You are correct to some extent but the topic is controversial. You need to throw out everything about refraction, axial length etc and focus instead on the staphyloma. You are right when you say that degeneration can occur in a "stable" eye but usually the staphyloma is STILL progressing and this may or may not impact axial length. It either expands, deepens or changes type and this can happen very slowly. It is very well known that the degree of degeneration is correlated strongly to the depth (grade) and type of staphyloma. You need to remember that axial length doesn't necessary include the staphyloma as it depends on how the measurement is taken. Stabilisation of the staphyloma will almost definitely stop atrophy from progressing. With the cross-linking, I wouldn't bet against it reducing axial length anyway as when it has been used in keratoconus, a large number of patients display regression of the condition. I think the effect may be even more dramatic in myopia.
In sum, the degree of degeneration is almost always correlated directly to staphyloma depth and type. Progressing staphy = progressing atrophy. Of course in later years there may be changes related more to ageing of the myopic eye.....but that is a different story. Of course, this may all come to late for you and I, but if you look at all the data, most people with pathological myopia continue to experience eye and staphy growth their entire lives so there is still reason to be positive. See my other recent post on 7-MX.
I guess one thing I don't understand is that degenerative changes can occur in an already-elongated eyeball independent of any further axial lengthening. So, if I'm already a high myope, and my prescription isnt' changing anymore, how would this treatment prevent degenerative changes in my eye induced by my ALREADY lengthened eyeball? In other words, this treatment may prevent FURTHER lengthening, but unless this treatment can reduce the length of the eyeball, you're still vulnerable to degen. changes due to your already-lengthened eyeball.
Unfortunately, you almost definitely have a staphyloma with that axial length and the appearance of atrophy that you mention. Please read more and educate yourself on this; it is important. There is plenty of data on this. Of course, I am very far from being a retina MD, but I guarantee I am better read than most retina MDs on this subject.
They are not easy to diagnose, despite what some might say. For many, they are low grade (grade 1 or 2) at a younger age and they can be very difficult to see at this stage and the only sign is a genralised "pallor and tessalation", which basically looks like a yellowing of the fundus areas (this is common to most myopic eyes, with or without a staphy). As we age, they tend to deepen and can become very obvious with sharp and steep margins. This is when they become obvious.
My doc says I do not have a stahpyloma either but that is total rubbish in my opinon. Rarely is chorioretinal atrophy like mine seen in the absence of a staphyloma; that is the cold hard truth of the available data I am afraid and I have only just come to terms with it myself. I do not believe I am one of the lucky ones who does not have a staphyloma. Also, it is important to stress that staphyloma development can occur in the absence of refractive changes. My refraction has been stable for 5 years or more, yet in the last two years degenerative changes have advanced significantly. It is not all doom and gloom. Many with staphys maintain good to decent vision all their lives. Keep your fingers crossed!
Having exchanged a number of e-mails with Dr Wollensak, he believes his treatment will work very well and thinks it will be available within 10 years in the USA but probably much sooner in Europe. He is testing it right now in myopia chicks and in human eyes that are to be removed for other reasons to rule out toxicitiy.
I'm just glad that SOMEONE in the world is investing in this type of research - even if it's not being done in the USA. The important thing is that the treatments be developed and available to those who want it!
Thanks dukey and kg, I enjoy reading and learning from your posts (and gaining reassurance as well).
Okay, just read your other post describing difficulty in diagnosing posterior staphylomas. What makes you believe that they are difficult to detect in early stages?
Found the studies on Pubmed. Do you have a posterior staphyloma? My retinal specialist says I do not have a staphyloma, yet I have atrophic damage. What gives? My axial length is nearly 30mm. The atrophy extends from the optic nerve to just short of fundus.
Well the degree of atrophy is almost always directly related to axial length so you stop one, you reduce the other. With the scleral buckle surgery, which basically aimed to do the same thing physically, once the lengthening had been halted, quite often the atrophic areas would begin to repair. This group have published five or six papers on this in the last year or two and god only knows why it is not getting more attention here (though one could easily speculate!).
I think it is very strong, not least because the technique is already approved, and widely used, for another ectatic disorder. In that disease, it halts progression in ALL patients. Following some more reading, it has been known for over 10 years that collagen was a problem in myopia...and it was discovered right here in the USA! Unbelievable.
Does this type of treatment aim to stop elongation of the eyeball, or actually prevent retinal atrophy in the elongated eyeball? or both?