Reversal of optic disc cupping in glaucoma.

AIM: To study whether reversal of optic disc cupping after intraocular pressure (IOP) reduction is related to risk of glaucoma progression. METHODS: In this prospective follow-up study, where 51 patients with exfoliation glaucoma and five with ocular hypertension combined with exfoliation syndrome were followed for 6 years after IOP reduction, 24 showed progression of glaucoma in visual fields or optic nerve head (ONH) stereophotographs. ONH topography was measured with the Heidelberg Retina Tomograph (HRT). A decrease in HRT parameter cup volume of more than 5% was considered cup reversal. Multiple logistic regression was used to model progression of glaucoma. RESULTS: Cup reversal (OR 0.226; 95% CI 0.055 to 0.918, p = 0.037), final IOP (OR 1.216; 95% CI 1.000 to 1.479, p = 0.050) and visual field mean defect at entry (OR 1.158; 95% CI 1.034 to 1.296, p = 0.011) were associated with progression. IOP change from study entry to 6-year control visit was not associated with progression (OR 0.964, 95% CI 0.850 to 1.092, p = 0.56). CONCLUSION: Cup reversal seemed to be an independent protective factor for progression of glaucoma.

Essential iris atrophy, pigment dispersion, and glaucoma in DBA/2J mice.

PURPOSE: To characterize ocular abnormalities associated with iris atrophy in DBA/2J mice and to determine whether mice of this strain develop elevated intraocular pressure (IOP) and glaucoma. METHODS: Different approaches, including slit-lamp biomicroscopy, ophthalmoscopic examination, ultrasound backscatter microscopy, and histology were used to examine the eyes of DBA/2J mice ranging from 2 to 30 months old. IOP was measured in DBA/2J mice of different ages. RESULTS: DBA/2J mice were found to develop pigment dispersion, iris transillumination, iris atrophy, anterior synechias, and elevated IOP. IOP was elevated in most mice by the age of 9 months. These changes were followed by the death of retinal ganglion cells, optic nerve atrophy, and optic nerve cupping. The prevalence and severity of these lesions increased with age. Optic nerve atrophy and optic nerve cupping was present in the majority of mice by the age of 22 months. CONCLUSIONS: DBA/2J mice develop a progressive form of secondary angle-closure glaucoma that appears to be initiated by iris atrophy and the associated formation of synechias. This mouse strain represents a useful model to evaluate mechanisms of pressure-related ganglion cell death and optic nerve atrophy, and to evaluate strategies for neuroprotection.