ocular effects of gases when injected into the anterior chamber of rabbit eyes . Arch Ophthalmol . 1991;92:571-575.Crossref 3. Eiferman RA, Wilkins EL. The effect of air on human corneal endothelium . Am J Ophthalmol . 1981;92:328-331. 4. Leibowitz HM, Laing RA, Sandstrom M. Corneal endothelium . Arch Ophthalmol . 1974;92:227-230.Crossref 5. Tsubota K, Laing RA, Chiba K, Kenyon KR. Effects of air and irrigating solutions on the corneal endothelium . Cornea . 1988;7:115-121.Crossref 6. Beesley RD, Olson RJ, Brady SE. The effects of prolonged phacoemulsification time on the corneal endothelium . Ann Ophthalmol . 1986;18:216-219, 222. 7. Craig MT, Olson RJ, Mamalis N, Olson RJ. Air bubble endothelial damage during phacoemulsification in human eye bank eyes: the protective effects of Healon and Viscoat . J Cataract Refract Surg . 1990;16:597-602.Crossref 8. Monson MC, Tamura M, Mamalis N, Olson RJ, Olson RJ, Protective effects of Healon and Occucoat against air bubble endothelial damage during ultrasonic agitation of the anterior chamber . J Cataract Refract Surg . 1991;17:613-616.Crossref 9. Norn MS. Corneal thickness after cataract extraction with air in the anterior chamber . Acta Ophthalmol (Copenh) . 1975;53:747-750.Crossref 10. Hirst LW, Snip RC, Stark WJ, Maumenee AE. Quantitative corneal endothelial evaluation in intraocular lens implantation and cataract surgery . Am J Ophthalmol . 1977;84:775-780. 11. McCarey BE, Edelhauser HF, Van Horn DL. Functional and structural changes in the corneal endothelium during in vitro perfusion . Invest Ophthalmol Vis Sci . 1973;12:410-417. 12. Fujino Y, Tanishima T. Actin in wound-healing of rabbit corneal endothelium, I: study by immunoperoxidase method . Jpn J Ophthalmol . 1987;31:384-392. 13. Fujino Y, Tanishima T. Actin in wound-healing of rabbit corneal endothelium, II: study by nitrobenzoxadiazole-phallacidin method . Jpn J Ophthalmol . 1987;31:393-404. 14. Kennedy JR, Williams RW, Gray JP. Use of Peldri II (a fluorocarbon solid at room temperature) as an alternative to critical point drying for biological tissues . J Electron Microsc Tech . 1989;11:117-125.Crossref 15. Kim EK, Geroski DH, Holley GP, Urken SI, Edelhauser HF. Corneal endothelial cytoskeletal changes in F-actin with aging, diabetes, and after cytochalasin exposure . Am J Ophthalmol . 1992;114:329-335. 16. Hills BA. The Biology of Surfactant . New York, NY: Cambridge University Press; 1988:171. 17. Weast RC, ed. CRC Handbook of Chemistry and Physics . 58th ed. Boca Raton, Fla: CRC Press Inc; 1977:C-270, F-43, F-45, F-47. 18. Dean JA, ed. Lange's Handbook of Chemistry . 13th ed. New York, NY: McGrawHill Book Co; 1985:sect 10. 19. Jacobson BS. Interaction of the plasma membrane with the cytoskeleton: an overview . Tissue Cell . 1983;15:829-852.Crossref 20. Lester GR. Contact angles of liquids at deformable solid surfaces . J Colloid Sci . 1961;16:315-326.Crossref 21. Adam NK. The Physics and Chemistry of Surfaces . Oxford, England: Clarendon Press; 1930:7. 22. Svensson B, Mellerio J. Phaco-emulsification causes the formation of cavitation bubbles . Curr Eye Res . 1994;13:649-653.Crossref 23. Holst A, Rolfsen W, Svensson B, Ollinger K, Lundgren B. Formation of free radicals during phacoemulsification . Curr Eye Res . 1993;12:359-365.Crossref 24. Olson LE, Marshall J, Rice NS, Andrews R. Effects of ultrasound on the corneal endothelium, I: the acute lesion . Br J Ophthalmol . 1978;62:134-144.Crossref 25. Zysset B, Fujimoto JG, Puliafito CA, Birngruber R, Deutsch TF. Picosecond optical breakdown: tissue effects and reduction of collateral damage . Lasers Surg Med . 1989;9:193-204.Crossref

