Archives of Ophthalmology

Carpel, Emmett F.

doi: 10.1001/archopht.1984.01040030522004pmid: 6721747

Abstract To the Editor. —I read with interest the recent article by Fuerst et al1 in the August Archives reporting the appearance of superior limbic keratoconjunctivitis in soft contact lens wearers. The appearance of superior conjunctival hyperemia, punctate epithelial and subepithelial opacities, and an irregular epithelium involving the superior one third to one half of the cornea has also been described by others.2,3 Although this condition has now been well reported, no definite etiology has been established.During the last several years, I have encountered a number of patients with clinical findings similar to the cases reported. In each case, after the symptoms and signs resolved—ever so slowly in some cases—I gave the patients a trial of the contact lenses. In all cases I could report that when symptoms and signs recurred, the contact lenses rode superiorly on the cornea, as if captured and held in place by the References 1. Fuerst DJ, Sugar J, Worobec S: Superior limbic keratoconjunctivitis associated with contact lens wear . Arch Ophthalmol 1983;101:1214-1216.Crossref 2. Miller RA, Brightbill FS, Slama SL: Superior limbic keratoconjunctivitis in soft contact lens wearers . Cornea 1982;1:293-299.Crossref 3. Conway ST, Wagdi SF: Corneal scarring associated with daily soft contact lens wear . Ann Ophthalmol 1983;15:868-871.

Raju, V. K.

doi: 10.1001/archopht.1984.01040030522002pmid: 6326719

Abstract To the Editor. —I read with interest the October Archives article by Margulies and Mannis1 in which they listed five causes of dendriform lesions of the cornea (herpes simplex, herpes zoster, systemic tyrosinemia, Thygeson's superficial punctate keratitis, and contact lens wear).During the last three years, we have seen two cases of dendriform lesions in adenovirus keratoconjunctivitis (Figure). In both, immunofluorescence and viral cultures for herpes simplex were negative. In both cases we were able to culture adenovirus, and the clinical manifestation and course were typical of adenoviral keratoconjunctivitis.Hence, adenoviral keratoconjunctivitis may be added to the list of dendriform lesions of the cornea. References 1. Margulies LJ, Mannis MJ: Dendritic corneal lesions associated with soft contact lens wear . Arch Ophthalmol 1983;101:1551-1553.Crossref

Mannis, Mark J.;Margulies, Linda J

doi: 10.1001/archopht.1984.01040030522003pmid: N/A

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. —We thank Dr Raju for adding yet another possible cause to the list of causes of dendritic lesions of the cornea. We have not seen dendritic lesions associated with adenoviral disease, and, of course, the one case in which the lesion was cultured in our study did not reveal adenovirus.

Rossi, Pietro;Ciurlo, Giuseppe

doi: 10.1001/archopht.1984.01040030522001pmid: 6721746

Abstract To the Editor. —In the April 1983 Archives Lindsey et al1 reported that an unplanned buckle removal resulted in a 43% rate of retinal redetachment in patients operated on for a retinal detachment. Other similar series report an even lower redetachment rate (from 40% to 33%).2,3 It may therefore be inferred that a permanent buckle is not needed to achieve the cure of a large number of retinal detachments.We read these reports with a great interest, since in 1978 we developed a method of temporary buckling for the management of retinal detachments with a single break.4The method essentially consists in cryocoagulating the break and indenting it transconjunctivally by means of a metallic plaque fixed to a ring. The ring is fixed to the eyeball by two polyester stitches passed radially through the sclera near the limbus and is held in place eight to 10 days, References 1. Lindsey PS, Pierce LH, Welch RB: Removal of scleral buckling elements: Causes and complications . Arch Ophthalmol 1983;101:570-573.Crossref 2. Hilton GF, Waleyn RH: The removal of scleral buckles . Arch Ophthalmol 1978;96:2061-2064.Crossref 3. Ulrich RA, Burton RC: Infection following scleral buckling procedures . Arch Ophthalmol 1974;92:213-215.Crossref 4. Ciurlo G, Rossi P: Transconjunctival buckling for retinal detachment . Ophthalmologica 1978;178:16-18.Crossref 5. Ciurlo G, Rossi P: Long-term evaluation of transconjunctival buckling for retinal detachment . Ophthalmologica 1980;181:149-151.Crossref

