You have raised a very good question regarding ocular hypertension (OHT) and pre-perimetric glaucoma. Before I answer your question I would like to summarize my hypothesis. I believe the disc starts sinking due to atrophy of the border tissue of Elschnig (BT) in both HTG and NTG. BT is supplied exclusively by ciliary circulation. Ciliary circulatory pressure and IOP are opposing forces. Normally the ciliary circulatory pressure should be higher than the IOP (10 -21) for the proper perfusion and healthy maintenance of BT.

However if this scenario is reversed: either the IOP becomes higher (due to an ocular disease) or the ciliary pressure becomes lower than IOP due to poor systemic problems like chronic hypotension then even that particular normal range IOP would take upper hand. In both scenarios the IOP would compress the ciliary circulation of the BT, resulting in chronic ischemia and its atrophy. In other words HTG is an ocular disease whereas NTG is a systemic disease but still the IOP is the cause of glaucoma in HTG and NTG.

If IOP is the main risk factor in both HTG and NTG then how can we call OHT a benign condition having high IOP ? If even a single case of OHT converts into glaucoma then we have moral and medico-legal obligation to treat every case of OHT as we could never predict which one would convert into glaucoma and which one not. Can we imagine internists skipping treatment to any of their hypertension and hypercholesterolemia patients thinking that skipped ones wouldn’t get stroke or cardiac problems? If not, then why should we skip treatment to any of OHT? Do we have a condition known as benign hypertension or benign hypercholesterolemia? If not, then why should we have the term ocular

hypertension. I think the term OHT is irrelevant which is unnecessarily causing confusion in glaucoma which is already a conundrum. I think we should call all cases of OHT as pre-perimetric glaucoma or glaucoma suspect as we know about 40% of the nerve fibers have to be lost before the fields defects occur.

If we start evaluating the disc for glaucoma in terms of sinking disc/severance of nerve fibers and its vasculature, we would be entering into new wealth of information which we had never seen before. All we need is to change the way we look at the glaucomatous disc (gestalt switch). Please try it and you would appreciate its value and thus you may support my hypothesis. Many thanks.

There is no connection between ciliary circulation and RGC’s. In fact the RGC’s are nourished by the central retinal artery and not by ciliary circulation. It is true that RGC’s are dying in glaucoma but not primarily due to apoptosis caused by raised raised IOP. Apoptosis can’t explain early peripheral field loss and selective destruction of the arcuate fibers and an orderly destruction of the nerve fibers, the peripheral first and central vision at the end.

I hypothesize that optic disc is sinking and as result the nerve fibers along with its vasculature are being stretched and broken (severed). RGC’s are dying as a result of retrograde degeneration of proximal end whereas distally the neurons of the LGN due to wallerian degeneration as a result of severance of the nerve fibers.

In nutshell the nerve fibers along with its vasculature are being severed, not atrophied in glaucoma. Analogy: the leg is atrophied, not amputated. Glaucoma may not be an optic disc neuropathy but an optic disc axotomy. I would welcome any feedback.

It is widely mentioned that there is apoptosis or suicide of the RGCs in glaucoma triggered by raised IOP. In glaucoma the nerve fibers or their RGCs are always being destroyed in a specific orderly fashion, starting with the peripheral fibers and ending with the central fibers. It never happens other way around or haphazardly. My answer to programmed suicide of RGCs: I don't believe our RGCs are smart enough to commit suicide in an orderly tandem fashion, always starting with those RGCs serving the peripheral vision and not commit suicide randomly. On this puzzling issue I can't convince myself that glaucoma can be a neurodegenerative disease, so why to worry about connection between RGCs and ciliary system.