Hu, Dan-Ning;McCormick, Steven A.;Ritch, Robert

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150091015pmid: 9006431

Abstract Objective: To culture iris pigment epithelium (IPE) from surgical iridectomy specimens of eyes with and without exfoliation syndrome. Methods: The IPE was treated to obtain a single cell suspension. Cells were cultured in Ham F12 nutrient mixture, which was supplemented with 30% fetal bovine serum, 50-mg/mL gentamicin, and 2-mmol/L glutamine. After confluence, the cells were detached using a 0.125% trypsin-0.01% edetic acid solution, resuspended, diluted, and subcultured. The IPE from primary cultures and subcultures was studied by transmission electron microscopy. Immunocytochemical staining was performed. Results: In the primary cultures of IPE from patients with exfoliation syndrome, curved, cross-banded, fine fibrils (diameter, 10-15 nm; periodicity, 10-14 nm) were found on the cell surface. Thicker fibrils (diameter, 24-48 nm; periodicity, 24-36 nm) were found external to the fine fibrils. Subcultures contained mainly fine fibrils. The IPE cells stained positively with anticytokeratin, S100 protein, and vimentin antibodies. Conclusion: Iris pigment epithelium can be successfully cultured from eyes with exfoliation syndrome. Studying the production of exfoliation material in vitro should provide information about the pathogenesis of exfoliation syndrome and about the nature of the exfoliation material. The cultivation of normal IPE from surgical specimens provides a source for the study of the growth regulation and pharmacophysiology of IPE in vitro. References 1. Ritch R. Exfoliation syndrome: the most common identifiable cause of openangle glaucoma . J Glaucoma . 1994;3:176-178. 2. Tenenbaum E, Kornblueth W. Cultivation of adult human iris in vitro . Arch Ophthalmol . 1958;60:312-318.Crossref 3. Barishak YR. In vitro behavior of the pigment cells of the retina and uvea of the adult human eye . Acta Ophthalmol Scand . 1960;38:339-346.Crossref 4. Ringvold A, Nicolaissen BJ. Culture of iris tissue from human eyes with and without pseudoexfoliation syndrome . Acta Ophthalmol Scand . 1990;68:310-316.Crossref 5. Hu D-N, McCormick SA, Pelton-Henrion K, Ritch R. Isolation and cultivation of human iris pigment epithelium . Invest Ophthalmol Vis Sci . 1993;33:2443-2453. 6. Prince AM. Streeten BW, Ritch R, et al. Preclinical diagnosis of pseudoexfoliation syndrome . Arch Ophthalmol . 1987;105:1076-1082.Crossref 7. Freddo T. Intercellular junctions of the iris epithelia in Macaca mulatta . Invest Ophthalmol Vis Sci . 1984;25:1094-1104. 8. Hu DN, DelMonte MA, Liu S. Maumenee IH. Morphology, phagocytosis, and vitamin A metabolism of cultured human retinal pigment epithelium . Birth Defects . 1982;18:67-79. 9. Runyon TE, McCombs WB, Holton OD, et al. Human ciliary body epithelium in culture . Invest Ophthalmol Vis Sci . 1983;24:687-696. 10. Smyth RJ, Kitada S, Lee DA. Growth of rabbit pigmented and nonpigmented ciliary body epithelium . Vision Res . 1994;34:137-141.Crossref 11. Hu DN, Ritch R, McCormick SA. Growth regulation of cultured human iris pigment epithelium . Invest Ophthalmol Vis Sci . 1993;34( (suppl) ):1389. 12. Ritch R. Exfoliation syndrome . In: Ritch R, Shields MB, Krupin T, eds. The Glaucomas . 2nd ed. St Louis, Mo: Mosby-Year Book Inc; 1996:993-1022. 13. Davanger M. Studies on the pseudoexfoliation material , von Graefe's Arch Clin Exp Ophthalmol . 1978;208:65-71.Crossref 14. Davanger M. On the ultrastructure and the formation of pseudo-exfoliation material . Acta Ophthalmol Scand . 1980;58:520-527.Crossref 15. Streeten BW, Gibson SA, Dark AJ. Pseudoexfoliative material contains an elastic microfibrillar-associated glycoprotein . Trans Am Ophthalmol Soc . 1986;84:304-320. 16. Streeten BW, Bookman L, Ritch R, et al. Pseudoexfoliative fibrillopathy in the conjunctiva: a relation to elastic fibers and elastosis . Ophthalmology . 1987;94:1439-1449.Crossref 17. Streeten BW, Dark AJ, Wallace RN, et al. Pseudoexfoliative fibrillopathy in the skin of patients with ocular pseudoexfoliation . Am J Ophthalmol . 1990;110:490-499. 18. Shimizu T, Futa R. Fine structure of pigment epithelium of iris in capsular glaucoma . von Graefe's Arch Clin Exp Ophthalmol . 1985;223:77-82.Crossref 19. Ringvold A. The distribution of exfoliation material in the iris from eyes with exfoliation syndrome (pseudoexfoliation of the lens capsule) . Virchows Arch . 1970;351:168-178.Crossref 20. Ghosh M, Speakman JS. The iris in senile exfoliation of the lens . Can J Ophthalmol . 1974;9:289-297. 21. Eagle RC Jr, Font RL, Fine BS. The basement membrane exfoliation syndrome . Arch Ophthalmol . 1979;97:510-515.Crossref 22. Asano N, Schlötzer-Schrehardt U, Naumann GOH. A histopathologic study of iris changes in pseudoexfoliation syndrome . Ophthalmology . 1995;102:1279-1290.Crossref

Brown, Jeremiah;Fingert, John H.;Taylor, Chris M.;Lake, Max;Sheffield, Val C.;Stone, Edwin M.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150097016pmid: 9006432

Abstract Objectives: To refine the dominant optic atrophy locus, OPA1, on chromosome 3q and to characterize the phenotype of a 6-generation family pedigree affected with this disease. Methods: Fifty-six family members had a complete eye examination. Clinical records of an additional 3 patients were reviewed. Goldmann perimetry and a 21-chip subtest of the Farnsworth-Munsell 100-Hue test were performed on selected patients. Affected patients, unaffected siblings, and potentially informative spouses were genotyped with short tandem repeat polymorphisms located on chromosome 3. The genotypic data were subjected to linkage analysis. Results: Thirty-four family members were found to be clinically affected. Most experienced vision loss (20/40 or poorer) in the first decade of life. Most (9 of the 16 eyes) progressed to 20/800 or poorer visual acuity by age 60 years, while 2 patients maintained visual acuities of 20/40 at that age. Affected patients had a 2- to 10-fold increase in the error score of a 21-chip subtest of the Farnsworth-Munsell 100-Hue test compared with age-matched unaffected family members. The optic nerve examination revealed temporal pallor and excavation in all affected individuals. Linkage analysis revealed significant lod scores with 9 markers. The highest lod score, 10.1 (u=0), was obtained with marker D3S2305. Analysis of recombinants narrowed the disease interval to approximately 3.8 centimorgans, flanked by D3S3669 (centromeric) and D3S1305 (telomeric). Conclusions: Most patients affected with dominant optic atrophy in this family progressed to legal blindness by middle age. Color vision testing is a sensitive method for detection of affected patients. The dominant optic atrophy locus, OPA1, has been refined by the identification of new flanking markers: D3S3669 (centromeric) and D3S1305 (telomeric). References 1. Kjer P. Infantile optic atrophy with dominant mode of inheritance: a clinical and genetic study of 19 Danish families . Acta Ophthalmol . 1959;54( (suppl) ):1-46. 2. Lyle WM. Genetic Risks . Waterloo, Ontario: University of Waterloo Press; 1993:360-367. 3. Eliott D, Traboulsi EI, Maumenee IH. Visual prognosis in autosomal dominant optic atrophy (Kjer type) . Am J Ophthalmol . 1993;115:360-367. 4. Hoyt CS. Autosomal dominant optic atrophy . Ophthalmology . 1980;87:245-250.Crossref 5. Johnston PB, Gaster RN, Smith VC, Tripathi RC. A clinicopathologic study of autosomal dominant optic atrophy . Am J Ophthalmol . 1979;88:868-875. 6. Kline LB, Glaser JS. Dominant optic atrophy: the clinical profile . Arch Ophthalmol . 1979;97:1680-1686.Crossref 7. Jacobson DM, Stone EM. Difficulty differentiating Leber's from dominant optic atrophy in a patient with remote visual loss . J Clin Neuro-ophthalmol . 1991;11:152-157. 8. Caldwell JBH, Howard RO, Riggs LA. Dominant juvenile optic atrophy . Arch Ophthalmol . 1971;85:133-147.Crossref 9. Smith P. Diagnostic criteria in dominantly inherited juvenile optic atrophy: a report of three new families . Am J Optom . 1972;49:183-200.Crossref 10. Eiberg H, Kjer B, Kjer P, Rosenberg T. Dominant optic atrophy (OPA1) mapped to chromosome 3q region. I . Hum Mol Genet . 1994;3:977-980.Crossref 11. Lunkes A, Hartung U, Magarino C. et al. Refinement of the OPA1 gene locus on chromosome 3q28-29 to a region of 2-8 cM, in one Cuban pedigree with autosomal dominant optic atrophy type Kjer . Am J Hum Genet . 1995;57:968-970. 12. Verriest G. Further studies on acquired deficiency of color discrimination . J Opt Soc Am A . 1963;53:185-195.Crossref 13. Stone EM, Nichols BE, Wolken MS, et al. New normative data for the Farnsworth-Munsell 100-Hue test . In: Drum B, ed. Color Vision Deficiencies, XI: Proceedings of the Eleventh Symposium of the International Research Group on Color Vision . Boston, Mass: Kluwer Academic Publishers; 1993. 14. Buffone GJ. Darlington GJ, Isolation of DNA from biological specimens without extraction with phenol . Clin Chem . 1985;31:164-165. 15. Heon E, Piguet B, Munier F, et al. Linkage of autosomal dominant radial drusen (Malattia leventinese) to chromosome 2p16-21 . Arch Ophthalmol . 1996;114:193-198.Crossref 16. Bassam BJ, Caetano-Anolles G, Gresshoff PM. Fast and sensitive silver staining of DNA in polyacrylamide gels . Anal Biochem . 1991;196:80-83.Crossref 17. Bonneau D, Souied E, Gerber S, et al. No evidence of genetic heterogeneity in dominant optic atrophy . J Med Genet . 1995;32:951-953.Crossref 18. Kjer P, Jensen OA, Klinken L. Histopathology of eye, optic nerve and brain in a case of dominant optic atrophy . Acta Ophthalmol . 1983;61:300-312.Crossref 19. Rice DS, Williams RW, Ward-Bailey P. et al. Mapping the Bst mutation on mouse chromosome 16 . Mamm Genome . 1995;6:546-548.Crossref