Sugar, Joel;Fuerst, David

doi: 10.1001/archopht.1984.01040030522005pmid: N/A

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. —We appreciate Dr Carpel's reply to our recent article. As he suggests, we saw the majority of our patients after they had ceased contact lens wear and thus cannot comment on his experience. With four of our patients in whom contact lenses were refit, however, we have not had recurrences, except for one patient who had a recurrence when preservative-containing solution were reinstituted. We continue to be intrigued by this syndrome and appreciate Dr Carpel's suggestions concerning etiology.

doi: 10.1001/archopht.1984.01040030524006pmid: N/A

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 Ophthalmology Day. —The annual Pediatric Ophthalmology Day of the Sainte-Justine Hospital in Montreal will be held Oct 12, 1984. There is no registration or tuition fee. The guest speaker will be Dr G. K. von Noorden of Houston. For further information, contact Dr Jean Milot, Department of Ophthalmology, Hôpital Sainte-Justine, 3175 Cote Ste-Catherine, Montreal, Quebec, Canada H3T 1C5. Meeting. —The annual meeting of the Canadian Implant Association will be held June 22-23, 1984, at the Queen Elizabeth Hotel, Montreal. The fee for the conference is $150, $50 for the extracapsular course, and $50 for the YAG laser course. For further information, contact Dr Marvin L. Kwitko, 5591 Cote des Neiges Rd, Suite 1, Montreal, Quebec, Canada H3T 1Y8. Workshop. —A conference and workshop on contact lens concepts will be held by the Department of Ophthalmology, College of Medicine, University of Kentucky, May 19-20, 1984, at Shaker Village, Pleasant Hill. For

Benson, William E.;Tasman, William

doi: 10.1001/archopht.1984.01040030525007pmid: 6721748

Abstract • We describe three cases of shallow posterior rhegmatogenous retinal detachment caused by tiny retinal tears. The clinical appearance of the detachments was very similar to that of idiopathic central serous chorioretinopathy or traction retinal detachment. However, the correct diagnosis was made by finding a tiny paravascular break. Vitrectomy without a thermal adhesion was successful in repairing the detachments. References 1. Margherio RR, Schepens CL: Macular breaks: I. Diagnosis, etiology and observations . Am J Ophthalmol 1972;78:219-222. 2. Schepens CL: Retinal Detachment and Allied Diseases. Philadelphia, WB Saunders Co, 1983, pp 497-556. 3. Adams ST: Retinal detachment due to macular and small posterior holes . Arch Ophthalmol 1961;66:528-533.Crossref

Jampol, Lee M.;Sieving, Paul A.;Pugh, David;Fishman, Gerald A.;Gilbert, Howard

doi: 10.1001/archopht.1984.01040030527008pmid: 6721749

Abstract • We examined 11 young patients with unilateral ocular findings that included multiple white dots at the level of the retinal pigment epithelium (RPE) or the deep retina, vitreal cells, RPE granularity in the macula, reduced visual acuity, electroretinogram (ERG) and early receptor potential (ERP) amplitudes, and fluorescein leakage from disc capillaries and late staining of the RPE. Recovery of visual function included a dramatic improvement in ERG and ERP amplitudes over several weeks. The etiology of this syndrome remains uncertain; there is no definite evidence of systemic involvement. References 1. Sieving PA, Fishman GA, Jampol LM, et al: Multiple evanescent white dot syndrome: II. Electrophysiology of the photoreceptors during retinal pigment epithelial disease . Arch Ophthalmol , 1984;102:675-679.Crossref 2. Gass JDM: Acute posterior multifocal placoid pigment epitheliopathy . Arch Ophthalmol 1968;80:177-185.Crossref 3. Ryan SJ, Maumenee AE: Birdshot retinochoroidopathy . Am J Ophthalmol 1980;89:31-45. 4. Gass JDM, Braunstein RA: Further observations concerning the diffuse unilateral subacute neuroretinitis syndrome . Arch Ophthalmol 1983;101:1689-1697.Crossref 5. Gass JDM: Stereoscopic Atlas of Macular Diseases: Diagnosis and Treatment , ed 2. St Louis, CV Mosby Co, 1977, pp 376-379. 6. Krill AE, Deutman AF: Acute retinal pigment epitheliitis . Am J Ophthalmol 1972;74:193-205. 7. Deutman AF: Acute retinal pigment epitheliitis . Am J Ophthalmol 1974;78:571-578.

