The influence of posterior capsule opacification on scanning laser polarimetry.
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Cataract↗
Biomedical subjects
M D Pinazo-Duran
Publications and source records attributed to M D Pinazo-Duran.
Effect of posterior capsular opacification removal on automated perimetry.
PURPOSE: Although posterior capsular opacification (PCO) is a common phenomenon in a considerable number of ophthalmologic patients, no prospective controlled trials assessing its influence on automated perimetry exist. This technique continues as a standard in the diagnosis of glaucoma and neuro-ophthalmological diseases. The aim of the present report is to investigate the effect of PCO on automated visual field examination. METHODS: A total of 26 PCO affected eyes of 26 patients had Humphrey SITA standard (program 24-2) immediately before, and between 1 and 8 weeks after Neodymium : YAG capsulotomy. The effect of learning associated with repeated testing was controlled with automated perimetry before enrollment and visual fields of the fellow eye. Best-corrected visual acuity (BCVA), intraocular pressure (IOP), and global perimetric pre- and post-laser indices were compared using the Student's t-test for paired samples. Correlation and linear regression analyses were also performed. RESULTS: BCVA and mean deviation (MD) improved following capsulotomy. Pattern standard deviation (PSD), an indicator of localized defects in the field, also improved significantly when PCO was solved. Moreover, a strong association among BCVA, MD, and PSD was shown both prior to and after capsulotomy. CONCLUSION: PCO is a heterogeneous mean opacity. This polymorphism may alter visual field results, and may even simulate the perimetric behaviour of other pathologies such as glaucoma. Consequently, the presence of PCO should be considered in the interpretation of any automated perimetry in pseudophakic patients. In addition, the values obtained before capsulotomy may partially predict the values obtained after capsulotomy.
Aged↗
Optic nerve alterations in apolipoprotein E deficient mice.
PURPOSE: To study the morphologic characteristics of the optic nerve (ON) by using an experimental model of knockout mice for expression of the ApoE gene. METHODS: Eyeballs with the retrobulbar ON attached were obtained from 24-week-old mice. Using morphologic and morphometric techniques and light and transmission electron microscopy, the ON characteristics were determined in three groups of mice: 1) wild type mice as the controls (CG; n = 15), 2) knockout mice for the ApoE gene (ApoE-G; n = 15), and 3) knockout mice for the ApoE gene that were fed a cholesterol-supplemented diet (ApoED-G; n = 15). RESULTS: The ON cross-sectional area was significantly higher in the ApoE-G than in the CG (p < 0.001) mice, whereas no significant changes were noticed between the ApoE-G and ApoED-G mice. Significant differences were noticed between those groups regarding the myelination index. Higher density of intra-axonal degeneration and myelin sheath alterations were found in both ApoE groups in respect to the CG. CONCLUSIONS: These results suggest that ApoE knockout mice have changes in ON morphology and myelination.
Animals↗
Lipid peroxidation in proliferative vitreoretinopathies.
PURPOSE: To study the lipid hydroperoxide activity in vasoproliferative and fibroproliferative retinal disorders. METHODS: Vitreous body samples from patients undergoing vitrectomy because of proliferative vitreoretinopathy (PVR; n = 12) or proliferative diabetic retinopathy (PDR; n = 15), and rhegmatogenous retinal detachment/macular hole/epiretinal membranes as the comparison group (CG; n = 14), were analysed for protein content and basal and induced lipid peroxidation (LPO), as determined by the thiobarbituric acid reactive substances (TBARS) test and LPO 586 commercial kit. The antioxidant activity for superoxide dismutase (SOD) and catalase (CAT) was also assayed. RESULTS: Malondialdehyde (MDA)-like metabolites and 4-hydroxynonenal (4-HNE) mean values were first measured to assess basal LPO, and found to be significantly higher in the PVR and PDR cases than in the CG (p < or = 0.0001). LPO induced by nicotine adenine dinucleotide phosphate iron (NADPH-Fe) was then assayed and the data showed that MDA mean values were 5-fold greater for the PVR and PDR eyes than in the case of basal LPO (p < or = 0.0001). SOD activity was significantly smaller in the PVR (p = 0.0010) and PDR (p < or = 0.0001) groups than in the CG. CAT levels displayed significantly lower values in the PVR and PDR cases than in the CG (p < or = 0.0001). No significant differences in free radical (FR) formation and antioxidant status between PVR and PDR patients were observed. CONCLUSIONS: Fibrovascular proliferative vitreoretinopathies correlate with increased FR formation and decreased antioxidant activity in the human vitreous body.