Johnston, Robert L.;Burdon, Michael A.;Spalton, David J.;Bryant, Stephen P.;Behnam, Joseph T.;Seller, Mary J.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150102017pmid: 9006433

Abstract Objectives: To perform DNA linkage studies in an extensive 5-generation British pedigree with dominant optic atrophy and to validate the efficacy of domiciliary screening for affected members. Methods: Family members received a domiciliary examination based on corrected visual acuity, color vision, visual field defects, and optic disc appearance; DNA linkage analysis was performed using 7 microsatellite markers on 3q27-qter. Results: Based on the results of the ophthalmic examination, 15 members could be classified as definitely affected, 1 probably affected, and 25 unaffected. Two-point linkage analysis gave significant maximum lod scores at u = 0.00, with the markers D3S3669, D3S3590, and D3S3642. A haplotype segregating with the disease was identified in affected individuals, including the probably affected subject. Informative meioses defined the disease interval between markers D3S1601 and D3S1265. Conclusions: Domiciliary screening was effective in identifying all 16 affected members of a British family with dominant optic atrophy. The typical clinical features were present. The location of the OPA1 gene in this new British family seems to be in the 3q27-28 region and is the same as that reported in Danish, Cuban, and French families, suggesting no genetic heterogeneity in this disorder. References 1. Lyle WM. Genetic Risks . Waterloo, Ontario: University of Waterloo Press; 1990. 2. Kjer P. Infantile optic atrophy with dominant mode of inheritance: a clinical and genetic study of 19 Danish families . Acta Ophthalmol . 1959;37( (suppl 54) ):1-146. 3. Hoyt CS. Autosomal dominant optic atrophy: a spectrum of disability . Ophthalmology . 1980;87:245-251.Crossref 4. Kline LB, Glaser JS. Dominant optic atrophy: the clinical profile . Arch Middle East Ophthalmol . 1979;97:1680-1686.Crossref 5. Eliott D, Traboulsi El, Maumenee IH. Visual prognosis in autosomal dominant optic atrophy (Kjer type) . Am J Ophthalmol . 1993;115:360-367. 6. Kjer P, Jensen OA, Klinken L. Histopathology of eye, optic nerve and brain in a case of dominant optic atrophy . Acta Ophthalmol . 1983;61:300-312.Crossref 7. Johnstone PB, Gaster RN, Smith VC, Tripathi R. A clinicopathologic study of autosomal dominant optic atrophy . Am J Ophthalmol . 1979;88:868-875. 8. McKusick VA. Mendelian Inheritance in Man . 10th ed. Baltimore, Md: The Johns Hopkins University Press; 1992. 9. Kivlin JD, Lovrien EW, Bishop T, Maumenee IH. Linkage analysis in dominant optic atrophy . Am J Hum Genet . 1983;35:1190-1195. 10. Eiberg H, Kjer B, Kjer P. Rosenberg T. Dominant optic atrophy (OPA1) mapped to chromosome 3q region, I: linkage analysis . Hum Mol Genet . 1994;3:977-980.Crossref 11. Lunkes A, Hartung U, Magarino C, et al. Refinement of the OPA1 gene locus on chromosome 3q28-q29 to a region of 2-8 cM, in one Cuban pedigree with autosomal dominant optic atrophy type Kjer . Am J Hum Genet . 1995;57:968-970. 12. Naylor SL, Moore S, Garcia D, et al. Mapping 638 STSs to regions of human chromosome 3 . Cytogenet Cell Genet . 1996;72:90-94.Crossref 13. Lathrop GM, Lalouel J-M. Easy calculations of lod scores and genetic risks on small computers . Am J Hum Genet . 1984;36:460-465. 14. Cottingham RW, Idury RM, Schaffer AA. Faster sequential genetic linkage computations . Am J Hum Genet . 1993;53:252-263. 15. Schaffer AA, Gupta SK, Shiram K, Cottingham RW. Avoiding recomputation in linkage analysis . Hum Hered . 1994;44:225-237.Crossref 16. O'Connell JR, Weeks DE. The VITESSE algorithm for exact multilocus linkage analysis via genotype set-recording and fuzzy inheritance . Nature Genet . 1995;11:402-408.Crossref 17. Dib C, Faure S, Fizames C, et al. A comprehensive genetic map of the human genome based on 5264 microsatellites . Nature . 1996;380:152-154.Crossref 18. Kjer B, Eiberg H, Kjer P, Rosenberg T. Dominant optic atrophy mapped to chromosome 3q region, II: clinical and epidemiological aspects . Acta Opththalmol Scand . 1996;74:3-7.Crossref 19. Bonneau D, Souied E, Gerber S, et al. No evidence of genetic heterogeneity in dominant optic atrophy . J Med Genet . 1995;32:951-953.Crossref

Leske, M. Cristina;Connell, Anthea M. S.;Wu, Suh-Yuh;Hyman, Leslie;Schachat, Andrew

