A hypothesis to explain ganglion cell death caused by vascular insults at the optic nerve head: possible implication for the treatment of glaucoma.

A hypothesis to explain ganglion cell death caused by vascular insults at the optic nerve head:... The pattern and progression of visual field loss in patients with glaucoma indicates that ganglion cells do not die at the same time. Both visual field loss and neuroretinal rim loss follow typical patterns, and there is experimental evidence of a preferential loss of ganglion cells in the peripheral retina. Sustained or intermittent vasogenic insults to groups of astrocytes in the optic nerve head region may explain these findings. Sufficient risk factors, including sustained elevation of the intraocular pressure (IOP), affect the quality of the blood supply in the optic nerve head. As a result, the nutritional supply to the optic nerve head is slowly compromised, particularly affecting astrocytes, microglia and ganglion cell axons. While the ganglion cell axon may be affected in the initial stages of the insult, the whole cell will eventually be affected with glutamate particularly being “non-physiologically” released into the extracellular space. Astrocytes and microglial cells also likely release a variety of “protective” and “damaging” factors. Increased glutamate is potentially toxic to many retinal cells. Muller cells eventually become inefficient, further increasing glutamate and GABA levels. The ganglion cells, being at a lower homeostatic status, are particularly susceptible. At a particular point, excessive glutamate will result in ganglion cell death. This death rate is variable, depending on the number of excitatory and inhibitory receptors associated with the neuron. This theory suggests that the initial insults to the ganglion cells occur in the optic nerve head. There are numerous vasoprotective/neuroprotective strategies that may be targeted for pharmacological intervention. These include prevention of toxic substance release from astrocytes/microglia, prevention of glutamate toxicity to retinal neurons, and administration of neurotrophic factors.—Hans E. Grossniklaus</P> http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Journal of Ophthalmology Elsevier

A hypothesis to explain ganglion cell death caused by vascular insults at the optic nerve head: possible implication for the treatment of glaucoma.

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Publisher
Elsevier
Copyright
Copyright © 2002 Elsevier Science Inc.
ISSN
0002-9394
DOI
10.1016/S0002-9394(01)01387-3
Publisher site
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Abstract

The pattern and progression of visual field loss in patients with glaucoma indicates that ganglion cells do not die at the same time. Both visual field loss and neuroretinal rim loss follow typical patterns, and there is experimental evidence of a preferential loss of ganglion cells in the peripheral retina. Sustained or intermittent vasogenic insults to groups of astrocytes in the optic nerve head region may explain these findings. Sufficient risk factors, including sustained elevation of the intraocular pressure (IOP), affect the quality of the blood supply in the optic nerve head. As a result, the nutritional supply to the optic nerve head is slowly compromised, particularly affecting astrocytes, microglia and ganglion cell axons. While the ganglion cell axon may be affected in the initial stages of the insult, the whole cell will eventually be affected with glutamate particularly being “non-physiologically” released into the extracellular space. Astrocytes and microglial cells also likely release a variety of “protective” and “damaging” factors. Increased glutamate is potentially toxic to many retinal cells. Muller cells eventually become inefficient, further increasing glutamate and GABA levels. The ganglion cells, being at a lower homeostatic status, are particularly susceptible. At a particular point, excessive glutamate will result in ganglion cell death. This death rate is variable, depending on the number of excitatory and inhibitory receptors associated with the neuron. This theory suggests that the initial insults to the ganglion cells occur in the optic nerve head. There are numerous vasoprotective/neuroprotective strategies that may be targeted for pharmacological intervention. These include prevention of toxic substance release from astrocytes/microglia, prevention of glutamate toxicity to retinal neurons, and administration of neurotrophic factors.—Hans E. Grossniklaus</P>

Journal

American Journal of OphthalmologyElsevier

Published: Feb 1, 2002

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