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      Analysis of Retinal Nerve Fiber Layer Thickness in Patients with Pseudoexfoliation Syndrome Using Optical Coherence Tomography

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          Abstract

          Objective: To evaluate the retinal nerve fiber layer (RNFL) thickness in patients with unilateral pseudoexfoliation syndrome (PXS) without glaucoma by using optical coherence tomography (OCT). Methods: 22 patients with unilateral PXS were evaluated. Group 1 included the eyes with the pseudoexfoliation, group 2 included the fellow eyes; 18 age-matched normal control eyes were assessed in group 3. The mean and segmental RNFL thickness in eyes with pseudoexfoliation and their fellow eyes in patients with unilateral PXS was compared to age-matched control subject eyes. Results: The RNFL in patients with PXS were significantly thinner than controls in all quadrants except the nasal quadrant with regard to segmental analysis (p < 0.05). This RNFL loss was apparent at 7, 10 and 11 o’clock of the PXS eyes with regard to clock hour position (p < 0.05). In the fellow eyes, no significant difference in RNFL measurement was found except the temporal quadrant when compared with the controls. In the analysis with regard to clock hour position, no significant reduction in RNFL thickness was found except in the 11-o’clock segment. In PXS eyes, RNFL thicknesses at the inferior quadrant and the 1-, 2- and 5-o’clock segments were significantly lower than in non-PXS eyes (p < 0.05). Conclusions: This study suggests that PXS without glaucoma may be associated with a thinner RNFL compared with those of age-matched control subjects and non-PXS fellow eyes. Further studies are needed to clarify the relationship between the decrease in RNFL thickness and the development of glaucomatous damage in eyes with pseudoexfoliation.

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          Most cited references 19

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          Exfoliation Syndrome

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            Pseudoexfoliation syndrome for the comprehensive ophthalmologist. Intraocular and systemic manifestations.

            Renewed interest in pseudoexfoliation syndrome (PEX) may be attributed to an increased awareness of many clinical risks not only for open-angle glaucoma and its recent recognition as a generalized disorder. This review summarizes the range of intraocular and extraocular manifestations. Involvement of all tissues of the anterior segment of the eye results in a spectrum of intraocular complications that have management implication for all practicing ophthalmologists. The study design was a review. Clinical diagnosis depends on biomicroscopy, biocytology, and laser-tyndallometry. Laboratory research methods range from light and electron microscopy, to immunohistochemical and molecular biologic approaches. Clinical-histopathologic correlations focus on the involvement of lens (PEX-phacopathy), zonular apparatus (zonulopathy), ciliary body (cyclopathy), iris (iridopathy), trabecular meshwork (trabeculopathy), and cornea (corneal endotheliopathy) leading to the following complications: (1) open-angle glaucoma as well as angle-closure glaucoma due to pupillary and ciliary block; (2) phacodonesis, lens dislocation, and increased incidence of vitreous loss in extracapsular cataract surgery caused by alterations of the zonular apparatus and its insertion into the ciliary body and lens; (3) blood-aqueous barrier breakdown (pseudouveitis), anterior chamber hypoxia, iris stromal hemorrhage, pigment epithelial melanin dispersion, poor or asymmetric pupillary dilatation, and formation of posterior synechiae due to involvement of all cell populations of the iris; and (4) early diffuse corneal endothelial decompensation explained by a damaged and numerically reduced endothelium. In view of the multitude of clinical complications, PEX is of relevance to comprehensive ophthalmologists, including specialists in glaucoma, cataract, cornea, neuro-ophthalmology, and retina. Special attention to the risks associated with PEX is advised before, during, and after surgery.
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              Neuroprotection in relation to retinal ischemia and relevance to glaucoma.

              Management of glaucoma is directed at the control of intraocular pressure (IOP), yet it is recognized now that increased IOP isjust an important risk factor in glaucoma. Therapy that prevents the death of ganglion cells is the main goal of treatment, but an understanding of the causes of ganglion cell death and precisely how it occurs remains speculative. Present information supports the working hypothesis that ganglion cell death may result from a particular form of ischemia. Support for this view comes from the fact that not all types of retinal ischemia lead to the pathologic findings seen in glaucomatous retinas or to cupping in the optic disk area. Moreover, in animal experiments in which ischemia is caused by elevated IOP, a retinal abnormality similar to that seen in true glaucoma is produced, whereas after occlusion of the carotid arteries a different pattern of damage is found. In ischemia, glutamate is released, and this initiates the death of neurons that contain ionotropic glutamate (NMDA) receptors. Elevated glutamate levels exist in the vitreous humor of patients with glaucoma, and NMDA receptors exist on ganglion cells and a subset of amacrine cells. Experimental studies have shown that a variety of agents can be used to prevent the death of retinal neurons (particularly ganglion cells) induced by ischemia. These agents are generally those that block NMDA receptors to prevent the action of the released glutamate or substances that interfere with the subsequent cycle of events that lead to cell death. The major causes of cell death after activation of NMDA receptors are the influx of calcium into cells and the generation of free radicals. Substances that prevent this cascade of events are, therefore, often found to act as neuroprotective agents. For a substance to have a role as a neuroprotective agent in glaucoma, it would ideally be delivered topically to the eye and used repeatedly. It is, therefore, of interest that betaxolol, a beta-blocker presently used to reduce IOP in humans, also has calcium channel-blocking functions. Moreover, experimental studies show that betaxolol is an efficient neuro protective agent against retinal ischemia in animals, when injected directly into the eye or intraperitoneally.
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                Author and article information

                Journal
                OPH
                Ophthalmologica
                10.1159/issn.0030-3755
                Ophthalmologica
                S. Karger AG
                0030-3755
                1423-0267
                2007
                August 2007
                30 August 2007
                : 221
                : 5
                : 299-304
                Affiliations
                Department of Ophthalmology, School of Medicine, Kocaeli University, Kocaeli, Turkey
                Article
                104759 Ophthalmologica 2007;221:299–304
                10.1159/000104759
                17728551
                © 2007 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Tables: 2, References: 31, Pages: 6
                Categories
                Original Paper

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