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150107018pmid: 9006434

Abstract Objective: To present population-based data on type and extent of age-related lens opacities in the predominantly black population of the Barbados Eye Study. Design: Prevalence study. Setting and Participants: The Barbados Eye Study included 4709 participants (84% of those eligible), who were identified from a random sample of Barbadian-born citizens aged 40 to 84 years. Data Collection: Lens gradings at the slit lamp, obtained with the use of the Lens Opacities Classification System II. Main Outcome Measure: Prevalence of posterior subcapsular, nuclear, and cortical opacities (defined as a grade ≥2 in either eye), as well as prevalence of any lens changes (including history of previous cataract surgery and/or cataract too advanced to grade). Results: Overall, 41% of the Barbados Eye Study population had any lens changes, including 3% with aphakia or an intraocular lens. Among the population of African descent, cortical opacities (34%) were most prevalent, followed by nuclear (19%) and posterior subcapsular (4%) opacities. Prevalence of all opacity types increased with age (P<.001). Cortical and nuclear opacities were more frequent in women than men. When prevalence of a single kind of opacity was considered, 21% of participants had cortical only, 6% had nuclear only, and 0.4% had posterior subcapsular only; 13% had mixed opacities. Visual acuity loss to worse than 20/40 in the more affected eye was present in 48%, 26%, and 18% of nuclear only, posterior subcapsular only, and cortical only types, respectively, and in 53% of mixed opacities. Conclusions: The Barbados Eye Study provides the first prevalence data on different types of lens opacities in a large, predominantly black population. Whereas nuclear opacities are most common in white populations, cortical opacities were the most frequent type in the Barbados Eye Study, a finding of possible etiologic relevance. Other results highlight a higher frequency of opacities in women than men and a high prevalence of visual acuity loss in affected eyes. References 1. Kupfer C. The conquest of cataract: a global challenge . Trans Ophthalmol Soc UK . 1984;104:1-10. 2. Leske MC, Sperduto R. The epidemiology of senile cataract: a review . Am J Epidemiol . 1983;118:152-165. 3. Kahn HA, Leibowitz HM, Ganley JP, et al. The Framingham Eye Study, I: outline and major prevalence findings . Am J Epidemiol . 1977;106:17-32. 4. Sperduto RD, Seigel D. Senile lens and senile macular changes in a populationbased sample . Am J Ophthalmol . 1980;90:86-91. 5. Klein BEK, Klein R, Linton KLP. Prevalence of age-related lens opacities in a population: the Beaver Dam Eye Study . Ophthalmology . 1992;99:546-552.Crossref 6. Sperduto RD, Hiller R. The prevalence of nuclear, cortical, and posterior subcapsular lens opacities in a general population sample . Ophthalmology . 1984;91:815-818.Crossref 7. Adamsons I, Munoz B, Enger C, Taylor HR. Prevalence of lens opacities in surgical and general populations . Arch Ophthalmol . 1991;109:993-997.Crossref 8. Chatterjee A, Milton RC, Thyle S. Prevalence and aetiology of cataract in Punjab . Br J Ophthalmol . 1982;66:35-42.Crossref 9. Hu T, Zhen Q, Sperduto RD, et al. Age-related cataract in the Tibet Eye Study . Arch Ophthalmol . 1989;107:666-669.Crossref 10. Hiller R, Sperduto RD, Ederer F. Epidemiologic associations with nuclear, cortical, and posterior subcapsular cataracts . Am J Epidemiol . 1986;124:916-925. 11. Leske MC, Chylack LT Jr, Wu SY, Lens Opacities Case-Control Study Group. The Lens Opacities Case-Control Study: risk factors for cataract . Arch Ophthalmol . 1991;109:244-251.Crossref 12. Klein BEK, Klein R. Cataracts and macular degeneration in older Americans . Arch Ophthalmol . 1982;100:571-573.Crossref 13. Hiller R, Sperduto RD, Ederer F. Epidemiologic associations with cataract in the 1971-1972 National Health and Nutrition Examination Survey . Am J Epidemiol . 1983;118:239-249. 14. Leske MC, Connell AMS, Schachat AP, Hyman L, Barbados Eye Study Group. The Barbados Eye Study: prevalence of open angle glaucoma . Arch Ophthalmol . 1994;112:821-829.Crossref 15. Chylack LT Jr, Leske MC, McCarthy D, Khu PM, Kashiwagi T, Sperduto R. Lens Opacities Classification System II (LOCS II) . Arch Ophthalmol . 1989;107:991-997.Crossref 16. Kleinbaum DG, Kupper LL, Morgenstern H. Epidemiologic Research: Principles and Quantitative Methods . New York, NY: Van Nostrand Reinhold; 1982. 17. Sommer A, Tielsch J, Katz J, et al. Racial differences in the cause-specific prevalence of blindness in East Baltimore . N Engl J Med . 1991;325:1412-1417.Crossref 18. Kahn HA, Leibowitz HM, Ganley JP, et al. The Framingham Eye Study, II: association of ophthalmic pathology with variables previously measured in the Framingham Heart Study . Am J Epidemiol . 1977;106:33-41. 19. Mohan M, Sperduto RD, Angra SK, et al. India-US case-control study of agerelated cataracts . Arch Ophthalmol . 1989;107:670-676.Crossref 20. Hiller R, Kahn H. Senile cataract extraction and diabetes . Br J Ophthalmol . 1976;60:283-286.Crossref 21. Ederer F, Hiller R, Taylor H. Senile lens changes and diabetes in two population studies . Am J Ophthalmol . 1981;91:381-395. 22. Leske MC, Connell AMS, Wu SY, Hyman L, Schachat AP, Barbados Eye Study Group. Risk factors for open-angle glaucoma: the Barbados Eye Study . Arch Ophthalmol . 1995;113:918-924.Crossref 23. Robertson JM, Donner AP, Trevithick JR. Vitamin E intake and risk of cataracts in humans . Ann N Y Acad Sci . 1989;570:372-382.Crossref 24. Hankinson SE, Stampfer MJ, Seddon JM, et al. Nutrient intake and cataract extraction in women: a prospective study . BMJ . 1992;305:335-339.Crossref 25. Sperduto R, Hu T-S, Milton RC, et al. The Linxian Cataract Studies: two nutrition intervention trials . Arch Ophthalmol . 1993;111:1246-1253.Crossref 26. Seddon JM, Christen WG, Manson JE, et al. The use of vitamin supplements and the risk of cataract among US male physicians . Am J Public Health . 1994;84:788-792.Crossref 27. Leske MC, Wu S, Hyman L, et al. Biochemical factors in the Lens Opacities Case-Control Study . Arch Ophthalmol . 1995;113:1113-1119.Crossref 28. Vitale S, West S, Hallfrisch J, et al. Plasma antioxidants and risk of cortical and nuclear cataract . Epidemiology . 1993;4:195-203.Crossref 29. Knekt P, Heliovaara M, Rissanen A, Aromaa A, Aarran R-K. Serum antioxidant vitamins and risk of cataract . BMJ . 1992;305:1392-1394.Crossref 30. Jacques PF, Chylack LT Jr, McGandy RB, et al. Antioxidant status in persons with and without senile cataract . Arch Ophthalmol . 1988;106:337-340.Crossref 31. Hyman L, Wu SY, Leske MC, Connell AMS, Schachat A, BES Group. Prevalence and causes of visual impairment in the Barbados Eye Study . Invest Ophthalmol Vis Sci . 1996;37( (suppl) ):942. Abstract.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150113019

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Hillis, Argye;Fine, Stuart L.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150114020pmid: 9006435

