Comparative Optic Disc Analysis in Normal Pressure Glaucoma, Primary Open-angle Glaucoma, and Ocular Hypertension

Tezel, Giilgim; Kass, Michael A.; Kolker, Allan E.; Wax, Martin B.

doi:10.1016/s0161-6420(96)30382-5

Cited by 99 publications

(62 citation statements)

References 30 publications

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“…In addition, IOP is not elevated in all of the eyes exhibiting characteristics of glaucomatous neurodegeneration. Similar clinical (Tezel et al, 1996) and histopathological findings (Wax et al, 1998a) in glaucomatous eyes either with elevated or normal IOP indicate that there is also an IOP-independent component of neuronal damage in glaucoma. Considerable evidence mostly from blood flow studies has illustrated that besides IOP, tissue hypoxia is also associated with the pathogenic mechanisms underlying glaucomatous neurodegeneration.…”

Section: Tissue Stress In the Glaucomatous Optic Nerve Head And Retinasupporting

confidence: 52%

Oxidative stress in glaucomatous neurodegeneration: Mechanisms and consequences

Tezel

2006

Progress in Retinal and Eye Research

615

449

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Reactive oxygen species (ROS) are generated as by-products of cellular metabolism, primarily in the mitochondria. Although ROS are essential participants in cell signaling and regulation, when their cellular production overwhelms the intrinsic antioxidant capacity, damage to cellular macromolecules such as DNA, proteins, and lipids ensues. Such a state of "oxidative stress" is thought to contribute to the pathogenesis of a number of neurodegenerative diseases. Growing evidence supports the involvement of oxidative stress as a common component of glaucomatous neurodegeneration in different subcellular compartments of retinal ganglion cells (RGCs). Besides the evidence of direct cytotoxic consequences leading to RGC death, it also seems highly possible that ROS are involved in signaling RGC death by acting as a second messenger and/or modulating protein function by redox modifications of downstream effectors through enzymatic oxidation of specific amino acid residues. Different studies provide cumulating evidence, which supports the association of ROS with different aspects of the neurodegenerative process. Oxidative protein modifications during glaucomatous neurodegeneration increase neuronal susceptibility to damage and also lead to glial dysfunction. Oxidative stress-induced dysfunction of glial cells may contribute to spreading neuronal damage by secondary degeneration. Oxidative stress also promotes the accumulation of advanced glycation end products in glaucomatous tissues. It is also evident that oxidative stress takes part in the activation of immune response during glaucomatous neurodegeneration, as ROS stimulate the antigen presenting ability of glial cells and also function as co-stimulatory molecules during antigen presentation. By discussing current evidence, this review provides a broad perspective on cellular mechanisms and potential consequences of oxidative stress in glaucoma.

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Section: Tissue Stress In the Glaucomatous Optic Nerve Head And Retinasupporting

confidence: 52%

Oxidative stress in glaucomatous neurodegeneration: Mechanisms and consequences

Tezel

2006

Progress in Retinal and Eye Research

615

449

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“…18,19 Other studies of glaucoma patients have shown abnormalities in blood rheology with increased blood viscosity and reduced erythrocyte deformability. 7,[20][21][22][23][24] In addition to the above clinical associations, a variety of experimental and clinical observations demonstrate circulatory aberrations of the anterior optic nerve, the peripapillary region, [25][26][27][28][29] the choroid, 27,30,31 and the retrobulbar vasculature [32][33][34][35][36][37][38][39][40] in eyes with GON. 33,[40][41][42][43] These apparent alterations in the circulation of the glaucomatous optic nerve may implicate dysfunction of vascular regulatory mechanisms.…”

Section: Glaucoma and Systemic Vascular Diseasementioning

confidence: 99%

Ischemic model of optic nerve injury

Cioffi

2006

American Journal of Ophthalmology

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“…The ImageNet system has been used to evaluate the characteristics of the optic nerve head of large normal and glaucomatous populations Tezel et al 1996). Comparison and good correlation between clinical evaluation and computerized analysis of the optic disc at one point on time has also been reported .…”

Section: Discussionmentioning

confidence: 99%

“…Qualitative or semiquantitative estimates of the optic nerve head by disc drawings or fundus photography (Lichter 1976;Klein et al 1985Klein et al , 1987Tielsch et al 1988;Varma et al , 1992Odberg & Rise 1985;Abrams et al 1994;Coleman et al 1996) and computerized quantitative techniques (Varma et al 1988;Dandona et al 1989;Dreher et al 1991;Burk et al 1993;Cioffi et al 1993;Weinreb et al 1993;Mikelberg et al 1993;Hoskins et al 1994;Varma et al 1994;Tezel et al 1996) can be used to record the appearance of the optic nerve head. Computerized disc analysis and laser scanning devices seem attractive but are expensive and their clinical utility has not been established yet in longitudinal studies.…”

mentioning

confidence: 99%

Detection of changes of the optic disc in glaucomatous eyes: Clinical examination and image analysis with the Topcon Imagenet system

Azuara‐Blanco

Katz

Spaeth

et al. 2000

Acta Ophthalmologica Scandinavica

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ABSTRACT.Purpose: This study was designed to evaluate the clinical agreement in the detection of optic disc changes and the ability of computerized image analysis to detect glaucomatous deterioration of the optic disc. Methods: Pairs of stereophotographs of 35 glaucomatous optic discs taken 5 years apart and of 5 glaucomatous discs photographed twice on the same day. Two glaucoma specialists examined the pairs of stereophotographs (35 cases and 5 controls) in a masked manner and judged whether the optic disc showed changes in the optic disc compatible with progression of glaucomatous damage. The stereophotographs of the five optic discs photographed twice on the same day (which by definition did not change) and of five cases judged to have deteriorated by both glaucoma specialists were analyzed by computerized image analysis with the Topcon ImageNet system. Intra-and inter-observer agreement in the detection of optic disc changes (evaluated using kappa statistic), and changes in the rim area to disc area ratio (evaluated using descriptive statistics and paired t-test). Results: Intra-observer agreement had a kappa value of 0.75 for observer 1 and 0.60 for the observer 2. Inter-observer agreement between the glaucoma specialists had a kappa value of 0.60. The image analyzer did not discriminate between controls and cases with clinically apparent glaucomatous change of the optic disc. Conclusion: Clinical agreement in detecting changes in the optic disc was moderate to substantial. Computerized image analysis with the Topcon ImageNet system appeared not to be useful in detecting glaucomatous changes of the optic disc.

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Comparative Optic Disc Analysis in Normal Pressure Glaucoma, Primary Open-angle Glaucoma, and Ocular Hypertension

Cited by 99 publications

References 30 publications

Oxidative stress in glaucomatous neurodegeneration: Mechanisms and consequences

Oxidative stress in glaucomatous neurodegeneration: Mechanisms and consequences

Ischemic model of optic nerve injury

Detection of changes of the optic disc in glaucomatous eyes: Clinical examination and image analysis with the Topcon Imagenet system

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