Sieving, Paul A.;Fishman, Gerald A.;Jampol, Lee M.;Pugh, David

doi: 10.1001/archopht.1984.01040030531009pmid: 6721750

Abstract • We performed electrophysiologic studies of photoreceptor function in three patients with multiple evanescent white dot syndrome. During the acute stage, while the visual acuity was impaired, the electroretinogram (ERG) a-wave and the early receptor potential (ERP) amplitudes were profoundly decreased. The ERP regeneration times, determined for one subject, were prolonged. These findings suggest that photoreceptor function was impaired (abnormal a-wave), the effective visual pigment optical density of the outer segments was markedly reduced (ERP amplitude), and visual pigment regeneration was abnormal (ERP regeneration kinetics). During the recovery stage, the ERG and ERP amplitudes and visual acuity returned to normal. Our patients' disease seemed to be primarily of the retinal pigment epithelium (RPE). The decreased visual pigment density and prolonged regeneration kinetics emphasize the physiologic dependence of the sensory retina on the RPE. References 1. Brown K, Watanabe K, Murakami M: The early and late receptor potentials of monkey cones and rods . Cold Spring Harbor Symp Quant Biol 1965;30:457-482.Crossref 2. Cone RA, Brown PK: Dependence of the early receptor potential on the orientation of rhodopsin . Science 1967;156:536. 3. Jampol LM, Sieving PA, Pugh D, et al: Multiple evanescent white dot syndrome: I. Clinical findings . Arch Ophthalmol , 1984;102:671-674.Crossref 4. Smith VC, Pokorny J, Ernest JTE, et al: Visual function in acute posterior multifocal placoid pigment epitheliopathy . Am J Ophthalmol 1978;85:192-199. 5. Hansen RM, Fulton AB: Cone pigments in acute posterior multifocal placoid pigment epitheliopathy . Am J Ophthalmol 1981;91:465-468. 6. Gass JDM: Acute posterior multifocal placoid pigment epitheliopathy . Arch Ophthalmol 1968;80:177-185.Crossref 7. Alpern M, Maaseidvaag F, Ohba N: The kinetics of cone visual pigments in man . Vision Res 1971;11:539-549.Crossref 8. Sieving PA: In vivo determination of visual pigment regeneration in humans by measurements of the early receptor potential (ERP), thesis. University of Illinois Medical Center, Chicago, 1981. 9. Sieving PA, Fishman GA, Alexander KR, et al: Early receptor potential (ERP) recordings in human ocular siderosis . Arch Ophthalmol 1983;101:1716-1720.Crossref 10. Osterberg G: Topography of the layers of rods and cones in the human retina . Acta Ophthalmol 1935;13( (suppl 6) ):11-102. 11. Sieving PA, Fishman GA: Rod contribution to the human early receptor potential (ERP) estimated from monochromats' data . Doc Ophthalmol Proc Series 1982;31:95-102. 12. Krill AE, Deutman AF: Acute retinal pigment epitheliitus . Am J Ophthalmol 1972;74:193-205. 13. Fishman GA, Rabb MF, Kaplan J: Acute posterior multifocal placoid pigment epitheliopathy . Arch Ophthalmol 1974;92:173-177.Crossref 14. Ryan SJ, Maumenee AE: Birdshot retinochoroidopathy . Am J Ophthalmol 1980;89:31-45. 15. Pak WL: Some properties of the early electrical response in the vertebrate retina . Cold Spring Harbor Symp Quant Biol 1965;30:493-499.Crossref 16. Brindley GS, Gardner-Medwin AR: The origin of the early receptor potential of the retina . J Physiol 1966;182:185-194. 17. Smith VC, Pokorny J, Diddie KR: Color matching and Stiles-Crawford effect in central serous choroidopathy . Mod Probl Ophthalmol 1978;19:284-295. 18. Weinstein GW, Hobson RR, Dowling JE: Light and dark adaptation in the isolated rat retina . Nature 1967;215:134-138.Crossref