Abstract Macular holes are a common cause of visual impairment. The randomized trial performed by Freeman et al1 for the Vitrectomy for Treatment of Macular Hole Study Group provides several pieces of important information about this prevalent condition. The results confirm that a large proportion of stage 3 and 4 macular holes close after vitrectomy, that such closure can occur even after a long duration, and that the anatomical results depend on the size and duration of the hole. The difference between the eyes assigned to vitrectomy (69% closure) and control eyes (4% closure) is statistically significant. The question then becomes whether this anatomical result translates into clinical visual improvement. The clinical results are mixed; improvements in visual acuity and serious adverse events were more common in the operated on eyes than in the control eyes, and both of these changes occurred in less than one quarter of these eyes. References 1. Freeman WR, Azen SP, Kim JW, El-Haig W, Mishell DR III, Bailey I, for the Vitrectomy for Treatment of Macular Hole Study Group. Vitrectomy for the treatment of full-thickness stage 3 or 4 macular holes: results of a multicentered randomized clinical trial . Arch Ophthalmol . 1997;115:11-21.Crossref 2. Park SS, Marcus DM, Dieker JS, et al. Posterior segment complications after vitrectomy for macular hole . Ophthalmology . 1995;102:775-781.Crossref 3. Kelly NE, Wendel RT. Vitreous surgery for idiopathic macular holes: results of a pilot study . Arch Ophthalmol . 1991;109:654-659.Crossref 4. Kim JW, Freeman WR, Azen SP, et al. Prospective randomized trial of vitrectomy for stage 2 macular holes . Am J Ophthalmol . 1996;121: (6) :605-614. 5. Bressler NM, Bressler SB. Indocyanine green angiography: can it help preserve the vision of our patients? Arch Ophthalmol . 1996;114:747-749.Crossref

Caprioli, Joseph

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150115021pmid: 9006436

Abstract Automated white-on-white static threshold perimetry, introduced some 20 years ago by Bebie and colleagues,1 has provided a new and generally higher standard of perimetric testing than was previously available. However, it has not met our initial expectations of providing sensitive and reliable evidence of early glaucomatous optic neuropathy. The first reproducible perimetric defects generally develop late in the disease, and the high rate of long-term fluctuation confounds our ability to detect disease progression. This realization has sparked a search for more reliable, early markers of glaucomatous optic neuropathy. Such markers would identify those patients who are most likely to benefit from treatment and spare others the costs and considerable morbidity of treatment. See also page 26 There have been proponents of structural and functional approaches toward the identification of early glaucomatous damage. Clinical and histological studies have suggested that detectable structural changes generally precede structural abnormalities detected with standard References 1. Bebie H, Fankhauser F, Spahr J. Static perimetry: accuracy and fluctuations . Acta Ophthamol . 1976;54:339-348.Crossref 2. Read RM, Spaeth GL. The practical clinical appraisal of the optic disc in glaucoma: the natural history of cup progression and some specific disc-field correlations . Trans Am Acad Ophthalmol Otolaryngol . 1974;78:OP255-OP274. 3. Sommer A, Pollack I, Maumenee AE. Optic disc parameters and onset of glaucomatous field loss, I: methods and progressive changes in disc morphology . Arch Ophthalmol . 1979;9:1444-1448.Crossref 4. Pederson JE, Anderson DR. The mode of progressive disc cupping in ocular hypertension and glaucoma . Arch Ophthalmol . 1990;98:490-495.Crossref 5. Yablonski ME, Zimmerman TJ, Kass MA, et al. Prognostic significance of optic disc cupping in ocular hypertensive patients . Am J Ophthalmol . 1980;89:585-592. 6. Odberg T, Riise D. Early diagnosis of glaucoma: the value of successive stereophotography of the optic disc . Acta Ophthalmol . 1985;63:257-263.Crossref 7. Sommer A, Katz J, Quigley HA, et al. Clinically detectable nerve fiber atrophy precedes the onset of glaucomatous field loss . Arch Ophthalmol . 1991;109:77-83.Crossref 8. Zeyen TG, Caprioli J. Progression of disc and field damage in early glaucoma . Arch Ophthalmol . 1993;111:62-65.Crossref 9. Mikelberg FS, Douglas GR, Schulzer M, et al. Reliability of optic disc topographic measurements recorded with a video-ophthalmograph . Am J Ophthalmol . 1984;98:98-102.Crossref 10. Shields MB, Martone JF, Shelton AR, et al. Reproducibility of topographic measurements with the optic nerve head analyzer . Am J Ophthalmol . 1987;104:581-586. 11. Caprioli J, Miler JM. Measurement of relative nerve fiber layer surface height in glaucoma . Ophthalmology . 1989;96:633-639.Crossref 12. Dreher AW, Tso PC, Weinreb RN. Reproducibility of topographic measurements of the normal and glaucomatous optic nerve head with the laser tomographic scanner . Am J Ophthalmol . 1991;111:221-229. 13. Brigatti L, Caprioli J. Correlation of visual field function with confocal laser disc measurements in glaucoma . Arch Ophthalmol . 1995;113:1191-1194.Crossref 14. Weinreb RN, Dreher AW, Coleman A, et al. Histopathologic validation of Fourierellipsometry measurements of retinal nerve fiber layer thickness . Arch Ophthalmol . 1990;108:557-560.Crossref 15. Schuman JS, Hee MR, Puliafita CA, et al. Quantification of nerve fiber layer thickness in normal and glaucomatous eyes using optical coherence tomography . Arch Ophthalmol . 1995;113:586-596.Crossref 16. Quigley HA, Dunkelberger GR, Green WR. Chronic human glaucoma causing selectively greater loss of large optic nerve fibers . Ophthalmology . 1988;95:357-363.Crossref 17. Glovinsky Y, Quigley HA, Dunkelberger GR. Retinal ganglion cell loss is size dependent in experimental glaucoma . Invest Ophthalmol Vis Sci . 1991;32:484-491. 18. Johnson CA. Selective vs nonselective losses in glaucoma . J Glaucoma . 1994;3:S32-S44. 19. Wall M, Jennisch CS, Munden PM. Motion perimetry identifies nerve fiber bundlelike defects in ocular hypertension . Arch Ophthalmol . 1996;114:26-33. 20. Silverman SE, Trick GL, Hart WM. Motion perception is abnormal in primary open-angle glaucoma and ocular hypertension . Invest Ophthalmol Vis Sci . 1990;31:722-729. 21. Bullimore MA, Wood JM, Swenson K. Motion perception in glaucoma . Invest Ophthalmol Vis Sci . 1993;34:3526-3533. 22. Baez KA, McNaught Al, Dowler JG, Poinoosawmy D, Fitzke FW, Hitchings RA. Motion detection threshold and field progression in normal tension glaucoma . Br J Ophthalmol . 1995;79:125-128.Crossref 23. Wall M, Ketoff KM. Random dot motion perimetry in patients with glaucoma and in normal subjects . Am J Ophthalmol . 1995;120:587-596. 24. Sample PA, Weinreb RN. Color perimetry for assessment of primary openangle glaucoma . Invest Ophthalmol Vis Sci . 1990;31:1869-1875. 25. Hart WM, Silverman SE, Trick GL, Nesher R, Gordon MO. Glaucomatous visual field damage: luminance and color-contrast sensitivities . Invest Ophthalmol Vis Sci . 1990;31:359-367. 26. Sample PA, Taylor JD, Martinez GA, Lusky M, Weinreb RH. Short-wavelength color visual fields in glaucoma suspects at risk . Am J Ophthalmol . 1993;115:225-233. 27. Johnson CA, Adams AJ, Casson EJ, Brandt JD. Blue-on-yellow perimetry can predict the development of glaucomatous visual field loss . Arch Ophthalmol . 1993;111:645-650.Crossref 28. Johnson CA, Adams AJ, Casson EJ, Brandt JD. Progression of early glaucomatous visual field loss as detected by blue-on-yellow and standard white-on-white automated perimetry . Arch Ophthalmol . 1993;111:651-656.Crossref 29. Johnson CA, Brandt JD, Khong AM, Adams AJ. Short-wavelength automated perimetry in low-, medium-, and high-risk ocular hypertensive eyes: initial baseline results . Arch Ophthalmol . 1995;113:70-76.Crossref 30. Felius J, de Jong LA, van den Berg TJ, Greve EL. Functional characteristics of blue-on-yellow perimetric thresholds in glaucoma . Invest Ophthalmol Vis Sci . 1995;36:1665-1674. 31. Wild JM, Moss ID, Whitaker D, O'Neill EC. The statistical interpretation of blueon-yellow visual field loss . Invest Ophthalmol Vis Sci . 1995;36:1398-1410.

