doi: 10.1001/archopht.1989.01070020803001pmid: 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.
doi: 10.1001/archopht.1989.01070020804002pmid: 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.
doi: 10.1001/archopht.1989.01070020805003pmid: N/A
Abstract To the Editor. —I write this letter to correct an error that appeared in the March 1988 issue of the Archives.1 I mistakenly described the patients as receiving cataract extractions with implantation of an intraocular lens. The patients in this study were aphakic and not pseudophakic. References 1. Flach AJ, Graham J, Kruger LP, Stegman RC, Tanenbaum L. Quantitative assessment of postsurgical breakdown of the blood-aqueous barrier following administration of 0.5% Ketorolac tromethamine solution: a double-masked, paired comparison with vehicle-placebo solution study . Arch Ophthalmol . 1988;106:344-347.Crossref
doi: 10.1001/archopht.1989.01070020805005pmid: 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. —The comments of Yuzbasiyan-Gurkan and Brewer concerning their clinical experiences with the relative safety of long-term oral zinc administration are illuminating. It is reasonable to recommend the consumption of a zinc preparation with less potential for gastric irritation so that the supplement may be taken at a time when its absorption is promoted. Additional supplementation with 1 mg of copper daily also appears reasonable.Yuzbasiyan-Gurkan and Brewer alluded to the variability of zinc uptake. This would likely be a problem regardless of the type of preparation. It is suspected, but not known with certainty, that the absorption of trace minerals may vary with age, as it does with a variety of disease processes. More needs to be understood concerning this matter.A single trace metal nutrient does not exist in vivo in isolation. It participates in metabolic and functional links involving a variety of other elements. It seems
Yuzbasiyan-Gurkan, Vilma;Brewer, George J.
doi: 10.1001/archopht.1989.01070020805004pmid: 2627236
Abstract To the Editor. —We read the article by Dr Newsome and colleagues1 with great interest. It was very exciting to learn that in such a well-designed, well-executed, and well-analyzed controlled study, zinc therapy had such a marked effect on reducing the progression of such an important and debilitating disease as macular degeneration. However, we were dismayed by the authors' emphasis on possible zinc toxicity. In their own terms, their abstract closes with, "Because of the pilot nature of the study and the possible toxic effects and complications of oral zinc administration, widespread use of zinc in macular degeneration is not now warranted." Elsewhere in the report the authors expresspecific concerns about anemia and worsening of cardiovascular disease.Our dismay arises from our team having spent the last 20 years administering zinc in relatively high doses to various types of patients and having a very difficult time identifying toxic effects. References 1. Newsome DA, Swartz M, Leone NC, Elston RC, Miller E. Oral zinc in macular degeneration . Arch Ophthalmol . 1988;106:192-198.Crossref 2. Prasad AS, Brewer GJ, Schoomaker EB. Hypocupremia induced by zinc therapy in adults . JAMA . 1978;240:2166-2168.Crossref 3. Oelshlegel FS Jr, Brewer GJ. Absorption of pharmacological doses of zinc . In: Brewer GJ, Prasad AS, eds. Zinc Metabolism: Current Aspects in Health and Disease . New York, NY: Alan R Liss Inc; 1977:299-311. 4. Brewer GJ, Yuzbasiyan-Gurkan V, Young AB. Treatment of Wilson's disease . Semin Neurol . 1987;7:209-220.Crossref
doi: 10.1001/archopht.1989.01070020806006pmid: 2597060
Abstract To the Editor. —In the June 1989 issue of the Archives, Gloor et al1 described a 19-month-old black female infant with a medical history of microcephaly, developmental delay, hypotonia, and seizures. The case was beautifully illustrated.Magnetic resonance imaging showed an arachnoidal cyst and partial agenesis of the corpus callosum. Funduscopic examination, according to the authors, revealed bilateral colobomatous discs. However, careful evaluation of the printed fundus photographs does not show optic disc colobomas but, rather, bilateral optic disc dysplasia and atypical peripapillary pigmentary changes. Moreover, the typical punched-out chorioretinal lesions were not present. These "punched-out" lesions are thought to be diagnostic of Aicardi's syndrome.2 Also, the electroencephalogram (EEG) in the case did not show a pure hypsarrhythmia, highly characteristic of the Aicardi syndrome,3,4 but a "pattern akin to it."Corpus callosum agenesis, arachnoidal cysts, and other neuroradiological midline anomalies have been described in patients with a References 1. Gloor P, Pulido JS, Judisch GF. Magnetic resonance imaging and fundus findings in a patient with Aicardi's syndrome . Arch Ophthalmol . 1989;107:922-923.Crossref 2. Aicardi J, Chevrie JJ, Rousselie F. Le syndrome spasmes en flexion, agenesie calleuse, anomalies chorio-retiniennes . Arch Fr Pediatr . 1969;26:1103-1120. 3. 3. Fariello RG, Chun RW, Doro JM, Buncic JR, Prichard JS. EEG recognition of Aicardi's syndrome . Arch Neurol . 1977;34:563-566.Crossref 4. Kellaway P, Frost JD Jr, Hrachovy RA. Infantile spasms . In: Morselli PL, Pippenger CE, Penry JK, eds. Antiepileptic Drug Therapy in Pediatrics . New York, NY: Raven Press; 1987:115-136.
