You have to remember we are working with criteria that were defined many decades ago and no one dares to change even if there are out dated.

CDR does not represent a risk factor it is a result of Nerve fiber loss.

CDR is a measurement of a void.

We know that a CDR 0.2 of a small disc is more significant than CDR 0.7 of a big disc.

CDR without optic disc measurement is meaningless.

CDR is a relic we are measuring a void. We should measure how much nerve fiber area we have, it is a much better criteria to monitor the Development of Glaucoma. Look at HRT and OCT and you see this is a very good criteria to diagnose and progress of glaucoma.

Whether CDR nor rim area are risk factors they represent changes due to damage to nerve fiber on the time scale

Dr. wegner, thank you for your intelligent response. I totally agree what you have said. The reason I posted this question was to create a curiosity: why should the vertical CDR be a risk factor and not the horizontal CDR. In fact I don’t agree at all with the concept of cupping mistakenly given in 1850s.

Most of the recent articles published in peer reviewed elite journals are mentioning that Vertical CDR is a risk factor for glaucoma without giving any explanation for it. My feeling is that since we are still working under 160 years old paradigm of cupping/atrophy of the nerve in glaucoma we can’t afford to abandon the sacred word of “cupping’.

However, if we review the embryology of the eye in Wolf’s anatomy we would learn that physiological cups of various sizes are produced by varying degree of atrophy of Bergmeister’s papilla. Some optic discs have none of this remnant tissue meaning ‘no cup’ and some have this remnant tissue as large as covering 90 % of the disc resulting in 0.9 cup. Base of the cup is identified as central connective tissue meniscus (CCTM) lying superficially on the surface of the nerve fibers and not even a part of it. If CCTM is made of fibrous tissue then why should it enlarge in response to raised IOP and why have we implicated it in glaucoma for so long?

Another big fallacy: the nerve fibers are concentrated in the rim area only whereas the central cupped area is empty and devoid of nerve fibers. Unfortunately there is not a single histology of any disc (normal or glaucomatous) supporting this doughnut shape arrangement of nerve fibers. I have no idea why are the researchers mentioning about cup/disc ratio and doughnut shaped arrangement of nerve fibers.

Your answer is interesting: “You have to remember we are working with criteria that were defined many decades ago and no one dares to change even if there are out dated”

I fully agree with your statement. However, I think if we don’t agree with something we have professional obligation to stand up and ask for the answers otherwise we would never find the truth and science would never progress.

C/D ratio definitely is a function of disc size. However, C/D ratio still has its implications. It was found that physiologic disc in normal population usually is rounded or horizontally oval, so the occurrence of vertical C/D ratio carries a statistical significance. Because loss of peripapillary RNFL loss occur preferentially at the superior & inferior poles of the disc , the cup enlarges vertically more than horizontally. Therefore Vertical C/D ratio has a clinical significance. Again I totally agree that Rim area is more important in evaluation as it represent more or less constant parameter. While Cupping whether horizontal or vertical belongs to disc size which is highly variable among normal with overlap between normal & abnormal

Dear Dr. Elbendary, thank you for your response. What I gather from your response is that normally the cups are round or horizontally oval but have become vertically oval due to preferential loss of nerve fibers at the superior and inferior poles of disc. This is what I also believe but then we shouldn’t call the VCDR a risk factor but we should call them early glaucoma cases. However I am certain there would be genuine cases which are born with larger VCDR so then how would we differentiate between the inherently large VCDR and those acquired due to glaucoma? I believe the whole subject of ‘cupping’ is conundrum which unfortunately is created by ourselves.

I have already conveyed my views about the concept of cupping in foregoing discussion. You also appear to be proponent of cupping theory in glaucoma. I would request the proponents of ‘cupping’ theory to review the embryology and histology of the normal disc in Wolf’s anatomy so they may find out that so called ‘physiological cups’ of varying sizes and shapes are nothing more than the remnants of the Bergmeister’s papilla. They have nothing to do with glaucoma. Moreover, there’s not a single histology showing cupping or doughnut shape arrangement of nerve fibers in the optic disc/LC. Many optic discs have no such cupping, then should we expect no glaucoma in such discs since there is no cup to enlarge ?

If after reviewing the embryology/histology of the disc, the proponents of the cupping theory still believe that different shapes or sizes of physiological cups which are in fact fibrous tissue remnants of Bergmeister’s papilla do have role in glaucoma then it is their decision but I am afraid I am unable to buy it.