Wiggs, Janey L.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150117022pmid: 9006437

Abstract Kjer DOMINANT optic atrophy (DOA) is a rare primary degeneration of the retinal ganglion cell. In this issue of the Archives, 2 articles describing the genetic analysis of single, large, affected families confirm the initial genomic mapping of this disease to chromosome 3q27-3q28 and refine the localization of the gene to a 4 to 7 centimorgan region.1,2 These mapping studies are important steps toward the cloning and characterization of the actual gene. Although this disorder is a rare cause of blindness, the genetic analysis of this disease will provide an opportunity to investigate one mechanism of optic nerve degeneration and to determine what role this gene may play in other degenerative disorders of the retinal ganglion cell and optic nerve. See also pages 95 and 100 Kjer DOA is inherited as an autosomal dominant trait with high penetrance. The responsible gene was initially mapped to chromosome 3q27-3q28 in 1994. References 1. Brown J Jr, Fingert JH, Taylor CM, Lake M, Sheffield VC, Stone EM. Clinical and genetic analysis of a family affected with dominant optic atrophy (OPA1) . Arch Ophthalmol . 1997;115:95-99.Crossref 2. Johnston RL, Burdon MA, Spalton DJ, Bryant SP, Behnam JT, Seller MJ. Dominant optic atrophy, Kjer type: linkage analysis and clinical features in a large British pedigree . Arch Ophthalmol . 1997;115:100-103.Crossref 3. Eiberg H, Kjer B, Kjer P, Rosenberg T. Dominant optic atrophy (OPA1) mapped to chromosome 3q region, I: linkage analysis . Hum Mol Genet . 1994;3:977-980.Crossref 4. Bennett SR, Alward WL, Folberg R. An autosomal dominant form of low-tension glaucoma . Am J Ophthalmol . 1989;108:238-244. 5. Ofner S, Samples JR. Low-tension glaucoma in identical twins . Am J Ophthalmol . 1992;114:764-765. Letter. 6. Wilensky JT, Podos SM, Becker B. Prognostic indicators in ocular hypertension . Arch Ophthalmol . 1974;91:200-202.Crossref 7. Wiggs JL. Complex disorders in ophthalmology . In: Michael Gorin, ed. Seminars in Ophthalmology . Philadelphia, Pa: WB Saunders Co. 1995;10:323-330.

Loewenstein, John I.;Hogan, R. Nick;Jakobiec, Frederick A.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150119023pmid: 9006438

Abstract A highly myopic patient had surgery for retinal detachment in both eyes. After 3 procedures, the left eye developed phthisis bulbi. After multiple procedures, the right eye underwent a vitrectomy for proliferative vitreoretinopathy. A plaque of preretinal tissue was removed. We found bone on pathologic examination. The retina remains attached, and visual acuity is 20/200. Ultrasonography showed additional evidence of calcification of both eyes, presumably metaplastic bone. References 1. Howes EL Jr. Basic mechanisms in pathology . In: Spencer WH, ed. Ophthalmic Pathology . Philadelphia, Pa: WB Saunders Co; 1985;1:13-14. 2. Samuels B. Ossification of the choroid . Trans Am Acad Ophthalmol Otol . 1938;43:193-244. 3. Kurz GH, Zimmerman LE. Vagaries of the retinal pigment epithelium . Int Ophthalmol Clin . 1962;2:441-464.Crossref 4. Yanoff M, Zimmerman LE, Davis RL. Massive gliosis of the retina . Int Ophthalmol Clin . 1971;11:211-229. 5. Allen CB, Ulshafer RJ, Ellis EA, Woodard JC. Scanning electron microscopic analysis of intraocular ossification in advanced retinal disease . Scanning Microsc . 1987;1:233-239. 6. Shields JA, Shields CL. Intraocular Tumors . Philadelphia, Pa: WB Saunders Co; 1992;261-271. 7. Gass JDM, Guerry RK, Jack RL, Harris G. Choroidal osteoma . Arch Ophthalmol . 1978;96:428-435.Crossref 8. Duke-Elder S, Perkins ES. Diseases of the Uveal Tract . St Louis, Mo: CV Mosby; 1966:740-748. 9. Duke-Elder S. The Eye in Evolution . St Louis, Mo: CV Mosby; 1958:401-403. 10. Machemer R, Laqua H. Pigment epithelial proliferation in retinal detachment (massive periretinal proliferation) . Am J Ophthalmol . 1975;80:1-23. 11. Machemer R, Van Horn D, Aaberg TM. Pigment epithelial proliferation in human retinal detachment with massive periretinal proliferation . Am J Ophthalmol . 1978;85:181-191.

Fick, A. Eugen

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150122024pmid: 9006439

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 Among the numerous diseases of the cornea, there are many which change its normal form; this results in the production of distorted or even completely blurred retinal images, and accordingly vision suffers. Now there is a group of alterations in the form of the cornea, of which the bad effects upon vision may be removed by the use of glasses; these are cases of regular astigmatism.... The matter begins to be more difficult when we deal with the alteration in the form of the cornea known as keratoconus [which causes irregular astigmatism]. The results of optical correction are, however, entirely unsatisfactory in cases in which defects of vision are due to irregular corneal astigmatism. Donders recommended the correction of such cases by stenopaeic glasses. He and his pupil, von Wijngarden, demonstrated that the improvement of [near] vision resulting from the use of stenopaeic glasses was often really astonishing, and that

Dabezies, Oliver H.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150123025

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Spraul, Christoph W.;Grossniklaus, Hans E.;Giles, Jackson T.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150124026pmid: 9006440

Abstract Cancers metastatic to the iris or ciliary body are rare.1,2 The most common carcinomas that metastasize to these structures arise in the breast, lung, or kidney.1,2 Malignant müllerian mixed tumors (MMTs) are rare, biphasic neoplasms of the uterus, cervix, and ovaries, and they contain both malignant glandular and stromal components, often including cartilage.3 We recently examined a patient with an MMT metastatic to the iris and ciliary body. Report of a Case. A 66-year-old woman complained of pain around her left eye for 2 weeks. Her right eye was clinically unremarkable (bestcorrected visual acuity, 20/50). Examination of her left eye showed a nodular tumor on the anterior surface of the iris between the 3- and 6-o'clock position, which contacted the posterior corneal surface and extended into the chamber angle (Figure 1).The patient's medical history was notable for a hysterectomy, with a bilateral salpingo-oophorectomy for a high-grade, References 1. Ferry AP, Font RL. Carcinoma metastatic to the eye and orbit, II . Arch Ophthalmol . 1975; 472-482. 2. Shields JA, Shields CL, Kiratli H, de Potter P. Metastatic tumors to the iris in 40 patients . Am J Ophthalmol . 1995;119:422-430. 3. To WW, Hgan HY. Malignant mixed müllerian tumor of the uterus . Int J Gynaecol Obstet . 1994;47:39-44.Crossref

