Dear Dr Husnain it seems true, therefore the term "optic disc sinking" is more appropriate than the presently used term "optic disc cupping".

Dr. Husnain, What is your take on it. I don't think your perspective will be that simple. Please add to my insight.

Dear Prof. Imtiaz and Muneeb.

In my humble opinion, Lamina Cribrosa (LC) just couldn’t be the primary site of injury in chronic glaucoma based on the orderly loss of NFs. There are several arguments against it, but I chose only the “orderly loss of NFs” thinking it should be more than enough.

It is an established fact that NFs in glaucoma are being destroyed in a predictable and an orderly tandem sequence from peripheral to central, never randomly, which is the reason we are doing visual field test.

It is inconceivable that the injury in the pores of the LC fastening the NFs in small bundles, so variable, intricate and disorderly placed would result in the orderly loss of NFs in glaucoma? It does not make any sense.

If the NFs are being destroyed in an orderly sequence then we should expect the mechanism for their destruction to be an orderly one as well.

Prerequisite for the orderly loss would be: the NFs should be loose so they can be easily separated individually and then destroyed in an orderly tandem fashion. It is only possible when the NFs are either in the retina or in the prelaminar area. But once the NFs have entered into the intricate meshwork of LC, the orderly loss of NFs can never be possible.

Other arguments against LC: 1. If cupping was taking place then the central most NFs should have been destroyed first but opposite is occurring since the peripheral NFs are being destroyed first and central at the end-stage.

Superior and inferior arcuate scotomas have very sharply defined margin as though they have been excised with a pair of scissors. If the production of arcuate scotoma was due to injury in the pores of LC, then, the margins of the arcuate scotoma would had been very irregular and serrated due to erratic placement of pores. I believe the LC being the site of injury as been theorized to satisfy the cupping paradigm given mistakenly 160 years ago.

Hi all,

Believing one mode or location of damage to nerve fibres in glaucoma is simplistic as previously noted. Multiple modalities have been proposed ranging from pressure induced, vascular based neuropathy and even accelerated aging of brain tissue.

Just because it is easy to visualise the damage at the Optic Nerve Head (ONH) doesn’t mean this is the site or cause of vision loss.. The area of neural fibre/rim at the ONH is more indicative of function than the actual cupping. There is a significant variation in the population but changes in ONH are more sinister.

OCT analysis shows loss in retinal fibres first before cupping and vice versa. Visual field losses may be recorded before a change at the ONH. Think of an optic neuritis field loss. There is low / normal tension glaucoma as well as high pressures glaucoma. Where is the compression in the former?

Limiting assessments to the ONH is a bit like saying wearing a raincoat will make it rain. But it is easy to access and assess and so has dominated our thinking for a long time.

Compression of nerve fibres at the ONH and vision loss is seen in patients with “Drusen of the ONH.” But even in these patients the amount of “Drusen” must be quite extensive before any field loss is noted. This suggests the the optic nerve may be more tolerant of compression than we believe, or perhaps our field assessment techniques are not as refined as we wou like to think.

Reducing pressures is the primary option for treatment but new research even points to the benefit of Vit B limiting visual losses. So....?

My opinion is clearly no. The elasticity modulus is higher than one of the ON. That's why the increase in IOP produces cupping of the ON.

Dear Julius& Ariciniegas

There is plethora of glaucoma theories ranging from time- honored 160 years old cupping theory and recently very popular neurodegeneration of RGCs. I am sorry to say that none of the prevalent glaucoma theory is able to explain the orderly loss of NFs, starting with the peripheral NFs and ending with the most central NFs, never randomly. The orderly and predictable loss of NFs is the hallmark of glaucoma and the reason for doing visual field test in glaucoma. If your theory or any other theory can explain the orderly loss of NFs in glaucoma, I will surely accept your views with thanks as it would have, then, solved the mystery of glaucoma.

Hi. Syed Hasnain,

Absolutely correct. There are as many theories as there are practitioners. There are generalities and common belief. But glaucoma is a multifaceted beast about which we think we know a lot but probably very little. So no simple answer to the question asked.

Hi Julius

I don’t think we should blame glaucoma but only ourselves. Everyone has his own reason for our failure in glaucoma. I attribute the failure entirely to our working under the wrong cupping paradigm which was given mistakenly 160 years ago. No questions were asked about its validity. Whatever glaucoma research we do, we have to fit its findings into cupping paradigm- a sacred conception.

There is no clear definition of cupping. Cup/disc ratio, bowing posteriorly of lamina cribrosa (cupping) have been theorized to fit into a cupping paradigm for which there is no histological proof. Although there is clear evidence of posterior migration of LC in the early stages of glaucoma but we are still calling the laminar displacement or laminar depth as cupping! How can a loosened and detached LC also become bowed posteriorly while migrating if posterior bowing of LC is the original definition of cupping?

Neuroretinal rim and doughnut shaped configuration of the optic disc have been created to justify cupping paradigm. Physiological cups are not doughnut shaped. Remnant of the Bergmeister,s papilla determines the size of so called cup. I have yet to find a single histology of any disc depicting doughnut shaped arrangement of NFs. All optic discs are packed with NFs from margin to the center. NFs are present underneath the fibrous tissue remnant as well. It is time to abandon the cupping paradigm along with all its associates like cup/disc ratio and so called neuroretinal rim.

We have failed to follow the most important lead of glaucoma “ orderly loss of NFs” which is the basis of our perimetry in glaucoma. It is said “ follow the money” but I would say follow the “orderly loss of NFs” and we would soon find the cause of glaucoma.

The reason why the peripheral NFs are lost first ,is because they are compressed against the sclera ring, by the IOP.

Dear Mr. Arciniegas, Thanks for your input.

Can you please explain: after the initial compression of peripheral NFs against the scleral ring by the IOP, then, how is the IOP compressing the rest of the NFs in an orderly sequence from peripheral to central until the end-stage?

The peripheral NFs, under compression, against the sclera ring, by the increase in IOP, disappear and they are replaced by the the NFs that are located immediately behind them; this process takes place again and again. At the same time, the central NFs , in the ON head, move horizontaly outwards producing the excavation of the ON. That's why the treatment of the ON excavation must be surgical.

I believe you meant that NFs are being compressed by the elevated IOP acting directly on the NFs again and again in an orderly sequence? But it is not possible that a million or so densely packed NFs in the optic disc could be destroyed in an orderly and predictable way by the direct effect of elevated IOP on the NFs and never would be destroyed randomly. And, how the central and other NFs would move at all if they are fastened in bundles in the fixed pores of lamina cribrosa !

Then, why are the NFs being destroyed in an orderly sequence?

This is the whole mystery of glaucoma that the direct action of elevated IOP couldn’t destroy the NFs in an orderly sequence.

We don’t have to answer only the orderly loss on NFs (although the most important) but also normal-tension glaucoma, higher incidence of glaucoma in myopia, sleep apnea, Raynaud’s disease and other conditions under the same yardstick. Thanks

There is not any "orderly sequence" . What happen is that the bigger the cupping of the ON, the bigger the force produced on the NFs, inside the cupping.

If you still believe in 160 years old concept of cupping and doughnut shaped configuration of optic disc for which there is no histological proof, then it is your prerogative and I have nothing more to say. Thanks

It is a logical an experimental way to focuse the problem