I have seen the patient with secondary postraumatic glaucoma in one eye -46 y.o., whose cupping was really reversed partially from 0.9 to 0.7 due to sudden medically controlled IOP inclusing neuroprotective agents topical brimonidine and oral nycergolin

Marianne, Greetings. I have two answers to your reply: First, in my opinion the exact measurements of cup size is very subjective and varies with each ophthalmologist. Was there any improvement of vision? If yes, then it would be a new discovery that vision lost in glaucoma can be regained.

Second, I am not convinced that cupping is occurring at all in glaucomatous discs according to the arrangement of nerve fibers in the retina/optic disc and the way the visual field defects are produced in glaucoma. The nerve fibers originating from the most peripheral retina lie deepest (closest to sclera) and exit closest to the scleral edge (rim) whereas the nerve fibers originating closest to the optic disc lie most superficial (closest to vitreous) and exit from the central most part of the disc. Cupping is defined as concentric enlargement of the physiological cups. Ironically, the physiological cups are remnants of the Bergmeister’s papilla –a tuft of hyaloid vessels in fetal life ( Wolf’s anatomy). I am puzzled: why should a fibrous plate enlarge concentrically in response to raised IOP, and why have we given so much importance to these remnant cups which are not even a part of neuronal tissue of the disc? I would leave this issue aside for time being but it is food for thought.

Returning to our real question: Since cupping implies that the pathology starts from the central most part of the disc and extends peripherally therefore if cupping was indeed occurring then the central fibers should be destroyed first resulting in loss of central vision (blindness) in the early stages and the peripheral vision at the end-stages of glaucoma. But in actuality the reverse is occurring, starting with the loss of peripheral vision and ending with the central vision in an orderly fashion. This fact alone contradicts the cupping theory.

If cupping may not be occurring then why should we use the term of reversal of cupping especially when it is not accompanied by regaining of any vision. I hypothesize that the physiological cups are not truly enlarging but disintegrating due to excavation (empty spaces) created from severance of the nerve fibers.

If my colleagues are still convinced that cupping is indeed occurring then I salute those who gave us the term cupping 150 years ago, keeping in view the time period when the ophthalmology was in infancy and ophthalmoscopes were rudimentary.

Dear prof. Hasnain,

Following your question my patient initially had VA 20/25 a little excentric and constricted visual field from nasal half , but latter on VA 20/25 and VF showed just a nasal step. I think that VA and VF findings correspon with cupping changes

My hypothesis of glaucoma is very simple and straight forward. Optic disc/lamina is detaching and sinking in the scleral canal – a mechanical failure. As a result the most peripheral fiber, since lying closest to the scleral edge would be stretched and broken (severed). Then the next in line nerve fiber would move towards the scleral edge and also get severed. This process would continue until the central most fiber has been severed. Thus there is continuous movement of nerve fibers from the central part to the periphery and this may explain the pseudo- enlargement of the cup. In fact the nerve fibers are being severed from the periphery to the central part and this is revealed by the glaucomatous field defects. I would rather call it an excavation (empty spaces) occurring as a result of severance of nerve fibers, rather than cupping.

Why is the Lamina detaching and sinking posteriorly? I am sure researchers would find out the answers. In glaucoma either the disc is cupping (center to periphery) or sinking (from periphery to center) but can’t have both ways.

Bottom line of my hypothesis: the nerve fibers along with its vasculature are being severed. Glaucoma may not be an optic disc neuropathy but an optic disc axotomy. If the nerve fibers are not being severed then of course my hypothesis would be wrong.

For more details of my views about glaucoma you may like to visit my facebook.

https://www.facebook.com/pages/Glaucoma-Paradigm-Shift-Project/516804278413418

Hi Syed. I agree with you regarding the subjectivity of estimating C/D ratio as well as cup sizes. However newer technologies can easily be used to partially eliminate this - OCT, HRT, RNFL analysis and so on. I would be interesting to see a study done using this technology. I also agree with your view regarding the loss of central vision if the central fibres are destroyed first. Maybe the axonal flow is just restored giving the appearance of a smaller cup when the pressure is reduced or if we follow your thinking, possibly the disc stops sinking giving the appearance of smaller cups?

Dirk, I am convinced that nerve fibers along with its vasculature are being severed in glaucoma. As a result excavation (empty spaces) are occurring in the glaucomatous disc. If someone would like to call this phenomenon of excavation as a cupping then it is their prerogative. Excavation, splinter hemorrhages, progressive thinning of the RNFL and finally the histology of the end-stage glaucomatous disc (ESGD) -an empty crater devoid of lamina cribrosa and nerve fibers all point in the direction that the nerve fibers are being severed, not atrophied in glaucoma.

I think this is the only missing card in the entire glaucoma mystery.

All we need is to look again the histology of the ESGD and then decide for ourselves: is the ESGD really 100% cupped lamina cribrosa/ physiological cups. My colleagues would agree that nothing has cupped in ESGD but it is a crater left over after the severance of the nerve fibers and vasculature. Physiological cups or lamina have either disintegrated or lying at the bottom of the crater. Time would tell whether I am right or wrong. I certainly thank you very much for your interest in my hypothesis.