Mootha, V. Vinod;Cowden, Thomas P.;Sires, Bryan S.;Dortzbach, Richard K.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150125027pmid: 9006441

Abstract Retrobulbar injection is a routine procedure for achieving akinesia and anesthesia prior to ophthalmic surgery. Previously reported complications to this procedure have included central nervous system toxic effects, globe perforation, retinal vascular occlusion, optic nerve damage, extraocular muscle palsies, ptosis, and retrobulbar hemorrhage.1 Visual loss has been reported following retrobulbar hemorrhage from retrobulbar and even peribulbar anesthesia.2 We report a case of subperiosteal orbital hemorrhage following a retrobulbar injection resulting in permanent severe visual loss. Report of a Case. An 81-year-old woman was transferred emergently for evaluation of a retrobulbar hemorrhage of her left eye that occurred within minutes of receiving a retrobulbar injection prior to a planned cataract extraction. The patient was not receiving any anticoagulant medications. A lateral canthotomy and inferior cantholysis had been performed by the referring ophthalmologist for intraocular pressure as high as 80 mm Hg. The patient had also been started on a References 1. Rubin AP. Complications of local anesthesia for ophthalmic surgery . Br J Ophthalmol . 1995;75:93-96. 2. Puustjarvi T, Purhonen S. Permanent blindness following retrobulbar hemorrhage after peribulbar anesthesia for cataract surgery . Ophthalmic Surg . 1992;23:450-452. 3. Cionni RJ, Osher RH. Retrobulbar hemorrhage . Ophthalmology . 1991;98:1153-1155.Crossref 4. Anderson RL. Bilateral vision loss after blepharoplasty . Arch Ophthalmol . 1981;99:2205.Crossref

Ryan, Edwin H.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150127028pmid: 9006442

Abstract Panoramic viewing during vitrectomy offers significant advantages over conventional viewing in many cases and is being used with increasing frequency. Two endoillumination probes that reduce the glare occurring with use of the existing panoramic endoillumination probes were developed. They allow easier viewing of the fundus in eyes with poor media and improve the visualization of the vitreous fibers adjacent to the probe in eyes with clear media. One probe is used for endoillumination alone, and the other has a pick to be used for bimanual dissection. The two probes have been used in more than 100 vitrectomies for various indications, and they give excellent illumination with reduced glare. References 1. Spitznas M, Reiner J. A stereoscopic diagonal inverter (SDI) for wide-angle vitreous surgery . Graef Arch Clin Exp Ophthalmol . 1987;225:9-12.Crossref 2. Bovey EH, Gonvers M. A new device for noncontact wide-angle viewing of the fundus during vitrectomy . Arch Ophthalmol . 1995;113:1572-1573.Crossref

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150128029

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Power, Michael H.;Regillo, Carl D.;Custis, Peter H.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150130030pmid: 9006443

References 1. Amarosi EL, Ultmann JE. Thrombotic thrombocytopenic purpura: report of 16 cases and review of the literature . Medicine . 1962;45:139-159. 2. Percival SP. The eye and Moschcowitz's disease (thrombotic thrombocytopenic purpura): a review of 182 cases . Trans Ophthalmol Soc U K . 1970;90:375-382. 3. Lewellen DR Jr, Singerman LJ. Thrombotic thrombocytopenic purpura with optic disk neovascularization, vitreous hemorrhage, retinal detachment, and optic atrophy . Am J Ophthalmol . 1980;89:840-844. 4. Gum KB, Carter KD, Vine AK. Massive bilateral retinal vascular occlusion secondary to thrombotic thrombocytopenic purpura . Retina . 1988;8:185-187.Crossref 5. Gass JDM. Stereoscopic Atlas of Macular Diseases: Diagnosis and Treatment . St Louis, Mo: Mosby-Year Book Inc; 1987:346-348, 558-559.

Cruz, Lyndon da;Constable, Ian J.;Barry, Christopher J.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150132031pmid: 9006444

References 1. Guyer DR, de Bustros S, Diener-West M, Fine SL. Observations on patients with idiopathic macular holes and cysts . Arch Ophthalmol . 1992;110:1264-1268.Crossref 2. Bidwell AE. Jampol LM. Macular holes and excellent visual acuity . Arch Ophthalmol . 1988;106:1350-1351.Crossref 3. Luckie A, Heriot W. Macular holes pathogenesis, natural history, and surgical outcomes . Aust N Z J Ophthalmol . 1995;23:93-100.Crossref 4. Wendel RT, Patel AC, Kelly NE, Salzano TC, Wells JW, Novack GD. Vitreous surgery for macular holes . Ophthalmology . 1993;100:1671-1676.Crossref

Hassin, Harold

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150134032pmid: 9006445

Abstract I read with anticipation Dr Javitt's editorial1 concerning the professional quandary in which contemporary ophthalmologists now find themselves, hoping he might shine a bright light on a previously ignored avenue. And, in truth, he did point the way by highlighting the disparity between the need for services from a public health perspective and the current demand. I believe, however, more detailed directions are required. By emphasizing the need for increased ethical marketing of eye care Dr Javitt takes us down a blind alley. What is the product of Dr Javitt's proposed education campaign? Surely, a population more keenly aware of the benefits of timely eye care but frustrated to find that these benefits are beyond their reach. It is clear that Dr Javitt is trying to show us that the path to a brighter future lies not in beggaring thy neighbor but in expanding the total market, so that References 1. Javitt JC. The RAND Manpower Study: retire, refract or re-educate? Arch Ophthalmol . 1996;114:476-477.Crossref

Javitt, Jonathan C.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150134033

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 Although I share Dr Hassin's disappointment in our national failure to pass comprehensive health care system reform, I disagree with his opinion that the market size for ophthalmologic services cannot be expanded in a meaningful way without comprehensive health care system reform and universal health insurance. While he refers to my suggestions as a "blind alley," his insistence on blaming the current situation on the failure of Congress to pass the Health Security Act takes the reader down afar murkier path. Moreover, he does a grave disservice to the many professional societies who either supported the legislation as written or would have done so based on achievable modifications. Health care system reform legislation was not passed because of many complex and tragic political reasons, but intractable physician opposition was not one of them.Dr Hassin cites no evidence to support his thesis that effective marketing would be useless

Peláez, Orfilio

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150135034pmid: 9006446

Abstract I have read the article titled "Evaluation of patients with Retinitis Pigmentosa Receiving Electric Stimulation, Ozonated Blood, and Ocular Surgery in Cuba," published in the May 1996 issue of the Archives (114:560-563). I am disappointed that such prestigious colleagues would conduct research about our procedure without previous notification or contact with us. If they had contacted us, we would have welcomed and contributed to their initiative, as we have done with other colleagues through the Retinitis Pigmentosa Foundation Fighting Blindness, Baltimore, Md, of which I am sure they are aware. I do not believe that this is a fair or ethical way to proceed. The study is not representative of "common forms of RP [retinitis pigmentosa]" because it included in such a small sample (N= 10 patients), 3 patients with X-linked recessive RP and 1 patient with Usher syndrome which are lower in frequency in the general population of patients References 1. Peláez O, Alemán T, Moreno N. Computerized evaluation of visual fields from retinitis pigmentosa patients operated on by revitalizing surgery: three years of follow up. Presented at the First Provincial Retinitis Pigmentosa meeting; June 1993; Havana, Cuba.

