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      Severe visual loss and recovery post trabeculectomy- A case report

      American journal of ophthalmology case reports
      Elsevier BV

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          Neuronal death in glaucoma.

          H Quigley (1998)
          Glaucoma is recognized to have its major detrimental effect upon the eye by killing retinal ganglion cells. The process of cell death appears to be initiated at the optic nerve head, though other sites of injury are possible but unsubstantiated. At present the injury at the nerve head seems related to the level of the eye pressure, but its detailed mechanism is as yet unexplained. There is a greater loss of ganglion cells from some areas of the eye, and this feature of glaucoma seems related to the regional structure of the supporting connective tissues of the optic nerve head. Larger retinal ganglion cells have been consistently shown to have somewhat greater susceptibility to injury in glaucoma, though all cells are injured, even early in the process. Ganglion cells die by apoptosis in human and experimental glaucoma, opening several potential areas for future therapies to protect them from dying. Neurotrophin deprivation is one possible cause of cell death and replacement therapy is a potential approach to treatment.
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            Ganglion cell losses underlying visual field defects from experimental glaucoma.

            To investigate the relationship between ganglion cell losses and visual field defects caused by glaucoma. Behavioral perimetry and histology data were obtained from 10 rhesus monkeys with unilateral experimental glaucoma that was induced by argon laser treatments to their trabecular meshwork. After significant visual field defects had developed, the retinas were collected for histologic analysis. The ganglion cells were counted by light microscopy in cresyl violet-stained retina sections, and the percentage of ganglion cell loss (treated to control eye counts) was compared with the depth of visual field defect (treated to control eye thresholds) at corresponding retinal and perimetry test locations. Sensitivity losses as a function of ganglion cell losses were analyzed for Goldmann III, white and Goldmann V, and short- and long-wavelength perimetry test stimuli. The relationship between the proportional losses of ganglion cells and visual sensitivity, measured with either white or colored stimuli, was nonlinear. With white stimuli, the visual sensitivity losses were relatively constant (approximately 6 dB) for ganglion cell losses of less than 30% to 50%, and then with greater amounts of cell loss the visual defects were more systematically related to ganglion cell loss (approximately 0.42 dB/percent cell loss). The forms of the neural-sensitivity relationships for visual defects measured with short- or long-wavelength perimetry stimuli were similar when the visual thresholds were normalized to compensate for differences in expected normal thresholds for white and colored perimetry stimuli. Current perimetry regimens with either white or monochromatic stimuli do not provide a useful estimate of ganglion cell loss until a substantial proportion have died. The variance in ganglion cell loss is large for mild defects that would be diagnostic of early glaucoma and for visual field locations near the fovea where sensitivity losses occur relatively late in the disease process. The neural-sensitivity relationships were essentially identical for both white and monochromatic test stimuli, and it therefore seems unlikely that the higher sensitivity for detecting glaucoma with monochromatic stimuli is based on the size-dependent susceptibility of ganglion cells to injury from glaucoma.
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              Reversal of lamina cribrosa displacement after intraocular pressure reduction in open-angle glaucoma.

              To compare the change in lamina cribrosa (LC) displacement in response to intraocular pressure (IOP) lowering in patients with open-angle glaucoma (OAG) using spectral-domain optical coherence tomography (SD-OCT). Observational case series. One hundred eyes of 100 patients with OAG in whom IOP at the follow-up examination had decreased by at least 20% compared with the baseline IOP. Serial horizontal B-scan images of the optic nerve head (ONH) were obtained from each eye using enhanced depth imaging SD-OCT. Approximately 65 B-scans covering the optic discs were obtained before and 3 to 6 months after lowering IOP. The baseline and follow-up LC depths (the distance from the Bruch's membrane opening plane to the level of the anterior LC surface) were measured in B-scan images from each eye. The mean and maximum amount of reductions in LC depth measured in the 7 selected B-scan images. Intraocular pressure decreased from 21.2±9.1 to 10.5±2.6 mmHg. The percent of IOP reduction was significantly related to the untreated IOP (P < 0.001). There was a significant decrease in the LC depth at the follow-up examination compared with the baseline value (P < 0.001). The magnitude of LC depth reduction was significantly associated with younger age, higher untreated IOP, higher baseline IOP, and greater percent of IOP reduction (all P < 0.02). Reversal of the LC displacement was observed after IOP-lowering treatment in OAG. The degree of LC displacement reversal was related to the amount of IOP lowering. Copyright © 2013 American Academy of Ophthalmology. Published by Elsevier Inc. All rights reserved.
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                10.1016/j.ajoc.2018.02.003
                http://creativecommons.org/licenses/by-nc-nd/4.0/

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