Gloor, Peter;Pulido, Jose S.;Judisch, G. Frank
doi: 10.1001/archopht.1989.01070020806007pmid: N/A
Abstract In Reply. —We thank Dr van Dalen for his comments. He feels that, based on the chorioretinal, optic disc, and EEG findings, the patient we presented probably does not have Aicardi's syndrome. We maintain that the patient does have Aicardi's syndrome.The fundus photographs in the photo essay clearly show the typical punched-out chorioretinal lesions found in Aicardi's syndrome (compare these photographs with those in a report by Weleber et al1).Typical colobomas of the optic disc are limited to the inferior portion of the disc. However, the colobomas sometimes found in Aicardi's syndrome are atypical, involving the entire circumference of the disc,2 as seen in the photographs of our patient.Hypsarrhythmia on EEG is a variable feature of Aicardi's syndrome. In a review of 43 reported cases of the syndrome, Bertoni et al3 found that only 27 patients had hypsarrhythmia. Fariello et al reviewed 32 EEGs References 1. Weleber RG, Lovrien EW, Isom JB. Aicardi's syndrome: case report, clinical features, and electrophysiologic studies . Arch Ophthalmol . 1978;96: 285-290.Crossref 2. Spencer WH. Optic nerve . In: Spencer WH, ed. Ophthalmic Pathology: An Atlas and Textbook . 3rd ed. Philadelphia Pa: WB Saunders Co; 1986:2355. 3. Bertoni JM, von Loh S, Allen RJ. The Aicardi syndrome: report of 4 cases and review of the literature . Ann Neurol . 1979;5:475-482.Crossref
doi: 10.1001/archopht.1989.01070020806008pmid: 2597061
Abstract To the Editor. —It is necessary to call attention to a major discrepancy in the case report by Greiner et al1 that appeared in the May issue of the Archives.The medical history recorded for the single patient whose case was reported should have led to one set of events. The laboratory results reported correspond to an entirely different set of events; two sets of clinical findings contradict each another. It would be unfortunate if this report were accepted unmodified as part of the methanol literature.According to the authors, the patient, a prisoner in an unnamed jail, was brought to an unnamed emergency department with a history of blurred vision and photophobia of about 10 hours' duration. The only other history recorded by the authors is that on the evening prior to admission to an unnamed hospital the patient drank "about a cupful" of fluid from cans References 1. Greiner JV, Pillai S, Limaye SR, Chu F. Sterno-induced methanol toxicity and visual recovery after prompt hemodialysis . Arch Ophthalmol . 1989:107:643.
Greiner, Jack V;Pillai, Sasikala;Limaye, Suresh R.;Chu, Fred
doi: 10.1001/archopht.1989.01070020806009pmid: 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. —The purpose of our Case Report describing Sterno-induced methanol toxicity and visual recovery after prompt hemodialysis was (1) to describe a case of decreased visual acuity associated with a vague medical history of alcohol ingestion and the importance of using anion and osmolal gaps to promptly diagnose methanol toxicity, and (2) to describe the potential use of prompt hemodialysis for visual recovery. The original manuscript stressed the importance of prompt diagnosis of methanol toxicity and extensively reviewed and discussed the use of anion and osmolal gaps in the diagnosis of methanol toxicity. The imposed length restriction for case reports required the deletion of many of the details and a chronology of events and findings elaborated on in the original manuscript.Regarding the amount of Sterno fluid consumed, the original manuscript described the patient's 3-month history of obtaining alcohol several times weekly. Although the amounts of alcohol consumed were
Kahlenborn, Chris;Sassani, Joseph W.;Sherrard, Maurice;Frankel, Carl A.
doi: 10.1001/archopht.1989.01070020807010pmid: 2597062
Abstract To the Editor. —There is a need in medical education for a simulator on which students and residents can practice the basic skills of ophthalmoscopy. Considerable time would be saved and patient discomfort and inconvenience reduced if the basic skills of ophthalmoscopy could be learned using a practical, inexpensive model system.Although model eyes do exist, they contain significant limitations. For example, some models depend on handpainted reproductions of pathologic findings as rendered on the posterior internal surface of the model.1 There is no flexibility to examine various fundus disorders without purchasing several models. One model uses slide transparencies of the viewing object, resulting in decreased resolution of fundus detail secondary to the inherent "graininess" of such transparencies.2 Finally, other models are too complex or expensive, such as one eye model that contains a photosensitive pupil that dilates in response to mydriatic eye drops.3We have developed References 1. Hamilton F, inventor; Optical education device. US patent 2 068 950. January 26, 1937. Int Cl (35/17). 2. Loeb MK, inventor; American Home Products Corp, assignee. Eye display and viewer, US patent 3177593. April 13, 1965.4 p. Int Cl (35/17). 3. Colenbrander A, Gordon SM, Patterson CD, inventors; University of Miami, assignee. Ophthalmological mannequin with funduscopic eyeground presentation. US patent 23 905130. September 16,1975. 5 p Int Cl G09b 23/ 32.
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