Berson, Eliot L.;Remulla, Juancho F. C.;Rosner, Bernard;Sandberg, Michael A.;Weigel-DiFranco, Carol

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150135035

Abstract In reply We conducted our study to see if informal claims of substantial improvement among those participating in the protocol in Cuba could be supported by measures of visual function. Dr Peláez was well aware of our investigation and corresponded with us about this in April 1995. It would seem that he and his coworkers would welcome an independent assessment of their work. Unfortunately, we could find no benefit based on our measurements of visual acuity, visual field area, and electroretinogram within the time frame of claimed improvement.1Our study sample seemed to be representative of the common forms of retinitis pigmentosa for severity of disease. As stated in the article, the average electroretinographic amplitude was consistent with data previously reported for patients with the common forms of this disease after considering their mean age. One of the 10 patients had Usher syndrome, type II; the prevalence of Usher References 1. Berson EL, Remulla JFC, Rosner B, Sandberg MA, Weigel-DiFranco C: Evaluation of patients with retinitis pigmentosa receiving electric stimulation, ozonated blood, and ocular surgery in Cuba . Arch Ophthalmol . 1996;114:560-563.Crossref

Abramson, David H.;Servodidio, Camille A.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150136036pmid: 9006447

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 response to the article titled "Metastatic Choroidal Melanoma to the Contralateral Orbit 40 Years After Enucleation" by Coupland et al in the June issue of the Archives (1996; 114:751-756)we also had a patient in whom metastatic choroidal melanoma to the contralateral orbit developed. Initially, a 27-year-old white man was seen with a loss of peripheral vision in his right eye. His condition was diagnosed as a choroidal melanoma measuring 8.5×16 mm. Results of a metastatic workup were negative. He was treated with a 20-mm iodine 125 plaque to his right eye. Five and one half years later, the right eye choroidal melanoma was undetectable on ultrasound scanning but the patient was seen with decreased visual acuity and peripheral vision, 2 mm of proptosis and papilledema of the left eye. B-scan and magnetic resonance imaging confirmed a left orbital mass. A metastatic workup revealed metastatic melanoma to the liver,

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150136037

Abstract We heartily endorse the concept of the "Patient-Physician Covenant" published by Crawshaw et al1 in the Journal of the American Medical Association. Medical care is, indeed, a "special kind of human activity" whose foundation is a promise, a profession, to be trustworthy. In times such as these when the means of providing care are in flux, it is useful, if not mandatory, to reflect on the basic elements of medical care that make it precious to a population. These basic elements cannot be ignored or negotiated if the public is to receive the care it deserves and requires. It is, indeed, our duty to advocate for the welfare of our patients by affirming our covenant to care. The generic elements of caring for the ill and infirm are constant. So are the temptations to material gain for the caregivers. The recipients of medical care are vulnerable because of their References 1. Crawshaw R, Rogers DE, Pellegrino ED, et al. Patient-physician covenant . JAMA . 1995;273:1553.Crossref

Williams, George A.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150137038

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150138039

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 Richard A. Saunders, MD, Has Been Named the N. Edgar Miles Professor of Ophthalmology at the Storm Eye Institute, Medical University of South Carolina, Charleston. Dr Saunders is professor and vice-chair of the Department of Ophthalmology. Dr Saunders is a recent recipient of honor awards from the American Association for Pediatric Ophthalmology and Strabismus and theAmerican Academy of Ophthalmology. He is serving his 19th year on the university's faculty. J. William Harbour Has Been Appointed Assistant Professor in the Department of Ophthalmology and Visual Sciences at the Washington University School of Medicine and has joined the Barnes Retina Institute in St Louis, Mo. Dr Harbour completed his residency at the Wills Eye Hospital in Philadelphia, Pa, a vitreoretinal fellowship at the Bascom Palmer Eye Institute, Miami, Fla, and an oncology fellowship at the University of California, San Francisco. Timothy Olsen, MD, Has Been Appointed Assistant Professor of Ophthalmology (Vitreoretinal

Egbert, James

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150139041

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 The purpose of this text is to describe the cognitive process that Drs von Noorden and Helveston use for diagnosing and treating patients with abnormalities of binocular vision. The format they have chosen is to use algorithms that are illustrated with arrows and boxes. The text includes 38 algorithms that are classified as preliminaries, and 59 that are classified as diagnostic and treatment decisions. I appreciated 7 algorithms conveying basic science information, 15 describing examination techniques, 40 describing the evaluation of specific clinical problems, 15 regarding treatment of particular disorders, and 20 combining the evaluation and treatment of disorders. On the page adjacent to the algorithms is a brief text that elucidates some but not all of the boxes within the algorithms. Approximately 50% of the references cited in the text consist of Drs von Noorden's and Helveston's clinical and basic science research. The reader is thus ensured of receiving

Barney, Neal P.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150139040

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 This is an excellent atlas of the cornea, external disease, and ocular adnexa diseases. It is likely to be one of the most complete collections of its kind. Drs Krachmer and Palay have included more than 800 of their own photographs and those from many contributors. Additionally, in their preface, they anticipate the likelihood of a second edition and welcome any additions for the atlas, or replacements of photographs currently published with better examples from their readers. The photographs depict various methods of slit-lamp photography, emphasizing the importance of careful observation that is needed in cornea and external disease diagnosis. This book is divided into 20 chapters or groupings of photographs and follows the order of subjects contained in the second and third volumes of the cornea text soon to be published by Dr Krachmer. Regardless of the number of illustrations or photographs contained in that 3-volume textbook, this will

Appen, Richard E.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150140042

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 this 2-book fifth volume of the most recent edition of Walsh and Hoyt's Clinical Neuro-Ophtholmology, Dr Miller has compiled a clinically pertinent and scientifically thorough conclusion to the 5-volume series. In 1947, Dr Walsh wrote what was to become the ultimate literary authority on neuro-ophthalmology. Later, Dr Hoyt collaborated with Dr Walsh to create an updated version of the textbook in 1969. Dr Miller has courageously undertaken the daunting task of updating this neuroophthalmology "Bible" in the modern era of knowledge explosion. In the fifth side of this literary pentagon, the first volume of which was published in 1982, he has completed his mission. clinically pertinent and scientifically thorough This volume, composed of 2 books of about 1000 pages each, considers the various infections and inflammatory disorders that probably are related to infection (eg, multiple sclerosis) that affect the nervous system and vision. An additional chapter considers nonorganic conditions.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150141043

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.

1997 Archives of Ophthalmology

doi: 10.1001/archopht.1997.01100150142044

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.