I may be an odd ophthalmologist who is firmly convinced that theory of cupping given in 1850s was a very unfortunate mistake which has derailed glaucoma for so long.

Another remark, It is always discussed with great amazement that typical visual field defects begin at upper visual field.

Just a quick look at the number/map receptors and ganglion cells gives the answer.

The place with the lowest number will be first to present with a defect.

Evolutionary we had to look at our level and down, in order to look for enemies therefore is the lower visual field the one with more reserves. We did not have to worry from air attacks so we have viewer reserves. A disease that has no preference to specific area like glaucoma the first visual defect will be in upper visual field.

No one wants to hear it.

I never believed in cupping. Our professors taught us that cupping represents glial atrophy while reduction of NRA represents axonal loss. According to the theory of preferential axonal loss at the poles, cupping is secondary to NRA loss. My attitude is to evaluate the NRA for generalized or localized changes, Whether It follows or deviate from ISNT rule. However, many ophthalmologist rely on (not necessarly believe) cupping because it it is easier to interpret C/D changes rather than to express NRA changes

Dear Drs. Wegner and Elbendary, I agree with you that no one listens to anyone. I think since glaucoma is a misunderstood disease and there is no consensus therefore everyone is managing glaucoma in his/her own way, which is very unfortunate. I think if something is so basically wrong then it is moral and professional obligation of everyone to liberate glaucoma from ‘cupping’. Concept of cupping given 160 years ago is creating havoc in glaucoma. Cup/disc ratio’s used in glaucoma diagnosis are grossly misleading and unfair to our patients.

Every day I see the subjects born with larger cups and normal IOP being treated as NTGs including children, whereas those with small cup and high IOP being ignored treatment as OHTs. We have to stand up and ask those who are controlling the dissemination of glaucoma knowledge to either prove us the phenomenon of ‘cupping’ or discard it altogether. We would be doing disservice to our profession if we don’t decide on this critical issue: YES or NO. We have heard enough of ‘cupping’ but now it is time to please show us the histological proof of physiological and pathological cupping.

The so called ‘cups’ are nothing more than vestigial fibrous tissue of Bergmeister’s papilla. Moreover, there is no such thing as cupped area being an empty hole. There is no histology to support this doughnut shaped misconception. The reason we don’t see the nerve fibers underneath is because they are covered by this remnant fibrous plate and not because of being empty hole, devoid of nerve fibers.

I propose the that the cups are not enlarging but breaking up due to creation of excavation (empty space) resulting from the severance of nerve fibers. The nerve fibers at the poles (arcuate fibers) have no special affinity for preferential loss. All the of nerve fibers are equally prone to damage since they are always being destroyed in an orderly fashion from peripheral to paracentral and ending with central fibers and never randomly.

I hypothesize that all the 360 degrees of nerve fibers are being severed simultaneously. However, the arcuate fibers being fewer in number compared to the rest would be depleted earlier giving rise to arcuate field defects. It is just the number game and not due to any different pore size of LC or undue sensitivity.

I ignore the cups and examines the glaucomatous discs in context of sinking disc/severance of nerve fibers and its vasculature. The amount of excavation, pallor, sloping, kinking of blood vessels provides enormous amount of information about the every stage of glaucoma. Notching is first sign of excavation in glaucoma. I find this simple method very exciting and correct and we may not need anything else.

My only regret: I wish I had known this in the beginning of my career 50 years ago. The essence is that the nerve fibers are being severed (not atrophied) in glaucoma. Histological proof of severance of nerve fibers lies in the histology of the end-stage glaucomatous disc- totally devoid of nerve fibers and no evidence of posteriorly bowed or cupped LC.

How interesting! I am obsessed with aetiology (all medicine) so have been following this thread with interest. Does this imply herniation of some sort causing the severance? Regards, Ayan

The most pathognomonic feature of glaucoma of glaucoma is: orderly loss of NFs from peripheral to central, never never haphazardly. If this was not true we would not be doing visual fields in glaucoma. Unfortunately no one talks about it in postulating their glaucoma theories. None of the prevalent theories are valid since there is no biological scenario which could cause the orderly loss of NFs in glaucoma including the direct role of elevated IOP on the NFs of the ONH. Yet, elevated IOP is the established cause of glaucoma without any doubt.

So, then how to solve this mystery? I propose that glaucoma is a two -stage disease. I have posted my this article on researchgate. Many thanks.