The term cupping implies that the physiological cups start enlarging concentrically due to raised IOP so turning them into pathological cups in glaucoma. Term cupping was originally given by Heinrich Muller in 1856 and given further credence by introducing the term cup- to - disc ratio for diagnostic purposes about 100 years later. However, the concept of cupping is unable to answer many puzzling questions raised in this discussion.
According to Wolf’s anatomy, the different size physiological cups are produced by the varying degree of atrophy of the Bergmeister papilla (BP), a tuft of hyaloid vessels supplying nutrition to the lens in fetal life. The remnant base of the BP is identified as central connective tissue meniscus lying superficially on the surface of the superficial nerve fibers layer, quite apart from Lamina Cribrosa (LC). If true: why should a fibrous plate get enlarged concentrically in response to raised IOP?
It is mentioned extensively that nerve fibers are present in the rim area whereas the central cupped area of the disc is empty. But the histology in none of the discs, normal or diseased, supports this doughnut arrangement of nerve fibers. It true, then it should also imply: someone born with 0.7 cup would become 100% cupped (totally blind) sooner compared to someone born with 0.2. If physiological cups are enlarging in glaucoma then what would enlarge in those born with no physiological cup?
It is also mentioned that there is posterior bowing of LC in response to raised IOP. Ironically, why would raised IOP cause posterior bowing of multi-layered rigid LC and not push it outward? What is the part of the disc really cupping? If the LC is also being cupped then we should expect a central missing area in LC, destroyed due to cupping.
My most puzzling question: the nerve fibers originating closest to the disc lie most superficial (closest to vitreous) and exit from the most central part of the disc. Therefore, these central fibers should be destroyed first resulting in concentric enlargement of the blind spot and not the initial loss of peripheral fibers if cupping was indeed occurring in glaucoma. I believe the term cupping was mistakenly given 150 years ago. I would welcome any feedback. Thank you.
Interesting and provocative thoughts.
However, I favor my (and others') observations with ophthalmology, imaging studies with ocular coherence tomography, histopathology, animal models, and other investigations that show cupping does exist and progress with glaucoma.
Dear John and Ahmad,
I am really very thankful for your reply to my question. The question of cupping has been bothering me ever since I started my residency in Ophthalmology in 1963. The term cupping was given in 1856 by pathologist Heinrich Muller and since then the term cupping has become synonymous with glaucoma. In fact the term cupping was given further credence in 1970s by introducing the term cup to disc ratio which instead of helping has created more confusion in glaucoma diagnosis, at least in my experience. After studying the subject of cupping, I have learned that cupping may not be occurring in glaucoma and the term cupping was mistakenly given in 150 years ago.
As I understand, the term cupping implies that the pathology starts from the central most part of the disc and extends peripherally. Let us now evaluate this phenomenon in the context of the arrangement of the nerve fibers in the retina and disc. The nerve fibers originating closest to the optic disc lie most superficial (closest to vitreous) and exit from the central most part disc whereas the nerve fibers originating from most peripheral retina lie deepest (closest to sclera) and exit closest to the edge of the scleral opening. Therefore if cupping was indeed occurring then these central most fibers should had been destroyed first resulting in concentric enlargement of the blind spot. But in actuality the peripheral nerve fibers are being destroyed first and the central fibers at the last in contradiction to cupping. If the cupping was occurring then glaucoma patients would have become totally blind much sooner due to destruction of central fibers in the early stages of glaucoma.
I have been unable to find even a single histology in which doughnut shaped arrangement ( cupping) of the nerve fibers exists. Let us look at the histology of end-stage glaucomatous disc again and decide for yourself: is the ESGD really a 100% atrophied cupped disc or a disc area left over after the total disappearance of nerve fibers – which according to my hypothesis is due to severance, not due to atrophy of the nerve fibers. Looking forward for feedback . Again many thanks for the interest in my question.
As regards Lamina Cribrosa changes, I think the underneath article would address your queries, somewhat.
Wang, B., Lucy, K.A., Schuman, J.S. et al. Tortuous Pore Path Through the Glaucomatous Lamina Cribrosa. Sci Rep 8, 7281 (2018). https://doi.org/10.1038/s41598-018-25645-9
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