It is widely mentioned that the end-stage glaucomatous disc (ESGD) is 100 % cupped. Textbooks describe the histology of the ESGD resembling a bean-pot, which appears much larger than the size of original disc. There is no evidence of either nerve fibers or of the Lamina Cribrosa (LC) in this empty bean-pot or ESGD. Where did the nerve fibers and LC go?
If cupping is due to atrophy of the nerve fibers then why is the cupping not occurring in non-glaucomatous optic atrophies? Why don’t we see atrophied or shrunken nerve fibers in ESGD as we see in the histology of optic atrophies due to other conditions such as multiple sclerosis? It is hard to believe that the nerve fibers in glaucoma would become so atrophied and shrunk that they become totally non-existent in contrast to nerve fibers in non-glaucomatous optic atrophies.
Second puzzling question: Where did the LC disappear in ESGD? There is no evidence of LC at the entrance of the bean-pot. Has the LC become so cupped that it has assumed the shape of huge belly of the bean-pot? In other words, the LC is so stretchable and distensible that it is cupped into the shape of huge bean-pot from its original size – an unlikely scenario. Then, why do we call ESGD a 100% cupped disc? I am very confused about the whole concept of cupping occurring in glaucoma dating back 150 years. I would appreciate if some one could explain: what structure of the disc has really cupped in ESGD? Thank you in advance.
Part 1: the axonal loss due to pressure effect , which occurs gradually leads to wallerian degeneration. If there are no inflammatory effects , there is usually no gliosis. Thus in glaucoma , which has progressive pressure effect on ganglion cells with no inflammation, leads to loss of axons with no replacement.
Non glaucomatous optic atrophies are usually acute and are associated with inflammation. This leads to gliosis, where in the lost axons are replaced by glial cells. thus they do not cause cupping , rather they cause white gliosis.
My real question was: why is the histology of the end-stage glaucomatous disc totally devoid of nerve fiber whereas the histology of non-glaucomatous optic atrophies reveal atrophied nerve fibers , shrunken and disorganized?
Where did the nerve fibers and lamina disappear in the end-stage glaucomatous disc?
What happened to the posteriorly bowed lamina which we documented in the early stages of glaucoma?
If the end-stage is really 100 % cupped disc then what structure of the disc has become hugely cupped if lamina and nerve fibers are no longer present in the end-stage glaucoma disc?
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