Bec, Pierre;Adam, Philippe;Mathis, André;Alberge, Yves;Roulleau, Jean;Arne, Jean Louis

doi: 10.1001/archopht.1984.01040030536010pmid: 6721751

Abstract • Optic nerve head drusen are rare, inherited concretions, which are almost always calcified; their appearance must be known because they represent one of the major causes of pseudopapilledema. The computed tomographic (CT) scan can show small and buried drusen, which are sometimes difficult to diagnose by the ophthalmoscopic examination. Four cases of drusen (two bilateral and two unilateral) were confirmed or diagnosed by high-resolution CT. The CT appearance of drusen is characteristic because the calcifications are well defined, punctate, and strictly located in the optic disc. The use of high-resolution CT scanners is very helpful. References 1. Daily MJ, Smith JL, Dickens W: Giant drusen (astrocytic hamartoma) of the optic nerve seen with computerized axial tomography . Am J Ophthalmol 1976;81:100-101. 2. Frisen L, Scholdstrom G, Svendsen P: Drusen of the optic nerve head: Verification by computerized tomography . Arch Ophthalmol 1978;96:1611-1614.Crossref 3. Trokel SL, Hilal SK: Submillimeter resolution CT scanning of orbital diseases . Ophthalmology 1980;87:412-417.Crossref 4. Edwards MK, Buncic JR, Harwood-Nash DC: Optic disc drusen . J Comput Assist Tomogr 1982;6:383-384.Crossref 5. Peyster RG, Hoover ED, Hershey BL, et al: High resolution CT of lesions of the optic nerve . AJNR 1983;4:169-174. 6. Turner RM, Gutman I, Hilal SK, et al: CT of drusen bodies and other calcific lesions of the optic nerve: Case report and differential diagnosis . AJNR 1983;4:175-178. 7. Hogan MJ, Zimmerman LE: Ophthalmic Pathology. Philadelphia, WB Saunders Co, 1962. 8. Hoyt WF, Pont ME: Pseudopapilledema: Anomalous elevation of the optic disc: Pitfalls in diagnosis and management . JAMA 1962;181:191-196.Crossref 9. Walsh FB, Hoyt WF: Clinical Neuro-Ophthalmology , ed 3. Baltimore, Williams & Wilkins Co, 1974. 10. Friedman AH, Beckerman B, Gold DH: Drusen of the optic disc . Surv Ophthalmol 1977;21:375-390.Crossref 11. Lorentzen SE: Drusen of the optic disc: A clinical and genetic study . Dan Med Bull 1967; 14:293-298. 12. Reese A: Relation of drusen of the optic nerve to tuberous sclerosis . Arch Ophthalmol 1940;24:187-205.Crossref 13. Friedman AH, Modi S, Gartner S: Drusen of the optic disc: A retrospective study in cadaver eyes . Br J Ophthalmol 1975;59:513-521. 14. Spencer WH: Drusen of the optic disc and aberrant axoplasmic transport . Am J Ophthalmol 1978;85:1-12. 15. Rubinstein K, Muntaz A: Retinal complications of optic disc drusen . Br J Ophthalmol 1982;66:83-95.Crossref 16. Trincao R, Cunha-Vaz JG, Pires JM: Astrocytic hamartoma of the optic disc in localized neuro-fibromatosis (von Recklinghausen's disease) . Ophthalmologica 1973;167:465-469.Crossref 17. Sundheim JL, Lapayowker MS: Calcification and ossification within the orbit . Radiology 1976;121:391-397. 18. Bullock JD, Campbell RJ, Waller RR: Calcification in retinoblastoma . Invest Ophthalmol Vis Sci 1977;16:252-255. 19. Brant-Zawadski M, Enzmann DR: Orbital computed tomography: Calcific densities of the posterior globe . J Comput Assist Tomogr 1979; 3:503-505.Crossref 20. Gass JDM, Guerry RK, Jack RL,et al: Choroidal osteoma . Arch Ophthalmol 1978;96:428-435.Crossref 21. Bisaria KK,Garg KC, Wahal KM: Calcifying orbital hemangioendothelioma . Am J Ophthalmol 1966;62:340-343. 22. Kollarits CR, Moss ML, Cogan DG, et al: Scleral calcifications in hyperparatyroidism: Demonstration by computed tomography . J Comput Assist Tomogr 1977;1:500-504.Crossref 23. Tayebi H: Ocular calcification and retrolental fibroplasia . AJR 1956;76:583-593.