Susceptibility to Neurodegeneration in a Glaucoma Is Modified by Bax Gene Dosage

In glaucoma, harmful intraocular pressure often contributes to retinal ganglion cell death. It is not clear, however, if intraocular pressure directly insults the retinal ganglion cell axon, the soma, or both. The pathways that mediate pressure-induced retinal ganglion cell death are poorly defined, and no molecules are known to be required. DBA/2J mice deficient in the proapoptotic molecule BCL2-associated X protein (BAX) were used to investigate the roles of BAX-mediated cell death pathways in glaucoma. Both Bax (+/−) and Bax (−/−) mice were protected from retinal ganglion cell death. In contrast, axonal degeneration was not prevented in either Bax (+/−) or Bax (−/−) mice. While BAX deficiency did not prevent axonal degeneration, it did slow axonal loss. Additionally, we compared the effects of BAX deficiency on the glaucoma to its effects on retinal ganglion cell death due to two insults that are proposed to participate in glaucoma. As in the glaucoma, BAX deficiency protected retinal ganglion cells after axon injury by optic nerve crush. However, it did not protect retinal ganglion cells from N-methyl-D-aspartate (NMDA)-induced excitotoxicity. BAX is required for retinal ganglion cell death in an inherited glaucoma; however, it is not required for retinal ganglion cell axon degeneration. This indicates that distinct somal and axonal degeneration pathways are active in this glaucoma. Finally, our data support a role for optic nerve injury but not for NMDA receptor-mediated excitotoxicity in this glaucoma. These findings indicate a need to understand axon-specific degeneration pathways in glaucoma, and they suggest that distinct somal and axonal degeneration pathways may need to be targeted to save vision

The Effect of Swimming Goggles on Intraocular Pressure and Blood Flow within the Optic Nerve Head

Purpose: Goggles are frequently worn in the sport of swimming and are designed to form a seal around the periorbital tissue orbit. The resultant pressure on the eye may have the potential to affect intraocular pressure and blood flow of the optic nerve head. This study evaluates the influence of wearing swimming goggles on intraocular pressure (IOP) and blood flow of the ocular nerve head (ONH) in normal subjects. Materials and Methods: Thirty healthy participants took part in this study. The IOP of each participant was measured using a Goldmann tonometer. Measurements were taken immediately before putting on swimming goggles, at 5, 10, 30, and 60 minutes after putting on swimming goggles, and then immediately after taking off the goggles. Blood flow of the ONH was measured using the Heidelberg retinal flowmeter. Results: The average IOP before, during and after wearing the swimming goggles were 11.88 ± 2.82 mmHg, 14.20 ± 2.81 mmHg and 11.78 ± 2.89 mmHg, respectively. The IOP increased immediately after putting on the goggles (p < 0.05) and then returned to normal values immediately after removal (p> 0.05). Blood flow of the ONH was 336.60 ± 89.07 Arbitrary Units (AU) before and 319.18 ± 96.02 AU after the goggles were worn (p < 0.05). Conclusion: A small but significant IOP elevation was observed immediately after the swimming goggles were put on. This elevated IOP was maintained while the goggles were kept on, and then returned to normal levels as soon as they were taken off. Blood flow of the ONH did not change significantly throughout the experiment. These facts should be considered for safety concerns, especially in advanced glaucoma patients

Specification of progression in glaucomatous visual field loss, applying locally condensed stimulus arrangements

The goal of this work was to (i) determine patterns of progression in glaucomatous visual field loss, (ii) compare the detection rate of progression between locally condensed stimulus arrangements and conventional 6° × 6° grid, and (iii) assess the individual frequency distribution of test locations exhibiting a local event (i.e., an abrupt local deterioration of differential luminance sensitivity (DLS) by more than -10dB between any two examinations). The visual function of 41 glaucomatous eyes of 41 patients (16 females, 25 males, 37 to 75 years old) was examined with automated static perimetry (Tuebingen Computer Campimeter or Octopus 101-Perimeter). Stimuli were added to locally enhance the spatial resolution in suspicious regions of the visual field. The minimum follow-up was four subsequent sessions with a minimum of 2-month (median 6-month) intervals between each session. Progression was identified using a modified pointwise linear regression (PLR) method and a modified Katz criterion. The presence of events was assessed in all progressive visual fields. Eleven eyes (27%) showed progression over the study period (median 2.5 years, range 1.3–8.6 years). Six (55%) of these had combined progression in depth and size and five eyes (45%) progressed in depth only. Progression in size conformed always to the nerve fiber course. Seven out of 11 (64%) of the progressive scotomata detected by spatially condensed grids would have been missed by the conventional 6° × 6° grid. At least one event occurred in 64% of all progressive eyes. Five of 11 (46%) progressive eyes showed a cluster of events. The most common pattern of progression in glaucomatous visual fields is combined progression in depth and size of an existing scotoma. Applying individually condensed test grids remarkably enhances the detection rate of glaucomatous visual field deterioration (at the expense of an increased examination time) compared to conventional stimulus arrangements