Adult↗
Gestational ethanol-induced changes in protein expression during the morphogenesis of the rat optic nerve.
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Abnormalities, Drug-Induced↗
Developmental changes in the optic nerve related to ethanol consumption in pregnant rats: analysis of the ethanol-exposed optic nerve.
Visual impairment is one of the most common ophthalmic abnormalities in fetal alcohol syndrome. Pathologic changes in optic nerve development related to alcohol consumption could be involved in this dysfunction. In order to assess the consequences of pre- and postnatal exposure to alcohol on the developing optic nerve, we administered an ethanol-containing liquid diet (5% w/v) before and during gestation and throughout lactation to rats and their offspring. A group of control animals were kept on a pair-fed isocaloric diet. The optic nerves were obtained at key stages from fetuses (21 days of gestation) and pups (4, 7, 14, 21 and 28 postnatal days). Samples of the optic nerve cross-section, behind the eyeball, were processed for analysis of gliogenesis, myelinogenesis, axonal growth, and remodelling events, using light and electron microscopy. Qualitative, morphometric, and immunocytochemical analyses, alternatively using anti-GFAP and anti-MBP antibodies, were carried out. Optic nerve cross-sections from prenatal and postnatal alcohol-exposed rats showed a decrease in size. Ultrastructural alterations and retarded development in macroglial cells, optic axons, and myelin sheath were also observed. The most prominent abnormalities were: damage of cytoplasmic organelles and disorganization of cytoskeleton in astrocytes; a decrease in free ribosome density and nuclear membrane inclusions in oligodendrocytes; and fragmentation of lamellae, aberrant myelin sheaths and intralamellar inclusions in myelin. These findings suggest that alcohol abuse during pregnancy is teratogenic to the optic nerve and closely related to the altered visual function.
Abnormalities, Drug-Induced↗
Optic nerve hypoplasia in fetal alcohol syndrome: an update.
Optic nerve hypoplasia was detected in up to one half of a group of Swedish children born to alcoholic mothers. Using an experimental model of pre- and postnatal alcohol exposure in rats fed a liquid diet, reduced optic nerve size from gestational day 21 (294 +/- 26 x 10(2) microns2 vs 502 +/- 16 x 10(2) microns2; n = 6; p < or = 0.001) to later in development was observed as a result of the daily mean blood alcohol levels achieved in dams and their offspring. Altered glial cells and degenerating and atrophic optic axons, myelin sheaths and ganglion cells were frequent in the alcohol-exposed optic nerves. Smaller optic nerve (1.918 +/- 61 x 10(2) microns2 vs 2.195 +/- 40 x 10(2) microns2; n = 4; p < or = 0.001), reduced gaglion cell and axonal densities, and ultrastructural damage to the macroglial cells and myelin sheaths were also detected in the treated group. All these changes remained in the retina and optic nerve of the oldest rats, as a consequence of the long-lasting effects of prenatal alcohol exposure. In summary, alcohol as a major teratogenic agent may induce dysmorphogenesis and irremediable damage to the retina and optic nerve, which frequently manifests itself as hypoplastic optic nerve.
Adult↗
Optic nerve alterations in PTEN +/- mice.
PURPOSE: To study the morphologic characteristics of the optic nerve (ON) by using an experimental model of knockout mice for the expression of the PTEN gene, mainly involved in cell cycle arrest, apoptosis control, and cell size regulation. METHODS: The eyeballs with the retrobulbar ON attached were obtained from 26-week-old mice. By using morphologic and morphometric techniques, light and electron transmission microscopy, the ON characteristics were determined in two groups of mice: 1) 'wild type' mice as the control group (C-G; n=15), 2) heterozygous knockout mice (+/-) for the PTEN gene (PTEN-G; n=15). Glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP) were studied using Western blot and immunoblotting approaches. RESULTS: The ON cross-sectional area was significantly higher in the PTEN-G than in the C-G (p<0.001). The axon sizes in mutant animals were much larger than in wild-type mice (p<0.001). No significant differences were noticed between those groups regarding the number of axons forming the ON and the presence of intra-axonal degeneration, myelin sheath alterations, or axoplasm density. No differences were detected in developmental marker protein expression. CONCLUSIONS: The morphologic and morphometric results suggest that heterozygous PTEN knockout mice had hypertrophic ON without ultrastructural alterations.
Animals↗