AAO Journal Archive
- Classification of Vitreous Seeds in Retinoblastoma
- Topical 5-Fluorouracil 1% as Primary Treatment for Ocular Surface Squamous Neoplasia
- Individualized Stabilization Criteria–Driven Ranibizumab versus Laser in Branch Retinal Vein Occlusion
- Correlation of Histologic Features with In Vivo Imaging of Reticular Pseudodrusen
- Pseudodrusen and Incidence of Late Age-Related Macular Degeneration in Fellow Eyes in the Comparison of Age-Related Macular Degeneration Treatments Trials
- Pharmacotherapies for Retinal Detachment
- Can Automated Imaging for Optic Disc and Retinal Nerve Fiber Layer Analysis Aid Glaucoma Detection?
- Suture Colonization Rate in Adjustable Strabismus Surgery
- Genetic and Dietary Factors Influencing the Progression of Nuclear Cataract
- Diagnostic Accuracy of Optical Coherence Tomography and Scanning Laser Tomography for Identifying Glaucoma in Myopic Eyes
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Corneal hydrops is an uncommon condition occurring in 2%−3% of patients with keratoconus. It is caused by a leak of aqueous into the cornea through a tear in Descemet's membrane causing severe corneal edema (Fig 1). Acute hydrops occurred in a 51-year-old man. The hydrops resolved over 4-months with conservative medical treatment, and a penetrating keratoplasty was performed. The histopathology (hematoxylin and eosin and periodic acid-Schiff) revealed thinning of the apical stroma (Fig 2, asterisk), breaks in Bowman's membrane (Fig 3, white arrow) and subepithelial bullae (Fig 4, open arrow).
Read more: Changes in the Corneal Architecture Following Corneal Hydrops
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We thank Dr Cullen for his interest in our editorial and thoughtful comments. With regard to the expressed notion that hyperemia and edema should indicate optic nerve head ischemia, one should recognize that in bona fide ischemic optic neuropathy such as in giant cell arteritis that Dr Cullen refers to in an earlier article from his Singapore series on ischemic optic neuropathy (ION),1 it is pallor rather than hyperemia that is the predominant sign. We believe that the noted hyperemia in so-called nonarteritic anterior ischemic optic neuropathy (NAION) is indicative of an altogether different process at hand.
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A 92-year-old woman had her right eye removed for a submacular choroidal melanoma. Four weeks before surgery her vision was counting fingers and intraocular pressure 17 mm Hg. The tumor measured 14.6×9.6 mm and was 4.4 mm thick. The nasal portion of the optic disc was visible and interpreted as normal (Fig A). In the laboratory, the eye was opened horizontally. Histologically, cavernous degeneration of the optic nerve was located nasally (N) opposite the melanoma (Figs B and C). Pial septi were widely dilated.
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Katz and associates are most appreciative of the new concept we propose in our editorial. That it is dynamic shear force injury due to epipapillary membrane vitreoglial separation from peripapillary and papillary axons that leads to pathology, heretofore described as nonarteritic anterior ischemic optic neuropathy (NAION). Their eloquent appraisal of our editorial and examples of other English misnomers is music to our ears.
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We read with relish the editorial of Parsa and Hoyt arguing for a change in prism through which we see what we had heretofore called nonarteritic anterior ischemic optic neuropathy (NAION).1 Their elegant and cogent summary of consequences and associations of vitreopapillary traction, when collated as they have done, convincingly argue their point. As the English horn is neither English nor a horn, so too, NAION is not ischemic, at least, not primarily so.